Surgical Patients
Postoperative sepsisPatients commonly develop SIRS in the immediate postoperative period 2° to ↑cytokine levels caused by the surgical tissue trauma. This is normally a self-limiting response that subsides within 48 hours. Persistent SIRS, or the development of end-organ dysfunction, should prompt examination and investigations to elucidate the cause.
Causes
A number of factors predispose patients to developing postoperative sepsis, including:
Preoperative:
Infection requiring surgery (e.g. bowel perforation, abscess)
Immunocompromised patients (e.g. RhA, malnutrition)
Intraoperative:
Peritoneal contamination
Gut ischaemia (e.g. thromboembolism, volvulus)
Reperfusion injury (e.g. aortic cross-clamping)
GU surgery (especially if indwelling catheter/stent and/or mucosal damage by calculus or instrumentation)
Surgery of infected area (e.g. debridement of burns, incision and drainage of abscess)
Postoperative:
Pneumonia (e.g. following thoracic/upper-GI surgery, prolonged immobility, or inadequate pain relief preventing deep breathing/coughing/mobilization)
Surgical wound infection
Presentation and assessment
(See also 
p.322.)
p.322.)
Pyrexia may be associated with other evidence of infection, including:
Tachypnoea, tachycardia, rigors, sweats
Complications of sepsis (see
p.322)
Raised WCC and inflammatory markers
Features of sepsis and end-organ dysfunction may be present.
After contaminated gut surgery, sepsis should be monitored for, particularly in the first 72 hours.
Investigations
ABGs (metabolic acidosis, lactataemia suggest impaired perfusion).
CRP (raised in response to inflammation).
Cultures:
Blood from indwelling lines and peripheral ‘stab’
Samples from all drains and any effusions that can be tapped
Sputum: consider bronchoscopy/BAL
Stool: C&S, C. difficile toxin if diarrhoea present
Wound swabs, if wound inflamed
LFTs (deranged if sepsis-induced hypoperfusion).
Serum glucose, phosphate, magnesium, calcium.
Serum amylase (raised in pancreatitis and other acute upper intra-abdominal conditions, e.g. cholecystitis).
CXR (new shadowing/consolidation).
Differential diagnoses
SIRS (no evidence of infection).
PE (hypoxia, hypotension, tachycardia, cool peripheries).
Haemorrhage (hypotension, tachycardia, cool peripheries).
Ongoing ischaemia (e.g. bowel ischaemia).
Immediate management
(See also sepsis, 
p.325.)
p.325.)
Invasive monitoring may be required to guide fluid management and deliver vasoactive support
Keep the patient NBM initially in case surgery required
Inform surgical team as urgent removal of infective source may be required
Assess blood loss and crossmatch blood for transfusion if necessary
Further management
(See also sepsis, 
p.326.)
p.326.)
Institute sepsis care management.
Consider:
Open wound drainage
Continuous wound irrigation
Multiple laparotomies for repeated washouts
In some conditions (e.g. necrotizing fasciitis) repeated surgical debridement may be required.
Monitor for, and treat, complications of sepsis (e.g. AKI).
Pitfalls/difficult situations
Multiple organ failure may occur if the source of infection is not aggressively treated.
Further reading
Monkhouse D. Postoperative sepsis. Curr Anaesth Crit Care 2006; 17: 65-70.
Rivers E, et al. Early Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345: 1368-77.
Wound dehiscenceThis is partial or complete opening of the surgical wound. Presentation and management vary with the site.
Causes
Predisposing factors include:
Wound infection.
Poor surgical technique.
Tension in the surgical incision site (ascites, ileus, obstruction).
Bleeding/haematoma formation.
Reduced tissue perfusion/oxygenation (‘shock’).
Tissue oedema/poor tissue strength (obesity, hypoalbuminaemia, uraemia, heart failure, liver failure, chemotherapy, radiotherapy).
Persistent coughing/vomiting.
Diabetes.
Smoking.
Long-term or high-dose steroid use.
Patient age >65 years.
Presentation and assessment
Early
Open wound noticed at dressings change or removal of clips/sutures.
Excessive soiling of dressings.
Inappropriate pain.
Investigations
Coagulation screen.
U&Es (raised urea/creatinine may suggest sepsis or excessive fluid loss).
Wound swabs.
Blood cultures if there are signs of generalized sepsis.
Immediate management
Invasive monitoring may be required to guide fluid management and deliver vasoactive support.
Keep the patient NBM initially in case surgery required.
Inform surgical team as urgent wound closure may be indicated.
Assess blood loss and crossmatch blood for transfusion if necessary.
Cover wound with sterile dressing.
In mechanically ventilated patients consider deepening sedation or commencing neuromuscular blockade to decrease likelihood of expulsion of abdominal contents.
Further management
Identify/avoid/treat any predisposing factors.
Continued invasive monitoring and correction of:
Fluid status
Electrolytes
Coagulation status
Antibiotic therapy may be required.
Surgical management will be required:
Dressing changes as appropriate
Wounds may require debridement and/or closure (which may have to be delayed)
Drainage of any associated collection
After re-closure of abdominal wound, pain relief will be extremely important; consider epidural infusion of local anaesthetics and opioids:
Involve the pain management team early
Re-closure of abdominal wound may also cause splinting of diaphragm—respiratory support is likely to be required.
Pitfalls/difficult situations
Sepsis and multiple organ failure may occur because the open wound is prone to infection. Strict sterile precautions are required.
Insensible fluid losses may be difficult to assess.
Further reading
Menke NB, et al. Impaired wound healing. Clin Dermatol 2007; 25: 19-25.
Penninckx FM, et al. Abdominal wound dehiscence in gastroenterological surgery. Ann Surg 1979; 189(3): 345-52.
Major postoperative haemorrhageThe loss of blood from the site of surgery may be obvious (e.g. from drains) or concealed. Hypovolaemic shock rapidly leads to 2° organ impairment.
Causes
Unnoticed haemostasis failure.
Massive transfusion coagulopathy.
Clip/suture migration.
