CHF ec DILATED RA-RV + OBESITAS

Presenter

: Ika Diamanda Apriano Amalia P Dewi

Day/Date Supervisor in charge

: Monday/ June 17th 2013 : 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 2007-200812.These findings, 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

Hawaiian school-aged children have the highest rates of obesity in this age group. Approximately 25% of black adolescents are obese. Rosen reported that obstructive 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

Follow up on May 22th- 9th June 2013 May 22th 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 <3 , Blood pressure 130/90 mmHg, Pitting oedem (+)

A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein

Laboratory result : May 22th 2013 May 22th 2013 Test Unit Complete Blood Count WBC 103/mm3 RBC 106/mm3 HGB g% HCT % MCV fL MCH Pg MCHC g% PLT 103/mm3 RDW CV % Neut % Lymph % Mono % Eos % Baso % Neu Absolute 103/L

Result 9,16 5,29 14,50 44,80 84,70 27,40 32,40 223 25,00 61,90 22,80 11,20 3,60 0,500 5,66

Reference 4,5-13,5 4,40-4,48 11,3-14,1 37-41 81-95 25-29 29-31 150-450 11,6-14,8 37-80 20-40 2-8 1-6 0-1 2,4-7,3

Lymph Absolute Mono Absolute Eos Absolute Baso Absolute Conclusion : Clinical Chemistry AGDA pH pCO2 pO2 HCO3 Total CO2 BE Saturation O2

103/L 103/L 103/L 103/L

2,09 1,03 0,33 0,05

1,7-5,1 0,2-0,6 0,10-0,30 0-0,1

mmHg mmHg Mmol/l Mmol/l Mmol/l %

7,474 36,6 182,9 26,2 27,4 2,8 99,4

7,35 - 7,45 38 42 85 100 22 26 19 25 (-2) (+2) 95 100 3,8 5,4 <200 <50 0,32-0,59 135 155 3,6 5,5 96 106

Liver Albumin gr/dl Carbohydrate Metabolism Glucose ad random mg/dl Renal Function Test (RFT) Ureum mg/dL Creatinin mg/dL Electrolyte Natrium mEq/L Calium mEq/L Cloride mEq/L Follow up on May 23th 2013

3,6 80,00 13,20 0,37 132 4,6 95

May 23th 2013 S Dyspnoe (-), fever (-), O Sensorium: compos mentis Temperature: 37,1C Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 102 bpm, reguler, no murmur RR : 24 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 <3 , Blood pressure 120/80 mmHg, Pitting oedem (+)

A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor

Treatment 1. O2 1 l/I nasal kanul 2. Furosemide 2x40 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein

Laboratory result : May 23th 2013 Maret 23th 2013 Test Unit URINALYSIS Complete Urine Analysis Colour Glucose Bilirubin Keton SG Ph Protein Urobillinogen Nitrit Blood Urine Sedimented Eritrocyte LPB Leucosyte LPB Epitel LPB Casts LPB Crystal LPB FECES Macroscopic colour Consistency blood Mucous Microscopic Egg warm LPB Amoeba LPB Eritrocyte LPB leucocyte LPB Conclution :

Result

Reference

Clear yellow Negative Negative Negative 1.015 8,0 Negative Negative Positive Negative 01 01 01 Negative Negative

Yellow Negative Negative Negative 1.005 1.030 5-8 Negative Negative Negative <3 <6 Negative

Yellow Soft Negative Negative Negative Negative 01 01

Negative Negative Negative Negative

Follow up on May 24th 2013 April 15th 2013 S Dyspnoe (-), fever (-), O Sensorium : compos mentis

Temperature: 37,0C Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 96 bpm, reguler, no murmur RR : 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 <3 , Blood pressure 120/80 mmHg, Pitting oedem (+)

A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein Planning 1. USG hepar, kandung empedu dan salurannya 2. USG ginjal dan saluran kemih 3. BNO

