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CHF ec DILATED RA-RV + OBESITAS

Presenter : Ika Diamanda Apriano

Amalia P Dewi

Day/Date : Monday/ June 17th 2013

Supervisor in charge : Dr. Hj. Melda Deliana Sp.A(K)

INTRODUCTION

Obesity is the most prevalent nutritional disorder among children and adolescents in

the United States. Approximately 21-24% of American children and adolescents are

overweight, and another 16-18% is obese; the prevalence of obesity is highest among specific

ethnic groups.1

Using body mass index (BMI) criteria, the most recent national surveys demonstrate

that 21-24% of American children and adolescents are overweight and that another 16-18%

are obese. A 2012 study noted a 16.9% prevalence of obesity in children and adolescents in

2009-2010, which is comparable to the prevalence rates reported in 2007-2008

12

.Thesefindings, indicate that the prevalence of overweight (BMI 85th percentile) children and

adolescents in the US has increased by 50-60% in a single generation, and the prevalence of

obesity has doubled. The prevalence of obesity in American Indians, Hawaiians, Hispanics,

and blacks is 10-40% higher than in whites.

International data reporting regarding childhood obesity varies, and accuracy may be

less than optimal; however, Eneli and Dele Davies reported that in 77% of the countries

analyzed, the prevalence rate for children who were overweight was at least 10%13

. Notably,

the highest rates for children at risk for obesity were found in Malta (25.4%) and the United

States (25.1%). Lithuania (5.1%) and Latvia (5.9%) had the lowest rates. A recent European

Youth Heart Study suggests Swedish children have a lower risk of becoming overweight or

obese in adolescence compared with Estonian children14.

Race and ethnicity are associated with increased rates of obesity in children and

adolescents. Puerto Rican, Cuban American, and Native American preschoolers have an

increased incidence of obesity; black, Native American, Puerto Rican, Mexican, and native
http://emedicine.medscape.com/article/123702-overviewhttp://emedicine.medscape.com/article/123702-overview


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Hawaiian school-aged children have the highest rates of obesity in this age group.

Approximately 25% of black adolescents are obese. Rosen reported thatobstructive sleep

apnea hypoventilation (OSA/H) is more commonly seen in black children than in Hispanic or

white children.14 Tonsils and adenoids are at their peak size, relative to the size of the

oropharynx, when children are aged 2-7 years.

During the second decade of life, females are more likely to be obese than males,

except for black teenagers, among whom males are more likely to be obese than females.

Although the male sex is associated with an increased incidence of OSA in adults, no

differences have been identified in children before puberty.

Adolescent obesity is predictive of adult obesity, with 80% of teenagers who are

obese continuing on to be obese as adults. Obesity is more likely to occur during specific

periods of life, such as when children are aged 5-7 years and during adolescence. A recent

European Youth Heart Study suggests male sex confers a higher risk of obesity in

adolescence13.

CASE
http://emedicine.medscape.com/article/1002703-overviewhttp://emedicine.medscape.com/article/1002703-overviewhttp://emedicine.medscape.com/article/1002703-overviewhttp://emedicine.medscape.com/article/1002703-overview


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Follow up on May 22th

- 9th

June 2013

May 22t 2013

S Dyspnoe (+), fever (+), oedem (+),

O Sensorium: compos mentis

Temperature: 37,6C

Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, oedema(+/+)

Ear, nose, and mouth : normal

Neck : lymph node was not palpable

Chest : Simmetrical fusiformis, no retraction

HR : 100 bpm, reguler, no murmur

RR : 22 breathes/minute, reguler, no ronkhi

Abdomen : Soepel, peristaltic (+) normal, hepar palpable mass in right hipocondria, size 6

x 5x 4 cm, immobile, venectation (+). Spleen indeterminate.

