POSTOPERATIVE PERICARDIAL EFFUSION-POSTPERICARDIOTOMY SYNDROME , TRÀN DỊCH MÀNG TIM SAU PHẪU THUẬT TIM

Postoperative pericardial effusion: frequent complication after HS. Early (15 th postoperative day): Postpericardiotomy syndrome Pericardial effusions resulting in cardiac tamponade (CT) are uncommon after open heart surgery (OHS).

POSTOPERATIVE PERICARDIAL EFFUSION- POSTPERICARDIOTOMY

SYNDROME

Buøi Gio An.MD

 Postpericardial injury syndrome (PPIS): Pericarditis or pericardial effusion that results from recent or earlier injury of the pericardium.

Postpericardiotomy

syndrome (PPS)

 A febrile illness with pericardial+/-pleural reactions, develops after surgery involving pericardiotomy.

 The term “ postpericardiotomy syndrome ” was substituted for the previous

“ postcardiotomy syndrome ”: syndrome can

occur after the pericardium is opened even if the heart is not invaded.EX: CA, insertion of

a pacing lead, ablation of an aberrant pathway…

 O Henry Janton (1952)-Louis A Soloff(1953): First

description of PPS in patient with rheumatic induced mitral valve stenosis who had undergone mitral valvuloplasty Reactivation of the rheumatic process!

 1956 -Dressler W: A post-AMI syndrome: idiopathic, recurrent, benign pericarditis

 1980-Engle: A possible etiology is autoimmune process +/- viral infection Anti-heart antibody-Antiviral antibody

 1980 Clapp SK: Relationship between postpericardiotomy syndrome and pericardial effusion

 1990-Horneffer PJ: A randomized placebo-controlled trial (RCT) of NSAIDs in treatment of postpericardiotomy syndrome after cardiac operations (J Thorac Cardiovasc Surg 1990 Aug;100(2):292-6)

 Life-threatening pericardial tamponade (1%)

 Cardiac repair ( CHD, Acquired HD), transluminal CA,

pacemaker insertion…

 Onset: Usually 1-6 weeks after surgery Median

postoperative time ~ 4 weeks ,range from 2 to 52 weeks

 Duration: Median 22 days, range from 2 to 100 days.

 Recurrence: 21% ,1-3months post-operative,7 year

follow-up

(Clinical features and long-term natural history of the postpericardiotomy

syndrome – Nishimura RA - Int J Cardiol - 01-NOV-1983; 4(4): 443-54 (From NIH/NLM MEDLINE)

 Frequency: vary

Antonio R Mott 2001,RCT,children

undergoing HS with CPB.n=246

CHANGE IN INCIDENCE OF PPS AND

post-PE

Incidence (cont) - Cheung

(6.7%)

PS-Multivariate analysis showed that postoperative warfarin is

a significant risk factor for post PE~adult result

Pericardium  Double-layered

fibroserous sac

 1–2 mm thick, separated by a space that normally contains 15–50 mL pericardial fluid (<1ml/kg).

 Intrapericardial pressure #pleural pressure :

inspiration

expiration

1 Blood supply from the internal mammary arteries.

2 Innervation from the phrenic nerve.

3 Drainage of pericardial fluid is via right lymphatic duct and

thoracic duct

Functions of the

Pericardium

1. Stabilization of the heart within

the thoracic cavity.

2. Protection of the heart from

mechanical trauma

3. Prevention of excessive dilation

of heart

Pathogenesis

 In era of rheumatic heart disease : PPS

Reactivation of the rheumatic process

 Unknown Autoimmune theory

antiheart-Ab, antiviral-Ab (Circulation 1974;69:401.)

 Maisch: Antisarcolemmal antibodies (primarily IgG), antifibrillary antibodies (predominantly IgM)

(Clin Exp Immunol 1979;38:189.)

