PURULENT PERICARDITIS IN INFANCY

(1)

PURULENT

PERICARDITIS

IN

INFANCY

Welton M. Gersony, M.D., and George H. McCracken Jr., M.D.

From the Department of Pediatrics, Children’s Medical Center, Universitij of Texas,

Southwestern Medica1 School, Dallas, Texas

(Submitted December 19, 1966; revision accepted for publication March 5, 1967.)

Presented at the Pediatric Cardiology Section of the American Academy of Pediatrics, October 1966.

PRESENT ADDRESS: (G.H.M.) National Institute of Child Health and Human Development, Bethesda, Maryland.

ADDRESS: (W.M.G.) 5323 Harry Hines Boulevard, Dallas 35, Texas.

P

IJBIJLENT PERICARDITIS in infancy is a

relatively infrequent but fatal disease unless recognized early and treated

aggres-sively. This report will present the

expe-rience at this institution with suppurative pericarditis in seven infants under 2 years

of age and a review of the literature. An

in-fant with purulent pericarditis due to

Neisseria meningitidLs was observed by the

authors and is reported in detail. To our

knowledge, meningococcal pericarditis has

not been described previously during

infancy.

CASE REPORT

This 13-month-old white girl (Case 5 of Table

I) was well until 4 days prior to admission. At

that time she developed fever, vomiting, and

lethargy, and there were “spots” over her entire

body. Although this rash began to fade without

treatment over the next 3 days, she became

in-creasingl lethargic and was admitted to

Chil-dren’s Medical Center on October 15, 1965.

Physical examination revealed an acutely ill,

ir-ritable infant. The temperature was 102#{176}F, pulse

was 160, respiration was 80, and blood pressure

was 110/70 with a 10 mm paradoxical pulse.

Positive findings included a high pitched cry,

nuchal rigidity, positive Brudzinski and Kemig

signs, distended neck veins, distant heart sounds,

a liver palpable 4 cm below the costal margin,

and fading petechiae over the extremities.

Laboratory data revealed a hemoglobin of 10.8;

a white blood count of 22,700/mm’ with 46

lymphocytes, 52 polymorphonuclear cells, and 2

mononuclear cells; and a normal urinalysis. A

spinal tap produced a cloudy fluid with 780 cells!

mm3, of which 77% were polyinorphonuclear cells.

The spinal fluid sugar was 9 mg/i#{174} ml with a

simultaneous blood sugar of 71 mg/100 ml.

Pro-tein was 20 rng/100 ml. Gram-negative

intracellu-lar diplococci were seen on direct smear. Cultures

of the spinal fluid and blood grew Neisseria

meningfticiis, Group B, sensitive by tube dilution

studies to sulfadiazine and ampicillin. The chest

film showed an enlarged heart with clear lung

fields, and the ECG revealed ST segment

eleva-tion in leads I, II, AVF, and V4-V6. There was

diminished voltage over the left precordial leads

(Fig. 1).

Therapy was initiated with ampicillin (200 mgI

kg/day), intravenously, and digitalis. Twelve

hours after admission a narrow pulse pressure

was noted and fluoroscopy revealed a virtually

pulseless cardiac silhouette. A pericardiocentesis

was performed with the removal of 60 cc of

pumlent material which contained 2,900 WBC’s/

mm’ with 79% polymorphonuclear cells, a sugar

of 4 mg/100 ml, and a protein of 4,200 mg/i00

ml. Smear revealed gram-negative intracellular

diplococci, which failed to grow on culture. After

this procedure, a widening of the pulse pressure

was noted, and a pericardial friction rub was

heard for the first time. During the next 2 days

four additional pericardiocertteses were

per-formed, and a total of 140 cc of seropurulent

material was removed. The infant became

afe-brile in 24 hours following admission and there

was rapid improvement in her condition.

Ampi-cillin was continued for 10 days. She was

dis-charged after 18 days; physical examination was

normal at this time. The electrocardiogram at

dis-charge revealed non-specific ST segment changes,

and the chest x-ray showed a normal sized

car-diac silhouette. Follow-up examination at 6

months revealed a well infant with a normal

chest x-ray and ECG.

