KETOASIDOSIS DIABETIKFatimah Eliana

Defisiensi insulin relatif/absolutPeningkatan hormon kontraregulator: glukagonkatekolamin kortisolgrowth hormonETIOLOGI

FAKTOR PENCETUS

InfeksiKebutuhan insulin mendadak naik pada keadaan infeksi, misalnya ISPA, pneumonia, ISK, absesPengobatan insulin dihentikanStress: IMA, strokeObat-obatanBanyak obat diketahui mengurangi sekresi insulin atau menambah resistensi insulin, hidroklotiazid, penghambat beta, penghambat kalsium, dilantin, kortisol (steroid)Alkohol mungkin menghambat sekresi insulin karena dapat menyebabkan pankreatitis subklinis dan mempengaruhi sel beta

PATOFISIOLOGI KAD

Pathogenesis of DKA and HHSStress, Infections and/or insufficient use of Insulin

DKA and HHSCurriculum Module III-6Slide of 55Insulin deficiencyGlucose uptakeLipolysisHyperglycaemiaGluconeogenesisGlycerolFree fatty acidsKetogenesisKetonemiaKetonuriaOsmotic diuresisUrinary water lossesElectrolyte depletionDehydrationAcidosisDiabetic ketoacidosisAdapted from Davidson 2001Glucosuria

DKA and HHSCurriculum Module III-6Slide of 55Ketones

Used as fuel when calories are restrictedPhysiological ketosis when fasting or with prolonged exerciseInsulin deficiency lypolysis and ketone production acidosisbeta-hydroxybutyrateacetoacetateacetone

DKA and HHSCurriculum Module III-6Slide of 55KetonesBeta-hydroxybutyrate predominant not detected by test strips or acetone tabletsKetoacidosis may be present without detectable urinary ketones Blood ketone testing may enable early identification of DKA

KRITERIA DIAGNOSIS:Klinis: Riwayat DM sebelumnyaTerdapat faktor pencetus yang biasa menyertaiKesadaran menurunPernapasan cepat dan dalam (kussmaul sign)Tanda-tanda dehidrasi

KRITERIA DIAGNOSIS:Laboratorium:Hiperglikemia (GDS > 250 mg/dl)Asidosis (PH < 7,3, bikarbonat < 15 mEq/L)Ketosis (ketonemia dan ketonuria)

DKA and HHSCurriculum Module III-6Slide of 55Earlier clinical symptoms and signs of DKA Polyuria Polydipsia Polyphagia Tiredness Muscle cramps Flushed facial appearance

DKA and HHSCurriculum Module III-6Slide of 55Later clinical symptoms and signs of DKA Weight loss Nausea and vomiting Abdominal pain Dehydration Acidotic breath Hypotension Shock Altered consciousness Coma

DKA and HHSCurriculum Module III-6Slide of 55DKA laboratory findings

Blood glucose>14mmol/L (252mg/dL)KetonesUrine: moderate to largeBlood: >3mmol/LOsmolalityIncreased high blood glucose and urea/creatinine, dehydrationElectrolytesLow/normal Na+ and Cl-Low/normal/high K+ (often misleading) Low HCO3 (normal 23-31) Anion gap>10 mild>12 moderate to severeBlood gasespH

DIAGNOSIS BANDINGKoma Hiperosmolar Non Ketotik (HONK)Koma hipoglikemikKesadaran menurun, GD < 60 mg/dlKoma uremikumKoma hepatikum

PEMERIKSAAN PENUNJANG

Foto toraks: tanda infeksi paruEKG: tanda infark miokard akutLaboratorium: DPLGD sewaktuaseton darah/urinanalisis gas darahelektrolittes fungsi hati tes fungsi ginjal.

PENATALAKSANAANSetelah diagnosis KAD ditegakkan maka pengobatan harus segera dimulai dan akan memberikan hasil yang baik bila dilakukan secara tepat dan intensif. Pemasangan Sonde HidungLambung; diperlukan untuk mengosongkan lambung supaya aspirasi isi lambung dapat dicegah bila pasien muntahKateter Urin, untuk memonitor jumlah cairan yang masuk dan keluarPemasangan kanula di vena perifer, namun bila memungkinkan pasang di vena sentral (CVC) terutama pada pasien usia lanjutPrinsip terapi:1. Rehidrasi2. Insulin3. Bikarbonat4. Kalium5. Antibiotika

PENATALAKSANAAN1. RehidrasiRehidrasi cepat merupakan tindakan awal yang harus segera dilakukan. Cairan yang dipilih adalah NaCl 0,9%, tapi bila kadar Natrium > 145 gunakan NaCl 0,45%. Pemberian cairan sebanyak 1 liter pada 30 menit pertama kemudian 0,5 liter pada 30 menit kedua, jadi berjumlah 3 liter pada jam pertama. Setelah itu cairan diberikan sesuai tingkat dehidrasi. Pada keadaan syok dapat digunakan plasma expander Bila kadar glukosa darah < 200 mg/dl, NaCl 0,9% segera diganti dengan dextrose 5%.

PENATALAKSANAAN2.InsulinInsulin mulai diberikan pada jam ke-2, dalam bentuk bolus (intravena) dosis 180 mU/Kg BB, dilanjutkan dengan drip insulin 90 m U/jam/kgBB dalam NaCl 0,9%. Bila glukosa darah < 200 mg %, kecepatan dikurangi menjadi 45 m U/jam/kg BB.Bila glukosa darah stabil sekitar 200-300 mg% selama 12 jam, dilanjutkan dengan drip insulin 1-2 unit/jam dan dilakukan sliding scale setiap 6 jam.

