MEDICAL GRANDROUNDS MEDICAL GRANDROUNDS IVY KATHRYN ILAGAN, MD IVY KATHRYN ILAGAN, MD August 21, 2008 August 21, 2008
Jan 05, 2016
MEDICAL MEDICAL GRANDROUNDSGRANDROUNDS
IVY KATHRYN ILAGAN, MDIVY KATHRYN ILAGAN, MD
August 21, 2008August 21, 2008
OBJECTIVESOBJECTIVES
To discuss an unusual To discuss an unusual presentation of infectious presentation of infectious mononucleosis.mononucleosis.
GENERAL DATAGENERAL DATA
RC RC 35 year old male35 year old male MarriedMarried FilipinoFilipino
CHIEF COMPLAINTCHIEF COMPLAINT
FEVERFEVER
HISTORY OF PRESENT HISTORY OF PRESENT ILLNESSILLNESS Apparently wellApparently well
8 days PTA8 days PTA intermittent fever (maximum intermittent fever (maximum
temperature 40.30C)temperature 40.30C) chillschillsHeadacheHeadacheNonproductive coughNonproductive cough
6 days PTA6 days PTA Consult doneConsult done CBC CBC normal normal systemic viral illness systemic viral illness sent home sent home
5 days PTA5 days PTA still has intermittent feverstill has intermittent fever epigastric painepigastric pain VomitingVomiting Loose watery stool, 4xLoose watery stool, 4x
4 days PTA4 days PTA Admitted in a private hospitalAdmitted in a private hospital Work-ups done:Work-ups done:
• CBC CBC leukocytosis, predominance of leukocytosis, predominance of lymphocyteslymphocytes
• CXR CXR bibasal pneumonia with bibasal pneumonia with
minimal pleural effusion, minimal pleural effusion, leftleft
• abdominal ultrasound abdominal ultrasound
minimal ascitesminimal ascites
normal liver size with normal liver size with diffuse patterndiffuse pattern
splenomegalysplenomegaly
cholecystitischolecystitis
• Malarial smear Malarial smear negative negative
• Chlamydia Chlamydia negative negative
• Blood and urine CS Blood and urine CS no growth no growth
Treated as pneumonia and acute Treated as pneumonia and acute gastroenteritisgastroenteritis
Fever, epigastric pain, vomiting, Fever, epigastric pain, vomiting, and diarrhea persisted, hence and diarrhea persisted, hence transferred in this institution transferred in this institution
REVIEW OF SYSTEMSREVIEW OF SYSTEMS
GeneralGeneral
(-) weight loss(-) weight loss
Head and neckHead and neck
(-) blurring (-) blurring
(-) visual changes(-) visual changes
(-) sorethroat(-) sorethroat
Chest and LungsChest and Lungs
(-) dyspnea(-) dyspnea
CardiovascularCardiovascular(-) chest pain(-) chest pain
(-) palpitations(-) palpitations
(-) easy fatigability(-) easy fatigability
(-) orthopnea(-) orthopnea
GastrointestinalGastrointestinal(-) hematemesis(-) hematemesis
(-) hematochezia(-) hematochezia
(-) melena(-) melena
GenitourinaryGenitourinary
(-) dysuria(-) dysuria
(-) hematuria(-) hematuria
HematologicHematologic(-) easy bruisability(-) easy bruisability
NeurologicNeurologic(-) changes in behavior(-) changes in behavior
PAST MEDICALL PAST MEDICALL HISTORYHISTORY Non-hypertensiveNon-hypertensive Non-diabeticNon-diabetic Non-asthmaticNon-asthmatic No history of pulmonary No history of pulmonary
tuberculosistuberculosis No known allergiesNo known allergies No history of traumaNo history of trauma
FAMILY HISTORYFAMILY HISTORY
Hypertension - paternal sideHypertension - paternal side Diabetes mellitus – maternal sideDiabetes mellitus – maternal side Asthma - maternal sideAsthma - maternal side No history of blood dyscrasiaNo history of blood dyscrasia
PERSONAL AND PERSONAL AND SOCIALSOCIAL
UnemployedUnemployed 15-pack year history of smoking15-pack year history of smoking Occasional alcoholic beverage Occasional alcoholic beverage
drinkerdrinker
PHYSICAL PHYSICAL EXAMINATIONEXAMINATION GENERAL SURVEYGENERAL SURVEY
Awake, conscious, coherent, not in Awake, conscious, coherent, not in respiratory distress.respiratory distress.
