Endocrine emergencies

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Endocrine emergencies

  1. 1. Endocrine Emergencies Professor Ikram S Ismail PhD (Wales) FRCP (Edin) FAMM FACE
  2. 2. Endocrine Emergencies <ul><li>Diabetic Coma </li></ul><ul><ul><li>Hypoglycaemia </li></ul></ul><ul><ul><li>Diabetic Ketoacidosis </li></ul></ul><ul><ul><li>Hyperosmolar nonketotic coma </li></ul></ul><ul><li>Thyroid storm </li></ul>
  3. 4. Diabetic Ketoacidosis <ul><li>Results from lack of insulin </li></ul><ul><li>Occurs in people with type 1 diabetes. Can also occur in type 2 DM in severe stress. </li></ul><ul><li>Medical emergency that needs urgent hospitalization </li></ul><ul><li>Accounts for approximately 5% mortality </li></ul>
  4. 5. Causes of DKA <ul><li>A. Absolute Insulin Deficiency: </li></ul><ul><li>Omission or reduction of insulin </li></ul><ul><li>Undiagnosed diabetes </li></ul>
  5. 6. Causes of DKA <ul><li>B. Relative Insulin Deficiency: (excess catabolic hormone secretion with fixed insulin dosage) </li></ul><ul><li>Acute illness: </li></ul><ul><ul><li>Infection </li></ul></ul><ul><ul><li>Myocardial infarction </li></ul></ul><ul><ul><li>Stroke </li></ul></ul><ul><ul><li>Trauma </li></ul></ul><ul><ul><li>Severe emotional disturbance </li></ul></ul><ul><li>Endocrine Disorders </li></ul><ul><ul><li>Steroid therapy </li></ul></ul><ul><ul><li>Adrenergic agonists </li></ul></ul><ul><ul><li>Phaeochromocytoma </li></ul></ul><ul><ul><li>Thyroid storm </li></ul></ul>
  6. 7. DKA: Pathophysiology
  7. 8. DKA: Pathophysiology
  8. 9. DKA - Symptoms <ul><li>Symptoms develop over several hours </li></ul>Thirst, Polyuria Osmotic Diuresis Fatigue Dehydration, protein loss Weight loss Protein loss, catabolism, dehydration Nausea, vomiting ?Ketosis, gastric stasis Abdominal pain ?ileus, gastric stasis, K deficit Muscle cramps ?K deficiency
  9. 10. DKA - Signs Dehydration Osmotic Diuresis, vomiting Tachycardia Dehydration Hypotension Dehydration, acidosis Warm skin Acidosis (peripheral vasodilatation) Hyperventilation Ketosis, acidosis Coma, drowsiness Hyperosmolality
  10. 11. DKA - Diagnosis <ul><li>Diagnostic procedures </li></ul><ul><li>Determine blood glucose level and test for ketones </li></ul><ul><li>Send blood to laboratory for estimation of glucose, urea, electrolytes,arterial pH, pO 2 , pCO 2, Hb, and WBC </li></ul><ul><li>Send for culture of blood, urine and lung secretions </li></ul>
  11. 12. Blood Ketone Testing <ul><li>Indications </li></ul><ul><li>Asymptomatic patients with glucose > 16.70 mM </li></ul><ul><li>Symptomatic patients with possible DKA </li></ul><ul><li>Monitoring in established DKA </li></ul><ul><li>To assist in making decision on admission </li></ul><ul><li>To assist in making decisions for intensive medical therapy </li></ul>
  12. 13. Established DKA >3.0 If concurrent stress and poor compliance - admit >1.5 Retest glucose and ketones in 2-4hrs 0.6 – 1.5 Check clinical status <0.6
  13. 14. DKA – Investigations Hyperglycaemia, hyperketonaemia Insulin deficiency Decreased pH, PCO2, bicarbonate Increased ketogenesis Hyponatraemia Hyperglycaemia Variable K Insulin deficiency, acidosis, urine loss Raised WCC Hyperketonaemia Raised haematocrit Dehydration
  14. 15. DKA - Deficits Water 5 to 8 liters Sodium 400-700 mmol Chloride 300-500 mmol Potassium 300-1000 mmol Calcium 100 mmol Magnesium 50 mmol Phosphate 50 mmol Bicarbonate 350 to 400 mmol
