Emergency Neurological Life Support

Subarachnoid Hemorrhage Protocol

Version 5.0

Authors
Sayona John, MD
William J. Meurer, MD, MS
Stephanie Qualls, RN, BSN, CNRN
Brian L. Edlow, MD

Last updated:
October 2022

Protocol developed by:

Sayona John, MD
Brian L. Edlow, MD
Subarachnoid Hemorrhage Algorithm
 Subarachnoid Hemorrhage Protocol

Checklist
☐ Airway, breathing, circulation
☐ Head computed tomography (CT)
☐ Laboratories: PT/INR, PTT, CBC, chemistries, troponin, toxicology screen
☐ 12 lead ECG
☐ Target SBP goal < 160 mmHg
☐ Consult neurosurgery/NCC team
☐ Address hydrocephalus if present

Communication
☐ Airway status
☐ Hemodynamic status and blood pressure control (BP goals)
☐ Clinical presentation (level of consciousness, motor examination, pupils)
☐ WFNS score and Hunt–Hess Grade
☐ Imaging findings /LP results
☐ Coagulopathy present?
☐ Hydrocephalus present?
☐ Medications given (dose and time administered), including sedatives, analgesics, seizure
prophylaxis, anti-hypertensives, and nimodipine
☐ Coordination of other vascular imaging

Sample sign off narrative:

“I am signing out a 56-year-old female with history of smoking and hypertension”.
“She complained of a sudden onset of severe headache that woke her up from her sleep GCS
on presentation was 14 and BP was 185/92.
We drew labs and sent him for a head CT”.
“CT completed at 8:30 AM showed diffuse subarachnoid hemorrhage, no intraventricular
hemorrhage or hydrocephalus. CTA shows an anterior communicating artery measuring 7
mm”.
“When she returned to the ED, he was sleepier, with a GCS of 5, so he was intubated using
rocuronium and etomidate”.
“Her labs came back with a Troponin of 0.9 and ECG with diffuse T wave inversions. Her chest
x-ray reveals mild volume overload”.
“Neurosurgery has been called, and they are on their way to see him. She is in ED
Resuscitation Room 3, intubated and sedated now on propofol at 30
mcg/kg/min and fentanyl 50 mcg/hr. His BP is 140/80 with no other treatment”.
“They are ready to take him in Bed 12 in the NCCU in 5 min. Nursing is also calling report”.

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 Subarachnoid Hemorrhage Protocol
Subarachnoid Hemorrhage (SAH)
Blood within the subarachnoid space

Subarachnoid Hemorrhage (SAH) is most commonly produced by trauma and next most
common by a ruptured intracranial aneurysm. For the latter, it is imperative that a timely
diagnosis is made because the prevention of aneurysm re-rupture can be lifesaving.

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Clinical Diagnosis of Subarachnoid Hemorrhage (SAH)
Clinical features

The diagnosis of traumatic SAH is based on history and brain imaging. The protocol for
management of traumatic SAH can be found under the ENLS protocol Traumatic Brain Injury.

Aneurysmal SAH has a classic presentation though signs and symptoms may vary.

Classic presentation:
• Abrupt onset of a sudden, severe headache; onset is typically less than 1 minute.
• The headache is a NEW, QUALITATIVELY DIFFERENT headache for the patient.
• May have neck pain, nausea and vomiting.
• The patient may transiently lose consciousness, or present in coma.
• The nature and onset of the headache is the key distinguishing feature from other
forms of stroke, syncope, and seizure.

Variant presentation:
• Headache is not reported as abrupt (the patient may not remember the event well).
• Headache responds well to non-narcotic analgesics or “anti-migraine” medications.
• Headache resolves on its own within hours.
• Approximately 50% of patients with SAH will have a normal neurological
examination. They may or may not have meningismus (which may take time to
develop) and do not necessarily appear acutely ill.

