Emergencies in Urology - part 7 pot

Lower urinary tract infection Upper urinary tract infection Organism cultured from fluid (other than urine) or tissue from the infected site. Abscess or other evidence of infection seen on examination, during surgery, or by histopathologic examination >38 °C Urgency Localized pain/ tenderness Hematuria Pyuria Organism isolated from culture Positive Gram stain Radiographic evidence of infection leukocytosis >12.000/µl leukopenia <400/µl Fibrinogen <1g/l Platelets <50.000 mm 3 PT 1.5–1.8 x control aPPT 1.5–1.8 x control Clinical signs Urine >38 °C Urgency Frequency Dysuria Pyuria Hematuria Pos. Gram stain Pus Suprabubic Tenderness > 3 leukocytes/high power field of unspun urine Positive dipstick (for leukocytes/nitrite) Urine culture ≥ 10 cfu/ml or two of the following Clinical signs Lap test Hypothermia <36 °C Hypothermia >38 °C Tachycardic >90/min Tachypnoe >20/min art. pCO 2 <4.3 kPa (33 mmHg) Ultrasound plain x-ray (abdomen) CT scan MRI Kidney Perinephric abscess Abscess of the kidney Retroperitoneal abscess Pyelonephritis Obstructive stones Tumor Lymphoma Pregnancy Extra/intraperitoneal Tumor Tbc Ureter Retroperitoneal abscess Retroperitoneal fibrosis Obstructive stones Obstructive tumor Extraluminal obstruction Lymphoma Pregnancy Extra/intraperitoneal Tumor Tbc Bladder Acute urinary retention Bladder stone Reflux Benign prostatic enlargement Diverticulum Bladder tumor Tbc Prostate Acute prostatitis Seminate vesicle abscess Epididymitis Orchitis Tbc Abscess drainage Double-J Mono-J Nephrostomy Zystostomy Transurethral catheter Operation Antibiotics (Table 18.1.27) + or Fig. 18.1.7. Workup and management of urinary tract infection 18.1 Acute Postoperative Complications 387 Table 18.1.28. Antimicrobial therapy of venous catheter- related bacteremia depend- ing on identity of pathogen therapy duration Pathogen Therapy Duration Staphylococcus aureus (oxacillin-sensitive) Isoxazolyl penicillin (penicillase-resistant penicillin) a At least 2 weeks i.v. b Staphylococcus aureus (oxacillin-resistant) Glycopeptide, linezolid, quinupristin + dalfopristin At least 2 weeks i.v. b Coagulase-negative staphylococci According to susceptibility pattern; glyco- peptide only in oxacillin-resistant cases For 5–7 days after defervescence Enterococci Aminopenicillin plus aminoglycoside For 5–7 days after defervescence Glycopeptide plus aminoglycoside in ampi- cillin-resistant cases Linezolid or quinupristin/dalfopristin in vancomycin-resistant cases Candida albicans Fluconazole 2weeks Alternative: amphotericin B or caspofungin Non-albicans Candida species Amphotericin B 2weeks Alternative: caspofungin or Voriconazole or itraconazole All other pathogens According to susceptibility pattern Not defined Follow-up blood cultures are always necessary after cessa- tion of antibiotic therapy in order to rule out persistence of infection From Fatkenheuer et al. (2003) a For oxacillin-sensitive strains (vast majority), treatment with penicillase- resistant penicillin is supe- rior to treatment with a glycopeptide. b High incidence of organ infection if treatment is continued for less than 2 weeks. Catheter removal is required whenever these pathogens are present Surgical Site Infection: Wound Management Despite prophylactic measures and good surgical tech- nique, a small percentage of patients will still experi- ence wound complications. SSIs require manual open- ing of the wounds to allow drainage. An open wound can be managed in two ways: secondary closure, sec- ondary intention with dressings or using negative pres- sure wound therapy. Secondary closure can be performed once a wound is free of infection or necrotic tissue and has started to granulate. This procedure is done within 1–4 days after evacuation of hematoma or seroma. The suture may be removed 7 days after reclosure. Several studies showed that patients who were treated with secondary closure required significantly fewer days to heal than patients who were allowed to heal by secondary intention. Modern wound care dressing selection considers fac- tors such as the phase of healing, the volume of exudate, and the presence of necrotic tissue to determine the type of dressing that willbe most supportiveofwound healing. The risk of infection can be reduced by using a nontoxic solutiontocleansethewound,e.g.,normalsaline(Ta- ble 18.1.29). Necrotic tissue can be removed by sharp de- bridement or daily applications of enzymatic debriders thatact onnecrotic tissue but have no effect on healthytis- sue. Drainage can be managed by using highly absorbent dressing material. Calcium alginate and foam are materi- als used in wound care that are highly absorbent. Negative pressure wound therapy also known as vacuum-assisted closure uses controlled levels of nega- tive pressure to assist and accelerate wound healing by evacuating localized edema with negative pressure. Bacterial colonization is reduced along with the evacu- ationofwounddrainage.Negativepressurealsoin- creases localized blood flow and oxygenation, thereby Table 18.1.29. Historically used dressing for wound cleansing Misconceptio ns about wound healing Agent Problem Povidone iodine Cytotoxic to white blood cells and other vital wound-healing compo- nents Iodophor gauze Delays wound healing Hydrogen peroxide Delays wound healing Keeping the wound dry Moist wounds promote autolytic debridement, support epithelial cell migration Table 18.1.30. Definition of infective endocarditis Definite infective endocarditis Pathologic criteria – Microorganisms demonstrated by culture or histologic examination of a vegetation, a vegetation that has embo- lized, or an intracardiac abscess, or – Pathologic lesions; vegetation or intracardiac abscess confirmed by histologic examination showing active en- docarditis Clinical criteria –2Majorcriteriaor – 1 Major criterion and 3 minor criteria or – 5 Minor criterion Possibleinfectiveendocarditis – 1 Major criterion and 1 minor criterion or – 3 Minor criteria Rejected – Firm alternative diagnosis explaining evidence of infec- tive endocarditis or – Resolution of infective endocarditis syndrome with anti- biotics therapy <4 days or – No pathologic evidence of infective endocarditis at sur- gery or autopsy, with antibiotic therapy for <4 days or – Does not meet criteria for possible infective endocarditis 388 18 Postoperative Complications promoting a nutrient-rich environment that stimulates granulation tissue growth. Such cellular proliferation encourages angioneogenesis, uniform wound size re- duction, and reepithelialization. 