Endocrine Emergencies - approach and management .pptx

Endocrine Emergencies - approach and management

1. Diabetic Ketoacidosis Dr Nazimal fikry

2. CONTENTS : INTRODUCTION DEFINITION CLINICAL FEATURES MANAGEMENTS

3. DIABETIC KETOACIDOSIS Is a biochemical triad of ketonemia, hyperglycemia and metabolic acidosis Consequences of absolute or relative insulin deficiency Accompanied by increase an counter regulatory hormones ( glucagon, cortisol, GH and cathecolamines ) This enhance hepatic gluconeogenesis and glycogenolysis resulting on severe hyperglycemia Enhance lipolysis increases serum fatty acid, leads to ketogenesis which results in accumulation of ketone bodies (acetone, 3-beta-hydroxybutyrate and acetoacetate)

4. CLINICAL FEATURES : Polyuria Polydipsia Excessive thirst Nausea Vomiting Abdominal pain

5. CAUSES OF DKA : MEDICATIONS : Missed medications Steroids, thiazides, sympathomimetics, antipsychotics INFECTIONS ENDOCRINE : Hyperthyroidism Pheochromocytoma Cushing’s disease SYSTEMIC : Cerebrovascular accidents Myocardial Infarction Pulmonary embolism Pancreatitis Gastrointestinal Hemorrhage Major trauma / Surgery

6. DIAGNOSTIC CRITERIA : ALL 3 CRITERIA MUST BE MET : CBG >11.1 mmol /L Serum ketone >3 mmol/L/ urine ketone =/>2+ VBG pH <7.3 and/or HCO3 <15 mmol /L

7. INDICATIONS FOR HDU ADMISSIONS : Elderly Pregnant Heart/ renal failure Severe DKA pH < 7.1 HCO3 <5 Serum ketone >6 Anion gap > 16 *Anion gap= ( Na+K )-(Cl+HCO3) Hypokalemia on admission (<3.5mmol/L) SpO2 <92 % (ABG required) GCS <12 PR >100/<60 Systolic BP <90mmHg

8. Principles of Management To set 3 IV lines on admission :- For maintenance fluid 125ml / hr ( 6pints in 24 hrs ) + potassium replacement Resuscitation line for NS : rate to be decided clinically based on blood pressure, degree of dehydration , urine output and CVL in some cases For IV insulin infusion : infused at 0.1u/kg/ hr until ketosis resolves

9. . Restoration of fluid depletion due to osmotic diuresis Use 0.9% NaCl ( normal saline ), with strict intake output charting. Cautious fluid replacement in patients whom are not in shock and have multiple co-morbidities. Hourly urine output, aim urine output at least 0.5ml/kg/hr. Suppression of Ketosis and reversal of metabolic acidosis Fixed Rate Insulin infusion ( FRII ) at 0.1U/kg/ hr enables rapid blood ketone clearance until ketosis resolves. The FRII should be continued until the bedside capillary ketone levels are less than 0.6 mmol/L, and the pH >7.32.

10. Monitoring progress and resolution of ketosis Use of serum ketone using bedside ketone meter for diagnosis and consider repeat serum ketones in order to monitor of resolution of DKA in situations where metabolic acidosis is not improving despite adequate hydration and adequate dose of insulin via FRII . Use of venous blood gas for monitoring for resolution of acidosis. Adequate potassium replacement to avoid Hypokalemia while in insulin infusion Maintain potassium level between 4-5mmol/L. Insulin therapy lowers serum potassium levels by promoting the movement of potassium back into the intracellular compartment. Identification and Management of any possible precipitating factors

11. MANAGEMENT :

12. HYPERGLYCEMIC HYPEROSMOLAR SYNDROME (HHS)

13. HHS Characterised by progressive hyperglycemia and hyperosmolarity found in : Debilitated patient with poorly controlled T2DM Limited access to water Precipitating illness

14. DIAGNOSTIC CRITERIA : CBG > 33.3 mmol /L pH >7.35/ HCO3 >15 Ketone neg /nil Marked hypovolemia, severe dehydration Serum osmolarity >320 mosmol /kg Calculation for osmolality: 2Na (corrected) + 2K + glucose + urea

15. PRECIPITATING FACTORS : Infections and sepsis Thrombotic stroke Intracranial hemorrhage Silent myocardial infarction Pulmonary embolism

16. CLINICAL FEATURES : MARKED HYPOVOLEMIA -cold peripheries, poor perfusion -loss skin turgor -sunken eyes -dry mucus membrane -hypotension

17. Principles of Management Replacement of fluid and electrolyte losses Fluid replacement alone (without insulin) will lower blood glucose which will reduce osmolality causing a shift of water into the intracellular space - initial rise in serum sodium (a fall in blood glucose of 5.5 mmol/L will result in a 2.4 mmol/L rise in sodium). This is not necessarily an indication to give hypotonic solutions. Rising sodium is only a concern if the osmolality is NOT declining concurrently. If the osmolality is no longer declining despite adequate fluid replacement with 0.9% sodium chloride solution AND an adequate rate of fall of plasma glucose of at least 5mmol/hour is not being achieved then 0.45% sodium chloride solution should be substituted.

