Chapter_17__Fluids_and_Electrolytes

Introduction

  • Sodium Zirconium Cyclosilicate is a potassium binder effective for hyperkalemia treatment (as of February 2021).

Fluids and Sodium: Pathophysiology

  • Total Body Water (TBW): Approximately 60% of total body weight.
    • Divided into Intracellular Fluid (ICF) and Extracellular Fluid (ECF).
    • ECF consists of intravascular fluid and extravascular (interstitial) fluid.
  • Homeostatic Equilibriums:
    • Osmotic equilibrium.
    • Electric equilibrium.
    • Acid-base equilibrium.
  • Sodium Concentration:
    • ECF: Approximately 140 mEq/L.
    • ICF: Approximately 10 mEq/L.
    • Capillary membrane between intravascular and interstitial fluid is permeable to water and electrolytes, thus sodium concentration is equal in both compartments of the ECF.
    • Cell membrane is permeable to water but not electrolytes.
    • Ionic pumps maintain constant intracellular sodium concentration around 10 mEq/L and potassium at 150 mEq/L.
  • Table 17-1: Lists electrolyte concentrations of body fluids and therapeutic solutions.
  • Table 17-2: Defines terms describing measures/characteristics of electrolytes and disorders.
  • Mole: 6.02×10236.02 × 10^{23} molecules of a substance.
  • Equivalent: Mass (in grams) of a mole divided by the charge of the substance.
  • Osmole: Amount of a substance that dissociates to form 1 mole of osmotically active particles.
  • Osmolarity: Solute concentration per unit volume of solvent (temperature-dependent).
  • Osmolality: Solute concentration per unit mass of solvent (preferred measure, constant with temperature changes).
  • Tonicity (Effective Osmolality): Osmotic pressure gradient between two solutions across a semipermeable membrane, affected only by non-permeable solutes.
    • Example: Urea or glucose do not affect tonicity.
    • Water moves across a membrane into the compartment with the more concentrated solution to equalize ion concentration and this movement is driven by osmotic pressure.
    • In human fluids, substances contributing most to osmotic pressure in ECF are sodium (Na+), bicarbonate (HCO3–), chloride (Cl–), and glucose.
  • Effective Osmolality/Tonicity Calculation:
    • 2×[Na+]+glucose/182×[Na+] + glucose/18 (normal range: 275-290 mOsm/L).
  • Effects of Fluid Addition to ECF:
    • 1 L free water: TBW expansion, slight osmolality reduction, water crosses into the ICF to equalize ECF osmolality.
    • 1 L isotonic saline (0.9%): ECF expansion only, no water movement into cells.
  • Fluid Loss and Osmolality Increase:
    • Osmoreceptors in the hypothalamus stimulate thirst and ADH (vasopressin) release from the pituitary gland.
    • Decreased blood volume activates low-pressure baroreceptors in great veins/right atrium, augmenting osmoreceptor effect, resulting in water reabsorption and vasoconstriction.
  • Plasma Sodium Concentration/Tonicity:
    • Hypertonic plasma: Draws water out of cells, causing cell shrinkage.
    • Hypotonic plasma: Cells swell with water.

Dehydration

  • Definition: Loss in TBW caused by water loss (hyperosmolality) or salt loss (hypo-osmolality).
  • Causes of Water Loss:
    • Inadequate fluid intake to replace insensible loss.
    • Excessive diuresis (e.g., hyperglycemia).
  • Causes of Salt Loss:
    • Vomiting, diarrhea, sweating, bleeding.
    • Chronic kidney failure.
  • Symptoms:
    • Thirst, fatigue, dizziness, confusion.
  • Signs:
    • Sunken eyes, dry mouth/tongue, skin tenting.
  • Elderly Patients:
    • Dehydration can cause delirium, cognitive deterioration, agitation, hallucinations, and delusions.
    • Rapid weight loss, dark urine, and behavioral changes are suggestive of dehydration.
  • Factors Precipitating Dehydration:
    • Chronic antihypertensive medication or diuretic use.
    • Exposure to high outdoor temperature.
    • Fever.
    • Acute illness with insufficient water intake.
  • Table 17-3: Screening checklist for dehydration risk.
    • Includes: Diuretics, end of life, high fever, yellow urine turns dark, dizziness (orthostasis), reduced oral intake, axilla dry, tachycardia, incontinence (fear of, reducing oral intake), oral problems, neurologic impairment, sunken eyes.

