Postoperative Fever and Wound Dehiscence After Colectomy
A 68-year-old man undergoes elective sigmoid colectomy for diverticular disease. On postoperative day 5, he develops a temperature of 38.6°C, tachycardia (110 bpm), and a swollen, erythematous midline laparotomy wound with serosanguinous discharge. His white cell count is 14.2 × 10^9/L, and CRP is 180 mg/L. Wound cultures grow Staphylococcus aureus and Escherichia coli. He is started on broad-spectrum antibiotics and the wound is partially opened. Two days later, the wound edges are separated, and granulation tissue is visible at the base. His albumin is 28 g/L, and he has a history of type 2 diabetes (HbA1c 8.5%).
1. Explain the pathophysiological sequence that led to wound dehiscence in this patient, integrating the concepts of inflammation, repair, and the effect of his comorbidities.
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The sequence begins with bacterial contamination at surgery, leading to a sustained acute inflammatory response. Neutrophils and macrophages release proteases (e.g., matrix metalloproteinases) and reactive oxygen species, which degrade newly deposited collagen and fibronectin in the provisional matrix. This impairs the transition to the proliferative phase. His diabetes causes microangiopathy and impaired neutrophil function, reducing delivery of oxygen and nutrients and allowing infection to persist. Hypoalbuminemia (28 g/L) limits collagen synthesis because wound repair requires amino acids and cofactors; collagen deposition is further compromised by poor glycaemic control, which promotes advanced glycation end-products that cross-link collagen and make it less compliant. The combination of infection, malnutrition, and diabetes weakens the fascial and dermal repair, so the wound edges separate (dehiscence) when tension is applied. Granulation tissue at the base indicates that repair is ongoing but insufficient to restore tensile strength. The key judgement is to recognise that dehiscence is not simply a mechanical failure but the outcome of an unfavourable balance between collagen synthesis and degradation, driven by persistent inflammation and metabolic derangement.
2. What are the priorities in managing this wound, and how would you monitor whether repair is progressing?
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Priorities are to control infection and provide optimal local and systemic conditions for repair. The wound should be opened and drained, necrotic tissue debrided, and the cavity packed to allow healing by secondary intention. Antibiotics should be guided by culture sensitivities; the presence of S. aureus and E. coli suggests a mixed aerobic and anaerobic flora, so broader cover may be needed until sensitivities return. Systemically, glycaemic control should be optimised (target HbA1c reduction over time, but acute glucose control now), and nutritional support with adequate protein (1.2–1.5 g/kg/day) and vitamin C and zinc should be provided. Monitoring includes serial measurement of wound dimensions, the amount and character of exudate, presence of healthy granulation tissue, and inflammatory markers (CRP, white cell count) trending downward. A rising CRP or persistent fever suggests uncontrolled infection or an undrained collection. Repeat debridement may be necessary if the wound remains static. The judgement is to balance aggressive local care with systemic optimisation, recognising that healing will be delayed and that secondary closure or skin grafting may be required once the wound is clean and granulating.