Surgical Infections & Wound Management

Physicians treat infection with drugs. Surgeons treat infection by removing the thing that is infected, and then give drugs to protect what remains.

The organising tool for this whole chapter is a single physiological fact: no antibiotic reaches a space with no blood supply.

Pus, dead tissue, a foreign body and an obstructed cavity all share that property. Blood cannot get in, so neither antibiotic nor white cell can, and the infection persists at full strength however impressive the prescription.

The same fact governs the second half of the chapter. A wound heals only where blood reaches it, so every factor that impairs healing does so by reducing perfusion, adding tension, adding infection or leaving something foreign behind.

1. Source Control Comes First

Source control means physically eliminating the focus of infection: draining pus, debriding dead tissue, removing an infected prosthesis, diverting a leaking anastomosis, or relieving an obstructed duct.

It is the intervention that changes outcome, and antibiotics are adjunctive. A patient with an undrained abscess on the correct antibiotic will not improve; a patient with a drained abscess will often improve before the culture returns.

That is why the classical aphorism survives: where there is pus, let it out.

The same logic explains several rules that look unconnected. Cholangitis needs drainage rather than stronger antibiotics. Infected pancreatic necrosis needs the collection drained. An infected mesh usually has to come out.

The corollary is equally important: intervening where there is no focus makes things worse. Draining sterile pancreatic necrosis introduces infection, and debriding viable tissue removes the perfusion the antibiotic depends on.

2. Classifying Wounds and Predicting Infection

Surgical site infection risk is predicted mainly by the degree of contamination at operation, and the classification is examined directly.

Surgical site infection is subdivided by depth into superficial incisional, deep incisional and organ or space infection, which matters because the management differs.

A superficial infection is usually treated by opening the wound and allowing drainage. An organ or space infection means a collection somewhere and requires imaging and drainage.

Patient factors compound the wound class: diabetes, obesity, smoking, malnutrition, corticosteroids, immunosuppression and prolonged preoperative stay all raise the rate.

Several preventive measures are examined because they are counterintuitive. Hair should be removed with clippers rather than a razor, or not at all, because razor shaving creates micro-abrasions that become colonised, and shaving the night before is worse than shaving immediately before.

Maintaining normothermia, adequate tissue oxygenation and glycaemic control during surgery all reduce infection, and all three work by protecting neutrophil function, which is oxygen-dependent.

3. Antibiotic Prophylaxis

Prophylaxis is intended to have a therapeutic drug concentration in the tissues at the moment of incision, and everything about its administration follows from that aim.

The dose is given within sixty minutes before incision, and redosed intraoperatively if the operation is prolonged beyond about two drug half-lives or if there is major blood loss.

Given too early, the concentration has fallen by the time of incision. Given after incision, the contamination has already occurred and the horse has bolted.

A single dose is sufficient for the great majority of operations, and prophylaxis is not continued after the operation ends. This is the point candidates most often get wrong, and it is supported by strong evidence: continuing prophylaxis postoperatively does not reduce surgical site infection.

Prolonging it does cause harm, selecting resistant organisms and predisposing to Clostridioides difficile infection, which is why the recommendation against it is strong.

Prophylaxis is indicated where infection is likely, as in clean-contaminated and contaminated surgery, or where infection would be catastrophic even if unlikely, as when a prosthesis is implanted.

The agent must cover the expected organisms: skin flora for clean surgery, so a first-generation cephalosporin, and additional anaerobic cover for colorectal surgery.

Note that antibiotics given for established infection, as in a dirty wound or a perforated viscus, are treatment rather than prophylaxis and follow a therapeutic course.

4. Abscess

An abscess is a collection of pus walled off by a pyogenic membrane, and its structure explains why it cannot be cured medically.

The wall is avascular granulation tissue and the centre is dead, so systemic antibiotic never reaches therapeutic concentration inside. The low pH and low oxygen tension within also impair the activity of several antibiotic classes and of neutrophils themselves.

Treatment is drainage, by incision or by image-guided catheter, with antibiotics reserved for surrounding cellulitis, systemic sepsis or an immunocompromised host.

Loculations must be broken down, because a multiloculated cavity that is only partly drained will simply reform.

A pilonidal abscess, a perianal abscess and a breast abscess all follow the same principle, though the breast abscess is increasingly managed by repeated ultrasound-guided aspiration rather than incision, which preserves cosmesis and allows continued feeding.

5. Necrotising Soft Tissue Infection

This is the surgical emergency of this chapter, and it is missed because early on it looks like cellulitis.

The cardinal feature is pain out of proportion to the visible signs, which recurs as a theme across surgery whenever tissue is dying beneath an intact-looking surface.

Other features are rapid progression over hours, systemic toxicity disproportionate to the local appearance, oedema extending beyond the erythema, skin anaesthesia from destruction of cutaneous nerves, crepitus, and skin necrosis or bullae appearing late.

Skin anaesthesia over an area of apparent cellulitis is close to diagnostic, because ordinary cellulitis is tender rather than numb.

