Rosen & Barkin's 5-Minute Emergency Medicine Consult (690 page)

• Activated charcoal: 1–2 g/kg up to 100 g PO
  
• Dextrose: D
  ₅₀
  W 1 amp: 50 mL or 25 g (peds: 1 to 2 mL/kg of D
  ₂₅
  W; infants: 2.5 to 5.0 mL/kg of D10%) IV
  
• Diazepam (benzodiazepine): 5–10 mg (peds: 0.2–0.5 mg/kg) IV. Not recommended <6 months of age
  
• Lorazepam (benzodiazepine): 2–6 mg (peds: 0.03–0.05 mg/kg) IV
  
• Nicardipine IV infusion at 5 mg/h titrate by 2.5 mg/h q5min to max. 15 mg/h
  
• Nitroprusside: 0.5--10 μg/kg/min IV (titrated to BP)
  
• Phenobarbital: 15–20 mg/kg at 25–50 mg/min until cessation of seizure activity; monitor for respiratory depression. Safety not established <6 years of age
  
• Phentolamine: 1–5 mg IV over 5 min (titrated to BP)
  
• Sodium bicarbonate: 1 or 2 amps (50 mEq/amp) (peds: 1–2 mEq/kg) IV push
  

FOLLOW-UP

• Admit all body packers or stuffers to hospital.
  
• Severe manifestations of toxicity to monitored bed:
  
  • Seizures
    
  • Dysrhythmias
    
  • Hyperthermia
    
  • Rhabdomyolysis
    
  • Severe hypertension
    
  • Altered mental status
    
• Ischemic chest pain
  

Mildly intoxicated patients can be observed and treated in ED until resolution of clinical manifestations.

Patients may need referral for chemical dependency rehab and detoxification

• Admit patients with severe or persistent symptoms
  
• Hyperthermia above 40°C may be life threatening:
  
  • Treat with aggressive sedation and active cooling
    
• Recognize rhabdomyolysis and hyperkalemia
  
• Avoid physical restraints in agitated patients if possible
  
• Consider associated emergency conditions:
  
  • Chest pain – acute coronary syndrome
    
  • Infection in altered patients with fevers and history of IV drug use
    
  • Traumatic injury with methamphetamine abuse
    
• Benzodiazepines are 1st-line therapy in symptomatic sympathomimetic intoxication
  

• Carvalho M, Carmo H, Costa VM, et al. Toxicity of amphetamines: An update.
  Arch Toxicol
  . 2012;86:1167–1231.
  
• Greene SL, Kerr F, Braitberg G. Review article: Amphetamines and related drugs of abuse.
  Emerg Med Australas
  . 2008;20:391–402.
  
• Prosser JM, Nelson LS. The toxicology of bath salts: A review of synthetic cathinones.
  J Med Toxicol.
  2012;8:33–42.
  
• Schep LJ, Slaughter RJ, Beasley DM. The clinical toxicology of metamfetamine.
  Clin Toxicol (Phila).
  2010;48:675–694.
  

CODES

971.2 Poisoning by sympathomimetics [adrenergics]

BASICS

• Transient loss of consciousness associated with loss of postural tone
  
• Ultimately, it is the lack of oxygen to the brainstem reticular-activating system, which results in a loss of consciousness and postural tone.
  
• Most commonly, an inciting event causes a drop in cardiac output.
  
• Cerebral perfusion is re-established by autonomic regulation as well as the reclined posture, which results from the event.
  
• Accounts for 3% of ED visits
  

• Pregnant patients frequently experience presyncope or syncope from various causes. 5% of patients experience syncope, 28% experience presyncope throughout their pregnancy.
  
• Placenta acts as an AV malformation, causing decreased SVR that potentiates orthostatic symptoms.
  
• Fetus lying on IVC can lead to neurogenic and hypovolemic syncope.
  
• Pregnant patients at higher risk of DVT/pulmonary embolism (PE), UTI, seizures (preeclampsia), valvular incompetencies. Must exclude these diagnoses in ED evaluation.
  

• Elderly with highest incidence as well as increased morbidity
  
• >1/3 will have numerous potential causes.
  

