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CPC

Laki-laki, 21 tahun dengan Ketoasidosis

Diabetikum, DM Tipe 1 dan Pneumonia

dr. Lia Sasmithae*

Dr. Laksmi Sasiarini, Sp.PD**

*Resident of Internal Medicine, Medical Faculty of Brawijaya University - Saiful Anwar GeneralHospital Malang

** Supervisor, Endocrine & Metabolic Disease, Internal Medicine Department BrawijayaUniversity- Saiful Anwar General hospital Malang


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KAD

Manifestasi awal dari DM tipe 1

infeksi, trauma, infark miokard, atau kelainan lainnya

hiperglikemia, asidosis metabolik, dan ketosis

Ketoasidosis diabetikum


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Kriteria KAD


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Patofisologi KAD


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DM tipe 1


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DM tipe 1


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Pneumonia


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Summary of Database

Mr. Supriadi, 21 years old, W. 26ward 27

Chief complaint : decrease of conciousness

Anamnesis : auto and heteroanamnesis (his older sister)

Patient suffered from decreased of consciousness, since 4 days before admission

and worsened a day before admission, gradually. He was found in weak condition

and couldnt be able to communicate well. Because of this complaint, he was

brought to Tumpang public health centre and his random blood sugar was about

600. That was the first time his family knew about the high blood sugar in the

patient.

Patient never knew that he had diabetes. But around 2 months before admission,

he started to feel thirsty easily. He drank a lot and his appetite increased. Patient also suffered from nausea and vomiting since 10 days before admission. He

vomit 2-3x/day, - glass/vomit, contained of fluid and food residual. At home, it

wasnt accompanied with blood nor mucous. But at ER, there was blood in his

vomiting.


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He also suffered from low grade fever since 20 days before admission,

intermittently, and relieved by drug that be given from a midwife. The fever

worsen at night and made him sweat a lot. His tongue was formed white plague

that painless. It was removed easily. Patient consumed Adem Sarito relieve it, but

there was no improvement.

Sometimes he had cough with whitish sputum. It was started since about a month

before admission.

His body weight decreased about 7 Kg in a month.

Family history:

Patients father died 15 years ago and he had diabetes.

Social history:

Patient was an employee in cassava factory, hasnt married yet. He denied about

multi partner sexual, alcohol consumption, nor intravenous drug usage.


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Physical ExaminationGeneral appearance : looked severely ill

GCS: 224 (ER)

At ward: 456

Patient looks underweight

Height: 165 cm

Weight: 50 KG BMI: 18.36 m2

BP : 110/70 mmHg PR : 96 bpm, strong,

regular

RR : 20 tpm Tax : 37 0C

Head Anemic (-) , icteric (-)

White plague at tongue, removed easily

Neck JVP R+0 cm H2O, 30 degree

Lymph node englargement (-)

Thorax : Cor Ictus invisible and palpable at ICS V MCL sinistra

LHM ~ ictus, heart waist + RHM: SL D

S1, S2 single with no murmur

Pulmo Symmetric, SF D = S, v v Rh - - Wh - -

v v - - - -

v v - - - -

Abdomen Flat, soefl, bowel sound N, liver span 8 cm, traubesspace tymphani

Extremities Warm acrals, CRT< 2, edema (-)


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b f d


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Laboratory finding

Lab Value Lab ValueLeukocyte 15,050 3.500-10.000/L Natrium

Osmolality

Na

Corrected

125

300

131

136-145 mmol / L

280-295 mOsm/kg

Haemoglobine

MCV

12.7

78.8

11,0-16,5 g/dl

80-97

Kalium 4.26 3,5-5,0 mmol / L

MCH 29.6 26,5-33,5 Chlorida 110 98-106 mmol / L

PCV

Trombocyte

Eo/Ba/Neu/Ly/

MoSGOT

SGPT

33.8

215,000

0.1/0.1/80.

0/12.0/7.248

25

35-50%

146.000-

390.000/L

0.4/0.1/51-67/

25-33/2-50-40 U/L

0-40 U/L

RBS 682

442

16998

171

< 200 mg/dL

Ureum 66.7 10-50 mg/dL BUN/Cr 22.26

Creatinine 1.40 0,7-1,5 mg/dL eGFR 67.99 mL/min/1.73 m2


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LAB VALUE LAB VALUE

Urinalysis Yellow, clear 10 x

PH 6.0 Epithelia 2.2

SG 1.015 Cylinder -

Glucose 3+ Hyaline -

Protein trace Granular -

Keton 2+ Leukocyte -

Bilirubin - Erythrocyte -

Urobilinogen - 40 xNitrite - Erythrocyte 10.2

Leucocyte - Leukocyte 3.0

Erythrocyte 3+ Crystal -

Bacteria 36.3 x 103

URINALYSIS


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BGA

O2 10 lpm via NRBM

PH 6.99 7.35-7.45PCO2 20.3 3545 mmHgPO2 163.4 80100 mmHgHCO3 5.0 2128 m mol/LO2 sat Art 97.5 > 95 %BE -26.8 (-3) - (+3) m mol/LTrue O2 38.1

Anion Gap 10.0 mEq/L

Conclusion: Severe acidosis metabolic partially

compensated with alkalosis respiratory and severe

hypoxemia


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ECG


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ECG

Sinus rhythm, Heart rate 100 bpm

Frontal Axis : normal

Horizontal Axis : normal

PR interval : 0.12

QRS complex : 0.08

QT interval : 0.36

Conclusion: Sinus rhythm with HR 100 bpm.


