lapkas gizi

Case Report

Marasmus in HIV-infected Children and Hemorrhagic Varicella

Presentator : Nanda Meutia

Fitri Rahmariani

Day, Date : 29 April 2013

Supervisor : dr. Hj. Tiangsa Br Sembiring, Sp.A (K)

Introduction

Marasmus is one of the three forms of serious protein-energy malnutrition

(PEM). The other two forms are kwashiorkor (KW) and marasmic kwashiorkor.

These forms of serious PEM represent a group of pathologic conditions associated

with a nutritional and energy deficit occurring mainly in young children from

developing countries at the time of weaning. Marasmus is a condition primarily

caused by a deficiency in calories and energy, whereas kwashiorkor indicates an

associated protein deficiency, resulting in an edematous appearance. Marasmic

kwashiorkor indicates that, in practice, separating these entities conclusively is

difficult; this term indicates a condition that has features of both.1

Marasmus is a serious worldwide problem that involves more than 50

million children younger than 5 years. According to the World Health

Organization (WHO), 49% of the 10,4 million deaths occurring in children younger

than 5 years in developing countries are associated with PEM.1

Marasmus is most frequently associated with acute infections, chronic

illnesses, or drastic natural or man made conditions.1 HIV infection is one of

chronic illnesses that can be attributed to marasmus. Human Immunodeficiency

Virus (HIV) is a retrovirus that can be transmitted vertically, sexually, or via

contaminated blood products or IV drug abuse. In an infection, HIV affects the

cells of the immune system, including helper T lymphocytes (CD4 lymphocytes),

monocytes and macrophages. The functions ofthese cells are diminished by HIV

infection, with profound affects towards both humoral and cell-mediated

http://www.who.int/en/

http://www.who.int/en/

immunity. In the absence of treatment, HIV infection causes deterioation of the

immune system, leading to conditions that is known as acquired

immunodeficiency syndrome (AIDS), and severe complications due to

vulnerability towards infections.3

Since the first cases of human immunodeficiency virus (HIV) were

identified, the number of children infected with HIV has risen dramatically in

developing countries, the result of an increased number of HIV-infected women

of childbearing age in these areas.3 The World Health Organization (WHO)

estimates that approximately 3,3 million children (<15 years) were living with

HIV infection as of 2011. In 2011, 330.000 children were newly infected and

230.000 children died because of AIDS.2 Most of these children acquire HIV from

their HIV-infected mothers during pregnancy, birth or breastfeeding.3

Information above shows that still many cases of marasmus and HIV

infections in children especially in developing countries. Based on Millennium

Development Goals (MDGs) 2015, the decreased of morbidity and mortality rate

due to malnutrition and HIV are indicators for monitoring progress of goals

achievement in eradicating extreme poverty and hunger, reducing child mortality,

and combating HIV/AIDS.4

Varicella (chickenpox) is caused by the varicella-zoster virus (VZV).

Chickenpox is largely a childhood disease, with more than 90% of cases occurring

in children younger than 10 years. The disease is benign in the healthy child, and

increased morbidity occurs in adults and immunocompromised patients.5 In

children with human immunodeficiency virus (HIV) infection or

immunocompromised patients, recurrent varicella or disseminated herpes zoster

can develop and hemorrhagic varicella is much more common.6

The explanation above shows that there is association between HIV

infection, marasmus, and varicella hemorrhagic.

Objective

The aim of this study is to explore more about the theoretical aspects on

malnutrition (marasmus), HIV infection, the association between marasmus and

HIV infection, hemorrhagic varicella, and to integrate the theory and application

of cases in daily life.

Case Report

MCS, 5 years 11 months 24 days old boy came to H. Adam Malik Hospital on 13th

March 2013 with main complaint of Diarrhea. The alloanamnese is taken from

patient’s grandmother.

- Patient has been experiencing diarrhea since 3 years ago with the

frequency of 3-5 times a day (watery diarrhea). Volume of diarrhea 125cc

per time.

- Fever is also experiencing by patient several times since 3 years ago. It is

not too high, and fever subside with antipyretic. Fever rises again after

few days. Shivering (-)

- History of Seizure (+) 5 days ago with frequency of 2 times a day. It is ± 5

minutes long. After the seizure, patient feels tired and unconscious.

- Patient weight has been reducing since 3 months ago. He has 12 kg before,

but now his weight is 11 kg.

- Patient has been experiencing skin rash since 1 month ago with bloody red

apperance.

- Oral trush also found, that shown since 2 month ago.

- History of Birth : SC, birth weight : 2600 gr. Cried spontaneously, no

history of Blue (-).

- History of Nutrition : 0-2nd month : breastfeeding. 2nd-6th month :

breastfeeding + complementary food , 6th-12th : breasfeeding + formula.

- History of Immunization : Unknown, BCG scar (+).

- History of Parents : patient’s father is HIV (+). Patient’s mother has died 3

years ago

- History of previous illness : Patient was diagnosed with tuberculosis in

Jakarta on Desember 2012 and given Anti Tuberculosis Drugs by doctor.

Drugs consumption was just 1 month because of the worsening patient’s

general condition.

- History of previous medications: Acyclovir, Anti Tuberculosis Drugs.

Physical Examination

Generalized status

Body weight : 11 kg,

Body length : 101cm

U. Arm Circumference: 110 mm

BW/age : 11/21 x 100% = 52,3 %

BL/age : 101/115 x 100% = 87,8 %

BW/BL : 11/16 x 100% = 68,7 % (<-3SD)

Presens status

Sensorium: Compos Mentis, Body temperature: 37,2 oC, Blood Pressure: 100/60

mmHg, Heart rate: 110 bpm, Respiratory Rate: 22 x/i. Anemic (-/-). Icteric (-/-).

Cyanosis (-/-). Edema (-/-).

Localized status

Head : Paleness of inferior palpebra conjunctiva (-/-). Icteric sclera (-/-).

Light reflex (+/+). Isochoric pupil. Papul Hyperpigmentation (+),

Crusta (+). Old Man Face (+). Ear/Nose : normal in appearance,

Mouth = Oral trush (+)

Neck :Lymph node enlargement (-), Papul Hyperpigmentation (+),

Crusta (+).

Thorax :Symmetrical fusiformis. Chest retraction (-). Papul

Hyperpigmentation (+), Crusta (+). Intercostal space seen clearly.

HR: 110 bpm, reguler, murmur (-). RR: 22 x/i, reguler, Crackles

(-/-).

Abdomen : Soepel. Peristaltic (+) normal. Liver/Spleen: Unpalpable, Papul

Hyperpigmentation (+), Crusta (+). Back : Baggy Pants (+)

Extremities : Upper extremities: Pulse 110 x/i, regular, adequate pressure and

volume, warm acral, CRT < 3”. Papul Hyperpigmentation (+),

Crusta (+). Loss subcutaneous fat (+). Lower extremities: oedem

(-/-), Papul Hyperpigmentation (+), Crusta (+). Loss subcutaneous

fat (+), Muscle Hypotrophy (+).

Urogenital : Male, Normal in appearance.

Working diagnosis : Severe malnutrition marasmic type + Varicella Hemmorhage

+ HIV

Therapy : - IVFD D5%, NaCl 0,45%, 30 gtt/i micro.

- Inj. Ceftriaxone 500 mg/12jam/iv

- Cotrimoxazole Syr 2 x 240 mg

- Nystatin drops 3 x 1 cc

- Acyclovir cream

- Dactanol 3 x 1

Plan

- Consult to Neurology division

- Consult to Respirology division

- Consult to Nutrition division

- Consult to Posyansus

- Complete blood count

- Liver function test

- Renal function test

- Electrolite

- Mantoux test

- Skin lesion culture

- Chest X-ray, A-P & Lateral

- CD-4

Immunophenotyping Result 13th March 2013

Immunodeficiency Profile Result Normal Value

CD4

CD4 % 1 31 – 60

CD4 Absolute 2 410 – 1590

FOLLOW UP

March 13st–March 17th

S: Diarrhea (+), Fever (+)

O:

Present Status :

Sensorium: Compos Mentis, Body temperature: 37,2 – 38,2 oC, Blood Pressure:

100/60 mmHg, Heart Rate: 110x/i, Respiratory Rate: 22 x/i. Anemic (-/-). Icteric (-/-).

