Electrolyte Disturbances

Electrolyte Disturbances:
Disorders of Sodium and Potassium, the two principle electrolytes, are the most common problems. Hypokalemia [ K+] is the most common. Hyperkalemia [¬ K+] occurs in special instances, primarily in renal patients. Hyponatremia [ Na+] and Hypernatremia [¬ Na+] generally occur in elderly and neurological patients.
Some patients come to the ED labeled as having an electrolyte disturbance, already detected by an earlier lab test, which we are expected to verify and treat accordingly. This can be due to a spurious lab result that is not matched by a redraw. Others come only with a presentation which coupled with their history suggests the possibility.
Common Causes of Spurious Lab Results:
• Rough handling of specimen tubes, tortuous passage of the blood through the needle, or splattering of the blood against the Vacutainer walls, even excessive "tourniquet time" can break up the erythrocyte walls causing a release of intracellular potassium that alters the test results. (A "small" needle is not the problem if the draw is gentle; --it is turbulence which destroys the cells.)
• Drawing the lab specimen proximal to an IV infusion, or drawing from a line and not discarding a "waste" of the volume representing the admixture within the lumen of cells, fluid, heparin, or medications.
• Misidentification of patient identity upon the specimen (results for wrong patient).
Hypokalemia:
Serum Potassium levels below 3.5 mEq/L leads to weakness, fatigue, cardiac arrhythmia and irritability. It typically occurs in older patients with excessive diuresis and inadequate dietary or supplementary potassium sources. If a potassium disorder ("hypo" or "hyper") is suspected, immediately do a stat. electrocardiogram and begin cardiac monitoring (checking for ECG changes is faster than the laboratory). How symptomatic a patient may depend more on the rate of change in serum level and the chronicity of it, than the absolute level?
Causes:
• Ongoing or severe fluid losses from the GI tract by vomiting, diarrhea, or nasogastric suction, are a major cause; chronic laxative abuse in the elderly; malnutrition may cause an inadequate dietary supply.
• Diuretics;  -adrenergic agonists e.g., Albuterol; Steroids; Theophylline; Aminoglycosides; are all implicated in lowering potassium levels.
• Renally mediated losses from Renal Tubular Acidosis or hyperaldosteronism, Magnesium depletion, and Leukemia.
• Insulin and alkalosis shift potassium out of circulation and into cells.
The patient may complain of palpitations due to arrhythmia; muscle weakness, cramps, fasiculations, or tetany; nausea and vomiting; constipation, ileus; paresthesias and paralysis; polyuria and polydipsia, altered mental status.
The physician of medications to spare potassium, and follow-up to recheck the level can treat mild hypokalemia with oral potassium (if tolerated), education upon dietary sources, possible change.
Symptomatic patients and more severe deficits will need careful and cautious intravenous replenishment of potassium.
Lab Studies:
Electrolytes, Serum Creatinine, Blood Urea Nitrogen, Glucose are basic; Calcium, Magnesium, Phosphate may be needed. Digoxin level is very important (whether hypokalemic or hyperkalemic) if patient is taking Digoxin due to enhancement of proarrhythmic or toxic properties. Alkalosis can shift K+ into cells; an ABG may be needed.
ECG Changes:
o T wave flattening or inverted T waves
o Prominence of U wave that appears as QT prolongation
o ST segment depression
o Ventricular arrhythmias (eg, premature ventricular contractions [PVCs], torsade de pointes, ventricular fibrillation)
o Atrial arrhythmias (e.g., premature atrial contractions [PACs], atrial fibrillation)
Source: [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذا الرابط]
Essential Points for Treatment:
1. Verify hypokalemia before giving Potassium.
2. Verify renal status before giving Potassium.
3. Do not use matrix tablets for acute replacement; they dissolve slowly and are for maintenance therapy. Use liquid or soluble potassium in chilled juice.
