✅ Lytes, Acid-Base, Injury, Vasculitis Flashcards Preview

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Acute urinary retention (AUR)

The major risk factors for development of AUR include:

  • Male sex (AUR rarely occurs in women)
  • Advanced age (~33% of men age >80 will develop AUR)
  • History of benign prostatic hyperplasia
  • History of neurologic disease (eg, mild cognitive impairment)
  • Surgery (especially abdominal surgery, pelvic surgery, and joint arthroplasty)
  • Medications (eg, anesthetics, opioids, anticholinergics) that are common precipitants.

In a patient with suspected AUR who is unable to void, the diagnosis is confirmed by bladder ultrasound demonstrating >300 mL of urine.  Treatment is with insertion of a Foley catheter, and urinalysis should be collected to rule out urinary tract infection (a potential cause of AUR).  Obesity, abdominal ascites, or tissue edema may render bladder ultrasound inaccurate; in such cases, Foley catheter insertion can be both diagnostic and therapeutic.

Postoperative oliguria (bladder scan (if available) to assess bladder volume.  Patients with significant urinary retention and likely distal obstruction require Foley catheterization to restore normal urine output and resolve or prevent hydronephrosis, tubular atrophy, and renal injury.  If catheterization does not relieve the patient's oliguria or if there is no significant urinary retention, the patient's AKI may be due to other etiologies (ie, intrinsic, pre-renal).  


Low Serum (plasma) Osmolality: 2 [Na+] + [BUN] / 2.8 + [glucose] /18

One approach to determining the etiology of hyponatremia is an assessment of the patient's volume status.  Evidence of volume overload (eg, peripheral edema, jugular venous distension) is consistent with hypervolemic hyponatremia, which occurs in heart failure, renal failure, and liver cirrhosis.  Evidence of volume depletion (eg, dry mucous membranes) suggests hypovolemic hyponatremia, which occurs in patients with dehydration. Euvolemic (eg, moist mucous membranes, absence of peripheral ADH (SIADH).

Hx: Symptoms occur at a serum sodium level of 110 meq/L and include obtundation, coma, seizures, and death (if untreated). In general, symptoms tend to be worse when the hyponatremia develops quickly.


🧂🧂🧂 3% NaCL?: Serum sodium level should be corrected to 120 meq/L at a rate of 1 to 2 meq/L/h; when this level is achieved, the rate of correction is slowed to 0.3 to 0.5 meq/L/h.

The quantity of sodium chloride required to increase the serum sodium concentration is calculated as:

TBW (L) × (Desired serum [sodium] − Actual serum [sodium]), where the desired [sodium] is 120 meq/L

Seizure and respiratory arrest, the main cause of permanent CNS damage in hyponatremia. ICU care, with frequent monitoring of the serum sodium level and CNS status, is critical. Once the Na has risen 4 to 8 mEq/L and the symptoms have improved, the rate of hypertonic saline infusion can be decreased.

🧂🧂🧂 Hypertonic saline is reserved for ❗ acute symptomatic hyponatremia. 

Correcting hyponatremia TOO rapidly can lead to osmotic demyelination syndrome (previously known as 🧠central pontine myelinolysis), which is characterized by flaccid paralysis, dysarthria, and dysphagia. The rate of sodium correction must be 0.3 to 0.5 meq/L/h or less. 10-12 in a 24 hour period for normal risk patients


"HYPERVOLEMIC" (High ECF volume)  w/ low EABV ("HYPOTONIC")

E = Extracellular

A = Arterial

Heart Failure, Liver Failure, Nephrotic syndrome, Renal Insufficency

The kidney is conserving both sodium and water because renal perfusion is compromised by poor cardiac output.


Liver Disease or HF ?

