NICE to Know Series: Aneurysmal SAH Care in the ED and Beyond (Neurological Interventional Care in Emergencies)

Aneurysmal subarachnoid hemorrhage (aSAH) is a must-not-miss diagnosis in the emergency department (ED). An aneurysm is a localized dilatation or ballooning of a blood vessel wall. Risk factors include hypertension, age >50, smoking and genetics (i.e., polycystic kidney disease, family history).¹ The rupture of an intracranial aneurysm leads to bleeding within the subarachnoid space, where cerebrospinal fluid circulates, which leads to various pathophysiological consequences, such as hydrocephalus, inflammation, vasospasm and ischemic injury.

The classic presentation for patients suffering from an aSAH is a thunderclap headache or a sudden, severe headache that reaches its maximum intensity within minutes. Some patients may have had a milder sentinel headache that occurred days or weeks earlier. Other symptoms may include neck pain or stiffness, photosensitivity, nausea/vomiting, loss of consciousness and neurological deficits.² This description typically prompts the evaluation for subarachnoid bleeding; however, up to 12% of presentations are still missed.^3,4 Kowalski 2004 analyzed 56/482 SAH patients that were missed in the ED and looked at the predictors associated with missed diagnosis. One of the interesting associations was that there was a longer interval between the onset of symptoms and presentation in missed cases.⁵ This points to a bias among providers who might be assuming that patients with aSAH would present on the day of aneurysm rupture.

SAH is a devastating condition with high morbidity and mortality; roughly two-thirds of untreated SAH patients die or have serious neurologic disabilities consequently.⁶ In the ED, clinicians are tasked with promptly identifying an aSAH and implementing treatments that are geared towards the prevention of aneurysm rebleeding and the deleterious effects of acute hydrocephalus. Here we will dive into how the ED clinician can effectively diagnose aSAH, treatments and what comes next once the patient leaves the ED.

Case Presentation

A 57-year-old female with a history of hypertension presented to the emergency department after a syncopal episode. She was shopping at the mall when she suddenly collapsed. There were no reports of head trauma. Upon arrival at the ED, she was very lethargic and slow to answer questions. She reported having an intense headache that came on suddenly prior to her collapse. She is a current smoker. She is not taking any anti-platelet or anti-coagulant medications. She was maintaining her airway and aside from her drowsiness, her neurological examination was non-focal.

Ok, I am getting a CT scan – will it provide me with the answers to my biggest question?

A non-contrast computed tomography of the head (NCHCT) is the initial test for evaluating any intracranial hemorrhage. The sensitivity of detecting subarachnoid blood is 100% within six hours of symptom onset and up to 90% within twenty-four hours.⁷ Once identified, it is important to take note of a few key radiographic features: the presence of hydrocephalus, distribution of blood, intraparenchymal involvement and the presence of global cerebral edema.⁷

Hydrocephalus arises from obstruction of the brain’s normal cerebrospinal fluid (CSF) flow dynamics. An increase in CSF due to obstruction will lead to an increase in intracranial pressure (ICP) and patients can quickly decline. Temporal horn enlargement, trans-ependymal edema and bowing of the third ventricle are CT findings suggestive of obstructive hydrocephalus.⁸ These findings in conjunction with the patient’s mentation and neurologic examination are an indication of an ICP crisis and necessitate immediate intervention.

Mild hydrocephalus can occasionally be tolerated if the patient remains easily arousable, although very close neuro monitoring must be maintained in an ICU level setting due to the risk for rapid worsening of hydrocephalus. The treatment for acute hydrocephalus in the setting of aSAH is emergent ventricular drain (EVD) placement. This procedure is performed by a trained neurosurgeon but may occasionally be done in the emergency department if necessary. Intubation is not absolutely necessary prior to EVD placement but should be performed at the discretion of the ED attending.

The distribution of blood on a NCHCT may help discern the underlying etiology or location of the patient’s vascular insult. However, this will need to be further assessed with a CT angiography (CTA) of the brain. CTA has a 98% sensitivity and specificity for the detection of aneurysms >3mm in size.¹ CTA is helpful for our neurosurgical and neuro-interventional colleagues in planning an open craniotomy for aneurysmal clipping or endovascular coiling, respectively. The presence of associated intraparenchymal hemorrhage or diffuse cerebral edema indicates a higher severity of brain injury and carries a high rate of morbidity and mortality.¹

To tap or not tap…that is the question!

Performing a lumbar puncture to exclude SAH when there is a negative NCHCT remains the standard of care. A hemorrhage on NCHCT may begin to appear less hyperdense, making a subarachnoid bleed difficult to diagnose. A LP is used to evaluate for the presence of red blood cells and xanthochromia or the yellowish discoloration in the CSF. Xanthochromia is a result of red blood cell (RBC) breakdown, develops within 6-12 hours after aSAH and has a 93% sensitivity and 95% specificity when present for aSAH.^9,10

Despite advanced imaging techniques (i.e., CTA, MRI/MRA, diagnostic angiography) becoming more readily available, the presence of an aneurysm on CTA after a negative NCHCT does not confirm rupture.

LP can yield false-negative results, partially if performed too early after symptom onset or if the blood is localized in a small area of the subarachnoid space.¹¹ Mark 2015 reported 49 of 58 patients undergoing LP had either visible xanthochromia or a CSF RBC count greater than 2000×106 /L which safely identified an aneurysmal cause of subarachnoid hemorrhage.¹²Both LP and CTA are great diagnostic tools when evaluating aSAH; however, LP remains the best test in diagnosing a ruptured aneurysm since the treatment for an unruptured aneurysm is different.

Holy crap…that is a big bleed…what comes next?