REVIEW OF CASES

The records of all infants under 2 years of age admitted with purulent pericarditis to Children’s Medical Center or the Pedia-tric Service at Parkland Hospital, Dallas,

Texas, from 1956 to 1966 were studied. The

diagnosis was established in each instance either by direct pericardial aspiration or at

postmortem examination. Purulent

pericar-ditis was considered to be due to a specific

bacterial agent when the organism was

(2)

FIG. 1. Case 5. The electrocardiogram recorded on the day of admission. Note the ST segment elevation in leads I, II, AVF, and V4-V6.

rectly recovered from the pericardial sac or

when isolated from infection elsewhere in

the presence of proved suppurative

pericar-ditis. Etiologic agents other than bacteria

were excluded on the basis of clinical data,

skin tests, and examination and culture of

pericardial fluid.

RESULTS

The records of seven patients with

puru-lent pericarditis were studied; the pertinent

clinical and laboratory data are

summa-rized in Table I. The ages ranged from 18

days to 15 months, and four of the seven

infants were female. Three infants

sue-cumbed to their illnesses; in each instance

the correct diagnosis was not made until

postmortem examination. In contrast in the

four surviving patients, the diagnosis of

pericarditis was made and therapy initiated

in 4 to 6 days following initial symptoms of

infection and within 72 hours after hospital-ization. In two infants the diagnosis of

pen-carditis was made immediately upon

ad-mission. The responsible bacteria were

Staphylococcus aureus in three,

Hemophi-1145 influenzae in two, and Neisseria men

in-gitidis in one. In one case the organism was

not defined.

Respiratory symptoms, including

tachy-pnea, dyspnea, and cough, were the initial

complaints in six of the seven infants. One

patient

(

Case 5

)

was admitted because of a

rash and frequent vomiting.

All of the infants were acutely ill, febrile, and markedly dyspneic on admission.

Physi-cal findings in the four patients in whom

the correct diagnosis was made included

evidence of cardiac tamponade. Pulsus

par-adoxus and hepatomegaly were noted in all

four infants; distended neck veins and

de-creased heart sounds were observed in

three. Each of these infants displayed pen-cardial friction rubs, but in two the rub be-came audible only after penicardiocentesis.

Cardiac murmurs were described in none.

Signs of meningitis were present in two

pa-tients

(

Cases 5 and 7

) ,

one of whom

(

Case 5) had a fading petechial rash suggestive of

(3)

PERICARDITIS

TABLE I

SUMMARY OF DATA FOR INFANTS WITH PURULENT PERICARDITIS SEEN AT CHILDREN’S MEDICAL CENTER

Case

Num-bee

and

.4ge } ear.

Days of Symptom. . .4asoeialed Prior to . illness Admis-.

Organism fource.

Therapy

Outcome

.

Per,-.

cordial .4ntibiotica. .

Sex aba Drainage

(F) 15 mo 19.56 1 pneiiinonitis None isolated - - tetracycline

penicillin

I)ied; autopsy: pen-canditis,

pneurnoni-tis. myocardial

ib-scesses.

(F) 13 mo 1956 3 upper

res-piratory

infection

Staphylococcus aureus

Blood C penicillin tetracycline chlorampheriicol

Recovered.

(M) 18 do 1957 pneumonitis Staphylococcus

aureus

Lung - penicillin

tetracycline

I)ied: ititopsy: pen-canditis. multiple

pulmonary il)SecSS-es.

4 (M) . wk 1959

I 1 pneixmonitis pleural effusion Staphylococcus aureus

Lung - chlonamplienicol bacitnacin

penicillin

I)ied; autopsy: pen-canditis, pulmonary

and myocardial

oh-scesses.

.5 (F) 13 mo 1965 4 meningitis Neisseria

rneningitidis

Blood CSF’

C ampicillin Recovened.

6 (M) 1-C mo 1965 4 none Hemophilus

influenzae

penicar-dium

0 ampicillin Recovered.

7 (F) 10mo 1966 3 meningitis pneumonitis

!Iemophilus

influenzae

penicar-dium

0 ampicillin Recovered.

S

C=Penicardiocenteses.

0 = Penicardiostomy with tube drainage.

0 =Cerebrospinal fluid.

with penicarditis due to Hemophilus

in-fluenzae had epiglottitis.

Electrocardiograms were obtained from

four of the infants. The initial tracings

(

within 48 hours of admission

)

in three

cases

(

Cases 2, 5, and 6

)

showed ST-T wave

elevations in leads II, III, AVF, and the left precordial leads. On the third hospital day one infant

(

Case 7

)

developed a transient

arrhythmia which alternated between a

nodal pacemaker and sinus rhythm with

nodal escape beats. It was not until the

eighteenth day that typical ST

abnormali-ties appeared. Significantly low QRS

vol-tage was apparent in three of the

pa-tients.