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CHEST X RAY


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CXR

AP position, symmetric, enough KV, enoughinspiration

Soft tissue and bone were normal

Trachea was in the middlle

Hemidiaphragm D/S were in domeshaped

Phrenicocostalis angle D/S were sharp

Cor: site was normal, size CTR 45%, shape was normal

Pulmo: bronchovascular pattern was normal

Conclusion : normal chest X-ray


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Dari anamnesa, pemeriksaan fisik dan

pemeriksaan penunjang, didiagnosa :1. Ketoasidosis diabetikum

2. DM tipe 1

3. hiponatremia hipoosmolar hypovolemia

3.1 dt no 1

3.2 GI loss

4. dyspepsia syndrome4.1 DM Gastroparese

4.2 SMRD

5. Lung infection

5.1 pneumonia

5.2 lung TB with secondary infection

6. Azotemia prerenal6.1 dt no 1

6.2 azotemia renal

6.2.1 Diabetic kidney disease


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20/04/2014; 01:00

RBS: High (lab: 682)Na/K/Cl: 125/4.26/110

BGA:

Ph: 6.99

HCO3: 5.0

Anion Gap: 10.0

Planning therapyRehydration 1L of NS

0,9% over first 1 h

Insulin short acting 0.1U/kg5iu (iv)

Line I: drip Insulin shortacting 0.1U/kg/hour (5

iu/hour)Line II: drip KCl 25 mEq

in 500 cc NaCl 0.9%

20/04/2014; 05:30

RBS: 442

Planning therapy

Line I: drip Insulin

short acting

0.1U/kg/hour (5

iu/hour)

Line II: drip KCl 25

mEq in 500 cc NaCl

0.9%

20/04/2014; 11:00

RBS: 98

Na/K/Cl: 133/3.11/119

BGA:

Ph: 7.24

HCO3: 8.8

Anion Gap: 5.2

Planning therapy

drip insulin was

stopped


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20/04/2014; 12:00RBS: 169

Na/K/Cl: 133/3.11/119

BGA:

Ph: 7.24

HCO3: 8.8

Anion Gap: 5.2

Planning therapy

Line I: drip Insulin short

acting 0.05U/kg/hour

(1 iu/hour)

Line II: drip KCl 25 mEq

in 500 cc NaCl 0.9%

20/04/2014; 15:00

RBS: 176

Na/K/Cl: 132/3.2/124

BGA:

Ph: 7.25

HCO3: 9.5

Anion Gap: 1.7

Planning therapy

Line I: drip Insulinshort acting0.05U/kg/hour (1iu/hour)

Line II: drip KCl 25mEq in 500 cc NaCl0.9%

20/04/2014; 21:00RBS: 179

Na/K/Cl: 134/4.30/122

BGA:

Ph: 7.28

HCO3: 9.8

Anion gap: 6.5

Planning therapy

Line I: drip Insulin shortacting 0.05U/kg/hour (1iu/hour)

Line II: drip KCl 25

mEq in 500 cc NaCl0.9%


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Diskusi

Pada pasien ini didiagnosa KAD karena:

Keton urin :+2 (ketosis)

BGA : asidosis metabolik (pH 6,99, HCO3:5,BE: -26,8, anion Gap: 10

GDA: 682 mg/dl

leukosit 15.050/L + tanda-tanda infeksi paru


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Infeksi yang paling sering menjadi penyebab KADadalah infeksi saluran kemih dan pneumonia.

infeksi ringan seperti skin lession atau infeksitenggorokan.

pasien ini didapatkan keluhan berupa demam, batuk,keringat malam, penurunan berat badandidiagnosasementara sebagai TB paru dengan sekunder infeksi(pneumonia)


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Dasar diagnosa DM tipe 1 :

penderita baru >50%: 20 tahun (pasienberusia 21 tahun)

penurunan beratbadan, polidipsia,dan

hiperglikemia

pasien mengalamipenurunan berat 7 kgdalam sebulan, cepatmerasa haus, danpernah periksa ke

puskesmas dengangula darah 600mg/dl)


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Prinsip Terapi

1. Terapi cairan

Prioritas utama pada penatalaksanaan KAD adalah terapi cairan.Terapi insulin hanya efektif jika cairan diberikan pada tahap awalterapi dan hanya dengan terapi cairan saja akan membuat kadargula darah menjadi lebih rendah. Studi menunjukkan bahwa selama

empat jam pertama, lebih dari 80% penurunan kadar gula darahdisebabkan oleh rehidrasi. Oleh karena itu, hal penting pertamayang harus dipahami adalah penentuan difisit cairan yang terjadi.Beratnya kekurangan cairan yang terjadi dipengaruhi oleh durasihiperglikemia yang terjadi, fungsi ginjal, dan intake cairan penderita.

