Hemorrhagic stroke

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Intracerebral hemorrhage is a medical emergency that requires immediate attention.[70] Arresting hematoma growth is a key objective for medical or surgical therapies.[21]

Initial stabilization and placement

Initial evaluation and management focuses on stabilization of airway, breathing, and circulation.[9]

For patients who are unable to protect their airway or who present with depressed level of consciousness (Glasgow Coma Score [GCS] ≤8), endotracheal intubation for airway protection is recommended.

Blood pressure (BP) is frequently elevated at presentation and requires treatment. Maintaining a systolic BP goal range of 130 to 150 mmHg is reasonable. Careful titration is recommended, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in systolic BP.[9]

All patients with acute hemorrhagic stroke should be admitted to a neuroscience intensive care unit (ICU) because of the following potential risks or requirements:

Hourly neurologic vital signs
Intubation with mechanical ventilation
Depressed consciousness
High risk for hematoma expansion
BP monitoring or control with continuous infusions
Need for external ventriculostomy catheter, intracranial pressure (ICP) monitor, or surgical intervention.

Some patients require urgent placement of an external ventriculostomy catheter due to acute hydrocephalus.

Regardless of bleed location (cerebellar versus noncerebellar), neurologically stable patients with strong vital signs may be observed, ensuring adequate hydration and nutrition as necessary.

Evaluation and treatment are best accomplished in the neuroscience ICU, or eventually in a dedicated stroke unit.[9][101][102] [ ]

Monitoring of all patients in a facility with 24-hour access to emergency neurosurgery coverage is recommended, in case of acute deterioration from hydrocephalus or mass effect. If 24-hour neurosurgery coverage is not available, the patient should be transferred to a hospital that has such coverage.

Tracheal intubation: animated demonstration

How to insert a tracheal tube in an adult using a laryngoscope.

Bag-valve-mask ventilation: animated demonstration

How to use bag-valve-mask apparatus to deliver ventilatory support to adults. Video demonstrates the two-person technique.

Surgical intervention

Surgical hematoma evacuation through craniotomy, minimally invasive approaches, or ventriculostomy is aimed at preventing further pressure-related injury and protecting against secondary physiological and cellular injury.[9]

Cerebellar hemorrhage

For patients with cerebellar intracerebral hemorrhage who are deteriorating neurologically, or have brainstem compression, or hydrocephalus from ventricular obstruction, or cerebellar intracerebral hemorrhage volume ≥15 mL, the American Heart Association and American Stroke Association (AHA/ASA) recommend immediate surgical removal of the hemorrhage with or without external ventricular drainage (EVD). Surgical intervention in these patients has been shown to reduce mortality, compared with medical management alone. The efficacy of surgical evacuation for improving functional outcomes, however, is uncertain and has not been demonstrated in retrospective studies.[9]

Noncerebellar hemorrhage

Limited data suggest that in patients with supratentorial intracerebral hemorrhage who are deteriorating, craniotomy for hematoma evacuation might be considered as a lifesaving measure.[9] However, randomized trials comparing standard surgery (craniotomy) with conservative management have not demonstrated a clear benefit for surgical intervention in patients with intracerebral hemorrhage.[9][106][107]

Minimally invasive surgery for intracerebral hemorrhage

Recommendations from the AHA/ASA include the following:[9]

For patients with supratentorial intracerebral hemorrhage of 20- to 30-mL volume with GCS scores in the moderate range (5-12), minimally invasive hematoma evacuation with endoscopic or stereotactic aspiration with or without thrombolytic use can be useful to reduce mortality compared with medical management alone.
For patients with supratentorial intracerebral hemorrhage of 20- to 30-mL volume with GCS scores in the moderate range (5-12) being considered for hematoma evacuation, it may be reasonable to select minimally invasive hematoma evacuation over conventional craniotomy to improve functional outcomes.
For patients with supratentorial intracerebral hemorrhage of 20- to 30-mL volume with GCS scores in the moderate range (5-12), the effectiveness of minimally invasive hematoma evacuation with endoscopic or stereotactic aspiration with or without thrombolytic use to improve functional outcomes is uncertain.