18.1.4.7 Special Conditions Fever Due to Infective Endocarditis Infective endocarditis accounts for about 1% of all cases of severe sepsis and is associated with a mortality rate of 33% (Angus et al. 2001). Diagnostic criteria for infective endocarditis, referred to as the Duke criteria, are based on microbiological data and echocardio- graphic imaging findings. According to these criteria, Table 18.1.31. Definitionofmajorandminorcriteriaofinfec- tive endocarditis Major criteria Blood culture positive for IE Typical microorganisms consistent with IE from two sepa- rate blood cultures: Streptococcus viridans, Streptococcus bovis,HACEKgroup, Staphylococcus aureus or Community-acquired enterococci in the absence of a primary focus or Microorganisms consistent with IE from persistently posi- tive blood cultures, defined as follows: At least two positive cultures of blood samples drawn >12 h apart or Allofthreeoramajorityoffourormoreseparatecul- tures of blood (with first and last sample drawn at least 1 h apart) Single positive blood culture for Coxiella burnetii or anti- phase I IgG antibody titer >1 : 800 Evidence of endocardial involvement Echocardiogram positive for IE (TEE recommended in pa- tients with prosthetic valves, rated at least “possible IE” by clinical criteria, or complicated IE (paravalvular abscess); TTE as first test in other patients), defined as follows: Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets or On implanted material in the absence of an alternative anatomic explanation or Abscess or New partial dehiscence of prosthetic valve New valvular regurgitation (worsening or changing of pre- existing murmur not sufficient) Minor criteria Predisposition, predisposing heart condition, or injection drug use Fever, temperature >37°C Vascular phenomena, major arterial emboli, septic pulmo- nary infarcts, mycotic aneurysm, intracranial hemor- rhage, conjunctival hemorrhages, and Janeway lesions Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evi- dence of active infection with organism consistent with IE Echocardiographic minor criteria eliminated IE infective endocarditis, TEE transesophageal echocardiogra- phy, TTE transthoracic echocardiography patients are classified into three diagnostic categories (definite, possible, and rejected endocarditis; see Ta- bles 18.1.30 and 18.1.31). Recently, modifications of the Duke criteria have been proposed to take into account several identified shortcomings of the original criteria, including the increasing diagnostic role of transesoph- ageal echocardiography and the relative risk of infec- tive endocarditis in bloodstream infections due to Staph ylococcus aureus (Li et al. 2000). Clinicians may appropriately and wisely decide to treatornottreatanindividualpatient,regardlessof whether they meet or fail to meet the criteria of “defi- nite” or “possible” infective endocarditis (IE) by the Duke schema. The Duke criteria are meant to be only a clinical guide for diagnosing IE and, certainly, must not Table 18.1.32. Diagnosis of infective endocarditis History Prior cardiac lesions Prior indwelling intravascular catheters Prior intravenous drug abuse Physical examination Auscultation of cardiac murmurs Neurologic impairment Petechiae Splinter hemorrhages Janeway lesions Osler’s nodes Roth spots Clinical evidence of emboli (fundi, conjunctivae, skin, and digits) Laboratory Blood cultures – a minimum of three blood cultures should be obtained Erythrocyte sedimentation rate ↑ CRP ↑ Leukocytes ↑ Rheumatoid factor ↑ (minor criteria in the Duke criteria) Red blood cell casts in urine plus a low serum complement level (minor criteria in the Duke criteria) Normochromic normocytic anemia Organism (see Table 18.1.33) Electrocardiogram Heart block Conduction delay Baseline electrocardiogram Chest x-ray Septic pulmonary emboli with few or multiple focal lung infiltrates Calcification in a cardiac valve Echocardiography a Detection of vegetations on valves Detectionofvalvulardysfunction Detection of hemodynamic dysfunction Detection of associated abnormalities (shunt or abscess) Histologic examination a Transthoracic echocardiography (TTE) may provide confirma- tion of the diagnosis of endocarditis. Transesophageal echocar- diography (TEE) has a higher spatial resolution than TTE and is much more sensitive for the detection of endocarditis 18.1 Acute Postoperative Complications 389 replace clinical judgment. In the clinical setting the di- agnosisisusuallyobviouswhenapatienthasthechar- acteristic findings of IE: Numerous positive blood cultures in the presence of a well-recognized predisposing cardiac lesion Absence of infection elsewhere Table 18.1.33. Modified therapy of infective endocarditis according to the American Heart Association Streptococcus viridans and Streptococcus bovis Aqueous crystalline 12–18 Million U/24 h IV either continuously or in four or six equally divided doses 4weeks Penicillin G sodium History of penicillin allergy Ceftriaxone sodium 2 g/24 h IV/IM in one dose 4 Relatively resistant to penicillin plus gentamicin sulfate 3 mg/kg per 24 h IV/IM in one dose 2 Penicillin-susceptible strains of S. pneumoniae and Streptococcus pyogenes Aqueous crystalline 24 Million U/24 h IV either continuously or in four or six equally divided doses 4 Penicillin G sodium Group B, C, G streptococci Ceftriaxone sodium 2 g/24 h IV/IM in one dose 4 Aqueous crystalline 24 Million U/24 h IV either continuously or in four or six equally divided doses 4 Penicillin G sodium 3 mg/kg per 24 h IV/IM in one dose 2 plus gentamicin