Electrolyte Imbalance

Electrolyte imbalance Beirut arab university 5th year medical school Salamtak workshop Done by Dr. Ahmad Al-kouzi

Composition of Body Fluids

• 50% of body weight is water in women • 60% of body weight is water in men • ICF:55-75% • ECF:25-45% including intavascular and extravascular in a ratio of 1:3 Major ECF particles: Major ICF particles: 1-sodium 1potassium 2-chloride 2-ATP

Water Balance • Plasma osmolality:275290mosmol/kg • Obligate water loss :Urine-Stool-skin and respiratory tract. • Minimum urine output of 500 ml/day is required for neutral solute balance • Water intake must equal water excretion

Water intake • Thirst osmolality

increase in effective or decrease in ECF

volume or blood pressure

Sensed by osmoreceptors

Water excretion A V P=ADH

Binds to V2 receptors of principal cells in the collecting duct The major stimulus for secretion is hypertonicity sensed by the osmoreceptors in antrolateral hypothalamus

Non osmotic factors that regulate AVP 1-effective circulating arterial volume 2-nausea,pain,stress,hypoglycemia 3-Pregnancy

Hypovolemia • Definition:”state of combined salt and water loss exceeding intake leading to ECF volume contraction” NB:The loss of Sodium may be renal or extrarenal Eg renal: diuretics-glucose-ureamannitoldiuretic phase of acute tubular

• Eg of Extrarenal: 1-GIT 2-SKIN 3-THIRD space accumulation

Pathophysiology • ECF volume contraction

Hypotension and diminished cardiac output Stimulates baroreceptors in carotid sinus and aortic arch sympathetic activation maintenance of cerebral and

• In respect to the Kidney: 1-increase PCT reabsorption of Sodium 2-Decrease GFR 3-increase reabsorption of Sodium by the collecting duct

Clinical Features: • Symptoms Signs: 2. Fatigue 3. Weakness hypotension 4. Thirst tachycardia 5. Postural dizziness 6. If

1. JVP 2.Postural 3.postural

Diagnosis: 1-BUN:creatinine=20:1(decreased GFR) However high BUN realtive to creatinine occurs in hyperalimentation and glucocorticoid therapy. 2-Urine sodium < 20 mmol/L However in ATN there is impaired Sodium reabsorption or in case of vomitting:see Cl 3-urine osmolality>450 mosmol/kg and specific gravity>1.015 However in DI SG and urine osmolalityare

Treatment • Mild:correct via the oral route • Severe:IV normal saline(154 mmol/L) However in Hypenatremia use half normal saline or 5% dextrose Patients with significant hemorrhage,anemia may require blood transfusion or dextran

Hyponatremia • Definition:Plasma sodium concentration<135 mmol/L Plasma Osmolality may be Decreased(hypotonic) Increased (hypertonic) Normal(isotonic)

Hypotonic hyponatremia • Primary water gain and secondary sodium loss:eg:1-Primary polydipsia 2-beer potomania 3-SIADH 4-Addison disease and hypothyroidism

• Primary sodium loss and secondary water gain

• Renal: 1-Diuretics(Thiazides) rarely loop. 2-Hypoaldosteronism 3-Salt wasting nephropathy • Extrarenal: 1-Intergumentary 2-GIT

Hyponatremia in ECF volume Expansion • By this there is Primary Na gain exceeded by secondary water gain 1-Heart Failure 2-Hepatic cirrhosis 3-Nephrotic Syndrome

Clinical features Mainly neurological: Brain cell swelling and cerebral edema Symtoms depend on : The severity of onset and the absolute decrease in plasma Na • Nausea and Malaise • Headache,lethargy,confusion • Stupor,seizures and coma(plasma Na <120mmol/L or decreases rapidly)

Diagnosis 1-Plasma osmolality 2-Urine osmolality 3-Urine Na 4-Urine K

Treatment 1-Raise plasma Na by restricting water intake and promoting water loss 2-Correct the underlying disorder 2 protocols In ECF volume volume contraction

In ECF

In ECF volume contraction • Na repletion in the form of isotonic saline The direct effect on the plasma Na is trivial however there is restoration of euvolemia and hence removing the hemodynamic stimulus of AVP allowing the excess free water to be excreted

In Edematous state • Restriction of Na and water • Correction of Hypokalemia • Promotion of Water loss in excess of Na

Correction (Desired plasma Na –Measured Plasma Na) X Weight X 0.6 in man or 0.5 in woman

Important: • Do not raise plasma Na more than 0.5 to 1 mmol/L/hour And no more than 10-12 mmol/L/day Except in altered mental status and seizures you are allowed up to 2 mmol/L/hour For fear of developping ODS

Osmotic demyelination syndrome • Flaccid paralysis • Dysarthria • Dysphagia Diagnosis:Clinically+neuroimaging studies Treatment:No treatment+high morbidity and mortality

Hypernatremia • Definition:plasma Na concentration >145mmol/L • Hypernatremia is a state of hyperosmolality which is usually mild unless impaired thirst(Primary hypodipsia) or limited access to water is present. • Causes:Primary Na gain(rare) or water deficit(common)

Non renal loss of water • In Profuse prespiration there is increase in solute free water loss • Diarrhea:osmotic not secretory(presents usually with hyponatremia or normal Na). • Mechanically ventilated patients and severe burns

Renal loss of water • Most common diuresis (DM)

osmotic Diabetes

insipidus

CDI NDI

Clinical features: • Contracted ICF volume • Decreased brain cell volume increasing risk of subarachnoid or intracerebal hemorrhage . • Neurologic manifestations: 1-altered mental status 2-weakness 3-seizures and coma

Treatment • Stop the ongoing water loss • And correct the water deficit • Correction: water deficit=[(Plasma Na concentration-140)/140]X TBW • TBW is 40% in women and 50%in men

• Do not correct more than 0.5 mmol/L/h • AND no more than 12mmol/L/h over the 24 hours

• The safest route is by mouth or via nasogastric tube • Half normal saline or dextrose can be given IV • CDI:desmopressin nasally • NDI:Thiazide.