VITAL SIGNSVITAL SIGNS BP 130/80mmHg BP 130/80mmHg HR 90bpm HR 90bpm RR 20cpm RR 20cpm T 39.2CT 39.2C
SKIN/HEAD/EYES/EARS/NOSE/NECK/THROATSKIN/HEAD/EYES/EARS/NOSE/NECK/THROAT Good skin turgorGood skin turgor
Pink palpebral conjunctiva, Pink palpebral conjunctiva, icteric icteric scleraesclerae
no tonsillopharyngeal congestionno tonsillopharyngeal congestion no cervical lymphadenopathyno cervical lymphadenopathy
CHEST AND LUNGSCHEST AND LUNGS Symmetrical chest expansion, no Symmetrical chest expansion, no
retractionsretractions Crepitant rales, bibasal areaCrepitant rales, bibasal area Decreased breath sounds, right lung Decreased breath sounds, right lung
basebase No wheezesNo wheezes
CVSCVS– Normal rate, regular rhythm, S1>S2 apex, Normal rate, regular rhythm, S1>S2 apex,
S2>S1 base, no murmurs, no S3, no S4S2>S1 base, no murmurs, no S3, no S4
ABDOMENABDOMEN– FlabbyFlabby– Normoactive bowel soundsNormoactive bowel sounds– SoftSoft– direct tenderness, epigastric areadirect tenderness, epigastric area– palpable liver, up to 4 cm from palpable liver, up to 4 cm from
subcostal linesubcostal line– dullness on 9th – 11dullness on 9th – 11thth ICS (obliterated ICS (obliterated
traube’s space) traube’s space)
EXTREMITIESEXTREMITIES– No gross lesionsNo gross lesions– No hematoma, petechiae, purpuraNo hematoma, petechiae, purpura– No cyanosisNo cyanosis– No edemaNo edema– Full and equal peripheral pulses Full and equal peripheral pulses
SALIENT FEATURESSALIENT FEATURES 35 year old male35 year old male
Previously treated in another hospital as pneumonia Previously treated in another hospital as pneumonia and acute gastroenteritisand acute gastroenteritis
Abdominal ultrasound done revealed ascitis, Abdominal ultrasound done revealed ascitis, cholecystitis, and splenomegalycholecystitis, and splenomegaly
On PE, On PE, – Febrile Febrile – IctericIcteric– crepitant rales, bibasal area; decreased breath sounds, crepitant rales, bibasal area; decreased breath sounds,
right lung baseright lung base– palpable liver, up to 4 cm from subcostal line, dullness palpable liver, up to 4 cm from subcostal line, dullness
on 9on 9thth-11-11thth ICS ICS
INITIAL IMPRESSIONINITIAL IMPRESSION
Community acquired pneumoniaCommunity acquired pneumonia Hepatosplenomegaly, etiology to Hepatosplenomegaly, etiology to
be determinedbe determined CholecystitisCholecystitis
COURSE IN THE COURSE IN THE WARDSWARDS
ABG ABG at room air, RR24at room air, RR24
pO2 pO2 81.1 81.1
pHpH 7.57.5
pCO2 pCO2 31.631.6
HCO3HCO3 24.824.8
O2 sat O2 sat 97%97%
BEBE +2.6+2.6
TCO2 TCO2 25.825.8
- respiratory alkalosis- respiratory alkalosis
CXR CXR – pneumonia, both lower lobespneumonia, both lower lobes– minimal pleural effusionminimal pleural effusion– mild left ventricular enlargementmild left ventricular enlargement
Pneumonia
5-Jun
Alkaline Phosphatase
543
TB 1.7
DB – IB 1.3 – 0.4
Na 0.8
Lipase 224
Amylase 28
CT scan of the whole abdomenCT scan of the whole abdomen – HepatosplenomegalyHepatosplenomegaly– Consider splenic infarctionsConsider splenic infarctions– Minimal ascitesMinimal ascites– Prominent retroperitoneal lymph Prominent retroperitoneal lymph
nodes, which may be reactive in nodes, which may be reactive in naturenature
– Minimal bilateral pleural effusion with Minimal bilateral pleural effusion with compressive atelectasis in both lower compressive atelectasis in both lower lobeslobes
CT scan of the CT scan of the whole abdomenwhole abdomen – HepatosplenomegalyHepatosplenomegaly– Consider splenic Consider splenic
infarctionsinfarctions
Lipase 224
Amylase 28
Alpha fetoprotein Alpha fetoprotein negativenegative
Pneumonia
Hepatosplenomegaly
Acute Cholecystitis
Pneumonia
Hepatosplenomegaly
Pneumonia
Hepatosplenomegaly
