Hypercalcemia, 275.42
Hyperkalemia, 276.7
Hypermagnesemia, 275.2
Hypernatremia, 276.0
Hyperphosphatemia, 275.3
Hypocalcemia, 275.41
Hypokalemia, 276.8
Hypomagnesemia, 275.2
Hyponatremia, 276.1
Hypophosphatemia, 275.3
Metabolic acidosis, 276.2
Metabolic alkalosis, 276.3
Respiratory acidosis, 276.2
Respiratory alkalosis, 276.3
HYPONATREMIA
I. Definition
A. Decreased serum sodium (Na+) concentration of less than 135 mEq/L; the norm is 135 to 145 mEq/L
B. Hypotonic hyponatremia (low serum osmolality)
1. State of body water excess, diluting all body fluids
2. Clinical signs arise from the water excess itself
C. Isotonic hyponatremia (normal serum osmolality)
1. Laboratory artifact that can be seen in extreme hyperlipidemia or hyperproteinemia
2. Body water is normal and patients are asymptomatic
D. Hypertonic hyponatremia (high serum osmolality)
1. State of dilution of sodium-containing extracellular fluids when high concentrations of nonsodium solute (e.g., glucose, mannitol) pull water from inside cells
II. Etiology/incidence/predisposing factors
A. 1% to 4% prevalence in hospitalized patients
B. Occurs when renal water excretion is insufficient for water intake because of impaired formation of dilute urine from decreased tubule function or ongoing antidiuretic hormone (ADH) concentration of urine
C. Hypervolemic hyponatremia: edematous state of excess total body sodium content, with or without hemodynamic deficiency, that stimulates ADH secretion
1. Congestive heart failure
2. Hepatic cirrhosis
3. Nephrotic syndrome
D. Hypovolemic hyponatremia: state of deficient total body sodium content, with or without hemodynamic insufficiency, that stimulates ADH secretion
1. Blood loss
2. GI fluid loss
a. Suction
b. Emesis
c. Diarrhea
3. Renal fluid loss
a. Excess diuresis
b. Aldosterone deficiency
4. Skin fluid loss
a. Excess sweating
b. Burns
E. Euvolemic hyponatremia
1. State of normal body sodium content
2. Edema-free and normal hemodynamic state with autonomous ADH secretion or reduced renal water formation
a. Syndrome of inappropriate ADH (SIADH)
b. Diuretics, especially thiazides in elderly females
c. Renal failure, acute or chronic
d. Cortisol deficiency
e. Hypothyroidism
f. Primary polydipsia or psychogenic water ingestion that exceeds capacity for renal water excretion
g. Beer potomania: inadequate solute (salt) intake, so kidney cannot make the quantity of dilute urine needed to excrete a large fluid (beer) intake
III. Subjective findings
A. Neurologic symptoms related to brain swelling from water excess; severity roughly parallels fall in serum Na+; more pronounced with acute (hours to 1-2 days) versus chronic (more than 2 days to weeks) development of hyponatremia
IV. Physical examination findings
A. General neurologic depression, rarely focal neurologic findings
B. Major findings may reflect the primary condition that caused hyponatremia
C. Cardiovascular focus: Determine volume status
1. Edema
2. Ascites
3. Pulmonary rales
4. Cardiac gallop
5. Standing and lying blood pressure and pulse
6. Jugular venous distention or collapse
V. Laboratory/diagnostic findings
A. Hypotonic hyponatremia
1. Serum Na+ less than 135 mEq/L and serum osmolality less than 270 mOsm/kg (normal, 280-295 mOsm/kg; serum [Osm] ≈ 2 × [Na+])
2. Urine osmolality (UOsm)
a. UOsm less than 100 mOsm/L: primary polydipsia (also seen when initial disorder that caused ADH secretion resolves)
