Initial approach, supportive care, risk stratification, and management of the troublesome complications for ruptured subarachnoid aneurysm, with Thomas Lawson (@TomLawsonNP), nurse practitioner in the neurocritical care unit at OSU Wexner Medical Center.
- SAH + shock or hypoxemia = suspect neurogenic pulmonary edema and/or Takotsubo cardiomyopathy.
- Aneurysmal SAH is much different from traumatic and other etiologies of SAH. Not only does it require securing the aneurysm (early rebleeding is associated with substantially increased mortality), it conveys generally greater morbidity.
- The “hanging chicken sign” at the base of the skull (across the basilar cisterns) is the most distinctive SAH finding on head CT. Look also for associated IPH or IVH, as well as signs of hydrocephalus, such as third ventricle enlargement or presence of a temporal horn in the lateral ventricles (normally just a faint C-shaped slit).
- Use either the Hunt and Hess or WFNS scores to prognosticate mortality, while considering the Modified Fischer score to assess risk of vasospasm, a complication usually occurring between 3–14 days (sometimes up to 21) days after onset of symptoms.
- With any acute neuro changes in the SAH patient, strongly consider the “stat stat” head CT to assess for rebleeding or worsening hydrocephalus. Also assess for functioning of an EVD, as an obstructed tube may indicate hydrocephalus as well.
- For deterioration in later timeframes, go with a CTA (or transcranial dopplers) to assess for vasospasm. If present, talk to your neurointerventionalists about offering catheter-directed vasodilators, such as verapamil or nicardipine; also, augment the BP to perfuse past the spasm.
- Many patients who spasm will continue to spasm. Watch diligently as some may need repeated neuro-intervention. IV milrinone and intra-thecal nicardipine (into an EVD) are available as last-ditch efforts.
- CTA will not show thrombosed aneurysms; such patients need a catheter angiogram and/or repeat imaging.
- “Triple H therapy” for SAH—hypertension, hypervolemia, and hypernatremia (or hemodilution) is dead. Just shoot for reasonable hypertension, plus euvolemia. Target a normal MAP and SBP <220.
- Polyuria should prompt concern for cerebral salt wasting, which is often followed by vasospasm. It can be distinguished from SIADH by the presence of hypovolemia.
- If a patient has no seizures noted, a 3–7 day course of anti-epileptics (e.g. levetiracetam) is reasonable. If they do seize, continue for longer.
- EVDs can come out when the daily drainage is dwindling. Then wean by raising the pop-off by about 5 cm H2o per day, monitoring the neuro exam and perhaps CT scans. Once at 20 cm H2O, clamp it, then consider removal. Occasionally patients may have permanent dysfunction of their arachnoid granulations and need a VP shunt, although this must usually be placed in a delayed fashion to avoid blockage by proteinaceous CSF early on.
Consensus guidelines: Grasso G, Alafaci C, Macdonald RL. Management of aneurysmal subarachnoid hemorrhage: State of the art and future perspectives. Surg Neurol Int. 2017 Jan 19;8:11. doi: 10.4103/2152-7806.198738. Erratum in: Surg Neurol Int. 2017 Apr 26;8:71. PMID: 28217390; PMCID: PMC5288992.
IV milrinone: Lannes M, Teitelbaum J, del Pilar Cortés M, Cardoso M, Angle M. Milrinone and homeostasis to treat cerebral vasospasm associated with subarachnoid hemorrhage: the Montreal Neurological Hospital protocol. Neurocrit Care. 2012 Jun;16(3):354-62. doi: 10.1007/s12028-012-9701-5. PMID: 22528278.