Critical Care Management
Pearls for the Management of Intracerebral Hemorrhage
Preventing clot growth is key to improving outcomes, especially in the first few hours after symptom onset.
Acute hypertension should probably be controlled. A systolic blood pressure of 140 to 160 mm Hg is reasonable.
Anticoagulation with vitamin K antagonists (e.g., warfarin) should be reversed immediately.
Nonconvulsive seizures should be excluded, but universal anticonvulsant prophylaxis is unlikely to benefit most patients.
Predicted poor outcome may lead to changes in goals of care and self-fulfilling prophecies.
Pearls for the Management of Subarachnoid Hemorrhage
The risk of aneurysm rebleeding should be minimized with acute blood pressure control, early aneurysm obliteration, and potentially with hemostatic therapy.
The incidence of vasospasm can be pharmacologically reduced.
Symptomatic vasospasm can often be treated with hyperdynamic therapy, alone or in conjunction with endovascular therapy (covered in Section IV of this book).
Nonconvulsive seizures should be excluded, but universal anticonvulsant prophylaxis is unlikely to benefit most patients.
Pearls for the Management of Elevated Intracranial Pressure
Elevated intracranial pressure may be related to mass, ischemia, insufficient nutrient delivery, or other potentially reversible causes.
A stepwise progression of therapies from short-acting (elevation of the head of the bed and titratable agents) to longeracting (barbiturates) should be quickly employed.
♦ Critical Care Management of Intracerebral Hemorrhage
Predictors of Outcome in Acute Intracerebral Hemorrhage
Several factors on admission are associated with worse outcome after intracerebral hemorrhage (ICH). Several similar prediction scores have been developed from prognostic variables.1
Intracerebral Hemorrhage Volume
An acute clot is a mass in the skull. As such, it may compress adjacent structures, increase intracranial pressure (ICP), and lead to hydrocephalus, herniation, and death. Larger volumes are associated with worse outcomes.
Intracerebral hemorrhage volume frequently increases after the diagnostic computed tomography (CT) scan. Approximately one third of patients have an increase in ICH volume of one third or more. When it occurs, ICH volume growth is associated with a worse outcome. Predictors of ICH volume growth include earlier time of the diagnostic CT scan, anticoagulation, larger ICH volume on the diagnostic scan, and acute hypertension.
Location of Intracerebral Hemorrhage
Intracerebral hemorrhage in the brainstem is especially deadly because it is likely to compress brain tissue involved in respiration, bronchial hygiene, and consciousness. A moderatesized cerebellar ICH may compress the brainstem and require neurosurgical decompression.
Age
Older age is associated with worse outcome. This is likely a combination of reduced recovery, limitations in goals of care, and reduced tolerance for cardiovascular stress if critical care is required.
Level of Consciousness and Neurologic Examination
The Glasgow Coma Scale and National Institutes of Health (NIH) Stroke Scale have both been shown to be predictors of outcome; any validated neurologic assessment is likely to be useful. A depressed level of consciousness may be related to increased ICH volume, hydrocephalus, or a seizure.
Intraventricular Hemorrhage
Hemorrhage in the basal ganglia, thalamus, or caudate nuclei more frequently extends into the third or a lateral ventricle. Intraventricular hemorrhage (IVH) leads to an increased risk of fever, hydrocephalus from obstructed flow of cerebrospinal fluid (CSF), and worse outcomes. Consultation with a neurosurgeon regarding ventricular drainage is advisable.
Blood Pressure Management for Acute Intracerebral Hemorrhage
Hypertension is a leading cause of ICH and is commonly abnormal on admission. The pathophysiology of elevated blood pressure may lead to increased ICP, a Cushing response (bradycardia with severe hypertension due to an intracranial mass), or a surge of catecholamines.
The available data generally show an association between acute hypertension and ICH volume growth. The presumed pathophysiology is that greater blood pressures lead to more acute bleeding from a small vessel and ICH volume growth. Case series of documented contrast extravasation on acute CT angiography (“spot sign”) and subsequent ICH volume growth lend support to this hypothesis.2
The optimal timing, potency, and choice of agent for blood pressure control have not been defined, and several clinical trials are in progress. One study found that “intensive” blood pressure control (target systolic blood pressure [SBP] 140 mm Hg, medication at the discretion of the treating physician) was associated with less clot growth than standard care (target SBP 180 mm Hg)3; a confirmatory trial is underway. For patients with severe hypertension an SBP of 160 mm Hg should be considered, although this may be modified by elevated ICP or tailored to therapy to optimize cerebral perfusion pressure (usually targeted at 60 to 80 mm Hg).
