Tirthankar Online: Topic of the month September 2008: Infective Endocarditis

September 05, 2008

Topic of the month September 2008: Infective Endocarditis

INFECTIVE ENDOCARDITIS: A RAPID REVIEW

What is Infective endocarditis (IE)?

-Infection of the endocardium, valve cusps or prosthetic valves
-May occur as acute infection (e.g. <24hrs after surgery)
-More commonly runs an insidious course : Subacute Bacterial Endocarditis (SBE)

Endocarditis is an infection that invades the innermost lining of the heart - the endothelium. It can damage the heart valves, the rings of connective tissue that surround the valves, as well as the inner linings of the heart chambers themselves.
In some congenital cardiac diseases, infection can also occur in the lining of the arteries that come out of the heart.

CONDITIONS PREDISPOSING TO IE
1. Structural cardiac abnormalities:
• AS
• AR
• MR
• VSD

2. Factors altering immunity:
• Immunosuppression
• AIDS
• Diabetes
• Chronic alcoholism

3. External factors:
• Prosthetic valves
• Indwelling vascular catheters
• Pacing wires (IV)

4. Factors causing bacteraemia:
• Oral/Dental surgery
• IV drug use
• Urogenital/GI operations

CARDIAC DISEASES IMMUNE TO IE
-ASD
-Heart failure
-VSD with reversal of shunt
-MS

WHAT ARE THE SIGNS AND SYMPTOMS?
The signs and symptoms of infective endocarditis depend on the causative organism. Symptoms may include fever, fatigue, weight loss, new rashes (either painful or painless), headaches, backaches, joint pains, and confusion.
A new heart murmur as well as new skin, fingernail, and retinal lesions are typical physical findings in endocarditis. We can make the diagnosis by finding microbial organisms in the blood and by performing an echocardiogram that shows evidence of endocarditis in the heart.

WHAT ARE THE COMPLICATIONS?
If not treated, most patients with infective endocarditis will die. Depending on when treatment is begun, there can be various complications. The infection can destroy the heart valves, resulting in congestive heart failure.
Small masses of bacteria or fungus, as well as platelets and fibrin can flick off the valves and cause problems throughout the body. These are called emboli. They can result in strokes, kidney failure, heart attacks, and damage to the gastrointestinal organs. Endocarditis can also result in heart arrhythmias and inflammation of heart tissue.
Finally, infective endocarditis can result in abscesses in the heart that are very hard to treat.

SUMMARY OF CLINICAL FEATURES AND COMPLICATIONS
A. General
1. Malaise
2. Fever
3. Night sweats
4. Anaemia
5. Clubbing
6. Weight loss
B. Eyes
1. Roth spots
2. Conjunctival splinter haemorrhages
C. Arthralgia
D. Splenomegaly
E. Skin
1. Osler’s nodes
2. Janeway lesions
3. Splinter haemorrhages
4. Petechiae
F. Cardiac
1. Murmurs
2. Cardiac failure
G. Cerebral emboli/abscess
H. Kidney
1. Glomerulonephritis
2. Haematuria

HOW IS INFECTIVE ENDOCARDITIS DIAGNOSED USING DUKE’S CRITERIA?

Duke clinical criteria
2 major criteria
Or
1 major & 3 minor criteria
Or
5 minor criteria

Major
i) Typical organism in 2 separate cultures or persistently +ve blood cultures (>3, >12 hrs apart)
ii) +ve echocardiogram (vegetation, abscess) or new valvular regurgitation
Minor
i) Predisposition
ii) Fever >38˚C
iii) Vascular/ immunological phenomena (splinter haemorrhages, Osler’s nodes)
iv) +ve blood cultures (not meeting major criteria)
v) +ve echocardiogram (not meeting major criteria)

INVESTIGATIONS FOR THE DIAGNOSIS OF IE

A. Routine – Blood, Urine, Ur, Cr, CXR, ECG
B. Special –
a. Blood culture
b. Echo-cardiography
c. Rheumatoid factor

HOW IS ENDOCARDITIS TREATED?
Infective endocarditis is treated with antibiotics and with surgery in some situations. Intravenous antibiotics are used for several weeks to eradicate the organism that caused the condition. But in more serious cases, urgent cardiac surgery is indicated to treat some patients.
Surgery is considered particularly when a patient has an artificial heart valve. However, there is new evidence to suggest that certain kinds of bacterial infections of prosthetic valves can be treated with just antibiotics.

IS ENDOCARDITIS PREVENTABLE?
Yes. As described above, infective endocarditis occurs when there is an infection in the blood. Antibiotics can prevent such an infection from occurring in the first place. Antibiotic prophylaxis is recommended before medical procedures with a high probability of introducing bacteria into the blood.
Dental procedures that cause bleeding from the gums (even a simple cleaning); rigid bronchoscopy; and surgery of the upper respiratory tract, urinary tract procedures, and gastrointestinal procedures all confer an increased risk of bacteremia, and therefore, an increased risk of infective endocarditis in those individuals with predisposing cardiac lesions.