4. Always use an infusion pump when giving intravenously.
5. Always dilute potassium; never inject potassium by push!
6. Peripheral Veins: use small cannula in large vein.
7. Central Veins: preferable to peripheral infusion; higher concentrations better tolerated. Do not use distal port of Pulmonary Artery Catheter (Swan-Ganz).
8. Infusion may be painful and phlebitic. Lidocaine may be given and warm packs may help. Infusion may need to be diluted further or slowed.
9. Cardiac Monitoring is desirable.
10. Be familiar with policy.
Dietary Sources rich in Potassium: Bananas, Tomatoes, Melons, Oranges, Peaches, and Avocado.
Hyperkalemia:
Acutely rising Serum Potassium threatens life. Symptoms are few and non-specific. A stat. electrocardiogram is essential for determining the effect of the hyperkalemia upon the heart. Most of our patients with hyperkalemia have renal failure (acute or chronic) and have been non-compliant with dialysis or have dietary indiscretions of food rich in potassium.
Causes: "Hyperkalemia results from the following:
o Decreased or impaired potassium excretion - As observed with acute or chronic renal failure (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
o Additions of potassium into extracellular space - As observed with potassium supplements (e.g., PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (e.g., venipuncture, blood transfusions, burns, tumor lysis)
o Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (e.g., acute digitalis toxicity, beta-blockers, succinylcholine)
o Factitious or pseudohyperkalemia - As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis"
Source: [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذا الرابط]
Symptoms:
Fatigue, weakness, paresthesias, paralysis, palpitations.
• ECG Changes: "ECG changes have a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows:
o Early changes of hyperkalemia include peaked T waves, shortened QT interval, and ST segment depression.
o The above changes are followed by bundle branch blocks causing a widening of the QRS complex, increases in the PR interval, and decreased amplitude of the P wave.
o Eventually, the P wave disappears and the QRS morphology widens to resemble a sine wave with ventricular fibrillation or asystole ultimately occurring.
o ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia."
Source: [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذا الرابط]
Lab Studies:
Electrolytes, Creatinine, Blood Urea Nitrogen, Glucose, Calcium, Digoxin level (if taking), Arterial Blood Gas (if acidosis), Urinanalysis (new renal problem?), Creatine Kinase [CK] (if rhabdomyolysis, e.g., "found on floor" or crush injury.
Treatment:
For severe hyperkalemia ( 7.0 mEq/L) with QRS widening, absent P wave, or arrhythmia:
Calcium Chloride 10% Solution: (preferred to Calcium Gluconate, as it is three times as potent as the gluconate) is given to stabilize cardiac membranes and activity; onset <5 minutes, duration 30-60 minutes. Generally 5-10 ml (500 mgm – 1 gm) for adults given slowly. May be repeated for continued wide QRS.
Insulin & Dextrose: 5 – 10 units of intravenous Regular Insulin are used to move glucose and potassium into the cells; 50% Dextrose (25 grams) follows to prevent hypoglycemia. Avoid extravasation of hypertonic dextrose that can cause sloughing.
Sodium Bicarbonate: (50-100 mEq at 1 mEq/kg) given slowly counters acidosis and enhances insulin effect in acidemic patients, and shifts K+ into cells. Causes tissue damage if extravasated. Infants receive half-strength, i.e., 4.2% solution instead of 8.4% solution; if none available, dilute 1:1 with sterile water.
Albuterol: Given as a series of or continuous nebulizer treatments causes a decrease of K+ and stimulates plasma insulin concentration pushing K+ into cells. Onset 30 minutes; duration 2 – 3 hours. Useful when concerned about sodium and fluid overloads, or poor IV access.
Sodium Polystyrene Sulfonate (Kayexalate) A resin that exchanges sodium and binds potassium when taken orally or rectally thus actually removing K+. Dispensed in 15-gram bottles. Dosed at 1 gram/kg. Slow onset and usually requires multiple doses.