Type 1 is polymicrobial with mixed aerobes and anaerobes, occurring in diabetics and the immunocompromised, and Fournier gangrene of the perineum is its best-known form. Type 2 is monomicrobial, classically group A Streptococcus, and can occur in healthy young people.

Investigations support the diagnosis but must not delay treatment. Imaging may show gas or fascial fluid, and scoring systems using laboratory values exist, but a negative score does not exclude the disease.

Treatment is immediate radical surgical debridement, repeated as often as necessary, with broad-spectrum antibiotics including an antitoxin agent such as clindamycin, and full organ support.

Mortality relates directly to the delay before the first debridement, which is why the diagnosis is clinical and the operation is not postponed for imaging.

6. Tetanus and Gas Gangrene

Tetanus is caused by the neurotoxin of Clostridium tetani, which blocks release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid at spinal inhibitory interneurons.

Removing inhibition produces unopposed motor activity, which is why the clinical picture is spasm rather than paralysis: trismus, risus sardonicus, opisthotonus and reflex spasms triggered by minimal stimuli, with a fully conscious patient.

Tetanus-prone wounds are those that are deep, contaminated with soil or faeces, devitalised, or presenting more than six hours after injury. Management combines wound debridement, human tetanus immunoglobulin, antibiotics and active immunisation.

Having tetanus does not confer immunity, because the amount of toxin required to cause disease is far below the amount needed to provoke an antibody response, so survivors must still be immunised.

Gas gangrene is caused by Clostridium perfringens, whose alpha toxin is a lecithinase that destroys cell membranes.

It presents with severe pain, a rapidly spreading brown discharge with a sweetish odour, crepitus, and profound systemic toxicity. Treatment is radical debridement or amputation with penicillin and clindamycin.

Crepitus is not specific to clostridial infection, since gas-forming coliforms and anaerobes produce it too, so its presence indicates urgency rather than a particular organism.

7. Sepsis in the Surgical Patient

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection, and septic shock is sepsis with vasopressor-requiring hypotension and a raised lactate despite fluid resuscitation.

The definition deliberately moved away from the older inflammatory response criteria, because those were too sensitive and identified patients who were not organ-dysfunctional.

Current guidance separates two situations by urgency. Where septic shock or a high likelihood of sepsis is present, antimicrobials are given immediately and ideally within one hour. Where sepsis is possible but there is no shock, a rapid time-limited assessment is made and antimicrobials given within three hours.

The distinction exists because immediate antibiotics for everyone with a possible infection causes measurable harm through overtreatment, while delay in true septic shock costs lives.

Cultures are taken before antibiotics where this does not delay them, fluid resuscitation is begun, lactate is measured and repeated, and vasopressors are started if the patient remains hypotensive.

None of that substitutes for source control, which should be achieved as soon as it is feasible, because a septic patient with an undrained source will not stabilise.

8. How a Wound Heals

Healing proceeds in overlapping phases, and knowing which phase a wound is in explains both its appearance and its strength.

Macrophages are the pivotal cell, not the neutrophil. Depleting neutrophils in experimental wounds barely delays healing, but depleting macrophages profoundly impairs it, because they orchestrate debridement, angiogenesis and fibroblast recruitment.

Wound strength is a separate question from wound appearance. Collagen content peaks at around three weeks, but tensile strength continues to rise for months as collagen is cross-linked and reorganised.

A healed wound never regains the strength of intact skin, reaching roughly seventy to eighty per cent at best. This is why an incisional hernia can appear a year after an apparently perfect closure.

Healing by primary intention means the edges are apposed and heal with minimal granulation. Secondary intention means the wound is left open and fills with granulation tissue, contracting as it heals. Tertiary or delayed primary intention means the wound is deliberately left open initially and closed after a few days once contamination has settled.

Factors impairing healing all act through the same four mechanisms: reduced perfusion, as in ischaemia, smoking and anaemia; impaired synthesis, as in malnutrition, vitamin C deficiency and zinc deficiency; suppressed inflammation, as with corticosteroids; and persistent injury, as in infection, foreign material or repeated trauma.

Vitamin C deficiency is instructive because it blocks hydroxylation of proline and lysine, so collagen cannot cross-link, and old healed scars break down.

9. Closure, Sutures and Drains

Suture materials are classified as absorbable or non-absorbable and as monofilament or braided, and the choice follows from what the tissue needs.

Braided sutures handle and knot better but have interstices that harbour bacteria, so monofilament is preferred in contaminated fields and for skin.

Absorbable sutures are used where support is temporary, as in bowel anastomosis and subcutaneous tissue. Non-absorbable sutures are used where permanent strength is needed, as in vascular anastomosis and mesh fixation.

Abdominal mass closure uses a continuous non-absorbable or slowly absorbable suture with a suture length to wound length ratio of about four to one, which places the bites far enough apart and deep enough to hold without strangling the tissue.

Wound dehiscence typically occurs around the fifth to eighth postoperative day, at the end of the inflammatory phase and before collagen has provided real strength.

The classic warning sign is a sudden discharge of serosanguinous fluid from the wound, often described as pink or salmon coloured, which precedes visible separation. Burst abdomen requires resuscitation, covering the bowel with saline-soaked packs, and return to theatre.

