Case Report - EBP To:

Non Infection Unit

CARDIAC TAMPONADE IN BOYS 15 YEARS OLD

Presentator : Muhammad Hidayat

Day / Date : / March 2019

Supervisor in charge : dr. Rizky Adriansyah ,M.Ked (Ped), Sp.A(K)

Supervisor : dr. Tina Christina L.Tobing, Sp.A(K)

dr. Muhammad Ali, Sp.A(K)

dr. Rizky Adriansyah ,M.Ked (Ped), Sp.A(K)

dr. Hafaz Zakky Abdillah, M.Ked (Ped), Sp.A (K)

dr. Putri Amelia, M.Ked (Ped), Sp.A

Introduction

A pericardial effusion refers to the accumulation of fluid in the pericardial sac

surrounding the heart. The pericardial sac is composed of the thin visceral pericardium which
consists of a single layer of cells adherent to the cardiac epicardium and the thicker and fibrous
parietal pericardium composed of collagen and elastin which is adherent to the lungs,
diaphragm, sternum, great vessels, and other mediastinal structures surrounding the heart. In a
healthy individual, the pericardial sac contains between 15 mL and 50 mL of serous
fluid.[1][2][3].(DA willner)

Cardiac tamponade occurs in approximately 2 out of 10.000 people.( buku Profesional

guide) .
 Pericardial effusions may develop rapidly (acute) or more gradually (subacute or
chronic). The normal pericardium can stretch to accommodate fluid increases in pericardial
volume, with the amount of stretch related to how quickly the effusion develops. The ability to
stretch is greater with slowly developing effusions. However, regardless of how quickly an
effusion develops, with ongoing accumulation of pericardial fluid into a closed space,
eventually the intrapericardial pressure begins to increase. When the intrapericardial pressure
becomes high enough to impede cardiac filling, cardiac function becomes impaired, and
cardiac tamponade can be considered to be present.(uptodate). Proper management and
treatment aims to reduce further damage to the heart and life-saving by immediate to
pericardiosyntesis if cardiac tamponade occurs. mou

The aim of this paper is to report the case of Pericardial Effusion in a 15 years old boys.

Case
SW, a 15 years old boy, was admitted to Pediatric Emergency Departement on Haji Adam
Malik General Hospital on December, 19th 2019, with chief complaint of shortness of breath
since 3 months ago. It related with activity such as going up and down the stairs, and said it
become better with rest. Chest pain has been felt in the last 1 month, radiating to the left
shoulders, it worsen when patient breathe deeply and gets better when the patient lean forward
Patient also complaint of dry cough which present since 3 months ago, and with no history of
fever. History contact with adult TB patients is denied. Enlarged abdomen experienced by
patients 3 months ago, and also decreased 5 kg of body weight in the last 3 months. History of
bluish lips and skin was not found, swelling was not found, history of sore throat is denied.
Urination and defecation was normal. No other symptom was reported.

Previous medical history:

The patient was referred from the hospital Karya Husada with the diagnosis of CHF ec DD /
RHD + presumption of pleural effusion and had received 4 days of treatment.
Previous drug history :
Injection of Ceftriaxon 1gram/12 hours, Furosemide injection 1 ampul/12 hours, Ambroxol 3x
1 tablet.

Physical Examination
Consciousness was alert, body weight: 54 kg (BW/A: 89% ), body height : 165 cm (BH/A:
96%), (BW/BH: 98%), with body temperature 37,1 oC, and nutritional statue was normoweight.
There was dyspnea on effort, no pale, icteric, cyanosis, and edema. Commented [u1]: jaundice

Head: Commented [MH2R1]:

Eyes : light reflexes (+/+), pupils were isochoric Ø 3 mm, pale at lower eyelid conjunctiva
(-/-),
Ears /Nose: within normal limit
Mouth : no cyanotic
Neck : with JVP R+5 cmH20
Chest : symmetrical fusiform, with retraction intercostal
Heart Rate : 110 bpm, muffled heart sound (+), no murmur was found (N: 60-10
bpm)
Respiratory Rate : 24 bpm, regular, no rales, wheezing and stridor (12-16 bpm)
Abdomen : distended, peristaltic was normal, liver palpable 5 cm below arcus costae and
spleen were not palpable
Extremities : Edema (-) pulse 110 bpm, regular, P/V adequate, capillary refill time < 2
seconds, blood pressure 80/50 mmHg (abnormal)

