Sunday, October 28, 2007

Diseases of Pericardium, by Dr. Sultan Mehmood

A 50 YRS OLD MAN PRESENTED WITH ILL HEALTH , ANOREXIA, LOW GRADE FEVER, WT. LOSS, PRECARDIALPAIN AND MILD DYSPNOEA FOR THE LAST 2 MONTHS.HIS PULSE WAS 110 BPM WITH MARKED PULSUS PARADOXUS,JVP 8CM VERTCALLY ABOVE STERNAL ANGLE. HEPATIC ENLARGEMNT 5CM, ASCITES AND PEDAL OEDEMA. HT. SOUNDS WERE FAINTLY AUDIBLE and LUNGS WERE CLEAR.
Q1. WHAT IS THE MOST LIKELY CLINICAL DIAGNOSIS
Q2. WHAT IS THE MOST LIKELY ETILOGICAL
DIAGNOSIS
Q3. WHAT WILL BE THE MOST HELPFUL IMEDIATE
INVESTIGATION
DISEASES OF PERICARDIUM

NORMAL PERICARDIUM
ØLUBRICATES THE SURFACE OF THE HEART
ØPREVENTS SUDDEN DEFORMATION OF THE HEART
ØACTS AS A BARRIER TO THE SPREAD OF INFECTION
ØPREVENTS DISLOCATION OF THE HEART

CLINICAL PRESENTATION OF PERICARDIAL DISEASE

1.ACUTE PERICARDITIS

2. PERICARDIAL EFFUSION

3. CONSTRICTIVE PERICARDITIS
CLASSIFICATION OF PERICARDITIS

•CLINICAL CLASSIFICATION

A. ACUTE PERICARDITIS (< 6 WEEKS)
1. FIBRINOUS OR DRY PERICARDITIS
2. EFFUSIVE PERICARDITIS
B. SUBACUTE PERICARDITIS (6 WEEKS TO 6 MONTHS)
1. EFFUSIVE
2. CONSTRICTIVE
C. CHRONIC PERICARDITIS (> 6 MONTHS)
1. CONSTRICTIVE
2. EFFUSIVE
3. ADHESIVE


ETIOLOGIC CLASSIFICATION

A. INFECTIOUS PERICARDITIS
1. VIRAL – COXSACKIE B
2. TUBERCULOUS
3. PYOGENIC
4. MYOCOTIC
5. OTHER INFECTIONS (SYPHILITIC, PARASITIC)

B. NON-INFECTIOUS PERICARDITIS
1. ACUTE MYOCARDIAL INFARCTION
2. URAEMIA
3. NEOPLASIA
A.PRIMARY TUMOR ( BENIGN OR MALIGNANT)
B. TUMORS METASTATIC TO PERICARDIUM
4. MYXOEDEMA
5. CHOLESTEROL
6. CHYLOPERICARDIUM

7. TRAUMA
A. PENETRATING CHEST WALL
B. NON – PENETRATING
8. AORTIC ANEURYSM (WITH LEAKAGE INTO PERICARDIAL SAC)
9. POST- RADIATION
10. FAMILIAL MEDITERANEAN FEVER
11. FAMILIAL PERICARDITIS
12. SARCOIDOSIS
13. ACUTE IDIOPATHIC
C. PERICARDITIS PRESUMABLY RELATED TO HYPERSENSITIVITY OR AUTO- IMMUNITY RHEUMATIC FEVER
COLLAGEN VASCULAR DISEASE
A. SYSTEMIC LUPUS ERYTHEMATOSUS
B. RHEUMATOID ARTHRITIS
C. SCLERODERMA
DRUG – INDUCED
A. PROCAINAMIDE
B. HYDRALAZINE
C. OTHER
POST CARDIAC INJURY
A. POST MYOCARDIAL INFARCTION (DRESSLER’S SYNDROME)
B. POST-PERICARDIOTOMY



ACUTE PERICARDITIS
COMMON CAUSES
MYOCARDIAL INFARCTION
VIRAL INFECTIONS – COXACKIE B VIRUS
TUBERCULOSIS
RHEUMATIC FEVER
URAEMIA
MALIGNANCY
CONNECTIVE TISSUE DISORDERS-SLE
POST PERICARDIOTOMY
POST RADIATION

SYMPTOMS
CHEST PAIN
•PRECARDIAL, SHARP
•REFERED TO THE NECK OR SHOULDER
•RELIEVED BY SITTING FORWARD , MADE WORSE BY LYING DOWN, MOVEMENT, RESPIRATION AND SWALLOWING
SIGNS
PERICARDIAL FRICTION RUB
•DIAGNOSTIC
•SUPERFICIAL, SCRATCHING, LEATHERY - HAVING “TO AND FRO” CHARACTER
•BEST HEARD TO THE LEFT OF THE LOWER STERNUM.

