Description

Many patients who are severely injured from an episode of trauma are unable to eat. There are many reasons for this not least a physical inability. Even those less severely injured patients, who are physically able, may not eat enough to support their metabolic state. Hospital food is notoriously unappealing and the injury associated pain together with the pain relief (usually opioids) may be such to cause marked anorexia and nausea. Metabolic deficits are difficult to make up and their influence on the natural history of the injury depends very much on the underlying nutritional state of the individual. It is important for the medical attendants to address this issue early on in the post-injury period.


Key points

Many patients who are severely injured from an episode of trauma are unable to eat.

The metabolic response to trauma


The metabolic response to injury involves a number of well described events triggered and influenced by various mediators. A catabolic state ensues designed to mobilise substrates that can be used by those regions of the body involved in the recovery from injury. This results in fat mobilisation, hyperglycaemia, salt and water retention and net protein breakdown (Meguid et al. 1974, Weissman 1990, Wilmore. 1991, Oppeheim et al. 1980). Fever, tachypnoea, tachycardia and a raised white cell count are the usual clinical correlates. Collectively this is known as the stress response or more recently the term “Systemic Inflammatory Response Syndrome” (SIRS) has been used (AMCP/SCCM 1992).

Key points

A catabolic state ensues designed to mobilize substrates that can be used by those regions of the body involved in the recovery from injury.

Mediators of the metabolic response


The mediators of the stress response can be broadly divided into two groups. Firstly, there are those that are released from stimulation of the neuroendocrine axis ie. hormones. Secondly, there are those with a primary immunological function such as cytokines. The response however is complex, involving the release of multiple mediators that are interconnected by amplification loops and negative feedback signals (Winmore 1991, Grimble 1996).


Key points

Mediators are neuroendocrine and immunological


The neuroendocrine axis

Hormones are released from afferent neuronal stimulation and also via cytokine release at the site of injury. A list of the major hormones involved in the stress response and their effects is seen in Table 36.1.



Cytokines and other mediators

Cytokines are a group of proteins or peptides released from a variety of cells in response to injury. They influence the immune response as well as producing widespread metabolic changes (Grimble 1996), (see Table 36.3). Cytokines may be considered pro-inflammatory or anti-inflammatory. Some pro- inflammatory cytokines such as IL-8, IL-1 and TNF- lead to the production of nitric oxide and other oxidant molecules which may damage the host. Furthermore cytokines such as IL-1 and TNF- induce further production of IL-6 and of themselves. Excessive or inappropriate production of cytokines has been associated with increased morbidity and mortality. Other cytokines such IL-4 and IL-10 are anti-inflammatory and inhibit IL-1 and TNF- production. A list of cytokines and other immune mediators are shown in Table 36.2.



Alteration of the stress response

The value of the stress response is evident by the poor outcome of sympathectomized and adrenalectomized animals when starved. However a prolonged stress response with production of cytokines is believed to contribute to the occurrence of multiple organ failure (Beal and Cerra 1994). The challenge lies in modulation of the stress response to the advantage of the host. This may be achieved by diminishing or preventing the signal at four levels;

The initial stimulus
Gene transcription and translation of the cytokines
Stimulation of effector cells
Transduction of the cell sig