So, you have cracked the case! You have identified the patient has an aSAH. Now what? As you begin to mobilize the cavalry (neurosurgery, neurology, neuro-ICU, neuro-interventional radiology) the ED provider must remember these key management considerations:

Antiepileptics

Seizures may be most frequent at the onset of aSAH.⁷ Several studies reported seizure activity in 6-26% of patients after aSAH.¹⁶ Seizure prophylaxis should be initiated and continued at least until after the aneurysm has been secured. The agent of choice is levetiracetam, with a loading dose upon arrival and a maintenance dose as patients transition to the intensive care unit (ICU). Seizure activity in the setting of an unsecured aneurysm increases the risk of aneurysm re-rupture carrying a high rate of mortality.¹⁶ Historically, phenytoin has also been used for seizure prophylaxis but recent data suggest that phenytoin is associated with worse neurologic and cognitive outcomes and should be avoided.¹⁷

External Ventricular Drains

An external ventricular drain (EVD) or ventriculostomy, is an invasive monitoring and therapeutic device that is inserted by a neurosurgeon. Placement of an EVD most frequently occurs in the ICU setting; however, there are cases where an increase in ICP and a decline in the patient’s mental status because of acute obstructive hydrocephalus (AOH) necessitates emergent placement in the ED. This device is carefully placed into the third ventricle by way of Kocher’s point (11cm posterior from the nasion and 3cm from the midline with a trajectory towards the ipsilateral medial canthus and a line extending coronally from the ipsilateral tragus).¹⁸An EVD is used to decrease ICP by diverting CSF from the intracranial compartment to an external drainage system. It is also used to quantify the ICP via a pressure transducer, which allows providers to swiftly treat any ICP elevations. This apparatus is closely managed by the neuro-intensivists and neurosurgical team.

During EVD placement, the ED attending has a critical role to play. BP management is paramount as spike in blood pressure during EVD placement may precipitate re-rupture of the aneurysm. For this reason, pain control, sedation and BP management are essential, in addition to airway control if necessary. ED management of these parameters allows the neurosurgeon to focus on proper placement of the ventricular drain.

Re-rupture

Re-rupture of an aneurysm and rebleeding occurs in ~15% of patients and carries a high mortality rate (50%).⁷ The risk of rebleeding increases over time in the setting of an unsecured aneurysm but highest in the first 24 hours. Factors associated with rebleeding include noxious stimuli, agitation, rapid drainage of CSF during ventriculostomy placement, agitation, hypertension and seizure activity.¹⁹ Only aneurysm securement is effective in definitively preventing rebleeding and should be performed as soon as possible.

Delayed Cerebral Ischemia (DCI) & Vasospasm

Vasospasm is the leading course of morbidity among patients who survive their initial SAH.²⁰The volume of blood located in the subarachnoid space can irritate the large arteries that reside there. This irritation can lead to vasospasm and decreased blood flow through the vessel causing ischemia to the downstream neuronal tissue. Nimodipine, a dihydropyridine calcium channel blocker, has a selective affinity for the calcium channels present in the smooth muscle cells of cerebral blood vessels. The vasodilation induced by nimodipine improves neurologic outcomes, likely through a neuroprotective mechanism. DCI may occur after 3-14 days with a peak around days 7-10.^13,19 Serial neurological examinations, transcranial Doppler and diagnostic angiography are methods used for DCI surveillance.

Disposition and Beyond

Patients with aSAH will always require the highest level of care in an ICU or a dedicated neuro-ICU. There are situations where patients will go directly to the operating room or the interventional radiology suite for securement of the ruptured aneurysm prior to admission to the ICU. Endovascular coiling of aneurysms has gained favor over neurosurgical clipping in recent years due to its safety profile and superior functional outcomes.^2,21 To note, aneurysms associated with intraparenchymal hematomas, broad neck aneurysms not amendable to coiling and patients with diffuse cerebral edema may benefit from open neurosurgical intervention.² Patients typically remain in the ICU for up to 21 days to closely monitor for DCI and treated for other systemic sequelae of ruptured aSAH, such as cerebral salt wasting, stress cardiomyopathy, neurogenic pulmonary edema and central fevers.

I am an ER doctor…what do I need to know?

• A good neuro-examination should be obtained upon arrival before any diagnostic or therapeutic interventions.
• A CT is 100% sensitive in detecting SAH within the first six hours, followed by a CTA if bleeding is present, to help identify the aneurysm and guide treatment planning.
• If after 12 hours of headache symptom onset and a negative CT, a lumbar puncture remains a useful diagnostic tool in revealing aSAH.
• Until the aneurysm is secured there is a high risk for re-rupture. To avoid rebleeding the ED provider should:
  • Treat pain aggressively
  • Obtain tight blood pressure control (goal SBP <120-140)
  • Administer anti-seizure prophylaxis
  • Obtain immediate neurosurgical consultation for EVD placement in the setting of acute obstructive hydrocephalus
  • Reverse coagulopathy
• Oral nimodipine should be used to prevent aSAH sequelae such as vasospasm and associated delayed cerebral ischemia but this is rarely a cause of patient deterioration in the emergency department.

Case Conclusion

Our patient was quickly transferred to the ICU where she received an EVD and subsequently underwent coiling of an anterior communicating artery aneurysm. She remained in the ICU for 21 days where close monitoring of her ICP was performed with the EVD in place and delayed cerebral ischemia was surveilled with daily transcranial dopplers (TCDs) and avoided with the use of nimodipine. She went home on hospital day 24 and has made a tremendous recovery.

References

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• Schievink WI. Intracranial aneurysms. N Engl J Med. 1997 Jan 2;336(1):28-40. doi: 10.1056/NEJM199701023360106. Erratum in: N Engl J Med 1997 Apr 24;336(17):1267. PMID: 8970938.
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