Laboratory Findings on Admission

Hemoglobin: gr/dL, Hematocrite%, Leucocytes: /mm3, Platelet: /mm3, MCV: fl, MCH: pg,
MCHC: g/dL, RDW
Sodium: mEq/L, Potassium : mEq/L, Chloride: mEq/L, Calcium: mg/dL
Glucose ad random: mg/dL

Electrocardiography Findings on Admission 19/2/19

Low voltage in all lead,
Differential Diagnosis
 DD/ - Cardiac Tamponade + Heart failure NYHA III-IV
- Cardiomyopathy

Working Diagnosis: Cardiac Tamponade + Heart failure NYHA III-IV

Therapy:
 02 Nasal canule 2 lpm
 IVFD D5% NaCl 0,45%  20 gtt/min micro
  Ceftriaxone injection 1gram/12 hour /IV
 Furosemide injection 40 mg/12 hour/IV
 Sprinolacton 2 x 25 mg
 Diet regular food 2100 kkal with 100 gr protein

Planning :
CBC, electrolyte, Glucose ad random, renal function test, liver function test, procalcitonin,
 Consult to Cardiology Division
 Echocardiography

Cardiology Division
Echocardiography Findings December, 19th 2019
Tamponade pericard
Planning :
-Pericardiosintesis Emergency
- Pericardial Fluid Analysis and fluid culture

Follow up patient post pericardiosintesis Emergency on 20/2/19

S : Shortness of breath decreses, pain was decreses

0 : There was dyspnea, no pale, icteric, cyanosis, and edema. Commented [u3]: jaundice

Head: Commented [MH4R3]:

Eyes : Light reflexes (+/+), pupils were isochoric Ø 3 mm, pale at lower eyelid conjunctiva
(-/-),
Ears /Nose: within normal limit
Mouth : no cyanotic
Neck : with JVP R+5 cmH20
Chest : symmetrical fusiform, with no retraction.
Heart Rate : 98 bpm, muffled heart sound, no murmur was found (N: 60-100 bpm)
Respiratory Rate : 20 cpm, regular, no rales and stridor (12-16 cpm)
Abdomen : distended, peristaltic was normal, liver palpable and spleen were not palpable
Extremities : Edema (-) pulse 98 bpm, regular, P/V adequate, capillary refill time < 2 seconds,
blood pressure 100/60 mmHg (normal)
A : Post pericardiosintesis ec Massive pericardial effusion ec dd/ Tuberculosis

Malignancy

+ CHF NYHA II-III

 P : 02 Nasal canule 2 lpm

 IVFD D5% NaCl 0,45%  20 gtt/min micro
 Ceftriaxone injection 1gram/12 hour /IV
 Furosemide injection 40 mg/12 hour/IV
 Sprinolacton 2 x 25 mg
 Diet regular food 2100 kkal with 100 gr protein

Lab result on HAM 20/02/19

Laboratory exam Result Laboratory exam Result

Hb 12,3
Eritrosit 5.190.000
leucoyte 9500
Hematocrit 39
Trombosit 439.000
E/B/N/L/M 0,8/6,98/15,9/73,3/8
Calcium 8,3 mEq/ml BUN 9 mg/dl
Natrium 134 mEq/ml Ureum 19 mg/dl
Kalium 3,8 mEq/ml Kreatinin Mg/dl
Chloride 104 mEq/ml
Procalcitonin 0,04 ng/ml
SGOT 17 U/L
SGPT 11 U/L

Pleural fluid Analysis 20/02/19

Colour Red RBC 2534

Total Protein 3,6 g/dl MN 89,9
LDH 146 U/L PMN 10,1
Glucose 52 mg/dl
 pH 8
WBC 1385

Follow up patient post pericardiosintesis 21/2/19

S : Shortness of breath decreses, pain was decreses

0 : There was dyspnea, no pale, icteric,cyanosis, and edema. Commented [u5]: jaundice

