Intracranial Hemorrhage
Authors: Flaherty, Alice W.; Rost, Natalia S.
Title: Massachusetts General Hospital Handbook of Neurology, The, 2nd Edition
Copyright 2007 Lippincott Williams & Wilkins
> Table of Contents > Adult Neurology > Intracranial Hemorrhage
Intracranial Hemorrhage
A. See also
CT signs of intracranial hemorrhage, p. 180; arterial diagrams in Cerebrovascular Ischemia, p. 20.
B. Epidural hematoma
1. H&P: Typically, head trauma with brief LOC; then lucid interval, then obtundation, contralateral hemiparesis, and ipsilateral pupil dilatation.
2. Cause: Injury to the meningeal artery or its branches.
3. Rx: Epidural hematomas should go to the OR immediately.
C. Subdural hematoma (SDH)
1. DDx: Epidural hematoma, subdural empyema, cerebral atrophy.
2. Causes:
a. Acute SDH: Usually follows trauma (injury to the bridging veins).
b. Chronic spontaneous SDH: In the elderly, especially with cerebral atrophy, alcoholism; or poor hemostasis.
3. Rx of SDH:
a. Symptomatic SDH should be surgically drained.
b. Asymptomatic SDH may be watched.
c. Seizure prophylaxis: If acute, s/p seizure, or s/p surgical intervention. Often started on AED for ~3 wk, then d/c if no seizures.
D. Subarachnoid hemorrhage (SAH)
1. Traumatic vs. spontaneous SAH: Nontraumatic SAH is an emergency; needs immediate angiogram to r/o aneurysm. Traumatic SAH
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can usually be watched. Make sure the head trauma preceded LOC, not vice versa.2. H&P in spontaneous SAH: Sudden, severe HA worst HA in my life. N/V, LOC, stiff neck, cranial nerve deficits (especially third nerve), obtundation, ocular hemorrhage.
3. Causes of SAH:
a. Trauma: Most SAH are traumatic.
b. Aneurysms: 75% of spontaneous SAH are ruptured aneurysms.
1) Location: 75% anterior circulation; 25% posterior. 25% have multiple aneurysms.
2) Associations with aneurysms: Polycystic kidney dz, fibromuscular dysplasia, AVMs, Ehlers-Danlos syndrome type IV, Marfan's, aortic coarctation, Osler-Weber-Rendu syndrome.
c. Idiopathic: 15% of all spontaneous SAH. Associated with cigarettes, oral contraceptives, HTN, alcohol.
d. Other: AVMs, vasculitis, carotid/vertebral artery dissection.
4. Tests in spontaneous SAH:
a. Blood: CBC, PT, PTT, blood bank sample with 6 units held for OR, DPH level if pt has received it.
b. EKG: For arrhythmia, MI, cerebral Ts, long QT, U waves.
c. Head CT: see p. 180 for CT appearance.
d. LP if CT negative: See CSF table (Table 3, p. 19). SAH has high opening pressure, blood that does not clear in successive tubes, xanthochromia if bleed >6 h. WBC may be secondarily high.
e. Emergent angiogram: For spontaneous SAH, to r/o correctable aneurysm. Consider calling angiographers to prepare them when you first know of pt. Angiogram and early intervention are especially indicated in pts with Hunt-Hess (H-H) grade 1-3 because of good prognosis. For H-H 4-5, prognosis is poor; thus, reassess frequently and consider treatment if pt improves after ventriculostomy.
1) Angiogram-negative spontaneous SAH: Repeat angio in 2 wk.
5. Prognosis in SAH:
a. Mortality: 30% die before reaching hospital; 10% more in first few days. 50% total in first month.
Table 11. Hunt-Hess clinical grading scale, diagnostic testing, and prognosis for subarachnoid hemorrhage.
H-H
GradeSAH Symptoms Tests and Prognosis 0 Unruptured aneurysm (incidental finding) F/u MRIs, ~1% a yr rupture 1 Mild HA, stiff neck 3 Drowsy/confused mild focal deficit 2 Severe HA/stiff neck cranial nerve sx 3 Drowsy/confused mild focal deficit 4 Stupor, hemiparesis, mild decerebration Angio only if pt better after EVD 5 Deep coma, decerebrate posturing Poor; usually palliative care b. Morbidity: 50%-60% have serious deficit even with successful clipping.
c. Rebleeding risk: With unclipped aneurysm, 15% rebleed in 14 d, 50% in 6 mo, then 3%/yr. Hypertension greatly increases rebleed risk.
d. Hunt-Hess (H-H) grading in SAH: Guides prognosis and rx.
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6. Rx of spontaneous SAH:
a. Immediate SBP control:
1) Place arterial line in the ER: SBP goal <140, MAP 70-100.
2) Nimodipine: 30 mg q2h to a total dose of 180 mg/d, as tolerated. Can use nicardipine drip for better control.
