Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

INITIAL

presumed hemorrhagic stroke

1st line – neurosurgical and neurocritical care evaluation

Back
INITIAL
|
presumed hemorrhagic stroke
1st line – 

neurosurgical and neurocritical care evaluation

Facilities are to have 24-hour availability of emergency neurosurgical consultation due to the potential need for surgical intervention. Most patients are admitted to an intensive care unit due to the frequent need for tracheal intubation or invasive monitoring of blood pressure or intracranial pressure.

Plus – admission to neuroscience intensive care unit or stroke unit

Back
INITIAL
|
presumed hemorrhagic stroke
Plus – 

admission to neuroscience intensive care unit or stroke unit

Treatment recommended for ALL patients in selected patient group

Treatment in a dedicated stroke unit is recommended.[102] [ Cochrane Clinical Answers logo ]

Neuroscience intensive care units and stroke units have multidisciplinary teams including physicians, nursing staff, and rehabilitation specialists.

Improved supportive care, avoidance of complications such as infection and deep venous thrombosis, and earlier initiation of rehabilitation therapy are among the mechanisms by which stroke units are hypothesized to produce better outcomes.

Studies of stroke units have predominantly included ischemic stroke patients, but it is reasonable to infer that hemorrhagic stroke patients also receive benefit.

Plus – airway protection

Back
INITIAL
|
presumed hemorrhagic stroke
Plus – 

airway protection

Treatment recommended for ALL patients in selected patient group

For patients who are unable to protect their airway or who present with depressed level of consciousness, endotracheal intubation for airway protection is recommended.

Tracheal intubation: animated demonstration
Tracheal intubation: animated demonstration

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

Bag-valve-mask ventilation: animated demonstration
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.

Plus – aspiration precautions

Back
INITIAL
|
presumed hemorrhagic stroke
Plus – 

aspiration precautions

Treatment recommended for ALL patients in selected patient group

Swallowing impairment is common in stroke 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. [ Cochrane Clinical Answers logo ] 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]

ACUTE

noncerebellar bleed: stable and alert

1st line – neurosurgical and neurocritical care evaluation

Back
ACUTE
|
noncerebellar bleed: stable and alert
1st line – 

neurosurgical and neurocritical care evaluation

Facilities are to have 24-hour availability of emergency neurosurgical consultation due to the potential need for surgical intervention. Most patients are admitted to an intensive care unit due to the frequent need for tracheal intubation or invasive monitoring of blood pressure or intracranial pressure.

Plus – admission to neuroscience intensive care unit or stroke unit

Back
ACUTE
|
noncerebellar bleed: stable and alert
Plus – 

admission to neuroscience intensive care unit or stroke unit

Treatment recommended for ALL patients in selected patient group

Treatment in a dedicated stroke unit is recommended.[102] [ Cochrane Clinical Answers logo ]

Neuroscience intensive care units and stroke units have multidisciplinary teams including physicians, nursing staff, and rehabilitation specialists.

Improved supportive care, avoidance of complications such as infection and deep venous thrombosis, and earlier initiation of rehabilitation therapy are among the mechanisms by which stroke units are hypothesized to produce better outcomes.

Studies of stroke units have predominantly included ischemic stroke patients, but it is reasonable to infer that hemorrhagic stroke patients also receive benefit.

Plus – supportive care

Back
ACUTE
|
noncerebellar bleed: stable and alert
Plus – 

supportive care

Treatment recommended for ALL patients in selected patient group

Supplemental oxygen should be provided only when blood oxygen saturation is <94%. Liberal use of oxygen is associated with increased mortality in acutely ill adults.[154][155]

Swallowing impairment is common in stroke and is associated with an increased risk of aspiration pneumonia.[118] 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]​​ Studies support early evaluation with a formal dysphagia screening tool. 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. [ Cochrane Clinical Answers logo ] 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]

In patients with spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 intensive care unit 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]

Plus – blood pressure control

Back
ACUTE
|
noncerebellar bleed: stable and alert
Plus – 

blood pressure control

Treatment recommended for ALL patients in selected patient group

The AHA/ASA recommend careful titration in patients with spontaneous intracerebral hemorrhage requiring acute blood pressure (BP) lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in systolic BP (SBP). This can be beneficial for improving functional outcomes.[9] Initiating 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.[9] 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.[9] 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] 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 and promote ischemia.[123]

Antihypertensive agents for noncerebellar hemorrhage have not been compared in controlled trials. Preference is given to the agent that is clinically deemed most likely to be effective for the given patient. Consult your local protocols.

