IR Acute Hepatitis B

medchiefs.bsd.uchicago.edu

IR Acute Hepatitis B

Intern Report

January 17, 17 2011

Bryan A. Smith

Jim Woodruff, MD


Case

• 68yo M presents with jaundice and decreased

appetite x 1 mo. mo

Questions?


More Info

• Began g feeling g sick 1 mo ago g after being g treated with

cipro for UTI

• Described symptoms of fever, chills, night sweats,

llethargy, h decreased d dappetite, ddark kcolored l durine and d

light stools

• One week previous, previous presented to OSH for laser

procedure to relieve prostate obstruction. Since then

has had bladder incontinence, dark red urine, clay

colored stools

• Patient reports weight loss of 10lbs in 1 mo


• PMHx

– PProstate t t ca‐ s/p / XRT

– Islet cell tumor of pancreas s/p

resection ‘06

– HTN

– BPH

– DM‐ insulin dependent

• PSHx

• Distal pancreatectomy/

splenectomy ’06‐ lymph nodes

neg, surgical margins free of dx.

• NKDA

• FHX

– noncontributory

Case (cont)

• Social

– Li Lives with ith wife if

– Retired, once worked in

pharmaceutical sales

– +tob‐ 25 pack‐years, social EtOH,

no illi illicits i

• Meds

– Enalapril 20mg BID

– Nifedipine p 90mg g dailyy

– Sildenafil 100mg daily

– Flomax 0.4mg daily

– Finasteride 5mg daily

– Glipizide 10mg daily

– Lantus


Differential?


Classification of Jaundice

UUnconjugated j t dHHyperbilirubinemia bili bi i CConjugated j t dHHyperbilirubinemia bili bi i

• Increased bilirubin production • Biliary Obstruction

– Extravascular hemolysis

– Et Extravasation ti of f bl blood d iinto t

tissues

– Intravascular hemolysis

– Dyserythropoiesis

y y p

• Impaired Hepatic Uptake

– Heart Failure

– Portosystemic Shunts

– Drugs

– Gilbert’s Syndrome

• Impaired conjugation

– Cil Crigler‐Najjar Njj SSyndrome d

– Gilbert’s Syndrome

– Hyperthyroidism

– Liver dx‐ dx chronic hepatitis,

advanced cirrhosis, Wilson’s

disease

– Choledocholithiasis

– Intrinsic and Extrinsic tumors

– Primary Sclerosing Cholangitis

– AIDS cholangiopathy

Acute/ chronic pancreatitis

– SStrictures‐ i s/pprocedures

/ d

– Parasitic infection

• Intrahepatic cholestasis

– Viral Hepatitis

– Alcoholic hepatitis

– Nonalcoholic steatohepatitis

– Primary biliary cirrhosis

– Drugs/ toxins

– Sepsis

– Infiltrative dx (amyloid, lymphoma, sarcoid,

TB)

– ESLD

• Hepatocellular Injury


Physical Exam

• Vitals: T: 37.4 P: 72 R: 18 BP: 158/74 O2sat: 97%RA

• GEN: NAD, well nourished

• HEENT: Scleral icterus, sublingual jaundice, moist mucus

membranes membranes, no oropharyngeal erythema/ exudate exudate, no LAD LAD,

no JVD

• CV: S1, S2, no MRG, RRR, PMI 5th ICS

• PULM: CTAB, normal respiratory effort

• GI: RUQ and epigastric mild TTP, soft, non‐distended, no

appreciable appecabeoga organomegaly, o egay, no o spider sp de angiomas a go as

• Neuro: A & O x 3, CN II‐XII intact, no asterixis

• Extremities: 2+ pulses, warm, well perfused, no LE edema


Evaluation of Jaundice

• 80% daily bilirubin

production from hemoglobin

• Normal serum concentration

of bilirubin < 1mg/dL g/

• Clinician cannot detect

jaundice until bilirubin >

2.0mg/dL

• Jaundice seen best in ocular

conjunctiva and in oral

mucus membranes (under

tongue, hard palate), and in

the skin.


Wh What labs lb would ld you lik like to order?

d ?


133 101 13

3.8 22 1.0

Labs and Studies

166

8.0

2.1

28 2.8

11.9

92 9.2 278 UA UA‐ + leuk esterase

33.1

N‐ 71

LL‐ 14

M‐ 15

MCV‐ 86.2

MCH MCH‐ 31

MCHC‐ 36.0

+ nitrite

2+ protein

3+ blood

3+ bilirubin

E‐ 0 RDW‐ 21.8 ‐ glucose

B‐0

trace ketones

PT‐ 17.8

INR‐ 1.4

7.1 2.9

21.0 16.4 / 4.6

994 1153

218

GGT‐ 351

Lipase‐ 47

Ammonia‐ 96


Wh What else l would ld you lik like to order?

d ?


• RUQ U/S

Additional Studies

– Partially distended gallbladder with gallbladder

wall thickness thickness. Sludge and gallstones within the

gallbladder noted.

– No hepatic vein thrombosis, no hepatomegaly, no

Budd‐Chiari syndrome


OSH workup arrives..

• CT abdomen/ pelvis w/ contrast‐ contrast

– s/p splenectomy and post op changes in uper abd

with clips in area of pancreas pancreas. No residual masses masses.

Thickening of gallbladder wall, may be 2/2 ascites.

No free air, no bowel obstruction.