Follow up on May 25th-26th 2013 May 25th-26th 2013 S Dyspnoe (+), fever (+), O Sensorium: compos mentis Temperature: 37,5C, weight 66 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 32 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 <3 , Blood pressure 120/80 mmHg, Pitting oedem (+) A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein Dipstick Urine 15.00 WIB Leu / Nit/ Uro/ Pro/ pH / Blo / SG / Ket / Bil / Glu / - / 0,2 / + / 6,0 / - / 1,010/ / + / Planning Kultur Urine to Microbiology Follow up on May 27th 2013 May 27 th -20th 2013 S Dyspnoe (+), fever (-), O Sensorium: compos mentis Temperature: 37,0C, weight 66 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 32 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 <3 , Blood pressure 120/80 mmHg, Pitting oedem (+) A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein Balance fluids 00.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 600 cc UOP = 500 Total : 600 cc 1800 Balance : Input Output = 600 1800 = -1200 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1200 = 2800 cc

Follow up on May 28th 2013 May 28 th -20th 2013 S Dyspnoe (+), fever (-),

O Sensorium: compos mentis Temperature: 36,9C, weight 65 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 30 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein Planning : Waiting for the results USG abdomen/ Conclusion USG abdomen = fatty liver and tumor abdomen Conclusion photos of BNO = innormal range in BNO photoss May 29 th -20th 2013 S Dyspnoe (+), fever (-), O Sensorium: compos mentis Temperature: 37,1C, weight 65 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 100 bpm, reguler, no murmur RR : 30 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 <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor P Treatment 1. O2 1 l/I nasal kanul

Follow up on May 29th 2013

2. Furosemide 2x40 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein Planning : CT Scan intraabdomen Follow up on May 30th 2013 May 30th 2013 S Dyspnoe (+), fever (-), O Sensorium: compos mentis Temperature: 36,1C, weight 65 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 30 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein May 31th 2013 S Dyspnoe (+), fever (+), O Sensorium: compos mentis Temperature: 36,8C, weight 63 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 30 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis :

Follow up on May 31th 2013

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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. 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 : Input Output = 550 1350 = 800 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 800 = 2400 cc

Follow up on June 1th 2013 June 1th 2013 S Dyspnoe (+), fever (-), O Sensorium: compos mentis Temperature: 36,9C, weight 66 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 30 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : 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 mg 3. Spironolacton 2x2,5mg 4. Digoxin 2x0,3mg 5. Diet MB 2000 kcal + 60 gr protein Balance fluids 00.00 WIB Input : IVFD = 100 Output : IWL = 1300 Diet = 550 cc UOP = 100 Total : 650 cc 1400 Balance : Input Output = 550 1400 = -750

Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 7500 = 2350 cc Follow up on June 2th 2013 June 2th 2013 S Dyspnoe (+), fever (-), O Sensorium: compos mentis Temperature: 37C, weight 63 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 94 bpm, reguler, no murmur RR : 36 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor P Treatment 1. Furosemide 2x40 mg 2. Spironolacton 2x2,5mg 3. Digoxin 2x0,3mg 4. Diet MB 1800 kkal Balance fluids 00.00 WIB Input : IVFD = Output : IWL = 1000 Diet = 250 cc UOP = 50 Total : 250 cc 1350 Balance : Input Output = 250 1350 = 1100 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1100 = 2700 cc Balance fluids 18.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 400 cc UOP = 300 Total : 400 cc 1600 Balance : Input Output = 400 1600 = -1200 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1200 = 2800 cc Follow up on June 3th 2013 June 3th 2013

S Dyspnoe (+), fever (-), O Sensorium: compos mentis Temperature: 37C, weight 63 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 94 bpm, reguler, no murmur RR : 36 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor P Treatment 1. Furosemide 2x40 mg 2. Spironolacton 2x2,5mg 3. Digoxin 2x0,3mg 4. Diet MB 1800 kkal Balance fluids 06.00 WIB Input : IVFD = Output : IWL = 1300 Diet = UOP = 200 Total : 0 cc 1500 Balance : Input Output = 0 1500 = -1500 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1500 = 3100 cc Balance fluids 18.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 600 cc UOP = 50 Total : 600 cc 1350 Balance : Input Output = 600 1350 = -750 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 750 = 2350 cc

