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Hemorrhagic Stroke. Lourdes James MS ACNP-BC CCRN The Johns Hopkins Hospital AACN Progressive Care Pathways Conference September 2013. Learning Outcomes. Identify the risk factors of hemorrhagic stroke Describe the etiology of hemorrhagic stroke

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Hemorrhagic stroke

Hemorrhagic Stroke

Lourdes James MS ACNP-BC CCRN

The Johns Hopkins Hospital

AACN Progressive Care Pathways Conference

September 2013

Learning outcomes
Learning Outcomes

  • Identify the risk factors of hemorrhagic stroke

  • Describe the etiology of hemorrhagic stroke

  • Relate the pathophysiological processes of hemorrhagic stroke to progressive care patient pathways and nursing care

Stroke definitions
Stroke Definitions

  • Stroke

    • Any damage to brain or CNS structures caused by abnormalities of the blood supply

    • Acute-onset of symptoms

  • Cerebrovascular Accident (CVA)

    • More general term

    • Does not define time (acute/chronic) in relation to brain injury

Stroke classification
Stroke Classification

  • Ischemic

    • 87% of all strokes

  • Hemorrhagic

    • Intracerebral Hemorrhage (ICH) – 10 to 15% of all strokes

    • Subarachnoid Hemorrhage (SAH) – 3%

    • Intraventricular Hemorrhage (IVH)

      • Rarely isolated

      • Typically extension of ICH

        • Occurs in 45% of patients with spontaneous ICH

Intracerebral hemorrhage
Intracerebral Hemorrhage

Ich definition
ICH: Definition

  • Non-traumatic, abrupt onset of severe headache, altered level of consciousness, or focal neurological deficit associated with a focal collection of blood within the brain parenchyma which is not due to trauma or hemorrhagic conversion of a cerebral infarction

Intraventricular Hemorrhage

Ich epidemiology
ICH: Epidemiology

  • Incidence rates in Western Hemisphere

    • 10 – 30 cases/100,000

  • Incidence rates are higher in Eastern Asia

  • Incidence greater in men than women

Ich location
ICH: Location

  • Location varies in populations

  • Deep cerebral hemorrhage

    • Most common in US, Europe and Australia

  • Lobar hemorrhages

    • Second to deep cerebral hemorrhage

    • ≅15% of ICHs

  • Cerebellar hemorrhages

    • ≅10% of ICHs

  • Brainstem hemorrhages

    • ≅5 – 10% of ICHs

A: Lobar: originating from penetrating cortical branches of the anterior, middle, or posterior cerebral arteries

B: Basal ganglia: originating from ascending lenticulostriate branches of the middle cerebral artery

C: Thalamus: originating from ascending thalmogeniculate branches of the posterior cerebral artery

D: Pons: originating from paramedian branches of the basilar artery

E: Cerebellum: originating from penetrating branches of the posterior inferior, anterior inferior, or superior cerebellar arteries

Ich risk factors
ICH: Risk factors

  • Hypertension

  • Age

  • Race

  • Cerebral Amyloid Angiopathy

  • Aneurysms/Vascular Malformations

  • Apolipoprotein E and CAA

  • Anticoagulants/Thrombolytics

  • Antiplatelets

  • Cerebral Microbleeds

  • Prior Cerebral Infarction

  • Hypocholesterolemia

  • Heavy Alcohol Use

  • Tobacco Use

  • Diabetes

  • Heritability

Ich etiology
ICH: Etiology

  • Hypertension

  • IVDA/Cocaine Use

  • Vascular malformations

    • AVM

    • Aneurysm

    • Cavernous angioma

  • Amyloid angiopathy

  • Coagulopathies

  • Neoplasm

  • Trauma

Ich pathophysiology
ICH: Pathophysiology

  • Damage to small penetrating arteries and arterioles (HTN)

  • Rupture of small penetrating arteries

  • Local pressure effect on surrounding capillaries and arterioles

  • Accumulation of hematoma

Ich clinical presentation
ICH: Clinical Presentation

  • Severe headache

  • Focal neurological deficits

  • Coma or decreased LOC

  • SBP > 200 mmHg

  • Vomiting

  • Given that symptoms are non-specific,

  • neuroimaging is a necessity

Ich neuroimaging
ICH: Neuroimaging

  • CT or MRI to distinguish between ischemic or hemorrhagic stroke

  • Hematoma expansion?

