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Surgical complications remain a frustrating and difficult aspect of the operative treatment of patients. Regardless of how techni­cally gifted and capable surgeons are, all will have to deal with complications that occur after operative procedures. The cost of surgical complications in the United States runs into millions of dollars; in addition, such complications are associated with lost work productivity, disruption of family life, and stress to employ­ers and society in general. Frequently, the functional results of the operation are compromised by complications; in some cases the patient never recovers to the preoperative level of func­tion. The most significant and difficult part of complications is the suffering borne by a patient who enters the hospital antici­pating an uneventful operation but is left suffering and compro­mised by the complication.

Complications can occur for a variety of reasons. A surgeon can perform a technically sound operation in a patient who is severely compromised by the disease process and still have a complication. Similarly, a surgeon who is sloppy or careless or hurries through an operation can make technical errors that account for the operative complications. Finally, the patient can be healthy nutritionally, have an operation performed meticu­lously, and yet suffer a complication because of the nature of the disease. The possibility of postoperative complications remains part of every surgeon’s mental preparation for a difficult operation.

Surgeons can do much to avoid complications by careful preoperative screening. When the surgeon sees the surgical can­didate for the first time, a host of questions come to mind, such as the nutritional status of the patient and the health of the heart and lungs. The surgeon will make a decision regarding perform­ing the appropriate operation for the known disease. Similarly, the timing of the operation is often an important issue. Some

operations can be performed in a purely elective fashion, whereas others must be done in an urgent fashion. Occasionally, the surgeon will require that the patient lose weight before the operation to enhance the likelihood of a successful outcome. At times, a wise surgeon will request preoperative consultation from a cardiologist or pulmonary specialist to make certain that the patient will be able to tolerate the stress of a particular procedure.

Once the operation has begun, the surgeon can do much to influence the postoperative outcome. Surgeons must handle tissues gently, dissect meticulously, and honor tissue planes. Performing the technical portions of the operation carefully will lower the risk for a significant complication. At all costs, sur­geons must avoid the temptation to rush, cut corners, or accept marginal technical results. Similarly, the judicious use of anti­biotics and other preoperative medications can influence the outcome. For a seriously ill patient, adequate resuscitation may be necessary to optimize the patient before giving a general anesthetic.

Once the operation is completed, compulsive postoperative surveillance is mandatory. Thorough and careful rounding on patients on a regular basis postoperatively gives the operating surgeon an opportunity to be vigilant and seek postoperative complications at an early stage, when they can be most effec­tively addressed. During this process, the surgeon will carefully check all wounds, evaluate intake and output, check temperature profiles, ascertain what the patient’s activity levels have been, evaluate nutritional status, and check pain levels. Over years of experience, the clinician can begin to assess these parameters and detect deviations from the normal postoperative course. Expedi­tious response to a complication makes the difference between a brief, inconvenient complication and a devastating, disabling one. In summary, a wise surgeon will deal with complications quickly, thoroughly, and appropriately.

Surgical Wound complicationS


CausesA seroma is a collection of liquefied fat, serum, and lymphatic fluid under the incision. The fluid is usually clear, yellow, and somewhat viscous and is found in the subcutaneous layer of the skin. Seromas represent the most benign complication after an operative procedure and are particularly likely to occur when

surgical wound complicationscomplications of thermal regulationrespiratory complicationscardiac complicationsrenal and urinary tract complicationsendocrine gland dysfunctiongastrointestinal complicationshepatobiliary complicationsneurologic complicationsear, nose, and throat complications

SurgiCal CompliCationSMahmoud N. Kulaylat and Merril T. Dayton

Chapter 13

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13-2  section ii  PerioPerative ManageMent

or associated with drainage of dark red fluid out of the fresh wound.

Hematoma formation is prevented preoperatively by cor­recting any clotting abnormalities and discontinuing medi­cations that alter coagulation. Antiplatelet medications and anticoagulants may be given to patients undergoing procedures for a variety of reasons. Clopidogrel is given after implantation of a coronary stent, ASA is given for the treatment of coronary artery disease (CAD) and stroke, and VKA is given after implan­tation of a mechanical mitral valve for atrial fibrillation, venous thromboembolism, and hypercoagulable states. These medica­tions must be temporarily discontinued before surgery. There are no specific studies that have addressed the issue of timing of discontinuation of such medications.

One must balance the risk of significant bleeding caused by uncorrected medication­induced coagulopathy and the risk of thromboembolic events after discontinuation of therapy. The risk of bleeding varies with the type of surgery or procedure and adequacy of hemostasis; the risk of thromboembolism depends on the indication for antithrombotic therapy and pres­ence of comorbid conditions.1 In patients at high risk for thromboembolism (e.g., those with a mechanical mitral valve or older generation aortic valve prosthesis, venous thromboem­bolism within 3 months, severe thrombophilia, recent atrial fibrillation [within 6 months], stroke or transient ischemic attack who are scheduled to undergo an elective major surgical procedure involving a body cavity), the VKA must be discon­tinued 4 to 5 days before surgery to allow the international normalized ratio (INR) to be lower than 1.5. In patients whose INR is still elevated (>1.5), low­dose vitamin K (1 to 2 mg) is given orally. Patients are then given bridging anticoagulation—that is, a therapeutic dose of rapidly acting anticoagulant, intra­venous (IV) UFH or to LMWH. Those receiving IV UFH (half­life, 45 minutes) can have the medication discontinued 4 hours before surgery and those receiving therapeutic dose LMWH SC (variable half­life) 16 to 24 hours before surgery. VKA is then resumed 12 to 24 hours after surgery (takes 2 to 3 days for anticoagulant effect to begin after start of VKA) and when there is adequate hemostasis. In patients at high risk of bleeding (major surgery or high bleeding risk surgery) for whom postoperative therapeutic LMWH or UFH is planned, initiation of therapy is delayed for 48 to 72 hours, low­dose LMWH or UFH is administered, or the therapy is completely avoided. Patients at low risk for thromboembolism do not require heparin therapy after discontinuation of the VKA. Patients on ASA or clopidogrel must have the medication with­held 6 to 7 days before surgery; otherwise, the surgery must be delayed until the patient has completed the course of treat­ment. Antiplatelet therapy is resumed approximately 24 hours after surgery. In patients with a bare metal coronary stent who require surgery within 6 weeks of stent placement, ASA and clopidogrel are continued in the perioperative period. In patients who are receiving VKAs and require urgent surgery, immediate reversal of anticoagulant effect requires transfusion with fresh­frozen plasma or other prothrombin concentrate and low­dose IV or oral vitamin K. During surgery, adequate hemo­stasis must be achieved with ligature, electrocautery, fibrin glue, or topical bovine thrombin before closure. Closed suction drainage systems are placed in large potential spaces and removed postoperatively when the output is not bloody and scant.


large skin flaps are developed in the course of the operation, as is often seen with mastectomy, axillary dissection, groin dissec­tion, and large ventral hernias or when a prosthetic mesh (polytetrafluoroethylene) is used in the repair of a ventral hernia.

presentation and managementA seroma usually manifests as a localized and well­circumscribed swelling, pressure or discomfort, and occasional drainage of clear liquid from the immature surgical wound. Prevention of seroma formation may be achieved with placement of suction drains under the flaps. Their premature removal often results in large seromas that will require aspiration under sterile conditions, followed by placement of a pressure dressing. A seroma that reaccumulates after at least two aspirations is evacuated by opening the incision and packing the wound with saline­moistened gauze to allow healing by secondary intention. In the presence of synthetic mesh, open drainage is best performed in the operating room, the incision is best closed to avoid exposure and infection of the mesh, and suction drains are placed. An infected seroma is also treated with open drainage. The presence of synthetic mesh in these cases will prevent the wound from healing. Management of the mesh depends on the severity and extent of infection. In the absence of severe sepsis and spreading cellulitis and the presence of localized infection, the mesh can be left in situ and removed at a later date when the acute infec­tious process has resolved. Otherwise, the mesh must be removed and the wound managed with open wound care.


CausesA hematoma is an abnormal collection of blood, usually in the subcutaneous layer of a recent incision or in a potential space in the abdominal cavity after extirpation of an organ (e.g., splenic fossa hematoma after splenectomy or pelvic hematoma after proctectomy). Hematomas are more worrisome than seromas because of the potential for secondary infection. Hematoma formation is related to inadequate hemostasis, depletion of clot­ting factors, or the presence of coagulopathy. A host of disease processes can contribute to coagulopathy, including myelopro­liferative disorders, liver disease, renal failure, sepsis, clotting factor deficiencies, and medications. Medications most com­monly associated with coagulopathy are antiplatelet drugs, such as acetylsalicylic acid (ASA, aspirin), clopidogrel, ticlopidine, eptifibatide, and abciximab, and anticoagulants, such as ultra­fractionated heparin (UFH), low­molecular­weight heparin (LMWH [e.g., enoxaparin, dalteparin sodium, tinzaparin]), and vitamin K antagonist (VKA [e.g., warfarin sodium]).

presentation and managementThe clinical manifestations of a hematoma may vary with its size, location, and presence of infection. A hematoma may manifest as an expanding, unsightly swelling and/or pain in the area of a surgical incision. In the neck, a large hematoma may cause compromise of the airway; in the retroperitoneum, it may cause a paralytic ileus, anemia, and ongoing bleeding caused by local consumptive coagulopathy; and, in the extremity and abdomi­nal cavity, it may result in compartment syndrome. On physical examination, the hematoma appears as a localized soft swelling with purplish blue discoloration of the overlying skin. The swell­ing varies from small to large and may be tender to palpation

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presentation and managementAcute wound failure may occur without warning and eviscera­tion makes the diagnosis obvious. A sudden, dramatic drainage of a relatively large volume of a clear, salmon­colored fluid precedes dehiscence in 25% of patients. More often, patients report a ripping sensation. Probing the wound with a sterile, cotton­tipped applicator or gloved finger may detect a partial dehiscence.

Prevention of acute wound failure is largely a function of careful attention to technical detail during fascial closure, such as proper spacing of the suture, adequate depth of bite of the fascia, relaxation of the patient during closure, and achieving a tension­free closure. For very high­risk patients, interrupted closure is often the wisest choice. Alternative methods of closure must be selected when primary closure is not possible without undue tension. Although retention sutures were used exten­sively in the past, their use is less common today, with many surgeons opting to use a synthetic mesh or bioabsorbable tissue scaffold.

Treatment of dehiscence depends on the extent of fascial separation and the presence of evisceration and/or significant intra­abdominal pathology (e.g., intestinal leak, peritonitis). A small dehiscence, especially in the proximal aspect of an upper midline incision 10 to 12 days postoper­atively, can be managed conservatively with saline­moistened gauze packing of the wound and use of an abdominal binder. In the event of evisceration, the eviscerated intestines must be covered with a sterile, saline­moistened towel and preparations made to return to the operating room after a very short period of fluid resuscitation. Similarly, if probing of the wound reveals a large segment of the wound that is open to the omentum and intestines, or if there is peritoni­tis or suspicion of intestinal leak, plans to take the patient back to the operating room are made.

Once in the operating room, thorough exploration of the abdominal cavity is performed to rule out the presence of a septic focus or an anastomotic leak that may have predisposed to the dehiscence. Management of that infection is of critical importance before attempting to close. Management of the incision is a function of the condition of the fascia. When technical mistakes are made and the fascia is strong and intact, primary closure is warranted. If the fascia is infected or necrotic, débridement is performed. The incision can then be closed with retention sutures; however, to avoid tension, use of a prosthetic material may be preferred. Closure with an absorbable mesh (polyglactin or polyglycolic acid) may be preferable because the mesh is well tolerated in septic wounds and allows bridging the gap between the edges of the fascia without tension, prevents evisceration, and allows the underly­ing cause of the patient’s dehiscence to resolve. Once the wound has granulated, a skin graft is applied and wound closure is achieved by advancing local tissue. This approach uniformly results in the development of a hernia, the repair of which requires the subsequent removal of the skin graft and use of a permanent prosthesis. An alternative method of closure is dermabrasion of the skin graft followed by fascial closure using the component separation technique. Attempts to close the fascia under tension guarantee a repeat dehiscence and, in some cases, result in intra­abdominal hypertension (IAH). The incision is left open (laparotomy), closed with a temporary closure device (open abdomen technique), closed

Evaluation of a patient with a hematoma, especially one that is large and expanding, includes assessment of preexisting risk factors and coagulation parameters (e.g., prothrombin time [PT], activated partial prothrombin time [aPTT], INR, platelet count, bleeding time) and appropriate treatment. A small hema­toma does not require any intervention and will eventually resorb. Most retroperitoneal hematomas can be managed by expectant waiting after correction of associated coagulopathy (platelet transfusion if bleeding time is prolonged, desmopressin in patients who have renal failure, and fresh­frozen plasma in patients who have an increased INR). A large or expanding hematoma in the neck is managed in a similar fashion and best evacuated in the operating room urgently after securing the airway if there is any respiratory compromise. Similarly, hema­tomas detected soon after surgery, especially those developing under skin flaps, are best evacuated in the operating room.

acute Wound Failure (dehiscence)

CausesAcute wound failure (wound dehiscence or a burst abdomen) refers to postoperative separation of the abdominal musculoapo­neurotic layers. It is among the most dreaded complications faced by surgeons and is of great concern because of the risk of evisceration, the need for some form of intervention, and the possibility of repeat dehiscence, surgical wound infection, and incisional hernia formation.

Acute wound failure occurs in approximately 1% to 3% of patients who undergo an abdominal operation. Dehiscence most often develops 7 to 10 days postoperatively but may occur anytime after surgery, from 1 to more than 20 days. A multitude of factors may contribute to wound dehiscence (Box 13­1). Acute wound failure is often related to technical errors in placing sutures too close to the edge, too far apart, or under too much tension. Local wound complications such as hematoma and infection can also predispose to localized dehiscence. In fact, a deep wound infection is one of the most common causes of localized wound separation. Increased intra­abdominal pressure (IAP) is often blamed for wound disruption and factors that adversely affect wound healing are cited as contributing to the complication. In healthy patients, the rate of wound failure is similar whether closure is accomplished with a continuous or interrupted technique. In high­risk patients, however, continu­ous closure is worrisome because suture breakage in one place weakens the entire closure.

Box 13-1  Factors associated With Wound Dehiscence

technical error in fascial closureemergency surgeryintra-abdominal infectionadvanced ageWound infection, hematoma, and seromaelevated intra-abdominal pressureobesitychronic corticosteroid usePrevious wound dehiscenceMalnutritionradiation therapy and chemotherapySystemic disease (uremia, diabetes mellitus)

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13-4  section ii  PerioPerative ManageMent

wound (macrodeformation) and removal of extracellular fluid (via decrease in bowel edema, evacuation of excess abdominal fluid, decrease in wound size), stabilization of the wound envi­ronment, and microdeformation of the foam­wound interface, which induces cellular proliferation and angiogenesis. The sec­ondary effects of the vacuum­assisted closure device include acceleration of wound healing, reduction and changes in bac­terial burden, changes in biochemistry and systemic responses, and improvement in wound bed preparation—increase in local blood perfusion and induction healing response through microchemical forces.3 This approach results in successful closure of the fascia in 85% of cases. However, the device is expensive and cumbersome to wear and may cause significant pain, cause bleeding (especially in patients on anticoagulant therapy), be associated with increased levels of certain bacteria, and be associated with evisceration and hernia formation. There is also an increased incidence of intestinal fistulization at enterotomy sites and enteric anastomoses, and in the absence of anastomoses.

Surgical Site infection (Wound infection)

CausesSurgical site infections (SSIs) still continue to be a significant problem for surgeons. Despite major improvements in antibiot­ics, better anesthesia, superior instruments, earlier diagnosis of surgical problems, and improved techniques for postoperative vigilance, wound infections continue to occur. Although some may view the problem as merely cosmetic, that view represents a shallow understanding of this problem, which causes signifi­cant patient suffering, morbidity, and even mortality, and is a financial burden to the health care system. Furthermore, SSIs represent a risk factor for the development of incisional hernia, which requires surgical repair. Currently, in the United States, SSIs account for almost 40% of hospital­acquired infections among surgical patients.

The surgical wound encompasses the area of the body, internally and externally, that involves the entire operative site. Wounds are thus categorized into three general categories:

1. Superficial, which includes the skin and subcutane­ous tissue

2. Deep, which includes the fascia and muscle3. Organ space, which includes the internal organs of

the body if the operation includes that areaThe Centers for Disease Control and Prevention has pro­

posed specific criteria for the diagnosis of surgical site infections (Box 13­2).4

Surgical site infections develops as a result of contamina­tion of the surgical site with microorganisms. The source of these microorganisms is mostly patients’ flora (endogenous source) when integrity of the skin and/or wall of a hollow viscus is violated. Occasionally, the source is exogenous when a break in the surgical sterile technique occurs, thus allowing contamina­tion from the surgical team, equipment, implant or gloves, or surrounding environment. The pathogens associated with a sur­gical site infections reflect the area that provided the inoculum for the infection to develop. The microbiology, however, varies, depending on the types of procedures performed in individual practices. Gram­positive cocci account for half of the infections (Table 13­1)—Staphylococcus aureus (most common), coagulase­negative Staphylococcus, and Enterococcus spp. S. aureus infections


with synthetic mesh or biologic graft (acellular dermal matrix), or closed by using negative­pressure wound therapy.

The open abdomen technique avoids IAH, preserves the fascia, and facilitates reaccess of the abdominal cavity. With laparotomy, the wound is allowed to heal with secondary inten­tion and/or subsequently closed with a skin graft or local or regional tissue. This approach is associated with prolonged healing time, fluid loss, and risk of complex enterocutaneous fistula formation as a result of bowel exposure, desiccation, and traumatic injury. Furthermore, definitive surgical repair to restore the integrity of the abdominal wall will eventually be required. A temporary closure device (vacuum pack closure) protects abdominal contents, keeps patients dry, can be quickly removed with increased IAP, and avoids secondary complica­tions seen with laparotomy. A fenestrated, nonadherent, poly­ethylene sheet is applied on the bowel omentum, moist surgical towels or gauze with drains are placed on top, and an iodophore­impregnated adhesive dressing is placed. Continuous suction is then applied. If the fascia cannot be closed in 7 to 10 days, the wound is allowed to granulate and then covered with a skin graft.

Absorbable synthetic mesh provides wound stability and is resistant to infection. It is associated with fistula and hernia formation repair, which is difficult and may require recon­struction of the abdominal wall. Repair with nonabsorbable synthetic mesh such as polypropylene, polyester, or polytetra­fluoroethylene (PTFE) is associated with complications that will require removal of the mesh (e.g., abscess formation, dehiscence, wound sepsis, mesh extrusion, bowel fistulization). Although PTFE is more desirable because it is nonadherent to underlying bowel, it is expensive, does not allow skin graft­ing, and is associated with chronic infections. An acellular dermal matrix (bioprosthesis) has the mechanical properties of a mesh for abdominal wall reconstruction and physiologic properties that make it resistant to contamination and/or infection. The bioprosthesis provides immediate coverage of the wound and serves as mechanical support in a single­stage reconstruction of compromised surgical wounds. It is bioactive because it functions as tissue replacement or scaffold for new tissue growth; it stimulates cellular attachment, migration, neovascularization, and repopulation of the implanted graft. A bioprosthesis also reduce long­term complications (e.g., erosion, infection, chronic pain). Available acellular materials are animal­derived (e.g., porcine intestinal submucosa, porcine dermis, cross­linked porcine dermal collagen) or human­derived (e.g., cadaveric human dermis). However, the rate of wound complications (e.g., superficial wound or graft infec­tion, graft dehiscence, fistula formation, bleeding) and hernia formation or literaxity of the abdominal wall is 25% to 50%.2

Negative­pressure wound therapy is based on the concept of wound suction. A vacuum­assisted closure device is most commonly used. The device consists of a vacuum pump, can­ister with connecting tubing, open­pore foam (e.g., poly­urethane ether, polyvinyl alcohol foam) or gauze, and semiocclusive dressing. The device provides immediate cover­age of the abdominal wound, acts as a temporary dressing, does not require suturing to the fascia, minimizes IAH, and prevents loss of domain. Applying suction of 125 mm Hg, the open­pore foam decreases in size and transmits the negative pressure to surrounding tissue, leading to contraction of the


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Box 13-2  centers for Disease control and prevention criteria for Defining a surgical site infection

Superficial incisionalinfection less than 30 days after surgery

involves skin and subcutaneous tissue only, plus one of the following:

• Purulent drainage• Diagnosis  of  superficial  surgical  site  infection  by  a 

surgeon• Symptoms of erythema, pain, local edema

Deep incisionalless than 30 days after surgery with no implant and soft tissue involvement

infection  less  than  1  year  after  surgery  with  an  implant; involves deep soft tissues (fascia and muscle), plus one of the following:

• Purulent drainage from the deep space but no exten-sion into the organ space

• abscess  found in the deep space on direct or radio-logic examination or on reoperation

• Diagnosis  of  a  deep  space  surgical  site  infection  by the surgeon

• Symptoms  of  fever,  pain,  and  tenderness  leading  to wound dehiscence or opening by a surgeon

organ Spaceinfection less than 30 days after surgery with no implant

infection less than 1 year after surgery with an implant and infection;  involves any part of  the operation opened or mani-pulated, plus one of the following:

• Purulent  drainage  from  a  drain  placed  in  the  organ space

• cultured organisms from material aspirated from the organ space

• abscess found on direct or radiologic examination or during reoperation

• Diagnosis of organ space infection by a surgeon

adapted from Mangram aJ, horan tC, pearson ML, et al: Guideline for prevention of surgical site infection. Infect Control hosp epidemiol 20:252, 1999.

normally occur in the nasal passages, mucous membranes, and skin of carriers. The organism that has acquired resistance to methicillin (methicillin­resistant S. aureus [MRSA]) consists of two subtypes, hospital­ and community­acquired MRSA. Hospital­acquired MRSA is associated with nosocomial infec­tions and affects immunocompromised individuals. It also occurs in patients with chronic wounds, those subjected to inva­sive procedures, and those with prior antibiotic treatment. Community­acquired MRSA is associated with a variety of skin and soft tissue infections in patients with and without risk factors for MRSA. Community­acquired MRSA (e.g., the USA300 clone) has also been noted to affect SSIs. Hospital­acquired MRSA isolates have a different antibiotic susceptibility profile—they are usually resistant to at least three β­lactam antibiotics and are usually susceptible to vancomycin, teico­planin, and sulfamethoxazole. Community­acquired MRSA is usually susceptible to clindamycin, with variable susceptibility to erythromycin, vancomycin, and tetracycline. There is

evidence to indicate that hospital­acquired MRSA is developing resistance to vancomycin (vancomycin intermediate­resistant S. aureus [VISA] and vancomycin­resistant S. aureus [VRSA]).5 Enterococcus spp. are commensals in the adult gastrointestinal (GI) tract, have intrinsic resistance to a variety of antibiotics (e.g., cephalosporins, clindamycin, aminoglycoside), and are the first to exhibit resistance to vancomycin.

In approximately one third of SSI cases, gram­negative bacilli (Escherichia coli, Pseudomonas aeruginosa, and Enterobacter spp.) are isolated. However, at locations at which high volumes of GI operations are performed, the predominant bacterial species are the gram­negative bacilli. Infrequent pathogens are group A beta­hemolytic streptococci and Clostridium perfringens. In recent years, the involvement of resistant organisms in the genesis of SSIs has increased, most notable in MRSA.

A host of patient­ and operative procedure–related factors may contribute to the development of SSIs (Table 13­2).6 The risk of infection is related to the specific surgical procedure performed and, hence, surgical wounds are classified according to the relative risk of surgical site infections occurring—clean, clean­contaminated, contaminated, and dirty (Table 13­3). In the National Nosocomial Infections Surveillance System, the risk of patients is stratified according to three important factors: (1) wound classification (contaminated or dirty); (2) longer duration operation, defined as one that exceeds the 75th percen­tile for a given procedure; and (3) medical characteristics of the patients as determined by the American Society of Anesthesiol­ogy score of III, IV, or V (presence of severe systemic disease that results in functional limitations, is life­threatening, or is expected to preclude survival from the operation) at the time of operation.7

presentationSSIs most commonly occur 5 to 6 days postoperatively but may develop sooner or later than that. Approximately 80% to 90%

From Weiss Ca, Statz CI, Dahms ra, et al: Six years of surgical wound surveillance at a tertiary care center. arch Surg 134:1041-1048, 1999.

table  13-1  pathogens  isolated  from  postoperative  surgical site infections at a University hospitalpathoGen percentaGe oF isoLates

Staphylococcus (coagulase-negative) 25.6

Enterococcus (group D) 11.5

Staphylococcus aureus 8.7

Candida albicans 6.5

Escherichia coli 6.3

Pseudomonas aeruginosa 6.0

Corynebacterium 4.0

Candida (non-albicans) 3.4

alpha-hemolytic Streptococcus 3.0

Klebsiella pneumoniae 2.8

vancomycin-resistant Enterococcus 2.4

Enterobacter cloacae 2.2

Citrobacter spp. 2.0

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13-6  section ii  PerioPerative ManageMent

patients are hospitalized for 6 days or less, 70% of postdischarge infections occur in that group.

Superficial and deep SSIs are accompanied by erythema, tenderness, edema, and occasionally drainage. The wound is often soft or fluctuant at the site of infection, which is a depar­ture from the firmness of the healing ridge present elsewhere in the wound. The patient may have leukocytosis and a low­grade fever. According to the Joint Commission (TJC), a surgical wound is considered infected if (1) there is drainage of grossly purulent material drains from the wound, (2) the wound spon­taneously opens and drains purulent fluid, (3) the wound drains fluid that is culture­positive or Gram stain–positive for bacteria, and (4) the surgeon notes erythema or drainage and opens the wound after determining it to be infected.

treatmentPrevention of surgical site infections relies on changing or dealing with modifiable risk factors that predispose to surgical site infections. However, many of these factors cannot be changed, such as age, complexity of the surgical procedure, and morbid obesity. Patients who are heavy smokers are encouraged to stop smoking at least 30 days before surgery, glucose levels in diabetics must be treated appropriately, and severely malnourished patients should be given nutritional supplements for 7 to 14 days before surgery.8 Obese patients must be encouraged to lose weight if the procedure is elective and there is time to achieve significant weight loss. Similarly, patients who are taking high doses of corticosteroids will have lower infection rates if they are weaned off corticosteroids or are at least taking a lower dose. Patients undergoing major intra­abdominal surgery are administered a bowel preparation in the form of a lavage solution or strong cathartic, followed by oral nonabsorbable antibiotic(s), particularly for surgery of the colon and small bowel. Bowel preparation lowers the patient’s risk for infection from that of a contaminated case (25%) to a clean­contaminated case (5%). Hair is removed by clipping immediately before surgery and the skin is prepped at the time of operation with an antiseptic agent (e.g., alcohol, chlorhexidine, iodine).

The role of preoperative decolonization in carriers of S. aureus undergoing general surgery is questionable, and the routine use of prophylactic vancomycin or teicoplanin (effective against MRSA) is not recommended. Although perioperative antibiotics are widely used, prophylaxis is generally recom­mended for clean­contaminated or contaminated procedures in which the risk of SSIs is high or in procedures in which vascular or orthopedics prostheses are used because the development of SSIs will have grave consequences (Table 13­4). For dirty or contaminated wounds, the use of antibiotics is for therapeutic purposes rather than for prophylaxis. For clean cases, prophy­laxis is controversial. For some surgical procedures, a first­ or second­generation cephalosporin is the accepted agent of choice. A small but significant benefit may be achieved with the pro­phylactic administration of a first­generation cephalosporin for certain types of clean surgery (e.g., mastectomy, herniorrhaphy). For clean­contaminated procedures, administration of preopera­tive antibiotics is indicated. The appropriate preoperative anti­biotic is a function of the most likely inoculum based on the area being operated. For example, when a prosthesis may be placed in a clean wound, preoperative antibiotics would include something to protect against S. aureus and streptococcal species.


Data from National Nosocomial Infections Surveillance Systems (NNIS) System report: Data summary from January 1992–June 2001, issued august 2001. am J Infect Control 29:404-421, 2001.

table 13-2  risk Factors for postoperative Wound infection

patient FactorsenVironMentaL Factors

treatMent Factors

ascites contaminated medications


chronic inflammation

inadequate disinfection/sterilization

emergency procedure


inadequate skin antisepsis

inadequate antibiotic coverage

Diabetes inadequate ventilation Preoperative hospitalization

extremes of age Presence of a foreign body

Prolonged operation



Peripheral vascular disease

Postoperative anemia

Previous site of irradiation

recent operation

remote infection

Skin carriage of staphylococci

Skin disease in the area of infection


table 13-3  classification of surgical Wounds

cateGorY criteriainFection  rate (%)

clean no hollow viscus entered 1-3Primary wound closureno inflammationno breaks in aseptic techniqueelective procedure

clean- contaminated

Hollow viscus entered but controlledno inflammation


Primary wound closureMinor break in aseptic techniqueMechanical drain usedBowel preparation preoperatively

contaminated uncontrolled spillage from viscus 20-25inflammation apparentopen, traumatic woundMajor break in aseptic technique

Dirty untreated, uncontrolled spillage from viscus


Pus in operative woundopen suppurative woundSevere inflammation

of all postoperative infections occur within 30 days after the operative procedure. With the increased use of outpatient surgery and decreased length of stay in hospitals, 30% to 40% of all wound infections have been shown to occur after hospital discharge. Nevertheless, although less than 10% of surgical

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contaminated instruments, avoidance of environ­mental contamination, such as debris falling from overhead)

7. Thorough drainage and irrigation of any pockets of purulence in the wound with warm saline

8. Ensuring that the patient is kept in a euthermic state, well­monitored, and fluid­resuscitated

9. Expressing a decision about closing the skin or packing the wound at the end of the procedure

The use of drains remains somewhat controversial in pre­venting postoperative wound infections. In general, there is almost no indication for drains in this setting. However, placing closed suction drains in very deep, large wounds and wounds with large wound flaps to prevent the development of a seroma or hematoma is a worthwhile practice.

Treatment of SSIs depends on the depth of the infection. For both superficial and deep SSIs, skin staples are removed over the area of the infection and a cotton­tipped applicator may be easily passed into the wound, with efflux of purulent material and pus. The wound is gently explored with the cotton­tipped applicator or a finger to determine whether the fascia or muscle tissue is involved. If the fascia is intact, débridement of any nonviable tissue is performed; the wound is irrigated with normal saline solution and packed to its base with saline­moistened gauze to allow healing of the wound from the base anteriorly, thus preventing premature skin closure. If widespread cellulitis or significant signs of infection (e.g., fever, tachycardia), are noted, administration of IV anti­biotics must be considered. Empirical therapy is started and tailored according to culture and sensitivity data. The choice of empirical antibiotics is based on the most likely culprit, including the possibility of MRSA. MRSA is treated with van­comycin, linezolid, or clindamycin. Cultures are not routinely performed, except for patients who will be treated with antibi­otics so that resistant organisms can be treated adequately. However, if the fascia has separated or purulent material appears to be coming from deep to the fascia, there is obvious concern about dehiscence or an intra­abdominal abscess that may require drainage or possibly a reoperation.