sulfate 2 Enterococcus – strains susceptible to penicillin, gentamicin, and vancomycin Ampicillin sodium 12 g/24 h IV in six equally divided doses 4–6 4–12 or Aqueous crystalline 18–30 Million U/24 h IV either continuously or in six equally divided doses 4–6 Penicillin G sodium plus gentamycin sulfate 3 mg/kg per 24 h IV/IM in three equally divided doses 4–6 Staphylococcus – strains suscepti- ble to oxacillin Nafcillin or oxacillin 12 g/24 h IV in four to six equally divided doses 6 In the absence of prosthetic materials with optional addition of gentamycin sulfate 3mg/kgper24hIV/IMintwoorthreeequallydi- vided doses 1 History of penicillin allergy Cefazolin 6 g/24 h IV in three equally divided doses 6 with optional addition of gentamycin sulfate 3mg/kgper24hIV/IMintwoorthreeequallydi- vided doses 1 Staphylococcus – strains resistant to oxacillin Vancomycin 30 mg/kg per 24 h IV in two equally divided doses 6 In the absence of prosthetic materials Staphylococcus – strains suscepti- ble to oxacillin Nafcillin or oxacillin 12 g/24 h IV in six equally divided doses 6 Therapy for prosthetic valve endocarditis plus Rifampin 900 mg per 24 h IV/PO in three equally divided doses 6 History of penicillin allergy plus gentamicin 3 mg/kg per 24 h IV/IM in two or three equally di- vided doses 2 Cefazolin 6 g/24 h IV in three equally divided doses 6 Staphylococcus – strains resistant to oxacillin Vancomycin 30 mg/kg 24 h in two equally divided doses Adjust vancomycin to achieve 1-h serum concentra- tion of 30–45 g/ml and trough concentration of 10–15 g/ml 6 6 Staphylococcus – strains resistant to oxacillin plus Rifampin 900 mg/24 h IV/PO in 3 equally divided doses 2 plusgentamycin 3mg/kgper24hIV/IMintwoorthreeequallydi- vided doses Therapy for both native and pros- thetic valve endocarditis caused by HACEK a Microorganisms Ceftriaxone sodium 2 g/24 h IV/IM in one dose 4 or ampicillin- sulbactam 12 g/24 h IV in four equally divided doses 4 a Haemophilus parainfluenzae, H. aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eik enella cor- rodens,andKingella kingae From Baddour et al. (2005) However,somepatientsdonothavepositivebloodcul- tures and 20%–30% of patients have no predisposing cardiac lesion. In this setting, the correct diagnosis may be delayed. UsuallythediagnosisofIEisbaseduponhistoryand physical examination, blood culture and laboratory re- sults, an electrocardiogram (ECG), a chest x-ray, and an echocardiogram (Table 18.1.32). 390 18 Postoperative Complications Medical treatment of native valve endocarditis is the domain of antibiotic administration. Basically, the du- ration of therapy hasto be sufficient to eradicate micro- organisms. The response to therapy should be assessed by obtaining repeat blood cultures 48–72 h after antibi- otics are begun. Thereafter, regular careful serial exam- inations should be performed to search for signs of heart failure, emboli, or other complications. Most pa- tients with IE generally become afebrile 3–5 days after treatment is begun with an appropriate antibiotic. Surgical therapy in patients with IE should be indi- vidualized, with input from both the cardiologist and the cardiovascular surgeon (Tables 18.1.33, 18.1.34). The incidence of reinfection of newly implanted valves in patients with active IE is 2%–3% (Mills et al. 1974) and is far less than the mortality rate for IE and conges- tive heart failure (CHF) without surgical therapy, which canbeashighas51%(SextonandSpelman2003). Complications of IE are CHF, which occurs more fre- quently in aortic valve infections (29%) than with mi- tral (20%) or tricuspid disease (8%). Systemic emboli- zation occurs in 22 %–50% of cases of IE. Emboli often involve the lungs, coronary arteries, spleen, bowel, and extremities. Up to 65% of embolic events involve the central nervous system. Most emboli occur within the first 2–4 weeks of antimicrobial therapy. Splenic ab- scessisararecomplicationofIE.Mycoticaneurysms (MAs) are uncommon complications of IE that result from septic embolization of vegetations to the arterial vasa vasorum or the intraluminal space, with subse- quent spread of infection through the intima and out- ward through the vessel wall. MAs occur most fre- quently in the intracranial arteries, followed by the vis- Table 18.1.34. Echocardiographic features that suggest poten- tial need for surgical intervention according to (Baddour et al. 2005) Ve g et a t io n Persistent vegetation after systemic embolization Anterior mitral leaflet vegetation, particularly with >10mm(surgerymayberequiredbecauseofriskof embolization) Embolic events during first 2 weeks of antimicrobial ther- apy (surgery may be required because of risk of emboli- zation) Increase in vegetation size despite appropriate antimicrobi- altherapy(surgerymayberequiredbecauseofriskof embolization, heart failure, or failure of medical therapy) Valvular dsyfunction Acuteaorticormitralinsufficiencywithsignsofventricu- lar failure Heart failure unresponsive to medical therapy Valve perforation or rupture Perivalvular extension Valvular dehiscence, rupture, or fistula New heart block Large abscess or extension of abscess despite appropriate antimicrobial therapy ceral arteries and the arteries of the upper and lower extremities. Neurological complications develop in 20%–40% of patients with IE. Intracranial MAs repre- sent an extremely dangerous subset of these complica- tions.TheoverallmortalityrateamongIEpatientswith intracranialMAsis60%.hantimicrobialtherapy.Ex- tracranial MAs (intrathoracic or intraabdominal) are often asymptomatic until leakage or rupture occurs. Presumably, most extracranial MAs (ECMAs) will rup- ture if not excised. Hematemesis, hematobilia, and jaundice suggest rupture of a hepatic artery MA, arteri- al hypertension and hematuria suggest rupture of a re- nal MA, and massive bloody diarrhea suggests the rup- ture of an ECMA into the small or large bowel (Baddour et al. 2005). Fever Due to Postoperative Appendicitis Theroleofincidentalappendectomyduringelective and nonelective surgery remains