Case conference November 13, 2015

Transcription

1 Case conference November 13, 2015

2 52-year-old Man CC: Fatigue and vomiting PMHx: Afib CAD s/p CABG HTN Hyperlipidemia GERD PUD Cirrhosis Pancreatitis DM II Low back pain OSA- does not use CPAP FHx: Mother: Pancreatic cancer, DM Brother: DM- double amputee Brother: SLE Father: CAD Social Unemployed Lives by himself, divorced, two children 0.5 pack/day smoker x 20 years ETOH: drinks ½ bottle of hard liquor a week No recent drug use

3 Medications: Amiodarone Furosemide Lisinopril Metformin Metoclopramide Metoprolol Nitro Omeprazole Percocet Ropinirole Simvastatin Spironolactone Trazodone HPI: Three weeks of fatigue Once-daily, bilious, non-bloody emesis Not associated with meals Decreased appetite Slowed thoughts Constipation with no BM for 5 days Recently drinking more, ~6 beers per day Was found by his friend, who called EMS

4 History from friend: Patient had been sleeping most of day for the past 3 weeks Fell down day prior to admission Discovered somnolent, confused at home No narcotics remaining in his bottle, prescription was filled 16 days prior Questions? Exam: BP 134/56, HR 59, T 97.5, R16, SpO2 99% RA Eyes: Pupils 4mm and symmetric Resp: CTAB CV: RRR with trace lower extremity edema Abd: Obese, BS hypoactive, tenderness RUQ, no rebound or guarding Neuro: Slow responses. Resting tremor in bilateral upper extremities. DTR s sluggish. Poor recent and remote memory. Psych: Poor insight

5 EKG

6 Labs & Imaging INR 1.2 Lipase 19 Tbili 4.3, Alk phos 115, AST 249 UA: Increased urobili, 1+ protein, LE+, 22 WBC, Hyaline casts TSH 2.05 Tylenol <5, salicylate <2.5 Utox: Opiates Abdominal US: Mild dilation of CBD with increased echogenicity of liver CT abdomen: Possible bowel wall thickening at the hepatic flexure, decompressed stomach, fatty hepatic infiltrate

7 HOSPITAL COURSE HD #2 Electrolytes replaced, treated conservatively Mentation improved Stated he had been using Percocet PTA but denied excessive use ETOH + fatty liver suspected cause of abnormal LFTs

8 HOSPITAL COURSE 9:30 PM RN Call: Patient acting goofy Inappropriate laughter Night Float Evaluates: BP 94/58, HR 120, RR 22 Alert, oriented, non-focal exam Plan: Continue to monitor 11:30 PM RN Call: Goofier Night Float Re-evaluates: BP 85/50, HR 140, RR 22 Oriented x 0, agitated Upset because people in the TV are telling him what to do

9 Now what? 1. STAT head CT 2. Hgb, bmp, troponin 3. Utox 4. Treat w/ ceftriaxone 5. Treat w/ Haloperidol 6. other

10 HOSPITAL COURSE Agitation escalated Code Green called Placed in restraints Initiated Alcohol Withdrawal Protocol HD #3 Continued agitation and confusion ETOH withdrawal vs hepatic encephaolopathy Ammonia 117 Lactulose started TID Hep C positive UC positive for E coli

11 Hospital course, cont. Overnight HD #3 Increasing respiratory rate Severe agitation Placed on lorazepam infusion Intubated Started on tube feeds HD #10 Slow to awaken, likely due to prolonged lorazepam infusion Extubated and transferred out of ICU Discharged to SNF on HD #13 CD evaluation as outpatient Patient not sure if he wanted to stop drinking

12 Alcohol Withdrawal

13 Epidemiology At some time in their lives, ~20% of men and 10% of women (in Western societies) will have an alcohol use disorder About 50% of persons with alcohol use disorders have symptoms of withdrawal with alcohol cessation or reduced intake About 5% with alcohol withdrawal delirium in placebo-treated alcohol dependent patients entered into clinical trials of inpatient drug treatment ~ 500,000 cases of withdrawal requiring medical treatment every year

14 Pathophysiology Short-term alcohol exposure Enhances CNS inhibition Binds at GABA receptor Decreases CNS excitation Inhibits glutamate at NMDA Chronic alcohol exposure Decreases inhibition GABA down-regulation Increases excitation NMDA up-regulation

15 Pathophysiology Alcohol withdrawal: Compensatory changes no longer opposed by alcohol Balance shifts towards excitability