• Neutrally mediated syncope:
  
  • Reflex response causing vasodilatation and bradycardia with resulting cerebral hypoperfusion
    
  • Vasovagal (common faint):
    
    • Often incited by pain or fear
      
    • Prodromal findings are usually present.
      
    • Typically lasts <20 sec
      
    • Tilt-table testing is the gold standard to diagnose.
      
  • Carotid sinus syncope:
    
    • Cough, sneeze
      
    • GI stimulation (e.g., defecation)
      
    • Micturition
      
• Orthostatic:
  
  • Positional changes cause abrupt drop in venous return to heart.
    
  • Volume depletion:
    
    • Severe dehydration (e.g., vomiting, diarrhea, diuretics)
      
  • Hemorrhage (see “Hemorrhagic Shock”)
    
• Autonomic failure:
  
  • Diabetic or amyloid neuropathy
    
  • Parkinson disease
    
  • Drugs (e.g., β-blockers) and alcohol
    
• Cardiac arrhythmias:
  
  • Typically sudden and without prodromal symptoms
    
  • Tachydysrhythmia or bradydysrhythmia
    
  • Inherited syndromes (e.g., long QT syndrome, Brugada syndrome)
    
  • Pacemaker/implantable cardioverter defibrillator malfunction
    
• Structural cardiac or cardiopulmonary disease:
  
  • Valvular disease (especially aortic stenosis)
    
  • Hypertrophic cardiomyopathy
    
  • Acute myocardial infarction
    
  • Aortic dissection
    
  • Pericardial tamponade
    
• Pulmonary embolus
  
• Neurologic:
  
  • Transient spike in intracranial pressure that exceeds cerebral perfusion pressure
    
  • Postsyncopal headache is almost universal
    
  • May be presentation of a subarachnoid hemorrhage
    
• Cerebrovascular steal syndromes
  

DIAGNOSIS

• Prodromal symptoms:
  
  • Lightheadedness
    
  • Diaphoresis
    
  • Dimming vision
    
  • Nausea
    
  • Weakness
    
• The following findings suggest an underlying life threat:
  
  • Sudden event without warning
    
  • Chest pain or palpitations
    
• 6 Ps of a syncope history:
  
  • 1. Preprodrome activities
    
  • 2. Prodrome symptoms—visual symptoms, nausea
    
  • 3. Predisposing factors—age, chronic disease, family history of sudden death
    
  • 4. Precipitating factors—stress, postural symptoms
    
  • 5. Passerby witness—what did they see?
    
  • 6. Postictal phase, if any—suggests seizure
    

• Evaluate for trauma
  
• Orthostatic vital signs
  
• Check for difference in BP in both arms suggesting aortic dissection or subclavian steal syndrome.
  
• Careful cardiovascular exam, including murmurs, bruits, and dysrhythmias
  
• Rectal exam to check for GI bleeding
  
• Urine pregnancy test in reproductive-age female
  
• Careful neurologic exam
  

• Warning signs of a potential serious underlying disease:
  
  • Syncope during exertion
    
  • Syncope to loud noise, fright, extreme stress
    
  • Syncope while supine
    
  • Family history of sudden death at young age (<30 yr)
    

• ECG immediately upon arrival to check for:
  
  • Ischemia
    
  • Dysrhythmias
    
  • Block
    
  • Long QT interval
    
  • Brugada syndrome
    
  • Wolff–Parkinson–White syndrome
    
• Detailed history and physical exam will determine diagnosis in 85% of those who eventually obtain a diagnosis.
  

• Driven by history and physical exam
  
• CBC in suspected occult hemorrhage
  
• Serum bicarbonate:
  
  • Normal with most syncopal events
    
  • Marked decreased bicarbonate obtained <1 hr after the event:
    
    • Suggestive of a grand mal seizure rather than syncope
      
    • If due to seizure, should normalize 1 hr after the event
      
• Cardiac enzymes in suspected ischemia
  
• Pregnancy test in reproductive-age female
  
• Electrolytes in patients with profound dehydration or diuretic use
  

• ECG and monitoring until cardiac etiology ruled out
  
• Chest radiograph ± CT angiography if congestive heart failure (CHF), dissection, or massive PE suspected
  
• Head CT if abnormal neurologic exam or transient ischemic attack suspected
  
• Echocardiogram if concern for structural defects