Extremities : pulse 100 bpm, reguler, pressure and volume were adequate, warm acral, CRT


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Lymph Absolute 10 /L 2,09 1,7-5,1

Mono Absolute 10 /L 1,03 0,2-0,6

Eos Absolute 10 /L 0,33 0,10-0,30

Baso Absolute 10 /L 0,05 0-0,1

Conclusion :

Clinical Chemistry

AGDA

pH 7,474 7,35 - 7,45

pCO2 mmHg 36,6 3842

pO2 mmHg 182,9 85100

HCO3 Mmol/l 26,2 2226

Total CO2 Mmol/l 27,4 1925

BE Mmol/l 2,8 (-2)(+2)

Saturation O2 % 99,4 95100

Liver

Albumin gr/dl 3,6 3,85,4

Carbohydrate Metabolism

Glucose ad random mg/dl 80,00


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P Treatment

1. O2 1 l/I nasal kanul2. Furosemide 2x40 mg3. Spironolacton 2x2,5mg

4. Digoxin 2x0,3mg5. Diet MB 2000 kcal + 60 gr protein

Laboratory result : May 23th

2013

Maret 23t

2013

Test Unit Result Reference

URINALYSIS

Complete Urine Analysis

Colour Clear yellow Yellow

Glucose Negative Negative

Bilirubin Negative Negative

Keton Negative Negative

SG 1.015 1.0051.030

Ph 8,0 5 - 8

Protein Negative Negative

Urobillinogen Negative

Nitrit Positive Negative

Blood Negative Negative

Urine Sedimented

Eritrocyte LPB 01


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Temperature: 37,0C

Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-,




HR : 96 bpm, reguler, no murmurRR : 26 breathes/minute, reguler, no ronkhi

Abdomen : Soepel, peristaltic (+) normal, hepar palpable mass in right hipocondria,

size 6 x 5x 4 cm, immobile, venectation (+). Spleen indeterminate.

Extremities : pulse 100 bpm, reguler, pressure and volume were adequate, warm acral,

CRT


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1. O2 1 l/I nasal kanul2. Furosemide 2x40 mg3. Spironolacton 2x2,5mg4. Digoxin 2x0,3mg5. Diet MB 2000 kcal + 60 gr protein

Dipstick Urine 15.00 WIBLeu / Nit/ Uro/ Pro/ pH / Blo / SG / Ket / Bil / Glu

/ - / 0,2 / + / 6,0 / - / 1,010/ / + / -

Planning

Kultur Urine to Microbiology


2013

May 27t -20t 2013

S Dyspnoe (+), fever (-),


Temperature: 37,0C, weight 66 kg










CRT


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Chest : Simmetrical fusiformis, no retractionHR : 98 bpm, reguler, no murmur





CRT


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2. Furosemide 2x40 mg3. Spironolacton 2x2,5mg4. Digoxin 2x0,3mg5. Diet MB 2000 kcal + 60 gr protein

Planning : CT Scan intraabdomen


2013

May 30t 2013













CRT


10/23

CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect

abdominal tumor

P Treatment

1. O2 1 l/I nasal kanul

2. Furosemide 2x40 mg3. Spironolacton 2x2,5mg4. Digoxin 2x0,3mg5. Diet MB 2000 kcal + 60 gr protein

Balance fluids 18.00 WIB

Input : IVFD = 50 Output : IWL = 1300

Diet = 500 cc UOP = 50

Total : 550 cc 1350

Balance : InputOutput = 5501350 = 800

Needs of fluids on 6 hours= Holiday segar Balance

= 1600 + 800

= 2400 cc

Follow up on June 1th

2013

June 1t 2013






Neck : lymph node was not palpableChest : Simmetrical fusiformis, no retraction






CRT


11/23


= 1600 + 7500

= 2350 cc


2013

June 2t 2013S Dyspnoe (+), fever (-),


Temperature: 37C, weight 63 kg










CRT


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Neck : lymph node was not palpableChest : Simmetrical fusiformis, no retraction






CRT


13/23

Temperature: 36,8C, weight 62,5 kg





HR : 90 bpm, reguler, no murmurRR : 30 breathes/minute, reguler, no ronkhi




CRT


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June 4t 2013


O Sensorium : compos mentis



Ear, nose, and mouth : normalNeck : lymph node was not palpable







CRT


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HBsAg Negative Negative

Hepatitis C

Anti HCV Negative Negative


2013

June 6t 2013S Dyspnoe (+), fever (-),

O Sensorium : compos mentis











CRT


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Balance : InputOutput = 4001700 = 2100


= 1600 + 2100

= 3700 cc

DISCUSSION

The identification of obesity and overweight in childhood may be an important aspect

of preventive pediatrics with implications for the promotion of physical, social, and

emotional health for children that may be effect in adulthood. Obesity is not a disease in itselfbut rather a symptom complex with a weak association to adult obesity with its correlates of

increased mortality, cardiovascular disease, atherosclerosis, and diabetes rates.

