Critical Care Problems in Kidney Transplant Recipients

Mark L. Sturdevant

Rainer W.G. Gruessner

Introduction

A kidney transplant (KTx) remains the most definitive and durable solution for patients reaching end-stage renal disease (ESRD). A successful transplant, as compared with dialysis, can provide a higher quality of life for a longer period at an overall lower cost for the more than 104,000 patients currently awaiting a KTx on the United Network for Organ Sharing waiting list [1,2]. In 2006, in United States KTx centers, the cumulative 1-year graft survival rate was 91.3% for deceased donor recipients and 96.4% for living donor recipients; an analysis of recipients transplanted in 2002 revealed a 5-year graft survival rate of 68.9% for deceased donor recipients and 81.5% for living donor recipients. The half-life graft survival time now projected for deceased donor recipients is approximately 10 years; for living related donor recipients, almost 18 years, depending on the human leukocyte antigen (HLA) match [3,4,5]. Despite these encouraging results, the waiting list continues to expand, and the living and deceased donor pools have fallen further behind; this divergence results in recipients who can be subjected to the ill effects of uremia and dialysis for more than 5 years pretransplant. Critical care providers therefore face a cohort of patients with a higher acuity of illness than seen even a decade ago. This chapter discusses the salient points of critical care that KTx recipients must receive to optimize their outcomes.

Pretransplant Evaluation

Thoughtful patient selection and a thorough pretransplant evaluation of transplant candidates are essential for optimal transplant outcomes; because hypertension, diabetes mellitus, and cardiovascular disease are ubiquitous in this group, risk stratifying is helpful. The pretransplant evaluation should be exhaustive (covering gastrointestinal, pulmonary, neurologic, genitourinary, and infectious disease concerns). The cardiovascular examination is the most important and possibly the most unreliable. Candidates at increased risk for coronary artery disease or cardiac dysfunction, especially those with diabetes, should undergo noninvasive cardiac stress testing. For those with reversible cardiac ischemia, coronary angiography is mandatory to elucidate the need for percutaneous coronary artery balloon dilation or even coronary artery bypass.

The problem lies in the most troublesome deficiency in noninvasive testing—that is, the suboptimal sensitivity for cardiac death and infarction. In a meta-analysis, the sensitivity of the pretransplant cardiac perfusion study for myocardial infarction was only 0.7; for cardiac death, only 0.8 [6,7]. Therefore, the onus remains on transplant physicians to have a high suspicion for life-threatening cardiovascular disease in this patient population; even uremic young adults (< 40 years old) should be heavily scrutinized, because more than 90% of them who
had renal insufficiency during childhood will have significant cardiac or carotid disease.

Even with an aggressive approach to pretransplant evaluation, cardiac complications occur in 6% of recipients during the first-month posttransplant [6]. Candidates with a history of stroke or transient ischemic attacks (TIAs) require a carotid duplex ultrasound to exclude critical carotid stenoses. Pulmonary function testing should be assessed in candidates with a history of pulmonary disease such as emphysema or asthma. Also, at least one group reported an abnormally high prevalence of pulmonary hypertension (40%) in recipients who were undergoing hemodialysis (HD) via an arteriovenous fistula [8].

Up to 10% of the HD population has antihepatitis C antibodies; therefore, all KTx candidates should be screened, and abnormal liver function test results should stimulate a more thorough evaluation [9]. Cholecystectomy should be considered for candidates with symptomatic cholelithiasis.

Gastrointestinal disease, ranging from gastritis and peptic ulcer disease to colonic diverticulosis, is more common in patients with ESRD. Liberal use of bidirectional endoscopy is justified in this population, and colonoscopy is mandatory in all candidates 50 years and older. Recurrent urinary tract infections or a history of bladder dysfunction mandates a urologic evaluation.

Candidates with a personal or family history of hypercoagulability should undergo a thrombophilia evaluation. If appropriate pretransplant evaluations are readily performed, therapeutic measures can begin in a timely manner to avoid many potential complications (some life threatening).

