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![TREATMENT OF HYPERNATREMIA
Treatment of hypernatremia is easier
1 Give 1-2 liters of saline in the first hour.
2. switching to DSW or half-normal saline
3. Recheck the serum sodium frequently since no matter HYDRATE and REPEAT
chemistries in 1-2 hours for severe disease.
4. Calculating free water loss (Cu rrent TBW x [Na+] - 1 40/ 1 40
For example, a 100 kg man with a sodium of only 160 (20 above normal) is
missing 9 liters of fluid.](https://image.slidesharecdn.com/electrolytedisorders-181031035334/75/Electrolyte-disorders-15-2048.jpg)
Uploaded byMohammad Omar Ansari
Electrolyte disorders
Sodium, potassium, and other electrolyte disorders can cause significant neurological and cardiac issues. Low sodium (hyponatremia) can cause symptoms ranging from nausea to seizures depending on severity. Treatment involves restricting water intake and using isotonic fluids or hypertonic saline. High sodium (hypernatremia) often causes confusion and is treated by rehydration. Low potassium (hypokalemia) commonly involves muscle weakness and cardiac arrhythmias, treated by oral or IV potassium replacement. High potassium (hyperkalemia) can alter the electrocardiogram and potentially cause fatal arrhythmias. Electrolyte levels must be closely monitored during treatment.
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Electrolyte disorders
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- 3. Sodium Disorders Allsodium disorders, whether from high or low sodium, cause neurologic abnormalities when severe. Look for: • Lethargy • Confusion • Altered mental status • Seizures and coma (severe cases) Sodium causes CNS problems, not rhythm disturbance.
- 4. hyponatremia Defined as aserum sodium concentration less than 1 3 5 mEq/L . hyponatremia is the most common electrolyte abnormality in hospitalized patients. Mild hyponatremia (130—134) Modrate hyponatremia ( 129---116) Sever hyponatremia (115)
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- 6. Clinical Findings dependson its severity and acuity. 1.Acute.( hours to days ) can be severely symptomatic. Mild hyponatremia ( 1 30- 135 mEq/L) is usually asymptomatic. mod hyponatremia;- nausea and malaise progress to headache, lethargy, and disorientation as the sodium concentration drops. serious symptoms :- R arest, seizure, coma, permanent brain damage, brainstem herniation, and death. Permanent brain injury from hyponatremic encephalopathy. 2.Chronic disease.-( weeks to months ) asymptomatic yet Na less 110meq because the brain has adapted by decreasing its tonicity over the months.
- 7. Treatment initial step restrictionof free water and hypotonic fluid intake. Hypovolumic Na isotonic fluids (NS or RL solution) Hypervolemic Na patients may require loop diuretics or dialysis, or both Pseudohyponatremia from hypertriglyceridemia or hyperproteinemia requires no therapy except confirmation. corect the eitiology.
- 8. Cont… symptomatic patients.First, 4-6 mEq/L /h in the S Na is necessary to reverse the neurologic manifestations. Second, acute hyponatremia (eg, exercise-associated hyponatremia) with severe neurologic manifestations can be reversed rapidly with 1 00 mL of 3% hypertonic saline infused over 10 minutes (repeated twice as necessary) . Third, correction rates for chronic hyponatremia are low ( 4-8 mEq/L per 24 hours in patients at high risk for demyelination) . For every 100 mg/dL above means sodium down 1.6 mEq Treatment is correction of the glucose level.
- 9. CONT… Symptomatic andsevere hyponatremia generally require hospitalization for careful monitoring of fluid balance DCmeds. hyponatremic patients at high risk for demyelination who are corrected too rapidly are candidates for treatment with a combination of DDAVP and intravenous dextrose 5% to relower the serum sodium. In severely symptomatic patients, the clinician should calculate the sodium deficit and deliver 3% hypertonic saline.
- 10. CONT… hyponatremic patientsat high risk for demyelination who are corrected too rapidly are candidates for treatment with DDAVP + dextrose 5% t In severely symptomatic patients, the clinician should calculate the sodium deficit and deliver 3% hypertonic saline. Sodium deficit =(TBW) x (Desired serum Na-Actual serum Na) not exceed 0.5 mL/kg body weight/h higher rates Hypertonic saline in hypervolemic patients can be hazardous (worsening volume overload, pulmonary edema, and ascites.)
- 11. CON… demeclocycline (300-600mg orally twice daily) inhibits the effect of ADH on the distal tubule. Onset of action may require 1 week. Cirrhosis may increase the nephrotoxicity of demeclocycline. Vasopressin antagonists have transformed the treatment of euvolemic and hypervolemic hyponatremia, especially in heart failure. oral selective vasopressin-2 receptor antagonists:-Tolvaptan, lixivaptan, and satavaptan are conivaptan is an intravenous agent.
- 12. Hypernatremia High sodiumlevels make patients confused and encephalopathic. Treatment of hypernatremia is easier because the initial therapy is always to hydrate the patient. At the beginning, any type of fluid will correct the sodium because the sodium level of saline is only 154 mEq/L.