Childhood obesity predisposes to insulin resistance andtype 2 diabetes,hypertension,

hyperlipidemia, liver and renal disease, and reproductive dysfunction. This condition also

increases the risk of adult-onset obesity and cardiovascular disease.1

Obesity in children is a complex disorder. Its prevalence has increased so significantly

in recent years that many consider it a major health concern of the developed world. The

National Health and Nutrition Examination Survey (NHANES) indicates that the prevalence

of obesity is increasing in all pediatric age groups, in both sexes, and in various ethnic and

racial groups. Many factors, including genetics, environment, metabolism, lifestyle, and

eating habits, are believed to play a role in the development of obesity. However, more than

90% of cases are idiopathic; less than 10% are associated with hormonal or genetic causes.

The BMI is a continuous, although imperfect, measure of body fatness. Calculated asweight (kg) divided by height (m2), BMI corrects for body size and can be readily and

reliably quantified in clinical settings. The BMI correlates closely with total body fat (TBF),

which is estimated using dual-energy x-ray absorptiometry (DEXA) scanning in children who

are overweight and obese.

Normal values for BMI vary with age, sex, and pubertal status, and standard curves

representing the 5th through the 95th percentiles for BMI in childhood and adolescence were

generated using data from the 1988-1994 NHANES2. Consensus committees have
http://emedicine.medscape.com/article/925700-overviewhttp://emedicine.medscape.com/article/889877-overviewhttp://emedicine.medscape.com/article/889877-overviewhttp://emedicine.medscape.com/article/925700-overview


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recommended that children and adolescents be considered overweight or obese if the BMI

exceeds the 85th or 95th percentiles, on curves generated from the 1963-1965 and 1966-1970

NHANES, or exceeds 30 kg/m2at any age3. McGavock et al demonstrated that low

cardiorespiratory fitness and reductions in fitness over time are significantly associated with

weight gain and the risk of being overweight in children aged 6-15 years. Analysis on a

cohort of 902 schoolchildren showed higher waist circumference and disproportionate weight

gain over a 12-month follow-up period in those children with low cardiorespiratory fitness.

The 12-month risk of overweight classification was 3.5-fold higher in youth with low

cardiorespiratory fitness, relative to fit peers4. Reductions in cardiorespiratory fitness were

significantly and independently associated with increasing BMI. Low levels of

cardiorespiratory fitness have also been associated with elevated depressive symptoms in

obese adolescents4.

One study suggests that a lack of adequate sleep time in young children is associated

with increased BMI; this observation is independent of other confounding variables (eg,

physical activity)5. Furthermore, data indicate that over a 5-year period an increase in BMI

among overweight children 6 to 11 years of age is associated with increases in both systolic

and diastolic blood pressure, as well as with a decrease in sleep time6.

Recognize that a loss of 5-20% of total body weight can reduce many of the health

risks associated with obesity in adults; however, whether modest weight loss or moderate

reductions in BMI can improve outcomes in pediatric patients or reduce the long-term risks

of obesity in adulthood is not known. Because dramatic reductions in BMI are difficult to

achieve and sustain in children and adolescents as well as adults, initiating counseling and

therapy may be prudent with realistic goals that emphasize gradual reductions in body fat and

BMI and maintenance of weight loss rather than a rapid return to ideal body weight.

Reductions in body weight are accompanied by equivalent reductions in energy expenditure.

Consequently, maintenance of a given weight in a patient with obesity necessitates a lower

energy intake than maintenance of an equivalent weight in a patient who has never been

obese.13

The most likely causes of pediatric congestive heart failure depend on the age of the c

hild. Congestive heart failure in fetus, or hydrops, can be detected by performing fetal echoca

rdiography. In older children, congestive heart failure may be caused by left sided obstructive

disease (valvar or subvalvar aortic stenosis or coarctation), myocardial dysfunction (myocard


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itis or cardiomyopathy), hypertension, renal failure, or, more rarely, arrhythmias or myocardi

al ischemia. Illicit drugs such as inhaled cocaine and other stimulants are increasingly precipit

ating causes of congestive heart failure in adolescents; therefore, an increased suspicion of dr

ug use is warrantened in unexplained congestive heart failure7.