  15. 16. Treatment of ketoacidosis <ul><li>Initiation of treatment must be immediate </li></ul><ul><li>Treatment includes </li></ul><ul><ul><li>Rehydration </li></ul></ul><ul><ul><li>Insulin administration </li></ul></ul><ul><ul><li>Electrolyte correction </li></ul></ul><ul><ul><li>Stabilization of cardiovascular and and renal function </li></ul></ul>
  16. 17. Treatment of ketoacidosis <ul><li>Fluids </li></ul><ul><ul><li>Most urgent and first line treatment </li></ul></ul><ul><ul><li>Rehydration alone will cause fall in glucose </li></ul></ul><ul><ul><ul><li>Increase urine flow </li></ul></ul></ul><ul><ul><ul><li>Allow perfusion </li></ul></ul></ul><ul><ul><li>Saline given rapidly </li></ul></ul><ul><ul><ul><li>1 L in 30min, then hourly for 3 hrs </li></ul></ul></ul><ul><ul><ul><li>CVP monitoring in elderly/CVS disease </li></ul></ul></ul>
  17. 18. Treatment of ketoacidosis <ul><li>Insulin </li></ul><ul><ul><li>Aim to switch off gluconeogenesis, lipolysis, ketogenesis </li></ul></ul><ul><ul><li>Insulin regimens </li></ul></ul><ul><ul><ul><li>Intramuscular: </li></ul></ul></ul><ul><ul><ul><ul><li>20 units stat, then 5U/hr </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Children: 0.25 U/kg stat, then 0.1 U/kg/hr </li></ul></ul></ul></ul><ul><ul><ul><li>Intravenous infusion </li></ul></ul></ul><ul><ul><ul><ul><li>Adults: 6 U/hr </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Children 0.1 U/kg/hr </li></ul></ul></ul></ul><ul><ul><li>Once glucose fallen to below 15 mmol/L, replace saline with 10%Dextrose with 20-40 mmol K, reduce insulin to 3 U/hr </li></ul></ul>
  18. 19. Treatment of ketoacidosis <ul><li>Potassium </li></ul><ul><ul><li>Hypokalemia most common cause of death </li></ul></ul><ul><ul><li>Potassium will fall during therapy: </li></ul></ul><ul><ul><ul><li>Move into cells resulting from insulin, correction of acidosis, and restoration of volume </li></ul></ul></ul><ul><ul><ul><li>Haemodilution </li></ul></ul></ul><ul><ul><ul><li>Urinary loss </li></ul></ul></ul><ul><ul><li>Begin with insulin treatment: 20 mmol/h </li></ul></ul>
  19. 20. Treatment of ketoacidosis Acid-base Hazards of acidosis pH<7 Hazards of alkali therapy <ul><li>Negative inotropism </li></ul><ul><li>Peripheral vasodilatation </li></ul><ul><li>Cerebral depression </li></ul><ul><li>Insulin resistance </li></ul><ul><li>Enzyme depression </li></ul><ul><li>Hypokalaemia </li></ul><ul><li>Increased anaerobic glycolysis </li></ul><ul><li>Impaired tissue oxygen delivery </li></ul><ul><li>Paradoxical fall in CSF pH </li></ul><ul><li>Rebound alkalosis </li></ul><ul><li>Sodium overload </li></ul>
  20. 21. Treatment of ketoacidosis <ul><li>Acid-base </li></ul><ul><ul><li>Give 100 mmoL with KCl 200 mmol when pH < 7, repeat until pH  7 </li></ul></ul><ul><ul><li>Symptomatic relief: 50 mmoL with KCl 10 mmol </li></ul></ul>
  21. 22. Treatment of ketoacidosis <ul><li>Clinical measures </li></ul><ul><ul><li>Gastric stasis: NG suction in drowsy pts </li></ul></ul><ul><ul><li>Infection: </li></ul></ul><ul><ul><ul><li>Usual signs lacking </li></ul></ul></ul><ul><ul><ul><li>Hyperglycaemia increases risk of sepsis </li></ul></ul></ul><ul><ul><ul><li>Use broad spectrum antibiotics after cultures </li></ul></ul></ul><ul><ul><li>Risk of thrombosis </li></ul></ul><ul><ul><ul><li>Prophylactic SC Heparin 5000 units q6-8hrly in the unconscious, elderly, hyperosmolar </li></ul></ul></ul><ul><ul><li>Hypotension: use plasma expanders </li></ul></ul><ul><ul><li>Clinical monitoring </li></ul></ul>