Cyanosis (-/-). Edema (-/-). Body weight: 11 kg, Body length: 101 cm. Loss appetite.

Localized status :

Head :Paleness of inferior palpebra conjunctiva (-/-). Icteric sclera (-/-).




Neck :Lymph node enlargement (-),Papul Hyperpigmentation (+), Crusta

(+).


Hyperpigmentation (+), Crusta (+). Intercostal space seen clearly. HR:

110 bpm, reguler, murmur (-). RR: 22 x/i, reguler, Crackles (-/-).

Abdomen :Soepel. Peristaltic (+) normal. Liver/Spleen: Unpalpable, Papul

Hyperpigmentation (+), Crusta (+). Back : baggy pants (+)

Extremities :Upper extremities: Pulse 110 x/i, regular, adequate pressure and

volume, warm acral, CRT < 3”. Papul Hyperpigmentation (+), Crusta

(+). Loss subcutaneous fat (+). Lower extremities: oedem (-/-), Papul

Hyperpigmentation (+), Crusta (+). Loss subcutaneous fat (+). Muscle

Hyportophy (+).


A: Malnutrition Marasmus type + HIV + Varicella hemorrhage

P: Management:

- O2 nasal canul1 L/i

- IVFD D5%, NaCl 0,45%, 20-30 gtt/i micro.

- Inj. Ceftriaxone 500 mg/12h/iv

- Inj. Acyclovir 500mg/m2/8h/iv ≈ 256 mg/8h/iv or 5 x 220 mg/oral


- Nystatin drops 3-4 x 1 cc

- Acyclovir zalf 3 x Appl I

- Zink 1x 20 g

- As. Folat 1 x 5 mg (first day, next 1 x 1 mg)

- Paracetamol 10-15mg/bw (Sprn)

- Vit-A 1 x 200.000 IV

- Diet F75 160cc/2h

- Multivitamin without Fe 1 x cth 1

- Dactanol gargl 3 x 1

- Fuson Cream 2 x appl I

Diagnostic Planning:

- Consul to Neurology division

- Consul to Respirology division

- Consul to Nutrition division

- Mantoux Test

- Gastric Lavage

- Thorax X-ray P-A

- Skin Swab

- CD 4

Result:

- 14/3/13 : CD 4 = 1 %

- CD 4 absolute = 2

- 16/3/13 : Thorax X-ray =

Perihiler infiltration, e.c Susp.

TB, Bronkopneumoni. CTR < 50

%

Laboratory Result:

15th January 2013

Parameters Unit Value Normal Value

Hematology

Hemoglobin g% 8,7 11,3-14,1

Eritrosit 106/mm3 3,37 4,40-4,48

Leukosit 103/mm3 2,98 6,0-17,5

Hematokrit % 26,50 37-41

Trombosit 103/mm3 303 217-497

MCV fL 78,6 81-95

MCH Pg 25,8 25-29

MCHC g% 32,8 29-31

RDW % 19,7 11,6-14,8

MPV fL 9,6 7,2-10

PCT % 0,29

PDW fL 9,9

Neutrofil % 78,2 37-80

Limfosit % 11,4 20-40

Monosit % 9,4 2-8

Eosinofil % 0,7 1-6

Basofil % 0,3 0-1

Neutrofil Absolut 103/µL 2,33 1,9-5,4

Limfosit Absolut 103/µL 0,34 3,7-10,7

Monosit Absolut 103/µL 0,28 0,3-0,8

Eosinofil Absolut 103/µL 0,02 0,20-0,50

Basofil Absolut 103/µL 0,01 0-0,1

Hemostatic

Ferritin ng/mL 1696 Child :15 - 240

Iron (Fe) Mg/dL 32 61-157

TIBC µg/dL 125 112-346

Liver Function Test

Bilirubin total Mg/dL 0,23 <1

Bilirubin direct Mg/dL 0,16 0-0,2

Fosfatase Alkali

(ALP)

U/L 452 <269

AST/SGOT U/L 369 <38

ALT/SGPT U/L 230 <41

Albumin g/dL 2,4 3,8-5,4

Renal Fuction Test

Ureum mg/dL 10,00 <50

Creatinine Mg/dL 0,19 0,24-0,41

Uric acid Mg/dL 3,3 <7,0

Electrolite

Calsium mg/dL 6,6 8,4-10,4

Natrium mEq/L 123 135-155

Kalium mEq/L 2,5 3,6-5,5

Chlorida mEq/L 100 96-106

Immunoserology

Qualitative CRP Positive

Procalcitonin ng/mL 0.14 <0,05

March 18th – March 22th

S: Diarrhea (+), Fever (-)

O:

Present Status :


100/60 mmHg, Pulse: 104x/i, Respiratory Rate: 20 x/i. Anemic (-/-). Icteric (-/-).

Cyanosis (-/-). Edema (-/-). Body weight: 10 kg, Body length: 101 cm. Reduced

diarrhea frequency. Appetite (+)

Localized status :






(+).





Hyperpigmentation (+), Crusta (+). Back : Baggy Pants (+).





Hypotrophy (+).



P: Management:


- IVFD D5%, NaCl 0,45%, 20-30 gtt/i micro.

- Inj. Ceftriaxone 500 mg/12h/IV

- Inj. Acyclovir 500mg/m2/8h/iv ≈ 256 mg/8h/iv or 5 x 220 mg/oral

- Inj. Ranitidine 10 mg/8h/IV

- Inj. Meropenem 400mg/8h/IV


- Nystatin drops 3-4 x 1 cc

- Acyclovir zalf cream 3 x Appl I

- As. Folat 1 x 1 mg

- Cetirizine 1 x 5 mg

- Zink 1x 20 g

- Paracetamol Syr 3 x cth 1 (sprn)

- Resomal 50cc/per vomit or per diarrhea

- Diet F100 modification 160cc/3h + mineral mix 3,2 cc (18th March)

- Diet F100 modification, Isomilk (164 g milk + 71 g sugar + 27,5 g oil) dissolve

in 1300 cc water, give per 3 hour) ≈ 165 cc/3h/Ngt + Mineral milk 3,3 cc (19th,

20,21,22, March)

- Ferriprox 1x 250 mg


- Fuson Cream


- Dactarin Oral Gel 3 x 1

- Ractin Oral Gel 3 x 1

Plan

- USG Abdomen

- Thorax-Xray Lateral

- Consul to Cardiology division

- EEG

March 23th–March 27th

S: Diarrhea (+), Cough (+), Fever (-)

O:

Present Status :

Sensorium: Compos Mentis, Body temperature: 36,5 – 37 oC, Blood Pressure: 100/60

mmHg, Pulse: 106x/i, Respiratory Rate: 26 x/i. Anemic (-/-). Icteric (-/-). Cyanosis

(-/-). Edema (-/-). Body weight: 11 kg, Body length: 101 cm. Reduced diarrhea

frequency. Appetite (+)

Localized status :






(+).





Hyperpigmentation (+), Crusta (+). Back : Baggy Pants (+).





Hyportophy (+).



P: Management:


- IVFD D5%, NaCl 0,45%, 24 gtt/i micro.

