Diagnosis of Hypernatremia clinical manifestations- Neurological manifestations predominate and are generally thought to result from cellular dehydration. Restlessness, lethargy, Hyperreflexia seizures, coma, and ultimately death may occur Rapid decreases in brain volume can rupture cerebral veins and result in focal intracerebral or subarachnoid hemorrhage.
TREATMENT OF HYPERNATREMIA The treatment of hypernatremia is aimed at restoring plasma osmolality to normal as well as correcting the underlying cause . Hypernatremia can be corrected by- Free water intake by oral or by nasogastric tube Hypotonic normal saline 0.45% NS Dextrose containing fluids Symptomatic hypernatremia - the water deficit should be reduced gradually by roughly 10 to 12 mEq /L/d chronic asymptomatic hypernatremia - the plasma [ Na+] should be lowered at a more moderate rate (between 5 and 8 mEq /L/d ).
Calculation for hypernatremia TBW is estimated by multiplying lean weight (in kilograms) by 0.5 in men and 0.4 in women.
Calculation for hypernatremia contd … Example-a patient 40 yr male has Na+ 1 7 0mEq/ l,his weigt is 60 kg. Desired Na+ is 145mEq/l Fluid for correction is 0.45%NS that contains 77 mEq /L =0+77-170/1+60*0.5 = -93/31=-3 The ∆[Na+] with 1 L of this fluid would be -3 mEq /L 4 L are necessary for a ∆ [Na+] -12 mEq /L/24 hours The hourly rate of infusion is 166 mL/ hr (4 L/day ∕ 24 hours/day = 0.166 L/hour )
Rapid correction of hypernatremia can result in seizures, brain edema, permanent neurological damage, and even death. In general, decreases in plasma sodium concentration should not proceed at a rate faster than 0.5 mEq/L/h. The goal of treatment is Na+ less than 145 mEq/L. Treatmet of hypernatremia contd …
HYPONATREMIA
HYPONATREMIA Na+ less than 135 mEq/L. Most common electrolyte disorder Hyponatremia is commonly caused by cellular edema with the presence of hypotonicity.
CAUSES OF HYPONATREMIA Renal Diuretics Mineralocorticoid deficiency Salt-losing nephropathies Osmotic diuresis (glucose, mannitol) Renal tubular acidosis EXTRA RENAL Vomiting Diarrhea Integumentary loss (sweating, burns)
Diagnosis f hyponatremia clinical manifestation- Patients with ([Na +] > 125 mEq/L) are frequently asymptomatic. Serious manifestation occur below 120 Early symptoms are typically nonspecific and may include anorexia, nausea, and weakness . Progressive cerebral edema, however, results in lethargy, confusion, seizures, coma, and finally death.
Treatment of hyponatremia • The treatment of hyponatremia directed at correcting both the is underlying disorder as well as the plasma [Na+]. • target plasma [Na+] is greater than 125 mEq /L .
the Na+ deficit, can be estimated by the following formula: Excessively rapid correction of hyponatremia has been associated with demyelinating lesions in the pons ( central pontine myelinolysis ), The following correction rates have been suggested: for chronic hyponatremia 0.5 mEq/L/h or less; for acute hyponatremia 1 mEq/L/h or less ; not correct greater than 10-12 mEq /day Treatment of hyponatremia contd …
Calculation for hyponatremia . Example-a patient 40 yr female has Na+ 108mEq/ l,her weigt is 80 kg complain of seizures. Fluid for correction is 3 %NS that contains 513 mEq /L . Rate of correction: She has symptomatic hyponatremia requiring an acute correction (1 to 2 mEq /L/ hr for the first 3 to 4 hours) but no more than 12 mEq /L corrected over 24 hours. Means of correction: ∆[Na+] = {513 - 108} / {80 * 0.5 +1 } =10 mEq /L(TBW=0.5*Body weight) One liter of this fluid 3%NS would increase [Na+] by 10 mEq /L. To prevent a change of >10 to 12 mEq /L over 24 hours, no more than 1 L of fluid should be given.
Treatment of hyponatremia . contd.. SIADH- Water restriction High dietary solute load-with high salt ,high protein dietor oral urea(30-60 gram) Vasopressin antagonist – IV conivaptan and oral tolvaptan
HYPOKALEMIA
HYPOKALEMIA Hypokalemia, defined as plasma [K +] less than 3.5 mEq/L. A decrease in plasma [K +] from 4 mEq/L to 3 mEq/L usually represents a 100- to 200-mEq deficit, whereas plasma [K +] below 3 mEq/L can represent a deficit anywhere between 200 mEq and 400 mEq.
