Kaiser Permanente Clinical Practice Guidelines

Brain Imaging for TIA and Stroke

Acute Evaluation and Management of Intracerebral Hemorrhage


Decisions regarding the acute management of intracerebral hemorrhage (ICH) are largely dependent upon the etiology, location, and size of the hemorrhage, as well as the clinical status of the patient. The purposes of this guidelines are to:

  • Provide prognostic information based on clinical status, ICH location, and ICH size;
  • Describe the likely etiologies of ICH;
  • Define the typical locations of hypertensive ICH;
  • Recommend the best medical treatments of ICH;
  • Identify the role of surgical treatment of ICH.

Hypertensive ICH:

The 6 main locations of hypertensive ICH are: putamen, subcortical cerebral lobe, thalamus, cerebellum, brainstem, and caudate nucleus. Each location may differ in clinical presentation, prognosis, and consideration for surgical treatment.

Putaminal Hemorrhage

The clinical presentation of putaminal hemorrhage may vary from relatively minor puremotor hemiparesis to profound weakness, sensory loss, eye deviation, hemianopsia, aphasia,and depressed level of consciousness. In this type of hematoma, intraventricularextension portends a poor prognosis, because the hematoma must be quite large to trackthrough the internal capsule and reach the ventricle.

Lobar Hemorrhage

Although hypertension is a common cause of cerebral lobar hemorrhage, avariety of other etiologies must be considered. This is the most common location forICH due to vascular malformation, tumor, and amyloid angiopathy. Clinical symptomsof lobar ICH depend largely on the location of the hemorrhage; for example, dominant lobetemporal hematomas may present with aphasia, and occipital hematomas may present withhomonymous hemianopsia. Further evaluation, such as angiography, needs to beconsidered in the context of the clinical presentation and CT findings. A significant rolefor surgery may exist in the treatment of certain lobar hematomas.

Thalamic Hemorrhage

Thalamic hemorrhage often presents with contralateral sensory loss. Due to the proximityof the internal capsule, motor defects are also quite common. Pupil and extraocularmovement defects may also be seen. Intraventricular hemorrhage or obstructivehydrocephalus may occur.

Cerebellar Hemorrhage

Cerebellar hemorrhage typically presents with abrupt onset of vertigo, headache, vomiting,and inability to walk without hemiparesis. Cranial nerve palsies may be associated. This type of hemorrhage may act as a posterior fossa mass, producing hydrocephalus and/orbrainstem compression, and is the most amenable to acute surgical intervention.

Brainstem Hemorrhage

Presentation of brainstem hemorrhage may be coma, posturing, loss of brainstem reflexes,and oculomotor abnormalities. It most commonly involves the pons and generally has adismal prognosis.

Caudate Hemorrhage

Hemorrhage into the caudate nucleus is rare. Because extension into the adjacent lateralventricle usually occurs, the most common presentation is that of a primaryintraventricular hemorrhage. Prognosis is generally good.

Non-Hypertensive ICH:

Not all ICH is due to hypertension. A variety of other etiologies need to be considered, even in cases with coexisting hypertension. The following are the most common causes of non-hypertensive ICH.

Vascular Malformation

Vascular malformation is a relatively common cause of ICH in non-hypertensive patients,especially in younger patients. Hemorrhage from a vascular malformation is the most commoncause of ICH in patients less than age 45. The two clinically important types ofvascular malformation related to ICH are arterioveneous malformations (AVM) and cavernoushemangiomas. Lobar ICH is the most common hemorrhage associated with both of thesevascular malformations.

AVM usually presents with ICH, which occasionally may haveassociated subarachnoid hemorrhage. The risk of repeat hemorrhage is substantial (6% inthe first year, 2% per year thereafter) (16). Neurosurgical evaluation is usuallyindicated. In cases believed to be surgically inaccessible, radiosurgery may be apotential treatment.

