*Resident of Internal Medicine, Medical Faculty of Brawijaya University - Saiful Anwar General Hospital Malang ** Supervisor, Endocrine & Metabolic Disease, Internal Medicine Department Brawijaya University- Saiful Anwar General hospital Malang
KAD Manifestasi awal dari DM tipe 1 infeksi, trauma, infark miokard, atau kelainan lainnya hiperglikemia, asidosis metabolik, dan ketosis Ketoasidosis diabetikum Kriteria KAD Patofisologi KAD DM tipe 1 DM tipe 1
Pneumonia Summary of Database Mr. Supriadi, 21 years old, W. 26 ward 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. 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 Sari to 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. Physical Examination General appearance : looked severely ill GCS: 224 (ER) At ward: 456 Patient looks underweight Height: 165 cm Weight: 50 KG BMI: 18.36 m 2
Tax : 37 0 C 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, traubes space tymphani Extremities Warm acrals, CRT< 2, edema (-)
Laboratory finding Lab Value Lab Value Leukocyte 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
Conclusion: Sinus rhythm with HR 100 bpm. CHEST X RAY CXR AP position, symmetric, enough KV, enough inspiration 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 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 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 1 6.2 azotemia renal 6.2.1 Diabetic kidney disease
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 therapy Rehydration 1L of NS 0,9% over first 1 h Insulin short acting 0.1 U/kg 5iu (iv) 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; 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
20/04/2014; 12:00 RBS: 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 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; 21:00 RBS: 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 short acting 0.05U/kg/hour (1 iu/hour) Line II: drip KCl 25 mEq in 500 cc NaCl 0.9% 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
Infeksi yang paling sering menjadi penyebab KAD adalah infeksi saluran kemih dan pneumonia. infeksi ringan seperti skin lession atau infeksi tenggorokan. pasien ini didapatkan keluhan berupa demam, batuk, keringat malam, penurunan berat badan didiagnosa sementara sebagai TB paru dengan sekunder infeksi (pneumonia) Dasar diagnosa DM tipe 1 : penderita baru >50% : 20 tahun (pasien berusia 21 tahun) penurunan berat badan, polidipsia,dan hiperglikemia pasien mengalami penurunan berat 7 kg dalam sebulan, cepat merasa haus, dan pernah periksa ke puskesmas dengan gula darah 600 mg/dl) Prinsip Terapi 1. Terapi cairan Prioritas utama pada penatalaksanaan KAD adalah terapi cairan. Terapi insulin hanya efektif jika cairan diberikan pada tahap awal terapi dan hanya dengan terapi cairan saja akan membuat kadar gula darah menjadi lebih rendah. Studi menunjukkan bahwa selama empat jam pertama, lebih dari 80% penurunan kadar gula darah disebabkan oleh rehidrasi. Oleh karena itu, hal penting pertama yang harus dipahami adalah penentuan difisit cairan yang terjadi. Beratnya kekurangan cairan yang terjadi dipengaruhi oleh durasi hiperglikemia 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)
Cairan fisiologis (NaCl 0,9%) diberikan dengan kecepatan 15-20 ml/kgBB/jam atau lebih selama jam pertama ( 1 - 1,5 liter). Sebuah sumber memberikan petunjuk praktis pemberian cairan sebagai berikut: 1 liter pada jam pertama, 1 liter dalam 2 jam berikutnya, kemudian 1 liter setiap 4 jam sampai pasien terehidrasi. 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 hidrasi pasien. Pilihan cairan selanjutnya tergantung dari status hidrasi,kadar elektrolit serum, dan pengeluaran urine 2. Terapi Insulin Sejak pertengahan tahun 1970-an protokol pengelolaan KAD dengan drip insulin intravena dosis rendah mulai digunakan dan menjadi popular. Cara ini dianjurkan karena lebih mudah mengontrol dosis insulin, menurunkan kadar glukosa darah lebih lambat, efek insulin cepat menghilang, masuknya kalium ke intrasel lebih lambat, komplikasi hipoglikemia dan hipokalemia lebih sedikit. Pada pasien diberikan terapi Insulin Insulin short acting 0.1 U/kg 5iu (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<3,3hold insulin and drip KCl 25mEq/h until K3,3 If initial 3,3<K<5drip KCl 20-30mEq/h If initial K5do not give KCl drip, check K/4 hour
Until RBG < 200/dl
Line I:drip Insulin short acting 0.02-0.05 U/kg/hr (2.5 i.u/h ) Line 2 D 5 1/2NS