Coagulopathy
Clotting limits the amount of bleeding into cerebral tissue. Anything that retards clotting may increase the risk of clot growth, IVH, and poor outcome. The more potent the inhibition of clotting, the more profound the risk.
Vitamin K Antagonists (Warfarin)
Warfarin (Coumadin), an antagonist of vitamin K, is commonly used for stroke prevention (especially in the setting of atrial fibrillation or artificial cardiac valves), and for the prevention of cerebrovascular and peripheral vascular disease. The intensity of anticoagulation is monitored with the international normalized ratio (INR), which corrects for variation in each laboratory’s prothrombin time (PT). An INR of 1 is considered normal, with 2 to 3 being the most commonly used therapeutic range. An elevated INR is strongly associated with more and later clot growth as blood continues to ooze.
A warfarin effect should be treated emergently. The best way to correct a warfarin effect has not been clearly determined, and different institutions use different protocols. The longer the time until the INR is corrected (1.4 or less is considered desirable, although the best target has not been prospectively defined), the greater the risk of clot growth and poor outcome. Several different options are available:
♦ Fresh Frozen Plasma
Fresh frozen plasma (FFP) replaces the factors inhibited by warfarin. The greater the intensity of anticoagulation, the more units are needed. Two to four units are usually given to start with follow-up of the INR.
♦ Prothrombin Complex Concentrates
Prothrombin complex concentrates (PCCs) have relatively high concentrations of vitamin K–dependent clotting factors. A variety of PCCs are available. PCC administration may be faster and require less volume than FFP, but the cost is significantly greater; the benefit as compared with FFP is attenuated if the INR is corrected quickly.4 One should consult in advance with a hematologist on the most appropriate PCC and dose required to avoid delay when a patient requires emergent treatment.
♦ Recombinant Factor VII
Recombinant factor VII (FVII) has been used in case series for the correction of warfarin. The INR is decreased quickly, but vitamin K–dependent clotting factors are not repleted. The effect on the INR is short-lived, so one should consider the concurrent administration of FFP or PCC.
♦ Vitamin K
Vitamin K is frequently given IV or PO. If anticoagulation is required again (such as for a mechanical cardiac valve), then the administration of vitamin K will complicate future use of warfarin, sometimes for weeks afterward. Vitamin K has a slow onset of action because clotting factors must be resynthesized by the liver, so it is not appropriate as monotherapy for warfarin-related ICH.
Heparin and Low-Molecular-Weight Heparins
Heparin is similar to warfarin in its impact on ICH, although not only the vitamin K–dependent clotting factors are involved. The risk of ICH is related to the intensity of anticoagulation, and unintentional over-anticoagulation increases the risk of cerebral hemorrhage. Unfractionated heparin should be reversed with protamine and discontinuation of heparin. Lowmolecular-weight heparins are incompletely corrected with protamine, and typically require administration of FFP or PCC.
Antiplatelet Agents (IIbIIIa Inhibitors, Aspirin, Thienopyridines [Clopidogrel])
Aspirin irreversibly acetylates a residue on platelets, which makes them less potent. Thienopyridines (of which clopidogrel is in widespread use and likely to be followed by others) inhibit platelet activation further downstream and are more potent. The classes are often combined, especially after the interventional treatment of acute coronary syndromes. Compared with monotherapy, combined antiplatelet therapy increases the risk of ICH.
Known antiplatelet medication use is generally associated with more ICH volume growth and worse outcome5; measurement of platelet activity may improve prediction.6 Platelet transfusion has been used to improve platelet activity, although data from randomized trials are not yet available. The utility of other agents (desmopressin, FVII) in this setting has not been well described.
Intravenous IIbIIIa inhibitors (e.g., abciximab, etanercept) may infrequently lead to cerebral hemorrhage. The risk of cerebral hemorrhage increases with elevated blood pressure, cerebral ischemia, and reperfusion. The antiplatelet agent should be discontinued and platelets administered, with potentially repeat treatment depending on the half-agent of the offending agent.