Head: Commented [MH6R5]:

Eyes : light reflexes (+/+), pupils were isochoric Ø 3 mm, pale at lower eyelid conjunctiva
(-/-),
Ears /Nose: within normal limit
Mouth : no cyanotic
Neck : with JVP R+3 cmH20
Chest : symmetrical fusiform, with no retraction.
Heart Rate : 100 bpm, muffled heart sound, no murmur was found (N: 60-100 bpm)
Respiratory Rate : 18 cpm, regular, no rales and stridor (12-16 cpm)
Abdomen : distended, peristaltic was normal, liver palpable and spleen were not palpable
Extremities : Edema (-) pulse 98 bpm, regular, P/V adequate, capillary refill time < 2 seconds,
blood pressure 100/60 mmHg (abnormal)

A : Post pericardiosintesis ec Massive pericardial effusion + CHF Nyha III

 P : 02 Nasal canule 2 lpm

 IVFD D5% NaCl 0,45%  20 gtt/min micro
 Ceftriaxone injection 1gram/12 hour /IV
 Furosemide injection 40 mg/12 hour/IV
 Sprinolacton 2x 1
Planning : tapping fluid

Discussion

Acute pericarditis may have many causes including infections, malignancy, collagen
vascular and autoimmune conditions, uremia, myocardial infarction, trauma, surgery,
hypothyroidism, and drugs such as hydralazine and procainamide. Idiopathic causes, which are
probably viral or autoimmune in most cases, are the prevalent etiologies in developed countries
[2].
Most common cause of pericardial effusion in children is viral infection is probably the
most common cause of pericarditis, particularly in infancy. Many viruses similar to those listed
in the section on myocarditis can cause pericarditis, acute rheumatic fever is a common cause
of pericarditis, especially in certain parts of the world (see also Chapter 20), bacterial infection
(purulent pericarditis) is a rare, serious form of pericarditis. Commonly encountered are
S. aureus, Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis, and
Streptococci, Tuberculosis is an occasional cause of constrictive pericarditis with an insidious
onset, heart surgery is a possible cause (see Postpericardiotomy Syndrome), collagen disease
such as rheumatoid arthritis (see Chapter 23), oncologic disease or its therapy, including
radiation and uremia (uremic pericarditis) is a rare cause in pediatric patient.

Table 1. Most common causes of pericardial effusion

Infectious Pericarditis
Staphylococcus aureus, Haemophilus influenzae,
Bacterial/Tuberculous
Neisseria meningitidis, Streptococcus pneumoniae β-
hemolytic streptococci, Mycoplasma pneumoniae,
Mycobacterium tuberculosis, Enterobacter cloacae,
Corynebacterium diphtheriae

Viral

Candida, Aspergillus, Histoplasma, coccidiomycosis

Fungal

Noninfectious Pericarditis

Cardiac Injury Postpericardiotomy syndrome, post myocardial infarction

Rheumatic fever, juvenile rheumatoid arthritis, systemic

Systemic Inflammatory Disease lupus erythematosus, inflammatory bowel disease,
Kawasaki disease, rheumatic fever, tumor necrosis factor
receptor–associated periodic syndrome (TRAPS), familial
Mediterranean fever

Leukemia, lymphoma, metastatic tumor, radiation pericarditis

Neoplasms

End-stage renal disease (uremia), dialysis

Renal
 Hypersensitivity to drugs/toxins (e.g., procainamide,
Miscellaneous
hydralazine, penicillins, cromolyn, dantrolene,
anthracyclines), amyloidosis, radiation

Additional Causes of Pericardial Effusion ± Pericarditis

Traumatic and Postoperative Blunt chest trauma, central line malposition,

catheterization/biopsy, rupture of coronary aneurysm
(such as with Kawasaki disease), early postoperative
hemorrhage

Superior vena cava syndrome, chylous effusion, primary

Elevated Central Venous Pressure/Low Plasma
Oncotic Pressure
pulmonary hypertension and right ventricular failure,
decompensated congestive heart failure, liver failure,
anorexia nervosa, bone marrow transplant/graft versus
host disease, hyperthyroidism/Hypothyroidism