b. UOsm greater than 100 mOsm/L: ADH effect or decreased renal tubule water formation
3. Urine Na+ (UNa)
a. UNa less than 20 mEq/L
i. Circulatory deficiency
ii. Seen in hypervolemic or hypovolemic states
b. UNa greater than 40 mEq/L
i. SIADH
ii. Diuretics
iii. Renal failure
iv. Hypothyroidism
v. Adrenal insufficiency
B. Isotonic hyponatremia
1. Serum Na+ less than 135 mEq/L, serum osmolality 280 to 290 mOsm/kg
2. Extreme hyperlipidemia (triglycerides greater than 1000-1500 mg/dl) or hyperproteinemia (protein greater than 12-15 g/dl), as in multiple myeloma
C. Hypertonic hyponatremia
1. Serum Na+ less than 135 mEq/L, serum osmolality greater than 290 mOsm/kg
2. Hyperglycemia: Each 100 mg/dl increment in serum glucose above 100 mg/dl decreases serum Na+ by approximately 1.6 mEq/L (e.g., for serum glucose, 900 mg/dl); serum Na+ falls by 8 × 1.6 mEq/L or by 13 mEq/L
3. Mannitol or glycerol in serum causes the same phenomenon
VI. Management
A. Only hypotonic hyponatremia requires treatment directed at serum Na+ itself
1. Therapy is guided by symptoms, level of serum Na+, and rapidity of development
2. Rate of correction of serum Na+ is critical; overcorrection or very rapid rise in serum Na+ may inflict further CNS injury, as is seen in the syndrome of pontine myelinolysis
B. Seizures or coma with serum Na+ less than 115 mEq/L, acute or chronic
1. Infuse 3% hypertonic saline at a rate to raise serum Na+ by 1 to 2 mEq/L/hour until serum Na+ rises by 12 to 15 mEq/L, or to a level of 120 mEq/L
2. Example: Na+ (mEq) required = 0.5 × body wt (kg) × (120 − serum [Na+])
a. For an 80-kg patient with serum Na+ of 107 mEq/L, Na+ required = (0.5 × 40) × (120 − 107) = 520 mEq
b. Infuse 1 L 3% saline (Na+ = 513 mEq/L) over 6 to 12 hours to correct acute hyponatremia
C. Lesser symptoms or serum Na+ less than 110 mEq/L, especially acute onset: Infuse 3% saline as above, or treat on the basis of volume status (below)
D. Mild or no symptoms, hypovolemic state: Infuse 0.9% normal saline (NS) at a rate to correct volume deficiency
E. Mild or no symptoms, hypervolemic state: Administer loop diuretic furosemide (Lasix), 40-80 mg IV or PO; use NS for IV fluid needs
F. All cases: Restrict water or total fluid intake to 1000 ml/24 hours or less
G. Associated hypokalemia: Supplement potassium PO or IV as needed
H. Underlying condition
1. Hypothyroidism: thyroid replacement
2. Adrenal insufficiency: cortisol therapy
3. SIADH: demeclocycline, 150-300 mg PO every 6 hours to antagonize ADH effect in chronic, pathologic ADH release
I. Monitor serum Na+ every 2 to 4 hours in all symptomatic patients
I. Definition
A. Increased serum sodium concentration
1. Serum Na+ greater than 150 mEq/L
2. The norm is 135 to 145 mEq/L
B. Hypernatremia always indicates hyperosmolality, a deficit of body water
C. Occurs with diuretic use, burn injuries, or when free access to water is limited or thirst is impaired
II. Etiology/incidence/predisposing factor
A. Occurs in 0.3% to 1% of hospitalized patients
B. Combination of excess water loss and inability to acquire water: more common in debilitated elderly, those with debility following CVA, and infants
C. Primary water loss
1. Central (pituitary) diabetes insipidus
2. Nephrogenic (renal) diabetes insipidus
3. Increased insensible loss in febrile states
D. Water loss in excess of sodium loss
1. Renal osmotic diuresis
