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ENDOCRINE EMERGENCIESPresented by: Dr. Stacy Arvinna Department : Emergency, HDOK.

HypoglycaemiaDiabetic KetoacidosisHyperosmolar Hyperglycaemic StatePituitary apoplexy Addisonian CrisisPhaeochromocytoma hypertensive crisisThyroid stormMyxoedema comaParathyroid glandHypo / hypercalcaemia

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OVERVIEWDIABETIC KETOACIDOSISHHSHYPOGLYCEMIATHYROID STORMMYXEDEMA COMAADRENAL INSUFFICIENCY

DIABETIC KETOACIDOSIS

DIABETIC KETOACIDOSIS

DKA is a triad of hyperglycaemia, ketosis and acidaemiaDKA is a potentially life threatening medical emergency due to absolute or relative insulin deficiency coupled with counter-regulatory hormones excess.Diagnostic criteria (ADA) : - Blood glucose > 13.8 mmol/l - pH < 7.3- Serum bicarbonate < 18mmol/l, - Anion gap > 10 - Ketonaemia

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Pathogenesis :- insulin deficiency- increased counter-regulatory hormones (glucagon, catecholamines, cortisol and GH)

This leads to increased glucose production by the liver and decreased utilisation in peripheral tissues. Lipolysis results in ketone body production and acidosis.

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Clinical Features : - Polyuria - Polydipsia - Weight loss - Vomiting - Abdominal pain - Weakness - Tachypnea - Altered mental statusPhysical findings:DehydrationHypotensionTachycardiaPoor skin turgorPrecipitating causes present (infection, vascular events, drug abuse etc)

Most patients usually present to emergency and ICU within 24 h of development of polyuria, polydipsia, weakness, and weight loss. There may be complaints of anorexia, abdominal pain, fatigue and muscle cramps. Intravascular volume depletion due to osmotic effects leads to dry mucous membranes, sunken eyeballs, tachycardia, orthostatic hypotension, and even supine hypotension. Tachypnea occurs to compensate the biochemical effects of metabolic acidosis. Infection and sepsis can aggravate the clinical effects of volume depletion. Altered sensorium ranging from mild confusion to coma may prevail.7

Laboratory Findings : - Hyperglycaemia (> 13.8 mmol/l) - Hyperosmolality [2x(Na+K) + Urea + Glucose] - Ketones - Widened anion gap metabolic acidosis (pH < 7.3) - Elevated urea and creatinine - Hyperkalaemia - Leucocytosis

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Differential diagnosis. Hyperglycemic hyperosmolar state is not associated with ketosis. Starvation and alcoholic ketoacidosis are not characterized by hyperglycemia >200 mg/dl and bicarbonate level 7 mmol/L) should be suspected. Ingestion of methanol, isopropyl alcohol, and paraldehyde can also alter anion gap and/or osmolality and need to be investigated.

ManagementA.Fluid therapy B.Insulin infusion C.Electrolyte management D.Treatment of underlying cause

According to ENDOCRINE UNIT HOSPITAL UNIVERSITI SAINS MALAYSIA KOTA BHARU, KELANTAN

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FLUID THERAPYRateActionFluidStep 11 pint over 30 min for 1 hourTo review1 litreStep 21 pint over 1 hour for 2 hourTo review1 litre

Step 31 pint over 2 hour for 4 hourTo review1 litre

Step 41 pint over 4 hour for 8 hourTo review1 litre

Fluid replacement is priority one in the treatment of DKA.Replace fluid deficit in DKA (~6 L) within 24-36 hours with the goal of 50% volume replacement within first 12 hours.

The first goal of therapy is to correct tissue hypo-perfusion, improve glomerular filtration and reverse the insulin resistance and deficiency. Note: 1.Starting point depend on severity ofdehydration. If a patient is not severely dehydrated, may start with Step 2or Step 3. 2.After each step, review the patient for adequacy of fluid replacement and evidence of fluid overload . a)Symptom eg. Breathlessness b)Sign eg. BP,PR, JVP, Lung Examination(for basal crepitation) c)Monitoring-Input/output chart (Aim for urine output ~1ml/min) -CVP (When indicated; aim for CVP reading 8-10cm H2O) d)Laboratory values-Hb, Hct,Urea (if available) 3.At review If patient still hemodynamicallyunstable ie. dehydrated and hypotensive with no urine output repeat same step If patient is improving, follow from step 1- step 4, and continue step 4 as maintenance If patient developed fluid overload, withhold fluid therapy and manage the fluid overload accordingly. Once stable, restart fluid therapy at slower rate ie. Skip the next step and go directly the step after that (eg. Step 2fluid overload-skip Step 3-go to Step 4) 4.Usual deficit in moderate DKA is 6L (range 4-8L)-aim 50% replacement in 6 hour, and total replacement within 24-48 hours. 5.In the acute stage, do not order fluid regimen for 24 hour. Always review after each steof fluid regime. 6.Caution in the elderly, those with heart failure or renal failure, slow replacementis imperative and frequent review is necessary to detect sign of fluid overload. 7.Use 0.45% NaCl (half normal saline) if serum Na>160mmol/L. 8.Once blood glucose level ~10mmol/L-change to 5% dextrose.