Chest x-rays revealed an enlarged cardiac silhouette in all of the infants, and, except

for those patients in whom pneumonitis

was present, the lung fields appeared to be

clear. In the four infants who were

fluoro-scoped, markedly decreased cardiac

pulsa-tions were described. One patient

(

Case 7)

was noted in retrospect to have had

cardi-omegaly on a chest film taken 1 month

prior to admission.

The four surviving infants were

dis-charged after 17 to 42 days. Penicardial

drainage was employed in all four

infants-two by continuous open drainage with a

penicardial window and two by multiple

penicardial taps. The patients infected with

Flemophilus influenzae and Neisseria

men-ingitidis were treated with ampicillmn, and the infant with staphylococcal penicarditis received penicillin, tetracycline, and

chlor-amphenicol. Two of the four patients were

digitalized. All recovered completely and

are well on follow-up examinations. In no

instance has evidence of constrictive

pen-carditis appeared.

Three infants in whom no pericardial

as-piration was carried out expired despite an-timicrobial therapy. Two received penicil-un and tetracycline in high doses. The third

was treated with chloramphenicol and

baci-tracin, with penicillin added later in the

(4)

::/:::. Total Number

::: of Patients

Deaths 13

12

11

C’) 10 I-z9

z -7

LA-06

cr5

ii

FIG. 2. Mortality related to

MONTHS

age in 50 reported infants with purulent pericarditis.

was not carried out in any of these three. All were digitalized. The two patients with proved staphylococcal disease showed

bilat-eral bronchopneumonia with abscess

for-mation at autopsy. One of these infants

(Case 4) , who died after a prolonged

flue-tuating illness, had a fibninopurulent

pericar-ditis with associated myocardial abscesses.

The other infant

(

Case 3) had purulent

pericarditis and mediastinitis. It appeared likely that the penicardial involvement oc-curred as a result of direct extension from the pulmonary abscesses in both patients. The third patient who died

(

Case 1

)

had no

bacteriologic diagnosis. Autopsy revealed a

fibrinopurulent pericarditis with myocardial

abscess formation but without pulmonary

abscesses.

COMMENT

Fifty infants with purulent pericarditis,

including the present series, have been

re-ported in the world literature since the turn

of the century.122 The children ranged in

age from 2 days to 24 months

(

Fig. 2

)

; and,

of the 46 patients in whom the sex was

specified, 26 were male and 20 female. The

mortality rate for purulent penicarditis

among these infants was 66%; but, if the

patients in whom the disease was not

rec-ognized clinically are eliminated, the

mor-tality was 47%. This figure is similar to the

mortality rate of 41% quoted by Boyle and

associates23 for all age groups in whom the

diagnosis was made during life. Recovery

occurred more often during the second year

of life. Only one infant with purulent

pen-carditis under the age of 1 month has been

documented to survive.’

Suppurative pericarditis has rarely been

found to be a primary infection. Rather, it

is usually observed in association with

in-fectious processes elsewhere, and it is

al-most invariably discovered subsequent to

the other illness. Pulmonary infection is the

most common accompanying condition

re-ported in older children and adults,2 and

this predominance holds true for infants as

well

(

Table II ). Suppurative pericarditis in

these patients may occur either by direct

extension from adjoining lung or may result

from hematogenous spread of organisms.

Although other associated illnesses are

re-corded less frequently, in some instances

(5)

this may have resulted from the failure to

search for them adequately. Suppurative

pericarditis as an isolated disease has been

reported in only 7 of the 50 infants, of

whom 5 recovered.

The differential diagnosis of penicarditis

has been well reviewed in the past,3’5 and

the diagnostic features among infants are

not different than those in older individuals.

Evidence of cardiac tamponade

(

pulsus

paradoxus, hepatomegaly, distended neck

veins

),

a quiet precordium with muffled

heart sounds and a pericardial friction rub

are the prominent physical findings. The

x-ray typically shows a large heart and clear

lung fields with poor cardiac pulsations at

fluoroscopy. The ECG reveals ST-T wave

changes with ST segment elevation being

the most typical abnormality found.

