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Morning

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

had diarrhea 1-2 times. He went to the outside ED where he received


fluids. Labs were sent and when his AST, ALT and bilirubin returned
elevated, he was sent to PCH as a direct admission.
PMH: mild intermittent asthma, broken collar bone s/p surgical repair

Medications: Omeprazole, Zofran PRN


Allergies: NKDA
Family history: negative for IBD, liver disease
Immunizations: UTD
Social Hx: Lives with parents and 2 siblings. He is a

senior in high school.


Exposure Hx: He is in boy scouts. Prior to the first illness,

he and other boy scouts drank from a stream. Scout


leader told them it was okay to drink the water. No
recent travel. No animal exposures except for chickens

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

Work-up from the


OSH

LABORATORY:

Complete Metabolic Panel: Na = 140, K = 3.2, Cl = 105, CO2 = 19,

BUN = 12, Cr = 1.01, Glucose = 87, Ca = 9.7, Protein = 7.5, Albumin


= 4.1, Bilirubin = 3, Alk. Phos. = 54, ALT = 251, AST = 858
PTT 27, PT 14/INR 1.1
Acute hepatitis panel: Nonreacitve
Monospot: negative
Lipase 13
CBC: WBC 14.3 (N 86, L 8.4, M 5.3), Hgb 16.2, Hct 47, Plts 247

IMAGING:
US Ab 11/22:Impression:

1. Dilated common bile duct.


2. Incidental small simple cyst in the right kidney.

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:

1. Persisting dilated common bile duct. No stone identified.


2. Gallbladder appears normal without stones.
3. Benign-appearing cystic lesion in the peripheral right
kidney, unchanged.
Renal doppler US 11/24:

IMPRESSION: Normal duplex ultrasound examination of the


kidneys, aorta and IVC.
AB Xray: Non-obstructive bowel gas pattern

Hospital course cont


Lipid panel: TC 100, LDL 55, HDL 29, TG 79; HgA1c

4.7; ANA negative; serum cerruloplasmin 19; EBV


panel negative; CMV qualitative negative; LKM AB
negative; Acute hepatitis panel negative; alpha 1antitrypsin phenotype M1M2; Anti-SM AB negative
Complete Metabolic Panel: Na = 138, K = 3.6, Cl =

108, CO2 = 22, BUN = 9, Cr = 0.88, Glucose = 135,


Ca = 9.4, Protein = 6.3, Albumin = 3.6 bilirubin =
3.9
Alk. Phos. = 44, ALT = 132, AST = 127
Amylase 64, Lipase 51
GGT 20

Hospital course
continues

Urine Tox: +THC

Diagnosis
Probable viral hepatitis +/exacerbating

Cannabinoid Hyperemesis Syndrome


Recent labs now show normal LFTs but

continues to have mildly elevated indirect


bilirubin (Gilberts/dehydration?)

Interpretation of
Liver Enzymes
AST(mitochondrial)/ALT (cytosolic)-

hepatocellular enzymes
Alkaline phosphatase- biliary enzyme also

comes from bones


GGT- biliary
High GGT and Alk phos = biliary source

(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

estimated that the cumulative, lifetime prevalence of cannabis use in the


US population is 42% to 46%2
Data from the National Institute on Drug Abuse's Monitoring the Future

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

nausea and vomiting

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

Essential for diagnosis:

History of regular cannabis use for years


Major clinical features of syndrome:

Severe nausea and vomiting


Vomiting that recurs in a cyclic pattern over months
Resolution of symptoms after stopping cannabis use
Supportive features:

Compulsive hot baths with symptom relief


Colicky abdominal pain
No evidence of gall bladder or pancreatic inflammation
Typically should not have lab abnormalities suggestive

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-

osplenomegaly were detected in 57.7%,


73.1% and 46.2%, respectively, of users of
marijuana on its own, with slight to moderate elevation of AST (42.3%), ALT (34.6%)
and AP (53.8%)6

Study limited by difficulty finding enough


people who were not poly-substance abusers

6. Borini, P., Guimaraes, R.C. Borini, S.B. Possible hepatotoxicity of chronic marijuana usage. Sao
Paulo Med J.. 2004. 122(3): 110-6.

Take Home Points


HEADSS
Interpretation of LFTs
CHS- chronic cannabis use, recurrent

vomiting, abdominal pain, relief with hot


showers