3) Other BP agents: Labetalol, nicardipine, or nipride. If pt. is also having an MI, consider nitroglycerine labetalol.
b. Oxygenation: If needed for airway protection, intubate pt after baseline exam. All other pts should get supplementary oxygen.
c. Monitoring: Cardiac monitor, arterial and central line, NG tube if altered consciousness. Neuro checks q1h. ABG, coags, glucose, electrolytes, and CBC qd. Euvolemia. (strict I&Os). Daily CXR: until stable to r/o neurogenic pulmonary edema.
d. Avoid all anticoagulants: Consider DVT prophylaxis after SAH stabilized/source treated (o/w, TEDs/P-Boots).
e. Vasospasm prophylaxis: Nimodipine 60 mg q4h PO (from 30 mg q2h, see above) 21 d, gentle volume expansion (e.g., D5NS + 20 KCl at 100 cc/h), but not at expense of keeping SBP low.
f. Seizure prophylaxis: DPH load 1 g, then 100 mg tid. If patient never had a seizure and has good mental status exam and aneurysm is secured, may d/c ACD.
g. ICU orders: Bedrest with HOB >30 degrees, pain drugs, normothermia, TEDs and airboots, stool softener. Minimize stimulation. Keep Na >135, Mg >2.0, glucose <120 (with IV insulin if necessary). Gastric prophylaxis. Ondansetron for N/V. No free water.
7. Complications of SAH:
a. Vasospasm:
1) Signs of vasospasm: Delayed neurological deficit, ~day 6-10; often abulia, poor attention, LE > UE weakness.
2) Tests: ABG to r/o hypoxia, electrolytes to r/o low Na, stat head CT, bedside transcranial ultrasound (TCD).
a) Consider repeat angiogram: ~day 6-7 in all pts. whose exam has worsened. Based on its results, consider hypertensive or endovascular treatment with nicardipine or milrinone, or angioplasty.
3) Triple-H therapy of vasospasm: Hypertension, hypervolemia, and hemodilution. Arterial line, MAP goal 70-120 (SBP 160-200). D/c antihypertensives, give blood (keep Hct <40%), albumin (q6h for CVP <8), then phenylephrine (neosynephrine), then fludrocortisone 0.2 mg bid.
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a) Contraindications: Unclipped aneurysm, severe brain edema or infarct, cardiac instability.
b) If poor exam (Fisher grade 2 or 3): Get angiogram on day 6 or 7. Based on the results, consider albumin (1 bottle q6h for CVP <8), HT treatment, angioplasty, or endovascular treatment with nicardipine or milrinone.
c) Other: Oxygen, consider ICP monitor, bid serum and urine electrolytes.
b. Hydrocephalus: EVD (q.v., p. 86) in the EW for all pts with H-H>grade 3. Others receive it as sx and scan warrant. See Rx of ICP, p. 68. Beware of lowering ICP quickly; it can cause rebleeding. Keep EVD at 18 cm above EAM (20 cm while aneurysm not secured), then can lower for ICP issues.
c. For focal signs of elevated ICP: Mannitol 1 g/kg (usually, 50-100 g) IV bolus, then 25 mg q6h for osms <310/serum Na <160, osmolal gap <10 (gap between serum osmolality and calculated serum osmolarity). Consider hypertonic NaCl (3% infusion or 23% bolus prn). Beware of lowering intracranial pressure quickly; it can cause rebleeding.
d. Hyponatremia:
1) Cause: Usually cerebral salt wasting (see p. 197), not SIADH.
2) Rx: For Na goal >140, hydration with NS salt tablets (up to 2 g tid) 3% NaCl 23% NaCl, as necessary. Florinef will help to retain Na and expand intravascular volume.
e. Ocular hemorrhage: Consult ophthalmology to follow intraocular pressures.
E. Parenchymal hemorrhage
AKA intracerebral (vs. intracranial) hemorrhage.
1. H&P: An acute parenchymal bleed is an emergency. Most significantly expand within 1st 1-3 h after onset (38% of hematomas expand; of those, 26% within 1 h vs. 12% within 1-24 h).
2. Tests: Stat noncontrast head CT, PT, PTT, INR, platelets, D-dimer, fibrinogen, electrolytes, BUN/Cr, glucose, LFTs, blood bank sample.
a. If alternative etiology is suspected (i.e., atypical for HTN ICH), consider further imaging when pt is stable [CTV/MRV to rule out venous sinus thrombosis; MRI w/susceptibilities to evaluate for CAA; with gadolinium to evaluate for tumor (but may need to delay up to 3 months)].
3. Causes: Location is guide to cause; see Ct signs of intracranial hemorrhage, p. 180.
a. Most common: Trauma, hypertensive bleed, amyloid angiopathy.
b. Hemorrhagic metastasis: Melanoma, renal clear cell CA, thyroid, choriocarcinoma .
c. Hemorrhagic transformation of infarct:
d. Other: Aneurysm, AVM, cavernous malformation, coagulopathy, cocaine, infection, vasculitis, vasculopathy (e.g., moya-moya), venous thrombosis.
4. Prognosis: Outcome depends on age, Glasgow Coma Scale (GCS) at presentation, and hematoma volume.
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Table 12. Distinguishing a primary parenchymal bleed from a hemorrhagic infarct.
