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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
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
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
slide12

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)
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
ad