Transcript The Shakes and the Horrors

*
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.
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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
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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?
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