controversial. Propo- nents of this practice argue with the technical ease, the low morbidity of the procedure, and the elimination of future risk and confusion over conflicting diagnosis and therefore for the prophylactic merits (Salom et al. 2003; Silvert and Meares 1976). Epidemiological stud- ies estimate a lifetime risk of acute appendicitis as 8.6% in men and 6.7% in women (Gupta et al. 2002; Hayes 1977). Addis et al. (1990) estimated that for a 60-year- old male, it would require 166 incidental appendecto- mies to prevent a single lifetime case of appendicitis. Since the cumulative lifetime risk for appendicitis de- creaseswithadvancingage(seeTable18.1.35)andpa- tients undergoing radical cystectomy and urinary di- version have a mean age of 64 years (Frazier et al. 1992), the lifetime risk of a postoperative appendicitis is very low (Gupta et al. 2002). The rationale for removing the appendix during urologic surgery is to prevent the fu- ture development of appendicitis since anatomical al- Table 18.1.35. Cumulative lifetime risk for acute appendicitis Age group (y) Men (%) Wo men (%) 0– 5 9.4 8.4 5– 9 9.2 8.3 10–14 8.6 7.8 15–19 7.2 6.7 20–24 5.9 5.4 25–29 4.9 4.5 30–34 4.1 3.8 35–39 3.4 3.1 40–44 2.8 2.5 45–49 2.3 2.0 50–54 1.9 1.7 55–59 1.6 1.2 60–64 1.2 0.9 65–69 0.8 0.6 70–74 0.4 0.3 From Wang and Sax (2001) 18.1 Acute Postoperative Complications 391 teration of viscera following urinary tract reconstruc- tion makes differential diagnosis of recurrent abdomi- nal pain in the right lower abdominal region difficult. But with the availability of the latest investigative mo- dalities (CT scan) over 95% of painful abdominal con- ditions can be detected. The value of computed tomog- raphy in the diagnosis of appendicitis has been well es- tablished in the past few years. This has been advocated as the imaging modality of choice because of its high sensitivity, accuracy, and negative predictive value in diagnosing appendicitis. In a study of patients with suspected appendicitis, computed tomography has shown its superiority in evaluating the extent of inflam- mation and in differentiating other intraabdominal pathologic findings by demonstrating a normal appen- dix (Balthazar et al. 1994; Levine et al. 1997). In a study performed by Gupta et al. (2002) on 160 consecutive radical cystectomy patients with urinary diversion in whom appendectomy was not done, patients present- ing with acute abdominal pain were easily diagnosed and managed. Moreover, none of the patients who were followed over a period of 10 years developed a appendi- citis postoperatively (Table 18.36). Therefore, routine appendectomy should be aban- doned in urologic surgery, due to the evolving role of the appendix in various urinary tract reconstructions and the very low risk of subsequent appendicitis (Gup- ta et al. 2002; Neulander et al. 2000; Santoshi et al. 2002). The incidence of incidental carcinoid tumors of the appendix between 0.4% and 2% should not change this way of proceeding (Silvert and Meares 1976). An- other important point that has not been well docu- mented to date is that, despite performing appendecto- my, the dilemma of acute abdominal pain may persist, as reported by varying studies on “stump appendicitis.” This is an entity in which inflammation occurs in the remnant tissue of the appendix after appendectomy. The incidence of stump appendicitis is underestimated, anditcanoccuranytimefromafewmonthsto20years after appendectomy (Feigin et al. 1993; Liang et al. 2006; Watkins et al. 2004). Table 18.1.36. Causes of acute abdominal pain on follow-up fol- lowing radical cystectomy Cause Incidence (%) Intestinal obstruction 11 Urinary retention 1.8 Neobladder perforation 0.6 Recurrent colic 1.3 Pyelonephritis 13 Stomal stenosis 1.3 Parastomal hernia 0.6 Postoperative appendicitis 0 Fever Due to Forgotten Foreign Body (Corpus Alienum: Rubber Drain, Gauze Sponge, Forceps, etc.) “Gossypiboma” refers to retained surgical sponge or swab and is derived from gossypi um (“cotton” in Latin) and boma (“place of concealment” in Swahili) (O’Con- nor et al. 2003). Because of legal implications, this con- dition is often underreported and the incidence has been estimated as 1 in 100–5,000 surgeries (Lauwers and Van Hee 2000). The most commonly retained for- eign body is the laparotomy sponge. It is often forgot- ten during operations in the lesser pelvis. Circum- stancesreportedtoexplainoperativelossofsponges are emergencies, hemorrhagic procedures, time-con- suming operations, sponge counting while closing, change in operating room personnel, and operations in anatomic regions that are difficult to reach. Fifty per- cent of gossypibomas are discovered 5 years or more af- ter surgery, and 40% are detected within the 1st year (Lauwers and Van Hee 2000; Rappaport and Haynes 1990). Migration of gauze sponge has been reported to oc- cur in ileum, duodenum, stomach, urinary bladder, and even by transdiaphragmatic migration into the lung causing lung abscess (Lone et al. 2005). The expul- sion of sponge has been seen to occur through laparot- omy wound and rectum. A sponge left in usually mani- fests within weeks to years and the longest duration of concealment has been 24 years (Kokubo et al. 1987). Retained sponge may produce various complications such as obstruction, fistula, peritonitis, abscess, trans- mural migration, or spontaneous extrusion. Two vari- ants of reaction have been studied. In one there is asep- ticfibrinousresponse,whichfollowsasilent,delayed course, and the second variant is an acute, exudative type leading to abscess formation including bacterial infection with anaerobes. Usual symptoms include unexplained abdominal distension and pain as well as palpable mass, nausea, vomiting, chronic anemia, rectal tenesmus and bleed- ing, diarrhea, discharge through a persistent sinus, in- testinal obstruction, and pseudotumoral syndrome (Tacyildiz and Aldemir 2004; Ben Meir et al. 2003). These symptoms are often accompanied with general symptoms such as fever and weight loss. Coughing and