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Subarachnoid Hemorrhage, Emergency Medicine


Basics


Description


  • Bleeding into the subarachnoid space and CSF:
    • Spontaneous:
      • Most often results from cerebral aneurysm rupture
      • Aneurysms that occur are more likely to rupture (>25 mm).
    • Traumatic:
      • Represents severe head injury

Epidemiology


  • Incidence is 6 " “16 per 100,000 individuals.
  • Affects 21,000 in US annually
  • Associated mortality in 30 " “50% of patients
  • Uncommon prior to 3rd decade; incidence peaks in 6th decade

Risk Factors


  • Previous ruptured aneurysm who have other aneurysms
  • Family history
  • Hypertension
  • Smoking
  • Alcohol abuse
  • Sympathomimetic drugs:
    • Cocaine, methamphetamine, and ecstasy (MDMA) use
  • Gender (female:male 1.6:1)

Genetics
  • 3 " “7-fold increased risk with 1st-degree relatives with subarachnoid hemorrhage (SAH)
  • Strongest genetic association represents only 2% of SAH patients:
    • Autosomal dominant polycystic kidney disease, Ehlers " “Danlos type IV, familial intracranial aneurysms

  • Most often due to arteriovenous malformation in children
  • Although rare in children, SAH is a leading cause of pediatric stroke.

Etiology


  • "Congenital, "  saccular, or berry aneurysm rupture (80 " “90%):
    • Occur at bifurcations of major arteries
    • Incidence increases with age.
    • Aneurysms may be multiple in 20 " “30%.
  • Nonaneurysmal perimesencephalic hemorrhage (10%)
  • Remaining 5% of causes include:
    • Mycotic (septic) aneurysm due to syphilis or endocarditis
    • Arteriovenous malformations
    • Vertebral or carotid artery dissection
    • Intracranial neoplasm
    • Pituitary apoplexy
  • Severe closed head injury

Diagnosis


Signs and Symptoms


History
  • Classically a severe, sudden headache:
    • Often described as "thunderclap "  or "worst headache of life " 
    • Headache is often occipital or nuchal, but may be unilateral.
    • Usually develops within seconds and peaks within minutes
    • Distinct from prior headaches
    • Headache often maximal at onset
  • Sentinel headaches and minor bleeding occur in 20 " “50%:
    • May occur days to weeks prior to presentation and diagnosis
  • Seizures, transient loss of consciousness, or altered level of consciousness occur in more than 50% of patients.
  • Vomiting occurs in 70%.
  • Syncope, diplopia, and seizure are particularly high-risk features for SAH.

Physical Exam
  • Focal neurologic deficits occur at the same time as the headache in 33% of patients:
    • 3rd cranial nerve (CN III) palsy (the "down and out "  eye) occurs in 10 " “15%.
    • Isolated CN VI palsy or papillary dilation may also occur.
  • Nuchal rigidity develops in 25 " “70%.
  • Retinal hemorrhage may be the only clue in comatose patient.

Essential Workup


  • Complete neurologic exam and fundoscopic exam
  • Emergent noncontrast head CT scan:
    • Diagnoses 93 " “98% of SAH if performed within 12 hr
    • Thin cuts (3 mm) through base of brain improve diagnostic yield.
    • CT is less sensitive after 24 hr or if hemoglobin <10 g/L.
  • Lumbar puncture (LP) and CSF analysis must be performed if CT negative and history suggests possibility of SAH.

  • Incidence slightly increased in pregnancy
  • Workup should include CT and LP

Diagnosis Tests & Interpretation


Lab
  • Baseline CBC and differential
  • Electrolytes, renal function tests
  • Coagulation studies
  • Cardiac markers:
    • Troponin I elevated in 10 " “40%
  • CSF analysis (see below)

Imaging
  • Chest radiograph for pulmonary edema:
    • Occurs in up to 40% with severe neurologic deficit
  • Traditional gold standard: 4-vessel digital subtraction cerebral angiography
  • Spiral CT angiography:
    • Useful for operative planning
    • Quite sensitive for detection of aneurysms >4 mm, less with smaller aneurysms
  • MR angiography:
    • MRI is less sensitive for hemorrhage
    • Quite sensitive for detection of aneurysms >4 mm, less with smaller aneurysms
  • Transcranial Doppler ultrasound:
    • May be useful in detecting vasospasm.