Renal conservation of sodium and water is documented by a low 🚽 urine sodium concentration (<10 [20] meq/L) and highly concentrated urine (frequently >450 mOsm/kg )


  • Treatment of the underlying cause
  • Dietary sodium restriction to 2 to 3 g/day
  • 🚱water restriction to 1 to 1.5 L/day
  • 🎡Diuretics 
    • Desire: Urine Na+ 60-80 w/ home dose (4 hours after)
    • Desire: Urine Na+ 80-120 w/ IV dose


HYPOVOLEMIC (Low ECF volume) w/ low EABV

E = Extracellular

A = Arterial

GI Loss, Vomiting, Diarrhea

In hypovolemic states, ADH release is stimulated by the decreased ECF volume status and leads to free-water retention.  

Remember that, even when ECF volume is decreased, hyponatremia almost always indicates free-water excess (hypotonicity).

GI Losses

🤮 Vomiting

Dx: If volume loss is due to vomiting, a low urine chloride concentration is corroborative.


Px: Dry mucous membranes, hypotension, and tachycardia. 


GI Loss

The urine indices reflect renal sodium conservation (🚽 urine sodium concentration <10 [20] meq/L) and water conservation (urine osmolality greater than the serum osmolality and frequently >450 mOsm/kg).


🧂 Intravenous (IV) normal saline as well as managing the condition that precipitated the volume loss.

🎡Diuretics, Renal Loss

Elevated 🚽 urine sodium (> 20 mEq/L) suggests salt wasting (early diuretic use)

Surreptitious diuretic use is sometimes employed as a means to lose weight. 


EUVOLEMIC (normal EABV) w/ low ECF

A = Arterial

E = Extracellular


Adrenal Insufficiency



Reset Osmostat

Inadequate Osmols




Renal defect in excreting free water.  

An increase in water intake does not produce an increase in water excretion because ADH release is relatively fixed.

Type A: Grossly elevated levels of ADH unresponsive to osmotic deviations

Type B: An abnormally low osmotic threshold for ADH release

Type C: ADH levels that are persistently in the physiologic range and are neither suppressed by a low plasma osmolality nor stimulated by a rising plasma osmolality.

Type D: Normal osmoregulation (ie, ADH secretion varies appropriately with the plasma osmolality), but the urine is concentrated even if ADH release is suppressed.

Type E: Decline in plasma ADH as the serum sodium concentration increases during infusion of hypertonic saline.


  • CNS disturbance (eg, stroke, hemorrhage, trauma)
  • Medications (eg, carbamazepine, SSRIs, NSAIDs)
  • Lung disease (eg, pneumonia)
  • Ectopic ADH secretion (eg, small cell lung cancer)
  • Pain &/or nausea

Clinical features

  • Euvolemia (eg, moist mucous membranes, no edema, no JVD)
  • Mild/moderate hyponatremia - nausea, forgetfulnessm [Serum sodium 130-135 mEq/L][Serum sodium 120-130 mEq/L may display mild symptoms (lethargy, forgetfulness)].
  • Severe hyponatremia - seizures, comaSerum sodium <120 mEq/L may have severe symptoms (eg, profound confusion, seizures, coma).  Cx: Cerebral edema and brainstem herniation.  

Laboratory findings

  • Hyponatremia
  • Serum osmolality <275 mOsm/kg H2O (hypotonic)
  • Urine osmolality >100 mOsm/kg H2O (and usually greater than 300 mOsm/kg H2O) WITHOUT evidence of hypovolemia [ADH prevents the kidneys from excreting dilute urine]
  • High Urine sodium >40 mEq/L [due to euvolemia]
  • Low serum uric acid  🧶
  • Low blood urea nitrogen (BUN) levels🍔


💀 Chest CRX and Head CT

🚱 Free water restriction for asymptomatic patients.  [Insensible and urinary water loss results in a rise in serum Na+ and serum osmolality and symptom improvement.]

🧂🧂🧂 Hypertonic saline (3% saline) is used to treat patients who are symptomatic [CNS symptoms such as confusion, obtundation, or seizures] Administered to raise the serum sodium out of the danger zone.   [Increase in the serum sodium level by approximately 4 to 6 mEq/L over the first 24 hours is sufficient.]

