Rosen & Barkin's 5-Minute Emergency Medicine Consult (691 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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DIFFERENTIAL DIAGNOSIS
  • Seizure is most commonly mistaken for syncope:
    • Key differentiating factor is postictal confusion.
    • Brief tonic movements and urinary incontinence may be seen with syncope.
  • Metabolic disorders (e.g., hypoxemia, hyperventilation, hypoglycemia)
  • Toxicologic
  • Stroke
  • Psychogenic syncope
  • Malingering
  • Breath-holding spells in children
TREATMENT
PRE HOSPITAL
  • Oxygen
  • Cardiac monitoring
  • IV access
INITIAL STABILIZATION/THERAPY
  • Advanced cardiac life support (ACLS) interventions for unstable patients
  • Oxygen
  • Cardiac monitoring
  • IV access with normal saline fluid bolus in suspected hypovolemia
  • Consider coma cocktail—dextrose, thiamine, and naloxone for persistent altered mental status
ED TREATMENT/PROCEDURES
  • ACLS interventions for dysrhythmias
  • Standard regimens for acute myocardial infarction
  • Control BP for subarachnoid hemorrhage and aortic dissection
  • Consider thrombolytics for submassive PE.
MEDICATION
  • Dextrose: D
    50
    W 1 amp (50 mL or 25 g) IV (peds: D
    25
    W 2–4 mL/kg IV)
  • Naloxone: 2 mg IV or IM (peds: 0.1 mg/kg)
  • Thiamine: 100 mg IV or IM (peds: 50 mg)
FOLLOW-UP
DISPOSITION
Admission Criteria
  • San Francisco Syncope Rule identifies patients at high risk for serious short-term outcomes (“CHESS”):
    • History of
      C
      HF
    • H
      ematocrit <30%
    • Abnormal
      E
      CG
    • Patient complaint of
      s
      hortness of breath
    • S
      ystolic BP <90
  • Other recommendations:
    • Suspected cardiac syncope must be admitted to monitored bed
    • GI bleeds consider intensive care unit bed
    • Admit elderly patients with syncope.
Discharge Criteria
  • Neutrally mediated syncope or orthostatic syncope from volume depletion may be evaluated on outpatient basis with close follow-up, if patient is reliable and has a good social structure.
  • Driving restrictions until cleared
PEARLS AND PITFALLS
  • Use of criteria such as the San Francisco Syncope Rule prevents unnecessary admissions.
  • Do not assume vasovagal cause in syncope associated with headache or chest pain.
ADDITIONAL READING
  • Brignole M, Alboni P, Benditt DG, et al. ESC guidelines on management (diagnosis and treatment) of syncope—update 2004. Executive summary.
    Eur Heart J
    . 2004;25(22):2054–2072.
  • Kessler C, Tristano JM, De Lorenzo R, et al. The emergency department approach to syncope: Evidence-based guidelines and prediction rules.
    Emerg Med Clin North Am.
    2010;28:487–500.
  • Massin MM, Bourguignont A, Coremans C, et al. Syncope in pediatric patients presenting to an emergency department.
    J Pediatr
    . 2004;145(2):223–228.
  • Saccilotto RT, Nickel CH, Bucher HC, et al. San Francisco Syncope Rule to predict short-term serious outcomes: A systematic review.
    CMAJ.
    2011;183(15):E1116–1126.
  • Yarlagadda S, Poma PA, Green LS, et al. Syncope during pregnancy.
    Obstet Gynecol.
    2010;115(2):377–380.
CODES
ICD9
  • 337.01 Carotid sinus syndrome
  • 427.89 Other specified cardiac dysrhythmias
  • 780.2 Syncope and collapse
ICD10
  • G90.01 Carotid sinus syncope
  • R00.1 Bradycardia, unspecified
  • R55 Syncope and collapse
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION (SIADH)
Matthew D. Bitner
BASICS
DESCRIPTION
  • Most common cause of hyponatremia in hospitalized patients (and doubles inpatient mortality in some studies)
  • A
    water balance problem more
    than 1 of sodium (Na) balance
