Emergencies in Urology - part 8 pdf

AFTER 2.5 Hr RENOGRAM AFTER 2.5 Hr and by reviewing the fluid balance charts of intake and output.USisaveryhelpfultoolinthedifferentialdiag- nosis of early oliguria or anuria. Gray-scale US excludes urological complications, while Doppler US is used for assessment of graft perfusion to exclude vascular thrombosis. If there are no urological or vascular problems, the next step is to assess the graft tissue by biopsy, which will differentiate between a variety of conditions such as ATN, rejection, drug toxicity, and early recurrence of the original kidney disease. The onset of a rejection episode on top of another complication such as ATN, urological complication, drug toxicity, or recurrence of the original kidney disease is confusing and renders the diagnosis more difficult. Nevertheless, repeated graft biopsy is very helpful in this situation. Volume Contraction Prerenal azotemia or volume contraction often may lead to allograft deterioration during the immediate postoperative period. Excessive diuretics and uncontrolled blood glucose are two of the commonest causes of the development of prerenal azotemia from volume contraction. Because most of these patients are already receiv- ing calcineurin inhibitors, which decrease renal blood flow, the concomitant insult of volume contraction may lead to an elevated level of blood urea nitrogen and serum creatinine, which may be difficult to distinguish from an episode of acute rejection. Careful attention to central venous pressure, daily weight, intake and output, and assessment of orthostatic blood pressure changes can reliably diagnose volume contraction as a contribut- ing factor for renal allograft dysfunction. Volume reple- tion with intravenous or oral fluid is indicated. Acute Tubular Necrosis Acute tubular necrosis (ATN) is the most frequent posttransplantation complication. Other than hyperacute rejection, ATN is the earliest posttransplantation complication. The incidence of ATN is significantly higher Fig. 18.4.4. Radioisotope renal scan ( 99m Tc-MAG 3 )ina patient with acute tubular necrosis (ATN) showing good perfusion, good uptake, and no excretion in cadaveric vs living donor transplants. An incidence of 25% for cadaver donors vs 5% for living donors has been reported (Shoskes and Cecka 1997). An increase in the incidence of ATN has also been noted with ad- vancing donor age. Prolonged cold ischemia time, up to 30 h, does not appear to have a significant impact on the incidence of ATN unless there is an episode of rejection. The diagnosis of ATN usually is apparent during the first 24 h after transplantation. Although some kidneys may produce urine initially, a fall off in urine output that is unresponsive to fluid challenge is the commonest clinical scenario indicating ATN. The major differential diagnostic consideration in a patient with a falling or absent urine output is an acute vascular or urological complication. The differential diagnosis can be deter- mined easily with urgent US and radionuclide renal scanning. Gray-scale US shows a large swollen graft, compressed pelvicalyceal system and an empty bladder. Moreover, Doppler US reveals perfect graft perfusion. A radioisotope scan may also help in diagnosis; typically, a transplantation with ATN shows good renal perfusion, good parenchymal uptake of 99-m Tc MAG 3 with poor or no renal excretion (Fig. 18.4.4). In caseof doubt, a biopsy is taken. Once the diagnosis of ATN is established, careful attention to fluid status is paramount to decrease the frequency and necessity for dialysis. The usual course of ATN is 10–14 days, and patients may re- quiresupportivedialysisformanagementoffluidand electrolyte disturbances. Moreover, the immunosuppressive drugs and antibiotics need to be modified. The major concern for transplant recipients with ATN is the potential onset of a concomitant acute rejection. The diagnosis of rejection in patients with ATN may be hindered because the primary clinical monitoring tool is a fall in serum creatinine. For this reason, some centers use antilymphocyte therapy to prevent early acute rejection in patients with ATN. Alternative- ly, frequent biopsies of patients with ATN have been proposed as a means for detection of acute rejection episodes. An early acute rejection episode after ATN 18.4 Emergencies Following Renal Transplantation 455 significantly lowers short- and long-term survival (Land 1998). Rejection Rejection that occurs early after transplantation includes