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with an atypical organism. Thus, a biopsy for culture and sensitivity testing is indicated.
Patient factors
Underlying disease can be considered from two viewpoints: disease arising due to the trauma that caused the wound to be sustained, and pre-existing concurrent disease. Trauma can cause a number of issues which will have a knock-on effect in respect to wound healing times including; shock, hypoperfusion, or dehydration, concurrent organ dysfunction, e.g. respiratory, renal, gastrointestinal compromise/damage. Patients may also have a concurrent disease process that can hinder wound healing. Hyperadrenocorticism (Cushing’s disease), diabetes mellitus, hypothyroidism, anaemia, are some of the disease processes, which can delay wound healing.
Nutritional status
Adequate nutritional intake is vital for wound healing
to occur, and should be a priority in all critical/ trauma patients. A catabolic state, attributable to malnutrition, is
a major contributing factor to nonhealing wounds. In this condition, the body does not have the necessary protein and energy sources (fats and carbohydrates); therefore, existing stores of protein are broken down to maintain basal functions. This means, the increased calorific and protein demands for healing are not available, and the wound becomes quiescent. Glucose and protein are important for normal progression of wound healing. Glucose is the primary source of energy for leukocytes and fibroblasts. It is the integral molecule within the ground substance that is laid down by the fibroblasts. Deposition of this is necessary before collagen formation. Thus, glucose deficiency can affect collagen formation and wound strength. Depletion of protein stores can
result in attenuated fibroplasia and prolonged healing time. It is vital that patients receive adequate protein levels, as they are necessary for animals undergoing healing. Sufficient protein levels help to prevent oedema and promote increased fibroplasia with increased wound strength. Zinc deficiency can result in lack of replication
of epithelial cells and fibroblasts, causing a weak wound and lack of epithelialization. At the other extreme, an elevated zinc concentration can inhibit macrophages, decrease phagocytosis, and interfere with collagen cross linking to have a negative effect on healing, and should be considered once other factors have been excluded. Ideally the patient’s nutritional status on admission to the practice should be noted, including a Body Condition Score and weight and this should be performed daily during the hospitalization period. If there is concern that the patient
is unable to achieve its resting energy requirement alone, then assisted feeding techniques such as the placement of oesophogostomy or gastrotomy tubes should be commenced. Many of these patients will require general anaesthesia as part of a wound management protocol,
An Urban Experience
e.g. wound debridement, and so the opportunity for
the placement of a feeding tube is likely to be available. For patients requiring sedation or anaesthesia over a prolonged period of time, nutritional status may also need to be addressed in terms of prolonged periods of starvation prior to anaesthesia, and in these cases the patient’s calorific requirements should be calculated and compared against the actual calorie intake of the patient.
Surgeon factors
The surgeon dealing with the wound management of the patient will ultimately have an effect on the likelihood of complications occurring. There are various issues that can be created during wound closure:
Postoperative haemorrhage and haematomas
The presence of post-operative haemorrhage, or haematoma formation, may delay wound healing
by putting pressure on suture lines, providing a rich environment for infection and cause discomfort to the patient, thus resulting in self-trauma. In addition to the indirect effect on wound tension, there is experimental evidence that postoperative hematoma formation
can directly affect flap survival where reconstructive surgery has been performed. Adherence to Halstead’s principles, including effective haemostasis, can help
to prevent this. Minor incisional haemorrhage can be controlled with direct manual pressure for 10 to 15 minutes, but moderate to severe haemorrhage will require further intervention. Conservative management involving placement of pressure bandages, movement restriction and fluid deficit replacement can be instituted initially if the patient is stable. In more severe cases of haemorrhage, or those not responding to conservative management, surgical intervention may be required to identify the source and provide definitive haemostasis.
Wound dehiscence
Dehiscence is defined as the breakdown of a surgically closed wound. Signs of a problem incision may be erythema, oedema or pain with signs of imminent wound dehiscence including necrosis of the skin edges, extensive cutaneous bruising, the presence of serum beneath the skin and serosanguinous discharge from the suture line. The most common causes of wound dehiscence include:
• Excessive tension
• Ischaemic or necrotic wound edges
• Inappropriate suture material or suture pattern selection
• Accumulation of moisture leading to tissue maceration
• Underlying pocket of infection, necrosis, foreign body or neoplasia
• Lack or inappropriate postoperative protection/ support (e.g. bandage, Elizabethan collar)

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