    • CTA or contrast-enhanced CT

  • Underlying structural lesions?

    • CTA/CTV, contrast-enhanced CT, contrast-enhanced MRI, MRA/MRV

  • Underlying vascular anomaly?

    • Cerebral angiography if high suspicion

Ich symptom progression
ICH: Symptom Progression

  • Worsening of symptoms during first 24 – 48 hours:

    • Continuation of bleeding

    • Hematoma enlargement

    • Cerebral edema

    • Herniation

Ich hematoma expansion
ICH: Hematoma Expansion

  • High rate of early neurologic deterioration due to bleeding occurring for hours after symptom onset

  • Head CT within 3 hours after symptom onset:

    • 28 – 38% have hematoma expansion of > 1/3

  • Predictive of neurologic deterioration and increased morbidity and mortality

Ich inpatient management
ICH: Inpatient Management

  • Obtain Hemostasis

    • Severe coagulation factor deficiency or thrombocytopenia

      • Replace factors and/or platelets

    • If INR elevated due to oral anticoagulation:

      • Hold warfarin (Coumadin)

      • Replace Vitamin K dependent factors (IV Vitamin K recommended)

      • Correct INR

Ich inpatient m anagement
ICH: Inpatient Management

  • General Monitoring

    • Initial monitoring in ICU

  • Blood Pressure (BP) Management

    • Incomplete efficacy evidence at present until ongoing trials of BP intervention

    • Patients with Systolic BP (SBP) 150 – 220mmHg, acute lowering to SBP < 140mmHg probably safe (Class IIa, Level B)

Stroke. 2010;41:2108-2129

Ich inpatient m anagement1
ICH: Inpatient Management

  • Temperature Management

    • Duration of fever linked to outcome, prognostic factor in patients surviving first 72H

    • Maintain normothermia

  • Seizure Prophylaxis

    • Treat with anti-epileptic drugs (AED) for patients with clinical seizures, electrographic seizures + change in MS

    • Prophylaxis with AED not recommended (Class III, Level B)

Ich inpatient m anagement2
ICH: Inpatient Management

  • Glycemic Control

    • Maintain normoglycemia

  • DVT prophylaxis

    • Intermittent pneumatic compression + elastic stockings

    • May consider low-dose LMWH after ICH stability established and 1-4 days from onset (Class IIb, Level B)

Ich inpatient m anagement3
ICH: Inpatient Management

  • Code Status

    • Aggressive full care early after ICH onset

    • Postponement of new DNR orders until at least the second full day of hospitalization is probably recommended

      (Class IIa,Level B)

    • Does not include patients with pre-existing DNR status

Icp monitoring treatment
ICP Monitoring & Treatment

  • ICP Monitoring Indications (Class IIb, Level C)

    • GCS ≤ 8

    • Transtentorial herniation

    • Significant IVH or hydrocephalus

  • CPP of 50 – 70 mmHg (Class IIb, Level C)

  • Ventricular drainage reasonable for treatment of hydrocephalus in patients with decreased LOC (Class IIa, Level B)

Ich surgical interventions
ICH: Surgical Interventions

  • Indications for Surgical Removal of Hemorrhage

    • Usefulness of surgery uncertain (Class IIb, Level C)

    • Cerebellar hemorrhage with evidence of neurological deterioration, or brain stem compression, and/or hydrocephalus (Class I, Level B)

    • Lobar clots > 30mL and within 1 cm of surface, supratentorial clot evacuation via craniotomy may be considered (Class IIb, Level B)

