18.1 Acute Postoperative Complications M

18 Postoperative Complications 18.1 Acute Postoperative Complications M. Seitz, B. Schlenker, Ch. Stief

18.1.1 Postoperative Bleeding 364 18.1.5 Abdominal Wound Dehiscence 403 18.1.1.1 Overview 364 18.1.5.1 Synonyms 403 18.1.1.2 Incidence and Risk Factors 365 18.1.5.2 Overview and Incidence 403 18.1.1.3 Detection and Clinical Signs 365 18.1.5.3 Risk Factors 404 18.1.1.4 Workup 366 18.1.5.4 Clinical Signs and Complications 404 18.1.1.5 Management 366 18.1.5.5 Prevention 405 18.1.1.6 Special Conditions 371 18.1.5.6 Management 405 18.1.2 Chest Pain and Dyspnea 373 18.1.6 Chylous Ascites 410 18.1.2.1 Overview 373 18.1.6.1 Overview 410 18.1.2.2 Cardiovascular System Disorders 373 18.1.6.2 Risk Factors and Pathogenesis 410 18.1.2.3 Postoperative Pulmonary Complications 373 18.1.6.3 Prevention 412 Pulmonary Embolism 373 18.1.6.4 Detection and Workup 413 Pleural Effusions 375 18.1.6.5 Management 413 Atelectasis 376 Infection/Pneumonia 376 18.1.7 Deep Venous Thrombosis 414 Tube Thoracostomy 376 18.1.7.1 Overview and Incidence 414 18.1.3 Acute Abdomen 377 18.1.7.2 Risk Factors 414 18.1.3.1 Initial Management 377 18.1.7.3 Detection and Clinical Findings 415 18.1.4 18.1.7.4 Management 415 Postoperative Fever 378 Unfractionated Heparin 415 18.1.4.1 Overview 378 Low-Molecular-Weight Heparin 415 18.1.4.2 Incidence 379 Long-Term Therapy 416 18.1.4.3 Definition 379 18.1.4.4 Risk Factors and Prevention 379 18.1.8 Lymphoceles 416 18.1.4.5 Detection and Work-Up 382 18.1.8.1 Anatomy and Physiology 416 Pulmonary 382 18.1.8.2 Overview 419 Urinary Tract 382 18.1.8.3 Risk Factors and Prevention 419 Central Venous Catheters and Catheter-Related 18.1.8.4 Clinical Signs 420 Infections 383 18.1.8.5 Diagnosis and Workup 420 Surgical(Wound)SiteInfection 383 18.1.8.6 Management 420 Intraabdominal Sepsis from Abscess 384 Bacteremia or Septicemia – Bloodstream References 421 Infection 384 18.1.4.6 Management 384 Current Treatment of Nosocomial Pneumonia 385 Treatment of CAUTI 385 18.1.1 Catheter-Related Infections 386 Postoperative Bleeding Surgical Site Infection: Wound Management 388 18.1.4.7 Special Conditions 389 18.1.1.1 Fever Due to Infective Endocarditis 389 Overview Fever Due to Postoperative Appendicitis 391 Fever Due to Forgotten Foreign Body Historically, major bleeding was a significant problem (Corpus Alienum: Rubber Drain, Gauze associated with radical retropubic prostatectomy and Sponge, Forceps, etc.) 392 cystectomy, TUR, and nephrectomy. Nowadays, major Fever Due to Intraabdominal Infections 393 life-threatening hemorrhage after urologic open and Fever Due to Skin and Soft-Tissue Infections 397 Fever Due to Impaired Drainage of Upper endoscopic surgery by expert surgeons is a rare event. Urinary Tract After Urologic Surgery 398 In some cases, the patient typically becomes hemody- Fever Due to Epididymitis After TUR, Brachythe- namicallyunstablesoonafterarrivalintherecovery rapy, Prostate Biopsy, and Open Surgery 399 room. On the other hand, sometimes hemorrhage Postoperative Fever of Unknown Origin 399 Appendix: How to Perform Blood Cultures 403 arises a few hours or days following the initial procedure. The surgeon must make a decision whether to 18.1 Acute Postoperative Complications 365 return immediately to the operating room or treat the 18.1.1.2 patient conservatively with blood and volume replace- Incidence and Risk Factors ment (Kaufman and Lepor 2005). Reasons for a significant major bleeding later on in the postoperative peri- See Table 18.1.1. od may be slipped ligatures or clips (e.g., from the renal pedicle or other major blood vessels) or in case of 18.1.1.3 partial nephrectomy, ruptured kidney. Also, removal Detection and Clinical Signs of drains days after surgery may induce significant bleeding, if the drains have been put primarily through Clinical findings that can be used to indicate the need a major blood vessel (e.g., epigastric). Reasons for for red cell transfusion may be subjective such as fa- early revisions may be insufficient ligatures or hemo- tigue and shortness of breath. Changes in respiratory stasis. rate and pulse can be difficult to interpret but can pos- Significant bleeding in a postoperative bleeding set- sibly be parameters indicating the need for blood ting is defined as patients requiring emergency blood transfusion. Estimated blood loss, blood pressure, as transfusion to maintain blood pressure during the well as the hemoglobin level must be taken into account postoperative period (Hedican and Walsh 1994; Kauf- since the decision to transfuse red cells is a complex man and Lepor 2005). one and depends on factors such as the patient’s ability to compensate for anemia, the likelihood of further

a Table 18.1.1. Incidence of Surgery Incidencea Incidenceb Author reintervention; incidenceb of blood transfusion Laparoscopic radical prosta- 0.5% 5% Rassweiler et al. 2006; Arai et tectomy al. 2003 Open radical prostatectomy 0.5%–1.2% 0.4%–2.4% Hedican and Walsh 1994; Kaufman and Lepor 2005; Koch and Smith 1996 Robotic radical prostatectomy 0%–0.5% 1%–1.3% Bhandari et al. 2005 Retropubic transvesical pros- 1.1%–3% 8.2% Adam et al. 2004; Serretta et tatectomy al. 2002 TURBT 0%–2.2% 2.3%–3.4% Collado et al. 2000; Nieder et al. 2005 TURP 2.2%–3.5% 2%–8.9% Gupta et al. 2006; Lim et al. 2004; Montorsi et al. 2004; Muzzonigro et al. 2004 Open nephron-sparing 2.6%–7.6% 5.3%–12% Becker et al. 2005; Heye et al. nephrectomy 2005; Steffens et al. 2005 Laparoscopic nephron-spar- 0.6%–3.5% 5.2%–17.8% Albaqami and Janet schek ing nephrectomy 2005; Desai et al. 2005; Guil- lonneau et al. 2003 Open radical nephrectomy 0%–2.7% 2.4%–9.8% Shuford et al. 2004 Laparoscopic radical nephrec- 1.6% 0.4% Vallancien et al. 2002; Wille tomy et al. 2004

Table 18.1.2. Classification of hypovolemic shock according to blood loss Class I Class II Class III Class IV Blood loss <15% (750 ml) 15%–30% (<1500 ml) 30%–40% (<2000 ml) >40% (>2000 ml) Blood pressure Systolic Unchanged Normal ↓↓↓↓ Diastolic Unchanged ↑↓↓↓↓ Pulse (beats/min) <100 100–120 120 (thready) >120 (very thready) Capillary refill Normal Slow (>2 s) Slow (>2 s) Undetectable Respiratory rate Normal Normal >20/min >20/min Urinary flow rate >30 ml/h 20–30 ml/h 10–20 ml/h 0–10 ml/h Extremities Normal Pale Pale Pale and cold Complexion Normal Pale Pale Ashen Adapted from Baskett 1990 366 18 Postoperative Complications

blood loss, and the severity of the hypovolemic shock 18.1.1.5 (Table 18.1.2). In the early postoperative period, blood Management loss via the drains may be an important sign as well as an increase in the abdominal girth, unpaired body Acute anemia caused by intra- and postoperative blood shape, and blood loss via the surgical incision. Mea- loss should be treated by blood and fluid replacement. surement of hemoglobin in the drained fluid may be Clinical experience has shown that losses of up to helpful. 30%–40% can be treated by crystalloids alone in During the very early postoperative period after young healthy patients. Estimation of actual and like- open urologic surgery, major hemorrhage, although lyfurtherbloodlossisanimportantconsideration rare,isthemostcommoncomplication.Patientsfol- in the decision to administer a red cell transfusion in lowing nephron-sparing nephrectomy may present thetreatmentofacutebloodloss.Thebenefitofred with massive hematuria after surgery. Blood loss after cell transfusion is usually considered in terms of in- partial or radical nephrectomy is associated with acute creasing the oxygen-carrying capacity of the blood, flank pain or a significant decrease in the hemoglobin but a more relevant consideration is the avoidance of level and signs of shock. Hemorrhage in the perirenal tissue hypoxia. General complications of blood trans- space can be found in these patients – recognized either fusion are listed in Table 18.1.4. Indications for trans- by adequately placed suction drains or by noninvasive imaging techniques such as sonography. Bleeding may Table 18.1.3. Workup with noninvasive and invasive proce- be from the kidney or renal pedicle but is occasionally dures from unrecognized injury to a neighboring structure Hemoglobin level Table 18.1.5 such as the spleen, the liver, or a mesenteric vessel. An- (Hb) giography after partial nephrectomy enables not only the exact visualization of extravasation of contrast ma- Classification of Table 18.1.2 hypovolemic shock terial, but also the superselective embolization of the feeding arteries within the kidney. Ultrasound Coagulum within TURP, TURBT the bladder Significant bleeding according to its definition following radical prostatectomy and cystectomy is a rare Fluid in the peri- Open and laparo- renal spaces, pel- scopic urologic event, with an incidence between 0.4% and 5% (Arai vic region surgery et al. 2003; Hedican and Walsh 1994; Kaufman and CT scan Visualization of Open and laparo- Lepor 2005; Koch and Smith 1996; Rassweiler et al. extravasation of scopic urologic 2006). contrast medium surgery Angiography Exact visualiza- Open and laparo- 18.1.1.4 tion of extravasa- scopic nephron- tion of contrast sparing nephrec- Workup medium tomy See Table 18.1.3. TURP transurethral prostatectomy, TURBT transurethral resection of bladder tumors

abc

Fig. 18.1.1. CT-scan of a 76 years old female patient 12 days post partial nephrectomy. Postoperatively, no complications were re- corded. Due to an elevated creatinine level the patient has not been discharged. On day 12 after the initial surgery she suddenly presented with acute flank pain and a significant decrease in the hemoglobin level. The CT-scan showed a massive retroperitoneal (a, c)andsubcutaneous(b) hematoma. Angio-CT did not show a active bleeding source, the patient remained unstable. Open surgery resulted in a total nephrectomy 18.1 Acute Postoperative Complications 367

Table 18.1.4. Complications of Complication Estimated risk per unit No. of deaths per blood transfusion million units Hepatitis A 1/1,000,000 0 Hepatitis B 1/50,000–1/170,000 0–0.14 Hepatitis C 1/200,000 <0.5 HIV <2,000,000 <0.5 Bacterial contamination 1/500,000 0.1–0.25 Acute hemolytic reactions 1/250,000–1/1,000,000 0.67 Delayed hemolytic reactions 1/1,000 0.4 Adapted from Murphy et al. 2001

Table 18.1.5. Indications for red cell transfusion and volume re- ting disorder, it may be necessary to temporarily pack placement in adults the wound with gauze, which can then be gradually re- Need based on estimation of blood loss moved after 24–48 h. Estimated blood loss >40% (>2000 ml) After partial nephrectomy, percutaneous supers- ↓ elective embolization (PSE) of the feeding arteries con- Rapid volume replacement, including RBC transfusion is tributing to the bleeding site is preferred to open sur- required, consider emergent control of bleeding source gery, which often results in a total nephrectomy (Albani Estimated blood loss 30%–40% (1,500–2,000 ml) and/or and Novick 2003; Van Poppel et al. 2001). PSE with mi- presence of symptoms of severe blood loss ↓ crocoils as the embolic agent after nephron-sparing re- Rapid volume replacement with crystalloids or synthetic nal surgery has a high success rate and a low complica- colloids is required, RBC will probably also be required tion (i.e., major parenchymal infarction) rate (Fisher et Estimated blood loss 15%–30% (800–1,500 ml) al. 1989; Maleux et al. 2003). It is, however, important to ↓ avoid occlusion of the proximal great vessels or the ad- Volume replacement with crystalloids or synthetic colloids; jacent smaller vessels to keep parenchymal loss to a need for RBC transfusion is unlikely unless the patient has minimum. In case of ruptured kidney, secondary ne- preexisting anemia, continuing blood loss, or reduced cardiovascular reserve phrectomy will not be avoidable. Estimatedbloodloss<15%(>750ml) Possible bleeding sources may depend on the surgi- ↓ calapproach(transperitonealorretroperitoneal)and Volume replacement or RBC transfusion only in the pres- surgical intervention. Partial or radical nephrectomy ence of co-morbid factors may develop hemorrhages from neighboring organs Need based on hemoglobin concentration such as spleen, adrenal, pancreas, bowel on the right Hb <7 g/dl hemiabdomen. On the contralateral side, duodenum, ↓ liver, and gallbladder injuries may contribute to post- RBC transfusion is indicated operative hemorrhage. In general, the bleeding point Inastablesettingthepatientshouldreceive2Uofpacked RBC in a hemodynamic relevant hemorrhage has to be se- Hb 7–10 g/dl cured (Tables 18.1.6, 18.1.7). Basically, the same ap- ↓ plies for retroperitoneal lymphadenectomy (Ta- No clear indication for RBC transfusion ble 18.1.8). Following radical prostatectomy, two ma- In a stable situation, the patient does not need blood re- jor sites may contribute to a postoperative hemor- placement rhage setting. First is the site of the pelvic lymphade- In the presence of clinical signs of blood loss, consider RBC transfusion nectomy at which slipped ligatures or clips may be re- Hb >10 g/dl sponsible for postoperative bleeding; second is the re- ↓ gion of the dorsal vein complex. Patients requiring RBC transfusion is not indicated acute transfusions for hypotension following radical High-risk patients prostatectomy should be explored to evacuate the pel- ↓ vic hematoma and decrease the likelihood of bladder Patients >65 years and/or those with cardiovascular or re- neck contracture and incontinence (Hedican and spiratorydiseasemaytolerateanemiapoorly.Suchpatients maybetransfusedwhenHb<8g/dl Walsh 1994). To secure the bleeding point, bipolar electrocoagulation as well as ligatures or clips can be Adapted from Murphy et al. 2001 used (Table 18.1.9). The possible causes of postoperative hemorrhage and its management in simple pros- fusion in the acutely bleeding patient are listed in Ta- tatectomy and radical cystectomy are listed in Ta- ble 18.1.5. bles 18.1.10 and 18.1.11. In some circumstances, it is best to reopen the In case of bleeding after TURP, venous and arterial wound, evacuate the hematoma, and secure the bleed- bleeding may be controlled conservatively. One can ing point. In the event of diffuse bleeding from a clot- overinflate the balloon of the catheter with 50–70 ml, 368 18 Postoperative Complications

Table 18.1.6. Right partial and radical nephrectomy with bleeding sources, diagnostic and therapeutic procedures Surgical Topographic anatomy and Diagnostic Clinical features procedure potential bleeding source procedures Right transperi- Cutis/subcutis PEa/Labb/USc Hb↓/swelling/hematoma toneal nephrec- Muscle PE/Lab/US Hb↓/swelling/hematoma tomy Omentum ⎫ Check for abnormal coagulation test (see Table 18.1.1.2) Peritoneum Psoas muscle Gall bladder Adrenal gland Hb↓/intraabdominal fluid/bleeding source/blood pres- ⎬ Lab/US/CT-scan Duodenum { sure↓,pulse↑ Bowel Testicular/ovarian Vessels ᭤ Consider relaparotomy in increasing unstable patient branches of lumbalis/ iliolumbalis vessels ⎭ Renal pedicle ᭤ Unstable patient Lumbar veins Urgent relaparotomy Right lumbar Cutis/subcutis PE/Lap/US Hb↓/swelling/hematoma nephrectomy Muscle PE/Lab/US Hb↓/swelling/hematoma Intercostal vessels PE/Lab/US Hb↓/swelling/hematoma Pleural cavity PE/Lab/US/x-ray Hb↓/respiratory rate↑/pleural effusion Peritoneum ⎫ ᭤ Consider drainage Psoas muscle Adrenal gland Hb↓/intraabdominal fluid/bleeding source/blood pres- ⎬ Lab/US/CT scan Testicular/ovarian vessels { sure↓,pulse↑ branches of lumbalis/ ᭤ Consider relaparotomy in increasingly unstable patient iliolumbalis vessels ⎭ Renal pedicle ᭤ Unstable patient Lumbar veins Urgent relaparotomy Partial lumbar/ Same as above ⎫ Consider PSE transperitoneal Additionally: PE/Lab/US/CT Consider double-J nephrectomy Branches of renal artery scan/CT angio- Condsider PSE and/or double-J Renal pelvis ⎬ graphy ᭤ Considerreoperationinincreasinglyunstablepatient ruptured kidney ⎭ ᭤ Unstable patient Urgent reoperation In our institution, although not evidence-based, hemorrhage after partial nephrectomy or nephrectomy is taken very seriously sincesuchconditionsmayrequireimmediateaction.EarlyCTscan(nephrectomy)orCTangiography(partialnephrectomy)is indicated a Physical examination b Laboratory c Ultrasound

placing it in the bladder, and put traction on it. This dure applies to drainage sites. As one approaches the compresses the prostate capsule with the remaining deeper operation field, hematoma must be evacuated prostatetissue,whichleadstosufficienthemostasis.A and adherent coagula removed. Washing with 2–3 l of second and technique that is also effective is placing the normal saline clears the surgical site and facilitates the balloon of the catheter in the resection cavity of the search for the bleeding source. Neighboring tissue and prostate and overinflate the balloon until the bleeding organs must be examined carefully. Smaller bleeding iscontrolledandtheirrigationfluidturnslightpink. sources may be secured by mono- or bipolar electroco- However, if the irrigation fluid has a continued red col- agulation; larger ones need to be clipped or ligated. In or one should reinsert the resectoscope and coagulate case of diffuse bleeding, one can use special devices the bleeding source. such as equine-derived, honeycomb-like collagen Practical aspects to approach a postoperative hem- sponge coated with a layer of coagulation factors: hu- orrhage surgically are to keep potential bleeding man fibrinogen and human thrombin. When applied sources in mind. After reopening the surgical site inci- tothesurfaceofbleedingtissue,thespongeprovides sion, one should pay attention to the muscle. Carefully, quick, reliable hemostasis. If surgical approaches fail, coagula should be removed in order to expose bleeding consider measures as described in Sect. 18.1.6, “Special sources from bruised muscle. Subtile mono- or bipolar Conditions.” coagulation should be performed. The same proce- 18.1 Acute Postoperative Complications 369

Table 18.1.7. Left partial and radical nephrectomy with bleeding sources, diagnostic and therapeutic procedures Surgical Topographic anatomy and Diagnostic Clinical features procedure potential bleeding source procedures Left transperito- Cutis/subcutis PEa/Labb/USc Hb↓/swelling/hematoma ↓ neal nephrecto- Muscle ⎫ PE/Lab/US Hb /swelling/hematoma my Omentum Check for abnormal coagulation test (see Table 18.1.1.2) Peritoneum Psoas muscle Spleen Adrenal gland Hb↓/intraabdominal fluid/bleeding source/blood pres- ⎬ Lab/US/CT-scan Bowel { sure↓,pulse↑ Pancreas Testicular/ovarian vessels ᭤ Consider relaparotomy in increasingly unstable patient Branches of lumbalis/ iliolumbalis vessels ⎭ Renal pedicle ᭤ Unstable patient Lumbar veins Urgent relaparotomy Left lumbar Cutis/subcutis PE/Lab/US Hb↓/swelling/hematoma nephrectomy Muscle PE/Lab/US Hb↓/swelling/hematoma Intercostal vessels PE/Lab/US Hb↓/swelling/hematoma Pleural cavity PE/Lab/US/X-ray Hb↓/respiratory rate↑/pleural effusion Spleen ᭤ Consider drainage Peritoneum ⎫ Psoas muscle Adrenal gland Hb↓/intraabdominal fluid/bleeding source/blood pres- ⎬ Lab/US/CT scan Testicular/ovarian vessels { sure↓,pulse↑ Branches of lumbalis/ ᭤ Consider relaparotomy in increasingly unstable patient iliolumbalis vessels ⎭ Renal pedicle ᭤ Unstable patient Lumbar veins Urgent relaparotomy Partial lumbar/ Same as above ⎫ Consider PSE transperitoneal additionally: PE/Lab/US/CT Consider Double-J nephrectomy Branches of renal artery scan/CT angio- IfPSEordouble-JfailscondsiderPSEanddouble-J Renal pelvis ⎬ graphy ᭤ Considerreoperationinincreasingunstablepatient Ruptured kidney ⎭ ᭤ Unstable patient Urgent reoperation In our institution, although not evidence-based, hemorrhage after partial nephrectomy or nephrectomy is taken very seriously sincesuchconditionsmayrequireimmediateaction.EarlyCTscan(nephrectomy)orCTangiography(partialnephrectomy)is indicated a Physical examination, b Laboratory, c Ultrasound

Table 18.1.8. Retroperitoneal lymphadenectomy with bleeding sources, diagnostic and therapeutic procedures Surgical Topographic anatomy and Diagnostic Clinical features procedure potential bleeding source procedures Retroperitoneal Cutis/subcutis PEa/Labb/USc Hb↓/swelling/hematoma lymphaden- Muscle (due to suture) PE/Lab/US Hb↓/swelling/hematoma ectomy Omentum ⎫ Check for abnormal coagulation test (see Table 18.1.1.2) Bowel Ureter Hb↓/extraperitoneal fluid/bleeding source/blood pres- Mesenterium ⎬ Lab/US/CT scan sure↓,pulse↑ Retroperitoneum { Psoas muscle ᭤ Consider conservative measures: Testicular vessels ⎭ See Table 18.1.5 RBC transfusion ᭤ Consider reoperation if conservative measures fail Spleen ⎫ Vessels in the node-bear- ingareas(caval,aortal, interaortocaval due to ⎬ slipped ligatures or clips) ᭤ Unstable patient Renal pedicle Urgent relaparotomy Lumbar veins ⎭ a Physical examination, b Laboratory, c Ultrasound 370 18 Postoperative Complications

Table 18.1.9. Radical prostatectomy with bleeding sources, diagnostic and therapeutic procedures Surgical Topographic anatomy and potential Diagnostic Clinical features procedure bleeding source procedures Radical retropubic Cutis/subcutis PEa/Labb/USc Hb↓/swelling/hematoma prostatectomy Muscle (due to suture or drainage) PE/Lab/US Hb↓/swelling/hematoma (open/extraperito- Pelvic vessels ⎫ Check for abnormal coagulation test (see neoscopic) Dorsal vein complex (due to Table 18.1.1.2) Plus pelvic lympha- slipped ligatures or clips) Hb↓/extraperitoneal fluid/bleeding source/ Lab/US/CT scan denectomy Bladder neck ⎬ { blood pressure↓,pulse↑ Seminal vesicle vessels ᭤ Consider conservative measures: Perirectal soft tissue See Table 18.1.5 Urethra ⎭ RBC transfusion ᭤ Consider reoperation in case of pelvic hematoma to prevent bladder neck contrac- ᭤ ture and incontinence Unstable patient Urgent reoperation Although recommended in the literature, we usually do not evacuate pelvic hematoma. In all of the rare cases of pelvic hematoma following radical retropubic prostatectomy that were treated conservatively, we did not find any bladder neck contracture or incontinence. But this a not an evidence-based opinion and prospective randomized trials on this issue are lacking. A condition in patients suspected of acute hemorrhage from pelvic vessels due to slipped ligatures or clips should be taken very seriously since immediate action may be required a Physical examination, b Laboratory, c Ultrasound

Table 18.1.10. Prostatectomy due to benign prostatic enlargement with bleeding sources, diagnostic and therapeutic procedures Surgical Topographic anatomy and Diagnostic Clinical features procedure potential bleeding source procedures Prostatectomy (Mellin/Freyer) Cutis/subcutis PEa/Labb/USc Hb↓/swelling/hematoma Muscle (due to suture or PE/Lab/US Hb↓/swelling/hematoma drainage) Check for abnormal coagulation test (see Table 18.1.1.2) Increase bladder irrigation ᭣ ᭤ Suprapubic cystostomy ⎫ site and bladder suture Expand transurethral catheter ᭣ ᭤ Suture of prostate capsule ⎬ Lab/US/CT scan Hb↓/extraperitoneal fluid/bleed- (50–100 ml) within the bladder and (Mellin) { ing source/blood pressure↓,pulse↑ put tension toward bladder neck ᭤ Consider conservative measures: Expand transurethral catheter ᭣ ᭤ Prostatic urethra (Freyer) ⎭ See Table 18.1.5 within the prostatic urethra (50– RBC transfusion 100 ml depending on enucleated ᭤ Consider reoperation if conserva- prostate volume) tive measures fail ᭤ Unstable patient Urgent relaparotomy a Physical examination, b Laboratory, c Ultrasound

