Fluid and electrolyte disorders following traumatic brain injury

Abstract

Abnormalities in salt and water balance are common following traumatic brain injury (TBI), manifesting clinically as either as hypo- or hypernatraemia. Dysnatraemia is associated with a greater risk of secondary brain injury from resultant changes in brain fluid levels, greater morbidity, longer length of hospital stay and in the case of hypernatraemia, greater mortality following TBI. Dysnatraemia occurs in the acute phase following TBI, is often transient and resolves in the majority of patients with recovery from the initial insult. Hyponatraemia secondary to the syndrome of inappropriate antidiuretic hormone is the commonest electrolyte disturbance following TBI although, iatrogenic causes and ACTH deficiency are important differentials to consider. Cerebral salt wasting syndrome is a rare cause of hyponatraemia following TBI. Acute symptomatic hyponatraemia predisposes to seizures and cerebral oedema and may be catastrophic, particularly if inappropriately treated. Hypernatraemia following TBI is most often due to AVP deficiency (AVP-D) and is an independent predictor of mortality. AVP-D is related to the severity of injury and is a poor prognostic indicator following TBI, often heralding rising intracranial pressure and death. In both hypo- and hypernatraemia early detection and prompt appropriate management is often life-saving. In this review we will discuss the pathophysiology of salt and water disorders following traumatic brain injury and provide detailed guidance on the approach to hypo- and hypernatraemia in this context.