Plus – deep venous thrombosis prophylaxis

Back
ACUTE
|
noncerebellar bleed: stable and alert
Plus – 

deep venous thrombosis prophylaxis

Treatment recommended for ALL patients in selected patient group

Prophylaxis against deep venous thrombosis using intermittent pneumatic compression devices, starting at the time of hospital admission, is recommended for nonambulatory patients with intracranial hemorrhage.[9][140][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]

Primary options

heparin: 5000 units subcutaneously every 8-12 hours

OR

enoxaparin: 40 mg subcutaneously once daily

Consider – antipyretic measures

Back
ACUTE
|
noncerebellar bleed: stable and alert
|
pyrexia
Consider – 

antipyretic measures

Treatment recommended for SOME patients in selected patient group

Fever has been associated with worse outcome after noncerebellar hemorrhage.[9] Treatment of fever is reasonable but unsupported by controlled trials.[9]

Acetaminophen is recommended.

Primary options

acetaminophen: 325-1000 mg orally every 4-6 hours when required, maximum 4000 mg/day

Consider – correction of coagulopathy

Back
ACUTE
|
noncerebellar bleed: stable and alert
|
pre-existing anticoagulation therapy
Consider – 

correction of coagulopathy

Treatment recommended for SOME patients in selected patient group

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 after diagnosis of spontaneous intracerebral hemorrhage to 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.

For patients with vitamin K antagonist (VKA)-associated spontaneous intracerebral hemorrhage whose international normalized ratio (INR) ≥2, 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.

For patients on intravenous unfractionated heparin, protamine is indicated.[9][127] It can also be used for 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, or with a history of vasectomy or protamine-containing insulin injections, are at risk for anaphylaxis and should be monitored carefully.[127]

Idarucizumab is the reversal agent for patients taking dabigatran.[128] In patients with dabigatran-associated spontaneous intracerebral hemorrhage, idarucizumab is reasonable to reverse the anticoagulant effect of dabigatran.[9] When idarucizumab is not available, activated PCC or PCCs may be considered to improve hemostasis.[9]

In patients with dabigatran- or factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, when the direct oral anticoagulant agent was taken within the previous few hours, activated charcoal may be reasonable to prevent absorption of the direct oral anticoagulant.[9] There is debate regarding the best approach for a patient with intracranial hemorrhage who is taking a direct thrombin inhibitor with no 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]

In patients with direct factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 the reversal agent for patients taking the factor Xa inhibitors apixaban and rivaroxaban.[129] It may be used off-label in some countries for other factor Xa inhibitors such as edoxaban and betrixaban. 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]

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]

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 platelet count of >100,000 per microliter of blood. There are no data to indicate the optimal minimum platelet level following noncerebellar 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]

noncerebellar bleed: decompensating

1st line – neurosurgical and neurocritical care evaluation

Back
ACUTE
|
noncerebellar bleed: decompensating
1st line – 

neurosurgical and neurocritical care evaluation

Facilities are to have 24-hour availability of emergency neurosurgical consultation due to the potential need for surgical intervention. All patients are admitted to an intensive care unit due to the frequent need for tracheal intubation or invasive monitoring of blood pressure or intracranial pressure.

Plus – admission to neuroscience intensive care unit or stroke unit

Back
ACUTE
|
noncerebellar bleed: decompensating
Plus – 

admission to neuroscience intensive care unit or stroke unit

Treatment recommended for ALL patients in selected patient group

Treatment in a dedicated stroke unit is recommended.[102] [ Cochrane Clinical Answers logo ]

Neuroscience intensive care units and stroke units have multidisciplinary teams including physicians, nursing staff, and rehabilitation specialists.

Improved supportive care, avoidance of complications such as infection and deep venous thrombosis, and earlier initiation of rehabilitation therapy are among the mechanisms by which stroke units are hypothesized to produce better outcomes.

Studies of stroke units have predominantly included ischemic stroke patients, but it is reasonable to infer that hemorrhagic stroke patients also receive benefit.

