An atypical case of large bowel obstruction
A 63-year-old woman self-presented to the emergency department with a week's history of worsening abdominal pain, distension, faeculent vomiting and two days of absolute constipation. She denied any urinary symptoms or previous urinary tract infections. There were no red flag symptoms for colonic malignancy.\nExamination revealed a soft distended abdomen, which was generally tender but more so in the left upper quadrant, with no palpable masses. Obstructive tinkling bowel sounds were heard on auscultation. Rectal examination and other system examinations were unremarkable.\nRoutine bloods were all within normal parameters, including white cells of 8.9, except for a marginally raised CRP of 28. Urinalysis on admission had a trace of protein and one plus of blood. Urine culture revealed no growth.\nAbdominal X-ray confirmed large bowel obstruction with a cut-off point in the proximal descending colon. A large staghorn calculus was evident in the left kidney with a second smaller well-defined area of calcification just lateral to the renal parenchyma. (Fig. )\nConservative management of bowel obstruction was initiated, a nasogastric tube was inserted and the patient was made nil by mouth while intravenous fluids were started.\nA subsequent CT scan confirmed the presence of xanthogranulomatous pyelonephritis and established that the second area of calcification was a 1.5 × 1.0 × 2.5 cm perforated extra-renal fragment of calculus positioned adjacent to the proximal descending colon.\nThis stimulated a diffuse inflammatory response in the left upper quadrant, resulting in a prominent thick-walled proximal descending colon with an abrupt calibre change in the mid descending colon, mesenteric fat stranding, a thickened ileo-psoas muscle with fragments of calculi in the left iliac fossa, gross lymphadenopathy and inflammatory changes around the spleen. (Fig. )\nThe patient's symptoms did not settle with conservative management, and as a result, she underwent an emergency left hemi-colectomy, left nephrectomy and extraction of the fragmented calculi. Recovery was uneventful. Histology confirmed an inflammatory stricture with hypertrophy and fibrosis but no malignancy. Stone analysis interestingly showed a struvite stone. Kidney histology revealed end-stage kidney disease with nephrosclerosis and chronic pyelonephritis. The parenchyma had been replaced with extensive fibro-fatty tissue and chronic inflammatory cell infiltrate with small areas of calcification. It contained thick-walled blood vessels and a few atrophic completely hyalinized renal glomeruli and various-size tubules with cast-like esosinophilic amorphous material. Many non-caseating granulomas were present in the hilar area with most containing a central calcification.