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Subarachnoid Hemorrhage

27

 

Charu Gauba and Pushpendra Nath Renjen

 

A 25-year-old woman had a sudden severe headache on waking up one morning. She described this as the worst headache she had ever experienced in her life. A few minutes later, she vomited and then fell unconscious. There was no witnessed seizure. She was arousable when she was brought to the emergency department and was talking coherently and obeying commands. There was no localizing sign, but she had neck stiffness.

Subarachnoid hemorrhage (SAH) should be suspected in patients presenting with severe headache of acute onset with an altered mental state. The most important cause of SAH is a ruptured aneurysm. Other causes include trauma, vascular malformations, hemorrhagic infarctions and hypertensive hemorrhages. The high morbidity and mortality associated with aneurysmal SAH mandates a high degree of suspicion to allow timely and appropriate treatment.

Step 1: Start resuscitation

Urgent airway protection is necessary in obtunded patients to avoid hypercarbia and rise in intracranial pressure.

In patients with suspicion of SAH, volume loading and vasopressors should be avoided during initial resuscitation to prevent aneurysmal rebleeding.

Step 2: Take focused history and perform clinical examination

The classic features of an SAH include a sudden explosive headache (often called a thunderclap headache). This may be accompanied by decreased consciousness, photophobia, neck pain, nausea and vomiting.

C. Gauba, M.D., D.N.B. (*) • P.N. Renjen, M.D., D.M.

Department of Neurology, Indraprastha Apollo Hospitals, New Delhi, India e-mail: charugauba@hotmail.com

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

223

DOI 10.1007/978-81-322-0535-7_27, © Springer India 2012

 

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C. Gauba and P.N. Renjen

 

Table 27.1 The Hunt and Hess scale

1.

Asymtomatic or, mild headache, slight neck rigidity

2.

Moderate-to-severe headache, neck rigidity, no neurological deficit other than cranial

 

nerve palsy

3.

Drowsiness/confusion, mild focal neurological deficit

4.Stupor, moderate-to-severe hemiparesis

5.Coma, decerebrate posturing

In SAH patients, history of trauma, hypertension, bleeding diathesis, use of antiplatelet agents or anticoagulants and drug abuse like cocaine should be taken.

Sentinel headaches occur in about half of patients before rupture.

Lateralizing signs may occur if there is an intracerebral hematoma.

Neck stiffness is a useful sign when present.

Close neurological monitoring and serial neuroexamination are essential as these patients might deteriorate suddenly.

Fundus examination may be carried out to rule out subhyaloid hemorrhage.

Step 3: Assess severity of SAH

The Hunt and Hess scale is one of the grading systems used to classify the severity of SAH based on the patient’s clinical condition. It is used as a predictor of the patient’s prognosis, with a higher grade correlating with lower survival rate (Table 27.1).

The Hunt and Hess scale is now used less frequently and has largely been replaced by the World Federation of Neurosurgical Societies classification, mentioned as follows:

1.Glasgow coma score (GCS) 15, motor deficit absent

2.GCS 13 or 14, motor deficit absent

3.GCS 13 or 14, motor deficit present

4.GCS 7–12, motor deficit absent or present

5.GCS 3–6, motor deficit absent or present

Step 4: Perform an urgent noncontrast CT scan of the head

CT is the imaging method of choice to diagnose an acute SAH. MRI is less effective in detecting blood early.

The sensitivity of CT for detecting SAH is 90–95% at 24 h and 80% at 72 h. A negative CT scan in a patient with a typical history of SAH should be followed by a lumbar puncture, which will show xanthochromia and crenated RBCs.

Step 5: Start initial treatment

Strict bed rest is advisable to prevent rebleeding of the aneurysm. Stool softeners, cough suppressants and a quiet environment are useful adjuncts.

Pain control should be achieved with titrated doses of opioids. Nonsteroidal anti-inflammatory drugs should be avoided.

27 Subarachnoid Hemorrhage

225

 

 

Rebleeding may be related to changes in blood pressure rather than absolute blood pressure. Rebleeding has been found to be more common in those with a systolic pressure of more than 160 mmHg. Blood pressure should be controlled (see Chap. 24) to balance the risk of hypertension-related rebleeding and to maintain cerebral perfusion pressure. Short-acting, continuous infusion intravenous agents with a reliable dose–response relationship and a good safety profile are desirable. Labetalol, nicardipine, and esmolol seem to meet these criteria the best. Intravenous nitroprusside is best avoided due to its tendency to raise intracranial pressure and cause toxicity with prolonged administration.

Mannitol is best avoided as it has been reported to precipitate rebleeding presumably by affecting transmural gradients across the aneurysm.

Step 6: Perform cerebral angiography

If CT or lumbar puncture test report is positive, imaging of the cerebral vessels is required to delineate the aneurysm.

The gold standard imaging modality is four-vessel cerebral digital subtraction angiography (DSA). All the vessels need to be included as multiple aneurysms occur in 20% patients.

Approximately 80–85% aneurysms arise from the anterior circulation and the remaining from the posterior circulation.

If DSA cannot be performed immediately, CT or MR angiography of the brain may be done initially. This needs to be followed up with DSA, however, to decide the ideal treatment modality for securing the aneurysm.

Measures to prevent contrast-induced nephropathy should be instituted for patients at risk.

Step 7: Take measures to prevent rebleeding

Early definitive treatment of the aneurysm improves outcome by decreasing rebleeding and enabling effective treatment of vasospasm once the aneurysm is secured.

Two forms of treatment may be used to secure the aneurysm—microsurgical clipping and endovascular coiling. Complete obliteration of the aneurysm is recommended whenever possible.

