Rosen & Barkin's 5-Minute Emergency Medicine Consult (731 page)

FOLLOW-UP

All patients

• Typical treatment for nongonococcal urethritis (e.g., azithromycin, doxycycline) does not treat T. vaginalis.
  
• Vaginitis in females not responding to treatment for bacterial vaginosis might be due to Trichomonas infection.
  
• Nongonococcal urethritis in males not responding to azithromycin or doxycycline might be due to Trichomonas.
  

• Centers for Disease Control and Prevention. 2011 Sexually transmitted diseases surveillance. Available at
  http://www.cdc.gov/std/stats11/other.htm#trich
  .
  
• Greer L, Wendel GD Jr. Rapid diagnostic methods in sexually transmitted infections.
  Infect Dis Clin North Am.
  2008;22:601–617.
  
• Sutton M, Sternberg M, Koumans EH, et al. The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001–2004.
  Clin Infect Dis
  . 2007;45:1319–1326.
  
• Wendel KA, Workowski KA. Trichomoniasis: Challenges to appropriate management.
  Clin Infect Dis.
  2007;44:S123–S129.
  
• Workowski KA, Berman S; Center for Disease Control and Prevention (CDC). Sexually transmitted diseases treatment guidelines, 2010.
  MMWR Recomm Rep
  . 2010;59(RR-12):1–110.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Gonococcal Disease
  
• Pelvic Inflammatory Disease
  
• Urethritis
  
• Vaginal Discharge/Vaginitis
  

CODES

• 131.01 Trichomonal vulvovaginitis
  
• 131.02 Trichomonal urethritis
  
• 131.9 Trichomoniasis, unspecified
  

BASICS

• Primary mechanism of tricyclic antidepressant (TCA) toxicity:
  
  • Sodium channel blocking effect (quinidine-like effect)
    
  • Inhibition of norepinephrine reuptake
    
  • α-blockade
    
  • Anticholinergic effect
    
• Selective serotonin reuptake inhibitors (SSRIs):
  
  • Wider margin of safety than TCA
    
  • Less CNS/cardiovascular toxicity
    
• Nonselective serotonin reuptake inhibitors:
  
  • Serotonin and norepinephrine reuptake inhibitors (SNRIs)
    
  • Can cause cardiac dysrhythmias or seizures
    
  • Venlafaxine (Effexor)
    
  • See “Antidepressants, Poisoning.”
    

• TCAs:
  
  • Amitriptyline
    
  • Nortriptyline
    
  • Imipramine
    
  • Doxepin
    
• Newer-generation antidepressants (nontricyclic):
  
  • Have different toxic profile than TCAs
    
  • See “Antidepressants, Poisoning.”
    
• Rapid deterioration may occur.
  

DIAGNOSIS

• Rapid deterioration may occur.
  
• Classic TCA compounds (imipramine, amitriptyline, nortriptyline)—greatest cardiovascular toxicity
  
• Newer agents (serotonergic agents)—less overall toxicity in overdose
  
• CNS:
  
  • Stimulation or depression
    
  • Stimulation:
    
    • Tremulousness
      
    • Agitation
      
    • Fasciculation
      
    • Seizures (resulting acidemia may lead to worsening cardiovascular toxicity)
      
  • Depression:
    
    • Drowsiness
      
    • Lethargy
      
    • Coma
      
• Cardiovascular system:
  
  • Hypotension
    
  • Tachycardia:
    
    • Early; owing to blockade of norepinephrine reuptake and anticholinergic effects
      
  • Bradycardia:
    
    • Late; owing to catecholamine depletion state
      
  • ECG changes:
    
    • QRS widening (>100–120 ms)
      
    • Rightward shift in terminal 40 ms in frontal plane axis (R wave >3 mm in aVR)
      
  • Dysrhythmias:
    
    • Supraventricular tachycardia (SVT)
      
    • Ventricular arrhythmias
      
• Anticholinergic effects (less common):
  
  • Dilated pupils
    
  • Decreased bowel sounds
    
  • Urinary retention
    

Substance ingestion in patient with access to TCA

• CNS:
  
  • Stimulation or depression
    
• Cardiovascular:
  
  • Tachycardia
    
  • Mydriasis or midrange pupils
    
  • Decreased bowel sounds
    
  • Urinary retention (rare)
    

• ECG: Factors associated with TCA poisoning:
  
  • Sinus tachycardia (almost always present at some time after poisoning)
    
  • QRS widening:
    
    • >100 ms associated with seizure
      
    • >160 ms associated with ventricular dysrhythmia
      
  • QT prolongation
    
  • PR prolongation
    
  • Rightward shifting of terminal 40 ms QRS axis
    
  • R-wave amplitude in aVR >3 mm
    
• Continuous cardiac monitor
  

• CBC
  
• Electrolytes, BUN, creatinine, glucose
  
• ABG
  
• Urine toxicology screen:
  
  • Rule out other toxins.
    
• TCA levels:
  
  • Not useful
    
  • Do not correlate well with degree of toxicity
    
  • Qualitative screen appropriate to confirm ingestion if necessary
    

Chest radiograph for aspiration pneumonia/pulmonary edema

• Drugs that cause coma:
  
  • Alcohols
    
  • Alcohol withdrawal
    
  • Anticholinergics
    
  • Lithium
    
  • Phencyclidine (PCP)
    
  • Opioids
    
  • Phenothiazines
    
  • Sedative hypnotics
    
  • Salicylates
    
• Cardiotoxic drugs:
  
  • Antidysrhythmics (category IA)
    
  • Digoxin toxicity
    
  • Sympathomimetics
    
  • Anticholinergics
    
• Drugs that cause seizures:
  
  • Alcohol withdrawal
    
  • Anticholinergics
    
  • Camphor
    
  • Isoniazid
    
  • Lindane
    
  • Lithium
    
  • Phenothiazines
    
  • Sympathomimetics
    
  • Toxic alcohols
    

TREATMENT

• Do not be lulled into false sense of security with well-appearing patient:
  
  • Rapid onset of altered mental status, seizures, and dysrhythmias occur.
    
• Perform endotracheal intubation if any evidence of compromise.
  
• Secure IV access.
  
• Administer sodium bicarbonate if any evidence of QRS widening (>100–120 ms):
  
  • 1 ampule in adults
    
  • 1–2 mEq/kg in children
    
• Ipecac contraindicated (risk for aspiration with development of depressed mental status or seizure)