160. Spontaneous Subarachnoid and Intracerebral Hemorrhage

Subarachnoid Hemorrhage

Risk Factors: HTN, smoking, alcoholics, polycystic kidney disease, family history of SAH, marfan/ehlers-danlos syndrome, coarctation of aorta.

Features: Acute onset within a few minutes, ‘thunderclap,’ previous history of similar headaches recently (sentinel bleed), 20% develop symptoms after exertion (exercise, sexual activity, defecation). Syncope alone should not raise suspicion for SAH.

Diagnosis: Noncontrast CT has same sensitivity if not better than MRI for blood. Better sensivity the earlier the CT is done. CSF analysis is still considered ‘gold standard’ after negative CT despite newer studies pointing against this. Two CSF tests: xanthochromia and RBC count. ┬áIt takes 12 hours to develop xanthochromia and remains present for almost 3 weeks. Traumatic LP results are still inconclusive and there is no general consensus on what number means true SAH. Generally, < 5 is definite no blood. CTA does not entirely rule out SAH (20% will have no aneurysm) and does not rule in SAH when aneurysm found (small % in population will be found incidentally).

Classification: Hunt-Hess Scale: I – mild headache, normal neuro exam; 2 – severe headache, normal neuro exam, may have CN deficit; 3 – confused, somnolent, may have CN deficit or mild neuro deficit; 4 – stupor, moderate to severe motor deficit, intermittent posturing; 5 – coma, reflex posturing or flaccid.

Treatment: Prevent complications: vasospasm (usually 2-21 days after, modest benefit with nimodipine 60mg PO q4), rebreeding (within first 24 hours, adequate BP control with MAP < 130mmHg, consider titratable labetolol), cerebral infarction, cerebral edema, hydrocephalus. 5-20% will have seizure – discuss with NSGY on need for prophylaxis.


Intracranial Hemorrhage

Risk Factors: 8-11% of all strokes, warfarin use, 3-9% of tPa use in ischemic stroke, long standing HTN, AV malformations, use of sympathomimetics (cocaine, phenylpropanolamine (decongestant).

Features: In hypertensive ICH, bleeding usually in putamen, thalamus, pons, or cerebellum (most common areas in ascending order).

Treatment: Management of elevated ICP: raise head of bed to 30 degrees, pain control/sedation, osmotic diuretics, mild hyperventilation with intubation. BP control if MAP > 150 or SBP > 180. Coagulopathy needs to be reversed. Warfarin reversal: Recombinant Factor VIIa or PCCs are mainstream now compared to FFP. Still need to add on Vitamin K, though slower.


References

Tintinalli, Chapter 160: Spontaneous Subarachnoid and Intracerebral Hemorrhage

Intracerebral Hemorrhage, Mike Abraham, The Crashing Patient Conference 2015

Subarachnoid Hemorrhage, Gunjan Parikh, The Crashing Patient Conference 2015

Unedited Notes:

ICH

Etiology of ICH: chronic HTN, cerebral amyloid agiopathy, sympathomimetics/cocaines, AVM, other vascular malformation.

Volume is a better predictor of morbidity than location.

Supratentorial: basal ganglia, lobar; infratentorial: pons, cerebellum; intraventricular involvement.

Calculate ABC/2 score. Calculate volume by taking the largest diameter, multiplying that by the total slices the bleed goes thru (0.5cm slices and on 6 slices would mean 3cm), then divide by 2 to get approximate volume.

ICH score: GCS, ICH volume, IVH, location, age: higher the number, the worse the prognosis. Score 6: 99% 30day mortality.

Main treatments: Look at BP and look at coagulopathy.

BP control: get SBP to 140, nicardipine/labetolol, try to achieve in 1 hour.

Coumadin: Vitamin K, give FFP. If C/I (hx/o CHF) to FFP, given PCCs.

Heparin: Protamine.

Antiplatelets: consider platelet transfusion, consider DDAVP.

Direct thrombin inhibitors: FFP, PCC, protamine. No improved outcomes any better even if the numbers look better in the studies.

Factor Xa inhibitors: FEIBA, dialysis. Antidote just approved. Outcomes still not that promising even if numbers are.

Secondary Treatment:

Seizures: routine prophylaxis not recommended. Treat all seizures aggressively if present. Continuous EEG monitoring may be helpful. Usually start with keppra (1-1.5g bolus).

SAH

CT scan: Thick blood in the cisterns. Sellate appearance of thick blood.

12-15% die before they reach the hospital. 50% survivors have persistent neuro deficits.

Females > males. Median age in the 50s.

Features: worst headache of life, neck pain/stifness, LOC (due to increased ICH at maximal on first rupture with brief loss of blood flow to the brain), nausea/vomiting.

Hunt and Hess Grading Scale. Grade 1-5.

Hunt and Hess Scale

EKG findings: peaked T, ST changes, Takosubos cardiomyopathy (contraction band necrosis, apical ballooning on echo).

Can be increased ICH during intubation: get everything right and get sedation/pain medications on early to prevent major changes in SBP. Use nicardipine for BP as well.

CT sensitivitiy drops over time. 98-100% within 12 hours.

CSF: Xanthochromia is present (minimal clearing of RBCs between tubes 1-4 (not completely valid either).

If CT positive, go ahead and get the CTA.

<20% have seizures. Guidelines recommend prophylaxis.

Worsening neuro decline: Rebleeding (number 1 cause), hydrocephalus, seizures cerebral edema, vasospasm (peak day 7) – nimodipine (not really necessary for ED), fever, hyponatremia.

SBP < 160, euvolemia. MAP > 70 or > 130 associated with poor outcome.

 

160. Spontaneous Subarachnoid and Intracerebral Hemorrhage

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