Intra Abdominal Abscess

An intra abdominal abscess is a localised collection of infected fluid or pus within the peritoneal cavity, retroperitoneum or an abdominal organ.

It commonly follows gastrointestinal perforation, appendicitis, diverticulitis, pancreatitis, trauma or abdominal surgery. A postoperative abscess should prompt consideration of an ongoing source such as an anastomotic leak, bowel injury or infected haematoma.

Antibiotics penetrate poorly into large established collections. Effective management therefore depends primarily on source control.

Presentation may be obvious or subtle. Persistent fever, abdominal pain, focal tenderness, anorexia and ileus are typical.

Postoperative clues include failure to recover as expected, persistent tachycardia, recurrent fever after initial improvement, prolonged ileus, increasing inflammatory markers or new organ dysfunction.

Deep pelvic or subphrenic collections may produce minimal abdominal findings.

Septic shock indicates uncontrolled infection until proven otherwise.

Check full blood count, renal function, electrolytes and C reactive protein. Measure lactate when systemic illness or hypoperfusion is present.
Blood cultures are particularly appropriate when fever is accompanied by hypotension, tachypnoea or delirium, or when resistant organisms are a concern.
CT abdomen and pelvis with IV contrast: investigation of choice in nonpregnant adults; confirm the collection and determine whether a safe percutaneous drainage route exists. IV contrast improves visualisation of the abscess wall.

There is no universal abscess diameter that independently determines drainage. Size must be interpreted with accessibility, loculation, clinical condition and response to antibiotics.

Source control is the central treatment.

A small collection in a stable patient may occasionally resolve with antibiotics alone, particularly when drainage would be difficult and there is no ongoing leak. A mature accessible collection causing systemic or persistent local infection should generally undergo image guided percutaneous drainage.

Send aspirated or operative fluid for bacterial culture when source control is performed.

A practical adult antimicrobial regimen for stable community acquired infection is:

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

For severe sepsis, healthcare associated infection or substantial resistant Gram negative risk:

Piperacillin tazobactam 4.5 g IV loading dose followed by 4.5 g IV every 8 hours by extended infusion, adjusted for renal impairment.

Operate when there is:

Generalised peritonitis
An uncontrolled perforation or anastomotic leak requiring repair
Bowel ischaemia or necrosis
A collection not amenable to percutaneous drainage with ongoing sepsis
Failed percutaneous drainage
Persistent physiological deterioration despite appropriate treatment

The operative objective is not merely drainage. Any continuing source of contamination must also be controlled.

After adequate percutaneous or operative source control, antibiotic treatment should generally be limited to 4 days, including higher risk patients with sepsis.

Persistent fever, leukocytosis or organ dysfunction after source control should trigger reassessment for inadequate drainage, another collection, fistula, retained foreign material or continued gastrointestinal leakage rather than automatic prolongation of antibiotics.

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

Bowel Infarction

Bowel infarction is irreversible transmural intestinal necrosis caused by sustained ischaemia.

It represents the end stage of several processes, including acute mesenteric arterial occlusion, mesenteric venous thrombosis, strangulated obstruction, volvulus, internal hernia and severe nonocclusive mesenteric ischaemia.

Once infarction is established, restoring perfusion alone is insufficient. Necrotic bowel must be removed while every possible centimetre of viable intestine is preserved.

Pain may initially be severe with limited physical findings if infarction follows vascular occlusion. As transmural necrosis progresses, the abdomen becomes tender with guarding and eventually generalised peritonitis.

Late manifestations include ileus, abdominal distension, gastrointestinal bleeding, fever, hypotension, metabolic acidosis, oliguria and septic shock.

In strangulated obstruction, a transition from intermittent colic to persistent focal pain should raise concern for evolving infarction.

Peritonitis in mesenteric ischaemia strongly predicts irreversible bowel injury.

CT angiography or contrast enhanced CT according to suspected cause: establishes the vascular or mechanical process and assesses bowel viability. Reduced or absent bowel enhancement, pneumatosis, portal venous gas or perforation support advanced irreversible injury, although operative assessment ultimately determines viability.

Check blood gas, lactate, full blood count, renal function, electrolytes and coagulation. Crossmatch blood.

Hyperkalaemia and worsening metabolic acidosis may become pronounced after extensive necrosis or reperfusion.

Bowel infarction is an emergency.

Begin balanced crystalloid resuscitation, correct major electrolyte and acid base disturbances and start broad spectrum antibiotics because mucosal barrier failure and necrosis cause bacterial translocation.

A practical adult regimen is:

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

If the mechanism is mesenteric vascular occlusion, administer full dose unfractionated heparin unless contraindicated and pursue revascularisation urgently.

Peritonitis, perforation or established necrotic bowel requires emergency exploration.

At surgery, first correct the reversible cause where feasible. Release strangulation, detorse volvulus or restore mesenteric arterial flow before deciding the final resection length.

Resect frankly necrotic bowel only. Marginal bowel may recover after restoration of blood flow, warming and physiological correction. Massive unnecessary resection can convert a survivable vascular catastrophe into permanent intestinal failure.

Primary anastomosis is appropriate only when bowel perfusion is clearly satisfactory and the patient is physiologically stable.

In severe shock, major contamination, bowel oedema or uncertain viability, use damage control principles. Leave stapled bowel ends in discontinuity if necessary, apply temporary abdominal closure and return for a second look operation in 24 to 48 hours.

Document residual small bowel length, presence of ileum, ileocaecal valve and remaining colon. These determine the subsequent risk and severity of short bowel syndrome.

When adequate source control has been achieved for associated intra abdominal infection, prolonged antibiotics are unnecessary. Current Surgical Infection Society guidance recommends no more than approximately 4 days after effective source control unless infection remains uncontrolled.

Intra Abdominal Abscess

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management