7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Spontaneous intracerebral hemorrhage: Acute treatment and prognosis : Guy Rordorf, MD, Colin McDonald, MD : Scott E Kasner, MD, Jonathan A Edlow, MD, FACEP, Alejandro A Rabinstein, MD, Glenn A Tung, MD, FACR : Richard P Goddeau, Jr, DO, FAHA All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: May 30, 2023. INTRODUCTION Intracerebral hemorrhage (ICH) is the second most common cause of stroke, following ischemic stroke, but accounts for a disproportionate amount of cerebrovascular mortality and morbidity. The goals of initial treatment include preventing hemorrhage expansion, monitoring for and managing elevated intracranial pressure, and managing other neurologic and medical complications ( table 1). The acute treatment and prognosis of spontaneous (atraumatic) intracerebral hemorrhage will be reviewed here. Other aspects of ICH are discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".) (See "Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis".) (See "Hemorrhagic stroke in children".) (See "Stroke in the newborn: Management and prognosis".) (See "Management of acute moderate and severe traumatic brain injury".) TRIAGE https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 1/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Prehospital management of acute ICH focuses on airway maintenance, cardiovascular support, and rapid transport to the nearest acute stroke care facility. Facilities without critical care units and expertise in stroke care should transfer stabilized patients with an acute ICH to an appropriate tertiary care center if possible. The initial steps of acute management in the emergency department include clinical evaluation and imaging-based diagnosis and are discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Evaluation and diagnosis' and "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Brain imaging'.) Admit to ICU or stroke unit Patients with acute ICH should be admitted to the hospital with expertise in neurology, neurosurgery, neuroradiology, and critical care to be monitored and managed in an intensive care unit (ICU) or dedicated stroke unit [1-5]. Multidisciplinary care and the use of ICH-specific treatment protocols can improve functional outcome in ICH [6]. Facilities without such expertise should transfer stabilized patients to an appropriate tertiary care center if possible. Patients with acute ICH are at risk for neurologic deterioration in the first several days due to complications including hematoma expansion, elevations in intracranial pressure, development of hydrocephalus, seizures, or brain herniation [7]. Initial aggressive care We generally provide initial aggressive care to all patients with acute ICH and delay prognostication or enacting new limitations in care for at least the first day. However, these measures do not apply to patients with preexisting "do not attempt resuscitation" (DNAR) orders nor to patients who present with catastrophic ICH and minimal brainstem function. There are inherent uncertainties in determining prognosis for individual patients with acute ICH. Severe neurologic impairment at initial evaluation may be due in part to reversible sources such as metabolic derangements or seizures. Additionally, early limitations to care including new DNAR orders may lead to a self-fulfilling prophecy of poor outcomes caused by clinical nihilism [8-10]. Clinical prediction scores may overestimate the likelihood of poor outcome due to these limitations [11]. MANAGEMENT OF ACUTE BLEEDING Cessation of bleeding occurs in ICH via intrinsic hemostatic pathways and vascular tamponade imposed by the rigid cranial vault [12]. Factors that delay this process by inhibiting hemostasis include exposure to antithrombotic medications and uncontrolled blood pressure. Prompt https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 2/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate control of these factors can reduce the risk of morbidity associated with hematoma enlargement. Reversal strategies differ by antithrombotic drug exposure. The management of uncontrolled blood pressure is reviewed below. (See 'Blood pressure management' below.) Reverse anticoagulation For patients who develop ICH, all anticoagulant and antiplatelet drugs should be discontinued initially. Medications to reverse the effects of anticoagulant drugs should be given immediately ( table 1). Medication-specific reversal agents include: Warfarin Four-factor prothrombin complex concentrate (4F PCC) is preferred for patients with acute ICH taking warfarin [5]. If 4F PCC is unavailable, three-factor prothrombin complex with recombinant activated factor VII or fresh frozen plasma (FFP) may be administered ( table 2). Intravenous vitamin K should also be given to sustain the short- acting effects of 4F PCC or FFP. Reversal of anticoagulation in this setting is discussed in detail separately. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Warfarin'.) Direct oral anticoagulants Reversal strategies for direct oral anticoagulants (DOACs) differ by agent and are presented separately ( table 3). (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Apixaban, edoxaban, and rivaroxaban' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'Dabigatran'.) Heparin and low molecular weight heparins Protamine sulfate is recommended for urgent treatment of patients with heparin-associated ICH [5]. The appropriate dose of protamine sulfate is dependent upon the type of heparin (unfractionated or low molecular weight agents), the dose of heparin given, and the time elapsed since that dose. Andexanet alfa may be used for patients taking low molecular weight heparin. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Unfractionated heparin' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'LMW heparin'.) Patients with severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement or platelet transfusion [5]. (See "Platelet transfusion: Indications, ordering, and associated risks", section on 'Actively bleeding patient'.) Limited role of platelet transfusion For most ICH patients on antiplatelet therapy, we suggest not using platelet transfusions because available data indicate this may be hazardous [13,14]. Platelet transfusions may be given to selected patients with ICH undergoing emergency surgery to reduce the risk of postoperative bleeding [5]. (See "Platelet transfusion: Indications, ordering, and associated risks", section on 'Antiplatelet agents'.) https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 3/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Other hemostatic strategies not recommended For ICH patients without coagulopathy and those not exposed to antithrombotic (anticoagulant or antiplatelet) therapy, we suggest not using specific hemostatic therapy outside the context of a clinical trial. While hemostatic therapy offers the theoretic potential to improve outcomes by stopping ongoing hemorrhage and preventing hemorrhage enlargement, the clinical benefits remain unproven [5,13] and these therapies may cause thromboembolic complications [15-17]. The two most studied hemostatic agents for use in spontaneous ICH are activated recombinant human factor VIIa (rFVIIa) and tranexamic acid. Recombinant factor VIIa rFVIIa promotes hemostasis by activating the extrinsic pathway of the coagulation cascade. Preliminary studies suggested that treatment with rFVIIa was safe and effective for ICH [18,19]. However, in the multicenter, double-blind Factor Seven for Acute Hemorrhagic Stroke (FAST) trial, rFVIIa failed to improve outcomes in patients with acute ICH [15]. The trial randomly assigned 841 patients with spontaneous ICH to receive either rFVIIa (20 or 80 mcg/kg) or placebo within four hours of symptom onset. Compared with placebo, treatment with rFVIIa produced a significant reduction in hematoma growth but did not result in improvement in death or severe disability at 90 days. Recombinant factor VIIa is associated with a risk of thrombosis from activation of the coagulation system [16]. In the FAST trial, the overall frequency of thromboembolic serious adverse events was similar among treatment groups, but the rate of arterial thromboembolic serious adverse events (myocardial infarction or cerebral infarction) was higher in the group assigned to 80 mcg/kg than those assigned to placebo (8 versus 4 percent) [15]. Similar findings were noted in an analysis of pooled data from three earlier randomized controlled trials of rFVIIa for spontaneous ICH [17]. Additionally, small open- label studies observed that rFVIIa treatment for ICH was associated with increased rates of troponin elevation and myocardial infarction [20] as well as higher-than-expected rates of posthemorrhagic hydrocephalus [21]. (See "Recombinant factor VIIa: Administration and adverse effects", section on 'Adverse events'.) The use of factor VIIa along with a prothrombin complex for patients with warfarin- associated ICH is discussed in detail separately. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Warfarin'.) Tranexamic acid Tranexamic acid inhibits fibrinolysis and the proteolytic activity of plasmin. Clinical trials have failed to show functional outcome or mortality benefit compared with placebo. The Tranexamic acid for hyperacute primary IntraCerebral Hemorrhage (TICH-2) trial randomly assigned over 2300 subjects with acute ICH to https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 4/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate treatment with tranexamic acid or matching placebo within eight hours of symptom onset [22]. At 90 days, there was no difference in functional status or mortality between the two treatment groups, despite early reductions in hematoma growth (at day 2) and death (at day 7). In another trial of patients with ICH who were treated within 4.5 hours of symptom onset, those assigned to tranexamic acid had a similar rate of ICH growth and functional outcomes as those assigned to placebo [23]. Managing hemorrhagic expansion Patients with acute ICH are at risk for hemorrhagic growth from continued or recurrent bleeding, most commonly within the first several hours after onset of ICH [24,25]. ICH growth can cause neurologic deterioration and increases the likelihood of developing elevated intracranial pressure (ICP). Medical and surgical strategies to manage patients with ICH growth and elevated ICP are discussed below. (See 'Intracranial pressure management' below.) Several imaging findings have been associated with the risk of