(Pada pasien ini dilakukan rehidrasi menggunakan cairan NS 0,9%

sebanyak 1 liter selama 1 jam di UGD)


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Cairan fisiologis (NaCl 0,9%) diberikan dengankecepatan 15-20 ml/kgBB/jam atau lebih selama jampertama ( 1 - 1,5 liter). Sebuah sumber memberikanpetunjuk praktis pemberian cairan sebagai berikut: 1liter pada jam pertama, 1 liter dalam 2 jam berikutnya,kemudian 1 liter setiap 4 jam sampai pasienterehidrasi.

Sumber lain menyarankan 1 -1,5 lt pada jam pertama,selanjutnya 250-500 ml/jam pada jam berikutnya.2

Petunjuk ini haruslah disesuaikan dengan status hidrasipasien. Pilihan cairan selanjutnya tergantung daristatus hidrasi,kadar elektrolit serum, dan pengeluaranurine


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2. Terapi Insulin

Sejak pertengahan tahun 1970-an protokolpengelolaan KAD dengan drip insulin intravena

dosis rendah mulai digunakan dan menjadipopular. Cara ini dianjurkan karena lebih mudahmengontrol dosis insulin, menurunkan kadarglukosa darah lebih lambat, efek insulin cepat

menghilang, masuknya kalium ke intrasel lebihlambat, komplikasi hipoglikemia dan hipokalemialebih sedikit.


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Pada pasien diberikan terapi Insulin

Insulin short acting 0.1 U/kg5iu (iv)

Line I: drip Insulin short acting 0.1 U/kg/hour(50 iu in 500mL NS 0,9% 50 mikrodrip/mnt5iu/h)Line II:If initial K


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Kriteria resolusi KAD

Kriteria resolusi KAD diantaranya adalah

kadar gula darah < 200 mg/dl, serum

bikarbonat 18 mEq/l, pH vena > 7,3, dan anion

gap 12 mEq/l.

(pada pasien ini sulit dimonitor resolusi dari KAD

karena pasien menolak untuk diperiksa kadar

gula darah, BGA dan SE rutinkarena faktor

biaya)


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3. Penatalaksanaan terhadap Infeksi yang Menyertai

Antibiotika diberikan sesuai dengan indikasi, terutamaterhadap faktor pencetus terjadinya KAD. Jika faktorpencetus infeksi belum dapat ditemukan, maka

antibiotika yang dipilih adalah antibiotika spektrumluas

(pada pasien ini saat masuk diberikan ceftriaxone 2 x 1gr sampai (H4) kemudian diganti dengan infusciprofloxacin 2 x 400 mg (intravena)) sumber infeksipada pasien dicurigai berasal dari lung infection


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28 April 2014

Kondisi pasien dilaporkan memburuk secaramendadak, pasien dilaporkan apnue, penurunankesadaranmeninggal

Diagnosa kematian :1. Aspirasi

2. Septic DIC

3. Intracranial bleeding

4. Hematologic malignancy


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PROGRESS NOTE

Blood Gas Analyse


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Blood Gas AnalyseBGA Value (O2 NRBM 10 lpm)

Blood Gas Analysis

Tanggal Normal 20/4 21/4 22/4 23/4

Jam 00:47 08:37 14:46 20:12 05:23 13:00 13:38 21:57 06:24 05:57

Oksigen Lpm 10 10 10 10 10 10 10 10 10 10

PH 7,35-7,45 6,99 7,24 7,25 7,28 7,25 7,30 7,32 7,34 7,36 7,38PCO2 35-45 20,3 20,5 21,5 20,6 19,1 19,9 19,1 20 20,4 23,3PO2 80-100 163,4 242,6 196,2 247,8 114,3 175,5 185 167,5 174,1 186,3HCO3 21-28 5 8,8 9,5 9,8 8,4 13,8 14,1 10,8 11,6 17,1Base Excess -3 until +3 -26,8 -18,8 -17,9 -17,2 -19,4 -14,3 -13,7 -15,2 -14 -9,4O2

saturation

True O2> 95% 97,5

34,66

99

51,46

98,3

41,61

99,1

52,56

98,4

24,23

99,1

37,22

96

38,24

98,8

35,53

94,1

36,93

96,6

39,51

Serum Electrolyte

Jam Normal 01:27 - 12:25 21:03 02:10 14:04 14:38 22:26 06:11 06:17 20:12

Na 136-145 125 - 135 132 134 131 130 128 128 133 121

K 3,5-5,0 4,26 - 3,10 3,20 3,62 5,27 3,59 3,39 3,16 3,39 2,56

Cl 98-106 110 - 134 124 122 128 125 123 119 114 121

Anion Gap 10 8,5 1,8 2,4 10,8 9,1 5,5 2,8 2

Blood Gas Analyse


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Blood Gas AnalyseBGA Value (O2 NRBM 10 lpm)

