CASE PRESENTATION

Dr. Kailash Raj

35 yr old female KHAIRUNNISA was admitted thru ER on 19oct 2010 with;

Fever 6 monthsGeneralized weakness

According to patient; she was in her usual state of health 6 months back that she started having low grade, on and off fever; associated with generalized weakness that patient’s routine activities were disturbed. For that she visited many general practitioners but got no ultimate relief. Besides that, from last 1 week she started having high grade fever that was associated with rigors, chills, headache and nausea. There is no h/o of joint pain, sore throat, palpitation, sweating, shortness of breath, skin rash, dysuria, hematuria, diarrhea and vomiting.

Case History

PM Hx: Not significant

PS Hx: Not significant

Personal Hx:Appetite---GoodBowel Habits---RegularMicturition ---- NormalThirst---- NormalWeight loss--- No

Family Hx:No history of T.B, D.M, HTN, Asthma

Parents: HealthySiblings: Healthy4 Children: Healthy

Socio-economic Hx:Fair

Case History

Physical examination

35 year old female of average height & built, lying comfortably on bed; oriented to time place and person

Pulse: 98/min B.P: 130/80 Resp: 16/min Temp:103FGen:

Anxious and worried, Anemia+ve, Jaundice –ve, Dehydration –ve, Cyanosis –ve, Clubbing –ve, osler nodes -ve, splintter hemmorhage-ve, janeway lesion -ve .

Neck:No JVD or hepatojugular reflux & no lymph nodes palpable

Cardiovascular:S1 and S2 audible, murmurs audible

Pulmonary:B/L NVB, No wheeze, crepts

Abd:Soft, non tender, hepato-spleenomegaly

Physical examination

CNS:

GCS 15/15 and neck stiffness-ve, other signs of meningeal irritation -veAt time of presentation CNS was fully intact; unfortunately on 3rd day of admission here in hospital she developed left sided weakness with dysarthriaBulk --- B/L NormalPower ---1/5 Lt side & 5/5 Rt sideTone --- Dec Lt sideReflexs--- Diminished Lt sidePlantars--- Rt ↓ ----- Lt- ↑

Laboratory Findings

CBCWBC: 10.9Hb:7.5PLT:137PCV:24.5MCV:80.2Hypochromia+, Anisocytosis++, Poikilocytosis++, Tear drop cells+.

Blood Sugar139mg/dl

Urea: 87Creatinine: 1.5Na: 130K: 3.9Cl: 110Bi carb: 21

LFTT.Protein:7.2Albumin: 3.1Globulin: 4.1T.Billi: 0.8GGT: 142Alk.Phos: 149SGPT: 184SGOT: 63

M.P: seenICT Malaria: +ve for P.Falciparum

Blood Culture: No growth seen.

Urine D/R: Normal Except Protein 1+, Hb 4+, WBC 2-3, RBC Many

Laboratory FindingsECG Heart rate 100, regular rhythm, No acute changes seen.

Ultrasound Upper Abdomen Enlarged liver Portal vein measures 1.0 cm Enlaged spleen Splenic vein is dilated

Echocardiography EF: 70% Moderate aortic stenosis Mild to moderate aortic regurgitation Moderte mitral regurgitation Mild tricuspid regurgitation Pulmonary artery hypertension Large freely mobile vegetation seen attached to non-coronary

cusp of aortic valve and to interventricular septum in lv outflow tract

DIFFERENTIALS

Inj. Benzyl penicillin Ҳ 3mega units Ҳ TIDInj. Genticin 120mg Ҳ ODInj. Arbinin 500 md Ҳ TIDInj. Risek 40mg Ҳ ODInj. Lasix 20mg × BDTb. Panadol × PRNTb. Folic acid 5mg ×ODTb. Lowplat 75mg × ODTb. Ascard 75mg × ODTb. Lexotanil 1.5mg × HS

