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Is a life-threatening acute complication of Is a life-threatening acute complication of diabetes mellitus. It occurs when insulin diabetes mellitus. It occurs when insulin therapy is absent, or becomes inadequate for therapy is absent, or becomes inadequate for the current physiological state, usually as a the current physiological state, usually as a result of intercurrent illness.result of intercurrent illness.

It is normally seen in type 1 diabetics and may It is normally seen in type 1 diabetics and may be a presenting feature of undiagnosed type 1 be a presenting feature of undiagnosed type 1 diabetes, particularly in children.diabetes, particularly in children.

However, it is not unheard of in type 2 diabetics.However, it is not unheard of in type 2 diabetics.

(1) (1) SymptomsSymptoms Nausea / vomiting.Nausea / vomiting. Thirst / polyuria.Thirst / polyuria. Abdominal pain.Abdominal pain. Shortness of breath.Shortness of breath.

(2) (2) physical findingsphysical findings Tachycardia.Tachycardia. Dehydration / hypotension.Dehydration / hypotension. Tachypnea / kussmaul respirations / Tachypnea / kussmaul respirations /

respiratory distress.respiratory distress. Abdominal tenderness ( may resemble Abdominal tenderness ( may resemble

acute pancreatitis or surgical abdomen)acute pancreatitis or surgical abdomen) Lethargy / obtundation / cerebral edema / Lethargy / obtundation / cerebral edema /

possibly coma.possibly coma.

(3) (3) precipitating eventsprecipitating events Inadequate insulinInadequate insulin administration.administration. Infection Infection

(pneumonia/UTI/gastroenteritis/sepsis)(pneumonia/UTI/gastroenteritis/sepsis) infraction infraction

(cerebral,coronary,mesenteric,peripheral)(cerebral,coronary,mesenteric,peripheral) Drugs (cocaine)Drugs (cocaine) Pregnancy.Pregnancy.

1. Inadequate insulin secretion hyperglycemia cellular starvation

2. Induce secretion of glucagon, catecholamine, cortical, & GH.

3. Stress response encourage proteolysis & lipolysis FFA convert to ketoacid, Acetoacetate, β-hydroxybutyrate & aceton metabolic acidosis

4. Encourage glycogenolysis, gluconeogenesis further glucose huge osmotic diuresis and gross dehydration

5. Dehydration tissue perfusion lactic acidosis

• Confirm diagnosis.Confirm diagnosis.• Admit to hospital.Admit to hospital.• Assess serum electrolytes & acid-base Assess serum electrolytes & acid-base

status .status .• Replace fluids.Replace fluids.• Administer short acting insulin.Administer short acting insulin.• Assess patient : what precipitate the episode Assess patient : what precipitate the episode • Replace K+.Replace K+.• Continue above until patient is stable.Continue above until patient is stable.• Administer intermediate or long actingAdminister intermediate or long acting

insulin as soon as patient is eating. insulin as soon as patient is eating.

1-1- Confirm diagnosisConfirm diagnosis

(plasma glucose, positive serum ketones, (plasma glucose, positive serum ketones, metabolic acidosis).metabolic acidosis).

2- 2- Admit to hospital:Admit to hospital:

intensive-care setting may be necessary for intensive-care setting may be necessary for frequent monitoring or if ph <7.00 orfrequent monitoring or if ph <7.00 or unconscious.unconscious.

3-3- Assess:Assess:serum electrolytes (K+ , Na+ , Mg+2 , Cl-, serum electrolytes (K+ , Na+ , Mg+2 , Cl-, bicarbonate , phosphate) acid-base status-bicarbonate , phosphate) acid-base status-pH, HCO3-, Pco2, pH, HCO3-, Pco2, ββ-hydroxybutyrate-hydroxybutyrate

4-4- Replace fluids: Replace fluids:2 -3 L of 0.9% saline over first 1-3 h (10-15 2 -3 L of 0.9% saline over first 1-3 h (10-15 ml/kg per hour); subsequently, 0.45% saline ml/kg per hour); subsequently, 0.45% saline at 150-300 ml/h; change to 5% glucose and at 150-300 ml/h; change to 5% glucose and 0.45% saline at 100-200 ml/h when plasma 0.45% saline at 100-200 ml/h when plasma glucose reaches 250 mg/dL (14 mmol/L).glucose reaches 250 mg/dL (14 mmol/L).

