1. Magdy Khalil, MD, EDIC Homeostasis

2. Principles of management Prompt recognition Identification and treatment of underlying process Correction (proportional to acuity and severity)

3. Hypokalaemia: recognition SymptomsForeseen  Arrhythmia  Fatigue, myalgia and muscular weakness with or without hypoventilation Renal losses diuretics GIT losses Diarrhoea, nasogastric aspirate Intracellular shift Metabolic alkalosis, B2 agonists, insulin K+ <3 mmol/L

4. Hypokalaemia:diagnosis History Lab. K+ metabolic alkalosis Mg+ +/- ECG ( in severe case)

5. Hypokalemia: management K+ supplementation Route/ Rapidity : Oral: safer (GI tract is available+ no serious complications) IV (severe and / or arrythmia) Access: peripheral line (10 mEq/hr) central venous catheter (>20 mEq/h) Preparation Saline rather than a dextrose-based solution KCl (alkalotics) K phosphate (acidotic and/or hypophosphataemic) Monitoring ECG Serum K+ Stop offending drugs Treat precipitating causes Correct hypoMg+

6. Hyperkalaemia: Recognition SymptomsForeseen Acute cardiac conduction disturbances and asystolic cardiac arrest Generalised symmetrical weakness with decreased reflexes. AKI (oliguric) Severe acidosis Rhabdomyolysis ( e.g. polytrauma) Tumour lysis syndrome Bowel necrosis Digitalis toxicity Adrenal insufficiency 5 mEq/L 6 mEq/L

7. Hyperkalemia: Diagnosis History S creatinine, BUN Ca+, P+, CK Urine analysis Cortisol/ACTH stimulation ECG Pseudohyperkalaemia

8. Hyperkalemia : management Cardiac arrhythmias, intravenous calcium (10 mL of 10% calcium gluconate, rapidly intravenously) This dose can be repeated up to a total of 30 mL Intravenous insulin ( 10 units of regular insulin/50–100 mL 50% dextrose over 20–30 minutes) Nebulised β 2-agonists (10–20 mg of salbutamol by nebuliser over 10 minutes [adults]) Alkalinisation: sodium bicarbonate or hyperventilation (for patients with significant acidosis) Loop diuretics Haemodialysis or haemofiltration may be necessary. Cationic-exchange resins :orally or as an enema Modify diet Treat cause D/C offending drugs

9. Hypothyrodism:Recognition Unexplained bradycardia Unexplained hypothermia Altered mental status and/or coma OSA (due to macroglossia) and hypercapnia Unexplained pleural and pericardial effusions. Dry coarse skin, puffy facies, macroglossia, periorbital oedema

10. Hypothyrodism: Diagnosis Clinical TSH and free T4 ↑ TSH, N or ↓ free T4 primary hypothyroidism ↓ TSH, ↓ free T4 secondary hypothyroidism TSH is an excellent screening test for hypothyroidism in the outpatient setting. However, in critically ill patients, this is not the case

11. Hypothyroidism: treatment Oral T4, once a day, 1.5 μ g/kg/day In myxoedema coma: T4: 500 μ g as a loading dose intravenously followed by 50– 100 μ g/day, or T3: 10–25 μ g can be given intravenously followed by 5–10 μ g /8h Supportive ttt: Hypothermia Hypercapnia Hypotension (careful vasoactive, avoid digoxin) Glucocorticoids

12. Euthyroid Sick Syndrome ↓ serum levels of thyroid hormones (T3±T4), ↑ rT 3, N/ ↓ /slight ↑ TSH Euthyroid patients with nonthyroidal systemic illness. Diagnosis is based on excluding hypothyroidism. Clinical judgment TSH, rT 3 Serum cortisol ( ↑ ) Treatment is of the underlying illness; thyroid hormone replacement is not indicated. Interpretation of abnormal thyroid function test results in ill patients is complicated by the effects of various drugs: Iodine-rich contrast agents Amiodarone Dopamine Corticosteroids

13. Hyponatraemia: recognition SymptomsForeseen neurologic: confusion and lethargy to stupor, convulsions and coma. Followin TURP, laparoscopic irrigation, or the utilisation hypotonic fluids for resuscitation. History of hypothyroidism, cirrhosis, chronic heart failure, SIADH and adrenal insufficiency plasma osmolality ≤240 mOsm/kg Mechanism:In hypotonic hyponatraemia of acute onset, brain swelling occurs Protective mechanisms follow: Extracellular fluid movement into the CSF Loss of solutes from the brain cells, Na+. K+, organic solutes Rapid correction of severe (chronic) hyponatraemia can lead to osmotic demyelination or central pontine myelinolysis ( dysphagia,dysarthria, quadriparesis, lethargy, seizures and coma)

14. Hyponatremia: types Hypotonic hyponatraemia (Commonest type) ↓ intravascular volume (with or without oedema) Congestive heart failure Cirrhosis Nephrotic syndrome Euvolaemic hyponatraemia SIADH Primary psychogenic polydipsia. (urine osmolality) Isotonic hyponatraemia Hyperlipidaemia hyperproteinaemia. Hypertonic hyponatraemia – Hyperglycaemia (↑ 100 mg/dL=↓ 1.6 mEq/L) Mannitol administration,

15. Hyponatremia: diagnosis Plasma osmolality Urine osmolality Plasma osmolar gap (difference between the calculated and measured osmolar Plasma uric acid level SIADH ↓ Volume depletion ↑ Cerebral salt wasting ↓ intravascular volume depletion+ ↓ serum uric acid Renal, adrenal and thyroid function (prerequisite for diagnosis of SIADH). Look for and identify diseases and/or drugs associated with SIADH (CNS disorders, tumours, major surgery, pulmonary disorders, drugs)

16. Hyponatremia: management Severe, acute symptomatic hyponatraemia: intravenous hypertonic saline, correction of <10–12 mmol/L/day. Plasma electrolytes should be closely monitored. Hypertonic saline should be discontinued when the patient becomes asymptomatic. Asymptomatic hyponatraemia, [Na] can be corrected more slowly at a rate of around 0.5 mmol/L/hr. Euvolaemic patients : water restriction in. Drugs associated with SIADH need to be discontinued. Hypovolaemic with haemodynamic compromise: correction of volume depletion by normal saline is a prerequisite to the normalisation of plasma Complications of therapy: Congestive heart failure Osmotic demyelination syndrome (ODS)