Congestive heart failure occurs when the heart can no longer meet the metabolic dema

nds of the body at normal physiologic venous pressures. Typically, the heart can respond to i

ncreased demands by means of 1 of the following :

1. Increasing the heart rate, which is controlled by neural and humoral input

2. Increasing the cintractility of the ventricels, secondary to circulating

catecholamines and autonomic input.

3. Augmenting the preload, medicated by constriction of the venous capacitate

vessels and the renal preservation of intravascular volume.

Many classes of disorders can result in increased cerdiac demand or impaired cardiac

function. Cardiac causes include arrythmias (tachicardia or bradycardia), structural heart dise

ase, and myocardial dysfunction (systolic or diastolic).

Cardiac rhythm disorders may caused by following :

Complete heart block

Supraventricular Tachycardia

Ventricular Tachycardia

Sinus node dysfunction

Volume overload may be caused by the following :

Structural heart defect

Anemia

Sepsis

Pressure overload may be caused by the following :

Structural heart defect

Hypertension

Systolic ventricular dysfunction or failure may be caused by the following :

myocarditis

dilated cardiomyophaty

malnutrition

ischemia

Diastolic ventricular dysfunction or failure may be caused by the following :


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hypertropic cardiomyophaty

restrictive cardiomyophaty

pericarditis

cardiac tamponade (pericardial effusion)8

Thorough history taking and physical examination, including an assessment of the up

per-extremity and lower-extremity blood pressures, are crucial in the evaluation of an infant o

r child with congestive heart failure.

Regardless of the etiology, the first manifestation of congestive heart failure is usually

tachycardia. An obvious exception to this finding occurs in congestive heart failure due to a

primary bradyarrhythmia or completeheart block.

As the severity of congestive heart failure increases, signs of venous congestion

usually ensue. Left-sided heart failure is generally associated with signs of pulmonary venous

congestion, whereas right-sided heart failure is associated with signs of systemic venous

congestion. Marked failure of either ventricle, however, can affect the function of the other,

leading to systemic and pulmonary venous congestion.

Later stages of congestive heart failure are characterized by signs and symptoms of

low cardiac output. Generally, congestive heart failure with normal cardiac output is called

compensated congestive heart failure, and congestive heart failure with inadequate cardiac

output is considered decompensated.

Signs of congestive heart failure vary with the age of the child. Signs of pulmonary

venous congestion in an infant generally include tachypnea, respiratory distress (retractions),

grunting, and difficulty with feeding. Often, children with congestive heart failure have

diaphoresis during feedings, which is possibly related to a catecholamine surge that occurs

when they are challenged with eating while in respiratory distress.

Right-sided venous congestion is characterized by hepatosplenomegaly and, less

frequently, by edema or ascites. Jugular venous distention is not a reliable indicator of

systemic venous congestion in infants, because the jugular veins are difficult to observe. In

addition, the distance from the right atrium to the angle of the jaw may be no more than 8-10

cm, even when the individual is sitting upright.
http://emedicine.medscape.com/article/151597-overviewhttp://emedicine.medscape.com/article/151597-overview


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Uncompensated congestive heart failure in an infant primarily manifests as a failure to

thrive. In severe cases, failure to thrive may be followed by signs of renal and hepatic failure.

In older children, left-sided venous congestion causes tachypnea, respiratory distress, and

wheezing (cardiac asthma). Right-sided congestion may result in hepatosplenomegaly,

jugular venous distention, edema, ascites, and/or pleural effusions. Older children with

uncompensated congestive heart failure may have fatigue or lower-than-usual energy levels.

Patients may complain of cool extremities, abdominal pain, nausea/vomiting, exercise

intolerance, dizziness, or syncope9.

If the underlying cause of the congestive heart failure cannot be immediately

corrected in a patient who is hemodynamically stable, outpatient management can be initiated

by using several agents. Afterload reduction using an ACE inhibitor is indicated in the

presence of left ventricular (LV) dysfunction, regardless of symptoms.

Afterload reduction is indicated in patients who have large left-to-right shunts at the

ventricular or arterial level (ventricular septal defect or patent ductus arteriosus), left-sided

regurgitant lesions (aortic insufficiency or mitral regurgitation), or poor systolic function

(myocarditis or dilated cardiomyopathy). ACE inhibitors are the medications of choice.

Alternatively, an angiotensin receptor blocker (ARB), such as losartan, may be used in

patients in whom ACE adverse effects (particularly cough) may be unacceptable10.