Table 18.1.11. Cystectomy with bleeding sources, diagnostic and therapeutic procedures Surgical Topog raphic anatomy Diagnostic Clinical features procedure and potential bleeding source procedures Cystectomy Cutis/subcutis PE*/Lab**/US*** Hb↓/swelling/hematoma (Mellin/Freyer) Muscle (due to suture or drainage) PE/Lab/US Hb↓/swelling/hematoma Male: Vessels in the node-bearing areas (iliac, ⎫ Check for abnormal coagulation test pelvic peritoneum obturator, caval, aortal, interaortoca- (see Table 18.1.1.2) ureteral stumps val due to slipped ligatures or clips) prostate Dorsal vein complex (due slipped seminal vesicles ligatures or clips) ↓ membranous urethra Omentum Hb /extraperitoneal fluid/bleeding ⎬ Lab/US/CT-scan ↓ ↑ Female: Bowel (anastomosis) { source/blood pressure ,pulse Uterus Ureter (anastomosis) ᭤ Consider conservative measures: Ovaries Mesenterium See Table 18.1.5 Fallopian tubes Perirectal soft tissue RBC transfusion vaginal vault Psoas muscle ᭤ Consider reoperation if conservative Urethra Testicular/ovarian vessels ⎭ measures fail ᭤ Unstable patient Urgent relaparotomy The indication for blood transfusion should be posed generously due to the limited prognosis of the underlying disease and Hb↓ is mostly due to diffuse bleeding. Patients generally benefit from RCB transfusion a Physical examination, b Laboratory, c Ultrasound 18.1 Acute Postoperative Complications 371

quired for oxygen transport and delivery. The use of 18.1.1.6 fresh frozen plasma (FFP) and/or platelet concentra- Special Conditions tion (PC) should depend on the results of coagulation Disorders responsible for postoperative hemorrhage testing and clinical judgment. A markedly prolonged are the disseminated intravascular coagulation (DIC) PT and aPTT as well as decreased levels of fibrinogen and massive transfusion (MT). MT is commonly de- will require the administration of FFP. Doses ranging fined as the replacement of the entire circulating vol- from 5 to 20 ml/kg body weight have been recommend- ume in a period of 24 h. A dynamic definition of MT, ed. In an adult, four units FFP (800–1,000 ml) should such as the transfusion of four or more red cell concen- be sufficient, initially (Erber 2002; Hardy et al. 2004; Hi- trates within 1 h when ongoing need is foreseeable, or ippala 1998). If the fibrinogen concentration remains the replacement of 50% of the total blood volume with- below 1.0 g/l despite therapy with FFP, the administra- in3h,ismorerelevantintheacuteclinicalsetting tion of cryoprecipitate, a concentrated source of fibrin- (Crosson 1996; Hardy et al. 2004). A high percentage of ogen, factor VIII, factor XIII, and von Willebrand fac- massively transfused patients will show evidence of de- tor may be indicated (10–20 U) (Pantanowitz et al. fective hemostasis. The pathophysiology of this phe- 2003). In Europe, cryoprecipitates are no longer avail- nomenaisascomplexasthediagnosisisdifficult.At ableandwhenfibrinogensubstitutionisrequired,vi- present there is no simple, reliable, and rapid diagnos- rus-inactivated fibrinogen preparations are adminis- tic test. The platelet count is the only indicator of coa- tered (e.g., Haemocomplettan 1–8 g IV; ZLB Behring, gulopathy that can be obtained rapidly through the use Bern, Switzerland). Platelets should be administered to of automated counters. The prothrombin time (PT) and correct a clinical coagulopathy associated with de- the activated partial thromboplastin time (aPTT) are creased platelet count and/or platelet function (Ta- expected to become elevated (Turi and Peerschke bles 18.1.12, 18.1.13). 1986). Of utmost importance for an intact hemostasis is Pharmacological agents are usually administered the fibrinogen concentration. According to the litera- relatively late in MT. Protamine sulfate (1,000–3,000 IE/ ture, fibrinogen concentration should be at least be- day) and desmopressin (Table 18.1.14) have been used, tween 0.5 and 1.0 g/l (Hiippala et al. 1995). especially in cardiac surgery. Aprotinin (Table 18.1.14) Approaches to treatment initially include crystalloids or colloids, which are infused to maintain normo- Table 18.1.14. Dosage regimes for hemostatic drugs after anti- volemia (Erber 2002). Basic recommendations include platelet therapy the maintenance of normothermia. A low hemoglobin concentration (Hb) should be corrected prior to the ad- Aprotinin 2 million kallikrein inhibitory units (KIU) IV over 20 min, followed by a continuous in- ministration of hemostatic blood products. The opti- fusion of 500,000 KIU for the entire duration mal Hb to sustain hemostasis in the context of MT re- of the procedure mains unknown but is probably higher than that re- Tranexamic 10 mg/kg IV initially, followed by a continu- acid ous infusion of 1 mg/kg for 10 h, alternative- Table 18.1.12. Abnormal coagulation tests in MT ly 15 mg/kg, with repeat dosing 4–6 h later Desmopres- 0.3 µg/kg IV, possibly repeated 4 h later (the Fibrinogen concentration <1.0 g/l sin thrombotic risk must be taken into account) Prothrombin time (PT) 1.5–1.8 times control Activated partial thromboplastin 1.5–1.8 times control Platelet Transfusion at a dosage of 0.5–0.7×1011, time (aPTT) transfusion i.e., the standard concentrate per 7 kg of Platelet count <50,000 mm3 body weight in adults

Table 18.1.13. Proposals for the administration of hemostatic blood products in the massively transfused patient Presence of Ye s No clinical bleeding Abnormal Yes Transfusion of FFP and PC according to the coagula- Possible transfusion of FFP and PC coagulation test tion tests if the hemorrhagic risk related to (Table 18.1.12) the surgical procedure is high No Search for a cause other than a hemostatic defect No indication to transfuse Reevaluate the importance of red cell transfusion and consider FFP and PC if transfusion is massive Repeat coagulation tests Unknown Transfusion guided by clinical probability of a specific No indication to transfuse hemostatic defect Obtain coagulation tests FFP fresh frozen plasma; PC platelet concentration 372 18 Postoperative Complications

hasbeensuggestedinthecontextofMTbutitsuseisnot receptor antagonists. Recognized indications for anti- supported by any controlled trial. Recombinant activat- platelet therapy (acetylsalicylic acid) are first acute ed factor VII (rFVIIa, Novoseven) is a promising hemo- myocardial infarction, which reduces mortality by ap- static agent under investigation. It is a safe and effective proximately 20%, and second acute coronary syn- tool for the treatment and prevention of hemorrhage in drome (minimum recommended initial dose is 160 mg, hemophiliacs with circulating inhibitors to replacement followed by a maintenance dose of 75–325 mg daily). factors, and patients with Glanzmann’s thrombasthenia The perioperative risk of bleeding with antiplatelet refractory to platelet transfusion. By restoring thrombin agents varies and depends on the surgical procedure generation on the surface of tissue-factor-bearing cells, (Bertrand et al. 2000). Recommendations with evi- such as activated platelets and monocytes, recombinant dence level I can only be given in hip and knee surgery. activated factor VII has the potential to effect hemosta- While in hip surgery low preoperative acetylsalicylic sis in the setting of many coagulopathic states (Hardy et acid doses increase the risk of hemorrhage and expo- al. 2004; Welsby et al. 2005). Case reports and case series sure to transfusion, this is not seen when acetylsalicylic report the successful off-label use of rFVIIa to treat acidisadministered,postoperatively.Inurology,only bleeding that could not be controlled by the administra- evidence levels II–III are available. Pre- and postopera- tion of hemostatic blood components, although only un- tive ticlopidine/acetylsalicylic acid increases postoper- derpowered studies addressing safety concerns have ative bleeding and transfusion requirements for TURP been conducted. Since factor VII must interact with tis- and prostate surgery via an abdominal approach. Still, suefactortoinitiatethegenerationofthrombin,coagu- themajorissueishowcanperi-andpostoperative lation occurs in the site of injury (Allen et al. 2002) and bleeding complications induced by certain antiplatelet the risk of thromboembolic effects appears minimal agents be avoided. Steroids to reduce or eliminate any (Hardy et al. 2004; Roberts 1998). In urology, one trial possible increase in perioperative blood loss are not has demonstrated decreasing blood loss and the need recommended Grade E (supported by only Level IV or for transfusion during retropubic prostatectomy (Frie- V studies). Also, prophylactic platelet transfusion derich et al. 2003). Since there is no established monitor- should not be given, but platelets must be readily avail- ing tool for the effect of rFVIIa, the cessation of bleeding able Grade C (supported by Level II studies). Nonspe- maybethebestandonlyindicatorofefficacy(Welsbyet cific methods to decrease perioperative blood loss are al. 2005). Official dosage recommendations for off-label recommendedbysomephysicianssuchasselectinga use of rFVII in surgical patients are not available, but surgical approach designed to achieve the most effec- dosesaslowas20µg/kgbodyweight(~60kIENovoSe- tive hemostatic control. If possible in consultation with ven) have been shown to have some effect, while doses the anesthesiologist, a controlled hypotension tech- around 40 µg/kg body weight (~120–180 kIE NovoSe- nique in normothermia should be used. However the ven) have been effective in many clinical settings. If inef- surgical procedure hemodilution should be restricted. fective,thedosecanberepeated,andlargerdosesdonot In addition, hematocrit levels should maintained to en- necessarily cause more thromboembolic complications sure normal biological hemostasis, usually at 30%. (Welsby et al. 2005). In cardiac surgery, established efficacious pharma- The pathophysiology is complex and coagulopathy cological modalities for reducing intra- and postopera- associated with MT requires a multidisciplinary ap- tive bleeding and transfusion exposure in patients on proach involving anesthesiologists, blood bankers, he- antiplatelet agents include aprotinin and tranexamic matologists, laboratory specialists, and urologists. acid (evidence level I) (Castati et al. 2001; Laupacis and Times have changed, blood products have changed, Fergusson 1997; Murkin 1994). Aprotinin may be re- and so has the management of the bleeding patient. sponsible for allergic reaction and even anaphylactic Nevertheless, standardized management may not al- shock (0.3% first exposure and 2.5%–3% after initial ways be possible in massively bleeding patients. Once contact).Tranexamicaciddoesnotinvolvethiskindof the initial hemorrhagic phase of coagulopathy is con- allergic risk and its cost–benefit ratio is more favorable. trolled, efforts should be directed toward the preven- While aprotinin has been documented with a very low tion of thrombotic complications related to the con- thrombotic risk, desmopressin, a third hemostatic sumption of coagulation factors associated with DIC. drug, is effective only in patients presenting with major Averyspecialsituationmaydevelopinpatientswho bleeding syndrome (evidence level III), and it is imper- experience intraoperative myocardial infarction and ative that its thrombotic risk potential be taken into ac- are in need of immediate therapy with antiplatelet count. Platelet transfusion to reduce or stop postopera- agents. So-called platelet inhibitors are drugs capable tive blood loss in patients treated with antiplatelets are of inhibiting platelet function, in particular activation effective despite the absence of level I or II evidence and aggregation. Currently available agents include as- (Table 18.1.14). pirin, dipyridamole, the thienopyridines (ticlopidine The lack of data in other types of urological surgery and clopidogrel), and the glycoprotein IIb/IIIa (IIb q 3) makes it impossible to formulate recommendations. 18.1 Acute Postoperative Complications 373

Whether a patient is in need of antiplatelet therapy pe- Table 18.1.15. Cardiovascular system disorders rioperatively should always be an on-site decision with Acute coronary syndrome/acute ischemia an experienced cardiologist, anesthesiologist, and Systolic dysfunction urologist. To stop the surgical procedure after subtile Valv ular disorders coagulation may be a choice if a cardiovascular inter- Pericardial diseases ventionisneeded.Guidelinesconcerningthisissuedo Anemia Thoracic aortic rupture not exist, nor are they wanted since guidelines restrict Deconditioning the margin of individual decisions. The literature reports two studies on ultrasound- guided transrectal biopsy, and three studies dealing 18.1.2.2 with aspirin-related bleeding complications after Cardiovascular System Disorders transurethral prostatectomy. Although red cell transfusion was never required after prostate biopsy, they were Table 18.1.15 gives an overview of frequent cardiac dis- givenin30%ofcontrolpatientsundergoingprostatec- orders.AnECGcanrevealacutemyocardialischemia, tomy:twocasesofmortalitywerereported.According arrhythmia, signs of left ventricular hypertrophy, bun- to the meta-analysis of Burger et al., aspirin increased dle branch block, or right ventricular strain. this risk of bleeding by a factor of 2.7. ThepresenceofSTsegmentelevationofmorethan 0.1 mV in at least two corresponding leads or a new complete left bundle branch block indicates a high like- 18.1.2 lihood of a blockage of a coronary artery with consecu- Chest Pain and Dyspnea tive myocardial infarction (Fig. 18.1.2). Reperfusion therapy by either primary percutaneous coronary in- 18.1.2.1 tervention (PCI) or thrombolysis can be initiated with- Overview out any further diagnostic tests, if there are no contra- Chest pain and dyspnea can be caused by a variety of indications due to the history of surgery (Hamm 2004). disorders. After surgery, they are most often due to dis- It must be remembered that the sensitivity of the orders of the respiratory or cardiovascular system but 12-lead ECG for detection of myocardial ischemia is can also be caused by gastrointestinal disorders (e.g., only about 50% (Lee et al. 1987; Giannitsis and Katus peptic ulcer disease) or musculoskeletal chest wall 2002). Therefore, the measurement of biochemical pain. The major purpose of diagnosis is to differentiate markers for myocardial necrosis in serum can be con- between cardiac and noncardiac disorders, acute and sidered as standard. Troponin T is widely used as a bio- chronic disorders, and benign and potentially life- chemical marker (Katus et al. 1991; Gerhardt et al. 1992; threatening disorders (Kurz et al. 2005). Diagnosis Bakker et al. 1994b); in addition, troponin I, myoglobin must be precise and quick to identify high-risk patients (Ohman et al. 1990; Stone et al. 1977), and creatine ki- and initiate the appropriate treatment. As symptoms nase MB (CK-MB) (Mair et al. 1991; Van Blerk et al. can be misleading, diagnosis should include the follow- 1992; Bakker et al. 1994a) are in use. ing for every patient presenting chest pain and/or dyspnea: 18.1.2.3 ) Evaluation of risk factors for respiratory or cardio- Postoperative Pulmonary Complications vascular disorders (e.g., history of myocardial in- Pulmonary complications are common during the hos- farction or thrombosis, diabetes, atherosclerosis, pital stay and a major cause of morbidity and mortality etc.) (Arozullah et al. 2000). The incidence in the periopera- ) Physical examination tive period ranges from 5% to 80% (Fisher et al. 2002; ) Vital signs (blood pressure, heart rate, respiratory Thompson et al. 2003). Table 18.1.16 gives an overview rate, oxygen saturation) of frequent postoperative pulmonary complications. In ) 12-Lead electrocardiogram (EKG) the following sections, management of the most fre- ) Complete blood count, electrolytes, creatinine, quent complications is described. D-dimer, troponin T ) Chest radiograph (CXR) (optional) ) Chest computed tomography (CT) angiogram Pulmonary Embolism (→ pulmonary embolism) (optional) Pulmonary embolism (PE) is a complication of deep venous thrombosis (see Chap. 18.1.6, “Deep Venous Thrombosis,” for etiology and therapy). Clinical signs include dyspnea, tachypnea, and tachycardia. As a consequence of right heart failure, the jugular veins are dis- 374 18 Postoperative Complications

Fig. 18.1.2. ST-Elevation in myocardial infarction

Table 18.1.16. Postoperative pulmonary complications block (Chan et al. 2001). However, the majority of patients with PE have normal or unspecific abnormal Pulmonary embolism Atelectasis echocardiograms (Challapalli et al. 2004). Bronchospasm Two-dimensional echocardiography can demon- Pleural effusions strate right ventricular hypokinesis with sparing of the Hypoxemia right ventricular apex (McConnell’s sign [Goldhaber Pneumothorax Noncardiogenic pulmonary edema 2002]), tricuspid regurgitation, and lack of collapse of Infection (e.g., pneumonia, bronchitis) theinferiorvenacavaduringinspiration.Spiralcom- Exacerbation of underlying chronic lung disease puted tomography is the first-line imaging technique Acute upper airway obstruction in many hospitals to secure the diagnosis of a PE Chemical pneumonitis (Fig. 18.1.4). Patients should be given up to 100% O If Abdominal compartment syndrome (ACS) 2. Tracheal laceration or rupture the patient is in pain or very distressed, morphine should be administered (10 mg IV). Guidelines suggest a bolus of unfractionated heparin (UFH) tended, an accentuated pulmonic heart sound and tri- 10,000 IU IV over 5 h, followed by a maintenance infu- cuspid regurgitation murmur can be monitored in the sion at 15–25 IU/kg/h as guided by aPTT (for most physical examination. commercial aPTT reagents, 1.8–3.0 times the control Plasma D-dimers have an excellent negative pre- value). Consider streptokinase in the postoperative dictive value (Janata 2003); elevated D-dimer levels, patient. however, are frequent after surgery and can be mis- The use of inferior vena cava filters reduces the inci- leading. dence of early pulmonary embolism during the first The electrocardiogram may show the classic S1Q3T3 12 days, but almost doubles the long-term risk of recur- pattern (Fig. 18.1.3) as a sign of acute cor pulmonale or rent DVT (Decousus et al. 1998). Therefore a vena cava a new complete or incomplete right bundle branch filter is only indicated in patients who have a contrain- 18.1 Acute Postoperative Complications 375

Fig. 18.1.3. S1Q3T3 pattern in pulmonary embolism

dication to anticoagulation or experience pulmonary embolism despite therapeutic anticoagulation (Bates and Ginsberg 2004; Ho et al. 2005).

Pleural Effusions After abdominal surgery, small pleural effusions can be monitoredinupto50%ofpatients(LightandGeorge 1976). Most patients have no symptoms: clinical signs due to a restrictive ventilatory defect (Gilmartin et al. 1985) include pleuritic chest pain, dyspnea, and dry nonproductive cough (Yataco and Dweik 2005). Frontalandlateralchestradiography(Ferrerand Roldan 2000) or sonographic study (McGahan 1985; McLoud and Flower 1991; O’Moore et al. 1987) is usually sufficient to detect a pleural effusion of at least Fig. 18.1.4. Spiral CT scan showing pulmonary embolism 250 ml of fluid (Yataco and Dweik 2005). In contrast to most other clinical situations, thoracentesis is not mandatory for small effusions after recent surgery but can tions for the placement of a tube thoracostomy include be indicated if the patient’s clinical condition deterio- pneumothorax, hemothorax, complicated parapneu- rates. Large and symptomatic effusions causing severe monic effusion, or empyema (Yataco and Dweik 2005). respiratory symptoms should be drained (Yataco and Additional pharmacological application of antibiotics Dweik 2005). A tube thoracostomy can be placed to and diuretics may be indicated. drain the pleural space continuously. Typical indica- 376 18 Postoperative Complications

and Huber 1976; Marini et al. 1979) mucolytic therapy Atelectasis cannot be definitively recommended (Jepsen et al. Atelectasisisoneofthemostfrequentpulmonarycom- 1989a, b). plications after abdominal surgery. Most often it is clinically insignificant. The incidence of clinically signifi- Infection/Pneumonia cant atelectasis is approximately 15%–20% (Celli et al. 1984; Craven et al. 1974; Platell and Hall 1997). Clinical See Chap. 18.1.3, “Postoperative Fever.” signs include increased work of breathing and hypoxemia. The development of atelectasis is caused by a va- Tube Thoracostomy riety of processes such as retained airway secretions, the altered compliance of lung tissue, and impaired re- A tube thoracostomy (Fig. 18.1.5) is used to drain air or gional ventilation (Platell and Hall 1997). Standard liquid from the pleural space. Indications to place a therapy remains continuous positive airway pressure tube thoracostomy include large, progressive or symp- (CPAP) (Squadrone et al. 2005; Fowler et al. 1978), tomatic pneumothorax, tension pneumothorax, hemo- whereas bronchoscopy may have a role in cases that are thorax, chylothorax, and complicated parapneumonic unresponsive to CPAP (Wanner et al. 1973; Feldman effusion or empyema.

Fig. 18.1.5. Placement of a tube thoracostomy 18.1 Acute Postoperative Complications 377

The silastic tube is most often inserted in the fourth Table 18.1.17. Differential diagnosis of acute abdomen or fifth intercostal space in the anterior axillary or mid- Intraabdominal axillary line (Miller and Sahn 1987; Symbas 1989). Generalized peritonitis: perforated viscus, primary infec- For the insertion, the patient’s arm is placed behind tive peritonitis, rupture of cyst the head (Fig. 18.1.5a). After disinfection and local an- Localized peritonitis: abscess, appendicitis, cholecystitis, esthesia (combined with general sedation and analgesia pancreatitis, salpingitis, Meckel diverticulitis Motility disorders: intestinal obstruction, biliary obstruc- if needed), a skin incision is made parallel to the inter- tion, ureteric obstruction, irritable colon, diverticulosis, costal space. To avoid injuries of nerves or vessels, it is uterine contraction, urinary retention performed immediately above the rib (b). A Kelly clamp Ischemia: acute myocardial infarction (AMI), mesenteric is used to penetrate through the intercostal muscle and ischemia/infarction/thrombosis, sickle cell crisis, splenic infarction, torsion of ovarian cyst/testicle/omentum, intothepleuralspace(c).Usingafinger,thecorrectpo- tumornecrosisofhepatoma/fibroid,vasculitides sition is confirmed and adhesions between the lung and Infective: urinary tract infection, malaria, tuberculosis, thepleuralsurfaceareremoved(d).Afterinsertingthe yersinia,cholera,typhoid chest tube (apically for a pneumothorax and inferiorly Other: peptic ulcer, inflammatory diseases (e.g., ulcerative colitis or Crohn disease), retroperitoneal tumors, ectopic for a pleural effusion or hemothorax), the distal end is pregnancy connected to the chest drainage unit (e). The tube is secured by a suture and/or tape (f) (Golden and Hiley Extraabdominal Thoracic: lung diseases (e.g., pulmonary embolism, pneu- 1998). There is no general recommendation on how monia), ischemic heart disease, esophageal disease, aor- much suction should be applied, although the most tic dissection commonly used pressure is 15–20 cm H2O. Vital signs Neurological: herpes zoster, spinal arthritis, radiculopathy (blood pressure, pulse, respiration rate, and oxygen sat- from tumors, tabes dorsalis, abdominal epilepsy Metabolic: diabetes mellitus, chronic renal failure, porphyria, uration) before and after placement of the tube should acute adrenal insufficiency, thyroid storm, hypercalcemia be monitored and compared. A chest x-ray must be tak- Abdominal wall: herniae, rectal sheath hematoma en to confirm the correct placement of the tube (Schul- Retroperitoneal pathologies: hematoma or abscess (with man et al. 2005). consecutive paralytic ileus) The drain can be removed when drainage has Nonspecific abdominal pain stopped or an x-ray shows that there is no air or fluid in the intrapleural space. There is controversy over wheth- ) Fever er the chest tube should be clamped for a few hours ) Free fluid in the abdomen before removal. In all events, the patient should have an ) Shaking chills x-ray immediately after removal to assess for lung reex- The characteristic expression of the face during an pansion. The x-ray should be repeated 24 h later. acute abdomen is called facies abdominalis. The patient’sfaceisanxious,furrowed,andpinchedwiththe 18.1.3 nose and upper lip drawn up. Acute Abdomen Case presentation acute abdomen A 63-year-old male is developing fever (39.1°C) and “Acuteabdomen”isacollectivetermforavarietyof abdominal pain beginning on the 5th day after cy- disorders, both of intra- and extraabdominal origin. In stectomy and ileum neobladder construction. The addition to all the above-mentioned complications af- abdomen is becoming increasingly rigid, the blood ter surgery, all non-surgery-related disorders (see Ta- drains (removed on the 2nd day after surgery) and ble 18.17) should be kept in mind as differential diag- blood count give no hint of prolonged bleeding. The nosis when approaching a patient presenting an acute patients face is pale and covered with cold sweat. He abdomen. has been complaining about abdominal distention Signs for an acute abdomen may include (see also and difficulties passing gas ever since surgery. The thecasepresentationbelow): vital signs show hypotension (75/45 mmHg) and an ) Abdominal pain accelerated pulse rate (100/min). The leukocyte ) Rigid abdomen count is 18.6 G/l, CRP is 23.2 mg/dl, troponin-T and ) Abdominal distention D-dimer levels are not elevated. The chest x-ray ) Point tenderness shows no sign for pneumonia; the urine analysis ) Nausea and vomiting shows a mild infection. The possible reason for acute ) Signs of shock abdomen: intestinal leakage. ) Hypotension ) Anuria Depending on the preceding type of surgery (open ) Inability to pass feces or gas surgery, transurethral surgery, ESWL), postoperative 378 18 Postoperative Complications