hyperacute, accelerated, and acute rejection. Hyperacute rejection occurs if renal transplantation is performed in the setting of an ABO mismatch or a posi- tive lymphocytotoxic crossmatch. Hyperacute rejection is manifested intraoperatively as soft blue kidney immediately after release of the vascular clamps. A hy- peracutely rejected kidney has no perfusion on Dopp- lerUSorrenalscanbecauseofthemicrovascular thrombosis. There is no effective treatment and the graft needs to be removed. Despite a negative T cell crossmatch test preopera- tively, some patients may develop an early aggressive form of rejection, termed accelerated vascular rejection. This rejection is seen most often in patients with a previous transplant or in those with high panel-reac- tive antibody. Accelerated rejection typically occurs within 2–5 days of the transplant. Histologically, renal transplant biopsy shows fibrin deposition and endo- theliitis. Accelerated rejection is poorly responsive to steroids and may be resistant to all forms of antirejec- tion therapy. Because of the likely contribution of the humoral immune response, a combination of plasmapheresis and anti-CD 20 monoclonal antibody (rituximab) have been recently used as a rescue therapy of accelerated rejection. The rationale of this combined therapy is that plasmapheresis gets rid of the existing antibodies, while rituximab prevents further formation of new antibodies through inhibition of B lymphocytes (Pescovitz, 2004; Garrett et al. 2002). Acute cellular rejection is the most common form of rejectionintheearlyposttransplantationperiod.Itis mediatedpredominantlybyhostlymphocytesre- sponding to the allogenic donor kidney. Acute rejection typically occurs 5–7 days after transplantation, but can occur at virtually any time thereafter. The highest incidence of acute rejection is within the first 3 months and overallratesofrejectionvaryfrom10%to50%within the first 6 months depending on HLA matching and the immunosuppressive protocol. The clinical manifesta- tion of acute rejection includes a rising serum creatinine, weight gain, fever, and graft tenderness. Since the introduction of cyclosporine and tacrolimus, the latter two signs are seldom present. The diagnostic gold stan- dard is kidney biopsy that shows cellular infiltration. The first line of treatment is bolus steroid therapy. Ap- proximately 85%–90% of acute cellular rejection episodes are steroid responsive. If the patient’s serum creatinine does not start decreasing by day 4 of therapy, alternative treatments should be considered, such as ALG or OKT 3 . Rejection that does not respond to treatment with steroids, ALG, or OKT 3 occurs in less than 5% of patients. This is observed more frequently in sensitized patients or retransplantations. Vascular T hrombosis Renal allograft vascular thrombosis is a serious complication of kidney transplantation that ultimately leads to graft loss. The reported incidence of thrombot- iccomplicationsvariesfrom0.8%to6%(Bakiretal. 1996; Groggel 1991). In our series, an incidence of 0.5% was observed (Osman et al. 2003). Many factors have been associated with thrombotic sequelae, such as pediatric recipients, preoperative hypercoagulable states, pretransplantation peritoneal dialysis, the type of fluid used for perfusion, and the pro-coagulant effect of OKT 3 or cyclosporine (van Lieburg et al. 1995; Murphy et al. 1994; Benoit et al. 1994). Thrombotic complications usually occur very early after transplantation and manifest by sudden anuria. The diagnosis is confirmed by Doppler US (Fig. 18.4.5a), MRA (Fig 18.4.5b), and/or radioisotope scan, which demonstrate absence of renal perfusion. Exploration must be performed immediately and rarely can the graft be salvaged by thrombectomy, but most cases will end in a graft loss. In a series of 1,200 consecutive live-donor renal transplantations, we recorded renal artery thrombosis in five patients (0.5%) and renal vein thrombosis in one (0.1%) (Osman et al. 2003). Patients with renal artery thrombosis were treated by graft nephrectomy in four and renal artery thrombectomy in one in whom the graft could be persevered. The patient with renal vein thrombosis was managed by graft nephrectomy (Os- man et al. 2003). Routine prophylactic heparinization has been great- ly debated over the years. Ubhi et al. (1989) recom- mended routine subcutaneous heparin to decrease postoperative thromboembolic complications in renal transplantation patients based in a prospective randomized study. Broyer et al. (1991) observed the effec- tiveness of low-molecular-weight heparin for decreasing the incidence of graft thrombosis in pediatric kidney transplantation. On the other hand, in a more recent study the role of intraoperative heparin was ques- tioned. Moreover, it was associated with a significant increase in postoperative hemorrhagic complications and the need for blood transfusion (Mohan et al. 1999). In our opinion, the use of posttransplantation anticoagulants must be reserved for patients at high risk of developing vascular thrombosis such as pediatric recipients, diabetics, patients with hypercoagulable state, orthosewithmultiplevessels. 