Hyponatremia

  • Definition: Serum [Na+] <138 mEq/L (symptomatic hyponatremia rarely occurs until [Na+] ≤135 mEq/L).
  • Prerequisite: High circulating ADH levels with normal water intake.
  • Urine osmolality: >100 mOsm/L H2O (except in psychogenic polydipsia).
  • Incidence:
    • Mild hyponatremia: 15%-30% in hospitalized patients.
    • [Na+] <126 mEq/L: 1%-4.5% of patients.
    • Heart failure patients: Approximately 20%.
    • Nursing home patients: At least 50% have had one or more episodes.
  • Evaluation:
    • Clinical evaluation of ECF volume status.
    • Comparison of measured and calculated plasma osmolalities.

Hyperosmolar Hyponatremia (Plasma Osmolality [POSM] >295 mOsm/kg H2O)

  • Cause: Accumulation of osmotically active solutes in the ECF space.
    • Net water movement from ICF to ECF, diluting ECF [Na+].
    • Commonly occurs with severe hyperglycemia.
      • Each 100 mg/dL increase in plasma glucose above the normal level of 100 mg/dL decreases serum [Na+] by 1.6 mEq/L.
    • Administration of osmotic agents: mannitol, glycerol, and maltose, causing an osmolar gap and hyponatremia.
  • Osmolar Gap: Difference between measured osmolality and calculated osmolality.
    • Normal difference: Around 10 mOsm/L.
    • >15 mOsm/L: Suggests a nondetectable agent with osmotic activity.
  • Consequence: Osmotic diuresis causing [Na+] deficit with volume depletion (treated with saline solution).

Iso-osmolar Hyponatremia (POSM 275 to 295 mOsm/kg H2O)

  • Pseudohyponatremia: Factitiously low [Na+] value due to severe hyperproteinemia or hyperlipidemia.
  • Mechanism: High concentrations of lipids or protein displace serum water.
  • Patient Presentation: Asymptomatic.
  • Treatment: Not needed.

Hypo-osmolar Hyponatremia (POSM <275 mOsm/kg H2O)

  • Causes: Classified according to volume status.
  • Mechanism: Osmol receptors in the hypothalamus react to low osmolality by secreting ADH (Antidiuretic hormone), which limits water excretion and increases water reabsorption.
  • Conditions: Heart failure, cirrhosis, and nephrotic syndrome, effective arterial blood volume decreases because water is distributed to interstitial space.
    • Na+ and water reabsorption are increased, and water excretion is reduced.
  • Table 17-4: Classification, differential diagnosis, and features of hyponatremia based on volume status.
    • Provides details on clinical conditions, orthostatic hypotension, edema, urine sodium (U[Na+]), and urine osmolality (UOSM).
  • Important Hyponatremic Disorders:
    • Syndrome of Inappropriate ADH Secretion (SIADH) and Cerebral Salt-Wasting Syndrome.
    • Diagnoses of exclusion after ruling out other causes.
    • Onset linked to chronic cerebral disease.
    • SIADH may also be caused by noncerebral diseases.
    • Volume Status:
      • SIADH: Normal volume status.
      • Cerebral Salt-Wasting Syndrome: Hypovolemia.
    • Treatment: Differ according to volume status.
  • Table 17-5: Causes of SIADH.
    • Includes neurologic/psychiatric disorders, drugs, lung diseases, non-CNS tumors, and MDMA intoxication.