The parietal and visceral surfaces of the pericardium are inflamed. Pericardial effusion
may be serofibrinous, hemorrhagic, or purulent. Effusion may be completely absorbed or may
result in pericardial thickening or chronic constriction (constrictive pericarditis). In this case
the fluid accumulation from first tapping is hemorrhagic with volume of 300 cc and collected
sample was sent for blood culture.
The pathogenesis of symptoms and signs of pericardial effusion is determined by two
Factors ; the speed of fluid accumulation and the competence of the myocardium. A rapid
accumulation of a large amount of pericardial fluid produces more serious circulatory
embarrassment. A slow accumulation of a relatively small amount of fluid may result in serious
circulatory embarrassment (cardiac tamponade) if the extent of myocarditis is significant. Slow
accumulation of the large amount of fluid may be accommodated by stretching of the
pericardium if the myocardium is intact.
With the development of pericardial tamponade, several compensatory mechanisms are
triggered, including systemic and pulmonary venous constriction to improve diastolic filling,
an increase in systemic vascular resistance to raise falling blood pressure, and tachycardia to
improve cardiac output. Heart murmur is usually absent, although it may be present in acute
rheumatic carditis (see Chapter 20). In children with purulent pericarditis, septic fever (101°–
105° F [38.3°–40.5°C]), tachycardia, chest pain, and dyspnea are almost always present, signs
of cardiac tamponade may be present: distant heart sounds, tachycardia, pulsus paradoxus,
hepatomegaly, venous distention, and occasional hypotension with peripheral vasoconstriction.
Pulsus paradoxus is characteristic of pericardial effusion with tamponade (MYUNG). Pulsus
paradoxus, defined as an exaggerated decrement in the arterial systolic pressure (>10 mm Hg)
during inspiration, occurs in tamponade primarily due to bulging of the interventricular septum
into the left ventricle (LV) as the right heart fills and the RV free wall is inhibited from
expanding anteriorly due to pericardial constraint. Exceptions to this occur when abnormal
communications exist between cardiac chambers (atrial septal defect; patent foramen ovale),
when there is alteration of normal ventricular pressure-volume relations (hypertrophic
cardiomyopathy, severe aortic stenosis, aortic insuf¬ficiency), 28-30 or when there is
decreased intravascular volume (low-pressure tamponade). (MOU2019) Cardiac tamponade
occurs more commonly in purulent pericarditis than in other forms of pericarditis. Just as
written in the literature, In this case we found that in physical examination theres no fever, on
the neck there is venous distension and in thorax we found dyspnea with respiratory rate 30x/
minutes that higher than normal, and we found pericardial friction rub, with tachycardia 110
beat/minutes. The blood pressure was 80/50 mmhg which is hypotension. In the abdomen,
hepatomegaly was found in physical eximination.
Pericardial effusion is commonly detected clinically and patients have to be suspected
of pericardial effusion when they develop cardiomegaly despite normal lung field on simple
X-ray [3]. To find causes of pericardial effusion from the beginning is not easy. The causes
need to be identified by relating the underlying diseases of patients or procedures history.
(Pericardial tamponade caused by massive fluid resuscitation in a patient with pericardial
effusion and end-stage renal disease -A case report-)
Pericaldial effusion may have a history of upper respiratory tract infection, precordial
pain (dull, aching, or stabbing) with occasional radiation to the shoulder and neck may be a
presenting complaint. The pain may be relieved by leaning forward and may be made worse
by the supine position or deep inspiration and fever of varying degrees may be
present.(myung). In this case the patient we found upper respiratory tract infection with
symptom dry cough for 3 months. The patient also complaint about dull pain with occasional
radiation to the left shoulder, and tend to sleep with two pillow support.
