KETOASIDOSIS METABOLIK

Oleh
Elok Nur Farida
Buddy Dayono
Restu Wulandari

Pembimbing
dr.

Kepaniteraan Klinik Fakultas Kedokteran

Universitas Tanjungpura
Stase Ilmu Penyakit Dalam
 Pendahuluan1
Ketoasidosis diabetik (KAD) adalah
dekompensasi kekacauan metabolik
Ditandai oleh trias hiperglikemia, asidosis, dan
ketosis
Faktor pencetus yang berperan untuk
terjadinya KAD adalah infeksi, infark miokard
akut, pankreatitis akut, penggunaan obat
golongan steroid, menghentikan atau
mengurangi dosis insulin.
1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al. Acute complications of diabetes mellitus.
Harrisons Principles of Internal Medicine 17th edition. USA : The McGraw-Hill Inc. 2008.
Pendahuluan
Amerika serikat
8 per 1000 pasien DM pertahun untuk semua kelompok umur
13,4 per 1000 pasien pada kelompok umur kurang dari 30
tahun
Angka kematian pasien dengan ketoasidosis diabetik di negara
maju kurang dari 5% pada banyak senter, beberapa sumber
lain menyebutkan 5-10%, 2-10%, atau 9-10%. Ketoasidosis
diabetik dilaporkan bertanggung jawab untuk lebih dari
100.000 pasien yang dirawat per tahun di Amerika Serikat.2
Indonesia
Data pasti belum ada, namun insiden KAD tidak sebanyak
dinegara barat karena prevalensi DM tipe 1 yang rendah.2

2. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
 Definisi1

Suatu kedaruratan medis akut pada penderita

DM yang disertai peningkatan kadar gula darah
yang tinggi disertai dengan adanya tanda dan
gejala asidosis dan plasma keton.

Sering terjadi pada DM tipe 1

Dapat terjadi pada DM tipe 2 akibat
adanya faktor pencetus.

1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al. Acute complications of diabetes mellitus.
Harrisons Principles of Internal Medicine 17th edition. USA : The McGraw-Hill Inc. 2008.
 Glikogenolisis
Pemecahan
glikogen glukosa
Glukoneogenesis
Makanan
Pembentukan glukosa
Karbohidrat
atau glikogen dari
(glucosa, fruktosa,
sumber non
galaktosa)
karbohidrat

Glukosa
Plasma

3. Tortora, G.J., Derrickson, B. Principles of anatomy & physiology. 14th ed. USA. 2014.
p:979-1022
3. Tortora, G.J., Derrickson, B. Principles of anatomy & physiology. 14th ed. USA. 2014.
p:979-1022
3. Tortora, G.J., Derrickson, B. Principles of anatomy & physiology. 14th ed. USA. 2014.
p:979-1022
Kontrol
Sekresi
Glukagon
dan Insulin

3. Tortora, G.J., Derrickson, B. Principles of anatomy & physiology. 14th ed. USA. 2014.
p:979-1022
 Glukosa
Lemak Elektrolit Protein
Air

Defisiensi Insulin

-Glukagon:
Glukoneogenesis Uptake glukosa Glukagon:
Lipogenesis Hiperglikemia Glukoneogenesis
FFA Glukosuria Katabolisme
Ketogenesis Poliuria protein
Ketonemia Hiperosmolaritas Sintesis protein

