7. A 43-year-old with acute severe epigastric pain after alcohol intake and ibuprofen

a. Diagnosis [1]

b. Investigations [3]

1. Baseline and resuscitation investigations
   • CBC: Hb, WBC count
   • Blood group, cross-match
   • Serum electrolytes, urea, creatinine, blood glucose
   • Liver function tests
   • Coagulation profile
   • ABG/VBG with serum lactate
   • Serum amylase/lipase to differentiate acute pancreatitis
   • Blood culture if febrile/septic
2. Imaging
   • Erect chest X-ray: free gas under diaphragm, especially right side.
   • Erect abdominal X-ray may show pneumoperitoneum.
   • Contrast-enhanced CT abdomen: most sensitive investigation, showing free intraperitoneal air, fluid, site of perforation, and excluding pancreatitis or other pathology.
   • If diagnosis remains uncertain and the patient is stable: water-soluble oral contrast study may show contrast leak.
3. Later
   • Test for H. pylori after stabilization, using stool antigen test or urea breath test.
   • Upper GI endoscopy after recovery, particularly if a gastric ulcer is suspected, to exclude malignancy.

c. Emergency management [3]

• Admit, call surgical team, assess with ABCDE.
• Keep patient nil by mouth.
• Give high-flow oxygen if needed; monitor pulse, BP, SpO₂, respiratory rate, temperature, and urine output.
• Insert two large-bore IV cannulae.
• Send blood tests and cross-match.
• Rapid IV crystalloid resuscitation, such as Ringer's lactate. Correct electrolyte abnormalities and acid-base disturbance.
• Insert nasogastric tube for gastric decompression and aspiration.
• Insert urinary catheter and target urine output at least 0.5 mL/kg/hour.
• Give titrated IV opioid analgesia and antiemetic.
• Start IV proton-pump inhibitor, for example pantoprazole.
• Start broad-spectrum IV antibiotics covering gram-negative and anaerobic organisms, for example ceftriaxone plus metronidazole, or piperacillin-tazobactam.
• Give DVT prophylaxis when appropriate.
• Obtain informed consent and arrange urgent operative source control.

d. Definitive management [3]

1. Operation
   • Laparoscopic repair in a stable patient where expertise is available.
   • Open upper midline laparotomy if unstable, delayed presentation, severe peritonitis, or laparoscopy is unavailable.
   • Peritoneal lavage and suction of food debris/pus.
   • Identify perforation.
   • For a small duodenal perforation: primary closure with interrupted sutures plus Graham omental patch.
   • Take biopsy from the edge of a gastric ulcer perforation to rule out malignancy. Large, suspicious, or non-closable gastric ulcers may require wedge excision or distal gastrectomy in selected patients.
2. Non-operative management
   • Not routine.
   • May be considered only in a carefully selected stable patient with a proven sealed perforation on water-soluble contrast study, no generalized peritonitis/sepsis, and close surgical observation available. WSES guidance advises against routine conservative treatment.
3. Postoperative and ulcer-directed treatment
   • Continue PPI.
   • Test and eradicate H. pylori if positive, then confirm eradication.
   • Stop ibuprofen and avoid all NSAIDs if possible. If unavoidable, use the lowest-risk option with PPI protection.
   • Stop smoking and reduce/avoid alcohol.
   • Follow-up endoscopy for gastric ulcer to confirm healing and exclude cancer.

Question 7

a. Diagnosis [1]

b. Investigations [3]

• CBC, blood group and cross-match
• Urea, electrolytes, creatinine, blood sugar
• Liver function tests and coagulation profile
• Serum amylase/lipase to exclude acute pancreatitis
• ABG/VBG and serum lactate in shocked or septic patient

• Erect chest X-ray: free gas under diaphragm.
• Erect abdominal X-ray: may show pneumoperitoneum.
• CECT abdomen: most accurate to identify free intraperitoneal air, site of perforation, fluid collection, and alternative diagnoses.
• Water-soluble contrast study if diagnosis remains uncertain and the patient is stable.

c. Management in emergency [3]

• Admit, urgent surgical referral, ABC assessment.
• Keep nil orally.
• Oxygen, continuous monitoring of pulse, BP, SpO₂, and temperature.
• Two large-bore IV cannulae; send blood and arrange cross-match.
• IV crystalloid resuscitation, correct electrolytes and acidosis.
• Insert NG tube for aspiration and gastric decompression.
• Insert Foley catheter and monitor urine output, target at least 0.5 mL/kg/hour.
• IV opioid analgesia and antiemetic.
• IV PPI, for example pantoprazole.
• Broad-spectrum IV antibiotics covering gram-negative and anaerobic organisms, such as ceftriaxone plus metronidazole or piperacillin-tazobactam.
• Prepare for urgent operative intervention.

d. Definitive management [3]

• Laparoscopic repair if haemodynamically stable and expertise is available.
• Open upper midline laparotomy if unstable, delayed presentation, severe contamination, or laparoscopic facilities are unavailable.
• Peritoneal lavage and removal of fluid/food debris.
• For a small duodenal perforation: primary closure with interrupted sutures and a Graham omental patch.
• For gastric ulcer perforation: take an edge biopsy to exclude malignancy; perform patch repair or gastric resection if the ulcer is large or suspicious.

• Continue PPI.
• Test for and eradicate H. pylori.
• Avoid NSAIDs such as ibuprofen, stop smoking, and avoid alcohol.
• Follow-up endoscopy is required for gastric ulcers to document healing and exclude cancer.

Question 6

• Significant weight loss
• Polyuria (increased frequency of urine)
• Polydipsia/dry mouth indicating severe dehydration
• Altered sensorium with reduced urine output indicating severe dehydration, acidosis, and possible shock

• Random blood glucose
• Urine or blood ketones, preferably blood beta-hydroxybutyrate
• Venous blood gas: metabolic acidosis, pH < 7.3 and bicarbonate < 18 mmol/L
• Serum electrolytes, urea, creatinine, and anion gap

• Weight loss + increased frequency of urination + dry mouth strongly suggest hyperglycaemia causing osmotic diuresis, which is classic for diabetes/DKA.
• Reduced urine output and altered sensorium can occur later in DKA because of profound dehydration, shock, and acidosis.
• The question mentions alcohol use, which can mislead toward liver disease, but alcohol use alone does not establish cirrhosis.

• Jaundice, ascites, pedal edema
• Spider nevi, palmar erythema, hepatosplenomegaly
• GI bleeding, infection, constipation, or other precipitant for encephalopathy
• Asterixis, fetor hepaticus
• Raised bilirubin/INR, low albumin
• Renal failure occurring in advanced cirrhosis with ascites, after excluding dehydration, sepsis, nephrotoxic drugs, etc.

Diabetic ketoacidosis due to newly diagnosed diabetes mellitus, with severe dehydration and altered sensorium.