Perioperative Care

Pretransplant Preparation

Proper pretransplant preparation in the days before the operation is essential for optimal graft and recipient outcome. Ideally, HD-dependent patients can undergo their routine HD session the day before their KTx; appropriate electrolyte panels should be checked within hours of anesthesia induction. Dialysis catheter sites require examination for infection; for recipients on peritoneal dialysis, culture and Gram stains of their peritoneal fluid should be obtained. Each recipient should undergo a repeat history and physical examination, electrocardiogram (ECG), chest x-ray (CXR), and laboratory examination within days before their transplant, to detect any interim health derangements since their last physician visit. A medication list review is mandatory to confirm the cessation of some drugs (e.g., warfarin) and the continuation of others (e.g., beta-blockers), which may affect intraoperative and postoperative outcomes. Bowel preparation occurs at some centers the evening before the operation.

Intraoperative Care

The type of invasive monitoring during the KTx should reflect the nature and degree of the individual recipient’s comorbidities. A central venous catheter is often introduced to facilitate monitoring of central venous pressure (CVP), thereby helping to guide intraoperative and postoperative fluid management (particularly in high-risk recipients). Continuous arterial blood pressure monitoring is considered mandatory at most centers, given the high prevalence of hypertension in this population as well as the importance of optimizing the blood pressure at the time of reperfusion. The indications for pulmonary artery pressure monitoring are more controversial, but it may be justifiable for those with significant cardiac dysfunction (e.g., ejection fraction < 30%), valvular abnormalities, or known pulmonary artery hypertension. A 20-Fr 3-way Foley catheter is placed in the bladder, which is then filled with saline and antibiotic solution. Compression stockings and sequential compression devices provide deep venous thrombosis prophylaxis.

Communication between the anesthesia and surgical teams is paramount during the KTx. Adequate intravascular volume, especially at the time of reperfusion, is critical to allow the graft to function immediately. The importance of immediate graft function, with avoidance of acute tubular necrosis (ATN) and of delayed graft function (DGF), cannot be overstated: both ATN and DGF have been found to be predictive of increased patient mortality [10]. CVP should be in the range of 10 to 15 mm Hg. Systolic blood pressure, ideally, should be greater than 120 mm Hg at the time of graft reperfusion. Vasopressors (except for low-dose dopamine) should be avoided in lieu of volume expansion. Mannitol at 1 g per kg, when combined with optimal volume expansion, has been shown to decrease the incidence of ATN; it is given concurrently with furosemide at many centers [11]. After the ureteral anastomosis is completed, urine output is measured frequently, which helps guide volume resuscitation in the immediate postoperative period.

Immediate Postoperative Care

Recipients with a higher acuity of illness may require admission to the intensive care unit (ICU) for optimal monitoring; however, the vast majority can receive appropriate care on a solid-organ transplant ward. Serial complete blood counts, coagulation profiles, and chemistries should be obtained; myocardial ischemia should be excluded with serial troponin measurements in the appropriate subgroup of recipients with cardiac risk factors. CXR and ECG are obtained in the immediate postoperative period. Electrolyte abnormalities (hyperkalemia, hypokalemia, hypomagnesemia, and hypocalcemia) are common and should be corrected.

For recipients with initial graft function, fluid management consists of equivalent replacement of urine output, which is measured hourly; if cardiac dysfunction is not present, urine output can initially be replaced milliliter for milliliter. For recipients with high-output diuresis (≥500 mL per hour), 1% dextrose with 0.45% normal saline solution should be administered; potassium replacement may also be necessary, but should not exceed 0.3 mEq per kg per hour intravenously; serum potassium levels should be serially monitored. For recipients with cardiac dysfunction and high-output diuresis (≥500 mL per hour), the volume of fluid replacement should be lower than urine output (i.e., 0.5 mL of replacement for 1 mL of urine). In general, within 24 hours posttransplant, urine output in recipients with initial high-output diuresis is frequently appropriate for the recipient’s weight and kidney function; fluid replacement is then converted to a continuous rate of 100 to 150 mL per hour. If initial urine output is less than 500 mL per hour, fluid replacement in nondiabetic recipients should consist of 5% dextrose with 0.45% normal saline solution. In diabetic recipients, 0.45% normal saline solution should be used.