In the Electrocardiography have low-voltage QRS complex caused by pericardial
effusion is characteristic but not a constant finding. QRS complexes on electrocardiogram and
electrical alternans, which is beat-to-beat alteration of the QRS complex amplitude and axis
due to the swinging motion of the heart within a large pericardial effusion (Fig. 28.3).26
Electrical alternans is considered specific but not sensitive for tamponade. The central venous
pressure waveform in tamponade classically shows an exaggerated x descent in ventricular
systole with a diminished or absent y descent in ventricular diastole (Fig. 28.4). This is because
in tamponade the intraluminal atrial or ventricular diastolic pressures (i.e., the downstream
pressures for venous return) are effectively determined by the pericardial pressure. Ejection of
blood in ventricular systole causes a decrease in total intrapericardial volume and subsequent
antegrade venous flow, whereas pericardial and atrial pressures remain elevated and unchanged
in ventricular. In this case we found the low voltage of ecg and with water-bottle-shaped in
thorax PA with the same as the literature.
The etiology of pericardial effusion varies widely by population studied; however,
purulent pericarditis appears to have become less common in the era of antibiotics and routine
vaccination against previously common bacterial pathogens. In a 20-year review of children
with pericardial effusion from a tertiary care center in the United States, bacterial infections
were found in only 3% of patients, with Haemophilus influenzae, Staphylococcus aureus, and
Neisseria meningitidis each reported. In this study 39% of patients with pericardial effusion
had associated neoplastic disease, 9% collagen vascular disease, 8% renal disease, 5% other
diagnoses (human immunodeficiency virus [HIV], viral sepsis, hypothyroidism, anorexia
nervosa), and 37% were classified as idiopathic.14 By contrast, a study of children with
pericardial effusion from a tertiary center in India demonstrated tuberculosis in 52%, other
bacteria in 23% (including S. aureus and Pseudomonas aeruginosa), viral causes in 12%,
idiopathic effusion in 8%, and only 4% with neoplastic disease.15 Similar findings have been
reported in adult studies of pericardial effusion, with 7% to 50% idiopathic, 10% to 37%
neoplastic, 2% to 20% infectious, 4% to 20% uremic, 5% to 15% collagen vascular, 0% to 20%
iatrogenic, 0% to 8% post myocardial infarction, and as high as 50% to 70% tuberculous in
some areas of the world.16-18 (MOU2019). Cardiac tamponade is a life-threatening clinical
condition that occurs when accumulation of material (such as fluid, blood, or air) in the
pericardium causes hemodynamic compromise. In this case we had collect the fluid for
bacterial culture and analyse the pericardial fluid. As the analysis of pericardial fluid we found
its exudate , lots of red blood cells and white blood cells with dominantly mononuclear.
The rate of fluid accumulation, effectiveness of compensatory mechanisms, and
stiffness of the pericardium affect the inflection point of the intrapericardial pressure curve and
thus the severity and timing of clinical manifestations.26 Therefore a slowly developing
pericardial effusion (such as in a systemic inflammatory state) may result in large volumes of
fluid before significant cardiovascular effect, whereas a rapidly accumulating process such as
a traumatic intrapericardial hemorrhage may quickly cause hemodynamic collapse.
Progression of hemodynamic changes in tamponade proceeds in a well-described
fashion. Increased pericardial pressure leads to increased cardiac diastolic pressure, reduced
myocardial transmural pressure, smaller cardiac chambers with decreased compliance, and
decreased preload and cardiac output. A compensatory sympathetic response results in
tachycardia, increased venous tone, and baroreflex-induced systemic arteriolar
vasoconstriction to compensate for the hypotension.27 Jugular venous distention,
hepatomegaly, and elevated central venous pressures may be evident. 31 In this patient we
found jugular venous distention and hepatomegaly.