A first­generation cephalosporin, such as cefazolin, would be appropriate in this setting. For patients undergoing upper GI tract surgery, complex biliary tract operations, or elective colonic resection, administration of a second­generation cephalosporin such as cefoxitin or a penicillin derivative with a β­lactamase inhibitor is more suitable. Alternatively, ertapenem can y be used for operations involving the lower GI tract. The surgeon will give a preoperative dose, intraoperative doses approximately 4 hours apart, and two postoperative doses appropriately spaced. The timing of administration of prophylactic antibiotics is crit­ical. To be most effective, the antibiotic is administered IV within 30 minutes before the incision so that therapeutic tissue levels have developed when the wound is created and exposed to bacterial contamination. Usually, a period of anesthesia induction, preparation, and draping takes place that is adequate to allow tissue levels to build up to therapeutic levels before the incision is made. Of equal importance is making certain that the prophylactic antibiotic is not administered for extended periods postoperatively. To do so in the prophylactic setting is to invite the development of drug­resistant organisms, as well as serious complications, such as Clostridium difficile–associated colitis.

At the time of surgery, the operating surgeon plays a major role in reducing or minimizing the presence of postoperative wound infections. The surgeon must be attentive to personal hygiene (hand scrubbing) and that of the entire team. In addi­tion, the surgeon must make certain that the patient undergoes a thorough skin preparation with appropriate antiseptic solu­tions and is draped in a sterile, careful fashion. During the operation, steps that have a positive impact on outcome are followed:

1. Careful handling of tissues2. Meticulous dissection, hemostasis, and débridement

of devitalized tissue3. Compulsive control of all intraluminal contents4. Preservation of blood supply of the operated organs5. Elimination of any foreign body from the wound6. Maintenance of strict asepsis by the operating team

(e.g., no holes in gloves, avoidance of the use of

From Kirby Jp, Mazuski Je: prevention of surgical site infection. Surg Clin North am 89:365-389, 2009.

table 13-4  prophylactic antimicrobial agent for selected surgical proceduresproceDUre recoMMenDeD aGent potentiaL aLternatiVe

cardiothoracic cefazolin or cefuroxime vancomycin, clindamycin

vascular cefazolin or cefuroxime vancomycin, clindamycin

gastroduodenal cefazolin cefoxitin, cefotetan, aminoglycoside, or fluoroquinolone + antianaerobe

open biliary cefazolin cefoxitin, cefotetan, or fluoroquinolone + antianaerobe

laparoscopic cholecystectomy none —

nonperforated appendicitis cefoxitin, cefotetan, cefazolin + metronidazole ertapenem, aminoglycoside, or fluoroquinolone + antianaerobe

colorectal cefoxitin, cefotetan, ampicillin-sulbactam, ertapenem, cefazolin + metronidazole

aminoglycoside, or fluoroquinolone + antianaerobe, aztreonam + clindamycin

Hysterectomy cefazolin, cefuroxime, cefoxitin, cefotetan, ampicillin-sulbactam

aminoglycoside, or fluoroquinolone + antianaerobe, aztreonam + clindamycin

orthopedic implantation cefazolin, cefuroxime vancomycin, clindamycin

Head and neck cefazolin, clindamycin —

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13-8  section ii  PerioPerative ManageMent

shock or with a severe illness often have associated vasoconstric­tion that results in poor perfusion of peripheral organs and tissues, an effect accentuated by hypothermia. In a high­risk patient, a core temperature lower than 35° C is associated with a twofold to threefold increase in the incidence of early postop­erative ischemia and a similar increase in the incidence of ven­tricular tachyarrhythmia. Hypothermia also impairs platelet function and reduces the activity of coagulation factors, thereby resulting in an increased risk for bleeding. Hypothermia results in impaired macrophage function, reduced tissue oxygen tension, and impaired collagen deposition, which predisposes wounds to poor healing and infection. Other complications of hypothermia include a relative diuresis, compromised hepatic function, and some neurologic manifestations. Similarly, the patient’s ability to manage acid­base abnormalities is impaired. In severe cases, the patient can have significant cardiac slowing and may be comatose, with low blood pressure, bradycardia, and a very low respiratory rate.

treatmentPrevention of hypothermia entails monitoring core tempera­ture, especially in patients undergoing body cavity surgery or surgery lasting longer than 1 hour, children and older adults, and patients in whom general epidural anesthesia is being con­ducted.9 Sites of monitoring include pulmonary artery blood, tympanic membrane, esophagus and pharynx, rectum, and urinary bladder. While the patient is being anesthetized, and during skin preparation, significant evaporative cooling can take place; the patient is kept warm by increasing the ambient temperature and using heated humidifiers and warmed IV fluid. After the patient is draped, the room temperature can be lowered to a more comfortable setting. A forced­air warming device that provides active cutaneous warming is placed on the patient. Passive surface warming is not effective in conserving heat. There is some evidence that a considerable amount of heat is lost through the head of the patient, so simply covering the patient’s head during surgery may prevent significant heat loss.

In the perioperative period, mild hypothermia is common­place and patients usually shiver because the anesthesia impairs thermoregulation. Many patients who shiver after anesthesia, however, are hypothermic. Treatment of the hypothermia with forced­air warming systems and radiant heaters will also reduce the shivering.9 In a severely hypothermic patient who does not require immediate operative intervention; attention must be directed toward rewarming by the following methods:

1. Immediate placement of warm blankets, as well as currently available forced­air warming devices

2. Infusion of blood and IV fluids through a warming device

3. Heating and humidifying inhalational gases4. Peritoneal lavage with warmed fluids5. Rewarming infusion devices with an arteriovenous

system6. In rare cases, cardiopulmonary bypass

Special attention must be paid to cardiac monitoring during the rewarming process because cardiac irritability may be a significant problem. Similarly, acid­base disturbances must be aggressively corrected while the patient is being rewarmed. Once in the operating room, measures noted earlier to keep the patient warm are applied.

Wound cultures are controversial. If the wound is small, superficial, and not associated with cellulitis or tissue necrosis, cultures may not be necessary. However, if fascial dehiscence and a more complex infection are present, a culture is sent. A deep SSI associated with grayish, dishwater­colored fluid, as well as frank necrosis of the fascial layer, raises suspicion for the presence of a necrotizing type of infection. The presence of crepitus in any surgical wound or gram­positive rods (or both) suggests the possibility of infection with C. perfringens. Rapid and expeditious surgical débridement is indicated in these settings.

Most postoperative infections are treated with healing by secondary intention, allowing the wound to heal from the base anteriorly, with epithelialization being the final event. In some cases, when there is a question about the amount of contamination, delayed primary closure may be considered. In this setting, close observation of the wound for 5 days may be followed by closure of the skin or negative­pressure wound therapy if the wound looks clean and the patient is otherwise doing well.

complicationS oF tHermal regulation


CausesOptimal function of physiologic systems in the body occurs within a narrow range of core temperatures. A 2° C drop in body temperature or a 3° C increase signifies a health emergency that is life­threatening and requires immediate intervention. Hypo­thermia can result from a number of mechanisms preoperatively, intraoperatively, or postoperatively. A trauma patient with inju­ries in a cold environment can suffer significant hypothermia, and paralysis can lead to hypothermia because of loss of the shiver mechanism.

Hypothermia develops in patients undergoing rapid resus­citation with cool IV fluids, transfusions, or intracavitary irriga­tion with cold irrigant, and in patients undergoing a prolonged surgical procedure with low ambient room temperature and a large, exposed operative area subjected to significant evaporative cooling. Almost all anesthetics impair thermoregulation and render the patient susceptible to hypothermia in the typically cool operating room environment.9 Advanced age and opioid analgesia also reduce perioperative shivering. Propofol causes vasodilation and significant redistribution hypothermia. Postop­eratively, hypothermia can result from cool ambient room tem­perature, rapid administration of IV fluids or blood, and failure to keep patients covered when they are only partially responsive. More than 80% of elective operative procedures are associated with a drop in body temperature, and 50% of trauma patients are hypothermic on arrival in the operating suite.

presentationHypothermia is uncomfortable because of the intense cold sen­sation and shivering. It may also be associated with profound effects on the cardiovascular system, coagulation, wound healing, and infection. A core temperature lower than 35° C after surgery triggers a significant peripheral sympathetic nervous system response, consisting of an increased norepinephrine level, vaso­constriction, and elevated arterial blood pressure. Patients in

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Once MH is suspected or diagnosed, the steps outlined in Box 13­3 are followed. Dantrolene is a muscle relaxant. In the solution form, it is highly irritating to the vein and must be administered in a large vein. When given intravenously, it blocks up to 75% of skeletal muscle contraction and never causes paralysis. The plasma elimination half­life is 12 hours. Dan­trolene is metabolized in the liver to 5­hydroxydantrolene, which also acts as a muscle relaxant. Side effects reported with dantrolene therapy include muscle weakness, phlebitis, respira­tory failure, GI discomfort, hepatotoxicity, dizziness, confusion, and drowsiness. Another agent, azumolene, is 30 times more water­soluble than and equipotent to dantrolene in the treat­ment of MH; like dantrolene, it does not affect the heart. Its main side effect is marked pulmonary hypertension. However, azumolene is not in clinical use at this time.

postoperative Fever

CausesOne of the most concerning clinical findings in a patient post­operatively is the development of fever. Fever describes a rise in core temperature, modulation of which is managed by the ante­rior hypothalamus. Fever may result from bacterial invasion or their toxins, which stimulate the production of cytokines. Trauma (including surgery) and critical illness also invoke a cytokine response. Cytokines are low­molecular­weight proteins that act in an autocrine, paracrine, and/or endocrine fashion to influence a broad range of cellular function and exhibit proin­flammatory and anti­inflammatory effects. The inflammatory

malignant Hyperthermia

CausesMalignant hyperthermia (MH) is a life­threatening hypermeta­bolic crisis manifested during or after exposure to a triggering general anesthetic in susceptible individuals. It is estimated that MH occurs in 1 in 30,000 to 50,000 adults. Mortality from MH has decreased to less than 10% in the last 15 years as a result of improved monitoring standards that allow early detec­tion of MH, availability of dantrolene, and increased use of susceptibility testing.

Susceptibility to MH is inherited as an autosomal domi­nant disease with variable penetrance. To date, two MH suscep­tibility genes have been identified in humans and four mapped to specific chromosomes but not definitely identified. The muta­tion results in altered calcium regulation in skeletal muscle in the form of enhanced efflux of calcium from the sarcoplasmic reticulum into the myoplasm. Halogenated inhalational anes­thetic agents (e.g., halothane, enflurane, isoflurane, desflurane, and sevoflurane) and depolarizing muscle relaxants (e.g., succi­nylcholine, suxamethonium) cause a rise in the myoplasmic Ca2+ concentration. When an MH­susceptible individual is exposed to a triggering anesthetic, there is abnormal release of Ca2+, which leads to prolonged activation of muscle filaments, culmi­nating in rigidity and hypermetabolism. Uncontrolled glycolysis and aerobic metabolism give rise to cellular hypoxia, progressive lactic acidosis, and hypercapnia. The continuous muscle activa­tion with adenosine triphosphate breakdown results in excessive generation of heat. If untreated, myocyte death and rhabdomy­olysis result in hyperkalemia and myoglobulinuria. Eventually, disseminated coagulopathy, congestive heart failure (CHF), bowel ischemia, and compartment syndrome develop.

presentation and managementMH can be prevented by identifying at­risk individuals before surgery. MH susceptibility is suspected preoperatively in a patient with a family history of MH or a personal history of myalgia after exercise, a tendency for the development of fever, muscular disease, and intolerance to caffeine. In these cases, the creatine kinase level is checked, and a caffeine and halothane contraction test (or an in vitro contracture test developed in Europe) may be performed on a muscle biopsy specimen from the thigh.10 MH­susceptible individuals confirmed by abnormal skeletal muscle biopsy findings or those with suspected MH susceptibility who decline a contracture test are given a trigger­free anesthetic (e.g., barbiturate, benzodiazepine, opioid, pro­pofol, etomidate, ketamine, nitrous oxide, nondepolarizing neuromuscular blocker).

Unsuspected MH­susceptible individuals may manifest MH for the first time during or immediately after the adminis­tration of a triggering general anesthetic. The clinical manifesta­tions of MH are not uniform and vary in onset and severity. Some patients manifest the abortive form of MH (e.g., tachy­cardia, arrhythmia, raised temperature, acidosis). Others, after intubation with succinylcholine, demonstrate loss of twitches on neuromuscular stimulation and develop muscle rigidity. An inability to open the mouth as a result of masseter muscle spasm is a pathognomonic early sign and indicates susceptibility to MH. Other manifestations include tachypnea, hypercapnia, skin flushing, hypoxemia, hypotension, electrolyte abnormali­ties, rhabdomyolysis, and hyperthermia.


Box 13-3  Management of Malignant hyperthermia

Discontinue the triggering anesthetic.Hyperventilate the patient with 100% oxygen.administer alternative anesthesia.terminate surgery.give dantrolene, 2.5 mg/kg, as a bolus and repeat every 5 min, 

then 1 to 2 mg/kg/hr until normalization or disappearance of symptoms.

check  and  monitor  arterial  blood  gas  and  creatine  kinase,  electrolyte, lactate, and myoglobin levels.

Monitor the electrocardiogram, vital signs, and urine output.adjunctive and supportive measures are carried out:

• volatile  vaporizers  are  removed  from  the anesthesia machine.

• carbon dioxide canisters, bellows, and gas hoses are changed.

• Surface  cooling  is  achieved with  ice packs  and  core cooling with cool parenteral fluids.

• acidosis  is  monitored  and  treated  with  sodium bicarbonate.

• arrhythmias  are  controlled  with  beta  blockers  or lidocaine.

• urine  output  more  than2 ml/kg/hr  is  promoted; furosemide (lasix) or mannitol and a glucose-insulin infusion  (0.2 u/kg  in  a  50%  glucose  solution)  are given  for  hyperkalemia,  hypercalcemia,  and myoglobulinuria.

the patient is transferred to the intensive care unit to monitor for recurrence.


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13-10  section ii  PerioPerative ManageMent

infections are preventable and are considered a “never” compli­cation by the Centers of Medicare and Medicaid Services.13 CR­BSI results from microorganisms that colonize the hubs or from contamination of the injection site of the central venous catheter (intraluminal source) or skin surrounding the insertion site (extraluminal source). Coagulase­negative staphylococci, hospital­acquired bacteria (e.g., MRSA, multidrug­resistant gram­negative bacilli, fungal species [Candida albicans]) are the most common organisms responsible for CR­BSI. S. aureus bac­teremia is associated with higher mortality and venous throm­bosis. Metastatic infections (endocarditis) are uncommon but represent a serious complication of CR­BSI. The duration of central venous catheter placement, patient location (outpatient versus inpatient), type of catheter, number of lumens and manipulations daily, emergent placement, need for total paren­teral nutrition (TPN), presence of unnecessary connectors, and whether best care practices are followed are risk factors for BSI.14

presentation and managementIn evaluating a patient with fever, one has to take into consid­eration the type of surgery performed, patient’s immune status, underlying primary disease process, duration of hospital stay, and epidemiology of hospital infections.

High fever that fluctuates or is sustained and that occurs 5 to 8 days after surgery is more worrisome than fever that occurs early postoperatively. In the first 48 to 72 hours after abdominal surgery, atelectasis is often believed to be the cause of the fever. Occasionally, clostridial or streptococcal SSIs can manifest as fever within the first 72 hours of surgery. Temperatures that are elevated 5 to 8 days postoperatively demand immediate atten­tion and, at times, intervention. Evaluation involves studying the six Ws: wind (lungs), wound, water (urinary tract), waste (lower GI tract), wonder drug (e.g., antibiotics), and walker (e.g., thrombosis). The patient’s symptoms usually indicate the organ system involved with infection; cough and productive sputum suggest pneumonia, dysuria and frequency indicate a UTI, watery foul­smelling diarrhea develops as a result of infec­tion with C. difficile, pain in the calf may be caused by deep venous thrombosis (DVT), and flank pain may be caused by pyelonephritis. Physical examination may show an SSI, phlebi­tis, tenderness on palpation of the abdomen, flank, or calf, or cellulitis at the site of a central venous catheter.

A complete blood count, urinalysis and culture, radiograph of the chest, and blood culture are essential initial tests. A chest radiograph may show a progressive infiltrate suggestive of the presence of pneumonia. Urinalysis showing more than 105 colony­forming units/milliliter (CFU/mL) in a noncatheterized patient and more than 103 CFU/mL in a catheterized patient indicates a urinary tract infection. The diagnosis of CR­BSI rests on culture data because physical examination is usually unreveal­ing. There is no gold standard for how to use blood cultures. Two simultaneous blood cultures or paired blood cultures (i.e., simultaneous peripheral and central blood cultures) are com­monly used. Peripheral blood cultures showing bacteremia and isolation of 15 CFUs or 102 CFUs from an IV catheter indicate the presence of a CR­BSI. In tunneled catheters, a quantitative colony count that is 5­ to 10­fold higher in cultures drawn through the central venous catheter is predictive of CRC­BSI. If paired cultures are obtained, positive culture more than2 hours before peripheral culture indicates the presence of CR­BSI. After removal of the catheter, the tip may be sent for quantitative


response results in the production of a variety of mediators that induce a febrile inflammatory response, also known as systemic inflammatory response syndrome.11 Hence, fever in the post­operative period may be the result of an infection or caused by systemic inflammatory response syndrome. Fever after surgery is reported to occur in up to two thirds of patients, and infection is the cause of fever in approximately one third of cases. Numerous disease states can cause fever in the postoperative period (Table 13­5).

The most common infections, however, are health care–associated infections—SSI, urinary tract infection (UTI), intra­vascular catheter–related bloodstream infection (CR­BSI), and pneumonia. Urinary tract infection is a common postoperative event and a significant source of morbidity in postsurgical patients. A major predisposing factor is the presence of a urinary catheter; the risk increases with increased duration of catheter­ization (>2 days). Endogenous bacteria (colonic flora, most common E. coli) are the most common source of catheter­related urinary tract infection in patients with short­term catheteriza­tion. With prolonged catheterization, additional bacteria are found. In the critically ill surgical patient, candiduria accounts for approximately 10% of nosocomial urinary tract infection. The presence of an indwelling catheter, diabetes mellitus, use of antibiotics, advanced age, and underlying anatomic urologic abnormalities are risk factors for candiduria.12

The use of central venous catheters carries a risk of CR­BSI that increases hospital stay and morbidity and mortality. The

table 13-5  causes of postoperative FeverinFectioUs noninFectioUs

abscess acute hepatic necrosis

acalculous cholecystitis adrenal insufficiency

Bacteremia allergic reaction

Decubitus ulcers atelectasis

Device-related infections Dehydration

empyema Drug reaction

endocarditis Head injury

Fungal sepsis Hepatoma

Hepatitis Hyperthyroidism

Meningitis lymphoma

osteomyelitis Myocardial infarction

Pseudomembranous colitis Pancreatitis

Parotitis Pheochromocytoma

Perineal infections Pulmonary embolus

Peritonitis retroperitoneal hematoma

Pharyngitis Solid organ hematoma

Pneumonia Subarachnoid hemorrhage

retained foreign body Systemic inflammatory

Sinusitis response syndrome

Soft tissue infection thrombophlebitis

tracheobronchitis transfusion reaction

urinary tract infection Withdrawal syndromes

Wound infection

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days. For patients with septic thrombosis or endocarditis, treatment is continued for 4 to 6 weeks. Catheter salvage is indicated in patients with tunneled catheters that are risky to remove or replace, or in patients with coagulase­negative staphylococci who have no evidence of metastatic disease or severe sepsis, do not have tunnel infection, or do not have persistent bacteremia. Catheter salvage is achieved by antibi­otic lock therapy whereby the catheter is filled with antibiotic solution for several hours.

reSpiratory complicationS

general considerationsA host of factors contribute to abnormal pulmonary physiology after an operative procedure. First, loss of functional residual capacity is present in almost all patients. This loss may be the result of a multitude of problems, including abdominal disten­tion, painful upper abdominal incision, obesity, strong smoking history with associated chronic obstructive pulmonary disease, prolonged supine positioning, and fluid overload leading to pulmonary edema. Almost all patients who undergo an abdom­inal or thoracic incision have a significant alteration in their breathing pattern. Vital capacity may be reduced up to 50% of normal for the first 2 days after surgery for reasons that are not completely clear. The use of narcotics substantially inhibits the respiratory drive, and anesthetics may take some time to wear off. Most patients who have respiratory problems postopera­tively have mild to moderate problems that can be managed with aggressive pulmonary toilet. However, in some patients, severe postoperative respiratory failure develops; this may require intu­bation and ultimately may be life­threatening.

Two types of respiratory failure are commonly described. Type I, or hypoxic, failure results from abnormal gas exchange at the alveolar level. This type is characterized by a low Pao2 with a normal Paco2. Such hypoxemia is associated with ventilation­perfusion ( � �V/Q) mismatching and shunting. Clinical conditions associated with type I failure include pulmonary edema and sepsis. Type II respiratory failure is associated with hypercapnia and is characterized by a low Pao2 and high Paco2. These patients are unable to eliminate CO2 adequately. This condition is often associated with excessive narcotic use, increased CO2 produc­tion, altered respiratory dynamics, and adult respiratory distress syndrome (ARDS). The overall incidence of pulmonary compli­cations exceeds 25% in surgical patients. Of all postoperative deaths, 25% are caused by pulmonary complications, and pul­monary complications are associated with 25% of the other lethal complications. Thus, it is of critical importance that the surgeon anticipate and prevent the occurrence of serious respira­tory complications.

One of the most important elements of prophylaxis is careful preoperative screening of patients. Most patients have no pulmonary history and need no formal preoperative evaluation. However, all patients with a history of heavy smoking, main­tained on home oxygen, unable to walk one flight of stairs without severe respiratory compromise, previous history of major lung resection, and older patients who are malnourished must be carefully screened with pulmonary function tests. Sim­ilarly, patients managed by chronic bronchodilator therapy for asthma or other pulmonary conditions also need to be assessed carefully. Although there is some controversy about the value of perioperative assessment, most careful clinicians will study a

culture. Serial blood cultures and a transesophageal echocardio­gram are obtained in patients with S. aureus bacteremia and valvular heart disease, prosthetic valve, or new onset of murmur. Patients who continue to have fever, slow clinical progress, and no discernible external source may require computed tomogra­phy (CT) of the abdomen to look for an intra­abdominal source of infection.

Prevention of urinary tract infection starts with minimiz­ing the duration of catheterization and maintenance of a closed drainage system. When prolonged catheterization is required, changing the catheter before blockage occurs is rec­ommended because the catheter serves as a site for pathogens to create a biofilm. The efficacy of strategies to prevent or delay the formation of a biofilm, such as the use of silver alloy or impregnated catheters and the use of protamine sulfate and chlorhexidine in reducing catheter­related UTIs has yet to be established.15

On the other hand, most if not all CR­BSIs are preventable by adopting maximal barrier precautions and infection control practice during insertion. Educational programs that stress best practice that targets those placing the catheter and those respon­sible for maintenance of the catheter are important. Removal of catheters when they are not needed is paramount. On placing the catheter, there must be strict adherence to aseptic technique, the same as in the operating room—hand hygiene, skin antisep­sis, full barrier precaution and stopping insertion when breaks in sterile technique occur. The subclavian vein is preferable to jugular and femoral vein. Involvement of a catheter care team for proper catheter care after insertion has proven effective in reducing the incidence of CR­BSIs. Antiseptic­ and antibiotic­impregnated catheters decrease catheter colonization and CR­BSIs but their routine use is not recommended.

treatmentManagement of postoperative fevers is dictated by the results of a careful workup. Management of the elevated temperature itself is controversial. Although the fever may not be life­threatening, the patient is usually uncomfortable. Attempts to bring the temperature down with antipyretics are recom­mended. If pneumonia is suspected, empirical broad­spectrum antibiotic therapy is started and then altered according to culture results.

A UTI is treated with removal or replacement of the cath­eter with a new one. In systemically ill patients, broad­spectrum antibiotics are started, because most offending organisms exhibit resistance to several antibiotics, and then tailored according to culture and susceptibility results. In patients with asymptomatic bacteruria, antibiotics are recommended for immunocompro­mised patient, patients undergoing urologic surgery, implanta­tion of a prosthesis, or patients with infections caused by strains with a high incidence of bacteremia. Patients with candiduria are managed in a similar fashion. The availability of fluconazole, a less toxic antifungal than amphotericin B, however, has encour­aged clinicians to use it more frequently.

The treatment of CR­BSI entails removal of the catheter, with adjunctive antibiotic therapy. A nontunneled catheter can be easily removed after establishing an alternative venous access. Single­agent therapy is sufficient and usually involves vancomycin, linezolid, or empirical coverage of gram­negative bacilli and Candida spp. in patients with severe sepsis or immunosuppression. Treatment is continued for 10 to 14

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13-12  section ii  PerioPerative ManageMent

ventilator­associated pneumonia. Tubes traversing the aerodiges­tive tract serve as conduits for bacteria to migrate to the lower respiratory tract.16 The most common pathogens encountered in patients with hospital­acquired pneumonia depend on prior antibiotic therapy. In patients with early hospital­acquired pneu­monia and no prior antibiotic therapy, the most common organ­isms are Streptococcus pneumoniae (colonizes upper airway), Haemophilus influenzae, Enterobacteriaceae spp. (E. coli, Klebsi-ella spp., and Enterobacter spp.), and S. aureus (mostly MRSA). Patients with early hospital­acquired pneumonia and recent antibiotic therapy and those with late hospital­acquired pneu­monia also have gram­negative bacilli involved. The bacteria are occasionally resistant to first­generation cephalosporins. The organisms in patients with late­onset hospital­acquired pneumo­nia and prior history of antibiotics exhibit multidrug resistance (P. aeruginosa, Acinetobacter baumannii, and MRSA).

DiagnosisThe most common cause of a postoperative fever in the first 48 hours after the procedure is atelectasis. Patients present with a low­grade fever, malaise, and diminished breath sounds in the lower lung fields. Frequently, the patient is uncomfortable from the fever but has no other overt pulmonary symptoms. Atelec­tasis is so common postoperatively that a formal workup is not usually required. With the use of incentive spirometry, deep breathing, and coughing, most cases of atelectasis will resolve without any difficulty. However, if aggressive pulmonary toilet is not instituted or the patient refuses to participate, frank devel­opment of pneumonia is likely. The patient with pneumonia will have a high fever and occasional mental confusion, and produces a thick secretion with coughing, leukocytosis, and chest radio­graph that reveals infiltrates. If the patient is not expeditiously diagnosed and treated, this condition may rapidly progress to respiratory failure and require intubation. Concurrently with the initiation of aggressive pulmonary toilet, inducted sputum for culture and sensitivity should be sent immediately to the labora­tory. Quantitative cultures of the lower airways obtained by blind tracheobronchial aspiration, bronchoscopically guided sampling (bronchoalveolar lavage [BAL]), or protected specimen brush allow more targeted antibiotic therapy and, most impor­tantly, decrease antibiotic use. Although pneumonia acquired in the hospital accounts for only 5% of all patients, particularly in older patients, the process may rapidly progress to frank respira­tory failure requiring intubation.

treatmentTo prevent atelectasis and pneumonia, smokers are encouraged to stop smoking for at least 1 week before surgery and the treat­ment of patients with chronic obstructive pulmonary disease, asthma, and CHF is optimized. Adequate pain control and proper pulmonary hygiene are important in the postoperative period. A patient­controlled analgesia device seems to be associ­ated with better pulmonary toilet, as does the use of an epidural infusion catheter, particularly in patients with epigastric inci­sions. Encouraging the patient to use the incentive spirometer and cough while applying counterpressure with a pillow on the abdominal incision site is most helpful. Rarely, other modalities such as intermittent positive­pressure breathing and chest phys­iotherapy may be required. Patients on the ventilator are best kept in a semirecumbent position and subjected to proper oral hygiene. Chlorhexidine rinse or nasal gel has been shown to


high­risk pulmonary patient before making an operative deci­sion. The assessment may start with posteroanterior and lateral chest radiographs to evaluate the appearance of the lungs. It serves as a baseline if the patient should have problems postoperatively.

Similarly, a patient with polycythemia or chronic respira­tory acidosis warrants careful assessment. A room temperature arterial blood gas analysis is carried out in high­risk patients. Any patient with a Pao2 lower than 60 mm Hg is at increased risk. If the Paco2 is more than 45 to 50 mm Hg, perioperative morbidity might be anticipated. Spirometry is a simple test that high­risk patients undergo before surgery. Probably the most important parameter in spirometry is the forced expiratory volume in 1 second (FEV1). Studies have demonstrated that any patient with an FEV1 higher than 2 liters will probably not have serious pulmonary problems. Conversely, patients with an FEV1 lower than 50% of the predicted value will probably have exer­tional dyspnea. If bronchodilator therapy demonstrates an improvement in breathing patterns by 15% or more, broncho­dilation is considered. Consultation with the patient includes a discussion about cessation of cigarette smoking 48 hours before the operative procedure, as well as a careful discussion about the importance of pulmonary toilet after the operative procedure.

atelectasis and pneumoniaThe most common postoperative respiratory complication is atelectasis. As a result of the anesthetic, abdominal incision, and postoperative narcotics, the alveoli in the periphery collapse and a pulmonary shunt may occur. If appropriate attention is not directed to aggressive pulmonary toilet with the initial symp­toms, the alveoli remain collapsed and a buildup of secretions occurs and becomes secondarily infected with bacteria, resulting in pneumonia. The risk appears to be particularly high in patients who are heavy smokers, are obese, and have copious pulmonary secretions.

Pneumonia is the most common nosocomial infection occurring in hospitalized patients. Pneumonia occurring more than 48 hours after admission and without antecedent signs of infection is referred to as hospital­acquired pneumonia. Aspira­tion of oropharyngeal secretion is a significant contributing factor in its development. Extended intubation results in another subset of hospital­acquired pneumonia, ventilator­associated pneumonia—pneumonia occurring 48 hours after but within 72 hours of the initiation of ventilation. Health care–associated pneumonia refers to pneumonia occurring in patients who had been hospitalized in the last 90 days, patients in nursing facilities or frequenting a hemodialysis unit, and those who have received recent antibiotics, chemotherapy, or wound care. Although some consider hospital­acquired pneumonia and health care–associated pneumonia to be the same disease process, because both have the same prevalent organisms, the prognosis is differ­ent. Hospital­acquired pneumonia arising early (<5 days) has better prognosis than that arising late (>5 days). Numerous factors are associated with increased risk for pneumonia: depressed immune status, concomitant disease, poor nutritional status, increased length of hospital stay, smoking, increasing age, uremia, alcohol consumption, prior antibiotic therapy, presence of an endotracheal, nasogastric (NG), or enteric tube, and therapeutic proton pump inhibitor (PPI). Used to prevent stress ulceration, PPI increases colonization of the stomach with pathogenic bacteria that can increase the risk of

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gastroesophageal reflux, even with the absence of an NG tube, and have altered GI motility. Prophylactic histamine 2 (H2) receptor antagonists or PPIs that increase gastric pH and allow the gastric contents to become colonized by pathogenic organ­isms, tracheostomy, reintubation, and previous antibiotic expo­sure are other factors associated with an increased risk for health care–related pneumonia. The risk of aspiration is high after extubation because of the residual effect of sedation, the NG tube, and oropharyngeal dysfunction.