5-5- Administer short-acting insulin: Administer short-acting insulin:IV (0.1 units/kg) or IM (0.3 units/kg), then IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by continuous IV 0.1 units/kg per hour by continuous IV infusion; increase 2-to3-fold if no response infusion; increase 2-to3-fold if no response by 2-4 h. If initial serum potassium is by 2-4 h. If initial serum potassium is corrected to >3.3 mmol/L (3.3.meq/L).corrected to >3.3 mmol/L (3.3.meq/L).

6-6- Assess patient:Assess patient:What precipitated the episode What precipitated the episode (noncompliance, infection, trauma, infraction, (noncompliance, infection, trauma, infraction, cocaine)? Initiate appropriate workup for cocaine)? Initiate appropriate workup for precipitating event(cultures,CXR,ECG).precipitating event(cultures,CXR,ECG).

7-7- Measure capillary glucose every 1-2 h; Measure capillary glucose every 1-2 h; measure electrolytes (especially K+, measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every bicarbonate, phosphate) and anion gap every 4 h for first 24 h.4 h for first 24 h.

8- Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1-4 h.

9-9- Replace K+: 10 meq/h when plasma K+<5.5 Replace K+: 10 meq/h when plasma K+<5.5 meq/L, ECG normal, urine flow and normal meq/L, ECG normal, urine flow and normal creatinine documented; administer 40-80 creatinine documented; administer 40-80 meq/h when plasma K+<3.5 meq/L or if meq/h when plasma K+<3.5 meq/L or if bicarbonate is given.bicarbonate is given.

• Very rarely k+ replacement may need to be Very rarely k+ replacement may need to be given before insulin if the patient profoudly given before insulin if the patient profoudly hypokalaemic to begin with e.g. k+ < 3.5 hypokalaemic to begin with e.g. k+ < 3.5 mmol/Lmmol/L

• If the patient is hyperkalaemic do not give K+ If the patient is hyperkalaemic do not give K+ therapy-recheck after 30 minute.therapy-recheck after 30 minute.

10- 10- Continue above until patient is stable, Continue above until patient is stable, glucose goal is 150-250 mg/dL, and acidosis glucose goal is 150-250 mg/dL, and acidosis is resolved. Insulin infusion may be is resolved. Insulin infusion may be decreased to 0.05-0.1 units/kg per hour.decreased to 0.05-0.1 units/kg per hour.

11-11- Administer intermediate or long-acting Administer intermediate or long-acting insulin as soon as patient is eating. Allow for insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous overlap in insulin infusion and subcutaneous insulin injection.insulin injection.

Mild diabetic ketosisMild diabetic ketosis If the patient is fully conscious & there has If the patient is fully conscious & there has

been no nausea or vomitting for at least 12 h been no nausea or vomitting for at least 12 h intravenous therapy is unnecessary it is intravenous therapy is unnecessary it is reasonable to give small doses of insulin s.c reasonable to give small doses of insulin s.c 4-6 hourly & fluids by mouth .4-6 hourly & fluids by mouth .

ComplicationsComplications Cerebral oedema – commoner in

children/adolescents where it affects around 1% of cases of DKA. Mortality is significant and estimated at 20-90%. Presents in first 24 hours with headache, behavioural changes and urinary incontinence progressing to abrupt neurological deterioration and coma.

Pulmonary oedema due to overzealous fluid replacement or as a spontaneous phenomenon.

Iatrogenic hypoglycaemia or hypokalaemia. Cardiac dysrhythmia due to electrolyte

disturbance(particularly K+)or metabolic asidosis.

Myocardial suppression due to metabolic acidosis.

Venous thromboembolism. Myocardial infraction(may be a cause of, or

complication of DKA). Diabetic retinopathic changes may be seen

prior to or after therapy for DKA . Hypophosphataemia- rarely has significant

clinical effects. Adult respiratory distress syndrome. Death still occurs.

ComplicationsComplications

PrognosisPrognosis Prognosis is excellent in cases that are

appropriately managed and which present before progression to coma.

Prognosis worsens with age and the severity of the underlying precipitating pathology (particularly MI, sepsis and pneumonia).

The presence of coma at presentation, hypothermia or persistent oliguria are poor prognostic indicators.