Splenic Infarct
Pneumonia
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Malignancy
Pneumonia
Hepatosplenomegaly
Splenic Infarct
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Infective Endocarditis
Atrial Fibrillation
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Leukemia
Polycythemia Vera
Protein C&S Deficiency
Salmonellosis
Infectious Mononucleosis
SLE
Infective Endocarditis
Atrial Fibrillation
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Leukemia
Polycythemia Vera
Protein C&S Deficiency
Salmonellosis
Infectious Mononucleosis
SLE
Infective Endocarditis
Day 2
6-Jun
Hgb 11.7
Hct 36.9
WBC 8.96
Seg 26
Lympho 56
Mono 17
Platelet ct 173T
MCV 83.9
MCH 26.6
Day 1 Day 2
5-Jun 6-Jun
Alkalinephosphata
se
543 439
TB 1.7 1.2
DB – IB 1.3 – 0.4
Na 0.8 141
K 3.3
BUN 6
Creatinine 0.8
CO2 29
Lipase 224
Amylase 28
Day 1 Day 2
5-Jun 6-Jun
SGOT 115
SGPT 129
Albumin 2.4
Corrected Ca
9.26
Glucose 89.91
Cholesterol
119.09
Hepatocellular/ Cholestatic Viral Hepatitis
Infectious Mononucleosis
SGOT 115
SGPT 129
Day 1 Day 2
5-Jun 6-Jun
Alkalinephosphatase
543 439
TB 1.7 1.2
DB – IB 1.3 – 0.4
Pneumonia
Hepatosplenomegaly
Splenic Infarct
Hepatocellular/ Cholestatic Viral Hepatitis
Infectious Mononucleosis
Day 1 Day 2
5-Jun 6-Jun
Alkalinephosphatase
543 439
Heat fractionation of alkaline Heat fractionation of alkaline phosphatase 45%phosphatase 45%Heated alkaline phosphatase at 560C: 216 U/LHeated alkaline phosphatase at 560C: 216 U/L
<25% osteoblastic<25% osteoblastic
>25% hepatic>25% hepatic
Day 2 Day 4
6-Jun 8-Jun
Hgb 11.7 11.7
Hct 36.9 36.3
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Leukemia
Polycythemia Vera
Protein C&S Deficiency
Salmonellosis
Infectious Mononucleosis
SLE
Hepatocellular/ Cholestatic Viral Hepatitis
Infectious Mononucleosis
Protein C Protein C normal 4.15normal 4.15 Protein SProtein S normal 17 normal 17
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Leukemia
Protein C&S Deficiency
Salmonellosis
Infectious Mononucleosis
SLE
Hepatocellular/ Cholestatic Viral Hepatitis
Infectious Mononucleosis
p-ANCAp-ANCA negative negative CryoglobulinCryoglobulin negative negative
Hepatocellular/ Cholestatic
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Leukemia
Salmonellosis
Infectious Mononucleosis
SLE
Viral Hepatitis
Infectious Mononucleosis
HbsAg HbsAg negatvenegatve Anti HCVAnti HCV non reactive non reactive
Hepatocellular/ Cholestatic
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Leukemia
Salmonellosis
Infectious Mononucleosis
Infectious Mononucleosis
Peripheral blood smear Peripheral blood smear – WBCs with atypical forms, platelets appear WBCs with atypical forms, platelets appear
increased and in clumps with some giant increased and in clumps with some giant platelets noted.platelets noted.
Bone marrrow culture – no growthBone marrrow culture – no growth Bone marrow biopsy - normalBone marrow biopsy - normal
Hepatocellular/ Cholestatic
Pneumonia
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Leukemia
Salmonellosis
Infectious Mononucleosis
Infectious Mononucleosis
Hepatocellular/ Cholestatic
Hepatosplenomegaly
Splenic Infarct
InfectiousSalmonellosis
Infectious Mononucleosis
Infectious Mononucleosis
Hepatosplenomegaly
Splenic Infarct
Infectious
Hematologic
Autoimmune
Infective Endocarditis
Blood cultureBlood culture
- - Streptococcus viridansStreptococcus viridans
C reactive protein -C reactive protein - positive up to positive up to 1:8 serum dilutions1:8 serum dilutions
2D Echocardiography with color 2D Echocardiography with color flow and Doppler study flow and Doppler study
- Normal, EF 70%. Mitral and - Normal, EF 70%. Mitral and tricuspid regurgitation are trivial.tricuspid regurgitation are trivial.