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INSULIN INFUSIONStart IVI at 0.1 unit/kg/ hr based on estimated body weight(50 units human soluble insulin;Actrapid/ Humulin R + 0.9% NaCl= 50 ml)Irrespective of blood glucose level Bolus insulin is not recommendedMonitor blood glucose level hourlyAim for blood glucose drop of 2-4mmol/L per hourInitially, aim for CBG~10mmol/L (range 8-12mmol/L) until DKA has improvedoWithold insulin infusion if serum potassium 6u/hr. oWithold insulin infusion if serum potassium 160mmol/L) use 0.45% NaCl (half normal saline) in fluid therapy Bicarbonate Bicarbonate replacement is not routinely indicated in the management of DKA Consider giving bicarbonate replacement if pH 320 mosmol/kg

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PATHOPHYSIOLOGYHHS and diabetic ketoacidosis (DKA) represent the two ends of the spectrum of markedly decompensated diabetes, differing mainly in severity of acidosis, ketosis and dehydration. HHS usually occurs with lesser degree of insulinopenia compared with DKA, but the pathophysiology is otherwise thought to be similar. In both entities, there is a decrease in net effective insulin action with concomitant elevation of counterregulatory hormones. In the setting of relative insulin deficiency, glucagon, catecholamines and cortisol stimulate hepatic glucose production though glycogenolysis and gluconeogenesis. High catecholamines and low insulin reduce peripheral glucose uptake. Unlike DKA, it is thought that there is adequate insulin available in HHS to restrain lipolysis and ketogenesis. However, there is significant hyperglycemia with resultant glycosuria leading to loss of water and electrolytes, dehydration, and ultimately decreased renal perfusion, decreased glucose clearance, and exacerbation of hyperglycemia.

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Precipitants : - Infection - Myocardial infarction / cerebrovascular accident- Inadequate insulin treatment / noncompliance - High sugar intake - Other endocrine disorders e.g. acromegaly - Drugs e.g. glucocorticoids, thiazides, loop diuretics, phenytoin

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Laboratory Findings : - Hyperglycaemia - Hyperosmolarity [2x(Na+K) + Urea + Glucose] - Hypo or hypernatraemia - Hyperkalaemia

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HYPOGLYCEMIA

HYPOGLYCAEMIAIN CONTEXT OF DIABETES; excess insulin in absence of enough carbohydrate. Most common in insulin treated patient.Low blood glucose concentrations lead to adrenergic activation and neuroglycopenia . Symptomatic hypoglycemia is diagnosed clinically using Whipples triad: symptoms of hypoglycemia, plasma glucose concentration 7.0 mmol/l)Patients post total pancreatectomy have more frequent and severe episodes because they have also lost their glucagon producing cells

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PATHOPHYSIOLOGYRedundant counter-regulatory mechanisms are in place to prevent or correct hypoglycemia. As glucose levels decline, major defenses include: a decrease in insulin secretion; an increase in glucagon secretion; an increase in epinephrine secretion. Increased cortisol and growth hormone secretion also occur. If these defenses fail, plasma glucose levels will continue to fall.In type 1 and longstanding type 2 diabetes these counter-regulatory responses to hypoglycemia are frequently impaired. This increases the risk of hypoglycemia and also contributes to hypoglycemia unawareness.

Causes :1. Drugs - insulin/oral hypoglycaemics - alcohol - salicylates - quinine - beta-blockers, pentamidine, disopyramide - prescription errors e.g. chlorpropamide for chlorpromazine 2. Tumours- Insulinoma- Retroperitoneal sarcomas

3. Miscellaneous- Liver dysfunction - adrenal insufficiency / hypopituitarism - renal failure - myxoedema

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Presentation :1. Autonomic (Blood glucose 3.3 3.6 mmol/l) - diaphoresis - anxiety - palpitations / tachycardia - tremor - warm feeling2. Neuroglycopenic (Blood glucose