dyspneaaswellasUTImaybetheresultofexogenous compression on the respiratory or urinary tract. Post- operative septic shock has been described (Lauwers and Van Hee 2000). Plain radiographs fail to delineate thespongeintheabsenceofaradiopaquemarker.Ab- dominal ultrasonography can demonstrate the gossy- piboma by an intense and sharply delineated acoustic shadow that can be present even in the absence of air and calcification. The diagnostic procedure of choice is the CT scan, which shows lesions with densely enhanc- ing wall and a central, low-density, whirl-like zone due 392 18 Postoperative Complications to gas trapped in the fiber meshwork of the gossypibo- ma. Differential diagnosis includes tumor or tumor re- currence, postoperative adhesions, invagination, in- traabdominal abscesses, volvulus, and hematoma. Treatment consists of thorough surgical exploration of the abdomen, removal of the gossypiboma, drainage of purulent fluid, and treatment of the accompanying lesions such as fistulizations. Complication of a gossy- piboma is the development of an angiosarcoma, late abscess formation, chronic fistulas, and erosion into blood vessels. Gossypiboma-associated mortality is as high as 11%–35% (Chorvat et al. 1976). When the for- eign body is diagnosed and removed during the imme- diate postoperative period, morbidity and mortality are low (Le Neel et al. 1994). A gossypiboma is poten- tially life-threatening. Therefore, extreme care in the handling of gauzes during surgical procedures is high- ly advisable. Repeated sponge counts before and after eachpartoftheoperativeprocedureandsystematic use of large sponges, one by one is recommended. Al- thoughthepresenceofradiopaquemarkersinall gauzes might give a false feeling of safety, their use is helpfulincaseofanincompletespongecountatthe end of an operative procedure (Lauwers and Van Hee 2000). Fever Due to Intraabdominal Infections Intraabdominal infection continues to be one of the ma- jor challenges in surgery and urology. While the term “peritonitis” means an inflammation of the peritoneum regardless of its etiology, intraabdominal infections en- compass all forms of bacterial peritonitis, intraabdomi- nal abscesses, and infections of intraabdominal organs. Several classification systems have been suggested for peritonitis and intraabdominal infections, respectively. However, neither phenomenological classifications nor classification systems with respect to the origin of bac- terial contamination have a proven relevance for the clinical course of this disease. Moreover, most of the studies dealing with secondary peritonitis or intraab- dominal infections are difficult to compare because of wide variations in inclusion criteria. Thus the true inci- dence of secondary bacterial peritonitis is difficult to assess. With respect to its etiology, perforation of hol- lowviscusistheleadingcausefollowedbypostopera- tive peritonitis, ischemic damage of bowel wall, infec- tion of intraabdominal organs, and translocation in nonbacterial peritonitis. The anatomic origin of bacte- rial contamination and microbiological findings are not major predictors of outcome. However, the preoperative physiological derangement, the surgical clearance of the infectious focus and the response to treatment are established prognostic factors. The pathogenesis of in- traabdominal infections is determined by bacterial fac- tors that influence the transition from contamination to infection. Intraabdominal adjuvants and the local host responsearealsoimportant.Bacterialstimulileadtoan almost uniform activation response, which is triggered by reaction of mesothelial cells and interspersed perito- neal macrophages and which also involves plasmatic systems, endothelial cells, and extra- and intravascular leukocytes.Thelocalconsequencesofthisactivation are the transmigration of granulocytes from peritoneal capillaries to the mesothelial surface and a dilatation of peritoneal blood vessels resulting in enhanced perme- ability, peritoneal edema, and lastly the formation of protein-rich peritoneal exudate. Clinically, peritonitis is often classified either as lo- cal or as diffuse. Local peritonitis refers to loculi of in- fection, usually walled-off or contained by adjacent or- gans, whereas diffuse is synonymous with generalized peritonitis, i.e., spread to the entire cavity. The pathogens (Table 18.1.37) normally detected in peritonitis are Gram-negative, e.g., E. c oli, and anaer- obes, e.g., Bacteroides fragilis. When peritonitis per- sists, however, other pathogens may be isolated, e.g., Pseudomonas aeruginosa, Enterobacter , En terococcus spp. Antimicrobial resistance of operative flora may correlatewithpostoperativeinfection.Theresponseto intraabdominal infection depends on five key factors: 1. Inoculum size 2. Virulence of the contaminating organisms 3. Presence of adjuvants within the peritoneal cavity 4. Adequacy of local, regional, and systemic host defenses 5. Adequacy of initial treatment The immune response mounted against the invading pathogens is the decisive element for outcome. When the inflammatory response gets out of control, multior- ganfailure(MOF)willensueandsurgerycannolonger limit the immune response, emphasizing the need for Table 18.1.37. The microbial flora of secondary peritonitis Type Organism Percent Aerobic bacteria E. coli 60 Gram-negative Enterobacter/Klebsiella 26 Proteus 22 Pseudomonas 8 Gram-positive Streptococci 28 Enterococci 17 Staphylococci 7 Anaerobic bacteria Bacteroides 72 Eubacteria 24 Clostridia 17 Peptostreptococcus 14 Peptococcus 11 Fungi Candida 2 From Hau et al. (1979) 18.1 Acute Postoperative Complications 393 timelyoperationinsuspectedperitonitis,themainstay of treatment. Factors affecting prognosis are age, fecal peritonitis, metabolic acidosis, blood pressure, preop- erative organ failure, serum albumin, malnutrition, malignoma, cause of infection, site of origin of perito- nitis, and the number of organs involved in multior- gan-failure (MOF). The diagnosis of intraabdominal infection is gener- ally made on physical examination