- Inj. Ceftriaxone 500 mg/12h/IV (aff 25th March)




- Candistatin drops 3-4 x 1 cc






- Diet F100 165cc/3 hour (23th March)

- Diet F100 175cc/3 hour (24th March)

- Diet F100 185cc/3 hour + mineral mix 3,7 cc (25th March)

- Diet F100 210cc/3 hour + mineral mix 4,2 cc (26, 27th March)

- Ferriprox 1x 250 mg


- Diet F100 modification 175cc/2h + mineral mix 3,3 cc

- Fuson Cream



Plan:

- Reconfirm Gastric Lavage

- CBC

- LFT

- RFT

- Electrolite

- USG Abdomen

Result:

- 25/03/13 : Gastric Lavage : BTA

(-)

- 25/03/13 : USG : Susp.

Hepatitis, Meteorismus

Laboratory Result

25th January 2013

Parameters Unit Value Normal Value

Hematology

Hemoglobin g% 10 11,3-14,1

Eritrosit 106/mm3 3,87 4,40-4,48

Leukosit 103/mm3 2,01 6,0-17,5

Hematokrit % 31,3 37-41

Trombosit 103/mm3 152 217-497

MCV fL 80,9 81-95

MCH Pg 25,8 25-29

MCHC g% 31,9 29-31

RDW % 20,3 11,6-14,8

MPV fL 10,5 7,2-10

PCT % 0,16

PDW fL 13,4

Neutrofil % 70,6 37-80

Limfosit % 21,9 20-40

Monosit % 6,00 2-8

Eosinofil % 1,00 1-6

Basofil % 0,500 0-1

Neutrofil Absolut 103/µL 1,42 1,9-5,4

Limfosit Absolut 103/µL 0,44 3,7-10,7

Monosit Absolut 103/µL 0,12 0,3-0,8

Eosinofil Absolut 103/µL 0,02 0,20-0,50

Basofil Absolut 103/µL 0,01 0-0,1

Renal Fuction Test

Ureum mg/dL 9,20 <50

Creatinine Mg/dL 0,17 0,24-0,41

Uric acid Mg/dL 2,0 <7,0

Electrolite

Calsium mg/dL 6,5 8,4-10,4

Natrium mEq/L 125 135-155

Kalium mEq/L 1,9 3,6-5,5

Phosphor mEq/L 2,4 3,4-6,2

Chlorida mEq/L 106 96-106

Magnesium mEq/L 1,57 1,4-1,9

Immunoserology

Qualitative CRP Positive

March 28th–April 1st

S: Diarrhea (-), Fever (-)

O:

Present Status :





Localized status :






(+).





Hyperpigmentation (+), Crusta (+). Back : Baggy Pants (+)





Hyportophy (+).


A: Malnutrition Marasmus type + HIV stad. III + Varicella hemorrhage

P: Management:



- Inj. Ceftriaxone 500 mg/12h/IV










- Diet F100 210cc/3 hour + mineral mix 4,2 cc (28th March)

- Diet F100 220 cc/3h/Ngt + Mineral milk 4,4 cc (30th March)

- Diet F100 330 cc/3h/Ngt + Mineral milk 6,6 cc (1st April)

- Multivitamin without Fe 1 x cth 1 (31 aprl aff)

- Multivitamin with Fe 1 x cth 1 (becefort)

- Fuson Cream


Plan:

- Mantoux test

- Thorax X-ray

Result:

- Thorax X-Ray : A-P: Infiltration

Perihiler e.c dd/ TB. BP

April 2nd–April 6th

S: Diarrhea (-), Fever (-)

O:

Present Status :





Localized status :






(+).





Hyperpigmentation (+), Crusta (+). Back : baggy pants (+).





Hyportophy (+).


A: Malnutrition Marasmus type + HIV stad. IV + Varicella hemorrhage + CMV

P: Management:









- Diet F100 330 cc/4h/Ngt + Mineral milk 6,6 cc (2nd April)

- Diet F100 340 cc/4h/Ngt + Mineral milk 6,8 cc (3th April)

- Diet F100 350 cc/4h/Ngt + Mineral milk 7 cc (5nd April)

- Multivitamin with Fe 1 x cth 1 (becefort)

- Fuson Cream





Plan:

- CBC

- Cytomegalo Virus Test

- Blood Culture

- Consul to Cardioloy Division

Result:

- 02/04/13 : Blood Culture : No

bacteria growth found

- Anti CMV IgG : 15 (reactive)

Anti CMV Ig M : 4,9 (reactive)

Discussion and Summary

Malnutrisi merupakan masalah kesehatan utama, khususnya pada negara

yang berkembang.7 Malnutrisi dapat dipengaruhi oleh beberapa faktor risiko atau

penyebab. Penyebab malnutrisi yang berbeda-beda ini saling terkait dan termasuk

penyebab langsung, penyebab, dan penyebab dasar. Semua faktor berjalan

bersama dan tidak saling bergantung.8

Gambar 1. Sebuah Model Konseptual Sederhana untuk Memahami Penyebab

Malnutrisi.9

Menurut kerangka ini, kekurangan gizi terjadi ketika asupan makanan

tidak memadai dan kesehatan tidak memuaskan, menjadi dua penyebab langsung

kekurangan gizi. Di negara berkembang, penyakit menular, seperti penyakit diare

(DD) dan penyakit saluran pernapasan akut (ISPA), bertanggung jawab untuk

sebagian besar nutrisi yang berhubungan dengan masalah kesehatan.10 Manifestasi

malnutrisi karena perbedaan antara jumlah nutrisi yang diserap dari makanan dan

jumlah nutrisi yang dibutuhkan oleh tubuh. Hal ini terjadi sebagai konsekuensi

dari mengkonsumsi terlalu sedikit makanan atau mengalami infeksi, yang

meningkatkan kebutuhan tubuh akan nutrisi, mengurangi nafsu makan, atau

mempengaruhi penyerapan nutrisi dari usus. Dalam prakteknya, kekurangan gizi

dan infeksi sering terjadi pada waktu yang sama. Malnutrisi dapat meningkatkan

risiko infeksi, sedangkan infeksi dapat menyebabkan kekurangan gizi yang

mengarah ke lingkaran setan. Seorang anak kurang gizi, yang tahan terhadap

penyakit yang lemah, jatuh sakit dan menjadi lebih kurang gizi, yang mengurangi

kemampuannya untuk melawan penyakit dan sebagainya.9

Penyebab malnutrisi dapat dikelompokkan dalam tiga kategori besar:

bahan pangan rumah tangga yabg tidak memadai, perawatan yang tidak memadai,

dan layanan kesehatan yang tidak memadai serta lingkungan rumah tangga yang

tidak sehat, seperti kurangnya akses ke air bersih dan sanitasi yang efektif. Bahan

pangan ada ketika semua orang setiap saat, memiliki akses fisik dan ekonomi

terhadap pangan yang cukup, aman dan bergizi untuk memenuhi kebutuhan

makanan mereka dan preferensi makanan untuk hidup aktif dan sehat. Perawatan

yang memadai termasuk ASI eksklusif dan makanan pelengkap yang memadai

dari sekitar usia enam bulan; perawatan kesehatan (khususnya, imunisasi); dan

dukungan emosional dan stimulasi kognitif serta makanan untuk tumbuh dan

berkembang dengan baik. Sebuah elemen penting dari perawatan kesehatan yang

baik adalah akses yang terjangkau, kualitas kuratif yang baik dan pelayanan

kesehatan preventif serta lingkungan rumah tangga yang sehat. Air cukup aman,

sistem sanitasi yang efektif, dan kondisi higienis adalah bagian dari rumah tangga

yang sehat environment.9 Penjelasan ini cocok untuk belajar yang menunjukkan

penghentian awal menyusui, kegagalan untuk menyelesaikan kursus utama

imunisasi, dan datang dari rumah tangga kurang mampu secara ekonomi adalah

risiko faktor malnutrisi energi protein berat pada anak.11

Manusia dan sumber daya lingkungan, sistem ekonomi serta faktor-faktor

politik dan ideologis adalah penyebab dasar yang berkontribusi terhadap

kekurangan gizi. Model ini berkaitan dengan faktor penyebab untuk di gizi buruk

dengan tingkat sosial-organisasi yang berbeda. Penyebab langsung mempengaruhi

individu, penyebab berhubungan dengan keluarga, dan penyebab dasar terkait

dengan masyarakat dan bangsa. Akibatnya, semakin banyak yang tidak langsung

adalah penyebabnya, lebih luas penduduk yang status gizi dipengaruhi.10

Pasien ini tinggal bersama neneknya. Ibunya sudah meninggal 3 tahun

yang lalu, dan ia berasal dari keluarga sosio-ekonomi menengah-rendah.