Clinical Features of Hyponatremia

  • Symptoms are primarily due to effects on the brain.
  • Classification (European clinical practice guideline):
    • Moderately Severe:
      • Plasma [Na+] <130 mEq/L.
      • Symptoms: Headache, nausea, disorientation, confusion, agitation, ataxia, and areflexia.
    • Severe:
      • [Na+] <120 mEq/L.
      • Symptoms: Intractable vomiting, seizures, coma, and respiratory arrest due to brainstem herniation.
      • Potential for irreversible brain injury.
  • The presence of hyponatremia-related symptoms which also defined hyponatremic encephalopathy dictates the therapeutic approach rather than the serum [Na+].
  • Symptom Onset and Brain Adaptation:
    • Symptoms are directly related to the rapidity of onset.
    • Initially, hypo-osmolality drives water into brain cells, causing swelling and intracranial hypertension.
    • After 48 hours, brain cells adapt by extruding Na+, K+, Cl–, and organic osmolytes (glycine and taurine), reducing cell osmolality and preventing further water uptake.
  • Impaired Adaptation:
    • Occurs in SIADH, children, menstruating women, and hypoxia.
    • Results in more severe and persistent symptoms.
Diagnosis of Hyponatremia
  • Based on clinical findings of volume status and specific laboratory values:
    • Serum [Na+].
    • Serum osmolality.
    • Volume status.
    • Urinary sodium (UNa+).
    • Urine osmolality (UOSM).
  • Acute vs. Chronic:
    • Acute: Onset time <24-48 hours.
    • Chronic: Onset time >24-48 hours.
    • If duration is unknown, treat as chronic with a longer correction time.
  • Estimating UOSM:
    • If UOSM unavailable, estimate using urinary specific gravity (π).
    • UOSM = (numerals in hundredths and thousandths decimal places of π) × 35.
    • Example: For π of 1.005, UOSM = 05 × 35 = 175 mOsm/L.
  • Table 17-4:Lists the values of UNa+ and UOSM in different classifications of hyponatremia according to volume status and the differential diagnosis for each classification.
  • UNa+:
    • Only in patients with edematous syndromes and in patients with vomiting and diarrhea will UNa+ be found to be <10 mEq/L.
  • Table 17-6: Diagnostic criteria for SIADH.
    • Hypotonic hyponatremia (POSM <275 mOsm/kg H2O).
    • Inappropriately elevated urinary osmolality (usually >200 mOsm/kg).
    • Elevated urinary [Na+] (typically >20 mEq/L).
    • Clinical euvolemia.
    • Normal adrenal, renal, cardiac, hepatic, and thyroid functions.
  • Exercise-Associated Hyponatremia:
    • Overhydration with hypotonic fluids during endurance exercise can cause hyponatremia.
    • Symptoms: Bloating, nausea, vomiting, and edema (check wrists and fingers).
    • Dehydration presents with excessive thirst, sunken eyes, poor skin turgor, and postural hypotension.
Treatment of Hyponatremia
  • Guided by four variables: severity of symptoms, rate of onset, volume status, and current serum [Na+].
  • Hypertonic saline infusion for severe neurologic symptoms (vomiting, seizures, reduced consciousness, cardiorespiratory arrest); treatment should be based on symptoms rather than serum [Na+].
  • Table 17-7: Treatment of Hyponatremia Symptomatic With Seizures or Coma.
    • Assess for indication for 3% hypertonic saline: severe symptoms in setting of acute or chronic hyponatremia.
    • Infuse 100-150 mL of 3% hypertonic saline IV over 15-20 min.
    • Measure serum sodium level after each 3% hypertonic saline infusion.
    • Stop infusion when symptoms improve or a target of a 5 mEq/L (range, 4-6 mEq/L) increase is achieved.
    • May repeat 150 mL of 3% hypertonic saline up to 3 total doses, or a total of 450 mL IV of 3% hypertonic saline.
    • Keep the IV line open with minimal volume of 0.9% normal saline until cause-specific treatment is started.
    • Limit increase in sodium level to no more than 8-12 mEq/L during the first 24 h or 18 mEq/L over 48 h.
  • Mild or Moderate Symptoms, Chronic Hyponatremia:
    • Slower [Na+] correction than acute hyponatremia.
    • Rapid correction increases risk for osmotic demyelination syndrome.
    • Correction rate should not exceed 6 mEq/24 h in high-risk patients and 12 mEq/24 h in low-risk patients.
    • Hypertonic (3%) saline can be given at a low infusion rate, 0.5 to 1 mL/kg/h, with frequent [Na+] checks.
  • Isotonic saline frequently used, especially for mild hyponatremia.
  • Loop diuretics (furosemide, starting with 20 mg IV) may be used with saline infusions.
  • Urine volume and [Na+] should be strictly measured.
  • Vaptans:
    • No definitive consensus on their role, safety, or tolerability.
    • Major concerns: Overcorrection risk, osmotic demyelination syndrome risk, and high cost.
  • Table 17-8: Cause-Specific Treatment for Hyponatremia.
    • Details therapies and cautions/comments for various clinical conditions.
    • Includes treatments for chronic heart failure, cirrhosis, nephrotic syndrome, kidney disease, psychogenic polydipsia, hypothyroidism, glucocorticoid deficiency, SIADH, diarrhea and vomiting, diuretics, mineralocorticoid deficiency, salt-losing nephropathies, and cerebral salt wasting.
Complications of Treatment
  • Osmotic Demyelination Syndrome
    • Caused by rapid correction of hyponatremia (>12 mEq/L/24 h).
    • Water moves from cells to ECF, yielding intracellular dehydration.
    • Risk factors: [Na+] <120 mEq/L, chronic heart failure, alcoholism, cirrhosis, hypokalemia, malnutrition, and treatment with vasopressin antagonists.
    • Symptoms: Dysarthria, dysphagia, lethargy, paraparesis/quadriparesis, seizures, and coma.
    • Treatment: 5% dextrose in water at 3 mL/kg/h, loop diuretics, and desmopressin.