INVESTIGATIONS
•ECG
ST ELEVATION WITH CONCAVITY UPWARDS IN AL THE LEADS FACING EPICARDIAL SURFACE.
LATER ST SEGMENT FALLS AND T- WAVE INVERSION OCCURS WHICH BECOMES NORMAL WITH RECOVERY
•DETECTION OF THE UNDERLYING CAUSE
MYOCARDIAL INFRACTION, VIRAL ANTIBODIES, TUBERCULOSIS, CT DISORDERS, URAEMIA, RHEUMATIC FEVER.
TREATMENT
•BED REST
•NSAIDS – ASPRIN, INDOMETHACIN
•STEROIDS IN SEVERE CASES
•TREATMENT OF THE UNDERLYING DISEASE
PURULENT – ANTIBIOTICS, PARACENTESIS,
MAY BE SURGICAL DRAINAGE
TUBERCULOUS – ANTITUBERCULOUS DRUGS
C.T. DISORDER – STEROIDS



PERICARDIAL EFFUSION

ØACCUMULATION OF FLUID IN THE PERICARDIAL SAC MAY ACCOMPANY ACUTE PERICARDITIS OR MAY OCCUR AS A CHRONIC CONDITION.

ØALMOST ALL THE AETIOLOGIES OF ACUTE PERICARDITIS MAY INDUCE THE FORMATION OF PERICARDIAL EFFUSION.

ØTHE SPEED OF ACCUMULATION OF FLUID IN THE PERICARDIUM IS IMPORTANT IN DETERMINING THE INTRA – PERICARDIAL PRESSURE.

ØWHEN THE ACCUMULATION IS SLOW, THE PERICARDIUM DISTENDS GRADUALLY AND THE INTRA – PERICARDIAL PRESSURE DOES NOT RISE MUCH EVEN IN THE PRESENCE OF A MASSIVE EFFUSION


ØWHEN THE FLUID ACCUMULATES RAPIDLY OR IS LARGER THAN THE CPACITY OF THE PERICADIAL SAC, THE INTRA – PERICARDIAL PRESSURE WILL RISE, CAUSING MECHANICAL COMPRESSION OF THE HEART AND PREVENTING VENTRICULAR FILLING RESULTING IN FALL OF CARDIAC OUTPUT- CARDIAC TEMPONADE

CLINICAL FEATURES
SYMPTOMS - NOT VERY MARKED:
ØPAIN OF PERICARDITIS MAY BE REPLACED BY SENSE OF PRECARDIAL OPPRESSION USUALLY WITH BREATHLESSNESS AS THE EFFUSION DEVELOPS.
ØSYMPTOMS DUE TO UNDERLYING CAUSE
SIGNS - VERY MARKED
ØRAISED JVP WITH OTHER SIGNS OF SYST. VENOUS HT
ØPULSUS PARADOXUS - PULSE VOLUME AND B.P FALLS DURING INSPIRATION
ØFRIEDREICH’S SIGN: SHARP DIASTOLIC COLLAPSE OF JVP
ØKUSSMAUL’S SIGN: INCREASED IN JVP DURING
INSPIRATION-VENOUS PULSUS PARADOXUS

APICAL IMPULSE MAY NOT BE PALPABLE, AREA OF CARDIAC DULLNESS MAY BE INCREASED AND HT. SOUNDS ARE SOFT
ØPERICARDIAL FRICTION RUB MAY BE AUDIBLE BUT DISAPPEARS AS THE FLUID SEPARATES THE VISCERAL AND PARIETAL LAYERS
ØSIGNS OF REDUCED CARDIAC OUTPUT MAY BE PRESENT

CARDIAC TAMPONADE
ØCOMPRESSION OF THE HEART BY A LARGE OR RAPIDLY DEVELOPING EFFUSION WHICH INTERFERES WITH DIASTOLIC FILLING OF THE HEART AND PRODUCES SEVERE MECHANICAL EMBARRASSMENT OF THE CIRCULATION; RESULTING IN FALL OF CARDIAC OUTPUT.
ØTHE JVP IS VERY HIGH, PULSUS PARADOXUS IS MARKED, URINARY OUTPUT FALLS AND CLINICAL PICTURE OF ACUTE CIRCULATORY FAILURE MAY DEVELOP.
ØPULMONARY OEDEMA USUALLY DOES NOT DEVELOP.

