Hypoglycemia, Electrolyte disturbances and acid-base imbalances

Transcription

1 Hypoglycemia, Electrolyte disturbances and acid-base imbalances Pediatric emergency PICU division Pediatric department Medical faculty, University of Sumatera Utara H. Adam Malik Hospital 1

2 Hypoglycemia Def : Plasma glucose < 45 mg/dl sweating, trembling, feeling of warmth, palpitations, anxiety, nausea, hunger, blurred or double vision, weakness Neuroglycopenic sypmtoms with prolonged hypoglycemia dizziness, confusion, tiredness, difficulty speaking, headache, inability to concentrate, nightmares, bizzare behaviour Criteria diagnostic for insulinoma (Whipple triad): - Hypoglycemic symptoms in fasting or exercising state - Low plasma glucose level - Relief of symptoms through correction of hypoglycemia 2

3 Insulin and C-peptide levels may help determine cause In nondiabetic hospitalized patients common etiologies include : - Renal insufficiency - Malnutrition - Liver disease - Infection - Sepsis Other causes : alcoholism, adrenal insufficiency, medications (insulin, sulfonylurea, pentamidine, trimethroprim sulfamethoxazole, salycilates, beta-blocking agents), insulin-secreting tumors. 3

4 Differential Diagnosis : o Delirium o Pheochromocytoma o Factitious hypoglycemia o Liver failure o Psychoneurosis o Sepsis syndrome o Myxedema coma 4

5 Treatment : - Glucose IV or orally (if awake & alert) Glucose 10% 5 ml/kgbw - Monitor blood glucose closely as patients may need continous dextrose infusion until precipitating cause removed - Glucagon & hydrocortisone can be given for refractory hypoglycemia - Identify & treat underlying disease or remove causative agent 5

6 Electrolyte disturbances 6

7 SODIUM Normal plasma level: mmol/l Hypernatraemia(greater than 150 mmol/l) Causes: vomiting/diarrhoea, excess water loss (e.g. diabetes insipidus, osmotic diuretics, burns), high sodium intake, iatrogenic fluid restriction (often combined with drugs containing sodium, near drowning (seawater) Presentation: lethargy, irritability, coma, seizures 7

8 Hypernatremia cont.. Treatment treat underlying cause slow rehydration using sodium containing fluid, e.g. 0.45% saline with dextrose (over at least 48 h). May need 0.9% saline. reduction of sodium level slowly mmol/l/h desmopressin (DDAVP) can be used in diabetes insipidus to reduce water loss 8

9 Hyponatraemia Causes Inappropriate ADH secretion decreased water clearance Water overload, e.g. iatrogenic, nephrotic syndrome Excessive sodium loss (e.g. diuretics, renal tubular dysfunction, diarrhoea and vomiting) Fluid sequestration, e.g. sepsis, burns Symptoms: range from non-symptomatic through lethargy to coma, nausea and vomiting, seizures usually below 125 mmol/l Therapy fluid restriction as therapy if symptomatic, 3% NaCl to return plasma sodium to 125 mmol/l 6 ml/kg of 3% saline increases body sodium by about 5 mmol/l 9

10 POTASSIUM Normal serum level is mmol/l Hypokalemia common causes: diarrhoea, alkalosis, diuretics, volume depletion, hyperaldosteronism, beta adrenergic agonists in asthma signs: ECG changes:t wave inversion, ST depression, predisposition to dysrhythmias, skeletal and smooth muscle excitability and weakness treatment: the cause, oral or IV replacement 10

11 Hyperkalemia causes: renal failure, metabolic acidosis, adrenal insufficiency, cell lysis, high intake hyperkalemia can be accompanied by hypovolaemia in sepsis Signs and symptoms: risk of arrhythmias particularly levels above 7.5 mmol/l can proceed to cardiac arrest peaked T waves, decreased R waves, widened QRS complex muscle weakness 11