Keep serum glucose between 150-200 mg/dl until resolution of DKA If patient ability to eat, Giving subcutaneous insulin: *insulin long acting 0-10iu *Insulin short acting 4iu-4iu-4iu Stop insulin drip after 2 hours 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) 3. Penatalaksanaan terhadap Infeksi yang Menyertai Antibiotika diberikan sesuai dengan indikasi, terutama terhadap faktor pencetus terjadinya KAD. Jika faktor pencetus infeksi belum dapat ditemukan, maka antibiotika yang dipilih adalah antibiotika spektrum luas (pada pasien ini saat masuk diberikan ceftriaxone 2 x 1 gr sampai (H4) kemudian diganti dengan infus ciprofloxacin 2 x 400 mg (intravena)) sumber infeksi pada pasien dicurigai berasal dari lung infection 28 April 2014
Kondisi pasien dilaporkan memburuk secara mendadak, pasien dilaporkan apnue, penurunan kesadaran meninggal Diagnosa kematian : 1. Aspirasi 2. Septic DIC 3. Intracranial bleeding 4. Hematologic malignancy
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 BGA 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 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 4.700 11.300 /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 142.000 424.000 /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 661 LED 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 <1,2 mg/dL 1,40 - - - 0,68 GDS 60-100 682 (01:27) - 261 (06:11) 219 (20:12) 190 171 (12:25) 218 (14:04) 2 249 (06:17) 176 (15:26) 179 (21:03 298 (22:26) LABORATORY FINDING (Follow Up) DATE; TIME S O A P 20/4/2014 05.30 Badan terasa lemas, mual, muntah GCS : 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/dl stop 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 1 6.2 azotemia renal 6.2.1 Diabetic kidney disease -bed rest -Sementara puasa -rehidrasa 3 liter NaCL 0.9%-->30 tpm Pasang NGT GL/8 jam Inj. Metocloperamid 3 x 10 mg Inj. Omeprazole 1 x 80 mg drip 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 kemudian Inj. Insulatard 10 IU (SC) Stop drip KCL MRS ruang 26 Tunda inj actrapid Drip KCl lanjut, cek SE/4 jam DATE; TIME S O A P 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 prerenal 6.1 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 intravena Plan 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 tpm inj 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; TIME S O A P
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: Diet cair 6 x 200 cc O2 nasal canul 2-4 lpm Inj insulatard 0-0-20 IU subcutan Inj actrapid 6x2 IU subcutan Ceftriaxone 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 jam GCS
DATE; TIME S O A P 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 Diet cair 6 x 200 cc 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; TIME S O A P 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 mmHg Nadi : 90 x/menit RR : 22x/menit Tax : 36,5 o C 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 prerenal 6.1 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 Inj insulatard 0-0-14 IU subcutan (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 tpm Plan monitoring : Subject, vital sign, cek SE 4 jam post koreksi pasien menolak untuk di BGA ulang
DATE; TIME S O A P 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 : 37 0 C 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. Azotemia prerenal 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 O2 nasal canul 2-4 lpm Diet lunak 1700 kcal/hari Inj insulatard 0-0-14 IU subcutan (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; TIME S O A P Visite seksi endocrinology - - pneumonia Plan diagnosa : Kultur sputum dan sensitivitas test BTA S-P-S LED Plan terapi : Bed rest O2 nasal canul 2-4 lpm Diet lunak 1700 kcal/hari IVFD NaCl 0,9% 20 tpm 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 intravena STOP Infus Ciprofloxacin 2 x 400 mg (intravena) (H1) Peroral : omeprazole 2 x 20 mg Plan monitoring : Subject, vital sign DATE; TIME S O A P 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 O2 nasal canul 2-4 lpm Diet lunak 1700 kcal/hari IVFD NaCl 0,9% 20 tpm 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 intravena STOP 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 stabil DL 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 Plan monitoring : Subj, vital sign DATE; TIME S O A P 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 2. Asidosis metabolik 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 7.1Asma dd bronkhitis akut 7.2Peumonia CAP 8. 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 O2 nasal canul 2-4 lpm Diet lunak 1700 kcal/hari IVFD NaCl 0,9% 20 tpm 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 intravena STOP Infus Ciprofloxacin 2 x 400 mg (intravena) (H3) Peroral : omeprazole 2 x 20 mg
