Surgical Patients



Surgical Patients






Postoperative sepsis

Patients commonly develop SIRS in the immediate postoperative period 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 unrelated to the operation (e.g. LRTI, UTI)


    • 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 image p.322.)



  • Pyrexia may be associated with other evidence of infection, including:



    • Tachypnoea, tachycardia, rigors, sweats


    • Complications of sepsis (see image 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).


  • FBC (/↓WCC, / platelets).


  • Coagulation screen ( APTT/PT and fibrinogen if DIC).


  • 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


    • Urine: dipstick, MSU/CSU


    • Stool: C&S, C. difficile toxin if diarrhoea present


    • Wound swabs, if wound inflamed



  • U&Es (raised urea/creatinine may suggest sepsis-induced AKI).


  • 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).


  • ECG (new onset AF).


  • CXR (new shadowing/consolidation).


  • Further imaging: consider US/CT of abdomen, pelvis, or chest (looking for evidence of perforation or collections) and plain films of joints if appropriate.


Differential diagnoses



  • SIRS (no evidence of infection).


  • MI (hypotension, tachycardia, hypoxia if LVF present, cool peripheries).


  • PE (hypoxia, hypotension, tachycardia, cool peripheries).


  • Haemorrhage (hypotension, tachycardia, cool peripheries).


  • Ongoing ischaemia (e.g. bowel ischaemia).



Further management

(See also sepsis, image 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 dehiscence

This 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.


Late



  • Signs of shock: hypotension, tachycardia.


  • Generalized sepsis.




Investigations



  • ABGs (metabolic acidosis/ lactate suggest impaired tissue perfusion).


  • FBC (/↓WCC, / platelets).


  • Coagulation screen.


  • U&Es (raised urea/creatinine may suggest sepsis or excessive fluid loss).


  • LFTs (↓protein/albumin may occur with SIRS/malnutrition).


  • Wound swabs.


  • Blood cultures if there are signs of generalized sepsis.


  • CXR or AXR may help identify alternate sources of infection.


  • Further imaging: a CT scan or a US scan of wound area may detect any fluid collection, or other source of infection.



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.


  • Patients are at high risk of developing resistant infections (e.g. MRSA, VRE, C. difficile).



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 haemorrhage

The loss of blood from the site of surgery may be obvious (e.g. from drains) or concealed. Hypovolaemic shock rapidly leads to organ impairment.


Causes



  • Unnoticed haemostasis failure.


  • Massive transfusion coagulopathy.


  • Clip/suture migration.

Jun 13, 2016 | Posted by in CRITICAL CARE | Comments Off on Surgical Patients

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