Plus – supportive care

Back
ACUTE
|
noncerebellar bleed: decompensating
Plus – 

supportive care

Treatment recommended for ALL patients in selected patient group

Supplemental oxygen should be provided only when blood oxygen saturation is <94%. Liberal use of oxygen is associated with increased mortality in acutely ill adults.[154][155]

For patients presenting with depressed level of consciousness, intubation for airway protection is recommended.

Patients should be placed "nothing by mouth" due to the potential need for emergency surgery. 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. [ Cochrane Clinical Answers logo ] 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]

In patients with spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 110 to 140 mg/dL (6.1 to 7.8 mmol/L) may be appropriate and acceptable if this can achieved without significant hypoglycemia.​​[136]

For patients admitted to an intensive care unit 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]

Tracheal intubation: animated demonstration
Tracheal intubation: animated demonstration

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

Bag-valve-mask ventilation: animated demonstration
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.

Plus – blood pressure control

Back
ACUTE
|
noncerebellar bleed: decompensating
Plus – 

blood pressure control

Treatment recommended for ALL patients in selected patient group

The AHA/ASA recommend careful titration in patients with spontaneous intracerebral hemorrhage requiring acute blood pressure (BP) lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in systolic BP (SBP). This can be beneficial for improving functional outcomes.[9] 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]

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. 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, intracranial pressure elevation, or compromised CPP.[9][124]

Antihypertensive agents for noncerebellar hemorrhage have not been compared in controlled trials. Preference is given to the agent that is clinically deemed most likely to be effective for the given patient. Consult your local protocols.

Plus – surgery

Back
ACUTE
|
noncerebellar bleed: decompensating
|
clots amenable to surgery
Plus – 

surgery

Treatment recommended for ALL patients in selected patient group

The American Heart Association and American Stroke Association (AHA/ASA) recommend that in patients with supratentorial intracerebral hemorrhage of 20- to 30-mL volume with Glasgow Coma Scale (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.[9] 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.[9] 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.[9] 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 technique (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]

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]

Plus – supportive management and/or external ventricular drainage

Back
ACUTE
|
noncerebellar bleed: decompensating
|
elevated intracranial pressure
Plus – 

supportive management and/or external ventricular drainage

Treatment recommended for ALL patients in selected patient group

Patients with intracranial hemorrhage are at risk of developing elevated intracranial pressure (ICP) from the effects of expanding hematoma, accumulating edema, or hydrocephalus. Patients with Glasgow Coma Scale (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 and increase complications.[9]

For patients with spontaneous intracranial hemorrhage, large intraventricular hemorrhage, and impaired level of consciousness, the American Heart Association and American Stroke Association 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]

Tracheal intubation: animated demonstration
Tracheal intubation: animated demonstration

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

Bag-valve-mask ventilation: animated demonstration
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.

Plus – antipyretic measures

Back
ACUTE
|
noncerebellar bleed: decompensating
|
pyrexia
Plus – 

antipyretic measures

Treatment recommended for ALL patients in selected patient group

Fever has been associated with worse outcome after noncerebellar hemorrhage.[156] Treatment of fever is reasonable but unsupported by controlled trials.[9]

Acetaminophen is recommended.

Primary options

acetaminophen: 325-1000 mg orally every 4-6 hours when required, maximum 4000 mg/day

Plus – anticonvulsants

Back
ACUTE
|
noncerebellar bleed: decompensating
|
seizures
Plus – 

anticonvulsants

Treatment recommended for ALL patients in selected patient group

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]

Evidence suggests that electrographic seizures (detected only on EEG) may be quite common, although the clinical significance is unclear.[9] The risk of early seizure is higher when the origin of the noncerebellar hemorrhage is in the cerebral lobes.[68] 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] Prophylactic use of anticonvulsants has not been shown to provide benefit, and is not recommended.[9][121]​​

Primary options

phenytoin: 15 mg/kg intravenously as a loading dose, followed by 4-6 mg/kg/day given in 2 divided doses, adjust dose according to response and serum phenytoin level

Plus – deep venous thrombosis prophylaxis

Back
ACUTE
|
noncerebellar bleed: decompensating
|
ongoing immobilization
Plus – 

deep venous thrombosis prophylaxis

Treatment recommended for ALL patients in selected patient group

Prophylaxis against deep venous thrombosis using intermittent pneumatic compression devices, starting at the time of hospital admission, is recommended for nonambulatory patients with intracranial hemorrhage.[9][140][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]

Primary options

heparin: 5000 units subcutaneously every 8-12 hours

OR

enoxaparin: 40 mg subcutaneously once daily

Consider – correction of coagulopathy

Back
ACUTE
|
noncerebellar bleed: decompensating
|
pre-existing anticoagulation therapy
Consider – 

correction of coagulopathy

Treatment recommended for SOME patients in selected patient group

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 after diagnosis of spontaneous intracerebral hemorrhage to 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.