The pathophysiology of aspiration pneumonitis is related to the pulmonary intake of gastric contents at a low pH associ­ated with particulate matter. The severity of lung injury increases as the volume of aspirate increases and its pH decreases. The process often progresses rapidly, may require intubation soon after the injury occurs, and later sets the stage for bacterial infec­tion. The infection is refractory to management because of the combination of infection occurring in an injured field. The pathophysiology of aspiration pneumonia is related to bacteria gaining access to the lungs.

presentation and DiagnosisA patient with aspiration pneumonitis often has associated vom­iting and may have received general anesthesia or had an NG tube placed. The patient may be obtunded or have altered levels of consciousness. Initially, the patient may have associated wheezing and labored respiration. Many patients who aspirate gastric contents have a cough or a wheeze. Some patients, however, have silent aspiration suggested by an infiltrate on a chest radiograph (CXR) or decreased Pao2. Others have cough, shortness of breath, and wheezing that progress to pulmonary edema and ARDS. In the great majority of patients with aspira­tion pneumonia, on the other hand, in a susceptible patient, the condition is diagnosed after a chest radiograph shows an infil­trate in the posterior segments of the upper lobes and the apical segments of the lower lobes.

treatmentPrevention of aspiration in patients undergoing surgery is achieved by instituting measures that reduce gastric contents, minimize regurgitation, and protect the airway. For adults, a period of no oral intake, usually 6 hours after a night meal, 4 hours after clear liquids, and a longer period for diabetics, is necessary to reduce gastric contents before elective surgery.17 Routine use of H2 antagonists or PPIs to reduce gastric acidity and volume has not been shown to be effective in reducing the mortality and morbidity associated with aspiration and hence is not recommended. When a difficult airway is encountered, awake fiberoptic intubation is performed. In emergency situa­tions in patients with a potentially full stomach, preoxygenation is accomplished without lung inflation, and intubation is per­formed after applying cricoid pressure during rapid­sequence induction. In the postoperative period, identification of an older or overly sedated patient, or a patient whose condition is dete­riorating, mandates instituting maneuvers to protect the patient’s airway. Postoperatively, it is important to avoid the overuse of narcotics, encourage the patient to ambulate, and cautiously feed a patient who is obtunded, older, or debilitated.

A patient who sustains aspiration of gastric contents needs to be placed on oxygen immediately and have a chest radiograph to confirm the clinical suspicions. A diffuse interstitial pattern is usually seen bilaterally and is often described as bilateral, fluffy

lower the rate of ventilator­associated pneumonia. Treatment with sucralfate as compared with a PPI for stress ulcer prophy­laxis may be considered for patients not at high risk for GI bleeding. Proper endotracheal tube care, elimination of secre­tions pooling around the endotracheal cuff, frequent suctioning with a closed suction technique, and use of protocols designed to minimize mechanical ventilation can lead to decreased ventilator­associated pneumonia. Once the diagnosis is made, and while awaiting culture results, treatment with empirical antibiotic therapy is associated with decreased mortality. The choice of antimicrobial agent depends on the patient’s risk factors, length of hospital stay, duration of mechanical ventila­tion, prior antibiotic therapy and culture results, and immuno­suppression.

aspiration pneumonitis and aspiration pneumonia

CausesAspiration of oropharyngeal or gastric contents into the respira­tory tract is a serious complication of surgery. Aspiration pneu­monitis (Mendelson’s syndrome) describes acute lung injury that results from the inhalation of regurgitated gastric contents, whereas aspiration pneumonia results from the inhalation of oropharyngeal secretions that are colonized by pathogenic bac­teria. Although there is some overlap between the two disease entities with regard to predisposing factors, their clinicopatho­logic features are distinct.

Factors that predispose patients to regurgitation and aspira­tion include impairment of the esophageal sphincters (upper and lower) and laryngeal reflexes, altered GI motility, and absence of preoperative fasting. A number of iatrogenic maneuvers place the patient at increased risk for aspiration in a hospital setting. In the perioperative period, aspiration is more likely with urgent surgery, in patients with altered levels of consciousness, and in patients with GI and airway problems. Trauma patients and patients with peritonitis and bowel obstruction may have a depressed level of consciousness and airway reflexes, a full stomach as a result of a recent meal or gastric stasis, or GI pathol­ogy that predisposes to retrograde emptying of intestinal con­tents into the stomach. Patients with depressed levels of consciousness as a result of high doses of narcotics and patients who have suffered cerebrovascular accidents are obtunded and have neurologic dysphagia and dysfunction of the gastroesopha­geal junction. Anesthetic drugs lower esophageal sphincter tone and depress the patient’s level of consciousness. Diabetics have gastroparesis and gastric stasis. Patients with an increased bacte­rial load in the oropharynx and depressed defense mechanisms as a result of an altered level of consciousness are at risk for aspiration pneumonia.

Older adults are particularly susceptible to oropharyngeal aspiration because of an increased incidence of dysphagia and poor oral hygiene. Patients with a NG tube or who are debili­tated are also at risk for aspiration because they have difficulty swallowing and clearing their airway. The risk for aspiration pneumonia is similar in patients receiving feeding via an NG, nasoenteric, or gastrostomy tube; patients receiving nutrition via a gastrostomy tube frequently have scintigraphic evidence of aspiration of gastric contents. The critically ill are at an increased risk for aspiration and aspiration pneumonia because they are in a supine position, have an NG tube in place, exhibit

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13-14  section ii  PerioPerative ManageMent

common manifestations of such injury are pulmonary edema, acute lung injury, and ARDS. The clinician’s ability to recognize and distinguish among these conditions is of critical importance because clinical management of these three entities varies con­siderably.

Pulmonary edema is a condition associated with accumula­tion of fluid in the alveoli. As a result of the fluid in the lumen of the alveoli, oxygenation cannot take place and hypoxemia occurs. As a consequence, the patient must increase the work of breathing, including an increased respiratory rate and exagger­ated use of the muscles of breathing. Pulmonary edema is usually caused by increased vascular hydrostatic pressure associated with CHF and acute myocardial infarction (MI). It is also commonly associated with fluid overload as a result of overly aggressive resuscitation (Box 13­4).

A consensus conference has identified acute lung injury and ARDS as two separate grades of respiratory failure second­ary to injury. In contrast to pulmonary edema, which is associ­ated with increased wedge and right­sided heart pressure, acute lung injury and ARDS are associated with hypo­oxygenation because of a pathophysiologic inflammatory response that leads to the accumulation of fluid in the alveoli, as well as thickening in the space between the capillaries and the alveoli. Acute lung injury is associated with a Pao2/Fio2 (fraction of inspired oxygen) ratio of less than 300, bilateral infiltrates on chest radiography, and a wedge pressure less than 18 mm Hg. It tends to be shorter in duration and not as severe. On the other hand, ARDS is associated with a Pao2/Fio2 ratio of less than 200 and also has bilateral infiltrates and a wedge pressure less than 18 mm Hg.

presentation and managementPatients with pulmonary edema often have a corresponding cardiac history, recent history of massive fluid administration, or both. In the presence of a frankly abnormal chest radiograph, invasive monitoring in the form of a Swan­Ganz catheter for evaluation of pulmonary capillary wedge pressure may be indi­cated. Patients with an elevated wedge pressure are managed by fluid restriction and aggressive diuresis. Administration of oxygen via face mask in mild cases and intubation in more severe cases is also clinically indicated. In most cases, the pulmonary edema resolves quickly after diuresis and fluid restriction.

Patients with acute lung injury and ARDS generally have tachypnea, dyspnea, and increased work of breathing, as mani­fested by exaggerated use of the muscles of breathing. Cyanosis is associated with advanced hypoxia and is an emergency. Aus­cultation of the lung fields reveals poor breath sounds associated with crackles and, occasionally, with rales. Arterial blood gas analysis will reveal the presence of a low Pao2 and high Paco2. Administration of oxygen alone does not usually result in improvement in the hypoxia.

In patients with impending respiratory failure, including tachypnea, dyspnea, and air hunger, management of acute lung injury and ARDS is initiated by immediate intubation plus careful administration of fluids; invasive monitoring with a Swan­Ganz catheter to assess wedge pressure and right­sided heart pressure is occasionally helpful. The strategy involves maintaining the patient on the ventilator with assisted breathing while the injured lung heals. A patient with severe acute lung injury or ARDS is initially placed on an Fio2 of 100% and then weaned to 60% as healing takes place. Positive end­expiratory pressure is a valuable addition to ventilator management of


infiltrates. Close surveillance of the patient is absolutely essen­tial. If the patient is maintaining oxygen saturation via a face mask without excessively high work of breathing, intubation may not be required. However, if the patient’s oxygenation dete­riorates or the patient is obtunded, the work of breathing increases, as manifested by an increased respiratory rate, and prompt intubation must be accomplished. After intubation for suspected aspiration, suctioning the bronchopulmonary tree will confirm the diagnosis and remove any particulate matter. Administration of antibiotics shortly after aspiration is con­troversial, except in patients with bowel obstruction or other conditions associated with colonization of gastric contents. Administration of empirical antibiotics is also indicated for a patient with aspiration pneumonitis that does not resolve or improve within 48 hours of aspiration. Corticosteroid adminis­tration does not provide any beneficial effects to patients with aspiration pneumonitis. Antibiotic therapy with activity against gram­negative organisms is indicated for patients with aspiration pneumonia.

pulmonary edema, acute lung injury, and adult respiratory distress Syndrome

CausesA wide variety of injuries to the lungs or cardiovascular system, or both, may result in acute respiratory failure. Three of the most

Box 13-4  conditions Leading to pulmonary edema, acute Lung injury, and adult respiratory Distress syndrome

increased Hydrostatic pressureacute left ventricular failurechronic congestive heart failureobstruction of the left ventricular outflow tractthoracic lymphatic insufficiencyvolume overload

altered permeability Stateacute radiation pneumonitisaspiration of gastric contentsDrug overdosenear-drowningPancreatitisPneumoniaPulmonary embolusShock statesSystemic inflammatory response syndrome and multiple organ 

failureSepsistransfusiontrauma and burns

mixed or incompletely understood pathogenesisHanging injuriesHigh-altitude pulmonary edemanarcotic overdoseneurogenic pulmonary edemaPostextubation obstructive pulmonary edemareexpansion pulmonary edematocolytic therapyuremia

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long bones and air embolism, often related to operative proce­dures and the presence of central lines.

presentation and DiagnosisThe physiologic response to PE depends on the size of the thrombus, coexisting cardiopulmonary disease, and various neu­rohormonal effects. More than 50% of DVTs are silent and PE may be the first manifestation of the disease. Most symptoms and signs associated with symptomatic PE are nonspecific and may be encountered with other disease states, such as MI, pneu­mothorax, and pneumonia (Box 13­5). CXR has limited value in the diagnosis of PE and is mainly used to rule out other causes of a patient’s symptoms. Approximately 5% to 10% of patients develop a massive PE that results in hemodynamic instability (hypotension, with or without shock) and death. The

patients with this injury. Similarly, tidal volume needs to be 6 to 8 mL/kg, with peak pressure kept at 35 cm H2O. Tidal volume is set at 10 to 12 mL/kg of body weight and the respira­tory rate is chosen to produce a Paco2 near 40 mm Hg. In addition, the inspiratory­to­expiratory ratio is set at 1 : 2. Most patients will require heavy sedation and pharmacologic paralysis during the early phases of recuperation.

Careful monitoring of oxygenation, improvement of the respiratory rate with intermittent mandatory ventilation, and general alertness will suggest when the patient is ready to be extubated. Criteria for extubation are listed in Table 13­6.

pulmonary embolism and Venous thromboembolism

CausesVenous thromboembolism describes DVT and pulmonary embolism (PE). PE is a serious postoperative complication that represents a source of preventable morbidity and mortality in the United States and is responsible for 5% to 10% of all in­hospital deaths. Undiagnosed PE has a hospital mortality rate as high as 30%, which falls to 8% if diagnosed and treated appropriately.

Venous thromboembolism (VTE) is caused by a perturba­tion of the homeostatic coagulation system induced by intimal injury, stasis of blood flow, and a hypercoagulable state. Risk factors for the development of VTE are listed in Table 13­7.18

Thrombophilia describes hereditary and acquired biochem­ical states that predispose to VTE. One in four fatal PE cases occurs in surgical patients. Survivors of VTE are at increased risk for recurrence. The highest risk of VTE occurs in patients hospitalized for surgery. The prevalence of PE in patients with malignancy is 11%. The incidence of relative risk of DVT and PE in patients with inflammatory bowel disease is approximately 5% and 3%, respectively. In major trauma victims, the incidence of DVT exceeds 50%, with fatal emboli occurring in 0.4% to 2% of cases. Critically ill and intensive care unit patients have multiple risk factors and are also at higher risk for VTE. Central venous catheter–related thromboses are more common with femoral placement. Thrombosis ranges from 4% to 28% after subclavian vein cannulation and 4% to 33% after internal jugular catheterization. In patients with subclavian or axillary vein thrombosis, PE is reported in 9.4%.

Most PEs originate from an existing DVT in the legs, and the iliofemoral venous system represents the site from which most clinically significant pulmonary emboli arise. Approxi­mately 50% of patients with proximal DVT develop a PE. Rare causes of PE include a fat embolus associated with fractures of

Box 13-5  symptoms and signs of pulmonary embolism

Pleuritic chest pain*Sudden dyspnea*tachypneaHemoptysis*tachycardia*leg swelling*Pain on palpation of the leg*acute right ventricular dysfunctionHypoxiaFourth heart sound*loud second pulmonary sound*inspiratory crackles*

*More common with pulmonary embolism.

table 13-6  criteria for Weaning from the VentilatorparaMeter WeaninG criteria

respiratory rate <25 breaths/min

Pao2 >70 mm Hg (Fio2 of 40%)

Paco2 <45 mm Hg

Minute ventilation 8-9 liters/min

tidal volume 5-6 ml/kg

negative inspiratory force −25 cm H2o

table 13-7  risk Factors for Venous thromboembolismcateGorY Factors

general factors advancing ageHospitalization or nursing home (with or 

without surgery)indwelling venous cathetersneurologic disease (plegia and paresis)cardiomyopathy, myocardial infarction, or 

heart failure secondary to valve diseaseacute pulmonary disease (adult respiratory 

distress syndrome and pneumonia)chronic obstructive lung diseasevaricose veins

inherited thrombophilia Protein c deficiencyProtein S deficiencyantithrombin iii deficiencyDysfibrinogenemiaFactor v leiden mutationProthrombin gene mutationHyperhomocysteinemiaanticardiolipin antibodyParoxysmal nocturnal hemoglobinemia

acquired thrombophilia Malignancyinflammatory bowel diseaseHeparin-induced thrombocytopeniatraumaMajor surgeryPregnancy/postpartumnephrotic syndromeBehçet’s syndromeSystemic lupus erythematosusHistory of venous thromboembolism

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In critically ill patients with high suspicion for PE and patients with suspected massive PE, the workup depends on their hemodynamic stability. In stable patients, anticoagulation is started if there are no contraindications, VUS is performed, and a spiral CT scan is obtained urgently. In unstable patients, anticoagulation is started and VUS and echocardiography are performed. If the echocardiographic results are positive, throm­bolytic therapy is started and, if negative, a pulmonary angio­gram is obtained.

treatmentMedications used in the treatment of venous thromboembo­lism are the heparins, fondaparinux, VKAs, and thrombolytic agents. Heparin prevents the thrombin­mediated conversion of fibrinogen to fibrin and stops propagation of the thrombus. UFH is inexpensive and highly effective, enhances antithrom­botic activity of antithrombin III and factor Xa, and has a short plasma half­life. LMWH primarily inactivates factor Xa and has a longer half­life and more predictable anticoagulant prop­erty. VKAs (e.g., warfarin) have a delayed onset of action and the potential to interact with other medications. Fondaparinux is a synthetic pentasaccharide that selectively inhibits factor Xa. Thrombolytic agents (e.g., streptokinase, urokinase, recombi­nant tissue plasminogen activator) are used in the treatment of massive PE.

Treatment of PE starts with prevention. Because the great majority of PEs originates from existing clots in the deep venous system of the legs in at­risk patients, identifying patients at risk for DVT plus applying preventive measures is the only way to decrease VTE­related morbidity and mortality. The intensity of prophylaxis must match the risk for VTE and potential compli­cations of the medication (e.g., bleeding, heparin­induced thrombocytopenia [HITT]). According to the American College of Clinical Pharmacy (ACCP), assessment of patients into low­, moderate­ and high­risk categories for VTE is based on the type of surgery performed, patient mobility, risk of bleeding, and VTE risk based on the presence of additional risk factors.20 Age is a significant risk factor, with the risk doubling with each decade beyond the age of 40 years. Most hospitalized patients have at least one risk factor for VTE and approximately 50% of them have more than three risk factors. Pharmacologic prophy­laxis is an accepted and effective strategy.21 In the critically ill, heparin is first­line prophylaxis. Prophylaxis is achieved with the administration of low­dose UFH given SC every 8 hours or LMWH given as a daily dose. Recent studies have suggested that LMWH is more effective prophylaxis than low­dose UFH in the critically ill and is associated a with reduced risk of major hem­orrhage. Overt bleeding and thrombocytopenia are contraindi­cations to chemical prophylaxis. In patients undergoing surgery, LDUF is administered (5000 U, 3 to 4 hours preoperatively and then every 8 hours). Fondaparinux has emerged as an alternative prophylactic after major orthopedic surgery. Nonpharmacologic prophylaxis can be achieved with elastic stockings, graduated compression stockings, intermittent pneumatic compression devices, or venous foot pumps. Compression devices are not associated with bleeding. They produce a satisfactory reduction in risk for DVT in high­risk surgical patients. However, little is known about their efficacy as sole prophylaxis in the critically ill and they may be most beneficial in combination with phar­macologic prophylaxis in the subset of high­risk patients or solely in patients for whom the risk of bleeding is high. The



probability of an individual having PE (pretest probability) is assessed by the sum of points given to VTE risk factors: the patient’s symptoms, signs, and laboratory results (e.g., electrocar­diogram [ECG], CXR, and arterial blood gas) most likely to be associated with PE. Using various scoring systems, patients are stratified into low­, moderate­, and high­probability categories.

Establishing the diagnosis of PE requires confirmatory tests (helical CT scan and/or a pulmonary angiogram) and ancillary tests (venous duplex ultrasound [VUS] and a D­dimer assay). Helical CT, also known as spiral CT or CT pulmonary angiog­raphy, has high specificity (92%) and sensitivity (86%), espe­cially for central PE (main pulmonary artery or subsegmental branches) and has replaced the � �V/Q scan as the initial test of choice. In addition to the findings listed in Box 13­5, spiral CT also allows diagnosis of other pulmonary causes of a patient’s symptoms. The test, however, requires IV contrast, may not be available after normal working hours, requires a cooperative patient to avoid artifacts, may miss emboli in subsegmental arteries, which account for 20% of all pulmonary emboli, and may be inconclusive in approximately 10% of cases. Pulmonary angiogram is the gold standard test because it visualizes the arte­rial tree directly and detects intravascular filling defects. It is used less commonly, however, because it is invasive, requires expertise, and after­hours availability is limited.

Echocardiography is a rapid, noninvasive, available bedside test that provides quick results in a critically ill or hemodynamically unstable patient. Transthoracic echocardiog­raphy (TTE) shows the hemodynamic consequences of acute ventricular pressure overload—namely, right ventricle dysfunc­tion (hypokinesia and dilation), interventricular septal flatten­ing and paradoxical motion, elevated tricuspid gradient, pulmonary hypertension, and a patent foramen ovale.19 Dys­function of the right ventricle (RV) occurs in 30% to 50% of patients with PE who undergo echocardiography. The trans­esophageal echocardiogram also shows secondary changes in cardiac chamber size and functions caused by hemodynamic effects of the PE and may reveal a proximal intrapulmonary or free­floating intracardiac clot. Echocardiography also rules out other causes of shock such as a pericardial tamponade. Trans­esophageal echocardiography is not always available and requires specialty training.

VUS of the extremities is used as an indirect test for diagnosing PE. Approximately one third of patients with PE will demonstrate lower extremity findings consistent with DVT, and 80% of PE patients have a DVT on the venogram. D­dimer is a degradation product of a cross­linked fibrin blood clot. Levels are typically elevated in patients with acute thromboembolism. Of the many D­dimer tests, enzyme­linked immunosorbent assay (ELISA) is the most sensitive, with quick results. A negative test excludes the diagnosis, but a positive test does not rule in the diagnosis.

Based on the pretest clinical probability, a patient suspected of having PE requires a CXR, ECG, arterial blood gas (ABG) analysis, and D­dimer assay. If leg symptoms are present, VUS is performed and, if positive, the patient is considered to have PE and receives anticoagulant medication because treatment is similar to that for PE. If leg symptoms are absent, the spiral CT approach may be used. If the findings on spiral CT are subop­timal or negative and there is a high clinical probability of PE, an angiogram is obtained. This approach is not appropriate for patients with iodinated dye allergy.


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and intra­abdominal procedures are most commonly associated with hypertensive events. Preoperatively, most hypertension is essential hypertension; much less common are cases associated with renovascular causes and, even rarer, vasoactive tumors. Intraoperatively, fluid overload and pharmacologic agents may cause hypertension. Postoperatively, a host of causative factors are associated with hypertension, including pain, hypothermia, hypoxia, fluid overload in the postanesthesia period caused by fluid mobilization from the extravascular compartment, and discontinuation of chronic antihypertensive therapy before surgery. Other causes of postoperative hypertension include intra­abdominal bleeding, head trauma, clonidine withdrawal syndrome, and pheochromocytoma crisis.

presentation and managementMost cases of hypertension are detected during the routine pre­operative workup. The observant surgeon will consider hyper­tension in the preoperative screening of patients, recognizing that failure to detect significant problems with hypertension can lead to needless hypertension­related complications. By defini­tion, any patient who has a diastolic blood pressure higher than 110 mm Hg must be assessed and treated preoperatively if elec­tive surgery is being contemplated. Patients taking chronic anti­hypertensive medications who are undergoing elective surgery are instructed to continue taking the medication up to the day of surgery. Patients receiving oral clonidine can be switched to a clonidine patch for at least 3 days before surgery. In emergency cases, the medications administered during induction and main­tenance of anesthesia will assist in bringing the blood pressure down. Intraoperatively, the anesthesiologist must carefully monitor blood pressure, make certain that it stays within accept­able limits, and avoid fluid overload, hypoxia, and hypothermia. In the postoperative period, the patient is given adequate analge­sia for pain control and long­term antihypertensive medications are resumed. In patients who are not able to take oral medica­tions, beta blockers, angiotensin­converting enzyme (ACE) inhibitors, calcium channel antagonists, or diuretics are given parenterally or clonidine is administered as a transdermal patch.

Although hypertension in the postoperative period is common, a hypertensive crisis is uncommon, especially after noncardiac surgery. A hypertensive crisis is characterized by severe elevation of blood pressure associated with organ dysfunction—cerebral and subarachnoid hemorrhage and stroke, acute cardiac events, renal dysfunction, and bleeding from the operative wound. This particularly appears to be the case in carotid endarterectomy, aortic aneurysm surgery, and many head and neck procedures. Diastolic hypertension (>110 mm Hg) is significantly associated with cardiac complica­tions and systolic hypertension (>160 mm Hg) is associated with an increased risk for stroke and death. In patients with new­onset or severe perioperative hypertension and patients with a hypertensive emergency, treatment with agents that have a rapid onset of action, short half­life, and few autonomic side effects to lower blood pressure is essential. Medications most commonly used in this setting include nitroprusside and nitro­glycerin (vasodilators), labetalol and esmolol (beta blockers), enalaprilat (useful for patients receiving long­term ACE inhibi­tors), and nicardipine (calcium channel blocker). It is crucial in the acute setting not to decrease blood pressure more than 25% to avoid ischemic strokes and hypoperfusion injury to other organs.

presence of leg ulcers and peripheral vascular disease precludes the use of mechanical devices.

Anticoagulation is the standard of care treatment for VTE. It prevents clot propagation and allows endogenous fibrinolytic activity to dissolve existing thrombi, a process that occurs over weeks and months. Incomplete resolution is not uncommon and predisposes to recurrent VTE. The initial treatment is with LMWH, UFH, or fondaparinux, followed by VKA, which is administered on the same day as LMWH or UFH, with overlap for 5 days or longer until the target INR is achieved. In patients with VTE and active cancer, anticoagulation is continued indef­initely. Surgical patients within 24 hours of surgery may be considered for a retrievable inferior vena cava filter until antico­agulation is initiated. In patients with a contraindication to anticoagulation, placement of an inferior vena cava filter pro­tects against PE.

UFH is given intravenously (a weight­adjusted bolus of 70 U/kg is followed by 1000 U/hr) to achieve a partial throm­boplastin time 1.5 to 2 times the control value. aPTT is deter­mined 6 hours after the loading dose and then on a daily basis, and the dose of heparin is adjusted accordingly. UFH is easily reversible and hence the agent of choice. LMWH is given SC once or twice daily (enoxaparin, 1.5 mg/kg/day, or dalteparin, 10,000 to 18,000 U/day, depending on weight). Monitoring of LMWH is not necessary. Both UFH and LMWH may be asso­ciated with HITT, and therefore the platelet count is monitored between days 3 and 5. Warfarin is given orally and this therapy is allowed to overlap with heparin therapy until the INR is therapeutic for 2 consecutive days before heparin is discontin­ued. Therapy is continued for more than 3 months, with the goal to reach an INR of 2.5.

In massive PE, the goal of therapy is to maintain hemody­namic stability, enhance coronary flow, and minimize right ven­tricular ischemia. Once suspected, resuscitation is initiated, oxygen administered, and IV UFH therapy started. In the hemodynamically unstable, IV vasoactive medications are required. Thrombolytic therapy, if not contraindicated, has the advantage of dissolving the clot rapidly, with rapid improvement in pulmonary perfusion, hemodynamic alterations, gas exchange, and right ventricular function. The role of surgical embolectomy is controversial. The transcatheter technique (with or without low­dose thrombolytic therapy) is another therapeutic approach. Placement of an inferior vena cava filter reduces the risk for recurrence of PE.

Novel anticoagulants under investigation include factor Xa inhibitors (direct inhibitor [hypermethylated derivative of fondaparinux with a long half­life given IV or SC] or indirect inhibitor mediated by antithrombin [given orally or parenter­ally]) and direct thrombin inhibitors.

cardiac complicationS

postoperative Hypertension

CausesHypertension is a serious problem that can cause devastating complications in the preoperative, intraoperative, and postop­erative periods. Perioperative hypertension (or hypotension) occurs in 25% of patients undergoing surgery. The risk of hyper­tension is related to the type of surgery performed and the presence of perioperative hypertension. Cardiovascular, thoracic,


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respiratory failure), increased heart rate (arrhythmias), change in mental status, or excessive hyperglycemia in diabetics. Many perioperative MIs are non–Q wave NSTEMI. Periprocedural MI is associated with the release of biomarkers of necrosis, such as MB isoenzymes of creatinine kinase (CK­MB) and troponins, into the circulation. The troponin complex consists of three subunits, T (TnT), I (TnI), and C (TnC). TnT and TnI are derived from heart­specific genes and are referred to as cardiac troponins (cTns). cTns are not present in healthy individuals; their early release is attributable to the cytosolic pool and late release to the structural pool.

Patients considered to have acute coronary syndrome should have a 12­lead ECG and placed in an environment with continuous electrocardiographic monitoring and defibrillator capability. Biomarkers of myocardial necrosis are measured. CK­MB has a short half­life and is less sensitive and less specific than cTns. Troponins can be detected in blood as early as 2 to 4 hours but elevation may be delayed for up to 8 to 12 hours. The timing of elevation of cTns is similar to CK­MB but cTns persist longer, for up to 5 to 14 days. Elevated cTn levels above the 99th percentile of normal in two or more blood samples collected at least 6 hours apart indicates the presence of myo­cardial necrosis. Equivalent information is obtained with cTnI and cTnT, except in patients with renal dysfunction, in whom cTnI has a specific role. Each patient should have a provisional diagnosis of acute coronary syndrome with UA (electrocardio­graphic changes of ischemia and no biomarkers in the circula­tion), STEMI, or NSTEMI. The distinction has therapeutic implications because patients with STEMI may be considered for immediate reperfusion therapy (fibrinolysis or percutaneous intervention).22

treatmentPreventing coronary ischemia is a function of identifying patients prospectively at risk for a perioperative cardiac complication. This will allow improvement of the condition of the patient, possibly lowering the risk, selection of patients for invasive or noninvasive cardiac testing, and identifying patients who will benefit from more intensive perioperative monitoring. Preop­erative cardiac risk assessment includes adequate history taking, physical examination, and basic diagnostic tests. The history is important to identify patients with cardiac disease or those at risk for cardiac disease, including previous cardiac revasculariza­tion, history of MI or stroke, and presence of valvular heart disease, heart failure, arrhythmia, hypertension, diabetes, lung disease, and renal disease. Unstable chest pain, especially cre­scendo angina, warrants careful evaluation and probable post­poning of an elective operation. Physical examination may reveal uncontrolled hypertension, evidence of peripheral artery disease, arrhythmia, or clinical stigmata of heart failure (HF). The CXR may show pulmonary edema, ECG may show an arrhythmia, blood gas analysis may reveal hypercapnia or a low Pao2, and blood tests may show abnormal kidney function. The patient who is found to have HF on physical examination or by history must have the problem treated before consideration for an elec­tive operative procedure. Guidelines for Perioperative Cardiovas-cular Evaluation for Noncardiac Surgery, published by the American College of Cardiology (ACA) and American Heart Association (AHA), have stratified clinical predictors of increased perioperative cardiovascular risk leading to MI, CHF, or death into major, intermediate, and minor risks (Table 13­8) and

perioperative ischemia and infarction

CauseApproximately 30% of all patients taken to the operating room have some degree of CAD. Older patients, patients with periph­eral artery disease, and those undergoing vascular, thoracic, major orthopedic, or upper abdominal procedures are at high risk for an acute coronary syndrome in the postoperative period. Major risk factors for developing CHD are smoking, family history, adverse lipid profiles, diabetes mellitus, and elevated blood pressure.22 Although management of nonoperative MI has improved, the mortality associated with perioperative MI remains approximately 30%. Perioperative myocardial compli­cations result in at least 10% of all perioperative deaths. In the 1970s, the risk for recurrence of MI within 3 months of an MI was reported to be 30% and, if a patient underwent surgery within 3 to 6 months of infarction, the reinfarction rate was 15%; 6 months postoperatively the reinfarction rate was only 5%. However, improved preoperative assessment, advances in anesthesia and intraoperative monitoring, and the availability of more sophisticated intensive care unit monitoring have resulted in improvement in the outcome of patients at risk for an acute cardiac event. Individuals undergoing an operation within 3 months of an infarction have an 8% to 15% reinfarction rate; between 3 and 6 months postoperatively, the reinfarction rate is only 3.5%. The general mortality associated with MI in patients without a surgical procedure is 12%.