In addition to afterload reduction (ACE inhibitor), low-dose furosemide (1

mg/kg/dose PO bid) may be initiated, with or without the addition of another agent for

inotropic effect (digoxin), or beta-blockade (carvedilol) to treat mild symptoms of congestive

heart failure The dose of digoxin (0.005-0.010 mg/kg/day PO divided twice daily, not to

exceed 0.125-0.250 mg PO qd) is almost never increased, either for effect or according to

digoxin levels, which are notoriously unreliable. However, the dose may be decreased in the

presence of signs of toxicity. The suspicion of digoxin toxicity should increase if an infant is

uninterested in feedings, gags, or vomits frequently. These symptoms are typically due to an

overdose or renal failure.

For more severe congestive heart failure, diuretic therapy with oral furosemide may

be increased to 2 mg/kg/dose orally 3 times daily or a second agent, such as

hydrochlorothiazide or metolazone, can be added. To be most effective, hydrochlorothiazide

and metolazone are best administered simultaneously with furosemide to achieve their

synergistic effect11.


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Reference

1. Ogden CL, Yanovski SZ, Carroll MD, Flegal KM. The epidemiology of

obesity. Gastroenterology. May 2007;132:2087-2102.

2. Fiore H, Travis S, Whalen A, Auinger P, Ryan S. Potentially protective factors

associated with healthful body mass index in adolescents with obese and non

obese parents: a secondary data analysis of the third national health and nutrition

examination survey, 1988-1994.J Am Diet Assoc. Jan 2006;106(1):55-64; quiz

76-9.

3. Flegal KM, Ogden CL, Wei R, et al. Prevalence of overweight in US children:

comparison of US growth charts from the Centers for Disease Control and

Prevention with other reference values for body mass index. Am J Clin Nutr. Jun

2001;73(6):1086-93

4. McGavock JM, Torrance BD, McGuire KA, Wozny PD, Lewanczuk RZ.

Cardiorespiratory fitness and the risk of overweight in youth: the Healthy Hearts


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Longitudinal Study of Cardiometabolic Health. Obesity (Silver Spring). Sep

2009;17(9):1802-7

5. Carter PJ, Taylor BJ, Williams SM, Taylor RW. Longitudinal analysis of sleep in

relation to BMI and body fat in children: the FLAME study.BMJ. May 26

2011;342:d2712.

6. Archbold KH, Vasquez MM, Goodwin JL, Quan SF. Effects of Sleep Patterns and

Obesity on Increases in Blood Pressure in a 5-Year Period: Report from the

Tucson Children's Assessment of Sleep Apnea Study.J Pediatr. Jan 25 2012

7. Rajagopal SK, et al. Pediatric heart failure and worsening renal function: Associat

ion with outcomes after heart transplantation.J Heart Lung Transplant. Oct 18 2011

8. Kaza AK, et al. Surgical interventions for anterioventricular septal defect subtypes

: The pediatric heart network experience. Ann Thorac Surg. Oct 2011; 92 (4) : 14

68-75

9. Erickson LC. Medical issues for the cardiac patient. Critical Care of Infants and

Children. 1996:259-62.

10.Konstam MA, Neaton JD, Poole-Wilson PA, Pitt B, Segal R, Sharma D, et al.

Comparison of losartan and captopril on heart failure-related outcomes and

symptoms from the losartan heart failure survival study (ELITE II).Am Heart J.

Jul 2005;150(1):123-31.

11.Rosenthal D, Chrisant MR, Edens E, Mahony L, Canter C, Colan S, et al.

International Society for Heart and Lung Transplantation: Practice guidelines for

management of heart failure in children.J Heart Lung Transplant. Dec

2004;23(12):1313-33.

12.(Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity and trends in body

mass index among US children and adolescents, 1999-2010. JAMA. Feb 1

2012;307(5):483-90. ).

13.(Eneli I, Dele Davis H. Epidemiology of childhood obesity. In: Dele Davis H, ed. Obesity

in Childhood & Adolescence. Vol 1. Westport, Conn: Praeger Perspectives; 2008:3-19.)


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14. .(Ortega FB, Labayen I, Ruiz JR, et al. Improvements in fitness reduce the risk of

becoming overweight across puberty. Med Sci Sports Exerc. Oct

2011;43(10):1891-7.)

15.

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