Salt Tablets

❌ Normal Saline: Normal saline (0.9%) and half normal saline (0.45%) have electrolyte concentrations of approximately 300 and 150 mOsm/kg H2O, respectively.  Intravenous infusion of either of these fluids would cause a net increase in total body free water and worsen the hyponatremia.

🏃🏽‍♀️Exercise-associated hyponatremia (EAH) is a recognized phenomenon that may occur in individuals participating in prolonged exercise (eg, marathons, triathlons).  Depending on the degree of hyponatremia, patients may be asymptomatic or mildly symptomatic (eg, lethargy, nausea) or may demonstrate severe symptoms (eg, seizures, profound confusion) that, when present, are indicative of life-threatening hyponatremia.

The largest contributing factor to EAH is the ingestion of large amounts of hypotonic fluid (eg, water, some sports drinks) during and immediately following prolonged exercise.  In addition, many individuals with EAH demonstrate temporary inability to excrete appropriately dilute urine (urine osmolality inappropriately remains >100 mOsm/kg H2O), which is consistent with syndrome of inappropriate antidiuretic hormone (SIADH).  In these individuals, excessive ADH secretion is triggered by nonosmotic stimuli (eg, exertion, pain, hypoglycemia, nausea) that occur during intense exercise.



Primary polydipsia is more common in patients with psychiatric conditions (eg, schizophrenia), possibly due to a central defect in thirst regulation.  These patients continue to drink water despite a decreased serum osmolality that should normally inhibit the thirst reflex. 

The kidney increases water excretion, which dilutes the urine maximally to an osmolality <100 mOsm/kg.  However, hyponatremia can develop if the water intake is higher than the kidney's ability to excrete water.  Patients with significant hyponatremia can develop confusion, lethargy, psychosis, and seizures.

The normal renal capacity for water excretion is approximately 15 L/day. A massive increase in water intake occurs in psychogenic polydipsia or, rarely, in hypothalamic diseases.

  • Urine sodium concentration >20 meq/L)
  • ADH levels are normal
  • Urine osmolality appropriately low (<100 mOsm/kg H2O)
  • Very dilute urine (ie, urine specific gravity of 1.001 or 1.002)

Tx: 🚱 Water restriction


Inadequate Osmoles

Severely decreased solute intake (in the setting of ongoing free water intake) and polydipsia.

At least 50 mOsm needed to excrete 1 L of water via the urinary tract; malnourished patients may not have adequate osmoles to excrete excess free water.

  • ADH levels are normal
  • Urine osmolality appropriately low (<100 mOsm/kg H2O)

Tx: Water restriction until nutrition can be corrected

"Tea and toast?" "Beer potomania?"


Glucocorticoid Deficiency

Renal defect in excreting free water.  increased ADH release

Mineralocorticoid deficiency typically presents with hyperkalemia and metabolic acidosis




Renal defect in excreting free water.   increased ADH release


Reset osmostat



HYPERTONIC (hyperosmolal) Hyponatremia


Measured sodium concentration can be corrected by the following calculation:

Corrected [Na+] = Measured [Na+] + 0.016 × ([Glucose] − 100)

! Other solutes capable of this effect include mannitol, radiographic contrast media, sorbitol, and glycine (sorbitol and glycine are used as irrigants during bladder or uterine surgical procedures)


ISOTONIC (pseudohyponatremia)

Measurement in a falsely large volume; an interfering substance displaces water in the sample.  

The most common space-occupying substances are:

Lipids (eg, severe hyperlipidemia) 

Paraproteins (eg, multiple myeloma).