Myocardial ischemia and MI result from the imbalance between myocardial oxygen supply and demand. Primary causes that reduce myocardial perfusion and therefore oxygen supply include coronary artery narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque, dynamic obstruction caused by spasm of an epicardial coronary artery or diseased blood vessel, and severe narrowing caused by progres­sive atherosclerosis. Secondary causes that increase myocardial oxygen requirements, usually in the presence of a fixed restricted oxygen supply (limited myocardial perfusion), are extrinsic cardiac factors that include fever and tachycardia (increased myocardial oxygen demand), hypotension (reduced coronary blood flow), and anemia and hypoxemia (reduced myocardial oxygen delivery). The increased circulating catecholamines asso­ciated with surgical stress further increase myocardial oxygen demand.

presentation and DiagnosisAcute coronary syndrome refers to a constellation of clinical symptoms that are compatible with myocardial ischemia and encompasses MI: ST­segment elevation myocardial infarction (STEMI) and depression (Q wave and non–Q wave), and unsta­ble angina (UA)/non–ST­segment elevation myocardial infarc­tion (NSTEMI). UA/NSTEMI is defined as ST­segment depression or prominent T wave inversion and/or positive bio­markers of myonecrosis in the absence of ST­segment elevation and in an appropriate clinical setting. The risk for myocardial ischemia and MI is greatest in the first 48 hours after surgery, and it may be difficult to make the diagnosis. The classic mani­festation, chest pain radiating into the jaw and left arm region, is often not present. Patients may have shortness of breath, increased heart rate, hypotension, or respiratory failure. Periop­erative myocardial ischemia and MI are often silent and, when they occur, are marked by shortness of breath (heart failure,


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stratified cardiac risk into high, intermediate, and low (Table 13­9).21

The ACC/AHA guidelines permit more appropriate use of preoperative testing (echocardiography, dipyridamole myocar­dial stress perfusion imaging, traditional exercise stress test, or angiography) and beta blocker therapy, with probable cancella­tion of the elective operative procedure.23 An algorithm for perioperative cardiovascular evaluation is presented in Figure 13­1. The role of preoperative coronary artery revascularization has yet to be determined. Percutaneous transluminal coronary angioplasty may be beneficial in reducing perioperative cardiac morbidity in a select group of patients.

Patients identified as being at high risk for myocardial events in the perioperative period are managed with beta blockers, careful intraoperative monitoring, maintenance of perioperative normothermia and vital signs, and continued post­operative pharmacologic management, including the adminis­tration of adequate pain medication. Given several days before surgery and continued for several days afterward, beta blockers (e.g., atenolol) have been shown to reduce perioperative myo­cardial ischemia by 50% in patients with CAD or CAD risk factors.24 Patients with chronic stable angina continue with their antianginal medications, and beta blockers are continued to the time of surgery and thereafter. An ECG is obtained before, immediately after, and for 2 days after surgery. Patients are monitored for 48 hours, and in high­risk patients for 5 days, after surgery and cardiac enzyme levels are also checked. Invasive hemodynamic monitoring is appropriate for patients with left ventricular dysfunction, fixed cardiac output, and unstable angina or recent MI.

Shortness of breath and chest pain remain the two postop­erative symptoms that must always be carefully evaluated and never written off as postoperative discomfort. Subtle changes in the ST segment and T wave hint of possible ischemia or MI. Evaluation of a patient suspected of having an intraoperative or postoperative MI includes immediate assessment by electrocar­diography and measurement of biomarkers of myocardial necro­sis. Constant electrocardiographic monitoring is required so that the development of any potentially lethal arrhythmia can imme­diately be treated. If the level of cardiac function is a concern, echocardiography is considered. Cardiac troponin levels identify patients with myocardial necrosis but do not identify the cause of necrosis. Cardiac­specific troponin levels begin to rise by 3 hours after myocardial injury. A troponin I level more than 1 ng/mL is specific, and elevations persist for 7 to 10 days. Troponin T elevations persist for 10 to 14 days after MI. Medical manage­ment of myocardial ischemia and MI includes immediate administration of high­flow oxygen, transfer to the intensive care unit, and early involvement of a cardiologist.

The goal of management of myocardial ischemia is to pre­serve the maximal amount of myocardial muscle possible, as well as improve coronary blood flow and decrease myocardial work. Immediate administration of beta blockers (oral or IV, dose­titrated to decrease heart rate to less than 70 beats/min) and aspirin (160 to 325 mg) is essential. Beta blockers are not indi­cated for patients with bradycardia, hypotension, severe left ventricular dysfunction, heart block, or severe bronchospastic disease. Nitroglycerin (given as a continuous IV infusion after a loading dose) alleviates pain and is beneficial for patients with MI complicated by HF or pulmonary edema. Systemic heparin­ization (or SC LMWH), if not contraindicated, is administered. In most cases, thrombolytic therapy is contraindicated in the postoperative period and can be used only in the situation in which minor surgery is performed. Studies have shown that emergency stricture dilation and coronary artery stenting may be more effective than thrombolytic therapy. ACE inhibitors may be given early after MI, especially anterior MI or with a


table  13-8  clinical  predictors  of  increased  perioperative  cardiovascular risk Leading  to Myocardial  infarction, heart Failure, or DeathLeVeL oF risK risK Factor

Major unstable coronary syndromes  acute or recent Mi with evidence of 

considerable ischemic risk as noted by clinical symptoms or noninvasive studies

  unstable or severe angina (canadian class iii  or iv)

Decompensated heart failureSignificant arrhythmias  High-grade atrioventricular block  Symptomatic ventricular arrhythmias in the 

presence of underlying heart disease  Supraventricular arrhythmias with an 

uncontrolled ventricular rateSevere valve disease

intermediate Mild angina pectoris (canadian class i or ii)Previous Mi identified by history or pathologic 

evidenceQ wavescompensated or previous heart failureDiabetes mellitus (particularly insulin dependent)renal insufficiency

Minor advanced ageabnormal electrocardiogram (e.g., left ventricular 

hypertrophy, left bundle branch block, St-t abnormalities)

rhythm other than sinus (e.g., atrial fibrillation)low functional capacity (e.g., inability to climb one 

flight of stairs with a bag of groceries)History of strokeuncontrolled systemic hypertension

From eagle Ka, Berger pB, Calkins h, et al: aCC/aha Guideline Update for peri-operative Cardiovascular evaluation for Noncardiac Surgery—executive Summary. a report of the american College of Cardiology/american heart association task Force on practice Guidelines (Committee to Update the 1996 Guidelines on peri-operative Cardiovascular evaluation for Noncardiac Surgery). anesth analg 94:1052-1064, 2002.

table 13-9  cardiac risk stratification for noncardiac surgical proceduresLeVeL oF risK risK Factor

High (cardiac risk often >5%)

emergency major operations, particularly in the elderly

aortic and other major vascular surgeryPeripheral vascular surgeryanticipated prolonged surgical procedures 

associated with large fluid shifts and blood loss

intermediate (cardiac risk generally <5%)

carotid endarterectomyintraperitoneal and intrathoracic surgeryorthopedic surgeryProstate surgery

low (cardiac risk generally <1%)

endoscopic proceduresSuperficial procedurescataract surgeryBreast surgery

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Other serious sequelae from acute MI include CHF, arrhyth­mias, and thromboembolic complications.

presentation and managementObservant physicians will watch a patient with an acute MI closely for evidence of the aforementioned complications. Car­diogenic shock usually develops rapidly over a short period and is marked by hypotension and respiratory failure. Aggressive management is required to save the life of a patient with this devastating condition. Immediate institution of mechanical ven­tilation with a high Fio2, and occasional monitoring with a Swan­Ganz catheter, is important. For patients who do not respond to pharmacologic and conservative management, intra­aortic balloon pumps and ventricular assist devices may be life­saving. For patients who have adequate myocardial reserve, coronary artery bypass may occasionally be indicated. Cardiac transplantation remains the gold standard treatment of end­stage HF.

low left ventricular ejection fraction, and probably continued as a long­term therapy. Angiography must be strongly considered if the patient has ongoing myocardial ischemia that does not respond to pharmacologic therapy.

cardiogenic Shock

CausesCardiogenic shock is one of the most serious sequelae of acute MI. Presumably, 50% or more of left ventricular muscle mass is irreversibly damaged, leading to a substantial reduction in cardiac output and resulting hypoperfusion. Other possible, less frequent causes of cardiogenic shock include ruptured papillary muscle or ventricular wall, aortic valvular insufficiency, mitral regurgitation, and ventricular septal defect. Cardiogenic shock is a highly lethal condition that results in the death of up to 75% of patients unless immediate management is instituted.

Figure 13-1  algorithm for perioperative cardiovascular evaluation for noncardiac surgery. Patients with major predictors of risk and patients with  intermediate predictors of  risk and a planned high-risk procedure undergo additional  testing and  resultant  indicated  treatment before elective surgery. CHF, congestive heart failure; MI, myocardial infarction. (adapted from eagle Ka, Brundage BH, chaitman Br, et al: guidelines for perioperative cardiovascular evaluation for noncardiac surgery. report of  the american college of cardiology/american Heart association task Force on Practice guidelines. J am coll cardiol 27: 910-945, 1996.)


No furthertesting

No furthertesting

Surgery Risk levelof surgery

High risk Intermediaterisk

Evaluation andtreatment beforeelective surgery

Major predictors of risk(unstable chest pain, CHF,symptomatic arrhythmias,

severe valvular disease)

Intermediate predictors of riskwith good to excellent function(prior MI, stable angina,compensated CHF)






Detailed risk assessmentdeferred to post-op period

Cardiacvascularizationin last 5 years

Risk factors andno recent cardiac


Cardiac evaluationin last 2 years, asymptomaticand stable

Elective or urgent


of risk

Proposed surgery

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rate are indicated in the treatment of arrhythmias that traverse the node and dangerous in those that do not. Beta blockers are avoided in patients with a low ejection fraction and bron­chospastic lung disease. The ultimate goal of therapy is to achieve sinus rhythm and, if not possible, prevention of com­plications associated with arrhythmias must be addressed (e.g., anticoagulants given to patients with atrial fibrillation for more than 48 hours). The management of postoperative arrhythmias is outlined in Box 13­6.

postoperative Heart Failure

CausesHeart failure is a clinical syndrome characterized by any struc­tural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.25 Several risk factors predispose to the development of heart failure, the most sig­nificant of which are CAD, hypertension, and increasing age. Poorly controlled heart failure represents one of the most serious cardiac risk factors for a preoperative patient, whereas patients with well­managed heart failure generally do well during an operation. Many factors can lead to new­onset heart failure or decompensation of preexisting heart failure in the perioperative period, including perioperative myocardial ischemia or MI, volume overload, hypertension, sepsis, occult cardiac valvular disease, PE, and new­onset atrial fibrillation. The risk for heart failure is greatest immediately after surgery and in the first 24 to 48 hours after surgery.

postoperative cardiac arrhythmias

CausesCardiac arrhythmias are common in the postoperative period and are more likely to occur in patients with structural heart disease. Cardiac arrhythmias are classified into tachyarrhyth­mia, bradyarrhythmia, and heart block. Tachyarrhythmia is further subdivided into supraventricular (sinus, atrial, nodal) and ventricular (premature ventricular contraction [PVC], ventricular tachycardia, ventricular fibrillation). Sustained supraventricular arrhythmia in patients undergoing major noncardiac surgery may be associated with an increased risk for a cardiac event (e.g., heart failure, MI, unstable angina) and cerebrovascular event.24 Factors associated with increased risk for supraventricular arrhythmias are increasing age, history of heart failure, and type of surgery performed. Sinus tachy­cardia and atrial flutter or fibrillation are the most common types of tachyarrhythmia. Sinus tachycardia is caused by pain, fever, hypovolemia, anemia, anxiety and, less commonly, heart failure, MI, thyrotoxicosis, and pheochromocytoma. Atrial flutter or fibrillation occurs commonly in patients with elec­trolyte imbalance, history of atrial fibrillation, and chronic obstructive lung disease.

Ventricular ectopy occurs in one third of patients after major noncardiac surgery and risk factors associated with an increased risk for PVCs include the presence of preoperative PVCs, history of CHF, and cigarette smoking. Postoperative risk factors include hypoxia, acute hypokalemia, and hypercapnia. Ventricular arrhythmias consist of largely benign and sustained ventricular tachycardia and fibrillation. Nonsustained ventricu­lar tachycardia commonly occurs during or after major vascular procedures.

presentationThe physiologic impact of an arrhythmia depends on its type and duration and the patient’s underlying cardiac status and ventricular response. Most arrhythmias are transient and benign and are not associated with symptoms or physiologic changes. Occasionally, sinus tachycardia may precipitate isch­emia and PVCs, and unsustained ventricular tachycardia may precipitate ventricular tachycardia. Arrhythmias may also rep­resent a prelude to hemodynamic compromise, especially in patients with severe heart disease or a history of MI or cardiomyopathy. Both bradyarrhythmia and tachyarrhythmia may decrease cardiac output. Symptoms associated with arrhythmias include palpitations, chest pain, shortness of breath, dizziness, loss of consciousness, cardiac ischemia, and hypotension.

treatmentThe patient’s underlying cardiac status is the key to manage­ment of arrhythmias. Arrhythmias may signal the presence of reversible causes or precipitating factors that must be sought and dealt with, and treatment is based on the presence of adverse hemodynamic effects of the arrhythmia, not its mere presence. In tachyarrhythmia, control of the ventricular response is essential, and distinction between arrhythmias that traverse the atrioventricular node (atrial fibrillation, ectopic atrial tachycardia) from those that do not (ventricular tachy­cardia, fibrillation) is paramount. Antiarrhythmics that alter atrioventricular node conduction and control the ventricular

Box 13-6  Management of postoperative cardiac arrhythmias

cardiology consultationMonitoring of the patient on a telemetry floor or in the intensive 

care unit12-lead ecg and long strip to differentiate between atrial and 

ventricular arrhythmiaclinical assessment• vital signs• Peripheral perfusion• cardiac ischemia and congestive heart failure• level of consciousness

treatment of arrhythmia• tachyarrhythmia

• unstable: cardioversion• Stable

Supraventricular  tachyarrhythmia:  Beta  blockers (esmolol),  ibutilide,  or  alternatives  (e.g.,  digoxin, calcium channel blockers, amiodarone)

Paroxysmal  supraventricular  tachyarrhythmia:  vagal stimulation or adenosine. Digoxin, amiodarone, or calcium channel blocker if adenosine fails

Multifocal  atrial  tachycardia:  Beta  blocker,  calcium channel blocker, or amiodarone

ventricular  tachycardia:  lidocaine,  procainamide,  or amiodarone

• Bradyarrhythmia• Sustained: atropine or β-adrenergic agonist• transient: no therapy

• Heart  block:  Persistent  high-grade  second-  or  third-degree block; insertion of a permanent pacemaker

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management of pain, including operative injection of local anes­thetics, may also diminish the incidence of urinary retention. Judicious administration of IV fluids during the procedure and in the immediate postoperative period, especially in patients who have undergone anorectal surgery for benign disease, may similarly diminish the likelihood of postoperative urinary reten­tion. Furthermore, awareness how much time has passed since the last voiding to the present time is crucial in preventing acute retention. Most patients should not go more than 6 to 7 hours without passing some urine, and an observant clinician will make certain that no patient goes longer than that before under­going straight catheterization.

General management principles for acute urinary retention include initial straight catheterization or placement of a Foley catheter, especially in older patients and patients who have undergone anterior resection because they may be unable to sense the fullness associated with retention. In high­risk patients, cystoscopy and cystometry may be required.

acute renal Failure

CausesAcute renal failure (ARF) is characterized by a sudden reduc­tion in renal output that results in the systemic accumulation of nitrogenous wastes. This hospital­acquired renal insuffi­ciency is more prevalent after major vascular procedures (rup­tured aneurysm), renal transplantation, cardiopulmonary bypass procedures, major abdominal cases associated with septic shock, and major urologic operations. It may also occur in procedures in which there is major blood loss, with transfu­sion reactions, in serious diabetics undergoing operations, in life­threatening trauma, with major burn injuries, and in mul­tiple organ system failure. Hospital­acquired renal insuffi­ciency adversely affects surgical outcomes and is associated with significant mortality, especially when dialysis is required. Two types of ARF have been identified, oliguric and nonoligu­ric. Oliguric renal failure refers to urine in which volumes less than 480 mL are seen in a day. Nonoliguric renal failure involves output exceeding 2 liters/day and is associated with large amounts of isosthenuric urine that clears no toxins from the bloodstream. Factors leading to ARF can be inflow, paren­chymal, or outflow, historically referred to as prerenal, renal, or postrenal, respectively (Table 13­10).

In normal kidneys, effective perfusion of the glomeruli is maintained by an autoregulatory mechanism involving the affer­ent and efferent arterioles. Any factor that interferes with or disrupts this mechanism results in ARF. Afferent constriction or efferent dilation decreases the glomerular filtration rate. Inflow, or prerenal, failure is secondary to hypotension, which causes afferent arteriolar constriction and efferent dilation, nonsteroidal anti­inflammatory drugs (NSAIDs), which inhibit afferent vaso­dilation, and gram­negative sepsis, which causes decreased peripheral vascular resistance while increasing renal vasocon­striction. Renal vascular stenosis and thrombosis can also be causes, although these are much less common. Outflow, or postrenal, ARF is caused by tubular obstruction from debris, crystals, or pigments, ureteric obstruction, or urinary bladder outflow obstruction. Ischemia, toxins, or nephritis cause paren­chymal ARF.

The incidence of contrast­induced nephropathy has been increasing. Tubular damage can occur within 48 hours of dye

presentationPatients with poorly controlled heart failure or new­onset heart failure suffer from shortness of breath and wheezing. Physical examination often reveals tachycardia, a narrow pulse pressure, low pressure or orthostatic hypotension, jugular venous disten­tion, peripheral edema, rales, and general evidence of poor peripheral perfusion. The ECG may reveal an MI, ventricular hypertrophy, atrial enlargement, or arrhythmias. A CXR may indicate cardiomegaly, pulmonary edema, and pleural effusion. Echocardiography assesses ventricular function and provides information about regional wall motion and valve function.

treatmentManagement of patients with heart failure is directed at optimiz­ing preload, afterload, and myocardial contractility. Afterload reduction is accomplished by lowering the vascular resistance against which the heart must contract, and ACE inhibitors are a cornerstone of therapy for heart failure. Nitrates (venodilator) and hydralazine (vasodilator) reduce excessive preload and are used as an alternative in patients who cannot tolerate ACE inhibitors. β­Adrenergic blockade (selective or nonselective) for heart failure has proved effective in reducing mortality in patients with ischemic and nonischemic heart failure.26 Digoxin (a sym­patholytic agent) has traditionally been used for patients with heart failure in sinus rhythm. Its use has decreased given the superior and definitive beneficial effects of ACE inhibitors and beta blockers. Diuretics are necessary in all patients with heart failure for the management of volume overload and relief of symptoms of congestion. Calcium channel blockers are used only for the treatment of hypertension or angina not adequately controlled with other agents, such as ACE inhibitors or beta blockers. Inotropes increase cardiac contractility and are used in the critically ill and patients with end­stage heart failure.

renal and urinary tract complicationS

urinary retention

CausesThe inability to evacuate a urine­filled bladder is referred to as urinary retention. This is a common postoperative complication seen with particularly high frequency in patients undergoing perianal operations and hernia repair. Urinary retention may also occur after surgery for low rectal cancer when an injury to the nervous system affects bladder function. Most commonly, however, the complication is a reversible abnormality resulting from discoordination of the trigone and detrusor muscles as a result of increased pain and postoperative discomfort. Urinary retention is also occasionally seen after spinal procedures and may occur after overly vigorous IV administration of fluid. Benign prostatic hypertrophy and, rarely, a urethral stricture may also be the cause of urinary retention.

presentation and managementPatients with postoperative urinary retention will complain of a dull constant discomfort in the hypogastrium. Urgency and actual pain in this area occur as the retention worsens. Percus­sion just above the pubis reveals fullness and tenderness.

To prevent urinary retention, the population at greatest concern, older adults and patients who have undergone low anterior resection, must be watched carefully. Adequate

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tcomplicated. Careful history taking may identify patients with preexisting renal dysfunction. Patients with large fluid losses from the GI tract (e.g., diarrhea, vomiting, fistula, high ileos­tomy output) often have associated profound dehydration. In such cases, the rise in the blood urea nitrogen (BUN) level is usually more than the rise in the creatinine level and the ratio of BUN to creatinine is more than 20. On the other hand, examination of the patient may reveal distended neck veins, rales in the lungs, and a cardiac gallop—all signs that a failing heart may be underperfusing the kidneys as the cause of the oliguria. Brown urine in the Foley bag in a trauma patient raises suspicion of myoglobinuria and requires rapid hydration, diuresis, and alkalinization of the urine. Evaluation of spun urine is helpful. The presence of hyaline casts indicates hypoperfusion and the presence of coarse granular casts indicates acute tubular necrosis. Lipoid casts are found with NSAID­ and contrast­induced nephropathy and white and red cell casts are found with pyelo­nephritis. In patients with prerenal azotemia, the concentrating ability of the nephrons is normal, thereby resulting in normal urine osmolality and fractional excretion of sodium (>50 mOsm/liter and FENa <1%, respectively). Conversely, with acute tubular necrosis, the concentrating ability of the kidney is lost and the patient produces urine with an osmolality equal to that of serum and high urine sodium levels (350 mOsm and >50 mOsm/liter, respectively; Table 13­11). The best laboratory test for discrimi­nating prerenal from renal azotemia is probably FENa. In prer­enal patients, FENa is 1% or less, whereas in renal azotemia patients it often exceeds 3%.

Once ARF is diagnosed, one has to ascertain whether the hypoperfusion of the kidney is caused by hypovolemia or cardiac failure. Distinguishing the two is critical because giving heart failure patients more fluid exacerbates an already failing system. Similarly, giving diuretics to a hypovolemic patient can worsen the renal failure. If the prerenal patient has no history of cardiac disease, administration of isosmotic fluid (normal saline or lac­tated Ringer’s solution, or blood in patients who have hemor­rhaged) is indicated. The IV fluid can be given rapidly (1 liter over a 20­ to 30­minute period) in young patients with healthy hearts and a Foley catheter in place to measure hourly urine output, and must be administered until the patient is producing a minimum of 30 to 40 mL/hr of urine. If fluid administration does not result in improvement of the oliguria, placement of a central venous pressure or Swan­Ganz catheter is indicated to measure left­ or right­sided heart filling pressure. In the presence of CHF, diuretics, fluid restriction, and appropriate cardiac medications are indicated. Ultrasound may show renal atrophy, reflecting the presence of chronic metabolic disease.


administration. Diabetic patients with vascular disease are at risk for major renal injury when contrast agents are administered. Administration of contrast to hypovolemic patients and those with preexisting renal dysfunction guarantees some degree of renal injury. The tubular injury is generally self­limited and reversible. Diabetic patients with creatinine clearance lower than 50 mL/min who receive 100 mL of contrast dye, however, can sustain severe tubular damage and may require dialysis. Blunt trauma with associated crush injuries place the patient at risk for ARF because of high serum levels of hematin and myoglobin, both of which are injurious to the renal tubules. ARF is a prominent feature in patients with acute compartment syn­drome.27 Growing awareness of this problem has led surgeons to intervene surgically, often resulting in dramatic improvement in renal function and preservation of renal filtering capacity.

presentation and managementPrevention of hospital­acquired renal insufficiency requires the following: identification of patients with preexisting renal dys­function; avoidance of hypovolemia, hypotension, and medica­tions that depress renal function; and judicious use of nephrotoxic drugs. In the presence of renal impairment, the dose of antibiot­ics given for serious infections must be adjusted. The risk for contrast­induced nephropathy is reduced by adequate hydration and premedication with a free radical scavenger (e.g., N­acetylcysteine) or the use of alternative contrast (e.g., gado­linium). Renal hypoperfusion is avoided by optimizing cardiac output and volume expansion. Administration of fluid must be particularly judicious in patients with a history of heart failure. Monitoring renal function in all surgical patients, at times including creatinine clearance, is a sound clinical practice. Early intervention in cases of postrenal obstruction and abdominal compartment syndrome can obviate the development of renal injury.

Anuria that suddenly develops postoperatively in an other­wise healthy individual with no preexisting renal disease is postrenal in nature until proven otherwise. A kink in the Foley catheter or obstruction must be cleared. In patients who have undergone major pelvic surgery, ligation of the ureters is suspect. If renal ultrasound or a CT scan shows hydronephrosis, imme­diate surgical treatment is indicated. Postrenal causes of ARF are the most dramatic and straightforward to diagnose and treat, with significant immediate improvement after treatment.

ARF is otherwise diagnosed when there is a rise in the serum creatinine level, decrease in creatinine clearance, and urine output less than 400 mL/day (<20 mL/hr). Distinguish­ing between prerenal and renal azotemia, however, is

table 13-10  causes of postoperative acute renal FailureinFLoW or prerenaL parenchYMaL or renaL oUtFLoW or postrenaL

Sepsis renal ischemia cellular debris (acute tubular necrosis)Medications Drugs (aminoglycosides, amphotericin) crystals  nonsteroidal anti-inflammatory drugs iodinated contrast media   uric acid  angiotensin-converting enzyme inhibitors interstitial nephritis   oxylateintravascular volume contraction Pigment  Hypovolemia   Myoglobin  Hemorrhage   Hemoglobin  Dehydration  atherosclerotic emboli  third spacing  cardiac failure

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corticosteroid secreted from the adrenal cortex, is under the influence of adrenocorticotropic hormone (ACTH) released from the pituitary gland, which in turn is under the influence of hypothalamic corticotropin­releasing hormone; both hor­mones are subject to negative feedback by cortisol itself. Cortisol is a stress hormone.

Chronic adrenal insufficiency may result from primary destruction of the adrenal gland or be secondary to a disease state or disorder involving the hypothalamus or anterior pitu­itary gland. Primary adrenal insufficiency is most frequently caused by autoimmune adrenalitis (Addison’s disease), in which the adrenal cortex is destroyed by cytotoxic lymphocytes. Sec­ondary adrenal insufficiency is most commonly caused by long­term administration of pharmacologic doses of glucocorticoids. Chronic use of glucocorticoids causes suppression of the hypothalamic­pituitary­adrenal axis, induces adrenal atrophy, and results in isolated adrenal insufficiency.

Acute adrenal insufficiency may occur as a result of abrupt cessation of pharmacologic doses of chronic glucocor­ticoid therapy, surgical excision or destruction of the adrenal gland (adrenal hemorrhage, necrosis, or thrombosis in patients with sepsis or antiphospholipid syndrome), or surgi­cal excision or destruction (postpartum necrosis) of the pitu­itary gland. In addition, so­called functional or relative acute adrenal insufficiency may develop in critically ill and septic patients.

presentation and DiagnosisThe clinical manifestations of adrenal insufficiency depend on the cause of the disease and associated endocrinopathies.29 Symptoms and signs of chronic primary and secondary adrenal insufficiency are similar and nonspecific—fatigue, weakness, anorexia, weight loss, orthostatic dizziness, abdominal pain, diarrhea, depression, hyponatremia, hypoglycemia, eosinophilia,

Treatment of ARF includes the management of fluid and electrolyte imbalance, careful monitoring of fluid administra­tion, avoidance of nephrotoxic agents, provision of adequate nutrition, and adjustment of doses of renally excreted medica­tions until recovery of renal function. Most urgent in manage­ment of ARF is treating hyperkalemia and fluid overload. Hyperkalemia can be managed with a sodium­potassium exchange resin, insulin plus glucose, an aerosolized β2­adrenergic agonist, and calcium gluconate. Insulin and β2­adrenergic ago­nists shift potassium intracellularly. Hyperkalemia­associated cardiac irritability (prolonged PR interval or peaked T waves) is urgently treated with the administration of a 10% calcium glu­conate solution over a 15­minute period, as well as simultaneous IV administration of glucose and insulin (10­U IV bolus with 50 mL of a 50% dextrose solution, followed by continuation of glucose to prevent hypoglycemia). A β2­adrenergic agonist is given as a nebulizer containing 10 to 20 mg in 4 mL of saline over a period of 10 minutes or as an IV infusion containing 0.5 mg. Calcium gluconate is given as 10 mL of a 10% solution over a 5­minute period to reduce arrhythmias. Refractory hyper­kalemia associated with metabolic acidosis and rhabdomyolysis requires hemodialysis. In less severe hyperkalemia, an ion exchange resin (sodium polystyrene [Kayexalate]) in enema form will help lower potassium levels. Phosphate levels also require careful monitoring. Hypophosphatemia can induce rhabdomy­olysis and respiratory failure and is treated with the oral admin­istration of Fleet Phospho­Soda. Hyperphosphatemia with hypercalcemia increases the risk for calciphylaxis and is treated with the administration of phosphorus binders (calcium carbon­ate) or dialysis. IV fluids are monitored with an emphasis on fluid restriction and occasional use of catheters to measure right­ and left­sided heart filling pressure to avoid fluid overload.

When supportive measures fail, consideration must be given to hemodialysis.28 Indications for hemodialysis are listed in Box 13­7. Although some hemodynamic instability may occur during dialysis, it is usually transient and may be treated with fluids. Dialysis may be continued on an intermittent basis until renal function has returned, which occurs in most cases.

endocrine gland dySFunction

adrenal insufficiency

CausesAdrenal insufficiency is an uncommon but potentially lethal condition associated with failure of the adrenal glands to produce adequate glucocorticoids. Cortisol, the predominant



Box 13-7  indications for hemodialysis

Serum potassium > 5.5 meq/literBlood urea nitrogen > 80-90 mg/dlPersistent metabolic acidosisacute fluid overloaduremic symptoms (pericarditis, encephalopathy, anorexia)removal of toxinsPlatelet dysfunction causing bleedingHyperphosphatemia with hypercalcemia

table 13-11  Diagnostic evaluation of acute renal FailureparaMeter prerenaL renaL postrenaL

urine osmolality >500 mosm/liter = Plasma variable

urinary sodium <20 mosm/liter >50 mosm/liter >50 mosm/liter

Fractional excretion of sodium <1% >3% variable

urine, plasma creatinine leve >40 <20 <20

urine, plasma urea level >8 <3 variable

urine, plasma osmolality <1.5 >1.5 variable

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without an obvious source of infection. Hyponatremia is usually present and does not respond to saline infusion. A sodium level less than 120 mmol/liter is dangerous and may lead to delirium, coma, and seizures. Hypoglycemia and azotemia may also be present. An ECG will occasionally reveal low voltage and peaked T waves. To diagnose the condition, cortisol and corticotropin concentrations are checked and the short corticotropin stimula­tion test performed.

treatmentPrevention and avoidance of adrenal insufficiency are achieved by a thorough preoperative history, detailed instruction of patients receiving chronic corticosteroid therapy regarding the dangers of abrupt termination of the medication, and adequate perioperative corticosteroid administration. Specific patients with rheumatoid arthritis, inflammatory bowel disease, or auto­immune disease and recipients of organ transplants are targeted. In the critically ill, a high index of suspicion can prevent a fatal outcome. A stress dose of hydrocortisone (100 mg) may be given with induction of anesthesia. For minor surgical procedures, the usual maintenance dose is continued postoperatively. For major surgical procedures, a stress dose (100 mg) is continued every 8 hours until the patient is stable or free of complications and then tapered to the usual maintenance dose.

Symptomatic patients are treated with hydrocortisone or cortisone. Fludrocortisone (substitute for aldosterone) is also administered to patients with primary disease. Patients who have received more than 20 mg of prednisone daily (or equivalent dose of another corticosteroid; Table 13­12) for more than 3 weeks within the previous year and patients with Cushing’s syndrome who are undergoing surgery are presumed to have hypothalamic­pituitary­adrenal axis suppression and must be treated in a similar fashion.