Table 18.1.18. Postoperative acute abdomen after radical cy- ) Vital signs (blood pressure, heart rate) stectomy ) Temperature Complications Incidence ) Complete blood count, electrolytes, creatinine ) Fluid balance Pyelonephritis (Joniau et al. 2005; Meller et al. 4%–23% ) 2002; Frazier et al. 1992; Gburek et al. 1998; Monitoring of blood drainage Madersbacher et al. 2003) If any of these findings are pathological or the patient Ileourethral stenosis (Joniau et al. 2005; Knap 3%–14% presents clinical signs of a postoperative complication et al. 2004; Frazier et al. 1992; Gburek et al. (e.g., pain or rigid abdomen), the diagnosis should be 1998; Madersbacher et al. 2003) extended, which may include: Urosepsis (Joniau et al. 2005; Hollenbeck et al. 2%–8% 2005; Rosario et al. 2000) ) Physical examination (auscultation, palpation, Ileus (Knap et al. 2004; Hollenbeck et al. 2005; 2%–10% percussion) Rosario et al. 2000)4,5,10 ) Vital signs (blood pressure, heart rate, respiratory Intestinal leakage (Eriksen et al. 2005; Mat- 2%–9% rate, oxygen saturation) thiessen et al. 2004; Nakada et al. 2004; Piso et ) 12-lead electrocardiogram (EKG) al. 2004) ) Complete blood count, electrolytes, creatinine, D-dimer, troponin T, amylase, lipase, glucose, clotting, Ca2+ acute abdomen is most often caused by bleeding, ab- ) Depending on the experience of the surgeon and scess, ileus, or intestinal leakage. Extraabdominal dis- indication:ultrasound(e.g.,bladder,kidneys,ab- orders induced by physical and mental stress must be domen), abdominal x-ray (AXR) or CT scan considered as well (acute myocardial infarction, pul- ) Blood and urine cultures monary embolism, peptic ulcer). Most of the surgery- Itmustbementionedthatnotallexaminationsare related complications make prompt reintervention mandatory and some complications such as bleeding necessary. may require immediate relaparotomy. Therefore all di- In urology, a postoperative acute abdomen most of- agnoses must be tailored to each patient and the indi- ten occurs after open surgery, in particular after radical vidual medical history. cystectomy.Thisstemsfromthelongdurationofsur- gery and somewhat high blood loss in combination with bowel surgery. Within the first 30 days after radi- 18.1.3.1 cal cystectomy, complications are reported in 19%– Initial Management 76% (Joniau et al. 2005; Tolhurst et al. 2005; Meller et al. 2002; Knap et al. 2004; Hollenbeck et al. 2005; Stein et As long as the underlying reason for an acute abdomen al. 2001), most of them may clinically present as acute is unknown, the initial management after surgery abdomen (see Table 18.1.18). should include: After transurethral surgery, an acute abdomen may ) Nothing by mouth (NBM) be attributable to intraperitoneal bladder perforation ) Intravenousfluids(fluidvolumeandelectrolytes) and bleeding (Nieder et al. 2005; Collado et al. 2000; ) Nasogastric tube Kondas and Szentgyorgyi 1992; Pycha et al. 2003). In ) Stress ulcer prophylaxis case of small extraperitoneal perforations, often pro- ) Antibiotics longed catheter drainage is sufficient therapy, whereas ) Analgesia larger or intraperitoneal perforations may require abdominal exploration. Further therapy depends on the cause of acute abdo- Acute abdomen after extracorporeal shockwave men (e.g., reintervention). lithotripsy (ESWL) is extremely rare, but small bowel perforation, rupture of the kidney, or perforation of the ureter may result in acute abdomen (Klug et al. 2001; 18.1.4 Kurtz et al. 1999; Alkibay et al. 1992; Geh et al. 1997; Postoperative Fever Holmberg et al. 1997). 18.1.4.1 The main goal after surgery is to monitor the patient Overview to detect early signs for any postoperative complication. According to the above-mentioned probability of Surgical patients are subjected to dramatic alterations postoperative acute abdomen patients with a high risk in body temperature during the intraoperative and (e.g., after cystectomy) should be monitored more postoperative periods (Sessler 1997). “Postoperative fe- closely than low-risk patients. The postoperative moni- ver” is a recognized term in the literature even though toring should include as a minimal standard: the syndrome has not been clearly characterized. An 18.1 Acute Postoperative Complications 379 important question is whether postoperative elevations 18.1.4.2 in body temperature represent true fever or hyperther- Incidence mia.Truefeverisanalterationofthethermoregulatory setpoint, which implies a feeling of cold discomfort and Depending on the definition of postoperative fever (see active vasoconstriction and shivering until the new set- Sect. 18.1.3.1), reviewed literature has estimated its in- point is attained. Hyperthermia occurs when heat gain cidence to be between 13% and 40%. In general, the (usually from an exogenous source) exceeds heat loss, procedures with longer surgical incisions and longer resultinginanelevatedTcthatisnotregulated. duration have the greatest postoperative increase in Tc. Elevated core temperature (Tc) in the postoperative Conversely, procedures with shorter incisions and du- period occurs commonly and the mechanism and clini- ration have less increase in core temperature (Frank et cal relevance is poorly understood. It seems that early al. 2000). postoperative elevation in Tc is a normal response after major surgical procedures due to tissue injury and pe- 18.1.4.3 rioperative stress that occurs in proportion to the dura- Definition tion of surgery and is associated with elevated levels of cytokines (Frank et al. 2000). This response satisfies the See Table 18.1.19. true definition of fever, i.e., a regulated increase in Tc setpoint. The setpoint for Tc is influenced by endoge- 18.1.4.4 nous substances, categorized as pyrogens (IL-1, IL-6, Risk Factors and Prevention tumor necrosis factor, interferon) or cryogens (gluco- corticoids, arginine vasopressin), which work by alter- Preoperative identification of risk factors (Table ing the thermoregulatory setpoint in the anterior hypo- 18.1.3.5) is the best prevention and the most important thalamus. The effect of endogenous pyrogens is to in- aspect of therapy. crease the Tc setpoint in the anterior hypothalamus. 1. Regarding the pulmonary tract, nosocomial pneu- Although traditional definitions of fever (38.3– monia is the second most common hospital-ac- 38.5°C) appear to correlate with infection in medical quired infection, after urinary tract infections, and patients (Bates et al. 1990), febrile surgical patients fre- accounts for between 27% and 47% of infections quentlyhavenoidentifiablesourceofinfection(Bellet within the intensive care unit (ICU) and reported al. 1978; Goodman et al. 1968). mortality rates between 30% and 70% (Kollef 2004). In the past, pulmonary atelectasis has classically Nosocomial pneumonia is usually defined as hospi- been described as the cause of postoperative fever, but tal-acquiredpneumoniathatoccursatleast48haf- morerecentstudiesindicatethatthecauseoffeverin ter admission to hospital but excludes any infection the postoperative period is equally likely to be infec- that was incubating at the time of admission (Cra- tious or noninfectious (Marik 2000; O’Grady et al. ven and Steger 195). Key risk factors include chronic 1998a, b). In other words, fever in the postoperative pe- lung disease, advanced age (>60 years), smoking, riod is neither sensitive nor specific as a clinical sign of prolongeddurationofmechanicalventilation, infection. supine position, and previous antibiotic therapy In summary, patients who undergo major surgical (Cook and Kollef 1998; Trouillet et al. 1998). Com- procedures experience a regulated increase in Tc set- mon pathogens responsible for early- (develops af- point in the early postoperative period, which fits the ter >2 days but <4 days of hospitalization) and late- classic definition of fever. The average Tc setpoint after onset nosocomial pneumonia are listed in Ta- surgery is elevated by 1.4°C (2.5°F) above the preopera- ble 18.1.20. tive baseline. A greater incidence of infection is well 2. Catheter-associated urinary tract infection (CAU- recognized when the duration of follow-up is longer. TI) is the most common nosocomial infection in The clinician should therefore use caution when inter- hospitals worldwide and the incidence has been preting fever occurring later in the postoperative reported to be approximately 35%. Although most course when fever may more likely be associated with CAUTIsareasymptomatic(TambyahandMaki infection. 2000), they often precipitate unnecessary antimi- Because fever is often the earliest and most easily de- crobial therapy. Numerous studies have document- tected sign of infection in the surgical patient, it is im- edahighprevalenceofresistantpathogensin portant that in clinical practice there is a clear defined CAUTI. The association between nosocomial work-up and management. CAUTI and surgical site infections has been made (Krieger et al. 1983). The most important risk factors have been prolonged catheterization and being female. Other 380 18 Postoperative Complications

Disorder Definition Table 18.1.19. Clinical diagnostic criteria of sepsis and Infection Presence of organisms in a normally sterile site that is usually, but not septic shock necessarily, accompanied by an inflammatory host response Bacteremia Bacteria present in blood as confirmed by culture may be transient Septicemia Same as bacteremia, but implies greater severity Clinical evidence of infection plus evidence of a systemic response to infection. This systemic response is manifested by two or more of the following conditions: Temperature>38°Cor<36°C Heart rate >90 beats/min Respiratory rate > 20 breaths/min or PaCO2 <32mmHg(<4.3kPa) WBC >12,000 cells/mm3 <4,000cells/mm3 or 10% immature (band) forms Sepsis syndrome Infection plus evidence of altered organ perfusion with at least one of the following: hypoxemia, elevated lactate, oliguria, altered mentation Hypotension A systolic blood pressure of <90 mmHg or a reduction of >40 mmHg from baseline in the absence of other causes of hypotension Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include but are not limited to lactic acidosis, oliguria, or an acute alteration on mental status Septic shock Sepsis with hypotension despite adequate fluid resuscitation along with thepresenceofperfusionabnormalitiesthatmayinclude,butarenot limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are on inotropic or vasopressor agents may not be hypoten- siveatthetimethatperfusionabnormalitiesaremeasured Systemic inflam- Response to a wide variety of clinical insults, which can be infectious, as matory response in sepsis but can be noninfectious in etiology (e.g., burns, pancreatitis) See Chap. 3 syndrome (SIRS) Adopted from Naber et al. (2001)

Table 18.1.20. Microbial etiology of nosocomial pneumonia obstructed catheters should be irrigated or if neces- Pathogen Onset of Frequency (%) sary, replaced. Meatal care, addition of antimicrobi- pneumonia* al agents in the drainage device, and vesical irrigation are useless (Leone et al. 2004). Antibiotics are in Streptococcus pneumoniae Early 10–20 Haemophilus influenzae Early 5–15 general protective, but the infections, when they oc- Anaerobic bacteria Early 10–30 cur, tend to be caused by antibiotic-resistant organ- Staphylococcus aureus Early/late 20–30 isms (Tambyah 2004). The best way of preventing a Gram-negative bacilli Late 30–60 CAUTI is to remove the catheter or to avoid its use. Pseudomonas aeruginosa Late 17 Suprapubic catheters are associated with a de- Klebsiella pneumoniae Late 7 Acinetobacter spp. Late 3 creased rate of CAUTI (Tambyah 2004). Escherichia coli Late 6 3. The use of central venous catheters (CVCs) has be- Enterobacter spp. Late 10 come an indispensable routine in modern medical Legionella pneumophila Late 0–15 practice. It has spread from ICUs and operating Adapted from Craven and Steger (1995) rooms to general wards and outpatient clinics. One of the most common and serious complications associated with CVCs is catheter-related infections riskfactorsidentifiedhaveincludedcatheterization (CRIs) (Hammarskjold et al. 2006; McGee and Gould outside the sterile environment of the operating 2003). The incidence of CRI varies between 2 and 30 room, having a urinary tract abnormality, other in- per 1,000 catheter days(Hammarskjold et al. 2006; fections, diabetes, malnutrition, and renal failure. Fraenkel et al. 2000). Known risk factors for CRI in- An important factor for preventing infection is the clude neutropenia, immunosuppression, ICU ad- maintenance of a closed sterile drainage system. On mission, shock, parenteral nutrition, long-term he- the urological ward, it is essential to allow the drain- modialysis, and insertion via the femoral or internal agetubetobeabovethelevelofthepatientandthe jugular vein (Polerman and Girbes 2002). The mor- collecting tube should be kept from kinking. The tality rate as a result of CRI is reported to be between collecting bag should be emptied regularly using a 0% and 25% (Polerman and Girbes 2002; Crnich separate collecting container. Poorly functioning or and Maki 2002)). The most common microbiologi- 18.1 Acute Postoperative Complications 381

Table 18.1.21. Risk and protective factors for central venous (Adam et al. 2004; Berger 2005; Hamasuna et al. 2004). catheter-related infections Microorganisms originating from the patient and the Risk factors Protective factors patient’s immediate environment are the primary sources for SSI (Staphylococcus epidermidis, S. aureus, Duration of catheterization Maximum asepsis Type of catheter (higher risk with Aseptic topical care MRSA[ Methicillin-resistant coagulase-negative S. au- multiple lumen catheter) reus], Escherichia coli, Proteus mirabilis, Pseudomonas Location of insertion (lower risk Antiseptic or antibiot- aeroginosa, Enterobacteriaceae) (Harbarth et al. 1999). with subclavian insertion, high- ic-coated devices The first step in prevention of wound infection starts er risk with femoral or internal jugular vein with the preparation of the operative site. Specifically, Emergent insertion avoidance of shaving the skin is emphasized, because Number of manipulations the use of a razor increases the risk of skin breakage, Age which can allow pathogens direct access to the blood- Disease (benign vs malignant) stream. A current review concerning the issue of hair Neutropenia Immunosuppression removal policies in clean surgery quotes four random- ICU admission ized, controlled trials, while no eligible meta-analysis Shock was found (Niel-Weise et al. 2005). When hair removal Parenteral nutrition wasconsiderednecessary,evidenceaboutthebesttime Long-term hemodialysis for removal was inconclusive. There was some evidence that hair removal by clipper is superior to removal by Table 18.1.22. Microbial etiology of central venous catheter-re- razor. A Cochrane Database Review in 2006 (Tanner et lated infections, al. 2006) questioned whether a preoperative hair re- Pathogen Total moval results in a fewer surgical site infections. Only two trials involving 358 patients matched the inclusion Coagulase-negative staphylococci ~60% Pseudomonas aeruginosa ~10% criteria of this review. Of people who were shaved, 9.6% Staphylococcus aureus 5%–6% developed an SSI compared with 6% who were not Enterobacter 5% shaved. There was no statistically significant difference Escherichia coli 2.5% between shaving and no hair removal; however, the Enterococcus faecalis 2.5% Klebsiella pneumoniae 2.5% studies were not of high quality and the comparison Candida albicans 5% was underpowered. The same applies to when depilato- ry cream was compared with no hair removal. When Adapted from Hammarskjold et al. (2006) and Paragioudaki et al. (2004) shaving was compared with clipping to reduce SSIs, the difference was statistically significant and shows that people are more likely to develop an SSI when they were cal agents responsible for CRI are Staphylococcus au- shaved than when they were clipped prior to surgery. reus, coagulase-negative staphylococci, Candida Unfortunately, no studies were identified which com- species, and various Gram-negative rods (O’Grady pared clipping with no hair removal. et al. 2002) (refer to Tables 18.1.21 and 18.1.22). A different objective is the effect on SSI rates of hair removal immediately before surgery compared with In our institution, the CVC are inserted using maximal hair removal more than 4 h before surgery. Tanner et al. sterile precautions (cap, mask, gown, gloves, large found no statistically significant difference in his Coch- drape) with a Seldinger technique by an anesthetic spe- rane Database Review. In conclusion, the review found cialist. The insertion site is treated with a solution con- insufficient evidence for an effect of preoperative hair taining 2% chlorhexidine. The site is dressed with a removal, but if hair removal is considered to be neces- transparent semipermeable dressing (Tegaderm HP, sary it should be performed with clippers because this 3M). Every 3rd day, dressings and stopcocks are results in fewer SSIs. changed and the insertion site is treated with the 2% Preoperative urinary tract infection (UTI) is the ma- chlorhexidine solution. In a trial performed by Ham- jorriskfactorforSSIinpatientsundergoingurological marskjöld et al., the median duration of catheterization surgery. Therefore, urine culture and sensitivities for the CRI group was 20 days and 15 days for those should be available, and UTIs should be treated with without infection. appropriate antibiotics preoperatively (Hamasuna et In terms of surgical wound infection, obesity, diabe- al. 2004). tes, corticosteroids, and stress are the major risk fac- The etiology of wound complications in obese pa- tors. The incidence of surgical site infection (SSI) in the tients is probably related to the poor vascularity of sub- urologic population varies in the literature, with rates cutaneousfat,serousfluidcollection,andhematoma ranging from 5.5% to 33% (Takeyama et al. 2005) in formation. Studies have shown that using a subcutane- patients receiving cystectomy and urinary diversion ous suture in all patients with greater than 2-cm subcu- 382 18 Postoperative Complications

Table 18.1.23. Risk factors for postoperative fever Table 18.1.24. Symptoms and workup in pneumonia Risk factors Measures taken to reduce risk Symptoms and Workup of infection clinical signs Category of surgical Prophylactic use of antibiotics Systemic upset Chest x-ray (infiltrate) procedure Fever U&E, FBC (with differential white Diabetes mellitus Bowel preparation cell count) Prosthetic heart valve Bowel preparation Pleuritic pain, cough, Blood cultures Stress Bowel preparation green sputum Obesity Bowel preparation Corticosteroids Bowel preparation Hemoptysis Expectorated sputum culture and Improvement in general state of microscopy (serology) patient: Confusion (in elderly) Endotracheal or bronchoscopic Chest physiotherapy aspirate Use of bronchodilators Crepitation Quantitatively cultured bronchoscopic bronchoalveolar lavage fluid taneous depth significantly reduces the risk of wound or brush catheter specimen disruption. Specifically, closure of excess subcutaneous Tachy pnea tissue eliminates dead space, thus reducing the forma- Sputum purulence tion of seromas. Impaired wound healing is frequently seen in pa- Degree of oxygenation impairment tients with diabetes. Cruse and Foord (Cruse and Foord 1973) reviewed infection rates in 23,649 patients and found that diabetics had five times the risk Pulmonary of infection of nondiabetics. Although increased levels of HgA1c do not seem to be positively correlated to All patients with suspected pneumonia should have a surgical site infections in one study, diabetes and post- chest x-ray to assess the severity and complications. operative hyperglycemia are independent risk factors Routinebloodculturesarealsorecommended,prefera- for a SSI. It was demonstrated that glucose levels above bly before initiating antimicrobial treatment. Sputum 200 mg/dl in the immediate postoperative period are examination including sputum culture, microscopy, associated with an increased SSI rate. Additionally, and serology for atypical pneumonia (Legionella, My- blood glucose levels above 200 mg/dl at 48 h after sur- coplasma, Chlamydia, Coxiella)shouldbeevaluated gery are significantly associated with deep wound in- (Table 18.1.24). fection. No specific recommendations other than avoidance Urinary Tract of hyperglycemia (blood glucose <200 mg/dl) and strict regulation of insulin to assist in wound healing Symptoms are not reliable for the diagnosis of CAUTI. canbemade(Table18.1.23). Sometimes it is hard to demonstrate a difference in presence of fever or symptoms related to the urinary tract in catheterized patients with and without CAUTI. 18.1.4.5 The catheter can itself be the source of symptoms. The Detection and Work-Up majority of cases of bloodstream infection associated Concerning etiology of postoperative fever in terms of with CAUTI are in patients where there is significant infection, six different predominant sites are consid- urinary obstruction. It has also been shown that pa- ered. tients with long-term indwelling catheters rarely have febrile episodes even though they have chronic significant amounts of bacteria in their urine. This changes when obstruction or encrustation occurs in that set- Site ting. 1 Pulmonary tract – most common in the immediate Suprapubic aspiration of the bladder represents the postoperative period gold standard in the diagnosis of urinary tract infec- 2 Urinary tract – common in patients with indwelling tion. It is, however, not performed routinely in clinical catheters practice in which urine samples are generally aspirated 3 Cellulitis in venous access sites 4 Surgical wound infections – generally present 3–7 days from the catheter itself or through a port designed spe- postoperatively cifically for that purpose. Disconnecting the catheter 5 Intraabdominal sepsis from abscess – generally present more than absolutely necessary is a violation of the after the 5th–7th postoperative day 6 closed drainage principle and is discouraged. The urine Bacteremia or septicemia sample should be sent immediately to the bacteriology 18.1 Acute Postoperative Complications 383 laboratory since bacteria will continue to proliferate in Table 18.1.25. Symptoms and workup in UTI/CAUTI the warm medium, leading to increased bacterial Symptoms and Workup counts. If such immediate referral is not possible, the clinical signs container should be transported in iced water and then Systemic upset Urinalysis and culture stored in a refrigerator at 40°C. Cooling stops bacterial growth, but the following day the bacteria can still grow Fever U&E, FBC (with differential white cell count) on culture medium. The definition of CAUTI is restrict- edtothepresenceofbacteriainthebladderofapatient Pyuria Fibrinogen <1 g/l, platelets <50,000 mm3,PTandaPTT with an indwelling catheter. Bacteriuria is defined as 1.5–1.8 × control thedetectionofmorethan105 cfu/ml organisms per milliliter of urine with no more than two species of or- Suprapubic pain Blood cultures ganism (contamination). Because of the prevalence of Frequency, urgency, Sonography of urinary bladder bacteriuria in patients with urinary catheters, some dysuria and kidney have advocated daily monitoring of urine in catheter- Costovertebral angle Consider plain x-ray (abdomen) ized patients. Routine monitoring of the urine from all pain catheterized patients is not an effective way to decrease Confusion (in elderly) Consider CT scan (abdomen) the incidence of symptomatic CAUTI (Garibaldi et al. Sepsis signs Consider MRI 1982). Thus, frequent microbiologic monitoring to detect early contamination of the urine in hope of pre- Table 18.1.26. Microbial etiology of UTI/CAUTI (Calandra and venting urosepsis cannot be recommended. Cohen 2005) From the clinical point of view, a CAUTI can manifest itself as bacteriuria, bacteremia, septicemia, or sep- Pathogens Frequency (%) sis syndrome. Sepsis syndrome is diagnosed when clin- Escherichia coli 53 ical evidence of infection is accompanied by signs of in- Enterococcus 20 flammation (fever, hypothermia, tachycardia, tachyp- Pseudomonas group 8.3 Staphylococcus aureus 6.6 nea, hypotension, oliguria, leukocyturia, or leukope- Proteus group 5 nia). Klebsiella 5 Asymptomatic bacteriuria or asymptomatic CAUTI Candida 3.3 is a microbiologic diagnosis from a patient without symptoms or signs referable to urinary tract infection. Central Venous Catheters and Catheter-Related Infections The usual quantitative definition is 105 cfu/mL or greater in two consecutive urine specimens (Rubin et al. The diagnosis of CRI is often a diagnosis of exclusion. 1992). Acute uncomplicated urinary tract infection is a Clinical findings are nonspecific to establish a diagno- symptomatic bladder infection characterized by fre- sis of catheter-related sepsis. Nevertheless, a diagnostic quency,urgency,dysuria,orsuprapubicpain,while algorithm is suggested in Fig. 18.1.6. A clinical suspi- acutenonobstructivepyelonephritisisarenalinfection cion of catheter infection in the presence of otherwise characterized by costovertebral angle pain and tender- unexplained severe sepsis or septic shock, however, ness, often with fever. In sedated patients, history, com- should prompt catheter removal and appropriate cul- plaints, and physical examination are limited. There- tures of the catheter tip, blood cultures, and exit-site or fore, urinalysis and culture should be taken; the same hub cultures depending on the presentation. The clini- applies for blood tests (Tables 18.1.25, 18.1.26). In any cal probability of CRI increases when a catheter has case, ultrasound of the bladder as well as the kidneys been in place 7 days. Local signs at the catheter exit site must be performed. Hydronephrosis, abscesses, and such as erythema, cellulitis along the subcutaneous urinary retention needs immediate intervention. If tract of the catheter, and pus also increase the clinical stones are suspected, plain x-ray or native CT scan probability of CRI, although the majority of CRI occurs should be considered. In case of perinephric abscess, in the absence of local symptoms. abscess of the kidney, or retroperitoneal abscess, a contrast-enhanced CT scan is advised because of the feasi- Surgical (Wound) Site Infection bility of a percutaneous intervention and the confirmation of the diagnosis. An algorithm is suggested in The diagnosis is SSI is a obvious clinical presentation Fig. 18.1.3.2. withcalor,dolor,rubor,andtumor (heat,pain,redness, and swelling) as known from textbooks of basic medicine. 384 18 Postoperative Complications

High probability of catheter-related infection

Fever and chills Bacteremia Hypotension Septcemia Hyperventilation Clinical presentation Sepsis syndrome Altered mental status in terms of severity Severe sepsis Nausea & vomiting & diarrhea Septic shock Thrombophlebitis SIRS Cellulitis

Signs of sepsis Patient becomes hypotensive when catheter is flushed Catheter in place ≥ 7 days or placed Clinical under nonsterile conditions Results Diagnosis probalibility Dysfunction of the catheter resulting from intraluminal clot Pus or cellulitis at exit site or tunnel tract infection

All cultures negative No catheter- related sepsis

Bacteremia with Paired blood culture and common skin catheter-related culture exite site and hub commensal AND sepsis with Diagnostic algorithm positive tip culture bacteriological and strategy Remove CVC and tip culture or exit site culture confirmation for same organism Replace CVC at new site

No bacteremia but Possible clinical positive culture of catheter-related tip, exit site or hub sepsis

Fig. 18.1.6. Modified diagnostic algorithm in the diagnosis of central venous catheter-related infection (Calandra and Cohen 2005) The patient has a recognized pathogen defined as a Intraabdominal Sepsis from Abscess microorganism different from a common skin con- Refer to Sect. 18.1.3.7.4. taminant (i.e., diphtheroids, Bacillus species, Propio- nibacterium species, coagulase-negative staphylococci, or micrococci) cultured from one or more blood Bacteremia or Septicemia – Bloodstream Infection cultures. Bloodstream infections (BSIs) account for 30%–40% Diagnosis is obtained by blood cultures; for manage- of all cases of severe sepsis and septic shock (Bochud et ment refer to Sect. 18.1.3.6.3. al. 2001). However, the incidence of BSI as a cause of severe sepsis is probably underestimated in the hospital setting,sincebloodculturesarefrequentlydrawnfrom 18.1.4.6 patients treated with broad-spectrum antibiotics. BSIs Management can be divided into two categories: Thetreatmentoftruefever(seeSect.18.1.3.3)should 1. Primary BSI comprising BSI of unknown origin in focus primarily on returning the setpoint toward nor- patients without an identifiable focus of infection, mal with antipyretics (acetaminophen or cyclooxyge- and intravascular catheter-related BSI (see nase inhibitors). Sect. 18.1.3.5.3 above). 2.SecondaryBSIdefinedasaBSIcausedbyamicro- organism related to an infection at another site. 18.1 Acute Postoperative Complications 385