456 18 Postoperative Complications a Fig. 18.4.5a, b. Renal artery thrombosis. a Power Dopp- ler US showing nonperfused transplanted kidney. b Mag- netic resonance angiography (MRA) showing nonvascula- rized right iliac renal allograft b Urinary Leakage The reported incidence of urinary leakage varies between 1.2% (Ghasemian et al. 1996; Makisalo et al. 1997) and 8.9% (Loughlin et al. 1984). In our series, an incidence of 3% was observed (El-Mekresh et al. 2001). Urinary leakage is generally evident early after transplantation and commonly caused by vascular insuffi- ciency secondary to inadvertent damage to the vessels that supply the ureter during organ harvesting. It may also occur as a result of technical problems during ur- eteroneocystostomy, particularly with transvesical procedures. The rate is slightly higher in patients who received kidneys from living donors than in those who received organs from cadavers (Loughlin et al. 1984; Ci- mic et al. 1997). This is presumably a result of more extensive hilar dissection required during harvesting from the living donor, with the attendant risks of injury to the blood supply of the ureter. With the early learn- ing curve of laparoscopic live-donor nephrectomy, the incidence of ureteral complications was significantly higher in comparison to open liver-donor nephrectomy (Rawlins et al. 2002; Ratner et al. 1999). The higher incidence of ureteral complications with laparoscopic nephrectomy was attributed to extensive dissections close to the wall of the ureter. With the current knowl- edge of the necessity for a meticulous preparation of the ureter and its surrounding fatty tissue, the propor- tion of ureteral complications no longer differs between laparoscopic and open live-donor nephrectomy. Some authors even describe fewer ureteral complications with the laparoscopic approach (Ratner et al. 1999). Symptoms of ureteric leak generally include sudden oliguria or anuria, an increasing serum creatinine level, and perigraft swelling. The urine may collect around the graft or leak from the wound or through the tube drain. Gray-scale US is important to diagnose a perigraft collection; if found, the collection should be drained. Determining the nature of the fluid collecting around the graft or leaking from the wound is para- 18.4 Emergencies Following Renal Transplantation 457 ab Fig. 18.4.6a, b. Urinary leakage. a Antegrade study showing leakage from the middle part of the ureter of the transplanted kidney. b AntegradestudyofthesamepatientafewdaysafterdrainageofthegraftbyPCNshowingintactpatentureterwithabsenceof extravasations mount. A quantitative estimation of the creatinine con- tent of this fluid differentiates between urine and lymph. If urine leakage is diagnosed, its possible sources could be either the site of the ureterovesical anastomosis or a ureteric fistula. A few days of watchful waiting with proper drainage of the wound and the bladder usually result in cessation of the urine leak if its source is the bladder. However, if urine continues to leak, then a ureteric fistula is suspected. The diagnosis is usually confirmed by fixation of a graft PCN and antegrade study (Fig. 18.4.6). Leakage from the urinary bladder is usually easily treated by prolonged catheter drainage. Almost half of ureteric leaks are managed by percutaneous techniques, which are currently used as the initial management in all cases. Open surgical revision can be used subsequently if this fails. The choice of the reconstructive procedure depends on the operative findings. Dis- tal pathologies can be corrected by ureterovesical reimplantation. For more proximal lesions, a Boari tube or ureteroureteral reanastomosis can be used. Early diagnosis and prompt treatment usually result in salvage of the graft with no harmful effect on either the graft or on the patient’s survival (Shokeir et al. 1993c). In a recent study, we