An experienced interventional radiologist and a neurosurgeon should be involved early in the management.

In the large prospective randomized international subarachnoid aneurysm trial (ISAT) trial, it was found that in patients equally suited for both treatment options, endovascular coil treatment produced substantially better patient outcomes than surgery in terms of disability-free survival at 1 year. The relative risk of death or significant disability at 1 year in patients treated with coils was 22.6% lower than in surgically treated patients, an absolute risk reduction of 6.9%.

However, the choice between coiling and clipping should be made after studying the characteristics of the aneurysm. Surgical intervention may be required with wide necked aneurysms or if there is an associated large intracerebral hematoma that requires evacuation.

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C. Gauba and P.N. Renjen

 

 

Step 8: Prevent, identify and manage vasospasm

Close neurological examination needs to be emphasized even after securing the aneurysm as vasospasm is a common and dreaded complication. This usually presents as a delayed focal neurological deficit but sometimes as an encephalopathy.

In patients with SAH, 32% of deaths occur due to delayed ischemia from vasospasm, 25% due to the direct effects of aneurysmal rupture and 18% due to rebleeding.

Onset of vasospasm typically occurs on days 3–5, peaks on days 5–14, and resolves over 2–4 weeks.

The Fisher scale (CT scan appearance) has been used to predict the likelihood of symptomatic cerebral vasospasm:

1. Grade 1: No bleeding is detected.

2. Grade 2: Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm.

3. Grade 3: Localized clots and/or vertical layers of blood 1 mm or greater in thickness.

4. Grade 4: Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present.

Diagnosis of vasospasm is made by clinical examination, presence of fresh infarct on CT or by angiography. Transcranial Doppler studies permit bedside diagnosis of vasospasm by detecting high blood flow velocities in intracranial vessels.

Oral nimodipine—an oral calcium channel antagonist, 60 mg 4-hourly for 21 days—is indicated to reduce poor outcome due to vasospasm. Side effects are infrequent and include peripheral edema, hypotension, tachycardia, abdominal discomfort, headache, and rash. The value of other oral or intravenous calcium antagonists remains uncertain. Benefit of nimodipine may be due to its neuroprotective property rather than to its vasodilatory property.

Early treatment of the aneurysm enables maintenance of normal circulating blood volume, which is essential for management of vasospasm.

Symptomatic cerebral vasospasm can be managed with “triple-H therapy,” that is, hypervolemia, induction of hypertension and hemodilution. This may be performed by infusing normal saline or colloids to increase the CVP to 10–12 cm of saline. If hypervolemia alone does not improve the patient’s condition, the systemic blood pressure is raised by withdrawing antihypertensives, if any, and giving dopamine infusion at 5 mg/Kg/min titrated to obtain a systolic BP of 160–180 mmHg. Hematocrit should be maintained at 30% ± 3%.

Hypervolemic and hypertensive therapy puts patients at increased risk of arrhythmias and pulmonary edema, which needs to be closely monitored.

Cerebral angioplasty and/or intra-arterial vasodilator therapy may be required, together with or in place of triple-H therapy in documented cases of vasospasm with deteriorating neurological status.

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Step 9: Manage hydrocephalus

Acute hydrocephalus occurs in 20% patients and appears within 3 days of the SAH. Delayed ventricular dilatation usually occurs after the tenth day and is seen in 23% patients.

Ventriculostomy can be beneficial in patients with ventriculomegaly and decreased level of consciousness after an acute SAH. However, it has been reported that abrupt lowering of the intracranial pressure could lead to rebleeding due to decreased transmural pressure or removal of the clot, sealing the previously ruptured aneurysm.

Temporary or permanent cerebrospinal fluid diversion is required in symptomatic patients with chronic hydrocephalus after SAH.

Step 10: Prevent and treat seizures

Because of the potential risk of rebleeding with a seizure, the administration of prophylactic anticonvulsants is recommended in the immediate (up to 3 days) posthemorrhage period. The long-term use of anticonvulsants is not routinely recommended for patients with no seizure episodes and should be considered only for patients with risk factors such as thick cisternal clot, prior seizure, hematoma, infarct or middle cerebral artery aneurysms. Phenytoin or fosphenytoin has been the most common agent that has been used for prophylaxis.

About 3–5% patients with SAH have seizures during their hospitalization. If seizures occur, they need to be treated like any other seizure (see Chap. 28).

Epilepsy develops in approximately 15% patients with SAH, and it develops within 18 months in more than 90% patients.

Risk factors for development of late epilepsy are poor neurological grades on admission, rupture of a middle cerebral artery aneurysm, cerebral infarction secondary to vasospasm and shunt-dependent hydrocephalus.

Step 11: Manage hyponatremia

The reported incidence of hyponatremia after SAH ranges from 10% to 30% and may be an independent risk factor for poor outcome.

Fluid restriction is required in patients with hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion. This can precipitate delayed ischemic deficits, and therefore, a careful balance has to be maintained.

Hyponatremia in many cases with SAH is due to the “cerebral salt-wasting syndrome.” This state is associated with features of volume depletion differentiating it from syndrome of inappropriate antidiuretic hormone (SIADH). Correction of hypovolemia with isotonic fluids is indicated in such cases.

Step 12: Manage neurogenic pulmonary edema

This is characterized by rapid onset of respiratory failure in the setting of raised intracranial pressure. It is thought to be due to pulmonary capillary endothelial damage.

Most of these patients are comatose.

Treatment includes reduction of intracranial pressure, mechanical ventilation with positive-end expiratory pressure and attaining the lowest central venous or pulmonary wedge pressure that maintains an effective cardiac output by cautious diuresis.

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