Treatment Being Given

Infective EndocarditisInfective Endocarditis

Definition

• Infective Endocarditis (IE):– A bacterial or fungal infection of

the valvular or endocardial surface of heart

– Microbial infection of the endothelial lining of the heart

Classification

• Classified into four groups: – Native Valve IE– Prosthetic Valve IE– Intravenous drug abuse (IVDA) IE– Nosocomial IE

Further Classification• Acute

– Affects normal heart valves

– Rapidly destructive

– Metastatic foci– Commonly

Staph.– If not treated,

usually fatal within 6 weeks

• Subacute– Often affects

damaged heart valves

– Indolent nature

– If not treated, usually fatal by one year

Pathophysiology1. Turbulent blood flow disrupts

the endocardium making it “sticky”

2. Bacteremia delivers the organisms to the endocardial surface

3. Adherence of the organisms to the endocardial surface

4. Eventual invasion of the valvular leaflets

Epidemiology

• Incidence difficult to ascertain and varies according to location, Estimated incidence: 1.6 to 6.0 / 100,000 person-per year.

• Much more common in males than in females, Male:female ratio is 1.7:1.

• May occur in persons of any age and increasingly common in elderly; 50% of cases are over 60yrs of age.

• Mortality ranges from 20-30%

Risk Factors

• Intravenous drug abuse• Artificial heart valves and pacemakers • Acquired heart defects

– Calcific aortic stenosis– Mitral valve prolapse with regurgitation

• Congenital heart defects• Intravascular catheters

Infecting Organisms• Common bacteria

– S. aureus– Streptococci – Enterococci

• Not so common– Fungi– Pseudomonas– HACEK

Symptoms• Acute

– High grade fever and chills

– SOB– Arthralgias/

myalgias– Abdominal

pain– Pleuritic chest

pain– Back pain

• Subacute– Low grade

fever– Anorexia– Weight loss– Fatigue– Arthralgias/

myalgias– Abdominal

pain

Signs

• Fever • Heart murmur• Nonspecific signs – petechiae,

subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes

• More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots

Petechiae1.Nonspecific2.Often located on extremities

or mucous membranes

Splinter Hemorrhages

1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail

bed4. Usually do NOT extend the entire length of the nail

Osler’s Nodes

1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. More common in subacute IE

• Osler’s Nodes:– 4 P’s:

• Pink• Painful• Pea-sized • Pulp of the fingers/toes.

– Immunologic origin

Janeway Lesions

1. More specific2. Erythematous, blanching macules 3. Nonpainful4. Located on palms and soles5. Septic emboli

Lab findings

• Hematology Anemia: normochromic, normocytic, low serum iron, low iron-

binding capacity (70-90%)– Thrombocytopenia (5-15%)– Leukocytosis (20-30%)– Histiocytes (>25%)– Elevated ESR, with mean value of 57mm/hr (90-100%)– Hypergammaglobulinemia (20-30%)

• Urinalysis– Proteinuria (50-65%)– Microscopic hematuria (30-60%)– Red cell casts (12%)

Lab findings

• Serology– Rheumatoid factor (40-50%)– Circulating immune complexes– Antinuclear antibodies– Complement

• Blood culture– Most important lab test– Positive cultures in 97% of cases

Imaging

• Chest x-ray – Look for multiple focal infiltrates and

calcification of heart valves• EKG

– Rarely diagnostic– Look for evidence of ischemia,

conduction delay, and arrhythmias• Echocardiography

Indications for Echocardiography

• Transthoracic echocardiography (TTE)– First line if suspected IE– Native valves – is rapid, noninvasive– specificity: 98%– sensitivity: <60%

• Transesophageal echocardiography (TEE)– Prosthetic valves– Intracardiac complications– higher ultrasonic frequencies, improve spatial resolution– specificity: 94% (prosthetic valve: 88-100%)– sensitivity: 76-100% (prosthetic valve: 86-94%)