Most KTx recipients are cared for on a surgical ward dedicated to solid-organ transplantation. ICU monitoring may become necessary if complications develop, at any time and at any stage posttransplant. The higher susceptibility of transplant recipients to complications is related to their comorbidities, immunosuppression intensity and duration, and immediacy of graft function. Thus, deceased donor recipients, with their accompanying higher DGF rate and increased immunosuppressant load, are more prone to complications than are living related donor recipients. Deceased donor recipients are also more likely to have felt the effects of prolonged uremia and dialysis, as compared with living donor recipients.

Many risk factors directly correlate with the incidence and severity of posttransplant complications. Between 15% and 30% of high-risk transplant recipients require specific critical care.

Critical Evaluation of Dysfunctional Grafts

Early graft function is affected by numerous factors, such as the quality of the donor (i.e., living vs. deceased), cold and warm ischemia times, and the recipient’s volume status and medical stability. Urine output is the most readily apparent parameter to gauge graft function in the initial hours posttransplant, but it may be influenced by a residual effect of diuretics infused during the operation or of urine produced by the recipient’s native kidneys. A consistent, downward trend in the serum creatinine level and brisk diuresis (> 100 to 200 mL per hour) confirm that the graft is functioning well.

Monitoring the function of an initially delayed or slow functioning graft is more difficult, because urine output is minimal, and the creatinine level may remain at baseline. Doppler ultrasound plays a vital role in surveillance of the newly transplanted kidney and is the most helpful modality in evaluating a dysfunctional graft. Intensivists must be aware of the medical and surgical complications that can occur in the early posttransplant period and that can result in an abrupt change in graft function; graft salvage is only possible with an efficient, expeditious evaluation leading to rapid therapeutic maneuvers.

Medical Complications Leading to Early Graft Dysfunction

Acute Tubular Necrosis

ATN is the most common cause of impaired kidney function immediately posttransplant. Although ATN is rare in living related donor recipients, its incidence averages 35% in deceased donor recipients. It may occur immediately after revascularization or, in grafts with initial diuresis, have a more delayed presentation; dysfunction may last from several days to several weeks. In deceased donor grafts, ATN is usually secondary to prolonged ischemia times, but may also occur in recipients with negative immunologic factors, for example, a high panel-reactive antibody percentage directed against HLAs, a retransplant, and a poor HLA match between donor and recipient. Donor factors such as age, underlying disease (e.g., hypertension), and use of vasopressors (during both procurement and the transplant operation) also contribute to ATN. As stated before, ATN has a detrimental effect not only on later graft function, but also on overall graft survival and postoperative morbidity [12].

Recipients with ATN have a higher incidence of acute rejection, which ultimately lowers graft survival rates by subjecting the kidney to higher rates, and more aggressive progression, of chronic allograft nephropathy [13]. ATN must be differentiated from a vascular catastrophe (renal artery or vein thrombosis) and early acute rejection. Thrombosis should be excluded within 24 hours posttransplant with a Doppler ultrasound to confirm vascular patency. For recipients with ATN, HD frequently must be reinstituted; after a few days to several weeks, kidney function recovers in more than 95% of recipients.

Acute Rejection

A complete discussion of acute kidney graft rejection is beyond the scope of this chapter, however, acute antibody-mediated rejection may lead to a rapid decline in early graft function and is therefore relevant. Alloantibodies may form in recipients with a history of blood transfusions, pregnancies, or previous organ transplants; these antibodies can be detected by cross-matching pretransplant, which may, in fact, preclude the transplant. Fortunately, desensitization protocols are in place at many centers that may allow highly sensitized KTx candidates to proceed with a transplant. They do, however, remain at much higher risk for rejection; when these preformed antibodies target capillary endothelium, the complement system may be activated, ultimately resulting in a rapid deterioration of graft function. Only a kidney graft biopsy can confirm the diagnosis; performing the biopsy via an open approach minimizes potential bleeding complications [14,15].