Treatment of functional acute adrenal insufficiency involves immediate, rapid administration of high­dose hydrocortisone or methylprednisolone, with appropriate monitoring until clinical improvement is seen. Hypovolemia and hyponatremia are cor­rected with saline infusion.



decreased libido and potency. Patients with primary hypoadre­nalism also show manifestations of elevated plasma levels of corticotropin and hyperpigmentation of the skin and mucous membranes. Patients with secondary disease, in contrast, ini­tially have neurologic or ophthalmologic symptoms (headaches, visual disturbances) before showing signs of hypothalamic­pituitary­adrenal axis disease (hypopituitarism). Manifestations of hypothalamic­pituitary­adrenal axis suppression include hypoadrenalism, decreased levels of corticotropin, and manifes­tations of other hormone deficiencies (e.g., pallor, loss of hair in androgen­dependent areas, oligomenorrhea, diabetes insipidus, hypothyroidism).

Laboratory test abnormalities, including hyponatremia, hyperkalemia, acidosis, hypoglycemia or hyperglycemia, normo­cytic anemia, eosinophilia, and lymphocytosis, are present to a variable extent. The diagnosis, however, is established by measur­ing the morning plasma cortisol concentration. A level higher than 19 µg/dL (525 nmol/liter) rules out adrenal insufficiency and less than 3 µg/dL (83 nmol/liter) indicates its presence. A basal plasma corticotropin level exceeding 100 pg/mL (22 nmol/liter), low or low­normal basal aldosterone level, and increased renin concentration are indicative of primary hypoadrenalism. The rapid corticotropin stimulation test to determine adrenal responsiveness is the diagnostic procedure of choice when testing for primary adrenal insufficiency (Box 13­8).

To confirm the diagnosis of secondary adrenal insuffi­ciency, the metyrapone test is performed. An insufficient increase in plasma 11­deoxycortisol and a low plasma cortisol concentration (<8 µg/dL) after the oral administration of metyrapone indicate the presence of secondary adrenal insuffi­ciency. Magnetic resonance imaging (MRI) allows evaluation of the pituitary­hypothalamic region in patients with neuro­logic and ophthalmologic symptoms and CT is used to evaluate the adrenal glands in patients with primary hypoadre­nalism.

The diagnosis of acute adrenal insufficiency can be espe­cially difficult to make in the critically ill. The condition is suspected in patients exhibiting manifestations of preexisting or undiagnosed chronic adrenal insufficiency in whom unexplained hypotension or hemodynamic instability develops despite fluid resuscitation, as well as ongoing evidence of inflammation

Box 13-8  rapid adrenocorticotropic hormone stimulation test in patients With adrenal insufficiency

• Determine baseline serum cortisol level.• give 250 µg cosyntropin iv (or iM).• Measure  serum  cortisol  levels  30  to  60 min  after 

cosyntropin is given.• results

• normal  adrenal  function:  Basal  or  postcorticotropin plasma  cortisol  concentration  is  at  least  18 µg/dl (500 nmol/liter)  or  preferably  20 µg/dl  (550 nmol/liter).

• Primary adrenal insufficiency: cortisol secretion is not increased.

• Severe secondary adrenal insufficiency: cortisol levels increase a little or not at all because of adrenocortical atrophy.

adapted from Druck p, andersen DK: Diabetes mellitus and other endocrine problems. In Stillman rM (ed): Surgery: Diagnosis and therapy, New York, 1989, Lange, p 205.

table 13-12  relative corticosteroid potency compared With hydrocortisone

GLUcocorticoiD actiVitY

MineraLocorticoiD actiVitY


Hydrocortisone 1 1

cortisone 0.8 0.8


Prednisone 4 0.25

Prednisolone 4 0.25

Methylprednisolone 5 trace

triamcinolone 5 trace


Dexamethasone 20 trace

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Definitive therapy for Graves’ disease is accomplished with radioactive iodine or surgery. Radioactive iodine has obvious advantages in older, high­risk patients but needs to be avoided in children, pregnant women, and patients with large toxic adenomas. By using doses of 123I in the range of 10 mCi (5 to 15 mCi) and subsequent levothyroxine, thyrotoxicosis can be successfully managed in 85% to 90% of patients. The main side effect of radioactive iodine is hypothyroidism. Surgery usually includes one of two operations, total thyroidectomy or a lobec­tomy on one side with a subtotal lobectomy on the other side. Total thyroidectomy is associated with a lower recurrence rate than subtotal thyroidectomy is (4% to 15%) but requires life­long T4 replacement postoperatively. Excision of the lesion is indicated for toxic adenoma, whereas total thyroidectomy is indicated for toxic multinodular goiter. Before surgery, patients must be made euthyroid with antithyroid drugs, and iodine is given for 7 days before surgery.


CausesHypothyroidism is characterized by low systemic levels of thyroid hormone and may be exacerbated in the postoperative period in patients with preexisting chronic hypothyroidism or as a result of severe stress. Severe illness, physiologic stress, and drugs may inhibit the peripheral conversion of T4 to T3 and induce a hypothyroid­like state. Hypothyroidism may be primary (e.g., surgical removal, ablation, disease of the thyroid gland), secondary (e.g., hypopituitarism), or tertiary (e.g., hypo­thalamic disease).

presentation and DiagnosisPatients with chronic hypothyroidism may be asymptomatic or, rarely, have the severe form (myxedema coma) characterized by coma, loss of deep tendon reflexes, cardiopulmonary collapse, and high mortality(≈40% to 50%). Most, however, demonstrate


Hyperthyroid crisis


Hyperthyroidism refers to a sustained increase in the synthesis of thyroid hormones, and thyrotoxicosis is a clinical syndrome that results from an abnormal elevation of circulating levels of thyroid hormone, regardless of cause. Thyroid hormones are under the influence of pituitary gland thyroid­releasing hormone, which in turn is under the influence of hypothalamic thyrotropin­releasing hormone; both are subject to negative feedback by the thyroid hormones. Thyroid hormones have physiologic effects on many organ systems, but the greatest effect is on the cardio­vascular system.

Thyroid crisis is a medical emergency that occurs in thy­rotoxic patients with toxic adenoma or toxic multinodular goiter, but most often in patients with Graves’ disease. The crisis is frequently precipitated by a stressful event and charac­terized by exacerbation of hyperthyroidism and decompensa­tion of one or more organ systems. Mortality is high, ranging from 20% to 50% if the crisis is unrecognized and left untreated.

presentation and DiagnosisClinical manifestations of hyperthyroidism include nervousness, fatigue, palpitations, heat intolerance, weight loss, atrial fibrilla­tion (in older patients), and ophthalmopathy characterized by eyelid retraction or lag, periorbital edema, and proptosis. The onset of thyroid crisis is sudden and manifested by accentuation of the symptoms and signs of thyrotoxicosis and organ system dysfunction, including hyperpyrexia, tachycardia out of propor­tion to fever, dehydration and collapse, central nervous system dysfunction (delirium, psychosis, seizure, coma), cardiac mani­festations, GI symptoms, and liver dysfunction.

The diagnosis of thyrotoxicosis requires demonstration of elevated levels of circulating thyroid hormone and suppressed thyroid­stimulating hormone (TSH) levels and identification of the cause of the thyrotoxicosis. Free thyroxine (T4) and triio­dothyronine (T3) represent the small unbound fraction of total thyroxine that is biologically active and correlate directly with the presence and severity of thyroid dysfunction. Thyroid scintigraphy with technetium pertechnetate (99mTcO4

−) or iodine 123 (123I) provides information about the functional anatomy of the gland. In Graves’ disease, there is diffuse uptake; in Plummer’s disease (toxic multinodular goiter), there is an inhomogeneous pattern with hot, cold, and warm areas, and with Goetsch’s disease (toxic solitary nodule), there is intense activity in the area of the nodule, with suppression of paranodular tissue.

treatmentIn addition to the identification and treatment of the precipitat­ing factor(s) and supportive care, specific medications (e.g., iodine, propylthiouracil, β­adrenergic blockers, dexamethasone) that target hormonal synthesis and release and block peripheral effects of the hormone are administered (Box 13­9).30 Steroids are required to block the peripheral conversion of T4 to T3 and as a supplement because there is increased steroid demand and turnover and decreased physiologic effectiveness. Cardioversion for supraventricular tachyarrhythmia is ineffective during the thyrotoxic storm.

Box 13-9  Management of thyroid crisis

identification and treatment of the precipitating factorSupportive care

• oxygen• iv fluid therapy• Sedation (chlorpromazine)• venous thromboembolism prophylaxis with heparin• Dexamethasone

Fever: antipyretics and coolingHeart failure: Digoxin and diureticsatrial fibrillation: iv heparinBeta blockers: oral propranolol, 60-80 mg/4 hr (or diltiazem), 

to reduce the heart rate below 100 beats/min. in very sick patients,  esmolol  is  given  iv  and  reserpine  is  given  to patients refractory to large doses of propranolol.

Propylthiouracil or methimazolelugol’s solution given 4 hr after propylthiouracilPlasmapheresis  and  charcoal  plasma  perfusion  or  exchange 

transfusion reserved for recalcitrant cases if no response in 24-48 hr

once euthyroidism achieved, definitive therapy must be consid-ered to prevent a second crisis


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criteria of SIADH include hyponatremia with hypotonicity of plasma, urine osmolality in excess of plasma osmolality, increased renal sodium excretion, absence of edema or volume depletion, and normal renal function.

treatmentManagement of SIADH includes treatment of the underlying disease process and removal of excess water (i.e., treatment of the hyponatremia). Fluid restriction is the mainstay of manage­ment of chronic SIADH. IV administration of normal saline is used only in significantly symptomatic patients with chronic SIADH or those with symptomatic acute SIADH, with a dura­tion of less than 3 days. Correction must occur at a rate of 0.5 mmol/liter/hr until the serum sodium concentration is 125 mg/dL or higher. Rapid correction leads to serious perma­nent neurologic damage. Diuretics such as furosemide occasion­ally help correct the imbalance. In some cases, IV administration of 3% saline solution may be required, but correction must be done in a constant, sustained fashion because overly rapid cor­rection can result in seizure activity.

gaStrointeStinal complicationS

ileus and early postoperative Bowel obstruction

CausesEarly postoperative bowel obstruction denotes obstruction occurring within 30 days after surgery. The obstruction may be functional (i.e., ileus), caused by inhibition of propulsive bowel activity, or mechanical as a result of a barrier. Ileus that occurs immediately after surgery in the absence of precipitating factors and resolves within 2 to 4 days is termed primary or postoperative ileus. On the other hand, ileus that occurs as a result of a pre­cipitating factor and is associated with a delay in return of bowel function is termed secondary, adynamic, or paralytic ileus.31 Mechanical bowel obstruction may be caused by a luminal, mural, or extraintestinal barrier.

The precise mechanism and cause of postoperative ileus are not completely understood. Several events that occur during an abdominal surgical procedure and in the perioperative period may interfere with or alter the contractile activity of the small bowel, which is governed by a complex interaction among the enteric nervous system, central nervous system, hormones, and local molecular and cellular inflammatory factors. Surgical stress and manipulation of the bowel result in sustained inhibitory sympathetic activity and release of hormones and neurotrans­mitters, as well as activation of a local molecular inflammatory response that results in suppression of the neuromuscular appa­ratus.32 In the immediate postoperative period, restricted oral intake and postoperative narcotic analgesia also contribute to altered small bowel motility. Opiates and opioid peptides in the enteric nervous system suppress neuronal excitability. After tran­section and reanastomosis of the small bowel, the distal part of the bowel does not react to the pacemaker (found in the duo­denum), and the frequency of contractions decreases. Other conditions listed in Box 13­10 are associated with or result in adynamic ileus.

Mechanical early postoperative small bowel obstruction is commonly caused by adhesions (92%), a phlegmon or abscess, internal hernia, intestinal ischemia, or intussusception. Intussusception occurring in the postoperative period is

cold intolerance, constipation, brittle hair, dry skin, sluggish­ness, weight gain, and fatigue. The impact of hypothyroidism is greatest on the cardiovascular system, with effects such as bra­dycardia, hypotension, impaired cardiac function, conduction abnormalities, pericardial effusion, and increased risk for CAD. In the critically ill (e.g., those with trauma or sepsis), hypothy­roidism is associated with worsening of pulmonary function, a predisposition to pleural effusion, and susceptibility to hypothermia.

The ECG usually shows bradycardia, low voltage, and pro­longed PR, QRS, and QT intervals. In patients with primary hypothyroidism, serum total T4, free T4, and free T3 levels are low, whereas the TSH level is elevated. In secondary disease, the TSH level, free T4 index, and free T3 are low. Distinguishing the two is important because adrenal insufficiency is present in secondary disease and administration of levothyroxine must be accompanied by cortisol or the disease could be exacerbated.

treatmentPatients with known hypothyroidism who are receiving replace­ment hormonal therapy and are in the euthyroid state do not require any special treatment before surgery but are instructed to continue taking their medications. In patients with symptom­atic chronic hypothyroidism, surgery is postponed until a euthy­roid state has been achieved.

Patients with myxedema coma or those showing clinical signs of significant hypothyroidism (e.g., severe postoperative hypothermia, hypotension, hypoventilation, psychosis, obtun­dation) are immediately treated with thyroid hormone, con­comitant with the IV administration of hydrocortisone, to avoid an addisonian crisis. IV levothyroxine or T3 may be given until oral ingestion is possible.

Syndrome of inappropriate antidiuretic Hormone Secretion

CausesThe syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of chronic normovolemic hyponatremia. Hyponatremia is defined as a serum sodium con­centration lower than 135 mmol/liter. SIADH is diagnosed in any patient who remains hyponatremic despite all attempts to correct the imbalance in the presence of persistent antidiuretic activity from elevated arginine vasopressin levels. Vasopressin is a naturally occurring antidiuretic hormone that regulates free water excretion. It is synthesized in the hypothalamus, trans­ported to the posterior pituitary, and stored until specific stimuli cause it to be secreted into the bloodstream. Thirst, hypovole­mia, nausea, hypoglycemia, and drugs are among the many stimuli for vasopressin. Disorders and conditions that predispose to this relatively rare condition include trauma, stroke, anti­diuretic hormone–producing tumors, drugs (ACE inhibitors, dopamine, NSAIDs), and pulmonary conditions.

presentationThe clinical features of SIADH include anorexia, nausea, vomit­ing, obtundation, and lethargy. With more rapid onset, seizures, coma, and death can result. Clinical expression of the syndrome is caused by hyponatremia and is a function of the degree of hyponatremia, as well as the rapidity of its onset. The cardinal

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The diagnosis of bowel obstruction is usually based on clinical findings and plain radiographs of the abdomen.33 However, in the postoperative period, differentiation between adynamic ileus and mechanical obstruction is imperative because the treatment is completely different. A CT scan, abdominal radiographs, and small bowel follow­through are variably used to establish the diagnosis and assist in treatment decision making. In adynamic ileus, abdominal radiographs reveal diffusely dilated bowel throughout the intestinal tract, with air in the colon and rectum. Air­fluid levels may be present, and the amount of dilated bowel varies greatly. With mechanical bowel obstruction, there is small bowel dilation with air­fluid levels and thickened valvulae conniventes in the bowel proximal to the point of obstruction and little or no gas in the bowel distal to the obstruction. A CT scan is more accurate for differentiating functional from mechanical obstruction by identifying the so­called transition point or cutoff at the obstruction site in cases of mechanical obstruc­tion. It also determines the level (high or low) and degree of obstruction (partial versus high­grade or complete), differenti­ates between uncomplicated and complicated (compromised bowel, perforation) obstruction, and identifies specific types of obstruction (closed­loop obstruction, intussusception). In addition, CT may identify other associated disease states (e.g., bowel ischemia, phlegmon, abscess, pancreatitis). Small bowel follow­through is indicated if the clinical picture of postopera­tive small bowel obstruction is confusing, radiographs of the abdomen are not diagnostic, or the response to expectant management is inadequate. A standard battery of laboratory tests is also obtained, including a complete blood cell count with differential, determination of amylase, lipase, electrolyte, magnesium, and calcium levels, and urinalysis.

treatmentPreventive measures must be started intraoperatively and con­tinued in the immediate postoperative period. A concerted effort must be made during any abdominal operation to minimize injury to the bowel and other peritoneal surfaces, the recognized source of adhesion formation. During the operation, the surgeon must handle the tissues gently and limit peritoneal dissection to only what is essential. The bowel must not be allowed to desic­cate by prolonged exposure to air without protection. Moist laparotomy pads must be used to cover the bowel and must be moistened frequently if contact with the bowel is prolonged. Instrument injury to the bowel must be avoided. Given the importance of adhesion formation and the large magnitude of serious problems related to adhesions, adjunctive measures, such as antiadhesion barriers, may be considered. A number of anti­adhesion barriers are available, including an oxidized cellulose product and a product that is a combination of sodium hyal­uronate and carboxymethyl cellulose. These agents may inhibit adhesions wherever they are placed. However, a decrease in the number of adhesions at the site of application does not necessarily translate into a decrease in the rate of small bowel obstruction.

In the postoperative period, electrolyte levels are monitored and any imbalance corrected. Alternative analgesia to narcotics, such as NSAIDs and placement of a thoracic epidural with local anesthetic, may be used when possible. Intubation of the stomach with an NG tube needs to be applied selectively. Routine intubation does not confer any appreciable effect and

relatively uncommon and is a rare occurrence after colorectal surgery. A phlegmon or abscess may be caused by leakage of intestinal contents from a disrupted anastomosis or by iatrogenic injury to the bowel during enterolysis or closure of laparotomy incision. With mechanical obstruction, there is an increased incidence of discrete, clustered contractions proximal to the obstruction that propel the intestinal contents past the point of obstruction (in cases of partial obstruction) and result in cramps. In high­grade or complete obstruction, the contents do not move distally, but accumulate in the proximal part of the bowel and initiate retrograde contractions that empty the small bowel contents into the stomach in preparation for expulsion during vomiting.

presentationPostoperative ileus affects the stomach and colon primarily. After laparotomy, small bowel motility returns within several hours, gastric motility within 24 to 48 hours, and colonic motility in 48 to 72 hours. Secretions and swallowed air are not emptied from the stomach, and gastric dilation and vomiting may occur. The return of bowel activity is heralded by the presence of bowel sounds, flatus, and bowel movements.

Patients with early postoperative small bowel obstruction do not show manifestations of bowel activity or have temporary return of bowel function. In adynamic ileus, the stomach, small bowel, and colon are affected. In mechanical obstruction, the obstruction may be partial or complete, may occur in the prox­imal part of the small bowel (high obstruction) or in the distal part of the small bowel (low obstruction), and may be a closed­loop or open­ended obstruction.33 There is stasis and progressive accumulation of gastric and intestinal secretions and gas; the bowel may lose its tone and dilate, thereby resulting in abdom­inal distention, pain, nausea and vomiting, and obstipation. The extent of the clinical manifestations varies with the cause, degree, and level of obstruction. Patients with high mechanical small bowel obstruction vomit early in the course and usually have no or minimal distention. The vomitus is generally bilious. Patients with distal obstruction, on the other hand, vomit later in the course and have more pronounced abdominal distention. The vomitus may initially be bilious and then becomes more fecu­lent. Differentiation between adynamic ileus and mechanical obstruction can be difficult. With adynamic ileus, patients have diffuse discomfort but no sharp colicky pain and a distended abdomen. They often have a quiet abdomen, with few bowel sounds detected on auscultation with a stethoscope. With mechanical obstruction, high­pitched, tinkling sounds may be detected. Fever, tachycardia, manifestations of hypovolemia, and sepsis may also develop.

Box 13-10  causes of intestinal paralytic ileus

Pancreatitisintra-abdominal infection (peritonitis or abscess)retroperitoneal hemorrhage and inflammationelectrolyte abnormalitieslengthy surgical procedure and prolonged exposure of abdom-

inal contentsMedications (e.g., narcotics, psychotropic agents)Pneumoniainflamed viscera

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microvascular permeability, exudation of fluid with resultant interstitial edema, bowel wall edema and ascites occurs.

In healthy individuals, IAP ranges from subatmospheric to 5 mm Hg and fluctuates with respiration, body mass index, and activity. Following uncomplicated abdominal surgery, IAP ranges from 3 to 15 mm Hg. IAP reflects intra­abdominal volume and abdominal wall compliance. With increased volume, there is a decrease in compliance and any further change in volume results in an increase in pressure, leading to IAH. In the early stages of IAH, changes in organ function are not detectable and of questionable clinical significance. With further increase in IAP, deleterious effects are observed in the intra­ and extra­abdominal organs and abdominal wall.27 Upward displacement of the diaphragm results in decreased thoracic volume and com­pliance and increased intrapleural pressure. This results in an increase in peak airway pressure (PAP), ventilation­perfusion (V­P) mismatch, hypoxia, hypercapnia, and acidosis. When IAP reaches 25 mm Hg, there is an increase in end­respiratory pres­sure to achieve a fixed tidal volume. However, modest IAH can exacerbate acute lung injury, inhalation injury, or respiratory distress syndrome. Compression of the inferior vena cava and portal vein occurs and results in decreased venous return, and therefore a decrease in preload and pooling of blood in the splanchnic and lower extremity vascular beds, and increased peripheral vascular resistance. Venus return decreases with IAP higher than 20 mm Hg. As a result, cardiac output (CO), cardiac index, and right atrial and pulmonary artery occlusion pressures decrease. Increased intrathoracic pressure also decreases left ventricular compliance, thus reducing contractility and further decreasing the CO. Ventricular compliance is reduced when IAP is higher than 30 mm Hg. Cardiac output decreases, despite normovolemia or apparent high filling pressures and a normal ejection when the IAP is 20 to 25 mmHg. Systemic delivery of oxygen (O2) decreases and whole body oxygen con­sumption is significantly reduced at an IAP higher than 25 mmHg.

Direct compression of the kidneys and obstruction of venous outflow, with resultant increase in prerenal vascular resistance and shunting of blood from the cortex to the medulla, results in a decrease in the glomerular filtration rate, renal plasma flow, glucose reabsorption, and urine output. In the postoperative patient admitted to the intensive care unit with an IAP higher than 18 mm Hg, renal function is impaired by 30%, independent of prerenal circulation. With an IAP higher than 25 mm Hg, renal output decreases in 65% of patients and in 100% of patients with an IAP higher than 35 mm Hg. Compression of the mesenteric vasculature leads to a decrease in splanchnic perfusion, mesenteric venous hypertension, and decreased hepatic arterial flow. This results in severe intramuco­sal acidosis, intestinal edema, and visceral swelling, increased intestinal permeability, and possible bacterial translocation. Gastric intramucosal acidosis develops with IAP higher than 20 to 25 cm H2O or 15 mm Hg. Elevated central venous pressure interferes with venous cerebral outflow, with consequent cere­bral pooling and increase in intracerebral pressure. Also, with diminished CO and increasing intracerebral pressure, cerebral perfusion pressure decreases. Interleukin 6 (IL­6) and IL­1B levels increase in response to increased IAP. Blood flow to the abdominal wall decreases with a progressive increase in IAP. This may result in an increased rate of abdominal wound com­plications.

is associated with discomfort, inhibits ambulation, and predis­poses to aspiration, sinusitis, otitis, esophageal injury, and elec­trolyte imbalance. The use of prokinetic agents does not alter the outcome after colorectal surgery and other pharmacologic manipulations, such as parasympathetic agents, adrenergic blocking agents, and metoclopramide, also have no impact on resolving postoperative ileus.32 The role of early postoperative feeding remains unclear.

Once early postoperative obstruction is suspected or diag­nosed, a three­step approach is essential to guarantee a favorable outcome—resuscitation, investigation, and surgical interven­tion.33 Emergency relaparotomy is performed if there is a closed­loop, high­grade, or complicated small bowel obstruction, intussusception, or peritonitis. Adynamic ileus is treated by resolving some of the abnormalities listed in Box 13­10 and waiting expectantly for resolution, with surgery not usually being required. Partial mechanical small bowel obstruction is also initially managed expectantly and for a longer period, 7 to 14 days, if the patient is stable and clinical and radiologic improvement continues. During this time, nutritional support is initiated and surgical intervention is performed if there are signs of deterioration or no improvement.

acute abdominal compartment Syndrome

CauseAbdominal compartment syndrome (ACS) describes increasing organ dysfunction or failure as a result of IAH. IAH is present when there is a consistent increased IAP value higher than 12 mm Hg, determined by a minimum of three measurements conducted 4 to 6 hours apart, measured at the end of expiration in a relaxed patient. ACS may be primary or secondary and develops when IAP is 20 mm Hg or higher, with or without abdominal perfusion pressure (APP) less than 50 mm Hg (at least three measurements performed 1 to 3 hours apart); it is associated with failure of one or more organ systems that was not present previously.

Primary ACS develops as a result of pathologic IAH caused by intra­abdominal pathology and secondary ACS develops in the absence of intra­abdominal primary pathology, injury, or intervention. Primary ACS is most commonly encountered in victims of multiple trauma, especially after damage control surgery, and develops as a result of ileus caused by bowel edema and contamination, continued bleeding, coagulopathy, packing used to control bleeding, capillary leak, and massive fluid resus­citation and transfusion. Closure of a noncompliant abdominal wall under tension in these situations is associated with IAH in 100% of cases. In nontrauma patients, IAH and possibly primary ACS have been reported to occur in patients with ascites, retro­peritoneal hemorrhage, pancreatitis, or pneumoperitoneum and after reduction of chronic hernias that have lost their domain, repair of ruptured abdominal aortic aneurysm, complex abdom­inal procedures, and liver transplantation. Secondary ACS is in part iatrogenic and commonly encountered in patients with shock requiring aggressive fluid resuscitation with crystalloids, thermally injured and shock trauma victims, critically ill hypo­thermic and septic patients, and those who have sustained cardiac arrest. Shock and ischemia increase capillary permeabil­ity; combined with excessive crystalloid resuscitation (leading to dilution of plasma) and gut reperfusion, which further increase

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decompression may be considered when the abdomen is tense and signs of extreme ventilatory dysfunction and oliguria develop. In grade IV IAH, with signs of ventilator and renal failure, decompression is indicated. In patients with severe head injury and IAP higher than 20 mm Hg, even without overt ACS, or intractable intracranial hypertension without obvious head injury, abdominal decompression must be considered. Unlike primary ACS, in which reopening of the preexisting laparotomy incision for decompression can be easily done, there is usually reluctance to perform a formal laparotomy for decompression in cases of secondary ACS, especially in the absence of primary intra­abdominal pathology. If nonoperative measures (see earlier) prove ineffective, fascial release without exposing the peritoneal cavity using minimally invasive tech­niques has proven effective in lowering IAP in experimental animals.34 Decompression (formal laparotomy) is an emergency and is performed in the operating room. Decompression leads to reduction of IAH, severe hypotension as a result of sudden decrease in systemic vascular resistance, and abrupt increase in the true tidal volume delivered to the patient, with washout of the byproducts of anaerobic metabolism from below the dia­phragm. This results in respiratory alkalosis, decrease in effec­tive preload, and a bolus of acid, potassium, and other

DiagnosisThe clinical manifestations of primary and secondary ACS are similar. However, the effects of secondary ACS are more subtle, so the diagnosis may be missed and the clinical deterioration of the patient is usually attributed to severity of the primary illness or occurrence of irreversible shock. Secondary ACS often occurs during aggressive fluid resuscitation in patients with burns, extra­abdominal injury, or sepsis. Patients with ACS have diffi­culty breathing or are difficult to ventilate and exhibit rising PAP, decreased volumes, hypoxia, worsening hypercapnia, and dete­riorating compliance. Oliguria rarely occurs in the absence of respiratory dysfunction or failure. The CO is reduced, despite apparent high filling pressures, and vasopressor therapy is required. The abdomen becomes distended and tense and neu­rologic deterioration may occur. The central venous pressure, pulmonary capillary wedge pressure (PCWP), and PAP become elevated and acidosis develops. Anuria, exacerbation of pulmo­nary failure, cardiac decompensation, and death ultimately occur.

Use of the urinary bladder catheter has been the gold stan­dard and is the indirect method used to measure IAP.28 IAP is measured in the following ways: (1) using a regular Foley cath­eter, disconnect from drainage tubing, directly inject 50 mL, clamp, insert needle, and measure; (2) a three­way Foley cath­eter with saline is injected into one port and IAP is measured through the other; or (3) a regular Foley catheter is serially con­nected to a three­way stopcock and a transducer. Other measure­ment kits have now become commercially available. Once measured, the pressure is graded: GI (IAP < 10 to 15 cm H2O), GII (IAP < 16 to 25 cm H2O), GIII (IAP < 26 to 35 cm H2O), and GIV (IAP > 36 cm H2O).

treatmentThe prevention of primary ACS entails leaving the peritoneal cavity open in patients at risk for IAH and after high­risk surgical procedures. Patients at risk for secondary ACS receiving crystal­loid resuscitation must be monitored closely and, when given more than 6 liters in a 6­hour period, IAP must be measured. In addition to blood pressure and urine output, monitoring APP (APP = mean arterial pressure − IAP) by continuously measuring IAP throughout resuscitation is a helpful indicator of the resus­citation end point. Routine measurement of IAP must also be considered in critically ill patients because IAH is the leading cause of chest wall impairment in ARDS. Monitoring gastric pH can detect cases of secondary ACS early after admission to the intensive care unit. A high incidence of suspicion is paramount, especially in cases of secondary ACS in which the onset is insidi­ous and manifestations are subtle. Patients exhibiting the prodro­mal phase of ACS benefit from timely intervention to relieve the IAH and prevent progression to ACS (Box 13­11). Conservative fluid resuscitation, administration of analgesia, sedatives and pharmacologic paralysis, patient positioning, drainage of intra­abdominal fluid, escharotomy, renal placement therapy, and diuretics are measures that may prevent progression to ACS.

Optimizing treatment and identifying patients with IAH­ACS likely to benefit from decompression is a challenging task. The decision to intervene surgically is not based on IAH alone but rather on the presence of organ dysfunction in asso­ciation with IAH. Few patients with a pressure of 12 mm Hg have any organ dysfunction, whereas IAP higher than 15 to 20 mmHg is significant in every patient. With grade III IAH,




Box 13-11  prevention of abdominal compartment syndrome

Patients at risk for iaH and abdominal compartment synd rome are  identified  (e.g.,  major  trauma,  complex  abdominal procedure).

organ function is monitored and assessed:• lungs: Hypercapnia, hypoxia, difficult ventilation, ele-

vated  pulmonary  artery  pressure,  drop  in  Pao2/Fio2 ratio,  decreased  compliance,  intrapulmonary  shunt, increased dead space

• Heart:  Decreased  cardiac  output  and  cardiac  index and need for vasopressors

• Kidneys: oliguria unresponsive to fluid therapy• central  nervous  system:  glasgow  coma  scale  score <10  or  neurologic  deterioration  in  the  absence  of neurotrauma

• abdomen: Distention; ct scan to check for fluid col-lections, narrowing of inferior vena cava, compression of the kidneys, and rounding of abdomen

intra-abdominal  pressure  is  measured  and  monitored  with  a urinary bladder or gastric catheter.

other tests to check organ dysfunction:• gastric mucosal pH• near-infrared  spectroscopy  to  measure  muscle  and 

gastric tissue oxygenation• abdominal  perfusion pressure = mean  arterial  pres-

sure − intra-abdominal pressure• renal filtration gradient = mean arterial pressure − 2× 

intra-abdominal pressure• ct scan

Measures to lower iaH:• Drainage of intra-abdominal fluid collections• Muscle relaxation

avoid  primary  closure  of  the  incision—laparotomy  or  mesh, Bogota bag, biomesh, or vacuum-assisted closure.