a. Glucosuria of diabetes mellitus
b. Mannitol therapy
c. Urea excretion in burns
d. Relief of urinary obstruction
2. GI fluid loss
a. Persistent diarrhea or emesis
b. Postsurgical drainage
3. Cutaneous fluid loss
a. Burns
b. Sweating
E. Hypertonic sodium gain
1. Hypertonic NaHCO3 with cardiopulmonary resuscitation (CPR)
2. Hypertonic NaCl IV or NaCl tablets PO
III. Subjective findings
A. Mostly neurologic
1. Related to brain shrinkage from water loss
2. Severity is relative to degree and rapidity of development of hypernatremia
B. Correlation with serum Na+
1. Serum Na+ 155 to 160 mEq/L
a. Acute: nausea, weakness, lethargy, confusion, or irritability
b. Chronic: none to mild CNS symptoms
2. Serum Na+ greater than 160 mEq/L
a. Acute: stupor, coma
b. Chronic: none to more severe CNS symptoms
D. Polyuria/nocturia
1. May indicate renal basis
2. Occurs with diabetes insipidus or osmotic diuresis (glucosuria in hyperglycemia)
IV. Physical examination findings
A. CNS depression, rare focal neurologic findings
B. Hypotension, tachycardia, or oliguria in volume-depleted states
C. Major findings reflect primary disorder that causes hypernatremia
V. Laboratory/diagnostic findings
A. Serum Na+ greater than 150 mEq/L: serum osmolality greater than 300 mOsm/L
B. Urine osmolality (UOsm)
1. UOsm less than 300 mOsm/L: central or nephrogenic diabetes insipidus
2. UOsm 300 to 400 mOsm/L: suggests osmotic diuresis
3. UOsm 400 mOsm/L: gastrointestinal, cutaneous, or insensible fluid (water) loss
C. Serum ADH levels during hypernatremia occasionally useful
D. Water deprivation test
1. Withhold all fluid intake
2. Monitor blood pressure (BP), serum Na+, and urine osmolality
3. When urine osmolality is nearly constant, inject aqueous vasopressin (AVP) 5 units subcutaneously; then, measure serum Na+ and urine osmolality in 1 hour
4. Central diabetes insipidus: less than 50% increase in urine osmolality
5. Nephrogenic diabetes insipidus: little or no increase in urine osmolality
VI. Management
A. Rapid lowering of serum Na+ indicated for acute, symptomatic hypernatremia; chronic hypernatremia must be treated more slowly
B. Estimate water deficit at approximately 0.4 × body wt (kg) × [(serum Na+/140) − 1]
C. Replace water at rate calculated to reduce serum Na+ by approximately 1 mEq/L/hour in acute hypernatremia; in chronic hypernatremia, to reduce serum Na+ by approximately one half of excess above 140 mEq/L over 24 hours
D. Enteral therapy: oral water preferable replacement in conscious patients
E. Intravenous therapy
1. Mild volume depletion
a. IV 5% dextrose in water (D5W)
b. Avoid hyperglycemia/glucosuria to prevent further renal water loss
2. Moderate volume depletion
a. IV one-half normal saline (½ NS)
b. Saline component restores ECF volume
c. Free water component repletes body water
F. Monitor serum Na+ every 2 to 4 hours in acute hypernatremia, every 4 to 6 hours in chronic hypernatremia
G. Treat diabetes insipidus, if present (see Chapter 53)
HYPOKALEMIA
I. Definition
A. Decreased serum potassium concentration: K+ less than 3.5 mEq/L; normal is 3.5 to 5.2 mEq/L
B. Serum levels may fall as the result of body loss due to cellular uptake of K+
II. Etiology/incidence/predisposing factors
A. Renal potassium loss
1. Diuretics
a. Acetazolamide
b. Loop diuretics
c. Thiazides
d. Osmotic diuretics (mannitol, glucose in diabetics)
2. Mineralocorticoid excess