  22. 23. Complications of treatment <ul><li>ARDS </li></ul><ul><ul><li>Sudden dyspnoea, hypoxaemia, diffuse pulmonary infiltrates </li></ul></ul><ul><ul><li>Younger pts, fatal </li></ul></ul><ul><ul><li>Mechanisms: </li></ul></ul><ul><ul><ul><li>Use of crystalloids </li></ul></ul></ul><ul><ul><ul><li>Alveolar defect caused by acidosis snf hyperventilation </li></ul></ul></ul><ul><li>Cerebral oedema </li></ul><ul><ul><li>High mortality </li></ul></ul><ul><ul><li>Use of hypotonic replacement fluids </li></ul></ul><ul><li>Abdominal pain </li></ul><ul><ul><li>Can mimic acute abdomen </li></ul></ul>
  23. 24. Hyperosmolar Non-ketotic Hyperglycaemia <ul><li>Accounts for 5-10% of hyperglycemic comas </li></ul><ul><li>Mortality 30-50%, usually from arterial or venous thrombosis </li></ul><ul><li>Occurs mainly in elderly persons with type 2 diabetes </li></ul><ul><li>When compared with DKA, it has: </li></ul><ul><ul><li>Higher mortality </li></ul></ul><ul><ul><li>Higher hyperglycemia </li></ul></ul><ul><ul><li>More severe dehydration </li></ul></ul>
  24. 25. HONK: Treatment <ul><li>Rehydration is the most important treatment </li></ul><ul><ul><li>Is performed under close observation of circulatory status </li></ul></ul><ul><li>Insulin concentration is usually low </li></ul><ul><ul><li>Blood glucose will drop in parallel with rehydration </li></ul></ul><ul><li>Patients should be monitored in a special intensive care unit </li></ul>
  25. 26. Hypoglycaemia <ul><li>Defined as blood glucose below 3 mmol/l </li></ul><ul><li>Some people with diabetes develop hypoglycaemic symptoms even when BG > 3 mmol/l </li></ul><ul><li>Some persons with diabetes do not have symptoms even at very low BG </li></ul><ul><ul><li>Hypoglycaemic unawareness </li></ul></ul>
  26. 27. Causes of Hypoglycaemia <ul><li>Administration of too much insulin. </li></ul><ul><li>Insufficient intake of carbohydrate. </li></ul><ul><li>Delay or omission of a snack or main meal. </li></ul><ul><li>Performing more exercise than usual. </li></ul><ul><li>Overdosing of sulphonylureas. </li></ul><ul><li>Over-indulgence in alcohol. </li></ul>
  27. 28. Hypoglycaemia : Symptoms and Signs
  28. 29. Hypoglycaemia : Classification <ul><li>Mild hypoglycaemia </li></ul><ul><ul><li>Activation of the autonomic nervous system </li></ul></ul><ul><ul><li>Symptoms: tremors, palpitations, sweating, hunger </li></ul></ul><ul><ul><li>The patients are able to treat themselves </li></ul></ul><ul><li>Severe hypoglycaemia </li></ul><ul><ul><li>Very low blood glucose level </li></ul></ul><ul><ul><li>Symptoms : confusion, drowsiness, coma, seizure </li></ul></ul><ul><ul><li>Help is needed from others or consciousness is lost </li></ul></ul><ul><ul><li>Acute professional assistance may be needed </li></ul></ul>
  29. 30. Nocturnal Hypoglycaemia <ul><li>Usually occurs between 2 and 4 am </li></ul><ul><li>Diagnosis through : </li></ul><ul><ul><li>Symptoms in the night and next morning </li></ul></ul><ul><ul><li>Blood glucose testing at the time of occurrence </li></ul></ul><ul><li>Treatment </li></ul><ul><ul><li>Add a snack before bedtime </li></ul></ul><ul><ul><li>Reduce dose of insulin </li></ul></ul><ul><ul><li>Adjust timing of insulin injection </li></ul></ul><ul><ul><li>Change the type of insulin </li></ul></ul>
