5.10 Nutritional Management

“Adequate nutrition for patients with severe head injury during primary care, as well as in the acute rehabilitation unit, is an important part of medical management” (Denes, 2004). While clinicians sometimes disregard a patient’s nutritional condition, it can often have a critical impact on the patient’s recovery process and final outcome (Elovic, 2000). The nutritional management of patients recovering from ABI presents many challenges. Despite the efforts of the clinicians, several factors make is difficult to avoid malnutrition in ABI patients, beginning with the metabolic changes that occur post-injury (Elovic, 2000).

In the event of ABI the damage to the metabolic control center causes more severe and protracted systematic responses than seen in many other forms of injuries, 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).  Loan (1999) noted that directly secondary to ABI, a catabolic and counterrregulatory hormone (glucagons and cortical) increase takes place.  “Deficienceies of follicle-stimulating hormones (FSH), leutenizing hormone (LH), and growth hormone (GH) indicate alteration in the hypothalamin-pituitary feed-back mechanism that normally regulates metabolism” (Loan 1999).Depending on the severity of the injury, nutritional requirements will be markedly increased while gastroparesis and ileus may delay the initiation of enteral nutritional support in mechanically ventilated patients.

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/day have been reported within the first week following injury (Young et al., 1985; Weekes & Elia, 1996; Bruder et al., 1994; Wilson et al., 2001). 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).

Dénes (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.  Dénes (2004)concluded that there has been little research done regarding the complications and effects of malnutrition during rehabilitation.

5.10.1 The Incidence of Malnutrition

The incidence of malnutrition following ABI is difficult to estimate. No consistent criteria have been used to define it and relatively few studies have examined the issue. Given that accidental brain injuries 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. However, substantial weight loss within the first several weeks has been reported and is certainly indicative of a compromised nutritional state. Brooke et al. (1989) reported an average weight loss of 13.2 kg from the time or injury to admission to a rehabilitation facility, while Weekes and Elia (1996) also reported a weight loss from the time of injury to day 19 (9.8 kg) among 4 previously healthy young males.  In the early rehabilitation phase, Brooke et al. (1989) reported that 60% of patients were considered underweight, while Haynes et al. (1992) reported 58%. However, obesity has also been reported among patients, typically in the chronic phase of recovery (Henson et al.,1993).

Individual Studies

Table 5.18 Nutritional Status of Brain-Injured Patients

D&B = Downs and Black (1998) quality assessment scale score.

Discussion

A single study was identified which reported the nutritional state of patients in the chronic phase of recovery (French & Merriman, 1999). The mean time from injury to admission to the unit was almost 6 years. Among studies evaluating the nutritional status of patients in the acute phase of injury, only changes, which were typically declines, in nutritional parameters were reported. No studies attempted to classify patients as well or malnourished.  Although they reported no malnutrition among a cohort of patients recovering from ABI, the authors did not define their criteria for malnutrition and used a body mass index (BMI) of 20 or greater to indicate the absence of nutritional deficit. Fifty-three percent of patients were classified as either overweight or obese and consumed more calories than required.

A survey conducted by Krakau et al. (2007) also found 68% of patients who had sustained a ABI showed signs of malnutrition within the first two months of injury.
When first admitted to hospital all patients (n=64) initially received nutrition parenterally (PN) for the first 19 days following injury.  The majority of these patients (86%) then received nutrition enterally (EN), while a small number (14%) immediately moved to oral feeding. Of the 56 patients receiving EN, 14 underwent a gastrostomy approximately 1 month after injury.  It was found that 6 months post injury 84% of patients were nutritionally independent.

Conclusions

Two studies were found assessing malnutrition in brain injured patients; however, only one reported seeing signs of malnutrition in patients within the first two months post injury.  The results of one study indicate the incidence of obesity was comparable to normal.

5.10.2 Hypermetabolism Post-ABI

Hypermetabolism is a well known metabolic sequalla 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 cytolines (Pepe & Barba, 1999).  Tremendous variability has been reported regarding the magnitude of the hypermaetabolic state post ABI. (see Table 5.19). The variations are likely due to the timing of the measurements, patient characteristics (initial level of injury, concomitant infections) and management (i.e. craniotomy, intubation and sedation and/or barbiturate use, ambient temperature).

Individual Studies

Table 5.19 Elevations in Resting Energy Expenditure (REE) Following ABI

D&B = Downs and Black (1998) quality assessment scale score.

Conclusions

Based on a series of studies, 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.