Diuresis Osmotik
Ketonuria Poliuria
BUN
Natrium Elektrolit imbaalns
Nitrogen urin
Mual, muntah Na, K, fosfat,
Balans nitrogen(-)
Bikarbonat
3. Tortora, G.J., Derrickson, B. Principles of
anatomy & physiology. 14th ed. USA.
2014. p:979-1022 pH serum Dehidrasi
Perfusi Jaringan
4. Silbernagl S, Lang F. Acute effect of Asidosis Hiperosmolaritas
Hipoksia Jaringan
insulin deficiency (diabetes mellitus). Hemokonsentrasi
Color Atlas of Pathophysiology. New York Kussmaul Asam laktat
Hipotensi
: Thieme. 2002;p288-289. Asidosis metabolik
5. Funk JL. Disoders of the endokrin
Ekskresi Aseton Perfusi renal
pancreas. Pathophysiology of Disease:
An Introduction to Clinical Medicine,
5thed. US : The McGraw-Hill Inc. Asidosis Metabolik, Syok, Koma, Kematian
 Symptoms Precipitating
Physical finding
event
Mual/Muntah Takikardi
Haus/poliuria Inadequate insulin Dehidrasi/hipotensi
Nyeri abdomen administration Takipnea/kussmaul
Sesak napas Infeksi Abdominal tenderness
Infark Penurunan Kesadaran
Kehamilan

1. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
 Kriteria Diagnosis KAD1,7
Tanda Biokimia Kadar
Hiperglikemia >250mg/dL
(gula darah)
Asidosis (pH <7,30
arteri)
Ketonemia Total keton
serum > 3mM

1. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic Syndrome and Obesity: Targets and
Therapy 2014:7 255264
Pemeriksaan Penunjang
Laboratorium
 Pemeriksaan Penunjang2,6
Ro Thorax (infeksi paru?)
Elektrokardiografi (EKG):cara cepat untuk
menilai hipokalemia atau hiperkalemia
Telemetri: Pasien dengan komorbiditas
(terutama jantung). Kelainan elektrolit yang
signifikan, dehidrasi berat, atau asidosis
mendalam.

2. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
6. Trachtenbarg DE. Management of Diabetic Ketoacidosis. American Family Physician. 2005;71(9):p1705-1714.
 Diagnosis Banding1,2

1. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
2. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
 Tatalaksana6
Penggantian cairan dan garam yang hilang
Menekan lipolisis sel lemak dan menekan
glukoneogenesis sel hati dengan pemberian
insulin.
Mengatasi stress sebagai pencetus KAD
Mengembalikan keadaan fisiologis normal dan
menyadari pentingnya pemantauan serta
penyesuaian pengobatan.

6. Trachtenbarg DE. Management of Diabetic Ketoacidosis. American Family Physician. 2005;71(9):p1705-1714.

 Tatalaksana6
Airway; bebaskan jalan
napas

Breathing; Oksigen

Circulation; IV line (pasang

kateter)

Penilaian Kegawatan

6. Trachtenbarg DE. Management of Diabetic Ketoacidosis. American Family Physician. 2005;71(9):p1705-1714.

 Tatalaksana6
Penilaian Kegawatan

Evaluasi Klinis -Cari etiologi, apakah ada

infeksi?, pemberian Obat
Hipoglikemik Oral atau
insulin inadekuat?
-Klinis dehidrasi
-Tingkat kesadaran
(Glassgow Coma Scale)
6. Trachtenbarg DE. Management of Diabetic Ketoacidosis. American Family Physician. 2005;71(9):p1705-1714.
 Management of DKA: Evaluation7
Complete Initial Evaluation
Including (but not limited to):
Medical history and physical Urine for urinalysis and ketones Adult patient Complete Initial
examination
with DKA Evaluation
Cultures as indicated (wound, blood,
Complete blood count with urine, etc.)
differential
Chest abdominal x-ray
Fingerstick blood glucose K+ Repletion
12-lead ECG
Serum chemistries (electrolytes, BUN,
Cr; serum ketones) Insulin Therapy
IV Fluids
Concurrently, begin empirical fluid resuscitation with 0.9% NaCl at
1000 mL/hr. Bicarbonate?

Consider volume expansions if hypovolemic shock is present.