and is supported by clinical signs, e.g., abdominal pain and tenderness, nausea, vomiting, diminished intestine sounds, fever, and shock. Prior performed surgery should raise the suspicion of a complication directly related to the pro- cedure itself (for example, a leak from an intestinal anastomosis or the inadvertent incorporation of a loopofbowelintotheabdominalwallclosure).Ahis- tory of hypotension may be suspicious of intestinal is- chemia or infarction, especially in patients with co-ex- isting peripheral vascular disease and general athero- sclerosis. After major surgery, perforation of a duode- nal ulcer is a not uncommon complication, particular- ly in the patient with known peptic ulcer disease. Oc- casionally, peritonitis may be due to devices within the peritoneal cavity such as dialysis cannulae or due to postoperative pancreatitis. The physiologic re- sponse to the trauma of surgery causes increased lev- els of antidiuretic hormone (ADH) and aldosterone, leading to fluid retention. In the absence of complica- tions, this process usually resolves by the 3rd day. Shouldapositivefluidbalancepersistafterthistime, the possibility of unrecognized complications should be suspected. Fluid retention is often manifested clini- cally by signs of organ dysfunction, such as tachypnea andhypoxemia,confusion,ortheonsetofanewsup- raventricular dysrhythmia (Marshall 2004). These clinical signs of surgical complications typically be- come evident on the 3rd postoperative day, but perito- nitis usually presents not until 7–10 days after the sur- gical procedure. Radiographic procedures are the cornerstone of di- agnosis and include plain x-ray (intraperitoneal free air, although air may normally be present for up to 7 days following a laparotomy; thumb-printing, which suggests ischemia; evidence of intestinal obstruction; contrast studies, which may demonstrate leaks or de- lineate the location of an obstruction), ultrasound, and CT scan. Computed tomography combined with oral and intravenous contrast medium is the most reliable imaging modality for evaluating the abdomen (intra- or retroperitoneal fluid collections, abscess formation, intestinal ischemia, clots within larger vessels, etc.) (Velmahos et al. 1999). MRI should also be considered with the possible exception of the evaluation of retro- peritoneal pancreatic pathology. Leukocytes and C reactive protein may be altered butarenotdirectsignsofperitonitis. Management principles (Marshall 2004) of the pa- tient with intraabdominal infection include three prin- ciples: Timely hemodynamic resuscitation and support of vital organ function Early administration of antimicrobial agents ap- propriatefortheinfectiousproblem Rapid anatomic diagnosis and the institution of adequate source control measures The cornerstone of timely hemodynamic resuscitation is the administration of adequate amounts of fluids to restoreadequateintravascularvolumeandthusopti- mize oxygen delivery to the tissues. There is no compel- ling evidence of the superiority of one type of fluid over another. Resuscitation should be guided by frequent as- sessment of heart rate and blood pressure. Urinary out- put is a simle and sensitive measure of intravascular volume filling and organ function; an hourly output of 30–50 ml/kg should be the minimal objective of thera- py. Patients who have significant co-morbidities, who present with more profound hemodynamic instability, or who fail to respond rapidly to fluid replacement shouldbemanagedinanICUsetting.Theamountof fluid required to achieve hemodynamic stability is var- iable, and frequently substantial, because of unappreci- atedthird-spacelossesintothefocusofinfectionand into the GI tract as a consequence of ileus (Madl and Druml 2003; Marshall 2004). Another mainstay is the early administration of systemic antibiotics (Ta- ble 18.1.38) without waiting for radiographic or micro- biologic confirmation. The spectrum should include Gram-negative aerobic organisms and anaerobes. The optimal duration of antibiotic therapy is unknown, and Table 18.1.38. Recommended antimicrobial regimens for patients with intraabdominal infections Single agents Infection Ampicillin/sulbactam Cefotetan Cefoxitin Ertapenem Imipenem/cilastatin Meropenem Piperacillin/tazobactam Ticarcillin/clavulanic acid Combination regimens Aminoglycoside plus an antianaerobe agent (clindamycin or metronidazole) Aztreonam plus clindamycin Cefuroxime plus metronidazole Ciprofloxacin plus metronidazole Third- or fourth-generation cephalosporin (cefepime, cefo- taxime, ceftazidime, ceftizoxime, or ceftriaxone) plus an antianaerobe anaerobe (clindamycin or metronidazole) from Malangoni (2005); Mazuski et al. (2002) 394 18 Postoperative Complications when antibiotics are used in association with adequate source control, the duration of therapy can be short (Wittmann and Schein 1996), and certainly no longer than 5–7 days (Wittmann and Schein 1996). The term “source control” can be defined as those physical measures undertaken to eradicate a focus of infection, eliminate ongoing microbial contamination, and render the local environment inhospitable to mi- crobial growth and tissue invasion (Jimenez and Mar- shall2001).Thisinvolvesoneormoreofthefollowing strategies: Drainage of abscesses or infected fluid collections Debridement of necrotic infected tissue Definitive measures to control a source of ongoing microbial contamination and to restore anatomy and function Drainage converts an abscess to a controlled sinus or fistula. This can be done by percutaneous techniques guided by radiographic imaging. In general, although no randomized control trial is available, percutaneous drainage seems to be as effec- tive as operative drainage and when percutaneous drainage is feasible it is the preferred initial approach becauseitistheleastinvasiveprocedure(Bufalarietal. 