Blood Gas Analysis

Tanggal Normal 24/4 25/4 26/4

Jam

Oksigen Lpm

PH 7,35-7,45

PCO2 35-45

PO2 80-100

HCO3 21-28

Base Excess -3 until +3

O2

saturation

True O2

> 95%

Serum Electrolyte

Jam Normal 11:23 09:40 15:00

Na 136-145 126 128 128

K 3,5-5,0 3,11 3,19 3,46

Cl 98-106 110 101 110

LABORATORY FINDING (Follow Up)


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Lab normal Tanggal

20/4 21/4 22/4 23/4 25/4 26/4 27/4

Jam 01:27 10:26 11:14

Leukocyte 4.70011.300 /L 15.050 - - - 6.840 9.080

Haemoglobine 11,4 - 15,1 g/dl 12,7 - - - 8,90 7,90

PCV 38 - 42% 33,8 - - - 23 22,1

Trombocyte 142.000424.000

/L

215.000 - - - 247.000 297.000

MCV 80-93 fl 78,8 - - - 74,9 79,5

MCH 27-31 pg 29,6 - - - 29 29,4

Eo/Bas/Neu/limf/Mo

n

0-4/0-1/51-67/25-

33/2-5

0,1/0,1/80/

12/7,2

- - - 2,3/0,3/56,1

/20,8/20,5

2,2/0,1/74,5

/14,5/8,7

SGOT 0-32 mU/dL 48 - - - 75 Retikulosit absolut 0,0809

Retikulosit 2,91%

PPT 11,3 (11,5-11,8)

INR 0,98 (0,8-1,30)

APTT 27,30 (27,4-28,6)

ALP Alkali phosphatase 86

Gamma GT 132, LDH 661LED 38 mm/jam, alb:3,3

SGPT 0-33 mU/dL 25 - - - 56

Ureum 16,6-48,5 mg/dL 66,7 - - - 33,8

Creatinin


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;

TIME

20/4/2014

05.30

Badan terasa

lemas, mual,

muntahGCS : 4-5-6

BP: 90/60 mmHg

HR 90 kali/ menit

RR : 24 kali/menit

Hb : 12,3 gr/dl

Hb : 12.7 gr/dl

(01.27)

Produksi urin 1000

cc/7 jam

05.30 GDA 442

mg/dl

11.00. GDA 98

mg/dlstop drip

insulin

12.00 GDA 169

mg/dl

17.00 SE

132/3.2/124

1.krisis

hiperglikemia

1.1 ketoasidosis

diabetikum

2. DM tipe 1

3. Hiponatremia

hipoosmolar

hypovolemia

3.1 dt no 1

3.2 GI loss

4. dyspepsia

syndrome

4.1 DM

Gastroparese

4.2 SMRD

5. Lung infection

5.1 pneumonia

5.2 lung TB with

secondary infection

6. Azotemia prerenal

6.1 dt no 16.2 azotemia renal

6.2.1 Diabetic kidney

disease

-bed rest

-Sementara puasa

-rehidrasa 3 liter NaCL 0.9%-->30 tpm

Pasang NGTGL/8 jam

Inj. Metocloperamid 3 x 10 mg

Inj. Omeprazole 1 x 80 mgdrip 80 mg/jam

Regulasi gula darah

Line 1: Drip insulin short acting 7 IU/hour

Line 2: Drip KCl 25 meq in 500 cc Nacl 0.9% 20 dpm

If RBG < 200 mg/dL

Line 1: Drip insulin short acting 3,5 IU/hour

Line 2: Drip KCl 25 Meq in 500 ccNacl 0.9% 20 dpm

If RBG < 150-200 mg/dL (+) 2 dari 3 : pH > 7,3,

anion gap 12, HCO315

Line 1 : drip actrapid 1 IU/jam

Line 2 : D51/2 NS

Jika: pH > 7,3, anion gap 12, HCO315

Mulai diet cair 6 x 200 cc

Inj. Insulatard 0-10 IU (SC)

Inj Actrapid 6x 2 IU (SC)

Stop actrapid 2 jam kemudianInj. Insulatard 10 IU (SC)

Stop drip KCL

MRS ruang 26

Tunda inj actrapid

Drip KCl lanjut, cek SE/4 jam

DATE; S O A P


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TIME

21/4/2014

(pagi)

