Subarachnoid hemorrhage – Doctor Guidelines

Subarachnoid hemorrhage (SAH) is characterized by bleeding into the subarachnoid space (between the pia and arachnoid mater). Half of the hemorrhagic strokes are subarachnoid hemorrhages, and its overall incidence is around 9/100.000 person-years. Relevant risk factors include hypertension, smoking and family history, among others (fibromuscular dysplasia, polycystic kidney disease).

CAUSES:

Different conditions may lead to subarachnoid bleeding. These include:

Head trauma (most cases)
Aneurysm rupture
Nonaneurysmal perimesencephalic hemorrhage (no visible vascular cause)
Arteriovenous malformation
Bleeding disorders (diseases or anticoagulation use)
Miscellaneous (sickle cell disease, pituitary apoplexy, drug abuse)

SIGNS & SYMPTOMS:

The classic symptom of a subarachnoid hemorrhage is a severe, sudden headache (thunderclap headache), the “worse headache of the patient`s life”. This headache is often severe enough to suddenly wake patients up during sleep. The headache is the most common symptom and is almost universally present (97%). Some patients with aneurysms (anywhere between 10-50%) may have a sentinel headache (also a sudden, severe but more bearable headache) some days before the rupture. The sentinel headache is, therefore, an important red flag.

Other symptoms may include various degrees of altered mental status (minor confusion to deep coma), seizures, nausea, vomiting and meningeal signs (e.g. neck stiffness). Signs of intracranial hypertension may also be present (bradycardia, bradypnea, hypertension, cranial nerve palsies).

DIAGNOSIS:

A history of sudden, severe headache should create an immediate alert for the possibility of imminent or undergoing intracranial bleeding. A focused physical examination should be performed with special attention to the neurological exam (particularly level of consciousness, pupillary abnormalities, cranial or peripheral deficits and meningeal signs). If the patient is stable enough (e.g. does not need immediate intubation and mechanical ventilation) brain imaging should be obtained.

Noncontrast CT scan is enough to establish the diagnoses in most cases. Few cases may have a normal CT scan. If the clinical suspicion is high, a lumbar puncture should be performed and it may shall xanthochromia, RBC levels that does not reduce from tube to tube and an increased opening pressure.

As soon as the diagnosis is established and the patient is stable, the etiology of the bleeding should be investigated. Digital subtraction angiography is the gold standard for diagnosis. CTA and MRA may be useful since these methods are more available and quicker (although they are not as good as digital subtraction angiography). If the cause is not clear on the angiography, the test should be repeated in 1-2 weeks, except in patients with perimesencephalic hemorrhage (blood in the cisterns), in which the location of the bleeding is often uncertain regardless of multiple studies.

Other relevant tests include CBC, CMP, ECG, coagulation studies, lipid panel and toxicological screening.

CLINICAL AND TOMOGRAPHIC SCALES:

Some scales are useful when assessing the severity of a subarachnoid hemorrhage and estimate prognosis and/or guide treatment.

A clinical scale that is often used is the Hunt and Hess Scale, in which the patient is classified as:

1. Asymptomatic, mild headache, slight nuchal rigidity
2. Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy
3. Drowsiness, confusion, mild focal neurologic deficit
4. Stupor, moderate or severe hemiparesis
5. Coma, decerebrate posturing

A CT scan scale that is often useful in clinical practice is the Fisher scale, which characterizes the patient according to the bleeding location. This scale may be helpful in predicting vasospasm risk. The Fisher scale is below:

Grade 1: No blood
Grade 2: Diffuse or thin layer of blood less than 1 mm thick (interhemispheric, insular, or ambient cisterns)
Grade 3: Localized clots and/or layers of blood greater than 1 mm thick in the vertical plane.
Grade 4: Intracerebral or intraventricular clots with diffuse or absent blood in basal cisterns.

TREATMENT:

First and foremost the A-B-C-D should be assessed and guaranteed. Cardiac and oxygen saturation monitoring should be provided, and a venous line should be obtained. The patient should be treated in a critical care environment.

After obtaining imaging and identifying the etiology, the specific treatment should be provided if possible. Otherwise, the patient should be kept stable and monitored for the possible complications.

If an aneurysm is identified as the etiology, it should be treated within 24-72h, usually with surgical clipping or endovascular coiling.

Vasospasm prophylaxis may be provided. Nimodipine 60mg q4h should be given to patients with spontaneous SAH (its effect is not as clear in patients with traumatic SAH). Statins may also help reducing the incidence of vasospasm (e.g. pravastatin 40mg daily). When present, vasospasm may be identified by changes on the physical examination, transcranial Doppler and angiography. There are specific measures to treat vasospasm (mentioned below).

Intracranial hypertension, if present, should be managed (see other article).

Prophylactic seizure treatment may be provided in some cases (e.g. patients with poor neurological status and large volume or intraparenquimatous bleeding), but should not be used for everyone.

Hypoglycemia should be avoided, as well as unreasonably high levels of glucose. A reasonable glucose level may be the one used in other critical conditions (140-180mg/dL).

Hypertension may be tolerated up to a SBP of 160mmHg and should not be treated to avoid reducing the brain perfusion.

VTE prophylaxis should be provided using pneumatic compression.

Fever should be avoided.

As mentioned before, during the whole course of management the provider should be aware of the complications and be proactive to avoid and/or control them as soon as they appear. Complications include:

Vasospasm (up to 30% of cases), which usually occurs after the 3rd day of bleeding (although it may happen earlier), is characterized by ischemia of a blain area and an associated neurological deficit. Vasospasm may cause delayed cerebral ischemia, often visible on the CT scan. Treatment of vasospasm: The strategies include the triple H = hypervolemia, hypertension and hemodilution (use of crystalloid solution) to increase perfusion. Vasopressors may be added. Ballon angioplasty or intra-arterial vasodilators may be used for patients that do not respond to other measures.

Rebleeding (up to 23% of cases), which occurs in the first 24h after the initial bleeding and manifests as acute neurological deterioration.

Hydrocephalus (may be manage with ventricular drainage)

Intracranial hypertension

Hyponatremia (SIADH or Cerebral Salt-Wasting syndrome)

Seizures

Cardiac abnormalities, probably due to ischemia (e.g. increases in BNP and troponin, ST segment depression, QT prolongation, T wave inversions, LV dysfunction)
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