The patient was a 31-year-old woman with a 15-year history of erythema on the cheek, swelling and pain of both knees, and abdominal distension. She had a history of idiopathic thrombocytopenia verified in December 1997. The patient had been maintained on prednisone 10 mg qd. In late March 2021, the patient suddenly stopped defecating, and this was accompanied by abdominal distension, intermittent nausea and retching. An indwelling gastric tube was placed in another hospital and the patient was treated with daily enemas. Gastric tube drainage was 300–400 ml per day. In mid-April, she was prescribed methylprednisolone 500 mg × 3 d shock treatment in addition to cyclophosphamide 0.2 g iv qod. The abdominal distension was relieved, but there was still no bowel movement. Finally, the patient came to our hospital on May 6 because of paroxysmal colic in the lower abdomen.
On admission, findings from physical examination were as follows: body temperature was 36.6 °C, pulse was 84/min, respiratory rate was 18/min, and blood pressure was 127/101 mmHg. The patient entered the room in a wheelchair with a gastric tube and a right subclavian central venous catheter. The patient's abdomen was extremely distended, with tenderness in the left lower quadrant (Fig. 1) but no rebound tenderness. The bowel sounds were very weak and hardly audible. Liver and spleen were not palpable in the subcostal and subxiphoid regions.
Blood tests showed positive antinuclear antibody (1:160); anti-dsDNA antibody, (−); antiRNP, (−); anti-Sm, (−); anti-SSA, (−); anti-SSB, (−); anti-ribosomal P, (−); anti-cardiolipin antibody, (−); and lupus anticoagulant, 1.2. In immunoserological testing, CRP was 33.08 mg/l; C3, 0.538 g/l; and C4, 0.408 g/l. Biochemical testing showed serum albumin was 27 g/l; ALT 40 U/L; TBil 10.7 μmol/L; DBil 6.6umol/L; Gamma-glutamyltransferase (GGT) 433 U/L; K, 3.4 mmol/L; Na, 137 mmol/L; Ca, 2.07 mmol/L, Fe 14 μg/dL; Cr 67 μmol/L; and Urea 6.13 mmol/L. Coombs test was positive, and total urine protein was 1.64 g/24 h.
A contrast-enhanced computed tomography (CT) scan (Fig. 2) on May 28 showed general dilated small and large bowel; dilated intrahepatic and extrahepatic bile ducts and dilated pancreatic ducts; significant enlargement of the gallbladder; bilateral dilatation of the renal pelvis, calyces and ureter; and localized stenosis of the sigmoid colon with dilatation of the upper intestinal canal with fluid flattening. Colonoscopy (Fig. 3) revealed a stenotic segment located 17–20 cm from the anus, with smooth local mucosa and extremely dilated anterior bowel. The pathological results of sigmoid stenosis also showed chronic mucosal inflammation.
Four days later, a catheter was inserted through the patient's anus to relieve intestinal obstruction, but the abdominal distension did not decrease and was accompanied by abdominal pain and dyspnoea. After several multidisciplinary discussions, we performed a transverse colostomy for this patient. We aspirated approximately 3000 ml of stool contents during the operation. After the operation, the patient's abdomen flattened, and abdominal distension improved significantly (Fig. 1). CT (Fig. 4) on June 7 showed that the patient's bowel dilatation had improved significantly. Gradually, voluntary bowel movements returned and the patient started enteral nutrition. In this case, early vigorous surgical intervention reversed her deteriorating condition and thus yielded a good outcome. A half year later, we performed a follow-up examination of her symptoms of abdominal distention, and we found that her symptoms did not recur. However, this patient strongly refused any further radical surgery. The histopathology of sigmoid stenosis is still unclear.