Minimally invasive surgical interventions require surgeon and center skill and experience as the basis for these recommendations. The literature supports that minimally invasive surgery may be considered to improve functional outcomes compared with conventional craniotomy.[9] However, the mortality benefit of minimally invasive surgery compared with craniotomy is uncertain since results from large randomized clinical trials have not been definitive.[9] Systematic reviews and meta-analyses have shown that patients subject to early evacuation using minimally invasive techniques (within 24 hours) are more likely to achieve functional independence.[108][109][110][111] One meta-analysis suggested that patients with superficial hematoma between 25 mL and 40 mL, treated within 72 hours, are most likely to benefit from a minimally invasive surgical approach.[112]

Minimally invasive surgery with thrombolysis for intracerebral hemorrhage

Meta-analyses indicate that stereotaxis plus thrombolysis can reduce mortality following intracerebral hemorrhage.[108] However, a subsequent open-label trial found that minimally invasive catheter evacuation followed by thrombolysis with alteplase (MISTIE) did not improve the proportion of patients with good response 365 days after a moderate to large intracerebral hemorrhage.[113]

Moyamoya disease: cerebral revascularization

Cerebrovascular bypass surgery can be performed in patients with Moyamoya disease, a rare progressive cerebrovascular disorder caused by blocked arteries at the base of the brain. Meta-analyses indicate that bypass surgery is more effective than conservative treatment for the prevention of stroke.[114][115][116] Direct bypass may be associated with better outcomes than indirect bypass.[115][117]

Management of elevated intracranial pressure (ICP)

Patients with intracranial hemorrhage are at risk of developing elevated ICP from the effects of expanding hematoma, accumulating edema, or hydrocephalus. Patients with GCS <8, clinical findings supporting transtentorial herniation, or significant intraventricular hemorrhage or hydrocephalus contributing to decreased level of consciousness might be considered for ICP monitoring and treatment.[9]

Corticosteroids should not be used, because they are not effective in intracerebral hemorrhage and increase complications.[9]

Consideration of surgery or ventricular drainage

Blood products or mass effect may cause obstruction of ventricular flow of cerebrospinal fluid, most commonly at the level of the aqueduct of Sylvius. Conversely, blood products may interfere with cerebrospinal fluid resorption by the arachnoid villi (i.e., communicating hydrocephalus). Neurosurgical consultation for consideration of surgery or ventricular drainage is required in these unstable patients.[106]

External ventricular shunt placement

For patients with spontaneous intracerebral hemorrhage, large intraventricular hemorrhage, and impaired level of consciousness, the AHA/ASA recommend external ventricular drainage (EVD). Surgical intervention in these patients has been shown to reduce mortality, compared with medical management alone. The efficacy of EVD for improving functional outcomes is not well established.[9]

For patients with cerebellar intracerebral hemorrhage and clinical hydrocephalus, EVD alone is, in theory, potentially harmful, especially if the basal cisterns are compressed.[9] EVD alone may be insufficient when intracranial hypertension impedes blood supply to the brainstem.[9]

Aspiration precautions

Swallowing impairment is common in stroke, regardless of clinical or neurologic stability or bleed location, and is associated with an increased risk of aspiration pneumonia that ranges from 20% to 60%.[118][119]

Guidelines support dysphagia screening by a speech-language pathologist or other trained healthcare provider before the patient begins eating, drinking, or receiving oral medications.[9][120] Early evaluation with a formal dysphagia screening tool is recommended.[9]

Patients who cannot take nutrition orally are hydrated with isotonic fluids (to decrease risk of brain edema) and receive enteral feeding by nasogastric, nasoduodenal, or percutaneous gastrotomy tube. [ ] However, patients fed via nasogastric tubes are at risk for developing pneumonia secondary to lower esophageal dysfunction, gastric reflux, and microaspiration exacerbated by the presence of the nasogastric tube.[119]

Seizure management

Anticonvulsants should be used to treat clinical seizures and patients with a change of mental status who are found to have electrographic seizures on electroencephalogram (EEG).[9]

New-onset seizures in the context of spontaneous intracerebral hemorrhage are relatively common (between 2.8% and 28%), and most of these seizures occur within the first 24 hours of the hemorrhage.[9]

The relationship between clinical seizures and neurologic outcome and mortality remains unclear.[9]

Prophylactic use of anticonvulsants has not been shown to provide benefit, and is not recommended.[9][121]

Blood pressure management

Hypertension is present in more than 70% of patients presenting with acute ischemic or hemorrhagic stroke and may reflect a response to cerebral injury.[122] Continuous arterial monitoring is helpful when BP is elevated in these patients. BP lowering has been hypothesized to reduce hematoma expansion but also to potentially reduce cerebral perfusion pressure (CPP) and promote ischemia.[123]