ICH growth in the acute setting. These are discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Predicting hemorrhage expansion'.) BLOOD PRESSURE MANAGEMENT Elevated blood pressure is common in patients with acute ICH. Patients may develop elevated blood pressure due to an increase in intracranial pressure (ICP) and pain from the mass effect of the hemorrhage. Additionally, many patients with acute ICH have high blood pressure due to comorbid baseline hypertension. Uncontrolled elevations in blood pressure and blood pressure variability are risk factors for hemorrhagic expansion and poor outcome [26-28]. We manage elevated blood pressure in acute spontaneous ICH as follows, in agreement with guidelines from the American Heart Association ( table 1) [5]: For patients with acute ICH who present with systolic blood pressure (SBP) between 150 and 220 mmHg, we suggest lowering of SBP to a target of 140 mmHg, ideally within the first one hour of presentation, provided the patient remains clinically stable [5]. This degree of blood pressure reduction appears safe in most patients and may improve functional outcome. For patients with acute ICH who present with SBP >220 mmHg, we suggest rapid lowering of SBP to <220 mmHg. Thereafter, the blood pressure is gradually reduced (over a period of hours) to a target range of 140 to 160 mmHg, provided the patient remains clinically stable. Patients who deteriorate clinically during this period may require reduction of acute https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 5/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate antihypertensive therapy. The optimal blood pressure goal is uncertain, but an SBP of 140 to 160 mmHg is a reasonable target for patients who remain clinically stable [5]. Medication selection should account for the rapidity and extent of blood pressure reduction, method of delivery (bolus versus infusion), individual patient comorbidities, potential adverse effects, and local experience [5]. We monitor all patients for neurologic deterioration during treatment. Reducing SBP below 130 mmHg in the first hours after ICH onset has not been shown clearly beneficial for reducing death or disability and may increase the risk of adverse events, including cerebral hypoperfusion and kidney injury [5]. For most patients with an initial SBP 160 mmHg, we prefer nicardipine for initial treatment because it is fast-acting and can be quickly titrated. Blood pressure is monitored every five minutes and patients are monitored at least hourly to assess for neurologic deterioration. For most patients with an initial SBP <160 mmHg, we start with labetalol for its ease of administration and long duration of effect. However, the choice of antihypertensive agent and the optimal rate of reduction depend upon patient-level factors and local experience; data to guide selection in this setting are lacking. Several intravenous medications may be used to control blood pressure in this setting including nicardipine, labetalol, clevidipine, esmolol, enalaprilat, and fenoldopam ( table 4). Nitroprusside and nitroglycerin are typically avoided because they may increase intracranial pressure. (See "Drugs used for the treatment of hypertensive emergencies".) The relationship between blood pressure and outcome in patients with ICH is complex, and data to specify optimal treatment strategies are lacking. The potential benefits of treating elevated blood pressure in patients with ICH in the acute setting must be balanced with the potential risks. The key competing issues are: Severely elevated blood pressure can worsen ICH by inciting continued or recurrent bleeding and by causing hemorrhage expansion and potentially worse outcomes [29,30]. Conversely, lowering the arterial pressure might mitigate these risks and possibly improve outcomes. Lowering blood pressure rapidly could cause further injury by promoting cerebral and systemic hypoperfusion [31]. Conversely, reducing elevated blood pressure slowly with stepwise reductions while monitoring for clinical deterioration might help prevent these complications by maintaining adequate cerebral and systemic perfusion. Clinical studies to assess these issues have shown that aggressive blood pressure lowering in acute ICH is associated with reduced hematoma growth [32-34]. Additionally, blood pressure https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 6/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate lowering does not appear to impair cerebral blood flow within the perihematomal region [35- 37]. The ischemic-appearing rim of low attenuation surrounding the hemorrhage visible on computed tomography imaging is caused by extravasated plasma and is not associated with markers of ischemia visible on magnetic resonance imaging [37]. Data from clinical trials have not demonstrated consistent safety and outcome benefits from acute blood pressure reduction. In the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial 2 (INTERACT2) trial, 2839 patients with acute ICH were assigned (within six hours of symptom onset) either to intensive blood pressure lowering or traditional management (target SBP <140 mmHg versus SBP <180 mmHg) [38]. The mean baseline SBP was 179 mmHg. There was a trend toward lower rates of death and severe disability