Hyperglycemia Patients with DKA can have pseudohyponatremia due to hyperglycemia;


Serum sodium concentration >145 meq/L

Central Diabetes Insipidus 🗿

Nephrogenic Diabetes Insipidus 🗿

Mineralcorticoid Excess

🧂🧂🧂 Hypertonic Saline (Iatrogenic)



💩GI losses

😰Skin losses 

💨 Respiratory Tract losses


GI losses

Most commonly, hypernatremia is due to loss of hypotonic fluids with inadequate water replacement. 

Associated with ICF contraction; Defective thirst mechanism, inadequate access to water, or a renal concentrating defect.  Patients with an intact thirst mechanism do not develop significant hypernatremia unless their access to water is restricted by unconsciousness, immobility, or an altered mental status.

Hx: GI, renal, cutaneous, or pulmonary losses. 

Weakness, lethargy, seizures, and coma.

Dx: Both thirst and ADH levels should be elevated

Tx: 0.9% NS replacement, 💧 free water replacement, and correction of the underlying problem leading to hypotonic fluid loss; ADH (desmopressin, vasopressin) administration.

The water deficit is estimated by the formula:

Water deficit = TBW – (Desired [sodium]/Current [sodium]) × TBW

Because of the presence of idiogenic osmoles created by the brain to protect ICF volume, correcting hypernatremia too quickly can lead to cerebral edema. Extreme care must be taken to correct serum sodium concentration at a rate ≤1 meq/L/h, with a goal of 50% correction at 24 to 36 hours and complete correction in 3 to 7 days.


Half normal saline and 5% dextrose are hypotonic solutions.  As such, they should NEVER be used for initial resuscitation because they quickly exit the intravascular system and lower the sodium too rapidly.  Precipitous drops in sodium levels can cause cerebral edema.


🗿 Nephrogenic Diabetes Insipidus

To distinguish between central (ADH deficiency) and nephrogenic (peripheral resistance to ADH action) diabetes insipidus, vasopressin (ADH by another name) is administered. If the urine osmolality rises and the urine output falls, the diagnosis is central DI. There will be little response to vasopressin in nephrogenic DI.

💊Lithium induces ADH resistance by impairing water reabsorption in the collecting duct.  Patients typically develop acute-onset nocturia, polyuria and polydipsia.  If water intake is inadequate, significant hypernatremia and central nervous system symptoms can develop.  Discontinuing lithium is recommended, with salt restriction and selected diuretics (eg, amiloride) as an alternative for patients who cannot stop lithium.

Hx: Drugs (eg, lithium, foscarnet), hypokalemia, hypercalcemia, sickle cell disease and trait, and amyloidosis.

Tx: The first step is to restore volume with isotonic fluids (0.9% saline).  Isotonic fluid is not usually used in hypernatremia, but it is recommended in patients with marked volume depletion and hemodynamic instability.  Once the patient is euvolemic, the fluid can be switched to a hypotonic fluid (5% dextrose preferred over 0.45% saline) for free water supplementation.  The serum sodium should be corrected by 0.5 mEq/dL/hr without exceeding 12 mEq/dL/24 hr

Cx: Cerebral edema can occur if the sodium is corrected too quickly.



Severe hypercalcemia (ie, serum calcium >14 mg/dL) can cause weakness, gastrointestinal distress, and neuropsychiatric symptoms (eg, confusion, stupor, coma), especially with a rapid rise in serum calcium.  Patients are typically volume-depleted due to polyuria and decreased oral intake.

Management of hypercalcemia

Severe (calcium >14 mg/dL) or symptomatic

  • Short-term (immediate) treatment
    • Normal saline hydration plus calcitonin 🤵🏼
    • Avoid loop diuretics unless volume overload (heart failure) exists
  • Long-term treatment
    • Bisphosphonate (zoledronic acid)

Moderate (calcium 12-14 mg/dL)

  • Usually no immediate treatment required unless symptomatic
  • Treatment is similar to that for severe hypercalcemia

Asymptomatic or mild (calcium <12 mg/dL)

  • No immediate treatment required
  • Avoid thiazide diuretics, lithium, volume depletion & prolonged bed rest

Patients with severe hypercalcemia require aggressive saline hydration to restore intravascular volume and promote urinary calcium excretion.  Calcitonin, by inhibiting osteoclast-mediated bone resorption, quickly reduces serum calcium concentrations and can be administered concurrently with saline.  Bisphosphonates (eg, pamidronate, zoledronic acid) also inhibit bone resorption and provide a sustained reduction in calcium levels.  However, the calcium-lowering effect of bisphosphonates is delayed, usually occurring over 2-4 days, and they are typically given after initial administration of saline and calcitonin).