Key aspects of the neurological examination:

• Glasgow Coma Scale (GCS)
• Pupillary exam
• Fundoscopic exam for subhyaloid hemorrhages
• Neck exam for meningismus
• Focal neurological deficits

Determine the clinical severity of the SAH using one of the scales below:

World Federation of Neurological Societies (WFNS) scale:

Grade 1: GCS 15
Grade 2: GCS 13-15 without neurological deficit
Grade 3: GCS 13-15 with neurological deficit
Grade 4: GCS 7-12
Grade 5: GCS 3-6

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Hunt-Hess Scale (increase by 1 grade for angiographic vasospasm or serious systemic
illness):
Grade 1. Asymptomatic, mild headache, slight nuchal rigidity
Grade 2. Moderate to severe headache, nuchal rigidity, no neurologic deficit other than
cranial nerve palsy
Grade 3. Drowsiness / confusion, mild focal neurologic deficit
Grade 4. Stupor, moderate-severe hemiparesis
Grade 5. Coma, decerebrate posturing

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Airway
Assess need for intubation

Factors contributing to necessity of intubation include:

• Inability to protect airway
• Hypoxia resistant to supplemental oxygen
• Expected decompensation during transport within hospital or to another hospital

See ENLS protocol Airway, Ventilation and Sedation.

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 Subarachnoid Hemorrhage Protocol

Prehospital Care
A variety of prehospital neurological examination tools, including the Cincinnati Prehospital
Stroke Scale, Los Angeles Prehospital Stroke Screen, National Institutes of Health Stroke
Scale, Miami Emergency Neurological Deficit Scale, and Glasgow Coma Scale, are used by
emergency medical services personnel. For patients presenting with isolated headache who
are neurologically intact, there are no specific prehospital interventions, apart from
consideration of analgesics. For patients presenting with a headache and neurological deficits,
pre-notification of the ED staff about the neurological deficits and the finger stick glucose are
important first steps. Patients who are severely encephalopathic, comatose, or vomiting
repeatedly may need to have their airway controlled by tracheal intubation in the field. Care at
a certified comprehensive stroke center that can provide neurosurgical and endovascular
consultation is recommended.

See ENLS protocol Acute Ischemic Stroke for prehospital protocol pertaining to SAH and other
types of stroke.

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Brain Imaging for SAH

If you suspect SAH by history, head imaging is the next step

Non-contrast CT imaging of the brain is the gold-standard for identifying SAH (Class1, LOE B).
• However, CT imaging is more sensitive in the first few days following a SAH and
becomes progressively less sensitive with the passage of time (by day 5 sensitivity
drops to 60-85%). Other reasons for a false negative CT include anemia, low
volume SAH and a technically poor scan.
• Some clinicians advocate for a CT angiogram (CTA) at the time of the CT scan to
look for an intracranial aneurysm. Although this is helpful if an aneurysm is seen,
the negative predictive value is less clear. One should not use a negative CTA
alone to rule out SAH.
• MRI is highly sensitive for intracranial hemorrhage but is most useful in patients who
present a few days following the SAH; hemosiderin sensitive sequences are most
useful in identification of SAH.

A CT image of an aneurysmal SAH is shown below:

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CT Confirms SAH
Blood is seen on the CT scan

The diagnosis of SAH is confirmed and cerebrospinal fluid analysis is not necessary.

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CT Scan is Negative - Perform Lumbar Puncture (LP) Next

Must perform an LP if the CT is negative

Recent data suggest that non-contrast CT imaging of the brain is close to 100% sensitive for
SAH if all of the following are true:
• The patient has a classic presentation with a thunderclap headache,
• The CT is done within 6 hours of headache onset,
• The patient is completely neurologically intact, and
• The CT is read by an attending radiologist (or someone with equivalent experience
reading brain CT scans)
If all of these criteria are met, clinicians can consider not doing an LP. The sensitivity of CT in
these patients is ~ 99.5% (may miss a SAH in 1-2 patients per 1,000 who fulfill all of these
criteria).

However, if these criteria are not met, one should perform an LP to determine if the patient has
a radiographically occult SAH.

