Drunk people – They are out to get to you

Abe Markin

Dec 2014 TBL

Outline

• Physiology • They’re out to get you • Management of intoxication in ED

– ABCs etc. – Do you have to check BAC? – Alcoholic Ketoacidosis

• Wernicke’s • Korsakoff’s • 4 Phases of withdrawal • Holiday Heart

Physiology

• Absorbed primarily in stomach (70%) and duodenum (25%)

• Distributed evenly throughout all organ systems

• Traditionally thought to be zero order kinetics

• First order kinetics for high levels, especially in heavy drinkers – 10% in gastric mucosa (first pass) – Remaining 90% in liver – Inducible CYP-450 enzymes in microsomal

ethanol oxidizing system (MEOS; 8–10%) – Catalase (0–2%)

• Respiratory depression, decreased airway responsiveness cause death

Rosen’s 7th Edition; Vonghia et al. (Eur J Intern Med, 2008)

How Drunks Might Get You

• Other causes of AMS – Other toxins (toxic alcohols, benzos) – Head bleed – Infection (meningitis, sepsis), – Metabolic disturbances (AKA, DKA, hypoglycemia,

hyponatremia, hepatic encephalopathy, uremia, hypoxia/CO2 narcosis)

– Seizures (post-ictal / status) – Withdrawal syndromes

• Missed injuries – Orthopedic, – C-spine – Intra-abdominal

• Vomiting while supine in 4 points

All drunks deserve…

• ABC, fluids, nutrition, consider withdrawal

• Benzos if needed

• Volume depletion – Give IVF (D5 0.9 NS)

• Nutrition – D5/food (No glycogen stores)

– Thiamine (100mg)

– Electrolytes: replace magnesium (1-2g/0-60min), potassium

– MVI

Slovis. (AAEM, 2007); Li et al. (Am J Emerg Med, 2008)

Should we get a BAC?

• Rosen: “Discharge (after excluding significant abnormal laboratory values or suspected head injury) can be considered when a patient is clinically sober and able to dress, walk, and function independently.”

• Tintinalli: “Patients with no other medical reason for admission may be discharged when their clinical intoxication has resolved to the extent that they do not constitute a danger to themselves or others. Clinical judgment should be used in deciding whether a patient is sober enough to discharge. As discussed above in Pathophysiology, intoxication does not correlate well with blood ethanol level in any given patient because there is such a wide range of tolerance.”

• UTD: “…disposition of these patients should not be based solely on the measured (or calculated) serum alcohol concentration. Patients with mild intoxication can be safely discharged when no longer clinically intoxicated and deemed by the clinician to be no danger to themselves or others.”

• Rate of clearance ranges from 9 - 36 mg/dL/hr • Assume 20 mg/dL/hr in intoxicated ED pt per Rosen’s

Rosen's Emergency Medicine; Tintinalli’s Emergency Medicine; Uptodate.com

Should we get a BAC?

• Recent legal precedent – Kowalski v. St. Francis Hospital and Health Centers

• Hospital has no right, and therefore no duty to restrain this person

• But… – NY, not MI

– Pt came in voluntarily, then pulled out IV and snuck out

Should we get a BAC?

True value is as a red flag if surprisingly low

and as a reason to keep psych pts who have rescinded their story

Hammond KB, Rumack BH, Rodgerson DO. "Blood ethanol: a report of unusually high levels in a living patient." JAMA 226.1 (1973): 63-64.

Johnson RA, Noll EC, Rodney WM. Survival after a serum ethanol concentration of 1 1/2%. Lancet 1982;2:1394.

Spontaneous bladder rupture

Parker H et al. Spontaneous bladder rupture in association with alcoholic binge: a case report and review of the literature. J Emerg Med 37.4 (2009): 386-389.

Alcoholic ketoacidosis: Features

• Occurs in malnourished drinkers, esp after 1-3 days of abstinence, vomiting, poor PO

• Features: – N/V, abdominal pain, tachypnea – Serum glucose usually < 200 – Ketones/BOHB present – 15% may have concomitant met alkalosis from vomiting, volume depletion

• Requires: – Dehydration – Low glycogen stores – No available carbohydrate – No available alcohol – A precipitating event

• Pathophys – Exact mechanism unknown – Acute on chronic starvation – Release of alcohol-induced block in ketogenesis – Increased NADH/NAD ratio predisposes to BOHB production and impairs

metabolism of lactate

Rosen’s Emergency Medicine, Medscape.com, Slovis (AAEM, 2007)

Alcoholic ketoacidosis: Differential

• DKA, starvation ketoacidosis

• Ethylene glycol, other toxic alcohols

• Renal failure

• Sepsis

Alcoholic ketoacidosis: Treatment

• Fluids • Carbohydrate (IV glucose) • Vitamins, minerals • K, Mg • Identify and treat underlying cause

