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* Grand Rounds: Delirium Tremens Connie Joylani, MD, R3 * Case Presentation * Delirium Tremens current therapies discussion * Historical approach * References * Question period * * PB: Patient is a 73 y.o. male with history of Asthma + recently diagnosed HTN who presented to ER with tongue swelling, sore throat and head/neck rash since morning of admission. He was started on Lisinopril and Verapamil for elevated BP. He reports taking lisinopril day prior, then Verapamil on morning of admission. Shortly after taking AM med, he noticed tongue swelling and red, itchy rash on his neck, head and back. He applied some alcohol to rash which helped with itching. He denied ever having breathing difficulties but mentions that the pitch of his changed Further denies fevers, chills, abdominal pain, N/V/D. * * ER Course * - Vitals stable. Airway patent. Voice changes were noted. * - NO labs done * - Lisinopril was d/c * - Given 125mg solumedrol+ 25mg benadryl + 40mg Pepcid for nausea * Upon admission, patient appeared comfortable and reported that he feels much better. He has noticed significant improvement in tongue swelling. He continued to deny breathing difficulties. Carries a history of asthma but denies wheezing, chest tightness or dizziness. Upon further questioning, he admits to alcohol use/abuse which resulted in incarceration for driving under influence. Last drink was yesterday. Reports drinking "quite a bit". Denies ever detoxing but experiences shakes and anxiety when sustains from drinking. No history of seizures * * A/P: * 1) Angioedema: Secondary to recently started Lisinopril for HTN. Improved upon discontinuation of lisinopril. Would continue to hold. He has been given one dose of solumedrol and benadryl, both of which has been shown to be ineffective. Would monitor vitals closely overnight. Low salt diet. Labs including, CBC, CMP, TSH ordered for AM. If sx reoccur however, would have low threshold for transferring to unit for closer monitoring. * 2) HTN: BP 120's-140's SBP, HR 80's. Since we are holding lisinopril and verapamil, would start HCTZ 12.5mg. He is African American so diuretic would be the better choice for HTN management. * 3) Alcohol abuse: CIWA started. CD consult. Patient seeking help. Also advised him to follow up with PCP for options to help with quitting alcohol. Folate and B12 level in AM * 4) Asthma: Stable. Would continue with home medications. * * * * * * * * * * * * * * * * Due to recurrence of airway symptoms within 6hrs of solumedrol, patient was transferred to the ICU and Intensivist became involved. Likely a classic allergic reaction. A/P: Check CBC with differential to look for eosinophils. I will check a urinalysis to check for urinary sediment. I will check IgE. I will check C1 esterase inhibitor. I am going to check CMP. I am going to order an ABG and his chest x-ray. The patient is going to be started on Solu-Medrol 125 mg q. 6 hours. The patient will be started on Benadryl 50 mg q. 6 hours. The patient will be started on famotidine 20 mg q. 6 hours. The patient will be started on racemic epinephrine for treatment given back to back x1 then q. 6 hours. The patient requires deep venous thrombosis and gastrointestinal prophylaxis. The patient will be started on oxygen. The patient will be started on D5 half normal saline at 75 mL per hour. * * 12/13 9AM: Pt starts to try to get out of bed, and becomes progressively more agitated. * Airway/allergic reaction issue continues to improve. * Transitioning to less frequent steroids, patient stabilizing from that standpoint. * * 12/13 9PM: Pt starts to hallucinate, tries to fight an invisible assailant in his room. * Code strong called. Patient restrained physically and chemically with geodon and ativan. * BP climbing, requiring hydralazine and labetalol. * On discussion with his wife, pt drinks 2 pints of whiskey everyday, and was admitted to an ICU and intubated 2 months ago for DTs. * * 12/14 AM: Pt continues to require high dose sedation and antihypertensives. * Intensivist sedates and intubates patient. * Versed and Fentanyl drips initiated. * Central and arterial lines instituted. * Cultures drawn. * * Neurology consulted for AMS, CT head negative. * Suspects metabolic encephalopathy. 12/15: sedation holiday attempted, pt remained agitated. Resedated, remains on ventilator. Tube feedings initiated. Nephrology consulted due to AKI, recommends continued hydration. * * 12/16: Still remains agitated, switched to proprofol sedation. * Pt noted to have copious secretions, but unimpressive CXR. Pt failing daily sedation holidays. * * LOS 7 days * 12/19: Patient remains ventilated, copious secretions are taking on a foul odor. Antibiotics initiated. CXR remains unimpressive. * * 12/20, LOS 8 days: Able to reduce propofol infusion. * Pt now able to follow commands. * Oral odor increasing, titrated antibiotics to Haemophilus sensitivity. * * 12/21, LOS 9 days: Pt weaned and extubated. * Is able to follow commands. * 12/22 LOS 10 days: Pt working with PT/OT, able to transfer to medical floor. * * 12/24, LOS 12 days: Pt had continued to progress well, worked with PT/OT, and was stable for DC after 7 days of intubation. * * 20% of men and 10% of women will have an alcohol use disorder in the span of their lives. * 50% of persons with alcohol use disorders have symptoms of alcohol withdrawal when they reduce or discontinue their consumption. * 3-5% of these persons have grand mal convulsions, delirium, or