Berdasarkan alloanamnese, ia memiliki asupan makanan yang tidak memadai dan

imunisasi yang tidak lengkap. Riwayat penyakit sebelumnya adalah TB. Dia

datang dengan keluhan utama diare dan juga didiagnosis dengan infeksi HIV (+).

Oleh karena itu, pasien ini memiliki faktor risiko gizi buruk.

Malnutrisi energi protein adalah hasil dari kehilangan protein, energi, atau

keduanya. Anak-anak yang kurus untuk tinggi badan mereka mungkin menderita

KEP akut (baru-baru ini kekurangan pangan yang parah), sedangkan anak-anak

yang pendek untuk usia mereka telah mengalami KEP kronis (kekurangan

makanan jangka panjang). KEP terjadi dalam dua bentuk: marasmus dan

kwashiorkor, yang berbeda dalam gambaran klinis mereka. Paragraf berikut

menyajikan tiga klinis sindrom-marasmus, kwashiorkor, dan kombinasi

keduanya.12

Marasmus mencerminkan kekurangan makanan dalam waktu yang lama

(KEP kronis). Sederhananya, orang tersebut kelaparan dan mengalami asupan

energi dan protein yang tidak memadai (dan asam lemak esensial yang tidak

memadai, vitamin, dan mineral juga). Anak marasmus terlihat seperti orang tua

kecil-hanya kulit dan tulang. Tanpa gizi yang cukup, otot, termasuk jantung,

waste dan melemah. Karena otak biasanya tumbuh hampir ukuran dewasa penuh

dalam dua tahun pertama kehidupan, marasmus merusak perkembangan otak dan

kemampuan belajar. Mengurangi sintesis hormon kunci memperlambat

metabolisme dan menurunkan suhu tubuh. Ada sedikit atau tanpa lemak di bawah

kulit untuk melindungi terhadap dingin. Karena anak-anak ini sering mengalami

keterlambatan perkembangan mental dan perilaku mereka, mereka juga

membutuhkan kasih sayang, lingkungan yang merangsang, dan perhatian

orangtua. Para anak yang kelaparan menghadapi ancaman terhadap kehidupan ini

dengan terlibat dalam sedikit kegiatan yang mungkin-bahkan tidak menangis

untuk makanan. Tubuh mengerahkan semua kekuatan untuk memenuhi krisis,

sehingga luka di atas setiap pengeluaran energi tidak diperlukan untuk fungsi

jantung, paru-paru, dan otak. Pertumbuhan berhenti; anak tidak lebih besar pada

usia empat tahun dibandingkan pada usia dua tahun. Enzim dalam pasokan

pendek dan lapisan saluran pencernaan memburuk. Akibatnya, anak tidak dapat

mencerna dan menyerap apa makanan yang dimakan.12 Pada marasmus, anak

tampak kurus dengan ditandai hilangnya lemak subkutan dan pengecilan otot.

Kulit xerotic, berkerut, dan longgar. Wajah monyet sekunder untuk hilangnya

bantalan lemak bukal adalah karakteristik dari gangguan ini. Marasmus mungkin

tidak memiliki dermatosis klinis. Namun, temuan kulit yang konsisten termasuk

halus, rambut rapuh; alopecia; gangguan pertumbuhan; dan fissuring pada kuku.13

Kwashiorkor biasanya mencerminkan kekurangan makanan yang tiba-tiba

dan baru-baru ini (KEP akut). Hilangnya berat badan dan lemak tubuh pada

kwashiorkor biasanya tidak separah seperti marasmus, tetapi beberapa pengecilan

otot dapat terjadi. Protein dan hormon yang sebelumnya dipelihara keseimbangan

cairan berkurang, dan cairan bocor ke dalam ruang interstitial. Tungkai dan perut

anak menjadi bengkak dengan edema, gambaran pembeda dari kwashiorkor.

Lemak hati berkembang karena kurangnya operator protein yang mengangkut

lemak dari hati. Lemak hati tidak memiliki enzim untuk membersihkan racun

metabolisme dari dalam tubuh, sehingga efek berbahaya mereka jadi lebih lama.

Peradangan dalam menanggapi racun ini dan infeksi lebih lanjut berkontribusi

terhadap edema yang menyertai kwashiorkor. Tanpa tirosin yang cukup untuk

membuat melanin, rambut anak kehilangan warnanya, dan sintesis protein yang

tidak memadai membuat kulit tambal sulam dan bersisik, sering dengan luka yang

gagal untuk sembuh.12 Saat hadir, perubahan kulit yang khas dan kemajuan selama

beberapa hari. Kulit menjadi gelap, kering, dan kemudian membagi terbuka saat

diregangkan, mengungkapkan daerah pucat antara celah-celah (yaitu, crazy

pavement dermatosis, enamel paint skin).13 Kurangnya protein untuk membawa

atau menyimpan besi meninggalkan besi yang bebas. Besi yang tidak terikat

adalah umum pada anak-anak dengan kwashiorkor dan dapat menyebabkan

penyakit dan kematian mereka dengan mempromosikan pertumbuhan bakteri dan

kerusakan akibat radikal bebas.12

Marasmus-Kwashiorkor adalah kombinasi marasmus dan kwashiorkor

yang ditandai dengan edema dari kwashiorkor dengan pemborosan marasmus.

Beberapa penelitian menunjukkan bahwa marasmus merupakan adaptasi tubuh

terhadap kelaparan dan kwashiorkor yang terjadi ketika adaptasi gagal. 12

Pasien memiliki penampilan seperti wajah orang tua, kurus dengan

ditandai hilangnya lemak subkutan dan pengecilan otot, dan juga tampilan seperti

celana baggy ditunjukkan. Ruang interkostal terlihat jelas atau tulang rusuk yang

menonjol. Penampilan ini menunjukkan kondisi marasmus.

Diagnosis malnutrisi (Malnutrisi Energi Protein) adalah dari anamnesis,

pemeriksaan fisik, dan pemeriksaan kesehatan lainnya (penilaian antropometri, uji

laboratorium, analisis makanan, dll).