Characteristic echocardiographic findings in pericardial effusion and tamponade are

depicted in Fig. 28.2. (MOU2019)

Management.
Management of pericardial effusion consists of treating the underlying disease, with
drainage performed when needed for diagnostic purposes or if progression to tamponade
appears imminent. Management of tamponade consists of immediate drainage of pericardial
fluid via percutaneous catheter pericardiocentesis or surgical pericardotomy/pericardectomy.
Volume loading with crystalloid or colloid solution may be considered as a temporizing
measure to augment preload, but definitive therapy should not be delayed. Diuretics may
worsen the patient’s condition by further reducing preload. Inotropic agents may be considered
but may have limited effect in the setting of an already brisk endogenous sympathetic response.
Endotracheal intubation and mechanical ventilation should be approached with extreme
caution because further cardiovascular compromise can occur with increased intrathoracic
pressure due to increased lung volumes, further reducing systemic venous return and increasing
total external constraint of the heart.33
Pericardiocentesis should be performed in an intensive care unit (ICU), operating room,
or catheterization laboratory with experienced personnel and resuscitation supplies present and
echocardiographic guidance if possible. An illustration of the technique of pericardiocentesis
using the Seldinger technique and a pigtail catheter is depicted in Fig. 28.5. The patient should
be positioned in the semiupright position. Local anesthesia with 1% or 2% lidocaine may be
used to facilitate puncture; systemic sedation/anesthesia should be used judiciously due to risk
of cardiovascular collapse even with administration of agents such as fentanyl or ketamine. An
18-gauge needle long enough to reach the effusion (often 6 cm) is used, with the best site of
puncture and angulation determined echocardiographically as the point at which the largest
fluid accumulation is closest to the body surface. In an emergency the subxiphoid approach
may be used with approximately 15-degree angulation off the skin directed toward the left
shoulder.14 In a retrospective series of 94 procedures in 73 pediatric patients, the optimal site
of puncture by echocardiographic guidance was determined to be para-apical (68.1%),
subxiphoid (17%), left axillary (5.3%), left parasternal (3.2%), right parasternal (2.1%),
posterolateral (1.1%), or unspecified (3.2%).34
Continuous suction is held until fluid is aspirated, at which point a 0.035- or 0.038-inch
guide wire is advanced, followed by dilation and insertion of a 7 Fr or 8 Fr pigtail catheter,
typically left in place for ongoing drainage until the underlying cause is resolved (see Fig.
28.5).21,34 Fluid may be sent to the laboratory for cell count with differential, determination
of glucose, protein, and lactate dehydrogenase levels, and bacterial/fungal culture if further
characterization is needed. A cardiac surgeon should be immediately available during the
procedure because complications of pericardiocentesis can include laceration/perforation of the
myocardium or coronary vessels with hemopericardium; however, intrapericardial fluid may
often be bloody even without cardiac puncture (56% of cases in one study).34 Bloody
pericardial fluid is nonclotting; additionally, bloody pericardial fluid usually sinks to the
bottom of a gauze sponge, whereas blood forms clots on the surface of the gauze.35
Approximately 2 to 5 mL of agitated saline may be instilled under echocardiographic guidance
to confirm placement. Other complications of pericardiocentesis include air embolism,
pneumothorax, pulmonary edema, arrhythmias (most commonly vasovagal bradycardia), or
puncture of the peritoneal cavity.36
After placement the pericardial catheter may then be flushed with saline to prevent
catheter plugging, and intermittent drainage (frequency dependent on reaccumulation rate and
hemodynamics; usual minimum, every 2 hours) is followed by sterile saline catheter flush to
maintain catheter patency. This is preferred over continuous drainage for maintenance of
catheter patency. Balloon pericardiotomy has been used in adults, and there is some experience
in children.37,38 Pericardial effusions also may be drained surgically via a subxiphoid
approach or laparoscopy.39,40 A pericardial window is a communication created surgically,
typically between the pericardial and pleural space. This allows ongoing drainage of effusion
and may be used for recurrent effusions (such as in malignancy) or to prevent tamponade after
cardiac surgery.16,4 (MYUNG) In this patient we had the pericardiosynthesis emergency
because the cardiac tamponade and we sent the fluid for blood culture and fluid analysis.
Figure 1. Schematic of pericardiocentesis technique.

Resume
We found with chief complaint of shortness of breath, cough within 3 months and dull
pain that radiate to left shoulder. The patient had symptoms of classic cardiac tamponade that
were hypotension, muffle heart sound, pericardial friction rub, jugular venous distention. We
found on the ECG that theres low voltage on all leads and from thorax photo we found water
bottle shaped. In echochardiography we conclude that theres fluid on pericardial sac.
In this case we had to immediately do the pericardiosynthesis for the emergency needs,
and after that we culture and analyse the fluid for determined the underlying cause.

Lippincott, William, wilkins. 2013. 10th edition. Wolters Kluwer : Philadelphia. P : 70