• Slovis Pearls

– No role for bicarbonate Unless pH <7.0, then r/o other causes of acidosis – No role for insulin in AKA

Even with hyperglycemia unless glucose >500 – Follow K, phos, pH – If pH falls once treatment has begun, this is NOT just AKA! – If serum phosphorus falls to below 1.5 - 1: Give 1/4 of potassium requirement as K2PO4

Wernicke’s Encephalopathy

• Thiamine deficiency present in 80% of alcoholics. • Wernicke’s develops in 12.5% • Classic triad of ataxia, encephalopathy, oculomotor disturbance

– May also have coma, miosis, hypothermia, hypotension, bradycardia

• Develops over hours to days • Reversible, with resolution of MRI changes in 7 days • 5 groups at risk

– Alcoholics, anorexia nervosa, hyperemesis gravidarum, malabsorption syndrome, chronic severe malnutrition

– Don’t look for triad. Give thiamine based on risk factors

• 10-20% case fatality, 80% of survivors develop Korsakoff’s • 100mg IV, 100mg PO QD x3d for possible case. Definite dx requires

higher doses

Agabio R. Thiamine administration in alcohol-dependent patients. Alcohol Alcohol. 40.2 (2005): 155-156. Martin, Singleton, Hiller–Sturmhöfel. The Role of Thiamine Deficiency in Alcoholic Brain Disease. http://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm

Shrinkage

Korsakoff’s Psychosis

• “Alcohol amnestic disorder”

• 13% of alcoholics at autopsy, 1 in 5 had prior dx

• Behavioral abnormalities, memory impairment, disorientation, confabulation

• Anterograde > retrograde amnesia

• "The Lost Mariner”

• Cerebellar degeneration distinct, more common (40% at autopsy)

Harper C. J Neuropathol Exp Neurol 57:101–110, 1998. Harper C, Rodriguez M, Gold J, Perdices M. Med J Aust 149:718–720, 1988.

The “French Paradox”

The “French Paradox”

The “French Paradox”

Withdrawal – 4 phases

• Tremulousness – 6-12 hrs post-cessation

• Seizures – 1-2 days

• Hallucinosis – 1-2 days – hallucinosis and Sz temporal overlap – up to 25% of drinkers who withdraw – usu. Visual – Auditory less likely to progress to DTs – Rx: benzos +/- haldol

• DTs – previously common, now very rare

Slovis C. Alcoholic Emergencies. AAEM. March 2007

Tremulousness

• Most frequent

• Hypersympathetic state like hyperthyroidism, cocaine intoxication, panic attack

• +/- N&V

• Choice of benzo: valium, ativan, versed. – Valium is longer acting, cannot be given IM

(erratic absorption, not water soluble)

• Don’t use beta blockers, benzos for tachycardia, hypertension, etc.

Rapid ED Benzodiazepine Titration

Valium Ativan 5 mgs IV 1 mg IV repeat 5 mgs IV in 5-10 min repeat 1 mg in 5-10 min if still agitated if still agitated wait 5-10 min wait 5-10 min 10 mgs IV 2 mgs IV repeat 10 mgs IV in 5 – 10 min repeat 2 mgs IV in 5-10 min if still agitated if still agitated wait 5 – 10 min wait 5 – 10 min 20 mgs IV 4 mgs IV repeat 20 mgs IV in 5 – 10 min repeat 4 mgs IV in 5-10 min if still agitated if still agitated 20 mgs IV Q 5-10 min 4 mgs IV Q 5-10 min until VS stable and patient calm until VS stable and patient calm

American Society of Addiction Medicine. Arch In Med. 2004. 164:1405-1412. via Slovis’ EM:RAP

• may use Haldol 5 mg IV/IM early in therapy for especially violent, mean or agitated patients • After 60 – 90 minutes of therapy in benzodiazepine refractory patients consider Propofol 25 mg/min slowly titrated to patients symptoms

Hallucinations

• Up to 10% of EtOH withdrawal pts

• 10-30 hrs after last drink

• Visual > auditory, olfactory or tactile

• Insomnia, hyperactivity

Seizures (Rum Fits)

• 6-48 hrs post-cessation

• Usually self-limited, generalized tonic-clonic, non-focal, non-status

• 6% intracranial problem. CT ‘em all.

• Status- ABCs NGT, benzo titration, start barbiturate, etomidate, or propofol

• Don’t give Dilantin unless some other cause

Earnest M, Feldman H, Marx J, et al. Intracranial lesions shown by CT scans in 259 cases of first alcohol related seizures. Neurology. 1988;38:1561-1565.