Hypernatremia

  • Definition: Serum or plasma [Na+] >145 mEq/L and hyperosmolality (serum osmolality >295 mOsm/L).
  • Cause: Deficit in TBW and/or net gain of Na+ (less common).
  • Mechanism: Normal subjects become thirsty and drink free water when [Na+] and osmolality increase.
  • Risk Factors:
    • Impaired thirst sense.
    • Limited water availability.
    • Limited kidney's ability to concentrate urine.
    • Increased salt intake.
  • At-Risk Populations: Elderly, decompensated diabetics, infants, and hospitalized patients.
  • Other causes may be the result of loss of free water in diarrheal stools or in the urine.
  • Onset and Brain Adaptation:
    • Symptoms more severe and evident with rapid onset.
    • After 48 hours, brain cells adapt with an increase in electrolytes and organic osmolytes and increased intracellular water.
  • Classification Based on Volume Status:
    • Hypovolemic hypernatremia: Decreased TBW and total body Na+.
    • Hypervolemic hypernatremia: Increased total body Na+ with normal or increased TBW.
    • Normovolemic hypernatremia: Near normal total body sodium and decreased TBW.
  • Table 17-9: Hypernatremia Classification and Features According to Volume Status.
    • Details clinical conditions, diagnosis, UOSM, and U[Na+] for each volume status.