PENATALAKSANAAN3. BikarbonatKoreksi natrium bikarbonat dilakukan bila pH

SKEMA PENATALAKSANAAN KAD

Penatalaksanaan:Secara skematis dapat dilihat pada skema dibawah ini. Slide *

JAM KE INFUS 1INFUS II (INSULIN)KOREKSI K+KOREKSI HCO30 2 kolf jam 1 kolf jam1 2 kolf2 1 kolf3 2 kolf4 kolf5 kolf6

d.s.t tergantung kepada kebutuhan

Jumlah cairan yang diberikan dalam 15 jam sekitar 5 liter.Bila Na0>155mEq/l ganti NaCl n

Pada jam ke 2 :Bolus 180 mU/KgBB dilanjutkan dengan drip insulin 90 mU/KgBB dalam NaCl 0.9%

Bila gula darah

PEMANTAUAN

Kadar glukosa darah tiap jam (glukometer)Elektrolit tiap 6 jam selama 24 jam, selanjutnya tergantung keadaanAnalisis gas darah; bila PH kurang dari 7 periksa kembali setiap 6 jam sampai PH lebih dari 7,1 selanjutnya tiap hari sampai stabilPengukuran TNSP: tekanan darah, tekanan nadi, frekuensi napas dan suhu tiap jamKeadaan hidrasi, balans cairanWaspada terhadap kemungkinan DIC

PROGNOSISBuruk bila tidak mendapat pengobatan dengan cepat

DKA and HHSCurriculum Module III-6Slide of 55DKA complicationsHypoglycaemia +/- hypokalaemiaAcidosis not improving consider continuing dehydration or infectionAspiration pneumoniaHeadache +/- falling level of awareness consider cerebral oedema and urgent treatment with Mannitol

This diagram shows the pathways in the development of DKA. The influence of counterregulatory hormones on gluconeogenesis and ketogenesis is not shown but is important.

Note the osmotic diuresis that promotes the severe degree of electrolyte depletion and dehydration.

DKA is the combination of dehydration and acidosis, both of which require treatment.It is important to recognize the difference between mild physiological ketosis and the more serious pathological production of ketones in DKA.

All of us have ketosis at times of fasting or when we are losing weight. In fact, some diet programmes require people to test for ketones in their urine to determine whether they are burning fat. This ketosis is physiological, does not represent a problem and does not cause illness.

Note: the normal blood ketone level is less than 0.5mmol/L.

In DKA, insulin deficiency leads to hyperglycaemia and the release of fatty acids from the breakdown (lipolysis) of fat stores. This produces excess ketones which are acidic hence ketoacidosis.

The three ketones produced are Beta-hydroxybutyrate which is the major ketone in the blood (and there are newer bedside methods of measuring this) Acetone (smelt on the breath and present in urine) Acetoacetate ( also excreted in the urine).The usual practice is to test urine for ketones (acetone and acetoacetate). Urine testing does not recognize beta-hydroxybutyrate, which is the main ketoacid in DKA. By the time urine tests positive for ketones, the level of beta-hydroxybutyrate may be quite high. Therefore, it is possible for a person to have DKA when the urine shows negative for ketones,.

It should be remembered that ketonuria takes many hours to clear and is not a good indicator of a persons well-being in the recovery phase of DKA.

As blood ketones change more quickly, these enable the early detection of DKA and, compared to ketonuria, may be a better indicator of clinical progress as a person recovers from DKA. Blood testing is expensive and not available everywhere.The early symptoms of DKA are the same as those for increasing levels of hyperglycaemia increased thirst and urination and, often, an increased appetite to cope with the catabolic phase of diabetes.

With regard to DKA, prevention is, of course, better than cure. The early recognition of these symptoms should alert us to a prompt diagnosis and urgent preventive treatment.If the early signs are ignored, rapid weight loss often more than 5 kg results from increased lipolyisis and dehydration.

By the time nausea and vomiting or abdominal pain develop, medical advice is required to either immediately adapt diabetes management in someone with established diabetes, or hospital treatment if new-onset diabetes is suspected.

Acidotic breath (with acetone smell) occurs with the accumulation of CO2 due to shifts in acid base (very low pH and blood bicarbonate). At this stage, hospital treatment is a urgently required.These are the results of clinical tests that may be seen in a person with DKA. Although ketoacidosis may be present with blood glucose levels within the normal range, blood glucose is usually above 14 mmol/l.

As mentioned previously, there are total body deficits in potassium (K+). Sodium (Na+) will also be low. However, the lab results may be misleading because high lipid levels in a person with uncontrolled diabetes may spuriously lower sodium levels. Vascular dehydration plus the escape of potassium from cells often raises potassium levels.

Treatment with insulin results in the rapid movement of potassium and glucose from the extra-cellular fluid back into the cells, thus potentially causing dangerous falls in potassium levels.

In treatment, therefore, it is most important to correct shock and severe dehydration (with renal impairment in older people) before adding potassium and then insulin. Serum bicarbonate (HCO3) will be low. The lower the HCO3 or blood pH, the more severe the ketoacidosis.*Although complications are not frequent, if these occur they are often serious and life-threatening.

With slower insulin infusions, hypoglycaemia is now much rarer; with careful potassium monitoring, cardiac arrhythmias with hypogycaemia or hyperkalaemia should be avoided.

The insertion of an NG tube to drain the stomach contents is very important in preventing continuing vomiting and aspiration pneumonia, especially in older people or those with impaired levels of consciousness.

If cerebral oedema is suspected, immediate Mannitol infusion is recommended before considering cerebral imaging.