Professional Documents
Culture Documents
Report 8/26
Hannah Duffey, PGY 3
Case Report
HPI:
17 yo male presenting with persistent vomiting in the setting of elevated
AST, ALT and bilirubin. 3 months prior to this presentation, he had cough,
runny nose and post-tussive emesis. After 5 days of symptoms,
presented to his doctor where he received steroids, antibiotics and an
inhaler. His symptoms improved except he was now just vomiting
without a cough. He went to an instacare where he has hypokalemic and
dehydrated. He received fluids and went home. Vomiting persisted he
went to an outside ED, where he was admitted for dehydration. At the
OSH an EGD showed erosive gastritis and esophagitis. He was placed on
antacids. Vomiting resolved after 2 weeks. Since that time he has had
weight loss (~5-6lbs) and fatigue.
This recent illness started 4 days prior to admission with vomiting. He
Physical exam
T 37.3. HR 62. RR 13. BP 156/72. SaO2 95% on Room Air.
WEIGHT - 75.7 Kg, (78%ile) HEIGHT - 167 cm, (11%ile), BMI 27.1 (92%)
GENERAL: tired, wakes up to talk to me
HEAD: normocephalic, atraumatic.
EYES: scleral icterus present, PERRL, EOMI.
EARS: normal external ears.
NOSE: no discharge or obstruction.
OROPHARYNX: moist mucus membranes, tonsils without exudate, no pharyngeal
erythema or lesions.
NECK: supple without lymphadenopathy or tenderness to palpation.
CARDIOVASCULAR: normal rate, rhythm, and S1/S2, without murmur or gallop. Pulses
appropriate. Capillary refill time 2-3 seconds.
LUNGS: clear to auscultation bilaterally, good air flow, no retractions.
ABDOMEN: soft, non-tender, non-distended with active bowel sounds and no masses
or hepatosplenomegaly.
EXTREMITIES: all extremities warm and well perfused. No cyanosis, clubbing, or
edema.
BACK: no abnormalities noted
GENITOURINARY: did not examine.
NEUROLOGIC: awake and alert, cranial nerves II-XII grossly intact, grossly normal
strength and tone, patellar tendon reflexes normal.
SKIN: jaundiced
LABORATORY:
IMAGING:
US Ab 11/22:Impression:
Differential Dx
17 yo M with recurrent, persistent vomiting in the setting of elevated
AST, ALT and bilirubin....
Differential
GI/Liver:
Acute abdomen
obstruction (intermittent
volvulus), perforated
appendix
Pseudo-obstruction
Cyclic vomiting
Alpha-1 anti-trypsin
deficiency, Wilsons
disease, auto-immune
hepatitis
Cholecystitis
Fatty liver
Hemochromatosis
ID:
Viral Hepatitis:
CMV, EBV,
Hepatitis A, B, C,
enterovirus,
adenovirus
Bacterial:
abdominal/liver
abscess
Parasite:
echinococcus
Differential continued
Ingestion/Exposure/dru
g/alcohol use
Tylenol
Excessive alcohol use
hyperemesis
cannabinoid
syndrome
Cocaine
Ecstasy
Unknown prescription
drug abuse
Heme/Onc:
leukemia,
lymphoma
MSK:
Rhabdomyolysis
CV:
Heart failure
Hospital course
Continued vomiting despite multiple anti-emetics
The patient showered 2-3 times per day during his stay
His liver enzymes trended down and Cr improved with IVF
Imaging:
AB US 11/24IMPRESSION:
Hospital course
continues
Diagnosis
Probable viral hepatitis +/exacerbating
Interpretation of
Liver Enzymes
AST(mitochondrial)/ALT (cytosolic)-
hepatocellular enzymes
Alkaline phosphatase- biliary enzyme also
(obstruction, infiltration)
PT/INR, Albumin = synthetic function
HEADSS Assessment
Home
Education, employment, environment
Activities
Drugs
Sexuality
Suicide/Depression
Cannabinoid Hyperemesis
Syndrome
Marijuana, cannabis, weed, grass, ganga, pot, herb, Mary Jane, reefer.
In 2004, Allen et al1 coined the term cannabinoid hyperemesis (CH)
after describing 9 patients with a cyclic vomiting illness that began in the
setting of long-term cannabis use and resolved after cessation of the drug
The 2008 World Health Organization World Mental Health Surveys
project show that only 44.1% of 12th graders believe regular marijuana
use is harmful3
More than 1/3 of high school seniors tried pot in 2012, and one in 15
3
itMoore
dailyG.M.,
1.smoked
llen J.H., de
Heddle R., and Twartz J.C.: Cannabinoid hyperemesis: cyclical
hyperemesis in association with chronic cannabis abuse. Gut 2004; 53: pp. 1566-1570
2. Degenhardt L., Chiu W.T., Sampson N., et al: Toward a global view of alcohol, tobacco,
cannabis, and cocaine use: findings from the WHO World Mental Health Surveys. PLoS
Med 2008; 5: pp. e141
3. Moyer, M.W. Scientific American . 2013; 308: 19
Symptoms/Clinical
Description
Current, heavy cannabis use
Abdominal pain
Recurrent episodes of severe nausea and
intractable vomiting
Compulsive bathing with symptom relief
Resolution of symptoms with cannabis cessation
Failure of standard antiemetics to resolve
Proposed mechanism
Tetrahydrocannabinol (THC), the active
compound in cannabis, binds to cannabinoid
receptors (CB 1 and CB 2 ). Antiemetic properties
are mediated by activation of CB 1 in the
hypothalamus, and nausea and vomiting
properties by activation of CB 1 in the enteric
nervous system. Hyperemesis in heavy cannabis
users is thought to occur because of the
accumulation of THC in fatty tissues, which
leads to enteric stimulation that overrides the
effects of the central nervous system4,5
4. Chen J., and McCarron R.M.: Cannabinoid hyperemesis syndrome: a result of chronic, heavy
cannabis use. Curr Psych 2013; 10: pp. 48-54
5. Galli J.A., Sawaya R.A., and Friedenberg F.K.: Cannabinoid hyperemesis syndrome. Curr Drug Abuse
Rev 2011; 4: pp. 241-249
C21H30O2
Tetrahydrocannabinol
Approach to
Diagnosis
of another process
Treatment
Supportive CESSATION of marijuana use
Cannabinoid
Hyperemesis
Syndrome
Patients with CHS may have
numerous visits with their
physician before diagnosis,
which highlights the
underrecognition of this
5
syndrome
5.
Galli J.A., Sawaya R.A., and Friedenberg F.K.:
Cannabinoid hyperemesis syndrome. Curr
Drug Abuse Rev 2011; 4: pp. 241-249
Possible hepatotoxicity
with chronic marijuana
use
Hepatomegaly, splenomegaly and hepat-
6. Borini, P., Guimaraes, R.C. Borini, S.B. Possible hepatotoxicity of chronic marijuana usage. Sao
Paulo Med J.. 2004. 122(3): 110-6.