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.
Vascular 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.
Ureteric complications
Urine leak
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
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 complications
Wound infection
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.
Wound dehiscence
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.
Lymphocoele
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).
