HPI

• 37 yo female with no medical history complains of one week of nonbloody intermittent vomiting
• She notes intermittent "electric shock" sensations down her arms into her hands
• She complains of tremors in her hands
• She notes gradual onset of yellowing of her sclera 
• Denies abdominal pain, fevers, diarrhea, urinary symptoms

Exam

Vitals: T 99.1 BP 144/120 HR 91 RR 20 Pox 100% on RA

• Appears agitated and tremulous
• HEENT: +scleral icterus
• Cardiac: no murmurs
• Pulm: Lungs clear
• Abd: Soft, nontender, +hepatomegaly
• Extrem: no edema
• Neuro: +resting tremor in hands

Pmhx:

• Denies medical history
• She does report taking an unknown medication for unclear psychiatric diagnosis in the past but not for several months

Social:

• Denies recreational drug use
• +heavy ETOH use daily last use within 24 hrs

Initial Differential Diagnosis

• ETOH withdrawal: +reported ETOH use with tremors, vomiting, elevated BP
• Acute hepatitis: new jaundice suggestive of viral or ETOH induced hepatitis or possible overdose of hepatotoxic medication 

Workup and Management

• IV access, cardiac monitor
• NS bolus 1 L
• FSBS: 101
• Chem basic, CBC. liver profile, acute hepatitis panel

Lab Results:

Lab intepretation:

• hypokalemia
• pancytopenia with macrocytic anemia
• elevated transaminases and bilirubin
• Overall picture suggestive of chronic ETOH abuse and alcohol induced pancreatitis

Case progression:

• Pt monitor shows this rhythm:

• Pt is found to be pulseless
• Rhythm is identified as polymorphic ventricular tachycardia: torsades de pointes
• Pt defibrillated at 200 J with return of spontaneous circulation, she regains consciousness and is at baseline mental status
• A subsequent ECG shows:

• QTc = 562 ms

Diagnosis and Management

• Prolonged QT from hypokalemia/hypocalcemia/hypomagnesemia from severe vomiting/malnutrition
• Acute alcoholic hepatitis
• Acute ETOH withdrawal
• Patient immediately treated with 4g IV magnesium, 2g calcium gluconate and 40 meq IV potassium chloride
• Admitted to intensive care unit for continued electrolyte replacement and monitoring
• 2 subsequent episodes of pulseless polymorphic VT treated with defibrillation
• She is started on a lidocaine infusion to shorten Qtc and considered for a transvenous pacemaker to attempt overdrive pacing
• Patient subsequently became agitated with visual hallucinatinons and had a brief seizure thought likely due to delerium tremens: treated with phenobarbital
• QT gradually decreases to 500 ms as electrolytes replaced

Learning Points

• Consider prolonged QTc in any patient who presents with vomiting and obtain an ECG early
• This is especially common in patients with alchohol abuse who are often malnourished 
• Treat markedly prolonged Qtc with aggressive intravenous replacement of potassium, magnesium, and calcium
• Consider isoproterenol to increase the HR which will shorten the QTc
• Consider overdrive pacing for unstable patients: placement of a transvenous pacemaker to artificially increase HR to shorten the QTc
• Treat unstable torsades as for unstable VT, with cardioversion for patients with a pulse and defibrillation in the absence of a pulse