Alcoholic Emergencies

That Drunk May Be More Than Just Drunk

by Adam Thompson, EMT-P

In prehospital emergency care, it is not uncommon to come across an intoxicated patient from time to time. We usually look at our partner with a smug and I've-had-enough manor and just say "E-T-O-H". EtOH stands for ethanol, which is a medical way for us to say alcohol without the patient thinking we are judgmental--even though we are. These patients may be the nicest patients or the meanest. They may say things to you that might make you want to send them from a standing to supine position. You may even want to do worse. Put the 16 gauge IV catheter away and empty that syringe you have filled with succs--I know it's tempting.

These patients are actually presenting with a form of altered mental status that we are writing off as drunk guy. You probably check a sugar on these patients because your EMT or paramedic instructor explained to you the common misdiagnosis of ketones for alcohol, and they may even teach this in online medical coding courses. So you try to rule out a diabetic in DKA even though you see two empty bottles of Jim Beam on the nightstand. You are also probably aware of the need for Thiamine with the administration of dextrose to these patients. Even though this patient might not be in DKA or hypoglycemic, he may be having a medical emergency.

Myth: Alcohol on the breath smells similar to ketones
Truth: Those are ketones

Drinking alcohol leads to a production of ketones through an oxidation process and you emit the fragrance of ketones.

It is often that chronic alcoholics will supplement food for alcohol. When they do this, they are subsequently getting all of their nutrition from the alcohol and the fats in their own body. Similar to a diabetic in DKA, these patients will go into a state of ketosis to get their body some energy. Ketosis is the state in which lipids (fats) are broken down for fuel. Ketones are produced. Those ketones are acidic, and that is where we get that lovely term ketoacidosis. These patients are suffering from a malnourished emergency, and should be treated accordingly.

Wernicke's Encephalopathy

Encephalopathy = Brain damage

Thiamine (vitamin b1) deficiency can lead to a condition known as Wernicke's Encephalopathy. This condition is characterized by ataxia, ophthalmoplegia, confusion, and impairment of short-term memory.

Ataxia - Gross lack of coordination of muscle movements. You know, like a drunk stumbling around.

Ophthalmoplegia - Paralysis of one or more of the extraocular muscles which are responsible for eye movement. Have your patient look left, then right.

When Wernicke's encephalopathy is accompanied by Korsakoff's syndrome, it is referred to as Wernicke-Korsakoff's Syndrome.

eMedicine [link]
Studies suggest that up to 80% of patients with Wernicke encephalopathy may not be diagnosed, which makes estimates of mortality rates unreliable. Wernicke encephalopathy is a significantly disabling and potentially lethal condition that can be prevented or reversed if treated early. Established Wernicke encephalopathy can have major long-term consequences among patients requiring permanent institutional care.
Other Possible Signs & Symptoms:
  • Hypothermia
  • Weakness
  • Foot droop
  • Decreased proprioception
  • Nausea/Vomiting
  • Abdominal pain
  • Hypotension
  • Coma
Possible Causes:
  • Prolonged alcohol abuse
  • AIDS
  • Hemodialysis
  • Infection
  • Starvation
Treatment = Thiamine and fluid replenishment

Pubmed [Link 1]
Wernicke encephalopathy is caused by thiamine deficiency in the central nervous system, and is defined by the triad of confusional symptoms, ocular alterations and ataxia. Some other factors may also predispose alcoholic patients to this deficiency. We report two patients with hyperglicaemia and ketoacidosis due to diabetes mellitus decompensation and chronic alcoholism who developed Wernicke encephalopathy before their hospital admission. The outcome was successful after intravenous thiamine administration and insulinotherapy. The presence of Wernicke encephalopathy in alcoholics with diabetic ketoacidosis, suggests that metabolic decompensation is essential in the onset of the disease.

Pubmed [Link 2]
BACKGROUND AND PURPOSE: Wernicke encephalopathy is a severe neurologic disorder that results from a dietary vitamin B1 deficiency. It is characterized by changes in consciousness, ocular abnormalities, and ataxia. This study was undertaken to analyze and compare findings on MR imaging and neurologic symptoms at clinical presentations of patients with Wernicke encephalopathy with and without a history of alcohol abuse. MATERIALS AND METHODS: A multicenter study group retrospectively reviewed MR brain imaging findings, clinical histories, and presentations of 26 patients (14 female, 12 male) diagnosed between 1999 and 2006 with Wernicke encephalopathy. The age range was 6-81 years (mean age, 46 .6+/-19 years). RESULTS: Fifty percent of the patients had a history of alcohol abuse, and 50% had no history of alcohol abuse. Eighty percent showed changes in consciousness, 77% had ocular symptoms, and 54% had ataxia. Only 38% of the patients showed the classic triad of the disease at clinical presentation. At MR examination, 85% of the patients showed symmetric lesions in the medial thalami and the periventricular region of the third ventricle, 65% in the periaqueductal area, 58% in the mamillary bodies, 38% in the tectal plate, and 8% in the dorsal medulla. Contrast enhancement of the mamillary bodies was statistically positively correlated with the alcohol abuse group. CONCLUSIONS: Our study confirms the usefulness of MR in reaching a prompt diagnosis of Wernicke encephalopathy to avoid irreversible damage to brain tissue. Contrast enhancement in the mamillary bodies is a typical finding of the disease in the alcoholic population.

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