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The key to the treatment of unconsciousness is an understanding of the underlying pathophysiology. Management of the unconscious patient should be targeted towards the diagnosis and treatment of the cause combined with supportive care of the patient, while the ultimate cause is elucidated. The basic tenants of emergency and critical care medicine—the ABC’s—apply to the unconscious patient with particular care if occult cervical spine injury is a possibility. The prognosis of disorders of consciousness depends heavily on the aetiology and accurate prognostication can be difficult even when the underlying cause has been determined.

Changes in consciousness are seen in a range of physiological and pathological settings including sleep, anaesthesia, brain lesions, metabolic disturbances, and complex partial or generalized seizures. In neurobiological terms, consciousness may be viewed as having an arousal dimension and an awareness dimension phenotypically expressed as the capacity to respond to self or environmental stimuli. Loss of consciousness is associated with lesions that disrupt neuronal systems in the brainstem and diencephalon that mediate arousal or thalamocortical or corticocortical systems that mediate awareness. As there are many causes of unconsciousness, a timely and focused history and neurologic examination are critical to defining the differential diagnosis.

Chapter 26 is an introduction to devoted to biological mechanisms underpinning organ dysfunction and repair in critical illness, and how research has generated fundamental insights into the biology of conditions, such as sepsis and ARDS, and has suggested important new therapeutic paradigms. It also specifically addresses issues surrounding genetic susceptibility, cognitive deficiency, frailty, myocardial ischaemia, muscle wasting, sepsis-associated encephalopathy (SAE), CIP, and structural muscle alterations.

The cognitive reserve hypothesis suggests that the structure and function of an individual’s brain can modulate the clinical expression of brain damage and illness. This chapter describes passive and active models of reserve, their impact on neurological illness, and how these effects can be assessed. Passive models focus on the protective potential of anatomical features, such as brain size, neural density, and synaptic connectivity, while active models emphasize the connectivity and efficiency of neural networks and active compensation by alternative networks. It is likely that both models represent features of a common biological substrate and could help in the development of strategies to improve outcome following critical illness.