Transesophageal Transesophageal echocardiographyechocardiography – No echocardiographic evidence of No echocardiographic evidence of
endocardial vegetations on the endocardial vegetations on the aortic, pulmonic, mitral and tricuspid aortic, pulmonic, mitral and tricuspid valves.valves.
– Intact interatrial septum.Intact interatrial septum.– No intracardiac thrombus formation. No intracardiac thrombus formation.
The diagnosis of infective The diagnosis of infective endocarditis is established with endocarditis is established with certainty only when vegetations certainty only when vegetations obtained at cardiac surgery, at obtained at cardiac surgery, at autopsy, or from an artery (an autopsy, or from an artery (an embolus) are examined embolus) are examined histologically and histologically and microbiologically.microbiologically.
The Duke criteria—has been The Duke criteria—has been developed on the basis of clinical, developed on the basis of clinical, laboratory, and echocardiographic laboratory, and echocardiographic findings.findings.
Documentation of two major Documentation of two major criteria, of one major and three criteria, of one major and three minor criteria, or of five minor minor criteria, or of five minor criteria allows a clinical diagnosis of criteria allows a clinical diagnosis of definite endocarditis. definite endocarditis.
The Duke criteriaThe Duke criteria
Major CriteriaMajor Criteria
1. Positive blood culture1. Positive blood cultureViridans streptococciViridans streptococci, ,
Streptococcus bovis, HACEK group, Streptococcus bovis, HACEK group, Staphylococcus aureus, community-acquired Staphylococcus aureus, community-acquired enterococci in the absence of a primary focusenterococci in the absence of a primary focus
2. Evidence of endocardial 2. Evidence of endocardial involvementinvolvement
- Positive echocardiogram- Positive echocardiogram
- New valvular regurgitation- New valvular regurgitation
Minor CriteriaMinor Criteria
1. Predisposition: predisposing heart 1. Predisposition: predisposing heart condition or injection drug usecondition or injection drug use
2. Fever 38.0°C2. Fever 38.0°C
3. Vascular phenomena: major arterial 3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, conjunctival hemorrhages, Janeway lesionshemorrhages, Janeway lesions
4. Immunologic phenomena: 4. Immunologic phenomena: glomerulonephritis, Osler's nodes, glomerulonephritis, Osler's nodes, Roth's spots, rheumatoid factorRoth's spots, rheumatoid factor
5. Microbiologic evidence: positive 5. Microbiologic evidence: positive blood culture but not meeting major blood culture but not meeting major criterion as noted previously or criterion as noted previously or serologic evidence of active infection serologic evidence of active infection with organism consistent with infective with organism consistent with infective endocarditis. endocarditis.
Hepatocellular/ Cholestatic
Hepatosplenomegaly
Splenic Infarct
InfectiousSalmonellosis
Infectious Mononucleosis
Infectious Mononucleosis
Hepatocellular/ Cholestatic
Hepatosplenomegaly
Splenic Infarct
Infectious
Infectious Mononucleosis
Infectious Mononucleosis
Hepatocellular/ Cholestatic
Hepatosplenomegaly
Splenic Infarct
Infectious
Infectious Mononucleosis
Monospot test - positiveMonospot test - positive
Started on Started on – piperacillin-tazobactam 4.5g IV q8piperacillin-tazobactam 4.5g IV q8– metronidazole 500 mg IV q8metronidazole 500 mg IV q8– vancomycin 1g IV q12vancomycin 1g IV q12
55thth HOSPITAL DAY HOSPITAL DAY
Blood CS Blood CS
- - Streptococcus viridansStreptococcus viridans
Sensitive to penicillin and Sensitive to penicillin and ampicillinampicillin
Resistant vancomycinResistant vancomycin Vancomycin and metronidazole Vancomycin and metronidazole
was then discontinued. was then discontinued.