Primary hyperparathyroidism

PTH [normally 10-65 pg/mL]

The most common cause of hypercalcemia diagnosed in the outpatient setting. 

Hx: This disorder also may be found during the evaluation of osteoporosis or nephrolithiasis. 

Increased 👨🏽‍🔬PTH

Increased 1,25-dihydroxy (vitamin 🔋D3) levels

Increased osteoclast-mediated bone resorption 🦴

Enhanced distal tubular reabsorption of calcium 🦴

Decreased proximal tubular reabsorption of phosphorus

Increased 🚽 urine phosphate and calcium levels. 

Increased 1α-hydroxylase 🤖 expression in the kidney, leading to increased production of 🤖 1,25-dihydroxy vitamin D, which further increases GI calcium absorption.

Dx: Associated with elevated serum calcium, low phosphate, PTH in the normal range (20%) or elevated (80%), normal or elevated alkaline phosphatase, and normal or elevated urine calcium.


Hypercalcemia of malignancy

Hypercalcemia of malignancy may be due to local osteolytic hypercalcemia or to humoral hypercalcemia of malignancy, in which a tumor that does not involve the skeleton secretes a circulating factor that activates bone resorption. 

Dx: Associated with elevated calcium, normal or low phosphate (elevated if GFR <35 mL/min/1.73 m2), normal or elevated PTHrP (not needed for diagnosis), normal or elevated alkaline phosphatase, and elevated urine calcium. Low PTH?


Asymptomatic or mild hypercalcemia (calcium <12 mg/dL) does not require urgent therapy, but hypercalcemia of malignancy may worsen over time.  

Control of the tumor with chemotherapy.

💦Saline diuresis (infusion): Normalization of intravascular volume with saline will improve delivery of calcium to the renal tubule and aid in excretion of calcium. As the kidneys excrete excess sodium from the saline, excretion of calcium will follow

Bisphosphonates (eg, zoledronic acid) inhibit the osteoclastic activity of bone, stabilizing destructive bony tumors and reducing the risk of skeletal-related events such as pathologic fracture and malignant hypercalcemia.


Metastatic bone disease

High calcium levels impair the ability of the nephron to concentrate urine, which results in inappropriate water loss from the kidney.  Hypercalciuria without hypercalcemia is most common.

Dx: Associated with elevated calcium, normal or elevated phosphate, elevated alkaline phosphatase (most cases), and variable PTHrP. Low PTH?


Multiple myeloma

Common cause of hypercalcemia in patients with decreased GFR and anemia.

Dx: Associated with elevated calcium, elevated phosphate, normal alkaline phosphatase, normal or low PTHrP, and abnormal serum protein immunoelectrophoresis. Low PTH?


Granulomatous disease (eg, sarcoidosis, tuberculosis)

Hypercalcemia can result from excessive ingestion or production of either 25-hydroxy vitamin D (calcidiol) or 1,25-dihydroxy vitamin D (calcitriol). The mechanism of hypercalcemia is the result of increasing GI calcium absorption and bone resorption.

Dx: Associated with elevated calcium, elevated phosphate, elevated alkaline phosphatase (but may not be of skeletal origin), elevated urine calcium, and elevated vitamin D. Low PTH?


