Rosen & Barkin's 5-Minute Emergency Medicine Consult (217 page)

Specific DIC treatment is usually not initiated in the ED. Underlying precipitating diseases should be treated initially:

• Heparin:
  
  • Low-dose regimen: 5–10 U/kg/h IV for causes where thrombosis predominates.
    

FOLLOW-UP

Severe precipitating illness in combination with DIC requires ICU admission.

None

Follow-up involves following platelets and coagulation factors.

• Suspect DIC as a complicating factor in severe, life-threatening illness.
  
• Establish early clinical suspicion since the sequelae of DIC can be devastating.
  
• Remember to consider treating the underlying cause of DIC when the thromboembolic and bleeding complications of the process seem to be dominating the clinical picture.
  

• Bick RL. Disseminated intravascular coagulation current concepts of etiology, pathophysiology, diagnosis, and treatment.
  Hematol Oncol Clin North Am
  . 2003;17(1):149–176.
  
• Levi M. Disseminated intravascular coagulation.
  Crit Care Med
  . 2007;35:2191–2195.
  
• Levi M, Toh CH, Thachil J, et al. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology.
  Br J Haematol
  . 2009;145(1):24–33.
  
• Levi M, van der Poll T. Disseminated intravascular coagulation: A review for the internist.
  Intern Emerg Med
  . 2013;8:23–32.
  
• Rodgers GM. Acquired coagulation disorders. In: Greer JP, Foerster J, Rodgers GM, et al., eds.
  Wintrobe’s Clinical Hematology
  . 12th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:1422–1455.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Sepsis
  
• Idiopathic Thrombocytopenic Purpura
  
• Thrombotic Thrombocytopenic Purpura
  

CODES

286.6 Defibrination syndrome

BASICS

• Inhibits various enzymes and its active metabolites exert additional effects.
  
• Disulfiram–ethanol reaction:
  
  • Usually occurs 8–12 hr after taking the drug; should not be observed >24 hr after dosing
    
  • Competitively and irreversibly inactivates aldehyde dehydrogenase
    
  • Ethanol metabolism is blocked, resulting in accumulation of acetaldehyde
    
  • Acetaldehyde produces release of histamine resulting in vasodilation and hypotension
    
  • Severe reactions may occur in drinkers with ethanol levels of 50–100 mg/dL
    
  • Severity and duration of reaction is proportional to amount of ethanol ingested
    
• Disulfiram blocks dopamine β-hydroxylase and limits synthesis of norepinephrine from dopamine:
  
  • Relative excess of dopamine may contribute to altered behavior
    
  • Relative depletion of norepinephrine may contribute to hypotension
    
• Disulfiram metabolite (carbon disulfide) interacts with pyridoxal 5-phosphate:
  
  • Diminishes concentration of pyridoxine available for formation of γ-aminobutyric acid (GABA) in CNS
    
  • Potentially lowers seizure threshold
    
  • Carbon disulfide is also cardiotoxic, hepatotoxic, and inhibits cytochrome P-450 (CYP2E1)
    
• Disulfiram metabolites may chelate important metals (copper, zinc, iron) essential in various enzyme systems
  
• Disulfiram metabolites may cause peripheral neuropathies that are dose and duration dependent
  

• Disulfiram is used as a deterrent in the treatment of chronic ethanol abuse
  
• Many users of the medication wear a medical alert bracelet
  
• Other agents producing disulfiram-like reactions:
  
  • Antibiotics:
    
    • Metronidazole
      
    • Cephalosporins (with nMTT side chain)
      
      • Cefoperazone, Cefotetan, Cefmetazole
        
    • Nitrofurantoin
      
  • Oral hypoglycemics:
    
    • Sulfonylureas
      
  • Industrial agents:
    
    • Carbon disulfide
      
    • Hydrogen sulfide
      
  • Mushrooms:
    
    • Coprinus atramentarius
      
    • Clitocybe clavipes
      

DIAGNOSIS

• Disulfiram–ethanol reaction:
  
  • Hypotension, tachycardia, tachypnea
    
  • Flushing of face, neck, torso
    
  • Pruritus, diaphoresis, sensation of warmth
    
  • Nausea, vomiting, abdominal pain, diarrhea
    
  • Headache, ataxia, confusion, anxiety, dizziness
    
  • Dyspnea, pulmonary edema, chest pain, dysrhythmias, myocardial infarction
    
• Disulfiram overdose:
  
  • Symptoms rare with <3 g ingested
    
  • 10–30 g may be lethal
    
  • May mimic shock and/or sepsis
    
  • Tachycardia, hypotension, tachypnea
    
  • Abdominal pain, diarrhea, garlic, or rotten-egg breath
    
  • Agitation, irritability, ataxia
    
  • Dysarthria, hallucinations
    
  • Lethargy, coma, seizures, flaccidity
    
  • Parkinsonism
    

Ingestion of disulfiram or agents listed above may provide essential clues to diagnosis

• Vital signs:
  
  • Hypotensive, tachycardic, tachypneic
    
• Cardiovascular:
  
  • Tachycardia, arrhythmias
    
• Pulmonary:
  
  • Pulmonary edema, dyspnea
    
• Abdominal:
  
  • Diffuse abdominal pain, nausea, vomiting
    
• Skin:
  
  • Flushed, diaphoretic
    
• Neurologic:
  
  • Dysphoria, confusion, signs of cerebellar dysfunction, seizures
    

Suspect disulfiram–ethanol reaction with the following:

• Typical signs and symptoms are present
  
• Treatment for chronic ethanol abuse in conjunction with recent ethanol ingestion, or exposure to ethanol-containing foods or medications, including mouthwash
  

• Ethanol level
  
• Electrolytes, BUN, creatinine, and glucose
  
• Liver function tests if hepatitis is suspected
  
• Creatine phosphokinase (CPK) if considering rhabdomyolysis in light of seizures or agitation
  
• Urinalysis (myoglobin)
  
• Serum levels of offending agent are NOT clinically useful
  

• ECG to assess cardiac ischemia or dysrhythmia
  
• CT scan or MRI:
  
  • Indicated with altered mental status/seizure
    
  • Basal ganglia ischemia and infarction have been reported
    
• EEG:
  
  • Diffuse slowing without focal abnormalities has been seen in cases of acute toxicity with coma
    

• Sepsis
  
• Meningitis, encephalitis
  
• Cardiogenic shock secondary to acute coronary syndrome
  
• Anaphylactoid/anaphylactic reaction
  
• Gastroenteritis/pancreatitis with dehydration
  
• Ethanol withdrawal
  

• Acute poisonings yield mainly severe CNS toxicity
  
• Ataxia, weakness, lethargy, seizures
  
• Reye syndrome-like encephalopathy in severe cases
  
• Adult symptoms may also be present
  

TREATMENT