Clinical Features of Hypernatremia

  • History: Varies based on the hypernatremia type.
    • May reveal nausea/vomiting, lethargy, weakness, increased thirst, low water intake, salt intake, polyuria (>3000 mL of urine/24 h), diabetes, hypercalcemia, hypokalemia, medications such as lactulose, loop diuretics, lithium, demeclocycline, or NSAIDs.
  • Physical Exam:
    • Hypovolemia: Hypotension, tachycardia, orthostatic blood pressures, sunken eyes, dry mucous membranes.
    • Any classification: Altered mental status.
    • Hypervolemic: Poor skin turgor or edema.
    • Cushing’s syndrome may be present.
  • Complications:
    • Without intervention: Coma, seizures, and shock.
  • Mortality:
    • Severe hypernatremia ([Na+] >150 to 160 mEq/L) yields a mortality of 75%.
Diagnosis of Hypernatremia
  • Based on clinical evaluation, volume status, and specific laboratory tests:
    • Serum electrolytes and osmolality.
    • Urine osmolality.
    • Urea/creatinine ratio.
    • Free water deficit.
  • BUN/Creatinine Ratio >40: Indicative of hyperosmolar dehydration.
  • Table 17-10: Urine Osmolality Findings in Selected Hypernatremic States.
    • Provides potential hypernatremic states based on urine osmolality (UOSM).
  • Free Water Deficit:
    • Calculated with phone application or Internet calculator.
Treatment of Hypernatremia
  • Initial Steps:
    • Treat shock, hypoperfusion, or volume deficits with isotonic (0.9%) saline.
    • Treat underlying cause (e.g., diabetes insipidus, vomiting, diarrhea, fever).
    • Correct the patient’s free water deficit at a rate reflecting the acuity or duration of the hypernatremia onset.
  • Acute hypernatremia with lethal sodium chloride ingestion/load (0.75 to 3.0 grams/kg) less than 6 hours prior to presentation may be replaced rapidly.
  • Rate of Correction:
    • Onset <48 hours: 1 mEq/L/h.
    • Onset >48 hours: No more than 0.5 mEq/L/h or 10 to 12 mEq/24 h to avoid cerebral edema.
  • Route of Administration:
    • Alert patient: Two-thirds free water orally and one-third IV.
  • Table 17-11: Treatment of Hypernatremia.
    • Details indications and comments for various treatments.
    • Includes isotonic saline, etiology-specific therapy, D5W or oral free water, 0.45% normal saline, and hemodialysis.

Diabetes Insipidus

  • Definition: Disease where the kidney’s ability to reabsorb free water is compromised.
  • Characteristics: Polyuria, polydipsia, increased volume of hypo-osmolar urine.
  • Hypernatremia: Present only when the thirst center is impaired or water intake is reduced.
  • Types:
    • Central (Neurogenic): Inadequate ADH secretion.
    • Renal (Nephrogenic): Normal or increased ADH, but kidney's collecting duct cells do not respond.
  • Etiology: Congenital or acquired.
  • Table 17-12: Classification of Diabetes Insipidus.
    • Details acquisition and pathophysiology for central and nephrogenic diabetes insipidus.
  • Congenital Forms:
    • Present during infancy.
    • Recurrent cellular dehydration causes cerebral calcifications and delayed intellectual advancement.
  • Symptoms and Signs:
    • Excessive thirst, polydipsia, and polyuria.
    • Nonspecific symptoms: Weakness, lethargy, myalgias, and irritability.
    • Infancy: Fatigue/weakness, vomiting, polyuria, sometimes fever.
  • Diagnosis:
    • Clinical presentation suggests diagnosis.
    • Requires prolonged test (4 to 18 hours).
    • Urine osmolality assessed after water deprivation.
    • May require assessment after desmopressin administration (water deprivation test).
    • Spot check: UOSM <300 mOsm/L.
  • Central Diabetes Insipidus:
    • MRI to evaluate hypothalamic-pituitary area.
    • Treatment: Desmopressin (nasal spray or PO).
  • Nephrogenic Diabetes Insipidus:
    • Low-salt, low-protein diet, adequate hydration.
    • Thiazide diuretic, potassium-sparing diuretic amiloride, and indomethacin.
    • Exogenous ADH may be used.