Drains are used to evacuate an existing collection or to detect a leak, not to prevent infection, and a drain left in an otherwise clean space is a route for bacteria to enter rather than a safeguard.

10. Abnormal Scars and Chronic Wounds

Hypertrophic scars remain within the boundaries of the original wound and often regress with time. Keloids extend beyond the original wound margins and do not regress, recurring readily after excision.

Both are commoner in darker skin and at particular sites: the sternum, shoulders, upper back and earlobes. Keloid management combines intralesional steroid, pressure, silicone and, where excision is unavoidable, adjuvant treatment to prevent recurrence.

A chronic wound is one that has failed to progress through the normal phases, and the commonest examples are venous, arterial, diabetic and pressure ulcers, each identifiable from its site and edge.

Venous ulcers sit in the gaiter area with sloping edges and surrounding pigmentation, and their treatment is compression. Arterial ulcers occur at the toes and pressure points with punched-out edges and absent pulses, and compression would make them worse.

Diabetic foot ulcers occur over pressure points in a neuropathic foot and require offloading, debridement and vascular assessment.

Marjolin ulcer is squamous cell carcinoma arising in a chronic wound or old burn scar and must be biopsied rather than dressed indefinitely.

11. Worked Examples

Example 1. A patient with cellulitis of the leg has pain far worse than the appearance suggests, is systemically unwell, and has an area of numb skin within the erythema.

Pain out of proportion to the signs, with systemic toxicity and skin anaesthesia, indicates necrotising soft tissue infection rather than cellulitis. The numbness reflects destruction of cutaneous nerves by the spreading fascial infection.

The correct action is immediate radical surgical debridement with broad-spectrum antibiotics including clindamycin. Waiting for imaging or for a laboratory risk score would delay the only intervention that alters mortality.

Example 2. A surgeon asks for prophylactic antibiotics to be continued for five days after an uncomplicated elective colectomy.

This is not supported. Prophylaxis is intended to provide tissue levels at the moment of incision, so a single preoperative dose within sixty minutes, redosed intraoperatively if the operation is long or bloody, is sufficient.

Continuing it postoperatively does not reduce surgical site infection and does select resistant organisms and predispose to Clostridioides difficile infection. The recommendation against prolongation is strong.

Example 3. On the seventh postoperative day after a laparotomy, a patient's wound discharges a large volume of pink serosanguinous fluid.

This is the classical warning sign of impending wound dehiscence, occurring at the point where the inflammatory phase has ended but collagen has not yet conferred strength.

The patient should be assessed urgently, the wound inspected, and preparation made for return to theatre. If frank evisceration occurs, the bowel is covered with saline-soaked packs, the patient is resuscitated, and closure is performed in theatre rather than on the ward.

Summary

• No antibiotic reaches a space with no blood supply; source control comes first.
• Pus, dead tissue, foreign bodies and obstructed cavities are all avascular.
• Intervening where there is no focus, such as sterile necrosis, causes harm.
• Wound class predicts infection: clean, clean-contaminated, contaminated, dirty.
• Surgical site infection is superficial, deep or organ and space, and management differs.
• Clip hair rather than shave, and do it immediately before surgery.
• Normothermia, oxygenation and glycaemic control protect oxygen-dependent neutrophils.
• Prophylaxis is given within 60 minutes before incision.
• Redose for long operations or major blood loss.
• A single dose suffices; postoperative continuation does not reduce infection.
• Prolonged prophylaxis selects resistance and causes Clostridioides difficile infection.
• An abscess cannot be cured by antibiotics because its wall is avascular.
• Loculations must be broken down or the abscess reforms.
• Breast abscess is increasingly aspirated rather than incised.
• Pain out of proportion to signs suggests necrotising infection.
• Skin anaesthesia within cellulitis is close to diagnostic.
• Type 1 necrotising infection is polymicrobial; type 2 is group A Streptococcus.
• Treatment is immediate radical debridement; imaging must not delay it.
• Tetanus toxin blocks glycine and GABA release, so spasm results, not paralysis.
• Surviving tetanus does not confer immunity.
• Clostridium perfringens alpha toxin is a lecithinase.
• Crepitus indicates urgency but not a specific organism.
• Antibiotics within one hour in septic shock, within three hours for possible sepsis.
• Sepsis will not resolve without source control.
• Macrophages, not neutrophils, are the pivotal cell in healing.
• Collagen peaks at three weeks but strength rises for months.
• A healed wound reaches only 70 to 80 per cent of original strength.
• Vitamin C deficiency prevents collagen cross-linking, so old scars break down.
• Monofilament is preferred in contaminated fields; braided sutures harbour bacteria.
• Mass closure uses a suture to wound length ratio of about four to one.
• Dehiscence occurs on days five to eight, heralded by pink serosanguinous discharge.
• Drains detect or evacuate collections; they do not prevent infection.
• Hypertrophic scars stay within the wound; keloids extend beyond it.
• Venous ulcers need compression; arterial ulcers are worsened by it.