Recommendations from the AHA/ASA include the following:[9]

In patients with spontaneous intracerebral hemorrhage requiring acute BP lowering, careful titration to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in systolic BP (SBP), can be beneficial for improving functional outcomes.
Initiating BP treatment within 2 hours of intracerebral hemorrhage onset and reaching target within 1 hour can be beneficial to reduce the risk of hematoma expansion and improve functional outcome.
In patients with spontaneous intracerebral hemorrhage of mild to moderate severity presenting with SBP between 150 and 220 mmHg, acute lowering of SBP to a target of 140 mmHg with the goal of maintaining in the range of 130 to 150 mmHg is safe and may be reasonable for improving functional outcomes. Acute lowering of SBP to <130 mmHg is potentially harmful in these patients.
In patients with spontaneous intracerebral hemorrhage presenting with large or severe intracerebral hemorrhage or those requiring surgical decompression, the safety and efficacy of intensive BP lowering are not well established.

These recommendations are based on two of the largest trials for early intensive BP lowering after intracerebral hemorrhage (INTERACT2 [Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial] and ATACH-2 [Antihypertensive Treatment of Acute Cerebral Hemorrhage II]), meta-analyses, and several post-hoc analyses of the INTERACT2 and ATACH-2 trials.[9]

A post-hoc analysis of one randomized controlled trial suggested that low CPP <60 and <70 mmHg was associated with increased mortality and poor functional outcomes, respectively, suggesting that BP modifications should be tailored to provide a CPP of 60 to ≥70 mmHg in patients with large intracerebral hemorrhage, ICP elevation, or compromised CPP.[9][124]

Correction of coagulopathy

In patients with anticoagulant-associated spontaneous intracerebral hemorrhage, anticoagulation should be discontinued immediately and rapid reversal of anticoagulation should be performed as soon as possible. These important actions improve survival.[9] Actions to correct hypocoagulant states include repletion of depleted clotting factors or platelets and antidotes to specific pharmacologic therapies.[9] A specific antidote may not be available for each anticoagulant agent; administration of the offending agent should be stopped in such cases.

Patients on a vitamin K antagonist (VKA; e.g., warfarin)

In patients with VKA-associated spontaneous intracerebral hemorrhage whose international normalized ratio (INR) is ≥2.0, 4-factor prothrombin complex concentrate (PCC) is recommended in preference to fresh frozen plasma to achieve rapid correction of INR and limit hematoma expansion.[9]

In patients with VKA-associated spontaneous intracerebral hemorrhage with INR of 1.3 to 1.9, it may be reasonable to use 4-factor PCC to achieve rapid correction of INR and limit hematoma expansion.[9]

All patients with intracranial hemorrhage should be given vitamin K intravenously directly after coagulation factor replacement (PCC or other) to prevent later increase in INR and subsequent hematoma expansion.[9]

By comparison with factor concentrates or recombinant activated factor VII, fresh frozen plasma normalizes INR less quickly, is infused more slowly, and requires higher infusion volumes.[125] INR should be checked postinfusion.

Human-derived 4-factor PCC contains the vitamin K-dependent clotting factors II, VII, IX, and X. It provides fast correction of INR with significantly less infusion of intravenous volume. INR should be checked after 15-60 minutes, then every 6-8 hours for the first 24-48 hours because of possible rebound of its effect.[126] If INR remains elevated, specialist advice on further management should be sought. Human-derived 4-factor PCC may be indicated.

Patients on heparin

The initial option for hypocoagulation caused by intravenous unfractionated heparin is protamine.[9][127] Protamine may also be used for correction of low molecular weight heparin (LMWH)-induced hypocoagulation.[9] Specific recommendations are provided in guidelines depending on time since LMWH administration.[9][127] Patients with fish allergy, history of vasectomy, or protamine-containing insulin injections are at risk for anaphylaxis and should be monitored carefully.

