Endocardial Infections
135Case 29 Aortic Valve Endocarditis
Table 29.2: Modified Duke’s diagnostic criteria of infective endocarditis Pathological criteria
The mainstay of the effective treatment of infective endocarditis (barring fungal endocarditis) is antibacterial drugs. Bactericidal drugs with low minimum inhibitory concentrations (MIC90) against the identified organism are chosen.
The intravenous route of administration is preferable to achieve high serum levels of the drug. This ensures adequate penetration of the antibiotic, since the vegetations are rich in necrotic tissue debris and therefore resist entry of the drug.
A combination of 3rd generation cephalosporin with an aminoglycoside may be initiated, even when culture reports are pending, and are generally effective against Streptococcal endocarditis. Infection caused by Staphylococcus aureus is treated with flucloxacillin or vancomycin along with gentamycin or amikacin.
Usually 2 to 4 weeks of treatment suffices in native valve Streptococcal infection while 6 weeks are required to treat Staphylococcal prosthetic valve endocarditis.
The indications for surgical intervention in endocarditis are prosthetic valve dehiscence, aortic root abscess, fistula formation, refractory heart failure and recurrent embolic events (Table 29.3).
136 Section 9 Endocardial Infections
Table 29.3: Indications for surgery in endocarditis
• Fungal or resistant organism causing endocarditis
• Prosthetic valve dehiscence or aortic root abscess
• Heart block (septal abscess) or a fistula formation
• Valve regurgitation leading to refractory heart failure
• Recurrent systemic emboli despite adequate therapy
RECENT ADVANCES
The clinical spectrum of infective endocarditis has undergone a major change in the last two decades, for several reasons. Prevalence of Staphylococcal infection has increased with the widespread use of catheters, venous lines and pacing leads and the rising incidence of intravenous drug abuse. An entirely new HACEK group of bacteria has been identified as also a range of intracellular bacteria that can cause endocarditis. With the growing number of valve replacements, prosthetic valve endocarditis is on the rise. Finally, immunocompromised hosts such as HIV-infected patients and organ transplant recipients on immunosuppressive drugs are more likely to be infected by fungal organisms.
C A S E
30 Tricuspid Valve
Endocarditis
CASE PRESENTATION
A 32-year old male came to the out-patient department of a charitable hospital, with history of fever for the last 3 weeks. The fever was high-grade and associated with chills and night sweats, but there were no rigors. He also felt fatigued and had lost his appetite, leading to significant weight loss. However, he was not aware of his exact past body-weight. He also had cough with scanty mucoid sputum for one month, but there was no history of burning micturition, vomiting, pain abdomen or passing loose stools. There was also no history of dyspnea, chest pain or hemoptysis. The patient was unmarried and he was not accompanied by any attendant. He was a college drop-out, presently not engaged in any gainful employment. He admitted smoking and taking alcohol as well as drug-snorts, whenever he could afford them.
He also sometimes abused intravenous illicit drugs.
On examination, the patient was emaciated, ill-looking, confused and febrile.
The pulse rate was 110 beats/min. with a BP of 96/70 mm Hg and a temperature of 101.60F. He was mildly anemic but not cyanosed or icteric and there was pitting edema over the ankles. The neck veins were engorged and showed rapid y descent.
There were multiple needle-prick marks over the veins on his forearms. On cardiac auscultation, a pansystolic murmur was heard over the lower left parasternal area;
no gallop sound was audible. There were scattered rhonchi and crepts over the lung fields. On examination of the abdomen, there was hepatomegaly. The liver edge was palpable 5 cm below the costal margin and it was pulsatile. There was no splenomegaly or ascites.
PERTINENT INVESTIGATIONS
The hemoglobin was 9.2 g/dL with a total leucocyte count of 13,600/cumm. of which 78% were neutrophils; the ESR was 64 mm in the 1st hour. Urine analysis showed albumin +1 with 2-3 WBCs and 8-10 RBCs per high power field. ASLO titre was 110 IU with a CRP value of 62 mg/L. The biochemical parameters were Glucose 78 mg/dl, Creatinine 1.4 mg/dl, Bilirubin 1.8mg/dl, SGOT 79 and SGPT 53 and Cholesterol 144 mg/dl. The hepatitis B surface antigen was negative but his HIV-status was unknown. Urine culture did not yield any bacterial growth.
Throat swab culture was negative for beta-hemolytic Streptococcus. Three sets
138 Section 9 Endocardial Infections
Table 30.1: Pathogens implicated in right-sided endocarditis
• Typical Staphylococcus aureus
• Atypical HACEK* group bacteria
• Fungal Candida, Aspergillus
*HACEK group: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella of blood cultures were obtained, including from the veins of the forearms that bore needle-prick marks. Two out of the three cultures grew coagulase negative Staphylococcus aureus. One of the cultures grew Candida albicans.
ECG showed sinus tachycardia with narrow QRS complexes and no ST-T changes. X-ray chest did not show any cardiomegaly, but the broncho-vascular markings were prominent over both lung fields. ECHO revealed normal left ventricular size and ejection fraction. The mitral and aortic valves were normal.
An irregular echo-reflective mass was observed, which appeared to arise from the tricuspid valve (Fig. 30.1). There was moderate degree of tricuspid regurgitation.
Keeping in mind the history of a prolonged febrile illness with intravenous drug abuse, positive blood cultures and demonstrable vegetations with tricuspid regurgitation, the most likely diagnosis in this case was of tricuspid valve endocarditis.
CLINICAL DISCUSSION
Endocarditis of the left-sided cardiac valves is more common than that of the right-sided valves. This is because of greater turbulence of blood flow in the left side of the heart and the fact that mitral and aortic valve disease is far more common than tricuspid valve disease. Tricuspid valve endocarditis usually occurs due to intravenous drug abuse. Staphylococcal aureus introduced by contaminated needles from the skin into the venous system, is the most common causative organism (Table 30.1).
Figure 30.1: ECHO showing a nodular mass attached to valve leaflet
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