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Electrolyte imbalance


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Published in: Health & Medicine

Electrolyte imbalance

  3. 3. HYPERNATREMIA  Sodium (Na+) concentration of greater than 145 mEq/L  Produces a state of hyperosmolality
  4. 4. CAUSES Impaired thirst Coma Essential hypernatremia Solute diuresis diabetic ketoacidosis nonketotic hyperosmolar coma, mannitol administration Excessive water losses Neurogenic diabetes insipidus Nephrogenic diabetes insipidus
  5. 5. 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.
  6. 6. TREATMENT  The treatment of hypernatremia is aimed at restoring plasma osmolality to normal as well as correcting the underlying cause.  Water deficit is calculated by  Free H2O deficit = {(plasma Na+/ 140) – 1} × TBW  correction should be done over 48 h with a hypotonic solution such as 5% dextrose in water
  7. 7.  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
  8. 8. ANESTHETIC CONSIDERATION  Hypernatremia has been demonstrated to increase the MAC for inhalation anesthetics  Elective surgery should be postponed in patients with significant hypernatremia (>150 mEq/L)  Both water and isotonic fluid deficits should be corrected prior to elective surgery.
  10. 10. HYPONATREMIA  Na+ less than 135 mEq/L.  Most common electrolyte disorder  Hyponatremia is commonly caused by cellular edema with the presence of hypotonicity.
  11. 11. 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) “Third-spacing”
  12. 12. 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.
  13. 13. TREATMENT • The treatment of hyponatremia is directed at correcting both the underlying disorder as well as the plasma [Na+]. • Correction of plasma [Na+] to greater than 125 mEq/L is usually suffi cient to alleviate symptoms.
  14. 14.  Desired value, the Na+ deficit, can be estimated by the following formula:  Na+ deficit =TBW ×(desired [Na+]−present [Na+]  Excessively rapid correction of hyponatremia has been associated with demyelinating lesions in the pons ( central pontine myelinolysis),  Th e following correction rates have been suggested: for  mild symptoms, 0.5 mEq/L/h or less; for  moderate symptoms, 1 mEq/L/h or less; and for  severe symptoms, 1.5 mEq/L/h or less.
  15. 15. ANESTHETIC CONSIDERATION  A plasma sodium concentration greater than 130 mEq/L is usually considered safe for patients undergoing general anesthesia.  In most circumstances, plasma [Na+] should be corrected to greater than 130 mEq/L for elective procedures, even in the absence of neurological symptoms.  Lower concentrations may result in significant cerebral edema that can be manifested intraoperatively as a decrease in MAC or postoperatively as agitation, confusion, or somnolence.
  17. 17. 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.
  18. 18. CAUSES EXCESS RENAL LOSS Mineralocorticoid excess Primary hyperaldosteronism (Conn’s syndrome) Renin excess Renovascular hypertension Diuresis Chronic metabolic alkalosis Renal tubular acidosisG.I LOSS Vomiting Diarrhea, ECF → ICF shifts Acute alkalosis Hypokalemic periodic paralysis Barium ingestion Insulin therapy
  19. 19. CLINICAL MANIFESTATION  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.
  20. 20.  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 .
  21. 21. TREATMENT  Intravenous replacement usually be reserved for patients with, or at risk for, significant cardiac manifestations or severe muscle weakness.  Because of potassium’s irritative effect on peripheral veins, peripheral intravenous replacement should not exceed 8 mEq/h.  Dextrose-containing solutions should generally be avoided because the resulting hyperglycemia and secondary insulin secretion may actually worsen the low plasma [K +].  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
  22. 22. ANESTHETIC CONSIDERATION  The decision to proceed with elective surgery is often based on lower plasma [K +] limits somewhere between 3 and 3.5 mEq/L.  In general, chronic mild hypokalemia (3–3.5 mEq/L) without ECG changes does not substantially increase anesthetic risk.
  23. 23.  The intraoperativelypotassium should be given if atrial or ventricular arrhythmias develop.  Glucose-free intravenous solutions should be used and hyperventilation avoided to prevent further decreases in plasma [K +].  Increased sensitivity to neuromuscular blockers (NMBs) may be seen; therefore dosages of NMBs should be reduced 25– 50%, and a nerve stimulator should be used to follow both the degree of paralysis and the adequacy of reversal
  25. 25. 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
  26. 26. CLINICAL MANIFESTATION  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.
  27. 27.  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.
  28. 28. TREATMENT  Hyperkalemia exceeding 6 mEq/L should always be corrected.  Treatment is directed to reversal of cardiac manifestations and skeletal muscle weakness, and to restoration of normal plasma [K+]  Calcium (5–10 mL of 10% calcium gluconate or 3–5 mL of 10% calcium chloride) partially antagonizes the cardiac effects of hyperkalemia and is useful in patients with marked hyperkalemia
  29. 29.  When metabolic acidosis is present, intravenous sodium bicarbonate (usually 45 mEq) will promote cellular uptake of potassium and can decrease plasma [K+] within 15 min  Β Agonists promote cellular uptake of potassium and may be useful in acute hyperkalemia associated with massive transfusions
  30. 30.  An intravenous infusion of glucose and insulin (30–50 g of glucose with 10 units of insulin) is also eff ective in promoting cellular uptake of potassium and lowering plasma [K+], but may take up to 1 h for peak effect.  Dialysis is indicated in symptomatic patients with severe or refractory hyperkalemia
  31. 31. ANESTHETIC CONSIDERATION  Elective surgery should not be undertaken in patients with significant hyperkalemia.  Succinylcholine is contraindicated, as is the use of any potassium containing intravenous solutions such as lactated Ringer’s injection.
  32. 32.  The avoidance of metabolic or respiratory acidosis is critical  Ventilation should be controlled under general anesthesia, and mild hyperventilation may be desirable.