Hyperglycemic Emergencies Dr. Miada Mahmoud Rady Ems/474 Endocrinal Emergencies Lecture 3

Lecture Topics 1.DKA. 2.HHNK.  Pathogenesis.  Predisposing factor  Clinical presentation.  Diagnosis.  Management.

Diabetic Ketoacidosis DKA

Introduction  DKA : Diabetic ketoacidosis is one of the major and may be life threatening complication of diabetes.  It is more common in type 1 diabetes, and so it is commonly seen in young and may be the first presenting symptoms.  Hall mark of DKA as illustrated by the way its has been called is hyperglycemia, ketosis and acidosis.  It develops rapidly usually over hours.

Pathophysiology  Mainly associated with type 1 diabetes : 1.Type 1 diabetes is characterized by absolute insulin deficiency. 2.In absence of insulin, the body cannot utilize glucose which is the primary source of energy so alternative sources are used (fatty acids ). 3.Excess fatty acids metabolism result in Increased ketone bodies which contribute to increased metabolic acids.

4.Hyperglycemia associated causes marked dehydration.

1.Hyperglycemia. 2.Ketosis 3.Metabolic acidosis. 4.Hyperkalemia.  These characteristic finding are responsible for clinical presentation of DKA. So DKA is characterized by………..

Predisposing factors 1.Missed insulin. 2.Heavy meal. 3.Acute pancreatitis. 4.Infection. 5.Trauma. 6.Surgery. 7.MI. 8.Pregnancy. Decreased insulin reserve Increased insulin requirement

Clinical Presentation 1.Polyuria and Polydepsia. 2.Marked dehydration. 3.Sweet, fruity breath odor (characteristic). 4.Kussmaul respiration (rapid and deep respiration). 5.Hyperkalemia induced cardiac arrhythmias. 6.Nausea, vomiting and abdominal pain. 7.Slow and Gradual decline in the mental status and finally coma.

Clinical Presentation Symptoms 1. Polyuria 2. Polydepsia 3. Nocturia. 4. Weakness, dizziness 5. Palpitation. 6. Dyspnea 7. Nausea, vomiting and abdominal pain. 8. Coma Signs 1. Warm, flushed skin. 2. Dry tongue. 3. Fruity smell of the mouth. 4. Hypotension and shock 5. Tachycardia and k induced arrhythmias. 6. Kussmaul breathing. 7. Abdominal tenderness. 8. Disturbed conscious level.

Laboratory Finding  Hyperglycemia : blood glucose level is more than 250mg/dl, ( usually more than 300mg/dl).  Ketonemia and ketonuria : Increase level of ketone bodies in the blood and its detection in urine.  Metabolic acidosis : PH ＜ 7.35  Hyperkalemia : increase serum potassium.

Clinical Tips 1.Abdominal pain of DKA may be so sever that it may simulate acute abdomen.  It is more common in children than adult.  It is commonly periumbilical. 2.Coma develops lately and only in very sever cases of DKA.

Management  Follow the general guidelines for patient care : 1.Airway :  Manage and maintain patent airway as indicated  If the patient is comatosed protect airway, be ware of vomiting and have suction ready. 2.Breathing :  Maintain adequate oxygenation and be prepared for intubation.

3.Circulation :  Record and continuously monitor cardiac rhythm and vital signs.  Obtain serial 12 lead ECG.  Measure blood glucose level.  Start an I.V line and Give 12.5 – 25 gm of 50% dextrose if blood glucose level is below 70 mg/dl or cannot be determined.  Start normal saline per local protocols. Management

 Cardiac rhythm monitoring in DKA :  Marked Hyperkalemia produce several ECG changes which is usually dangerous and potentially fatal :  Sharply peaked T waves may indicate high levels of potassium and so sodium bicarbonate may be necessary.  The QRS complex will widen and may blend with the t wave, developing into a sine wave and becoming bradycardic : calcium chloride or gluconate may be indicated. Management

ECG changes of Hyperkalemia

Management 3.Transport patient rapidly. 4.Insulin has no rule in the field treatment of DKA.

DKA Definition DKA = 3 letters= triad of D K A Diabetic glucose >250 mg/dL (usually ) Keto ketones produced  ketones : both in urine and in serum  acetoacetate, acetone, betahydroxybutyrate  fruity smell, not often encountered in real life) Acidosis metabolic acidosis; HCO3- <15, pH<7.30 Rapid deep breathing and hyperkalemia

Insulin Deficiency Glucose uptake Lipolysis Free Fatty Acids Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Polyuria Polydepsia Fruity breath (acetone smell) Kussmaul breathing (acidotic) Mental status changes Dehydration Dry tongue Tachycardia Hypotension Abd pain Electrolyte imbalance Clinical manifestations