Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist...

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Teaching program 5 th year 2010/2011 . در وي ق لاح ص دConsultant Physician, Endocrinologist Medical Department Tripoli Central Hospital

Transcript of Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist...

Page 1: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Teaching program5th year 2010/2011

قويدر. صالح دConsultant Physician, Endocrinologist

Medical DepartmentTripoli Central Hospital

Page 2: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Endocrine Emergencies

Page 3: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Endocrine Emergencies:Diabetic emergencies ( DKA, NKHOC,

Hypoglycemia)

Thyrotoxic crises, Myxoedema coma.

Adrenal crises.

Pituitary failure, Diabetes Insipidus, SIADHS.

Calcium related emergencies.

Page 4: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Case History:

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

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

Positive clinical & Lab. Data:Pulse: 110/min, BP 90/60, Temp. 38.5 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

Page 6: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Diagnosis:

Diabetic Keto acidosis 450 mg/dl Ketonuria PH 7.1

Page 7: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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/dlBlood pH < 7.3Ketones in serum > 5 meq/L

Page 8: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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

Page 9: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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.

Page 10: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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).

Page 11: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Hyperglycemia leads to1. Glycosuria 2. Polyuria (osmotic diuresis)3. Polydipsia4. Polyphagia5. Weight loss6. Dehyrdation

Ketone bodies lead to7. Metabolic acidosis

Page 12: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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

Page 13: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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.

Page 14: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Symptoms: Polyuria, nocturia, thirstRapid weight lossMuscular weaknessVisual disturbanceAir hungerAbdominal pain, nausea, vomitingLeg crampsAltered sensorium

Page 15: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Signs Acetone breathAir hungerImpaired consciousness

Hyperglycemia, osmolarityCerebral edema if sensorium worsens during

treatmentHypotension: due to peripheral vasodilatation due to

acidosis

Hypothermia Succussion splashMay mimic surgical emergency

Page 16: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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, HCO3<15mEq/L)

Increase in Anion gab = ( Na + K)- (Cl + Hco3) 8 – 16 mmol/l

supporting features are volume depletion and Kussmaul’s breathing.

Page 17: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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

Page 18: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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.

Page 19: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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 1000 1-3 cm 500 4-8 cm 250 9-12 cm 100

The pt. may require 5-6 l in the first 8 hrs. Infuse 5% dextrose when the sugar reaches 250 mg/dl .

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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.

Page 21: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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.

Page 22: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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/l K- substitution mmol/hr

< 3 20-25

3-4 15-20

4-5 10-15

Page 23: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

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.

Page 24: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

HypoglycemiaDef: blood sugar < 40 mg/dl

OR blood sugar <45mg/dl.

Whipple Triads symptoms of hypo.

correction with Glucose.

Page 25: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

CausesFasting 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.

Page 26: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

TreatmentElimination of precipitating factors.

Mild cases : conscious pat. Oral glucose as grape juice, cola, 20 gm sugar.

Severe cases : 25- 100 ml 40% glucose i.v, repeat after 20 min. Or 5% dextrose infusion ( blood sugar 200mg/dl)

Glucagon 1 mg i.m.

Page 27: Teaching program 5 th year 2010/2011 د. صلاح قويدر Consultant Physician, Endocrinologist Medical Department Tripoli Central Hospital.

Hypercalcaemia:Forceful diuresis ( 0.9% Nacl 3 to 6 litres +

frusemide) Bisphosphonate.Corticosteroids.Calcitonin.

Hypocalcaemia: calcium gluconate 10 % i.v ( 20-30 ml) calcium and vitamin D orally.