Patients on direct thrombin inhibitors

In patients with dabigatran-associated spontaneous intracerebral hemorrhage, idarucizumab is reasonable to reverse the anticoagulant effect of dabigatran.[9] Idarucizumab, a monoclonal antibody fragment that binds dabigatran, quickly and completely reversed the effect of dabigatran in 88% to 90% of patients in one study.[128] When idarucizumab is not available, activated PCC or PCC may be considered to improve hemostasis.[9] In patients with dabigatran- or factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, if the direct oral anticoagulant was taken within the previous few hours, activated charcoal may be reasonable to prevent absorption.[9]

There is debate regarding the best approach for a patient with intracranial hemorrhage who is taking a direct thrombin inhibitor with no specific antidote. Various strategies have been suggested, including administration of activated charcoal in patients who present within 2 hours of taking an oral direct thrombin inhibitor. Other recommendations include administration of PCC, activated PCC, and emergency hemodialysis.[126]

Patients on factor Xa inhibitors

In patients with direct factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, the AHA/ASA recommend that recombinant coagulation factor Xa (andexanet alfa) is reasonable to reverse the anticoagulant effect of factor Xa inhibitors.[9] Recombinant coagulation factor Xa (andexanet alfa) is a modified human factor Xa decoy protein that is a reversal agent for the factor Xa inhibitors apixaban and rivaroxaban. It may be used off-label in some countries for other factor Xa inhibitors such as edoxaban and betrixaban. One multicenter, prospective, open-label, single-group study showed that treatment with recombinant coagulation factor Xa (andexanet alfa) markedly reduced anti-factor Xa activity in patients with acute major bleeding associated with use of a factor Xa inhibitor; 82% of patients had excellent or good hemostatic efficacy at 12 hours.[129]

In patients with direct factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, the AHA/ASA recommend that a 4-factor PCC or activated PCC may also be considered to improve hemostasis.[9]

Patients on thrombolytic therapies

In patients with symptomatic intracranial bleeding occurring within 24 hours of administration of intravenous alteplase for ischemic stroke, the alteplase infusion should be stopped.[120] Cryoprecipitate (which includes factor VIII) should be infused over 10-30 minutes.[120] An additional dose should be administered if fibrinogen levels are low (<150 mg/dL).[120] Tranexamic acid or aminocaproic acid may be beneficial for some patients, but particularly when blood products are contraindicated or declined by patient/family or if cryoprecipitate is not available in a timely manner.[120] Hematology and neurosurgery consults should be considered.[120]

Prognosis for people with tPA-related hemorrhage is poor, and data to guide coagulation management in this setting are inadequate. A hematology consult should be considered due to the complex nature of the coagulopathy.

Platelet transfusion

For patients with spontaneous intracerebral hemorrhage being treated with aspirin and who require emergency neurosurgery, the AHA/ASA recommend that platelet transfusion may be useful to reduce postoperative bleeding and mortality.[9]

Platelet infusion is indicated for thrombocytopenia to achieve a platelet count of >100,000 per microliter of blood. There are no data to indicate the optimal minimum platelet level following intracerebral hemorrhage, but a level >100,000 per microliter of blood is reasonable for the first 24 hours following onset, when risk of hemorrhage expansion is highest.

For patients with spontaneous intracerebral hemorrhage being treated with aspirin and not scheduled for emergency surgery, platelet transfusions are potentially harmful and should not be administered.[9][130] Antiplatelet medications tend to reduce platelet activity and predispose patients to easy bruising and bleeding complications. This functional reduction has been associated with early clot growth and worse 3-month outcome after intracerebral hemorrhage.[131][132] Platelet infusion to ameliorate the effects of antiplatelet therapy and minimize intracerebral hemorrhage expansion increased risk of death or disability, compared with standard care, in one randomized controlled trial.[130][133]

Management of fever

Fever is common after intracerebral hemorrhage, especially intraventricular hemorrhage. Longer duration of fever has been associated with worse outcomes and has been established as an independent prognostic factor.[9] Post-hoc analysis of a randomized controlled trial in patients with acute ischemic stroke or intracerebral hemorrhage found that treatment with acetaminophen was associated with improved outcome in patients with baseline body temperature 98.6°F to 102.2°F (37°C to 39°C).[134] A follow-up multicenter, randomized, double-blind, placebo-controlled clinical trial was stopped prematurely because of slow recruitment and lack of funding.[135] Despite lack of definitive evidence, treatment to reduce temperature during fever seems reasonable.[9]

Glucose control

In patients with spontaneous intracerebral hemorrhage, the AHA/ASA recommend to treat hypoglycemia (<40-60 mg/dL [<2.2-3.3 mmol/L]) to reduce mortality. In patients with spontaneous intracerebral hemorrhage, treating moderate to severe hyperglycemia (>180-200 mg/dL [>10.0-11.1 mmol/L]) is reasonable to improve outcomes.[9]