Acute Hemodialysis: The ultimate and definitive treatment of hyperkalemia especially in the context of acute or chronic renal failure. Not done in our ED; admitted and dialyzed in rooms with special plumbing or in critical care (possibly short "23 hour" stay if no other issues). Chronic renal failure dialysis patients with hyperkalemia may have above treatments to  K+ as a temporizing measure and be discharged to have acute dialysis at their regular dialysis center; planned in consultation with patient’s Attending Nephrologist.
Furosemide (Lasix): Slow in onset and unpredictable in amount of K+ lowered. Lasix may be given at double the usual oral dose slow IV if the patient is neither anuric or hypovolemic. 20 – 40 mgms, if it has not previously taken.
Hyponatremia:
In good health, the body to a range of 135 – 145 mEq/L and serum osmolarity of 290 ( 10) mOsm/kg finely regulates sodium balance through mechanisms of thirst, secretion of Anti Diuretic Hormone by the posterior pituitary gland, the renin-angiotensin-aldosterone system, and kidney responses to sodium. Changes in sodium and osmolarity can affect volume of intracellular fluid and the functioning of cells. This is especially so with rapid or acute changes, as slower chronic change may be better tolerated to a point. Cerebral cells are especially vulnerable to increases of intracellular volume as the skull provides no relief for edema and pressure increases until brain herniation occurs. The very young and the very old are more severely affected. Attempts to rapidly alter sodium level and osmolarity can have severe adverse effects such as fluid overload, or in chronic hyponatremia when compensatory changes have occurred too rapid correction can produce Central Pontine Myelinolysis (CPM) in which focal demyelination occurs in the pons and extrapontine areas.
Causes and Work-up:
Not all hyponatremia is alike. Different causes and approaches to treatment exist due to acuity, volume status, total body water amount (TBW), and osmolarity. The full work-up may extend beyond the ED to inpatient or outpatient status, diagnostic studies, and consultations.
o Infants given only tap water during gastroenteritis.
o Hyperglycemia and Diabetic Ketoacidosis.
o Psychogenic polydipsia.
o Beer Alcoholism with malnutrition.
o Recreational use of MDMA "Ecstasy".
o Congestive Heart Failure.
o Malignancy.
o CNS disease.
o Pulmonary disease, Tuberculosis.
o Drug effects (good medication history is needed).
o Renal disorders.
o Hepatic Cirrhosis.
o Hypothyroidism.
o Adrenal Insufficiency.
o Syndrome of Inappropriate Antiduretic Hormone (SIADH).
o Iatrogenic replacement of fluid losses with hypotonic solutions.
Lab Studies:
Electrolytes, Creatinine, BUN, Glucose (Hyperglycemia can cause a pseudohyponatremia by a factor of 1.6 mEq/L for each ¬ 100 mg/dl of glucose, which is self-correcting as patient becomes normoglycemic.), Serum Osmolarity; Calcium, Magnesium, Phosphate may be requested; Urine Sodium and Osmolarity; additional tests may include lipids, thyroid function tests, serum cortisol and ACTH stimulation test.
Chest X-Ray to look for malignancy. Head CT to check for cerebral edema, herniation, and possible tumor.
Presentation:
The patient seems to have "failure to thrive" with anorexia, nausea, headache, cramps, or "altered mental status" ranging to confusion, status seizures, coma, and death. If sodium has declined gradually, compensatory changes will have occurred, the patient may have mild symptoms, and may tolerate serum sodium of 110 mEq/L. If change has occurred in 24-48 hours, then patients will be symptomatic at  120 mEq/L and risk of herniation increases with continued fall.
Nursing Approach:
1. Assess the patient. Get a sense of baseline. Determine the acuity and severity of change. Neurological abnormalities indicate the severest derangement and potential disaster.
2. Notify Attending Emergency Physician of Altered Mental Status stat.
3. ABCs Stat. SpO2, Blood Glucose. Consider Naloxone (Narcan); Dextrose; Thiamine. IV access and send lab studies.
4. Continue assessment of cardiopulmonary status and hydration status (hypovolemic, euvolemic, or hypervolemic and edematous).
