“The Heart of the Problem”. A Case of Acute Renal Failure, Infective Endocarditis and Poor...

“The Heart of the Problem”

A Case of Acute Renal Failure, Infective Endocarditis

and Poor Nutrition

Professor Oliveira’s firm:

Jane Miller, Kristina Antonova, Lav Joshi, Madeline Butcher

and Mark Bowers

The Plan

1) Present the case of Mr. CC

2) Discuss the topic of infective endocarditis

The case of Mr. CC

History

• PC– protracted vomiting

– renal failure (incidental)

• HPC– 2-3/52 vomiting, appetite ?cause

– GP organised OGD mild gastritis , H. pylori, contd vomiting hospital

• PMH– Hx of learning difficulties

– Vitiligo, Seborrhoeic keratosis, Fibromyalgia

• DH– nil, NKDA

• SH– Council house living with 3

siblings

– retired motor mechanic

– non-smoker, no alcohol

• FH– nil of note

• SE– Resp - chest infection

– CVS - nil

– ABDO - constipation BWO

– Neuro - nil else

Examination

• Unkempt, Cachectic, °JACCOL

• CVS– HS I + II + 0

– HR 80 reg

– JVP – No oedema

• Resp– Good air entry L=R

– good expansion

– RR =14

• Abdo– Soft, non-tender

– Faecal loading LIF

– dark urine

• Neuro– CN I - XII normal

– Tone, power, reflexes, coordination and sensation

– plantars - down-going

Plan and Investigations

• 1) Bloods - recheck Ca, needs PTH

• 2) Fluids

• 3) Antiemetics

• 4) Urine dipstick MSU

• 5) Fluid balance

• 6) Keep catheter in

• 7) Abdo USS

• 8) CXR

Na 145 Bili 21

K 3.9 ALT 17

Cl 109 Alk P 70

HCO3 23 Alb 21

Ur 50.7 Ca 2.26

Cr 563 P04 1.64

CRP 105.2 Adj Ca 2.64

Hb 9.0 WCC 9.3

Plts 157

Management and Progress• Transfuse - 2 units blood

• USS Kidney (22/4)• large 13.5 corticomedullary differentiation in keeping with acute tubular

necrosis (ATN).

• CXR and subsequent clinical signs indicated chest infection.Rx Antibiotics: Augmentin and Erythromycin

• Haemodialysis started

• Renal biopsy (1/5)• ATN, some crescents. Some form of immune complex disease

?endocarditis

• not a small vessel disease

• IgG & C3 complexes seen - prednisolone started

Management and Progress 2• Blood cultures (1/5)

• taken - but pt on AB. Advice from microbiology stop AB and repeat BC

• Echo (1/5)• marked thickening of leaflet tip with small mobile lesion

• AR Murmur heard (10/5)• Normal PR interval on ECG

• IV gentamicin and benzylpenicillin started

• Splinter Haemorrhage right toe (13/5)

• Bilateral small pleural effusions (13/5)

Management and Progress 3

• Rash over both shins- non blanching (16/5)

• Intermittently pyrexial, referred to cardiologist (22/5)

• TOE- broad jet of severe AR arising from the left coronary cusp (23/5)

• Plan: Replace aortic valve

• MaxFax review (23/5)• Oral hygiene very poor

• pre-op oral scale and polish and antibiotic cover

• AV replacement carried out (24/5)

Progress to Date

• Pt has had 23% wt loss since admission

• Pt refusing oral nutrition, and unable tolerate NG tube

• PEG tube inserted (17/7)

Infective Endocarditis

Topic of interest:

Definition

• Infection of the endocardium, vascular endothelium of the heart or intracardiac foreign bodies.

• May occur as acute infection (e.g. <24hrs after surgery)

• More commonly runs an insidious course : Subacute Bacterial Endocarditis (SBE)

Incidence

• Approx. annual incidence in UK is 6-7 per 100,000.

