Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital

Endocrine Emergencies

Endocrine Emergencies: Diabetic emergencies ( DKA, NKHOC, Hypoglycemia) Thyrotoxic crises, Myxoedema coma. Adrenal crises. Pituitary failure, Diabetes Insipidus, SIADHS. Calcium related emergencies.

Case History: 21 years old girl, presented with 2 days history of abdominal pain, vomiting, preceded by significant wt. loss, polyuria and polydepsia.

Positive clinical & Lab. Data: Pulse: 110/min, BP 90/60, Temp c °, RR: 30/min Signs of dehydration. RBS: 450 mg/dl, urea: 110 mg/dl, K: 5.5 mmol/l, Na: 150 mmol/l, WBC: 18000/μl Urine positive for Ketons. ABG: PH: 7.1, P02: 110, Pco2: 30, Hco3: 12 mmol/l

Diagnosis: Diabetic Keto acidosis 450 mg/dl Ketonuria PH 7.1

Definition: One of the most serious acute metabolic complications of diabetes. Occurs more commonly in patients with insulin- dependent diabetes mellitus (IDDM) Characterized by: Blood glucose level > 250 mg/dl Blood pH < 7.3 Ketones in serum > 5 meq/L

Epidemiology: Mortality rate was 100% in 1922 but has since come down to 5% with improvements in health care Common cause of death in type 1 diabetics Can occur in type 2 as well 25% as first presentation of type 1 DM

Pathogenesis: Ineffectiveness of insulin. Elevations in glucagon, catecholamines & cortisol. Hepatic gluconeogenesis, glycogenolysis, and lipolysis are affected by this hormone imbalance. Fat, liver and muscle can survive without glucose but Brain must maintain use of glucose.

Hyperglycemia results from Increased gluconeogenesis. Conversion of glycogen to glucose. Inadequate use of glucose by peripheral tissues. Ketone bodies result from Increase triglyceride breakdown to FFA and glycerol. Beta oxidation of FFA. Decreased concentrations of malonyl coA (an inhibitor of ketogenesis).

Hyperglycemia leads to 1. Glycosuria 2. Polyuria (osmotic diuresis) 3. Polydipsia 4. Polyphagia 5. Weight loss 6. Dehyrdation Ketone bodies lead to 1. Metabolic acidosis

Hyperglycemia Lipolysis Hyperosmolarity Ketosis Acetone smell, vomiting Intracellular Osmotic diuresis Kussmaul”s Breathing Dehydration Electrolyte loss loss of extracellular consciousness dehydration Acute renal failure + Shock Insulin deficiency Metabolic acidosis Hypovolemia

Precipitating factors: Infection : Pneumonia and UTI most commonly. Inadequate use of insulin: Not taking insulin. Small dose. Use of OAD. New onset diabetes. Medical, surgical or emotional stress. Drugs: Corticosterioids, thiazide diuretics. Pancreatitis.

Symptoms:  Polyuria, nocturia, thirst Rapid weight loss Muscular weakness Visual disturbance Air hunger Abdominal pain, nausea, vomiting Leg cramps Altered sensorium

Signs Acetone breath Air hunger Impaired consciousness Hyperglycemia, osmolarity Cerebral edema if sensorium worsens during treatment Hypotension: due to peripheral vasodilatation due to acidosis Hypothermia Succussion splash May mimic surgical emergency

Diagnosis: Diagnosis of DKA in IDDM patient is not that difficult. Diagnostic criteria for DKA: hyperglycemia (>250 mg/dl) ketosis (ketonemia or ketonuria) metabolic acidosis (pH<7.3, HCO 3 <15mEq/L) Increase in Anion gab = ( Na + K)- (Cl + Hco3) 8 – 16 mmol/l supporting features are volume depletion and Kussmaul’s breathing.

Other investigations: Sodium, Potassium, Leucocytosis, high urea, increase of Hb. Ht.

Management: General measures :  control of Breathing, circulation, input, output chart.  central venous line, urinary catheter, NGT.  decubitus and thromboembolism prophylaxis.  control of sugar hourly, K, ABG every 2 hours. Specific treatment:  correction of dehydration.  insulin therapy.  correction of acidosis.  electrolytes replacement.

Fluid replacement: Use isotonic saline ( normal saline ) 0.9% NaCl. if Na > 155 mmol/l use hypotonic saline 0.45% NaCl. in case of collapse use plasma proteins or albumin. 1 hour 1000 ml. After that according to CVP: CVP ml fluid/ hr 0 cm cm cm cm 100 The pt. may require 5-6 l in the first 8 hrs. Infuse 5% dextrose when the sugar reaches 250 mg/dl.

Insulin: Soluble insulin ( regular, rapid) i.v, 20 units stat. followed by 5-10 units /hr through infusion pump. Slowly reduction not more than 100mg/dl/hr. Keep the sugar around 250 mg/dl.( 2 iu+ 5% dextrose) Hypoglycemia, hypokalemia, brain edema.

Correction of acidosis: Under insulin the acidosis will be reversed due to inhibition of lipolysis. If pH < 7.1 give 1/3 of HCO3 deficit. NaHCO3= -ve base excess x wt.kg/3. Risk of hypokalemia is there.

Electrolytes replacement: Na: Initially plasma sodium concentrations are low or normal despite water losses due to osmotic shift of water. So will be replaced through i.v fluids. K : concentrations may be normal or elevated, because of: Acidosis and lack of insulin causes potassium shift. Serum – K- mmol/lK- substitution mmol/hr <

Non-ketotic Hyperosmolar coma: Common in type II. Blood sugar usually > 600 mg/dl. Rarely to have acidosis.( small amount of insulin enough to inhibit acidosis). Hyperosmoarity > 600 mosmol/kgH₂O. Management as DKA.

Hypoglycemia Def: blood sugar < 40 mg/dl OR blood sugar <45mg/dl. Whipple Triads symptoms of hypo. correction with Glucose.

Causes Fasting hypoglycaemia:. Insulinoma..severe liver diseases..Hypoadrenalism, hypopituitarism..ß- cell hyperplasia( Nesidioblastosis) Reactive hypoglycaemia :.early stage of DM..diab. Gastro paresis( autonomic N.).Dumping syndrome after gastric surgery.. Increase vagus tone. Exogenous hypoglycaemia:.overdose of insulin or sulfonylurea drugs..factious hypoglycaemia..Alcohol.

Treatment Elimination of precipitating factors. Mild cases : conscious pat. Oral glucose as grape juice, cola, 20 gm sugar. Severe cases : ml 40% glucose i.v, repeat after 20 min. Or 5% dextrose infusion ( blood sugar 200mg/dl) Glucagon 1 mg i.m.

Hypercalcaemia: Forceful diuresis ( 0.9% Nacl 3 to 6 litres + frusemide) Bisphosphonate. Corticosteroids. Calcitonin. Hypocalcaemia: calcium gluconate 10 % i.v ( ml) calcium and vitamin D orally.