Making the Diagnosis

• Pelletier and Petersdorf criteria (1977)– Classification scheme of definite, probable, and

possible IE– Reasonably specific but lacked sensitivity

• Von Reyn criteria (1981)– Added “rejected” as a category– Added more clinical criteria– Improved specificity and clinical utility

• Duke criteria (1994)– Included the role of echocardiography in diagnosis– Added IVDA as a “predisposing heart condition”

Duke Criteria for IE diagnosis

Duke Criteria for IE diagnosis

Modified Duke Criteria

• Definite IE– Microorganism (via culture or histology) in a valvular

vegetation, embolized vegetation, or intracardiac abscess

– Histologic evidence of vegetation or intracardiac abscess

• Possible IE– 2 major– 1 major and 3 minor– 5 minor

• Rejected IE– Resolution of illness with four days or less of antibiotics

Therapy

• Complete eradication takes weeks, relapses may occur. This is due to:1. The infection exists in an area of impaired host defense

and is tightly encased in a fibrin meshwork2. The bacteria reach very high population densities, such

that the organism may exist in a state of reduced metabolic activity and cell division

• Aspirin may decrease the growth of vegetative lesions and prevent cerebral emboli

Therapy: General principles

• Etiologic agent must be isolated in pure culture. • Parenteral antibiotics are recommended over oral drugs• Bacteriostatic antibiotics are generally ineffective• Antibiotic combinations should produce a rapid effect• Selection of antibiotics should be based on susceptibility tests,

and treatment should be monitored clinically and with antimicrobial blood levels

• Blood cultures should be obtained during the early phase of therapy to ensure eradication

• Use of anticoagulants during therapy for native valve IE is not recommended. With mechanical valves, anticoagulation should be maintained (if indicated) within therapeutic range

Surgical therapy:Indications

• refractory CHF• >2 serious systemic embolic episode• uncontrolled infection• physiologically significant valve dysfunction as

demonstrated by echo• ineffective antimicrobial therapy• resection of mycotic aneurysms• most cases of prosthetic valve IE (caused by more

antibiotic-resistant pathogens)• local suppurative complications including perivalvular or

myocardial abscesses

Prognostic factors

• S. aureus, fungal infections• Previous IE• Cyanotic heart disease• CHF• Embolic phenomena• Rupture of a mycotic aneurysm• Lack of response to antimicrobial therapy• Prosthetic valve endocarditis• Periannular extension of infection

Complications

• Four etiologies– Embolic– Local spread of infection– Metastatic spread of infection– Formation of immune complexes –

glomerulonephritis and arthritis

Embolic Complications

• Occur in up to 40% of patients with IE• Predictors of embolization

– Size of vegetation– Left-sided vegetations– Fungal pathogens, S. aureus, and Strep.

Bovis• Incidence decreases significantly

after initiation of effective antibiotics

Embolic Complications

• Stroke• Myocardial Infarction

– Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia

• Ischemic limbs• Hypoxia from pulmonary emboli• Abdominal pain (splenic or renal

infarction)

Septic Pulmonary Emboli

Septic Retinal Embolus

Local Spread of Infection

• Heart failure– Extensive valvular damage

• Paravalvular abscess (30-40%)– Most common in aortic valve, IVDA, and S. aureus– May extend into adjacent conduction tissue

causing arrythmias– Higher rates of embolization and mortality

• Pericarditis• Fistulous intracardiac connections

Local Spread of Infection

Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations.

Acute S. aureus IE with mitral valve ring abscess extending into myocardium.

Metastatic Spread of Infection

• Metastatic abscess – Kidneys, spleen, brain, soft tissues

• Meningitis and/or encephalitis• Vertebral osteomyelitis• Septic arthritis

Summary• IVDA and the elderly are at greatest risk of

developing IE.

• The signs and symptoms of IE are nonspecific and varied.

• A thorough but timely evaluation (including serial blood cultures, adjunct labs, and an echo) is crucial to accurately diagnose and treat IE.

• Beware of life-threatening complications.

Thank you.