Rosen & Barkin's 5-Minute Emergency Medicine Consult (684 page)

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

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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ED TREATMENT/PROCEDURES
  • Acute
  • Early neurosurgical intervention (<4 hr) in comatose patients shows reduced mortality:
    • Burr holes may be used as temporizing measure in deteriorating patients.
    • ICP monitoring is indicated for patients with abnormal CT who are intubated.
    • Subdural evacuating port system has been shown to be equivalent to Burr hole for acute treatment of SDH
  • Nonoperative treatment may be indicated for small SDH:
    • <20 mL of blood, <1 cm, midline shift <5 mm, no mass effect, no neurologic deficit
    • This requires frequent neurologic reassessment.
    • 10% go on to require operative intervention.
  • Maintain euvolemic state with isotonic fluids:
    • Arterial line placement to monitor MAP, PO
      2
      , and PCO
      2
    • Foley catheter to monitor I/O status
  • Control ICP:
    • Prevent pain, posturing, and increased respiratory effort:
      • Sedation with benzodiazepines
      • Neuromuscular blockade with vecuronium or rocuronium in intubated patients
      • Etomidate is a good induction agent.
    • Mannitol may be used once euvolemic:
      • Shown to increase MAP > cerebral perfusion pressure and CBF as well as decrease ICP
    • Keep osmolality between 295 and 310.
    • Use furosemide (Lasix) as an adjunct only if normovolemic.
    • Treat HTN:
      • Labetalol, nicardipine, or hydralazine
    • Treat coagulopathy
    • Use fresh frozen plasma 4+ units
    • Use prothrombin complex concentrate
    • Treat hyperglycemia if present:
      • Associated with increased mortality in traumatic brain injury
    • Treat and prevent seizures:
      • Diazepam and phenytoin (Dilantin), levetiracetam: Prophylactic anticonvulsants not indicated
MEDICATION
  • Diazepam: 5–10 mg (peds: 0.2–0.3 mg/kg) IV/IM q10–15min PRN; max. 30 mg (peds: 10 mg)
  • Dilantin: Adults and peds: Load 18 mg/kg at 25–50 mg/min
  • Etomidate: 0.3 mg/kg IV for induction of RSI
  • Fentanyl: 2–4 μg/kg
  • Hydralazine: 10–20 mg (peds: 0.1–0.5 mg/kg IV) q2–4h 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)
  • Lasix: Adults and peds: 0.5 mg/kg IV
  • Levetiracetam: 1,500 mg PO/IV q12h
  • Lidocaine: As preinduction agent, 1.5 mg/kg IV
  • Mannitol: Adults and peds: 0.25–0.5 g/kg IV q4h
  • Midazolam: 1–2 mg (peds: 0.15 mg/kg IV × 1) IV q10min PRN
  • Nicardipine: 5–15 mg/h IV continuous infusion (peds: Safety not established)
  • Pentobarbital: 1–5 mg IV q6h
  • Prothrombin complex concentrate: 50 U/kg IV
  • Rocuronium: 1 mg/kg for induction
  • Thiopental: As induction agent, 20 mg/kg IV
FOLLOW-UP
DISPOSITION
Admission Criteria
  • Acute SDH patients should be admitted to the operating room or ICU by the neurosurgical service.
  • Subacute subdurals should be admitted to a monitored setting.
Discharge Criteria

Patients with chronic SDH often can be managed as outpatients in conjunction with neurosurgery, adequate home resources, and appropriate follow-up.

Issues for Referral

All patients need neurosurgical evaluation immediately.

PEARLS AND PITFALLS

The following factors predict prognosis:

