Emergency care of an acute stroke
Emergent management of acute stroke parallels care of people with acute myocardial infarction. Cardiovascular and cerebrovascular events have numerous similarities. Both of those life-threatening diseases of arterial origin are accompanied by serious complications that add to morbidity and mortality.
Both diseases can be treated successfully and outcomes can be improved. Like management of those with acute heart disease, modern stroke (and if you only suspect a stroke) care requires urgent treatment.
General Emergency Care of a stroke
Airway and Breathing
Basic administration of life support is the critical first step; emergent management of patients with acute stroke should begin as follows:
Protect the airway with an endotracheal tube in patients with:
- Depressed consciousness
- Bulbar dysfunction
- Prominent vomiting
- Give ventilatory assistance and supplemental oxygen
- Bronchopulmonary toilet
- Monitor cardiac rhythm
- Treat life-threatening arrhythmias
- Start intravenous fluids (normal saline) via access
- Treat seizures with anticonvulsants.
Most stroke patients do not need immediate endotracheal intubation, ventilatory assistance, or emergent cardiac care. However, patients with massive brain damage leading to a decreased level of consciousness or with a stroke causing prominent bulbar dysfunction likely will need intubation to secure the airway.
Patients having seizures secondary to acute stroke will also need protection of the airway.
Many patients with intracranial hemorrhage or infarctions in the brain stem or cerebellum will vomit and securing the airway forestalls the complication of aspiration pneumonia. An oropharyngeal or nasopharyngeal airway usually is not adequate.
Abnormalities in respiratory rate and rhythm are prominent in people who have depressed consciousness. The respiratory disturbances can be secondary to dysfunction of the respiratory centers in the brain stem or delayed responses to hypoxia or hypercarbia.
While respiratory arrest occurs most commonly with massive hemorrhages, hypoventilation can develop in a large number of patients. The resulting hypercarbia and hypoxia can worsen the neurologic status and aggravate development of increased intracranial pressure (ICP) by promoting vasodilation. Supplemental oxygen and ventilatory assistance should be prescribed liberally.
Fever is uncommon during the first hours after stroke. It can result from complications such as aspiration pneumonia or an infectious cause of stroke, such as endocarditis.
Less commonly, people with intracranial bleeding can have an elevated temperature secondary to disturbances of thermoregulatory centers in the hypothalamus. While “central” fever does occur, another source of the elevated temperature should be sought and the cause treated. An elevated temperature can potentiate ischemia, and measures to lower the fever are recommended.
Potentially life-threatening cardiac arrhythmias develop during the first 24 to 48 hours after stroke, especially among patients with intracranial hemorrhage. Cardiac monitoring to detect abnormal rhythms is part of the initial observation of all patients with possible stroke. If serious arrhythmias are detected, medications should be prescribed using the rules of advanced cardiac life support.
A clinically silent myocardial infarction can be the cause of an embolic stroke. Myocardial infarction also is a potential complication of stroke, particularly among those with subarachnoid hemorrhage (SAH). Both electrocardiogram (ECG) and serum enzyme changes consistent with acute myocardial ischemia can be found.
Most patients have an elevated blood pressure during the first hours after stroke.[6,69] The high blood pressure can be from:
- Pre-existing hypertension
- Increased ICP
- Stress of the stroke.
The high pressure also can be a compensatory mechanism to maintain adequate perfusion to the brain. Cerebrovascular autoregulation is lost in the ischemic bed, and blood flow becomes pressure-dependent. The brain may need a high blood pressure to limit the scope of the vascular injury, and sudden lowering of the blood pressure can result in worsening of the neurologic signs.
Information is lacking about what level of blood pressure is too high in the setting of stroke or about the best response to the finding of arterial hypertension. The best approach lies in not lowering the blood pressure too steeply or too rapidly. Rather, blood pressure measurements should be obtained at frequent intervals and responses based on sustained elevations of pressure.
Arterial blood pressures often are extremely high in people with acute intracranial hemorrhage. The values may be so high that the diagnosis of hypertensive encephalopathy is considered. However, hypertensive encephalopathy is relatively uncommon and should not be diagnosed until an intracranial vascular event has been excluded.
Because severe hypertension can exacerbate intracranial bleeding, the blood pressure in those with hemorrhage is treated more aggressively than among those with ischemic stroke. For patients with ischemic stroke, the values that should lead to treatment are > 220 mm Hg systolic or > 130 mm Hg mean (sum of the systolic pressure and 2 times the diastolic pressure divided by 3).
Occasionally, other serious diseases will mandate aggressive lowering of the blood pressure in people with an ischemic stroke, such as:
- Acute myocardial infarction
- Acute renal failure
- Dissection of the aorta.
Generally, hypertension declines spontaneously during the first hours after stroke. If medications are needed, oral medications are preferred. One approach is to restart use of antihypertensive drugs taken before the stroke. The aim will be to cautiously lower the blood pressure by 15% during the first 24 hours. Parenteral agents are given to rapidly lower pressures in more urgent situations.