Milk-alkali syndrome

MAS is caused by excessive intake of calcium and absorbable alkali (eg, calcium carbonate preparations used in patients with osteoporosis).  The resulting hypercalcemia causes renal vasoconstriction and decreased glomerular blood flow.  In addition, inhibition of the Na-K-2Cl cotransporter (due to activation of calcium-sensing receptors in the thick ascending loop) and impaired antidiuretic hormone activity lead to loss of sodium and free water.  This results in hypovolemia and increased reabsorption of bicarbonate (augmented by the increased intake of alkali).

Consider in healthy persons in whom primary hyperparathyroidism has been excluded.  Excessive ingestion of calcium carbonate to treat osteoporosis or dyspepsia can result in hypercalcemia, metabolic alkalosis, and kidney insufficiency. Metabolic alkalosis stimulates the distal tubule to reabsorb calcium, contributing to hypercalcemia. 

Hx: Medications that raise the risk of MAS include thiazide diuretics, ACE inhibitors/angiotensin II receptor blockers, and nonsteroidal anti-inflammatory drugs.  In addition to hypercalcemia, metabolic findings in MAS include hypophosphatemia, hypomagnesemia, metabolic alkalosis, and acute kidney injury.  Parathyroid hormone levels are suppressed.

Dx: Associated with elevated calcium, elevated phosphate, elevated creatinine, normal alkaline phosphatase, elevated bicarbonate, and variable urine calcium. Low PTH?



Hypercalcemia of immobilization is likely due to increased osteoclastic bone resorption.  The risk is increased in patients with a pre-existing high rate of bone turnover (eg, younger individuals, Paget disease). 

Occurs in persons with high bone turnover before an immobilizing event (eg, untreated primary hyperparathyroidism, hyperthyroidism, Paget disease of bone).

Dx: Associated with elevated calcium, elevated phosphate, elevated alkaline phosphatase, and elevated urine calcium. Low PTH?

The onset of hypercalcemia is usually around 4 weeks after immobilization, although patients with chronic renal insufficiency may develop hypercalcemia in as little as 3 days.

The onset of hypercalcemia due to immobilization is often insidious, and the presenting symptoms can be nonspecific.  Bisphosphonates inhibit osteoclastic bone resorption and are effective in treating hypercalcemia of immobilization and reducing the associated bone loss.



Hypercalcemia is a frequent incidental finding in hyperthyroidism, which results from direct stimulation of osteoclasts by thyroxine or triiodothyronine. Low PTH?


Benign familial hypocalciuric hypercalcemia

Constitutive overexpression of the calcium-sensing receptor gene.

Dx: Elevated calcium, low phosphate, and a calcium-creatinine clearance ratio <0.01 [calculated as (Urine calcium ÷ Serum calcium) × (Serum creatinine ÷ Urine creatinine)]. Normal PTH?



Calcium normally 9-10.5 mg/dL


  • Neck surgery (parathyroidectomy)
  • Pancreatitis
  • Sepsis
  • Tumor lysis syndrome
  • Acute alkalosis
  • Chelation: blood (citrate) transfusion, EDTA (ethylenediaminetetraacetic acid), foscarnet

Clinical features

  • Muscle cramps
  • Chvostek & Trousseau signs
  • Paresthesias
  • Hyperreflexia/tetany
  • Seizures


  • IV calcium gluconate/chloride

Decreased 👨🏽‍🔬PTH production

Hypomagnesemia causes decreased production of 👨🏽‍🔬PTH as well as decreased end-organ response to the hormone.  🍻 Alcohol causes increased urinary losses of magnesium which then leads to the mentioned effects on PTH and ultimately to hypocalcemia.  Hypomagnesemia alone would 🅿increase phosphorus by decreasing parathormone effect.


Approximately 40% of circulating calcium is bound to proteins (predominantly albumin).  Hypoalbuminemia will lower the total serum calcium level; therefore, measured calcium levels are corrected upward based on the extent of hypoalbuminemia.  Conversely, hyperalbuminemia is associated with an increase in total calcium. 

