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Teaching program 5 th year 2010/2011

Teaching program 5 th year 2010/2011. د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital. Endocrine Emergencies. Endocrine Emergencies:. Diabetic emergencies ( DKA, NKHOC, Hypoglycemia) Thyrotoxic crises, Myxoedema coma. Adrenal crises.

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Teaching program 5 th year 2010/2011

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  1. Teaching program5th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital

  2. Endocrine Emergencies

  3. Endocrine Emergencies: • Diabetic emergencies ( DKA, NKHOC, Hypoglycemia) • Thyrotoxic crises, Myxoedema coma. • Adrenal crises. • Pituitary failure, Diabetes Insipidus, SIADHS. • Calcium related emergencies.

  4. Case History: 21 years old girl, presented with 2 days history of abdominal pain, vomiting, preceded by significant wt. loss, polyuria and polydepsia.

  5. Positive clinical & Lab. Data: • Pulse: 110/min, BP 90/60, Temp. 38.5 c°, RR: 30/min • Signs of dehydration. • RBS: 450 mg/dl, urea: 110 mg/dl, K: 5.5 mmol/l, Na: 150 mmol/l, WBC: 18000/μl • Urine positive for Ketons. ABG: PH: 7.1, P02: 110, Pco2: 30, Hco3: 12 mmol/l

  6. Diagnosis: Diabetic Ketoacidosis 450 mg/dl KetonuriaPH 7.1

  7. Definition: One of the most serious acute metabolic complications of diabetes. Occurs more commonly in patients with insulin-dependent diabetes mellitus (IDDM) Characterized by: • Blood glucose level > 250 mg/dl • Blood pH < 7.3 • Ketones in serum > 5 meq/L

  8. Epidemiology: • Mortality rate was 100% in 1922 but has since come down to 5% with improvements in health care • Common cause of death in type 1 diabetics • Can occur in type 2 as well • 25% as first presentation of type 1 DM

  9. Pathogenesis: Ineffectiveness of insulin. Elevations in glucagon, catecholamines & cortisol. Hepatic gluconeogenesis, glycogenolysis, and lipolysis are affected by this hormone imbalance. Fat, liver and muscle can survive without glucose but Brain must maintain use of glucose.

  10. Hyperglycemia results from Increased gluconeogenesis. Conversion of glycogen to glucose. Inadequate use of glucose by peripheral tissues. Ketone bodies result from Increase triglyceride breakdown to FFA and glycerol. Beta oxidation of FFA. Decreased concentrations of malonylcoA (an inhibitor of ketogenesis).

  11. Hyperglycemia leads to • Glycosuria • Polyuria (osmotic diuresis) • Polydipsia • Polyphagia • Weight loss • Dehyrdation Ketone bodies lead to • Metabolic acidosis

  12. Insulin deficiency Hyperglycemia Lipolysis Hyperosmolarity Ketosis Acetone smell, vomiting Intracellular Osmotic diuresisKussmaul”s Breathing Dehydration Electrolyte loss loss of extracellular consciousness dehydration Acute renal failure + Shock Metabolic acidosis Hypovolemia

  13. Precipitating factors: • Infection : • Pneumonia and UTI most commonly. • Inadequate use of insulin: • Not taking insulin. • Small dose. • Use of OAD. • New onset diabetes. • Medical, surgical or emotional stress. • Drugs: Corticosterioids, thiazide diuretics. • Pancreatitis.