16 Question What is the typical timeframe for the onset of delirium tremens? A. At the peak BAL B. 2-6 hours after last drink C hours after last drink D hours after last drink E. 1-2 weeks after last drink

17 Withdrawal Timeframe

18 Minor Withdrawal Symptoms Apparent 6-8 hours after last drink May occur while patients still have a significant BAL Resolve in 24 to 48 hours if not progressive CNS hyperactivity: Insomnia Tremulousness Mild anxiety GI upset Headache Diaphoresis Palpitations

19 Withdrawal SEIZURE 6-48 hours after last drink Generalized tonic-clonic Usually singular, sometimes a flurry in quick succession Recurrent or prolonged seizures should lead to further evaluation Untreated, 1 / 3 go on to DTs

20 ALCOHOLIC HALLUCINOSIS hours after last drink Resolves in 1 to 2 days Commonly visual hallucinations; can be auditory or tactile Not the same as DTs: Mental status overall intact Vital signs typically normal

21 DELIRIUM TREMENS ~ 5% of withdrawal patients hours after last drink Lasts up to 7 days Symptoms: Disorientation / AMS Hallucinations Agitation Tachycardia Hypertension Fever Diaphoresis

22 Delirium tremens Risk factors: Prior history of DTs Sustained drinking Withdrawal during high BAL Concurrent illness Age > 30 Longer time period since last drink Mortality rate: Old data: ~15% Newer data: 0-1% Cause of death: Dysrhythmia Complicating illness Aspiration pneumonia Missing the illness that led to alcohol cessation Pancreatitis, hepatitis, CNS infection, &c

23 Diagnosis H&P may need input from spouse, family etc Consider symptoms in regard to timeframe Consider the differential Delirium otherwise Infections Head trauma Metabolic Drugs GIB Hepatic failure

24 Symptom Management Benzodiazepines are the agents of choice Work at GABA receptor as does alcohol Safe and effective Reduce psychomotor agitation Reduce seizures Reduce incidence of delirium Reduce severity and help prevent progression of withdrawal Be aggressive in severe withdrawal!

25 Benzodiazepines: half-lives Lorazepam approximately 12 hours Diazepam hours if active metabolites included Chlordiazepoxide longer yet than Diazepam. Parent compound, hours but metabolites hours

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27 Symptom-triggered Care Score: Mild < 8 Moderate 8 15 Severe > 8 q10-15min evaluation in severe withdrawal on IV benzos q1h evaluation once symptoms controlled q4-6h evaluation for mild symptoms Symptom-triggered treatment results in less total medication and in shorter treatment

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29 Further Management Supportive care: IVF Volume depleted due to diaphoresis, hyperthermia, vomiting and tachypnea Correct fluid deficits with isotonic fluids Dextrose-containing IVF when euvolemic and after thiamine Correct electrolyte derangements Potassium Magnesium (dysrhythmia, seizures) Phosphorus (cardiac failure, rhabdomyolysis) Thiamine 100 mg IV daily initially MVI with folate Nutritional support

30 If refractive to massive benzodiazepine dosing Hypothesized that perhaps GABA-A receptors that respond to Ativan/Valium and their ilk become saturated Mainstay has been barbiturates similar GABA effect vs. benzodiazepines but at a different receptor Propofol combined GABA/NMDA effect Less studied: Dexmedetomidine (Precedex) - central alpha-2 antagonist (similar to clonidine) Also baclofen (GABA-B receptor)

31 Adjunctive role for antipsychotics? No clear guidance Haldol decreases seizure threshold Frequently administered (part of our order set) Did not find trials for atypical agents Uptodate: should not be used routinely in the withdrawing alcoholic Perhaps a role if EtOH withdrawal atop decompensated thought disorder

32 Wernicke Encephalopathy Acute disorder due to B1 deficiency Seen in alcoholism, malnutrition The triad: Encephalopathy Ataxia Occulomotor dysfunction Nystagmus, lateral rectus palsy, dysconjugate gaze Do not need all of them (rare) Encephalopathy alone probably most common sign Treatment = B1 (Thiamine) Give (IV) prior to glucose-containing solutions so as not to trigger or worsen Wernicke s Even if recognized/treated, permanent deficits are to be expected

33 Korsakoff SYNDROME Chronic, develops out of Wernicke s Marked deficit in ante- and retrograde memory Apathy Intact sensorium Confabulation but social interactions may, to the uninitiated, seem normal No effective medical treatment