Subarachnoid and Intracerebral hemorrhage

1. Description of the problem

What every clinician needs to know

Broadly classified as subtypes of stroke, subarachnoid and intracerebral hemorrhage are commonly seen in the critical care unit.

Intracerebral Hemorrhage (ICH)

Defined as a hemorrhage into the brain parenchyma; usually arises in the region of the small arteries that supply the basal ganglia, thalamus, and brainstem. ICH is divided into different subgroups based on the etiology of the bleed:

1. Hypertensive (spontaneous) ICH: secondary to uncontrolled hypertension, the most common locations for this kind of ICH are basal ganglia, thalamus, brainstem and cerebellum.

2. Lobar ICH: most commonly secondary to amyloid angiopathy (a neurodegenerative process), with increased age being the most common risk factor. Tumors and vascular malformations must also be considered, as well as atypical presentations of hypertensive or aneurysmal hemorrhage.

3. Hemorrhagic conversion of ischemic stroke: more common in embolic large-vessel strokes, it occurs in approximately 6% of patients after IV t-PA.

4. Venous infarct-associated ICH: mostly seen in hypercoagulable states, dehydration and postpartum. These hemorrhages are suspected when in characteristic anatomic locations (such as in the medial frontal or parietal lobe adjacent to the sagittal sinus). Counterintuitively, these hemorrhages are treated with full-dose anticoagulation.

5. Arteriovenous malformations (AVMs) and cavernous angioma-associated ICH: typically seen in younger patients who often have a with history of seizures or headaches.

6. Illicit drug-induced ICH: mostly with sympathomimetic drug abuse like cocaine, methamphetamine or any illicit drug that can cause a severe elevation in blood pressure.

7. Neoplasms: seen in primary tumors like GBM, but more common in metastatic tumors like melanoma, lung, renal, thyroid and choriocarcinomas.

8. Hemorrhage contusion after traumatic brain injury. These lesions may be non-hemorrhagic initially and convert into hemorrhagic contusions over the first 24-48 hrs.

Subarachnoid Hemorrhage (SAH)

Defined by hemorrhage into the subarachnoid space, with or without intraparenchymal hemorrhage, and can be divided into:

1. Aneurysmal SAH

2. Non-aneurysmal SAH (most commonly traumatic SAH)

Distinguishing ICH from SAH

ICH should be suspected in any patient who presents with a sudden onset of focal neurological deficit in the setting of headaches and hypertension. The diagnosis is determined by an emergent CT scan of the head without contrast.

SAH presentation is often different: the most common complaint is that of severe headache that is the “worst headache of my life.” Often patients present with a warning or “sentinel” headache that precedes the severe “thunderclap” headache. Neck stiffness, photophobia and meningeal symptoms occur, as can focal neurological deficit. SAH is a cause of sudden death and should be considered in comatose patients after cardiac arrest.

2. Emergency Management

Emergent management of both ICH and SAH centers around rapid diagnosis, blood pressure management, and referral to a center with the appropriate neurosurgical and neurocritical care capabilities. Patients may be obtunded to the point that they require intubation for airway protection. If necessary, this should be accomplished with good hemodynamic control.

Blood pressure should be kept below 160 mmHg systolic, and newer evidence suggests that below 140 mmHg is safe). The presence of coagulopathy should trigger appropriate correction (i.e. platelets, plasma, prothrombin concentrate, vitamin K, recombinant activated factor VII). Hematoma expansion in ICH and rebleeding in aneurysmal SAH are very common over the first 24 hours.

3. Diagnosis

1. CT Head (non-contrast): the study of choice to diagnose the bleed, its size, and its location. CT angiography can be added at medical centers with this capability in order to look for underlying vascular lesions. For SAH: approximately 90% of hemorrhages are visible on CT within 24 hours of the ictus; the thickness of the clot and the presence of intraventricular hemorrhage predict the risk of vasospasm. Lumbar puncture is used to look for hemorrhage in patients with negative head CT but suspected SAH. CT can be used to assess the volume of the ICH by the A*B*C/2 method (length x width x depth), and can show expansion of the bleed by comparing the repeat CT to the initial.

2. MRI: as sensitive as CT to diagnose the bleed, but more difficult to interpret because the appearance of the ICH changes as blood products age (requiring more expertise). MRI is a great study in that it provides additional data that are helpful in determining if there is an underlying lesion that caused the bleed, such as a neoplasm or acute stroke.