1. History Taking

In children, the findings of poor weight gain or weight loss; slowing of

linear growth; and behavioral changes, such as irritability, apathy, decreased

social responsiveness, anxiety, and attention deficit may indicate protein-energy

malnutrition. In particular, the child is apathetic when undisturbed but irritable

when picked up. Kwashiorkor characteristically affects children who are being

weaned. Signs include diarrhea and psychomotor changes.13

2. Physical Examination

Physical findings that are associated with PEM include the following:14

a. Decreased subcutaneous tissue: Areas that are most affected are the legs, arms,

buttocks, and face

b. Edema: Areas that are most affected are the distal extremities and anasarca

(generalized edema)

c. Oral changes: Cheilosis, angular stomatitis, and papillar atrophy

d. Abdominal findings: Abdominal distention secondary to poor abdominal

musculature and hepatomegaly secondary to fatty infiltration

e. Skin changes: Dry, peeling skin with raw, exposed areas; hyperpigmented

plaques over areas of trauma

f. Nail changes: Fissured or ridged nails

g. Hair changes: Thin, sparse, brittle hair that is easily pulled out and that turns a

dull brown or reddish color

3. Workup

WHO recommends diagnostic laboratory studies include blood glucose,

examination of blood smears by microscopy or direct detection testing ,

hemoglobin, urine examination and culture, stool examination by microscopy for

ova and parasites, serum albumin, HIV test (this test must be accompanied by

counseling of the child's parents, and strict confidentiality should be maintained),

and electrolytes.13

Stool specimens should be obtained if the child has a history of abnormal

stools or stooling patterns or if the family uses an unreliable or questionable

source of water.14

Other studies may focus on thyroid functions or sweat chloride tests,

particularly if height velocity is abnormal.14

Practical nutritional assessment includes complete history, including a

detailed dietary history; growth measurements, including weight and

length/height; head circumference in children younger than 3 years; and complete

physical examination.14

Severe malnutrition is defined in WHO guidelines as the presence of

severe wasting (<70% weight-for-height or <-3SD) and/or oedema.15

Our patient had body weight : 11 kg, body length : 101cm, and BW/BL :

62%. It this, patient indicated very low body weight. From CDC chart, body

weight-for-height was below 70%. According to was diagnosed with severe

malnutrition.

The WHO guidelines for severe malnutrition treatment are divided in five

sections:15

a. General principles for routine care (the’10 steps’)

b. Emergency treatment of shock and severe anaemia

c. Treatment of associated conditions

d. Failure to respond to treatment

e. Discharge before recovery is complete

There are ten essential steps: treat/prevent hypoglycaemia, treat/prevent

hypothermia, treat/prevent dehydration, correct electrolyte imbalance,

treat/prevent infection, correct micronutrient deficiencies, start cautious feeding,

achieve catch-up growth, provide sensory stimulation and emotional support, and

prepare for follow-up after recovery.15

Table 1. Time-Frame for the Management of a Child with Severe Malnutrition16

Step 1. Treat/prevent hypoglycaemia

Hypoglycaemia and hypothermia usually occur together and are signs of

infection. Check for hypoglycaemia whenever hypothermia (axillary<35.00C;

rectal<35.50C) is found. Frequent feeding is important in preventing both

conditions.15

Treatment:

If the child is conscious and dextrostix shows <3mmol/l or 54mg/dl give:

1. 50 ml bolus of 10% glucose or 10% sucrose solution (1 rounded teaspoon of

sugar in 3.5 tablespoons water), orally or by nasogastric (NG) tube. Then feed

starter F-75 (see step 7) every 30 min. for two hours (giving one quarter of the

two-hourly feed each time)

2. Antibiotics (see step 5)

3. Two-hourly feeds, day and night (see step 7) 15

If the child is unconscious, lethargic or convulsing give:

1. IV sterile 10% glucose (5ml/kg), followed by 50ml of 10% glucose or sucrose

by Ng tube. Then give starter F-75 as above

2. Antibiotics

3. Two-hourly feeds, day and night15

Monitor:

1. Blood glucose: if this was low, repeat dextrostix taking blood from finger or

heel, after two hours. Once treated, most children stabilise within 30 min. If

blood glucose falls to <3 mmol/l give a further 50ml bolus of 10% glucose or

sucrose solution, and continue feeding every 30 min. until stable

2. Rectal temperature: if this falls to <35.50C, repeat dextrostix

3. Level of consciousness: if this deteriorates, repeat dextrostix15

Prevention:

1. Feed two-hourly, start straightaway (see step 7) or if necessary, rehydrate first

2. Always give feeds throughout the night15

There was no test for blood glucose level in this patient, but according to

guideline, he still got treatment for hypoglycemia with IVFD D5% NaCl 0,45%.

Step 2. Treat/prevent hypothermia

Treatment:

If the axillary temperature is <35.00C, take the rectal temperature using a

low reading thermometer. If the rectal temperature is <35.50C (<95.90F):

1. feed straightaway (or start rehydration if needed)

2. rewarm the child: either clothe the child (including head), cover with a warmed

blanket and place a heater or lamp nearby (do not use a hot water bottle), or put

the child on the mother’s bare chest (skin to skin) and cover them

3. give antibiotics (see step 5) 15

Monitor:

1. body temperature: during rewarming take rectal temperature twohourly until it

rises to >36.5oC (take half-hourly if heater is used)

2. ensure the child is covered at all times, especially at night

3. feel for warmth

4. blood glucose level: check for hypoglycaemia whenever hypothermia is

found15

Prevention:

1. feed two-hourly, start straightaway (see step 7)

2. always give feeds throughout the day and night

3. keep covered and away from draughts

4. keep the child dry, change wet nappies, clothes and bedding

5. avoid exposure (e.g. bathing, prolonged medical examinations)

6. let child sleep with mother/carer at night for warmth15

Patient’s temperature when admitted to the hospital was 37,7 C and treated

with antipyretic, but monitoring of his temperature was still done to prevent

hypothermia.

Step 3. Treat/prevent dehydration

Low blood volume can coexist with oedema. Do not use the IV route for

rehydration except in cases of shock and then do so with care, infusing slowly to

avoid flooding the circulation and overloading the heart. 15

Treatment:

The standard oral rehydration salts solution (90 mmol sodium/l) contains

too much sodium and too little potassium for severely malnourished children.

Instead give special Rehydration Solution for Malnutrition (ReSoMal). 15

It is difficult to estimate dehydration status in a severely malnourished

child using clinical signs alone. So assume all children with watery diarrhoea may

have dehydration and give:

1. ReSoMal 5 ml/kg every 30 min. for two hours, orally or by nasogastric tube,

then

2. 5-10 ml/kg/h for next 4-10 hours: the exact amount to be given should be

determined by how much the child wants, and stool loss and vomiting. Replace

the ReSoMal doses at 4, 6, 8 and 10 hours with F-75 if rehydration is

continuing at these times, then

3. continue feeding starter F-75 (see step 7) 15

During treatment, rapid respiration and pulse rates should slow down and

the child should begin to pass urine. Monitor progress of rehydration: Observe

half-hourly for two hours, then hourly for the next 6-12 hours, recording pulse

rate, respiratory rate, urine frequency, and stool/vomit frequency. 15

Return of tears, moist mouth, eyes and fontanelle appearing less sunken,

and improved skin turgor, are also signs that rehydration is proceeding. It should

be noted that many severely malnourished children will not show these changes

even when fully rehydrated. 15

Continuing rapid breathing and pulse during rehydration suggest

coexisting infection or overhydration. Signs of excess fluid (overhydration) are

increasing respiratory rate and pulse rate, increasing oedema and puffy eyelids. If

these signs occur, stop fluids immediately and reassess after one hour. 15

Prevention:

To prevent dehydration when a child has continuing watery diarrhoea:

1. Keep feeding with starter F-75 (see step 7)

2. Replace approximate volume of stool losses with ReSoMal. As a guide give

50-100 ml after each watery stool. (Note: it is common for malnourished

children to pass many small unformed stools: these should not be confused

with profuse watery stools and do not require fluid replacement)

3. If the child is breastfed, encourage to continue15

Patient’s urine output was adequate and there was no sign for dehydration.

However, patient came with diarrhea condition and treated with ReSoMal 50 cc

per diarrhea or vomitting to prevent dehydration.