Seksi endokrin

TD: 140/90 ,,Hg

N : 96 kali per menit

RR : 20 kali per

menit

Tax : 36,3 0 C

GDA pukul 05.00

213 mg/dl

SE : 134/3.62/122

Hb : 8.5 gr/dl (13.38)

Hb : 10.3 gr/dl

(21.57)

1.krisis hiperglikemia

1.1 ketoasidosis

diabetikum

2. DM tipe 1

3. Hiponatremia

hipoosmolar

hypovolemia

3.1 dt no 1

3.2 GI loss

4. dyspepsia

syndrome

4.1 DM

Gastroparese

4.2 SMRD

5. Lung infection

5.1 pneumonia

5.2 lung TB with

secondary

infection

6. Azotemia

prerenal6.1 dt no 1

6.2 azotemia

renal

6.2.1 Diabetic

kidney disease

PDx: GDA, SE, BGA ulang

Puasa

Line 1 : drip actrapid 1 IU/jam

Line 2 : drip KCl 25 meq dalam 500 cc NaCl

0.9%20 tpm (K : > 5.2 stop drip KCl)

Jika GDA 150-200 mg/dl

pH 7.3

HCO3 15

Diet cair 6 x 200 cc

Inj insulatard 10 IU (SC)

Inj Actrapid 6 x 2 IU (SC)

Drip insulin stop 2 jam post subcutan

Inj. Ceftriaxone 2 x 1 gr (skin test)

Inj metocloperamid 3 x 10 mg intravena

Inj omeprazole 1 x 40 mg intravenaPlan monitoring :

GDA per jam

BGA per 6 jam

SE per 6 jam

Oksigen nasal canul 2-4 liter permenit

Inj ceftriaxone 2 x 1 gram intravena

Inj metocloperamide 3 x 10 mg intravena

Inj omeprazole 1 x 40 mg intravena

iVFD NS 0.9%30 tpminj insulatard 10 IU subcutan

inj. Actrapid 5x4 IU subcutan

diet DM 5 x 200 cc

2 jam post koreksi drip stop

Plan monitoring

GDS, SE, BGA

Pindah keruang biasa R27

DATE; S O A P


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TIME

Pukul 10.30

(visite seksi R26)

Pukul 10.20 GDS 178 cc pindah ke ruang biasa

Line 1:Drip insulin 1 IU/ jam

Line 2 : drip Kcl meq dalam 500 cc

NaCl 0.9%20 tpm

(K > 5.5 stop drip KCl)

Diet cair 6x 200 cc (dapat dimulai)

Inj. Insulatard 0-0-10 IU (subcutan)

Inj. Actrapid 6x2 IU (subcutan)

Drip insulin stop 2 jam post

subcutan

Target GDA 150-200 mg/dl

pH7.3

HCO3 15

pH GDA per 6 jam

BGA dan SE per 4 jam

Plan diagnosa :

GDA per jam

BGA, SE per 4 jam

Plan terapi:


O2 nasal canul 2-4 lpm

Inj insulatard 0-0-20 IU subcutan

Inj actrapid 6x2 IU subcutanCeftriaxone 2 x 1 gram (skin test)

Inj metocloperamid 3 x 10 mg

intravena (Kalau perlu)

Inj Omeprazole 1 x 40 mg intravena

ganti oral Omeprazole 2 x 20 mg

Plan monitoring

Vital sign, subjectif per 6 jam

GDA per jam

BGA, SE per 4 jamGCS

DATE; S O A P


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TIME

22/4/2014 Nyeri saat menelan Hb : 10.8 (06.24)GCS : 456

TD 130/80 mmHg

N : 88 kali per menit

RR 20 kali per menit

Same as

above

Plan diagnosis :

Cek BGA/24 jam

SE per 6 jam

GDA per 2 jam

Plan terapi :

Bed rest


Inj insulatar 0-0-14 IU subcutan

Inj actrapid 3x4 IU subcutan

Inj ceftriaxone 2 x 1 gr itravena (H2)

Inj metocloperamin 3 x 10 mg

(intravena ) (K/P)

Peroral :

Omeprazole 2 x 20 mg

Plan monitoring :

Subject, vital sign, GDA/2 jam, BGA,

se/ 6 jam, GCS

DATE; S O A P


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TIME

23/4/2014

(05.35)

Badan lemas dan

lemah

Pasien menolak

untuk diambil darah

lagi

Hb : 11 gr/dl (05.57)

Hb : 11 gr/dl ( 12.15)

Pukul 20.00

TD : 150/100 mmHgNadi : 90 x/menit

RR : 22x/menit

Tax : 36,5oC

SE :133/3.39/114

(06.00)

SE : 121/2.56/121

(20.12)

1.krisis hiperglikemia

1.1 ketoasidosis

diabetikum

2. DM tipe 1

3. Hiponatremia

hipoosmolar

hypovolemia

3.1 dt no 1

3.2 GI loss

4. dyspepsia

syndrome

4.1 DM

Gastroparese

4.2 SMRD

5. Lung infection

5.1 pneumonia

5.2 lung TB with

secondary

infection

6. Azotemia

prerenal6.1 dt no 1

6.2 azotemia

renal

6.2.1 Diabetic

kidney disease

Plan diagnosa :

