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Case Presentation

Alcohol Withdrawal
by

Laila Sayeed

on 20 January 2014

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Transcript of Case Presentation

Case Presentation
Past Medical History:
A laborer/driver by profession who is married and has 03 children
History of smoking Hash for about 30 years
History of drinking Vodka and Whiskey for about 30 years
roughly one bottle every night(30 units).He had suddenly stopped
drinking about a month ago.
Family History:
GPE:
A 57 year old man lying unconcious in bed.
CVS:
Pulse 92/min. Regular and of good volume. BP 96/60. No JVD. No Edema.
AB 5ICS MCL. No Parasternal heave or thrills. H.S S1+S2+ no murmurs
Chest:
Resp rate 15/min. O2 Saturation 88% on room air. No central cyanosis. Trachea central. No intercostal recessions. Expansion reduced and symmetrical. Percussion notes resonant. B.S Harsh vesicular breath sounds with B/L crepts
Abdomen:
Soft. Distended with previous scar of umbilical hernia repair. No visceromegaly Bowel sounds present.
CNS:
Unconcious with GCS 7/15 E2V1M5. Pupils: BERL Constricted b/l upto 1.5mm Fundi: Retinal hemorhages. Reflexes intact. Both plantars downgoing. Kernig's sign Positive. No signs of cerebellar involvement.
CBC: Hb 17.8mg/dl.RBC 6.54x10^12/L. TLC 8.80x10^9/L. Platelets 228x10^9/L. MCV 90fl. PCV 58.9%
COAGULATION PROFILE:
PT 12.5 sec(against 10 sec). APTT 25.2(against 25 sec). INR 1.26
ELECTROLYTES: Na 138.4mmol/L.
K 6.39mmol/L
. Cl 99.4mmol/L. HCO3 32.8mmol/L
RENAL FUNCTION:
Urea 66mg/dl
. Creatinine 0.86mg/dl. eGFR 97.42ml/min/1.73m^2
LIVER FUNCTION TESTS: Bilirubin Total 0.34mg/dl. Bilirubin Direct 0.06mg/dl. Gamma GT 11U/L.
AST 51U/L. ALT 85U/L.
URIC ACID: 6.2mg/dl. CALCIUM: 9.4mg/dl.
PHOSPHORUS: 7.9mg/dl
. MAGNESIUM: 2.3mg/dl

What would be your differential diagnosis
HISTORY
Aggression - 30 Days
Altered Mentation - 14 Days
Abnormal Jerky Movements - 07 Days
Unconciousness - since Morning
By: Laila Sayeed
House Officer MICU

A 57 year old male patient presented to the ER at 11:20am
Chief Complaints:
History Of Presenting Illness:
According to the attendant of the patient this 57 year old male was on anti-psychotic medication on/off for the past 14 years with poor compliance. He is also a known asthmatic/COPD since ten years using regular nebulization and inhalers. He hadn't been well for long but for the past one month he developed aggressive behaviour with episodes of confused speech. He became bed bound because he found it difficult to walk after which he developed jerky movements of the whole body.That morning he was found unconcious in bed.