37
37.5
38
38.5
39
39.5
Day 1 Day 2 Day 3 Day 4 Day 5Hospital Day
Te
mp
era
ture
(C
elc
ius
)
piperacillin-tazobactam 4.5g IV q8
Repeat CXR Repeat CXR – partial resolution of the bibasal partial resolution of the bibasal
pleural effusionpleural effusion– subsegemntal atelectasis are now subsegemntal atelectasis are now
seen at seen at
right paracardiac and left basal right paracardiac and left basal regions regions
66thth HOSPITAL DAY HOSPITAL DAY
Tazocin was discontinued Tazocin was discontinued Penicillin G 3M units IV every 4 Penicillin G 3M units IV every 4
hourshours Gentamicin 70 mg IV every 8 Gentamicin 70 mg IV every 8
hours.hours.
37
37.5
38
38.5
39
39.5
Day 1 Day 2 Day 3 Day 4 Day 5 Day 6
Hospital Day
Te
mp
era
ture
(C
elc
ius
)
piperacillin-tazobactam 4.5g IV q8
37
37.5
38
38.5
39
39.5
Day 1 Day 2 Day 3 Day 4 Day 5 Day 6
Hospital Day
Te
mp
era
ture
(C
elc
ius
)
Pen G 3M U IV q4Gentamycin 70mg
IV q8
88thth HOSPITAL DAY HOSPITAL DAY
Day-1 afebrileDay-1 afebrile
No note of recurrence of fever on No note of recurrence of fever on the subsequent days.the subsequent days.
35
35.5
36
36.5
37
37.5
38
38.5
39
39.5
Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7 Day 8 Day 9 Day 10 Day 11 Day 12 Day 13
Hospital Day
D2- Pen G
D2- Genta
Day 2 Day 4 Day 6 Day 7 Day 8
6-Jun 8-Jun 10-Jun 11-Jun 12-Jun
Hgb 11.7 11.7 12.2 12.7 12.5
Hct 36.9 36.3 38 40.2 39.5
WBC 8.96 7.05 8.07 9.01 8.79
Seg 26 40 38 41 49
Lympho 56 46 50 49 44
Mono 17 13 11 8 7
Platelet ct
173T 270T 257T 532T 500T
MCV 83.9 82.9 83.2 84.1 84.9
MCH 26.6 26.7 26.7 26.6 26.9
Day 1 Day 2 Day 4 Day 8
5-Jun 6-Jun 8-Jun 12-Jun
Alkalinephosphata
se
543 439 480
TB 1.7 1.2 1
DB – IB 1.3 – 0.4 0.5 – 0.5
Na 0.8 141 138 135
K 3.3 3.9 3.5
BUN 6 13.01
Creatinine 0.8 1.5
Day 1 Day 2 Day 4 Day 8 Day 12
5-Jun 6-Jun 8-Jun 12-Jun 16-Jun
Alkalinephosphata
se
543 439 480 251
TB 1.7 1.2 1 0.7
DB – IB 1.3 – 0.4 0.5 – 0.5 0.2 – 0.5
Na 0.8 141 138 135 136
K 3.3 3.9 3.5 4.1
BUN 6 13.01 16.99
Creatinine 0.8 1.5 1.5
CO2 29
Lipase 224
Amylase 28
SGOT 115 38
SGPT 129 71
FINAL DIAGNOSISFINAL DIAGNOSIS
Infectious mononucloesisInfectious mononucloesis
Streptococcus viridansStreptococcus viridans bacteremia bacteremia
INFECTIOUS INFECTIOUS MONONUCLEOSISMONONUCLEOSIS
Pfeiffer's diseasePfeiffer's disease MonoMono – Kissing disease – Kissing disease Glandular feverGlandular fever
Epstein-Barr virus Epstein-Barr virus
– The cause of heterophile-positive The cause of heterophile-positive infectious mononucleosis (IM)infectious mononucleosis (IM)
– Also associated with several human Also associated with several human tumors, including nasopharyngeal tumors, including nasopharyngeal carcinoma, Burkitt's lymphoma, carcinoma, Burkitt's lymphoma, Hodgkin's disease, and (in patients Hodgkin's disease, and (in patients with immunodeficiencies) B cell with immunodeficiencies) B cell lymphoma. lymphoma.
- Family HerpesviridaeFamily Herpesviridae- Consists of a linear DNA coreConsists of a linear DNA core- Two types of EBV that are widely Two types of EBV that are widely
prevalent in nature are not prevalent in nature are not distinguishable by conventional distinguishable by conventional serologic tests.serologic tests.