BGA, SE / 12 jam, GDA/ 24 jam

Plan terapi :

Bed rest

O2 nasal canul2-4 liter per menit

Diet DM lunak 1700 kcal/hari


(pukul 22.00 wib)

Inj. Actrapid 3x4 IU (subcutan)

sebelum makan

Inj. Metocloperamid 3 x 10 mg

kalau perlu

Inj ceftriaxone 2 x 1 gram intravena

(H3)

Per oral :Omeprazol 2x20 mg

Plan monitoring:

Subject, vital sign, BGA,SE, GDA

Plan terapi :

Drip KCl 20 Meq dalam 500 cc Nacl

0.9%--> 20 tpmPlan monitoring :

Subject, vital sign, cek SE 4 jam post

koreksi

pasien menolak untuk di BGA ulang

DATE; S O A P


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TIME

24/4/2014 Batuk, badan

lemas

GCS ; 4-5-6

SE : 126/3.11/110

Post koreksi SE (11.23)

TD : 130/70 mm Hg

Nadi 92 kali per menit

RR 28 kali per menit

Tax : 370C

Post krisis 1.krisis

hiperglikemia

1.1 ketoasidosis

diabetikum

2. DM tipe 1

3. Hiponatremia

hipoosmolar

hypovolemia

3.1 dt no 1

3.2 GI loss

4. dyspepsia

syndrome

4.1 DM

Gastroparese

4.2 SMRD

5. Lung infection

5.1 pneumonia

5.2 lung TB with

secondary

infection

6. Azotemiaprerenal

6.1 dt no 1

6.2 azotemia

renal

6.2.1 Diabetic

kidney disease

Plan diagnosis :

Cek BGA, SE/ 12 jam

Cek GDA per 24 jam

Plan terapi :

Bed rest


Diet lunak 1700 kcal/hari


(pukul 22.00)

Inj. Actrapid 3x4 IU subcutan

sebelum makan

Inj. Metocloperamid 3x10 mg (IV)

(K/P)

Inj. Ceftriaxone 2 x 1 gr intravena

(H4)Peroral : omeprazole 2 x 20 mg

Plan monitoring :

Subject, vital sign, BGA, SE,

GDS

DATE; S O A P


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TIME

Visite seksi

endocrinology

- - pneumonia

Plan diagnosa :

Kultur sputum dan sensitivitas test

BTA S-P-S

LED

Plan terapi :

Bed rest



IVFD NaCl 0,9%20 tpm


(pukul 22.00)

Inj. Actrapid 4-4-4 IU subcutan

sebelum makan

Inj. Metocloperamid 3x10 mg

(intravena) (K/P)

Inj. Ceftriaxone 2 x 1 gr intravena

STOP

Infus Ciprofloxacin 2 x 400 mg

(intravena) (H1)

Peroral : omeprazole 2 x 20 mgPlan monitoring :

Subject, vital sign

DATE; S O A P


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TIME

25/4/2014 (05.30) Batuk berdahak

warna putih

Hb : 8.9

gr/dl

1. Post krisis

hiperglikemia

1. ketoasidosis

diabetikum

2. Asidosis metabolik

1. dt no 1

3. hipokalemia

hipoosmolar

hypovolemia

4.1dehydration

5. dyspepsia

syndrome

5.1 DM Gastroparese

5.2 dt no.3

6. Hipokalemia

6.1 dehydration

7. lung infection

7.1Asma dd bronkhitis

akut

7.2Peumonia CAP

Plan diagnosis :

Tunggu hasil Kultur sputum dan sensitivitas antibiotik, BTA

S-P-S, LED, konsul paru

Plan terapi :

Bed rest




Inj insulatard 0-0-14 IU subcutan (pukul 22.00)

Inj. Actrapid 4-4-4 IU subcutan sebelum makan

Inj. Metocloperamid 3x10 mg (intravena) (K/P)

Inj. Ceftriaxone 2 x 1 gr intravenaSTOP

Infus Ciprofloxacin 2 x 400 mg (intravena) (H2)

Peroral : omeprazole 2 x 20 mg

Hasil konsul paru :

Diagnosa paru :

1. Asma DD bronkhitis akut

2. Pneumonia CAP

Plan diagnosis :

Sputum gram/ kultur dan sensitivity

Spirometri bila stabilDL ulang

Chest X ray PA ulang

Plan terapi Paru :

O2 1-2 lpm nasal canul (bila sesak)

Inj ceftriaxone sesuai IPD

NAC 3 x 200 mg

Ferbivent nebulizer 3x per hari

Pulmicort nebulizizer 2x/hari

Lain-lain sesuai IPD

DATE; S O A P


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TIME

26/4/2014

(05.00)-

Mimisan 2x tetapi

berhenti sendiri

Hb : 7.9 gr/dl

(11.14)