Step 4. Correct electrolyte imbalance

All severely malnourished children have excess body sodium even though

plasma sodium may be low (giving high sodium loads will kill). Deficiencies of

potassium and magnesium are also present and may take at least two weeks to

correct. Oedema is partly due to these imbalances. Do NOT treat oedema with a

diuretic. Give:

1. extra potassium 3-4 mmol/kg/d

2. extra magnesium 0.4-0.6 mmol/kg/d

3. when rehydrating, give low sodium rehydration fluid (e.g. ReSoMal)

4. prepare food without salt15

The extra potassium and magnesium can be prepared in a liquid form and

added directly to feeds during preparation. Adding 20 ml of this solution to 1 litre

of feed will supply the extra potassium and magnesium required. The solution can

also be added to ReSoMal. 15

From laboratory test, hyponatremia, hypokalemia, and Hypocalcemia was

found. Patient was treated with IVFD D5% NaCl 0,45% (maintenance).

Step 5. Treat/prevent infection

In severe malnutrition the usual signs of infection, such as fever, are often

absent, and infections are often hidden. Therefore give routinely on admission:

1. broad-spectrum antibiotic(s) AND

2. measles vaccine if child is > 6m and not immunised (delay if the child is in

shock) 15

Some experts routinely give, in addition to broad-spectrum antibiotics,

metronidazole (7.5 mg/kg 8-hourly for 7 days) to hasten repair of the intestinal

mucosa and reduce the risk of oxidative damage and systemic infection arising

from the overgrowth of anaerobic bacteria in the small intestine. 15

Choice of broad-spectrum antibiotics:

a) if the child appears to have no complications give: 15

Co-trimoxazole 5 ml paediatric suspension orally twice daily for 5 days (2.5 ml

if weight <6 kg). (5 ml is equivalent to 40 mg TMP+200 mg SMX).

OR

b) if the child is severely ill (apathetic, lethargic) or has complications

(hypoglycaemia; hypothermia; broken skin; respiratory tract or urinary tract

infection) give:

Ampicillin 50 mg/kg IM/IV 6-hourly for 2 days, then oral amoxycillin 15

mg/kg 8-hourly for 5 days, or if amoxycillin is not available, continue with

ampicillin but give orally 50 mg/kg 6-hourly

AND

Gentamicin 7.5 mg/kg IM/IV once daily for 7 days

If the child fails to improve clinically within 48 hours, add

Chloramphenicol 25 mg/kg IM/IV 8-hourly for 5 days. 15

Where specific infections are identified, add specific antibiotics if

appropriate and antimalarial treatment if the child has a positive blood film for

malaria parasites. 15

If anorexia persists after 5 days of antibiotic treatment, complete a full 10-

day course. If anorexia still persists, reassess the child fully, checking for sites of

infection and potentially resistant organisms, and ensure that vitamin and mineral

supplements have been correctly given. 15

Patient got prophylaxis antibiotic with cotrimoxazole dose adjusted.

Step 6. Correct micronutrient deficiencies

All severely malnourished children have vitamin and mineral deficiencies.

Although anaemia is common, do not give iron initially but wait until the child

has a good appetite and starts gaining weight (usually by the second week), as

giving iron can make infections worse. 15

1. Give: vitamin A orally on Day 1 (for age >12 months, give 200,000 IU; for age

6-12 months, give 100,000 IU; for age 0-5 months, give 50,000 IU) unless

there is definite evidence that a dose has been given in the last month.

2. Give daily for at least 2 weeks:

a) Multivitamin supplement

b) Folic acid 1 mg/d (give 5 mg on Day 1)

c) Zinc 2 mg/kg/d

d) Copper 0.3 mg/kg/d

e) Iron 3 mg/kg/d but only when gaining weight

Patient got multivitamin without iron until week 2 and switched to

multivitamin with iron after that. He also got folic acid 5 mg (day 1), 1 mg

(next) , and viamin A 200.000IU (single dose).

Step 7. Start cautious feeding

In the stabilisation phase a cautious approach is required because of the

child’s fragile physiological state and reduced homeostatic capacity. Feeding

should be started as soon as possible after admission and should be designed to

provide just sufficient energy and protein to maintain basic physiological

processes. The essential features of feeding in the stabilisation phase are: 15

1. small, frequent feeds of low osmolarity and low lactose

2. oral or nasogastric (NG) feeds (never parenteral preparations)

3. 100 kcal/kg/d

4. 1-1.5 g protein/kg/d

5. 130 ml/kg/d of fluid (100 ml/kg/d if the child has severe oedema)

6. if the child is breastfed, encourage to continue breastfeeding but give the

prescribed amounts of starter formula to make sure the child’s needs are met.

Monitor and note:

1. amounts offered and left over

2. vomiting

3. frequency of watery stool

4. daily body weight15

Patient got formula WHO 75, energy required 130 kkal/gBW/day with the

calculation:

• F 75 = 130 x 1100/ 75 per 24 hours

• F 75 = 1906,67 ml / 24 hours

• For the stabilization phase, F 75 should be given every 2 hours, then the patient

needed:

• F 75 = 1906,67 / 12 times

• F 75 = 158 cc (rounded to be 160 cc/ 2hours)

Step 8. Achieve catch-up growth

In the rehabilitation phase a vigorous approach to feeding is required to

achieve very high intakes and rapid weight gain of >10 g gain/kg/d. The

recommended milk-based F-100 contains 100 kcal and 2.9 g protein/100 ml.

Modified porridges or modified family foods can be used provided they have

comparable energy and protein concentrations.15

Readiness to enter the rehabilitation phase is signalled by a return of

appetite, usually about one week after admission. A gradual transition is

recommended to avoid the risk of heart failure which can occur if children

suddenly consume huge amounts.15

To change from starter to catch-up formula: 15

1. replace starter F-75 with the same amount of catch-up formula F- 100 for 48

hours then,

2. increase each successive feed by 10 ml until some feed remains uneaten. The

point when some remains unconsumed is likely to occur when intakes reach

about 30 ml/kg/feed (200 ml/kg/d).

In the patient, F-75 was replaced with the same amount of formula F-100

on day 5 (17th March 2013).

Monitor during the transition for signs of heart failure: 15

1. respiratory rate

If respirations increase by 5 or more breaths/min and pulse by 25 or more

beats/min for two successive 4-hourly readings, reduce the volume per feed

(give 4-hourly F-100 at 16 ml/kg/feed for 24 hours, then 19 ml/kg/feed for 24

hours, then 22 ml/kg/feed for 48 hours, then increase each feed by 10 ml as

above).

2. pulse rate

After the transition give: 15

1. frequent feeds (at least 4-hourly) of unlimited amounts of a catchup formula

2. 150-220 kcal/kg/d

3. 4-6 g protein/kg/d

4. if the child is breastfed, encourage to continue

Monitor progress after the transition by assessing the rate of weight gain: 15

1. weigh child each morning before feeding.

2. each week calculate and record weight gain as g/kg/d

If weight gain is: 15

1. poor (<5 g/kg/d), child requires full reassessment

2. moderate (5-10 g/kg/d), check whether intake targets are being met, or if

infection has been overlooked

3. good (>10 g/kg/d), continue to praise staff and mothers

Step 9. Provide sensory stimulation and emotional support

In severe malnutrition there is delayed mental and behavioural

development. Provide: 15

1. tender loving care

2. a cheerful, stimulating environment

3. structured play therapy 15-30 min/d

4. physical activity as soon as the child is well enough

5. maternal involvement when possible (e.g. comforting, feeding, bathing, play)

Step 10. Prepare for follow-up after recovery

A child who is 90% weight-for-length (equivalent to -1SD) can be

considered to have recovered. The child is still likely to have a low weight-for-age

because of stunting. Good feeding practices and sensory stimulation should be

continued at home. Show parent or carer how to: 15

1. feed frequently with energy- and nutrient-dense foods

2. give structured play therapy

Advise parent or carer to: 15

1. bring child back for regular follow-up checks

2. ensure booster immunizations are given

3. ensure vitamin A is given every six months

Diarrhoea is a common feature of malnutrition but it should subside during

the first week of treatment with cautious feeding. In the rehabilitation phase,

loose, poorly formed stools are no cause for concern provided weight gain is

satisfactory. 15

Mucosal damage and giardiasis are common causes of continuing

diarrhoea. Where possible examine the stools by microscopy. Give metronidazole

(7.5 mg/kg 8-hourly for 7 days) if not already given. 15

Lactose intolerance. Only rarely is diarrhoea due to lactose intolerance.