reported 37 cases of urinary leakage among 1,200 live-donor renal transplantations. The conservative management of vesical leaks by pro- Fig. 18.4.7. MRU following a Boari flap from the bladder to the pelvis of the graft for treatment of extensive fibrosis of the ureter longed catheter drainage was successful in six patients. Three patients (with ureters reimplanted using the Po- 458 18 Postoperative Complications litano-Leadbetter technique) required open repair and closure in two layers. Several methods were used to manage ureteric leaks. For minor leaks at the vesicou- reteric junction, definitive treatment by PCN drainage was attempted in 14 patients. Two patients required subsequent reconstructive procedures. Open surgical revision was required in 16 patients. For distal pathologies, a ureterovesical reimplantation was possible. Leaks resulting from more ischemic damage of the ureter required either a ureteroureteric anastomosis (five), a Boari flap ureteroneocytostomy (two) (Fig. 18.4.7) or an anastomosis between the renal pelvis of the donor’s kidney and the ureter of the recipient (one patient). In one patient with total necrosis of the ureter, interposi- tion of a segment of ileum between the renal pelvis and the bladder was necessary (El-Mekresh et al. 2001). Drug Toxicity Both of the calcineurin inhibitors, cyclosporine and tacrolimus, are effective in preventing acute rejection episodes but clearly can lead to nephrotoxicity, primar- ily by decreasing renal blood flow in the afferent arteri- ole, leading to tubular injury (Pirsch and Friedman 1994). Because of variability in intestinal absorption in the early transplant period, underdosing may result in rejection episodes and overdosing can lead to nephrotoxicity. Although there are many clinical parameters that have been advocated to differentiate calcineurin inhibitor nephrotoxicity from rejection, most clinical parameters are not of sufficient sensitively to predict the cause of the transplant dysfunction confidently. In patients with ATN, it is be more difficult to diagnose acute rejection or calcineurin nephrotoxicity reliably. Monitoring cyclosporine andtacrolimus levels is of val- Fig. 18.4.8. Fine needle aspiration cytology showing cyclosporine nephrotoxicity with the characteristic fine vacuoles in the renal tubules ue in preventing significant increases in blood levels, which may lead to nephrotoxicity. Controversy remains regarding the time of sample collection for monitoring of cyclosporine level using either a trough level sample (12hafterthepreviousdose)oraC 2 level sample (2 h after the previous dose). The most reliable way of differentiating calcineurin nephrotoxicity from rejection is percutaneous renal allograft biopsy. Early functional nephrotoxicity is manifested most often by evidence of tubular injury characterized by vacuolation (Fig. 18.4.8). In patients with established calcineurin nephrotoxicity, lowering the dose or temporary discontinuation of cyclosporine or tacrolimus can lead to reversal of the renal injury. Recurrence of the Original Kidney Disease Most causes of renal failure do not recur in the transplant kidney, when they do, it is usually later in the posttransplant course. Two diseases may occur in the immediate posttransplant period and lead to significant graft dysfunction or graft loss if not treated ag- gressively. These include focal segmental glomerulosclerosis (FSGS) and hemolytic uremic syndrome. FSGS is the commonest glomerulonephritis that can recur in the immediate postoperative period (Artero et al. 1994). The diagnosis is established by the development of nephrotic-range proteinuria in a patient with a pretransplant diagnosis of FSGS and is confirmed by biopsy. Electron microscopy shows diffuse foot process effacement, which is diagnostic in this setting. Various strategies have been employed to treat recurrent FSGS, including high-dose calcineurin inhibitors, predni- sone, and plasmapheresis. Hemolyticuremicsyndromecanrecurintheimme- 18.4 Emergencies Following Renal Transplantation 459 diate postoperative period (Kaplan et al. 1998). It is characterized clinically by a fall in hematocrit and/or platelet count with evidence of a microangiopathic process on peripheral blood smear, increased lactate dehy- drogenase and transplant allograft dysfunction. Kid- ney biopsy shows fibrin clot in the small arterioles of the kidney. Hemolytic uremic syndrome has been noted to be induced by cyclosporine or tacrolimus. Dis- continuation of the calcineurin inhibitor and plasmapheresis have been beneficial in some series (Kaplan 1999, 2003). The use of anticoagulants and aspirin is of uncertain benefit. 