a. Primary hyperaldosteronism of adrenal disease
b. Secondary aldosterone excess in hypovolemic states
c. Secondary aldosterone excess in renovascular hypertension
3. Renin-secreting tumor
4. Cushing’s syndrome or adrenal hyperplasia
5. Exogenous mineralocorticoid effect: high-dose prednisone therapy, fludrocortisone, authentic licorice ingestion
6. Renal tubular disorders
a. Renal tubular acidosis (RTA), types I and II
b. Bartter’s, Gitelman’s, or Liddle’s syndrome
7. Hypomagnesemia
B. Nonrenal potassium loss
1. Emesis and nasogastric suction; both GI and renal losses may occur
2. Diarrhea, especially from laxative abuse, and secretory diarrheas
C. Potassium uptake into cells
1. Insulin therapy: common in the treatment of diabetic ketoacidosis
2. Catecholamine excess: epinephrine or adrenergic therapy
3. Metabolic diseases
a. Familial periodic paralysis
b. Thyrotoxic paralysis
D. Inadequate dietary potassium intake: rare
E. Occurs in up to 20% of hospitalized patients and in 10% to 40% of outpatients who are taking diuretics (incidence correlates with diuretic dose)
IV. Physical examination findings
A. Muscle tenderness or weakness
B. Cardiac rhythm changes or extrasystoles
V. Laboratory/diagnostic findings
A. Serum K+ less than 3.5 mEq/L
B. Electrocardiogram: T-wave flattening, appearance of U wave
C. Urinary K+ excretion
1. Greater than 25 mEq/L/24 hours: renal potassium wasting
2. Less than 25 mEq/L/24 hours: nonrenal potassium losses
D. Increased serum HCO3−: suggests mineralocorticoid excess
E. Serum Mg++
1. Normal is 1.6 to 2.2 mg/dl
2. Decreased in up to 40% of hypokalemic patients
VI. Management
A. Body deficits are poorly correlated with serum K+; estimate 100 mEq K+ loss for each 0.3-mEq/L decrease in serum K+ less than 4.0 mEq/L
B. Intravenous KCl: Patients with cardiac arrhythmias (especially on digitalis therapy) or hepatic encephalopathy, or those unable to take oral potassium
1. Maximum solution concentration
a. Peripheral vein infusion: 40 mEq/L
b. Central vein infusion: 60 mEq/L
i. Rate of infusion: maximum 10 to 20 mEq/hour; continuously monitor ECG
C. Oral K+: Cl− salt most effective, especially in metabolic alkalosis
1. KCl (K-Lor and others), 10-40 mEq/day in 1 or 2 doses
2. KCl extended-release (K-Dur, Micro-K Extencaps), dose as above
D. Potassium-sparing diuretics: usually given in combination with other diuretics
1. Spironolactone (Aldactone), 25-100 mg PO daily
2. Amiloride (Midamor), 5 mg PO daily
3. Eplerenone (Inspra), 25-50 mg PO daily
E. High-potassium diet: nuts, dried fruits, tomatoes, potatoes, oranges
HYPERKALEMIA
I. Definition
A. Increased serum potassium concentration
B. Serum levels may rise from decreased renal excretion, decreased cellular uptake, or increased cellular release of K+
II. Etiology/incidence/predisposing factors
A. Decreased renal excretion
1. Renal failure—acute or chronic
2. Decreased aldosterone synthesis
a. Adrenal insufficiency
b. Heparin therapy
3. Decreased renal aldosterone effect
a. Potassium-sparing diuretics
b. Certain renal diseases (diabetic, obstructive, sickle cell nephropathies)
B. Renin-angiotensin system disruption
1. Hyporeninemia-hypoaldosteronism, most commonly from early diabetic nephropathy
2. ACE inhibitor therapy
3. Angiotensin receptor blocker (ARB) therapy
4. NSAID therapy
5. Cyclosporine therapy
C. Decreased cell uptake/increased cell release
1. Insulin deficiency as in diabetic hyperglycemia