Ich recurrence prevention
ICH: Recurrence Prevention

  • BP Management

    • BP should be well-controlled after acute ICH

      • BP <140/90mmHg, <130/90mmHg if DM or CKD (Class IIa, Level B)

  • Anticoagulation

    • Avoid long-term anticoagulation for non-valvular atrial fibrillation after lobar ICH (Class IIa, Level B)

    • Anticoagulation after non-lobar ICH and anti-platelet therapy after all ICH might be considered when definite indication (Class IIB, Level B)

Ich recurrence prevention1
ICH: Recurrence Prevention

  • Avoidance of heavy alcohol usage (Class IIa, Level B)

  • Insufficient data to recommend restrictions for:

    • Statins

    • Physical activity

    • Sexual activity

Ich nursing considerations
ICH: Nursing Considerations

  • Neurological monitoring

    • Change in exam?

      • Hematoma expansion?

      • Worsening cerebral edema/herniation?

      • Increased ICP?

      • Seizure?

  • ICP/Cerebral perfusion pressure (CPP) monitoring

  • BP management and hemodynamic monitoring

  • Airway maintenance

  • Maintain normothermia

  • Maintain normoglycemia

  • Prevention of complications

Subarachnoid hemorrhage sah
Subarachnoid Hemorrhage (SAH)

  • Bleeding into the subarachnoid space (between the arachnoid layer and pia mater)

Sah etiology
SAH: Etiology

  • Trauma

    • Most common

  • Ruptured cerebral aneurysm

    • Most described in literature

    • Aneurysmal subarachnoid hemorrhage (aSAH)

Asah epidemiology
aSAH: Epidemiology

  • US incidence: 9.7/100,000

  • 14.5 discharges/100,000

  • US mean mortality rate: 32%

    • Death occurs in 12-15% of cases before reaching hospital

    • True incidence may be higher?

  • Average age of onset ≥ 50

  • Incidence higher in females than males

  • African Americans and Hispanics have higher incidence

Asah behavioral risk factors
aSAH: Behavioral Risk Factors

  • Hypertension

  • Tobacco Use

  • Alcohol Abuse

  • Sympathomimetic drugs (cocaine)

Asah non modifiable risk factors
aSAH: Non-modifiable Risk Factors

  • Female gender

  • Unruptured aneurysm

    • Symptomatic

    • Larger in size

    • Posterior communicating artery or vertebrobasilar location

  • Previous aSAH

  • Familial aneurysms

    • At least 1 first-degree relative, especially ≥ 2 first degree relatives

  • Genetic syndromes

Asah clinical presentation
aSAH: Clinical Presentation

  • “Worst headache of life”

    • Described by ≈ 80% of patients

  • Onset of headache may be associated with:

    • Nausea

    • Vomiting

    • Nucchal rigidity

    • Photophobia

    • Focal neurological deficits

    • Loss of consciousness

Asah diagnosis
aSAH: Diagnosis

  • Clinical presentation

    • High level of suspicion with acute onset severe headache

  • Neuroimaging

    • CT for suspected SAH

      • Lumbar Puncture (LP) if CT negative

    • CTA may be used to detect aneurysm

      • if inconclusive, will need cerebral angiogram

    • Cerebral angiography for +SAH to identify presence of aneurysm if not detected on noninvasive angiogram

    • MRI may be reasonable for diagnosis, would still need LP

Asah prognosis
aSAH: Prognosis

  • SAH Grading Scales

    • Hunt and Hess Scale

    • Fisher Scale

  • Degree of neurological impairment associated with prognosis

Asah prevention of rebleed
aSAH: Prevention of Rebleed

  • BP Management (SBP < 160mmHg)

  • Bedrest

  • Antifibrinolytic therapy?