  • GCS on admission
  • Time to treatment
  • Pupil abnormalities
  • CT volume of hematoma and presence of midline shift
  • Midline shift > hematoma volume
ADDITIONAL READING
  • Beslow LA, Licht DJ, Smith SE, et al. Predictors of outcome in childhood intracerebral hemorrhage: A prospective consecutive cohort study.
    Stroke
    . 2010;41(2):313–318.
  • Chittiboina P, Cuellar-Saenz H, Notarianni C, et al. Head and spinal cord injury: Diagnosis and management.
    Neurol Clin.
    2012;30(1):241–276, ix.
  • Huh JW, Raghupathi R. New concepts in treatment of pediatric traumatic brain injury.
    Anesthesiol Clin
    . 2009;27(2):213–240.
  • Krupa M. Chronic subdural hematoma: A review of the literature. Part 2.
    Ann Acad Med Stetin
    . 2009;55(3):13–19.
  • Kubal WS. Updated imaging of traumatic brain injury.
    Radiol Clin North Am
    . 2012;50:15–41.
  • Zhu GW, Wang F, Liu WG. Classification and prediction of outcome in traumatic brain injury based on computed tomographic imaging.
    J Int Med Res
    . 2009;37(4):983–995.
CODES
ICD9
  • 432.1 Subdural hemorrhage
  • 767.0 Subdural and cerebral hemorrhage
  • 852.20 Subdural hemorrhage following injury without mention of open intracranial wound, unspecified state of consciousness
ICD10
  • I62.00 Nontraumatic subdural hemorrhage, unspecified
  • P10.0 Subdural hemorrhage due to birth injury
  • S06.5X0A Traum subdr hem w/o loss of consciousness, init
SUDDEN INFANT DEATH SYNDROME (SIDS)
Genie E. Roosevelt
BASICS
DESCRIPTION
  • Sudden, unexpected death of an infant <1 yr old who was typically well before being placed down to sleep
  • Death remains unexplained after being thoroughly investigated by autopsy, exam of the death scene, investigation of the circumstances, and review of the family and infant medical histories.
  • Leading cause of death in infants 1 mo–1 yr of age; the incidence has declined markedly since the initiation of the “Back to Sleep” program in 1994:
    • 1992: 120 deaths/100,000 live births (US)
    • 2001: 56 death/100,000 live births (US)
    • No change from 2001–2006
  • Peak occurrence of SIDS at 1–4 mo of age:
    • 90% occur <6 mo of age
    • 2% occur >10 mo of age
  • Ethnic differences: 2006 rates per 100,000 live births: All populations, 54.5; non-Hispanic white, 55.6; non-Hispanic black, 103.8; American Indian/Alaska Natives, 119.4; Asian American or Pacific Islander, 22.8; Hispanic, 27.
  • Sleeping on back (supine) reduces incidence significantly (“Back to Sleep”). Practice of infants sleeping on their backs began initially in Europe and then in US
ETIOLOGY
  • Most likely multifactorial
  • SIDS infants likely have predisposing conditions that make them more vulnerable to both internal and external stressors.
  • Potential stressors include anemia, congenital diseases, dysrhythmias, electrolyte abnormalities, genetic defects, infection, metabolic disorders, neurologic events, suffocation, trauma, upper airway obstruction.
  • Maternal and antenatal risk factors:
    • Alcohol and illicit drug use
    • Intrauterine growth restriction
    • Lower socioeconomic status
    • Poor prenatal care
    • Prior sibling death secondary to SIDS
    • Shorter interval between pregnancies
    • Smoking
    • Younger age
  • Infant risk factors:
    • Bed sharing
    • Exposure to environmental smoking
    • Gastroesophageal reflux (GER)
    • Hyperthermia
    • Low birth weight, prematurity
    • Male gender
    • Soft bedding, soft sleeping surface
    • Recent febrile illness
  • Supine sleeping position, breast-feeding, and pacifier use are protective.
  • Home monitoring has not been shown to prevent SIDS.
DIAGNOSIS
SIGNS AND SYMPTOMS
History
  • No significant pre-existing signs or symptoms to alert caretakers
  • Unpredictable
  • Most infants appear normal when put to bed.
  • Death occurs while the infant is sleeping.
  • Typically the event is silent with no signs of struggling.
  • No clinical or pathologic explanation for death.
  • Apparent life-threatening event (ALTE) is an acute event that is frightening to the caretaker:
    • Characterized by apnea (either central or obstructive) causing changes in skin color—cyanosis, pallor, or erythema with limpness, choking, and/or gagging.
    • Infant should be transported to hospital for evaluation and monitoring.
    • Appears well when evaluated by clinicians after recovery from ALTE.
    • Associated with an increased risk of SIDS.
Physical-Exam
  • Prior to the event, the infant is seemingly healthy and well appearing, well developed, and well nourished.
  • If event was brief and self-limited, may appear well when evaluated after the episode.
  • Potential complications for surviving infants include pulmonary edema, aspiration pneumonia, and neurologic sequelae secondary to hypoxia including seizures.

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