INVESTIGATIONS
ØX-RAY CHEST: INCREASINGLY LARGE, GLOBULAR HEART WITH SHARP OUTLINES AND RELATIVELY DRY LUNG FIELDS.
ØECG :SMALL COMPLEXES, TACHYCARDIA, Electrical alternans is pathognomonic- due to the heart swinging within the large effusion
ØECHOCARDIOGRAPHY : THE MOST USEFUL TEST TO DIAGNOSE PERICARDIAL EFFUSION BY SHOWING ECHO-FREE ZONE BETWEEN THE POSTERIOR WALL OF THE L. VENTRICLE AND THE PERICARDIUM.
ØCT SCAN / MRI
ØPERICARDIAL FLUID ANALYSIS
ØPERICARDIAL BIOPSY


TREATMENT

1.PERICARDIOCENTESIS
vDIAGNOSTIC
vTHERAPEUTIC
- XIPHISTERNAL APPROACH
- APICAL APPROACH
vFOR CONTINUOUS DRAINAGE, PLASTIC CANNULA MAY BE LIFT IN PLACE

2. PERICARDIAL FENESTRATION : SUGICAL CREATION OF A WINDOW IN THE PERICARDIUM WHEN FLUID ACCUMULATES REPEATEDLY.
3. SPECIFIC THERAPY :
v ANTIBIOTICS IN PYOGENIC FLUID
vANTITUBERCULOUS DRUGS IN TUBERCULOUS EFFUSION.
vSTEROIDS : SLE, AUTOIMUNE DISORDERS,OCCASIONALLY USED TO PREVENT
THE DEVELOPMENT OF CONSTRICTIVE PERICARDITIS


CONSTRICTIVE PERICARDITIS
FOLLOWING TUBERCULOUS PERICARDIAL EFFUSION,
HAEMOPERICARDIUM, PYOGENIC PERICRDITIS OR
ACUTE PERICARDITIS DUE TO VIRAL INFECTION AND
POST RADIATION PERICARDITIS, THE
PERICARDIUM MAY BECOME THICK, FIBROUS AND
ULTIMATELY CALCIFIED AND RIGID.
THE HEART IS THEN ENCASED IN A RIGID SHELL AND
CANNOT EXPAND AND FILL IN DIASTOLE.

CLINICAL FEATURES
Ø BREATHLESSNESS IS NOT PROMINENT AS THERE IS NOT MUCH PULMONARY CONGESTION
ØSIGNS OF SYSTEMIC VENOUS HYPERTENSION -
RAISED JVP, HEPATOMEGALLY, ASCITES AND DEPENDENT OEDEMA
ØSIGNS OF IMPAIRED V. FILLING
KUSSMAUL’S SIGN, PULSUS PARADOXUS AND FRIEDRIECH’S SIGN
ØATRIAL FIBRILLATION IS COMMON
ØPERICARDIAL KNOCK – A LOUD EARLY THIRD HEART SOUND
ØTHE APICAL IMPULSE IS NOT FORCEFUL AND HEART SOUNDS ARE QUIET- “SMALL QUIET HEART”.
INVESTIGATIONS
ØX-RAY CHEST
RELATIVELY SMALL HEART WITH SHAGGY HEART BORDERS AND PERICARDIAL CALCIFICATION ON THE LATERAL FILM
Ø ECG
LOW QRS COMPLEXES AND INVERTED T – WAVES.
Ø ECHOCRDIOGRAM
THICKENED PERICARDIUM, RELATIVE IMMOBILITY OF THE
HEART WALLS.
Ø CT SCAN / MRI SCAN
THICKENED PERICARDIUM, CALCIFICATION
TREATMENT
ØPERICARDIECTOMY
SURGICAL RESECTION OF PERICARDIUM PRODUCES RAPID IMPROVEMENT

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