In critically ill patients who are persistently hyperglycemic (≥180 mg/dL [≥10.0 mmol/L] confirmed on two occasions within 24 hours), a variable rate intravenous insulin infusion should be initiated. A target glucose range of 140 to 180 mg/dL (7.8 to 10.0 mmol/L) is recommended for most critically sick patients with hyperglycemia.[136] A target glucose range of 110 to 140 mg/dL (6.1 to 7.8 mmol/L) may be appropriate and acceptable in selected patients (e.g., critically sick postsurgical patients), if this can be achieved without significant hypoglycemia.[136] For patients admitted to an ICU who present with high blood glucose, an intravenous insulin protocol could also be considered. See local specialist protocol for insulin dosing guidelines.

Untreated hyperglycemia is independently associated with poor prognosis in patients with intracerebral hemorrhage.[137][138] Consequently, prompt glucose correction is recommended despite a lack of evidence for improving outcomes.[9]

Tight glucose control may increase the incidence of hypoglycemia, which may result in poor outcomes. Therefore, glucose should be monitored closely and both hyperglycemia and hypoglycemia should be avoided.[9]

Deep venous thrombosis (DVT) prophylaxis

The risk of venous thromboembolism may be higher in patients with hemorrhagic stroke than in patients with ischemic stroke.[139] The presence of intracerebral hemorrhage makes it challenging to determine the most appropriate approach for prophylaxis against DVT and/or pulmonary embolism.

Intermittent pneumatic compression significantly reduces the risk of DVT following hemorrhagic stroke and should be started at the time of hospital admission for patients with intracranial hemorrhage.[9][140][141][142] Graduated compression stockings of knee-high or thigh-high length alone are not beneficial for venous thromboembolism prophylaxis in these patients.[9]

Early mobilization is recommended, but efficacy is unproven in randomized controlled trials.[9]

Low-dose unfractionated or low molecular weight heparin may be considered as long as there is no evidence of continued bleeding.[9][140][143]

If patients develop DVT or pulmonary embolism, systemic anticoagulation or inferior vena cava filter placement may be considered, but the risks versus benefits should be understood. The time from hemorrhage, hematoma stability, cause of hemorrhage, and patient's clinical appearance are important factors in decision making.[9]

Rehabilitation

Many patients experience limited ambulation and mobility, which reduces their quality of life. Additionally, immobility-related complications (i.e., DVT, pulmonary embolism, aspiration pneumonia) are common early after stroke.[144]

The objective of rehabilitation is to enable the person to return to an acceptable social and/or working lifestyle. Early rehabilitation after stroke is recommended.[9][144] However, one trial found no benefit attributable to very early, intense mobilization (e.g., multiple out-of-bed sessions) within 24 hours of stroke onset (ischemic or hemorrhagic) compared with usual standard of care.[145] [ ] [Evidence B] Smaller studies have found that starting rehabilitation within 24 to 48 hours of intracerebral hemorrhage improves survival and functional outcomes after 3 to 6 months' follow-up.[146]

Multidisciplinary stroke rehabilitation

There is strong evidence that rehabilitation outcomes are better when a multidisciplinary team with experience in stroke rehabilitation is involved.[147] Practice guidelines provide recommendations related to every aspect of stroke rehabilitation, from early-acute therapy to community reintegration.[9][144]

About one-third of patients who have a stroke develop aphasia. Speech and language therapy is crucial in order to increase the degree of functional communication. Differences in functional outcome when comparing specific therapy regimens (i.e., intensity, dosage, and duration) are being investigated.

Interventions to improve motor function

Mental practice describes a training method that uses cognitive rehearsal of activities to improve performance of those activities - an individual repeatedly mentally rehearses an action or task in their imagination (e.g., picking up a cup or reaching out with their arm) without physically performing the action or task. Randomized controlled trials support the use of mental practice, in addition to conventional physical rehabilitation treatment, in improving upper extremity impairment after stroke.[148]

Several studies have investigated the use of pharmacotherapy to improve motor recovery. Amphetamines, levodopa, and selective serotonin reuptake inhibitors (SSRIs) have been the most widely studied. Fluoxetine, an SSRI, did not improve functional outcomes in randomized controlled trials and meta-analyses of patients with acute stroke, including hemorrhagic stroke.[149][150][151]

Virtual reality allows stroke patients with disabilities to engage in specific tasks in a computer-generated visual environment. There is some evidence that the use of virtual reality can improve functional balance, various aspects of gait, and other functions.[152][153]

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