both. * * Alcohol is a CNS depressant, rapidly increases GABA in the brain. * Repeated exposure to alcohol causes the brain to adapt with changes in receptors and proteins. * This requires higher doses of alcohol to achieve similar depressant states. * * Withdrawal symptoms can include insomnia, anxiety, tachycardia, hypertension, tachypnea, tremor, seizures or hallucinations/delirium. * Because ethanol is short acting, withdrawal symptoms usually begin within 8hrs after blood levels decrease, peak at 72hr and are reduced by day 5 through 7 of abstinence. * * The CIWA (Cinical Institue Withdrawal Assessment of Alcohol Scale) was developed to aid in close monitoring of withdrawal and timely therapies. * * Most studies estimate that 3-5% of patients admitted for withdrawal meet DT criteria. * These include delirium (rapid-onset fluctuating * disturbance of attention and cognition, sometimes with hallucinations) plus alcohol withdrawal. * * Withdrawal delirium usually begins about 3 days after appearance of symptoms of alcohol withdrawl. * Lasts from 1 to 8 days or more. * 1-4% of these patients will die. * Death usually results from hyperthermia, cardiac arrhythmias, complications of withdrawal seizures, or concomitant medical disorders. * * Delirium during alcohol withdrawal is predicted * by the following: CIWA-Ar scores above 15 * (especially in association with a systolic blood * pressure >150 mm Hg or a pulse rate >100 beats * per minute), recent withdrawal seizures (seen in * 20% of persons with delirium), prior withdrawal * delirium or seizures, older age, recent misuse of * other depressant agents, and concomitant medical * problems. * * Concomitant medical problems can include: Electrolyte abnormalities (e.g., low levels of potassium, magnesium, or both), low platelet counts, and respiratory, cardiac, or gastrointestinal disease. * * Treatment: * Treat the concomitant medical issues. * Control agitation * Decrease risk of seizures * Often the best treatment is within the ICU * Suggested Treatment of Alcohol Withdrawal Delirium (Delirium Tremens). * The mainstay of pharmacologic treatment of DTs is depressants such as benzodiazepines. No single agent has shown to be superior to another. * Diazepam has a longer half life and lorazepam shorter. * Doses vary dramatically among patients, e.g. >2000mg of diazepam in the first 2 days in one patient. * * In patients who doe not have a response to high doses of benzodiazepines, propofol may be administered. * E.g. 0.3 to 1.25mg/kg up to 4mg/kg/hr for up to 48 hrs. * Another adjunctive medication is dexmedetomidine (Precedex), an alpha2 adrenergic agonist, which sedates (but allows pts to be arousable) and decreases sympathetic tone. Doses up to 0.7mcg/kg per hour may be required. * Maintain sedation until patient tolerates sedation holidays without agitation/hallucination/seizure activity. * * September 1892 (JAMA): * Favored the use of liquor ammoniae acetatis, given every hour. Milk, beef juice, broth and coffee also administered. * Subsequent attacks and seizures were treated with opium and bromides, forcing a “narcotic sleep.” * Of course a padded room of the nearest workhouse was the next option. * * April 1909 (JAMA): * Bromids were used most extensively – equal parts sodium, potassium, and ammonium bromid. Mortality was 45.5%, which the paper suggested was due to too large doses too frequently repeated. * Chloral (first synthetically produced sedative-hypnotic drug) was also used, which was found to be “of no service.” And was found to actually increase mortality. * At this time, Whiskey was falling out of favor as a treatment as it too increased mortality and dependence. * * August 1911 (JAMA): * Purgation added to the treatment course. * Purgation was initiated early and actively to combat the “faulty elimination” commonly seen in DTs. * Included calomel (mercury chloride a yellowish-white solid, also used as an insecticide), saline, and cathartic pills plus a “cleansing enema.” * * August 1916 (JAMA): * This report suggested lumbar puncture with varying quantities of CSF removed (10 to 40cc) and a solution of magnesium sulphate was introduced via syringe through the lumbar puncture needle into the canal. * Surprisingly only 2 of the 10 patients studied suffered death as an ADR. * * August 1942 (JAMA) (last one): * Patients were given no sedation but “remained strapped in bed, straining against his bonds and raising considerable disturbance.” * Initiated injections of (what would eventually evolve to become our banana bag) dextrose, vitamin B1 and insulin, all at once. * “Further investigation in the field of chemical determinations of the blood may help to decide the exact roles played by Vitamin B1, insulin and dextrose.” * * N Engl J Med 2014;371:2109-13. DOI: 10.1056/NEJMra1407298 * NON-NARCOTIC TREATMENT OF DELIRIUM TREMENS.. JAMA. 1892;XIX(10):291-292. doi:10.1001/jama.1892.02420100023003. * * Wholey CC. Purgation in Delirium Tremens. JAMA. 1911;LVII(8):672. doi:10.1001/jama.1911.04260080236019. * RANSON S. THE RESULTS OF DRUG TREATMENT IN FIVE HUNDRED CASES OF DELIRIUM TREMENS. JAMA. 1909;LII(16):1224-1227. doi:10.1001/jama.1909.25420420004002. * LEONARD EA, Jr.. INTRASPINAL INJECTIONS OF MAGNESIUM SULPHATE * IN DELIRIUM TREMENS. JAMA. 1916;LXVII(7):509-510. doi:10.1001/jama.1916.02590070033011. Cannon EA, Modarelli WH, DeVincenzo FR, Swiney MM, III. THE TREATMENT OF DELIRIUM TREMENS. JAMA. 1942;119(17):1418. doi:10.1001/jama.1942.72830340005008d. * *Thank you! *Questions? *