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Endocrine Emergencies. Christian Hariman. Objectives. Diabetic Emergencies • Recognise and participate in the management of diabetic ketoacidosis • Recognise and participate in the initial management of honk • Recognise and manage hypoglycaemia
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Endocrine Emergencies Christian Hariman
Objectives • Diabetic Emergencies• Recognise and participate in the management of diabetic ketoacidosis • Recognise and participate in the initial management of honk • Recognise and manage hypoglycaemia • Other Metabolic Disorders• Recognise the symptoms and signs of thyrotoxicosis • Manage thyrotoxicosis using medical therapy• Recognise and initiate the immediate management of Addisonian crisis• Initiate investigation of hypo and hyper natraemia and hypo and hyperkalaemia initiate management of these conditions • Recognise the circumstances when hypercalcaemia may occur and initiate the management of hypercalcaemia
Diabetes Emergencies • Diabetes Ketoacidosis • Hyperosmolar Non Ketosis (Hyperosmolar Hyperglycaemic state) • Hypoglycaemia
Case Rose Smith
Loss of Beta cell function in pancreas Loss of beta cell function is gradual over time “Honeymoon period” alpha-cell beta-cell
Symptoms and signs Nausea Vomiting Abdominal pain Often preceding polyuria, polydipsia, weight loss Drowsiness/confusion/coma (severe) Kussmaul respiration - hyperventilation ‘Pear drops’ breath Sign of associated systemic illness (MI, infection, etc)
Diabetic Ketoacidosis:Pathophysiology MUSCLE Normal – glucose in blood B L O O D
Diabetic Ketoacidosis:Pathophysiology MUSCLE Normal Mechanism B L O O D Insulin
Diabetic Ketoacidosis:Pathophysiology Liver Glucagon MUSCLE • Insulin deficiency • *lack of glucose in muscle • glucagon excess • *increase in gluconeogenesis B L O O D Insulin
Diabetic Ketoacidosis:Pathophysiology MUSCLE 3. Rapid lipolysis into free fatty acids and ketone bodies release of Beta-hydroxybutyrate ketones makes you sick B L O O D ketones ketones ketones ketones
Diabetic Ketoacidosis:Pathophysiology MUSCLE 4. Hypovolaemia – vomitting + osmotic diuresis Increases concentration of ketones + glucose ketones B L O O D ketones
How do I diagnose DKA? • Diagnosis requires all 3 of the following: • High blood sugar (i.e diabetes) Glucose > 11 mmol • *Finger-prick blood glucose can be normal* • Ketones (blood or urine ≥ +++) • Acidosis (pH<7.30 or HCO3<15mmol)
How do I Manage DKA? • ABC – if impaired – consider early ITU input / central venous access • Replace fluids • Resolution of ketonaemia / insulin • Replace electrolytes • Look for cause • Close monitoring • Consider Low molecular weight heparin
Replacing fluids Initial management • 1L 0.9% NaCl • 30 mins* • 1hr • 2hr • 4 hr Then continue NaCl 0.9% as dictated by fluid status *beware of elderly patients Later • Once blood glucose <14 mmol/L – give 10% dextrose alongside 0.9% Normal Saline at 125ml / hour
Resolution of ketonaemiaInsulin infusion • Insulin infusion • 50units actrapid made to 50ml with NaCl 0.9% • Rate: 0.1 units/kg/hour • E.g 70kg = 7 units/hour • Aim for fall in serum ketone of 0.5 mmol/L per hour • OR rise in serum HCO3- by 3 mmol/hr or reduction of Blood glucose by 3 mmol/hr • Increase rate of insulin by 1 unit per hour if above not achieved • Continue infusion until blood ketones <0.3, venous pH >7.3 and/or HCO3- >18
Replace electrolytes • K+ is most important • Insulin shifts K+ into cells therefore K+ will fall as rehydrate • Serum K+ ≥ 5.5 • No potassium supplement • Serum K+ 3.5 - 5.4 • Add 20mmol per litre • Serum K+ <3.5 • Add 40mmol per litre • Hyponatraemia may occur due to osmotic effect of glucose - it will correct with treatment of DKA
Monitoring • Monitor urine output and vital signs closely • catheterize • Repeat U&E, glucose, VENOUS bicarbonate – ABG PAINFUL • 2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours • Repeat ABG at 2 hours if not improving • ? Alternative cause for acidosis e.g. lactate
Case Nicholas Brown
Hyperosmolar Hyperglycaemic State (HHS) (the artist formerly known as Hyperosmolar Non Ketotic – HONK)
Features of HHS Possibly osmotic symptoms Dehydration around 10L deficit Decreased level of conciousness Signs of underlying infection in up to 50% +/- thrombo-embolism in up to30% 2/3 cases previously undiagnosed As high as 50% mortality – higher than DKA
HHS:Pathophysiology MUSCLE • Insulin production markedly reduced but NOT absent. • No switch to fat metabolism and therefore no ketones or acidosis • Gluconeogenesis • Loss of intravascular volume B L O O D Insulin
Diagnosis • Diagnosis requires ALL of the following: • Raised blood glucose (usually >30mmol) • Absence of ketones (or + or ++ only) • Serum osmolality >350mmol
Is the treatment the same as DKA? • 1L 0.9% NaCl • 1 hr* • 2 hr • 4 hr • 8 hr Then continue NaCl 0.9% as dictated by fluid status *half the rate of DKA • Fluid replacement – SLOWER (may be a marker of population not pathology) • Electrolyte replacement (pseudohyponatraemia) • Insulin – ‘slower’ scale – normally very responsive to IV insulin • Search for cause • ANTICOAGULATION • Monitor