CLINICAL MANIFESTATION OF HYPOKALEMIA Most patients are asymptomatic until plasma [K +] falls below 3 mEq/L. Cardiovascular effects are most prominent and include an abnormal ECG , arrhythmias, decreased cardiac contractility, and a labile arterial blood pressure due to autonomic dysfunction.
Chronic hypokalemia has also been reported to cause myocardial fibrosis. ECG manifestations are primarily due to delayed ventricular repolarization and include T-wave flattening and inversion, an increasingly prominent U wave, ST- segment depression, increased P- wave amplitude, and prolongation of the P–R interval . CLINICAL MANIFESTATION OF HYPOKALEMIA Contd..
ECG of hypokalemia 3.9mEq/l 2.7mEq/l 1.3mEq/l
TREATMENT OF HYPOKALEMIA Correction of the K+ deficit can be made with either oral or IV therapy . A 20mEq/dose[ K+]will raise the [ K +] by 0.25mEq/L Oral therapy- when hypokalemia is mild and the patient can tolerate oral administration . Oral doses of 40 mEq are generally well tolerated and can be given as often as every 4 hours. Traditionally , 10 mEq of potassium salts are given for each 0.10 mEq /L decrement in serum [ K+].
IV Therapy - Patients with imminently life-threatening hypokalemia like cardiac manifestation and those who are unable to take anything by mouth require IV replacement therapy with KCl . The maximum concentration of administered K+ should be no more than 40 mEq /L via a peripheral vein or 100 mEq /L via a central vein. The rate of infusion should not exceed 20 mEq / hr unless paralysis or malignant ventricular arrhythmias are present More rapid intravenous potassium replacement (10–20 mEq /h) requires central venous administration and close monitoring of the ECG . Intravenous replacement should generally not exceed 240 mEq /d TREATMENT OF HYPOKALEMIA Contd …
HYPERKALEMIA
HYPERKALEMIA Hyperkalemia exists when plasma [K +] exceeds 5.5 mEq/L. kidneys can excrete as much as 500 mEq of K +per day. So hyperkalemia rarely occurs in normal individuals
CLINICAL MANIFESTATION OF HYPERKALEMIA Th e most important effects of hyperkalemia are on skeletal and cardiac muscle. Skeletal muscle weakness is generally not seen until plasma [K +] is greater than 8 mEq/L, Cardiac manifestations are primarily due to delayed depolarization, and are consistently present when plasma [K +] is greater than 7 mEq/L.
ECG changes characteristically progress sequentially from symmetrically peaked T waves →widening of the QRS complex →prolongation of the P–R interval →loss of the P wave →loss of R- wave amplitude →ST-segment depression →an ECG that resembles a sine wave, before progression to ventricular fibrillation and asystole. Hypocalcemia, hyponatremia, and acidosis accentuate the cardiac effects of hyperkalemia. HYPERKALEMIA CONTD…
ECG OF HYPERKALEMIA S i n e w a ve
TREATMENT OF HYPERKALEMIA Hyperkalemia exceeding 6 mEq/L should always be corrected. Calcium (10 mL of 10% calcium G luconate infused over 2-3 minutes ) given if there is ECG changes found . An intravenous infusion of glucose and insulin (30–50 g of glucose with 10 units of insulin) 50% 50ml dextrose is commonly used
When metabolic acidosis is present, intravenous sodium bicarbonate (usually 45 mEq ) is used Β - Agonists promote cellular uptake of P otassium Loop diuretics-furosemide Cation exchange resins , such as sodium polystyrene sulfonate ( Kayexalate ),promote the exchange of Na+ for K+ in the GI tract Dialysis is indicated in symptomatic patients with severe or refractory Hyperkalemia TREATMENT OF HYPERKALEMIA Contd..
Take home message Hyponatremia is the most common cause of electrolyte imbalance Hyponatremia or hypernatremia corrected after calculation of deficit or Na+ excess G.i loss vomiting diarrhea is common cause of hypokalemia h ypokalemia can be corrected with oral or iv therapy depending on the severity of hypokalemia Hypo and hyperkalemia can be diagnosed by ecg Calcium gluconate is the first line of treatment of hyperkalemia