Parenchymal Bleed Hemorrhagic Infarct Symptoms Progressive Max. at onset CT appearance Dense, homogeneous Mottled, petechial Onset of blood At time of first deficit Often days to weeks after Ventricular blood Common Rare Mass effect Usually milder Prominent 1) ABC/2 estimate of bleed volume: On head CT, let A = largest diameter of hematoma in cm, B = diameter perpendicular to A, C = 1/2 of the # of CT scan slabs with blood in them (each CT slab is ~0.5 cm). An ellipsoid approximation gives bleed volume ABC/2.
Table 13. ICH volume predicts mortality. (Adapted from Broderick J, et al. Stroke. 1993;24:987-993.)
GCS ICH Vol (cc) 30-Day Mortality (%) <30 19 8 30-60 46 >60 75 <30 44 <8 30-60 74 >60 91 2) Bleed volume is best mortality predictor:
3) Modifiers: Intraventricular bleed or hydrocephalus makes prognosis worse.
4) In anticoagulated pts, ABC/2 tends to overestimate bleed size; best to use ABC/3.
5. If risk of vascular anomaly: (Pt young, without traditional risk factors, bleed is near Sylvian fissure, has SAH component, has heterogeneous appearance, etc.) Get stat CTA of head and neck and neurosurgery consultation.
6. Rx of parenchymal bleed:
a. SBP control: Usual SBP goal ~140-160; however, official guidelines recommend MAP <130, SBP <180 (more liberal to prevent drop in CBF and further ischemia). Treat hypotension aggressively with fluids or vasopressors (if SBP <90 or CPP <60).
b. Correct coagulopathy: Stat reversal of anticoagulation with FFP (2-4 U) and IV vit K (10 mg 1) for goal INR <1.3. If pt is on warfarin and ASA, give 6 U of platelets. Check coags q4h for 24 h, and repeat FFP/vit K as needed. For other coagulopathies, use institutional protocols, i.e., consult hematology/transfusion
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medicine services for help (e.g., heparin/LMWH protamine; direct thrombin inhibitors -aminocaproic acid; etc.). For platelet disorders, transfuse as needed.c. Consider early hemostatic Rx: Recombinant activated factor VII (rFVIIa) is currently available, although expensive. Consider thrombotic risk.
d. Rx of mass effect: If evidence of secondary hydrocephalus, midline shift, poor neuro exam, acute deterioration, significant IVH, pt will require stat:
1) EVD placement by neurosurgery: Goal CPP >70, ICP <20 (adjust EVD settings accordingly). Prophylactic antibiotics while EVD is in place (cefazolin or vancomycin).
2) If mass effect progresses after EVD: Hypertonic agents (mannitol, 3% and 23% NaCl), hyperventilation, or even hemicraniectomy with clot removal (especially if R-sided). But no data that hemicraniectomy helps anyone but young pts with superficial clots, especially if cerebellar bleeds >3 cm.
3) Monitoring: If neuro exam unrevealing, follow with serial head CTs.
e. Normoglycemia, normothermia, euvolemia: May need insulin drip, acetaminophen, cooling blanket, NS, strict I&Os.
f. DVT prophylaxis: Pneumo-boots (after leg ultrasounds if in hospital >24 h); can use SQ heparin in ~48 h.
g. Seizure prophylaxis: Controversial; not necessary for small, deep bleeds without subarachnoid component.
h. Steroids: Useless in management of swelling from hemorrhage.
i. Disposition and outcomes: Neuro-ICU with frequent neuro checks, close EVD management. Discuss prognosis with family depending on exam, bleed volume, clinical course (secondary events).
F. Vascular malformations
1. Arteriovenous malformations (AVM): Congenital direct connection between arteries and veins. CNS sites: intraparenchymal > subarachnoid (~5% of all SAH) > intraventricular > subdural.
a. H&P: Hemorrhage (~4%/yr; rarely associated with early rebleeding or vasospasm), seizures, headache, focal deficits, cranial bruits.
b. Tests: May be seen on MRI (susceptibilities/gradient echo series) or MRA, but arteriogram is needed to characterize an AVM's blood supply.
c. Rx: Endovascular embolization, XRT, or surgery.
2. Venous angiomas: No arterial inputs. Lower bleed risk than with AVMs. Usually seen on MRI.
3. Cavernous malformations: Sinusoidal vessels without intervening neural tissue. Present with seizures, focal neurological deficit, HA. Often not seen on angiogram because of low flow and presence of thrombosis.
4. Dural-based AV fistulae: Vascular malformations in one of the major venous sinuses. Typically acquired due to change in cerebrovascular hemodynamics or intracranial pressure changes. Sx depend on lesion site (papilledema with superior sagittal sinus involvement; pulsatile tinnitus in transverse/sigmoid sinus; seizures in cortical lesions). Angiogram w/external carotid artery injection is diagnostic.
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G. Intraventricular hemorrhage
Usually hypertensive, possible other small-vessel arteriopathy (CAA, AVM) or aneurysm. Prognosis is worse due to risk of hydrocephalus; pt will usually need an EVD.
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