Potassium • Major intracellular cation • Normal:3.5-5mmol/L • For balance:matching ingestion with excretion. • Immediately following a meal K⁺ enters cells as result of insulin and initial elevation of plasma K⁺. • Eventually however excess is excreted in urine

Potassium excretion • 90% of filtered K⁺ is reabsorbed by PCT and loop of Henle.(TALH) • K⁺ delivery to the distal nephron approximated dietary intake • Regulation by ALDOSTERONE and HYPERKALEMIA

Hypokalemia • Definition:plasma potassium concentration<3.5mmol/L • Causes 1-decreased intake 2-shift into cells 3-increased net loss

Redistribution into cells • • • • • •

In metabolic alkalosis Insulin treatment of DKA Uncontrolled DM from osmotic diuresis ß₂ adrenergic agonist Anabolic states Transfusion of frozen RBCs

NB:hypokalemic periodic paralysis is a rare condition in which there is recurrent episodic weakness or paralysis

Loss of Potassium

• Non renal: 1-Excessive sweating(renal) 2-ECF contraction and hyperaldosteronism 3-Secretory diarrhea 4-Vomitting due to metabolic alkalosis and volume depletion

• Renal: 1-Primary hyperaldosteronism 2-Hyperreninemia in Malignant hypertension(+tumors) 3-Liddle’s syndrome(rare) 4-Bartters syndrome. 5-Most important:Diuretic abuse.

Clinical features • Fatigue ,myalgias and muscular weakness of the lower extremities. • Progressive weakness,hypoventilation and complete paralysis • ECG changes: 1-flattening or inversion of T wave 2-Prominent U wave 3-ST depression 4-Prolonged QU interval If severe: Prolonged PR and widening QRS

Hypokalemia Metabolic alkalosis

Diagnosis • Diuretic and laxative abuse • Surreptitious vomitting • Marked leucocytosis(AML) Pseudohypokalemia • TTKG

Treatment • Correct K⁺ deficit and minimize losses • In intracellular shifts use oral preparations. • In DKA there may be an underestimation of the K⁺ deficit. • Use KCl and rarely Bicarbonate formulas.

Hyperkalemia • Definition: plasma K⁺ concentration > 5 mmol/L • Causes: 1-Decreased renal loss 2- increased potassium release from the cells. Pseudohyperkalemia:PROLONGED use of a tourniquet-hemolysis-marked leucocytosis and thrombocytosis.

• Renal failure • Decreased distal flow • Decreased K⁺ secretion : A-Impaired Na reabsorption 1-Primary hypoaldosteronism 2-secondary hypoaldosteronism 3-Resistance to aldosterone B-Enhanced Chloride reabsorption: 1-Gordon’s syndrome(Cl shunt) 2-Cyclosporine

Clinical features • Weakness,flaccid paralysis and respiratory arrest • Metabolic acidosis • Cardiac toxicity ECG changes: 1-increased T wave amplitude or tented T wave 2-increased PR interval and widening of QRS 3-loss of P wave

ECG

Diagnosis • • • •

Exclude pseudohyperkalemia Symptoms Plasma K ECG

Treatment • Depends on Plasma K conc +ECG changes+associated muscular weakness • If >7.5 severe and may be fatal so emergency treatment: 1-Administration of Ca gluconate(rule of 10) dose may be repeated if no changes in ECG 2-insulin +GLUCOSE 3-IV NaHCO3 (specifically in metabolic acidosis)

Removal of K⁺ • If renal function is adequate: Loop and thiazide diuretics • Na polystyrene sulfonate(SPS) • If renal function is impaired :Hemodialysis

Calcium • Normal calcium level:8.9-10.1 g/dl • Regulation by PT glands+VitD • Regulating diverse physiological processes

Hypercalcemia • Causes: 1- Excess PTH 2-FHH (CaSR mutations) 3-PTHrP 4-Sarcoidosis 5-Hyperthyroidism 6-Osteolytic metastasis

Clinical manifestations • If mild asymptomatic however be careful of neuropshychiatric changes. • PUD • Nephrolithiasis • If severe >12-13 mg/dl lethargy stupor or coma+GIT symptoms • ECG changes:AV block-bradycardiashort QT interval

Diagnosis • Note the albumin concentration 50% ionized-50% bound to albumin If there is hypoalbuminemia add 0.8mg/dl for every 1g/dl albumin decrement and opposite for increase in albumin • PTH level • Renal function

Treatment • In severe hypercalcemia : 1-Hydration 4-6 L IV saline in 24 hours 2-Loop diuretics 3-Bisphosphonates 4-Calcitonin 5-Dialysis 6-IV phosphate

In sarcoidosis and other granulomatous disease: • Glucocorticoids IV or oral • Ketoconazole,chloroquine may be occasionally used

Hypocalcemia • PTH levels:

If High: If LOW Secondary Hypoparathyroidism Renal failure

Clinical manifestaions • Paresthesias:finger,toes,circumoral regions • Carpopedal spasm • Chvostek sign • Trousseau sign • QT prolongation