Chronic Mesenteric Ischaemia

Chronic mesenteric ischaemia is insufficient intestinal blood flow during increased metabolic demand, most commonly caused by atherosclerotic stenosis of the superior mesenteric and coeliac arteries.

Extensive collateral circulation means symptoms usually develop only when perfusion reserve becomes significantly impaired. Symptomatic disease is important because continued weight loss and malnutrition are common and plaque thrombosis can cause acute on chronic mesenteric ischaemia.

A symptomatic isolated stenosis of approximately 70% or more may be clinically relevant. In multivessel disease, a superior mesenteric artery stenosis of approximately 50% or more may be clinically significant when symptoms are convincing.

The typical syndrome is postprandial epigastric or central abdominal pain beginning after food intake and lasting from tens of minutes to several hours.

Progressive food avoidance produces weight loss. Weight loss greater than 5% with typical postprandial symptoms should increase suspicion substantially. Diarrhoea, nausea and early satiety may accompany the syndrome.

The classical triad of postprandial pain, weight loss and abdominal bruit has poor sensitivity. Its absence does not exclude disease.

Sudden intensification of chronic symptoms, continuous pain or development of tenderness should trigger immediate assessment for acute thrombosis.

CT angiography: first line anatomical investigation; defines coeliac and superior mesenteric artery disease and guides revascularisation planning. Contrast enhanced MR angiography is appropriate when CT contrast cannot be used.

Duplex ultrasound can screen for proximal arterial stenosis in experienced centres but a positive result requires definitive cross sectional vascular imaging.

Chronic mesenteric ischaemia should not be diagnosed from an incidental stenosis alone. Correlate arterial disease with a compatible symptom complex and exclude competing gastrointestinal causes.

Symptomatic atherosclerotic chronic mesenteric ischaemia requires revascularisation rather than nutritional treatment alone.

Do not delay revascularisation solely to achieve weight restoration. The postprandial perfusion deficit is the reason the patient cannot maintain nutrition.

Endovascular revascularisation is generally preferred because of lower early procedural morbidity. Angioplasty with stenting is preferred over angioplasty alone for atherosclerotic mesenteric lesions. When one vessel is targeted, the superior mesenteric artery is the priority vessel.

Open mesenteric bypass remains appropriate in fit patients with anatomy unsuitable for endovascular treatment, failed endovascular therapy or durable reconstruction requirements.

After mesenteric artery stenting, a practical antiplatelet regimen is:

Aspirin 75 to 100 mg orally once daily plus clopidogrel 75 mg orally once daily for at least 1 month, followed by lifelong single antiplatelet therapy, usually aspirin.

Patients already requiring therapeutic anticoagulation generally need only one additional antiplatelet agent for approximately 4 weeks after stenting rather than prolonged triple therapy.

Treat the systemic atherosclerotic disease aggressively with smoking cessation, blood pressure control, diabetes management and high intensity lipid lowering therapy according to cardiovascular prevention targets. Secondary cardiovascular prevention should begin as soon as atherosclerotic chronic mesenteric ischaemia is diagnosed.

Recurrent postprandial symptoms after treatment should prompt evaluation for restenosis using duplex ultrasound or CT angiography.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Perforated Peptic Ulcer

Also known as: Perforated ulcer

Perforated peptic ulcer is full thickness perforation of a gastric or duodenal ulcer with leakage of gastroduodenal contents into the peritoneal cavity.

Major causes include Helicobacter pylori, nonsteroidal anti inflammatory drugs and smoking.

Most perforations occur in the anterior duodenum or stomach. Posterior duodenal ulcers more commonly bleed because of proximity to the gastroduodenal artery.

Perforation produces chemical peritonitis followed rapidly by bacterial contamination and secondary intra abdominal infection.

Classically there is sudden severe epigastric pain that rapidly becomes generalised.

The patient often lies still because movement worsens peritoneal pain.

Important findings include:

Board like abdominal rigidity
Generalised percussion tenderness
Tachycardia
Reduced bowel sounds
Progressive dehydration
Sepsis or shock in delayed presentation

Older adults and immunosuppressed patients may have limited guarding despite significant contamination.

Resuscitation and operative preparation should occur simultaneously.

Keep fasting.

Establish large bore IV access and use balanced crystalloid according to perfusion response. Correct potassium, magnesium and significant acid base disturbance.

Insert a urinary catheter in shock or major sepsis.

Nasogastric decompression is useful with substantial gastric distension or persistent vomiting.

Give:

Pantoprazole 40 mg IV every 12 hours.

Start antibiotics promptly.

A practical stable community acquired regimen is:

Ceftriaxone 2 g IV every 24 hours plus metronidazole 500 mg IV every 12 hours.

For septic shock or major contamination:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

Nonoperative management

Routine conservative treatment of a free perforation is inappropriate.

A highly selected patient may undergo nonoperative management only when:

Haemodynamics are stable
There is no diffuse peritonitis or sepsis
Imaging demonstrates a contained perforation
Water soluble contrast assessment confirms that the perforation has sealed
Continuous monitoring and immediate access to surgery are available

Clinical deterioration requires immediate source control.

Operative management

Stable patients are suitable for laparoscopic repair when expertise is available.

For a perforation below 2 cm, primary suture closure is generally sufficient. An omental patch can be added where the tissue is friable or the surgeon believes reinforcement is useful, but it is not mandatory for every small perforation.

For a gastric ulcer, inspect carefully for malignant features. Large, indurated or irregular ulcers require tissue diagnosis. Wedge resection or gastrectomy may be preferable when malignancy is strongly suspected and the patient is physiologically suitable.

For a large duodenal defect above approximately 2 cm, simple closure may be unsafe. Depending on location and tissue quality, options include reinforced repair, pyloric exclusion with gastrojejunostomy, antrectomy, Roux en Y duodenojejunostomy or another tailored reconstruction. Tube duodenostomy is reserved for exceptional destructive defects where safer reconstruction is impossible.

In septic shock, choose the shortest operation that reliably controls contamination. Complex acid reducing ulcer surgery should not be added routinely to emergency source control.

After adequate source control, continue antibiotics for approximately 4 days unless sepsis remains uncontrolled.

Ulcer eradication

Treat Helicobacter pylori after recovery when present.

A practical 14 day bismuth quadruple regimen is:

Proton pump inhibitor standard dose orally twice daily
Bismuth subsalicylate 524 mg orally four times daily
Tetracycline 500 mg orally four times daily
Metronidazole 500 mg orally three to four times daily

Stop nonsteroidal anti inflammatory drugs where possible. If long term treatment remains unavoidable, maintain appropriate gastroprotection.

Confirm Helicobacter pylori eradication after treatment.

Patients with a gastric ulcer require interval endoscopic reassessment, usually after healing, to ensure malignancy has not been missed. Persistent symptoms, recurrent pain, fever or postoperative ileus should trigger evaluation for repair failure or intra abdominal collection.

Chronic Mesenteric Ischaemia

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management