For patients with vitamin K antagonist (VKA)-associated spontaneous intracerebral hemorrhage whose international normalized ratio (INR) ≥2, 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.

For patients on intravenous unfractionated heparin, protamine is indicated.[9][127] It can also be used for 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, or with a history of vasectomy or protamine-containing insulin injections, are at risk for anaphylaxis and should be monitored carefully.[127]

Idarucizumab is the reversal agent for patients taking dabigatran.[128] In patients with dabigatran-associated spontaneous intracerebral hemorrhage, idarucizumab is reasonable to reverse the anticoagulant effect of dabigatran.[9] When idarucizumab is not available, activated PCC or PCCs may be considered to improve hemostasis.[9]

In patients with dabigatran- or factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, when the direct oral anticoagulant agent was taken within the previous few hours, activated charcoal may be reasonable to prevent absorption of the direct oral anticoagulant.[9] There is debate regarding the best approach to a patient 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]

In patients with direct factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 the reversal agent for patients taking the factor Xa inhibitors apixaban and rivaroxaban.[129] It may be used off-label in some countries for other factor Xa inhibitors such as edoxaban and betrixaban. 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]

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]

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 platelet count of >100,000 per microliter of blood. There are no data to indicate the optimal minimum platelet level following noncerebellar 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]

<3 cm cerebellar bleed: alert

1st line – neurosurgical and neurocritical care evaluation

Back
ACUTE
|
<3 cm cerebellar bleed: alert
1st line – 

neurosurgical and neurocritical care evaluation

Facilities are to have 24-hour availability of emergency neurosurgical consultation due to the potential need for surgical intervention. All patients are admitted to an intensive care unit due to the frequent need for tracheal intubation or invasive monitoring of blood pressure or intracranial pressure.

Plus – admission to neuroscience intensive care unit or stroke unit

Back
ACUTE
|
<3 cm cerebellar bleed: alert
Plus – 

admission to neuroscience intensive care unit or stroke unit

Treatment recommended for ALL patients in selected patient group

Treatment in a dedicated stroke unit is recommended.[102] [ Cochrane Clinical Answers logo ]

Neuroscience intensive care units and stroke units have multidisciplinary teams including physicians, nursing staff, and rehabilitation specialists.

Improved supportive care, avoidance of complications such as infection and deep venous thrombosis, and earlier initiation of rehabilitation therapy are among the mechanisms by which stroke units are hypothesized to produce better outcomes.

Studies of stroke units have predominantly included ischemic stroke patients, but it is reasonable to infer that hemorrhagic stroke patients also receive benefit.

Plus – supportive care

Back
ACUTE
|
<3 cm cerebellar bleed: alert
Plus – 

supportive care

Treatment recommended for ALL patients in selected patient group

Supplemental oxygen should be provided only when blood oxygen saturation is <94%. Liberal use of oxygen is associated with increased mortality in acutely ill adults.[154][155]

Swallowing impairment is common in stroke and is associated with an increased risk of aspiration pneumonia.[118] Guidelines support dysphagia screening by a speech-language pathologist or other trained healthcare provider before the patient begins eating, drinking, or receiving oral medications.[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. [ Cochrane Clinical Answers logo ] 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]

In patients with spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 ill 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 ill postsurgical patients), if this can be achieved without significant hypoglycemia.[136]

For patients admitted to an intensive care unit 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]

Plus – blood pressure control

Back
ACUTE
|
<3 cm cerebellar bleed: alert
Plus – 

blood pressure control

Treatment recommended for ALL patients in selected patient group

The AHA/ASA recommend careful titration in patients with spontaneous intracerebral hemorrhage requiring acute blood pressure (BP) lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in systolic BP (SBP). This can be beneficial for improving functional outcomes.[9] Initiating 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.[9] 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.[9] 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 and promote ischemia.[123]

Antihypertensive agents for intracranial hemorrhage have not been compared in controlled trials. Preference is given to the agent that is clinically deemed most likely to be effective for the given patient. Consult your local protocols.

