Surgical Complications Of Kidney Transplantation
Post-transplant surgical complications usually present in the first days to weeks following transplantation. They can be divided into three broad categories:
1 vascular complications
2 ureteric complications
3 wound complications.
Renal artery thrombosis
This is a rare (<1% of transplants) and usually catastrophic complication. Endothelial damage during brain death and retrieval surgery may predispose to thrombosis, but most are due to technical complications with the anastomosis. Patients usually present in the first week post-transplant with a rapid decline in graft function and anuria. Diagnosis may be delayed in patients with post-transplant acute tubular necrosis (ATN), where these features are not discriminatory, or who have a good urine output from their own kidneys. Doppler ultrasound demonstrates a lack of renal perfusion. The patient should be taken back to theatre immediately in an attempt to remove the clot and restore perfusion to the graft. This is rarely successful, and most commonly the graft has already infarcted necessitating transplant nephrectomy.
Renal vein thrombosis
Renal vein thrombosis is also uncommon, occurring in around 2–5% of transplants. As with arterial thrombosis, the patient presents with declining graft function and oligo-anuria in the early post-transplant period. Venous thrombosis may also cause graft swelling, pain, and macroscopic haematuria and rupture of the kidney. Treatment is by urgent thombectomy, but the prognosis is poor. A number of aetiological factors have been suggested, including damage to the vein during retrieval, poor anastomotic technique, post-operative hypotension and venous compression by haematoma or lymphocoele. Patients with a history of previous venous thromboembolism or a known thrombophilic tendency should be carefully monitored or prophylactically anticoagulated, as they are at increased risk of this complication.
Renal artery stenosis
Renal artery stenosis is far more common (∼5%) than vascular thromboses and usually presents much later, at around 3 to 6 months post transplant. The stenosis usually occurs just beyond the arterial anastomosis. Clinical features include refractory hypertension, a gradual decline in renal function or a sharp decline following the introduction of ACE inhibitors. Examination may reveal a bruit over the graft, but this is relatively non-specific. The diagnosis is confirmed by angiography and treatment is percutane- ous balloon angioplasty. Recurrence occurs in one-third of cases, requiring further angioplasty, stent insertion or even surgical intervention. Anastomotic renal artery stenosis occurs mainly in live donor transplants where no Carrel patch is present.
Urinary leaks usually present in the first days/weeks post transplant, often when the urinary catheter is removed. They mostly occur due to leakage at the site of anastomosis of donor ureter to bladder. It is either due to poor surgical technique or ureteric necrosis. The latter complication often results from over-enthusiastic stripping of the adventitial tissue from around the ureter during preparation for implantation. Patients present with discharge of fluid from the wound, which should be sent for bio-chemical analysis. Urine has a high creatinine and urea concentration (much higher than serum), whereas lymph has similar concentrations to serum. Anterograde pyelography/cystography allows identification of the leak.
Urine leaks are managed by decompressing the bladder by re-insertion of the urinary catheter. If a urinary stent is in situ, then catheterisation may be sufficient to limit the leak and allow healing to occur, although subsequent stricture formation is common. If there is no stent present, then percutaneous nephrostomy may be required as a prelude to surgical revision once the site of the leak is identified.
Ureteric obstruction may occur early post-transplant if a ureteric stent is not inserted. Causes include anastomotic strictures, luminal blood clot and extrinsic compression due to a lymphocoele. Obstruction presenting later (>3 months post transplant) is invariably due to a ureteric stricture, usually caused by ureteric ischaemia, possibly due to division of a small lower pole artery that supplied the ureter. Other causes of ureteric stenosis include infection (particularly BK virus infection) and rejection, particularly chronic rejection. Patients present with urinary leak (if obstruction occurs early) or a decline in renal function, and ultrasound demonstrates transplant hydronephrosis. Percutaneous nephrostomy is required to decompress the kidney, and allows an anterograde nephrostogram to be performed, which will delineate the site and severity of the stricture. Short strictures (<2 cm) may be dilated and stented; more significant lesions require surgical intervention, with excision of the stricture and reimplantation of the ureter, or by anastomosis of the native ureter to the transplant ureter or collecting system.
Wound infections may be limited to the skin and subcutaneous tissue or may extend deeper into the fascia and muscle layers. More superficial infections present with erythema and swelling around the wound. Ultrasound may be useful in identifying deeper collections. Such patients may also have systemic symptoms such as fever. Treatment is with systemic antibiotics and surgical drainage of any collections.
Superficial wound dehiscence may occur if there is infection or tension. Once infection is cleared, healing usually occurs spontaneously, and may be assisted by application of a vacuum dressing. Deeper dehiscence with disruption of the muscle layer is less common and requires surgical repair.
Lymphatics draining the transplant kidney, together with those surrounding the recipient’s blood vessels, are divided as part of the transplant process. Lymph may leak from these and collect, forming a lymphocoele. Lymphocoeles are common, occurring in up to 20% of transplants but are mostly small (<3 cm) and asymptomatic. Larger collections may result in swelling or persistent discharge from the wound. Occasionally, collections may compress adjacent structures such as the ureter (resulting in hydronephrosis and transplant dysfunction) or the iliac vein (resulting in leg swelling or deep vein thrombosis). Small, asymptomatic lymphocoeles are left to resolve spontaneously. Larger collections require percutaneous drainage; if they recur (which is common), then surgical drainage is required, and involves making a window in the peritoneum to allow the lymphocoele to drain into the peritoneal cavity (a ‘fenestration’ procedure).