ALCOHOLS

 

ETHANOL 

Few rules:

  • If  the pt is a "frequent flyer" alcoholic, do not get comfortable, see if labs were drawn last week  and if not, get routine lytes + Mg, Ca.
     
  • On a known alcoholic, checking ETOH level may put you occasionally in an awkward position.  You can't dc pt with ETOH level above the legal limit, yet waiting for the level to be in legal range puts pt in risk of developing DT which is a medical emergency, especially if pt was dc and didn't have a chance to "retank" him/herself with alcohol. The best way is to wait for pt to wake up and if AAOx3 and not ataxic, dc to his/her environment.

Pathophysiology:

  • ETOH is metabolized by alcoholdehydrogenase to acetaldehyde that in turn is metabolized to acetate by aldehydehydrogenase. Acetate is finally broken to CO2 and H2O in TCA cycle.  Along its various metabolic steps, ETOH metabolism requires Thiamine as a cofactor and this depletes rapidly.

S & S:

  • Classically pt  acts intoxicated, i.e. slurred speech, ataxia, disinhibited behavior. Not all intoxicated pts have to have high alcohol level. Some show aggressive, disinhibited behavior after ingesting only  small, legal amount of alcohol. This is known as -Idiosyncratic alcohol toxicity.
     
  • Naïve drinker metabolizes alcohol at 15-20 mg/dL/hr while seasoned drinker  - 30-35 mg/dL/hr. This is zero order kinetics and guides health care provider as to time needed for pt to be sober and ready for dc.

 Treatment

  • of ETOH intoxicated pt c/o IVF "banana bag"(contains MVi), Thiamin 100 mg IM x 1 prn. H2-blocker (e.g. famotidine 20 mg IV or ranitidine 150 mg IV) can be given to  chronic alcoholic and, if severe N/V are present, prochlorperazine or other anti-emetic should be  administered to avoid  Mallory-Weiss tear.

 Complications in the ER:

  1. 1) AKA
     
    • Alcoholic ketoacidosis develops 2ry to starvation that promotes metabolism of FFA.  Ketone bodies form and pt develops anion gap acidosis. Glucose level < 300 mg/dL and no ETOH consumption for 24-72 hrs, differentiates this entity  from DKA.
       
  2. 2) WD/Etc.
     -
    • W/D-can occur within hrs after sobriety and c/o tremor, HR, diaphoresis, BP, +/- SZ.
       
    • DT- (see also "Neurology" chapter) can occur in 48-100 hrs. Symptoms as above in addition to wax and wane MS.
       
    • Rum fit - (see "Neurology" chapter) are grand mal seizures that develop 8-48 hrs after WD from ETOH.
       
    • ETOH w/d hallucinosis - pt develops this entity  within 48 hrs of abstinence. Pt does not manifest other  S&S of w/d and the only symptoms are auditory hallucinations. Wernicke and Korsakoff must be considered in differential.
       
  3. Wernicke- see "Neurology" chapter
     
  4. Beriberi
     
    • Is considered high output cardiac failure. Initially described in Chinese nobleman, the Mandarin, who would consume  rice after peeling it. The peel, being rich in vit B1 (thiamine), would cause B1 depletion and the consequent Beriberi. Pts develop cardiomyopathy (edema, effusion, tachycardia),  neurodeficit (degeneration to posterior columns, paresthesias, burning feet at night, cramps to calves, Wernicke's). Treatment c/w Thiamine 100 mg.
       
  5. Subdural hemorrhage- see "Trauma" chapter.

 

 

ETHYLENE  GLYCOL:

Etiology:

  • Found in antifreeze, coolants, paints, detergents and other chemical/ pharmaceuticals. Absorbed orally.

Pathophysiology:

  • When metabolized it produces toxic substances (glycoaldehyde, glycolate, oxalate) that in turn interfere with  oxidation at mitochondria level and give AG acidosis.  Many of  EgOH steps are metabolized by same enzymes as EtOH. Oxalate compounds can precipitate at the level of kidney in form of CaOxalate and cause both Hypocalcemia (QT >) and kidney damage (RBC, proteinuria, and envelope- and/or needle-shaped birefringent crystals on UA).

S&S:

  1. CNS - symptoms develop in 1-8 hrs and can manifest with any of  neurological symptoms (intoxication, coma, ataxia, hallucination, ocular nerve paralysis). It is speculated to be 2ry  to CaOxalate deposition in the brain and 2ry to ­ AG acidosis and ­ Osmolality.
     
  2. CV - occurs 12-48 hrs after ingestion and manifests with  tachycardia/
    tachypnea/CHF, QT> 2ry to     ¯ Ca. AG acidosis contributes to toxicity.
     