Anti-heart antibodies (exposed in HS)Heart antigen

PERICARDITIS

Immune system

PERICARDIAL EFFUSION

TAMPONADE (0.1% to 6%)

Immune complex

HEMODYNAMICS OF PERICARDIAL EFFUSION

 A - Acute Effusion, e.g traumatic injury of the heart

 B - Chronic Effusion, e.g., viral pericarditis, tuberculosis

IPP

Pericardial pressure-volume (or strain-stress) curves

? 10-20mmHg

Spodick D Acute cardiac amponadeNew Engl J Med 2003;349:684– 90

?

Figure 64-4  Beat-to-beat changes in pulmonary arterial and aortic stroke

volume (as percentage of control) following abrupt production of cardiac

tamponade (at arrow)

pericarditis +/- pleuritis, worsening with inspiration and supine position

 General symptoms: Malaise, irritability, decreased appetite, arthralgias

CLINICAL: Physical exam

 Pericardial friction rub, sometime absent, scratchy superficial sound, heard most strongly along the left parasternal edge.

Triphasic:

 (1) an atrial systolic rub,precedes S1

 (2) a ventricular systolic rub between S1 and S2

 (3) an early diastolic rub after S2

 Pleural friction rub, change with breath cycle.

 Systemic fluid retention

 Hepatomegaly can occur.

 Tachycardia

Physical exam: Pericardial effusion

 Asymptom

 Tachycardia

 Tachypnae with clear lungs

 Heart sounds may be distant or faint

 Jugular venous pressure is elevated

 Liver may be enlarged, peripheral

edema

 Symptom of low cardiac output…

Physical exam: Cardiac

tamponade

1 Beck’s triad (usually acute tamponade, first

described in 1953)

 Hypotension

 Quiet heart sounds

 Raised jugular venous pressure

2 Compensatory tachycardia

3 Pulsus paradoxus

4 Other: hepatomegaly, dyspnoea or

tachypnoea with clear lungs

Atrial

contraction

Raised jugular venous pressure

Atrial relax Ventricular contraction

Atrial filling

Empty into ventricle

Physical exam: Cardiac

tamponade

Upper limit: +7mmHg

Upper limit: +12mmHg

PARADOXICAL PULSE

Blood sample

 Leukocytosis with a shift to the left

 Elevated erythrocyte sedimentation rate and CRP.

 Antiheart antibodies: high titer

 TNF-alpha, Cardiac enzyme testing: usually not helpful Ex: troponin I

(cTnI), creatinine kinase (CK),

creatinine kinase isoenzyme MB

(CKMB).

Pericardial fluid analysis

 Bacteriologic studies were negative

http://chestjournal.org/cgi/content/abstract/83/3/500

Chest X_ray

 Ranging from normal to

“water bottle” heart shadow.

 +/- Pleural effusion, especially on the left

 Enlarged cardiac silhouette with clear lungs

ECG findings: Pericarditis

 Stage I: anterior and inferior concave ST segment elevation PR segment deviations opposite to P polarity.

 Early stage II: ST junctions return to the baseline, PR deviated.

 Late stage II: T waves progressively flatten and invert

 Stage III: generalised T wave inversions

 Stage IV: ECG returns to prepericarditis state.

ECG findings: PE-CT

 Sinus tachycardia

 Low voltage of the QRS complexes: total amplitude of the QRS complexes in each

of the six limb leads is <=5 mm (0.5 mV)

 CT- Electrical alternans; relatively specific but not sensitive; beat-to-beat alterations

in the QRS complex and other electrocardiographic waves  swinging

of the heart in the pericardial fluid

2:1 ratio

Echocardiography

Horowitz classification

 Type A: No effusion

 Type B: Separation of epicardium and pericardium (3–

16 ml)

 Type C 1: Systolic and diastolic separation of epicardium and pericardium (small effusion >16 ml)

 Type C 2: Systolic and diastolic separation of epicardium and pericardium with attenuated pericardial motion

 Type D: separation of epicardium and pericardium with large echofree space

 Type E: Pericardial thickening (>4 mm).

 The size of effusions can be graded as:

 Small: echo-free space in diastole <10 mm

 The echo image at the level of the aortic root (Ao) and left atrium (LA) demonstrates a large echo free space representing a pericardial effusion (PE) behind the LA.