K : 2,56

Hb : 8.6 g/dl

1. Post krisis

hiperglikemia

1. ketoasidosis

diabetikum


1. dt no 1

3. Hiponatremia

hipoosmolar

hypovolemia

3.1 GI loss

4. dyspepsia

syndrome

Syndrome

4.1 DM Gastroparese

4.2 dt no.3

6. Hipokalemia

6.1 dehydration

7. lung infection


akut

7.2Peumonia CAP8. Epistaksis

8.1 hematologic

malignancy

8.2 plexus kiesselbach

Plan diagnosis :

Tunggu hasil kultur sputum dan sensitivity,

tunggu hasil BTA S-P-S

Plan terapi :

Bed rest




Inj insulatard 0-0-14 IU subcutan (pukul

22.00)

Inj. Actrapid 4-4-4 IU subcutan sebelum

makan

Inj. Metocloperamid 3x10 mg (intravena)

(K/P)


Infus Ciprofloxacin 2 x 400 mg (intravena)

(H3)


Plan monitoring : Subj, vital sign

Plan diagnosis :Blood smear, reticulosit count, FH, FOBT,

determinan test

Drip KCl 20 Meq dalam 500 cc NaCl 0,9%

20 tetes per menit

Lain-lain menunggu hasil lab

DATE; S O A P


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TIME

26/4/2014

(05.00)-

Mimisan 2x tetapi

berhenti sendiri

Hb : 7.9 gr/dl

(11.14)

K : 2,56

Hb : 8.6 g/dl

1. Post krisis

hiperglikemia

1. ketoasidosis

diabetikum


1. dt no 1

3. hipokalemia

hipoosmolar

hypovolemia

4.1dehydration

5. dyspepsia

syndrome

Syndrome

5.1 DM Gastroparese

5.2 dt no.3

6. Hipokalemia

6.1 dehydration

7. lung infection


akut

7.2Peumonia CAP8. Epistaksis

8.1 hematologic malignancy

8.2 plexus kiesselbach

Plan diagnosis :



Plan terapi :

Bed rest





22.00)


makan


(K/P)



(H3)




determinan test


20 tetes per menit


DATE; S O A P


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TIME

28/4/2014 (06.00) Batuk berdahak (+)

Hb : 7.9 gr/dl

(11.14)

K : 2,56

Hb : 8.6 g/dl

1. Post krisis

hiperglikemia

1. ketoasidosis

diabetikum


1. dt no 1

3. hiponaterima

hipoosmolar

hypovolemia

3. Dt no 1

3.2 GI loss

4. dyspepsia

syndrome

4.1 DM Gastroparese

4.2 dt no.3

5 Hipokalemia

5.1 GI loss

6. lung infection


akut

6.2Peumonia CAP

Plan diagnosis :



Plan terapi :

Bed rest





22.00)


makan


(K/P)



(H3)




determinan test


20 tetes per menit



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DATE;

TIME

S O A P

28/4/14

08.15

Dilaporkan penurunan

kesadaran

GCS 1 1 1

BP:160/90

Nadi:98x/mnt

RR:34x/mnt

Rhonki (+) padaapeks dan medial

paru kanan dan

kiri.

Produksi urin 350

cc selama 3 jam

Edema tungkai

kanan dan kiri

serta tangan

kanan dan kiri

GDA:495

Cek BGA, SE cito

Rehidrasi Nacl 0,9% 500cc

O2 NRBM 10lpm

08.25 Sesak bertambah GCS 111

Nadi melemah,

kecil dan cepat

RR:16x/mnt

CPR 5 siklus

Gagal

Jam 08.30 meninggal, midriasis maximal, nadi

tidak teraba, RR (-)Kemungkinan penyebab:

1.aspirasi,

2. Hematologic malignancy

3. Intracranial bleeding


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MODY Clinical Presentation

Some forms of MODY produce significanthyperglycemia and the typical signs and symptoms ofdiabetes: increased thirst and urination (polydipsia andpolyuria).

In contrast, many people with MODY have no signs orsymptoms and are diagnosed either by accident, whena high glucose is discovered during testing for otherreasons, or screening of relatives of a person

discovered to have diabetes. Discovery of mildhyperglycemia during a routine glucose tolerance testfor pregnancy is particularly characteristic.


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Presentation

Mild to moderate hyperglycemia (typically 130250 mg/dl, or 7

14 mmol/l) discovered before 30 years of age. However, anyone under 50can develop MODY.

A first-degree relative with a similar degree of diabetes.

Absence of positive antibodies or other autoimmunity (e.g., thyroiditis) inpatient and family.

Persistence of a low insulin requirement (e.g., less than 0.5 u/kg/day) past

the usual honeymoon period. Absence of obesity (although overweight or obese people can get MODY)

or other problems associated with type 2 diabetes or metabolic syndrome(e.g., hypertension, hyperlipidemia, polycyctic ovary syndrome)

Insulin resistance very rarely happens.