at 90 days with intensive blood pressure lowering, although this was not statistically significant (52 versus 55.6 percent). In addition, intensive blood pressure lowering was associated with improved measures of disability according to modified Rankin scale scores. The rates of acute neurologic deterioration and other adverse events were similar in the patient groups. The Antihypertensive Treatment of Acute Cerebral Hemorrhage 2 (ATACH-2) trial found no differences in death or disability rates among 1000 patients with acute ICH assigned in an earlier time window (within 4.5 hours) to a more intensive target SBP of 110 to 139 mmHg versus a standard target SBP of 140 to 179 mmHg (39 versus 38 percent) [31]. Additionally, the rate of acute neurologic deterioration in patients assigned to intensive treatment was similar to those assigned standard treatment. However, the rate of adverse kidney events was higher in the intensive treatment group (9 versus 4 percent). Failure to achieve goal blood pressure was also more frequent in the intensive group (12 versus 1 percent). In a subsequent analysis of patients by actual blood pressure attained, the rates of neurologic deterioration at 24 hours and cardiac- related adverse events were higher among patients who achieved and sustained SBP <140 mmHg [39]. In a post-hoc analysis using individual patient data of the INTERACT2 and ATACH-2 trials, each 10 mmHg reduction in SBP in the first 24 hours was associated with a 10 percent increased odds of better functional recovery, down to a threshold as low as 120 to 130 mmHg [40]. In this analysis, the combined mean baseline blood pressure was 178 mmHg and the mean ICH volume was 11 mL. It is unclear if these improved outcomes would be applicable to patients with more severe elevations in baseline blood pressure, those with more severe ICH, or those treated beyond the acute time intervals applied in the trials. INTRACRANIAL PRESSURE MANAGEMENT https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 7/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Patients with space-occupying lesions such as acute ICH are at risk for progressive neurologic impairment from brain compression due to increased intracranial pressure (ICP). Acute ICH may lead to elevated ICP due to several mechanisms. These include: Mass effect of the initial hematoma Expansion or rebleeding of the ICH Cerebral edema surrounding the hemorrhage Hydrocephalus from ventricular outflow obstruction The risk of developing increased ICP is highest in the first several days after ICH but may vary depending on the size and location of the hemorrhage and patient-level factors. (See 'Assessing elevated ICP' below.) Basic measures outlined below should be instituted initially for all patients with ICH; indications for ICP monitoring and treatment interventions (eg, cerebrospinal fluid drainage and osmotic therapy) are discussed in the sections that follow ( algorithm 1). Select patients with ICH may benefit from surgical interventions ( table 1). Identifying patients with an indication for emergent surgery Some patients with ICH may present with clinical evidence of, or imaging features concerning for, rapidly progressive neurological impairment due to elevated ICP. For these selected patients, emergent surgical consultation is indicated to assess whether surgery may be lifesaving. Such ICH features may include: Cerebellar hemorrhage that is either greater than 3 cm in diameter or associated with acute neurological deterioration, brainstem compression, or hydrocephalus due to ventricular obstruction. (See 'Cerebellar hemorrhage' below.) Intraventricular hemorrhage with ventricular enlargement associated with acute neurologic deterioration. (See 'Cerebrospinal fluid drainage for obstructive hydrocephalus' below.) Supratentorial (hemispheric) hemorrhage associated with acute neurological deterioration and life-threatening brain compression or hydrocephalus; however, not all patients will benefit from surgery. Treatment decisions for these patients should be individualized based on assessments of prognosis with and without surgical therapy. (See 'Supratentorial hemorrhage' below.) Preventive measures for all other patients For patients who do not require immediate surgical evaluation, preventive measures should be enacted to mitigate the morbidity associated https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 8/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate with elevated ICP. The following measures should be initiated unless a specific contraindication exists [5]: Elevation of the head of the bed to 30 degrees Mild sedation for agitated patients, typically to a goal Richmond Agitation-Sedation Scale (RASS) score of 0 to -2 ( table 5) (see "Sedative-analgesic medications in critically ill adults: Selection, initiation, maintenance, and withdrawal") Antipyretic medications if core temperature is >38 degrees Celsius Head positioning and device placement at the neck to facilitate cerebral venous outflow; these include avoiding neck rotation, internal jugular central line placement, and tight device securement (eg, device ties, endotracheal tube holder, or intravenous line dressings) Isotonic solutions such as normal saline for maintenance and replacement fluids; hypotonic