EpidemiologyEpidemiology
Occurs worldwide. Occurs worldwide. Most common in early childhood, with Most common in early childhood, with
a second peak during late a second peak during late adolescence. adolescence.
By adulthood, more than 90% of By adulthood, more than 90% of individuals have been infected and individuals have been infected and have antibodies to the virus. have antibodies to the virus.
Spread by contact with oral secretionsSpread by contact with oral secretions More than 90% of asymptomatic More than 90% of asymptomatic
seropositive individuals shed the virus seropositive individuals shed the virus in oropharyngeal secretions. in oropharyngeal secretions.
SymptomsSymptoms Sore throatSore throat 75 % 75 % MalaiseMalaise 4747 HeadacheHeadache 38 38 Abdominal pain, nausea, or Abdominal pain, nausea, or
vomitingvomiting 1717 ChillsChills 1010 DiarrheaDiarrhea
ManifestationsManifestations
SignsSigns LymphadenopathyLymphadenopathy 95%95% FeverFever 9393 Pharyngitis or tonsillitisPharyngitis or tonsillitis 8282 SplenomegalySplenomegaly 5151 HepatomegalyHepatomegaly 1111 RashRash 1010 Periorbital edemaPeriorbital edema 1313 Palatal enanthemPalatal enanthem 77 JaundiceJaundice 55
SPLENIC INFARCTIONSPLENIC INFARCTION
Splenic infarction during IM is very rare;Splenic infarction during IM is very rare; To our knowledge, only five cases have previously been reported To our knowledge, only five cases have previously been reported The pathogenesis of splenic infarction during IM remains unclear. The pathogenesis of splenic infarction during IM remains unclear. In one case report of IM associated with splenic infarction, transient In one case report of IM associated with splenic infarction, transient
elevation of antiphospholipid antibodies was found and thought to elevation of antiphospholipid antibodies was found and thought to be responsible for the splenic infarct. be responsible for the splenic infarct.
Acute EBV infection should be considered in the differential Acute EBV infection should be considered in the differential
diagnosis of splenic infarction. This diagnosis should also be diagnosis of splenic infarction. This diagnosis should also be considered in patients presenting with unexplained acute abdominal considered in patients presenting with unexplained acute abdominal pain. pain.
--Scottish Medical Journal, 2007Scottish Medical Journal, 2007Splenic infarction due to infectious mononucleosis Splenic infarction due to infectious mononucleosis K Ashawesh, R Abdulqawi, BN Chandrappa, K.S. K Ashawesh, R Abdulqawi, BN Chandrappa, K.S.
Srinivasan Srinivasan Department of medicine, Princess Royal Hospital, Department of medicine, Princess Royal Hospital,
Telford, UK Telford, UK
Splenic infarction is a rare feature of infectious Splenic infarction is a rare feature of infectious mononucleosis mononucleosis
Splenic infarction during acute EBV infection Splenic infarction during acute EBV infection associated with the transient induction of associated with the transient induction of antiphospholipid antibodies. antiphospholipid antibodies.
Once other more common causes of splenic Once other more common causes of splenic infarction, such as endocarditis and lymphoma, infarction, such as endocarditis and lymphoma, have been excluded, the possibility of viral-have been excluded, the possibility of viral-induced antiphospholipid antibodies should be induced antiphospholipid antibodies should be considered.considered.
- Journal of clincal virology, 2006Journal of clincal virology, 2006Splenic infarction due to transient antiphospholipid Splenic infarction due to transient antiphospholipid antibodies induced by acute Epstein-Barr virus antibodies induced by acute Epstein-Barr virus infectioninfection
18 year old Japanese man, with hereditary 18 year old Japanese man, with hereditary spherocytosis (HS) known to have developed splenic spherocytosis (HS) known to have developed splenic infarction following infectious mononucleosis (IM). infarction following infectious mononucleosis (IM).
On day 4 of admission, the patient complained of On day 4 of admission, the patient complained of severe abdominal pain. Abdominal CT scan revealed severe abdominal pain. Abdominal CT scan revealed findings of splenic infarction. Two months after the findings of splenic infarction. Two months after the occurrence of splenic infarction, a splenectomy was occurrence of splenic infarction, a splenectomy was performed. performed.