5. The hypovolemic patient (continuing loss with replacement by free water or hypotonic solutions) with tachycardia,  turgor, light-headedness, dry membranes, possible orthostasis, may need gentle hydration with Normal Saline as ordered by the physician.
6. The euvolemic patient without dehydration or edema will need fluid restriction and other actions as ordered by the physician.
7. The edematous and congested patient will need fluid and sodium restriction, other studies, and actions as ordered by the physician.
8. Anticipate admission.
Treatment Options:
Fluid Restriction: Limiting access to free water when patients have ¬ Total Body Water as in Syndrome of Inappropriate Anti-Diuretic Hormone.
Fluid Replacement with Isotonic Solutions (Normal Saline): Eliminate hypotonic solutions when patient is hypovolemic or has continuing loss.
Hypertonic Saline (3%): Giving "extra" sodium is reserved for obtunded patients with impending brain stem herniation or status epilepticus. An infusion pump is necessary. Hypertonic saline is given until symptoms no longer progress (about 4-6 mEq/L increase in serum sodium, over 1-2 hours, and terminated as soon as possible.
Hypernatremia:
Hypernatremia (serum sodium >145 mEq/L) can be a significant electrolyte disturbance, especially in the elderly, with up to 50% mortality. Excessive sodium and hypertonicity or hyperosmolarity is ordinarily well regulated by thirst (given access to water) and ADH mechanism. When it occurs water extraction from brain cells can cause neurological change, and even protective compensatory transport of electrolytes and generation of solutes inside the cell to protect the cell structure impairs the functioning of the neuron. Brain shrinkage pulling on dural veins and sinuses can cause intracranial hemorrhage.
Endogenous sodium gain as in Cushing’s Syndrome of mineralocorticoid excess, or exogenous sources such as Hypertonic Saline infusions, Salt or Sodium contaminated ingestants, or Sodium Bicarbonate administration may cause a problem.
Water losses greater than sodium loss through diarrhea, vomiting or burns, or through renal disease or diuresis and osmotic diuresis may lead to hypernatremia.
Disorders of thirst regulation by the hypothalamus, or of ADH regulation as in Central (neural) or Nephrogenic Diabetes Insipidus.
Medication effects and other systemic diseases as causes mandate a thorough drug and medical history.
Signs & Symptoms:
Thirst, dry membranes, apathy, confusion, restlessness, fever, decreased or absent urine output, hyperventilation, muscle twitching or spasticity, progressive decrease in mental status.
Lab Studies:
Electrolytes, Creatinine, BUN, Glucose, Osmolarity; Urine Osmolarity and Electrolytes.
Other Studies:
Head CT to rule out Intracranial Hemorrhage or tumor. CXR. Weight. Intake & Output.
Nursing Approach:
1. Assess the patient. Get a sense of baseline. Determine the acuity and severity of change. Neurological abnormalities indicate the severest derangement and potential disaster.
2. Notify Attending Emergency Physician of Altered Mental Status stat.
3. ABCs Stat. SpO2, Blood Glucose (to consider and rule out Hyperglycemic Hyperosmolar Non-Ketotic Coma). IV access, and send lab studies.
4. Continue assessment of cardiopulmonary status and hydration status (hypovolemic, euvolemic, or hypervolemic and edematous).
5. The hypovolemic patient with tachycardia and hypotension may need hydration with Normal Saline or ½ Normal Saline to stabilize, until free fluid deficits can be corrected with D5%Water as ordered by the physician; dialysis may be needed in some cases.
6. The euvolemic patient may have free fluid deficits replaced by D5%Water as calculated and ordered by the physician.
7. Patients with Diabetes Insipidus ( ADH inability to concentrate urine) will need hydration and correction with Vasopressin (Pitressin) (given IV/IM/SC) which is synthetic ADH or with Desmopressin (DDAVP) (given IV/SC/IntraNasal Insufflation) to control the abnormality as ordered by the physician.
8. Anticipate admission.