Ensuring patients with ABI have adequate nutrition is an important part of their medical management (Denes 2004), as it has a critical impact on the patient’s recovery process and final outcome (Elovic 2000). Denes (2004) stated that rehabilitation problems associated with severely malnourished ABI patients include an increased occurrence of complications, a greater challenge in patient mobilization, an increased frequency for the need to operate on contractures and a longer length of stay in a rehabilitation unit. Despite clinicians’ efforts several factors make is difficult to avoid malnutrition in patients with ABI patients, beginning with the metabolic changes that occur post injury (Elovic 2000). Post ABI, the damage to the metabolic control center causes more severe and protracted systematic responses than seen in many other forms of injuries. The former is a possible consequence of the change in feedback mechanisms post injury and the brains’ critical role in triggering the metabolic response (Young et al. 1992).
Secondary to ABI, a catabolic and counter regulatory hormone (glucagons and cortical) increase takes place (Loan 1999). Deficiencies of follicle-stimulating hormones (FSH), leuteinizing hormone (LH), and growth hormone (GH) indicate alteration in the hypothalamic-pituitary feed-back mechanism that normally regulates metabolism (Loan 1999). As a result of hypermetabolism and hypercatabolism, both energy and protein requirements will be elevated in the first several weeks following injury. Negative energy and nitrogen balance, which may exceed 30 grams per day, have been reported within the first week following injury (Bruder et al. 1994; Weekes & Elia 1996; Wilson et al. 2001; Young et al. 1985). Unfortunately, although muscle wasting occurs as a consequence of bed rest and immobilization, only a portion of these losses are responsive to nutritional interventions (Behrman et al. 1995).
The Incidence of Malnutrition
The incidence of malnutrition following ABI is difficult to estimate as there are no consistent criteria used, and relatively few studies have examined the issue. Given that ABI tend to occur in younger, previously healthy individuals, it is unlikely that pre-existing nutritional deficits are prevalent at the time of injury. Therefore, declines in nutritional parameters are most likely directly related to the metabolic effects of the injury. Brooke et al. (1989) reported an average weight loss of 13.2 kg from injury to rehabilitation admission, while Weekes and Elia (1996) reported 9.8 kg of weight loss from the time of injury to day 19 in four previously healthy young males. In the early rehabilitation phase, a substantial amount of patients are underweight (approximately 60%; Brooke et al. 1989; Haynes 1992); however, obesity has also been reported among patients, typically in the chronic phase of recovery (Henson et al. 1993).
A single study was identified which reported the nutritional state of patients in the chronic phase of recovery and found individuals had adequate nutrition (French & Merriman 1999). The mean time from injury to admission to the unit approached six years. However, a survey conducted by Krakau et al. (2007) found 68% of patients who had sustained an ABI showed signs of malnutrition within the first two months of injury. When first admitted to hospital all patients initially received nutrition parenterally for the first 19 days following injury. The majority of these patients (86%) then received nutrition enterally (Krakau et al. 2007).
Following an ABI, malnutrition may be present in patients with severe injuries within the first months post injury.
The incidence of obesity in the chronic stages of injury was comparable to the normal population.
Hypermetabolism is a well-known metabolic sequelae of ABI. Hypermetabolism has been defined as an increase in metabolic rate above that which is predicted using equations, which take into account age, sex, height, and weight (Souba & Wilmore 1999). The hypermetabolic state, which is characterized by increased oxygen consumption and nitrogen excretion following injury, is thought to be mediated by an increase in i) counterregulatory hormones such as epinephrine, norepinephrine and cortisol; ii) corticosteroids; and iii) proinflammatory mediators and cytokines (Pepe & Barba 1999). Tremendous variability has been reported regarding the magnitude of the hypermaetabolic state post ABI. The variations are likely due to the timing of the measurements, patient characteristics (i.e., initial level of injury, concomitant infections) and management (i.e., craniotomy, intubation and sedation and/or barbiturate use, ambient temperature).
There is Level 4 evidence of a hypermetabolic state in the acute period following ABI. The extent of the response can be moderated by barbiturates.
Patients with ABI are often acutely hypermetabolic.