Insulin • 50units actrapid made to 50ml with NaCl 0.9% • Rate: 0.1 units/kg/hour • 70kg = 7 units/hour • More insulin sensitive • Reduce rate if Blood glucose falls >10 mmol / hour • Consider halving the rate within the first 1-2 hours • Stop when patient is recovered
Case Daniel Walters
Causes Insulin / medications Liver disease Insulinoma
Features of Hypoglycaemia • Autonomic: • sweating, palpitations, tremor, hunger • Neuroglycopenic • confusion, clumsiness, behavioural changes, seizures • Non-specific • nausea, headache, tiredness • Symptoms may not present at the same level of blood glucose • Diagnosis with serum/capillary glucose (<3.0) • *beware may not be accurate*
Treatment of hypoglycaemia • If able to eat • glucose: e.g 3 dextrosol tabs / 200mls of orange juice/ sugar drinks • followed by long acting carbohydrate eg toast/ sandwich • In the community: 1mg glucagon im and long acting carbohydrate on recovery • Hospital options- • I.M. glucagon 1mg • I.V. 20ml of 50% dextrose* • Other: hypostop
Other Metabolic Disorders • Thyrotoxicosis • Addisonian Crisis • Initiate investigation of hypo and hyper natraemia and hypo and hyperkalaemia initiate management of these conditions • Recognise the circumstances when hypercalcaemia may occur and initiate the management of hypercalcaemia
Case Joanna Webbley
Thyrotoxicosis • Sweating • Tachycardia with or without AF • Nausea, vomiting and diarrhea • Tremulousness and delirium, occasionally apathetic • Diarrhoea • Exopthalmos (only in graves disease) • Hyperpyrexia ( >40 0C )
Causes • Graves Disease • Thyroiditis (Hashimoto’s, de Quervain’s, etc) • Primary hyperthyroid (multinodular goitre, single nodule, etc) • Exogenous thyroid
Diagnosis • Free T4, Free T3 elevated • TSH suppressed • Thyroid antibodies (if autoimmune) present
Treatment • Anti-thyroid medication • Carbimazole (CMZ), Propylthiouracil (PTU) • Beware of CMZ in pregnancy • Beware of aggranulocytosis • Beta blocker • CMZ / PTU takes 2 weeks • Beta blockade patient if symptomatic for 2-3 weeks
Thyroid Storm • rare • A-E of resuscitation, treat hyperthermia • Call senior help / ITU • May require parentral beta blockade and anti-thyroid medications • Can give lugol iodine to block thyroid release
Case Brian Walker
Hypothalamus-pituitary-adrenal axis Hypothalamus CRH Pituitary ACTH Adrenals Negative feedback Glucocorticoids
Features • rare • Lack of cortisol • Orthostatic hypotension, lethargy, faintings • If autoimmune – dark/pigmented skin • Causes: • Iatrogenic : Adrenelectomy, sudden stop of long term glucocorticoids • Autoimmune • Hypothalamic disease, pituitary disease, adrenal disease
Diagnosis • Low random cortisol (not accurate) • Short Synachten test • Cortisol time 0 • Synacthen (artificial ACTH) Intramuscular • Cortisol time 30 mins • Interpretation • Normal: increment of >200 nmol/L and 30min test >600 nmol/L
Treatment • Give Cortisol • Intravenous 200 mg Hydrocotisone • Oral Hydrocortisone • 10mg – 10/5mg – 5mg routine • Normal adult required 20-30mg HC daily • Remember: • Sick patients require more cortisol • 5mg Prednisolone = 20mg Hydrocortisone • STEROID CARD
Hyperkalaemia • Normal range 3.5 – 4.5 • Danger of atrial / ventricular fibrillation • Assess patient (A-E of resus) • Re-check the Potassium levels (lab + blood gas) • Stop offending drugs (spironolactone, amiloride)
Hyperkalaemia treatment • Urgent • ECG – tall t waves / widening QRS • Cardiac compromise or impending • Emergency call if cardiac compromise • 10mL Calcium gluconate (10%) over 2 min • 50mL of 50% dextrose + 10 units Actrapid over 20-30 mins • Consider dialysis / filtration • Non urgent • Nebulised Salbutamol • Calcium resonium • 50mL of 50% dextrose + 10 units Actrapid over 20-30 mins
Hyper + Hypo natraemia • Assess patient’s fluid status • Hypovolaemia, euvolaemia, hypervolaemia • Hypernatraemia • Hyponatraemia • Beware of acute vs chronic hyper/hyponatraemia
Hyponatraemia • Common in elderly • If asymptomatic + chronic – may not need treatment • Investigate cause: Addisons, SIADH • Consider stopping the offending drug • ACE-i, diuretics, omeprazole • Main treatment: • Fluid restrict if euvolaemia / hypervolaemia • If unable to tolerate – consider V2 receptor antagonist • If hypovolaemia– slow fluid resuscitation • BEWARE – too quick replacement can cause Central Pontine Myelinolysis
Hypernatraemia Assess fluid status Commonest cause is pure water loss Chronic vs acute Investigate cause: Conn’s, Diabetes insipidus Fluid replacement – slowly if chronic
Hypercalcaemia • Behavioural change, tetany, seizures • Investigate cause – Primary hyperPTH, malignancy, recent bone radiotherapy, Familial Hypercalcaemia hypocalciuria • Beware of true calcium levels in hypoalbuminaemia • Corrected Ca = measured Ca + 0.02 x (40-albumin)