Analisis Gas Darah Dan Pem Lab Neonatus

7/26/2019 Analisis Gas Darah Dan Pem Lab Neonatus

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GANGGUAN KESEIMBANGAN

ASAM BASA, CAIRAN, DAN

ELEKTROLIT

dr. Agustyas Tjiptaningrum, SpPK


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Acid Base Disorders


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ACID-BASE REGULATION

The body attempts to maintain a pH

between 7.35 and 7.43 (hydrogen ionconcentration between 35 and 45 nmol/L.

This is achieved despite considerable

variation in acid-base intake


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Elimination of volatile acids

Volatile hydrogen ion are eliminated by

the lungsas CO2 based on:

H+

+ HCO3-

H2CO3 CO2+ H2O


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Sources of nonvolatile acids

Diet, about 30 mEq of H ion is added to the

body daily. (this can increase with a very

high animal protein intake)

Incomplete metabolism, about 30mEq/day

(ketoacids,betahydroxybutyrate etc)

Stool loss of Bicarbonate, around 20mEqbicarbonate is lost in stools daily.


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Elimination of acid-baseLungs.

The lungs eliminatea large amount of volatileacidas CO2.This can be greatly increased ormodestly decreased if the lungs are normal.

Kidneys.

Acid excretionand alkali excretionNormallythe kidneys are called on to excrete 70 to 100

mEq acid/day. This can be reduced to 0 orincreased to fourfold. If faced with an alkalineload,the kidneys can excrete hundreds mEq ofbicarbonate.


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Abnormal States

Lungs: Abnormalities can lead to reducedCO2or too much CO2.

Kidneys: Deficient or excess H ion excretion.Excess HCO3regeneration or loss.

Metabolic abnormalities: Diabetes, poor

tissue perfusion, anaerobic metabolism.Gastrointestinal abnormalities: Vomiting,diarrhea.


8/64Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Buffer systems

Respiration Renal function

Maintain tight control within range 7.35 7.45

Disturbances of Acid-base Balance


9/64Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.11a

The Central Role of the Carbonic Acid-Bicarbonate Buffer System in the Regulation of

Plasma pH


10/64Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.11b

The Central Role of the Carbonic Acid-Bicarbonate Buffer System in the Regulation of

Plasma pH


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Measurements and Calculations

Hydrogen concentration (pH)

Bicarbonate concentration (HCO3)

pCO2

Anion Gap (AG).


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The bodys buffer system.

Carbonic acidbicarbonate system

Hemoglobin

Protein


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The HendersonHasselbalch

equation

Clinically, the carbonic acidbicarbonate

system is most important. By applying

the law of mass action to the followingreaction:

CO2+ H2O H2CO3H++HCO3

-

one obtains the classic equation:

pH = 6.1 + log [HCO3] / pCO2


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The HendersonHasselbalch

equation

The classic equation:

pH = 6.1 + log [HCO3] / pCO2

The practical equation:[H+] = 24 x pCO2 / [HCO3

-]

pH = 7.40

[HCO3-] = 24 mEq/L[H+] = 40 nmol/L

pCO2= 40 mmHg


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Specific Disturbances

Metabolic acidosis (a fall in pH and adecrease in HCO3-)

Metabolic alkalosis (a rise in pH and anincrease in HCO3-)

Respiratory acidosis (a fall in pH resulting

from a primary increase in pCO2)Respiratory alkalosis (a rise in pH from adecrease in pCO2)


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Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.6

Figure 27.6 The Basic Relationship between PCO2and Plasma pH


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Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory acid-base disorders

Result when abnormal respiratory function

causes rise or fall in CO2in ECF Metabolic acid-base disorders

Generation of organic or fixed acids

Anything affecting concentration ofbicarbonate ions in ECF

Acid-Base Disorders


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Respiratory acidosis Results from excessive levels of CO2in body

fluids

Respiratory alkalosis Relatively rare condition

Associated with hyperventilation

Respiratory acid-base disorders


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Compensation.

Metabolic disorders:

The pulmonaryresponsewill attempt to

correct the pH.Respiratory correction occurs

immediately.

Respiratory disorders:The kidneys regulatesbicarbonate levels

It takes several hoursto respond


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Respiratory Acid-Base Regulation

Figure 27.12a


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Respiratory Acid-Base Regulation

Figure 27.12b


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Incomplete Compensation

When compensation failsto occur, it is

because of disease in that system.

This is then termed a mixed or combined

disorder


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Anion Gap

In the blood, when measured, cations

seem to exceed anions in number. This

is due to the plasma proteins, thedifference amounts to about 1012

mEq/L.

Anion Gap = [Na+](Cl-+ HCO3-)


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Anion Gap

An increased AG alwaysmeans a

metabolic acidosisis present.

An increased AG implies that the cause of

acidosis must be retention of some acid

other than HCl.