A pathohistologic examination of the resected spleen A pathohistologic examination of the resected spleen revealed no evidence of thrombosis or arterial revealed no evidence of thrombosis or arterial occlusion. We assume that the cause of splenic occlusion. We assume that the cause of splenic infarction was insufficient blood flow to oxygenate the infarction was insufficient blood flow to oxygenate the entire spleen during the acute enlargement of the entire spleen during the acute enlargement of the spleen. spleen.
- Splenic infarction after Epstein-Barr virus infection in a - Splenic infarction after Epstein-Barr virus infection in a patient with hereditary spherocytosis patient with hereditary spherocytosis Suzuki YSuzuki Y, , ShichishimaShichishima T T, , MukaeMukae M M, , OhsakaOhsaka M M, Hayama M, , Hayama M, Horie R, Togano T, Miyazaki K, Ichinoe M, Iwabuchi K, Fujii Horie R, Togano T, Miyazaki K, Ichinoe M, Iwabuchi K, Fujii H, Higashihara M. H, Higashihara M. Department of Hematology, Kitasato University School of Department of Hematology, Kitasato University School of Medicine, Sagamihara, Japan Medicine, Sagamihara, Japan
LABORATORY LABORATORY FINDINGSFINDINGS
WBC usually elevated and peaks WBC usually elevated and peaks at 10,000–20,000/L during the at 10,000–20,000/L during the second or third week of illness.second or third week of illness.
Lymphocytosis with >10% Lymphocytosis with >10% atypical lymphocytes.atypical lymphocytes.
Low-grade neutropenia and Low-grade neutropenia and thrombocytopenia are common thrombocytopenia are common during the first month of illness.during the first month of illness.
Liver function is abnormal in Liver function is abnormal in >90% of cases.>90% of cases.
Aminotransferases and alkaline Aminotransferases and alkaline phosphatase are usually mildly phosphatase are usually mildly elevated. elevated.
Bilirubin is elevated in ~40% of Bilirubin is elevated in ~40% of cases.cases.
Monospot testMonospot test
Positive for infectious Positive for infectious mononucleosismononucleosis
Specific for heterophile Specific for heterophile antibodies, not EBV. antibodies, not EBV.
~75% sensitive and ~90% ~75% sensitive and ~90% specific compared with EBV-specific compared with EBV-specific serologies. specific serologies.
Can also be positive in patients Can also be positive in patients with lumphoma, systemic lupus with lumphoma, systemic lupus erythematosus, viral hepatitis, erythematosus, viral hepatitis, malaria, and some GI cancersmalaria, and some GI cancers
SPECIFIC TEST FOR SPECIFIC TEST FOR EBVEBV
Epstein-Barr Virus (EBV) viral Epstein-Barr Virus (EBV) viral capsid antigen IgG and IgM and, capsid antigen IgG and IgM and, EBV nuclear antigen IgG by EBV nuclear antigen IgG by immunofluorescenceimmunofluorescence
Epstein-Barr virus antibody titers Epstein-Barr virus antibody titers to help distinguish acute infection to help distinguish acute infection from past infection with EBV from past infection with EBV
TREATMENTTREATMENT
Self-limitingSelf-limiting Symptomatic and/or supportive Symptomatic and/or supportive
treatments treatments
Rest is recommended during the acute Rest is recommended during the acute phase of the infection, but activity phase of the infection, but activity should be resumed once acute should be resumed once acute symptoms have resolved. symptoms have resolved.
Nevertheless heavy physical activity Nevertheless heavy physical activity and contact sports should be avoided and contact sports should be avoided to abrogate the risk of splenic rupture, to abrogate the risk of splenic rupture, for at least one month following initial for at least one month following initial infection and until splenomegaly has infection and until splenomegaly has resolved, as determined by ultrasound.resolved, as determined by ultrasound.
MORBIDITY AND MORBIDITY AND MORTALITYMORTALITY Fatalities from mononucleosis are Fatalities from mononucleosis are
near impossible in developed near impossible in developed nations. nations.
CNS: CNS: – Meningitis, encephalitis, hemiplegiaand Meningitis, encephalitis, hemiplegiaand
transverse myelitis. transverse myelitis. – Proposed as a risk factor for the Proposed as a risk factor for the
development of multiple sclerosis, but development of multiple sclerosis, but this has not been affirmed. this has not been affirmed.
Hematologic: Hematologic: – Autoimmune hemolytic anemia Autoimmune hemolytic anemia
(direct Coombs test is positive) and (direct Coombs test is positive) and various cytopenias.various cytopenias.
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