1996). Contraindications for percutaneous drainage in- clude diffuse peritonitis due to the lack of localization oftheinfectiousprocess,multipleabscesses,andana- tomic inaccessibility. Debridement is the physical re- moval of infected or necrotic tissue and can be accom- plished by surgical excision and irrigation. Early ag- gressive debridement is associated with an improved clinical outcome. Debridement encompasses the exci- sion of necrotic intestine, the removal of feces or fibrin from the peritoneal cavity, and the excision of necrotic and infected fat. Clear demarcation between viable and nonviable tissues is a prerequisite to successful de- bridement (Marshall et al. 2004). Removal of extensive fibrin deposition on the peritoneal surface of loops of bowel shows no improvement in the clinical outcome. Intraoperative peritoneal lavage, although well entren- ched in modern surgical practice, has not yet demon- strated that it decreases clinical mortality. No absolute proof exists that the addition of antibiotics to intraope- rative lavage increases the survival rate (Hudspeth 1975). Definitive measures to correct the anatomic de- rangement are an integral part of source control man- agement. Whether definitive measures should be un- dertaken during the initial management of the septic episode or preferentially delayed and performed elec- tively when the patient has recovered depends on the stability of the patient and the nature of the interven- tion that is needed: in general, the simplest interven- tion that accomplishes the source control objective is the best option. There is a trend in the literature to make a stoma in cases of anastomotic dehiscence and peritoneal infection. While there is general agreement that on-table bowel preparation and primary anasto- mosis is safe in the presence of localized peritonitis, its use in the presence of generalized peritonitis is contro- versial and most surgeons opt for a Hartmann’s proce- dure in this situation. Intestinal reanastomosis is in most instances not performed in peritonitis. The ap- proach employed to treat the immediate problem must take into consideration the consequences of that deci- sion for later reconstruction. Open abdomen ap- proaches, for example, commit the patient to a series of reconstructive procedures to repair abdominal wall herniasortocloseenterocutaneousfistulae.Thecrea- tion of a stoma requires a subsequent procedure if the stoma is to be closed, and the morbidity associated with such procedures can be substantial (Hackam and Rotstein 1995a, b). If a stoma is created, a loop enteros- tomy or colostomy is easier to close than an end stoma, for it can be accomplished locally without the need for a full laparotomy. There is increasing evidence that laparoscopy may play a definite role in patients with peritonitis. In pa- tients with generalized peritonitis resulting from per- forated diverticular disease, treatment by laparoscopy and peritoneal lavage was successful. However, laparo- scopic management of generalized peritonitis needs further assessment. The most common cause of peritonitis in the hospi- talized patient is intraperitoneal infection as a conse- quence of prior abdominal surgery (Table 18.1.39). If the GI tract has been entered as in radical cystectomy and urinary diversion, then the possibility of an anas- tomotic leak should be considered. Risk factors for this complication include excessive tension on the suture line, hematoma at the suture line, ischemia related to Table 18.1.39. Causes of peritonitis in the hospitalized patient Type Cause Postoperative peritonitis Anastomotic leak (Fig. 18.1.3.4) Procedural complications Inadvertent or missed intestinal injury Infected hematoma Intestinal injury secondary to laparo- scopic trocar Spontaneous GI perforation Perforation of gastric or duodenal ulcer Intestinal ischemia Delayed ischemia secondary to low- flow mesenteric venous thrombosis Acalculous cholecystitis Device-related infection CAPD peritonitis Infected ventriculoperitoneal shunt Hematoma Insufficient coagulation Slipped clips or ligatures Coagulopathy 18.1 Acute Postoperative Complications 395 History PE* Clinical signs Labarotory tests Abdomen CT scan Origin still unknown? Differential Diagnosis INFECTIOUS Surgical side Infections Pneumonia CAUTI UTI CRI Antibiotic associated diarrhea Sinusitis Otitis media Parotitis Abdominal abscess Meningitis Acalculous cholocystitis Transfusion associated viral infections Foreign body infection Osteomyelitis Endocarditis (Table 18.1.32) NONINFECTIOUS Seroma/Hematoma at surgical site Suture reaction Deev vein thrombosis Pulmonary embolism Gout/pseudogout Pancreatitis Cerebral infarction Subarachnoid hemorrage Myocardial infarction Bowel ischemia/infarction Drug/alcohol withdrawal Transfusion reaction Transfusion rejection Rheumatic fever Lymphome Solid tumor Sarcoid Lupus Rheumatoid arthritis Giant coil arteritis Neoplastic fever Drug fevar Factitious fover What kind of surgery? Previous [. . . ], UTI (Fig. 18.1.3.2) CRI (Table [. . . ]) SSI? Endocarditis (Table18.1.22) Local pain or tenderness? Transfusion? Predisposing heart condition or infection drug use? Previous deep vain thrombosis? Previous gout? Previous rheumatic fever? Lupus? [. . . ]? Animal exposure Chest (Table 18.1.3.41) Heart (IE) Abdomen (Table 24 + 26) Retroperitoneum (Table 18.1.3.45) Skin and soft tissue [. . . ] exit pito Lymphnodes Upper and lower extremities consider eyes (IE) Fever and chills Hypotension Hyperventilation Altered mental status Nausea & vomiting & diarrhea Abdominal pains. Thrombophlebitis Celulitis Refer to Table 18.1.19, 18.1.24, 18.1.25 Postoperative fever of unknown origin 67-Gallium scintigraphy or 111-Indium- labeled- leukocoytes scintigraphy Consider: Endocrinologist Rheumatologist Surgeon ORL Cardiologist Dentist Complete blood count Differential count Platelet count Routine blood chemistries liver enzymes Bilirubin Urine analysis Urine culture Erythrocyte sedimentation rate Blood cultures Hepatitis serology Locate dehydroge- nase Tuberculin skin test (AFB smear and NAA)*1 HIV viral load HIV antibody assay Rheumatoid factor Antinuclear antibodies Mycobacterial Tbc AFB smear (Acid fast bacilli smear) NAA (Nucleic acid amplification