Cavernous hemangiomas comprise most of the lesion previouslydescribed as occult cerebrovascular malformations (OCVM). They may occur in multiplelocations and may be familial (40). These lesions carry a substantial risk of repeathemorrhage (4-5%/yr), and may be amenable to surgical treatment.


Although usually a cause of subarachnoid hemorrhage, a ruptured saccular aneurysm may insome cases be the cause of ICH or intraventricular hemorrhage. The temporal and frontallobes are the most common locations for ICH resulting from a ruptured saccular aneurysm.

Intracranial Tumor

Bleeding into a tumor is the cause of hemorrhage in 6-10% of patients presenting with ICH.This is most commonly seen in malignant glioma, metastatic melanoma, metastatic renal cellcarcinoma, metastatic choriocarcinoma, or metastatic bronchogenic carcinoma. Clues to thiscause of ICH include papilledema at presentation, multiple lesions, or disproportionateassociated edema(31).

Amyloid Angiopathy

Amyloid angiopathy is a relatively common cause of ICH in elderly patients (52). Lobar ICHis the most common hemorrhage associated with amyloid angiopathy. Hemorrhage from amyloidangiopathy tends to be recurrent; a prior history of ICH in an elderly person,particularly a prior lobar ICH, raises a strong suspicion of amyloid angiopathy. There isan association of amyloid angiopathy with Alzheimer’s disease.


ICH is patients receiving anticoagulation tends to carry a poor prognosis (50-60%mortality in one study) due to the often large size of the resultant hemorrhage. Hypertension, intensity of anticoagulation, and age are risk factors for development ofICH in anticoagulated patients (10,24,59). Some series have reported a relatively high percentage of anti-coagulant-related hemorrhage to be located in the cerebellum. Anticoagulation with heparin is reversible with protamine sulfate, and anticoagulationwith warfarin may be reversed by administration of fresh frozen plasma and vitamin K (10).

Thrombolytics (e.g. t-PA, streptokinase)

ICH associated with thrombolytics tends to be lobar in location, and has a high mortalityrate (44-66%) (15,26). The risk is relatively low in myocardial infarction treatment(0.4-1.3%), but considerably higher in acute stroke patients (48). Symptomatic ICH within36 hours of treatment occurred in 6.4% of t-PA treated patients in the NINDS t-PA study(47). Hypertension may increase the risk of hemorrhage with thrombolytic therapy (30).

ICH associated with thrombolytics usually occurs early in he courseof thrombolytic therapy, either during the infusion or with a few hours after the infusionis completed. After the infusion is stopped, the duration of thrombolytic activityremaining is four minutes for t-PA, and 15-20 minutes for streptokinase and urokinase.Replacement of fibrinogen with cryoprecipitate may partially reverse the thrombolyticeffect (10).


The sympathomimetics most often associated with ICH are cocaine and amphetamines, althoughphenylpropanolamine (found in decongestants and appetite suppressants) has alsooccasionally been implicated (9,19,25,228,29). Direct vessel injury or acute hypertensionmay be the mechanisms. The location tends to be lobar or involve the thalamus or putamen.


Vasculitis usually is associated with ischemic infarction, but hemorrhage may also occurin both systemic and isolated central nervous system vasculitis (5).

Cerebral Venous Thrombosis

Cerebral venous thrombosis may also be present as ICH due to the associated increasedvenous pressure. It most often occurs during pregnancy and the post-partum period, withthe use of birth control pills, and with underlying systemic disease such as cancer andsystemic inflammatory conditions.

Review of Medical Treatment:

Intubation/Hyperventilation: Intubation provides airway protection, allows correction of hypoxemia, and enables thehyperventilation. Hyperventilation produces an immediate and temporary reduction inintracranial pressure (ICP), but has not been proven to affect outcome.

Corticosteriods: A randomized prospective trial has shown that corticosteroids increase complication rateand do not improve outcome in ICH (37).