  30. 31. Hypoglycaemia Caused by Sulphonylureas <ul><li>More common with longer acting sulphonylureas </li></ul><ul><ul><li>Chlorpropamide </li></ul></ul><ul><ul><li>Glibenclamide </li></ul></ul><ul><li>Treatment with glucose </li></ul><ul><li>Hospitalisation with severe hypoglycaemia </li></ul><ul><li>Alternative diabetic treatment </li></ul><ul><ul><li>Shorter acting sulphonylureas </li></ul></ul><ul><ul><li>Metformin </li></ul></ul>
  31. 32. Hypoglycaemic Unawareness <ul><li>Low blood glucose without symptoms </li></ul><ul><li>Associated with </li></ul><ul><ul><li>Long duration of diabetes </li></ul></ul><ul><li>Condition requires frequent blood glucose monitoring </li></ul>
  32. 33. Treatment of Mild Hypoglycaemia <ul><li>Relieved by </li></ul><ul><ul><li>1 glass of fruit juice or soft drink </li></ul></ul><ul><ul><li>3 heaped teaspoon of sugar, honey or 3-5 sweets </li></ul></ul><ul><ul><li>Dextrose tablets of 5 g </li></ul></ul><ul><li>Repeat if symptoms are not relieved after 5 to 10 minutes </li></ul><ul><li>If next meal not immediately due, take 30 g of complex carbohydrate i.e. an apple or a slice of bread after recovery </li></ul>
  33. 34. Treatment of Severe Hypoglycaemia <ul><li>Confirm diagnosis with a portable meter </li></ul><ul><li>Administer 1 mg of glucagon intramuscularly for adults and for children >25 kg (children < 25kg, give 0.5 mg or 0.02 mg/kg body weight) </li></ul><ul><li>If next meal not immediately available, give 30 g complex carbohydrate </li></ul><ul><li>If the patient does not recover consciousness within 5-10 minutes, admit to hospital </li></ul>
  34. 35. Thyroid Storm <ul><li>Life threatening exacerbation of hyperthyroid state with evidence of decompensation in one or more organ systems. </li></ul><ul><li>Incidence : 10% of patient hospitalized for thyrotoxicosis </li></ul><ul><li>Fatal if not treated </li></ul><ul><li>Mortality 20-30% </li></ul>
  35. 36. Pathophysiology: <ul><li>Levels of thyroid hormones </li></ul><ul><li>Rate of rise of thyroid hormone </li></ul><ul><li>Development of tissue intolerance </li></ul><ul><li>Role of adrenergic activation </li></ul>
  36. 37. Pathophysiology <ul><li>Levels of thyroid hormones </li></ul><ul><li>Most older studies found no difference in thyroid hormone levels </li></ul><ul><li>Newer studies measuring free hormone levels showed higher levels of free T4 in thyroid storm </li></ul>
  37. 38. Pathophysiology <ul><li>Rate of rise of thyroid hormone </li></ul><ul><li>Related to the change in levels of binding proteins noted in systemic illness and postoperatively </li></ul><ul><li>Production of T4 binding inhibitors resulting in decreased binding affinity of T4 and increase free T4 levels </li></ul><ul><li>Rapid release of T4 into the circulation could saturate binding capacity </li></ul>
  38. 39. Pathophysiology <ul><li>Development of tissue intolerance </li></ul><ul><ul><li>Homeostatic decompensation despite similar hormone levels. </li></ul></ul><ul><li>Role of adrenergic activation </li></ul><ul><ul><li>Normal plasma levels of adrenaline noted </li></ul></ul><ul><ul><li>But T 4 causes increased  receptors in some tissues </li></ul></ul><ul><ul><li>Post receptor action to alter responsiveness to catecholamine </li></ul></ul>