Follow up on June 4th 2013 June 4th 2013 S Dyspnoe (-), fever (-), O Sensorium : compos mentis

Temperature: 36,8C, weight 62,5 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 90 bpm, reguler, no murmur RR : 30 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 90 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor P Treatment 1. Furosemide 2x40 mg 2. Spironolacton 2x2,5mg 3. Digoxin 2x0,3mg 4. Diet MB 1800 kkal + 134 gr protein Balance fluids 00.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 500 UOP = 70 Total : 0 cc 1370 Balance : Input Output = 500 1370 = -870 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 870 = 2470 cc Balance fluids 06.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 500 cc UOP = 100 Total : 500 cc 1400 Balance : Input Output = 500 1400 = -900 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 900 = 2500 cc Balance fluids 18.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 750 cc UOP = 200 Total : 500 cc 1500 Balance : Input Output = 500 1500 = -1000 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1000 = 2600 cc Follow up on June 5th 2013

June 4th 2013 S Dyspnoe (+), fever (-), O Sensorium : compos mentis Temperature: 37C, weight 61 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 100 bpm, reguler, no murmur RR : 28 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 <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor P Treatment 1. Furosemide 2x40 mg 2. Spironolacton 2x2,5mg 3. Digoxin 2x0,3mg 4. Diet MB 1800 kkal + 134 gr protein Balance fluids 06.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 100 UOP = Total : 100 cc 1300 Balance : Input Output = 100 1300 = -1200 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1200 = 3000 cc Laboratory result : June 5th 2013 June 5th 2013 Test Unit Liver functionTest (LFT) Total Bilirubin mg/dl Bilirubin direct mg/dl Alkali fosfatase U/L (ALP) AST/SGOT U/L ALT/ SGPT U/L Renal Function Test (RFT) Ureum mg/dL Creatinin mg/dL Uric Acid Mg/dl IMUNOSEROLOGY Hepatitis

Result 14.48 13.01 166 64 35 46,80 0,30 5,5

Reference <1 0-0.2 <300 <32 <31 <50 0,39 0,73 <5,7

HBsAg Hepatitis C Anti HCV Follow up on June 6th 2013

Negative Negative June 6th 2013

Negative Negative

S Dyspnoe (+), fever (-), O Sensorium : compos mentis Temperature: 36,8C, weight 61 kg Head : Eyes : Light reflexes : +/+, isocoric, conjunctiva palpebra pale -/-, Ear, nose, and mouth : normal Neck : lymph node was not palpable Chest : Simmetrical fusiformis, no retraction HR : 98 bpm, reguler, no murmur RR : 28 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 98 bpm, reguler, pressure and volume were adequate, warm acral, CRT <3 , Blood pressure 130/80 mmHg, Pitting oedem (+) A Working Diagnosis : CHF ec dilated RA-RV + moderated PI +n moderated TI + obesitas + suspect abdominal tumor P Treatment 1. Furosemide 2x40 mg 2. Spironolacton 2x2,5mg 3. Digoxin 2x0,3mg 4. Diet MB 1800 kkal + 134 gr protein Balance fluids 00.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 250 UOP = 100 Total : 250 cc 1400 Balance : Input Output = 250 1400 = -1150 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1150 = 2750 cc Balance fluids 06.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 250 UOP = --Total : 250 cc 1300 Balance : Input Output = 250 1300 = -1050 Needs of fluids on 6 hours= Holiday segar Balance = 1600 + 1050 = 1650 cc Balance fluids 12.00 WIB Input : IVFD = Output : IWL = 1300 Diet = 400 UOP = 400 Total : 400 cc 1700

Balance : Input Output = 400 1700 = 2100 Needs of fluids on 6 hours= Holiday segar Balance = 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 itself but 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 and type 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 as weight (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

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/m2 at 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

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 :

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 complete heart 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.

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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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 20 11 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
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