3. Cerebral angiography: the gold standard in SAH (and ICH for that matter) to rule out an aneurysmal cause of the bleed. Immediate endovascular treatment of the aneurysm can be delivered as well depending on the anatomic characteristics of the aneurysm (location, neck size, etc.) and the availability of appropriately trained neurointerventionalists. About 1 in 7 patients with SAH have a negative angiogram (so-called angiogram-negative SAH). These patients may have low-risk venous hemorrhages or may be found to have aneurysm(s) on subsequent follow-up angiograms.

4. CT angiogram: a very useful noninvasive study with high sensitivity for aneurysms over a few millimeters in size.

5. Lumbar puncture: should be performed on any patient with suspected SAH and a negative CT head, xanthochromia can be seen within 12 hours of ictus and can last for 2 weeks afterwards.

Check the medication history, as many patients are on antiplatelet therapy. All patients with ICH/SAH should have a complete blood count, type and screen, prothrombin/INR/partial thromboplastin time, chemistry panel, liver function test and toxicology screen checked. Cardiac enzymes and electrocardiograms should be obtained as well.

4. Specific Treatment

ICH/SAH is a medical (and in some cases surgical) emergency. It should be promptly recognized, diagnosed and treated in a critical care setting.

Recognizing the reason for the bleed is crucial in the management. All the patients with ICH/SAH should be admitted and treated in a highly monitored setting (usually an ICU) with frequent neurological examinations. A cerebral imaging study, usually a CT scan, should be performed and repeated to follow up on the size of the bleed and if there is any volume expansion, usually within 24 hours. CT angiography or conventional cerebral angiography is typically used to detect any underlying lesion or any aneurysm as the cause of the bleed and should be done as soon as the patient is stable from a respiratory and cardiovascular standpoint.

Blood pressure control is very important. Keeping SBP <140 is safe according to the most recent AHA/ASA recommendations. An antihypertensive IV drip can be used if needed to target that goal (such as nicardipine).

In aneurysmal SAH, securing the aneurysm via clipping or coiling is the definitive treatment. Early deterioration of the SAH patient is most commonly due to obstructive hydrocephalus or, secondarily, to rebleeding. Hydrocephalus is treated with an external ventricular drain (ventriculostomy). The decision to clip or coil the aneurysm to avoid rebleeding is made on a variety of issues, including the morphology of the aneurysm, the location of the aneurysm, and the capabilities/experience of the center where the patient is being treated. This is performed urgently, usually within the first 24 hours.

After the aneurysm has been secured, delayed ischemic deficits due to vasospasm are the primary concern. Patients are watched with frequent neurologic examinations and daily transcranial Doppler studies. The period of observation is usually 14 days but can be individualized based on the patient’s condition and risk for delayed ischemic deficits. Nimodipine, a dihydropyridine calcium channel blocker, is the only medication that is proven to improve the outcome after SAH. It should be given for the first 21 days after the bleed in a dose of 60 mg q4 hours. Statin therapy is commonly used as well, but the evidence base is weak at present.

As in any hemorrhagic disorder, correcting any bleeding diathesis is essential. This can be accomplished using platelet transfusion if the patient has platelet dysfunction, most commonly due to aspirin or clopidogrel therapy. For patients with prolonged INR’s, usually due to coumadin therapy or liver disease, fresh frozen plasma, prothrombin complex concentrate, vitamin K, and recombinant activated factor VII should be considered.

There is concern with the use of rFVIIa due to a risk for drug-induced thromboembolic events, and that it corrects the INR artificially without supplementing the clotting factors that are needed for normal coagulation. It must be stressed, however, that the risk:benefit ratio of rFVIIa is unknown in this setting.

Prophylactic antiepileptic medication is not recommended for routine use in patients with ICH/SAH. However, if the patient is thought to be at a very high risk for seizures, as in lobar/cortical ICH or diffuse SAH, post-craniotomy for aneurysm repair, or if seizure activity occurred in the patient around the time of presentation, antiepileptic medications should be considered.

Surgical hematoma evacuation should be considered on an individual basis but is generally not recommended for supratentorial ICH. Patients with superficial lobar ICHs are more likely to benefit from surgical evacuation than those with deep hypertensive hemorrhages (STITCH trial). All patients with cerebellar ICH >3 cm who are deteriorating neurologically or have brainstem compression or hydrocephalus from ventricular obstruction should have surgical removal urgently.

Patients with a depressed level of consciousness usually require intracranial pressure monitoring with an external ventricular drain or other intracranial pressure monitor (such as a parenchymal bolt). Elevated ICP is treated with cerebrospinal fluid drainage, hyperosmotic therapy, sedation, and other measures.