How-ever, variations from this clinical picture are frequent. The pericardial friction rub is

often transient, may not be audible at all,

or may be present only after

pericardiocen-tesis has been carried out. The ECG

changes are often non-specific, may be

identical with those found in myocarditis,

and may not appear until relatively late in

the course of the illness. The most reliable

sign of cardiac tamponade appears to be

TABLE II

ASSOCIATED ILLNESSES IN 50 INFANTS REPORTED

WITH PURULENT PERICARDITIS

illness Number

Pulmonary infectiont 34

Meningitis 4

Osteomyelitis 3

Myocardial abscesses

3

Pyelonephritis

Congenital heart disease Liver abscess

Pulmonary infarction 2

Kwashiorkor I

Diphtheria I

Retropharyngeal abscess I

Peritonitis

1

Endocarditis I

None 7

* Twelve patients had more than one condition.

t Includes pneumonitis, empyema, and pulmonary

abscesses.

the presence of a pulsus paradoxus of >20

mm. Values between 10 mm and 20 mm are

considered to be suspicious but not

diag-nostic. In small infants it is often

technical-ly difficult and time consuming to obtain an

auscultatory blood pressure, which is neces-sary to demonstrate the paradoxical pulse. Thus, in most instances, the early diagnosis

of penicarditis is not made unless a high

index of suspicion is present and the signs are searched for diligently.

The organisms responsible for purulent

pericarditis reported among infants are

shown in Figure 3. The incidence of the

various agents according to age is

present-ed in Figure 4. Staphylococcus aurens

ac-counted for almost one half of the cases and

was responsible for 73% of the deaths. The

pneumococcus, once the most common

cause of suppurative pericarditis in

chil-dren,25 has not been reported in infancy

since the advent of antibiotics and repre-sents only 10% of the total cases. #{176}The one patient in the present series with meningo-coccal pericarditis (Case 5) is the first such case reported in infancy. Only five children under the age of 15 years with penicarditis due to this agent have been described in the

literature. The pertinent data relative to

these patients are presented in Table III.

Purulent pericarditis occurs as a relatively

late complication of meningococcal

infec-tion and it is likely that its rarity is related to the usually fulminate nature of the

men-ingococcemia. Most patients either expire

relatively early in the illness or are treated

and recover promptly. The recent

appear-ance of resistant strains of Neisseria

men-ingitidL#{176} could conceivably lead to an

in-creased incidence of penicarditis by

pro-longing the clinical course of infection.

The results of therapy of purulent

pen-carditis in the 50 infants are presented in

Table IV. A striking preponderance of

sun-0 Since this paper was completed, a

12-month-old infant with primary purulent pericarditis due

to pneumococcus was successfully treated at

Chil-dren’s Medical Center with penicillin and open

(6)

5-(I)

iii1

Number of Cases

!

Mortality

[.

_rIrkIr-

Staph. Pneumococcus H. Unknown Others*

aureus influenzae

*Strep. pyogenes, Pa ra colon, N.meningitidis , Bacteroides, Salmonella

and E. coli.

FIG. 3. Infectious agents in 50 infants reported with purulent pericarditis.

(‘use

, .lufbzor

.‘ U1fl()C

1 Trace and BerkovitzN 1931 l

3

L4JC 811(1 1)iaiiiond27 1945

Weis afl(l Sillier28

Outcome

Recovered.

Year Sex .lge

Syr

F

l3yr

1961 F 4 yr

1963

\l

15 yr

1964 F’ S yr periear(liostomv, 1)CIii- lte(overe(l.

(illili

229

25

20

15

-10

-

0-vivals is noted among the infants who were

treated with both penicardial drainage and

antimicrobial agents. There were no

recov-enies among patients who received

antibiot-ics alone, and only three of twelve infants survived who had drainage of the

pericardi-urn without antimicrobial therapy. Thus it

vould appear that both modes of treatment

are crucial in the therapeutic regimen for

purulent pericarditis. It has been stated#{176}

that, in the modern era, antibiotics alone

are sufficient to treat this disease, since

overwhelming infection accounts for the

mortality among the great majority of

pa-tients with punulent penicarditis, whereas

cardiac tamponade is a relatively rare

oc-currence. The present study does not

sup-port this view. Each of our own four

surviv-ing patients had acute tamponade, which

was relieved by pericardial drainage.

Fur-thermore, recovery with antibiotics alone

has not been reported in a single infant

with suppurative pericarditis. On the basis of these data, immediate pericardiocentesis

TABLE III

REPORTEI) (‘AMES CW IEIIICARDITIS I)uE TO .VEJSSER!.-1 .IIE.V!.VGJTJD!S IN (‘IIIrDnEN

4 lleiiziiig, III, aII(1

l’iill)l8Il2

5 Staiiiey2#{176}

Therapy

pericardiocenteses,

iii-trapericardial anti-serum

periear(liostomy,

lwIli-(‘illifl

peIIi(illiII

j)CIiiCiLIiIl

Iteenvered.