18.4.3.3 Late Graft Dysfunction Late graft dysfunction is defined as gradual and progressive deterioration of the renal function after at least 2 months of stable function. This could be due to renal artery stenosis, ureteral obstruction, lymphocele, or chronic rejection. Renal Artery Stenosis Transplant renal artery stenosis is a primary and po- tentially reversible cause of hypertension and graft loss. The reported incidence is 1%–16% (Lo et al. 1996; Halimi et al. 1999) and 0.4% in our series (Osman et al. 2003), with a mean incidence of around 6% for ab Fig. 18.4.9a, b. Renal artery stenosis (RAS). a Intraarterial angiography showing RAS before treatment. b Intraarterial angiography of the same patient after percutaneous angioplasty showing resolution of the stenosed segment live-donor and cadaveric transplantations (Sutherland et al. 1993). Zaontz et al. (1988) summarized the etio- logicalfactorsofrenalarterystenosisasfaultysurgical technique, trauma to the donor kidney from the perfusion cannula or intimal tears from overstretching the artery, intimal injury during end-to-end anastomosis, or artery angulation secondary to excessive length from end-to-end anastomosis with the hypogastric artery. The disease usually manifests late after transplantation by severe persistent hypertension. Diagnosis is confirmed by intraarterial angiography (Fig. 18.4.9). The role of Doppler US and magnetic resonance angiography is still controversial. The disease can be managed by percutaneous angioplasty or surgical correc- tion. Ureteric Obstruction The reported incidence of intrinsic ureteric obstruction is 1.3% (Ghasemian et al. 1996) to 10.2% (Rigg et al. 1994) and 1.9% in our series (El-Mekresh et al. 2001). Ureteric obstruction may occur in either the early or the late postoperative period. Most of the ob- structions involve the distal ureter or the ureterovesical junction. Various causes are possible in the pathogene- sisofthiscomplication,amongwhichischemiaofthe ureter is the most common (Rigg et al. 1994; Shokeir et al. 1993a). Other causes including technical problems (Ghasemian et al. 1996), urinary leaks with periureteric 460 18 Postoperative Complications a b Fig. 18.4.10a, b. Ureteric obstruction. a Antegrade study showing distal ureteric obstruction. b Antegrade study of the same patient after ureterovesical reimplantation showing resolution of the ureteric obstruction fibrosis (Rigg et al. 1994), and ureteritis resulting from acute rejection episodes (Katz et al. 1988; Schweizer 1977) were all implicated. The diagnosis of ureteric obstruction is usually suspected by a progressive increase in the serum creatinine level and dilatation of the graft pelvicaliceal system by routine ultrasonography. Further investigations include diuretic radioisotope renography and magnetic resonance urography. The diagnosis is confirmed by antegrade pyelography after fixation of a graft percutaneous nephrostomy (PCN) tube (Fig. 18.4.10). Percutaneous drainage with antegrade dilatation and stenting can be attempted as initial management of ureteric obstruction. For failures, open surgical revision is necessary and should involve the use of a healthy, well-vascularized proximal segment. Uretero- ureteric, pelviureteric, and pyelovesical anastomosis can all be used. The replacement of the ureter by an iso- lated ileal segment was successfully used in three patients in our series in whom there was extensive ischemic damage of the ureter (Shokeir et al. 1993c) (Fig. 18.4.11). Prolonged use of azathioprine may result in formation of uric acid stones, which may obstruct the ureter (Fig. 18.4.12a). In this situation, the stone could be removed through antegrade ureteroscopy (Fig. 18.4.12b). Lymphocele Lymphocele may be an asymptomatic incidental find- ing, but when it becomes large enough to compress ad- jacent structures it may cause a variety of clinical mani- festations, some of which may result in serious morbidity. The incidence of lymphocele is 0.6%–41% (Boed- ker et al. 1990; Stephenian et al. 1992) and 1.4% in our series (El-Mekresh et al. 2001). The cause of lymphocele is not fully recognized, but most authors believe it emanates either from unligated lymphatics from the iliac dissection in the recipient or from interrupted channels of the donor kidney itself (Stephenian et al. 1992). In clinical practice, a lymphocele usually presents later than a urinary leak. The former may be recognized as early as the 18th posttransplantation day or as lateasthe17thmonthaftersurgery(Meyersetal. 