Abstract Urinary tract obstruction is a common problem associated with many complications. Decompression of an enlarged bladder has been associated with several complications, mainly vesicular bleeding. We report a case of a 42-year-old male patient who developed bilateral renal subcapsular hematomas secondary to relief of an extremely enlarged bladder.
Urinary tract obstruction (UTO) is a relatively common problem. Obstruction of urinary flow might be acute or chronic, unilateral or bilateral, and might occur at any site in the urinary tract. Urinary tract obstruction is associated with many complications related to the obstructed kidney or to the decompression of an enlarged bladder.1 In this report we will describe for the first time an unusual complication of decompression of an extremely enlarged bladder and hydronephrotic kidneys, namely bilateral subcapsular hematoma. Other causes for this complication will also be discussed briefly.
A 42-year-old man presented with back pain. A magnetic resonance imaging scan (MRI scan) showed an enhancing lesion in the spinal cord at the level of L3-L4; the patient was prescribed a course of steroids to treat this problem. Blood pressure and renal function were normal. The patient's pain did not improve and a repeat MRI showed only modest resolution of the spinal lesion. Past medical and surgical histories were negative. The patient had a negative physical exam except for mild lumbar spine tenderness.
The patient then defaulted on follow up. He re-presented some 9 months later with a 1-month history of paraparesis, an increase in abdominal girth and a decrease in urine output. He reported that only with pressure over his suprapubic area was he able to urinate.
On physical examination the patient was now hypertensive (blood pressure was 180/90 mmHg). There was severe abdominal distention with dullness on percussion over the suprapubic area extending to the level of the umbilicus. There was also severe bilateral lower extremity pitting edema. Neurological examination showed neurological deficit in the lower extremities consistent with an upper motor neuron lesion.
Investigation showed renal failure (plasma creatinine, 6.7 mg/dL). A computerized tomography scan (CT scan) of the abdomen showed a hugely distended urinary bladder, with bilateral hydroureters and hydronephrosis (Fig. 1). A Foley catheter was inserted and the patient drained 14 L of bloody urine over 3 days. As a result, the plasma creatinine normalized, but the hemoglobin concentration fell sharply over 3 days from 11.5 g/dL to 8.6 g/dL, and the patient remained mildly hypertensive. A repeat CT scan of the abdomen, carried out after 3 days, showed a large right subcapsular renal collection with signal intensity and appearance of a right renal subcapsular hematoma measuring 13.6 × 8 × 4.5 cm and a smaller left subcapsular hematoma. There was significant resolution of the bilateral hydronephrosis (Fig. 2). The patient was diagnosed with Toxocara induced myelitis, which was causing his paraparesis, and was started on albendazole PO.
Urinary tract obstruction can affect people of all ages. In childhood it is mainly secondary to anatomical abnormalities (e.g. urethral valves). In adults, calculi, tumors and prostatic enlargement are the typical causes.1 Urinary tract obstruction in its early stages can be asymptomatic, but when more severe it is often complicated by renal insufficiency, hypertension and pain.2
Management of an obstructed urinary tract involves imaging, to detect the level and nature of the obstruction, and decompression (e.g. urinary catheterization, percutaneous nephrostomy). These interventions have well-documented complications (e.g. gross hematuria and reflex hypotension after decompression of an enlarged bladder).3 However, to the best of our knowledge, no one has previously documented bilateral subcapsular hematoma as a complication of the relief of UTO by bladder catheterization.
The fact that the subcapsular hematoma was bilateral in our patient, who initially had severe bilateral hydronephrosis, alerted us to the possibility that his condition might have been caused by a mechanism similar to that which causes gross vesicle hematuria after urinary catheterization. In the bladder, the sudden expansion and rupture of attenuated, compressed, submucosal bladder wall veins is the cause of bleeding.4 We postulate that the same mechanical forces can apply to the kidneys, although in this case the compressed veins are in the capsule.
Documented causes of subcapsular hematoma are diverse. The most common cause is idiopathic. However, acceptance of a spontaneous bleed can only occur after a rigorous search for an underlying cause, such as underlying renal pathology or a systemic disease. These secondary causes are listed in Table 1.5–9
Table 1. Differential diagnosis of renal subcapsular hematomas
Causes of renal subcapsular hematoma
Renal cancer (angiomyolipoma, adenocarcinoma, hypernephroma)
Extra corporeal shock wave lithotripsy
Internal ureteral catheterization
Lumbar plexus block
Paravertebral injection of local anesthetics
Subcapsular hematomas can present with severe flank pain that mimic renal colic, or they can be painless. If the hematoma is large enough to compress the kidney, the renin-angiotensin system can be activated and hypertension can ensue. This situation is known as Page kidney.10
The two most common diagnostic imaging modalities are ultrasound and CT scanning. These techniques have the advantage of being able to detect underlying kidney pathology (e.g. tumors, aneurysms). Renal angiography, MRI, and plain films can also be used with variable degrees of success.
Treatment of subcapsular hematoma is controversial and depends on many factors. Nephrectomy is indicated in cases of hypernephroma. If malignancy is ruled out, the options are either an expectant policy (spontaneous resolution of hematoma has been reported after 1.5 years of injury), or an active interventional policy, with options of operative liberation, or laparoscopic removal of hematoma. Longstanding hematoma can organize into fibrous pseudocapsules, or can cause irreversible renal parenchymal damage.10
In our case, because the patient had stable controlled blood pressure and stable creatinine levels after 3 months follow up, a conservative approach was selected as the most appropriate treatment.