I)ie1 ; autopsy :

(011-strictive pericar(litis with cor(Ius

(7)

A

.

A

0

v#{149} #{149}L1&

A Staph. aureus

#{174}N. meningitidis

. Pneumococcus

yE. coli

. Unknown

0 H. influenzae

Strep. pyogenes

? Bacteroides

Salmonella

U Paracolon

<1 mo. 1-12 mos. 12-24 mos.

FIG. 4. Incidence of infecting organisms according to age in 50 infants reported with purulent pericarditis.

230

* Patients reported iii the pee-antibiotic era.

t Three cases reported in the pre-antibiotic era.

12

11

10

U)

z

-7 LL 06

cr5

2

is strongly recommended when the

diag-nosis of purulent penicarditis is suspected.

Survival does not appear more likely

whether multiple taps or pericardiostomies

are employed; the crucial factor is that of

adequate drainage to relieve frank or

im-pending cardiac tamponade and prevent its

recurrence. However, surgical

pericardios-tomy may be preferred in that loculation of

exudate is less likely, and constant drainage prevents reaccumulation of fluid.

The proper selection of an antimicrobial agent in the treatment of infants with

puru-TABLE IV

RESULTS OF THERAPY IN 50 INFANTS REPORTED

WITH PURtTLENT PERICARDITIS

Treatment Recoveries Deaths

Antibiotics and iericardial

drainage 14 3

Antibiotics alone 0 17

Pericardial drainage alone5 3 9

No treatmentt 0 4

lent pericarditis depends in part on the

clinical course of illness, the gram stain

and culture of the penicardial fluid, as well

as familiarity with the microbial agents

most commonly responsible for penicarditis in this age group. The antistaphylococcal penicillins are the drugs of choice in treat-ing infants with severe staphylococcal dis-ease when the organism is resistant to

peni-cihin. Penicillin G remains the most

ap-propriate agent in treating

penicillin-sensi-tive staphylococcal and pneumococcal

in-fections. Ampicillin is, at present, the drug of choice in infections due to Hernophilus influenzae and Neisseria meningitidis.

When at the outset of illness the etiologic agent is uncertain, more than one antibiotic

(

for example, methicillin and ampicillin)

may be appropriate to ensure coverage

against the most likely microbes. Combined therapy should be continued until results of the culture and sensitivities are available and selection of the best therapeutic agent can be made.

There have been no reported cases of

constrictive penicarditis as a sequela of

pu-rulent penicarditis in infancy. Reports

(8)

some authors have denied that this compli-cation occurs.#{176}-82 Boyle, et al.,23 in a review of 274 cases of constrictive penicarditis,

could find only six poorly documented

in-stances in which there was said to be a

pu-rulent origin. However, Weis and Silber28

did observe a 4-year-old child who

de-veloped constriction during the healing

phase of meningococcal penicarditis and

subsequently died

(

Table IV, Case 3).

Thomas, et also reported a well studied

case of constrictive pericarditis in a

4%-year-old child with staphylococcal

infec-tion. Both of these patients developed

con-striction within 2 to 3 weeks after their

initial illnesses. This unusual type of

“acute” constriction is in contrast to the

months or years described as the common

temporal sequence of nonpurulent

con-strictive pericarditis. Although certainly an unexpected complication, constriction should be considered in any infant with pu-rulent pericarditis if signs of cardiac failure

persist or recur despite optimal therapy

having been carried out in the initial phases

of the disease.

SUMMARY

Seven patients less than 2 years of age

vith purulent pericarditis were

encoun-tered. Four infants survived, including the

first infant reported with meningococcal

penicarditis. Including the present patients, 50 infants with suppurative penicarditis

have been described in the literature. The

overall mortality was 67%; it was 47%

among patients in whom the diagnosis was

made clinically. Staphylococcus aureus was

the most common infecting organism, and

it was responsible for the greatest number

of deaths. Pulmonary infection was by far

the most frequently observed associated

ill-ness, whereas purulent penicarditis

occur-ring as a primary infection was rare.

Survival from purulent penicarditis

de-pends upon adequate pericardial drainage

with antimicrobial therapy. Antibiotics

alone have not been successful in the

treat-ment of this disease.

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(9)

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Acknowledgment

The authors wish to thank Mrs. Patricia Smith

for her efforts in the preparation of this

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1967;40;224

Pediatrics

Welton M. Gersony and George H. McCracken, Jr.