Treat only if continuing diarrhoea is preventing general improvement. Starter F-

75 is a low-lactose feed. In exceptional cases: substitute milk feeds with yoghurt

or a lactose-free infant formula and reintroduce milk feeds gradually in the

rehabilitation phase. 15

Osmotic diarrhoea may be suspected if diarrhoea worsens substantially

with hyperosmolar starter F-75 and ceases when the sugar content is reduced and

osmolarity is <300 mOsmol/l. In these cases: use isotonic F-75 or low osmolar

cereal-based F-75 and introduce F-100 gradually. 15

Severe weight loss and wasting were some of the earliest recognized signs

of human immunodeficiency virus (HIV) infection, and in many African countries

HIV was called “slim disease” because of the prominence of this feature. Wasting

and weight loss are common features of HIV infection, especially in resource-

limited settings, with some studies showing 40%-44% of adults and 59% of

children having wasting and malnutrition as a part of their disease manifestations.

There is a complex relationship between nutrition and HIV infection.

Malnutrition, even without HIV, can compromise the immune system, and CD4 T

cells can be decreased in malnourished, HIV-negative individuals. Nutritional

status may indicate disease severity and may help indicate response to

antiretroviral therapy (ART). Both macronutrient and micronutrient deficiencies

are important in HIV-infected patients. For all these reasons, an assessment of

nutritional status should be a routine part of the care of every HIV-infected

patient. Prevention and management of nutritional deficiencies and malnutrition

are crucial parts of the comprehensive management of HIV-infected children and

adults. Metabolic abnormalities, usually related to ART, are common but will not

be discussed in this chapter (see the chapter on metabolic abnormalities).17

HIV berkontribusi untuk malnutrisi dalam berbagai cara dan bisa langsung

atau tidak langsung mengakibatkan penurunan asupan kalori, meningkatkan

hilangnya nutrisi, dan meningkatan penggunaan nutrisi / energi. Faktor-faktor

yang dianggap berkontribusi untuk wasting dan malnutrisi pada orang dengan

HIV / AIDS meliputi perubahan metabolik, infeksi, demam, perubahan

gastrointestinal (GI) dan penyakit, masalah perkembangan / neurologis, dan isu-

isu ekonomi dan psikososial. HIV juga tampaknya mempengaruhi tubuh kurus

atau massa otot lebih agresif daripada infeksi lain, mengakibatkan hilangnya otot

yang tidak proporsional dibandingkan dengan lemak selama pengembangan

malnutrisi.17

Setiap infeksi, dan infeksi HIV pada khususnya, mengubah metabolisme

energi, karbohidrat, lemak, protein, vitamin, dan mineral, meningkatkan

kebutuhan tubuh akan nutrisi. Demam dapat meningkatkan pemanfaatan protein

dan meningkatkan kebutuhan kalori sebesar 12% untuk setiap derajat Celsius di

atas normal dan 7% untuk setiap derajat Fahrenheit di atas normal. Meskipun ada

beberapa kontroversi, diperkirakan bahwa infeksi HIV dapat meningkatkan

pengeluaran energi istirahat (jumlah energi yang digunakan tubuh untuk

menjalankan fungsi jaringan sel dasar dan saat istirahat), yang dapat menyebabkan

wasting. Peningkatan produksi sitokin dalam infeksi HIV juga dapat

menyebabkan wasting pada infeksi HIV.17

Interaksi HIV dengan saluran pencernaan dapat sangat mempengaruhi

status gizi. Diare meningkatkan kebutuhan kalori sebesar 25% dan sering

mengarah ke penurunan asupan oral. Malabsorpsi, ketidakmampuan tubuh untuk

menyerap nutrisi dari saluran pencernaan, dapat berhubungan dengan diare atau

terjadi tanpa diare karena perubahan metabolik yang berhubungan dengan HIV.

Hal ini dapat menyebabkan vitamin, mineral, protein, lemak, dan karbohidrat

hilang serta penurunan asupan oral. Dehidrasi akibat diare dapat menyebabkan

kehilangan berat yang akut dari kehilangan air dan dapat menjadi komplikasi diare

yang mengancam jiwa. Kandidiasis oral yang berat (ragi), kandidiasis esofagus,

herpes gingivostomatitis, esofagitis virus, dan gastritis bisa membuat sulit makan

dan nyeri, yang menyebabkan penurunan asupan oral atau penolakan makan.

Mual dan muntah yang disebabkan oleh obat-obatan, infeksi, dan / atau penyakit

dapat mengakibatkan asupan mulut yang buruk, dehidrasi, dan kehilangan

nutrisi.17

Anak-anak dan orang dewasa dengan HIV / AIDS dapat mengembangkan

masalah makan, sering karena kerusakan saraf yang berhubungan dengan infeksi

HIV, yang menyebabkan kurangnya asupan nutrisi. Bayi dengan HIV dapat

mempunyai isapan yang lemah, mengakibatkan kurangnya asupan ASI atau susu

formula. Anak-anak dapat mengembangkan mengunyah dan kemampuan makan

yang buurk. Kesulitan menelan dapat menyebabkan asupan oral buruk atau

penolakan untuk makan. Ada risiko aspirasi dan pneumonia dengan masalah

menelan.17

Masalah ekonomi yang mengarah ke asupan gizi yang tidak memadai

merupakan kontributor sering kekurangan gizi di banyak rangkaian. Isu-isu ini

termasuk pasokan makanan yang terbatas, hilangnya pendapatan rumah tangga

atau mata pencaharian (seperti pertanian) karena sakit, serta memasak dan fasilitas

penyimpanan yang terbatas. Dewasa yang terinfeksi HIV mungkin terlalu sakit

atau tidak tertarik untuk merawat diri mereka sendiri dan anak-anak mereka.

Depresi pada orang dewasa atau anak juga dapat menyebabkan penurunan nafsu

makan dan asupan gizi yang buruk.17

Interaksi antara gizi buruk dan HIV sangat kompleks. Menyadari

kekurangan gizi ini penting karena dapat memprediksi perkembangan penyakit

dan risiko morbiditas dan mortalitas lebih tinggi. Kehadiran malnutrisi merupakan

prediktor hasil yang lebih buruk pada orang dewasa dan anak-anak yang terinfeksi

HIV. Pada anak-anak yang terinfeksi HIV, pengukuran seperti kecepatan

pertumbuhan tinggi dan berat badan rendah untuk usia memprediksi kelangsungan

hidup dan perkembangan penyakit. Malnutrisi mungkin akibat sekunder penyakit

HIV lanjut. Malnutrisi primer juga dapat mempercepat perkembangan penyakit

HIV. Malnutrisi yang tidak tergantung infeksi HIV memiliki morbiditas dan

mortalitas yang tinggi, dan efek ini mungkin berlebihan pada orang HIV-positif.17

