Surgical Site Infection

Surgical site infection is infection involving the operative incision, deeper soft tissues or operated organ space.

Clinically divide it into:

Superficial incisional infection involving skin and subcutaneous tissue
Deep incisional infection involving fascia or muscle
Organ space infection involving the operated cavity or organ

Management becomes progressively more source control dependent as infection extends deeper.

Superficial infection causes wound pain, erythema, warmth, swelling or purulent drainage.

Deep infection may produce increasing wound pain, induration, wound breakdown or deep purulent discharge.

Organ space infection may present predominantly with fever, tachycardia, ileus, abdominal pain or sepsis with little external wound abnormality.

Rapid progression, disproportionate pain, bullae, crepitus, skin necrosis or systemic toxicity should trigger immediate evaluation for necrotising infection.

The primary treatment of a superficial purulent surgical site infection is opening the incision and draining infected material. Antibiotics alone do not adequately treat a closed infected wound.

Remove sufficient sutures or staples to allow complete drainage. Debride devitalised tissue.

Systemic antibiotics are not required for every small superficial wound infection after effective drainage if there is minimal surrounding cellulitis and no systemic response. IDSA supports antibiotics when there is significant systemic response or extensive surrounding inflammation.

For cellulitic infection after a clean operation where methicillin susceptible staphylococci and streptococci are likely:

Cefazolin 2 g IV every 8 hours in a hospitalised adult with normal renal function.

Where MRSA risk is substantial, use vancomycin with dosing guided by weight, renal function and AUC monitoring. For serious MRSA infection, the target vancomycin AUC is 400 to 600 mg hour/L.

Following gastrointestinal or perineal surgery, antimicrobial therapy must also cover enteric Gram negative organisms and anaerobes. A reasonable severe regimen is:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion.

Deep fascial infection requires operative assessment because fascial necrosis or dehiscence may coexist.

Organ space infection requires drainage or other definitive source control. Once adequate intra abdominal source control is achieved, prolonged antibiotics are usually unnecessary and therapy should generally be limited to 4 days.

Oesophageal Perforation

Oesophageal perforation is full thickness disruption of the oesophageal wall with leakage of oesophageal and gastric contents into the neck, mediastinum, pleural cavity or peritoneum.

Common causes are endoscopic instrumentation, dilation, surgery, spontaneous rupture, foreign bodies and trauma.

The absence of a protective serosal layer and proximity to the mediastinum allow rapid contamination, mediastinitis, pleural sepsis and shock.

Outcome is determined by location, size, underlying oesophageal disease, extent of contamination, physiological state and speed of source control.

Thoracic perforation commonly produces severe chest or upper abdominal pain, dyspnoea and systemic toxicity.

Cervical perforation may present with neck pain, dysphagia, odynophagia, cervical tenderness or subcutaneous emphysema.

Abdominal oesophageal perforation produces epigastric pain and peritonitis.

Tachycardia may be the earliest physiological abnormality. Progressive fever, respiratory distress, hypotension and organ dysfunction indicate uncontrolled contamination.

Keep strictly fasting.

Establish IV access, correct hypovolaemia and begin broad spectrum antimicrobial therapy immediately.

A practical adult regimen is:

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

Add antifungal treatment only when there is a specific risk such as prolonged critical illness, immunosuppression, established Candida infection or another strong clinical indication. Routine empirical antifungal therapy is not required for every perforation.

Give acid suppression, for example:

Pantoprazole 40 mg IV every 12 hours.

Establish early nutrition, preferably distal enteral feeding when feasible.

A stable patient with an early, contained perforation, minimal contamination and no sepsis may be managed without open surgery provided intensive surgical, endoscopic and radiological support is immediately available. This still requires antibiotics, fasting, nutritional support and drainage of any collection.

Small iatrogenic defects, particularly below approximately 2 cm, may be closed with endoscopic clips when recognised early.

Larger defects can be treated with fully covered self expanding oesophageal stents or endoscopic vacuum therapy in selected patients. Endoscopic therapy must be combined with drainage of contaminated mediastinal or pleural spaces where necessary.

Operate urgently for:

Haemodynamic instability
Free uncontained leak
Extensive pleural or mediastinal contamination
Established sepsis not controlled by drainage
Necrotic oesophageal tissue
Failed endoscopic treatment
Underlying pathology that cannot be adequately treated conservatively

Primary repair is preferred when tissue can hold sutures. Debride devitalised margins, close the defect without tension, reinforce the repair with vascularised tissue where appropriate and provide generous external drainage.

Extensive destruction, delayed presentation with nonrepairable tissue or severe underlying oesophageal disease may require exclusion, diversion or oesophagectomy.

Delay should not be accepted simply because the perforation is more than 24 hours old. Viable repairable tissue can still be primarily repaired in selected delayed cases, but contamination control becomes increasingly important.

Surgical Site Infection

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management