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or platelet inhibitor therapy will identify patients at high risk for postoperative bleeding.

In general, bright red blood is considered to come from a colonic or distal small bowel source. Melanotic stools suggest a gastric cause of the bleeding. However, rapid bleeding at any site may result in bright red blood. Bleeding from the anastomosis may be a slow ooze or a rapid hemorrhage that can lead to hypotension. Patients who appear to have lost a significant amount of blood have associated tachycardia or hypotension or have a significant decrease in hematocrit level.

treatmentTo prevent stress ulceration and decrease the risk for bleeding, patients at risk must receive aggressive fluid resuscitation to improve oxygen delivery and prophylaxis that neutralizes or reduces gastric acid. Patients with respiratory failure and coagu­lopathy benefit the most from prophylaxis. Maintaining the gastric pH above 4 is essential to minimize gastric mucosal injury and propagation of injury by acid. This can be achieved with antacids, H2 blockers, M1 cholinoreceptor antagonists, sucralfate, or PPIs.

The basic principles of management of postoperative GI bleeding include the following:

1. Fluid resuscitation and restoration of intravascular volume

2. Checking and monitoring clotting parameters and correcting abnormalities, as needed

3. Identification and treatment of aggravating factors4. Transfusion of blood products5. Identification and treatment of the source of the

bleedingIn general, management of GI bleeding is best conducted

in the intensive care unit setting. Fluid resuscitation with isos­motic crystalloids is begun after securing venous access. Blood samples are sent to assess the hematocrit, platelet count, pro­thrombin time, partial thromboplastin time, and INR. If the INR is elevated, vitamin K and fresh­frozen plasma are admin­istered. Platelet transfusion is administered to patients with a prolonged bleeding time or to those who have been taking antiplatelet drugs; desmopressin acetate may also be given to patients in renal failure. Hypothermia, if present, is corrected.

Blood transfusion is recommended when tachycardia and hypotension refractory to volume expansion are present, with a hemoglobin concentration in the 6­ to 10­g/dL range and the extent of blood loss is unknown, a hemoglobin concentration less than 6 g/dL, and rapid blood loss more than 30%, as well as in patients at risk for ischemia or those with an oxygen extrac­tion ratio more than 50%, with a decrease in Vo2.35 An NG tube is placed and the effluent checked for the presence of blood. Nonbloody bilious drainage almost rules out a gastroduodenal source of the bleeding. If blood is present, lavage with saline at room temperature is performed.

Identification and treatment of the source of bleeding can be achieved with endoscopy, angiography or, occasionally, lapa­rotomy. Endoscopic control of bleeding can be achieved with an injection of epinephrine, electrocoagulation, laser coagulation, heater probe, argon plasma coagulator, clip application, banding, or any combination of these modalities, depending on the source of bleeding. Visceral angiography is indicated for patients who are actively bleeding or when endoscopy fails to control the bleeding. Once an actively bleeding vessel is identified,

byproducts delivered to the heart, where they cause arrhythmia or asystolic arrest. Hence, decompression is performed after adequate preload with volume has been established. Most patients respond to decompression and survive. Once stable, the patient may be returned to the operating room for defini­tive closure. If primary closure is not possible, closure may be effected with skin flaps only, composite mesh, bioprosthesis, bilateral medial advancement of rectus muscle and its fascia with lateral skin relaxation incisions, or tissue expanders and myocutaneous flaps.

postoperative gastrointestinal Bleeding

CausesPostoperative GI bleeding is one of the most worrisome com­plications encountered by general surgeons. Possible sources in the stomach include peptic ulcer disease, stress erosion, a Mallory­Weiss tear, and gastric varices, in the small intestine, arteriovenous malformations and bleeding from an anastomosis and, in the large intestine, anastomotic hemorrhage, diverticu­losis, arteriovenous malformations, and varices.

In the critically ill, GI bleeding caused by stress ulceration is a serious complication. The incidence of bleeding from stress ulceration has decreased in the past 15 years, mainly because of improved supportive care, superior acid suppression, and enhanced resuscitative measures. Clinically significant bleeding that leads to hemodynamic instability, the need for transfusion of blood products, and occasionally operative intervention occurs in less than 5% of cases and is associated with significant mortality. Risk factors for stress ulceration are listed in Box 13­12.

presentation and DiagnosisWhen considering the source of the hemorrhage, a previous history is important when assessing the patient. A history of peptic ulcer disease and previous upper GI bleeding lead one to consider a duodenal ulcer. Severe trauma, major abdominal surgery, central nervous system injury, sepsis, or MI may be associated with stress ulceration. An antecedent history of violent emesis leads to consideration of a Mallory­Weiss tear, and a history of portal hypertension or variceal bleeding is a clue regarding the presence of esophageal varices. A previous history of diverticulosis may indicate that the hemorrhage is diverticular in nature. With a recent surgical history of intestinal anastomo­sis, oozing from the suture or staple line may be the source of GI bleeding. In distal colorectal anastomoses, bleeding may be the first sign of anastomotic breakdown. A previous history of aortic aneurysm repair may indicate the presence of an aorto­duodenal fistula. A history of intake of NSAIDs or anticoagulant

Box 13-12  risk Factors for Development of stress erosions

Multiple traumaHead traumaMajor burnsclotting abnormalitiesSevere sepsisSystemic inflammatory response syndromecardiac bypassintracranial operations

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dermal layer of skin, excessive bowel tension, or peristomal infection.

Stomal prolapse is most alarming to the patient and can result in incomplete diversion of stool, interfere with the stoma appliance, lead to leakage of stool, or become associated with obstructive symptoms and incarceration. Parastomal hernia for­mation occurs to some degree in most patients. A peristomal fistula is often a sign of Crohn’s disease, may result from a deep suture used to mature the stoma, or may be caused by trauma from an appliance.

Chemical dermatitis is caused by contact of the stoma effluent with peristomal skin as a result of a large opening in the faceplate or leakage from an ill­fitted faceplate. Chemical der­matitis is initially manifested as erythema, ulceration (ileostomy effluent), encrustation (urostomy effluent), or pseudoepithelio­matous hyperplasia. Infectious dermatitis may be caused by fungus, bacteria, tinea corporis, or C. albicans. Allergic derma­titis may be related to any of the stomal equipment (e.g., face­plate, tape, belt), with skin manifestations appearing at the site of contact. Traumatic dermatitis occurs during change of the stomal device, from stripping of adhesive, or as a result of fric­tion or pressure from the stomal device or supportive belt. Traumatic dermatitis is manifested as erythema, erosion, and ulceration.

Stoma patients are at risk for diarrhea and dehydration. The risk for dehydration depends on the type of stoma, under­lying primary disease process, and any concomitant bowel resec­tion; it commonly occurs in older patients, in hot weather, during strenuous exercise, and in association with short bowel syndrome.

Cutaneous manifestations of the disease may develop in the damaged peristomal skin in patients afflicted with certain skin conditions, such as psoriasis. Pyoderma gangrenosa may develop in patients with inflammatory bowel disease, and parastomal varices may develop in patients with liver disease.

treatmentTo prevent most stomal complications, adherence to sound sur­gical technique is imperative. Application of the technical points shown in Box 13­13 ensures the construction of a healthy and well­positioned stoma in patients undergoing surgery. In emer­gencies and difficult cases such as the obese, distended bowel, and shortened mesentery, to ensure delivery of a viable stoma free of tension, the fascial aperture may be made larger, the bowel may have to be extensively mobilized, the ileocolic artery and inferior mesenteric artery may have to be divided at their origin, windows may need to be created in the mesentery, the stoma may be brought out at a site with less subcutaneous fat (above the umbilicus), or alternative stomas may be selected.

After construction of a stoma, a dusky appearance indicates some degree of ischemia. The ischemia may be mucosal or full thickness, and the extent and depth of ischemia dictate the need for immediate revision of the stoma. Viability of the stoma is checked with a test tube and a flashlight or endoscopy. Necrosis extending to and beyond the fascia requires immediate reopera­tion. Ischemia limited to a few millimeters is observed and may not result in any long­term sequelae. Repair of stomal retraction often requires laparotomy.

Skin­level stenosis can be repaired locally and stenoses from other causes can be repaired via laparotomy. Complete separa­tion or detachment usually requires revision. Repair of end

embolization (e.g., with Gelfoam, autologous blood clot, coils) often controls the bleeding. Infusion of vasopressin may be used in patients with severe stress ulceration, diverticulosis, and ongoing bleeding. Bleeding from an intestinal anastomosis and stress ulceration usually cease with expectant management. Rarely, a patient with an anastomosis may require a reoperation to resect the anastomosis and reconnect the bowel. Similarly, surgery for stress ulceration is reserved for patients who fail medical management. Usually, a generous gastrotomy is per­formed to evacuate the blood clots and oversew sites of active bleeding; uncommonly, total or subtotal gastrectomy, with or without vagotomy, is performed. Recurrence with both approaches is prevented in 50% to 80% of cases.

Stomal complications

CausesStomas are widely used in the treatment of colorectal, intestinal, and urologic diseases. An intestinal stoma can be an ileostomy, colostomy, or urostomy, end, loop, or end­loop, temporary or permanent, diverting or decompressing, or continent or incon­tinent. A tube cecostomy and a blowhole are considered tempo­rary decompressing colostomies performed in emergencies. Stomal complications are the result of several causative factors. Technical factors are most important in minimizing the compli­cation rate of stoma construction and are largely preventable. Stomal complications are numerous (Table 13­13) and range from a bothersome problem with fit of the stomal appliance to major skin erosion and bleeding. Early complications are con­sidered those that occur within 30 days after surgery.

presentation and DiagnosisIschemic necrosis results from impaired perfusion to the termi­nal portion of the bowel as a result of a tight aperture, overzeal­ous trimming of mesentery, or mesenteric tension. Stomal retraction occurs early as a result of tension on the bowel or ischemic necrosis of the stoma. Late retraction is caused by increased thickness of the abdominal wall with weight gain. Stenosis occurs as a result of a small aperture, so­called natural maturation, ischemia, recurrence of Crohn’s disease, or develop­ment of carcinoma. Mucocutaneous separation develops as a result of ischemia, inadequate approximation of mucosa to the


table 13-13  stomal complicationsComplication

cateGorY earLY Late

Stoma Poor location Prolapseretraction* Stenosisischemic necrosis Parastomal herniaDetachment Fistula formationabscess formation* gasopening wrong end odor

Peristomal skin excoriation Parastomal varicesDermatitis* Dermatoses

cancerSkin manifestations of 

inflammatory bowel disease

Systemic High output* Bowel obstructionnonclosure

*May also develop as a late complication.

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bacterium C. difficile. Several factors are associated with increased risk for CDC (Table 13­14). There has been an increased inci­dence and diagnosis rate of C. difficile infection (CDI) in hos­pitalized patients, as well as an increase in severity, requiring admission to the intensive care unit, treatment failure of the disease, colectomies, and 30­day mortality (4.7% in 1992 to 13.8% in 2003).36,37 These changes are caused by increased awareness of the disease, advanced age of inpatients, with numer­ous comorbidities, ubiquitous use of antibiotics, and emergence and spread of a hypervirulent strain. Historically, cephalospo­rins, clindamycin, and ampicillin­amoxicillin were most com­monly associated with CDI. Fluoroquinolones, as a class of antibiotics, have emerged as the most prone and at increased risk to cause CDI, and the increased use of newer generation fluo­roquinolones is implicated in outbreaks of a fluoroquinolone­resistant strain. Since 2000, a hypervirulent toxinotype III strain of C. difficile (designated BI/NAP1/027 strain) has been identi­fied in Canada, the United States, and England. Virulence of the wild­type C. difficile bacteria is related to enterotoxin A and cytotoxin B encoded by the genes tcdA and tcdB. Polymorphisms or partial deletions (18­base pair deletion) in tcdC may lead to increased production of toxins A and B at levels 16 and 23 times higher than the wild type.

Antibiotic use continues to precede almost all cases of infection. Of patients contracting CDC, 90% have received antibiotic therapy and 70% have been treated with multiple antibiotics. Patients receiving prolonged courses of antibiotic therapy are particularly susceptible, and those receiving prophy­laxis are also at risk. Prolonged hospital stay allows exposure to contaminated environmental surfaces by more susceptible people. Intensive care and long­term facility units are not only sites of heavy environmental contamination, but also house critically ill and vulnerable patients. Impaired host immune defense as a result of advanced age, surgery, immunosuppressive medications, HIV, and chemotherapy are major risk factors. The proportion of immunocompromised patients infected with C. difficile has increased from 20% to 30% in the past decade. Surgical patients account for 45% to 55% of CDC, and the highest rates of infection are noted in patients undergoing general and vascular surgery. C. difficile is a gram­positive anaer­obic spore­forming bacillus; approximately 5% to 35% of bac­teria do not produce toxins and thus do not cause colitis. The


stomal prolapse can be achieved locally by making a circumfer­ential incision at the mucocutaneous junction, excision of redundant bowel, and rematuration. Repair of loop stomal pro­lapse is achieved by local revision to an end stoma. Laparotomy may be required for the treatment of recurrent prolapse and prolapse associated with a parastomal hernia. Large permanent or complicated parastomal hernias are treated by relocating the stoma or reinforcing the fascia ring with mesh (synthetic or biomaterial). Treatment of a peristomal fistula entails resection of the diseased or involved segment of bowel and relocation of the stoma. Treatment of mucosal islands ranges from ablation with electrocautery to relocation of the stoma.

Treatment of chemical dermatitis entails cleaning the damaged skin, the use of barriers, and a properly fitting stomal management system. Candida dermatitis is best treated with nystatin powder. Allergic dermatitis is treated by removal of the offending item and symptomatic relief is produced by oral anti­histamine or topical or oral steroid therapy. Traumatic dermati­tis is treated by patient education and application of a skin barrier under the tape is used to secure the faceplate in place. Occasionally, in cases of severe dermatitis, the patient will have to be admitted to the hospital and placed on TPN while the skin around the stoma heals enough to allow subsequent place­ment of an appliance.

Clostridium difficile colitis

CausesC. difficile colitis (CDC) is an inflammatory bowel disease caused by toxins produced by unopposed proliferation of the

Box 13-13  technical aspects of stoma construction

abdominal Wall apertureexcision of circular piece of skin approximately 2 cm in sizePreservation  of  subcutaneous  fat  to  provide  support  for  the 

stomatransrectus muscle placement of the stomaFascial aperture to admit two fingersStomaSelection of normal bowel for the stomaadequate mobilization of bowel to avoid tension on the stomaPreservation of blood supply to end of bowel (marginal artery 

of  the colon and  last vascular arcade of small bowel mes-entery must be preserved)

Small bowel serosa must not be denuded of >5 cm of mesen-tery

maturationPrimary maturation of end stoma or afferent limb of loop ileos-

tomyavoidance of traversing skin with sutures during maturation

other maneuvers*tunneling of bowel through extraperitoneal space of abdominal 

wallMesenteric-peritoneal closureFixation of mesentery or bowel to fascial ringuse of supportive rod with loop stomas

*May be performed but have not been proved to be effective in preventing post-operative complications.

table 13-14  Factors associated With increased risk for Clos-tridium difficile colitiscateGorY risK Factors

Patient-related factors increasing agePreexisting renal diseasePreexisting chronic obstructive lung diseaseimpaired immune defenseunderlying malignancyunderlying gastrointestinal disease

treatment-related factors

Preoperative bowel cleansingantibiotic useimmunosuppressive therapySurgeryProlonged hospital stay

Facility-related factors intensive care unitscaregiverslong-term facilities

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more prominent and are associated with systemic signs of toxic­ity. Diarrhea may be absent in 5% to 12% of cases; the WBC count may be depressed but is most commonly increased with a rapid elevation (>20,000 cells/mm3) and bandemia (>30%). A leukemoid reaction is a prominent feature that may suggest CDC or herald the onset of fulminant disease. Frank peritoneal signs and toxic megacolon may develop and rapidly progress to shock. Toxic megacolon usually develops slowly and is charac­terized by obstipation, a dilated colon, and systemic toxicity. In fulminant disease, the toxin assay is negative in 12.5% of cases. CT scanning is diagnostic and typically shows a boggy, edema­tous, and thickened colon wall (>3 mm) in 88%, pancolitis in 50%, serous ascites in 35%, pericolic inflammation in 35%, a clover leaf or accordion sign in 20%, and megacolon (transverse colon >8 cm) in 25% of cases. Sigmoidoscopy shows pseudo­membranes in 90% of cases versus 23% in mild cases.

treatmentTreatment of CDC starts with prevention. However, this is dif­ficult because disinfectants may eliminate C. difficile but not the highly resistant spores, antibiotics are ineffective in clearing stools of carriers and although effective, steam sterilization is expensive. Judicious use of antibiotics, application of standard hygiene measures to hospital staff, use of disposable gloves and single­use disposable thermometers, and ward closure and decontamination in case of outbreaks are important for decreas­ing the mortality and morbidity associated with CDC.

Once a diagnosis of CDC is made, medical therapy and timely surgical intervention improve recovery and lower the mortality rate. Death is related to delay in diagnosis, reliance on negative toxin assay, less than total abdominal colectomy, and additional patient­related factors. Infections with C. difficile usually follow a benign course. Although some patients respond to discontinuation of antibiotic therapy, others require treat­ment and respond within 3 to 4 days, and symptoms resolve in 95% to 98% within 10 days. Vancomycin (125 mg, four times/day) is given orally, down the NG tube or given or as an enema, or metronidazole (Flagyl) is given orally (250 mg, four times/day) or IV (500 mg, three times/day) for 2 weeks. Antimotility agents and narcotics are avoided. IV fluid therapy is instituted to correct dehydration. In the absence of ileus, oral intake is allowed. Approximately 25% to 30% of patients develop recur­rent disease as a result of reinfection with a second strain or reactivation of toxigenic spores that persist in the colon. Treat­ment of relapse is similar to that of the primary infection. In patients with recurrent attacks, pulsed vancomycin therapy, combination therapy with vancomycin and rifampicin, or the administration of competitive organisms (e.g., Lactobacillus aci-dophilus and Saccharomyces cerevisiae) may be tried.

Most patients with CDI respond to medical treatment but, occasionally, the disease progresses to a more severe form, such as fulminant colitis, despite appropriate and timely medical treatment. Fulminant colitis is characterized by severe systemic inflammatory response (fever, hypotension, tachycardia, leuco­cytosis, and/or requirement for volume resuscitation), shock, multiple organ failure, and death caused by toxin­induced inflammatory mediators (e.g., IL­8, macrophage inflammatory protein­2, substance P, tumor necrosis factor­α [TNF­α]) released locally in the colon. Hypotension that requires vasopres­sor support despite adequate volume resuscitation, lactate level 5 mmol/liter or higher, respiratory failure and ventilator support,


organism produces a capsule that resists degradation by phago­cytes. The spore is heat­resistant, persists in the environment for months and years in a dormant phase, and survives on inanimate objects. Approximately 3% to 5% of the general population has the organism in their stool. This increases to 8.6% of patients with hematologic malignancies and 10% to 25% of adults during hospitalization.

Antibiotic use leads to a disturbance in the microflora of the colon and allows the nosocomial organism to grow, prolifer­ate, and produce toxins. Toxin A, an enterotoxin, causes cell rounding, mucosal damage and inflammation, and release of inflammatory mediators. Toxin B is a potent cytotoxin that causes identical cell rounding and activates the release of cyto­kines from human monocytes. The toxins translocate to the portal circulation. Phagocytosis of toxins by macrophages in the liver results in the elaboration of several cytokines that act in the propagation of the systemic septic response.

presentation and DiagnosisOvergrowth of the toxigenic strain of C. difficile results in a variety of disease states, with varied clinical courses. Watery diarrhea is the hallmark symptom and usually starts during or shortly after antibiotic use. One dose of antibiotic can result in the disease, but the incidence with prophylactic antibiotics increases with extended use of antibiotics beyond the recom­mended period. Approximately 25% to 40% of patients become symptomatic 10 weeks after completion of antibiotic therapy. The stools are foul­smelling and may be positive for the presence of occult blood. In mild to moderate cases, systemic signs of infection are absent or present to a mild degree. In severe colitis, the diarrhea becomes associated with abdominal cramps and anorexia, abdominal tenderness, dehydration, tachycardia, a raised leukocyte (white blood cell [WBC]) count, and bandemia (>10%). Pseudomembranous colitis is the more dramatic form of the disease and develops in 40% of patients who are signifi­cantly symptomatic.

Cell cytotoxin assay in tissue culture is a highly sensitive and specific test for the detection of toxin B (rounding effect) and is the gold standard diagnostic test for CDC. ELISA that detects toxin A or B in stool is highly sensitive and specific. Unlike the stool cytotoxic test, which requires 24 to 48 hours, results with ELISA are obtained within hours, the test is less expensive, and does not require specific training. Endoscopy reveals nonspecific colitis in moderate disease (mucosal edema and patchy erythema) or pseudomembranes in severe disease. The presence of pseudomembranes may be limited to the prox­imal colon in 10% of cases and the rectum may be spared in 60% of cases. Radiographs of the abdomen may be normal or show adynamic ileus, colonic dilation, thumb printing, or haus­tral thickening. CT scans may show a thickened and edematous colon wall and free peritoneal fluid.

Approximately 2% to 5% of patients develop fulminant colitis, despite timely medical therapy, and may succumb to cytokine­mediated cardiovascular collapse and death. This fre­quently develops in hospitalized and postoperative patients but may occur in the out of hospital setting. At­risk patients are the immunocompromised or those taking multiple antibiotics, patients with a previous diagnosis of C. difficile infection, those with vasculopathy, older adults, those with chronic obstructive pulmonary disease, and those in renal failure. In fulminant colitis, abdominal cramps, distention, and tenderness become

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prophylaxis, modern surgical techniques, and advances in patient care, the need for mechanical bowel preparation has been questioned. Studies have shown that mechanical bowel prepara­tion results in adverse physiologic changes and structural altera­tions in the colonic mucosa and inflammatory changes in the bowel wall. Furthermore, some studies have suggested that its use in elective cases is not only unnecessary but also associated with increased anastomotic leaks, intra­abdominal and wound infections, and reoperation.39 Proponents of intraoperative lavage have also become content with simply decompressing the dilated colon and milking away fecal matter in the area of the anastomosis instead of aggressive cleansing. Although there is a trend toward elimination of cleansing of the colon in elective and emergent colon resection, one must be cautioned against abandoning the practice completely, especially for anterior resec­tions, in which the presence of stool in the rectum poses a problem with the use of staplers.

The level of the anastomosis in the GI tract is important. Although small bowel, ileocolic, and ileorectal anastomoses are considered safe, esophageal, pancreaticoenteric, and colorectal anastomoses are considered high risk for leakage. In the esopha­gus, lack of serosa appears to be a significant contributing factor. In the pancreas, the texture of the gland and size of the pancre­atic duct, presence of pancreatic duct obstructive lesions, experi­ence of the operating surgeon, and probably the type of enteric anastomosis are implicated (see later). In the rectum, the highest leak rate is found in anastomoses in the distal rectum, 6 to 8 cm from the anal verge.

Adequate microcirculation at the resection margins is crucial for the healing of any anastomosis. Factors interfering with the perianastomotic microcirculation include smoking, hypertension, locally enhanced coagulation activity as a result of surgical trauma, perianastomotic hematoma, and presence of macrovascular disease. In colorectal anastomoses, relative isch­emia in the rectal remnant is a factor because its blood supply is derived from the internal iliac artery via the inferior hemor­rhoidal vessels, contribution from the middle hemorrhoidal artery is minimal and, at best, variable because the vessels are mostly absent and, when present, are unilateral. Total mesorec­tal excision, neoadjuvant therapy, and extended lymphadenec­tomy with high ligation of the inferior mesenteric artery are additional contributing factors.

Intraluminal distention is believed to be responsible for rupture of an anastomosis. The mechanical strength of the anas­tomosis is important and, in the early period, is dependent on sutures or staples, with endothelial cells and fibrin­fibrinonectin complex additionally contributing to the tension force. Con­struction of a watertight and airtight anastomosis is therefore essential. Antiadhesive agents may predispose to leaks because they isolate the anastomosis from the peritoneum and omentum and, as found in animal studies, decrease anastomotic bursting pressure and hydroxyproline levels.40

Intra­abdominally placed open rubber drains are not helpful and, if left for more than 24 to 48 hours, are associated with an increased risk of infection. In the pelvis, drains have been shown in some studies to be associated with a higher leak rate. Conversely, drains may remove blood, cellular debris, and serum that act as good culture media for perianastomotic sepsis or abscess formation. Local sepsis affects the integrity of the anastomosis negatively as it reduces collagen synthesis and increases collagenase activity, which results in increased lysis of

and an increase in organ dysfunction are alarming premortem signs.36,38

Colectomy is indicated when medical treatment fails or when the patient develops hemodynamic instability, fulminant disease, toxic megacolon, or peritonitis. The timing of interven­tion is not well established. Although the end point of failure of medical therapy is not known, a 24­ to 48­hour trial is consid­ered minimal. Early intervention commits the patient to a major surgical procedure and an ileostomy, and a delayed intervention is associated with high mortality (35% to 75%).36­38

Once the patient develops fulminant CDC, multiple organ failure, and hypotension, surgical intervention is less likely to be beneficial. Mortality is also increased with advanced age (>65 years), prolonged duration of CDI, length of medical treatment, and elevated serum lactate levels.36­38 Consequently, to lower mortality of severe CDI, patients at risk for fulminant disease are identified and the clinical features of the disease must be recognized. Most importantly, surgical intervention must be considered during a critical window that precedes the onset of multiple organ failure and hemodynamic collapse from prolonged septic shock. Early surgical intervention noted in recent years (2000­2006 versus 1995­1996) has changed the outcome, with a decrease in mortality from 65% to 32%.36,37 The procedure of choice is total abdominal colectomy and ileos­tomy. Lesser procedures are less effective and associated with high mortality (70%) compared with 11% with abdominal colectomy.

anastomotic leak

CausesNumerous factors can cause or are associated with an increased risk for anastomotic leak (Table 13­15). Mechanical bowel prep­aration has long been considered a critical factor in preventing infectious complications after elective colorectal surgery. In emergencies, surgeons have resorted to on­table colonic lavage to cleanse the colon and primary anastomosis, with good results. With decreased morbidity rates as a result of effective antibiotic

table 13-15  risk Factors associated With anastomotic LeakDeFinitiVe Factors iMpLicateD Factors

technical aspects: Mechanical bowel preparationDrainsadvanced malignancyShock and coagulopathy

  Blood supply  tension on the suture line  airtight and watertight 


location in the gi tract: emergency surgery  Pancreaticoenteric Blood transfusion  colorectal Malnutrition    above the peritoneal obesity reflection    Below the peritoneal gender reflection

local factors: Smoking  Septic environment Steroid therapy  Fluid collection neoadjuvant therapy

Bowel-related factors: vitamin c, iron, zinc, and cysteine deficiency  radiotherapy

  compromised distal lumen Stapler-related factors:  crohn’s disease   Forceful extraction of the stapler

  tears caused by anvil or gun insertion

  Failure of the stapler to close

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leakage of intestinal contents. The leakage may be diffuse throughout the peritoneal cavity (uncontrolled leak) or become walled off by omentum, abdominal wall, and contiguous loops of bowel, pelvic wall or adhesions from prior operations. If a surgical drain is present, intestinal contents are discharged onto the skin. Intra­abdominal fluid collections may contain intesti­nal contents, frank pus, or pus mixed with intestinal contents. If the fluid collection is drained surgically or percutaneously, there is an initial discharge of purulent material followed by feculent material heralding the formation of an enterocutaneous fistula (controlled fistula). If allowed to drain through the surgi­cal incision or abdominal wall, surgical wound infection and dehiscence with evisceration or an abdominal wall abscess may occur. If the fluid collection burrows into a contiguous structure such as the urinary bladder or vagina, spontaneous drainage occurs, with the formation of an enterovesical or enterovaginal fistula.

Hence, after the index surgery, a patient may have an initial normal postoperative course or may not have been progressing as expected. The early warning signs of anastomotic leak are malaise, fever, abdominal pain, ileus, localized erythema around the surgical incision, and leukocytosis. Patients may also develop bowel obstruction, induration, and erythema in the abdominal wall, rectal bleeding, or suprapubic pain. There may be an initial excessive drainage from the surgical wound or surgical wound dehiscence and/or evisceration. An intra­abdominal fluid collec­tion or abdominal wall abscess may be identified and drained surgically or percutaneously. Patients may also experience pneu­maturia, fecaluria, and pyuria. Once a fistulous communication is established, problems related to the loss of intestinal contents, perifistula skin, surgical wound, and malnutrition soon ensue.

Sepsis is a prominent feature of anastomotic leakage and results from diffuse peritonitis or localized abscess, abdominal wall infection, or contamination of a sterile site with intestinal contents. Abdominal wall infection develops as a result of contact of purulent material with the muscle and subcutaneous tissue, tissue necrosis associated with fascial sutures, and/or contact of corrosive intestinal juices with the abdominal wall, resulting in chemical erosion and extension of the infectious process. Nonclostridial necrotizing infections of the abdominal wall occur, particularly with fistulas of the lower GI tract that contain high concentrations of Enterobacteriaceae, nongroup A beta­hemolytic streptococci, and anaerobic cocci or penicillin­sensitive Bacteroides spp. Contamination of the urinary bladder with intestinal contents (enterovesical fistula) results in urosepsis.

treatmentTreatment of anastomotic leakage starts with prevention. In elective cases, nutritional support for 5 to 7 days is appropriate for patients who are malnourished or have lost significant amounts of weight. Mechanical and chemical bowel prepara­tions are still recommended by many surgeons prior to colorec­tal resection. In patients receiving or who have received bevacizumab, the appropriate interval between the last dose administered and the surgery is not known. The terminal half­life of the medication is long—20 days—so wound healing complications are documented up to 56 days after treatment. It is advisable to delay elective surgery for at least 4 to 8 weeks or, preferably, three half­lives (60 days) after treatment. In patients with newly constructed anastomoses who are candidates for

collagen at the anastomosis. Defunctioning or protective stomas do not decrease the overall leak rate but rather minimize the severity and sequelae of perianastomotic contamination and decrease the reoperation rate. Defunctioning stomas, however, deprive the colon of short­chain fatty acids, resulting in exclu­sion colitis and delay in epithelialization of the anastomosis, and are associated with altered collagen metabolism observed in left­sided anastomoses.

Bevacizumab, an angiogenesis inhibitor, is associated with increased risk for surgical site complications. It is a humanized monoclonal antibody that targets vascular endothelial growth factor (VEGF). VEGF is a critical factor for the survival of endothelial cells and is selectively present in the neovasculature of growing tumors. Bevacizumab binds with high specificity and affinity to VEGF, inhibiting the binding of VEGF to its recep­tors and negatively affecting angiogenesis and/or the remodeling of the existing network of blood vessels. Bevacizumab is used in combination with standard chemotherapy IFL (irinotecan, 5­fluorouracil [FU], and leucovorin) in the treatment of patients with metastatic colorectal cancer. In animal studies, antiangio­genic cancer therapy inhibits dermal wound healing in a dose­related fashion and compromises healing of colonic anastomoses. In patients with metastatic colorectal cancer, it increases the risk of surgical site complications—spontaneous dehiscence of primary anastomosis and colocutaneous fistula formation from an anastomosis. Such complications may occur up to 2 years after surgery.41 The mechanism is probably related to micro­thromboembolic disease leading to bowel ischemia, inhibition of angiogenesis in the microvascular bed of the new anastomosis, inhibition of neoangiogenesis in postradiated tissue, and reduc­tion in the number of newly formed vessels in granulation tissue surrounding anastomotic sites. Risk factors for delayed anasto­motic complications include a history of anastomotic complica­tions, radiotherapy, and rectal location of anastomoses.