• Differing ages, mainly middle-age/elderly.• More common in men.• St. George’s: range of between 6-17 cases seen

per year (between 1991-1999)

Diagnosis

• New regurgitant murmur

+• Continuous/remitting fever

=• Endocarditis until proven otherwise

Diagnosis

• Duke clinical criteria. 2 major criteria

or 1 major & 3 minor criteria

or 5 minor criteria

Dukes CriteriaMajor • Typical organism in 2 separate cultures or

persistently +ve blood cultures (>3, >12 hrs apart)• +ve echocardiogram (vegetation, abscess) or new

valvular regurgitationMinor • Predisposition • Fever >38˚C• Vascular/ immunological phenomena (splinter

haemorrhages, Osler’s nodes)• +ve blood cultures (not meet major criteria)• +ve echocardiogram (not meet major criteria)

AetiologyAgent Prevalance

Streptococci . . 60-80%

Viridan . . . 30-40%

Enterococci . . . 5-18%

Other Strep. . . . 15-25%

Staphlococci . . 20-35%

Coagulase +ve . . . 10-27%

Coagulase -ve . . . 1-3%

Gram -ve aerobic bacilli . 1.5-3%

Fungi . . . . 2-4%

Miscellanous Bacteria . <5%

Mixed . . . . 1-2%

Culture -ve . . . <24%

Pathogenesis

Damaged endocardium

Adherence of vWF Adherence of platelets

Adherence of bacteria Platelets bind fibrin

Vegetation formation

• Vegetations usually form on the edge of valves.• The organisms destroy the valves.

Conditions Predisposing to IEStructural cardiac

abnormalities• AS, AR• Bicuspid aortic valves• MS, MR• Senile mitral ring

calcificationFactors altering

immunity• Immunosuppression• Diabetes• Chronic alcoholism

External factors• Mechanical valves• Indwelling vascular

catheters• Pacing wires (IV)

Factors causing bacteraemia

• Dental work• IV drug misuse• Urogenital/GI

operations

Clinical Features of SBEGeneral• Malaise• Fever• Night sweats• Anaemia• Clubbing• Weight lossEyes• Roth spots• Conjunctival splinter

haemorrhagesArthralgia

Skin• Osler’s nodes• Janeway lesions• Splinter haemorrhages• PetechiaeCardiac• Murmurs• Cardiac failureSplenomegalyHaematuriaCerebral emboli/abscessKidney• Glomerulonephritis

Stigmata of SBE

• Clubbing (2%)• Roth spots• Conjunctival splinter haemorrhages• Osler’s nodes• Janeway lesions• Splinter haemorrhages• Petechiae

Janeway lesions appear as flat, painless, red to bluish-red spots on the palms and soles.

Janeway Lesions

Osler’s Nodes

Clubbing

Splinter Haemorrhages

Roth Spots

Investigations• Non-specific Tests

– FBC: normocytic normochromic anaemia, neutrophil leucocytosis

– U+E’s (Mg2+), LFT’s– ESR/CRP: elevated– Urinalysis: microscopic haematuria

• Blood Cultures: at least 3 set from different sites at different times (take BEFORE AB administered)

• Echocardiography: TTE or TOE• ECG: prolonged P-R interval• CXR: cardiomegaly

Management

• Pathogens embedded in vegetation– partially protects from cellular & humoral

defence mechanisms• Prolonged high dose combination of IV

antibiotics (for at least 4wks - less in uncomplicated Strep. viridans)

Management contd

• Cidal drugs Usually penicillin & gentamicin, if IVDA/hospital aquired/on haemodialysis use vancomycin instead of penicillin ( add rifampicin with coagulase -ve staph. or Staph. aureus, use ampicillin/amoxycillin instead of penicillin for Enterococci)

• Tailour AB’s in light of culture results

• Role of Surgery (consider early)– MR at presentation

– Not controlled by AB’s

[Antibiotic treatment of streptococcal, enterococcal, and staphlyoccal endocarditis. Heart 1998;79:207-210]

Complications

• Cardiac– Valve incompetence (Ao>M)– Intracardiac fistulae/abscesses– Mycotic aneurysm rupture

(pyohaemopericardium, pericardial tamponade, ASD, VSD, aortopulmonary communication)

• Extra cardiac– Arterial embolism (CNS, kidney)– Diffuse immune complex mediated nephritis– Focal embolic glomerularnephritis– Drug hypersensitivity

Prognosis

• 30% mortality with Staphylococcus

• 14% mortality with bowel organisms

• 6% mortality with sensitive Streptococcus• VT/VF/Sudden death < 1%• Poorer prognosis if develop CCF from acute severe Ao

regurge• Thromboembolic complications:

– more in mitral than Ao valve disease– greater risk with mobile &/or large vegetations

Prevention

• Prevent Rheumatic fever• Pre-existing valve lesions

– Good oral hygiene– Antibiotic prophylaxis for surgery & dental

procedures

• Pts in hospital– Care of IV lines/catheters etc

• IVDA– Education, needle exchange programmes

Thank you

Any Questions ?