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Metabolic Acidosis

Metabolic acidosis results from three

types of disorders:

excess acid load

decreased acid excretionby the

kidney

alkali (bicarbonate) loss


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Metabolic acidosis

Normal AG(hyperchloremic metabolic acidosis)

A. Excess intake (HCl, NH4Cl)

B. Bicarbonate loss1. GI tract

Diarrhea

Fistulas

2. Proximal renal tubular acidosis

C. Decreased renal acid secretion. (distalrenal tubular acidosis)


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Metabolic acidosis

Increased AG

A. Ketoacidosis

1. Diabetes mellitus

2. Alcohol

B. Lactic acidosis (usually due to shock)

C. Poisons

D. Renal failure

M t b li id b di d


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Major causes of metabolic acidosis are:

Depletion of bicarbonate reserve

Inability to excrete hydrogen ions at kidneys

Production of large numbers of fixed / organic

acids Bicarbonate loss due to chronic diarrhea

Metabolic alkalosis

Occurs when HCO3-concentrations becomeelevated

Caused by repeated vomiting

Metabolic acid-base disorders

Th R t M t b li A id i


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The Response to Metabolic Acidosis


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Workup of metabolic acidosis.

high pH

Respiratory alkalosis

Increased Gap

ketoacidosis

lactic acidosis

uremia

Normal Gap

Renal tubular acidosis

GI disease

Acid intake

2. Determine AG

low pH

Metabolic acidosis

1. Measure pH

low Bicarbonate


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Workup of normal AG

metabolic acidosis1. Serum K

Decreased Increased or Normal :Early uraemic acidosis

Obstructive nephropathy

Mineralocorticoid deficiency

Infusion / ingestion: HCl, NH4Cl2. Urinary pH

pH >5.5 pH


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Metabolic Alkalosis


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Causes of metabolic alkalosis

HCl loss

a. Gastrointestinal

b. Increased urine acidification

Excess alkali intake

a. Alkali abuse

b. Treatment of acidosis

Severe potassium depletion


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Primary causes of alkalosis

ECV

Vomiting/Diuretics

Aldosterone BicarbonateReabsorbtion

H+secretion

Alkalosis

HCl

Alkalosis

Vomiting/Diuretics

KCl

H+Shift

into cells


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Secondary causes of alkalosis

K

Depletion

ECF

Contraction

AKALOSIS

Shift H+Into cells

Proximal TubuleBicarbonate

Reabsorbtion

Acid

Urine

Aldosterone

Exchange Na for

H in Distal

Tubule

Exchange Na for

K in Distal

Tubule


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Workup of metabolic alkalosis

low pH

Respiratory acidosis

ECV depletion

a. GI losses

b. Diuretics

c. severe K depletion

ECV normal

a. aldosteronism

b. alkali intake

c. severe K depletion

2. Assess ECV

a. history

b. exam

c. urine Na

high pH

Metabolic alkalosis

1. measure pH

elevated Bicarbonate


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Respiratory disorders

Respiratory Acidosis

This disorder results from hypoventilation.

Because chemical buffering is limited.Acute respiratory failureis associated with

severe acidosiswith little increasein plasma

bicarbonate.

Chronic respiratory failurecauses increased

renal generation of bicarbonate.


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Causes of respiratory acidosis

Depression of respiratory centerStroke, Tumors, Encephalitis, Drugs

Limitation of chest wall movementNeuromuscular disorders, Trauma, Surgery, Fixation of ribs

Pulmonary diseaseChronic bronchitis, Chronic emphysema, Asthma, Pneumonia


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Depression of respiratory

centerStrokes

Tumors

Encephalitis

Drugs : narcotics

sedatives

tranquilizers


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Limitation of chest wall

movementNeuromuscular disorder :

myasthenia gravis

GuillainBarrtetanus

Trauma and surgery

Fixation of ribs


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Pulmonary disease

Chronic bronchitis

Chronic emphysema

Asthma

Pneumonia


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Respiratory alkalosis

This disorder results from hyperventilationdue

to a variety of causes.

Acute hypocapniacauses release of Hionsfrom tissue buffers, this tends to minimizethe

reduction of plasma bicarbonate.

Chronic hypocapniastimulates renaladaptation

with reduced bicarbonate generation, thuslowering plasma bicarbonateconcentration.


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Causes of respiratory

alkalosisDirect stimulation of respiratory center.

Psychogenic, CNS disease, Sepsis, Hypermetabolic state,

Exercise, Liver failure, Drugs

Reflex stimulation of respiratory center.Pneumonia, Pulmonary edema, Pulmonary fibrosis, Asthma,

Cyanotic heart disease

Excessive mechanical ventilation

Direct stimulation of respiratory


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Direct stimulation of respiratory

center

Psychogenic

CNS disease : stroke, encephalitis

SepsisHypermetabolic state: fever, thyrotoxicosis.