Consider – antipyretic measures

Back
ACUTE
|
<3 cm cerebellar bleed: alert
|
pyrexia
Consider – 

antipyretic measures

Treatment recommended for SOME patients in selected patient group

Fever has been associated with worse outcome after intracranial hemorrhage.[156] Treatment of fever is reasonable but unsupported by controlled trials.[9]

Acetaminophen is recommended.

Primary options

acetaminophen: 325-1000 mg orally every 4-6 hours when required, maximum 4000 mg/day

Plus – deep venous thrombosis prophylaxis

Back
ACUTE
|
<3 cm cerebellar bleed: alert
|
ongoing immobilization
Plus – 

deep venous thrombosis prophylaxis

Treatment recommended for ALL patients in selected patient group

Prophylaxis against deep venous thrombosis using intermittent pneumatic compression devices, starting at the time of hospital admission, is recommended for nonambulatory patients with intracranial hemorrhage.[9][140][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]

Primary options

heparin: 5000 units subcutaneously every 8-12 hours

OR

enoxaparin: 40 mg subcutaneously once daily

Consider – correction of coagulopathy

Back
ACUTE
|
<3 cm cerebellar bleed: alert
|
pre-existing anticoagulation therapy
Consider – 

correction of coagulopathy

Treatment recommended for SOME patients in selected patient group

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 after diagnosis of spontaneous intracerebral hemorrhage to 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.

For patients with vitamin K antagonist (VKA)-associated spontaneous intracerebral hemorrhage whose international normalized ratio (INR) ≥2, 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.

For patients on intravenous unfractionated heparin, protamine is indicated.[9][127] It can also be used for 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, or with a history of vasectomy or protamine-containing insulin injections, are at risk for anaphylaxis and should be monitored carefully.[127]

Idarucizumab is the reversal agent for patients taking dabigatran.[128] In patients with dabigatran-associated spontaneous intracerebral hemorrhage, idarucizumab is reasonable to reverse the anticoagulant effect of dabigatran.[9] When idarucizumab is not available, activated PCC or PCCs may be considered to improve hemostasis.[9]

In patients with dabigatran- or factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, when the direct oral anticoagulant agent was taken within the previous few hours, activated charcoal may be reasonable to prevent absorption of the direct oral anticoagulant.[9] There is debate regarding the best approach to a patient 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]

In patients with direct factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 the reversal agent for patients taking the factor Xa inhibitors apixaban and rivaroxaban.[129] It may be used off-label in some countries for other factor Xa inhibitors such as edoxaban and betrixaban. 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]

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]

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 platelet count of >100,000 per microliter of blood. There are no data to indicate the optimal minimum platelet level following noncerebellar 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]

>3 cm cerebellar bleed or drowsy/unstable

1st line – neurosurgical and neurocritical care evaluation

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
1st line – 

neurosurgical and neurocritical care evaluation

For patients presenting with depressed level of consciousness, intubation for airway protection is recommended.

Facilities are to have 24-hour availability of emergency neurosurgical consultation due to the potential need for surgical intervention. All patients are admitted to an intensive care unit due to the frequent need for tracheal intubation or invasive monitoring of blood pressure or intracranial pressure.

Tracheal intubation: animated demonstration
Tracheal intubation: animated demonstration

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

Bag-valve-mask ventilation: animated demonstration
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.

Plus – admission to neuroscience intensive care unit or stroke unit

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
Plus – 

admission to neuroscience intensive care unit or stroke unit

Treatment recommended for ALL patients in selected patient group

Treatment in a dedicated stroke unit is recommended.[102] [ Cochrane Clinical Answers logo ] ​​

Neuroscience intensive care units and stroke units have multidisciplinary teams including physicians, nursing staff, and rehabilitation specialists.

Improved supportive care, avoidance of complications such as infection and deep venous thrombosis, and earlier initiation of rehabilitation therapy are among the mechanisms by which stroke units are hypothesized to produce better outcomes.