Potassium: Pathophysiology

  • Potassium (K+) is the major intracellular cation.
    • 98% of total body K+ is intracellular.
    • 70%-75% of total K+ is in muscle tissues.
    • Normal intracellular concentration averages 150 mEq/L.
    • Normal extracellular concentration: 3.5 to 5.0 mEq/L.
  • Excretion:
    • Predominantly by the kidneys (80%-90%).
    • Filtered freely through the renal glomerulus.
    • Reabsorbed in the proximal and ascending tubules.
    • Secreted in the distal tubule in exchange for Na+.
    • Healthy individuals can excrete up to 6 mEq/kg/d.
  • Accurate calculation of total body K+ is difficult due to intracellular location.
  • Estimated Potassium Deficit Equation:
    • Estimated K+ deficit in mEq/L = (expected serum [K+] in mEq/L – measured serum [K+] in mEq/L) × ICF (calculated as 40% of total body weight).
    • Reliable only for healthy subjects.
  • Potassium shifts are crucial for maintaining is the most important determinant of neuromuscular and cardiovascular excitability.
    • Resting membrane potential and the ratio of intracellular to extracellular K+.
  • Acid-Base Imbalance:
    • Inverse proportionality between serum pH and [K+].
    • [K+] rises about 0.6 mEq/L for every 0.1 decrease in pH and vice versa, through an exchange between H+ and K+.
  • Duration of hypo- and hyperkalemia influences clinical response.
  • Chronic potassium depletion or surplus allows adaptation through shifts in intra-/extracellular K+ concentration.
  • Potassium derangements are becoming more frequent in the ED (up to 11%) and should be promptly and correctly addressed.

Hypokalemia

  • Definition: Serum [K+] <3.5 mEq/L.
  • Causes:
    • Insufficient dietary intake.
    • Intracellular shifts.
    • Increased losses.
  • Table 17-13: Causes of Hypokalemia.
    • Transcellular shifts.
    • Decreased intake.
    • GI loss.
    • Renal loss.
    • Other.
  • Clinical Manifestations:
    • Result from abnormalities in membrane polarization.
    • Particularly dangerous in the myocardium.
    • Hypokalemia makes the resting potential more electronegative, thus enhancing depolarization.
    • The reduction in [K+] conduction delays repolarization, causing prolonged QTc, flattened T waves, and U waves in the ECG.
  • ECG Changes.

Clinical Features of Hypokalemia

  • Symptoms usually start when serum concentrations reach 2.5 mEq/L
  • Cardiac arrhythmias, usually tachyarrhythmias (atrial fibrillation, torsades de pointes, ventricular tachycardia, and ventricular fibrillation), can be life threatening.
  • Table 17-14:Symptoms and Signs of Hypokalemia
    • Cardiovascular
    • Neuromuscular
    • GI
    • Renal
    • Metabolic
    • Endocrine
Diagnosis of Hypokalemia
  • Made with serum chemistry measurements.
  • Etiology investigated with additional testing.
  • ECG should be obtained.
  • Blood gas analysis when alkalosis is suspected.
  • Spot urinary electrolytes can be obtained before starting K+ replacement
  • UNa+, UOSM(urine osmolality), and POSM(plasma osmolality) should be measured, a UNa+ value <30 mEq/L and a UOSM value less than POSM suggest polyuria.
  • Table 17-15: Interpretation of Urinary Potassium
  • Transtubular K+ gradient = (Urinary K+ × POSM)/(UOSM × Plasma K+), with normal values of 8 to 9 mEq/L
    • Values <5 mEq/L suggest hyperaldosteronism.
    • If paralysis is present, values <3 mEq/L suggest hypokalemic periodic paralysis.
  • A calcium/phosphate ratio >1.7 on a spot urine is 100% sensitive and 96% specific for thyrotoxic hypokalemic periodic paralysis.
Treatment of Hypokalemia
  • Replacement of K+ should be done orally in stable patients with mild hypokalemia (>3.0 mEq/L) who are able to tolerate oral intake.
  • Foods rich in K+ (fruits, dried fruits, nuts, vegetables, and meat) can be suggested at discharge from ED, as well as salt substitutes or K+ supplements that should be prescribed with abundant fluids and/or food to prevent gastric irritation.
  • IV replacement is indicated in patients with severe (<2.5 mEq/L) hypokalemia and in symptomatic patients with moderate (2.5 to 3 mEq/L) hypokalemia, patients with cardiac arrhythmias or prolonged QTc or when oral replacement is not tolerated or not feasible.
  • Monitor the patient’s rhythm when treating with IV K+.
  • Table 17-16: Common Medications Known to Prolong QTc
  • General principles in hypokalemia correction
    • Use potassium chloride and avoid administering K+ in glucose solution.
    • Potassium is irritating to the endothelium. adequate dilution is mandatory to prevent pain and phlebitis.
    • Reassessing serum [K+] should be adjusted to infusion rate and coexisting factors
    • ECG monitoring is recommended.
    • In most cases, hypokalemic patients are also hypomagnesemic. Magnesium (20 to 60 mEq/24 h) may be added to the infusion.