    • For patients with unavoidable delay in surgical/endovascular treatment

    • < 72 hours of therapy

    • tranexamic acid or aminocaproic acid is reasonable

Asah prevention of rebleed1
aSAH: Prevention of Rebleed

  • Surgical/endovascular treatment of ruptured aneurysm

    • Surgical clipping of cerebral aneurysm

    • Stent/coiling of cerebral aneurysm

  • Should be performed as early as possible

  • Complete obliteration recommended

Asah complications
aSAH: Complications

  • Cerebral Vasospasm and Delayed Cerebral Ischemia (DCI)

  • Hydrocephalus

  • Hyponatremia and Volume Contraction

  • Seizures

  • Cerebral edema

  • Rebleed

  • Neurogenic Stress Cardiomyopathy

Asah cerebral v asospasm dci
aSAH: Cerebral Vasospasm/DCI

  • Clinical vs Angiographic Vasospasm

  • Transcranialdoppler (TCD)

  • Management:

    • Oral nimodipine (Nimptop)

    • Maintain euvolemia

    • Prophylactic hypervolemia not recommended

    • Induced HTN recommended for DCI, unless HTN at baseline or poor cardiac status

Asah cerebral v asospasm dci1
aSAH: Cerebral Vasospasm/DCI

  • Symptomatic Vasospasm

    • Triple-H Therapy

      • Hypervolemia

      • Hypertension

      • Hemodilution

    • Cerebral angioplasty/IA vasodilator therapy

Asah hydrocephalus
aSAH: Hydrocephalus

  • CSF diversion

    • Temporary or permanent

  • Ventriculostomy

    • Ventriculomegaly and LOC

Asah seizures
aSAH: Seizures

  • Prophylactic AED therapy in immediate posthemorrhagic period

  • Routine long-term use of AED not recommended, unless otherwise indicated

Asah hyponatremia volume c ontraction
aSAH: Hyponatremia & Volume Contraction

  • Avoid hypotonic solutions and intravascular volume contraction

  • Volume contraction treatment

    • Isotonic solutions

  • Hyponatremia treatment

    • Hypertonic solutions

    • Fludrocortisone (Florinef)

Asah hyponatremia volume c ontraction1
aSAH: Hyponatremia & Volume Contraction

  • Volume status monitoring

    • Central Venous Pressure (CVP)

    • Pulmonary Artery Wedge Pressure (PAWP)

    • Fluid balance

    • Body weight

Asah neurogenic stress cardiomyopathy
aSAH: Neurogenic Stress Cardiomyopathy

  • Secondary cardiomyopathy and/or regional wall motion abnormality (RWMA) associated with intracranial hemorrhage

    • Most common after aneurysmal SAH

  • Reversible cardiomyopathy

  • No evidence of underlying obstructive CAD

  • Asah neurogenic stress cardiomyopathy1
    aSAH: Neurogenic Stress Cardiomyopathy

    • Epidemiology:

      • Nearly 20 – 30% of patients with SAH have evidence of a secondary cardiomyopathy and/or regional wall motion abnormality (RWMA)

      • Pulmonary edema noted in approximately 10% of patients with SAH

      • Sudden death occurs in 12% of patients with SAH

    Asah neurogenic stress cardiomyopathy2
    aSAH: Neurogenic Stress Cardiomyopathy

    • Clinical Findings:

      • ECG changes

      • Arrhythmias

      • RWMA

      • Elevated cardiac enzymes

      • BNP elevation

      • Chest x-ray abnormalities

    Asah management of other c omplications
    aSAH: Management of Other Complications

    • DVT prophylaxis

    • Anemia

      • Treat with PRBC for those with concern for cerebral ischemia

      • Optimal Hgb goal not established

    • Maintain normothermia

    • Avoid hypoglycemia

    Asah nursing considerations
    aSAH: Nursing Considerations

    • Neurological monitoring

      • Change in exam?

        • Cerebral vasospasm?

        • Hydrocephalus?

        • Seizure?

    • ICP/CPP monitoring

    • Monitoring the airway

    • Evaluating hemodynamic status

    • Monitoring fluid and electrolytes

    • Pain management

    • Preventing complications

    • Allow for calm environment

    Speaker Contact Information:Lourdes James MS ACNP-BC CCRNThe Johns Hopkins HospitalNeurosciences Critical [email protected]