Subarachnoid hemorrhage

Background

Pearls

1. Obtain GCS before intubation
2. If intubate prevent hypertension (rebleeding)
   1. Pretreatment
      1. Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)
      2. Fentanyl 200mcg (sympatholytic)
   2. Sedation
      1. If pt has high BP - use propofol
      2. If pt has adequate BP - use etomidate
3. Treat pain
   1. Prevents incr catacholamines/ incr BP

Epidemiology

• Of All pts in ED who p/w HA:
  • 1% will have SAH
  • 10% will have SAH if c/o worst HA of life
  • 25% will have SAH if c/o worst HA of life + any neuro deficit

Risk Factors

1. Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
2. Hypertension
3. Atherosclerosis
4. Cigarette smoking
5. Alcohol
6. Age >50
7. Cocaine use
8. Estrogen deficiency

Etiology of Spontaneous SAH

1. Ruptured aneurysm (85%)
2. Nonaneurysmal (15%)
   1. Perimesencephalic hemorrhage (10%)
   2. Other
      1. Tumor, coagulopathy, dissection, vasculitis, sickle cell, venous sinus thrombosis

Clinical Features

1. Sudden, severe headache (97% of cases)
   1. Sudden onset is more important finding than worst HA
2. May be associated with syncope, seizure, nausea/vomiting, and meningismus
   1. Meningismus may not develop until several hrs after bleed (blood breakdown -> aseptic meningitis)
3. Retinal hemorrhage
   1. May be the only clue in comatose patients
4. 30-50% will have sentinel bleed/HA 6-20d before SAH

Diagnosis

If concerned for SAH, must do BOTH CT and LP

1. Non-Contrast Head CT
   1. 90%-98% sensitive if performed w/in 24 hours of bleed
   2. 91% sensitive in patients w/ normal neuro exam
      1. Decreases to ~50% sensitive by day 5
   3. Not as sensitive/specific for minor bleeds
   4. SAH 2/2 aneurysm (90%) - look in cisterns (especially suprasellar cistern)
   5. SAH 2/2 trauma - Look at convexities of frontal & temporal cortices
2. Lumbar Puncture
   1. Findings:
      1. Elevated RBC count that doesn't decrease from tube one to four
         1. (Decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl)
      2. Opening pressure > 20 in 60% of patients with SAH
         1. Can help differentiate from a traumatic tap (opening pressure expected to be normal)
         2. Elevated opening pressure also seen in cerebral venous thrombosis, IIH
      3. Xanthrochromia
         1. May help differentiate between SAH and a traumatic tap
         2. Takes at least 2 hours after the bleed to develop (beware of false negatives)
         3. Sensitivity (93%) / specificity (95%) highest after 12 hours
   2. If unable to obtain CSF consider CTA

Treatment

1. Nimodipine
   1. Associated with improved neuro outcomes and decreased cerebral infarction
   2. Give 60mg q4hr PO or NGT only! (never IV)
2. BP control
   1. No consensus on HTN (incr BP may maintain CPP but may also increase rate of bleeding)
      1. If pt is alert this means CPP is adequate so consider lowering sbp to 120-140
         1. If pt has history of HTN consider lowering sbp to ~160
      2. If pt is ALOC consider leaving BP alone as the ALOC may be 2/2 reduced CPP
   2. If BP control is necessary use NICARDIPINE, LABETALOL, or ESMOLOL
      1. Avoid vasodilators such as nitroprusside or NTG (increase cerebral blood volume > increased ICP)
   3. Avoid hypotension
      1. Maintain MAP > 80
         1. Give IVF
         2. Give pressors if IVF ineffective
3. Discontinue/reverse all anticoagulation
   1. Coumadin - give (prothrombin complex conc or FFP) and vit K)
   2. Aspirin - give DDAVP
   3. Plavix - give platelets
4. Seizure prophylaxis
   1. Controversial; 3 day course may be preferable
   2. Phenytoin load
5. Glucocorticoid therapy
   1. Controversial; evidence suggests is neither beneficial nor harmful
6. Glycemic control
   1. Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
7. Keep head of bed elevated

Complications

1. Rebleeding
   1. Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours
   2. Usually diagnosed by CT after acute deterioration in neuro status
   3. Only aneurysm treatment is effective in preventing rebleeding
2. Vasospasm
   1. Leading cause of death and disability after rupture
   2. Typically begins no earlier than day three after hemorrhage
   3. Characterized by decline in neuro status
   4. Aggressive treatment can only be initiated after the aneurysm has been treated (sx or intraluminal tx)
      1. Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia)
3. Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
   1. Ischemia
      1. Elevated troponin (20-40% of cases)
      2. ST segment depression
   2. Rhythm disturbances
      1. Torsades, a fib, a flutter
   3. QT prolongation
   4. Deep, symmetric TWI
   5. Prominent U waves
4. Hydrocephalus
   1. Consider ventricular drain placement for deteriorating LOC + no improvement within 24 hours
5. Hyponatremia
   1. Usually due to SIADH
      1. Treat via isotonic, or if necessary, hypertonic saline (do not treat via water restriction!)

Prognosis

Hunt and Hess

• Grade 0: Unruptured aneurysm
• Grade 1: Asymptomatic or mild HA and slight nuchal rigidity
  • Grade 1a: No acute meningeal/brain reaction, with fixed neurological def
• Grade 2: Moderate to severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
• Grade 3: Mild mental status change (drowsy or confused), mild focal neurologic deficit
• Grade 4: Stupor or moderate to severe hemiparesis
• Grade 5: Coma or decerebrate rigidity

^Grade 1 or 2 have curable dz, if dx missed pts return w/ higher grade (ie 3 or 4), 2/3 will be dead or vegetative at 6 mos if grade 3 or 4!

^Add one grade for serious systemic dz (HTN, DM, severe atherosclerosis, COPD)

World Federation of Neurosurgical Societies (WFNS)

Grade	GCS	Major Focal Deficit
0 (unruptured)	NA	NA
1	15	Absent
2	13-14	Absent
3	13-14	Present
4	7-12	Present/absent
5	3-6	Present/absent

See Also

Intracranial Hemorrhage

Source

UpToDate

EB Emergency Medicine, July 2009

EMCrit Podcast 8