Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
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 Diabetic Ketoacidosis (DKA) 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 Normal – glucose in blood Diabetic Ketoacidosis:Pathophysiology Normal Mechanism Diabetic Ketoacidosis:Pathophysiology 1. Insulin deficiency *lack of glucose in muscle 2. glucagon excess *increase in gluconeogenesis Diabetic Ketoacidosis:Pathophysiology 3. Rapid lipolysis into free fatty acids and ketone bodies release of Beta-hydroxybutyrate ketones makes you sick Diabetic Ketoacidosis:Pathophysiology 4. Hypovolaemia – vomitting + osmotic diuresis Increases concentration of ketones + glucose 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? 1. 2. 3. 4. 5. 6. 7. 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 ketonaemia Insulin 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 Serum K+ 3.5 - 5.4 Add 20mmol per litre Serum K+ <3.5 No potassium supplement 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 to 30% 2/3 cases previously undiagnosed As high as 50% mortality – higher than DKA HHS:Pathophysiology 1. Insulin production markedly reduced but NOT absent. No switch to fat metabolism and therefore no ketones or acidosis 2. Gluconeogenesis 3. Loss of intravascular volume 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? 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 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 Insulin 50units actrapid made to 50ml with NaCl 0.9% Rate: 0.1 units/kg/hour More insulin sensitive Reduce rate if Blood glucose falls >10 mmol / hour 70kg = 7 units/hour Consider halving the rate within the first 1-2 hours Stop when patient is recovered Case Daniel Walters Hypoglycaemia 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 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 antithyroid medications Can give lugol iodine to block thyroid release Case Brian Walker Addison’s Disease & Crisis 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) Hypercalcaemia Treat underlying cause if possible ABC of resus IV fluids Correct hypomagnasaemia / hypokalaemia Consider diuretics once rehydrated Bisphosphonates – takes 2-3 days, max 1 week Inhibits osteoclast + bone resorption Thank you [email protected]