Continue fluid resuscitation until volume status and cardiovascular When Serum Glucose
parameters (pulse, BP) have been restored. Reaches 200 mg/dL

7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic Continuing
Syndrome and Obesity: Targets and Therapy 2014:7 255264 Management
18
 Management of DKA: K+ Repletion7
Potassium (K+) Repletion
Obtain baseline serum potassium. Obtain 12-lead ECG.
Adult patient Complete Initial
K+ 5.5 mEq/L K+ < 5.5 mEq/L and adequate urine output with DKA Evaluation

Hold K+ therapy Add K+ to IV fluids (use KCI and/or Kphos)

Treat hyperkalemia if ECG K+ = 4.5 5.4: add 20 mEq/L IV fluids K+ Repletion
changes present K+ = 3.5 4.4: add 30 mEq/L IV fluids
K+ < 3.5 : add 40 mEq/L IV fluids
Recheck K+ in 2 hours Insulin Therapy

Follow serum K+ every 2-4 hours until stable: anticipate rapid drop of serum K+ IV Fluids
during therapy, due to dilution and intracellular shifting.
Bicarbonate?
Ensure adequate urine output to avoid over-repletion and hyperkalemia.

Continue K+ repletion until serum K+ is stable between 4-5 mEq/L.

If refractory hypokalemia, ensure concurrent magnesium repletion. When Serum Glucose

Reaches 200 mg/dL
K+ repletion may need to be continued for several days, as total body losses may
reach up to 500 mEq.
Continuing
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic Management
Syndrome and Obesity: Targets and Therapy 2014:7 255264 19
 Management of DKA: IV Fluids7
IV Fluids
Adult patient Complete Initial
Based on corrected serum sodium.* with DKA Evaluation

If high/normal, use 0.45% NaCl

K+ Repletion
If low/normal, use 0.9% NaCl.

Continue IV fluids at 250-1000 mL/hr depending on volume Insulin Therapy

status, cardiovascular history, and cardiovascular status IV Fluids
(pulse, BP).
Bicarbonate?
Children: more susceptible to cerebral edema; go slow

When Serum Glucose

*Sodium correction: Serum sodium should be corrected for Reaches 200 mg/dL
hyperglycemia. For every 100 mg/dL of glucose elevation above 100
mg/dL, add 1.6 mEq/L to the measured sodium value; this will yield
the corrected serum sodium concentration.
Continuing
Management
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic 20
Syndrome and Obesity: Targets and Therapy 2014:7 255264
 Management of DKA: Insulin Therapy7

Adult patient Complete Initial

Insulin Therapy with DKA Evaluation

Regular insulin bolus 0.15 U/kg.

K+ Repletion
IV infusion, 0.10 U/kg/hr.
Insulin Therapy
Check serum glucose hourly should fall by 50-80 mg/dL/hr.
IV Fluids

If serum glucose falling too rapidly, back off on insulin Bicarbonate?

infusion.

If serum glucose rising or falling too slowly, increase insulin

infusion rate by 50-100%. When Serum Glucose
Reaches 200 mg/dL

Continuing
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic Management
Syndrome and Obesity: Targets and Therapy 2014:7 255264 21
 Management of DKA: Bicarbonate
Therapy7
Bicarbonate Therapy
Adult patient Complete Initial
Obtain arterial blood gas. with DKA Evaluation
Obtain baseline serum bicarbonate.
pH < 6.9 6.9 pH < 7.0 pH 7.0
K+ Repletion
88 mEq/L 44 mEq/L Assess need for
(2 amps) (1 amp) bicarbonate
NaHCO3 NaHCO3 Insulin Therapy
over 2 hours over 1 hour IV Fluids

Bicarbonate?
Repeat arterial blood gas after bicarbonate administration.

Repeat NaHCO3 therapy until pH 7.0, then discontinue

therapy. When Serum Glucose
Reaches 200 mg/dL
Follow serum bicarbonate q4h until stable.

Continuing
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic Management
Syndrome and Obesity: Targets and Therapy 2014:7 255264 22
 Management of DKA: Glucose7
Adult patient Complete Initial
with DKA Evaluation
When Serum Glucose Reaches 200
mg/dL
K+ Repletion
Add dextrose to IV fluids at 150-250 mL/hr and adjust insulin
infusion to maintain serum glucose at 140-200 mg/dL until
Insulin Therapy
metabolic control is achieved.
IV Fluids
Continue until anion gap has closed and acidosis has Bicarbonate?
resolved.