The duration of antibacterial treatment should be Current Treatment of Nosocomial Pneumonia limited to the shortest effective course of therapy, to re- There are various published guidelines and recommen- duce the risk of creating resistance. Seven days of thera- dations for the treatment of nosocomial pneumonia. py for VAP should be sufficient and could prevent recol- Generally, nosocomial pneumonia is divided into three onization with resistant pathogens (Kollef 2004), al- levels of severity (Kollef 2004): though no prospective randomized controlled trials exist. ) Group (1): – Mild/moderate without risk factors, any time of onset (early/late) Treatment of CAUTI – Severe without risk factors, early onset From expert opinion, asymptomatic bacteriuria does ) Group (2): not require treatment (Cravens and Zweig 2000). In- – Mild/moderate with risk factors, any time of dwelling catheters can be changed in this setting, al- onset (early/late) though no evidence is available in the literature. In a ) Group (3): randomized comparison of active management includ- – Severe pneumonia without risk factors, late ingashortcourseofantibioticandthereplacementof onset indwelling catheter vs control, no benefit was associat- – Severe pneumonia with risk factors, any time of ed with the active management, and a trend to multire- onset (early/late) sistant bacterial superinfection was observed in this group (Leone et al. 2004). Group 1 Antibiotics There are only a few specific studies of urinary tract Enteric Gram-negative Third-generation cephalosporins bacteria (cefotaxime/ceftriaxone) infection (UTI) in populations of ICU patients with se- Escherichia coli If Enterobacter suspected: vere sepsis/septic shock, and although both bacterial Klebsiella spp. – q -lactam/ q -lactamase inhibitor CAUTI and candiduria are very common, CAUTI is the combination most common nosocomial infection. According to the Proteus spp. Ampicillin/sulbactam International Conference for the Development of a Serratia marcescens Ticarcillin/clavulanate Haemophilus influenzae Piperacillin/tazobactam Consensus on the Management and Prevention of Se- Methicillin-sensitive If allergic to penicillin: vere Candidal Infections, colonized patients without S. aureus – Fluoroquinolone evidence of infection do not require treatment. Never- Streptococcus pneumo- – Clindamycin plus aztreonam theless, candiduria can occasionally be the only acces- niae sible evidence of deep candidiasis. Candiduria is rare in 2 Group Antibiotics normal healthy adults, and even in an unselected hos- Group 1 organism plus Group 1 antibiotics plus Anaerobes – Clindamycin or q -lactam/ q -lac- pital population only about 2% of urine samples re- tamase inhibitor combination ceived in the laboratory will show candiduria, although Staphylococcus aureus – Vancomycin (until methicillin- this number rises to 3%–15% in the ICU in catheter- resistant S. aureus excluded) ized patients (Leone et al. 2003b; Tissot et al. 2001). Legionella –Erythromycin Candida albicans and Candida glabrata are found in Pseudomonas aerugi- – Antipseudomonal penicillin nosa (pieracillin, titarcillin) 46% and 31% of cases, respectively (Leone et al. 2003a). There is considerable uncertainty about the cri- Group 3 Antibiotics Group 1 organism plus Group 1 antibiotics plus teria to be used in interpreting the finding of candidu- Acinetobacter spp. – Aminoglycoside or fluoroquino- ria. The early work of Goldberg et al. (1979) suggesting lone plus one of the following: that Candida speciescountsof104/ml represent clini- Pseudomonas aerugi- Anti-pseudomonal penicillin cally significant infection has been supported by oth- nosa (pieracillin, titarcillin) Methicillin-resistant q -lactam/ q -lactamase inhibitor ers, although there are certainly reports suggesting that S. aureus combination lower counts can be associated with symptoms and in- Aztreonam deed that lower counts often quickly increase to higher – Imipenem/meropenem ± vanco- counts if untreated. Hence, in the clinical setting, and in mycinllin) particular on the ICU, clinicians will rarely rely on microbiology alone to decide on the significance of candi- Appropriate empiric antibacterial treatment should duria. They will have to integrate other clinical infor- be initiated as soon as infection is suspected, since a mation. Fluconazole may be the best option for treating delay in starting treatment will reduce the effectiveness candiduria Edwards et al. 1997), but only if the species of therapy and increase the risk of mortality (Iregui is C. albicans. Voriconazole may be more effective et al. 2002; Luna 1997). Following initial therapy, labo- against non-albicans species. ratory data on the identification and susceptibility In the clinical setting, infected hydronephrosis due profileofthecausativepathogenallowspecifictherapy. toanycause,kidneyorperinephricabscessesare 386 18 Postoperative Complications

Table 18.1.27. Recommendations for antimicrobial therapy in urology Diagnosis Frequent Initial, empiric antimicrobial therapy Therapy duration pathogens UTI with complicating E. coli – Cephalosporin, third-generation (cefotaxime, 3–5 Days after defervescence factors ceftazidime) or control/elimination of complicating factor Nosocomial UTI Enterococcus – Fluoroquinolone (ofloxacin, levofloxacin) Pyelonephritis, acute, Staphylococcus –Anti-Pseudomonas active Acylaminopenicllin/ complicated BLI Urosepsis Klebsiella –Carbapenem Proteus – Meropenem Enterobacter ±Aminoglycoside Pseudomonas Candida Serratia Modified according to Naber et al. (2005) BLI q -lactamase inhibitor

dreaded pathologies because of their potential to turn aeruginosa,andBacillus spp.Inthesecases,itisessen- into severe sepsis. In these cases, it is of utmost impor- tial to follow patients up carefully. Attempts to preserve tance to come to a rapid diagnosis in order to prelude the catheter in patients with CRI due to S. aureus have adequate source control measures. Usually infected hy- no more than a 20% chance of success (Marr et al. dronephrosis needs to be drained either by a double-J 1997). Catheter preservation is inadvisable in patients catheter combined with a transurethral catheter or a with S. aureus bacteremia also because of the high risk percutaneous nephrostomy. Early administration of of secondary complications (endocarditis, osteomyeli- appropriate antimicrobial agents is equally essential. tis). Catheter removal is likewise necessary in patients Both kidney and perirenal abscesses need to be drained with CRI due to Candida spp. by inserting a tube (e.g., a pigtail catheter) guided by Sincemorethan60%ofCRIsarerelatedtostaphylo- ultrasound or CT scan. In severe cases, emergency ne- cocci (coagulase-negative staphylococci), vancomycin phrectomy may be indicated in individual cases (refer (15mg/kgi.v.every12h,ifrenalfunctionisnormal) to Table 18.1.27 and Fig. 18.1.27). should be administered as empirical treatment. When cultures grow, a pathogen treatment should be amended accordingly. Catheter-Related Infections The impact of S. aureus bacteremia on clinical man- ThetherapyforlocalCRIsuchasinfectionoftheinser- agement has to be stressed specifically. Sufficiently long tion site or thrombophlebitis is removing the catheter. treatment periods are necessary to adequately address Catheter removal is also necessary if Staphylococcus the risk of seeding (e.g., endocarditis, osteomyelitis). aureus is detected in blood cultures. An exchange of the Accordingly, 2–4 weeks of treatment with intravenous CVC using a guidewire at the infected insertion site antibiotics are recommended (Raad and Sabbagh may result in bacteremia and septic emboli and there- 1992). Therapy with penicillase-resistant penicillin is fore should be omitted. In thrombophlebitis and inser- more effective and therefore preferable to treatment tion site infection, local and systemic administration of with glycopeptide antibiotics (Siegman-Igra et al. antibioticsisnotrequiredunlesstemperaturerises 1997). Glycopeptides are indicated only in patients with above 38°C and signs of infection such as purulence are penicillin allergy or methicillin-resistant staphylococ- present and cultures are negative. Warm soaks and ele- ci. Newer drugs directed against Gram-positive bacte- vation of the extremity should be sufficient. If any sign ria (linezolid, quinupristin/dalfopristin) should be re- of systemic infection is seen, antimicrobial therapy for served for patients who are intolerant or infected with 7daysorlessshouldbesufficient.IftherapyviaCVC organisms resistant to glycopeptide antibiotics. Ta- continues to be necessary and an alternative site for in- ble 18.1.28 gives an outline of treatment of the most serting the CVC is unavailable, antimicrobial therapy common catheter-related infections. without removal of the CVC is reasonable in the absence of signs or symptoms of sepsis in the presence of the following pathogens: coagulase-negative staphylococci, Corynebacterium jeikeium, Acinetobacter bau- mannii, Stenotrophomonas maltophilia, Pseudomonas 18.1 Acute Postoperative Complications 387

Lower urinary tract Upper urinary tract infection infection

Positive dipstick (for Organism cultured >38 °C >38 °C Clinical from fluid (other than Urgency Urgency leukocytes/nitrite) signs urine) or tissue from Localized pain/ Frequency or the infected site. tenderness Dysuria > 3 leukocytes/high Abscess or other Hematuria Pyuria power field of evidence of infection Pyuria Hematuria + unspun urine seen on examination, Organism isolated Pos. Gram stain during surgery, or by from culture Pus histopathologic Positive Gram stain Suprabubic ≥ Urine culture 10 examination Radiographic evidence Tenderness cfu/ml Urine or two of the following of infection

Clinical signs Hypothermia <36 °C leukocytosis >12.000/µl Hypothermia >38 °C leukopenia <400/µl Tachycardic >90/min Fibrinogen <1g/l Tachypnoe >20/min Platelets <50.000 mm3 art. pCO <4.3 kPa 2 PT 1.5–1.8 x control (33 mmHg) aPPT 1.5–1.8 x control Lap test

Ultrasound plain x-ray (abdomen) CT scan MRI

Kidney Ureter Bladder Prostate Perinephric abscess Retroperitoneal abscess Acute urinary retention Acute prostatitis Abscess of the kidney Retroperitoneal fibrosis Bladder stone Seminate vesicle Retroperitoneal abscess Obstructive stones Reflux abscess Pyelonephritis Obstructive tumor Benign prostatic Epididymitis Obstructive stones Extraluminal obstruction enlargement Orchitis Tumor Lymphoma Diverticulum Tbc Lymphoma Pregnancy Bladder tumor Pregnancy Extra/intraperitoneal Tbc Extra/intraperitoneal Tumor Tumor Tbc Tbc

Abscess drainage Double-J Mono-J Nephrostomy Zystostomy Transurethral catheter Operation

Antibiotics (Table 18.1.27)

Fig. 18.1.7. Workup and management of urinary tract infection 388 18 Postoperative Complications

Pathogen Therapy Duration Table 18.1.28. Antimicrobial therapy of venous catheter- Staphylococcus aureus Isoxazolyl penicillin (penicillase-resistant At least 2 weeks i.v. b related bacteremia depend- (oxacillin-sensitive) penicillin)a ing on identity of pathogen therapy duration Staphylococcus aureus Glycopeptide, linezolid, quinupristin + At least 2 weeks i.v. b (oxacillin-resistant) dalfopristin Follow-up blood cultures are Coagulase-negative According to susceptibility pattern; glyco- For 5 –7 days after always necessary after cessa- staphylococci peptide only in oxacillin-resistant cases defervescence tion of antibiotic therapy in Enterococci Aminopenicillin plus aminoglycoside For 5–7 days after order to rule out persistence defervescence of infection From Fatkenheuer et al. (2003) Glycopeptide plus aminoglycoside in ampi- a cillin-resistant cases For oxacillin-sensitive Linezolid or quinupristin/dalfopristin in strains (vast majority), vancomycin-resistant cases treatment with penicillase- resistant penicillin is supe- Candida albicans Fluconazole & 2weeks rior to treatment with a Alternative: amphotericin B or caspofungin glycopeptide. Non-albicans Candida Amphotericin B & 2weeks b High incidence of organ species infection if treatment is Alternative: caspofungin or Voriconazole continued for less than 2 or itraconazole weeks. Catheter removal is required whenever these All other pathogens According to susceptibility pattern Not defined pathogens are present

Surgical Site Infection: Wound Management Table 18.1.29. Historically used dressing for wound cleansing Despite prophylactic measures and good surgical tech- Misconceptions about wound healing nique, a small percentage of patients will still experi- Agent Problem ence wound complications. SSIs require manual open- Povidone iodine Cytotoxic to white blood cells and ing of the wounds to allow drainage. An open wound other vital wound-healing compo- can be managed in two ways: secondary closure, sec- nents ondary intention with dressings or using negative pres- Iodophor gauze Delays wound healing sure wound therapy. Hydrogen peroxide Delays wound healing Secondary closure can be performed once a wound Keeping the wound Moist wounds promote autolytic is free of infection or necrotic tissue and has started to dry debridement, support epithelial cell granulate. This procedure is done within 1–4 days after migration 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 Table 18.1.30. Definition of infective endocarditis required significantly fewer days to heal than patients Definite infective endocarditis who were allowed to heal by secondary intention. Pathologic criteria Modern wound care dressing selection considers fac- – Microorganisms demonstrated by culture or histologic tors such as the phase of healing, the volume of exudate, examination of a vegetation, a vegetation that has embo- and the presence of necrotic tissue to determine the type lized, or an intracardiac abscess, or – Pathologic lesions; vegetation or intracardiac abscess of dressing that will be most supportive of wound healing. confirmed by histologic examination showing active en- The risk of infection can be reduced by using a nontoxic docarditis solutiontocleansethewound,e.g.,normalsaline(Ta- Clinical criteria ble 18.1.29). Necrotic tissue can be removed by sharp de- –2Majorcriteriaor bridement or daily applications of enzymatic debriders – 1 Major criterion and 3 minor criteria or that act on necrotic tissue but have no effect on healthy tis- – 5 Minor criterion sue. Drainage can be managed by using highly absorbent Possibleinfectiveendocarditis dressing material. Calcium alginate and foam are materi- – 1 Major criterion and 1 minor criterion or als used in wound care that are highly absorbent. – 3 Minor criteria Negative pressure wound therapy also known as Rejected vacuum-assisted closure uses controlled levels of nega- – Firm alternative diagnosis explaining evidence of infective endocarditis or tive pressure to assist and accelerate wound healing by – Resolution of infective endocarditis syndrome with anti- evacuating localized edema with negative pressure. biotics therapy <4 days or Bacterial colonization is reduced along with the evacu- – No pathologic evidence of infective endocarditis at sur- ationofwounddrainage.Negativepressurealsoin- gery or autopsy, with antibiotic therapy for <4 days or creases localized blood flow and oxygenation, thereby – Does not meet criteria for possible infective endocarditis 18.1 Acute Postoperative Complications 389 promoting a nutrient-rich environment that stimulates patients are classified into three diagnostic categories granulation tissue growth. Such cellular proliferation (definite, possible, and rejected endocarditis; see Ta- encourages angioneogenesis, uniform wound size re- bles 18.1.30 and 18.1.31). Recently, modifications of the duction, and reepithelialization. Duke criteria have been proposed to take into account several identified shortcomings of the original criteria, including the increasing diagnostic role of transesoph- 18.1.4.7 ageal echocardiography and the relative risk of infec- Special Conditions tive endocarditis in bloodstream infections due to Fever Due to Infective Endocarditis Staphylococcus aureus (Li et al. 2000). Infective endocarditis accounts for about 1% of all Clinicians may appropriately and wisely decide to cases of severe sepsis and is associated with a mortality treatornottreatanindividualpatient,regardlessof rate of 33% (Angus et al. 2001). Diagnostic criteria for whether they meet or fail to meet the criteria of “defi- infective endocarditis, referred to as the Duke criteria, nite” or “possible” infective endocarditis (IE) by the are based on microbiological data and echocardio- Duke schema. The Duke criteria are meant to be only a graphic imaging findings. According to these criteria, clinical guide for diagnosing IE and, certainly, must not

Table 18.1.31. Definitionofmajorandminorcriteriaofinfec- Table 18.1.32. Diagnosis of infective endocarditis tive endocarditis History Major criteria Prior cardiac lesions Blood culture positive for IE Prior indwelling intravascular catheters Typical microorganisms consistent with IE from two sepa- Prior intravenous drug abuse rate blood cultures: Physical examination Streptococcus viridans, Streptococcus bovis,HACEKgroup, Auscultation of cardiac murmurs Staphylococcus aureus or Neurologic impairment Community-acquired enterococci in the absence of a Petechiae primary focus or Splinter hemorrhages Microorganisms consistent with IE from persistently posi- Janeway lesions tive blood cultures, defined as follows: Osler’s nodes At least two positive cultures of blood samples drawn Roth spots >12 h apart or Clinical evidence of emboli (fundi, conjunctivae, skin, Allofthreeoramajorityoffourormoreseparatecul- and digits) tures of blood (with first and last sample drawn at least 1 h apart) Laboratory Single positive blood culture for Coxiella burnetii or anti- Blood cultures – a minimum of three blood cultures should phase I IgG antibody titer >1 : 800 be obtained Erythrocyte sedimentation rate ↑ Evidence of endocardial involvement ↑ Echocardiogram positive for IE (TEE recommended in pa- CRP Leukocytes ↑ tients with prosthetic valves, rated at least “possible IE” by ↑ clinical criteria, or complicated IE (paravalvular abscess); Rheumatoid factor (minor criteria in the Duke criteria) TTE as first test in other patients), defined as follows: Red blood cell casts in urine plus a low serum complement Oscillating intracardiac mass on valve or supporting level (minor criteria in the Duke criteria) structures, in the path of regurgitant jets or Normochromic normocytic anemia On implanted material in the absence of an alternative Organism (see Table 18.1.33) anatomic explanation or Abscess or Electrocardiogram New partial dehiscence of prosthetic valve Heart block New valvular regurgitation (worsening or changing of pre- Conduction delay existing murmur not sufficient) Baseline electrocardiogram Minor criteria Chest x-ray Predisposition, predisposing heart condition, or injection Septic pulmonary emboli with few or multiple focal lung drug use infiltrates Fever, temperature >37°C Calcification in a cardiac valve Vascular phenomena, major arterial emboli, septic pulmo- Echocardiographya nary infarcts, mycotic aneurysm, intracranial hemor- Detection of vegetations on valves rhage, conjunctival hemorrhages, and Janeway lesions Detectionofvalvulardysfunction Immunologic phenomena: glomerulonephritis, Osler’s Detection of hemodynamic dysfunction nodes, Roth’s spots, and rheumatoid factor Detection of associated abnormalities (shunt or abscess) Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evi- Histologic examination

dence of active infection with organism consistent with IE a Echocardiographic minor criteria eliminated Transthoracic echocardiography (TTE) may provide confirmation of the diagnosis of endocarditis. Transesophageal echocar- IE infective endocarditis, TEE transesophageal echocardiogra- diography (TEE) has a higher spatial resolution than TTE and phy, TTE transthoracic echocardiography is much more sensitive for the detection of endocarditis 390 18 Postoperative Complications

replace clinical judgment. In the clinical setting the di- However,somepatientsdonothavepositivebloodcul- agnosisisusuallyobviouswhenapatienthasthechar- tures and 20%–30% of patients have no predisposing acteristic findings of IE: cardiac lesion. In this setting, the correct diagnosis may be delayed. ) Numerous positive blood cultures in the presence UsuallythediagnosisofIEisbaseduponhistoryand of a well-recognized predisposing cardiac lesion physical examination, blood culture and laboratory re- ) Absence of infection elsewhere sults, an electrocardiogram (ECG), a chest x-ray, and an echocardiogram (Table 18.1.32).

Table 18.1.33. Modified therapy of infective endocarditis according to the American Heart Association Streptococcus viridans and Aqueous crystalline 12–18 Million U/24 h IV either continuously or in 4weeks Streptococcus bovis Penicillin G sodium four or six equally divided doses 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. Aqueous crystalline 24 Million U/24 h IV either continuously or in four 4 pneumoniae and Streptococcus or six equally divided doses pyogenes 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 4 or six equally divided doses Penicillin G sodium 3 mg/kg per 24 h IV/IM in one dose 2 plus gentamicin sulfate 2 Enterococcus – strains susceptible Ampicillin sodium 12 g/24 h IV in six equally divided doses 4–6 4–12 to penicillin, gentamicin, and or vancomycin Aqueous crystalline 18–30 Million U/24 h IV either continuously or in 4–6 Penicillin G sodium six equally divided doses plus gentamycin sulfate 3 mg/kg per 24 h IV/IM in three equally divided 4–6 doses Staphylococcus – strains suscepti- Nafcillin or oxacillin 12 g/24 h IV in four to six equally divided doses 6 ble to oxacillin In the absence of prosthetic with optional addition of 3mg/kgper24hIV/IMintwoorthreeequallydi- 1 materials gentamycin sulfate vided doses History of penicillin allergy Cefazolin 6 g/24 h IV in three equally divided doses 6 with optional addition of 3mg/kgper24hIV/IMintwoorthreeequallydi- 1 gentamycin sulfate vided doses Staphylococcus – strains resistant Vancomycin 30 mg/kg per 24 h IV in two equally divided doses 6 to oxacillin In the absence of prosthetic materials Staphylococcus – strains suscepti- Nafcillin or oxacillin 12 g/24 h IV in six equally divided doses 6 ble to oxacillin Therapy for prosthetic valve plus Rifampin 900 mg per 24 h IV/PO in three equally divided 6 endocarditis doses History of penicillin allergy plus gentamicin 3 mg/kg per 24 h IV/IM in two or three equally di- 2 vided doses Cefazolin 6 g/24 h IV in three equally divided doses 6 Staphylococcus – strains resistant Vancomycin 30 mg/kg 24 h in two equally divided doses 6 to oxacillin Adjust vancomycin to achieve 1-h serum concentra- 6 tion of 30–45 g/ml and trough concentration of 10–15 g/ml Staphylococcus – strains resistant plus Rifampin 900 mg/24 h IV/PO in 3 equally divided doses 2 to oxacillin plusgentamycin 3mg/kgper24hIV/IMintwoorthreeequallydi- vided doses Therapy for both native and pros- Ceftriaxone sodium 2 g/24 h IV/IM in one dose 4 thetic valve endocarditis caused or ampicillin- sulbactam 12 g/24 h IV in four equally divided doses 4 by HACEKa Microorganisms a Haemophilus parainfluenzae, H. aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella cor- rodens,andKingella kingae From Baddour et al. (2005) 18.1 Acute Postoperative Complications 391

Medical treatment of native valve endocarditis is the ceral arteries and the arteries of the upper and lower domain of antibiotic administration. Basically, the du- extremities. Neurological complications develop in ration of therapy has to be sufficient to eradicate micro- 20%–40% of patients with IE. Intracranial MAs repre- organisms. The response to therapy should be assessed sent an extremely dangerous subset of these complica- by obtaining repeat blood cultures 48–72 h after antibi- tions.TheoverallmortalityrateamongIEpatientswith otics are begun. Thereafter, regular careful serial exam- intracranialMAsis60%.hantimicrobialtherapy.Ex- inations should be performed to search for signs of tracranial MAs (intrathoracic or intraabdominal) are heart failure, emboli, or other complications. Most pa- often asymptomatic until leakage or rupture occurs. tients with IE generally become afebrile 3–5 days after Presumably, most extracranial MAs (ECMAs) will rup- treatment is begun with an appropriate antibiotic. ture if not excised. Hematemesis, hematobilia, and Surgical therapy in patients with IE should be indi- jaundice suggest rupture of a hepatic artery MA, arteri- vidualized, with input from both the cardiologist and al hypertension and hematuria suggest rupture of a re- the cardiovascular surgeon (Tables 18.1.33, 18.1.34). nal MA, and massive bloody diarrhea suggests the rup- The incidence of reinfection of newly implanted valves ture of an ECMA into the small or large bowel (Baddour in patients with active IE is 2%–3% (Mills et al. 1974) et al. 2005). and is far less than the mortality rate for IE and congestive heart failure (CHF) without surgical therapy, which Fever Due to Postoperative Appendicitis canbeashighas51%(SextonandSpelman2003). Complications of IE are CHF, which occurs more fre- Theroleofincidentalappendectomyduringelective quently in aortic valve infections (29%) than with mi- and nonelective surgery remains controversial. Propo- tral (20%) or tricuspid disease (8%). Systemic emboli- nents of this practice argue with the technical ease, the zation occurs in 22%–50% of cases of IE. Emboli often low morbidity of the procedure, and the elimination of involve the lungs, coronary arteries, spleen, bowel, and future risk and confusion over conflicting diagnosis extremities. Up to 65% of embolic events involve the and therefore for the prophylactic merits (Salom et al. central nervous system. Most emboli occur within the 2003; Silvert and Meares 1976). Epidemiological stud- first 2–4 weeks of antimicrobial therapy. Splenic ab- ies estimate a lifetime risk of acute appendicitis as 8.6% scessisararecomplicationofIE.Mycoticaneurysms in men and 6.7% in women (Gupta et al. 2002; Hayes (MAs) are uncommon complications of IE that result 1977). Addis et al. (1990) estimated that for a 60-year- from septic embolization of vegetations to the arterial old male, it would require 166 incidental appendecto- vasa vasorum or the intraluminal space, with subse- mies to prevent a single lifetime case of appendicitis. quent spread of infection through the intima and out- Since the cumulative lifetime risk for appendicitis de- ward through the vessel wall. MAs occur most fre- creaseswithadvancingage(seeTable18.1.35)andpa- quently in the intracranial arteries, followed by the vis- tients undergoing radical cystectomy and urinary diversion have a mean age of 64 years (Frazier et al. 1992), Table 18.1.34. Echocardiographic features that suggest poten- the lifetime risk of a postoperative appendicitis is very tial need for surgical intervention according to (Baddour et al. low (Gupta et al. 2002). The rationale for removing the 2005) appendix during urologic surgery is to prevent the future development of appendicitis since anatomical al- Ve ge t at i on Persistent vegetation after systemic embolization Anterior mitral leaflet vegetation, particularly with Table 18.1.35. Cumulative lifetime risk for acute appendicitis >10mm(surgerymayberequiredbecauseofriskof embolization) Age group (y) Men (%) Women (%) & Embolic events during first 2 weeks of antimicrobial therapy (surgery may be required because of risk of emboli- 0– 5 9.4 8.4 zation) 5– 9 9.2 8.3 Increase in vegetation size despite appropriate antimicrobi- 10–14 8.6 7.8 altherapy(surgerymayberequiredbecauseofriskof 15–19 7.2 6.7 embolization, heart failure, or failure of medical therapy) 20–24 5.9 5.4 25–29 4.9 4.5 Valvular dsyfunction 30–34 4.1 3.8 Acuteaorticormitralinsufficiencywithsignsofventricu- 35–39 3.4 3.1 lar failure 40–44 2.8 2.5 Heart failure unresponsive to medical therapy 45–49 2.3 2.0 Valve perforation or rupture 50–54 1.9 1.7 Perivalvular extension 55–59 1.6 1.2 Valvular dehiscence, rupture, or fistula 60–64 1.2 0.9 New heart block 65–69 0.8 0.6 Large abscess or extension of abscess despite appropriate 70–74 0.4 0.3 antimicrobial therapy From Wang and Sax (2001) 392 18 Postoperative Complications