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; TIME S O A P 26/4/2014 (05.00) - Mimisan 2x tetapi berhenti sendiri
Plan diagnosis : Tunggu hasil kultur sputum dan sensitivity, tunggu hasil BTA S-P-S Plan terapi : Bed rest O2 nasal canul 2-4 lpm Diet lunak 1700 kcal/hari IVFD NaCl 0,9% 20 tpm 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 intravena STOP Infus Ciprofloxacin 2 x 400 mg (intravena) (H3) Peroral : omeprazole 2 x 20 mg
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; TIME S O A P 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 2. Asidosis metabolik 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 6.1Asma dd bronkhitis akut 6.2Peumonia CAP Plan diagnosis : Tunggu hasil kultur sputum dan sensitivity, tunggu hasil BTA S-P-S Plan terapi : Bed rest O2 nasal canul 2-4 lpm Diet lunak 1700 kcal/hari IVFD NaCl 0,9% 20 tpm 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 intravena STOP Infus Ciprofloxacin 2 x 400 mg (intravena) (H3) Peroral : omeprazole 2 x 20 mg
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; 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 (+) pada apeks 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 Terima kasih MODY Clinical Presentation Some forms of MODY produce significant hyperglycemia and the typical signs and symptoms of diabetes: increased thirst and urination (polydipsia and polyuria). In contrast, many people with MODY have no signs or symptoms and are diagnosed either by accident, when a high glucose is discovered during testing for other reasons, or screening of relatives of a person discovered to have diabetes. Discovery of mild hyperglycemia during a routine glucose tolerance test for pregnancy is particularly characteristic. Presentation Mild to moderate hyperglycemia (typically 130250 mg/dl, or 7 14 mmol/l) discovered before 30 years of age. However, anyone under 50 can develop MODY. A first-degree relative with a similar degree of diabetes. Absence of positive antibodies or other autoimmunity (e.g., thyroiditis) in patient 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 onset before six months of age. Liver adenoma or hepatocellular carcinoma in MODY type 3 Renal cysts, rudimentary or bicornuate uterus, vaginal aplasia, absence of the vas deferens, epidymal cysts in MODY type 5 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 insulin sensitivity. Sulfonylureas are effective in the K ATP channel forms of neonatal-onset diabetes. Diagnosis for LADA C-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 the disease 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 diabetes
and 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 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 to minimally obese. Often, but not always, a lack of family history for T2DM (family history for type 2 diabetes is sometimes involved regarding a latent autoimmune diabetic adult) Persons with LADA are insulin resistant like, but at prevalence levels less than Type 2. Human leukocyte antigen (HLA) genes associated with type 1 diabetes 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 require insulin injections around three to 12 years after diagnosis .
C-Peptide C-peptide measurement has a key role in the correct diagnosis of the type of diabetes in adults. [8] and in children. [9] In type 1 diabetes, the majority of patients become severely insulin deficient within 5 years of diagnosis (23 years in children), [10] whereas in MODY and type 2 diabetes C-peptide persists. C-peptide testing is most useful beyond 23 years of diabetes and can not discriminate MODY from type 2 diabetes. Measuring C-peptide C-peptide can be measured in plasma or serum, fasting or following stimulation. Blood samples need 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 is more reproducible. [11] On the other hand, it is cumbersome, requires an overnight fast, and is rarely performed 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 clinical care . A spot urine sample measuring urinary C-peptide creatinine ratio (UCPCR) may provide a useful non-invasive alternative, a particular advantage for children 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. The main roles for C-peptide testing are in the discrimination of diabetes subtypes, which in turn informs correct management and to monitor interventions aimed at preserving beta cell function. Terima kasih