Hypoglycemia,Electrolyte disturbances and acid-base

imbalances

Pediatric emergency – PICU division

Pediatric department

Medical faculty, University of Sumatera Utara –

H. Adam Malik Hospital

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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 hypoglycemiaNeuroglycopenic 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 hypoglycemia2

Insulin and C-peptide levels may help determine cause

In nondiabetic hospitalized patients common etiologiesinclude :- Renal insufficiency- Malnutrition- Liver disease- Liver disease- Infection- Sepsis

Other causes : alcoholism, adrenal insufficiency, medications(insulin, sulfonylurea, pentamidine, trimethroprim –sulfamethoxazole, salycilates, beta-blocking agents),insulin-secreting tumors.

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Differential Diagnosis :

o Deliriumo Pheochromocytomao Factitious hypoglycemiao Liver failureo Psychoneurosiso Sepsis syndromeo Sepsis syndromeo Myxedema coma

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Treatment :

- Glucose IV or orally (if awake & alert)Glucose 10% � 5 ml/KgBW

- Monitor blood glucose closely as patients may need continousdextrose infusion until precipitating cause removed- Glucagon & hydrocortisone can be given for refractoryhypoglycemia- Identify & treat underlying disease or remove causative agent

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Electrolyte disturbances

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• Normal plasma level:133–144 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

SODIUM

insipidus, osmotic diuretics, burns), high sodium intake, iatrogenic

fluid restriction (often combined with drugs containing sodium, near

drowning (seawater)

• Presentation: lethargy, irritability, coma, seizures

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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 0.5–1 mmol/l/h• reduction of sodium level slowly 0.5–1 mmol/l/h

• desmopressin (DDAVP) can be used in diabetes

insipidus to reduce water loss

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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, • 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

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POTASSIUM

Normal serum level is 3.5–5.5 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

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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 • 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

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Treatment of hyperkalemia

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CALCIUMNormal level 2.1–2.56 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

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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

ACID-BASE DISORDERS

• pH is normally within the range of 7.35–7.45

• 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

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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+

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• 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):

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

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• 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

Respiratory alkalosis

• Characterised by lowered PaCO2

• Causes: Hyperventilation:

– Salicylate poisoning

– Fever, sepsis

– Encephalopathy

– Hypoxic and acidotic patients may hyperventilate

– Overventilated by mechanical ventilation

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– 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

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

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– Renal failure

– Ingestion, e.g. salicylates, methanol

– Ketoacidosis, e.g. diabetic ketoacidosis

– Lactic acidosis

•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

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– Diabetes mellitus

– Hepatic failure

– Severe infection

– Drugs (e.g. salicylates)

– Toxins (e.g. ethanol)

– Inborn errors of metabolism

• 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

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–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

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, Post-

hypercapnia

• Increased HCO3-– administration• Increased HCO3-– administration

• Large citrate load, e.g. massive blood transfusion

• Treatment: Treat cause if possible (e.g. stop diuretics)

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Thank You

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