Diagnostic Procedures/Surgery
  • LP:
    • Presence of erythrocytes in CSF indicates SAH or traumatic tap:
      • If traumatic tap suspected, LP should be performed 1 interspace higher.
      • Diminishing erythrocyte count in successive tubes suggests but does not firmly establish a traumatic tap.
      • Xanthochromia is diagnostic of SAH if performed 12 hr after onset.
    • An elevated opening pressure may indicate SAH, cerebral venous sinus thrombosis, or pseudotumor cerebri.
  • ECG:
    • ST-segment elevation or depression
    • QT prolongation
    • T-wave abnormalities
    • Often mimics ischemia or infarction
    • Symptomatic bradycardia, ventricular tachycardia, and ventricular fibrillation

Differential Diagnosis


  • Neoplasm
  • Arterial dissection
  • Aneurysm (unruptured)
  • Arteriovenous malformation
  • Migraine
  • Pseudotumor cerebri
  • Meningitis
  • Encephalitis
  • Hypertensive encephalopathy
  • Hyperglycemia or hypoglycemia
  • Temporal arteritis
  • Acute glaucoma
  • Subdural hematoma
  • Epidural hematoma
  • Intracerebral hemorrhage
  • Thromboembolic stroke
  • Sinusitis
  • Seizure disorder
  • Cerebral venous sinus thrombosis
  • Cavernous sinus thrombosis

Treatment


Pre-Hospital


  • Initial assessment and history:
    • Level of consciousness
    • Glasgow Coma Scale score
    • Gross motor deficits
    • Other focal deficits
  • Patients with SAH may need emergent intubation for rapidly deteriorating level of consciousness.
  • IV access should be established.
  • Provide supplemental oxygen.
  • Monitor cardiac rhythm.
  • Patients should be transported to a hospital with emergent CT and ICU capability.

Initial Stabilization/Therapy


  • Manage airway, resuscitate as indicated:
    • Rapid-sequence intubation
    • Pretreat with lidocaine and defasciculating dose of nondepolarizing paralytic to blunt increase in intracranial pressure (ICP) during intubation.
    • Cardiac monitoring and pulse oximetry
    • Establish adequate IV access
  • Obtain urgent neurosurgical consultation

Ed Treatment/Procedures


  • Prevent rebleeding:
    • Risk of rebleeding highest in the 1st few hours after aneurysmal rupture
  • Manage ICP:
    • Elevate head of bed to 30 ‚ °.
    • Prevent increases in ICP from vomiting and defecation with antiemetics and stool softeners.
    • Treat increased ICP with controlled ventilation and mannitol.
    • Maintain central venous pressure >8 mm Hg and urine output >50 mL/hr
  • BP control:
    • Balance HTN-induced rebleeding vs. cerebral hypoperfusion
    • Goal mean arterial pressure 100 " “120 mm Hg, systolic BP <160:
      • Labetalol, hydralazine, nitroprusside, or nicardipine for hypertension
    • Correct hypovolemia:
      • Should start within 96 hr of SAH
      • Treat hypotension with volume expansion.
  • Cerebral vasospasm:
    • May cause secondary ischemia and infarction after SAH:
    • Oral nimodipine improves functional outcome:
      • Discuss with neurosurgeon prior to administration
    • Monitor with transcranial Doppler.
  • Adequately treat pain.
  • Seizures:
    • Manage with IV benzodiazepine
    • Consider prophylactic anticonvulsants in immediate posthemorrhagic period
  • Correct temperature, electrolyte, glucose, or pH abnormalities.
  • Treat coagulopathy, thrombocytopenia, and severe anemia.
  • Monitor for and correct pulmonary edema and cardiac arrhythmias.
  • Antifibrinolytic therapies:
    • Discuss with neurosurgeon prior to initiation
    • Consider administration immediately after aneurysmal rupture in patients at high risk of rebleeding when this is combined with treatment of aneurysm and monitoring for hypotension.
  • When patient is stable, expedited transfer to hospital with neurosurgical capabilities is mandatory.

