mdc preliminary 10062010 eve

8/8/2019 MDC Preliminary 10062010 Eve

1/47

MDC10/07/2010

Revathi C Belur


2/47

CaseCC: Right Flank, RUQ painHPI: 50 yo woman with a h/o ALL s/p stem cell

transplant in 2 007 , DM, RA, GERD, fatty liver disease, and fibromyalgia presents to her PCP with R flank, RUQ pain. Pt stated thatthe pain began 4 nights ago following fever to10 1. 7 , chills, sore throat, HA, and diarrhea inthe morning. She took 8 00 mg ibuprofen atthat time w/o relief.


3/47

PMHx

Pre B Cell ALL s/p stem cell transplant 2 007

DMRAGERDFatty liver disease

FibromyalgiaCarpal tunnel syndrome


4/47

PSHx

Cholecystectomy 1984C-sectiontubal ligationknee/ankle arthroscopic surgeries


5/47

Hom e Medicati on s

amitriptyline 2 5 mg QHSaspirin 81 mg Dailyergocalciferolglipizideibuprofen 6 00 mg PO TID PRNmagnesium oxide 2 50 mg Dailymetformin 1, 000 mg PO BIDmycophenolate mofetil 1, 000 mg PO BID


6/47

Hom e Medicati on snaproxen 500 mg PO BIDomeprazole 4 0 mg PO Dailysimvastatin 2 0 mg PO QHS


7/47

HistoryFamHx:

Mother and father - HL and HTNSister CVA

SocHx:

Denies tobacco, EtOH and illicitsLives with her sister and 2 daughtersDisabled and no working


8/47

Review of SystemsDaily HA, occasional electrical sensationacross her chest, muscle spasms of her Feet. Denied CP, SOB, F/C, D/C,heat/cold intolerance, bleeding disorder,

weight changes.


9/47

General Medicine Consult1.How should we approach abdominal

pain/flank pain in the outpatient settingand what immediate work-up/examneeds to be/can be done?

2. When should we admit?


10/47

Further careShe was sent to the ED to r/o pyelonephritis,nephrolithiasis, or other intraabdominal

process. W/U at that time was notable for aWBC to 14.6 and negative CXR and CT abdand pelvis. She was given diazepam,morphine, and ketorolac in the ED anddischarged. She presented again 2 dayslater with the same complaints and was given4mg IV morphine x4 with minimal relief of her pain.


11/47

CT of abdomen, pelvis


12/47


13/47


14/47


15/47


16/47


17/47


18/47


19/47

ImagingCT abdomen/pelvisMild hyperdensity within the bilateralcollecting systems is likely the sequelaof recent IV contrast administration.There is no evidence of renal calculi or

another acute intra-abdominal process.


20/47

Imaging

U/S AbdomenUnremarkable ultrasound of the right

upper quadrant.CXR

No active cardiopulmonary disease.


21/47

In ERRepeat CT abd and pelvis and abd US

were negative. Her leukocytosis of 2days ago had resolved. She deniedtaking any Tylenol or Tylenol containingnarcotics. She vomited x1 after receiving her last dose of morphine.She denies trauma and post-prandialvariation. She stated that the pain wasunlike her fibromyalgia pain.


22/47

Further w/

uin ER

Hepatitis serologies checked: Hep A, Hep B,Hep C negative.

UA with small blood.


23/47

Physical Exam on Floor Admitted for intractable right

flank/RUQ pain.Vitals:Temp: 98 deg FahrenheitBP:12 7 /7 8 HR: 9 0 RR:18


24/47

Physical Exam on Floor General: awake, alert, NADHEENT: PERRL, MMM, OP clear

Neck: no LADHeart: RRR, S1 S2, no murmursLungs: CTA-B

Abdomen: +NABS, nondistended, tendernessto deep palpation in RUQ, no HSM

Pain with palpation of R CVA, no paraspinaltenderness

Ext: no edema, cyanosis, or clubbing


25/47

Labs138 | 1 0 3 | 18-------------------------12.7

/37

.7


26/47

LabsPT 13.2PTT 28.2

INR 0 .9 5

Tbili 0 .6Dbili 0 .1

Alk Phos 112 AST - 119 (29 ytd) ALT - 1 55 (34 ytd)

albumin 3.3


27/47

Labs

lipase 1 7

Hep A-C serology negative

UA - small blood with 4 RBCs, traceprotein


28/47

D ifferential D iagnoses of Right F lank Pain/RUQ pain

Right Flank painUrolithiasisRadic u lar/m u scu lar PyelonephritisHerpes Zoster Renal AbscessRenal Vein T hrombosis

