Electrolyte disorder 2018, Hyponatremia, Hypernatremia By Dr. Omar Ansari

1. ELECTROLYTE
DISORDERS
Sodium Disorders

2. TB FLUID
d

3. Sodium Disorders
 All sodium 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 a serum 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)

5. 2Na+gl/18+BUN/2.8=

6. Clinical Findings
 depends on 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 restriction of 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 and severe 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 patients at 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 (300-600 mg 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 sodium levels 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
 typical findings;- 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
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.

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 of hypokalemia
 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 potassium l 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 causes cardiac 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
 mild to 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 potassium level 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 causes of 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
 Hyperkalemia impairs 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 interval prolongation
peaked T waves, QRS widening
biphasicQRS-T complexes.
Conduction disturbances (BBB and AV block)
terminal events (VF,CA).

31. K-LEVEL -ECG

36. Refferences
 CURRENT MEDICAL DIAGNOSIS & TREATMENT
 ICU FOR DR
 NET