  39. 40. Clinical presentation <ul><li>All of usual features of thyrotoxicosis - usually exaggerated and severe </li></ul><ul><li>History of previous thyroid disease partially treated or a history of symptoms suggestive of thyrotoxicosis </li></ul><ul><li>Fever typically present </li></ul><ul><li>Sweating profuse initially, later dry when become dehydrated </li></ul><ul><li>Pulse pressure widened </li></ul>
  40. 41. <ul><li>Atrial arrhythmias </li></ul><ul><li>Nausea, vomiting, diarrhea </li></ul><ul><li>Increase motor and psychic restlessness  confusion, delirium, agitation </li></ul><ul><li>Unusual presentation reported </li></ul><ul><ul><li>acute abdomen </li></ul></ul><ul><ul><li>status epilepticus, coma </li></ul></ul><ul><ul><li>stroke </li></ul></ul>Clinical presentation
  41. 42. Clinical Presentation <ul><li>Occasionally few or no thyrotoxic features  GI, cardiovascular or neurologic features predominate </li></ul><ul><li>May be impossible to distinguish between severe hyperthyroidism with concurrent illness and thyroid storm. </li></ul><ul><li>Usually thyroid storm, the fever and tachycardia tends to be out of proportion to the illness </li></ul>
  42. 43. Precipitating events <ul><li>Infection </li></ul><ul><li>Surgery </li></ul><ul><li>Radioactive iodine </li></ul><ul><li>Withdrawal of anti-thyroid drugs </li></ul><ul><li>Amiodarone, thyroid hormone ingestion </li></ul><ul><li>DKA, CCF, Hypoglycemia </li></ul><ul><li>PET, parturition </li></ul><ul><li>Vigorous palpation of the thyroid gland </li></ul>
  43. 44. Diagnosis <ul><li>Mainly clinical </li></ul><ul><li>Diagnostic criteria to aid clinical diagnosis </li></ul><ul><ul><li>Thermoregulatory Dysfunction </li></ul></ul>
  44. 45. Diagnosis <ul><ul><li>Central Nervous system Effects </li></ul></ul>
  45. 46. Diagnosis <ul><ul><li>Gastrointestinal-hepatic Dysfunction </li></ul></ul>
  46. 47. Diagnosis <ul><ul><li>Cardiovascular dysfunction </li></ul></ul>
  47. 48. Diagnosis <ul><li>Clinical Diagnostic Criteria </li></ul><ul><ul><li>A score of 45 or more is highly suggestive of a storm </li></ul></ul><ul><ul><li>A score of 25-44 is suggestive of impending storm </li></ul></ul><ul><ul><li>A score below 25 is unlikely to represent storm </li></ul></ul>
  48. 49. Laboratory Criteria <ul><li>No lab criteria for a storm </li></ul><ul><ul><li>Biochemical evidence of thyrotoxicosis i.e.  T 3 , T 4 ,  TSH </li></ul></ul><ul><ul><li>Free T 4 tends to be higher but no criteria as yet </li></ul></ul><ul><ul><li>Do not wait for lab confirmation </li></ul></ul><ul><ul><li>If diagnosis not clear and no known history of hyperthyroidism, 2 hour RAI uptake useful </li></ul></ul><ul><ul><li>Other suggestive features include hyperglycemia, leukocytosis, hypercalcemia,  AST,  LDH. </li></ul></ul>
  49. 50. Treatment <ul><li>Correct hyperthyroidism </li></ul><ul><ul><li>Block synthesis of additional hormones </li></ul></ul><ul><ul><li>Block release of thyroid hormones </li></ul></ul><ul><ul><li>Inhibit peripheral conversion </li></ul></ul><ul><ul><li>Direct measures to reduce levels of hormones </li></ul></ul><ul><ul><li>Definitive treatment </li></ul></ul><ul><li>Normalizing homeostatic decompensation </li></ul><ul><li>Treat precipitating event </li></ul>