teration of viscera following urinary tract reconstruc- Fever Due to Forgotten Foreign Body (Corpus Alienum: tion makes differential diagnosis of recurrent abdomi- Rubber Drain, Gauze Sponge, Forceps, etc.) nal pain in the right lower abdominal region difficult. But with the availability of the latest investigative mo- “Gossypiboma” refers to retained surgical sponge or dalities (CT scan) over 95% of painful abdominal con- swab and is derived from gossypium (“cotton” in Latin) ditions can be detected. The value of computed tomog- and boma (“place of concealment” in Swahili) (O’Con- raphy in the diagnosis of appendicitis has been well es- nor et al. 2003). Because of legal implications, this con- tablished in the past few years. This has been advocated dition is often underreported and the incidence has as the imaging modality of choice because of its high been estimated as 1 in 100–5,000 surgeries (Lauwers sensitivity, accuracy, and negative predictive value in and Van Hee 2000). The most commonly retained for- diagnosing appendicitis. In a study of patients with eign body is the laparotomy sponge. It is often forgot- suspected appendicitis, computed tomography has ten during operations in the lesser pelvis. Circum- shown its superiority in evaluating the extent of inflam- stancesreportedtoexplainoperativelossofsponges mation and in differentiating other intraabdominal are emergencies, hemorrhagic procedures, time-con- pathologic findings by demonstrating a normal appen- suming operations, sponge counting while closing, dix (Balthazar et al. 1994; Levine et al. 1997). In a study change in operating room personnel, and operations in performed by Gupta et al. (2002) on 160 consecutive anatomic regions that are difficult to reach. Fifty per- radical cystectomy patients with urinary diversion in cent of gossypibomas are discovered 5 years or more af- whom appendectomy was not done, patients present- ter surgery, and 40% are detected within the 1st year ing with acute abdominal pain were easily diagnosed (Lauwers and Van Hee 2000; Rappaport and Haynes and managed. Moreover, none of the patients who were 1990). followed over a period of 10 years developed a appendi- Migration of gauze sponge has been reported to oc- citis postoperatively (Table 18.36). cur in ileum, duodenum, stomach, urinary bladder, Therefore, routine appendectomy should be aban- and even by transdiaphragmatic migration into the doned in urologic surgery, due to the evolving role of lung causing lung abscess (Lone et al. 2005). The expul- the appendix in various urinary tract reconstructions sion of sponge has been seen to occur through laparot- and the very low risk of subsequent appendicitis (Gup- omy wound and rectum. A sponge left in usually mani- ta et al. 2002; Neulander et al. 2000; Santoshi et al. fests within weeks to years and the longest duration of 2002). The incidence of incidental carcinoid tumors of concealment has been 24 years (Kokubo et al. 1987). the appendix between 0.4% and 2% should not change Retained sponge may produce various complications this way of proceeding (Silvert and Meares 1976). An- such as obstruction, fistula, peritonitis, abscess, trans- other important point that has not been well docu- mural migration, or spontaneous extrusion. Two vari- mented to date is that, despite performing appendecto- ants of reaction have been studied. In one there is asep- my, the dilemma of acute abdominal pain may persist, ticfibrinousresponse,whichfollowsasilent,delayed as reported by varying studies on “stump appendicitis.” course, and the second variant is an acute, exudative This is an entity in which inflammation occurs in the type leading to abscess formation including bacterial remnant tissue of the appendix after appendectomy. infection with anaerobes. The incidence of stump appendicitis is underestimated, Usual symptoms include unexplained abdominal anditcanoccuranytimefromafewmonthsto20years distension and pain as well as palpable mass, nausea, after appendectomy (Feigin et al. 1993; Liang et al. vomiting, chronic anemia, rectal tenesmus and bleed- 2006; Watkins et al. 2004). ing, diarrhea, discharge through a persistent sinus, intestinal obstruction, and pseudotumoral syndrome (Tacyildiz and Aldemir 2004; Ben Meir et al. 2003). Table 18.1.36. Causes of acute abdominal pain on follow-up fol- These symptoms are often accompanied with general lowing radical cystectomy symptoms such as fever and weight loss. Coughing and Cause Incidence (%) dyspneaaswellasUTImaybetheresultofexogenous compression on the respiratory or urinary tract. Post- Intestinal obstruction 11 Urinary retention 1.8 operative septic shock has been described (Lauwers Neobladder perforation 0.6 and Van Hee 2000). Plain radiographs fail to delineate Recurrent colic 1.3 thespongeintheabsenceofaradiopaquemarker.Ab- Pyelonephritis 13 dominal ultrasonography can demonstrate the gossy- Stomal stenosis 1.3 piboma by an intense and sharply delineated acoustic Parastomal hernia 0.6 Postoperative appendicitis 0 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 18.1 Acute Postoperative Complications 393 to gas trapped in the fiber meshwork of the gossypibo- tors that influence the transition from contamination to ma. infection. Intraabdominal adjuvants and the local host Differential diagnosis includes tumor or tumor re- responsearealsoimportant.Bacterialstimulileadtoan currence, postoperative adhesions, invagination, in- almost uniform activation response, which is triggered traabdominal abscesses, volvulus, and hematoma. by reaction of mesothelial cells and interspersed perito- Treatment consists of thorough surgical exploration neal macrophages and which also involves plasmatic of the abdomen, removal of the gossypiboma, drainage systems, endothelial cells, and extra- and intravascular of purulent fluid, and treatment of the accompanying leukocytes.Thelocalconsequencesofthisactivation lesions such as fistulizations. Complication of a gossy- are the transmigration of granulocytes from peritoneal piboma is the development of an angiosarcoma, late capillaries to the mesothelial surface and a dilatation of abscess formation, chronic fistulas, and erosion into peritoneal blood vessels resulting in enhanced perme- blood vessels. Gossypiboma-associated mortality is as ability, peritoneal edema, and lastly the formation of high as 11%–35% (Chorvat et al. 1976). When the for- protein-rich peritoneal exudate. eign body is diagnosed and removed during the imme- Clinically, peritonitis is often classified either as lo- diate postoperative period, morbidity and mortality cal or as diffuse. Local peritonitis refers to loculi of in- are low (Le Neel et al. 1994). A gossypiboma is poten- fection, usually walled-off or contained by adjacent or- tially life-threatening. Therefore, extreme care in the gans, whereas diffuse is synonymous with generalized handling of gauzes during surgical procedures is high- peritonitis, i.e., spread to the entire cavity. ly advisable. Repeated sponge counts before and after The pathogens (Table 18.1.37) normally detected in eachpartoftheoperativeprocedureandsystematic peritonitis are Gram-negative, e.g., E. coli, and anaer- use of large sponges, one by one is recommended. Al- obes, e.g., Bacteroides fragilis. When peritonitis per- thoughthepresenceofradiopaquemarkersinall sists, however, other pathogens may be isolated, e.g., gauzes might give a false feeling of safety, their use is Pseudomonas aeruginosa, Enterobacter, Enterococcus helpfulincaseofanincompletespongecountatthe spp. Antimicrobial resistance of operative flora may end of an operative procedure (Lauwers and Van Hee correlatewithpostoperativeinfection.Theresponseto 2000). intraabdominal infection depends on five key factors: 1. Inoculum size Fever Due to Intraabdominal Infections 2. Virulence of the contaminating organisms 3. Presence of adjuvants within the peritoneal cavity Intraabdominal infection continues to be one of the ma- 4. Adequacy of local, regional, and systemic host jor challenges in surgery and urology. While the term defenses “peritonitis” means an inflammation of the peritoneum 5. Adequacy of initial treatment regardless of its etiology, intraabdominal infections encompass all forms of bacterial peritonitis, intraabdomi- The immune response mounted against the invading nal abscesses, and infections of intraabdominal organs. pathogens is the decisive element for outcome. When Several classification systems have been suggested for the inflammatory response gets out of control, multior- peritonitis and intraabdominal infections, respectively. ganfailure(MOF)willensueandsurgerycannolonger However, neither phenomenological classifications nor limit the immune response, emphasizing the need for classification systems with respect to the origin of bacterial contamination have a proven relevance for the clinical course of this disease. Moreover, most of the Table 18.1.37. The microbial flora of secondary peritonitis studies dealing with secondary peritonitis or intraab- Type Organism Percent dominal infections are difficult to compare because of wide variations in inclusion criteria. Thus the true inci- Aerobic bacteria E. coli 60 Gram-negative Enterobacter/Klebsiella 26 dence of secondary bacterial peritonitis is difficult to Proteus 22 assess. With respect to its etiology, perforation of hol- Pseudomonas 8 lowviscusistheleadingcausefollowedbypostopera- Gram-positive Streptococci 28 tive peritonitis, ischemic damage of bowel wall, infec- Enterococci 17 tion of intraabdominal organs, and translocation in Staphylococci 7 nonbacterial peritonitis. The anatomic origin of bacte- Anaerobic bacteria Bacteroides 72 rial contamination and microbiological findings are not Eubacteria 24 major predictors of outcome. However, the preoperative Clostridia 17 physiological derangement, the surgical clearance of Peptostreptococcus 14 Peptococcus 11 the infectious focus and the response to treatment are established prognostic factors. The pathogenesis of in- Fungi Candida 2 traabdominal infections is determined by bacterial fac- From Hau et al. (1979) 394 18 Postoperative Complications

timelyoperationinsuspectedperitonitis,themainstay Management principles (Marshall 2004) of the pa- of treatment. Factors affecting prognosis are age, fecal tient with intraabdominal infection include three prin- peritonitis, metabolic acidosis, blood pressure, preop- ciples: erative organ failure, serum albumin, malnutrition, ) Timely hemodynamic resuscitation and support of malignoma, cause of infection, site of origin of perito- vital organ function nitis, and the number of organs involved in multior- ) Early administration of antimicrobial agents ap- gan-failure (MOF). propriatefortheinfectiousproblem The diagnosis of intraabdominal infection is gener- ) Rapid anatomic diagnosis and the institution of ally made on physical examination and is supported adequate source control measures by clinical signs, e.g., abdominal pain and tenderness, nausea, vomiting, diminished intestine sounds, fever, The cornerstone of timely hemodynamic resuscitation and shock. Prior performed surgery should raise the is the administration of adequate amounts of fluids to suspicion of a complication directly related to the pro- restoreadequateintravascularvolumeandthusopti- cedure itself (for example, a leak from an intestinal mize oxygen delivery to the tissues. There is no compel- anastomosis or the inadvertent incorporation of a ling evidence of the superiority of one type of fluid over loopofbowelintotheabdominalwallclosure).Ahis- another. Resuscitation should be guided by frequent as- tory of hypotension may be suspicious of intestinal is- sessment of heart rate and blood pressure. Urinary out- chemia or infarction, especially in patients with co-ex- put is a simle and sensitive measure of intravascular isting peripheral vascular disease and general athero- volume filling and organ function; an hourly output of sclerosis. After major surgery, perforation of a duode- 30–50 ml/kg should be the minimal objective of thera- nal ulcer is a not uncommon complication, particular- py. Patients who have significant co-morbidities, who ly in the patient with known peptic ulcer disease. Oc- present with more profound hemodynamic instability, casionally, peritonitis may be due to devices within or who fail to respond rapidly to fluid replacement the peritoneal cavity such as dialysis cannulae or due shouldbemanagedinanICUsetting.Theamountof to postoperative pancreatitis. The physiologic re- fluid required to achieve hemodynamic stability is var- sponse to the trauma of surgery causes increased lev- iable, and frequently substantial, because of unappreci- els of antidiuretic hormone (ADH) and aldosterone, atedthird-spacelossesintothefocusofinfectionand leading to fluid retention. In the absence of complica- into the GI tract as a consequence of ileus (Madl and tions, this process usually resolves by the 3rd day. Druml 2003; Marshall 2004). Another mainstay is the Shouldapositivefluidbalancepersistafterthistime, early administration of systemic antibiotics (Ta- the possibility of unrecognized complications should ble 18.1.38) without waiting for radiographic or micro- be suspected. Fluid retention is often manifested clini- biologic confirmation. The spectrum should include cally by signs of organ dysfunction, such as tachypnea Gram-negative aerobic organisms and anaerobes. The andhypoxemia,confusion,ortheonsetofanewsup- optimal duration of antibiotic therapy is unknown, and raventricular dysrhythmia (Marshall 2004). These clinical signs of surgical complications typically become evident on the 3rd postoperative day, but perito- Table 18.1.38. Recommended antimicrobial regimens for nitis usually presents not until 7–10 days after the sur- patients with intraabdominal infections gical procedure. Single agents Radiographic procedures are the cornerstone of di- Infection agnosis and include plain x-ray (intraperitoneal free Ampicillin/sulbactam air, although air may normally be present for up to Cefotetan Cefoxitin 7 days following a laparotomy; thumb-printing, which Ertapenem suggests ischemia; evidence of intestinal obstruction; Imipenem/cilastatin contrast studies, which may demonstrate leaks or de- Meropenem lineate the location of an obstruction), ultrasound, and Piperacillin/tazobactam Ticarcillin/clavulanic acid CT scan. Computed tomography combined with oral and intravenous contrast medium is the most reliable Combination regimens Aminoglycoside plus an antianaerobe agent (clindamycin imaging modality for evaluating the abdomen (intra- or metronidazole) or retroperitoneal fluid collections, abscess formation, Aztreonam plus clindamycin intestinal ischemia, clots within larger vessels, etc.) Cefuroxime plus metronidazole (Velmahos et al. 1999). MRI should also be considered Ciprofloxacin plus metronidazole with the possible exception of the evaluation of retro- Third- or fourth-generation cephalosporin (cefepime, cefo- peritoneal pancreatic pathology. taxime, ceftazidime, ceftizoxime, or ceftriaxone) plus an Leukocytes and C reactive protein may be altered antianaerobe anaerobe (clindamycin or metronidazole) butarenotdirectsignsofperitonitis. from Malangoni (2005); Mazuski et al. (2002) 18.1 Acute Postoperative Complications 395 when antibiotics are used in association with adequate peritoneal infection. While there is general agreement source control, the duration of therapy can be short that on-table bowel preparation and primary anasto- (Wittmann and Schein 1996), and certainly no longer mosis is safe in the presence of localized peritonitis, its than 5–7 days (Wittmann and Schein 1996). use in the presence of generalized peritonitis is contro- The term “source control” can be defined as those versial and most surgeons opt for a Hartmann’s proce- physical measures undertaken to eradicate a focus of dure in this situation. Intestinal reanastomosis is in infection, eliminate ongoing microbial contamination, most instances not performed in peritonitis. The ap- and render the local environment inhospitable to mi- proach employed to treat the immediate problem must crobial growth and tissue invasion (Jimenez and Mar- take into consideration the consequences of that deci- shall2001).Thisinvolvesoneormoreofthefollowing sion for later reconstruction. Open abdomen ap- strategies: proaches, for example, commit the patient to a series of reconstructive procedures to repair abdominal wall ) Drainage of abscesses or infected fluid collections herniasortocloseenterocutaneousfistulae.Thecrea- ) Debridement of necrotic infected tissue tion of a stoma requires a subsequent procedure if the ) Definitive measures to control a source of ongoing stoma is to be closed, and the morbidity associated microbial contamination and to restore anatomy with such procedures can be substantial (Hackam and and function Rotstein 1995a, b). If a stoma is created, a loop enteros- Drainage converts an abscess to a controlled sinus or tomy or colostomy is easier to close than an end stoma, fistula. This can be done by percutaneous techniques for it can be accomplished locally without the need for guided by radiographic imaging. a full laparotomy. In general, although no randomized control trial is There is increasing evidence that laparoscopy may available, percutaneous drainage seems to be as effec- play a definite role in patients with peritonitis. In pa- tive as operative drainage and when percutaneous tients with generalized peritonitis resulting from per- drainage is feasible it is the preferred initial approach forated diverticular disease, treatment by laparoscopy becauseitistheleastinvasiveprocedure(Bufalarietal. and peritoneal lavage was successful. However, laparo- 1996). Contraindications for percutaneous drainage in- scopic management of generalized peritonitis needs clude diffuse peritonitis due to the lack of localization further assessment. oftheinfectiousprocess,multipleabscesses,andana- The most common cause of peritonitis in the hospi- tomic inaccessibility. Debridement is the physical re- talized patient is intraperitoneal infection as a conse- moval of infected or necrotic tissue and can be accom- quence of prior abdominal surgery (Table 18.1.39). If plished by surgical excision and irrigation. Early ag- the GI tract has been entered as in radical cystectomy gressive debridement is associated with an improved and urinary diversion, then the possibility of an anas- clinical outcome. Debridement encompasses the exci- tomotic leak should be considered. Risk factors for this sion of necrotic intestine, the removal of feces or fibrin complication include excessive tension on the suture from the peritoneal cavity, and the excision of necrotic line, hematoma at the suture line, ischemia related to and infected fat. Clear demarcation between viable and nonviable tissues is a prerequisite to successful debridement (Marshall et al. 2004). Removal of extensive Table 18.1.39. Causes of peritonitis in the hospitalized patient fibrin deposition on the peritoneal surface of loops of Type Cause bowel shows no improvement in the clinical outcome. Postoperative Anastomotic leak (Fig. 18.1.3.4) Intraoperative peritoneal lavage, although well entren- peritonitis ched in modern surgical practice, has not yet demon- Procedural Inadvertent or missed intestinal injury strated that it decreases clinical mortality. No absolute complications proof exists that the addition of antibiotics to intraope- Infected hematoma rative lavage increases the survival rate (Hudspeth Intestinal injury secondary to laparo- 1975). Definitive measures to correct the anatomic de- scopic trocar rangement are an integral part of source control man- Spontaneous GI Perforation of gastric or duodenal ulcer agement. Whether definitive measures should be un- perforation dertaken during the initial management of the septic Intestinal ischemia Delayed ischemia secondary to low- episode or preferentially delayed and performed elec- flow mesenteric venous thrombosis tively when the patient has recovered depends on the Acalculous cholecystitis stability of the patient and the nature of the interven- Device-related CAPD peritonitis tion that is needed: in general, the simplest interven- infection Infected ventriculoperitoneal shunt tion that accomplishes the source control objective is Hematoma Insufficient coagulation the best option. There is a trend in the literature to Slipped clips or ligatures make a stoma in cases of anastomotic dehiscence and Coagulopathy 396 18 Postoperative Complications

Differential Diagnosis What kind of surgery? Complete blood Immediate Previous [. . . ], count (within hours of INFECTIOUS UTI (Fig. 18.1.3.2) Differential count surgery) Surgical side CRI (Table [. . . ]) Platelet count Drug fever Infections SSI? Routine blood Malignant hyperther- Pneumonia Endocarditis chemistries liver mia CAUTI Postoperative fever (Table18.1.22) enzymes Transfusion reaction UTI Local pain or of unknown origin Bilirubin Trauma to surgery CRI tenderness? Urine analysis Antibiotic associated Transfusion? Urine culture Acute diarrhea Predisposing heart Erythrocyte (onset within the first Sinusitis condition or sedimentation rate week) Otitis media infection drug use? Blood cultures Pneumonia Parotitis Previous deep vain UTI Abdominal abscess thrombosis? Hepatitis serology CAUTI Meningitis Previous gout? Locate dehydroge- CRI Acalculous Previous rheumatic nase SSI cholocystitis fever? Tuberculin skin test Transfusion Lupus? History (AFB smear and Subacute associated viral [. . . ]? NAA)*1 (onset from 1 to 4 infections HIV viral load Animal exposure weeks Foreign body HIV antibody assay following surgery) infection Rheumatoid factor Pneumonia Chest (Table PE* Osteomyelitis Antinuclear SSI 18.1.3.41) antibodies Endocarditis Heart (IE) CRI (Table 18.1.32) Abdomen (Table 24 Thrombophlebitis NONINFECTIOUS + 26) Antibiotic-associate Seroma/Hematoma Retroperitoneum Mycobacterial diarrhea at surgical site (Table Tbc Drug fever Suture reaction 18.1.3.45) AFB smear (beta-lactan, Deev vein thrombosis Skin and soft tissue (Acid fast bacilli antibiotics, [. . . ] exit pito smear) sulforamides, H2- Pulmonary embolism Clinical signs Gout/pseudogout Lymphnodes NAA blockers, procain- Pancreatitis Upper and lower (Nucleic acid amide, Cerebral infarction extremities amplification phenytoin, heparin) Subarachnoid consider eyes (IE) assay) Deep venous hemorrage thrombosis Myocardial infarction Fever and chills pulmonary Bowel Hypotension Labarotory tests emblosm ischemia/infarction Drug/alcohol Hyperventilation Delayed Altered mental status withdrawal Infection Transfusion reaction Nausea & vomiting & diarrhea Due to blood Transfusion rejection transfusion Rheumatic fever Abdominal pains. Abdomen (CMV, HIV, Hepatitis) Lymphome Thrombophlebitis CT scan Chest Solid tumor Celulitis x-ray SSI Sarcoid Refer to Table 18.1.19, Lupus 18.1.24, 18.1.25 Rheumatoid arthritis Differential diagnosis Giant coil arteritis based on Origin still unknown? Ecectrocardiogram Neoplastic fever the basis of timing of Drug fevar fever Factitious fover TTE*2 Consider: TTE*3 Endocrinologist Refer to Table 67-Gallium *1 AFB smear = Acid fast bacilli 18.1.3.43 Rheumatologist scintigraphy 18 F-FDG smear; NAA = Nucleic acid Surgeon or 111-Indium- amplification assay PET/CT ORL labeled- *2 TTE = Transthoracic Cardiologist echocardiography leukocoytes *3 TEE = Transesophageai Dentist scintigraphy echocardiography Fig. 18.1.8. Algorithm for postoperative fever of unknown origin

underlying vascular disease, obesity, excessive devas- tions of blood within the peritoneal cavity support the cularization of the intestine at the site of the anastomo- proliferation of bacteria shed at the time of surgery, sis, or intestinal distension at the suture line, and tech- and is one of the most common predisposing factors to nical errors in the creation of the anastomosis. Collec- postoperative abscesses (Fig. 18.1.8). Their anatomic 18.1 Acute Postoperative Complications 397 location reflects the preceding operative procedure: the process and to identify deep sites of infection. The following nephrectomy, for example, postoperative ab- classification of skin and soft-tissue infections can be scesses are typically found in the subhepatic or sub- subdivided into surgical and nonsurgical infections. splenicspacesoralongthepsoasmuscle,whereasan Surgical site infection is an infection that arises within abscess developing following radical prostatectomy or 30 days of an operative procedure and at the site of sur- cystectomy most commonly occurs in the pelvis. The gical intervention. Nonsurgical skin and soft-tissue in- same applies to lymphatic fluid and collection from fections comprise erysipelas, impetigo, folliculitis, cel- which infected lymphoceles and infected chylogenous lulitis, pyodermas, abscess, necrotizing cellulitis or fas- ascites can develop (refer to Chaps. 18.1.5, 18.1.7). Un- ciitis or myositis, and myositis/pyomyositis/myonecro- recognized intraoperative tear of a segment of bowel or sis. the inadvertent incorporation of a loop of bowel into Cellulitis is defined as an acute spreading infection theabdominalwallclosuremaybeanothercauseofa of the skin and underlying soft tissue suggested by the postoperative peritonitis. Such complications are more presence of a rapidly expanding erythema, local ten- frequent in reoperative surgery, since scarring and ad- derness, pain, swelling, lymphangitis, and lymphade- hesions distort the intraabdominal anatomy and neces- nopathy, which is frequently accompanied by systemic sitate a more extensive dissection. Less common com- signs and symptoms including malaise, fever (temper- plications should also be considered: trocar injury fol- ature 38.0°C), and chills. lowing laparoscopic surgery, inadvertent passage of a Necrotizing cellulitis and fasciitis are defined as drain through a loop of intestine, etc. The morbidity acute, rapidly progressing, and life-threatening de- and mortality of postoperative peritonitis is substan- structive (i.e., necrotizing) infections of the subcutane- tial,withmortalityratesofupto60%forpatientshav- ous tissues dissecting along tissue planes. Although ing diffuse peritonitis (Bohnen et al. 1983; Marshall these two clinical entities exhibit some distinctive clini- 2004; Marshall et al. 2004). cal and microbial characteristics, they share common features. The symptoms and signs suggestive of necrotizing cellulitis or fasciitis are intense local pain (a car- FeverDuetoSkinandSoft-TissueInfections dinal feature), exquisite tenderness, erythema (initially Infectionsoftheskinandsofttissuearecommonand discrete but evolving to red-purple and then blue-gray encompass a spectrum of illness severity, from focal cutaneous lesions often with hemorrhagic bullae), cellulitis producing only mild symptoms to life-threat- swelling,edema,crepitations(inthecaseofnecrotizing ening necrotizing infections resulting in extensive tis- cellulitis), and extensive tissue necrosis, which are as- sue loss and substantial acute morbidity and mortality. sociated with prominent systemic toxicity (toxic shock Local signs of inflammation are the hallmark of a syndrome, severe sepsis, or septic shock). soft tissue infection. Features of severe sepsis rarely ac- Microbiologically confirmed skin and soft tissue in- company a superficial skin and soft tissue infection and fection is defined by the isolation by culture or Gram suggest concomitant tissue necrosis, a deep skin and stain of a microorganism from a skin aspirate or biopsy soft tissue infection, or a particularly virulent infecting of the subcutaneous tissues of an erythematous skin le- organism. Fluctuance suggests a subcutaneous abscess. sion or wound. Probable skin and soft tissue infection Necrotizing infection is suggested by the presence of is defined as compelling clinical and laboratory evi- pain (usually severe and constant in the case of necro- dence (such as spreading cutaneous erythema and tizing fasciitis), discoloration of the overlying skin, bul- blanching, or drainage of purulent material on opening lous lesions, or soft tissue crepitus; these findings, how- a surgical wound, with or without lymphangitis, in as- ever, are neither sensitive nor specific for the recogni- sociation with fever 38.0°C, or leukocytosis) of the tion of tissue necrosis, and extensive necrotizing infec- presence of a skin and soft tissue infection based on ration of the subcutaneous tissues may be present with diographic, clinical, and surgical findings but without only minimal findings in the overlying skin. The diag- microbiological confirmation. Possible skin and soft nosis of infection of the skin and soft tissues is most tissue infection is defined as clinical (such as mild cuta- commonly accomplished by direct examination, ob- neous erythema associated with fever of 38.0°C), labo- taining cultures to identify the infecting organisms and ratory (such as leukocytosis), or radiographic findings toaidintheselectionofanoptimalantimicrobial suggestive of the presence of a skin and soft tissue in- agent. A microbiological diagnosis of cellulitis can fection but with insufficient evidence to confirm diag- sometimes be made by aspiration of the involved area. nosis. Infections are further classified as superficial or Biopsy can be used to determine whether tissue necro- deep, based on whether the deep fascia or muscle layers sis is present and to facilitate quantitative culture, a are involved. In mild to moderate cases, antibiotic ther- technique that is useful in the diagnosis of burn wound apy should be sufficient, while in severe cases radical infection. Radiologic examination – particularly com- surgical debridement is required. puted tomography – is of value to define the extent of 398 18 Postoperative Complications