fluids are contraindicated Maintain serum sodium >135 mEq/L Assessing elevated ICP Patients with acute ICH should be monitored until improvement in or stabilization of the neurologic exam and imaging findings (eg, hemorrhage and associated edema). The risk of neurologic deterioration from elevated ICP is typically highest in the first several days after ICH onset but may vary depending upon the presence of associated risks including the size and location of the ICH, ICH extension or rebleeding, or comorbid features (eg, fever, hyperglycemia, hypervolemia, and/or hypoosmolar fluid status). ICP is typically assessed and monitored by serial clinical examinations. We repeat urgent imaging with computed tomography (CT) of the head for deteriorating patients with suspected ICP elevation to help guide treatment and evaluate for an indication for surgery. Serial imaging is also sometimes used to monitor changes that may indicate progressive elevation of ICP; however, other modalities are preferred because progressive elevation of ICP may occur in the setting of a stable head CT. Invasive ICP monitoring is used for some deteriorating patients when the neurologic examination may be unreliable due to baseline deficits or other treatments (eg, sedative medications). (See 'Invasive ICP monitoring when clinical exam is unreliable' below.) For patients with rapid, life-threatening clinical deterioration or when imaging may be delayed, we give an initial dose of osmotic therapy prior to imaging. (See 'Identifying patients with an indication for emergent surgery' above and 'Osmotic therapy' below.) https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 9/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Clinical exam findings Serial examinations to identify progressive neurologic impairment are generally performed hourly for the initial few days or otherwise when the risk of deterioration is highest. Serial examinations may be less useful for comatose patients and others with severe baseline impairment (eg, hemiplegia). For these patients, we use invasive monitors and imaging to evaluate for elevated ICP. (See 'Invasive ICP monitoring when clinical exam is unreliable' below and 'Serial imaging for other patients' below.) Examination findings in a patient with acute ICH concerning for a progressive elevation in ICP include new or worsening: Pupillary changes, including impaired reactivity to light Abducens nerve (cranial nerve VI) palsy; alert patients may report horizontal diplopia Progressive drowsiness Cushing triad consisting of bradycardia, respiratory depression, and hypertension Focal symptoms related to herniation syndromes ( table 6) The clinical manifestations of elevated intracranial pressure are also discussed separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Clinical manifestations'.) Invasive ICP monitoring when clinical exam is unreliable We use invasive monitoring for select deteriorating patients unable to participate in serial clinical examinations due to severe baseline deficits or sedation (eg, those with Glasgow Coma Scale score <8 ( table 7)), those with clinical evidence of transtentorial herniation, and those with midline lesions or otherwise at risk for developing obstructive hydrocephalus [5]. Measuring ICP directly allows directed treatment of ICP and blood pressure with a goal of maintaining a cerebral perfusion pressure (CPP) of 50 to 70 mmHg. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Physiology'.) However, there are no high-quality data showing that ICP monitoring or management of elevated ICP improves outcomes in patients with ICH [41,42]. In addition, the use of invasive monitors is associated with a small risk of infection and intracranial bleeding. Noninvasive ICP monitoring techniques such as transcranial doppler, optic nerve sheath diameter analysis, and ocular ultrasound have been used as alternatives when invasive options are contraindicated or unavailable. However, these techniques have not been shown effective in large trials [43-45]. ICP monitoring is discussed in detail separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'ICP monitoring'.) https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 10/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Serial imaging for other patients We typically repeat imaging for deteriorating patients with suspected ICP elevation to help guide treatment and evaluate for an indication for surgery. (See 'Identifying patients with an indication for emergent surgery' above.) Serial imaging may also be used to monitor some patients for changes in the first days after acute ICH related to a progressive elevation of ICP. As examples, repeat surveillance imaging may be performed for patients who are deeply sedated to treat coexisting status epilepticus, patients receiving neuromuscular blocking medications, and those with a poor baseline neurologic exam due to a brainstem hemorrhage. However, serial neurologic examination or direct ICP monitoring are preferred strategies when feasible because progressive elevation of ICP may occur in the setting of a stable head CT. Such imaging findings that may be suggestive of a progressive elevation in ICP and associated with neurologic deterioration include: Increasing shift of brain tissue