Hypersmolar Therapy

Mannitol is the agent usually used for hyperosmolar therapy, and has often been utilizedto treat increased intracranial pressure associated with ICH. However, no randomizedcontrolled trials have been performed to evaluate its utility in this setting. Althoughmannitol reduces intracranial pressure, this effect is temporary, and upon withdrawal ofmannitol, rebound intracranial hypertension may occur. Additionally, by shrinkingsurrounding normal brain, the possibility of promoting extension of the ICH exists.Mannitol is best used as a temporizing measure when definitive surgical treatment isanticipated.

ICP Monitoring

The role of ICP monitoring and its effect on outcome in ICH has not been defined.

Antihypertensive Therapy

Elevated blood pressure is often the causative factor for ICH; however, whether acutereduction of blood pressure is helpful or harmful is a difficult question to answer (2,38). A recent retrospective study found that both an elevated initial blood pressure onadmission (mean arterial pressure > 145 torr), and blood pressure poorly controlledafter admission (mean arterial pressure > 125 torr) are associated with poor outcome. However, it is unclear whether uncontrolled as opposed to uncontrollable hypertension wasrelated to the poor outcome.

Review of Surgical Treatment:

Most patients with ICH do not require surgical management. Factorswhich influence the decision regarding surgical treatment include the clinical status ofthe patient, and the location and size of the hemorrhage. Surgical treatment is usuallyconsidered in the setting of cerebellar hemorrhage, and may also be considered in somecases of lobar hemorrhage. In addition, neurosurgical consultation should be considered inany patient with a potential underlying vascular lesion such as aneurysm, or for thetreatment of hydrocephalus.

Cerebellar Hemorrhage

Surgery needs to be considered in all cases of cerebellar hemorrhage. Because of thelimited space of infratentorial compartment, sudden deterioration can occur withcerebellar ICH. However, if the hematoma is small (1-2 cm), prognosis is generally goodand surgery is usually not necessary. Hematomas 3 cm or larger, particularly with fourthventricular compression, hydrocephalus, brainstem signs, or quadrigeminal cisterneffacement should be considered for immediate surgical treatment in all cases, unless thepatient is in deep stupor or coma (11,32,45). If the patient is comatose, mortality isgreater than 80% even with surgical treatment, and surgery is not likely to be beneficial(36).

Lobar Hemorrhage

Lobar hematomas are generally the only supratentorial ICH where acute surgical treatmentis considered potentially helpful. Even so, well controlled prospective studies arelacking. Patients with intermediate-sized hemorrhages (25-50cc, corresponding to a maximumdiameter of 3.6 – 4.6 cm for a spherical hematoma), particularly with GCS scores of 6-8,have improved outcome with surgical treatment in some studies. this observation may beparticularly true for temporal lobe hematomas. Patients with smaller hematomas improvewithout surgical treatment; patient with larger hematomas do poorly regardless oftreatment (23, 53).

Other Locations

Although there have been occasional reports of surgical benefit in highly selected series,putaminal hemorrhages are generally not benefited from surgical treatment (4,20,25,35).



  1. Level of consciousness and neurological status should be routinely assessed and documented for all patients with ICH. (Expert Opinion: Strong Consensus)
  1. CT scan should be obtained and both location and size (diameter measured in cm) of the hemorrhage should be document. Presence of mass effect and/or shift should also be noted. (Expert Opinion: Strong Consensus)

Medical Treatment

  1. Any patient who is obtunded is a candidate for intubation for airway protection. The prognosis and wishes of the patient in such circumstances should be considered in making the decision regarding intubation. (Expert Opinion: Strong Consensus)
  1. Corticosteroids are not recommended in the treatment of ICH. (Research Evidence: Grade B)
  1. Mannitol is recommended only as a temporary measure to reduce cerebral edema in patients for whom surgery is anticipated. The recommended dosage is 0.5-1.0 gm/kg. The value of the routine use of mannitol outside this setting is uncertain. (Expert Opinion: Strong Consensus)
  1. Routine treatment of elevated blood pressure is not recommended. (Expert Opinion: Strong Consensus)
  1. If ICH occurs in the setting of thrombolytic, anticoagulant, or antiplatelet therapy, immediate cessation of the active agent is indicated. Reversal of thrombolytic or anticoagulant activity may also be considered. (Expert Opinion: Strong Consensus)