tients because bacteria are more easily able to colonize Fever Due to Impaired Drainage of Upper Urinary Tract the neobladder formation in comparison to the normal After Urologic Surgery urinary bladder. Additionally, incomplete emptying of Urinary tract infection due to urinary diversion with the neobladder may promote infection, even with no- and without cystectomy due to benign and nonbenign nadherent microorganisms. Finally, excessive mucus diseases is a common problem in this setting. The ileal production by the bowel epithelium accompanying an conduit is colonized postsurgically through the cutane- established infection prevents effective clearance of mi- ous opening. During the initial 10-day period after op- croorganisms. Microbial flora includes E. coli strains eration, both ureters are stented and antibiotic therapy (60%), Klebsiella species, Proteus mirabilis, Enterococ- is discontinued after removal of the ureteral stents in cus species, Pseudomonas species, and Citrobacter spe- our institution. When fever stemming from impaired cies. In neobladders, bacterial colonization correlates drainage of the upper urinary tract occurs in these first with residual urine, thus optimal evacuation decreases 10 days, ultrasound of the kidney may reveal hydrone- the bacterial burden as residual volumes reaches 20 ml phrosis and urinalysis and culture should be obtained. or less. Controversy exists regarding the appropriate Correct replacement of the ureteral stent or percutane- treatment of asymptomatic bacteriuria in patients with ous nephrostomy should be performed. When cultures ileal neobladder. Wood et al. (2003) stated that al- grow, a pathogen treatment should be amended ac- though small bowel intestine appears to promote cordingly. asymptomatic bacterial colonization (39%), urosepsis A mixed population of yeast and Gram-positive cocci occurs in 12% of the patients with UTI. The estimated (Streptococcus species, Staphylococcus epidermis, and 5-year probability of UTI and urosepsis according to enterococci) subsequently develops in the conduit. As Wood et al. (2003) is around 58% and 18%, respective- antibiotic protection is withdrawn, Gram-negative or- ly.Urineculturewithgreaterthan105 cfu bacteria and ganisms (E. coli and Proteus, Pseudomonas,andKlebsi- femalegenderaretheonlyfactorspredictiveofUTI. ella species) become part of the mixed microbial flora. Recurrent UTI in this trial is the only predictor for ur- Electron microscopic examination showed no bacteria osepsis. Intermittent catheterization or hydronephro- adhering to columnar cells of the conduit, but mucus sis are not related to urinary tract infection or urosep- was heavily colonized with microcolonies of Gram-pos- sis. Therefore, prophylactic antibiotics are recom- itive and Gram-negative bacteria (Bruce et al. 1984; mended only for patients with recurring UTIs (Wood et Chan et al. 1984), whereas cultures from colonic con- al. 2003; Falagas and Vergidis 2005). duits most often grow a single bacterial species. Because In patients with continent nonorthotopic urinary conduit urine is bacteriuric in most cases, clinicians diversion (pouch) pouchitis is a rare complication have to decide when to provide antibiotic coverage and caused by infection of the urine reservoir. It is mani- when to drain the upper urinary tract. Treatment fested by sudden explosive loss of urine through the should be instituted if symptoms suggest upper urinary continence mechanism, associated with pain in the re- tract infection such as fever, costovertebral pain or ten- gion of the pouch. The explosive urine discharge results derness, pathologic blood test, and coagulopathy (see from pouch hypercontractility. Mucus production is Fig. 18.1.3.2). Antibiotics should be administered as increased in these infections. Although this is an ex- mentioned above (Table 18.1.3.9), and in case of infect- pected protective response of the intestinal segment to ed hydronephrosis and/or impaired renal function, ure- inflammation, the resultant excessive mucus produced teral stents or percutaneous nephrostomy must be im- potentially contributes to the persistence of the micro- plemented. Prophylactic antibiotic treatment is justi- organisms (Falagas and Vergidis 2005; N’Dow et al. fied in patients with the history of recurrent pyelone- 2004). The infection must be treated with appropriate phritis. The incidence of UTI after noncontinent uri- antimicrobial treatment for at least 10 days. Benson nary diversion varies according to the literature and is andOllson(BensonandOllson2002;FalagasandVer- estimated by Madersbacher et al. to be roughly 23% gidis 2005) reported that short courses of antibiotics with a median follow-up of 98% (Madersbacher et al. usually are not successful in pouch infections (Falagas 2003); causes associated with UTI are anastomotic stric- and Vergidis 2005). ture, stomal stenosis, and urolithiasis. Postoperativefeverduetoimpaireddrainageofthe Basically, as for ileal or colonic conduit, the same ap- upper urinary tract system may also occur after radical plies for orthotopic urinary diversion in terms of clini- prostatectomy, prostatectomy due to benign prostatic cal signs, diagnostic procedure, and management. A enlargement, TURP, and TURBT. After open surgery standard 3- to 5-day course of antibiotics (see Ta- (radical prostatectomy, prostatectomy due to benign ble 18.1.27), after removal of the urinary catheter prostatic enlargement), a surgical failure such as su- placed intraoperatively after formation of a neoblad- tures may contribute to obstruction of distal/prevesical der, usually sterilizes urine. However, in the following ureter. Ultrasound and urinalysis as well as creatinine period there is an increased risk for UTIs in this pa- levels will guide the diagnosis. Management include 18.1 Acute Postoperative Complications 399

Table 18.1.40. Microorganisms isolated and recommended treatment in different types of urinary diversion Type of Diversion Microorganisms isolated Treatment Noncontinent urinary Gram-positive mixed skin flora (Streptococ- No treatment for asymptomatic bacteriuria, unless diversion cus species, Staphylococcus epidermidis) history of recurrent pyelonephritis Gram-negative Enterobacteriaceae (Ecoli, Proteus species, Pseudomonas species) Enterococcus faecalis Continent nonorthoto- Chronic bacteriuria as patient performs No treatment for asymptomatic bacteriuria pic urinary diversion intermittent self-catheterization Orthotopic urinary di- E. coli and other Gram-negative Enterobac- No treatment for asymptomatic bacteriuria (contro- version teriaceae versy) Treat for urea-splitting organisms, such as Proteus species, even if asymptomatic (potential for stone formation) From Falagas and Vergidis (2005) transurethralureteralstentsandpercutaneousnephro- should consider bed rest, scrotal elevation, and cooling. stomy. Violation of the ureteral orifice at TURP or Also recommended are analgesics and NSAIDs. In men TURBT may also lead to infected hydronephrosis and with epididymitis caused by probable urinary patho- when infected has to be drained as described above gens, the use of quinolone antibiotics such as ciproflo- (Fig. 18.1.17; Table 18.1.40). xacin 500 mg twice daily for 10–14 days or doxycycline 100 mg twice daily for 10–14 days is recommended. In severe infections with systemic disturbance or features Fever Due to Epididymitis After TUR, Brachytherapy, suggesting bacteremia, initial intravenous therapy may Prostate Biopsy, and Open Surgery be indicated. Although epididymitis after TURP and TURBT is an event with an incidence of less than 1% (Uchida et al. Postoperative Fever of Unknown Origin 1993, 1999), such testicle pathologies may contribute to postoperative fever. Even in patients receiving brachythe- Physical examination usually starts with the respirato- rapy of the prostate due to prostate cancer develop post- ry system. The respiratory examination is normally implantation epididymitis, for example in only 1% of a performed according to Osler’s classic sequence of in- large patient cohort with 517 patients, and when admin- spection, palpation, percussion, and auscultation. All istered preoperative antibiotics, epididymitis drops to lobes of the lung should be systematically examined. 0.5% (Hoffelt et al. 2004). In TRUS-guided biopsy of the Findings should be compared left with right, upper prostate, Donzella et al. (2004) estimated the incidence of with lower, and anterior with posterior. Percussion of approximately 1% and an onset of weeks to months after the thorax attempts to assess the state of the pulmonary the procedure, particularly in older patients or those with parenchyma. Auscultation assesses the state of the air- a greater number of prostate biopsies taken. ways and provides additional information about the After open surgery such as transvesical prostatecto- state of the lung parenchyma. Pulmonary disorders are my,theincidenceofepididymitisasanearlycomplica- listed in Table 18.1.41, whereas consolidation and tion has been reported to be around 1.8%–11.5% (Di- pneumonia secondary to atelectasis and pleural effu- allo et al. 2001; Tan et al. 1991). For the diagnosis of epi- sion may be the major causes of postoperative fever. didymitis and orchitis, a scrotal ultrasound must be Congenital abnormalities of the heart, previous en- carried out. On physical examination, epididymal docarditis, and valvular disease are typically associated swelling and pain and erythema of the scrotal skin may with increased risk of IE. The presence of a new, chang- be present. Clinical features also include dysuria, fever, ing or altered murmur has been reported in as few as and chills. Laboratory tests will assess leukocytosis and 40% of IE patients (Stamboulian and Carbone 1997), elevated CRP levels and a positive urine bacterial cul- but still the auscultation of the heart is essential when ture. In epididymitis, B-mode ultrasonography shows dealing with a patient with postoperative fever. When an enlarged, echo-poor epididymis; color-flow Doppler IE is suspected, examination of the nails, which may ultrasonography shows hypervascularity. Bacteriuria- show splinter hemorrhages, should be performed; the associated causes of acute epididymitis include the fol- eyes may show retinal hemorrhages and petechiae in lowing organisms: E. coli, Proteus species, Klebsiella the conjunctiva on examination may be present. Jane- pneumoniae, Pseudomonas aeruginosa, H. influenzae way lesions are seen in people with acute bacterial en- type b, Staphylococcus spp., and Streptococcus spp. docarditis.Theyappearasflat,painless,redtobluish- In the management of acute epididymitis, one redspotsonthepalmsandsoles. 400 18 Postoperative Complications

Table 18.1.41. Major diagnostic complexes in the evaluation of Table 18.1.42. Causes of splenomegaly pulmonary disorders Vascular congestion Percus- Transmis- Quality/ Adventi- Cirrhosis sion sion intensity tious Splenic vein thrombosis sounds Portal vein thrombosis Consolidation Dull ↑↑↑ Bronchial Rales Reticuloendothelial hyperplasia ↓ Acute infections (e.g., bacterial endocarditis) Atelectasis Dull ± ↓ Rales Subacute or chronic infections Pleural fluid Dull Egophony Vesic ular Rub Collagen vascular diseases and abnormal immune responses ↓ ↓ (e.g., systemic lupus erythematosus) Pneumothorax Tympa- ↓ Vesic ular – ↓ Work hy per trophy nitic Hemolytic anemias Infiltrative or replacement processes Nonmalignant hematologic disorders (e.g., polycythemia Lymph nodes should be examined in a systematic vera, myelofibrosis) fashion. Lymph nodes that are smooth and relatively Leukemias soft,butslightlyenlarged,maybenormalormayshow Lymphomas hyperplasia. Enlarged lymph nodes that have an irreg- Metastatic solid tumors Abscess ularshapeandarubbery,hardconsistencymaybein- filtrated by malignant cells. Tender nodes are suggestive of an inflammatory process. Matted nodes or Table 18.1.43. Timeofonsetofpainandfeverinabdominaldis- nodes fixed to underlying structures should raise the orders question of malignancy or infection; freely movable Sudden onset Perforation of the gastrointestinal tract nodes are more likely to occur in benign conditions. (duodenal ulcer, a colonic diverticulum, Lymphadenitis may occur if the glands are over- or a foreign body) whelmed by bacteria, virus, fungi, or other organisms Mesenteric infraction Ruptured aortic aneurysm and infection develops within the glands. The location of the affected lymph nodes is usually associated with Rapid onset Cholecystitis Pancreatitis thesiteoftheunderlyinglesion.Theskinoveranode Intestinal obstruction may be reddened and hot. Lymphangitis secondary to Diverticulitis lymphadenopathy involves the lymph vessels, with re- Appendicitis sultant pain and systemic and localized symptoms. It Ureteral stone Penetrating gastric or duodenal ulcer commonly results from an acute streptococcal or staphylococcal infection of the skin (cellulitis), or from Gradual onset Neoplasms Chronic inflammatory processes an abscess in the skin or soft tissues. Lymphangitis Large bowel obstruction presents with red streaks from infected area to the armpit or groin and throbbing pain along the affected area. oftheumbilicus.Thesenodeshavetheeponym“the Beginning with the lymph nodes of the neck, cervi- node of Sister Mary Joseph” and are a signal of signifi- cal lymph node chains should be evaluated including cant intraabdominal lymphadenopathy, usually associ- the preauricular, posterior auricular, occipital, superi- ated with malignant processes or massive abdominal or cervical, posterior cervical, submaxillary, submen- infection. Finally, the inguinal region should be care- tal, inferior deep cervical, and supraclavicular. En- fully evaluated for significant lymphadenopathy. It is largement of specific cervical lymph node groups can not uncommon for adults to have firm, unfixed lymph be helpful diagnostically. For example, oropharyngeal nodesthatarelessthan1cmindiameterfromrecur- and dental infections can cause cervical adenopathy. rent infections and insults to the feet and legs. Unilater- Right-sided supraclavicular nodes drain parts of the al enlarged and tender nodes in this region suggest an lung and mediastinum and are signals of intrathoracic infection of an ipsilateral lower extremity. Inguinal lesions (lung and esophagus). Left-sided supraclavicu- adenopathy can also be part of systemic processes such larnodes(Virchow’snodes)areclosetothethoracic as lymphoma or leukemia. duct and often signal intraabdominal lesions, particu- Thespleen(Table18.1.42)ispartofthelymphatic larly from the stomach, ovaries, testes, or kidneys. The system and should be carefully evaluated in any patient patient should then be examined for axillary adenopa- in whom other lymphadenopathy is present. thy. Axillary adenopathy may be part of a generalized The workup in postoperative fever and pain con- process or may be localized and secondary to infection cerningtheabdomenincludessixfeatures:onset,pro- in the upper extremity. Next, the patient should be eval- gression,migration,character,intensity,andlocation uatedforlymphnodesthatcanbefoundinthevicinity (Table 18.1.43). 18.1 Acute Postoperative Complications 401

Table 18.1.44. Common Anatomical Abnormality Common condition abnormalities of abdominal structure examination Umbilicus Mass, pain, or protrusion Hernia Abdominal wound dehiscence Surgical site infection Sister Mary Joseph’s node Prominent veins Portal hypertension Stomach Mass or pain in left upper quadrant Gastric carcinoma Gastric outlet obstruction Ulcer perforation Pancreas Mass or pain in right upper quadrant Pancreatic carcinoma Pancreatitis Gallbladder Mass or pain in right upper quadrant Cholecystolithiasis Hydrops of gallbladder Carcinoma of gallbladder Acute cholecystitis Small intestine Mass or pain, decreased bowel sounds Ileus, anastomosis leakage Mass or pain, increased bowel sounds Obstruction Liver Increased size Hepatitis Metastatic carcinoma Cirrhosis Abscess Decreased size Budd-Chiari Nodularity Cirrhosis Metastatic carcinoma Cirrhosis Spleen Increased size See Table 18.1.3.24 Peritoneal space Presence of ascites Portal hypotension Metastatic disease Congestive heart failure Lymphocele (infected) Chylogenous ascites Anus and rectum Anal or rectal mass or pain Anal carcinoma Rectal perforation Douglas abscess Prostatitis Fissure Fistula

Table 18.1.45. Cause of flank pain and postoperative fever For examination of the gastrointestinal system and Acute ureteral obstruction Chronic ureteral obstruction abdomen, a sequence of steps should be followed (auscultation, palpation, percussion, check for ascites, rec- Stone Congenital anomaly Blood clot Tumor tal examination, inguinal examination). Common Papillary necrosis Stricture of ureter abnormalities of the abdomen are described in Ta- Previous surgery ble 18.1.44. Radiation therapy The characteristic of flank pain is very helpful in de- Retroperitoneal fibrosis termining the cause. Important characteristics include Stone Renal inflammation local or referred pain, acute or chronic or recurrent Acute pyelonephritis pain, degree of severity, and duration. Associated Perinephric abscess Gallbladder disease symptoms such as fever, nausea and vomiting, and atri- Renal tumor Appendicitis al fibrillation often help in making the correct diagno- Renalcellcarcinoma Diverticulitis Transitional cell carcinoma Other gastrointestinal disease sis (Table 18.1.45). Wilms tumor Chest disease For the evaluation of the suprapubic region, there Kidney trauma Salpingitis may be tenderness referring to injury to the bladder or Renal infarction urine leakage mostly in combination with hematuria Vesicoureteral reflux (bladder augmentation, psoas bladder hitch, Boari 402 18 Postoperative Complications

plastic, etc.). Other causes may stem from lymphoceles al changes have occurred, and it can also differentiate after radical cystectomy, prostatectomy, and retroperi- between necrotic and viable tissues. Therefore, it has toneal lymphadenectomy. higher sensitivity than anatomical imaging techniques Evaluation of the external genitalia in males in- (CT, MRI). When performing a 67Ga scintigraphy or a cludes examination of the penis, scrotum, and scrotal single photon emission computerized tomography contents. Postoperatively, most common are epididy- (SPECT), some facts should be remembered. Gallium mitis, orchitis, and paraphimosis. is normally distributed in bone marrow and gut excre- For a diagnostic algorithm refer to Fig. 18.1.9. tion. Also, a faint salivary gland and renal activity is The imaging diagnostic approach in postoperative normal. This normal contribution of gallium as well as fever of unknown origin (FUO) includes not only con- the poor resolution and the high dosimetry of this im- ventional radiographic studies such as plain x-rays, CT aging modality was the impetus to develop 111In-oxide- scans, or MRI. It has been reported that gallium-67 and labeled leukocyte scintigraphy. A significant disadvan- 111-indium-labeled leukocyte scanning have an over- tage of the 111In-oxide-labeled leukocytes scintigraphy all higher yield than CT for detecting sites of FUO is the need for in vitro isolation of blood cells, which (Knockaert et al. 1994; Syrjala et al. 1987). At the mo- exposes the patient to an infection hazard (Peters ment gallium-67 scanning is a commonly used radio- 1998). Positron emission tomography (PET and PET/ tracer for the evaluation of postoperative FUO because CT) has the potential to replace other nuclear medicine it has the advantage of detecting changes at the molec- imaging techniques in the evaluation of patients with ularlevelintheearlystagesbeforeanyvisiblestructur- FUO. The tracer 18-fluoro-deoxy-glucose (18F-FDG) is

Fig. 18.1.9a–c. CT scan in patients with postoperative fever due to abdominal infection. a Patientonday10followingrad- ical cystectomy with urinary diversion (ileal conduit) with an anastomotic leakage. Note free fluid in the pelvis and upper abdomen. b, c Patient following radical cystectomy with urinary diversion (ileal neobladder); a relaparotomy was required because of an acute abdomen and peritonitis due to necrotic neobldder. After conversion to ileal conduit, the pa- c tient presented 9 days postoperatively with fever due to abscess formation in the subhepatic (b) and lesser pelvic (c) spaces 18.1.5 Abdominal Wound Dehiscence 403 a nonspecific tracer of increased glucose metabolism should be disinfected by swabbing concentrically with and does not accumulate only in sites of infection and 70% alcohol, from the venipuncture site outward. The inflammation. Indeed, its high sensitivity for the detec- site should be cleansed once again, this time with 10% tion of malignant cells has led to its successful and ex- povidone-iodine again in a circular motion. Iodine tensive use in oncology. Therefore, 18F-FDG-PET is ad- should be dried completely before puncture, which vantageous over gallium-67 and 111-In-oxide labeled takes between 1 and 2 min. In the meantime, the rubber leukocyte scintigraphy because it can image the whole stopper of the blood culture bottle should be decon- body in a short time, has high spatial resolution and taminatedwith70%alcohol.Oneshouldwithdraw provides high-quality images, and delivers a relatively 20 ml of blood from the puncture site. Changing the low radiation dose to the patient (Sugawara et al. needles between venipuncture and inoculation of the 1998). Several authors reported sensitivity rates of bottles, or between bottles, should be omitted because 81%–98%, specificity of 75%–100%, and accuracy of there might be a chance of needlestick injury without 91% for FDG-PET(-CT), while scintigraphy revealed lessening the chance of contamination (Little et al. sensitivity rates of 67%, specificity of 78%, and accura- 1999). cy of 84%–86% in patients with suspected infections If at all possible, blood for cultures should not be (El-Haddad et al. 2004; Meller et al. 2000; Stumpe et al. drawn through an intravenous or intraarterial cathe- 2000). ter. If blood cultures are drawn from an intravenous In spite of its high spatial resolution, the anatomic line, a second culture should be drawn from a periph- information available with stand-alone PET remains eral venipuncture. Single sets of blood cultures should limited. Integrated PET/CT systems provide “hard- notbeusedtoevaluateanypatientwithsuspected ware” coregistered metabolic and structural data. Such bacteremia or candidemia. The optimal yield is ob- a correlated acquisition of metabolic and anatomic da- tained with two – including at least one set of central ta may benefit the precise detection of infected sites. In and peripheral blood cultures taken simultaneously – a feasibility trial with 18F-FDG-labeled leukocyte PET/ (in suspected intraabdominal sepsis or pneumonia) CT depending on the standardized uptake value (SUV), or three (in suspected infective endocarditis) sets of Dumarey et al. showed a sensitivity of 86%, a specifici- blood cultures but no more than three blood cultures ty of 86%, a PPV of 92%, a NPV of 85%, and an accura- within a 24-h period. There is a direct relationship be- cy of 86% in imaging infection (Dumarey et al. 2006). tween the volume of blood obtained and the yield of a In another current publication comparing PET with blood culture set. A total of 20 ml of blood should be FDG-labeled leukocytes vs 111In-oxine-labeled leuko- obtainedperbloodculturebottle(MermelandMaki cyte scintigraphy, the authors found a sensitivity of 1993). 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 nec- 18.1.5 essary to evaluate the superiority of FDG-labeled leu- Abdominal Wound Dehiscence kocyte PET/CT over 111In-oxine-labeled leukocyte scin- 18.1.5.1 tigraphy (Rini et al. 2006). Synonyms Synonyms for abdominal wound dehiscence include Appendix burst abdomen, open abdomen, and ruptured abdomen. How to Perform Blood Cultures No microbiologic test is more important for the clini- 18.1.5.2 cian than the blood culture. Although only 5%–15% of Overview and Incidence blood cultures drawn in febrile patients are positive, the finding of pathogenic microorganisms in the The open abdomen, although uncommon, is associated bloodstream often provides critical clinical informa- with significant morbidity and mortality (Barker et al. tion that in turn leads to specific, often life-saving ther- 2000). Long-term sequelae include enterocutaneous apy. fistula formation, ventral hernia development, and es- Blood cultures should be drawn prior to beginning thetic problems. Deep abdominal dehiscence involving antibiotics whenever possible. If an empiric treatment fascia,otherwiseknownasaburstabdomen,may is an emergency, blood cultures should be drawn as occur following a laparotomy. The incidence ranges soon as possible after beginning antibiotics. There are between 0.4% and 3%, and the mortality rate is no data to suggest that the timing of culture in relation 15%–20% (Knight and Griffen 1983; Pool 1985; Swan to appearance of fever or chills will maximize the yield. and Banwell 2005). In some instances, the abdomen is After the vessel site is selected, a 5-cm area of skin left open after laparotomy when surgical reexploration 404 18 Postoperative Complications

(second look) is foreseeable, for example if repeated ance and secretion mobilization there should not be an drainage of infectious material is indicated, or in cases attempt to inhibit this reflex by drugs because coughing of abdominal compartment syndrome where immedi- decreases the incidence of pneumonia by reducing the ate closure is contraindicated. probability of developing postoperative atelectasis. Some authors even propagandize the two-stage cough inthepostoperativesetting.Thefirstcoughraisesthe 18.1.5.3 secretions, the second cough facilitates expectoration. Risk Factors One may use splinting techniques for coughing, splint- Postoperative nausea and vomiting (PONV) continues ing the surgical incision with the use of a pillow or tobeacommoncomplicationofsurgeryandoneofthe hands. leading causes of postoperative abdominal wound dehiscence. Other risk factors are listed in Table 18.1.46. 18.1.5.4 Prevention means reducing risk factors. Local factors Clinical Signs and Complications such as infection and surgical technique can be influenced easily by the physician in attendance. Systemic From clinical experience, open abdominal wounds can factors can be assessed but usually cannot be treated be classified by the wound type and its clinical impor- before the surgical procedures. Therefore, attention tance. Superficial skin defects, also known as surgical should be directed to prevent PONV (see also Chap. 3, site infection (SSI), involves only skin and subcutane- “New Developments in Anesthesia”) and postoperative ous tissue of incision and occurs within 30 days after coughing. the operation and at least one of the following features An important goal in prevention is to identify pa- are present: tients at high risk for PONV (Table 18.1.47). The con- ) Purulent drainage (culture documentation is not sensus guidelines for managing PONV of the Interna- required) tional Anesthesia Research Society differentiates be- ) Organisms are isolated from tissue or fluid of the tween patient-specific, anesthetic, and surgical risk superficial incision factors (Gan et al. 2003). A reduction of baseline risk ) At least one sign of inflammation (pain or tender- factors can significantly reduce the incidence of PONV. ness, induration, erythema, local warmth of the Approaches for this context are the use of regional an- wound esthesia, the use of propofol, supplemental oxygen, and hydration. Nitrous oxide and volatile anesthetics Table 18.1.47. should be avoided. Minimization of intraoperative and Risk factors for PONV postoperative opioids as well as neostigmine is recom- Patient-specific risk factors mended. Female sex Antiemetic therapy for PONV prophylaxis (doses Nonsmoking status History of PONV/motion sickness and timing) is shown in Table 18.1.48. Since coughing represents a way for airway clear- Anesthetic risk factors Use of volatile anesthetics within 0–2 h Nitrous oxide Table 18.1.46. Risk factors for abdominal wound dehiscence Use of intraoperative and postoperative opioids Surgical risk factors Local factors Duration of surgery (every 30-min increase in duration in- Infection creases PONV risk by 60% Surgical technique Type of incision Type of surgery (laparoscopy, laparotomy) Closure technique Suture type From Gan et al. (2003) Surgeon’s experience Mechanical Abdominal distension Table 18.1.48. Pulmonary complication Antiemetic doses and timing for administration in adults Systemic factors Obesity Drug Dose Evi- Timing Malnutrition dence Medication Steroids level Immunosuppression Ondansetron 4–8 mg i.v. IA At end of surgery Smoking Dolasetron 12.5–50 mg i.v. IA At end of surgery Anemia Granisetron 0.35–1 mg i.v. IA At end of surgery Hyperbilirubinemia Tropisetron 2 mg i.v. IA At end of surgery Postoperative factors Dexamethasone 5–10 mg i.v. IIA Before induction Coughing Droperidol 0.625–1.25 mg IA At end of surgery Vomit ing i.v. 18.1 Acute Postoperative Complications 405