  14. Symptoms: • Polyuria, nocturia, thirst • Rapid weight loss • Muscular weakness • Visual disturbance • Air hunger • Abdominal pain, nausea, vomiting • Leg cramps • Altered sensorium

  15. Signs • Acetone breath • Air hunger • Impaired consciousness • Hyperglycemia, osmolarity • Cerebral edema if sensorium worsens during treatment • Hypotension: due to peripheral vasodilatation due to acidosis • Hypothermia • Succussion splash • May mimic surgical emergency

  16. Diagnosis: • Diagnosis of DKA in IDDM patient is not that difficult. • Diagnostic criteria for DKA: • hyperglycemia (>250 mg/dl) • ketosis (ketonemia or ketonuria) • metabolic acidosis (pH<7.3, HCO3<15mEq/L) • Increase in Anion gab = ( Na + K)- (Cl + Hco3) 8 – 16 mmol/l • supporting features are volume depletion and Kussmaul’s breathing.

  17. Other investigations: Sodium, Potassium, Leucocytosis, high urea, increase of Hb. Ht.

  18. Management: General measures : • control of Breathing, circulation, input, output chart. • central venous line, urinary catheter, NGT. • decubitus and thromboembolism prophylaxis. • control of sugar hourly, K, ABG every 2 hours. Specific treatment: • correction of dehydration. • insulin therapy. • correction of acidosis. • electrolytes replacement.

  19. Fluid replacement: • Use isotonic saline ( normal saline ) 0.9% NaCl. if Na > 155 mmol/l use hypotonic saline 0.45% NaCl. in case of collapse use plasma proteins or albumin. • 1 hour 1000 ml. After that according to CVP: CVP ml fluid/ hr 0 cm 1000 1-3 cm 500 4-8 cm 250 9-12 cm 100 • The pt. may require 5-6 l in the first 8 hrs. • Infuse 5% dextrose when the sugar reaches 250 mg/dl .

  20. Insulin: • Soluble insulin ( regular, rapid) i.v, 20 units stat. • followed by 5-10 units /hr through infusion pump. • Slowly reduction not more than 100mg/dl/hr. • Keep the sugar around 250 mg/dl.( 2 iu+ 5% dextrose) • Hypoglycemia, hypokalemia, brain edema.

  21. Correction of acidosis: • Under insulin the acidosis will be reversed due to inhibition of lipolysis. • If pH < 7.1 give 1/3 of HCO3 deficit. NaHCO3= -ve base excess x wt.kg/3. • Risk ofhypokalemiais there.

  22. Electrolytes replacement: Na: Initially plasma sodium concentrations are low or normal despite water losses due to osmotic shift of water . So will be replaced through i.v fluids. K : concentrations may be normal or elevated, because of: Acidosis and lack of insulin causes potassium shift.

  23. Non-ketoticHyperosmolar coma: • Common in type II. • Blood sugar usually > 600 mg/dl. • Rarely to have acidosis.( small amount of insulin enough to inhibit acidosis). • Hyperosmoarity > 600 mosmol/kgH₂O. • Management as DKA.

  24. Hypoglycemia • Def: blood sugar < 40 mg/dl OR blood sugar <45mg/dl. Whipple Triads symptoms of hypo. correction with Glucose.

  25. Causes Fasting hypoglycaemia: . Insulinoma. .severe liver diseases. .Hypoadrenalism, hypopituitarism. .ß- cell hyperplasia( Nesidioblastosis) Reactive hypoglycaemia : .early stage of DM. .diab. Gastro paresis( autonomic N.) .Dumping syndrome after gastric surgery. . Increase vagus tone. Exogenous hypoglycaemia: .overdose of insulin or sulfonylurea drugs. .factious hypoglycaemia. .Alcohol.

  26. Treatment Elimination of precipitating factors. Mild cases : conscious pat. Oral glucose as grape juice, cola, 20 gm sugar. Severe cases : 25- 100 ml 40% glucose i.v, repeat after 20 min. Or 5% dextrose infusion ( blood sugar 200mg/dl) Glucagon 1 mg i.m.

  27. Hypercalcaemia: Forceful diuresis ( 0.9% Nacl 3 to 6 litres + frusemide) Bisphosphonate. Corticosteroids. Calcitonin. Hypocalcaemia: calcium gluconate 10 % i.v ( 20-30 ml) calcium and vitamin D orally.

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