  3. ARF - occurs 24-72 hrs after ingestion. It is 2ry to CaOxalate precipitation and consequent ATN.

DX:

  1. ­Osmolar gap, ­ AG acidosis, no ketosis,  ­EgOH (hard to perform).  Osmolality is calculated by following formula:

                2(Na) + Glu/18 + Bun/2.8 + EgOH/4.3
     
  2. EKG (may show  > QT) and ¯ Ca are helpful in establishing the diagnosis.
     
  3. UA may not show any changes if pt presents prior to onset of RF. If pt ingested EgOH from antifreeze, urine will be fluorescent on Wood's lamp exam.
    Note! Osmolar  gap is present also in AKA and DKA but is generally  < 20 vs. >20 in case of EgOH and/or MetOH.

Treatment:

  1. Correct the AG with HCO3 and low Ca is corrected with CaCl.
     
  2. B6 (100 mg IV) and B1 (100 mg IV) are given since they promote EgOH detoxification.
     
  3. EtOH is given when EgOH intoxication is suspected .The dose is 10 ml/kg the loading dose  followed by 1.5 mg/kg/hr and maintained at serum alcohol  level of 100-150 mg/dL. Same treatment is for MetOH (see below)
     
  4. Hemodialysis is indicated when EgOH is >25-50 mg/dL, liver failure, CV manifestations, RF, acidosis.  Both  in case of  EgOH and MetOH,  EtOH infusion must be doubled during HD to keep it at 100-150 mg/dL level.

ISOPROPANOL:

  • Found in rubbing alcohol. Absorbed by GI and lungs. Metabolized by same enzymes as EtOH to acetone that is responsible for:
     
    1) CNS - intoxication, lethargy, coma 
    2)GI - N/V, abdo pain, GI bleed (hemorrhagic gastritis)
    3)CV -    ¯ BP, tachycardia.

S&S:

  • CNS (confusion), GI (N/V) and CV (tachycardia) symptoms may be prolonged since the T1/2 of  acetone is 30 hr. Symptoms are very similar to  intoxication/inebriation.

DX:

  • Isopropanol is suspected in a hard-core alcoholic when pt presents with prolonged           symptoms, (-)ve serum EtOH level, ­ Osmolar gap, (-)ve acidosis, (+) ketosis (ketonemia, ketonuria). Osmolality is calculated by following :
            
                        2(Na)+ Glu/18+Bun/2.8+IpOH/5.9

    and the value obtained is subtracted from measured osmolality to detect the "gap".

Treatment:

  • Supportive treatment and HD is suggested only if pt shows severe hemodynamic compromise or extremely high levels of  IpOH.

 

METHANOL:

  • Found in  paint solvent, sterno.
     
  • Can cause toxicity from GI, skin and respiratory route.
     
  • Metabolized into formaldehyde and formate by same enzymes implicated in ETOH metabolism. Formate is responsible for AG acidosis since it blocks cellular oxidation at the mitochondria level. Formate is also responsible for  visual changes due to its accumulation in optic nerve.

S&S:

  • can occur  within 1-48 hr. and present with intoxication/AMS/lethargy or normal mental state,
     
  • blurry vision and/or snowstorm vision, photophobia.
     
  • N/V and abdo pain are described and occur  2ry to acidosis, gastritis and pancreatitis (in combination or separately).

DX is established by demonstrating:

  •     ­ MetOH, ­Osmolar Gap,­ AG and no ketosis . Osmolality is calculated by :
    2(Na)+Gluc/18+BUN/2.8+MetOH/2.6.
     
    The value obtained from this formula  (calculated) is subtracted from the value given by lab report (measured). If the difference is > 10 mOsm/L (generally >20), methanol toxicity is likely in proper clinical setting.

Treatment:

  • Standard decontamination techniques (lavage)
     
  • HCO3 if severe acidosis,
     
  • Folic acid (1mg/kg up-to 50 mg IV and then the same dose q 4 hr x 24 hr.). This increases the metabolism of  formate.
     
  • Since ETOH has affinity to same enzymes that metabolize methanol, administration of this will prevent further formate formation. The loading dose of EtOH is 10 ml/kg of 10% EtOH IV over 30-60 min.  Then maintenance dose is given that varies from 0.8 ml/kg/hr for naïve drinker and double that amount  for chronic alcoholic. Yet the best approach is by monitoring serum ETOH level that must be kept  at 100-150mg/dL. Glucose and B1 should be given and FS must be performed during EtOH infusion.
     
  • Hemodialysis (HD) is reserved for MetOH level  of  25-50mg/dL, liver  failure, severe MS changes. EtOH infusion  rate must be doubled during Hd.

[BACK]