Organ transplantation involves dissection of vascular and lymphatic channels in the targeted areas of implantation in both the recipient and the donor. This process together with the derangements resulting from antecedent pathophysiologic processes associated with end-organ failure necessitating transplantation in the first place invites a specific set of venous and lymphatic disorders that complicate the care of transplant patients in both the pre- and posttransplant phases. Although seemingly unrelated because of different anatomical locations and organ systems; these disorders are linked by the disorders of coagulation that eventually govern their occurrence. The scope of discussion in this chapter addresses only disorders that are common and vexing.

Lymphocele after Kidney Transplantation

Lymphocele is a lymphatic fluid collection in the postoperative field outside of the parietal peritoneum, which is a non-epithelized cavity. This complication has been believed to be from inadequate ligation of lymphatic vessels coursing over the recipient’s iliac vessels or lying over the hilum of the renal allograft. In the early literature, the incidence of lymphoceles, based on clinical presentation, was estimated around 2%.^1,2 As ultrasonographic surveillance has become part of routine postoperative follow-up, the incidence has been shown to be as high as 50%.³ Diagnosis of lymphocele can be made with ultrasonography and computed tomography (CT) scan to document the size, location, and compression of adjacent structures.⁴

Meticulous ligation of overlying lymphatics during mobilization of iliac vessels is crucial for prevention of lymphocele.⁵ Increased incidence of lymphocele seems to be associated with recipient obesity and use of mammalian target of rapamycin (mTOR) inhibitors as part of the immunosuppression regimen.^6,7

Although most lymphoceles are asymptomatic, some of them become clinically significant because of pressure on adjacent structures, including the ureter, iliac vein, or lower extremity lymphatics. In severe cases, the patient may develop hydronephrosis and resultant azotemia, urinary frequency, a protruding mass, or ipsilateral leg edema. Less frequent presentations are deep venous thrombosis (DVT) caused by compression of iliac vein and infected lymphocutaneous fistula through the incision.^8,9,10,11 Larger collections may become clinically evident at 2 weeks to 6 months after transplantation (peak incidence, 6 weeks).

Small and asymptomatic lymphoceles may resolve without treatment.¹² Unnecessary intervention may lead to infective complications. Although simple image-guided aspiration may be curative, prolonged drainage through a percutaneous catheter often becomes necessary.¹³ Use of sclerosing agents such as tetracycline or povidone–iodine has been advocated by some authors.¹⁴ The major drawback of both prolonged percutaneous drainage and injection of sclerosing agents is an increased risk of infectious complications. After a failure of percutaneous drainage, the most preferred approach is surgical drainage of lymphocele into the peritoneal cavity by fenestration of lymphocele through a transperitoneal approach to drain lymphatic fluid into the peritoneal cavity, where it will be reabsorbed by the peritoneum.^15,16 This procedure can be done either laparoscopically or through a lower midline incision.^17,18 A preoperative CT scan is necessary to localize adjacent structures, including the ureter and iliac vessels. An indwelling catheter is mandatory during the procedure to decompress the bladder, and the procedure should be done when the cavity of lymphocele is full (i.e., not immediately after drainage) to facilitate drainage and prevent complications.

Deep Venous Thrombosis after Kidney Transplantation

In the early literature of kidney transplantation without the use of DVT prophylaxis, the incidence of DVT was reported to be 8.3%. The peak incidence was at 4 months after surgery and was often associated with another event necessitating bedrest or a lymphocele.^19,20 Renal transplant patients are at a low risk for DVT in the early posttransplant phase because of the protective effect of platelet dysfunction resulting from pretransplant uremia. However, after achieving stable renal allograft function, the recipients are at the same risk of thromboembolic complication as individuals without uremia. In cases of DVT, proximal extension of thrombus above the anastomosis between the allograft and iliac vein is rare, probably because of increased blood flow from drainage of allograft renal vein into the iliac vein from the allograft. It is nevertheless possible and associated with a poor outcome.²¹ The universal use of DVT prophylaxis with intermittent pneumatic compression devices on the lower extremities during and after renal transplantation seems to be beneficial. Subcutaneous heparin should be added for prophylaxis, especially for obese patients or patients who are not on dialysis before preemptive transplantation.²²

Portal Vein Thrombosis

The presence of portal vein thrombosis (PVT) in a patient was once considered to be a contraindication to liver transplantation because of the higher degree of technical difficulty of the transplantation and its resultant higher mortality rate.²³

As more experience has been accumulated with better surgical technique and preoperative imaging, liver transplantation in patients with PVT has become amenable in most cases. Although the results have significantly improved, these patients with PVT are still considered at “high risk.”²⁴ Surgical techniques used for transplantation of patients with PVT include balloon thrombectomy of the portal vein, thrombovenectomy up to splenomesenteric confluence, venous conduit from the superior mesenteric vein (SMV), an alternate source of portal inflow such as the inferior vena cava (IVC), or varices. In extreme cases with intractable gastrointestinal (GI) bleeding from diffuse mesenteric venous thrombosis secondary to hypercoagulable disorder resulted from the liver, simultaneous replacement of liver and GI tract by way of multivisceral transplantation has been performed.²⁵