Hyperkalemia: Pathophysiology

  • Hyperkalemia is defined as measured serum [K+] of >5.5 mEq/L.
  • The most common cause is factitious hyperkalemia due to release of intracellular potassium caused by hemolysis during phlebotomy.
  • Table 17-17: Causes of Hyperkalemia
    • Pseudohyperkalemia
    • Intracellular to extracellular potassium shift
    • Potassium load
    • Decreased potassium excretion
  • Clinical manifestations of hyperkalemia result from disordered membrane polarization.
  • Cardiac manifestations are the most serious
  • Table17-18: ECG Changes Associated with Hyperkalemia
  • Calcium administration does not affect potassium levels. Rather, calcium antagonizes the effects of hyperkalemia at the level of the cell membrane.

Clinical Features of Hyperkalemia

  • Cardiac dysrhythmias, such as ventricular fibrillation, sinoatrial and atrioventricular blocks until complete heart block, and asystole, may occur.
  • Other common symptoms include neuromuscular dysfunctional weakness, paresthesias, areflexia, ascending paralysis, and GI effects (nausea, vomiting, and diarrhea).
Diagnosis of Hyperkalemia
  • A stat ECG is essential in all hyperkalemic patients
  • if ECG changes are present, emergency treatment of hyperkalemia should start immediately.
  • A symptomatic patient with a relatively small elevation of [K+] (5.0 to 6.0 mEq/L) requires identification and treatment of the underlying cause.
  • elevated spot urine K+ (>20 mEq/L) suggests an extrarenal cause
  • low urine K+ output (<10 mEq/L) suggests oliguric kidney failure or drug effect, such as angiotensin–converting enzyme inhibitors or angiotensin II receptor blockers.
Treatment of Hyperkalemia
  • Emergency treatment includes continuous ECG monitoring and immediate intervention with several therapeutic medications which based on the action mechanism can be divided into three modalities with different onset time and duration:
    • Membrane stabilization
    • Intracellular shift of K+
    • Removal/excretion of K+ from the body
  • Table 17-19: Emergency Therapy of Hyperkalemia
  • General principles in treatment of hyperkalemia
    • Immediate cessation of further K+ administration, reduction of dietary intake, and suspension of drugs impairing K+ renal excretion.
    • Fluid administration enhances K+ renal excretion
    • ECG continuous monitoring should be used to confirm the effects of therapy, thus reducing the frequency of rechecking [K+].

Magnesium

  • The total body content of magnesium (Mg2+) is 24 grams, or 2000 mEq, 50% to 70% of which is fixed in bone and only slowly exchangeable.
  • Normal serum [Mg2+] ranges between 1.5 and 2.5 mEq/L (0.7 to 1.1 mmol/L or 1.7 to 2.7 milligrams/dL).
  • Circulating Mg2+ is 25% to 35% bound to proteins (mainly albumin), 10% to 15% complexed, and 50% to 60% ionized, which is the active portion.
  • The normal dietary intake of Mg2+ is approximately 240 to 336 milligrams/d and is found in vegetables such as dry beans and leafy greens, meat, and cereals.
  • Sixty percent of excreted Mg2+ is through stool, with the remainder via the urine
  • Magnesium is effective therapy in severe asthma when added to standard therapy.