Renal InfarctionAbdominal Aortic Ane u rysm (AAA)RUQ painBiliary: calc u li, infection, inflammation, neoplasmHepatic: hepatitis, abscess, hepatic congestion, neoplasm, tra u ma.Gastric: peptic u lcer disease (PU D ), pyloric stenosis, neoplasm, alcoholic gastritis, hiatal

herniaPancreatic: pancreatitis, neoplasm, stone in pancreatic d u ct or amp u llaRenal: calc u li, infection, inflammation, neoplasm, r u ptu re of kidneyPu lmonary: pne u monia, p u lmonary infarction, right-sided ple u risyIntestinal: retrocecal appendicitis, intestinal obstr u ction, high fecal impaction, divertic u litisC ardiac: myocardial ischemia (partic u larly involving the inferior wall), pericarditisC u taneo u s: Herpes Zoster T rau maF

itz-Hu

gh-C u

rtis syndrome (perihepatitis)


29/47

D ifferential D iagnoses of elevated

LF T sLiver disease (e.g., viral hepatitis, cirrhosis, Reyes syndrome)Alcohol ab u seD r u gs (e.g., acetaminophen, statins, NSAI D s, fenofibrates, antibiotics, anabolic steroids,

narcotics, heparin, labetalol, amiodarone, chlorpromazine, phenytoinHepatic congesionsInfectio u s monon u cleosis, sepsis, CM V infection, HIV infectionLiver metastasesAu toimm u ne hepatitisM IM yocarditisSevere m u scle tra u maD ermatomyositis or polymyositisPrimary liver malignancyRenal and P u lmonary infarctionC onvu lsionsEclampsiaD ehydration (relative increase)C hinese herbs


30/47

HospitalD

ay 1Since pt had RA and on cell cept,Rheumatology was consulted.Q uestions for Rheumatology consult1. Can RA, either directly or in relation to

treatment, lead to liver function

abnormalities?2. How do you diagnose RA-related(autoimmune?) hepatitis?


31/47

Fu rther development

Pt was noted to have erythematous rashon right flank.

Labs continued to show elevatedtransaminases and alk phos.


32/47

Hospital Day 2Liver enzymes continue to trend upwards.

Antimitochondrial antibody sent

Antismooth muscle antibody sentCMV, HCV, EBV, HSV type 1, VZV PCR sent.

P retra n spla n t ser o log ies 5/2007

+CMV+VZV+EBV+HSV I/II


33/47

Lab Results Antimitochondrial antibody - Negative Antismooth muscle antibody - NegativeCMV - None detectedHCV None detectedEBV None detected

HSV type 1 None detectedVZV PCR - 61 00


34/47

InterpretationPt had disseminated VZV infection andVZV hepatitis. Liver biopsy to confirm theVZV hepatitis was deferred.


35/47

Liver Consult

What are the causes of elevated LFTs ina person on cellcept with RA?

How common is the liver infection causedby non-hepatotropic virus?


36/47

Heme Onc ConsultIn a patient with stem cell transplant, on

immunosuppressant therapy, what are the

most common causes of elevated LFTs?

What would make you suspect GVHD versusinfectious hepatitis?

How would you treat GVHD?


37/47

Transplant ID consultHow common is hepatitis in transplant

patients?

How common is hepatitis by non-hepatotropic virus?

How is the diagnosis of VZV hepatitismade?


38/47

Evidence BasedM

edicineT here are many case reports, reporting the

infection of the liver by VZV in pts who are

imm u nos u ppressed.


39/47

EBM

Case ReportsIn a case report and review of literat u re review by Pishvaian

et al p u blished in D igestive D iseases and Sciences in J u ly2006, reported a fatal case of VZV hepatitis.


40/47

Disseminated VZV and hepatitis

Pts herpes zoster vesic u lar rash was on thesame dermatome that corresponded to thenerve distrib u tion of liver also.