The LP is done to look for xanthochromia. Xanthochromia is the yellowish discoloration of

CSF by heme breakdown products (chiefly bilirubin). It takes several hours for blood in the
subarachnoid space to break down, so the presence of xanthochromia is time dependent and
is nearly universally present after 12 hours from onset of hemorrhage.
• If the CSF shows xanthochromia, the diagnosis of SAH is confirmed (CSF protein
exceeding 100 mg/dl can lead to a false positive).
• If the CSF is clear of RBCs and xanthochromia is absent, it is highly unlikely that the
patient had a subarachnoid hemorrhage. However, a rapidly expanding aneurysm
without subarachnoid rupture can present with a classic thunderclap headache
(‘sentinel headache’ which typically occurs about 2-8 weeks prior to overt
subarachnoid hemorrhage). If there is ongoing clinical suspicion for an aneurysm on
clinical grounds, emergent neurosurgical consultation is recommended.

In summary, the typical findings of SAH on cerebrospinal fluid analysis are:

• Presence of RBCs (generally in the thousands)
• < 5 WBCs
• WBC:RBC ratio 1:700
• Xanthochromia is present
• Minimal clearing of RBCs between tubes 1 and 4 (fewer than 2000 x 106/L RBCs in
the final tube and the absence of xanthochromia had a negative predictive value of
100% (95% confidence interval 99.2 to 100%) for excluding SAH).

Note:
• The sensitivity of all tests for SAH are dependent upon the time from the bleed. CT
is more sensitive early and less so with time. RBCs in the spinal fluid is also more

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likely to be seen early and will clear with time. Xanthochromia is absent early and
nearly always present by 12 hours after the bleed.
• Spectrophotometry is more sensitive (but much less specific) for xanthochromia than
is visual inspection (spin down CSF, compare to water in neutral light; see figure
below); however visual inspection is the only test available at most hospital labs.

Typical appearance of xanthochromia (left) compared to water (right). CSF is centrifuged first
to take any RBCs out of solution.

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SAH is Confirmed
CT or LP evidence of SAH

Diagnosis of SAH is confirmed. The goal is to reduce the chance of aneurysm re-rupture and
expedite treatment of the aneurysm while preventing any medical complications.

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Initial Orders
First steps

Once SAH is confirmed, in addition to the items outlined below (neurosurgical consultation,
seizure prophylaxis, reverse coagulopathy, treatment of anxiety and pain, and blood pressure
management):
• Bed rest with cardiac monitoring
• 12-lead electrocardiogram
• Labs
o Blood: CBC, coagulation tests (prothrombin time, partial thromboplastin time,
international normalized ratio), electrolytes, renal function tests, troponin, and a
type and screen
o Urine: toxicology screen

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Neurosurgical Consultation
Definitive therapy is obliteration of the aneurysm, by either endovascular coiling or surgical
clipping. Both of these therapies isolate the aneurysm from the cerebrovascular circulation
and should be carried out as soon as feasible, ideally within the first 24 h of presentation.

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Seizure Prophylaxis
Should one prescribe anticonvulsants now?

• Approximately 20% of SAH patients have seizures prior to hospital arrival, and another
5–10% experience seizures after admission.
• Early seizures may increase the risk of aneurysm re-rupture and elevated intracranial
pressure (ICP).
• Acute seizures should be treated with antiseizure medications.
• In patients with persistent altered mental status, non-convulsive status epilepticus may
be present, which can only be diagnosed by continuous electroencephalography (EEG).
• Both the AHA and NCS guidelines suggest consideration of antiseizure medications in
the immediate post-hemorrhage period.
• A very short course of prophylactic antiseizure medications may be recommended in
the period following diagnosis and before definitive aneurysm treatment because of a
concern for seizure-related aneurysm re-rupture.
• As phenytoin may lead to worse long-term cognitive outcomes, the use of a different
agent should be considered. Refer to ENLS Pharmacology module for more
information.

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Reverse Coagulopathy
Coagulopathy should be urgently treated.
• Patients taking Vitamin K antagonists including warfarin with an INR ≥ 1.4 should be
treated with some combination of IV vitamin K (10 mg IV), and prothrombin complex
concentrates.
• Fresh Frozen Plasma (FFP) is an alternative for reversal if PCC is unavailable.
• Thrombocytopenia (platelets < 100,000) can be treated with platelet transfusions.