Delirium Tremens

• Abstinence day 3-5 • Medical emergency requiring ICU care • Features

– Hypertension, tachycardia, hyperventilation, hyperthermia

• Another time they’re out to get you – r/o PNA, GIB, hypoglycemia, other toxins/ metabolic causes,

meningitis/sepsis, head bleed

• If present in DTs: – Hypotension = dehydration – Bradycardia = overmedicated; elevated ICP – Hypoventilation = overmedicated; elevated ICP – Hypothermia = sepsis, CNS trauma, Wernicke's

• Mortality from oversedation, electrolyte abnormalities

Holiday Heart

• In 1978 Philip Ettinger described "Holiday heart syndrome"

• New ventricular and atrial tachyarrhythmia (esp. A fib) in non-alcoholics after acute ingestion

• Usu. presents w/ palpitations, precordial pressure or pain, syncope, and dyspnea

Tonelo, Providência, & Gonçalves. (Arquivos Brasileiros de Cardiologia, 2013)

Holiday Heart: Proposed Mechanisms

Lean

AKA: Sizzurp, syrup, purple drank, drank, barre, purple jelly, Texas tea, and Tsikuni. Double cup.

They say don't drink and sip that lean but I mix em up Turnt up to the max, real ratchet s*** - “Codeine cups” by Juicy Jay

A Cure for Drunk?

• Metadoxine: – Pyrrolidone carboxilate

and pyridoxine

– RCT showing single dose 900mg IV significantly faster sobriety • decreased the half-life of

ethanol in blood (from 6.70 +/- 1.84 to 5.41 +/- 1.99 hr; p < 0.013)

• Median recovery 56 min vs 2hr 20 min

Shpilenia LS et al. Meta- doxine in acute alcohol intoxication: a double-blind, randomized, placebo-controlled study. Alcohol Clin Esp Res 2002;26:340–6.

Thank you!

References

• Li, Siu Fai, et al. "Vitamin deficiencies in acutely intoxicated patients in the ED."The American journal of emergency medicine 26.7 (2008): 792-795.

• Vonghia, Luisa, et al. "Acute alcohol intoxication." European Journal of Internal Medicine 19.8 (2008): 561-567.

• World Health Organization. "Alcohol and injury in emergency departments: summary of the report from the WHO Collaborative Study on Alcohol and Injuries." (2007).

• Parker H et al. Spontaneous bladder rupture in association with alcoholic binge: a case report and review of the literature. J Emerg Med 37.4 (2009): 386-389.

• Johnson RA, Noll EC, Rodney WM. Survival after a serum ethanol concentration of 11⁄2%. Lancet 1982;2:1394.

• Godbout, Brandon J., et al. "Yield of head CT in the alcohol-intoxicated patient in the emergency department." Emergency radiology 18.5 (2011): 381-384.

• Hammond, Keith B., Barry H. Rumack, and Denis O. Rodgerson. "Blood ethanol: a report of unusually high levels in a living patient." JAMA 226.1 (1973): 63-64.

• McGuire, L. C., A. M. Cruickshank, and P. T. Munro. "Alcoholic ketoacidosis."Emergency medicine journal 23.6 (2006): 417-420.

• Mayo-Smith, Michael F., et al. "Management of alcohol withdrawal delirium: an evidence-based practice guideline." Archives of internal medicine 164.13 (2004): 1405-1412.

References

• Chikritzhs TN et al. Mortality and life-years lost due to alcohol: a comparison of acute and chronic causes. Med J Aust 2001;174:281–4.

• Martin, Singleton, Hiller–Sturmhöfel. The Role of Thiamine Deficiency in Alcoholic Brain Disease. http://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm

• Weathermon, Ron, and David W. Crabb. "Alcohol and medication interactions."Alcohol Res Health 23.1 (1998): 40-54.

• Agabio, Roberta. "Thiamine administration in alcohol-dependent patients."Alcohol and alcoholism 40.2 (2005): 155-156.

• Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Mosby/Elsevier; 2010

• Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011

• Tonelo, D., Providência, R., & Gonçalves, L. (2013). Holiday heart syndrome revisited after 34 years. Arquivos brasileiros de cardiologia, 101(2), 183-189.

• Shpilenia LS, Muzychenko AP, Gasbarrini G, Addolorato G. Meta- doxine in acute alcohol intoxication: a double-blind, randomized, placebo-controlled study. Alcohol Clin Esp Res 2002;26:340–6.

Pain meds in alcoholics

• NSAIDs – Risk of gastritis, ulcers, UGIB increased by EtOH

– Anti-platelet effect may be enhanced by alcohol use

• Acetaminophen – Toxic metabolite production by CYP2E1 +/- CYP3A

– CYP2E1 enhanced by chronic EtOH

– Liver injury at as low as 2-4g/day

• Opiates – sedation

Weathermon R, Crabb DW. Alcohol Res Health 23.1 (1998): 40-54.