Additional Labs

• Blood cx‐ negative • Hepatitis Panel

• Urine cx‐ negative

• AAnti‐mitochondrial ti it h d i l ab b ‐


Hepatitis B

• Affects 1.25 million people in the US and 350‐400 million worldwide

• After WHO recommended hep B vaccine included in infant immunization in 1992,

incidence has dropped from 252,000 to 51,000 cases annually in the US

• 0.1 ‐ 0.2% carriers in low prevalence areas‐ U.S., Canada, Western Europe

• 10‐20% carriers in high prevalence areas‐ southeast Asia, China, sub‐Saharan Africa

• In low prevalent areas, most acute HBV infections occur during adolescence or

early adulthood due to risky behavior

• In high prevalent areas, perinatal transmission results in chronic infection in 90%


Risk Factors

• High Prevalent Areas‐ Perinatal transmission most

common and vertical transmission as high as 90%

• Intermediate Prevalence Areas‐ common age 1‐5

– Horizontal transmission common via breaks in skin and

mucous membranes, close body contact

• Low prevalence areas‐ most common age 25‐44

– SSexual liintercourse t with ith iinfected f t diindividual di id l

• Heterosexual transmission‐39%

• MSM‐ 24%

– IV ddrug use‐ 16%

– Others‐ accupuncture, tattoo, body piercings

– Blood transfusion‐ risk 1:63,000


• Belongs to

hepadnavirus family

• Genome‐ Genome relaxed

partially dsDNA

replicates by reverse

transcriptase

Hepatitis B Virus

• Comprised of envelope of viral encoded proteins

(HBsAg) and core of nucleocapsid protein (HbcAg),

viral genome, DNA polymerase protein


Acute Hepatitis B

• Exposure‐ HBV enters bloodstream, circulates to liver

• Incubation period‐ Pt is asymptomatic, normal liver transaminases

– HBV replicates within hepatocytes, immune response initiated, HBV DNA rises

– May last 1‐6mo, with avg duration of 60 days

• Prodrome‐ non‐specific symptoms of anorexia, malaise, nausea, vomiting, abd pain

Acute phase‐ 70% have subclinical hepatitis, while 30% develop icteric hepatitis

– Avg time from infection to jaundice 90 days.

– Labs reveal elevations in AST and ALT up to 1000‐2000 IU/L, with ALT>AST

• Resolution‐ Associated with decline in liver transaminases and symptomatic resolution

– Transaminases normalize within 2‐8 weeks

– Among those who recover, virus cleared by antiviral antibodies and cytotoxic T lymphs

– Resolution associated with elimination of virus and appearance of anti‐ HBs, conferring

lifelong immunity from re‐infection


Serologic Markers

• HBsAg‐ serologic hallmark of infection (acute and chronic)

– Detectable after 4‐10wk incubation period before symptoms and rise in ALT

– Typically becomes undetectable after 4‐6mo

– Persistence >6mo implies chronic hep B

• Anti‐HBs‐ Follows disappearance of HBsAg and persists for life

– May not be detectable during window period for few weeks –months during which

no HBsAg or anti‐HBs are detectable

• HBcAg‐ intracellular antigen expressed in hepatocytes but not expressed in serum

– Can be detected by immunohistochmical staining of liver histological specimens

• IgM anti‐HBc‐ shortly follows HBsAg positivity

– Positive during window period‐ HBsAg undetectable and anti‐HBs may not be positive

– Indication of acute HBV infection

– May remain detectable up to two years after acute infection

– May also be positive in exacerbations of chronic HBV

• IgG anti‐HBc‐ persists for life in pt with acute or chronic HBV infection


Serologic Markers (cont)

• HBeAg‐ protein marker indicating HBV replication and infectivity

– Associated with high levels of HBV DNA in serum and high rates of

transmission from carrier mothers to babies

– HBeAg seroconversion to anti‐Hbe occurs early in acute HBV, typically

before HBsAg seroconversion to anti anti‐ HBs

– Seroconversion may take months to years in pt with chronic HBV but

indicates decrease of serum HBV DNA and remission

• HBV DNA

– Most assays use real time PCR, reporting in IU/mL

– Recovery from acute hepatitis accompanied by disappearance of HBV

DNA in i serum

– Low levels HBV DNA detectable in the blood for many years


Acute Hepatitis B Treatment

• Treatment for acute HBV mainly supportive‐ progression to fulminant hepatic

failure


Over course of admission…

• Pt spiked daily fevers to 38.9 thought to be 2/2 hep B. Blood

cultures lt remained i dnegative, ti no other th source of f acute t infection. i f ti On O

ceftriaxone x 3 days for UTI.

• Symptomatic improvement‐ abdominal pain resolved, nausea

resolved resolved, pt able to tolerate PO

• Total bilirubin trended from 21.0 19.1, ALT 1153 1060, AST

994 916

• GI consult‐ consult no additional w/u indicated, follow up as outpatient

with symptomatic management for acute hepatitis B

• Surgery consult signed off

• UTI‐ pt p ggiven 3 days y of ceftriaxone and d/cwoabx /

• Source of infection remained unclear‐ pt denies any risky sexual

behavior, IVDU, recent blood transfusions, etc.


2 week follow up

• Total bilirubin: 21.0 7.4

• ALT 1153: 144

• AST: 994 71

• Albumin: 2.9 3.5

• HHepatitis titi B viral i llload: d 282199 247

• Still admits to dark urine and some fatigue but

abd bd pain i resolved l dand d feeling f li much h better btt

• Regular follow up per GI


Take Home Points

• Most acute Hepatitis p B infections are self‐limiting g and

will resolve with symptomatic management in 6mo 6

• Active infections need follow up in clinic to trend

transaminases, bilirubin, and serology

• Pts should refrain from sexual activity until they

develop anti‐HBs, which may take up to 6mo

• Those with chronic hepatitis B have increased risk of

developing cirrhosis and hepatocellular carcinoma


Thanks!

Questions?

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