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Answers to your questions

2. Short note on SSSS.(Deborshi)

Ans:
Definition:

Staphylococcal scalded skin syndrome (SSSS) is an acute epidermolysis caused by a staphylococcal toxin.

Newborns and children are most susceptible. Symptoms are widespread bullae with epidermal sloughing. Diagnosis is by examination and sometimes biopsy. Treatment is antistaphylococcal antibiotics and local care. Prognosis is excellent with timely treatment.

Staphylococcal scalded skin syndrome (SSSS) almost always affects children < 6 yr (especially infants); it rarely occurs in older patients unless they have renal failure or are immunocompromised. Epidemics may occur in nurseries, presumably transmitted by the hands of personnel in contact with an infected infant or who are nasal carriers of Staphylococcus aureus. Sporadic cases also occur.
SSSS is caused by group II coagulase-positive staphylococci, usually phage type 71, which elaborate exfoliatin (also called epidermolysin), a toxin that splits the upper part of the epidermis just beneath the granular cell layer. The primary infection often begins during the first few days of life in the umbilical stump or diaper area; in older children, the face is the typical site. Toxin produced in these areas enters the circulation and affects the entire skin.

Symptoms and Signs

The initial lesion is usually superficial and crusted. Within 24 h, the surrounding skin becomes painful and scarlet, changes that quickly spread to other areas. The skin may be exquisitely tender and have a wrinkled tissue paper–like consistency. Large, flaccid blisters arise on the erythematous skin and quickly break to produce erosions. Intact blisters extend laterally with gentle pressure (Nikolsky's sign). The epidermis may peel easily, often in large sheets. Widespread desquamation occurs within 36 to 72 h, and patients become very ill with systemic manifestations (eg, malaise, chills, fever). Desquamated areas appear scalded. Loss of the protective skin barrier can lead to sepsis and to fluid and electrolyte imbalance.

Diagnosis

· Biopsy
· Cultures may be useful in adults

Diagnosis is suspected clinically, but confirmation usually requires biopsy (frozen section may give earlier results). Specimens show noninflammatory superficial splitting of the epidermis. In children, skin cultures are seldom positive; in adults, they are frequently positive. Cultures should be taken from the nose, conjunctiva, throat, and nasopharynx.

Differential diagnosis:

Differential diagnosis includes drug hypersensitivity, viral exanthemas, scarlet fever, thermal burns, genetic bullous diseases (eg, some types of epidermolysis bullosa), acquired bullous diseases (eg, pemphigus vulgaris, bullous pemphigoid), and toxic epidermal necrolysis. Stevens-Johnson syndrome is characterized by mucosal involvement, which is absent in SSSS.

Differentiating Staphylococcal Scalded Skin Syndrome (SSSS) and Toxic Epidermal Necrolysis (TEN)

SSSS

i)Patients affected - Infants, young children, immunocompromised adults

ii)Patient history - Recent staphylococcal infection, renal failure

iii) Level of epidermal cleavage (blister formation)* - Within the granular cell (outermost) layer of the epidermis

TEN

i)Patients affected - Older patients

ii)Patient history - Drug use

iii)Level of epidermal cleavage (blister formation)* - Between the epidermis and dermis or at the level of the basal cell

*Determined by Tzanck test or by a frozen section of a fresh specimen.

Treatment

· Antibiotics
· Corticosteroids not recommended
· Gel dressings for weeping lesions

With prompt diagnosis and therapy, death rarely occurs; the stratum corneum is quickly replaced, and healing usually occurs within 5 to 7 days after start of treatment.Penicillinase-resistant antistaphylococcal antibiotics given IV must be started immediately.

1. Comment: carcinoma usually spreads through lymphatics. (Himel)

Answer: It is a common dictum that carcinomas usually spread via lymphatics, and sarcomas usually spread through blood vessels. Most carcinomas metastasise by lymphatics, which include Ca breast, Ca stomach, Ca uterus, etc. However, it is not a universal dictum, as some Ca preferencially spreads via blood vessels, like renal cell carcinoma.

Recent research has thrown light on the probable reason behind this peculiar preference. The tumors that spread via blood vessels produce sufficient local angiogenesis, so that the tumor is well supplied by micro vessels that help in hematogenous spread. However, tumors that metastasise through lymphatics are rarely supplied with micro lymphatics. Instead, they have a surrounding chain of lymphatics outside the tumor mass. The spread into these vessels is facilitated if the surface area of the micro lymphatics can be increased or if the growth of intra-tumor lymphatics can be facilitated.. It is seen that the carcinomas that spread via lymphatics secrete higher amounts of VEGF-C, VEGF-D, VEGF-A and PDGF-BB, the growth factors that increase the number and the surface area of the lymphatics and facilitates the invasion by tumor cells. The higher expression of VEGF gene in carcinomas compared to sarcomas may explain why carcinomas more often spread via lymphatics.