  50. 51. Treatment <ul><li>Correct hyperthyroidism </li></ul><ul><ul><li>Block synthesis of additional hormones </li></ul></ul><ul><ul><ul><li>PTU, carbimazole orally, NG. </li></ul></ul></ul><ul><ul><ul><li>Block iodine incorporation within 1 hour </li></ul></ul></ul><ul><ul><ul><li>PTU loading dose 600-1000 mg, then 200-250 mg q4hr </li></ul></ul></ul><ul><ul><ul><li>Carbimazole 20 mg Q4H </li></ul></ul></ul><ul><ul><li>Block release of thyroid hormones </li></ul></ul><ul><ul><ul><li>Inorganic iodine only after carbimazole. Orally or nasogastric. Lugol’s iodine 30 drops daily </li></ul></ul></ul><ul><ul><ul><li>Ipodate (Oragrafin) 1 g tds. Also inhibit T4 conversion </li></ul></ul></ul><ul><ul><ul><li>Lithium only if allergic to iodine </li></ul></ul></ul>
  51. 52. Treatment <ul><ul><li>Inhibit peripheral conversion </li></ul></ul><ul><ul><ul><li>PTU </li></ul></ul></ul><ul><ul><ul><li>Ipodate </li></ul></ul></ul><ul><ul><ul><li> blockers with MSA e.g. propanolol </li></ul></ul></ul><ul><ul><ul><li>steroids </li></ul></ul></ul><ul><ul><li>Direct measures to reduce levels of hormones </li></ul></ul><ul><ul><ul><li>Plasmapheresis, PD, exchange transfusion </li></ul></ul></ul><ul><ul><li>Definitive treatment </li></ul></ul><ul><ul><ul><li>Radioiodine must be delayed 6 months as iodine can inhibit uptake </li></ul></ul></ul>
  52. 53. Treatment <ul><li>Normalizing homeostatic decompensation </li></ul><ul><ul><li>IV Fluids to rehydrate </li></ul></ul><ul><ul><li>Glucose for calories and restore glycogen storage </li></ul></ul><ul><ul><li>Multivitamins </li></ul></ul><ul><ul><li>Treatment of arrhythmias, CCF. </li></ul></ul><ul><ul><li>Pressors/invasive monitoring if indicated </li></ul></ul><ul><ul><li>Supplemental oxygen </li></ul></ul>
  53. 54. Treatment <ul><ul><li>Treat hyperthermia </li></ul></ul><ul><ul><ul><li>Central thermoregulation Paracetamol. Aspirin can displace T4 from binding proteins </li></ul></ul></ul><ul><ul><ul><li>Peripheral measures </li></ul></ul></ul><ul><ul><ul><li>icepacks, cooling blanket </li></ul></ul></ul><ul><ul><li>Glucocorticoids </li></ul></ul><ul><ul><ul><li>Relative adrenal insufficiency due to increased degradation of cortisol </li></ul></ul></ul><ul><ul><ul><li>Absolute adrenal insufficiency associated with Graves Disease </li></ul></ul></ul><ul><ul><ul><li>Inhibit T4 to T3 conversion </li></ul></ul></ul>
  54. 55. Treatment <ul><ul><li>Cardiac failure </li></ul></ul><ul><ul><ul><li>CCF usual treatment </li></ul></ul></ul><ul><ul><ul><li>Arrhythmias: most common AF </li></ul></ul></ul><ul><ul><ul><li>Large doses of digoxin needed </li></ul></ul></ul><ul><ul><ul><li>Significant risk of embolism: anticoagulate if no contraindications </li></ul></ul></ul><ul><ul><li>Anti adrenergic agents </li></ul></ul><ul><ul><ul><li>Propanolol result in dramatic improvement 20-40 mg Q6h </li></ul></ul></ul><ul><ul><ul><li> 1 selective, esmolol (short acting during perioperative period). </li></ul></ul></ul>
  55. 56. Treatment <ul><li>Treat precipitating event </li></ul><ul><ul><li>Identify and treat aggressively </li></ul></ul><ul><ul><li>Infections </li></ul></ul>
  56. 57. Treatment <ul><li>Response </li></ul><ul><ul><li>Clinical response within 12-24 hours - defervesence, reduced pulse. </li></ul></ul><ul><ul><li>Full recovery in 7-8 days </li></ul></ul><ul><ul><li>Mental status good marker for recovery. </li></ul></ul>

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