Summary: Gastroparesis is a syndrome characterized by delayed gastric emptying in the absence of mechanical obstruction. The most common underlying aetiology is diabetes mellitus; however, many cases are idiopathic. Pregnancy per se is associated with gastrointestinal neuromuscular dysfunction; however, reports of gastroparesis arising during pregnancy are rare. We report a case of severe gastroparesis and proximal small bowel paresis presenting during pregnancy.Keywords: gastroenterology, high-risk pregnancy
CASE REPORTA 24-year-old primigravida, at 10 weeks gestation, presented with nausea, vomiting, colicky right lower quadrant pain and an elevated white cell count. There was no history of fevers. She underwent uncomplicated laparoscopic appendicectomy; however, she was found to have congenital malrotation of the bowel, and the appendix, located in the right upper quadrant, was normal on histology. No cause of the right lower quadrant pain was identified.Post appendicectomy, the patient had ongoing symptoms and developed intractable large volume vomitus, initially containing 'old' food, and absence of bowel motions with minimal flatus. Two weeks later the patient presented to the emergency department with ongoing symptoms and 7 kg weight loss (8.1% of initial body weight, body mass index 31.6). The vital signs showed a blood pressure of 110/70 ( postural drop of 20 mmHg in systolic blood pressure), heart rate 96 beats per minute and temperature 37.18C. On examination the patient appeared unwell with clinical signs of dehydration and right lower quadrant abdominal tenderness with abdominal distension. There were no clinical features consistent with an autonomic or peripheral neuropathy. Laboratory tests were notable for the presence of a marked electrolyte disturbance, acute renal impairment with an elevated urea/ creatinine ratio (in keeping with dehydration) and deranged liver function tests (Table 1). The lipase and lactate were normal.The patient was prescribed antiemetic medication (metoclopramide, prochlorperazine and ondansetron), vitamin supplementation (thiamine and multivitamin), intravenous fluid therapy and kept nil by mouth. With hydration there was resolution of the postural drop, normalization of the renal and electrolyte disturbances, and improvement of the liver function tests. There was little change in symptomatology.An abdominal ultrasound showed a normal gallbladder, pancreas, spleen, kidneys and ureters with diffuse fatty infiltration of the liver (likely secondary to rapid weight loss). On day 8, an upper endoscopy performed showed a dilated stomach with a large amount of fluid residue. No focal abnormality was detected. The first and second parts of the duodenum were grossly dilated with an apparent transition point between segments D2 and D3 with no mucosal abnormality visualized. The distal D3 segment appeared normal. Gastric mucosal biopsy was normal. A diagnostic laparoscopy on day 9 revealed a dilated stomach with inflammatory adhesions at the duodenum, thought to be a point of obs...