Table 18.1.49. Pathogens associated with wound infections Table 18.1.50. Complications of the open abdomen Pathogen Frequency Early Late (%) Evisceration Ventral hernia Staphylococcus aureus 20 Peritoneal contamination Enterocutaneous fistulae Coagulase-negative staphylococci 14 Third-space fluid loss Intraabdominal abscesses Enterococci 12 Necrotizing fasciitis Suture sinus/incision pain Escherichia coli 8 Intestinal ileus Pseudomonas aeruginosa 8 Death Enterobacter species 7 Proteus mirabilis 3 Klebsiella pneumoniae 3 18.1.5.5 Other streptococci 3 Candida albicans 3 Prevention Group D streptococci 2 Despite of advances in surgical technique and materi- Other Gram-positive aerobes 2 Bacteroides fragilis 2 als, abdominal fascial closure has remained a procedure that often reflects a surgeon’s personal preference with a reliance on tradition and anecdotal experience. Deep incisional SSI also occurs within 30 days of the Thebestabdominalclosuretechniqueshouldbefast, operation or within 1 year if an implant is present. It in- easy, and cost-effective, while preventing both early volves deep soft tissue such as fascia and/or muscle and and late complications. A meta-analysis by Rucinski at least one of the following features apply: delineatestheoptimalclosuretechniqueoftheabdom- inal midline fascia incision. The continuous all-layer ) Purulent drainage is present from the deep incision closurewithabsorbablemonofilamentsuturematerial but without organ or space involvement looped or double-looped (Nasir and Baker 2001) (Poly- ) Fascial dehiscence dioxanone[PDS],Ethicon,Inc.,Somerville,NJ;Polyg- ) A deep abscess identified by direct examination or lyconate,Maxon,USSurgical,andDavis&Geck,Inc., by radiologic examination Danbury,CT)with#1or#2suturewithasuture- Open abdomen with fascial dehiscence may show ex- length-to-wound-length ratio of 4:1 (placing the su- posed bowel or omentum, and in a rather complex turesapproximately2cmawayfromfascialedgeand form the patient presents with intraabdominal sepsis approximately 2 cm from one another) is the optimal or enteric fistulae. Pathogens commonly associated technique for fascial closure after laparotomy and with wound infections and their frequency of occur- therefore the best prevention of a ruptured abdomen rence is listed in Table 18.1.49. (Rucinski et al. 2001). Usually, the abdominal wound dehiscence is an on- site diagnosis. Organisms should be isolated by aseptic 18.1.5.6 culturing technique. Any sign of infection should lead Management the surgeon to open the incision site deliberately. Man- ually, palpation is performed to ensure the continuity In the management of open abdomen, primary clo- of the closure of the fascia. Any discontinuity in terms sure, as long as it is performed without tension and of fascial dehiscence (exposed bowel or omentum, any does not lead to abdominal compartment syndrome sign of intraabdominal abscess or sepsis) is a danger- (ACS),isthepreferableformofdefinitiveclosure.Al- ous complication that requires emergency operative though difficult to quantify, the risks of infection, ent- intervention. Most patients are in poor condition since erocutaneous fistula, and recurrent wound problems the cause is mostly an intraabdominal infection. Coa- appear to be lower if primary closure is possible gulopathy can manifest as diffuse microvascular (Rutherford et al. 2004). As the patient’s overall status bleeding, with abnormal clotting studies and throm- improves and edema lessens, primary closure can of- bocytopenia (Ferrara et al. 1990; Valeri et al. 1987). ten be performed days to weeks after the original lapa- Necrotizing fasciitis is a dreaded condition. This rap- rotomy. idly progressive, infective process affecting the deep Primary closure of the abdomen without tension is a fascia, with secondary involvement of the subcuta- main goal, preferable as soon as possible after diagno- neoustissues,isassociatedwithhighmorbidityand sis. In most circumstances, the rectus sheath as well as mortality. Early, aggressive surgical debridement is the ventral fascia of the rectus muscle are identifiable. If necessary. Early and late complications are listed in tension-free closure can be performed one should use Table 18.1.50. the same technique as mentioned above (prevention) after aggressive surgical debridement thoroughly removing necrotic tissue (skin, subcutaneous tissues, fascia, muscle) and cleaning the wound with normal sa- 406 18 Postoperative Complications

line or antiseptic fluids (Lavasept). Sometimes it may andasfarlaterallyaspossible.Therectusmusclesare be necessary to recreate a neofascia by mobilization of advanced medially and sutured to close the defect. Ad- skin and subcutaneous tissue. If tension-free closure is ditional mobility in each location can be gained by sep- not achievable, component separation, described by arating the rectus muscle from the posterior rectus Ramirez et al. in 1990, reconstructs the midline defect sheath. Bilateral advancement yields enough mobility with an innervated advancement of muscle and fascia. to close defects of 10 cm in the epigastrium, 20 cm at The external oblique is transected approximately 2 cm the umbilicus, and 6 cm at the suprapubic level. Some- lateral to its insertion into the rectus sheath and sepa- timesitmaybenecessarytoplaceaVicrylbandbe- rated from the internal oblique (Fig. 18.10). This sepa- tween fascia closure and subcutaneous tissue in order ration extends 5–7 cm cephalad to the costal margin, to strengthen the abdominal wall. The skin is closed

Fig. 18.1.10. a Cross-sectional view of the normal anatomy of the abdominal wall. RM rectus abdominis muscle, EO external oblique muscle, IO internal oblique c muscle, TA transversus abdominis muscle. b Open abdomen with ventral hernia. c Arrows demonstrate the line of dissection between the external oblique muscle and the overlying subcutaneous tissue. Incision in the ex- ternalobliquemusclelateral to the rectus sheath. Another incision into the posterior sheath. d Completed proce- d dure of the components separation 18.1 Acute Postoperative Complications 407 over closed-suction drains, which remain in place hydrochlorideandsilvercarbonatepreservative 1–2 weeks. Necrosis of the overlying skin can be a com- agents, biologic materials – porcine small intestinal mon complication because of the extensive mobiliza- submucosa, human acellular dermis), vacuum-assisted tion of skin that is required. Component separation can closure, or plastic surgical techniques (tissue expand- be used in the acute setting, or in a delayed fashion. In ers, flaps, component separation [Ramirez et al. 1990]), times of evidence-based medicine, steel sutures, al- anticipating a hernia (Fig. 18.1.11). though recommended by some authors, should no lon- Totalparenteralnutrition(TPN)andenteralnutri- ger be used as reinforcement sutures and are aban- tion are available routes of nutritional support in the doned in our institution. recovery of critically ill patients. In patients who have If primary closure is not possible, the options in- enterocutaneous fistulas, lack of intestinal continuity, clude closure with a permanent prosthesis (polypro- dysmotility disorders, or mechanical bowel obstruc- pylene, polytetrafluoroethylene [PTFE], composite tion, TPN remains the first choice (Rutherford et al. materials – a sandwich of polypropylene and ePTFE, 2004) (Table 18.1.51), although typical complications antiseptic-impregnated materials using chlorhexidine such as intravenous catheter sepsis, hepatic failure,

Surgical site infection (SSI)

Abdominal wound Superficial SSI Deep SSI dehiscense

– Purulent drainage – Involvement of deep soft – Organisms are isolated tissue (fascia/muscle) and from tissue/fluid at least one of the follow- – Continuity of the fascia ing features: – at least one sign of • Purulent drainage from inflammation: deep incision without • Pain or tenderness organ/space involvement • Induration • Fascial dehiscence • Erythema • Deep abscess by • Lokal warmth raidiologic examination

Clinical sign Ultrasound CTscan MRI

Primary closure skin graft Vacuum-assisted Autologous reconstruction Non- autologous closure of muscolofascial defect reconstruction

Primary closure composition Prosthetic repair component Delayed skin graft Local flaps* Distant flaps** Skin graft

Fig. 18.1.11. Algorithm for * Local flaps: rectus abdominis muscle, external oblique muscle, internal oblique muscle surgical repair of abdominal ** Distant flaps: tensor fasclae latae, rectus femoris muscle, latissimusdorsi muscle, gracillis muscle wall defects 408 18 Postoperative Complications

Table 18.1.51. Indications for TPN Braunschweig et al. (2001) published a meta-analy- Severe short bowel syndrome, i.e., less than 100 cm of small sis of prospective, randomized, controlled trials to de- bowel termine both infectious and noninfectious complica- Severe radiation enteritis, including nonoperative strictures tions associated with EN and TPN in clinical practice. Gastrointestinal fistulas Aggregated results showed a significantly lower rate of Persistent postoperative ileus, mechanical bowel obstruction, infection with tube feeding (0.66; 95% confidence in- dysmotility disorders Lack of intestinal continuity terval[CI],0.56–0.79)comparedwithTPN.Thislower risk of infection with enteral feeding is independent of whethercathetersepsisisincludedintheanalysis. and metabolic bone disease should be kept in mind. Noncatheter infections include pneumonia, abdomi- Tight control of blood sugars in the range of nal abscess, and empyema. The higher risk of infection 80–110 mg/dl should be maintained (Rutherford et al. in TPN patients may be partially explained by a higher 2004). incidence of hyperglycemia since increased serum glu- Findings from a review of the available data pub- cose concentrations are a known risk factor for sys- lished by Jeejeebhoy (2004) show the benefits of enteral temic infection of hospitalized patients. In terms of nutrition (EN). Enteral diets are usually less expensive, noninfectious complications, a significantly higher are nutritionally complete, and have a more physiolog- risk of nutrition-support complications (parenteral ical administration than intravenous feeding. EN is as- and enteral nutrition technical problems, diarrhea, vo- sociated with a higher frequency of gastrointestinal miting, aspiration) was found with tube feeding com- adverse effects than parenteral nutrition, but the ef- pared with TPN (relative risk [RR], 1.36; 95% CI, fects are usually mild (Bozzetti et al. 2001). Patients on 0.96–1.83). Although many of the complications asso- EN have significantly fewer complications and a short- ciated with EN such as diarrhea and abdominal bloa- er postoperative stay than patients on TPN. Further- ting occur, they are considered less severe than cathe- more, EN seems to be favored in terms of duration of ter sepsis. complications, time required to recover bowel func- If catheter sepsis is included as a nutrition support tion, and mortality. A cumulative incidence curve of complication in this meta-analysis, the difference in postoperative complications comparing TPN with EN complications between EN and TPN are eliminated was published by Bozzetti (Fig. 18.1.12) (Bozzetti et al. (RR, 1.05; 95% CI, 0.79–1.4). 2001). Reasons in this context may be the so-called Others share these observations (Scolapio 2004) and bacterial translocation, which means that the migra- results published in this meta-analysis and speak about tion of bacteria from the intestinal lumen to the sys- downplaying tube feeding complications. Aspiration of temic circulation is limited, thus reducing the inci- tube feeds, misplaced nasal gastric feeding tubes into dence of sepsis. Therefore, prevention of bacterial the lungs, perforation and local infection associated translocation with the use of enteral nutrition is the with percutaneous endoscopic gastrostomy (PEG) tube premise of why enteral nutrition may be associated insertion, and inadequate nutrition delivery secondary with fewer infectious complications than TPN (Scola- to tube feeding interruption are just a few examples. pio 2004). Therefore, one can say that EN has advantages over TPN in terms of infections complications, but never- thelessENhassomelimitationswithrespecttoitsad- verse effects and contraindications. Irrespectiveofthemodeofnutritionsupport,critically ill patients are also at risk for the development of stress-related mucosal disease that can lead to significant upper gastrointestinal bleeding (Fennerty 2002). Stress gastritis prophylaxis for these patients is strong- ly recommended with histamine-2-receptor antagonists(H2RA)orevenmoresufficientwithprotonpump inhibitors [PPIs]) (Rutheford et al. 2004). Some ICUs still use sucralfate. Messori et al. (2000) showed in a meta-analysis of placebo-controlled trials of ranitidine or sucralfate a picture of poor effectiveness. Only a few prospective randomized placebo-controlled studies on sucralfate exist, showing rather disappointing results in prophy- Fig. 18.1.12. Cumulative incidence of postoperative complica- lactic treatment (Ruiz-Santana et al. 1991). The meta- tions(TPNvsEN) analysis of the trials on ranitidine also showed no dif- 18.1 Acute Postoperative Complications 409 ference compared with placebo. Another meta-analy- dine three had positive results, one had significant re- sis has been published by Cook et al. (1996). In their sultsinpatientsatlowrisk,andonehadnegativere- assessment of effectiveness of H2RA in terms of stress sults. ulcer prophylaxis, Cook included five trials that used The results of three meta-analyses that evaluated cimetidine and three trials with negative results that pneumonia were contradictory in some respects (rani- used ranitidine. Cimetidine is probably effective at tidine vs placebo and sucralfate vs placebo had the statistical levels, as out of the trials that used cimeti- same incidence of pneumonia; for ranitidine vs sucral-

Table 18.1.52. Recommended antibiotics in an abdominal wound dehiscence setting Cephalosporin first-generation Drug name Cefazolin Description First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, including Staphylococcus aureus. Typically used alone for skin and skin-structure coverage. IV and IM dosing regimens are similar Adult dose 250 mg to 2 g IV/IM, 6–12 h depending on severity of infection; not to exceed 12 g/day Pediatric dose 25–100 mg/kg/d IV/IM divided 6–8 h depending on severity of infection; not to exceed 6 g/day Contraindi- Documented hypersensitivity cations Interactions Probenecid prolongs effect; coadministration with aminoglycosides may increase renal toxicity; may yield false-positive urine dip test for glucose Pregnancy Usually safe but benefits must outweigh risks Precautions Adjust dose in renal impairment; superinfections and promotion of nonsusceptible organisms may occur with 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. In- fections caused by cephalosporin- or penicillin-resistant Gram-negative bacteria may respond to cefoxitin Adultdose 1–2gIV6–8h Pediatric dose Infants and children: 80–160 mg/kg/d IV divided every 4–6 h; higher doses for severe or serious infections; not to exceed 12 g/day Contraindi- Documented hypersensitivity cations Interactions Probenecid may increase effects of cefoxitin; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function) Pregnancy Usually safe but benefits must outweigh the risks Precautions Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis Drug name Cefotetan (Cefotan) Description Second-generation cephalosporin indicated for infections caused by susceptible Gram-positive cocci and Gram-negative rods Dose and route of administration depend on condition of patient, severity of infection, and susceptibility of causative organism Adult dose 1–2 g IV/IM 12 h for 5–10 days Pediatric dose 20–40 mg/kg/dose IV/IM 12 h for 5–10 days Contraindi- Documented hypersensitivity cations Interactions Consumption of alcohol within 72 h of cefotetan may produce disulfiram-like reactions; cefotetan may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (e.g., loop diuretics) or aminoglycosides may increase Pregnancy Usually safe but benefits must outweigh the risks Precautions Reduce dose by one-half if CrCl <10–30 ml/min and by one-fourth if CrCl <10 ml/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy 410 18 Postoperative Complications

fate, there was a significantly higher incidence of pneu- 18.1.6 monia with ranitidine, p=0.012) (Messori et al. (2000). Chylous Ascites The large trial by Cook et al. showed a trend toward an 18.1.6.1 increased incidence of pneumonia with ranitidine vs Overview sucralfate. PPIs are the most potent and reliable acid suppres- Chylous ascites (CA), an uncommon disease with an in- sants available, are well tolerated, and offer the versa- cidence of 1 in 20,000 hospital admissions (Aalami et al. tility of i.v. administration. Thus, their use in the peri- 2000) (Table 18.1.53) usually caused by obstruction or operative setting should be considered when manag- rupture of the peritoneal or retroperitoneal lymphatic ing patients at high risk for acid-related complications glands, is defined as the accumulation of chyle in the (Pisegna and Martindale 2005). When comparing peritoneal cavity (Browse et al. 1992). It is a difficult H2RA with PPI therapy in critical care, nosocomial disorder because of the serious mechanical, nutrition- pneumonia developed in 14% and 3% of patients al, and immunological consequences of the constant treated with ranitidine and omeprazole, respectively loss of protein and lymphocytes (Leibovitch 2002). (Levy et al. 1997). An evaluation of nosocomial pneu- Most investigators believe that the incidence of CA is monia after trauma demonstrated no difference in pa- increasingbecauseofmoreaggressivethoracicandret- tients receiving famotidine i.v. or omeprazole suspen- roperitoneal surgery and with the prolonged survival sion, despite more frequent risk factors for pneumonia of patients with cancer (Huang et al. 2004). Some new intheomeprazolegroup(Mallowetal.2004).Ade- techniques,suchaslaparoscopicsurgeryandtrans- quate prevention of venous thromboembolic disease plantation, also have led to increased postoperative CA in this setting must be an important goal, since autopsy (Huang et al. 2004; Shafizadeh et al. 2002). series showed an incidence of deep venous thrombosis The response to conservative treatment is low, and (DVT)ashighas65%anda3.8%-to20%-incidenceof resolution of the fistula cannot be guaranteed; invasive pulmonary embolism (Rogers 2001). Still, route and treatments, including reoperation of the patient, in- dose of prophylaxis are debatable, but LMWH (low- volve additional trauma and may not be successful, and molecular-weight heparin) should be initiated early in protein malnutrition and immune dysfunction develop the patient’s course of treatment when the risk of from persistent lymph wasting (Giovannini et al. 2005). bleeding is deemed acceptable (Rutherford et al. 2004). Infection remains a feared complication in these high- Table 18.1.53. Incidence of CA after RPLND and LLDN in the risk patients, since they harbor risk factors that in- literature crease their septic morbidity, such as hemorrhagic shock, intestinal injuries, and age. With massive vol- Surgery CA rate in % ume resuscitation, the potential for antibiotic washout RPLND (primary and 2–15a exists and redosing should be considered. In patients secondary) with open abdomen without intestinal injury, a first- LLDN (laparoscopic life 7 reported cases in literature generation cephalosporin or equivalent is recom- donor nephrectomy) mended. In patients suffering from open abdomen in a Baniel and Sella (1999); Sexton et al. (2003) combination with intestinal injury a second-generation cephalosporin or equivalent is recommended (Ta- ble 18.1.52). Unfortunately, studies are lacking in this 18.1.6.2 population of patients that address antibiotic type, Risk Factors and Pathogenesis dosage, and duration of therapy. Physicians caring for these patients must be vigilant in the search for infec- Although CA is a rare condition in urology, reviewing tion, but should exercise judgment and common sense the literature there are some reports on CA, predomi- in antibiotic usage, since excessive antibiotic use may nantly as casuistics in patients following radical prosta- lead to toxicity and resistance (Fabian 2002; Ruther- tectomy, retroperitoneal lymphadenectomy for testis ford et al. 2004). (Heidenreich et al. 2005), and renal carcinomas (Leibo- vitch et al. 2002), as well as laparoscopy nephrectomy, including donor and hand-assisted donor nephrectomy (Caumartin et al. 2005; Wu et al. 2004). Fig- ure 18.1.13 illustrates schematically the lymphatic drainage in relation to a human torso. Figure 18.1.14 demonstrates the cisterna chyli, which is the origin of the thoracic duct, lies in the retrocrural space. It arises from several confluent lumbar (right and left lumbar truncal,syn.truncuslumbarisdextraetsinistra),intes- 18.1 Acute Postoperative Complications 411

Fig. 18.1.13. Lymphatic vessels in relation to the torso Fig. 18.1.14. Cisterna chyli and thoracic duct: confluence of lumbar, intestinal, and intercostal lymphatic channels (Fig. 18.1.13 and 18.1.14 from: Sobotta, Atlas der Anatomie des Menschen, 19. Auflage © 1988 Elsevier GmbH, Urban & Fischer Verlag München) tinal (intestinal truncal, syn. truncus intestinalis), and rived from the transudation of plasma and proteins intercostal lymphatic channels, and can be seen during through capillary membranes into the peritoneal cavi- lymphangiography and at surgery. It is located to the ty. A delicate balance between the production and reab- right of the aorta and anterior to the first and second sorption regulates the volume of peritoneal fluid. The lumbar vertebrae. Surgical dissections have revealed a fluid is removed exclusively by way of the lymphatic range of 5–7 cm in length. Figure 18.1.15 illustrates the capillaries lining the diaphragmatic peritoneum. Un- anatomy of the retroperitoneal vessels and in combina- der normal conditions, the peritoneal fluid and parti- tion with the intestinal lymph vessels, it is easy to un- cles are brought to the right hemidiaphragm by a clock- derstand that any surgical intervention to the abdomi- wise current. Respiratory movements and elevation of nalcavityandretroperitonealspacecancausecrucial the diaphragm create this current such that a relative damage to this rather little known anatomical struc- vacuum is created in the upper quadrants. From the di- ture. aphragm, 80% of the lymphatic fluid drains by way of The peritoneal cavity normally contains a small vol- anterior mediastinal retrosternal channels to the right ume of free-circulating fluid. The peritoneal fluid is de- thoracic trunk, which ultimately empties into the right 412 18 Postoperative Complications

Fig. 18.1.15. Retroperitoneal lymphatic system and cisterna chyli. Anatomic relation of lymphatic system to blood supply and retroperitoneal muscle (From: Sobotta, Atlas der Anatomie des Menschen, 19. Auflage © 1988 Elsevier GmbH, Urban & Fischer Ver- lag München)

subclavian vein. The principal mechanisms of ascites present. One can imagine that these small lymphatic formation are lymphoperitoneal fistula or leakage from vessels can be managed by monopolar or bipolar coagu- the small bowel and mesenteric lymphatics or through lation. Collecting lymphatics, with a diameter of more the walls of the retroperitoneal megalymphatics (Amin than 0.2 mm, consist of a tunica intima (endothelium 2002). with basement membrane), tunica media (muscular layer), and tunica adventitia (fibrous fibers). Following the management of blood vessels, collecting lymphatics 18.1.6.3 should be clipped or tied by the surgeon with increasing Prevention diameter. The intraoperative application of fibrin glue To prevent the formation of chylogenous ascites, some does not reduce the rate of lymphoceles or chylogenous urologists recommend monopolar and/or bipolar elec- ascites (Pepper et al. 2005; Scholz et al. 2002). Drains trocautery dissection with placement of multiple lym- routinely placed after surgery to evacuate blood should phatic ligatures to decrease postoperative lymphorrhea. be used carefully after intraabdominal node dissection, No prospective comparative studies of the efficacy of astheabsorptivesurfaceoftheperitoneumusually these measures have been reported (Olszewski 1991) serves to mobilize and clear lymphorrhea without stasis (see Chap. 18.1.7). If one looks at the histology of lym- or infection. However, some authors recommend their phatic vessels at the light microscopy level, the lymphat- use routinely to minimize lymphocele formation. In our ic capillaries (initial lymphatics) have diameters be- institution, drains are usually removed on the 2nd to 3rd tween 10 and 80 µm, whereas the precollectors have a postoperative day independent of the amount of re- caliber between 100–200 µm. Both lack a basement moved fluid. Suction drains with negative pressure are membraneandmusclelayers,butreticularfibersare contraindicated in these conditions. 18.1 Acute Postoperative Complications 413

Table 18.1.54. Clinical findings and workup of CA Symptoms and clinical Workup findings Nausea Ultrasound Lack of appetite Bipedal lymphangiography Weight gain/weight loss Lymphoscintigraphy Shortness of breath/dyspnea CT scan Increase in abdominal girth Distended abdomen Total serum protein ↓ (normal, 61–80 g/l) Dullness to percussion Albumin ↓ (normal, 30–48 g/l) Leg swelling (plus upward involving scrotum) Diagnostic paracentesis Milky in color CA culture/microscopy/ cytology CA cytochemical: Totalproteinlevel2.5–7.0g/dl Triglyceride level >200 mg/dl Specific gravity >serum

