Bryant’s sign as a manifestation of a retroperitoneal paraduodenal bleed and subsequent small bowel obstruction

Background

The ‘blue scrotum sign of Bryant’, now commonly known as Bryant’s sign, is the phenomenon of penile or scrotal ecchymosis associated with a retroperitoneal bleed or ruptured aortic aneurysm. It was first described by Bryant in 1903 on analysing postmortem reports of patients with abdominal aneurysms.1

Bryant’s sign has been noted to have several clinical variations. It may be continuous or patchy, unilateral or bilateral and may also extend down the legs.2 Variations have also been reported with timing, occurring as soon as hours, days or even weeks after the retroperitoneal bleed.3 4

Case presentation

A previously well man in his 60s presented to the emergency department of our tertiary institution with 4 days of atraumatic scrotal tenderness, bruising and swelling. This was on a background of 1 week of lower abdominal pain, nausea and general malaise. On examination, his observations were stable and within normal limits (respiratory rate 16, oxygen saturation>95% on room air, pulse rate 70 and blood pressure 140/80 mm Hg, afebrile). His abdomen was soft with mild lower abdominal pain and no peritonism. Genitourinary examination revealed Bryant’s sign (figure 1) and blood 1+ on urinalysis. He was initially diagnosed with epididymitis or a haematocele and was discharged on trimethoprim with outpatient follow-up imaging.

He re-presented 3 days later with upper abdominal pain and further history taking revealed intermittent non-steroidal anti-inflammatory drug (NSAID) use for back pain over the past 2 months. Outpatient genitourinary ultrasound had been unremarkable and his observations remained within normal limits. A portal-venous phase abdominal CT scan showed a heterogenous collection around the third part of the duodenum (D3). This appearance was initially thought to be most consistent with either a contained duodenal perforation or inflammatory peripancreatic collection given some associated minor pancreatic head fat stranding. The uncinate process of the pancreas indented the superior aspect of the collection, however no focal pancreatic abnormality was identified and there was no evidence to suggest chronic pancreatitis. Biochemistry was unremarkable. The patient was admitted under general surgery and managed with clear fluids orally, antibiotics and a proton pump inhibitor. He improved clinically and was discharged 1 day later with a plan for outpatient endoscopy and interval CT scan.

Unfortunately, he re-presented within 24 hours of discharge as he was unable to tolerate oral diet with profuse vomiting. Once again, his observations remained within normal limits and his abdominal examination showed only mild upper abdominal pain without peritonism.

Investigations

Blood results showed a haemoglobin of 114 (115–160 g/L), platelets 266 (150–400×10⁹/L) and international normalised ratio 0.8 (0.9–1.3). The white cell count was 5 (4.00–11.00×10⁹/L) with a C reactive protein of 34 (<5.0 mg/L). Renal function and liver function tests were within normal limits and the lipase was 62 (<60 U/L).

A triphasic CT angiography (CTA) of the abdomen (figure 2) reported the known retroperitoneal collection was causing extrinsic compression on D3 causing mechanical duodenal obstruction. All previous radiology were re-reviewed with a senior radiologist and the final diagnosis of a contained rupture of a microaneurysm of the pancreaticoduodenal arterial arcade and associated presence of a low-grade coeliac artery stenosis (Sutton-Kadir syndrome) was made. Mild calcification of the posterior intima of the abdominal aorta was also noted. Subsequent endoscopy showed extraluminal compression from the second part of the duodenum to the duodenojejunal flexure.

Differential diagnosis

This case highlights a broad, evolving differential diagnosis. The initial diagnosis of epididymitis or a haematocele was not well supported by the history, urinalysis or blood investigations. Median arcuate ligament syndrome can compress the origin of the coeliac artery, however the history and imaging features did not support this diagnosis. Subsequent CT scan of the abdomen raised the suspicion for a diagnosis of pancreatitis with an acute inflammatory collection or a duodenal perforation. Pancreatitis is a potential unifying diagnosis explaining the acute pancreatic collection, aneurysm and obstruction. Although an atypical indolent history, in keeping with diagnostic criteria this was supported by symptoms and imaging. An underlying peripancreatic malignancy also required consideration.

Treatment

The patient remained haemodynamically stable in hospital with ongoing gastric decompression, nasojejunal feeding and close observation for refeeding syndrome. Given the possibility of an underlying malignancy, ongoing assessment with serial imaging and clinical review was performed. Repeat CT scan showed interval reduction in the retroperitoneal haematoma size with craniocaudal dimensions of 43 mm decreasing to 19 mm over 2 weeks. There was no evidence of ongoing bleeding and a barium swallow showed interval resolution of duodenal obstruction.

Given the rarity of this presentation, an upper gastrointestinal multidisciplinary discussion was requested in order to provide optimal patient care. There was consensus among the upper gastrointestinal surgical consultants and radiologists regarding the high likelihood of an underlying pancreaticoduodenal arterial arcade microaneurysm, which decreased in size in keeping with known resorption rates and guiding the subsequent supportive treatment.

Outcome and follow-up

The duodenal obstruction resolved over 4 weeks and at 6 weeks post admission, the patient was back at his baseline and tolerating a normal diet. Reassuringly, MRI of the pancreas and serial abdominal CT scans did not demonstrate underlying malignancy. For completeness, an endoscopic ultrasound was performed which showed no abnormalities.