Preoperative knowledge of extent of PVT can greatly facilitate better operative strategy, selection of appropriate deceased donor organ, and obtaining additional venous conduit during organ recovery. The anesthesia team and the blood bank must communicate preoperatively regarding the possibility of more blood loss than usual and the resultant requirement of more blood products. Therefore, a detailed assessment of the anatomical extent of PVT must be made as a part of the liver transplantation evaluation. All liver transplant candidates require color Doppler ultrasonography as a part of preoperative evaluations.^26,27 In any suspected case of PVT, further imaging with dynamic triphasic contrast CT scan or magnetic resonance angiography must be obtained both for confirmation and assessment of anatomical extent of PVT.^28,29 With the use of multidetector row CT scan with three-dimensional vascular reconstruction capability, triphasic dynamic contrast CT scan can be equally accurate to assess vascular anatomy.³⁰ The choice between these two modalities depends on local expertise and possible limitation to use iodinated intravenous (IV) contrast for CT scans in patients with renal insufficiency.

In the case of a partial PVT with a non-obstructing thrombus, preemptive placement of a transjugular intrahepatic portosystemic shunt (TIPS) can be helpful to prevent progression of PVT through maintaining blood flow through the portal vein.³¹ Spontaneous portosystemic collaterals such as a recanalized umbilical vein could be protecting the portal vein from progression of PVT.³² However, large spontaneous splenorenal shunts seem to be associated with diminished portal venous flow and a resultant risk of PVT.³³

The anatomical extent of PVT can be confirmed during operative dissection proximally with palpating a “soft part” of the portal vein. After obtaining proximal and distal control of portal flow, restoration of portal venous flow can be performed. Balloon thrombectomy through a transverse incision on the portal vein can be done in a case with fresh thrombus in a short segment of the portal vein. If there is any organized thrombus, thrombovenectomy must be performed. After securing corners of the portal vein with atraumatic clamps or stay sutures, the thrombus can be separated off the venous wall using an endarterectomy spatula. While grabbing the thrombus with tonsil clamps, the venous wall can be gently everted as more room is created between the wall and the thrombus (Figure 38-1). Then the thrombus can be gently pulled off the lumen. After removal of thrombus, the distal edge of the thrombus should look feathery, and a brisk bleeding from the lumen is observed. Sometimes probing of the lumen with Pean clamps or the surgeon’s little finger may be necessary for confirmation of wide lumen after thrombectomy.

With more successful application of thrombovenectomy, the necessity of using a venous conduit from the SMV seems to be decreasing in recently published series.³⁴ In cases of diffuse thrombosis of portal vein beyond splenomesenteric confluence, preoperative planning in advance can save significant operating time and blood loss with avoidance of futile attempts of thrombovenectomy to restore portal flow. In this case, alternate strategies to obtain portal inflow should be considered. When a venous graft is found to be necessary, a portion of SMV must be exposed below transverse mesocolon and lateral to the small mesenteric artery (SMA) in the root of mesentery. A segment of SMV 3 to 4 cm long should be dissected where the vessels feels patent and soft. Then the anastomosis between the venous conduit and SMV can be performed in end-to-side fashion. Correct orientation and sharp beveling of the proximal end of the venous conduit are extremely important to avoid angulation or kinking of the graft.³⁵ In very rare occasions with complete cavernous transformation of the recipient’s portal vein that is not amenable for thrombovenectomy, there could be large enough coronary vein or other collaterals for alternate source of portal inflow for the hepatic allograft.³⁶ Because of the extremely thin wall of these collaterals, great deal of caution should be used in dissecting and suturing them. An alternative approach to complete thrombosis beyond splenomesenteric confluence has been cavoportal hemitransposition. The inflow to the allograft portal vein comes through either end-to-end or side-to-end anastomosis between the recipient portal vein and the donor IVC.³⁷ There are a few limitations to this approach. Persistent portal hypertension after transplantation carries a significant risk of variceal bleeding and has been treated with gastric devascularization, splenectomy, or endoscopic variceal ligation. Persistent ascites and lower extremity edema can be potential problems.^38,39

Although initially the reported outcome of transplantation for patients with PVT was worse than for ordinary transplant patients, some recent large series have reported comparable survival of these patients.^34,40 Many reports have shown increased morbidity and transfusion requirements after transplantation for these patients. The outcome after portocaval hemitransposition seems definitely worse because of persistent portal hypertension. As the last resort for intractable episodes of GI bleeding from varices with diffusely thrombosed mesenteric vein as a result of liver-originated hypercoagulable disorder such as protein C deficiency, en bloc transplantation of the stomach, pancreas, intestine, and liver could be performed.