Hemorrhage After Alteplase (Tissue-Type Plasminogen Activator) for Ischemic Stroke
Cerebral hemorrhage after alteplase (tissue-type plasminogen activator [tPA]) administration for acute ischemic stroke is infrequent (approximately 5%). Centers that follow the National Institute of Neurological Disorders and Stroke (NINDS) tPA protocol have hemorrhagic conversion rates similar to that in the original tPA trial. When it occurs, the hemorrhages tend to be severe and in ischemic or reperfused brain tissue. The risk is increased by older age, hypertension, longer time from symptom onset to treatment, greater amount of ischemic brain tissue (involvement of one third or more of the middle cerebral artery distribution increases the risk), and protocol violations (e.g., early administration of aspirin or heparin, severe hypertension).7 Drug administration should be stopped whenever hemorrhage is suspected (change in mental status, new headache, etc.) and excluded with CT. When ICH occurs, FFP is typically given.
Acute Hemostatic Therapy
The documentation of ICH volume growth in the first hours after symptom onset implies that if clot growth could be stopped, then outcomes might be improved. There have been two randomized clinical trials with FVII as an acute hemostatic agent after ICH. In both trials, treatment led to less ICH volume growth, although functional outcomes at 90 days were improved only in the first trial.8
Surgical Decompression and Catheter-Based Clot Lysis
Surgical decompression and catheter-based clot lysis are covered in Section III of this book.
Seizures and Anticonvulsant Medication Use After Intracerebral Hemorrhage
There are widely varying quoted rates of seizures after ICH, from 5% to >20%. Seizures usually occur soon after ICH. A substantial number of seizures are only detected on prolonged electroencephalogram (EEG) monitoring, and such monitoring should be considered for comatose patients to exclude nonconvulsive seizures and status epilepticus. Other risk factors for seizures include cortical location, an associated subdural hematoma, and previous cerebral infarction.9
If a patient does not have seizures within a few days of ICH, is at low risk for seizures, or if seizures have been excluded with EEG, then the potential benefits of anticonvulsant therapy are probably low. Prophylactic anticonvulsant therapy, especially phenytoin, has been associated with more fever and worse functional outcomes.10
Self-Fulfilling Prophecies in Intracerebral Hemorrhage
Intracerebral hemorrhage is known to have the worst prognosis of the subtypes of stroke. Confidence in prognosis can be counterproductive, however, because clinicians who are certain of a poor outcome may direct their care away from intervention and rehabilitation toward restriction of critical care and comfort. In patients with equivalent severity of neurologic illness scores, hospitals that have higher rates of do-not-resuscitate orders have higher mortality.11 Patients with a good outcome may, early on, be thought to have no reasonable chance of functional independence. This does not mean that intensive care is always appropriate, but rather that clinicians should be aware of their potential biases in discussions with decision makers. If you are convinced the case is hopeless, you can usually prove yourself correct.
Web Resources
Updated guidelines from the American Heart Association for the management of acute ICH are available at:
http://stroke.ahajournals.org.easyaccess2.lib.cuhk.edu.hk/cgi/content/full/38/6/2001
Ongoing clinical trials in ICH can be found at:
♦ Critical Care Management of Subarachnoid Hemorrhage
Predictors of Outcome in Aneurysmal Subarachnoid Hemorrhage
The features that predict poor outcome in subarachnoid hemorrhage (SAH) are similar to those described for ICH. Advanced age, impaired level of consciousness, focal neurologic deficits, hemorrhage burden, and the presence of IVH are associated with poor outcome. Markers of physiologic derangement on admission, including the presence of increased A-a gradient, metabolic acidosis, hyperglycemia, hypotension, and hypertension, have been reported to predict poor outcome (Table 4.1).12 Prevention of rebleeding (see below) is important to maximize the chances of good neurologic outcome.
Management of Subarachnoid Hemorrhage Prior to Aneurysm Obliteration
Early management of SAH focuses on treating elevated ICP through medical management and CSF diversion, limiting hemorrhage burden through prevention of rebleeding, and reversing physiologic derangement through aggressive resuscitation.
Airway Management
Patients with a normal level of consciousness generally do not require invasive airway control. Patients with a reduced level of consciousness are at risk for aspiration, and endotracheal intubation for poor bronchial hygiene should be considered. After intubation, effective sedation should be achieved with a short-acting sedatives and analgesics. Coughing and ventilator asynchrony may produce sharp increases in ICP and blood pressure and potentially increase the risk of aneurysm rebleeding.
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