1977). In our series, the earliest lymphocele was ob- 18.4 Emergencies Following Renal Transplantation 461 a b Fig. 18.4.11. a Antegrade study showing arrest of dye at the site of pelviureteric junction due to extensive fibrosis of the ureter. b Antegrade study after ileal replacement of the transplanted ureter served after 3 weeks and the majority during the 3rd month (Shokeir et al. 1993b). Ultrasonography is the method of choice for the diagnosis and follow-up of lymphoceles. The technique is noninvasive and can be performed without difficulty even when renal function is seriously impaired. Other investigations that complement US include IVU and CT (Fig. 18.4.13) (when the renal function permits) and MRU. An analysis of the chemical composition of a fluid collection is also useful, because lymph constituents are similar to those of plasma, whereas urinary creatinine, potassium, and urea nitrogen concentrations are higher than in lymph. Single percutaneous needle aspiration is ineffective in the treatment of symptomatic lymphocele and should be done only for diagnostic purposes. Percuta- neous catheter drainage with the use of a sclerosant (tetracyeline, providone-iodine, ampicillin, and fibrin) may be a safe and successful alternative (Shokeir et al. 1993b) (Fig. 18.4.14). Should catheter drainage fail or the lymphocele recurs, surgical marsupializati- on by laparoscopic or open techniques usually be effective. Chronic Rejection Chronic rejection is currently referred to as chronic allograft nephropathy because the etiology includes factors that can be considered both immune, or alloantigen-dependent, and nonimmune, or alloantigen-inde- pendent. An example of the former factor is previous acute rejection and examples of the latter factors are chronic ischemia and use of cyclosporine. Chronic allograft nephropathy is an important cause of graft failure inthelateposttransplantationperiod.Clinically,itusu- allypresentsasafindinginpatientsundergoingbiopsy for gradually declining renal function or proteinuria. Chronic rejection is characterized by stenosis of the peripheral arteries with magnetic resonance angiography. No effective treatment is currently available. Nev- ertheless, some measures could be used for prophylaxis against chronic rejection such as prevention of attacks of acute rejection by induction therapy and use of po- tent immunosuppressive drugs, early detection of rejection by protocol biopsy and avoidance of calcineurin inhibitor nephrotoxicity. 462 18.4 Emergencies Following Renal Transplantation ab Fig. 18.4.12a, b. Ureteric stones. a Antegrade study showing a filling defect of a stone in the ureter of a transplanted kidney. b Ante- grade ureteroscopy for removal of the ureteric stone Fig. 18.4.13. CT showing large lymphocele displacing the urinary bladder and obstructing the ureter of a transplanted kidney 18.4.3.4 Surgical Complications Related to Immuno- suppressive Drugs Some recent kidney transplantation prospective ran- domizedtrialshavedemonstratedhighersurgical wound complication rates with sirolimus immunosup- Fig. 18.4.14. Percutaneous drainage of lymphocele pression in comparison to other types of immunosuppressive drugs (Dean et al. 2004; Troppmann et al. 2003). A surgical wound complication is defined as any complication directly related to the surgical transplant wound that needs reintervention, such as hematoma and lymphocele requiring relaparotomy, seroma re- 18.4.3 Recipients: Surgical and Nonsurgical Emergencies 463 quiring repeated aspirations, delayed healing requiring serial wound debridement, and incisional hernia requiring surgical repair. Mycophenolate mofetil (MMF) has been used successfully since 1995 as an adjunct immunosuppressive agent for the prevention of acute rejection in renal transplantation. However, hematologic and GI side ef- fects are a concern with MMF-containing immunosuppressive regimens. Diarrhea, abdominal pain, nausea, vomiting, intestinal bleeding, and perforation oc- curred more frequently in the MMF-treated group than in placebo or azathioprine-treated groups in phase III clinical trials (Sollinger et al. 1995; European Study Group 1995; MMF Study Group 1996; Hardinger et al. 2004). Hemorrhagic cystitis is one of the complications of prolonged use of cyclophosphamide. Sometimes the hematuriaissoseverethatitcausesclotretention.Im- provement usually