Rosen & Barkin's 5-Minute Emergency Medicine Consult (69 page)

TREATMENT

• ABCs:
  
  • Cardiac monitor
    
  • Isotonic crystalloids as needed for hypotension
    
• Naloxone, thiamine, and dextrose (D50W) as indicated for altered mental status
  
• Cardiovascular:
  
  • Vasopressors if refractory hypotension is present
    
  • Central venous pressure monitoring to prevent pulmonary/cerebral edema
    
  • Avoid type IA, IC and III antidysrhythmic agents, which worsen QTc prolongation
    
  • Continuous cardiac monitoring for QTc prolongation
    
• Neurologic:
  
  • Treat seizures with benzodiazepines
    
  • Assist ventilation for respiratory failure from neuromuscular weakness
    
• Renal:
  
  • Hemodialysis for renal failure
    
• Alimentary:
  
  • Dextrose, enteral or parenteral feeding may be beneficial
    

• Decontamination:
  
  • Orogastric lavage or aspiration may be helpful within the 1st hr of ingestion
    
  • Activated charcoal does not bind arsenic
    
  • If opacities are seen on abdominal film, administer whole bowel irrigation (polyethylene glycol) at 1–2 L/hr until repeat radiographs are clear
    
  • If dermal exposure, decontaminate skin as 1st step in management
    
• Ensure that no one else is contaminated and environment is evaluated
  
• Ensure that electrolytes such as calcium, magnesium, and potassium are replaced
  
• Evaluate need for chelation therapy, based on levels, acuity of exposure, clinical symptoms:
  
  • Consult with medical toxicologist/poison center
    
  • Agents
    
    • Dimercaprol (British anti-Lewisite)
      
    • DMSA (succimer)
      
• Elimination:
  
  • Hemodialysis not routinely effective
    
    • Consider for patient with renal failure or other hemodialysis indications
      
    • Continue chelation throughout hemodialysis sessions
      

• Dimercaprol (British anti-Lewisite): 3 mg/kg deep IM q4h for 24 h, then q6h for the next 24 h, then q12h until able to tolerate PO
  
  • Caution: Contraindicated in patients with peanut allergies
    
• Dextrose 50%: 25 g (50 mL) (peds: 0.5 g/kg D
  ₂₅
  W) IV for hypoglycemia
  
• DMSA (succimer): 10 mg/kg PO q8h for 5 d, then q12h for 14 d
  
• Sodium bicarbonate: 1 mEq/kg IV bolus, followed by infusion of 150 mEq in 1 L of D
  ₅
  W at 150 mL/h
  
  • Used to treat rhabdomyolysis
    
  • Ensure that potassium and other electrolytes are monitored and replaced during infusion
    
• Naloxone: 0.4–2.0 mg (peds: 0.1 mg/kg) IV, may repeat up to 10 mg for suspected opioid intoxication
  
• Thiamine: 100 mg IM or IV (peds: 1 mg/kg)
  
• Vasopressors after sufficient fluids
  
  • Dopamine 5 μg/kg/min, increase by 5–10 μg/kg/min (q10–30min) Max.: 20 μg/kg/min
    
  • Norepinephrine 0.01–3 μg/kg/min, start at 2 μg/min, titrate to MAP 65–90 mm Hg
    
• Max.: 20 μg/min
  

FOLLOW-UP

Symptomatic arsenic exposures should be admitted to an intensive care setting.

• Asymptomatic patients with a spot urinary arsenic level <50 μg/L may be discharged
  
• Suspected chronic exposures who do not require admission should be referred for outpatient evaluation and 24 hr urine collection
  
• Ensure that home environment is safe for patient prior to discharge
  

• Psychiatric follow-up for intentional overdoses
  
• Primary care follow-up for cancer screening and monitoring
  

• Arsenic poisoning results in a myriad of signs and symptoms
  
  • Suspect acute arsenic poisoning when patients present with gastrointestinal distress and neurologic findings.
    