  • Normal regulation of water balance:
    • Antidiuretic hormone (ADH):
      • Integral controller of water balance
      • Increases water permeability of the collecting tubules, resulting in free water reabsorption
      • Synthesized by hypothalamus but secreted by posterior pituitary
    • Water deprivation (increased plasma osmolality) stimulates secretion as sensed by:
      • Osmoreceptors/atrial stretch receptors
      • Carotid baroreceptors
      • Aortic arch/pulmonary veins
  • Hyponatremia:
    • Mild
      : Serum sodium <135 mEq/L
    • Moderate
      : Serum sodium <130 mEq/L
    • Severe
      : Serum sodium <125 mEq/L
    • Excess extracellular water
      relative
      to Na
    • Depletional hyponatremia:
      • Sodium depletion can be caused by diet, GI losses, diuretic use, and renal or adrenal disease.
      • Often accompanied by extracellular fluid volume depletion
      • Hyponatremia associated with clinical signs of hypovolemia
      • Increased Hct, BUN, Cr
      • Urinary sodium excretion <20 mEq/L
    • Dilutional hyponatremia:
      • Increased extracellular water in presence of normal or increased total body sodium
      • Can be caused by increased fluid intake (oral, IV), drugs, or medical conditions
      • Euvolemia with edema
      • Normal or decreased Hct, BUN, Cr
      • Urinary sodium excretion >20 mEq/L
      • Inappropriate ADH secretion is a form of dilutional hyponatremia.
  • Definition of SIADH:
    • ADH secretion in absence of hyperosmolality or hypovolemia
  • Criteria for definition:
    • Essential features:
      • Hyponatremia
        —despite correction for hyperglycemia, hyperproteinemia, or hyperlipidemia
      • Euvolemia
        —no clinical signs of volume depletion (orthostasis, tachycardia) or volume overload (edema, ascites)
      • Hyposmolality
        of the plasma—<275 mOsm/kg of water
      • Normal renal, adrenal, and thyroid function
      • No recent diuretic use
      • Urine Osm >100 mOsm/kg of water
    • Supplemental features:
      • Plasma uric acid <4 mg/dL
      • BUN <10 mg/dL
      • FENa >1%
      • Failure to correct hyponatremia after an infusion of normal saline (NS) 0.9%
      • Abnormal water load test (inability to excrete ≥90% of a 20 mL/kg water load in 4 hr)
ETIOLOGY
  • Malignant disorders:
    • ADH-producing tumors
    • Cancer (Small-cell lung, pancreatic, prostate)
    • Pituitary tumors
    • Thymoma
    • Lymphoma
  • Pulmonary disorders:
    • Pneumonia
    • TB
    • Lung abscess
    • COPD
  • CNS disorders:
    • Meningitis/encephalitis
    • CVA
    • Head injury
  • Medications:
    • Thiazides
    • Chlorpropamide
    • Vincristine
    • Anticonvulsants (carbamazepine)
    • Antidepressants (tricyclics, SSRIs)
    • Antipsychotics
    • NSAIDs
    • Ecstasy (MDMA)
    • Vasopressin analogs (DDAVP, oxytocin, vasopressin)
  • Transient:
    • Endurance exercise
    • General anesthesia
    • Pain
    • Stress
  • Other:
    • Hereditary
    • Positive-pressure ventilation
    • HIV/AIDS
    • Idiopathic
ALERT

Cerebral salt-wasting syndrome (CSWS) can mimic SIADH.

  • Seen in patients with cerebral tumors or subarachnoid hemorrhage and in neurosurgical patients
  • Etiology unclear
  • Represents appropriate water resorption in the face of salt wasting (urine Na >30–40 mmol/L)
  • Fluid restriction can help differentiate the 2:
    • In SIADH: Hypouricemia will correct
    • In CSWS: Hypouricemia will persist
  • Treatment of CSWS may differ from that of SIADH:
    • Infusion of NS
    • May benefit from fludrocortisones therapy
DIAGNOSIS

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