41/47

VZV HepatitisVaricella zoster vir u s (VZV), a member of the Herpesviridae family, also hasthe potential to ca u se hepatitis. Primary varicella infection (chickenpox) ismost often seen in children, and it consists of a febrile illness associated withvesic u lar rash. Hepatitis is u ncommon in primary infection inimm u nocompetent hosts altho u gh a mild derangement of liver enzyme tests issometimes present in children d u ring chickenpox infection.Beca u se of the high prevalence of varicella expos u re in ad u lt pop u lation, VZVinfection in ad u lt transplant recipients is u su ally the res u lt of the reactivationof latent infection, and it u su ally presents as typical herpes zoster or shingles,which are most often clinically evident as a vesic u lar rash in a dermatomaldistrib u tion. Occasionally, a nondermatomal distrib u tion of the rash isobserved; this may indicate generalized a high risk of associated visceral

involvement, incl u ding hepatitis. D isting u ishing this presentation fromdisseminated HSV may be clinically diffic u lt, and scraping of a c u taneo u svesicle, followed by imm u nofl u orescent examination to detect the presence of antigens, is req u ired to confirm the diagnosis. Liver involvement by VZV inthe absence of c u taneo u s disease is rare, b u t it has been occasionally describedas part of a generalized visceral VZV infection witho u t rash.


42/47

VZV HepatitisPrimary infection u su ally occ u rs in pediatric recipients altho u gh seronegativeadu lts are also at risk. Aggressive antiviral treatment with acyclovir may

prevent its dissemination and the associated visceral complications.Vaccination has been recommended for nonimm u ne patients beforetransplantation. Beca u se this is a live atten u ated varicella vaccine,administration to SO T recipients is not recommended by the C D C . However,this has been given to small n u mbers of patients u su ally as postexpos u re

prophylaxis with mixed res u lts.Liver involvement by VZV is s u ggested by a typical varicella or zoster rashthat is accompanied with liver f u nction abnormalities, fever, and abdominal

pain. In HSV hepatitis, elevated aminotransferases that are more than fivetimes the ULN are the predominant biochemical abnormality, b u t the bilir u bin

may also be moderately increased to as m u ch as three to fo u r times the ULN.Liver biopsy findings are similar to those seen in HSV hepatitis, with focalcoag u lative necrosis and an inflammatory infiltrate. Viral incl u sions may be

present, b u t their absence does not excl u de the diagnosis.Imm u nohistochemistry or in sit u hybridization can help to disting u ish betweenHSV and VZV hepatitis.


43/47

VZV inT

ransplant pts. That VZV infection tends to occ u r later in the post-

transplantation period than HSV, u su ally approximately 4to 5 months after transplantation b u t most often within a

year of the procedu

re, is worth noting.M

any of the reportsof liver involvement by VZV indicate that this occ u rsrelatively early in posttransplantation period, reflecting themore intense state of imm u nos u ppression at that time thatallows dissemination of the vir u s. Hepatic VZV, like other visceral VZV infections, sho u ld be treated with high dose

IV acyclovir. M ortality from disseminated VZV infectionhas been red u ced with, b u t not eradicated by , acyclovir treatment, th u s highlighting the potentially serio u s nat u reof hepatic involvement by VZV in this gro u p of patients.


44/47

VZV infection of allograftsHerpes Simples and VZV viral hepatitisHerpes simplex (types I and II) vir u s and varicella-zoster vir u s (VZV)have been identified as potential ca u ses of liver allograft hepatitis.Allograft involvement may occ u r as early as 3 days after transplant or at any time thereafter. T he clinical feat u res incl u de fever, vesic u lar rashes, fatig u e, and body pain, combined with serologic evidence of hepatic inj u ry. If HSV hepatitis is u nrecognized, it can lead tosu bmassive or massive hepatic necrosis, hypotension, disseminatedintravasc u lar coag u lopathy, and metabolic acidosis q u ite rapidly.Fu lminant cases occ u r more often in patients who do not haveevidence of prior antibody-mediated imm u nity. Early recognitionu sing needle biopsy sampling is partic u larly cr u cial beca u se effective

pharmacologic therapy is available.


45/47

Management

Pt was started on IV acyclovir.

Pt was transferred to Hematology service.

Pts L F T s trended down and dischargedhome.


46/47

ReferencesTr ansplant I nfections

By Raleigh A Bowden, Per Lj u ngman, D avid R SnydmanSchiff's diseases of the live r, Volume 1

By E u gene R. Schiff, M ichael F . Sorrell, Willis C . M addrey


47/47

AcknowledgementT hanks to:D r. Zar

D r. T u lleyD r. PeaceD r. AramiD r. BerkesD r. ReidD r. ZibelmanT eam B

mdc preliminary 10062010 eve

Documents