What is the treatment for neurostorming?

Treatment of Neurostorming (Paroxysmal Sympathetic Hyperactivity)

Neurostorming should be treated with a multimodal pharmacologic approach combining sedation (propofol or midazolam), opioid analgesia (fentanyl), beta-blockade (labetalol or propranolol), and dopamine agonists (bromocriptine), while simultaneously minimizing external stimuli and avoiding frequent neurological checks that can trigger episodes. 1

Immediate Pharmacologic Management

First-Line Agents

• Administer labetalol as the primary beta-blocker to control acute hypertension and tachycardia during storming episodes 1
• Initiate continuous sedation with either propofol or midazolam to suppress sympathetic outflow and reduce the frequency of episodes 1
• Provide continuous opioid analgesia with fentanyl infusion to blunt pain-mediated sympathetic responses 1
• Add dexmedetomidine for its central alpha-2 agonist effects, which reduce sympathetic tone without respiratory depression 1

Second-Line Agents for Refractory Cases

• Bromocriptine (dopamine agonist) should be added when first-line agents fail to control episodes, as it helps restore hypothalamic-brainstem regulation 1
• Propranolol can be used as an alternative or adjunct to labetalol for more sustained beta-blockade 1

Environmental and Supportive Measures

Minimize Triggering Stimuli

• Reduce the frequency of neurological examinations and vital sign checks to the minimum necessary, as these are potent triggers for sympathetic storms 1
• Limit unnecessary patient manipulation, including routine turning, suctioning, and bathing during acute phases 1
• Maintain a quiet, low-stimulation environment with minimal lighting and noise 1

Temperature Management

• Treat hyperthermia aggressively as it both results from and exacerbates sympathetic storming 1
• Note that hypothermia protocols can mask the manifestations of paroxysmal sympathetic hyperactivity, so be vigilant when rewarming patients as storming may emerge 1

Monitoring and Recognition

Clinical Features to Monitor

• Acute onset of nonstimulated tachycardia, hypertension, tachypnea, hyperthermia, external posturing, and diaphoresis occurring in paroxysms characterize sympathetic storming 1
• Episodes occur without external provocation but can be triggered by routine care activities 1

Associated Conditions

• Neurostorming is most frequently associated with severe traumatic brain injury but can occur with subarachnoid hemorrhage (especially with vasospasm), intracranial tumors, hydrocephalus, severe hypoxic brain injury, and intracerebral hemorrhage 1
• Vasospasm may be a precipitating factor in SAH-related cases 1

Important Caveats

Masking Factors

• Neuromuscular paralysis and therapeutic hypothermia can completely mask the clinical manifestations of sympathetic storming, leading to delayed recognition when these interventions are discontinued 1
• Clinicians must maintain high suspicion when weaning sedation or rewarming patients with severe brain injury 1

Duration and Resolution

• Sympathetic storming can be prolonged, lasting weeks in some cases despite aggressive treatment 1
• Timely adjustment of medications combined with minimization of exogenous stressors is essential for resolution 1
• Intermittent recurrence is common even with treatment, requiring sustained vigilance 1

Relationship to Intracranial Pressure

• While sympathetic storming can occur with elevated ICP, the treatment priorities differ from standard ICP management 2, 3
• If elevated ICP is present concurrently, maintain cerebral perfusion pressure >60 mmHg through volume replacement and/or catecholamines as needed 4
• Standard ICP treatments (mannitol, hypertonic saline, hyperventilation) should be employed if ICP elevation is documented, but these do not directly treat the sympathetic storming 2, 3