Recurrence of Kidney Disease

Most acute kidney diseases rarely recur, but focal segmental glomerulosclerosis (FSGS) and hemolytic uremic syndrome (HUS) deserve special mention for their ability to cause profound, early graft dysfunction. Posttransplant nephrotic range proteinuria (i.e., > 3.5 g per day) in a recipient with known FSGS should prompt an immediate biopsy, which will likely show diffuse foot process effacement [16]. When graft dysfunction is accompanied by signs of microvascular trauma (i.e., low haptoglobin levels, elevated lactate dehydrogenase levels, and the presence of schistocytes on blood smears), HUS should be suspected. It may be recurrent or de novo: calcineurin inhibitors (CNIs) (i.e., tacrolimus, cyclosporine) have been long implicated as a causative agent [17].

Surgical Complications Leading to Early Graft Dysfunction

Hemorrhage from the venous or arterial anastomosis is rare. Most postoperative bleeding emanates from small vascular tributaries in the renal hilum or from diffuse hemorrhage in the retroperitoneal dissection field. In the confined retroperitoneal space, bleeding usually tamponades, so reexploration is seldom required. Subcapsular bleeding, albeit less common, is considerably more morbid and can lead to significant and irreversible kidney damage if not quickly recognized and controlled. Bleeding should be suspected if recipients are tachycardic, hypotensive, or oliguric, or if they require several units of blood in the early posttransplant period.

Although the incidence of vascular thrombosis is low (0.7% to 5%), it almost invariably results in graft loss [18]. Any sudden change in urine output or creatinine levels in the first several weeks posttransplant should prompt urgent Doppler sonography. The best opportunity for graft salvage occurs if the thrombosis is discovered while the patient is in the recovery room; after several hours, salvage is unlikely and nephrectomy is usually necessary.

Causative factors for renal artery thrombosis include unidentified intimal flaps, perfusion or preimplantation arterial or graft damage, size discrepancy between donor and recipient vessels, hypotension or hypoperfusion (especially in pediatric recipients with adult donors), and technical difficulties in kidneys with multiple arteries [18]. Other arterial complications include aneurysms and stenosis. Aneurysms may be anastomotic (pseudoaneurysm) or infected (mycotic). Magnetic resonance angiography can usually confirm the diagnosis without exposing the kidney to nephrotoxic contrast; conventional angiography is reserved for equivocal cases. Aneurysms require surgical repair, which can result in graft loss. For recipients with iliac or renal artery stenosis, percutaneous balloon dilation is the treatment of choice; if unsuccessful, surgical repair is necessary.

Renal vein thrombosis, a complication in 0.3% to 4.2% of KTx recipients, may be caused by kinking of the anastomosis, intimal injury during organ procurement, pressure on the vein
secondary to a fluid collection (i.e., lymphocele, urinoma, or hematoma), compartment syndrome, and extension of an iliofemoral thrombosis [19]. Renal vein thrombosis usually occurs within the first few posttransplant days and may be characterized by sudden onset of pain and graft swelling, hematuria, and, in the case of iliofemoral thrombosis, an edematous leg. The diagnosis is confirmed by Doppler ultrasound, which will show a pulsatile renal artery (with reversal of blood flow) running into the hilum of an enlarged kidney, possibly surrounded by hematoma. If thrombosis is complete, nephrectomy is necessary, although recovery of function after surgical embolectomy or thrombolytic therapy has been report. If thrombosis is incomplete, immediate thrombectomy is recommended (or, as an alternative, urokinase, and heparin treatment).

Urologic complications are rarely life threatening, but can add significant morbidity and can lead to inferior graft survival rates if not handled in a systematic manner. The incidence of urologic complications ranges from 5% to 14% in most KTx series [20].