Surgical Treatment

    1. Neurosurgical consultation should be considered:
    • In cases of cerebellar ICH, particularly in patients with intermediate of larger sized hematomas with evidence of mass effect and brainstem signs. By the time coma occurs, it is usually too late for surgical treatment to be beneficial. (Expert Opinion: Strong Consensus);
    • In cases of intermediate-sized cerebral lobar hematomas in patients with moderately impaired neurologic status. (Expert Opinion: Strong Consensus);
    • In patients with a potential surgical vascular lesion, in which case angiography will need to be performed. (Expert Opinion: Strong Consensus);
    • In some cases of ICH with intraventricular hemorrhage or hydrocephalus, where ventricular drainage may be indicated. (Expert Opinion: Strong Consensus).

Initial Evaluation of Suspected Subarachnoid Hemorrhage


Subarachnoid hemorrhage (SAH) is an acute life-threatening medical emergency associated with high mortality and morbidity. Outcome can be significantly improved with rapid diagnosis and triage to neurosurgical treatment. The clinical management goals of these guidelines are to:

  • Identify patients with clinical suspicion of subarachnoid hemorrhage;
  • Proceed promptly with the appropriate evaluation of these patients;
  • Arrange for speedy triage and referral of patients with SAH to a neurosurgical center.

Initial Presentation:

The sudden onset of the “worst-ever” headache with transient impairment ofconsciousness followed by nausea, vomiting, nuchal rigidity, and focal neurological signsis the classic presentation of SAH. The headache can vary in character, being eithergradual or step-wise in evolution and localized or holocranial in location. Disturbancesin consciousness as a result of the hemorrhage, secondary seizures, or hydrocephalus maybe manifested by confusion and transient of prolonged coma. Autonomic symptoms such aslow-grade fever, diaphoresis, shivering, hypertension, and cardiac arrhythmia are alsocommon. Sighs and symptoms of meningeal irritation, as manifested by neck of back pain andstiffness, are occasionally more prominent that the headache itself.

Neuroophthalmo logic manifestations such as photophobia, blurred vision, eye pain, and limitations ofextraocular movement may be present. Focal neurological symptoms can result from the mass effect of the aneurysm or hematomas and cerebral ischemia. Since the overall presentation is often not classic, a delay in diagnosis and referral for neurosurgical care often occurs. Even in large medical centers, misdiagnosis has occurred in up to 50% of patients. (8-11)

A substantial proportion of patients with ruptured cerebral aneurysms have warning symptoms. The interval from the initial warning to a major aneurysm rupture is typically from six to 20 days. Although patients with a warning sign, e.g. a “sentinelleak,” appear less ill than patients with a larger sub arachnoid hemorrhage, their prognosis with treatment is better, making the need fro correct diagnosis more urgent. (15)

Thunderclap headache is a paroxysmal, excruciating headache which clinically resembles SAH. However, no evidence of subarachnoid hemorrhage is found on CT scan or lumbar puncture. The prognosis for these patients is extremely good and cerebral angiography is not indicated. (16)

Diagnostic Tests:

The sudden onset of the “worst-ever” headache with transient impairment of consciousness followed by nausea, vomiting, nuchal rigidity, and focal neurological signs is the classic presentation of SAH.

A CT scan of the brain without contrast is the diagnostic procedure of choice for suspected SAH and should be obtained urgently.

When the CT scan is negative, lumbar puncture (LP) must be done in cases of suspected SAH.