2. Cellular disruption
a. Hemolysis during venipuncture
b. Rhabdomyolysis in muscle ischemia or crush injury
c. Tumor lysis syndrome after chemotherapy
3. Pseudohyperkalemia: occurs in venipuncture tube only
a. Thrombocytosis, platelet count greater than 500,000/mm3
b. Leukocytosis, WBC count greater than 100,000/mm3
4. Metabolic acidosis: usually hyperchloremic variety
5. Digitalis poisoning
D. Increased intake
1. Oral: K+ supplements or dietary salt substitutes
2. IV: overly aggressive replacement, K+ salts of drugs
III. Subjective findings
A. Muscle weakness to paralysis
B. Symptoms of underlying disorder often dominate
IV. Physical examination findings
A. Muscle weakness
B. Signs of underlying disorder
V. Laboratory/diagnostic findings
A. Serum K+ greater than 5.2 mEq/L
B. ECG: progression of peaked T waves, widened QRS complex, disappearance of P wave, fusion of QRS and T to form sine wave
C. Elevated BUN and serum creatinine identify renal failure
E. Plasma K+: measured in heparinized tube; normal in pseudohyperkalemia
VI. Management
A. Urgency and level of intervention based on absence or severity of ECG changes
B. All cases
1. Repeat serum (or plasma) K+.
2. Seek and limit sources of K+ intake.
3. Discontinue drugs that limit K+ excretion.
4. Obtain ECG.
C. ECG normal
1. Furosemide (Lasix), 40-80 mg IV, to increase renal K+ excretion
2. Sodium polystyrene resin (Kayexalate), 40-60 g with osmotic cathartic (70% sorbital or lactulose), to increase GI K+ excretion
3. Hemodialysis or peritoneal dialysis to remove K+ in renal failure
D. ECG abnormal; monitor ECG until normal
1. Absent P wave, QRS widening, or sine waves
a. Calcium gluconate 10%: 10 ml IV infusion over 1 to 2 minutes to antagonize hyperkalemic effect; immediate onset; repeat in 3 to 5 minutes if needed to normalize ECG
b. Regular insulin (10 units) IV over 2 to 5 minutes to increase cellular K+ uptake
i. Add glucose (50 g) if euglycemic
ii. Effect in 15 to 30 minutes
iii. Insulin drip plus D10W may follow
c. Albuterol (20 mg) via inhalation over 10 minutes to increase cellular K+ uptake; effect in 15 to 30 minutes
d. NaHCO3 (50 mEq) IV over 1 to 2 minutes
i. May help if metabolic acidosis present
ii. Onset over 1 hour
iii. Variable efficacy
e. Diuretic, resin, dialysis as above to enhance removal
2. Peaked T waves alone
a. Insulin/glucose or albuterol as above to increase cellular K+ uptake
b. Diuretic, resin, dialysis as above to enhance removal
HYPOCALCEMIA
I. Definition
A. Decreased serum calcium concentration: Ca++ less than 8.6 mg/dl
1. Normal is 8.6 to 10.2 mg/dl
2. Portion of total calcium binds to serum albumin, so that total serum Ca++ can be corrected upward by 0.8 mg/dl for each 1 g/dl decrease in serum albumin
II. Etiology/incidence/predisposing factors
A. Hypoparathyroidism, usually surgical post thyroidectomy
B. Hypomagnesemia, especially with serum Mg++ less than 1 mEq/L
C. Pancreatitis (40%-70% incidence in acute pancreatitis)
D. Vitamin D deficiency
1. Malnutrition, especially in infants and the elderly
2. Fat malabsorption
a. Pancreatic insufficiency
b. Regional enteritis
c. Jejunoileal bypass
d. Hepatobiliary disease
3. Chronic renal failure
E. Acute pancreatitis
F. Chronic alcoholism
G. Drugs
1. Phenytoin
2. Cisplatin
3. Estrogen therapy
III. Subjective findings
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A. Mental changes