Begin exhaustive search for precipitant of metabolic

decompensation. When Serum Glucose
Reaches 200 mg/dL

Continuing
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic Management
Syndrome and Obesity: Targets and Therapy 2014:7 255264 23
 Management of DKA: Continuing
Management7
Adult patient Complete Initial
Continuing Management: with DKA Evaluation

Follow and replete serum electrolytes (including divalent

cations) q2-4h until stable.
Insulin Therapy
After resolution of hyperglycemic state, follow blood glucose IV Fluids
q4h and initiate SC insulin regimen.
Potassium Bicarbonate?
Convert IV insulin to SC injections, ensuring adequate
overlap.

Begin clear liquid diet and advance as tolerated. Encourage When Serum Glucose
resumption of ambulation and activity. Reaches 200 mg/dL

Review and update diabetes education, with special attention

to sick day rules. Continuing
Management

7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes, Metabolic

Syndrome and Obesity: Targets and Therapy 2014:7 255264 24
 Komplikasi2
Edema serebri
Disaritmia jantung
Edema paru

2. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
 Prognosis2
Prognosis pasien diobati dengan ketoasidosis
diabetes sangat baik, terutama pada pasien yang
lebih muda jika infeksi intercurrent tidak ada.
Prognosis terburuk adalah biasanya diamati pada
pasien yang lebih tua dengan penyakit
intercurrent parah, misalnya, infark miokard,
sepsis, atau pneumonia.s
Kehadiran koma mendalam pada saat diagnosis,
hipotermia, dan oliguria merupakan tanda-tanda
prognosis buruk.
2. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti
Setiati. Buku Ajar Ilmu Penyakit Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
Kesimpulan
KAD merupakan komplikasi metabolik akut
serius pada pasien DM.
Manifestasi utama berupa kekurangan insulin,
hiperglikemia yang berat, dehidrasi, asidosis
metabolik.
Diagnosis ditegakkan bila ditemukan
hiperglikemia ketonemia, dan asidosis
Kesimpulan
Terapi bertujuan mengoreksi kelainan
patofisiologis yang mendasari, yaitu gangguan
keseimbangan cairan dan elektrolit, kadar
glukosa darah, gangguan asam basa, serta
mengobati faktor pencetus.
Komplikasi KAD dapat berupa edema paru,
edema serebri dan disaritmia jantung.
 Daftar Pustaka
1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al. Acute
complications of diabetes mellitus. Harrisons Principles of Internal Medicine 17th
edition. USA : The McGraw-Hill Inc. 2008.
2. Soewondo, Pradana. Ketoasidosis Diabetik. In: Sudoyo, Aru W., Bambang
Setyohadi, Idrus Alwi, Marcellus Simadibrata, Siti Setiati. Buku Ajar Ilmu Penyakit
Dalam Jilid III Ed 5. 2009. Jakarta: Interna Publishing.
3. Tortora, G.J., Derrickson, B. Principles of anatomy & physiology. 14th ed. USA.
2014. p:979-1022
4. Silbernagl S, Lang F. Acute effect of insulin deficiency (diabetes mellitus). Color
Atlas of Pathophysiology. New York : Thieme. 2002;p288-289.
5. Funk JL. Disoders of the endokrin pancreas. Pathophysiology of Disease: An
Introduction to Clinical Medicine, 5thed. US : The McGraw-Hill Inc. 2006;513-540.
6. Trachtenbarg DE. Management of Diabetic Ketoacidosis. American Family
Physician. 2005;71(9):p1705-1714.
7. Gosmanov AR, et al. Management of adult diabetic ketoacidosis. Diabetes,
Metabolic Syndrome and Obesity: Targets and Therapy 2014:7 255264