Medication


  • Diazepam: 5 " “10 mg (peds: 0.2 " “0.3 mg/kg) IV/IM q10 " “1min PRN; max. 30 mg (peds: 10 mg)
  • Fentanyl: 1 " “3 Ž Όg/kg (adults and peds) IV q1 " “4h PRN
  • Fosphenytoin: 15 " “20 phenytoin equivalents (PE) per kg (adults and peds) IV ƒ — 1; maintenance 4 " “6 mg/kg/d IV
  • Hydralazine: 10 " “20 mg (peds: 0.1 " “0.5 mg/kg IV) q30min " “4h PRN
  • Labetalol: 20 mg IV bolus, then 40 " “80 mg q10min; max. 300 mg; follow with IV continuous infusion 0.5 " “2 mg/min (peds: 0.4 " “1 mg/kg/h IV continuous infusion; max. 3 mg/kg/h)
  • Lidocaine: 1 " “1.5 mg/kg IV ƒ — 1 (adults and peds)
  • Lorazepam: 2 " “4 mg (peds: 0.03 " “0.05 mg/kg/dose; max. 4 mg/dose) IV q15min PRN
  • Midazolam: 1 " “2 mg (peds: 0.15 mg/kg IV ƒ — 1) IV q10min PRN
  • Morphine: 2 " “10 mg (peds: 0.05 " “0.2 mg/kg IV) q2 " “4h PRN
  • Nicardipine: 5 " “15 mg/h IV continuous infusion (peds: Safety not established)
  • Nimodipine: 60 mg PO/NGT q4h; (peds: Safety not established)
  • Nitroprusside: 0.25 " “10 Ž Όg/kg/min IV continuous infusion (adults and peds)
  • Ondansetron: 4 " “8 mg (peds: 0.1 " “0.15 mg/kg max. 4 mg) PO/IM/IV TID PRN
  • Phenytoin: 15 " “20 mg/kg IV load at max. 50 mg/min; max. 1.5 g; maintenance 4 " “6 mg/kg/d IV; (adult and pediatric)
  • Promethazine: 12.5 " “25 mg (peds >2 yr old: 0.25 " “1 mg/kg; max. 25 mg/dose) PO/IM/IV q4 " “6h PRN

Surgery/Other Procedures


  • Per neurosurgical consultant
  • Early operative or endovascular intervention may prevent vasospasm and improve outcome.

Follow-Up


Disposition


Admission Criteria
  • All patients with SAH should be admitted to an ICU.
  • Patients with negative CT findings and equivocal LP findings should be admitted for observation.

Discharge Criteria
  • Patients with negative CT and LP findings and onset of symptoms <2 wk
  • Outpatient follow-up for headache treatment and further evaluation

Issues for Referral
Early referral to center with access to neurosurgeons and endovascular specialists (if none at practicing institution) ‚  

Prognosis


  • Mortality is 12% before arrival to hospital.
  • Ultimately fatal in more than 50%.
  • In cases of "sentinel bleed "  or early detection of aneurysmal rupture, outcomes are improved with early surgical or interventional approaches.

Pearls and Pitfalls


  • Failure to consider SAH in differential diagnosis for new, acute headache
  • Failure to assess previous headache workup as complete (CT and LP)

Additional Reading


  • Bederson ‚  JB, Connolly ‚  ES Jr, Batjer ‚  HH, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke.  2009;40:994 " “1025.
  • Edlow ‚  JA, Malek ‚  AM, Ogilvy ‚  CS. Aneurysmal subarachnoid hemorrhage: Update for emergency physicians. J Emerg Med.  2008;34(3):237 " “251.
  • Rabinstein ‚  AA. The AHA Guidelines for the Management of SAH: What we know and so much we need to learn. Neurocrit Care.  2009;10(3):414 " “417.
  • Uysal ‚  E, Yanbulo „ Ÿlu ‚  B, Ert ƒ Όrk ‚  M, et al. Spiral CT angiography in diagnosis of cerebral aneurysms of cases with acute subarachnoid hemorrhage. Diagn Interv Radiol.  2005;11(2):77 " “82.
  • Wolfson ‚  A. Blunt neck trauma. In: Wolfson ‚  AB, Hendey ‚  GW, Hendry ‚  PL, et al., eds. Harwood-Nuss ' Clinical Practice of Emergency Medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.

Codes


ICD9


  • 430 Subarachnoid hemorrhage
  • 852.00 Subarachnoid hemorrhage following injury without mention of open intracranial wound, unspecified state of consciousness

ICD10


  • I60.9 Nontraumatic subarachnoid hemorrhage, unspecified
  • S06.6X0A Traum subrac hem w/o loss of consciousness, init

SNOMED


  • 21454007 Subarachnoid intracranial hemorrhage (disorder)
  • 262955000 Traumatic intracranial subarachnoid hemorrhage (disorder)
  • 270907008 Spontaneous subarachnoid hemorrhage
  • 230719004 intracranial subarachnoid hemorrhage due to ruptured aneurysm (disorder)
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