See the ENLS Pharmacology protocol regarding reversal of Factor Xa and thrombin inhibitors.

For patients with SAH taking oral anti-platelet agents, such as aspirin, clopidogrel or prasugrel,
NCS and SCCM management recommendations include:
• Anti-platelet agents can potentially increase the risk and severity of aneurysm re-
rupture, as well as neurosurgical complications.
• Platelet transfusion is recommended for patients with aspirin- or adenosine diphosphate
(ADP) inhibitor-associated SAH who will undergo a neurosurgical procedure.
• Platelet transfusion is not recommended if no neurosurgical procedure is planned.
• The risk–benefit ratio of anti-platelet therapy reversal using other hemostatic agents
such as desmopressin (DDAVP) should be considered for individual patients.

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Treat Pain and Anxiety

An uncomfortable patient can re-rupture his or her aneurysm

It is important to avoid straining, Valsalva maneuver, and writhing, as this can cause re-rupture
of an unsecured aneurysm. One must also be careful to not over-sedate the patient as this
could mask the symptoms of hydrocephalus (obtundation).

• Use IV medications with short half-lives (fentanyl for example).

• Liberal use of anti-emetics is justified especially if vomiting occurs.
• Blood pressure control is enhanced with adequate analgesia.
• If anxiety is present, consider small doses of an anxiolytic such as lorazepam.

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Blood Pressure Management: SPB <160

Avoid hypertension to prevent re-rupture

General principles:
• Current guidelines suggest treating severe hypertension in patients with an unsecured
ruptured aneurysm.
• Modest hypertension [mean arterial pressure (MAP) < 110 mmHg] may not require
treatment.
• Premorbid BPs should be considered and used to inform the risks and benefits of
treatment.
• Antihypertensive medications that are short acting, titratable, and can be administered
as a continuous infusion, such as nicardipine or clevidipine, to reduce the systolic
pressure < 160 mmHg, or the MAP < 110 mmHg, should be used, keeping in mind the
principles mentioned above.
• Nitroprusside and nitroglycerine should be avoided because these agents may cause
cerebrovascular dilation and thereby increase ICP.

See the ENLS Pharmacology protocol.

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Decline in Neurological Exam

Worsening neurological examination?

There are several immediate causes of early (within the first hour) neurological
decompensation.
• Re-rupture of the aneurysm: repeat head CT is diagnostic
• Worsening hydrocephalus: repeat head CT is diagnostic; need for external
ventricular drain (EVD) is now paramount; give mannitol while arranging for EVD
placement
• Seizure: treat with phenytoin or levetiracetam load
• Cardiopulmonary cause: neurogenic pulmonary edema, catecholamine
cardiomyopathy manifesting with worsening hypoxia or hypotension.
Echocardiography is diagnostic of cardiomyopathy.

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Hydrocephalus
Are the ventricles dilated?

Hydrocephalus is caused by blockage of CSF absorption and is diagnosed by interpreting the

head CT scan. If the patient is obtunded or comatose, it is important to provide ventricular
drainage by having an external ventricular drain placed. This both treats the hydrocephalus
and provides a monitor of ICP.

• If a neurosurgeon is not available at your hospital and hydrocephalus is present,

consider treating the patient with mannitol 1 gm/kg and expediting transfer to a
facility with neurosurgical capability within the next hour.

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Consider Antifibrinolytic Agents

Preventing re-rupture

Preventing re-rupture bleeding of the aneurysm is a major goal of initial therapy.

• Antifibrinolytic agents such as aminocaproic acid and tranexamic acid can reduce
aneurysmal re-rupture bleeding. However, these agents also raise the risk of deep
venous thrombosis (DVT), pulmonary embolus (PE), and ischemic stroke if they are
continued. If the patient is free of recent myocardial infarction, DVT/PE or any
known hypercoagulable state, many centers administer antifibrinolytic agents until
the aneurysm can be secured; this may be an appropriate strategy but should be
discussed with the consultant.

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