Emergency bowel surgery is associated with high morbidity and mortality, in part because of sepsis and anastomotic leakage. This is related to the poor nutritional status of the patient, pres­ence of underlying malignancy, immunocompromised state, presence of intra­abdominal contamination or sepsis, and hemo­dynamic instability. Transfusion, on the one hand, causes impaired cell­mediated immunity and predisposes to infection and, on the other hand, alleviates anemia and improves the oxygen­carrying capacity of red blood cells that may have a positive impact on healing. Obesity increases the difficulty and complexity of the surgery, has been shown to be associated with increased postoperative complications, and is an independent risk factor for an increasing leakage rate, especially after a low colorectal anastomosis. Steroids affect healing by decreasing col­lagen synthesis, delaying the appearance of the inflammatory reaction, and reducing the production of transforming growth factor­β and insulin­like growth factor in wounds, which are essential for wound healing.

presentation and DiagnosisAnastomotic leak is a dreadful complication to encounter. It results in sepsis and enteric fistula formation, leads to reopera­tion and a possible permanent stoma, and is associated with decreased survival and increased local recurrence rate after cura­tive resection of cancer, and possibly leads to death.42

The clinical manifestations are the result of a cascade of events that start with loss of integrity of the anastomosis and

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Drains and octreotide can be used when an anastomosis is per­formed to a soft pancreas with a small duct and in lower surgi­cal volume centers or centers with a high leak rate (>10%). Pancreatic duct stents (placed intraoperatively) continue to be used, despite the lack of data to suggest that they decrease the leak rate.43 A pancreatic stent placed prior to a distal pancreatec­tomy decompresses the pancreatic duct by abolishing the pres­sure gradient between the pancreatic duct and duodenum and may decrease the risk of fistula formation, thus allowing the site of a leak to seal.

Once an anastomotic leak is suspected or diagnosed, resuscitation is started immediately because patients are in the postoperative period and have been without nutrition. Further­more, they have a contracted intravascular volume because of third spacing and lost intestinal contents, and may have an electrolyte imbalance. Intravascular volume is restored with crystalloid fluids and a blood transfusion if anemia is present and electrolyte imbalances are corrected. Oral intake is stopped and the bowel is put at rest to decrease luminal contents and GI stimulation and secretion. A NG tube is placed if obstruc­tive symptoms are present. Infected surgical wounds are opened, and any abdominal wall abscesses are incised and drained. Reoperation is indicated if there is diffuse peritonitis, intra­abdominal hemorrhage, suspected intestinal ischemia, major wound disruption, or evisceration. Reoperation is a major undertaking and is associated with significant mortality and morbidity. The procedure is bloody and carries the risk of bowel injury. Primary closure of the leaking point only is avoided because failure is certain.

The management of duodenal and proximal jejunal leaks is a challenging task. In these situations, transgastric placement of a jejunal tube helps divert gastric and biliopancreatic secre­tions and placement of drains in close proximity to the leak allows external drainage of the intestinal contents. Pyloric exclu­sion and gastrojejunostomy should be used judiciously in these situations. Management of jejunal, ileal, and colorectal leaking anastomoses depends on the severity and duration of contamina­tion, condition of the bowel, and hemodynamic stability of the patient. In a critically ill and unstable patient, especially one with fecal peritonitis, a damage control type of procedure is performed—the anastomosis is taken down, the ends of the bowel are stapled, peritoneal lavage is performed, and the inci­sion is left open. A second­look laparotomy with stomal forma­tion is performed in 24 to 48 hours or once the patient is more stable. Otherwise, in the small bowel, an anastomosis may be performed or the ends of the bowel are delivered as stomas; in the colon, the proximal end of the colon is brought out as a colostomy and the distal end closed or brought out as a mucous fistula; and, in the rectum, the distal end is closed and the proximal end of the colon delivered as a stoma. A proximal diverting stoma with drainage of the pelvis is not adequate treat­ment of leaking colorectal anastomoses associated with diffuse peritonitis. If the abdomen is left open, covering the bowel with the greater omentum (if available) or a biologic implant protects the bowel and prevents desiccation and spontaneous fistula for­mation. Negative­pressure wound therapy is best avoided when bowel is exposed, especially in the presence of unprotected suture or staple line.44

In the absence of diffuse peritonitis and evisceration, a CT scan may identify single or multiple abscesses, pneumoperito­neum, ascites and, at times, extravasation of oral contrast into

bevacizumab therapy, evaluation of the anastomosis prior to initiation of therapy with fine­cut CT scanning, barium enema, and colonoscopy allows identification of patients at risk for anastomotic complications. In emergencies, especially in hemo­dynamically unstable, immunocompromised, and nutritionally depleted patients, in the presence of fecal peritonitis, significant bowel dilation, and edema, an anastomosis is best avoided because a leak may prove fatal.

Construction of an anastomosis that is at low risk for dis­ruption requires the following:

1. Adequate exposure, gentle handling of tissues, aseptic precaution, and meticulous, careful dissection

2. Adequate mobilization so that the two attached organs have a tension­free anastomosis

3. Correct technical placement of sutures or staples with little variance

4. Matching of the lumina of the two organs to be con­nected, which can be done by various techniques

5. Preservation of the blood supply to the ends of struc­tures to be anastomosed

Sufficient microcirculation is essential for healing of the anastomosis. In intestinal anastomoses, the marginal artery of the colon and last vascular arcade of small bowel mesentery must be preserved. The small bowel serosa must not be denuded of mesentery more than 3 to 4 cm for hand­sewn anastomoses. In the distal colon, to ensure a tension­free anastomosis, the may be required: inferior mesenteric artery may be divided at its origin, windows created in the mesentery of the small bowel up to the third portion of the duodenum, and small branches inter­rupted between the arcades, creating mesenteric windows and dividing the ileocolic vessels at their origin. For intestinal and colorectal anastomoses, there is no difference in the rate of anastomotic leakage between hand­sewn and stapled anastomo­ses and among various stapling techniques, provided that sound surgical technique is followed. The decision to construct a one­ or two­layer intestinal anastomosis is a matter of preference. A colorectal anastomosis is easier to perform in one layer. However, since the advent of stapling devices, an anastomosis deep in the pelvis has most commonly been stapled. The technique is not only faster but also improves asepsis because the anastomosis is performed in a closed fashion compared with a hand­sewn anas­tomosis, which is considered an “open anastomosis” and allows for more contamination. In low anterior resection, the omentum may be advanced to the pelvis and placed around the colorectal anastomosis. This maneuver may lower the rate of anastomotic leak or disruption but mostly appears to decrease the severity of the complication. Drainage of a colorectal anastomosis is advisable in difficult cases and when technical problems are encountered, or when neoadjuvant therapy has been used. Defunctioning stomas are used for extraperitoneal anastomoses, when technical difficulties are encountered, or after neoadjuvant therapy.

When constructing a pancreaticoenteric anastomosis, a pancreaticojejunostomy is equivalent to pancreaticogastrostomy. An end to side–duct to mucosa pancreaticojejunostomy is asso­ciated with a lower leak rate compared with an end­to­end invaginating pancreaticojejunostomy; obliteration of the main pancreatic duct with protamine gel or human fibrin sealant, or suture closure of the remnant pancreas without an anastomosis, is associated with the highest leak rate.43 The routine placement of drains in proximity to pancreatic anastomoses is controversial.

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course. They then start showing the manifestations of leakage of intestinal contents (see earlier). The seriousness and severity of these manifestations depend on the surgical anatomy and phys­iology of the fistula. Anatomically, the fistula may originate from the stomach, duodenum, small bowel (proximal or distal), or large bowel. The tract of the fistula may erode into another portion of the intestines (enteroenteric fistula) or another hollow organ (enterovesical), thus forming an internal fistula, or into the body surface (enterocutaneous and pancreatic fistula) or vagina (enterovaginal fistula), thus forming an external fistula. A mixed fistula describes an internal fistula associated with an external fistula. A superficial fistula drains on top of an open or granulating wound; in a deep fistula, the tract traverses the abdominal cavity and drains onto the skin. Physiologically, the fistula is classified as high or low output on the basis of the volume of discharge in 24 hours. The exact definition of low and high output varies from 200 to 500 mL/24 hr. However, three different categories are recognized—low output (<200 mL/24 hr), moderate output (200 to 500 mL/24 hr), and high output (>500 mL/24 hr). The ileum is the site of the fistula in 50% of high­output fistulas. The discussion in this section focuses mainly on external fistulas.

Sepsis is a prominent feature of postoperative intestinal fistulas and is present in 25% to 75% of cases. As noted earlier, sepsis is the result of diffuse peritonitis or localized abscess, abdominal wall or necrotizing infection, or contamination of a sterile hollow organ with intestinal contents.

Loss of intestinal contents through the fistula results in hypovolemia and dehydration, electrolyte and acid­base imbal­ance, loss of protein and trace elements, and malnutrition. In a high intestinal fistula, it also results in loss of the normal inhibi­tory effect on gastric secretion, thus resulting in a gastric hyper­secretory state. With high­output enterocutaneous fistulas, there is also intrahepatic cholestasis related to the loss of bile salts, disruption of enterohepatic circulation, and bacterial overgrowth in the defunctionalized intestine. Malnutrition results from loss of protein­rich secretions, lack of nutrient intake, loss of absorp­tion caused by bypass of the gut (e.g., gastrocolic, duodenocolic, high enterocutaneous fistulas), and sepsis that sets the stage for nutritional deficiency and rapid breakdown of body muscle mass. In gastroduodenal and proximal small bowel fistulas, the output is high and the fluid loss, electrolyte imbalance, and malabsorp­tion are profound. In distal small bowel and colonic fistulas, the output is low and dehydration, acid­base imbalance, and malnu­trition are uncommon. Significant electrolyte imbalance occurs in 45% of patients and malnutrition occurs in 55% to 90%.

Skin and surgical wound complications develop as a result of contact of GI effluent with skin or the wound. Effluent der­matitis results from the corrosive effect of intestinal contents, which cause irritation, maceration, excoriation, ulceration, and infection of the skin. Fecal dermatitis is marked by erythema and desquamation and may encourage skin sepsis. Superficial and deep surgical wound and necrotizing infections also develop. Pain and itching by contact of effluent with unprotected skin is intolerable and affects the morale of the patient.

treatmentPostoperative intestinal fistulas are not a new problem but rather continue to be a challenging clinical scenario. Their etiogenesis has changed and their management continues to evolve. In the past, the main focus of management involved suctioning of the

the peritoneal cavity. Multiple abscesses require open drainage, a single intra­abdominal abscess can be drained percutaneously, and a pelvic abscess can be drained transrectally or transvagi­nally. Following drainage, an external fistula may develop. The management of a controlled fistula is outlined in the next section. If percutaneous drainage fails to control sepsis, reopera­tion is indicated. At the time of open drainage of a pelvic abscess, if there is any doubt about the origin of the abscess (de novo abscess versus abscess secondary to a small anastomotic leak that has sealed), a defunctioning stoma is constructed unless there is complete disruption of the anastomosis. In that case, the ends of the bowel are exteriorized as a stoma. A pancreaticojejunos­tomy leak, if small, can be treated by placing a drain next to the leak. However, for an anastomosis that has almost fallen apart, the patient will probably require completion pancreatectomy. A patient who has a bile duct leak will require drainage of the infection and placement of a drain next to the leak or, in the case of a large leak, may require bile duct reconstruction.

intestinal Fistulas

CausesA fistula represents an abnormal communication between two epithelialized surfaces, one of which is a hollow organ. In the GI tract, a fistula may develop between any two digestive organs or between a hollow organ and the skin and may be develop­mental or acquired. Acquired fistulas account for most GI fistu­las and can be traumatic, spontaneous, or postoperative in nature.

GI fistulas are most commonly iatrogenic, develop after an operation, and may occur anywhere in the GI tract. Esophageal, aortoenteric, and rectal fistulas are not discussed in this section. In the past, acquired GI fistulas most commonly developed as a result of a difficult appendectomy. At present, they commonly occur as the result of anastomotic breakdown, dehiscence of a surgically closed segment of stomach or bowel, unrecognized iatrogenic bowel injury following adhesiolysis, or during closure of a laparotomy incision. Occasionally, they develop after instru­mentation or drainage of a pancreatic, appendiceal, or diver­ticular fluid collection or abscess. The presence of intrinsic intestinal disease, such as Crohn’s disease, radiation enteritis, distal obstruction, or a hostile abdominal environment, such as an abscess or peritonitis, are predisposing factors for fistula for­mation. The risk is also higher in emergencies when the patient may be malnourished or poorly prepped.

Gastric fistulas are uncommon and frequently occur after resection for cancer and less frequently after resection for peptic ulcer disease, necrotizing pancreatitis, an antireflux procedure, or bariatric surgery. Pancreatic fistulas develop as a result of disruption of the main pancreatic duct or its branches secondary to trauma or postoperatively following pancreatic biopsy, distal pancreatectomy, pancreaticoduodenectomy, pancreatic necro­sectomy, and surgery on the stomach, biliary tree, or spleen. Intestinal fistulas develop after resection for cancer, diverticular disease, inflammatory bowel disease, or closure of a stoma.

presentation and DiagnosisEnterocutaneous fistulas are usually associated with a triad of sepsis, fluid and electrolyte imbalance, and malnutrition. Patients are usually in the postoperative period and may not be progress­ing as expected or may have an initial normal postoperative

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also associated with a decreased rate of healing of GI fistulas. Infected surgical wounds are opened and drained, abdominal wall abscesses are incised and drained, and intra­abdominal fluid collections are drained percutaneously or surgically. Percutane­ous drainage is tolerated better and allows changing a complex fistula (fistula associated with an abscess) to a simple fistula that has a better chance of spontaneous closure. A small pigtail cath­eter may be changed to a larger catheter that allows irrigation of the abscess cavity, later injection of contrast to assess resolution of the abscess, and study of the anatomy of the fistula.

Nutrition is one of the most important factors contributing to a successful outcome in the management of intestinal fistulas. TPN must be started early after the correction of electrolyte imbalance and repletion of volume. TPN allows bowel rest, which decreases output, eliminates negative nitrogen balance, improves the patient’s nutritional status, allows better timing of the operation when needed, increases the rate of recovery, and may slightly improve the closure rate once sepsis is controlled. Trace elements, multivitamins, vitamin K, and medications such as octreotide may be added to the TPN. TPN is the initial nutritional support for any patient with a fistula and is contin­ued in patients with high­output fistulas or patients who cannot tolerate oral intake. Somatostatin (SMS) analogues (e.g., octreo­tide, with a long half­life) help in management of the fistula by reducing GI secretions and inhibiting GI motility, thus control­ling and reducing its output. Their value in healing intestinal fistulas is yet to be proven and routine use is limited because they are not without side effects. Somatostatin leads to cellular apoptosis, villous atrophy, and interruption of intestinal adapta­tion, and may be associated with acute cholecystitis. Enteral nutrition (low­residue diet, elemental diet, liquid whole protein diet) is administered to patients with low­output small bowel and colonic external fistulas. Fistuloclysis (i.e., infusion of nutri­tion directly through the fistula into the bowel distal to the fistula) is another option to deliver enteral nutrition to patients whose fistula has not healed spontaneously, provided there is more than 75 cm of healthy bowel distal that is in continuity with the fistula.45 Fistuloclysis is safer and less expensive than TPN and prevents atrophy of the bowel distal to the fistula.

intestinal effluent and early surgical intervention. This approach has proven ineffective and is associated with significant patient morbidity and mortality and a high reoperation rate. At present, management requires the involvement of a surgeon, nutritionist, enterostomal therapist, interventional radiologist, and gastroen­terologist; it entails initial medical treatment to allow spontane­ous healing of the fistula, early surgical intervention in a select group of patients, and planned definitive surgery for patients whose fistulas have failed to heal. External intestinal fistulas result in prolonged hospital stays and enormous cost to the hospital and are associated with significant patient disability, morbidity, and mortality (6% to 30%). Although spontaneous closure occurs in 40% to 80% of cases, operative intervention may be required in 30% to 60% of cases.

The first step in the management of a GI fistula is to prevent its occurrence. Reducing the likelihood of an anasto­motic leak requires adherence to sound surgical principles and proper techniques (see earlier). Should a fistula form, manage­ment involves several phases that are applied systematically and simultaneously (Table 13­16).

Once a leak is diagnosed or suspected, management involves resuscitation, TPN, correction of electrolyte imbal­ances, and transfusions, as appropriate. Oral intake is stopped and the bowel is put at rest, thus decreasing luminal contents and reducing GI stimulation and secretion. An NG tube is placed if obstructive symptoms are present. Routine NG place­ment is not helpful and subjects the patient to complications, such as sinusitis and aspiration. Broad­spectrum IV antibiotic therapy is started and later adjusted according to cultures.

The indications for early surgical intervention have been discussed earlier. Otherwise, resuscitation is continued. Treat­ment with H2 antagonists or PPI helps decrease peptic ulceration and may decrease fistula output but does not aid in the closure of fistula. Accurate measurement of output from all orifices and the fistula is paramount in maintaining fluid balance. Effective control of all sources of sepsis is important because continued sepsis is a major source of mortality that results in a state of hypercatabolism and the failure of exogenous nutritional support to restore and maintain body mass and immune function; it is

table 13-16  Factors affecting healing of external intestinal FistulasFactors FaVoraBLe UnFaVoraBLe

Surgical anatomy of the fistula long tract, >2 cm Short tract, <2 cmSingle tract Multiple tractsno other fistulas associated internal fistulaslateral fistula end fistulanonepithelialized tract epithelialized tractorigin (jejunum, colon, duodenal stump, and 

pancreaticobiliary)origin (lateral duodenum, stomach, and ileum)

no adjacent large abscess adjacent large abscess

Status of the bowel no intestinal disease intrinsic intestinal disease (crohn’s disease, radiation enteritis, recurrent or incompletely resected cancer)

no distal bowel obstruction Distal bowel obstructionSmall enteral defect, <1 cm large enteral defect, >1 cm

condition of the abdominal wall

intactnot diseased

Disrupted (fistula opens into the base of the disrupted incision)infiltrated with malignancy or intestinal disease

no foreign body Foreign body (mesh)

Physiology of the patient no malnutrition Malnutritionno sepsis Sepsis

output of the fistula no influence influence

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intra­abdominal inflammatory reaction occurs 10 to 21 days after surgery and lasts for 6 to 8 weeks before starting to resolve. A 6­month period is required for a neoperitoneal cavity to develop in fistulas within a laparoscopy wound. A simple fistula—single fistula with direct communication between the bowel and skin, a short tract and small enteral opening, and associated with other favorable factors—can be closed 12 weeks after the index surgery. A complex fistula—a fistula with a long tract and associated with other internal fistulas, large abscess cavity, fistula that opens into the base of a disrupted wound, or other unfavorable factors—is closed 6 to 12 months after the index surgery. Complex fistulas associated with intrinsic intesti­nal disease require definitive surgical intervention once the initial sepsis is controlled because spontaneous closure is highly unlikely and extirpation of the diseased bowel is essential. In patients with Crohn’s disease, infliximab (Remicade) may also be used to aid in closure of the fistula in a select group of patients.

A controlled ECF that opens into the base of an inter­rupted wound requires abdominal wall construction at the time of definitive repair of the fistula. The fistulizing segment must not be excluded or bypassed to avoid the risk of blind loop syndrome. The fistula is excised, continuity of the GI tract rees­tablished, and freshly constructed anastomosis wrapped with omentum, if available. Gastric, duodenal, and proximal jejunal fistulas that cannot be resected without major surgical procedure are best managed with a Roux­en­Y intestinal anastomosis. The laparotomy incision is closed primarily or with durable well­vascularized coverage. Autogenous tissue reduces the risk of infection. Pedicle or free flaps with microvascular reconstruction may be considered; however, component separation when the rectus muscle is intact, with or without augmentation with acel­lular dermal matrix or synthetic mesh, is the preferred proce­dure.47 Postoperative morbidity, ventral hernia formation, and recurrent ECFs develop in approximately 20% to 25% of cases. Biologic material (e.g., acellular human or porcine dermal matrix, porcine submucosa) used for visceral overlay protection or reconstruction is another viable option in this setting of compromised operative field because the implant resists infec­tion and, when postoperative infection occurs, removal of the implant is not necessary. However, the product is expensive and the procedure is associated with a high rate of hernia formation and abdominal wall laxity.48 Occasionally the incision is closed in stages. The incision may be left open (laparotomy), an absorb­able mesh (polyglactin or polyglycolic acid) may be used to bridge the fascial defect, or negative­pressure wound therapy can be instituted. Once granulation tissue is formed, a split­thickness skin graft is applied.

New innovative approaches, such as transcatheter injection of diluted thrombin, endoscopic tissue sealant or clip applica­tion, and porcine small intestinal submucosa have been used in recalcitrant cases or as adjunctive therapy to hasten healing of the intestinal fistula, with some success.

pancreatic FistulasOverall, the physiologic classification, diagnosis, management, and outcome of postoperative external pancreatic fistulas are similar to that for external intestinal fistulas. However, pancre­atic fistulas have additional distinctive features. Following pan­creaticoduodenectomy, texture of the pancreas, size of the pancreatic duct, blood supply to the stump, and volume of pancreatic juice produced are the most significant risk factors

Early control of fistula output is essential to protect the perifistula skin from the corrosive effects of intestinal effluent, promote healing of damaged skin and surgical wounds, and facilitate nursing care of the patient. Early involvement by an enterostomal therapist and wound care team cannot be overem­phasized. Protection of the skin is achieved with barriers, seal­ants, adhesives, and pouches. Negative­pressure wound therapy another treatment strategy whereby the continuous suction of fistula output minimizes contact between intestinal contents and surrounding tissue. Hence, it protects perifistula skin, reduces the need for dressing changes, promotes wound healing, and even accelerates fistula closure, especially in deep fistulas. Closure has been reported to occur in 46% to 84% of cases.46

Once initial sepsis is controlled, nutrition provided, and wound and fistula care provided, studies are performed to define the surgical pathology of the fistula (origin, course, length of the fistula) and condition of the bowel (presence of intrinsic intes­tinal disease, presence of distal obstruction, continuity of the bowel) and to evaluate resolution of the intra­abdominal abscess. A fistulogram is performed by injecting a water­soluble contrast medium or barium through an existing drain or by inserting a 5 Fr pediatric feeding tube or a Foley catheter into the external opening of the fistula. A fistulogram delineates the anatomy of the fistula and identifies associated cavities, other fistulas, and distal obstructions. A contrast enema demonstrates the presence of a colocutaneous fistula in 90%, a colovesical fistula in 34%, and a coloenteric fistula in most cases. Enteroclysis allows eval­uation for intrinsic intestinal disease. Cystoscopy identifies the fistula opening in 40% of enterovesical fistulas but the findings of localized bullous edema, with erythema and possible ulcer­ation, are suggestive of the diagnosis in most patients. GI endos­copy allows direct visualization of colonic, intestinal, and gastroduodenal mucosa. A CT scan allows evaluation for the resolution of intra­abdominal abscesses and presence of intrinsic intestinal disease.

With such an orchestrated approach, most external fistulas heal spontaneously. Factors associated with spontaneous healing or failure to close are listed in Table 13­16. After control of sepsis, approximately 60% to 90% of external intestinal fistulas with favorable factors will close spontaneously with medical management, 90% will close within 4 to 6 weeks, and less than 10% in months 2 and 3. There are limited therapeutic options for ECFs that fail to close—accept the fistula as a stoma await­ing optimal time for definitive closure or attempt direct closure.

Direct repair is applicable to a superficial bud fistula whereby limited dissection is performed to identify and close the edges of the fistula extraperitoneally and protect the suture line with a biologic dressing, with or without tissue adhesive. Although several attempts may be required to achieve successful closure of the fistula, the surgery is a local low­risk procedure and can be repeated. Definitive repair requires careful planning and may be a daunting task. Definitive closure requires a waiting period of 8 to 12 weeks, and requires that sepsis be controlled, nutrition provided, and skin is protected. The waiting period is crucial to allow recovery of immunologic competence, improve­ment of nutritional status, and resolution of the period of dense inflammatory reaction. There are no well­established guidelines to help in determining the timing of surgery. However, the expe­rience of the surgeon, general condition of the patient, softness of the abdominal wall and abdominal cavity, and surgical anatomy of the fistula must be taken into consideration. A dense


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for most postoperative biliary injuries and strictures. The rate of major bile duct injury after laparoscopic cholecystectomy ranges from 0.4% to 0.7%, as opposed to 0.2% after open cholecys­tectomy.49 Bile leak may be caused by a bile duct injury, cystic duct stump leak, divided accessory duct, or injury to the intes­tine. Acute cholecystitis, a foreshortened cystic duct, anomalies of the biliary tree, hemorrhage from injury to the cystic or hepatic artery, dissection with thermal instruments in the triangle of Calot, and failure to define the anatomy in the tri­angle of Calot clearly are among the most important factors associated with a higher frequency of duct injury after laparoscopic cholecystectomy.

The most common injury sustained during the laparo­scopic procedure is complete transection at or below the hepatic duct bifurcation. Other less complex injuries include occlusion of the duct with a clip, thermal injury, avulsion of the cystic duct, and partial laceration.

presentation and diagnosisMost bile duct injuries are not identified at the time of surgery. Early in the postoperative period, patients may have manifesta­tions related to a bile leak or have signs of a bile duct stricture later. Bile leaking from a lacerated divided duct may accumulate in the subhepatic space and form a biloma or seep into the peritoneal cavity and result in bile ascites. Patients in this situ­ation have right upper quadrant pain, fever, nausea, abdominal distention, and malaise. The bile, on the other hand, may drain through an intraoperatively placed drain and be manifested as a bile leak. In this setting patients, may have leukocytosis and a slightly elevated bilirubin level. Patients with a clipped bile duct do not usually have symptoms but do have elevated liver enzyme levels. Bile duct strictures are usually accompanied by cholangi­tis, pain, fever, chills, and jaundice.

Diagnosis of bile duct injury requires the use of nuclear medicine imaging to demonstrate the presence of a leak or obstruction, a CT scan to identify bile collections or ascites, and ERCP to define the type and level of injury accurately. Percuta­neous transhepatic cholangiography is indicated in cases of com­plete transection to define the proximal anatomy and site of injury. Magnetic resonance cholangiopancreatography is becom­ing the test of choice to diagnose late strictures and define the bile duct anatomy.

treatmentPrevention of bile duct injury starts with proper surgical tech­nique and adequate identification of the anatomy. The anatomic variability associated with severe inflammation creates a low threshold for converting a laparoscopic to an open cholecystec­tomy. During laparoscopic cholecystectomy, the infundibulum of the gallbladder must be retracted laterally and inferiorly to expose the triangle and widen the cystic–common bile duct angle. Dissection of the cystic duct and artery must commence close to the infundibulum of the gallbladder. The cystic duct and artery are divided once the anatomy is clearly delineated. Excessive traction on the gallbladder must be avoided because it will result in tenting of the common duct. If there is bleeding in the area of the cystic duct, blind clipping and cautery must be avoided and adequate exposure must be achieved, even if placement of another port is required. If there is an unexpected bile leak, unusual anatomy, or a second bile duct identified, or when technical difficulties and excessive bleeding are

for fistula formation. Pulmonary problems, autodigestion, and erosion into adjacent organs are additional significant morbidi­ties associated with pancreatic fistulas. Sepsis and hemorrhage are associated with significant mortality (20% to 40%) and result in prolonged hospitalization and increased hospital expense. Postoperative pancreatic fistula is diagnosed when there is drain output of any measurable volume of fluid after postop­erative day 3 with an amylase content more than three times the serum amylase activity. More often, the fluid amylase content is in the tens of thousands. The fistula is demonstrated on a fistu­logram or CT scan.

Efforts to decrease the morbidity and mortality of pan­creatic fistulas after pancreaticoduodenectomy focus on pre­venting, decreasing, and controlling pancreatic leaks at the pancreatic­enteric reconstruction (see earlier, “Anastomotic Leak”). The benefit of perioperative somatostatin or its ana­logue have been evaluated in two meta­analysis studies. One study noted that somatostatin and octreotide reduce the rate of biochemical fistula but not the incidence of clinical anasto­motic dehiscence, whereas the other noted a significant reduc­tion in pancreatic fistula rate but no significant difference in postoperative mortality. Intraoperatively, a modified side to end pancreaticojejunal anastomosis provides a tension­free anastomosis to a pancreatic stump, with adequate blood supply and unobstructed flow of pancreatic juice in optimal. Common to this modified pancreaticojejunostomy is mobili­zation of the pancreatic stump to allow invagination of 3 to 4 cm of pancreatic stump into the jejunum, ablation of the jejuna mucosa in the area of the jejunum­pancreas interface, suturing the capsular edge of the pancreatic stump to mucosa of the everted jejunum, or the use of traction sutures between the capsular edge and jejunum proximal edge to avoid slip­page of the stump out of the jejunum.

Once a pancreatic fistula has formed, medical treatment results in spontaneous closure in almost all fistulas after a pan­creaticoduodenectomy and in up to 80% of all other cases of pancreatic fistulas. Octreotide therapy is beneficial because it significantly reduces fistula output and decreases the time to fistula closure. Endoscopic retrograde cholangiopancreatogra­phy (ERCP) is valuable because it defines the pancreatic duct anatomy and ductal obstruction and allows the placement of a stent that bypasses the high­resistance areas of the sphincter of Oddi, ductal strictures, and calculi, thus allowing pancreatic secretions to follow the path of least resistance. The stent may also block the ductal opening of the fistula. Operative treat­ment of a benign pancreaticocutaneous fistula depends on the location of the fistula (proximal versus distal portion of the pancreas) and status of the pancreatic duct (dilated versus ste­notic duct). High excision of the fistula with fistuloenteros­tomy has been associated with the best results. Pseudocyst enterostomy is associated with an unacceptable recurrence and failure rate.

HepatoBiliary complicationS

Bile duct injuries

CausesThe most dreaded complication of gallbladder surgery is injury to the extrahepatic bile duct system. Cholecystectomy accounts





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consciousness and changes in cognition. They may have reduced ability to focus, decreased levels of awareness, and difficulty with attention. In addition, they may have hallucinations and altered psychomotor activity and sleep­wake cycle. These changes have a tendency to fluctuate during the course of the day and are worse at night (sundowning). The severity of these manifesta­tions depends on the underlying cause.

The incidence of postoperative delirium and cognitive dis­orders in geriatric patients varies with the type of surgery per­formed and preexisting dementia. Postoperative anemia (secondary to acute blood loss), electrolyte imbalance, sepsis, malnutrition, bladder catheterization, physical restraints, extended duration of anesthesia, infection, and respiratory com­plications are significant precipitating factors.