Hematuria from the distal ureter or the cystostomy suture line generally ceases within the first 12 to 24 hours posttransplant, but it may result in clot formation in the bladder, especially in grafts with poor initial diuresis. Bladder clots or debris may lead to obstructive uropathy, which presents with a sudden cessation of urine output; obstructive uropathy is the most common cause of new-onset anuria in the immediate postoperative period and should be readily remedied with catheter irrigation. If anuria persists, emergent Doppler ultrasound will (1) confirm renal artery and vein patency and (2) rule out a large retroperitoneal hematoma causing hydronephrosis or a retroperitoneal compartment syndrome. Persistent hematuria due to a bleeding diathesis or technical error in the ureteroneocystostomy may lead to the formation of large bladder clots, which may present with suprapubic pain and “bladder spasms” or with frequent Foley catheter occlusions; if continuous bladder irrigations do not restore diuresis, manual hematoma evacuation is performed via a 20-Fr 6-eye Foley catheter. If hematuria is caused by a posttransplant biopsy, with subsequent clot formation in the renal pelvis, temporary percutaneous placement of a nephrostomy tube may be necessary. Most hematuria-related complications require close urine output monitoring, but rarely ICU admission.

Urine leaks most commonly occur at the ureteroneocystostomy anastomosis and can present in the first few postoperative days (technical error) or during the first several weeks (ureteral necrosis). Symptoms and signs of a urine leak may include graft swelling and tenderness, fever, wound drainage, oliguria, scrotal or labial edema, and ipsilateral thigh swelling. Diagnostic studies that confirm the diagnosis include nephroscintigraphy, retrograde cystography, or pelvic computed tomography (CT) scans. Perirenal fluid collections can be aspirated and sent for fluid creatinine level testing to confirm the diagnosis. Minor urine leaks may spontaneously resolve after several weeks with Foley catheter decompression. Recipients with significant leaks in the early postoperative period are best served by immediate exploration and reimplantation of the ureter. Other investigators advocate for an initial percutaneous maneuvers, namely, a percutaneous nephrostomy and stent placement for 4 to 8 weeks; success rates up to 90% have been reported in some centers with this approach [21,22].

Ureteral stenosis becomes evident months posttransplant and may be secondary to rejection, ischemia, infection, or a tight ureteroneocystostomy. Recipients usually have an elevated creatinine level and hydronephrosis (visualized on ultrasound). A percutaneous nephrostomy elucidates the location and degree of the stenosis and is typically followed by a balloon dilatation with a temporary stent tube. If balloon ureteroplasty and stenting fail, operative repair is required (but fortunately only in the vast minority of recipients). A localized distal ureteral stenosis can be repaired by reimplanting the transplanted ureter, but most stenoses require a ureteroureterostomy (to the native ureter) or an ureteropyelostomy (native ureter to the graft’s renal pelvis) because of extensive adhesions and lack of graft mobility [22].

Lymphoceles or hematomas can cause compression of the iliac veins (leading to leg edema or deep venous thrombosis) as well as compression of the ureter (leading to hydronephrosis and impaired graft function). Lymphoceles are a collection of lymph in the retroperitoneal space secondary to disruption of lymphatic vessels along the external iliac artery. The incidence can be decreased with careful ligation of the lymphatic vessels during dissection of the iliac vessels. Symptomatic lymphoceles can be diagnosed by ultrasound and treated with percutaneous drainage. Recurrent lymphoceles are approached laparoscopically [23] or, less commonly, by open laparotomy, to create a peritoneal window for decompression of the lymph leak.

Non-Renal Post-Transplant Complications

Cardiovascular Complications

The incidence of cardiac complications, the most common cause of death posttransplant [24], depends on the extent of underlying cardiac disease, on the efficacy of the preoperative cardiac evaluation, and on the function of the newly transplanted kidney. Correction of uremia by immediate posttransplant graft function improves the cardiac index, stroke volume, and ejection fraction [25]. In contrast, recipients with ATN experience persistent uremia and oliguria, which may lead to perioperative fluid overload and congestive heart failure if immediate HD is not performed to correct fluid retention and electrolyte derangements. Recipients with diabetes, hypertension, and significant coronary disease are more likely to develop cardiac complications if there is no urine output immediately posttransplant; therefore, such recipients require perioperative ICU monitoring, especially if their left ventricular function is poor (e.g., ejection fraction < 30%). Pulmonary artery catheter (PAC) placement to optimize hemodynamics might be prudent, especially in diabetic recipients with coronary artery disease.

