41. Acute stroke



Download 2.22 Mb.
Date04.06.2018
Size2.22 Mb.

Initial management


  • Key in management is determining timing of onset and ruling out hemorrhage.

  • Arrange stat I head CT by calling neurorads (pager 39991). Acute stroke takes precedence over all other imaging in the queue.

  • Ruling out hemorrhage is essential to determining treatment.

  • Consult the stroke service via pager 34CVA (34282), who will determine role of thrombolysis or anticoagulation.

  • Call neurosurgery consult early if you suspect a bleed clinically (anticoagulation, brain metaseses, seizure, headache, etc.) Arrange to reverse anticoagulation/coagulopathy if present (order FFP).

  • Coma/unresponsiveness or inability to protect airway are indications for intubation.

  • Intubation may also be indicated for blood pressure control in the setting of hemorrhage, or hyperventilation for treatment of increased ICP.

Non-hemorrhagic acute stroke management


  • Thrombolysis. IV tPA remains the treatment of choice for acute stokes within 3 hours of onset of symptoms (0.9 mg/kg total dose, max dose 90 mg, contraindicated if age >80 or SBP>180). Intra-arterial tPA or clot removal may be delivered via interventional neuroradiology catheterization within 6 hours.

  • Anticoagulation. IV heparin without a bolus is given with thrombolysis. It is also often indicated if thrombolysis cannot be given. Heparin may be bolused if the neurological deficits appear to be fluctuating or brainstem ischemia is suspected.

  • Antiplatelet agents. Aspirin 325 mg should be given if thrombolysis is not; clopidogrel may be added if ASA is already being taken.

  • Blood pressure management. Blood pressure may be autoregulated for at least 10 days, up to SBP of 200 unless other emergencies present (MI, CHF, aortic dissection)

Hemorrhagic acute stroke management


  • Neurosurgical intervention. Should be considered for any hemorrhage with significant mass effect and any cerebellar bleed greater than 3 cm in size.

  • Correction of anticoagulation. Immediately administer fresh frozen plasma and vitamin K if indicated, transfuse platelets if antiplatelet agents on board.

  • Blood pressure management. Control BP <140/100 (goal MBP <130) via invasive blood pressure monitoring.

  • Seizure prevention. Give phenytoin IV 1 g load (over 20 minutes; consider fosphenytoin if hypotensive) for hemorrhage involving cortex or ventricles.

Major threats to life


  • Transtentorial herniation occurs primarily in the following situations:

  • Massive hemispheric infarction or hemorrhage

  • Intraventricular extension of ICH or SAH.

  • Cerebellar infarction or hemorrhage. All patients with large cerebellar lesions require neurosurgical evaluation because emergent decompression can be lifesaving.

  • Aspiration. All patients should be considered to have impaired swallowing until proven otherwise.

  • Myocardial infarction. MI complicates approximately 3% of acute ischemic strokes.

Etiologies


  • Ischemic: 80% of all strokes

  • Embolus

    • Cardiac (60% of all strokes, 20% known source, 40% unidentifiable)

    • Paradoxical embolus, artery-to-artery, fat, air

  • Thrombosis

    • Large artery (about 15% of infarctions)

    • Penetrating artery (lacunar stroke, also known as hypertensive lipohyalinosis)

  • Intracerebral hemorrhage

  • Hypertensive

  • AVM

  • Amyloid angiopathy

  • Bleeding metastasis

  • Subarachnoid hemorrhage (5% of all strokes)

  • Miscellaneous (venous infarct, carotid/vertebral dissection, CNS vasculitis, migraine, drug abuse (cocaine or amphetamines), hematologic disorders (sickle cell, polycythemia, leukemia), MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke)

Common stroke syndromes


  • Left MCA stroke. Aphasia with right hemiplegia of lower face and arm.

  • Right MCA stroke. Decreased attentiveness with left hemiplegia of lower face and arm, language usually intact, impaired spatial visualization.

  • Subcortical stroke. Extrapyramidal motor signs (chorea, athetosis), unilateral weakness of face/arm/leg (internal capsule) or unilateral sensory loss (thalamus).

  • Cerebellar stroke. Appendicular ataxia (cerebellar hemisphere) or truncal ataxia (midline).

  • Brainstem stroke. Unilateral (face/arm/leg) weakness/sensory loss with cranial nerve involvement.

Differential diagnosis


  • Stroke mimics: spinal cord lesion, peripheral nerve injury (e.g. Bell’s palsy, Saturday night palsy), Todd’s paralysis (post-seizure), multiple sclerosis flare, vasculitis, hemiplegic migraine, transient global amnesia, hypoglycemia

Helpful studies and laboratory information (Do Not Edit)


  • Blood: glucose, CBC, lytes, PT/PTT, ESR. Consider lipid panel, homocysteine, CRP, hypercoagualation panel, D-dimer, RPR. Be aware that CPK rises 4-7 days after stroke.

  • Emergent head CT to rule out bleed, then follow-up MRI/MRA of head and neck (to assess vascular obstruction, stenoses) with DWI within 72 hours.

  • Vascular studies: CNI, TCD may be employed to follow effects of treatment or if MRI/CTA contraindicated.

  • Cardiac workup: EKG, TTE with agitated saline to evaluate for PFO. Eventually, may need cardiac risk stratification with ETT because TIA is a risk factor for MI.


Alexander Morss, M.D.


(
Figures from JAMA 1985;253:1420.
Do Not Edit This Line This is Hidden Text)





MGH Medical Housestaff Manual



Share with your friends:


The database is protected by copyright ©dentisty.org 2019
send message

    Main page