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