  1. A CT scan should be done urgently in all patients with suspected SAH. The scan should be interpreted immediately by an experienced physician. (Expert Opinion: Strong Consensus)
  1. When the CT scan is negative, a lumbar puncture must be done by an experienced physician. (Expert Opinion: Strong Consensus)
  1. The results of CT and/or LP must be obtained and interpreted as soon as possible,and a clinical diagnosis determined. If the diagnosis of SAH is made, the patient should be referred immediately to the regional neurosurgical center. (Expert Opinion: Strong Consensus)

Tissue Plasminogen Activator for Acute Ischemic Stroke


Tissue plasminogen activator (t-PA) may play a role in minimizing damage from acute ischemic stroke and preserving functional status in selected patients. The purposes of this guideline are to:

  • Provide a framework for the treatment of ischemic stroke with t-PA in appropriate patients;
  • Provide appropriate rigorous exclusion criteria to minimize risk associated with t-PA use.


The NINDS study has shown that t-PA to be effective in the treatmentof acute stroke for a select group of patients, if initiated within three hours of initialsymptom onset. The FDA has approved t-PA for this indication. The benefit of treatmentwith t-PA has been demonstrated to outweigh the attendant risk only in patients who meetrigorous inclusion and exclusion criteria. Patients not qualifying by the followingcriteria should not be treated with t-PA. (Research Evidence: Grade A)

Whenever possible, the risks versus potential benefit of the use of t-PA should be discussed with the patient and family before treatment is initiated. Documentation of this discussion is recommended.

Inclusion Criteria for t-PA in Acute Stroke:

All of the following inclusion criteria should be met; treatment should be initiated within three hours of the initial onset of stroke symptoms.

  1. Diagnosis is acute ischemic stroke.
  1. There is a definite time of initial symptom onset.
  1. Patient has a significant acute focal neurologic deficit.
  1. Neurologist has been consulted (at least by telephone) and concurs with t-PA use. Neurology will participate in ongoing inpatient management.
  1. CT scan has been obtained and interpreted by an experienced physician.

Exclusion Criteria for t-PA in Acute Stroke:

Patients with any of the following conditions should not be treated with t-PA.

  1. Time of onset of stroke symptoms is unknown or unclear (includes patients waking from sleep with symptoms), or more than three hours has elapsed since initial symptom onset.
  1. Sustained blood pressure greater than 185/110 at time t-PA treatment is to be initiated. Treatment of blood pressure to attain this level is not recommended without prior discussion with neurology.
  1. CT scan shows any evidence of intracranial hemorrhage.
  1. Significant spontaneous improvement of neurologic deficits prior to initiation of t-PA administration (includes TIAs).
  1. Minor neurologic deficit, such as isolate sensory symptoms, isolated limb ataxia, or isolated mild limb weakness as the only clinical finding.
  1. Suspected subarachnoid hemorrhage.
    1. Common disorders mimicking stroke, such as:
    • Seizure at the onset of stroke.
    • Glucose concentrations below 50 mg/deciliter or above 400 mg/deciliter.
    1. Any other contraindication to t-PA including:
    • Active internal bleeding.
    • History of intracranial hemorrhage.
    • Prior stroke within previous three months.
    • Recent myocardial infarction.
    • Serious head trauma within previous three months.
    • GI or GU hemorrhage within previous 21 days.
    • Major surgery within previous 14 days.
    • Arterial puncture at a noncompressible site within previous seven days.
    • Ongoing anticoagulant therapy at the time of stroke onset. (Antiplatelet therapy is NOT an exclusion criterion.)
    • Heparin within 48 hours preceding onset of stroke, if associated with an elevated partial-thromboplastin time (PTT).
    • Prothrombin time (PT) > 15 seconds. (Treatment need not be delayed for the results of PT if patient not recently on oral anticoagulants or suspected of having a coagulopathy.)
    • Platelet count below 100,000/cubic millimeter.
  1. Any condition or circumstance in which the treating physician assesses that t-PA treatment would pose a significant hazard, e.g., end-stage organ failure, endocardidtis, other serious underlying medical condition, or intracranial lesion predisposing to intracerebral hemorrhage such as aneurysm, vascular malformation, or neoplasm.

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