INTRACRANIAL HEMORRHAGE


See also "Neonatal Intracranial Hemorrhage"

I. Etiology

  1. Vascular anomalies
    1. AVM
    2. Angioma
    3. Aneurysm
      1. More common in first-degree relatives of pts with h/o ruptured intracranial aneurysms, though screening such relatives not recc'd as of 2000 (NEM 341:1344, 1999--JW; BMJ 320:141, 2000--JW)
  2. Abnormal arteries (arteritis, amyloid angiopathy)
  3. Bleeding diatheses
  4. Head trauma
  5. Bleeding into preexisting lesions, e.g. tumor
  6. "Spontaneous"--more common in elderly; us. in subcortical WM, basal ganglia, cerebellum & pons; traditionally attributed to chronic HTN, but no h/o HTN in about 50% of pts! Acute rises in BP and reperfusion of ischemic areas may play roles. (edit. in Neurol. 38:624, 4/88)

II. Intracranial hemorrhage associated with IV heparin:

  1. Heparin for Tx of ischemic CVA associated with 0.8% incidence of hemorrhagic stroke; 3.1% incidence of hemorrh. anywhere, with 16% mortality among these
  2. Most pts with hemorrh. complications (anywhere) have PTTs in therapeutic range
  3. Independent risk factors for IC hemorr. secondary to IV Hep post-CVA (or post-TIA or "RIND"):
  1. Rapid (<24 post-sx-onset) onset of CT evidence of cerebral infarction on presentation
  2. Hep loading doses >100U/kg
  3. Total Hep dose >35U/kg/h in 1st 4h
  4. "Severe" neurol. deficits

III. Subdural hematoma

  1. Occurs as the result of tearing of "bridging veins" between the dura and arachnoid typically due to trauma (deceleration injuries-most commonly falls in elderly, MVAs in younger patients)
  2. More common in elderly and pts with brain atrophy (e.g. due to alcohol abuse)
  3. Typically unilateral
  4. Found in 25% of pts presenting unconscious to an ED after a head injury
  5. Overall mortality 40-60%
  6. Associated with persistent congnitive dysfunction after recovery
  7. Clinical presentation-Depends on location of the hematoma and the rate of accumulation
    1. Mental status changes including drowsiness (most common sign in the elderly) or coma,
      1. Up to 50% of patients are initially conscious after injury then mental status deteriorates as hematoma accumulates
    2. Headache
      1. Usually sudden-onset, severe, worsened with coughing or straining, and often accompanied by nausea and vomiting
      2. Mild generalized headache present in 90% of elderly pts
    3. Seizures (rare)
    4. On Px:
      1. Focal neurologic deficits, including pupillary abnormalities (present in 30-50%)
      2. Papilledema
      3. Asymmetric reflexes
      4. Babinski sign
      5. Aphasia or dysphasia
      6. Gait abnormalities
      7. Neck stiffness
      8. etc.
    5. In infants: irritability, vomiting, bulging anterior fontanelle
    6. Can result in brain herniation and death
  8. CT findings: hyperdensity from the hematoma, usually concave towards the brain ("crescent"-shaped) and crossing suture lines, in contrast to epidural hemorrhage which is typically convex towards the brain and does not cross suture lines
  9. Indications for surgical evatuation of subdural hematoma
    1. Hematoma thickness > 10mm
    2. Midline shift > 5mm
    3. Glascow coma score < 9 AND any of:
      1. GCS decrease of > 1 point from time of injury to hospital admission
      2. Pupillary asymmetry
      3. Pupils fixed and dilated
      4. Intracranial pressure > 20mm Hg
  10. Chronic subdural hemorrhage
    1. Slow bleeding can delay clinical presentation
    2. Incidence greatly increased after age 70yo or use of antithrombotics
    3. Other risk factors: blotting disorders, leukemia, hepatic or renal disease, alcohol abuse, seizure disorder, loc intracranial pressure, hemodialysis, birth trauma
    4. Can be seen in toddlers (typically form abuse)
    5. Can grow in size over time due to recurrent bleeding
    6. Often no clear h/o trauma
    1. Management
      1. Check coag studies and hepatic and renal panels
      2. Brain imaging with CT or MRI (serial scans until stable unless treating surgically)
      3. Seizure prophylaxis typically with phenytoin (continue post-operatively if treating surgically)
      4. Immediate reversal of anticoagulation, if anticoagulated
      5. Surgical trainage

IV. Subarachoid hemorrhage

  1. 80% result from rupture of Intracranial Aneurysms
  2. Usually treated with external ventricular drains
  3. Cerebral vasospasm is common and can cause ischemic deficits after initial presentation; usually dx'd by transcranial doppler.  Tx's used to prevent this:
    1. Hypervolemic hypertensive hemodilutional (HHH) therapy
    2. Endovascular papaverine
    3. Angioplasty are typically used
    4. Intrathecal sodium nitroprusside and thiosulfate--Experimental as of 2002
  4. 15-20% of pts with subarachnoid hemorrhage have delayed ischemic neurologic deficits ("DINDs") within 2wks of the SAH, due to vasospastic reaction.
  5. In a study in 80 pts with aneurysmal subarachnoid hemorrhage randomized to pravastatin 40mg QD vs. placebo started within 72h of onset of symptoms and continued x 14d, the Pravastatin group had sig. lower incidence of DIND (5% vs. 30%) and sig. lower mortality (5% vs. 20%) (Stroke 36:1627, 2005--JW)

V. Intracerebral hemorrhage

  1. Treatment
    1. In a study in 1,033 pts with spontaneous intracerebral hemorrhage <72 s/p onset randomized to surgery within 24h of presentation vs. conservative treatment, at 6mos, there were no sig. diffs. in mortality or disability scores, though the subgroup whose hematomas were 1cm or less from cortical surface did show sig. better outcomes with surgery than conservative tx (Lancet 365:387, 2005--JW)
    2. 399 pts with spontaneous intracerebral hemorrhage presenting < 3h after symptom onset randomized to recombinant activated Factor VII ("NovoSeven," one dose, at various doses) within 1h after diagnosis. Repeat CT at 24h showed sig. less 90-day incidence of (death or severe disability) in Factor VII recipients c/w placebo (49-55%, depending on dose, vs. 69% w/placebo). Serious arterial thromboembolic events were sig. more likely in Factor VII recipients (5% vs. 0%) (NEJM 352:777, 2005--JW)
(Sources include Core Content Review of Family Medicine, 2012)