Agents that have immediate effects when started or stopped are preferred. Potent, long-acting agents, such as sublingual nifedipine, should be avoided.
Some agents mandate placement of an intra-arterial catheter to continuously monitor changes in blood pressure. After the neurologic condition is stable, a maintenance antihypertensive regimen can be administered.
The current guidelines for the use of thrombolytic agents in the treatment of acute ischemic stroke do not recommend their use in patients whose systolic blood pressure is > 185 mm Hg or diastolic blood pressure is > 110 mm Hg.
Thus, physicians may be tempted to rapidly lower the blood pressure so that recombinant tissue-type plasminogen activator (rt-PA) can be administered. Given the current relatively short window of time for the safe and effective use of rt-PA, management of an elevated blood pressure becomes problematic. In most instances, time will not be sufficient to determine if the blood pressure is stabilized at a desired level before giving rt-PA. The potential risks of exacerbating the ischemia by lowering the blood pressure also may counteract any benefits in treating with rt-PA.
The possibility of an elevated blood pressure exacerbating the risk of hemorrhagic transformation of the infarction after treatment with rt-PA requires aggressive monitoring and control of hypertension during and after the use of the agen.
Some of the recommended interventions are best administered when the blood pressure is monitored by an intra-arterial catheter, but placement of the monitor can be difficult immediately after the use of a thrombolytic agent.
Seizures complicate approximately 5% of strokes, but status epilepticus is uncommon. Frequent seizures can intensify the brain injury from the stroke, and seizures are a neurologic emergency in their own right.
Seizures are most frequent among people with SAH or cortical infarctions secondary to embolism. In the former situation, a transient loss of consciousness at the time of aneurysmal rupture may be misinterpreted as a seizure. The sudden increase in ICP secondary to intracranial bleeding can exceed the mean arterial pressure and lead to transient global brain hypoperfusion and a period of unresponsiveness.
Besides basic life support measures, emergent parenteral administration of anticonvulsants is advised. Patients who are not actively seizing but who have had a seizure with their ictus also should be treated.
Phenytoin is the most commonly prescribed drug. Fosphenytoin can be given to those who need parenteral anticonvulsants. Depending upon the extent of seizure activity, the medication can be given rapidly or administered over the first 4 to 6 hours.
Short-acting benzodiazepines can be given to patients who are having active seizures. Prophylactic administration of anticonvulsants to those with a recent stroke, but who have not had a seizure, is not needed. Some physicians will give anticonvulsants to all patients with SAH secondary to a ruptured aneurysm because of concern that a seizure can induce a recurrent hemorrhage.
The utility of this approach is not established.
Increased Intracranial Pressure
Patients with a multilobar infarction or large hemorrhage are at high risk for a severely elevated ICP. High ICP can worsen brain ischemia by reducing blood flow and perfusion. In addition, pressure gradients between compartments in the cranial vault lead to herniation and secondary brain injury. Elevations in ICP result from:
- Brain edema
- Mass effect of the vascular lesion
The mass effects of the brain hematoma or acute hydrocephalus secondary to blockage of cerebrospinal fluid (CSF) pathways by clots mean that marked rises in ICP during the first hours after stroke are largely a problem among those with hemorrhagic stroke.
Usually, the course of brain edema and increased ICP is slower in patients with ischemic stroke; the symptoms evolve over days in people with large hemispheric infarctions. Those with large hematomas or infarctions of the cerebellum or brain stem can develop signs of increased ICP rapidly. In this situation, the mass effects of the vascular lesion cause both hydrocephalus and brain stem compression.
Papilledema, the usual hallmark of increased ICP, appears over several hours; thus, it often is not seen in patients with acute stroke. Signs of herniation, such as a unilateral oculomotor (III) nerve palsy, appear late in the course. An alert or drowsy patient with a III cranial nerve palsy probably does not have an uncal herniation syndrome.
A more likely scenario will be a ruptured aneurysm of the posterior communicating artery or basilar artery, directly affecting the nerve. Computed tomography (CT) and magnetic resonance imaging (MRI) can detect:
- Mass effect
These tests are recommended before therapeutic interventions are started.
Management of increased ICP after stroke includes both prophylactic and urgent treatment.
Patients with small- to moderate-sized strokes, as reflected by the nature and severity of the neurologic impairments or the size of the lesion on brain imaging studies, usually do not need measures to control ICP because of the low risk of clinically significant brain edema. However, early use of prophylactic measures to control edema and ICP is critical among those with major neurologic impairments suggesting:
- Multi-lobar hemispheric infarction
- Large intracerebral hemorrhage
- Large brainstem infarction or hematoma
- Large cerebellar hemorrhage or infarction.
These patients should have close observation for changes in neurologic status. In particular, declines in consciousness should be monitored. In addition, placement of an ICP monitor expedites observation for changes in pressure that will precipitate emergent treatment.