Myocardial infarction is uncommon in the perioperative period. It is mostly seen in diabetic recipients with preexisting coronary artery disease who have complicated posttransplant courses with resultant hypotension. ICU admission, serial troponin evaluations, and close monitoring of their hemodynamic parameters are mandatory, especially when complicated by postoperative ATN. Although uncommon in the early posttransplant period, myocardial infarction is one of the major causes of death long-term in transplant recipients. In diabetic recipients, the duration of their diabetes and the presence of preexisting coronary artery disease have an impact on the incidence and severity of posttransplant myocardial infarction, which is the main cause of death in this subgroup. Data suggest that maintaining the hematocrit above 30% is prudent in diabetic recipients: doing so is associated with a 24% decrease in cardiac morbidity in the initial 6 months posttransplant [26].

The incidence of pericarditis in the early posttransplant period is 1% to 3% [27]. It has been attributed to infections (e.g., cytomegalovirus [CMV]), fluid overload, and certain medications (e.g., minoxidil). The main factor, however, is uremia. Most episodes of viral or uremic pericarditis occur during the first 8 weeks posttransplant. In contrast, the less frequent bacterial pericarditis develops later, often in recipients with advanced septic complications. Bacterial pericarditis usually requires, besides antibiotic treatment, surgical or ultrasound/CT–guided drainage. Pericardiocentesis is mandatory if cardiac failure, hypotension, or cardiac tamponade develops. Recipients with clinical symptoms of pericarditis require ICU monitoring.

Although hypertension is the most common long-term complication posttransplant, with an incidence of up to 50%, it may also require aggressive management immediately posttransplant. Overzealous perioperative hydration may lead to postoperative exacerbation of baseline hypertension. Abrupt cessation of antihypertensive medications should be avoided as well; however, most clinicians do advocate removal of angiotensin-converting enzyme (ACE) inhibitors from the perioperative regimen. CNIs, a part of virtually every immunosuppressive regimen, may also lead to hypertension, especially when they reach toxic levels. The pathophysiology of CNI-induced hypertension has not been fully elucidated, but appears to be multifactorial. CNIs directly lead to systemic vascular constriction by reducing prostacyclin and nitric oxide production while increasing serum levels of endothelin-1; this imbalance favors widespread constriction. Afferent arteriole vasoconstriction in the kidney leads to diminished glomerular filtration, which enhances sodium retention and exacerbates hypertension. Calcium-channel blockers appear to be superior at obviating the renal vasoconstriction induced by CNIs [28,29,30].

More intensive blood pressure monitoring is warranted in recipients with systolic blood pressure greater than 180 mm Hg or diastolic pressure greater than 100 mm Hg. Treatment often is simply to restart their home regimen, which is typically a combination of calcium-channel blockers, vasodilators, and diuretics. Unless a strong contraindication is noted, perioperative β-blockade is mandatory in this high-risk cohort of surgical patients in order to minimize perioperative cardiac events [31]. Consensus has not been reached on the optimal antihypertensive regimen, given that many drugs interfere with kidney function and CNI metabolism; treatment is based on each individual’s response. ICU monitoring and intravenous (IV) antihypertensive infusions (e.g., titration with sodium nitroprusside) may be required, but early posttransplant hypertension can usually be controlled with appropriate oral antihypertensive medications [32].