12 Treatment of hyperkalemia 12

13 CALCIUM Normal level mmol/l Hypercalcemia rare causes: childhood malignancy, hyperparathyroidism, iatrogenic administration effects: polyuria, kidney stone formation, hypertension, shortened QT interval and dysrhythmias treatment: hydration with or without diuretics, reduce Ca intake, phosphate infusion Hypocalcemia causes: severe septicaemia, rickets, hypoparathyroidism, pancreatitis rhabdomyolysis, citrate infusion (massive blood transfusion), acute and chronic renal failure treatment: IV calcium,may need infusion via central line, high phosphate (especially in renal failure) may prevent rise 13

14 ACID-BASE DISORDERS ph is normally within the range of Normal ph is maintained by buffers in the body solutions which contain a weak acid and its conjugate base and are relatively resistant to changes in ph Two main categories are bicarbonate and non-bicarbonate The non-bicarbonate forms almost 50% of the buffering capacity of whole blood haemoglobin, plasma proteins and organic and inorganic phosphates However, the bicarbonate buffer system along with plasma proteins are able to form the immediate response to an increase in acid or base 14

15 The bicarbonate buffer system is dependent on the equation: CO2 (the acid component) is removed by the lungs HCO3 _ (the base component) is regulated by the kidney, by the retention of HCO3 _ from the urine, greater production of HCO3 _ and increased H+ excretion Full compensation by either mechanism is unusual Acute rises in [H+] leads to an increase in intra-cellular cation leading to K+ leaving the cell causing hyperkalaemia The anion gap can be used to estimate negative ions not measured regularly (Normal is around 12 mmol/l): 15

16 Respiratory acidosis Characterised by raised PaCO2 Causes: Hypoventilation due to respiratory depression, obstructive and restrictive respiratory disease, neuro-muscular weakness causing respiratory failure, inadequate mechanical ventilation Increased CO2 production; seizures, malignant hyperpyrexia Chronic respiratory acidosis is associated with a partially compensated picture with raised PaCO2 and bicarbonate Treatment: Improve respiratory function by ventilatory support Need to be careful in patients with chronic respiratory acidosis 16

17 Respiratory alkalosis Characterised by lowered PaCO2 Causes: Hyperventilation: Salicylate poisoning Fever, sepsis Encephalopathy Hypoxic and acidotic patients may hyperventilate Overventilated by mechanical ventilation Treatment: Treat cause in order to reduce respiratory rate and depth Reduction of ventilation or increase in dead space may help if ventilated 17

18 Metabolic acidosis Characterised by a rise in serum H+ Causes: Normal anion gap HCO3 - lost: From GI tract, e.g. diarrhoea, fistulae From renal tract, e.g. proximal renal tubular acidosis Increased anion gap acidosis: Renal failure Ingestion, e.g. salicylates, methanol Ketoacidosis, e.g. diabetic ketoacidosis Lactic acidosis 18

19 Causes of lactic acidosis: Association with hypotension and/or severe tissue hypoxia Shock from any cause Respiratory failure Cyanide or carbon monoxide poisoning Severe anaemia Associated with impaired mitochondrial respiration and increased lactate production Diabetes mellitus Hepatic failure Severe infection Drugs (e.g. salicylates) Toxins (e.g. ethanol) Inborn errors of metabolism 19

20 Sign of metabolic acidosis: stimulation of respiration, may become deep and sighing (Kussmaul s respiration), myocardial depression, reduced cardiac output, peripheral vasodilatation leading to hypotension, confusion and drowsiness, reduced activity of inotropic agents Treatment: Treatment of the cause Intra-venous fluids Sodium bicarbonate, but beware due to the left shift of the oxygen dissociation curve, inhibition of oxygen release from Hb may occur Renal replacement therapy 20

21 Metabolic alkalosis Characterised by gain of HCO3 - or loss of H+ Causes: Loss of H+: Vomiting, Gastric losses from nasogastric tube, Renal losses e.g. diuretic therapy, Increased mineralocorticoids, Posthypercapnia Increased HCO3 - administration Large citrate load, e.g. massive blood transfusion Treatment: Treat cause if possible (e.g. stop diuretics) 21

22 Thank You 22