Prophylactic measures include elevation of the head of the bed and positioning of the head in order to expedite venous drainage. Modest fluid restriction is often prescribed; the usual 24-hour restriction is 1.5 to 2 liters. Hypo-osmolar fluids, such as 5% dextrose in water, are avoided. Measures to treat fever, hypoxia, and hypercarbia are important baseline steps; controlling nausea, vomiting, pain, anxiety, or agitation also can help.
Contrary to the situation in brain tumors, corticosteroids (dexamethasone or methylprednisolone) have not been effective in controlling brain edema.
Clinical trials have not demonstrated benefit from treatment with either conventional or large doses of corticosteroids.
However, these trials have shown increased risk of infectious complications with the use of corticosteroids in seriously ill patients with stroke. Based on the lack of efficacy and the potential for increasing infectious complications, corticosteroids are not recommended for treatment of those with stroke.
Most patients at risk for markedly elevated ICP will have been intubated. If not, those with deterioration secondary to ICP and brain edema should have emergency endotracheal intubation. Hyperventilation to lower the blood level of the partial pressure of carbon dioxide (pCO2) can rapidly lower ICP. Carbon dioxide is a potent vasodilator and lowering its concentration will cause constriction of the vascular compartment and a drop in ICP.
Excessive lowering of the pCO2 will lead to increased ischemia; thus, the goal should be to drop the pCO2 to 25 mm Hg to 30 mm Hg. Hyperventilation has an immediate but nonsustained effect; it must be followed by other therapies.
Intravenous administration of furosemide (20 mg to 40 mg) can lower intracranial pressure through its diuretic effects. It can be given in an emergency situation, but furosemide should be considered as an adjunct to other measures to control ICP and brain edema. Osmotic therapy (mannitol or glycerol) is given to patients with signs of clinically significant brain edema and elevated ICP following stroke. Clinical trials show that these drugs lessen morbidity and mortality.
Mannitol is administered intravenously over a 20-minute period in a dose of 0.5 g/Kg. Subsequent doses can be given every 4 to 6 hours. The usual maximal daily dose is 2 g/Kg. Intracranial pressure can be lowered within 20 minutes of starting the infusion and the effects will last 4 to 6 hours.
A hyper-osmolar state is a potential complication of repeated use of mannitol. In order to lessen the risk of this side effect, intravenous fluids can be administered to compensate for losses occurred during the previous 6 hours. The level of monitored ICP can be used to time subsequent doses of mannitol. Glycerol is less widely used in the United States. Oral glycerol is very sweet, and many patients cannot tolerate the medication. Intravenous glycerol causes hemolysis of red blood cells.
Patients with secondary hydrocephalus can have drainage of CSF via an intraventricular catheter and removal of a small amount of fluid can lower ICP. Continuous drainage of CSF is often done, especially in patients with SAH.
Repeated lumbar punctures can be performed in patients without masses; SAH is the only likely situation. Administration of large doses of barbiturates to induce a hypometabolic coma has been used to lower ICP following stroke. This intervention is very aggressive, and treated patients require extensive cardiovascular monitoring. The usefulness of barbiturate-induced coma in treatment of stroke patients has not been established.
Large Intracerebral Hematoma or Infarction Causing Mass Effects
Large (> 2.5 cm in diameter) infarctions or hematomas of the cerebellar hemisphere are especially amenable to surgical treatment.
Operative evacuation of a large hematoma or infarction can be a life-saving measure. Secondary compression of the brain stem or hydrocephalus can be eased by prompt operative removal of the cerebellar mass.
Because decompensation can occur rapidly, patients with large cerebellar strokes should be monitored intensively and surgery performed immediately if deterioration is detected.
Operative evacuation of deep hemorrhages arising in the thalamus or basal ganglia has been associated with considerable morbidity and mortality. Stereotactic evacuation of a hematoma is a potential alternative measure that is under study. Large (> 3 cm to 5 cm in diameter) lobar hematomas can be treated operatively, especially if the hemorrhage is located close to the cortical surface.
The most dangerous hematomas are located in the frontal, temporal, and parietal lobes. Large hematomas in the frontal or occipital poles are less likely to cause herniation. Large subarachnoid clots also can be evacuated; in most instances, a ruptured saccular aneurysm or vascular malformation also can be treated.
Surgery can be offered to patients with multi-lobar infarctions who have not responded to medical measures to control ICP.
During the operation, the surgeon removes a section of infarcted brain, most commonly the temporal lobe, to provide room for adjacent tissues that are swelling. In addition, the section of bone removed during the craniotomy is not re-inserted in order to give additional space for swelling. Decompressive craniectomy without resection of infarcted brain tissue can be done also. In this operation, a large piece of bone (diameter > 10 cm) is resected to avoid venous compression when the brain herniates through the hole in the skull. These operations can be life-saving measures for critically ill patients. Still, they often are not recommended for many patients because survival can be accompanied by major neurologic sequelae.
Operations are advised most frequently for younger patients with nondominant hemisphere infarctions.