Cystic kidney disease in patient or close relatives.

Non-transient neonatal diabetes, or apparent type 1 diabetes with onsetbefore six months of age.

Liver adenoma or hepatocellular carcinoma in MODY type 3

Renal cysts, rudimentary or bicornuate uterus, vaginal aplasia, absence ofthe vas deferens, epidymal cysts in MODY type 5


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MODY Treatment

In MODY2, oral agents are relatively

ineffective and insulin is unnecessary.

In MODY1 and MODY3, insulin may be more

effective than drugs to increase insulinsensitivity.

Sulfonylureas are effective in the KATPchannel

forms of neonatal-onset diabetes.

Di i f LADA


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Diagnosis for LADAC-peptide

This test measures residual beta cell function by determining the level of insulin secretion.

Persons with LADA typically have low, although sometimes moderate, levels of C-peptide as thedisease progresses. Patients with insulin resistance or type 2 diabetes are more likely to, but will

not always, have high levels of C-peptide due to an over production of insulin.

Autoantibody panel

Glutamic acid decarboxylase autoantibodies (GADA), islet cell autoantibodies (ICA), insulinoma-

associated (IA-2) autoantibodies, and zinc transporter autoantibodies (ZnT8). Glutamic acid

decarboxylase antibodies are commonly found in diabetes mellitus type 1.Islet cell antibodies (ICA) tests

Islet Cell IgG Cytoplasmic Autoantibodies, IFA; Islet Cell Complement Fixing Autoantibodies,

Indirect Fluorescent Antibody (IFA); Islet Cell Autoantibodies Evaluation; Islet Cell Complement

Fixing Autoantibodies - Aids in a differential diagnosis between LADA and type 2 diabetes.

Persons with LADA often test positive for ICA, whereas type 2 diabetics only seldom do.

Glutamic acid decarboxylase (GAD) antibodies tests Microplate ELISA: Anti-GAD, Anti-IA2, Anti-GAD/IA2 Pool - In addition to being useful in making

an early diagnosis for type 1 diabetes mellitus, GAD antibodies tests are used for differential

diagnosis between LADA and type 2 diabetesand may also be used for differential diagnosis of

gestational diabetes, risk prediction in immediate family members for type 1, as well as a tool to

monitor prognosis of the clinical progression of type 1 diabetes.

Other characteristics of LADA that may


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Other characteristics of LADA that may

aid in differential diagnosis include

Onset usually at 25 years of age or older Initially mimics non-obese type 2 diabetes (patients are usually thin

or of normal weight, although some may be overweight tominimally obese.

Often, but not always, a lack of family history for T2DM (family

history for type 2 diabetes is sometimes involved regarding a latentautoimmune diabetic adult)

Persons with LADA are insulin resistant like, but at prevalence levelsless than Type 2.

Human leukocyte antigen (HLA) genes associated with type 1diabetes are seen in LADA but not in type 2 diabetes.

Although some people having type 2 diabetes may inject insulin,this only rarely happens; in contrast, people with LADA requireinsulin injections around three to 12 years after diagnosis .


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C-Peptide

C-peptide measurementhas a key role in the correct diagnosis of the type of diabetes inadults.[8]and in children.[9]In type 1 diabetes, the majority of patients become severely insulindeficient within 5 years of diagnosis (23 years in children),[10]whereas in MODY and type 2diabetes C-peptide persists. C-peptide testing is most useful beyond 23 years of diabetes and cannot discriminate MODY from type 2 diabetes.

Measuring C-peptide

C-peptide can be measured in plasma or serum, fasting or following stimulation. Blood samplesneed to be taken on ice and processed immediately to prevent degradation by blood peptidases,

which limits testing to a hospital setting with on-site laboratory facilities . Stimulated C-peptide secretion can be assessed in response to a standard mixed meal tolerance

test (MMTT) or following glucagon injection. The MMTT is better tolerated, with less nausea, and ismore reproducible.[11]On the other hand, it is cumbersome, requires an overnight fast, and is rarelyperformed in routine clinical practice. Its main use is in intervention trials.

Fasting C-peptide correlates well with stimulated C-peptide, and is more routinely used in clinicalcare . A spot urine sample measuring urinary C-peptide creatinine ratio (UCPCR) may provide auseful non-invasive alternative, a particular advantage for children
http://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabeteshttp://www.diapedia.org/type-1-diabetes-mellitus/c-peptide-in-type-1-diabetes


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C-peptide is a useful measure of endogenous

insulin secretion in insulin-treated diabetes. C-

peptide can be measured in blood or urine,

during a fasting or stimulated sample. Themain roles for C-peptide testing are in the

discrimination of diabetes subtypes, which in

turn informs correct management and tomonitor interventions aimed at preserving

beta cell function.


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