assay) Refer to Table 18.1.3.43 Immediate (within hours of surgery) Drug fever Malignant hyperther- mia Transfusion reaction Trauma to surgery Acute (onset within the first week) Pneumonia UTI CAUTI CRI SSI Subacute (onset from 1 to 4 weeks following surgery) Pneumonia SSI CRI Thrombophlebitis Antibiotic-associate diarrhea Drug fever (beta-lactan, antibiotics, sulforamides, H2- blockers, procain- amide, phenytoin, heparin) Deep venous thrombosis pulmonary emblosm Delayed Infection Due to blood transfusion (CMV, HIV, Hepatitis) SSI Differential diagnosis based on the basis of timing of fever Chest x-ray Ecectrocardiogram TTE* 2 TTE* 3 18 F-FDG PET/CT *1 AFB smear = Acid fast bacilli smear; NAA = Nucleic acid amplification assay *2 TTE = Transthoracic echocardiography *3 TEE = Transesophageai echocardiography Fig. 18.1.8. Algorithm for postoperative fever of unknown origin underlying vascular disease, obesity, excessive devas- cularization of the intestine at the site of the anastomo- sis, or intestinal distension at the suture line, and tech- nical errors in the creation of the anastomosis. Collec- tions of blood within the peritoneal cavity support the proliferation of bacteria shed at the time of surgery, and is one of the most common predisposing factors to postoperative abscesses (Fig. 18.1.8). Their anatomic 396 18 Postoperative Complications [...]... tube feeding (0.66; 95 % confidence interval [CI], 0.56 – 0 .79 ) compared with TPN This lower risk of infection with enteral feeding is independent of whether catheter sepsis is included in the analysis Noncatheter infections include pneumonia, abdominal abscess, and empyema The higher risk of infection in TPN patients may be partially explained by a higher incidence of hyperglycemia since increased... prolonged use or repeated therapy Cephalosporin second-generation Drug name Cefoxitin (Mefoxin) Description Second-generation cephalosporin indicated for Gram-positive cocci and Gram-negative rod infections Infections caused by cephalosporin- or penicillin-resistant Gram-negative bacteria may respond to cefoxitin Adult dose 1 – 2 g IV 6 – 8 h Pediatric dose Infants and children: 80 – 160 mg/kg/d IV divided... 18.1.9 The imaging diagnostic approach in postoperative fever of unknown origin (FUO) includes not only conventional radiographic studies such as plain x-rays, CT scans, or MRI It has been reported that gallium- 67 and 111-indium-labeled leukocyte scanning have an overall higher yield than CT for detecting sites of FUO (Knockaert et al 1994; Syrjala et al 19 87) At the moment gallium- 67 scanning is a commonly... only minimal findings in the overlying skin The diagnosis of infection of the skin and soft tissues is most commonly accomplished by direct examination, obtaining cultures to identify the infecting organisms and to aid in the selection of an optimal antimicrobial agent A microbiological diagnosis of cellulitis can sometimes be made by aspiration of the involved area Biopsy can be used to determine whether... NPV of 85 %, and an accuracy of 86 % in imaging infection (Dumarey et al 2006) In another current publication comparing PET with FDG-labeled leukocytes vs 11 1In- oxine-labeled leukocyte scintigraphy, the authors found a sensitivity of 87 % vs 73 %, a specificity of 82 % vs 86 %, a PPV of 72 % vs 73 %, a NPV of 92 % vs 86 %, and an accuracy of 84 % vs 81 % Further investigations and larger trials are... 5-cm area of skin should be disinfected by swabbing concentrically with 70 % alcohol, from the venipuncture site outward The site should be cleansed once again, this time with 10 % povidone-iodine again in a circular motion Iodine should be dried completely before puncture, which takes between 1 and 2 min In the meantime, the rubber stopper of the blood culture bottle should be decontaminated with 70 ... nonspecific tracer of increased glucose metabolism and does not accumulate only in sites of infection and inflammation Indeed, its high sensitivity for the detection of malignant cells has led to its successful and extensive use in oncology Therefore, 18F-FDG-PET is advantageous over gallium- 67 and 111 -In- oxide labeled leukocyte scintigraphy because it can image the whole body in a short time, has high... examination, inguinal examination) Common abnormalities of the abdomen are described in Table 18.1.44 The characteristic of flank pain is very helpful in determining the cause Important characteristics include local or referred pain, acute or chronic or recurrent pain, degree of severity, and duration Associated symptoms such as fever, nausea and vomiting, and atrial fibrillation often help in making... patients, since they harbor risk factors that increase their septic morbidity, such as hemorrhagic shock, intestinal injuries, and age With massive volume resuscitation, the potential for antibiotic washout exists and redosing should be considered In patients with open abdomen without intestinal injury, a firstgeneration cephalosporin or equivalent is recommended In patients suffering from open abdomen in. .. 21.1 – 34.2 0.5 – 0.69 0.56 – 0.82 Albumin 29.0 34.0 – 87. 0 29.4 – 42.0 0.52 0. 57 – 1.0 0.93 Total protein Albumin 30.0 – 41.0 12.4 – 25.5 0.46 – 0.65 0.4 – 0.68 Total protein Albumin Hepatic Intestinal Total protein L:S Table 18.1.59 Incidence of symptomatic lymphoceles depending on surgical intervention Surgery L:S lymph to serum ratio cells, lipoproteins, auto- and foreign antigens encoded by RNA . superiority in evaluating the extent of inflam- mation and in differentiating other intraabdominal pathologic findings by demonstrating a normal appen- dix (Balthazar et al. 1994; Levine et al. 19 97) . In. with only minimal findings in the overlying skin. The diag- nosis of infection of the skin and soft tissues is most commonly accomplished by direct examination, ob- taining cultures to identify the infecting. plus aminoglycoside For 5 7 days after defervescence Glycopeptide plus aminoglycoside in ampi- cillin-resistant cases Linezolid or quinupristin/dalfopristin in vancomycin-resistant cases Candida