beyond midline Ventricular or brainstem compression Obstructive hydrocephalus Herniation (transtentorial, parafalcine, uncal, central, tonsillar) of brain structures ( figure 1) For most patients, we prefer head CT because it is typically more readily available and a faster imaging modality compared with brain magnetic resonance imaging (MRI). However, MRI may be performed as an alternative modality and may be preferred in circumstances where other causes of neurological deterioration may be not be adequately assessed by head CT. Such circumstances include assessing acute ischemic stroke and measuring interval changes in cerebral edema volume. Surgical approaches vary by specific imaging findings including the location of the ICH. (See 'Surgical approaches for selected patients' below.) Treatment measures for patients who have severe or progressive ICP elevation For patients who have severe signs or symptoms of elevated ICP or for those with milder symptoms that progress despite initial measures, we use osmotic therapy. We also repeat imaging to assess for structural sources that may be corrected with invasive and surgical options. For patients with rapid, life-threatening clinical deterioration or when imaging may be delayed, we give an initial dose of osmotic therapy prior to imaging. (See 'Assessing elevated ICP' above and 'Surgical approaches for selected patients' below.) https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 11/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate Glucocorticoids should not be used to lower the ICP in most patients with ICH due to lack of benefit and risk of infection and hyperglycemia [46]. Osmotic therapy Acute ICP elevation or life-threatening mass effect can be treated with hypertonic saline or mannitol [47]. Osmotic therapy is effective for lowering ICP but has not been shown to improve outcomes in patients with acute ICH [48]. There is no compelling evidence to support the superiority of either agent, although some studies in patients with traumatic brain injury suggest that hypertonic saline may be more effective [49-52]. Either agent may be used depending upon local protocol and physician experience. Hypertonic saline is an effective hyperosmolar agent for the control of elevated ICP [52]. For patients with evidence of life-threatening or progressive deterioration (including patients with herniation syndromes and those awaiting emergent surgery), we use high- concentration (23.4 percent) saline as an intermittent bolus via a central intravenous line, typically 15 to 30 mL every six hours. For other patients with milder signs or symptoms, we use a continuous infusion of 3 percent saline (via peripheral or central intravenous line) titrated to a sodium goal of approximately 145 to 155 mEq/L. (See "Management of acute moderate and severe traumatic brain injury", section on 'Osmotic therapy'.) Serial measurement of electrolytes is performed at six-hour intervals to monitor and prevent excessive elevation of sodium and chloride levels and to detect and correct other derangements such as hypokalemia. Other potential adverse effects include circulatory overload, pulmonary edema, and a non-anion gap metabolic acidosis. Intravenous mannitol has also been shown to effectively lower ICP [53]. For initial therapy and for patients with evidence of life-threatening or progressive deterioration (including patients with herniation syndromes and those awaiting emergent surgery), we use mannitol 1 g/kg as a bolus via a central intravenous line. For other patients, we use mannitol at a dose of 0.25 to 0.5 g/kg every six hours. The goal of therapy is to force water to exit the brain while maintaining an adequate plasma volume [54]. The plasma osmolal gap should not be allowed to exceed 55 mosmol/kg; higher doses can cause reversible acute kidney injury. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Osmotic therapy and diuresis' and "Complications of mannitol therapy".) The osmolal gap peaks rapidly after mannitol infusion and typically normalizes from diuresis within hours. Therefore, the serum osmolality and electrolytes to calculate the osmolal gap should be drawn prior to subsequent doses to verify renal clearance of the previous dose as well as to monitor, prevent, and correct metabolic derangements and https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 12/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate acute kidney injury. Other potential adverse effects of mannitol therapy include hypotension and intravascular volume depletion [55]. (See "Complications of mannitol therapy" and "Serum osmolal gap".) Surgical approaches for selected patients The role of surgery in patients with acute ICH varies with the site of the bleed. Cerebrospinal fluid drainage for obstructive hydrocephalus Ventricular drainage of cerebrospinal fluid (CSF) with an external ventricular drain can help reduce elevated ICP for selected patients with hydrocephalus, particularly when associated with a decreased level of consciousness [5]. Obstructive hydrocephalus may occur when hemorrhage or mass effect obstructs CSF ventricular outflow. This may commonly be seen with ICH in the following locations: Thalamic hemorrhage (with third ventricle compression) Cerebellar hemorrhage (with fourth ventricle compression) (see 'Cerebellar hemorrhage' below) ICH with intraventricular extension (see "Intraventricular hemorrhage", section on 'External ventricular drain') For patients with neurologic deterioration who develop ventricular enlargement due to a large cerebellar hemorrhage, craniectomy with hematoma evacuation along with CSF drainage is the preferred intervention to treat both hydrocephalus and brainstem compression. In this setting, external drainage alone, without posterior fossa decompression, may create the theoretical risk of upward herniation of the cerebellar mass. (See 'Cerebellar hemorrhage' below.) For other ICH patients, a ventriculostomy catheter may be used with an external ventricular drainage to remove CSF and intraventricular blood to lower and monitor ICP. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Removal of CSF'.) The management of patients with intraventricular hemorrhage is discussed in greater detail separately. (See "Intraventricular hemorrhage", section on 'Management'.) Surgical decompression Cerebellar hemorrhage The indications for evacuation of a cerebellar hematoma depend on the ICH size and location, the time since onset, and the clinical status of the patient [5,56,57]. As examples, patients presenting acutely with a cerebellar hemorrhage greater than 3 3 cm in diameter (volume of at least 14 cm ) and brainstem compression will typically require https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 13/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate urgent surgical decompression of the cerebellum with craniectomy and hematoma evacuation. Some patients with smaller acute cerebellar hematomas may also warrant surgical decompression if they are deteriorating neurologically or have brainstem compression and/or hydrocephalus due to ventricular obstruction. Other patients with small, subacute cerebellar hematomas that do not exert mass effect on the brainstem may be managed medically with close monitoring. These recommendations are in broad agreement with published guidelines. Patients with cerebellar hemorrhage are at risk for rapid deterioration and fatal herniation due to the bony and tentorial confines of the posterior fossa. For patients selected for surgical decompression of a cerebellar hematoma, we suggest craniectomy and hematoma evacuation rather than ventriculostomy without posterior fossa decompression. External drainage alone may create the theoretical risk of upward herniation of the cerebellar mass. Observational evidence suggests that surgical evacuation of hematoma is associated with decreased mortality in patients with cerebellar hemorrhage. In a 2019 meta-analysis with individual patient data from four observational studies including 304 patients with cerebellar hemorrhage, surgical hematoma evacuation was associated with an increased probability of survival at three months compared with conservative treatment (78 versus 61 percent; absolute risk difference [ARD] 18.5 percent, 95% CI 13.8-23.2) [58]. This association was sustained at 12 months. The overall likelihood of a favorable functional outcome was similar for patients who had a hematoma evacuation or conservative treatment (31 versus 36 percent; ARD -3.7 percent, 3 95% CI -8.7 to 1.2). However, for patients with a hematoma volume of 12 cm , the likelihood of a favorable outcome was lower with surgical evacuation (31 versus 62 percent; ARD 35 percent). 3 By contrast, in the subgroup of patients with a hematoma volume of 15 cm , a favorable outcome was more likely with hematoma evacuation than with conservative treatment (75 versus 45 percent). Limitations to this meta-analysis include retrospective design, lack of randomization, small sample size for subgroup analyses, and a high number of patients on oral anticoagulant therapy at baseline, which impacts the generalizability of the findings. Supratentorial hemorrhage Surgical hematoma evacuation for supratentorial ICH is controversial because the potential benefits of hematoma evacuation may be offset by surgical morbidity in many cases. The subset of patients who may benefit from surgical treatment have not been conclusively defined [5]. We reserve surgical therapy for patients with life-threatening mass effect from supratentorial ICH, individualizing treatment decisions based on assessments of prognosis with and without surgical therapy. Limited data suggest that supratentorial hematoma evacuation might reduce mortality for patients who are comatose, have a large hematoma with significant midline shift, or have elevated ICP refractory to medical management [5]. Supratentorial decompression with https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-acute-treatment-and-prognosis/print 14/79 7/5/23, 12:24 PM Spontaneous intracerebral hemorrhage: Acute treatment and prognosis - UpToDate hematoma evacuation and/or decompressive hemicraniectomy may reduce mortality but not improve functional outcomes. It should only be considered as a life-saving procedure to treat refractory increases in ICP; even in these instances, decisions should be addressed on an individual basis: Surgery should not be considered for patients who are either fully alert or deeply comatose. Patients with intermediate levels of arousal (obtundation-stupor) are more