General critical care considerations: Prophylactic venous thromboembolism treatment with subcutaneous low-molecular-weight or unfractionated heparin may be considered after 3-4 days from onset of the ICH or SAH (individualized for the patient based on the type of bleed, etiology, neurosurgical interventions, etc.). Sequential compression devices can be used from the time of admission to reduce deep venous thrombosis formation.

Fevers are common in this patient population. The patient should be investigated for infection, and the fever should be treated with antipyretic medication and/or cooling devices to maintain normothermia and minimize secondary brain injury.

Early mobilization of the patient is essential when possible.

Aspiration should be avoided by careful evaluation of swallowing function and elevation of the head of bed.

Finally, hyponatremia is very common in SAH and ICH, either due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or to cerebral salt wasting (CSW). SIADH is a hyponatremic normovolemic condition while CSW is a hyponatremic hypovolemic condition. Hyponatremia can be corrected by administration of hypertonic saline if necessary (along with volume replacement in CSW), remembering to avoid overly rapid correction of the sodium (>8-10 meq/24 hours).

Epidemiology

ICH: occurs in 12-30 per 100,000 people each year in the United States, accounts for 10% of all strokes, with a mortality rate of 30-50%.

SAH accounts for 5% of all strokes. It affects 30,000 individuals per year in the United States. Approximately 10% of those patients die before receiving medical attention, and another 20% die after hospitalization.

Prognosis

SAH: 10% of patients die before reaching the hospital, another 20% die after hospitalization, and a majority of survivors have some neurocognitive impairments. There are several predictors for poor outcome following SAH, including Glasgow Coma Scale score on presentation, Hunt-Hess grade, aneurysm size, age, rebleeding, vasospasm, hydrocephalus, hyponatremia and seizures.

ICH:Morbidity and mortality rates are high in this disease as well. Overall prognosis depends on the patient age, size of the hematoma, location of the bleed, intraventricular extension and level of consciousness on presentation. The ICH score is a useful tool in determining the prognosis:

Glasgow Coma Scale score: 3-4, 2 points; 5-12, 1point; 13-15, 0 points
ICH size: >30 cm, 1point; <30, 0 points
IVH: Yes, 1point; No, 0 points
AGE: >80, 1 point; <80, 0 points
LOCATION: infratentorial, 1point; supratentorial, 0 points
Total score = % mortality: 0 = 0%, 1 = 13%, 2 = 26%, 3 = 72%, 4 = 97%

Special considerations for nursing and allied health professionals.

Watch for dysphagia, aspiration, inability to protect the airway.

What's the evidence?

Gebel, JM. “Intracerebral hemorrhage”. Neurol Clin. vol. 18. 2000. pp. 419-38.

Broderick, J, Connolly, S. “Guidelines for management of spontaneous ICH in adult”. Stroke. vol. 38. 2010. pp. 2001-23.

Hemphill, JC. “Reliable grading scale for ICH, ICH score”. Stroke. vol. 32. 2001. pp. 891-7.

Mast, H. “Risk of spontaneous hemorrhage after diagnosis of AVM”. Lancet. vol. 350. 1997. pp. 1065-8.

Stapf, C. “Predictors of hemorrhage in patients with untreated AVM”. Neurology. vol. 66. 2006. pp. 1350-5.

“TpA for acute ischemic stroke”. N Engl J Med. vol. 333. 1995. pp. 1581-7.

Sansing, LH. “Prior antiplatelet use does not affect hemorrhage growth or outcome after ICH”. Neurology. vol. 72. 2009. pp. 1397-402.

Drake, CG. “Report of World Federation of Neurological Surgeons Committee on a universal SAH grading”. J Neurosurg. vol. 68. 1988. pp. 985-6.

Tidswell, P, Dias, PS. “Cognitive outcome after aneurysm rupture: Relationship to aneurysm site and perioperative complications”. Neurology. vol. 45. 1995. pp. 875-82.

Le Roux, PD. “Predicting outcome in poor-grade patients with subarachnoid hemorrhage”. Neurosurgery. vol. 59. 2006. pp. 21-7.

Anderson, CS. “Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT)”. Stroke. vol. 41. 2010 Feb. pp. 307-12.

Bederson, JB. “Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association”. Stroke. vol. 40. 2009 Mar. pp. 994-1025.

Mendelow, AD. “Early surgery vs. initial conservative treatment in patients with spontaneous supratentorial intracerebral hematomas in the International Surgical Trial in Intracerebral Hemorrhage”. Lancet. vol. 365. 2005 Jan 29-Feb 4. pp. 387-97.

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