Exercise

Liver faillureDrugs: salicylates, ammonia, progesterone

Reflex stimulation of respiratory


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Reflex stimulation of respiratory

center

Pneumonia

Pulmonary edema

Pulmonary fibrosis

Asthma

Cyanotic heart disease

Detection of acidosis and alkalosis


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Diagnostic blood tests

Blood pH

PCO2 Bicarbonate levels

Distinguish between respiratory and metabolic

Detection of acidosis and alkalosis

A Diagnostic Chart for Acid-Base Disorders


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A Diagnostic Chart for Acid-Base Disorders

Aging and Fluid Electrolyte and Acid-base


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Reduced total body water content

Impaired ability to perform renal compensation

Increased water demands

Reduced ability to concentrate urine Reduced sensitivity to ADH/ aldosterone

Net loss of minerals

Inability to perform respiratory compensation

Secondary conditions that affect fluid, electrolyte, acid-base balance

Aging and Fluid, Electrolyte, and Acid-baseBalance


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KESIMPULAN


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KESIMPULAN

Terdapat 4 macam gangguan keseimbangan asam basa :

1. Asidosis metabolik pH, [HCO3-]akibat keluarnya bicarbonat dari tubuhatau penambahan hidrion yg akan bereaksi dg bicarbonat asam karbonat CO2 dan H2O

2. Alkalosis metabolikpH , [HCO3-]akibat hilangnya HCL mll muntah atau

sekresi lambung

3. Asidosis respiratorikpH, PCO2 hipoventilasi

4. Alkalosis respiratorik pH , PCO2hiperventilasi

Tubuh akan mengkompensasi setiap gangguan keseimbangan asam basa

GANGGUAN METABOLIK Baik asidosis maupun alkalosis respon paru

Asidosis hiperventilasi PCO2 , [H+]

Alkalosis hipoventilasi PCO2 , [H+] kembali N kompensasi ini terba

tas karena dapat menyebabkan hipoksia (PO2


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KESIMPULAN

GANGGUAN RESPIRATORIK

Kompensasi oleh ginjal pengaturan kadar bikarbonat Asidosis respiratorik produksi dan retensi HCO3-

Alkalosis respirarorik ekskresi HCO3-, [HCO3-] plasma pH N

Kompensasi oleh ginjal berjalan lambat (beberapa jam)

Bila kompensasi tidak komplet gangguan asam basa

Anion Gap perbedaan kation mayor (sodium) dan anion mayor (Cl dan bikarbonat)

AG asidosis metabolik retensi asam selain HCL

GANGGUAN KOMPENSASIAsidosis metabolik

Alkalosis metabolik

Asidosis respiratorik akut

Alkalosis respiratorik akut

Asidosis respiratorik kronik

Alkalosis respiratorik kronik

Setiap 1 mEq [HCO3-], PCO2 1-1.3 mmHgSetiap 1 mEq [HCO3-], PCO2 0.6 mmHgSetiap 1 mm PCO2 , [HCO3-] 0.1 mEqSetiap 1 mm PCO2 , [HCO3-] 0.2 mEqSetiap 1 mm PCO2 , [HCO3-] 0.35 mEqSetiap 1 mm PCO2 , [HCO3-] 0.5 mEq


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PEMERIKSAAN LABORATORIUM

PADA NEONATUS


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Ikterus neonatorum

Ikterus neonatorum secara fisiologis dapat terjadi

akibat:

Peningkatan produksi bilirubin karena pemecahan

eritrosit masa janin (fetal erythrocyte) karena

masa hidup fetal erythrocyte memendek Kapasitas ekskresi hepar untuk bilirubin ini masih

rendah pada neonatus karena masih sedikitnya jumlah

protein yang mengikat bilirubin untuk dibawa masuk

ke hepar dan masih rendahnya aktivitas enzim

glucoronyl transferase

IKTERUS NEONATORUM


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IKTERUS NEONATORUM

Kuning pada bayi baru lahir akibat penimbunan bilirubin

unconjugated pada kulit dan sklera

ETIOLOGI

ONSET < 24 JAM

1. Biasanya patologik2. Sering pd

inkompatibilitas

ABO rhesus

3. Bukan sepsis

4. Inkompatibilitas

golongan darahyang lain

5. Defisiensi G6PD

6. Defek membran

eritrosit (sferositosis

herediter

ONSET > 10 HARI

1. Conjugatedhyperbilirubinemia

hepatitis neonatal

idiopatik, TORCH, VHB,

malformasi condenital

spt atresia biliar, defisiensi

AAT-1, atau GSD tipe IV2. Sepsis

3. Hipotiroid

4. Hemolisis

5. Ikterik akibat ASI

ONSET 24J-10 HARI1. Fisiologis

2. Sepsis

3. Hemolisis

4. Polisitemia

5. Perdarahan

6. Peningkatansirkulasi

enterohepatik

pada obstruksi

usus

Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.

Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9 6


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PATOGENESIS

Produksi sepertipada perdarahan

atau hemolitik

intravaskuler Ambilanoleh hati

Sirkulasi

enterohepaptikGangguan aliran

empedu padakolestasis

Gangguanekskresibilirubin

Konjugasioleh hati

Merckmanual. Neonatal hyperbilirubinemia. 2009. Diunduh dari: http://www.merckmanuals.com.Pada tanggal 29 Desember 2010

PATOFISIOLOGI
http://www.merckmanuals.com/http://www.merckmanuals.com/http://www.merckmanuals.com/


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Kern icterus

Bilirubin unconjugated >>>

Kapasitas albumin untuk

mengikat terbatas

Neurotoksik

PATOFISIOLOGI

Bilirubin unconjugated bebas(larut dalam lipid membran sel)

Menembus sawar otak

Merckmanual. Neonatal hyperbilirubinemia. 2009. Diunduh dari: http://www.merckmanuals.com. Pada tanggal 29 Desember 2010

Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010
http://www.merckmanuals.com/http://www.merckmanuals.com/


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GEJALA KLINIK

Bila terdapat bilirubin encephalopathy terdapat gejala:

Hipotonia

Letargi Kejang

koma

PEMERIKSAAN FISIK

Ikterik pada sklera dan kulitPenilaian derajat ikterik menggunakan Kramers rules

Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9.

American Academic of Pediatrics. Clinical practice guidelines:management of hyperbilirubinemia in the newborn infant 35 or more weeks gestation. Pediatrics. 2004;114(1):297-316.

( mg/dL) 5,9 8,8 11,7 14,6 >14,6



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1. KIMIA:

Bilirubin total, direk, dan indirek2. HEMATOLOGI

Hematologi lengkap

Gambaran darah tepi

Retikulosit

Golongan darah ABO/rhesus

Coombstest

G6PD3. URINALISIS

4. KULTUR bila dicurigai sepsis

Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9.


DIAGNOSIS


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DIAGNOSIS

Diagnosis ditegakkan berdasarkan anamnesis, pemeriksaan fisik, dan

pemeriksaan laboratorium

Indikasi pemeriksaan billirubin serum :

1. Ikterik tampak pada 24 jam pertama neonatus

2. Ikterik tidak sesuai dengan umur neonatus

3. Keraguan derajat ikterus, terutama kulit gelap

4. Ikterik berkelanjutan hingga 2 minggu (aterm) dan > 3 minggu (preterm)

5. Ikterus pada neonatus dengan kondisi klinis yang tidak baik Mencari faktor risiko :

1. Hemolitik isoimun

2. Defisiensi G6PD

3. Asfiksia

4. Letargi

5. Suhu tubuh tidak stabil

6. Sepsis

7. Asidosis

8. Kadar albumin serum


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Resiko sedang

1. Neonatus cukup bulan

(>38 minggu) dengan

faktor risiko

2. Neonatus kurang bulan(35-37 6/7 mgg) sehat

Risiko Neonatus



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DETEKSI HIPOTIROIDISME PADA NEONATUS

Prevalensi hipotiroidism pada neonatus sekitar 1dalam 3000-5000

Deteksi dini hipotiroidism pada neonatus sangatpenting untuk mengeliminasi retardasi mental beratakibat defisiensi hormon tiroid

Pemeriksaan untuk skrining hipotiroid pada neonatusadalah TSH dan T4 darah

Bahan pemeriksaan dry blood spot atau darah talipusat

Pada bayi dengan berat badan lahir yang sangatrendahdisarankan pengulangan tes pada 2minggu dan 4-6 minggu berikutnya untuk mendeteksilate-onsettransient hypothyroidism

Henryjs clinical laboratory


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DETEKSI HIPOTIROIDISME PADA NEONATUS

Nilai rujukan pada initial TSH tali pusat 20 mIU/L maka perlu

dilakukan evaluasi endokrin untuk menegakkandiagnosis hipotiroid neonatus

False positive pada pem T4 dapat terjadi prematur

atau kelainan kongenital berupa tidak terdapatnya

TBG sehingga pemeriksaan T4 saja tidak cukupuntuk menegakkan diagnosis hipotiroid tapi harus

disertai dengan pemeriksaan TSH

Henryjs clinical laboratory


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SEPSIS NEONATORUM

Sepsis terjadi bila terdapat bakteriemia

Pemeriksaan laboratorium pada sepsis neonatorum

adalah:

Pemeriksaan darah lengkap neutrofilia shift to theleft

IT ratio yaitu ratio antara Immature-TotalNeutrophilnormal


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Analisis Gas Darah Dan Pem Lab Neonatus