18. Normalise the osmolality Aim for gradual decline in serum osmolality at rate of 3 mOsm /kg to 8mOSm/kg per hour. (normal plasma osmolality ranges between 275-295 mOsm /kg). The best approximation to measured osmolality can be calculated using the formula 2Na + 2K + glucose + urea using serum sodium level corrected for hyperglycaemia (corrected Na) Corrected Na = Laboratory measured [Na] + [(Glucose – 5 )÷3.5] Normalise the blood glucose Establish fluid replacement first. Fluid replacement alone with 0.9% sodium chloride solution will result in falling blood glucose and because most patients with HHS are insulin sensitive there is a risk of lowering the osmolality precipitously. Low dose IV insulin (0.05 units/kg/ hr ) should be commenced using FRIII.

19. 4. Prevention of complications and electrolyte imbalance Maintain potassium level between 4-5mmol/L. Ensure monitoring 6 hourly using laboratory values or reliable blood gas analyzer potassium value. Rising sodium is only a concern if the osmolality is NOT declining concurrently. If the osmolality is no longer declining despite adequate fluid replacement with 0.9% sodium chloride then 0.45% sodium chloride solution should be substituted 6. Identify and treat precipitating Factors Stroke / MI/ Acute coronary syndrome / infection / missed medication

20. THYROID STORM

21. THYROID STORM An extreme manifestation of thyrotoxicosis which is defined as : -acute severe life threatening hypermetabolic state of thyrotoxicosis -caused either by : Excessive release of thyroid hormone causing adrenergic hyperactivity OR Altered peripheral response to thyroid hormones following the presence of precipitant (hormones vs receptors sensitivity)

22. PRECIPITANTS OF THYROID STORM Systemic insult : Infection Trauma Surgery Endocrinal insult : DKA Cardiovascular insult : MI CVA Pulmonary embolism Drug/hormone related : Withdrawal of anti-thyroid drugs Excess iodine Ingestion of thyroid hormone Unknown etiology -up to 25% of cases

23. pathophysiology Involve the adregenic hyperactivity either via increased thyroid hormone production or increased receptor sensitivity When there is excess of thyroid hormones, circulating T4 & T3 are taken into cytoplasm of the cell T4 is converted into its active form, T3 T3 then bind into thyroid hormone receptors to induce gene activation and transcription.

24. CLINICAL FEATURES :

25. Diagnostic criteria BURCH & WARTOFSKY 1993 Criteria/clinical tools for diagnosis : Score of >45 highly suggestive of thyroid storm 25-45 impending storm <25 unlikely

26. Management : Supportive care : general – cardiac monitoring, oxygen cooling : acetaminophen 325-650mg (regular dose) fluid – iv NS / glucose iv dextrose 5% cardiac decompensation – AF/ CCF treat precipitating factors

27. Inhibition of thyroid hormone release a) prevention of thyroid hormone synthesis Propylthiouracil(PTU) 600-1000mg loading dose then 200-250mg 4hrly Carbimazole 60-120mg/day in 3-4 divided dose PTU is preferred than carbimazole as it has additional action --inhibit peripheral conversion of T4 to T3 b) blockage of thyroid hormone release Lugol's iodine can be given 30-40 drops/day divided to 3-4x/day Given at least 1 hr after thioamides to inhibit thyroid hormone release into circulation –cause thyroid hormone spike

28. Inhibition peripheral conversion of T4 to T3 Propranolol – IV 1-2mg in slow bolus,may be repeated every 10-15 minutes until desired effect is achieved Oral propranolol : 20-120mg/dose Esmolol - 500mcg/kg IV bolus followed by maintenance 50-200 mcg/kg/min Steroids : IV hydrocortisone 100mg 8hrly or IV dexamethasone 2mg 6hrly

29. REFERENCES : Tintinalli’s Emergency Medicine, 8 th Edition Clinical Practice Guidelines, Management of Type 2 Diabetes Mellitus, 5 th Edition. Shirley Ooi , Peter Manning; Guides to the Essentials in Emergency Medicine