Hernia repair: 5-6 years ago
No past history of hospitalization
Personal History:
Medication/Drug History:
Bupropion
Haloperidole
Procyclidine
Allergy:
No history of allergy noted
Travel History:
On Examination:
Differential Diagnosis:
Hypoglycemia
Drug Overdose
Encephalitis
Meningitis
Electrolyte Imbalance
Investigations:
Respiratory Failure/ CO2 Retention
Malignancy with brain mets
Hepatic/Hypertensive/Uremic Encephalopathy
Head Trauma
Acute Liver failure
Diagnosis: Alcohol Withdrawal - Delirium Tremens
OVERVIEW
DEFINITION
Latin for " Shaking Frenzy". Also known as "The horrors" and "The shakes"
Most severe form of alcohol withdrawal. It is manifested by global
confusion and autonomic hyperactivity leading to circulatory collapse.
It's a medical emergency making early recognition and treatment essential.
ETIOLOGY
EPIDEMIOLOGY:
About 09% of US adults meet the criteria for an alcohol-use disorder.
Less than 50% of alcohol dependant persons will develop withdrawal symptoms requiring pharmacological treatment.
The life time risk for developing DTs among chronic alcoholics is about 5-10%.
Only 5% of those that develop withdrawal symptoms progress to DTs.
PROGNOSIS:
Complications: Oversedation, Respiratory distress, arrest or intubation, Aspiration pneumonia and Cardiac arrhythmias.
The current mortality rate from DTs ranges from 5-15% but should be closer to 5% with modern ICU management.
Prior to the era of intensive care the mortality was as high as 35%.
Greater risk for death: Extreme fever, fluid and electrolyte imbalance or an intercurrent illness such as trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis or Wernicke-Korsakoff syndrome.
CLINICAL PRESENTATION
HISTORY
Alcohol withdrawal syndrome is divided into four categories:
1.Minor withdrawal occurs within 6-24hours following last drink; this is withdrawal tremulousness.
2.Major withdrawal occurs 10-72 hours after last drink; characterized by hallucinations.
3. Withdrawal seizures(rum fits) occurs 6-48 hours of alcohol cessation: these are major motor seizures, generalized and brief.
4. DTs is the most severe form of alcohol withdrawal occuring 3-10 days following last drink. Clinical manifestation includes include agitation, global confusion, disorientation, hallucinations, fever, diaphoresis and autonomic hyperactivity.
Assessment Tool: the Clinical Institute Withdrawal Assessment for Alcohol, Revised(CIWA-Ar)
PHYSICAL EXAMINATION:
No specific findings are diagnostic for DTs.
However DTs often presents with a co-existing illness which should be uncovered. Patient should be assessed for stigmata of CLD and signs of trauma.
Clinical findings associated with DTs may include the following:
Tachycardia
Hyperthermia
Hypertension
Tachypnea
Diaphoresis
Tremors
Mydriasis
Altered Mental status
Severe Psychomotor Agitation
Fever
Chronic Alcohol intake affects several neurotransmitters. Most important of them are :
GABA and NMDA receptors.
GABA is an inhibitory neurotransmitter and alcohol leads to its increased receptor activation.
It also leads to up regulation of NMDA receptors.
When a person stops taking alcohol it leads to two folds effect.
1st there is loss of GABA receptor activation and this leads to diaphoresis, anxiety, tachycardia
and seizures. Then there is disinhibition of NMDA receptors which leads to delirium and
seizures.
Past episodes leads to increased frequency and severity of DTs, a phenomenon known
as KINDLING.
Positional nystagmus
Global confusion
Disorientations
WORKUP
SERUM CHEMISTRY STUDIES
OTHER LABS
IMAGING STUDIES
LUMBAR PUNCTURE
Includes; electrolytes, BUN, Creatinine
Magnesium, Phosphorus, LFTs,
CPK(some patients develop Rhabdomyolysis),
Lipases and Ketones
Serum glucose
CBC with differentials
Drug screen.
Chest radiograph
Trauma screen
CT scanning of the head if any indication
WERNICKE - KORSAKOFF SYNDROME
MANAGEMENT
GENERAL MEASURES
Admit the patient to a medicine bed
Correct electrolyte abnormalities and dehydration
Treat any co-morbid disorder
Give parenteral Thiamine slowly(250mg daily for 3-5 days in the absence of W-K Syndrome)
Give parenteral Thiamine slowly(500mg daily for 3-5 days in the presence of W-K Syndrome)
Give prophylactic phenytoin or carbamezapine if previous history of withdrawal fits.
SPECIFIC DRUG TREATMENT
One of the following orally
Diazepam 10-20mg
Chlordiazepoxide 30-60mg
Repeat one hour after last dose depending on response
FIXED SCHEDULE REGIMENS
Diazepam 10mg every 6 hours for 4 doses, then 5 mg 6 hourly for 8 doses
Chlordiazepoxide 30mg every 6 hours for 4 doses, then 15mg 6 hourly for 8 doses
Provide additional Benzodiazepine when symptoms and signs are not controlled
When learning and memory deficits are present in patients with Wernicke Encephalopathy then it is called WERNICKE-KORSAKOFF SYNDROME.
In 1881 Carl Wernicke described an illness that consisted of paralysis of eye movements, ataxia and confusion. Sergie Korsakoff described the disturbance of memory during the course of chronic alcoholism in his study during 1887-91. In 1897 Murawieff postulated that a single etiology was responsible for both syndromes.
Deficiency of Thiamine (B1) is responsible for this symptom complex and any condition that results in poor nutritional state places patients at risk.
Alcohol interferes with gastrointestinal transport, activation and storage of thiamine however this syndrome can occur without exposure to alcohol.
Thiamine is involved as cofactor in various biochemical reactions. Its deficiency leads to impaired lipid and carbohydrate metabolism leading to focal brain damage.
Initially patient should be treated as Wernickes encephalopathy with high dose parental thiamine for 7 days followed by oral thiamine for as long as the patient is taking alcohol.
As much as 25% of the patients will need long term supervised care.
No significant family history of note
Travel to Japan about 20 years ago.
CRP: 0.49mg/dl. HBA1C 6.2%.TROP I: 0.10ng/ml. LACTIC ACID: 15.1mg/dl. VIROLOGY:Non-Reactive.
THYROID FUNCTION TESTS: TSH 2.23miu/l. Free T4: 0.97ug/dl
URINE R/E: Albumin +, Pus cells 03-04/HPF, Red cells 01-02/HPF. Casts 00-01/HPF.C/S No growth.
ABGs:
pH 7.10, pCO2 130mmHg, pO2 79.3mmHg
ECG: Normal
CXR: Normal
CSF R/E: Glucose 122mg/dl.Protein 24mg/dl.RBC 50/cmm.TLC <5/cmm.No microorganisms or AFB seen
ABDOMINAL U/S: Renal parenchymal Disease Grade-1.
ECHO: Ejection fraction 65%. Normal LV/RV systolic function. LV diastolic dysfunction.
CT SCAN BRAIN WITH CONTRAST: Normal study.
CONCLUSION ??
Thank You
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