Case Report Kardiologi Tamponade.docx

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 Bacterial/Tuberculous

Staphylococcus aureus, Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae βhemolytic streptococci, Mycoplasma pneumoniae, Mycobacterium tuberculosis, Enterobacter cloacae, Corynebacterium diphtheriae

Viral

Fungal

Candida, Aspergillus, Histoplasma, coccidiomycosis

Noninfectious Pericarditis

Cardiac Injury

Systemic Inflammatory Disease

Neoplasms

Renal

Postpericardiotomy syndrome, post myocardial infarction

Rheumatic fever, juvenile rheumatoid arthritis, systemic 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

End-stage renal disease (uremia), dialysis

Miscellaneous

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

Additional Causes of Pericardial Effusion ± Pericarditis Traumatic and Postoperative

Elevated Central Venous Pressure/Low Plasma Oncotic Pressure

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 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