  • Suspect chronic arsenic poisoning in patients who present with neurologic deficits, nonspecific wasting, and hyperkeratotic skin lesions.
    
• Consult a medical toxicologist/poison center regarding the need for chelation therapy.
  

A special thanks goes to Dr. Gerald Maloney Jr, who contributed to the previous edition.

• Agency for Toxic Substances and Disease Registry. Toxicologic Profile for Arsenic. US Department of Health and Human Services. August 2007.
  
• Chen Y, Parvez F, Gamble M, et al. Arsenic exposure at low-to-moderate levels and skin lesions, arsenic metabolism, neurological functions, and biomarkers for respiratory and cardiovascular diseases: Review of recent findings from the Health Effects of Arsenic Longitudinal Study (HEALS) in Bangladesh.
  Toxicol Appl Pharmacol
  . 2009;239:184–192.
  
• Hughes MF, Beck BD, Chen Y, et al. Arsenic exposure and toxicology: A historical perspective.
  Toxicol Sci
  . 2011;123(2):305–332.
  
• Munday SW, Ford M. Arsenic. In:
  Goldfrank’s Toxicologic Emergencies
  . 9th ed. New York, NY: McGraw-Hill; 2010.
  
• Tournel G, Houssaye C, Humbert L, et al. Acute arsenic poisoning: Clinical, toxicological, histopathological, and forensic features.
  J Forensic Sci
  . 2011;56(suppl 1):S275–S279.
  

CODES

985.1 Toxic effect of arsenic and its compounds

BASICS

• Results when air bubbles enter the pulmonary venous return from ruptured alveoli, then propagate through the systemic vasculature:
  
  • Clinical manifestations depend on location of air bubbles in systemic vasculature system.
    
• Also known as dysbaric air embolism or cerebral air embolism
  
• Caused by overpressurization of lung tissue, causing pleural tear with air entering the vascular circulation:
  
  • Trapped air (in lungs with closed glottis) expands on diver ascent.
    
  • Boyle law: At a constant temperature, pressure (P) is inversely related to volume (V):
    
    • PV = K (constant) or P
      ₁
      V
      ₁
      = P
      ₂
      V
      ₂
      
  • As pressure increases/decreases, volume decreases/increases.
    

• Pulmonary atrioventricular (AV) shunts, or as paradoxical embolism via a patent foramen ovale
  
• Breath holding during ascent:
  
  • Symptoms attributable to a shower of bubbles and multiple blood vessel involvement
    
• Iatrogenically during placement of central venous pressure (CVP) lines, cardiothoracic surgery, or hemodialysis
  
• Penetrating injuries to heart, with emergent repair of cardiac wound
  

DIAGNOSIS

• Cerebral:
  
  • Rapid onset:
    
    • Almost all cases of AGE present within 1st 5 min of surfacing, although most often symptoms are evident in 1st 2 min
      
  • Dive-related stroke
    
  • 2 main presentations:
    
    • Apnea and full cardiopulmonary arrest
      
    • Any combination of neurologic deficits
      
  • Presentation depends on arterial distribution of gas embolism:
    
    • Stupor or confusion (24%)
      
    • Coma without seizure (22%)
      
    • Coma with seizures (18%)
      
    • Unilateral motor deficits (14%)
      
    • Visual disturbances (9%)
      
    • Vertigo (8%)
      
    • Unilateral sensory deficits (8%)
      
    • Bilateral motor deficits (8%)
      
    • Collapse (4%)
      
  • Spontaneous improvement minutes after initial deficits may occur:
    
    • High incidence of relapse
      
    • Improvement may be transiently related to postural changes that affect distribution of bubbles flowing to brain.
      
• Pulmonary:
  
  • Dyspnea
    
  • Hemoptysis, pleuritic chest pain
    
  • Subcutaneous air
    
• Cardiac:
  
  • MI owing to air in coronary vessels
    
  • Reduced cardiac output owing to air trapped in ventricle
    
  • Hamman sign: Crepitus on auscultation of heart
    
• Renal:
  
  • Renal infarction owing to air embolism