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 meHEAD: 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 notedGENITOURINARY: 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 Dx17 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, Wilson’s 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/

drug/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 rightkidney, unchanged.

Renal doppler US 11/24: IMPRESSION: Normal duplex ultrasound examination of thekidneys, 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 1-antitrypsin 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 = 127Amylase 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 smoked it daily31. llen J.H., de Moore G.M., 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 mechanismTetrahydrocannabinol (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 system4,54. Chen J., and McCarron R.M.: Cannabinoid hyperemesis syndrome: a result of chronic, heavy cannabis use. Curr Psych 2013; 10: pp. 48-545. Galli J.A., Sawaya R.A., and Friedenberg F.K.: Cannabinoid hyperemesis syndrome. Curr Drug Abuse Rev 2011; 4: pp. 241-249

C21H30O2Tetrahydrocannabinol

Approach to Diagnosis

Essential for diagnosis:History of regular cannabis use for years

Major clinical features of syndrome:Severe nausea and vomitingVomiting that recurs in a cyclic pattern over months Resolution of symptoms after stopping cannabis use

Supportive features:Compulsive hot baths with symptom reliefColicky abdominal painNo evidence of gall bladder or pancreatic inflammation

Typically should not have lab abnormalities suggestive of another process

TreatmentSupportive CESSATION of marijuana use

Cannabinoid Hyperemesis SyndromePatients with CHS may have numerous visits with their physician before diagnosis, which highlights the underrecognition of this syndrome5

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 moder- ate 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