Menyadari kekurangan gizi juga penting agar perawatan khusus diarahkan

pada peningkatan status gizi yang dapat digunakan. Pengendalian infeksi HIV

menggunakan obat-obatan antiretroviral (ARV) dan intervensi diarahkan pada

kekurangan gizi, seperti suplemen nutrisi, sering keduanya diperlukan untuk

perawatan yang cukup untuk individu yang terinfeksi. Penggunaan ARV tanpa

dukungan nutrisi, atau dukungan nutrisi tanpa ARV, akan sering mengakibatkan

respon dan hasil yang buruk. Dengan pengobatan ARV dan peningkatan jumlah

CD4 dan viral load, berat dan beberapa massa tubuh tanpa lemak dapat

dikembalikan. Namun, beberapa pasien melihat sedikit atau tidak ada perbaikan

dalam massa tubuh tanpa lemak, jadi salah satu harus mencoba untuk

mempertahankan status gizi yang baik pada pasien HIV-positif dari saat

didiagnosis.17

Selain itu, pasien didiagnosis dengan HIV (+). HIV merupakan salah satu

penyakit kronis yang berhubungan dengan marasmus. Wasting (marasmus) pada

pasien dengan infeksi HIV mungkin menandakan perkembangan penyakit atau

kekurangan gizi yang mendasarinya. Diagnosis infeksi HIV didasarkan pada

beberapa pertimbangan. Pertama, riwayat HIV (+) dari orang tuanya terbukti. Dari

diskusi, kami menganggap infeksi HIV ini ditularkan secara vertikal dari orang

tuanya. Kedua, pasien menunjukkan beberapa tanda dan gejala infeksi HIV

pediatrik, seperti infeksi jamur yang berulang (kandidiasis oral atau oral trush),

infeksi virus yang berat (hemoragik varicella), dan wasting (marasmus). Temuan

laboratorium juga menunjukkan bukti bahwa CD4 menurun.

Pada anak dengan HIV / AIDS, pemulihan yang baik dari gizi buruk

adalah mungkin meskipun mungkin memakan waktu lebih lama dan kegagalan

pengobatan mungkin terjadi. Intoleransi laktosa terjadi pada parah diare kronis

terkait HIV. Pengobatan harus sama seperti untuk anak HIV negatif.15

Infeksi virus berulang atau sangat berat, seperti herpes simpleks berulang

atau disebarluaskan atau infeksi zoster atau sitomegalovirus (CMV) retinitis,

terlihat dengan defisiensi kekebalan seluler sedang hingga berat.3 Pasien ini juga

didiagnosis dengan hemoragik varicella. Hemoragik varicella merupakan varicella

yang berat yang dapat ditemukan dalam beberapa kasus, seperti pada anak dengan

immunocompromised. Anak-anak dengan status immunocompromised beresiko

untuk varicella yang parah dan rumit dan tingkat kematian mereka lebih tinggi

dari pada anak-anak imunokompeten.18

Pada pasien ini, agen antivirus diberikan untuk hemoragik varicella.

Jika rekomendasi diterapkan, anak-anak dengan marasmus harus diatasi

dengan cepat, berat badan secara teratur, dan kembali ke status perkembangan

yang sesuai dengan usia. Biasanya, respon yang buruk terhadap pengobatan

karena asupan yang tidak memadai atau infeksi yang mendasarinya, terutama HIV

atau TB. Namun, respon yang buruk terhadap terapi memerlukan penilaian ulang

lengkap dari situasi, bukan hanya menambahkan obat atau zat gizi mikro, yang

biasanya tidak efektif.1

Prognosis tergantung pada usia serta lama dan tingkat keparahan

kekurangan gizi, dengan anak-anak muda yang memiliki tingkat tertinggi

komplikasi jangka panjang dan kematian.19 Kecuali untuk komplikasi, prognosis

marasmus berat baik jika pengobatan dan perawatan tindak lanjut yang benar

dilakukan.1 Kematian biasanya disebabkan oleh infeksi (misalnya, diare dan

dehidrasi, pneumonia, sepsis gram negatif, malaria, infeksi saluran kemih) atau

penyebab lainnya (misalnya, gagal jantung terkait dengan anemia, kelebihan

larutan rehidrasi, atau kelebihan protein dalam hari-hari pertama pengobatan;

hipotermia; hipoglikemia; hypokalemia; hipofosfatemia).1 Selain itu, infeksi HIV

dikaitkan dengan prognosis yang buruk.13

Kematian anak-anak yang dirawat di rumah sakit dengan marasmus yang

tinggi, khususnya selama beberapa hari pertama rehabilitasi. Tingkat mortalitas

dapat bervariasi dari kurang dari 5% hingga lebih dari 50% anak, tergantung pada

kualitas perawatan.1 Selain itu, anak HIV-positif secara bermakna lebih mungkin

meninggal dibandingkan anak negatif.20

Dalam kasus ini, diagnosis pasien adalah marasmus dengan infeksi HIV

yang mendasarinya dan dikaitkan dengan prognosis buruk.

REFERENCES

1. Rabinowitz, S. S. Marasmus. 2012. Available at:

http://emedicine.medscape.com/article/984496-overview#showall

2. Global Summary of the AIDS Epidemic. 2011. Available at:

http://www.who.int/hiv/data/2012_epi_core_en.png

3. Greenfield, R. A. Pediatric HIV Infection. 2012. Available at:


4. Millennium Development Goals (MDGs). Available at:

http://www.alliance2015.org/fileadmin/user_upload/MDGs.pdf

5. Papadopoulus, A. J. Chickenpox. 2012. Available at:


6. American Academy of Pediatrics. Summaries of Infectious Disease:

Varicella-Zoster Infections. 2009. Available at:

http://redbookarchive.aappublications.org/cgi/content/extract/2009/1/3.150

7. World Health Organization (WHO). Water Sanitation Health: Water-related

Diseases; 2013. Available at:

http://www.who.int/water_sanitation_health/diseases/malnutrition/en/

8. De Lange, J. C. Factors Contributing to Malnutrition in Children 0-60 Months

Admitted to Hospitals in the Northtern Cape. [Dissertation]. Bloemfontein,

South Africa: Faculty of Health Sciences, Department of Nutrition and

Dietetics University of the Free State; 2010.

9. Maxwell, S. Module 5: Causes of Malnutrition. In Harmonised Training

Package (HTP): Resource Material for Training on Nutrition in Emergencies.

Version 2.Oxford: Emergency Nutrition Network (ENN); 2011.

10. Food Security and Nutrition. Conceptual Framework of Malnutrition.

Cambodia: Council for Agricultural and Rural Development; 2011. Available

at: http://www.foodsecurity.gov.kh/conceptual-framework-malnutrition

11. Owor, M., Tumwine, J. K., and Kikafunda, J. K. Socio-Economic Risk

Factors for Severe Protein Energy Malnutrition among Children in Mulago

Hospital, Kampala. East African Medical Journal. 2000 September; 77(9).

xx

12. Rolfes, S. R., Pinna, K., and Whitney, E. Chapter 6. Protein: Amino Acids.

In Understanding Normal and Clinical Nutrition. Eighth Ed. Canada:

Wadsworth Cengage Learning; 2009. p. 196-198.

13. Scheinfeld, N. S. Proein-Energy Malnutrition. 2013. Available at:


14. Shashidhar, H. R. Malnutrition. 2013. Available at:


15. Ashworth, A., Khanum, S., Jackson, A., and Schofield, C. Guidelines for the

Inpatient Treatment of Severely Malnourished Children. Geneva: World

Health Organization (WHO); 2003.

16. World Health Organization (WHO). Of Severe Malnutrition: A Manual For

Physicians And Other Senior Health Workers. Geneva: World Health

Organization (WHO); 1999.

17. Gracia-Prats, A. J., McMeans, A. R., and Ferry, G. D. Nutrition and

HIV/AIDS.

18. Bechtel, K. A. Pediatric Chickenpox Clinical Presentation. 2012. Available

at: http://emedicine.medscape.com/article/969773-clinical#showall

19. Encyclopedia of Children’s Health. Marasmus. Encyclopedia of Children’s

Health; 2013. Available at:

http://www.healthofchildren.com/M/Malnutrition.html

20. Maayer, T. D. The Impact of HIV on Severe Childhood Malnutrition.

[Thesis]. Johannesburg: Faculty of Health Sciences, University of the

Witwatersrand; 2010.