1 Phrenic nerve, 2 Inferior vena cava, 3 Minor and major splanchnic nerves, 4 Vagus nerve, 5 Inferior phrenical artery and inferior diaphragmatic lymph nodes, 6 Suprarenal plexus, 7 Coeliac ganglion and plexus with coeliac lymph nodes, 8 Renal plexus, 9 Superior mesenteric plexus with central mesenteric lymph nodes, 10 Sympathetic trunc, 11 Aortic plexus, 12 Left lumbal lymph nodes, 13 Inferior mesenteric plexus with inferior mesenteric lymph nodes, 14 Superior hypogastric plexus, Fig. 18.1.17. Scheme of saphenoperitoneal shunt 15 Internal iliac plexus, 16 Promontory lymph nodes, 17 Left inferior hypogastric plexus, 18 Sympathetic trunc, 19 Right lumbal lymph nodes, 20 Phrenic ganglion firmed by the diagnostic paracentesis, which shows Fig. 18.1.16. Relationship between lumbar and iliac lymph milky fluid with a specific gravity higher of that in se- nodes and vegetative nervous system, ganglia, and sympa- rum as well as total protein levels between 2.5–7.0 g/dl thetic trunk (black, lymph nodes) (From: Földi/Földi/Kubik: and triglyceride levels above 200 mg/dl. Lehrbuch der Lymphologie, 6. Auflage © 2005 Elsevier GmbH, Urban & Fischer Verlag München) 18.1.6.5 Management 18.1.6.4 Conservative treatment of chylous ascites involves pa- Detection and Workup racentesis and a medium chain triglyceride (MCT) -based diet. Patients should be supplemented with Clinical findings vary from nausea, lack of appetite, MCToil,15mlorallythreetimesaday.Totalparenteral and shortness of breath to distended abdomen. These nutrition (TPN) is recommended after dietary manip- findings, in combination with ultrasound and CT scan ulation has failed (nonprotein calories, 25 kcal/kg/day; results, usually indicate the diagnosis. Other symptoms nitrogen, 0.2–0.25 g/kg/day; glucose:fat ratio, 6:4 via and clinical signs as well as diagnostic procedures are central vein) and somatostatin therapy (continuous in- listedinTable18.1.54.Thediagnosisisusuallycon- travenous infusion at a dose of 6 mg/24 h) is attempted 414 18 Postoperative Complications

only if chylous ascites has been refractory to all conser- Table 18.1.55. Surgical management and prevention of CA vative measures. It will take several weeks to 2 months Technique Clips to close the lymphatic fistula adequately with routine Sutures, direct ligation conservative regimens (Aalami et al. 2000). Others pre- Coagulation fer TPN with somatostatin as first-line therapy, which Biological gluea should be started as soon as possible. Fasting, together Placement of peritoneovenous shunt withTPN,candecreasethelymphflowinthoracicduct a Pepper et al. (2005); Scholz et al. (2002) dramatically from 220 ml/kg/h to 1 ml/kg/h. Further- more, TPN restores nutritional deficits and balances metabolic impairments (Huang et al. 2004). The resolu- Surgical exploration to repair the cisterna chyli is most tion rate of chyloperitoneum by conservative manage- successful when a discrete leak can be found by lymph- ment is approximately 50%–60% (Caumartin et al. angiogram. Outcome data are limited to retrospective 2005). case studies, but all patients that were treated surgically Surgery should usually be considered after failure of with direct ligation or placement of a peritoneovenous conservative treatment (Leibovitch 2002). Recently, the shunt were reported to be successful (Aalami et al. laparoscopic approach has been used successfully to re- 2000; Almakdisi et al. 2005; Dewdney et al. 2005) solve postoperative CA (Caumartin et al. 2005) and is (Table 18.1.55). thoughttobelessinvasivethantheconventionalsurgi- cal technique. The timing for surgical repair remains controversial. Surgical management of patients with 18.1.7 CA should be addressed after 4 weeks of conservative Deep Venous Thrombosis management. This delay will permit small fistula to 18.1.7.1 heal (Baniel et al. 1993; Busch et al. 2000). Overview and Incidence Surgical options include placement of a peritoneovenous shunt (Schumpelick and Riesener 1993; Utikal Venous thromboembolism (VTE) is common risk for et al. 2004) (Fig. 18.1.14) or repair of the cisterna chyli. hospitalized patients, especially in general and urologi- Peritoneovenous shunts are considered for patients in cal surgery. The annual incidence of VTE is approxi- whom a definitive leak cannot be identified. A perma- mately 0.1%–0.2%, most often presented as deep ve- nent peritoneal cavity drainage with return of ascitic nous thrombosis (DVT) or pulmonary embolism (PE) fluid into the circulation based on positive pressure (Oger 2000). The annual incidence of VTE among gradient between peritoneal cavity with ascites and youngadultsisabout0.01%,increasingtoabout1% central venous pressure is the principle. The long sa- among people who are 60 years and older (Nordstrom phenousveinisusedasadrainagesystem.One-way et al. 1992; Silverstein et al. 1998). ascites flow is ensured by a natural valve in the saphenous orifice. A suitable long saphenous vein with suf- 18.1.7.2 ficient orificial valve is required. The procedure is per- Risk Factors formed under general anesthesia. The long saphenous vein is exposed through vertical incision, its branches Several factors – inherited and acquired – influence the are ligated and it is divided at 20 cm. In a simple me- risk for developing a VTE (Table 18.1.56). These risk chanical manner, (catheterization with saline solution factors accumulate and increase the individual risk for flush) the central patency of the saphenus vein and the aVTE. sufficiency of its orificial valve (no backflow from the The most effective way to reduce the morbidity of femoral vein) should be checked. The inguinal canal is VTE is to identify patients who present the above-men- exposed through an oblique incision and the parietal tioned risk factors and to institute an appropriate indi- peritoneum is disclosed after division of the internal vidual primary prophylaxis (Heyers et al. 2001; Hirsh oblique muscle fibers laterally from the spermatic and Hoak1996). cord (funiculus) in the internal ring. This is the place In urology and general surgery, no consensus on the for incision in the peritoneum. The proximal cut end ideal prophylaxis exists. While in Europe pharmacologi- of the long saphenous vein is turned upward and calthromboprophylaxisinpatientsundergoingmajor pulled through the subcutis above the inguinal liga- pelvic surgery can be considered as standard, in the Unit- ment. A slight curve is formed in the venous orifice to ed States intermittent pneumatic compression and early prevent a sharp bend. The peritoneum is cut and a wa- ambulation often is favored (Galvin et al. 2004; Koya et al. tertight anastomosis is performed with an obliquely 2005). Pharmacological thromboprophylaxis by low- cut saphenous end using a continuous Prolene 6-0 su- dose unfractionated heparin (LDUH) or low-molecular- ture. The wounds are closed in layers with no drain- weight heparin (LMWH) seems to be the most effective age. (Kakkar et al. 1993, 1997; Nurmohamed et al. 1995). 18.1 Acute Postoperative Complications 415

Table 18.1.56. Risk factors for venous thromboembolism Table 18.1.57. Contraindications for anticoagulation Inherited conditions Absolute contraindications Protein C, protein S, antithrombin III deficiency Active bleeding Factor V Leiden mutation Relative contraindications G20210A prothrombin-gene mutation (heterozygous) Recent bleeding, gastrointestinal bleeding (within 2 weeks), Dysfibrinogenemia intracranial bleeding (within 3 months) Acquired conditions Bleeding diathesis Major surgery or major trauma Coagulation defect Previous venous thromboembolism Severe thrombocytopenia Antiphospholipid antibodies Platelet function defect Cancer (chemotherapy) Recent major trauma Major medical illness Uncontrolled hypertension Age Endocarditis Obesity Leg paralysis Estrogen therapy Pregnancy or puerperium continuous intravenous UFH. It can be administered Major medical illness subcutaneously without laboratory monitoring in Hereditary, environmental or idiopathic conditions most patients and is more convenient to use (Ho et al. High plasma homocysteine 2005). High plasma coagulation factors VIII, IX, XI There are contraindications for anticoagulation (Ta- ble 18.1.57), but most of them are relative. 18.1.7.3 Detection and Clinical Findings Unfractionated Heparin Classic signs of a DVT are pain, tenderness, and swell- After an initial loading dose, UFH is given intravenous- ing of the leg. However, these symptoms can be mis- ly by continuous infusion. Laboratory monitoring of leading and can be caused by nonthrombotic disorders the activated partial thromboplastin time (aPTT) is (Hull et al. 1984; Nicolaides et al. 1971). Therefor, it is necessary, because the anticoagulant response varies essential to confirm the diagnosis of venous thrombo- duetovariablebindingofUFHtoplasmaproteins sis by reliable objective tests. These objective tests in- (Hirsh et al. 2001). There exist many different applica- clude venography (Lensing et al. 1992), impedance tion schemes for UFH. The therapeutic range is for plethysmography (IPG) (Buller et al. 1991; Hull et al. most commercial aPTT reagents 1.8–3.0 times the con- 1990a), and venous ultrasonography. Today, compres- trol value (Monreal et al. 1989) although for less sensi- sion ultrasonography can be considered as the diag- tive reagents it is 1.5–2.0 (Hirsh and Hoak 1996; Basu et nostic test of choice in clinical practice, because it is al. 1972; Bjornsson and Nash 1986). Tomaintain antico- noninvasive, reliable, and widely available (Hirsh and agulation within this therapeutic range, weight-based Hoak 1996; Kearon et al. 1998). In patients with clinical heparin nomograms can be used (Raschke et al. 1996). symptoms and negative results on ultrasonography, as- Other guidelines suggest a bolus of 5,000 IU i.v. when a cending contrast venography may be additionally per- DVTissuspected,followedbyareboluswithUFH formed. Another way is to perform a D-dimer assay, 80 IU/kg i.v. and a maintenance infusion at 18 IU/kg as but since after surgery the D-dimer test is often false soon as a DVT is confirmed7. Monitoring of the aPTT positive, its value is limited in the diagnosis of DVT for after 4 h is mandatory. The duration of heparin therapy surgical patients. shouldbe4–5daysforpatientswithDVT(Gallusetal. 1986; Hull et al. 1990b). It should be only extended to a 7- to 10-day course in case of large iliofemoral vein 18.1.7.4 thrombi or major pulmonary embolism(Hirsh and Ho- Management ak 1996). The initial therapy of DVT should be a combination of unfractionated (UFH) or low-molecular-weight hepa- Low-Molecular-Weight Heparin rin (LMWH) followed by oral anticoagulants (Hirsh and Hoak 1996; Brandjes et al. 1992). Thrombolytic Administration of LMWH in a fixed dose by subcutane- treatment and surgical thrombectomy is usually only ous injection once or twice daily in weight-adjusted indicated for patients with massive iliofemoral throm- doses provides some important advantages compared bosis or pulmonary embolism (Hyers et al. 2001; Hey- toUFH.LMWHshaveproventobeatleastaseffective mans et al. 1998; Verhaeghe et al. 1997). LMWH has be- and safe as UHF (Monreal et al. 1994; Hull et al. 1992; come the standard for the initial treatment of DVT be- Siragusa et al. 1996; Gould et al. 1999). In addition, they causeithasbeenshowntobeaseffectiveandsafeas seem to cause less heparin-induced thrombocytopenia 416 18 Postoperative Complications

(Hirsh et al. 2001; Warkentin et al. 1995) and a lower in- 18.1.8 cidence of osteoporosis than heparin (Monreal et al. Lymphoceles 1994; Pettila et al. 2002). As they need no monitoring, 18.1.8.1 LMWHs are more convenient to administer and make Anatomy and Physiology an effective outpatient therapy possible (Koopman et al. 1996; Levine et al. 1996). As there are numerous The lymphatic system is an anatomical structure com- LMWH agents on the market, no general advice on the posed of channels, where the principal function is to dosage can be given. maintain the blood volume by returning fluid and protein molecules that leak from blood capillaries to the interstitial space to the general circulation. In addition, Long-Term Therapy there are circulating lymphocytes and lymphoid organs Initial therapy of venous thromboembolism by either that play an important role in the process of defense LMWH or UFH should be followed by oral anticoagula- against infection and tumor growth (Olszewski 1991). tion for secondary prophylaxis and to reduce risk of re- The lymph draining system of the body is composed currence (Hyers et al. 2001; Prins et al. 1999). Heparin of thin-walled channels that are classified according to therapy is overlapped with initiation of warfarin or an- the histotopographical position. The smaller channels, other coumarin until the therapeutic range, indicated commonly called lymphatic capillaries (initial lym- by an international normalized ratio (INR) of 2.0–3.0, phatics), form the roots of this vascular system. Within is reached for 2 consecutive days. In case of massive the organs, the initial lymphatics communicate to pre- thrombosis, an extended course of heparin for collector ducts. Outside of parenchymatous organs, the 7–14 days should be considered (Bates and Ginsberg lymph is drained by collecting vessels that carry the 2004; Schulman 2003). Because of an increased bleed- lymphtotheregionalnodes.Thesevesselsarereferred ing risk, it can be essential to delay coumarin therapy to as prenodal collecting vessels. After intranodal pas- after surgery. sage of one node or a set of successive nodes, the lymph The duration of oral anticoagulation treatment is drained by postnodal collecting lymphatics, which should be adapted to the individual patient. In general, converge to larger lymphatic trunks that finally drain a course of 3–6 months is recommended (Hyers et al. into the lymphatic ducts. The largest of them, the tho- 2001). Extending therapy beyond 6 months may be ad- racic duct, joins the angle between the left subclavian visable for patients with multiple recurrent episodes of vein and the internal jugular vein (Földi et al. 2005; Ols- idiopathic VTE or with active malignant disease-asso- zewski 1991). Figures 18.1.19 and 18.1.20 illustrate the ciated VTE or antithrombin deficiency (Levine et al. decisive lymphatic vessels and nodes physicians en- 1988; Hirsh 1995). counter in urology. At the light microscopy level, initial lymphatic vessels show highly variable diameters, between 10 and 80 µm,

a b

Fig. 18.1.18a–d. CT scan of a patient on day 6 following open radical retropubic prostatectomy with a large (>5 cm) lymphocele in the left pelvic region presenting with pain in the left lower abdomen. White arrows show the extension of the lymphocele. Black arrows show a partial compression of the common iliac vein (a). On the CT scan (b), the black arrows indicate the stasis of the common iliac vein with no signs of thrombosis. The grey arrow is placed to show a small epifascial hematoma 18.1 Acute Postoperative Complications 417

Fig. 18.1.18. c A dilated common iliac vein without thrombosis. d Ultrasound of the same patient showing the lymphocele with a diameter of more than 5 cm which clearly exceed that of blood capillaries, that lack a basement membrane, but reticular fibers are present. The precollectors have a larger caliber (100–200 µm) than the initial lymphatics but the fundamental mor- phology is similar in both types of vessels. Lymphatic channels have numerous valves and are often slightly distended at these sites. Collecting lymphatics with a diameter of more than 0.2 mm usually have three layers: tunica intima (endothelium with basement membrane), tunica media (muscular layer with no clear division into circular or longitudinal coats), and tunica adventitia (fibrous fibers). A longitudinal muscular layer is present in the right lymphatic and thoracic ducts. The lymphatic system is an organized network composed of function- ally interrelated lymphoid tissue, and trans- portation pathways of tissue fluid, or lymph, andlymphoidcels.Itsmaincomponentsare 1. Migrating dendritic cells, macrophages and lymphocytes, organized lymphoid tis- suesuchaslymphnodes,thymus,spleen,

Fig. 18.1.19. Lymphatic drainage of the pelvic region 1 Superficial inguinal lymph nodes, 2 Profund in- 10 Lateral sacral lymph nodes, 10a Medial guinal lymph nodes, 3 External iliac lymph nodes, sacral lymph nodes, 11 Lumbal lymph nodes, 3a Lateral lacunar lymph node, 3b Intermedial lacu- 12 Left lumbal trunk, 13 Right lumbal trunk, nar lymph node, 3c Medial lacunar lymph node, 14 Cisterna chyli, 15 Thoracic duct, 16 Cross- 3d Lateral interiliac lymph node, 3e Medial interili- over, 17 Presacral cross-over, 18 Deep lymph ac lymph node, 3f Principal lymph node, 4 Obtura- vessels of the lower extremity, 19 Inguinal tor canal lymph node, 5 Obturator fossa lymph bypass, 20 Iliac bypass, 21 Lumbal bypass nodes, 6 Common iliac lymph nodes, 7 Promontory (From: Földi/Földi/Kubik: Lehrbuch der lymph nodes, 8 Superior gluteal lymph nodes, 9 In- Lymphologie, 6. Auflage © 2005 Elsevier ferior gluteal lymph nodes, GmbH, Urban & Fischer Verlag München) 418 18 Postoperative Complications

Fig. 18.1.20. Lymphatic drainage of the extraperitoneal region 1 Intercostal lymph node, 2 Juxtavertebral lymph node, 3 Laterocaval lymph nodes, 4 Precaval lymph nodes, 5 Retro- caval lymph nodes, 6 Intermedial lumbal lymph nodes, 7 Preaortic lymph nodes, 8 Lateroaortic lymph nodes, 9 Common iliac lymph nodes, 10 Intermedial external iliac lymph nodes, 11 Internal iliac lymph nodes, 12 Medial external iliac lymph nodes, 13 Intercalary lymph node (From: Földi/Földi/Kubik: Lehrbuch der Lymphologie, 6. Auf- lage © 2005 Elsevier GmbH, Urban & Fischer Verlag München

Inaddition,itisenrichedinproductsofcellmetabo- bone marrow, and lymphoid tissue in gut and lism.Thustheexactcompositionoflymphisdictated lungs, liver lymphoid cells, and the dend- by capillary filtration rate, permeability of the capillary ritic cell network of nonlymphoid organs wall, the metabolic state of parenchymal cells, and tis- 2. Vessels (intercellular space, lymphatics, suefluid,andlymphtransportawayvialymphatics.All and perivascular spaces) these factors change depending on the actual function- 3. Fluids (tissue fluid and lymph). al state of the tissue or organ from which the lymph is The lymphatic system can be divided into the following drained. The average amount of proteins is approxi- compartments: peripheral (from the interstitial space mately 20 g/l but shows dependence on the topographi- to and within the nearest lymph node) and central (ef- cal areas (Table 18.1.58). ferent lymphatics, cisterna chyli, and the thoracic duct, The tissue fluid and lymph constitute a 12-l water all lymphoid organs). Organs and tissues with the most and electrolyte compartment containing immune cells active afferent arm of the lymphatic system are skin, and free cellular components, apoptotic bodies, cell ly- gut, and lungs. These are the body structures exposed sates, exosomes, bacteria, viruses or virus-like anti- to the external environment (Földi et al. 2005; Olszew- gens, intracellular pathogens, and proteins (soluble, ski 1991). particulate, or complexed with immunoglobulins, heat The daily production of lymph goes beyond 2 l/24 h shock proteins, complement factors, coagulation fac- under normal conditions. The chemical composition of tors, cytokines and chemokines, and their receptors lymphistoalargedegreedifferentfromthatofplasma. and inhibitors, free DNA from the host’s destroyed 18.1 Acute Postoperative Complications 419

Table 18.1.58. Proteins in lymph of humans Table 18.1.59. Incidence of symptomatic lymphoceles depending on surgical intervention Source of lymph Protein Value g/l L:S Surgery Incidence (sympto- Thoracic duct Total protein 35.0 matic)a 11–16, 10, 17 31.0–48.9 0.5–0.69 Albumin 21.1–34.2 0.56–0.82 Renaltransplantation 0.6%–18% RPLND 25% Hepatic Total protein 29.0 0.52 Open pelvic lymph node dissection 4.7%–14.8% 34.0–87.0 0.57–1.0 Laparoscopic pelvic lymph node 1%–3% Albumin 29.4–42.0 0.93 dissection Intestinal Total protein 30.0–41.0 0.46–0.65 Inguinal lymphadenectomy 7.5%–30% Albumin 12.4–25.5 0.4–0.68 RPLND retroperitoneal lymph node dissection L:S lymph to serum ratio a Sogani et al. (1981); Bailey et al. (2003); Corvin et al. (2004); Jacobelis (2003); Janetschek et al. (1999); McCullough et al. (1991); Nelson et al. (2004); Solberg et al. (2003) cells, lipoproteins, auto- and foreign antigens encoded by RNA or DNA, and ectoenzymes) (Olszewski 2005). Mechanisms regulating extravascular coagulation in In renal transplantation, lymphatics can be disrupted slow-moving extravascular fluids (interstitial fluids in the hilum of the graft either during procurement or and lymph) are poorly understood since data dealing graft preparation. Lymphoceles develop in up to 61% with this aspect are rare in the literature. Whereas con- of patients undergoing renal transplantation or pelvic siderable data are available on coagulation factor levels surgery. However, only a small portion of these lym- in thoracic duct lymph, which is not surprising, since phoceles are clinically significant (Table 18.1.59), lymph from the liver, the site of synthesis of most he- causing venous obstruction with subsequent edema mostatic factors, very few data are available on the lev- and thromboembolic complications (Yablon et al. els of hemostatic factors in peripheral lymph. A recent 2004). study on hemostatic factors in peripheral rabbit lymph Most lymphoceles are asymptomatic and resolve by Le et al. (1998) showed a mean lymph fibrinogen lev- spontaneously (Pepper et al. 2005; Sogani et al. 1981). el of almost 30% of the mean plasma level. Since fibrin Drainage or ablation may be necessary if lymphoceles degradation products were not detectable, the authors are large (~5 cm), become infected, are associated with concluded that fibrin does not form under normal pain, or cause compression of adjacent structures (e.g., physiological conditions, despite a substantial concen- ureter, urinary bladder, iliac veins) (Pepper et al. 2005; tration of fibrinogen in this slow-moving fluid. Addi- Sogani et al. 1981). The development of lymphoceles tionally, the data are compatible with a basal factor VI- depends on: Ia tissue factor-catalyzed extravascular activation of 1. The number of injured lymphatics and insufficient factor X, which is prevented from progressing to gener- closure of lymph vessels ation of fibrin in limb interstitial fluid and lymph by 2. The speed of development of new lymphatic con- low levels of factor VIII and factor V and by the inhibi- nections tory activity of antithrombin and tissue factor pathway 3. The coexistence of deep thrombophlebitis with ve- inhibitor (TFPI). nous blood stasis and subsequent lymph overpro- A different study conducted by Olszewski (Olszew- duction ski 2005) investigated 17 healthy men and their lymph: 4. The preexistence of idiopathic lymph stasis plasma ratios. Activated factor VII (FVIIa) and TFPI- 5. Postischemic capillary permeability with high in- Xa complex concentrations were higher in lymph than filtration rate and augmented lymph production. plasma. Fibrin degradation products were higher in lymph than plasma, up to five times as high. This high level may indicate proteolysis of fibrinogen and may in- 18.1.8.3 directly show hemostatic activity, which may explain Risk Factors and Prevention the ability of the lymphatic system of spontaneous coagulation following injury or surgery. The incidence of lymphoceles can be minimized by me- ticulous surgical technique and attention to sealing the lymph vessels during lymph node dissection (Pepper et 18.1.8.2 al. 2005; Sogani et al. 1981). The most common nodal Overview operation performed in urology are groin, pelvic, and Lymphoceles are a collection of lymphatic fluid with- retroperitonealnodedissection.Lymphnodedissec- out an epithelial lining occurring as a consequence of tionsareperformedsimilarlybymostsurgeons.The surgical dissection and inadequate closure of afferent margins of dissection are exposed, cleaned of fat and lymphatic vessels and subsequent leakage of lymph. interlying lymphatic structures are removed en bloc. 420 18 Postoperative Complications

Table 18.1.60. Risk factors for lymphoceles in surgical urology Table 18.1.61. Clinical findings and workup

Repeat transplantation Clinical findings Acute graft rejection Distension or abdominal pain Cadaveric donor kidney Secondary infection Sirolimus immunosuppression Edema of the lower extremity or genitalia Adult polycystic kidney disease Compressive effect on ureter Previous chemotherapy Deep vein thrombosis Low-molecular-weight heparin Graft dysfunction Surgical techniques Diagnostic procedure Extension of pelvic lymph node dissection Ultrasound/duplex sonography (Fig. 18.1.21) CT scan (Fig. 18.1.18–18.1.20) The skin incision is placed along the lines of skin ten- Lymphocele aspirate (microbiology/culture) sion and crossing the major flexion of the groin at right angles is avoided. The margins of dissection are dis- 18.1.8.5 sected sharply and blood vessels are tied or clipped. Diagnosis and Workup Some surgeons recommend both monopolar and bipolar electrocautery dissection with placement of multi- Ultrasound is simple and effective in confirming the po- ple lymphatic ligatures to decrease postoperative lym- sitionandsizeofthefluidcollection.OccasionallyCT phorrhea. No prospective comparative studies of the scans are used to diagnose lymphoceles (Fig. 18.1.18). efficacy of these measures have been reported (Olszew- Cytologicalandbiochemicalanalysisoftheaspiratecan ski 1991). Suction drains are routinely placed in the be used to aid in their diagnosis. Fluid chemistry is par- groin area after dissection to evacuate blood and lymph ticularly helpful in differentiating lymphoceles from ur- from divided vessels and to coapt the skin to the ex- inoma since lymphocytes usually can be detected. posed structures beneath. The drains used are sterile, While electrolytes and creatinine are serum isotone in closed systems that produce a constant negative pres- lymphoceles, in urinoma high creatinine levels are the sure of 20–50 mmHg. They are removed when the tis- rule. If there is a discontinuation of the lymphatics in sue adheres well and the fluid removed is minimal the upper retroperitoneum (celiac axis area), chylous (<30 ml/day) and without obvious infection. Drains fluidcollects.Incaseofchillsandfever,theaspirate are not always placed after intraabdominal node dis- should be cultured. section, as the absorptive surface of the peritoneum usually serves to mobilize and clear lymphorrhea with- 18.1.8.6 out stasis or infection. However, some authors recom- Management mend their use routinely to minimize lymphocele formation. In our institution, suction drains are used as Pelvic lymphoceles after radical or transplant surgery described above for lymphadenectomy of the groin. can be treated by single or recurrent percutaneous For extraperitoneal and intraabdominal procedures, drainage (Pepper et al. 2005; Zanetta et al. 1993), with themanagementisidentical.Drains(withoutsuction) or without sclerotherapy (Table 18.1.62), percutaneous are removed at day 2 or 3 after surgery independent of catheter drainage (Pepper et al. 2005; Kim et al; 1999), the amount of fluid removed. Lymphadenectomy is laparoscopic surgery (Pepper et al. 2005; Fallick and performed by using clips and/or bipolar electrocoagu- Long 1996; Thurlow et al. 1996) or open surgical drain- lation. age (Pepper et al. 2005; Gruessner et al. 1995). Risk factors are listed in Table 18.1.60 (Koch and Jr 1997; Lundin et al. 2002). Table 18.1.62. Suggested agents for sclerotherapy of lymphoceles 18.1.8.4 Sclerosant Clinical Signs Tet rac ycline The symptoms of a lymphocele depend on the site, size, Doxycycline (e.g., 500 mg doxycycline hyclate powder re- constituted in 100 ml 0.9% NaCl combined with 5 ml 1% and the presence of infection. A visible or palpable pel- lidocaine for 60 min) vic mass may be present, resulting in abdominal or pel- Bleomycin (e.g., 60,000 units of bleomycin in 50 ml 0.9% vicpain.Symptomsorsignsmaystemfromvenousor NaCl for 2 – 3 h) ureteric compression resulting in unilateral leg edema Ethanol (e.g., 10–100 ml absolute alcohol for 30 min) Povidone iodine (e.g., 20 ml 5% povidone iodine for and leg pain, hydronephrosis with deterioration in re- 20 min) nal function, and deep vein thrombosis. Fever and Talcum(e.g.,1gasbestos-free,sterilizedtalcin50–100ml chills should raise the suspicion of an infected collec- 0.9% NaCl for 60 min) tion. Differential diagnosis includes urinoma, hemato- Fibrin glue (e.g., 5 ml fibrin sealant (Tissucol, Tisseel, ma, and abscess formation (Table 18.1.61). Vivostat) References 421

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