Hypomagnesemia

  • Table 17-20:Causes of Hypomagnesemia
    • Redistribution
    • Extrarenal loss
    • Decreased intake
    • Renal loss
    • Endocrine disorders
  • IV hyperalimentation or treatment of diabetic ketoacidosis without adequate provision of Mg2+, especially in a previously malnourished patient, can cause an abrupt fall in plasma Mg2+ levels.
  • Concomitant hypomagnesemia and hypokalemia may coexist.

Clinical Features

  • Due to the essential role of Mg2+ in enzyme regulation in multiple body systems, hypomagnesemia may result in a wide variety of neuromuscular, GI, and cardiovascular effects
  • Table 17-21: Symptoms and Signs of Hypomagnesemia
    • Neuromuscular
    • GI
    • Cardiovascular
    • Miscellaneous
Diagnosis of Hypomagnesemia
  • Hypomagnesemia is common in acute illness; it has been found in 12% of hospitalized patients and in up to 65% of medical intensive care patients.
  • The diagnosis of hypomagnesemia in the presence of normal serum calcium levels is suggested by increased neuromuscular irritability, Hypomagnesemia should be suspected in patients with alcoholism or cirrhosis or those requiring IV fluids or hyperalimentation for prolonged periods.
  • Low total [Mg2+] can also be secondary to hypoalbuminemia.
  • The ECG changes may be similar to those caused by hypokalemia and/or hypocalcemia because they may be due to Mg2+ deficiency altering cardiac intracellular potassium content.
Treatment of Hypomagnesemia
  • Hypokalemia, hypocalcemia, and hypophosphatemia are often present with severe hypomagnesemia and must be monitored carefully.
  • General principles in treatment of hypomagnesemia
    • Treat or stop the cause of hypomagnesemia.
    • For asymptomatic patients (including ECG changes), magnesium supplements should be administered orally, in multiple low doses during the day, to avoid diarrhea.
    • For severe and symptomatic hypomagnesemia, urgent IV replacement is mandatory.

Hypermagnesemia

  • Hypermagnesemia is rarely encountered in emergency medicine practice, because the kidney can increase the fractional excretion of Mg2+ up to nearly 100%.
  • The most common cause for hypermagnesemia can be found in patients with renal insufficiency or renal failure who ingest Mg2+­containing drugs.
  • Table 17-22: Causes of Hypermagnesemia
    • Renal Failure
    • Increased magnesium load
    • Increased renal magnesium absorption
  • Mg2+ decreases the transmission of neuromuscular messages and thus acts as a CNS depressant and decreases neuromuscular activity.
  • Table 17-23: Symptoms and Signs of Hypermagnesemia

Treatmentof Hypermagnesemia

  • Immediate cessation of Mg2+ administration is required.
  • If renal failure is not evident, dilution by IV fluids may be indicated.
  • Calcium directly antagonizes the cardiac effects of magnesium. Patients with renal failure may benefit from dialysis using a decreased [Mg2+] bath that lowers serum [Mg2+].

Calcium Pathophysiology

  • Calcium (Ca2+) is the most abundant mineral in the body [Ca2+] is 15 grams/kg of body weight, or about 1 kg in an average sized adult 99% bound in bone as phosphate and carbonate mineral Total intake = 800 to 3000 milligrams of Ca2+ [one third] absorbed primarily in the small bowel by active and passive absorption
  • Secretion of Ca2+ is primarily via the stool
  • Cell content to 10,000 times lower than the plasma and is maintained by Ca-ATPase, Ca2+-specific channels
  • Plasma Level - 8.5-10.5 milligrams/dL, ionized 50%
  • Total Serum= ionized with albumin Alkalosis decreases the fraction, no change in total.
  • Role is crucial for muscles, conduction, co-factors - leads to dys