15–33% of patients following severe traumatic brain injury (GCS 8 or less) can develop an exaggerated stress response which goes by many names in the literature such as dysautonomia, paroxysmal autonomic instability with dystonia, autonomic dysfunction syndrome and diencephalic seizures. All refer to the sequelae of an overactive, under-inhibited sympathetic nervous system. The exact pathophysiology is unknown, but there is an imbalance or disassociation between the sympathetic and parasympathetic nervous systems. The incidence of sympathetic storming appears to be greater in patients with diffuse axonal injury and brain stem injury.

Clinical diagnosis

Various diagnostic criteria exist but Blackman et al (2005) include:
• temperature of 38.5°c or greater
• hypertension
• tachycardia > 130bpm
• respiratory rate > 40 breaths per minute
• intermittent agitation
• diaphoresis
• dystonia

These features need to occur for at least three days with at least one cycle per day for a diagnosis to be made and not all of these symptoms may occur. Episodes are often unprovoked, but can be precipitated by routine care tasks, eg. turning and suctioning. Early episodes may be masked by sedation or the use of paralysing drugs. Autonomic storming occurs with a mean duration of 74 days post injury, hence it may happen after transfer outside of critical care and in a rehabilitation setting.

Adverse effects

There is a risk of secondary brain insult from the widespread effects of untreated sympathetic storming, including hypertension, cerebral hypoxia, hyperglycaemia, hyperthermia, arrhythmias, hypernatraemia and rhabdomyolysis.

Clinical management

Treatment is symptomatic. As with many other brain injury related conditions, the symptoms are treated independently, and there is no specific treatment of the underlying cause (neural damage).

Due to the wide array of neurotransmitters that are involved in the management of the sympatmetic nervous system, a wide array of medications that impact upon those neurotransmitters may be useful. Opiate receptor agonists, dopamine agonists, beta-blockers, alpha blockers, GABA agonists and sedatives are all used. The NCCU staff will be well versed in treating this condition and can offer advice for patients outside the NCCU setting.

Educating and supporting the patient’s family is very important as these events look very alarming and they may fear that an irreversible deterioration has taken place.