occurs with discontinuation of the drug. In conclusion, emergencies following live-donor renal transplantation need integration of urologists, ne- phrologists, radiologists, and pathologists for proper diagnosis and treatment. Early diagnosis and prompt management can save the graft as well as the patient. Improper diagnosis will result in mismanagement that may aggravate the condition. Therefore, the key to suc- cess is to start the proper treatment inthe optimal time. References Artero ML, Sharma R, Savin VJ, Vincenti F (1994) Plasmaphe- resis reduces proteinuria and serum capacity to injure glo- meruli in patients with recurrent focal glomerulosclerosis. Am J Kidney Dis 25:574 BaghossianT,HenriM,DubeS,BendavidY,MorinM(2005) Laparoscopic nephrectomy donor death due to cerebral gas embolism in a specialized transplant center; risk zero does not exist. Transplantation 79:258 Bakir N, Sluiter WJ, Ploeg RJ, van San WJ, TegzessAM (1996) Pri- mary renal graft thrombosis. Nephrol Dial Transplant 11:140 BenoitG,JaberN,MoukarzelM,DouguetD,BensadounD, Bensadoun H, Blanchet P et al (1994) Incidence of vascular complications in kidney transplantation: is there any inter- ference with the nature of the perfusion solution? Clin Transplant 8:485 Blohme I, Fehrman I, Norden (1992) Living donor nephrectomy complication rates in 490 consecutive cases. Scand J Urol Nephrol 26:149 Boedker A, Roikjaer O, Rasmussen F, Loekkegaard H (1990) Lymphocele following renal transplantation: a clinical study. Transplant Proc 22:54 BroyerM,GognadouxMF,SierroA,FischerAH,NiaudetP (1991) Preventive treatment of vascular thrombosis after kidney transplantation in children with low molecular weight heparin. Transplant Proc 23:1384 CimicJ,MeulemanEJH,OosterhofGON,HoitsmaAJ(1997) Urological Complications in renal transplantation: a comparison between living-related and cadaveric grafts. Eur Ur- ol 31:433 DeanPG,LundWJ,LarsonTS,PrietoM,NybergSL,Ishitani MB et al (2004) Wound-healing complication after kidney transplantation: a prospective randomized comparison of sirolimus and tacrolimus. Transplantation 77:1555 El-Mekresh M, Osman Y, Ali-El-Dein B, El-Diasty T, Ghoneim MA (2001) Urological complications after living-donor renal transplantation. BJU Int 87:295 European Mycophenolate Mofetil Study Group (1995) Placebo- controlled study of mycophenolate mofetil combined with cyclosporine and corticosteroids for prevention of acute rejection. Lancet 345:1321 Garret ED Jr, Groshart K, Duvall-Seaman D, Combs D, Stuggs R (2002) Treatment of humoral rejection with rituximab. Ann Thorac Surg 74:1240 Ghasemian SMR, Guleria AS, Khawand NY,Light JA (1996) Di- agnosis and management of the urologic complications of renal transplantation. Clin Transplant 10:218:23 Groggel GC (1991) Acute thrombosis of the renal transplant artery: a case report and review of the literature. Clin Nephrol 36:42 HalimiJM,Al-NajjarA,BuchlerM,BirmeleB,TranquartF,Ali- son D et al (1999) Transplant renal artery stenosis: potential role of ischemia renal reperfusion injury and long-term outcome following angioplasty. J Urol 161:28 Hardinger KL, Brennan DC, Lowell J, Schnitzer MA (2004) Long-term outcome of gastrointestinal complications in renal transplant patients treated with mycophenolate mofetil. Transpl Int 17:609 Huynth PN, Hollander JB (2005) Trends toward laparoscopic nephrectomy at a community hospital. J Urol 173:547 Jacobs SC, Cho E, Foster C, Liao P, Bartlett ST (2004) Laparo- scopic donor nephrectomy: the university of Maryland 6- year experience. J Urol 171:47 Kaplan AA (1999) Therapeutic apheresis for renal disorders. Ther Apher 3:25 Kaplan AA (2003) The use of apheresis in immune renal disorders. Ther Apher 7:165 Kaplan BS, Meyers KE, Schulman SL (1998) The pathogenesis and treatment of hemolytic uremic syndrome. 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Transplant Proc 29:152 Matas AJ, Bartlett ST, Leichtman AB, Delmonico FL (2003) Morbidity and mortality after living kidney donation, 1999 survey of United States transplant centers. Am J Transplant 3:830 Meyers AM, Levine E, Myburgh JA, Goudie E (1977) Diagnosis and management of lymphoceles after renal transplantation. Urology 10:497 Mohan P, Murphy DM, Counihan A, Cunningham P, Hickey DP (1999) The role of intraoperative heparin in cyclosporine 464 18.4 Emergencies Following Renal Transplantation [...]... Libertino 18. 5.1 Introduction 466 18. 5.2 Indications 466 18. 5.3 18. 5.3.1 18. 5.3.2 18. 5.3.3 18. 