Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

Rosen & Barkin's 5-Minute Emergency Medicine Consult (682 page)

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult

11.64Mb size Format: txt, pdf, ePub

Read Book Download Book

ads

Pediatric Considerations

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.

Pregnancy Considerations

Incidence slightly increased in pregnancy
Workup should include CT and LP

DIAGNOSIS TESTS & NTERPRETATION
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 μg/kg (adults and peds) IV q1–4h PRN
Fosphenytoin: 15–20 phenytoin equivalents (PE) per kg (adults and peds) IV × 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 × 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 × 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 μg/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