Hypotension, either intraoperatively or immediately posttransplant, is the single most detrimental nonimmunologic event associated with an increased incidence of graft loss or severe dysfunction. Intraoperative hypotension is usually related to volume depletion or anesthetic agents. Intravascular volume status is assessed most accurately via CVP monitoring, before unclamping, to avoid poor graft perfusion. Posttransplant hypovolemia, especially in recipients with immediate graft function, is often caused by inadequate fluid replacement and should be treated accordingly. Cardiac dysfunction and bleeding must be excluded in recipients with early posttransplant hypotension. Induction immunosuppression (e.g., Thymoglobulin) may lead to hypotension, which is readily reversed by slowing the infusion rate.

As compared with the general population, uremic recipients are more prone to deep venous thrombosis (DVT) posttransplant. The incidence of DVT ranges from 1% to 4%. DVT has been linked both to high-dose corticosteroid therapy early posttransplant and to “rebound” hypercoagulability, which is attributed to overcorrection of impaired platelet aggregation and thrombin generation (both associated with uremia). Thrombophilic events of concern within the first few weeks posttransplant include decreased fibrinolytic activity and an increase in plasminogen activation inhibitors. Other risk factors for the development of DVT are postoperative immobilization, increased blood viscosity from posttransplant erythrocytosis, cyclosporine use, and posttransplant hematoma and lymphocele formation (both of which diminish the venous return from the leg and may result in stasis and ultimately thrombosis).

In contrast, neither transient marked elevation nor moderate sustained elevation of hemoglobin levels per se seem to be directly associated with an increased incidence of thromboembolic complications; DVT rarely occurs during periods of peak hemoglobin elevation. Elevated hemoglobin levels (in combination with increased whole blood viscosity, iron deficiency, or hypertension), as well as older recipient age and diabetes, contribute to the occurrence of thrombotic events posttransplant. Aggressive therapeutic phlebotomy to maintain the hematocrit level at less than 55% has been recommended in such recipients. The diagnosis is made clinically and confirmed by Doppler ultrasound to assess the extent of DVT and the potential involvement of the kidney graft in the thrombotic event. Because the kidney is a “high-flow” organ, DVT usually stops at the level of, or distal to, the renal vein anastomosis. About two-thirds of the time, DVT occurs on the graft side.

Once the diagnosis of DVT has been established, standard therapy is systemic heparinization followed by warfarin administration for 3 to 6 months. If DVT occurs in the immediate postoperative period, when heparinization can cause major bleeding, an inferior vena cava filter is an appropriate alternative. Surgical intervention is indicated only if phlegmasia cerulea dolens develops. Venous thrombectomy (with or without creation of a temporary arteriovenous fistula) and, if necessary, fasciotomy are the treatments of choice in that rare situation [33,34,35].

Pulmonary embolism is rare (< 1%) after a KTx, yet more common than in the uremic nontransplant population. In kidney recipients, especially those who were uremic pretransplant, the coagulation system is activated and enhanced during the first-week posttransplant, which may explain the overall higher incidence of pulmonary embolism. In general, quick recovery posttransplant lowers the rate of pulmonary embolism. Pulmonary embolism as a result of DVT occurs in fewer than 1% of kidney recipients, but, if it does occur, the mortality rate is about 40%.

Pulmonary Complications

Most KTx recipients do not require ventilator support postoperatively, but prolonged support may be indicated in case of pulmonary dysfunction secondary to intraoperative fluid overload, cardiac dysfunction, or underlying lung disease.

Pulmonary edema usually is the result of overresuscitation intraoperatively and is more likely to occur in recipients who underwent inadequate pretransplant HD and/or overzealous volume infusion accompanied by a poorly functioning graft. As discussed previously, poor early graft function requires much more precise fluid management to optimize volume status for the graft, without placing the recipient at unacceptable risk for cardiopulmonary complications. Chest radiography in the recovery room to assess pulmonary status should be routine, particularly when anti-CD3 murine monoclonal antibody (OKT3) is given intraoperatively; fluid-overloaded recipients can respond to their first dose of OKT3 with flash pulmonary edema [36,37]. Fortunately, few modern immunosuppressive regimens include OKT3 for induction; its primary role is to combat acute rejection. Recurrent pulmonary edema may be an atypical manifestation of a kidney graft renal artery stenosis.

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