5.3.4 Infectious Peritonitis 4 68 Intraabdominal Abscess 470 Anastomotic Leaks 471 Injury to the Colon and Rectum 473 Laparoscopic Bowel Injury 475 18. 5.4 Postoperative Bleeding 476 18. 5.4.1 Delayed Bleeding 476 18. 5.4.2 Planned Reoperation 477 18. 5.5 18. 5.5.1 18. 5.5.2 18. 5.5.3 Stomal Complications 4 78 Necrosis... 69 40 – 54 Below 40 4 Points 3 Points 2 Points 0 Points 2 Points 3 Points 4 Points 6 Respiratory rate Over 49 35 – 49 25 – 34 12 – 24 10 – 11 6–9 Below 6 4 Points 3 Points 1 Points 0 Points 1 Points 2 Points 4 Points 7 Oxygenation (use PaO2 if FiO2< 50 %, otherwise use A-a gradient) A-a gradient over 499 4 Points A-a gradient 350 – 499 3 Points A-a gradient 200 – 349 2 Points A-a below 200 (if FiO2 over... Points 4 Points 4 Points 3 Points 2 Points 0 Points 2 Points 12 Hematocrit Over 59.9 50 – 59.9 46 – 49.9 30 – 45.9 20 – 29.9 Below 20 4 Points 2 Points 1 Points 0 Points 2 Points 4 Points 13 White blood count Over 39 20 – 39.9 15 – 19.9 3.0 – 14.9 1.0 – 2.9 Below 1.0 4 Points 2 Points 1 Points 0 Points 2 Points 4 Points 14 Minus the Glasgow Coma Score (maximum GCS =15) Motor response Verbal Eye opening... 4 78 Stenosis 479 Parastomal Hernias 479 18. 5.6 Bowel Obstruction 479 18. 5.7 Dehiscence 480 18. 5 .8 Abdominal Compartment Syndrome 481 18. 5.9 Cutaneous Ureterostomy 18. 5.10 Conclusions References 482 483 483 18. 5.1 Introduction There are limited reports of open salvage procedures in the urological literature Surgical outcome reports from institutions across the world are readily available; however, in- depth... patient 5 Points Yes, and elective postoperative patient 2 Points No 0 Points 3 Rectal Temperature Over 40.9 39 – 40.9 38. 5 – 38. 9 36 – 38. 4 34 – 35.9 32 – 33.9 30 – 31.9 Below 30 4 Points 3 Points 1 Points 0 Points 1 Points 2 Points 3 Points 4 Points 4 Mean arterial pressure (mm Hg) Over 159 130 – 159 110 – 129 70 – 109 50 – 69 Below 50 4 Points 3 Points 2 Points 0 Points 2 Points 4 Points 5 Heart... 0 Points pO2 = 61 – 70 1 Points pO2 = 55 – 60 3 Points pO2 below 55 4 Points 8 Arterial pH Over 7.69 7.60 – 7.69 7.50 – 7.59 7.33 – 7.49 7.25 – 7.32 7.15 – 7.24 Below 7.15 4 Points 3 Points 1 Points 0 Points 2 Points 3 Points 4 Points 9 Serum sodium (mmol/l) Over 179 160 – 179 155 – 159 150 – 154 130 – 149 120 – 129 111 – 119 Below 111 4 Points 3 Points 2 Points 1 Points 0 Points 2 Points 3 Points... found in postoperative patients without bacteremia Differentiating these patients from those who are septic is critical Systemic inflammatory response syndrome (SIRS) is a transition to sepsis and is linked to a complex cascade of inflammatory mediators and cytokines The most widely studied pro-inflammatory cytokines include tumor necrosis factor (TNF), interleukin-1 (IL1), and interleukin -8 (IL -8 ) The... appropriate monitoring devices (e.g., a Swan-Ganz catheter and arterial line), the patient can be mobilized to the operating room The goals of surgical intervention include: (1) controlling the source of infection, (2) evacuating bacterial inoculum (peritoneal washout), (3) treating and preventing abdominal compartment syndrome, and (4) preventing or treating recurrent or persistent infection (Marcello... Saver (Haemonetics, Inc, Braintree, MA, USA) A surgeon needs a broad spectrum of instruments in managing arterial bleeding These should include vascular forceps and needle holders, 5-0 and 6-0 sutures, bulldog clamps, partial and total occlusion clamps for the aorta and inferior vena cava, in addition to umbilical and silastic loops for arterial control (Zinman and Libertino 1 988 ) Following adequate anesthesia,... Surg 28: 137 Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM (19 98) Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis incidence and clinical relevance of gastric mucosal pH, abdominal compartment syndrome J Trauma 44:1016 Kelleher CM, Curci JA, Blinder MA (2005) Hemostasis and transfusion therapy In: Klingensmith ME, Amos KD, Green DW, Halpin VJ, . factor (TNF), interleukin-1 (IL- 1), and interleukin -8 (IL -8 ) . The anti-inflammatory cytokines are interleukin-6 (IL-6) and interleukin-10 (IL- 10) (Clarke 2001; Christman et al. 1991). Patients. is linked to a complex cascade of inflammatory mediators and cytokines. The most widely studied pro-inflammatory cytokines include tumor necrosis factor (TNF), interleukin-1 (IL- 1), and interleukin -8 . Complications 4 78 18. 5.5.1 Necrosis 4 78 18. 5.5.2 Stenosis 479 18. 5.5.3 Parastomal Hernias 479 18. 5.6 Bowel Obstruction 479 18. 5.7 Dehiscence 480 18. 5 .8 Abdominal Compartment Syndrome 481 18. 5.9 Cutaneous