Echocardiography:CT

 The subcostal view

echocardiogram shows a large pericardial effusion encircling the heart

 "swinging" motion during the cardiac cycle

 Diastolic collapse of the right atrium and ventricle, a result of tamponade

 Intrapericardial pressure is also raised,virtually identical

to RA pressure (both pressures fall in inspiration)

 RV mid-diastolic pressure raised and equal to the RA and pericardial pressures (no dip-and-plateau configuration)

 Pulmonary artery diastolic pressure is slightly raised

 Pulmonary capillary wedge pressure is also raised and nearly equal to intrapericardial and right atrial pressure

 LV systolic and aortic pressures may be normal or reduced

 Mild cases: Bed rest is all enough

 Life-threatening CT: Immediate pericardiocentesis

 Nonsteroidal anti-inflammatory agents

1 Aspirin

• First-line medication

• Inhibits prostaglandin synthesis

• Pediatric Dose:80-120 mg/kg/d PO divided q6h

• Diagnosis: at least two of the following: fever,

anterior chest pain, and friction rub

• Drug efficacy: resolution of at least two of

these criteria within 48 hours of drug

initiation

• Ibuprofen and indomethacin significantly

more effective than placebo.

• Prednisone

• Reserved for treating severe cases or

relapses, contraindications or failure of NSAIDs.

• Result in faster resolution of symptoms

• Pediatric Dose

 2 mg/kg/d PO; tapered over 2-4 wk

Corticosteroids

Wilson NJ (Pediatric cardiology;1994 Mar-Apr,15(2):62-5)

 Randomized Controlled Trial.

 Prednisone 2 mg/kg/day reducing to zero over 14 days (n = 12) vs placebo (n = 9).

 Measures of efficacy: number of patients in remission

at 72 h and at 1 week.

 Result:

• No difference in remission rates 72 h,

• Remission rate significantly at 1 week prednisone group

• Prednisone hastens the recovery,but PE may increase

despite the use of corticosteroids

The optimal method for

prevention of PPS?

Mott AR (Journal of the American College of Cardiology,2001

May;37(6):1700-6)

 Randomized Controlled Trial.

 Children undergoing cardiac surgery CPB

 Pre-CPB intravenous methylprednisolone (1 mg/kg) plus four additional intravenous doses over 24 h vs placebo.

 Result:

• Intravenous methylprednisolone: standard

anti-inflammatory dose neither prevents nor attenuates PPS in children

• Short-term Short-term pre-CPB pre-CPB and and post-CPB post-CPB

methylprednisolone treatment may complicate PPS

The optimal method for

prevention of PPS?

Finkelstein Y (Herz,2002 Dec;27(8)791-4)

 Randomized Controlled Trial.

 On the 3rd postoperative day: colchicine (1.5 mg/day) or placebo for 1 month

 Follow up for the first 3 postoperative months for PPS

 N=111 patients who completed the study

 Result

• PPS was 5/47 cases (10.6%) in the colchicine

group and 14/64 (21.9%) in the placebo group

• Colchicine may be efficacious

Recurrent case? Unknow

G Wendelin: case report

 A 12-year-old girl with surgical closure of a secundum atrial septal defect in July 1999

 Recurrence of PE 2 weeks post-operated  treated successfully with ASA

 Massive pericardial effusion with pericardial tamponade

3 weeks post-operated drained and prednisone 2 mg/kg/day for 4 days, tapered gradually over 10 days

 2 days after steroid discontinuation: fever, chest pain, relapse of PEnot respond to ASA, rapidly improved with prednisone

 Following 22 months, recurrences of PPS whenever prednisone was reduced to less than 0.3 mg/kg/day All anti-myocardial antibody and anti-viral antibody tests normal

 After 8 th relapse of PPS treatment with IVIG, 2 g/kg was administered over 24 hoursall symptoms resolved

 Follow-up of 54 months, no further recurrences

 Pericardial+/-pleural reactions, develops after surgery involving pericardiotomy.

process.

 Pericarditis occur late in post-operated

period, most >1w, after patient has

discharged frome hospital  CT  death.

No data for effect prevention.

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