Studies of stroke units have predominantly included ischemic stroke patients, but it is reasonable to infer that hemorrhagic stroke patients also receive benefit.

Plus – supportive care

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
Plus – 

supportive care

Treatment recommended for ALL patients in selected patient group

Supplemental oxygen should be provided only when blood oxygen saturation is <94%. Liberal use of oxygen is associated with increased mortality in acutely ill adults.[154][155]

Patients should be placed "nothing by mouth" due to the potential need for emergency surgery. 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. [ Cochrane Clinical Answers logo ] 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]

In patients with spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 intensive care unit 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]

Plus – deep venous thrombosis prophylaxis

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
Plus – 

deep venous thrombosis prophylaxis

Treatment recommended for ALL patients in selected patient group

Prophylaxis against deep venous thrombosis using intermittent pneumatic compression devices, starting at the time of hospital admission, is recommended for nonambulatory patients with intracranial hemorrhage.[9][140][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]

Primary options

heparin: 5000 units subcutaneously every 8-12 hours

OR

enoxaparin: 40 mg subcutaneously once daily

Plus – surgery

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
Plus – 

surgery

Treatment recommended for ALL patients in selected patient group

For patients with cerebellar intracerebral hemorrhage who are deteriorating neurologically, or brainstem compression and/or hydrocephalus from ventricular obstruction, or cerebellar intracerebral hemorrhage volume ≥15 mL, the 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] EVD alone may be insufficient when intracranial hypertension impedes blood supply to the brainstem.[9]

Plus – blood pressure control

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
Plus – 

blood pressure control

Treatment recommended for ALL patients in selected patient group

The AHA/ASA recommend careful titration in patients with spontaneous intracerebral hemorrhage requiring acute blood pressure (BP) lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in systolic BP (SBP). This can be beneficial for improving functional outcomes.[9] Initiating 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.[9] 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.[9] 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 and promote ischemia.[123]

Antihypertensive agents for intracranial hemorrhage have not been compared in controlled trials. Preference is given to the agent that is clinically deemed most likely to be effective for the given patient. Consult your local protocols.

Plus – antipyretic measures

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
|
pyrexia
Plus – 

antipyretic measures

Treatment recommended for ALL patients in selected patient group

Fever has been associated with worse outcome after cerebellar hemorrhage.[156] Treatment of fever is reasonable but unsupported by controlled trials.[9]

Acetaminophen is recommended.

Primary options

acetaminophen: 325-1000 mg orally every 4-6 hours when required, maximum 4000 mg/day

Consider – correction of coagulopathy

Back
ACUTE
|
>3 cm cerebellar bleed or drowsy/unstable
|
pre-existing anticoagulation therapy
Consider – 

correction of coagulopathy

Treatment recommended for SOME patients in selected patient group

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 after diagnosis of spontaneous intracerebral hemorrhage to 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.

For patients with vitamin K antagonist (VKA)-associated spontaneous intracerebral hemorrhage whose international normalized ratio (INR) ≥2, 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.

For patients on intravenous unfractionated heparin, protamine is indicated.[9][127] It can also be used for 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, or with a history of vasectomy or protamine-containing insulin injections, are at risk for anaphylaxis and should be monitored carefully.[127]

Idarucizumab is the reversal agent for patients taking dabigatran.[128] In patients with dabigatran-associated spontaneous intracerebral hemorrhage, idarucizumab is reasonable to reverse the anticoagulant effect of dabigatran.[9] When idarucizumab is not available, activated PCC or PCCs may be considered to improve hemostasis.[9]

In patients with dabigatran- or factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, when the direct oral anticoagulant agent was taken within the previous few hours, activated charcoal may be reasonable to prevent absorption of the direct oral anticoagulant.[9] There is debate regarding the best approach to a patient 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]

In patients with direct factor Xa inhibitor-associated spontaneous intracerebral hemorrhage, the American Heart Association/American Stroke Association (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 the reversal agent for patients taking the factor Xa inhibitors apixaban and rivaroxaban.[129] It may be used off-label in some countries for other factor Xa inhibitors such as edoxaban and betrixaban. 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]

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]

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 platelet count of >100,000 per microliter of blood. There are no data to indicate the optimal minimum platelet level following noncerebellar 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]

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