The most immediately threatening disorder encountered by physicians is delirium tremens, which may occur 48 hours to 14 days after acute alcohol withdrawal. In addition, delirium tremens is associated with extreme autonomic hyperactivity. Early signs of delirium tremens include fever, tremor, and tachy­cardia, and late signs include confusion, psychosis, agitation, and seizures. Because of the serious underlying nutritional and medical deficiencies, these patients have s moderately high mor­tality, which approaches 20% in some series.

encountered, intraoperative cholangiography helps identify the anatomy and any injuries. Early conversion to an open proce­dure must also be considered.

Once a leak is diagnosed intraoperatively, immediate repair must be performed. The procedure is converted to an open one and the extent of duct injury is assessed. An acces­sory duct can be ligated, partial transection of the common duct can be repaired over a T tube, a divided duct or almost circumferential transection of the common duct can be repaired with an end­to­end anastomosis over a T tube, and a high injury can be repaired with a Roux­en­Y biliary enteric anastomosis. If repair of a high duct injury is difficult, drains are placed in the subhepatic space and the patient is referred to a tertiary center.

A leak or injury identified early in the postoperative period is treated as follows. The biloma is drained percutaneously, and a sphincterotomy is performed, a stent is placed, or both can be done if ERCP demonstrates a leak or partial narrowing. Surgical intervention is indicated for patients with major obstruction of the bile duct, major injury, or suspicion of a bowel injury. After adequate resuscitation, administration of antibiotics, and ade­quate drainage, patients are watched for a few days to make certain that they are not septic at the time of the operation. If there is evidence of adequate control of the leak, the surgeon may wait up to 5 to 7 days for inflammation in the area to subside before undertaking operative repair. Meticulous and careful dissection is required in this area because there is usually loss of common bile duct substance. After identifying the source of the bile extravasation, dissection plus débridement of nonvi­able common bile duct is prudent. Once it has been ascertained that there is tissue with good integrity, a Roux­en­Y limb can be anastomosed to the common bile duct. Multiple drains are left around the site of the repair.

neurologic complicationS

delirium, cognitive disorder, and psychosis

CauseDelirium refers to a state of acute confusion and is a common complication of surgery. Numerous factors are implicated in causing delirium (Box 13­14). The presence of a structural brain disorder (infarct) increases the individual’s susceptibility to delir­ium. Anticholinergic medications and conditions that decrease the production of acetylcholine can precipitate delirium. In addition, a planned operation with loss of the patient’s routine schedule, stress of the disease process, fear of the operation, loss of personal control, placement in an unfamiliar environment, addition of mind­altering pain medications, and pain can lead to dramatic alterations in behavior in postoperative patients. At particularly high risk for behavioral disorders in the postopera­tive period are older patients, patients with a previous history of substance abuse or psychiatric disorders, and children.

presentation and DiagnosisEarly in the postoperative period, a patient may become acutely agitated, uncooperative, and confused. Patients with a previous psychiatric disorder may, however, become more withdrawn and depressed. Some patients may become noncommunicative and emotionally flat and may withdraw from any emotional exchange. Patients may also show an altered level of

Box 13-14  causes of acute Delirium

advanced agealcohol intoxication and withdrawalDrugs (overdose or withdrawal)

• anticholinergic  drugs  (tricyclic  antidepressants, antihistamine)

• oral hypoglycemic agents• antibiotics (cephalosporins)• Histamine receptor blocking agents• anti-inflammatory drugs (e.g., steroidal, nonsteroidal)• anticonvulsant medications• anxiolytics (diazepam)• narcotics• cardiac medications (beta blockers, digoxin)

Structural brain abnormalities (e.g., edema, transient  ischemic attack, neoplasm)

Metabolic and hemodynamic disturbances• electrolyte imbalance• Hypoglycemia• Hypoxemia• Hypovolemia

endocrine dysfunction• thyrotoxicosis• Hypothyroidism• adrenocortical insufficiency

Sepsis and infectionsrespiratory  dysfunction  (e.g.,  respiratory  failure,  pulmonary 

embolism, chronic obstructive pulmonary disease)liver, renal, cardiac disease (e.g., congestive heart failure, renal 

failure)trauma (surgical or otherwise)critical illness and intensive care unit stay

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presentation and managementSeizures characterized by convulsions, rhythmic myoclonic activity, loss of consciousness, and change in mental status are often associated with fecal and urinary incontinence, lack of neurologic responsiveness, and postevent amnesia. On recogniz­ing evidence of seizure activity, the patient must be carefully restrained so that injury is not sustained during convulsions and is carefully observed. Administration of IV benzodiazepines is essential to stop the seizure activity and is the standard for immediate care. Phenytoin (Dilantin) is the most commonly used anticonvulsant for new­onset generalized or focal seizures. It may be administered IV during acute convulsions or PO for maintenance. Phenytoin has several side effects, including rash and liver dysfunction. Occasionally, phenobarbital may be used but, because of sedation, is not an agent of choice. The two most commonly used agents for maintenance after seizures or for someone with status epilepticus are carbamazepine (Tegretol) and valproic acid. Neither of these agents can be given IV and thus are used for maintenance only. Gabapentin can be admin­istered when the patient’s condition is refractory to other agents. After adequate control of the seizure, a diagnostic workup for its cause is initiated. This includes a detailed history and physi­cal examination, history of previous medication and drug use, WBC count to rule out occult infection, and electrolyte and metabolic assessment. CT or MRI is indicated for a patient with new­onset seizure activity because tumors are often the cause. Similarly, an electroencephalogram is obtained at some point to look for abnormal waveform activity.

Stroke and transient ischemic attacks

CausesA stroke in the perioperative period is devastating and correlates with the type of operative procedure performed, age of the patient, and presence of risk factors for cardiovascular disease. Strokes are more commonly associated with cardiovascular pro­cedures. Although older adults with cardiovascular disease are at a higher risk for a stroke, younger individuals are not exempt, especially those with an underlying inherited thrombophilia.

Postoperative strokes may be ischemic or hemorrhagic in nature. Ischemic strokes most commonly result from periopera­tive hypotension or overzealous control of hypertension, or from cardioemboli in patients with atrial fibrillation. Other sources of cardioemboli include MI and bacterial endocarditis. An embolus arising from DVT and traversing a patent foramen ovale (i.e., paradoxical embolization) may be responsible for strokes of unknown cause. Hemorrhagic strokes are less common and are mostly related to therapy with anticoagulants. Factors related to coagulation disorders, such as chronic abuse of alcohol, acquired immunodeficiency syndrome (AIDS), cocaine use, bleeding diathesis, and preexisting cerebrovascular anomalies, are associated with an increased risk for hemorrhagic stroke.

presentation and managementIn all cases of stroke, the neurologic changes represent a dramatic departure from normal patient function. A focal alteration in motor function, alteration in mental status, aphasia, or occasion­ally unresponsiveness may be noted. Hemorrhagic strokes are uncommon, and their effect can be more devastating than isch­emic strokes that are transient (occurring for seconds to minutes) or reversible (occurring for minutes to hours). In truly

treatmentManagement of delirium and cognitive disorders in a postop­erative patient is a frustrating and challenging clinical scenario. Prevention starts with the identification of high­risk individuals before surgery and careful follow­up thereafter. Minimizing the dose or eliminating medications that interrupt mental function must be considered. Optimizing fluid status, providing nutrition and adequate pain control, and removing restraints early, includ­ing the Foley catheter, are essential. Early ambulation and trans­fer from the intensive care unit are encouraged.

Treatment of patients with acute confusion or a sudden change in behavior after surgery requires the following:

1. Recognition of the disorder2. Close observation and monitoring3. Identification and elimination of the precipitating

factor4. Treatment of any associated laboratory abnormalities5. Selective use of imaging or other studies to rule out

an organic brain lesion6. Application of measures to protect the patient and

staff7. Treatment

A history of drug or alcohol abuse and of cardiac, pulmo­nary, renal, or liver disease or psychiatric illness must be sought. A list of medications used in the perioperative period must be checked. Clinical evaluation is performed to look for evidence of sepsis or a recent neurologic event. A thorough neurologic examination is performed while focusing on the level of con­sciousness and presence of focal neurologic deficits, ataxia, paresis, or paralysis. Cognitive tests are conducted. Blood samples are sent to check for evidence of infection and to iden­tify metabolic, electrolyte, nutritional, and blood gas abnor­malities. A CXR and urinalysis are performed to look for a source of infection. An ECG is obtained to look for evidence of MI. CT or MRI, and occasionally a spinal tap, may be helpful in select cases.

Measures to protect the patient and staff may include the occasional use of physical restraints, reassurance by speaking to the patient, and allowing family members to be involved in patient care. Medical therapy includes haloperidol, a neuroleptic (0.5 to 2 mg, given IV or IM to achieve a rapid effect and then PO for maintenance therapy). Benzodiazepines are the drug of choice for acute alcohol withdrawal. Other medications, includ­ing haloperidol (to control psychosis), beta blockers (to control autonomic manifestations), and clonidine (to control hyperten­sion) are given in addition to benzodiazepine to patients with acute alcohol withdrawal.

Seizure disorders

CausesSeizures are caused by paroxysmal electrical discharges from the cerebral cortex and may be primary or secondary. Primary causes include intracranial tumor, hemorrhage, trauma, and idiopathic seizure activity. Secondary causes include metabolic derange­ment, sepsis, systemic disease processes, and pharmacologic agents. Patients at particularly high risk for postoperative seizure include those with a previous history of epilepsy and patients acutely withdrawing from alcohol or medications or receiving other pharmacologic agents, including antidepressants, hypogly­cemic agents, and lidocaine.


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refractory case. If the bleeding fails to stop, packing for an extended period with petroleum jelly–covered strip gauze may be required. Removal of the packing in 1 to 3 days is usually associated with successful treatment of refractory epistaxis, along with treatment of the underlying condition or reversal of anticoagulation.

A more serious scenario is posterior nasal septal bleeding, which on occasion can be life­threatening. If all attempts to stop anterior nasal septal bleeding are unsuccessful, one may infer the probability of a posterior nasal hemorrhage, which may necessitate placement of a posterior pack of strip gauze covered in petroleum jelly ointment. For particularly refractory cases, a Foley catheter with a 30­mL balloon can be passed through the nasal passages and, after the pack is placed, pres­sure can be applied to it by pulling on the Foley catheter. This type of epistaxis may require concomitant anterior nasal packing to be successful. The packs on a difficult hemorrhage such as this may need to be left in place for 2 to 3 days. For epistaxis that defies all attempts at conservative management, ligation of the sphenopalatine artery or anterior ethmoidal artery may be required.

acute Hearing lossAbrupt loss of hearing in the postoperative period is an uncom­mon event. An immediate physical examination is performed to ascertain the degree of hearing loss. Unilateral hearing loss is generally associated with obstruction or edema related to an NG or feeding tube. Bilateral hearing loss is more often neural in nature and is usually associated with pharmacologic agents, such as aminoglycosides and diuretics. Examination with an otoscope will often reveal the presence of cerumen impaction or edema from a middle ear infection. If the otologic examination is com­pletely normal, neural injury related to the agents just men­tioned should be suspected. These drugs need to be discontinued immediately and hearing monitored over the ensuing 2 to 3 days to see whether recovery occurs. For cerumen impaction, use of a delicate speculum under direct vision is indicated. If the hearing loss is associated with edema related to an NG tube, merely removing the NG tube will result in resolution of the edema.

nosocomial SinusitisNosocomial sinusitis is a recognized complication in the criti­cally ill. Left untreated, sinusitis may be complicated by brain abscess formation, postorbital cellulitis, and nosocomial pneu­monia. Patients at high risk for sinusitis are those receiving ventilatory support via a nasotracheal tube and those with nasal colonization with gram­negative bacteria. Also at risk are patients with facial trauma, those with an NG or feeding tube, and patients who have received antibiotic therapy.

Most nosocomial sinusitis occurs in the second week of hospitalization, and the maxillary sinuses are the most com­monly affected. The classic signs encountered with community­acquired sinusitis (e.g., facial pain, malaise, fever, and purulent nasal discharge) may not be present because the patient is usually unconscious and intubated, has other sources of infection, and is receiving analgesics and antipyretics. The diagnosis is often made when CT is performed to look for a source of fever and the sinuses are included in the cuts. The CT scan generally shows thickened mucosa and the presence of an air­fluid level or opaci­fication of the sinus.

irreversible injury, the impact on the patient’s overall health is immeasurable, and the patient’s ability to function and enjoy a good quality of life is severely compromised.

Prevention of a perioperative stroke starts with the identi­fication of at­risk patients. Patients with hypertension must receive adequate treatment, and overzealous correction must be avoided. Patients with atrial fibrillation benefit from prophylaxis with anticoagulants. Patients with a carotid bruit must be eval­uated with noninvasive vascular studies and treated accordingly. Patients undergoing a high­risk surgical procedure (e.g., carotid endarterectomy) may be monitored intraoperatively with tran­scranial Doppler and electroencephalography. Adequate hydra­tion and monitoring in the perioperative period to avoid hypotension and fluctuations in blood pressure are essential to avoid ischemic strokes.

On recognizing the clinical signs and symptoms of a stroke, the patient must have an IV line placed and be monitored for cardiac arrhythmias. Coagulation parameters are assessed for the presence of a coagulopathy, and blood is sent for culture and determination of the sedimentation rate to check for bacteremia and bacterial endocarditis. A diagnostic workup is started imme­diately to distinguish between hemorrhagic and ischemic stroke with a CT scan or MRI of the brain. Further tests depend on the clinical scenario, such as echocardiography to assess the heart for structural disease, carotid duplex scanning to assess patency of the carotid artery, and cerebral angiography to evaluate for vascular anomalies. Therapy is dictated by the underling mech­anism of the stroke. A hypertensive hemorrhagic stroke is treated by aggressive control of the hypertension, an embolic stroke (cardiogenic or secondary to inherited thrombophilia) is treated by anticoagulation (in the absence of a contraindication) to prevent recurrence, and a hemorrhagic stroke is treated by rever­sal of the coagulopathy with protamine, if secondary to heparin, or platelet transfusion, if secondary to antiplatelet therapy. Man­nitol and dexamethasone are given to reduce cerebral swelling. Treatment of any underlying cardiac arrhythmia is imperative to prevent recurrent embolization. Surgical intervention is indi­cated for patients with a localized hematoma or vascular anomaly, depending on the location and size of the hematoma, status of the patient, and accessibility of the aneurysm. Thrombolytic therapy (recombinant tissue plasminogen activator) is effective in restoring cerebral blood flow and minimizing brain injury if instituted early after the onset of an embolic event. Otherwise, low­dose aspirin therapy is the standard for acute ischemic infarction and, in patients who continue to have symptoms, antiplatelet agents (e.g., clopidogrel bisulfate, ticlopidine hydro­chloride) are added.

ear, noSe, and tHroat complicationS

epistaxisEpistaxis may be associated with primary blood dyscrasias such as leukemia and hemophilia, excessive anticoagulation, and hypertension. Epistaxis is divided into two general catego­ries, anterior and posterior. Anterior trauma is often caused by contusion or laceration of the nasal septum or turbinates during insertion of an NG or endotracheal tube. Firm pres­sure applied between the thumb and index finger to the nasal ala and held for 3 to 5 minutes is generally successful in stop­ping most cases of anterior epistaxis. Occasionally, packing with strip gauze for 10 to 15 minutes will aid in a particularly

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Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emer­gency Medicine. J Am Coll Cardiol 50:e1–e157, 2007.

Patients with angina, particularly unstable angina, represent a high-risk group for surgery. The paper provides practical guidelines for the man-agement of this challenging group of patients.

Anderson DJ, Kaye KS, Classen D, et al: Strategies to prevent surgi­cal site infections in acute care hospitals. Infect Control Hosp Epide­miol 29(Suppl 1):S51–S61, 2008.

Surgical site infections (SSIs) remain a serious cause of significant post-operative morbidity, increased cost, and poor outcomes. This paper provides a realistic strategy for lowering or preventing SSIs in the acute care hospital setting.

Cooper MS, Stewart PM: Corticosteroid insufficiency in acutely ill patients. N Engl J Med 348:727–734, 2003.

This paper discusses the topic of functional adrenal insufficiency in critically ill patients and outlines the workup and treatment strategies.

Dronge AS, Perkal MF, Kancir S, et al: Long­term glycemic control and postoperative infectious complications. Arch Surg 141:375–380, 2006.

This paper addresses the importance of glycemic control as it relates to postoperative infections.

Eagle KA, Berger PB, Calkins H, et al: ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluations for Noncardiac Surgery—Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. (Committee to Update the 1996 Guidelines on Periop­erative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg 94:1052–1064, 2002.

This important report from the ACC and AHA carefully outlines the management of patients with cardiac risk factors who will undergo a noncardiac operation.

Geerts WH, Bergqvist D, Pineo GF, et al: Prevention of venous thromboembolism: American College of Chest Physicians Evidence­Based Clinical Practice Guidelines (8th Edition). Chest 133:381S– 453S, 2008.

The ACCP offers evidence-based guidelines for preventing deep vein thrombosis in postoperative patients.

Heller L, Levin SL, Butler CE: Management of abdominal wound dehiscence using vacuum­assisted closure in patients with compro­mised healing. Am J Surg 191:165–172, 2006.

This paper deals with the concept of integration of vacuum-assisted closure systems in the management of wound dehiscence.

Lin HJ, Spoerke N, Deveney C, et al: Reconstruction of complex abdominal wall hernias using acellular human dermal matrix: A single institution experience. Am J Surg 197:599–603, 2009.

Once diagnosed or suspected, nasal tubes are removed, decongestant is administered, and antibiotic therapy targeting the two most common organisms, S. aureus and Pseudomonas spp., is given. Other organisms that play a major role in noso­comial infections, such as MRSA and vancomycin­resistant Enterococcus and Acinetobacter spp., are also included in the coverage. With such treatment, clinical response occurs in 48 hours and a clinical and radiologic cure occurs in two thirds of patients. Failure of medical therapy leads to surgical drain­age of the sinus involved. In rare cases, severe intractable sinusitis may require a drainage procedure via an operative technique.

parotitisParotitis most commonly occurs in an older man with poor oral hygiene and poor oral intake, with an associated decrease in saliva production. The pathophysiology involves obstruction of the salivary ducts or an infection in a diabetic or immuno­compromised patient. The patient is noted to have significant edema and focal tenderness surrounding the parotid gland, which eventually progresses to involve edema of the floor of the mouth. If left undiagnosed and untreated, the parotitis can cause life­threatening sepsis. In the worst case scenario, the infection can dissect into the mediastinum and cause stridor from partial airway obstruction. Patients with advanced parotitis will have dysphagia and some respiratory occlusion. If the diagnosis of parotitis is being entertained, the patient receives IV, high­dose, broad­spectrum antibiotics with good coverage of Staphylococcus, the most common agent cultured from this disease. In the presence of a fluctuant area, incision plus drainage is indicated, with care taken to avoid the facial nerve. Rarely, advanced disease may even require emergency tracheostomy. Most patients with parotitis will have the condi­tion arise 4 to 12 days after the initial operation. Because of the rapid progression of this disease, one must be aware of the diagnosis and, when present, institute immediate therapy, including occasional emergency surgery for patients with an obvious fluctuant area.

Selected reFerenceSAlmanaseer Y, Mukherjee D, Kline­Rogers EM, et al: Implementa­tion of the ACC/AHA guidelines for preoperative risk assessment in a general medicine preoperative clinic: Improving efficiency and pre­serving outcomes. Cardiology 103:24–29, 2005.

This paper describes the clinical predictors of increased cardiovascular risk leading to acute cardiac events in surgical patients. Implementation of these predictors may also allow better selection of patients who require more specific preoperative cardiac evaluation and beta blocker therapy.

Anderson JL, Adams CD, Antman EM, et al: ACC/AHA 2007 guidelines for the management of patients with unstable angina/non­ST­Elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non­ST­Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardio­vascular Angiography and Interventions, and the Society of Thoracic



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13-46  section ii  PerioPerative ManageMent

repair in a compromised surgical field. Arch Surg 144:209–215, 2009.

3. Heller L, Levin SL, Butler CE: Management of abdominal wound dehiscence using vacuum­ assisted closure in patients with com­promised healing. Am J Surg 191:165–172, 2006.

4. Mangram AJ, Horan TC, Pearson ML, et al: Guideline for preven­tion of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol 20:250–278, 1999.

5. Awad SS, Elhabash SI, Lee L, et al: Increasing incidence of methicillin­resistant Staphylococcus aureus skin and soft­tissue infections: Reconsideration of empiric antimicrobial therapy. Am J Surg 194:606–610, 2007.

6. National Nosocomial Infections Surveillance (NNIS): System Report, Data Summary from January 1992–June 2001, issued August 2001. Am J Infect Control 29:404–421, 2001.

7. Culver DH, Horan TC, Gaynes RP, et al: Surgical wound infec­tion rates by wound class, operative procedure, and patient risk index. National Nosocomial Infections Surveillance System. Am J Med 91:152S–157S, 1991.

8. Anderson DJ, Kaye KS, Classen D, et al: Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 29(Suppl 1):S51–S61, 2008.

9. Buggy DJ, Crossley AW: Thermoregulation, mild perioperative hypothermia and postanaesthetic shivering. Br J Anaesth 84:615–628, 2000.

10. Rosenberg H, Antognini JF, Muldoon S: Testing for malignant hyperthermia. Anesthesiology 96:232–237, 2002.

11. Jawa RS, Kulaylat MN, Baumann H, et al: What is new in cyto­kine research related to trauma/critical care? J Intensive Care Med 21:63–85, 2006.

12. Bukhary ZA: Candiduria: A review of clinical significance and management. Saudi J Kidney Dis Transpl 19:350–360, 2008.

13. Centers for Medicare and Medicaid Services (CMS), HHS: Medi­care program; changes to the hospital inpatient prospective payment systems and fiscal year 2008 rates. Fed Regist 72: 47129–48175, 2007.

14. Edwards JR, Peterson KD, Andrus ML, et al: National Healthcare Safety Network (NHSN) Report, data summary for 2006, issued June 2007. Am J Infect Control 35:290–301, 2007.

15. Ksycki MF, Namias N: Nosocomial urinary tract infection. Surg Clin North Am 89:475–481, ix–x, 2009.

16. American Thoracic Society; Infectious Diseases Society of America: Guidelines for the management of adults with hospital­acquired, ventilator­associated, and healthcare­associated pneumonia. Am J Respir Crit Care Med 171:388–416, 2005.

17. Practice guidelines for preoperative fasting and the use of pharma­cologic agents to reduce the risk of pulmonary aspiration: applica­tion to healthy patients undergoing elective procedures: A report by the American Society of Anesthesiologist Task Force on Preop­erative Fasting. Anesthesiology 90:896–905, 1999.

18. Heit JA, Silverstein MD, Mohr DN, et al: Risk factors for deep vein thrombosis and pulmonary embolism: a population­based case­control study. Arch Intern Med 160:809–815, 2000.

19. Goldhaber SZ: Echocardiography in the management of pulmo­nary embolism. Ann Intern Med 136:691–700, 2002.

20. Geerts WH, Bergqvist D, Pineo GF, et al: Prevention of venous thromboembolism: American College of Chest Physicians Evidence­Based Clinical Practice Guidelines (8th Edition). Chest 133:381S–453S, 2008.


The development of a biologic prosthesis that can be placed in a con-taminated field during hernia repair has provided a relatively new treat-ment paradigm for the management of these complex patients. This paper is a retrospective review of a single institute’s experience with one type of biologic prosthesis.

Migneco A, Ojetti V, Testa A, et al: Management of thyrotoxic crisis. Eur Rev Med Pharmacol Sci 9:69–74, 2005.

This paper outlines the manifestations and treatment of an uncommon but potentially devastating complication of thyrotoxicosis.

Moore AFK, Hargest R, Martin M, et al: Intra­abdominal hyper­tension and the abdominal compartment syndrome. Br J Surg 91: 1102–1110, 2004.

This paper is important because it details the pathophysiology of intra-abdominal hypertension and abdominal compartment syndrome and attempts to provide guidelines for medical and surgical management of patients in whom these complications develop.

Perry SL, Ortel TL: Clinical and laboratory evaluation of thrombo­philia. Clin Chest Med 24:153–170, 2003.

This review outlines the causes and workup of patients with a hyperco-agulable state and provides recommendations for testing this high-risk group of patients.

Sailhamer EA, Carson K, Chang Y, et al: Fulminant Clostridium difficile colitis: Patterns of care and predictors of mortality. Arch Surg 144:433–439, 2009.

This recent description of a more virulent, resistant, and aggressive form of C. dificile makes this paper highly relevant.

Simon TL, Alverson DC, AuBuchon J, et al: Practice parameter for the use of red blood cell transfusions: Developed by the Red Blood Cell Administration Practice Guideline Development Task Force of the College of American Pathologists. Arch Pathol Lab Med 122: 130–138, 1998.

This paper is the result of a consensus conference held by the College of American Pathologists regarding blood transfusion and its usefulness for the treatment of surgical patients.

Slim K, Vicaut E, Panis Y, et al: Meta­analysis of randomized clinical trials of colorectal surgery with or without mechanical bowel prepara­tion. Br J Surg 91:1125–1130, 2004.

This paper sheds light on the usefulness of mechanical bowel prepara-tion before colorectal surgery.

reFerenceS1. Douketis JD, Berger PB, Dunn AS, et al: The perioperative man­

agement of antithrombotic therapy: American College of Chest Physicians Evidence­Based Clinical Practice Guidelines (8th Edition). Chest 133:299S–339S, 2008.

2. Diaz JJ, Jr, Conquest AM, Ferzoco SJ, et al: Multi­institutional experience using human acellular dermal matrix for ventral hernia

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and problem­oriented, New York, 2001, Zuckschwerdt, pp 102–113.

34. Kirkpatrick AW, Balogh Z, Ball CG, et al: The secondary abdom­inal compartment syndrome: Iatrogenic or unavoidable? J Am Coll Surg 202:668–679, 2006.

35. Simon TL, Alverson DC, AuBuchon J, et al: Practice parameter for the use of red blood cell transfusions: Developed by the Red Blood Cell Administration Practice Guideline Development Task Force of the College of American Pathologists. Arch Pathol Lab Med 122:130–138, 1998.

36. Seder CW, Villalba MR, Jr, Robbins J, et al: Early colectomy may be associated with improved survival in fulminant Clostridium difficile colitis: An 8­year experience. Am J Surg 197:302–307, 2009.

37. Sailhamer EA, Carson K, Chang Y, et al: Fulminant Clostridium difficile colitis: Patterns of care and predictors of mortality. Arch Surg 144:433–439; discussion 439–440, 2009.

38. Pepin J, Vo TT, Boutros M, et al: Risk factors for mortality fol­lowing emergency colectomy for fulminant Clostridium difficile infection. Dis Colon Rectum 52:400–405, 2009.

39. Slim K, Vicaut E, Panis Y, et al: Meta­analysis of randomized clinical trials of colorectal surgery with or without mechanical bowel preparation. Br J Surg 91:1125–1130, 2004.

40. Uzunkoy A, Akinci OF, Coskun A, et al: Effects of antiadhesive agents on the healing of intestinal anastomosis. Dis Colon Rectum 43:370–375, 2000.

41. August DA, Serrano D, Poplin E: “Spontaneous,” delayed colon and rectal anastomotic complications associated with bevacizumab therapy. J Surg Oncol 97:180–185, 2008.

42. Branagan G, Finnis D: Prognosis after anastomotic leakage in colorectal surgery. Dis Colon Rectum 48:1021–1026, 2005.

43. Stojadinovic A, Brooks A, Hoos A, et al: An evidence­based approach to the surgical management of resectable pancreatic adenocarcinoma. J Am Coll Surg 196:954–964, 2003.

44. Orgill DP, Manders EK, Sumpio BE, et al: The mechanisms of action of vacuum­assisted closure: More to learn. Surgery 146: 40–51, 2009.

45. Teubner A, Morrison K, Ravishankar HR, et al: Fistuloclysis can successfully replace parenteral feeding in the nutritional support of patients with enterocutaneous fistula. Br J Surg 91:625–631, 2004.

46. Wainstein DE, Fernandez E, Gonzalez D, et al: Treatment of high­output enterocutaneous fistulas with a vacuum­compaction device. A ten­year experience. World J Surg 32:430–435, 2008.

47. Wind J, van Koperen PJ, Slors JF, et al: Single­stage closure of enterocutaneous fistula and stomas in the presence of large abdominal wall defects using the components separation tech­nique. Am J Surg 197:24–29, 2009.

48. Lin HJ, Spoerke N, Deveney C, et al: Reconstruction of complex abdominal wall hernias using acellular human dermal matrix: A single institution experience. Am J Surg 197:599–603, 2009.

49. Krahenbuhl L, Sclabas G, Wente MN, et al: Incidence, risk factors, and prevention of biliary tract injuries during laparoscopic cholecystectomy in Switzerland. World J Surg 25:1325–1330, 2001.

21. Eagle KA, Berger PB, Calkins H, et al: ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncar­diac Surgery—Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg 94:1052–1064, 2002.

22. Anderson JL, Adams CD, Antman EM, et al: ACC/AHA 2007 guidelines for the management of patients with unstable angina/non­ST­Elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non­ST­Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physi­cians, the Society for Cardiovascular Angiography and Interven­tions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Reha­bilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol 50:e1–e157, 2007.

23. Almanaseer Y, Mukherjee D, Kline­Rogers EM, et al: Implemen­tation of the ACC/AHA guidelines for preoperative cardiac risk assessment in a general medicine preoperative clinic: improving efficiency and preserving outcomes. Cardiology 103:24–29, 2005.

24. Polanczyk CA, Goldman L, Marcantonio ER, et al: Supraven­tricular arrhythmia in patients having noncardiac surgery: clinical correlates and effect on length of stay. Ann Intern Med 129: 279–285, 1998.

25. Hunt SA, Baker DW, Chin MH, et al: ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: Executive summary. J Heart Lung Transplant 21:189–203, 2002.

26. Bonet S, Agusti A, Arnau JM, et al: Beta­adrenergic blocking agents in heart failure: benefits of vasodilating and non­vasodilating agents according to patients’ characteristics: A meta­analysis of clinical trials. Arch Intern Med 160:621–627, 2000.

27. Moore AF, Hargest R, Martin M, et al: Intra­abdominal hyper­tension and the abdominal compartment syndrome. Br J Surg 91:1102–1110, 2004.

28. Karsou SA, Jaber BL, Pereira BJ: Impact of intermittent hemodi­alysis variables on clinical outcomes in acute renal failure. Am J Kidney Dis 35:980–991, 2000.

29. Cooper MS, Stewart PM: Corticosteroid insufficiency in acutely ill patients. N Engl J Med 348:727–734, 2003.

30. Migneco A, Ojetti V, Testa A, et al: Management of thyrotoxic crisis. Eur Rev Med Pharmacol Sci 9:69–74, 2005.

31. Postoperative Ileus Management Council: Proceedings of Con­sensus Panel to Define Postoperative Ileus. Colorectal surgery consensus report, Atlanta, 2006, Thomson American Health Consultants.

32. Schwarz NT, Kalff JC, Turler A, et al: Selective jejunal manipula­tion causes postoperative pan­enteric inflammation and dysmotil­ity. Gastroenterology 126:159–169, 2004.

33. Kulaylat MN, Doerr RJ: Small bowel obstruction. In Holzheimer RG, Mannick JA, editors: Surgical treatment—evidence­based

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