- 13. Etiology of Hypernatremia Free water loss: • Skin: sweating, burns, skin loss • Urine: diuretics without free water replacement • GI: diarrhea without free water replacement • Diabetes insipidus 1. Central: head trauma, hypoxia, infection, tumor, granulomatous disease 2. Nephrogenic: low potassium, high calcium, sickle cell disease or trait
- 14. Clinical Findings typicalfindings;- dehydrated,orthostatic hypotension and oliguria early signs;- Lethargy,irritability, and weakness . Sever hypernatremia;- Hyperthermia, delirium, seizures, cerebral demyelination and coma ( Na> 1 5 8 mEq/L) .
- 15. TREATMENT OF HYPERNATREMIA Treatmentof hypernatremia is easier 1 Give 1-2 liters of saline in the first hour. 2. switching to DSW or half-normal saline 3. Recheck the serum sodium frequently since no matter HYDRATE and REPEAT chemistries in 1-2 hours for severe disease. 4. Calculating free water loss (Cu rrent TBW x [Na+] - 1 40/ 1 40 For example, a 100 kg man with a sodium of only 160 (20 above normal) is missing 9 liters of fluid.
- 16. TREATMENT OF HYPERNATREMIA 1 . Hypernatremia with hypovolemia:- isotonic 0.9% normal saline or 0.45% saline or 5% dextrose (or both) in Milder volume deficits 2. Hypernatremia with euvolemia:-Water ingestion or IV 5% dextrose 3. Hypernatremia with hypervolemia- includes 5% dextrose+ Loop diuretics to promote natriuresis In severe rare cases with kidney disease, hemodialysis may be necessary to correct the excess total body sodium and water.
- 17. Potasium disorder Potassium(K) abnormalities are extremely common in the hospital. Whether the level is up or down, potassium causes:Arrhythmias that can easily be fatal Muscle weakness Arrhythemia K abnormality, always recheck the level after you have treated it(3-6h)+CON ECG. Do not wait until the next day to recheck potassium abnormality.
- 20. The causes ofhypokalemia Decreased potassium intake Potassium shift into the cell Increased postprandial secretion of insulin Alkalosis Trauma (via beta-adrenergic stimulation?) Periodic paralysis (hypokalemic) Barium intoxication Extra rena l potassium l oss Vomiting, dia rrhea, laxative abuse Potassium causes cardiac problems, not CNS disturbance. TTKG= UK x PK/UOSMxPOSM
- 21. Renal potassiuml oss Primary hypera ldosteronism Secondary al dosteronism (dehydration, heart fa i l u re) Renovascular hypertension Malignant hyperten Increased aldosterone (mineralocorticoid) Diuretics (furosemide, thiazide) Hypomagnesemia Renal tubular acidosis (type I or I I ) Metabolic alkalosis (bicarbonaturia)
- 23. Cont.. Low potassium causescardiac and muscular problems . • In intensive care, 20-30 mEq/hr can be given with continuous cardiac monitor. • 10 mEq KCl IV raises blood level by 0.1 mEq/L If you replace lots of potassium but the level does not go up. check the magnesium level. Low magnesium will cause urinary leakage of potassium, thereby preventing potassium correction. EKG will show "U" waves, broad T wave, decrease amplitude & ST dep
- 25. Clinical Findings mildto moderate hypokalemia :- Muscular weakness, fatigue, and muscle cramps.constipation or ileus. severe hypokalemia (less than 2 . 5 mEq/L):- Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis . The presence of HTN is a clue to the diagnosis of hypokalemia from aldosterone or mineralo corticoid excess Renal manifestations include nephrogenic DI and interstitial nephritis.
- 26. Hyperkalemia Serum potassiumlevel greater than 5 m Eq/L Hyperkalemia may develop in patients taking ACE inhibitors/ARB. potassium-sparing diuretics, or their combination. The ECG may show pea ked T waves, widened QRS and biphasic QRS-T complexes, or may be normal.
- 27. CAUSE HYPERKALEMIA The causesof hyperkalemia are: • Renal failure/insufficiency • Medications 1. ACE inhibitors/ARBs 2. Aldosterone antagonists (spironolactone, eplerenone) 3. Beta blockers • Acidosis (metabolic more common) • Diabetes, especially DKA • Cell breakdown Tumor lysis Rhabdomyolysis Hemolysis
- 28. Clinical Findings Hyperkalemiaimpairs neuromuscular transmission, causing muscle weakness, flaccid paralysis, and ileus. Electrocardiography ;->6.5 mEq/L will manifest ECG changes. include bradycardia, PR interval prolongation, peaked T waves, QRS widening, and biphasicQRS-T complexes. Conduction disturbances, such as bundle branch block and atrioventricular block, may occur. Ventricular fibrillation and cardiac arrest are terminal events
- 29. ECG CHANGES bradycardia PR intervalprolongation peaked T waves, QRS widening biphasicQRS-T complexes. Conduction disturbances (BBB and AV block) terminal events (VF,CA).
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- 36. Refferences CURRENT MEDICALDIAGNOSIS & TREATMENT ICU FOR DR NET