The serum calcium concentration INCREASES by 0.8 mg/dL for every 1 g/dL decrease in serum albumin; the corrected calcium level can be calculated using the following formula:

Corrected calcium = (measured total calcium) + 0.8 × (4.0 g/dL − serum albumin in g/dL)

"Add 0.8 mg/dL to the observed calcium level for every 1 g reduction in the albumin level (from 4 used as normal)"

An ionized calcium level is consistent and accurate regardless of the albumin level of a patient.  Direct measurement of ionized calcium is performed in many clinical laboratories, but it requires special handling and may not be readily available.  

Plasma calcium exists in 3 forms: ionized calcium (45%), albumin-bound calcium (40%), and calcium bound to inorganic and organic anions (15%).  Homeostasis of these forms is significantly influenced by the extracellular pH level.  An increased extracellular pH (due to respiratory alkalosis ) causes hydrogen ions to dissociate from albumin molecules, thereby freeing up the albumin to bind with calcium.  This increase in the affinity of albumin for calcium leads to decreased levels of ionized calcium.

Ionized calcium is the only physiologically active form, which means that a decrease in ionized calcium can result in the clinical manifestations of hypocalcemia (eg, crampy pain, paresthesias, carpopedal spasm) even though total calcium is unchanged.

  • Chvostek sign
  • Trousseau sign 

🍊 Citrate in transfused blood binds ionized calcium, which is the biologically active fraction (total calcium levels will not be significantly affected).  Hypocalcemia is uncommon following blood transfusion in patients with normal liver function as citrate is rapidly metabolized by the liver; however, 🐄 hepatic dysfunction can.  Other infused substances that can chelate calcium in the blood include lactate, foscarnet, and sodium ethylenediaminetetraacetic acid (EDTA).


Oral calcium (carbonate or citrate) supplementation

Intravenous calcium guconate/chloride more rapidly increases the serum calcium level and may be indicated in patients with very low (< 7.5 mg/dL) calcium levels or more significant clinical findings associated with the hypocalcemia, such as severe musculoskeletal weakness, tetany, or electrocardiographic conduction abnormalities.

Recombinant form of parathyroid hormone (teriparatide) is available, although its primary use is in the treatment of advanced osteoporosis in selected patients. Although teriparatide holds promise as a potential therapy for chronic hypoparathyroidism, its safety and long-term effectiveness for this indication have not been established, and it does not have Food and Drug Administration approval for treatment of acute hypoparathyroidism.



Hypophosphatemia is defined as a serum phosphorus concentration less than 2.5 mg/dL  and is most common in patients with a history of chronic 🍻 alcohol use, critical illness, or malnutrition.

Respiratory alkalosis is one of the commonest causes of hypophosphatemia; it results from shift of phosphate from the extracellular to the intracellular space.

Dx: Most patients with hypophosphatemia are asymptomatic, but symptoms of weakness may manifest at serum phosphorus levels < 2.0 mg/dL. Levels less than 1.0 mg/dL may result in respiratory muscle weakness, hemolysis, rhabdomyolysis or tumor lysis. Serum uric acid >15 mg/dL suggests rhabdomyolysis or TLS.

🍗Refeeding syndrome is caused by an intracellular shift of 🅿phosphorus; calories provided to a patient after a prolonged period of starvation serve as a stimulus for cellular growth, which consumes phosphorus in the form of phosphorylated intermediates such as adenosine triphosphate. 

Hx: Persons who chronically 🍻abuse alcohol frequently may develop refeeding syndrome, largely because of underlying poor nutrition. The syndrome may also be the result of intravenous infusion IV of glucose in malnourished patients.  Such patients have clear clinical evidence of malnutrition.  In addition, malnutrition almost always causes hypoalbuminemia.

Tx: If the refeeding syndrome occurs, the level of nutritional support should be reduced, and the hypophosphatemia, hypokalemia, and hypomagnesemia should be corrected.  Moderately to severely ill patients with marked edema or a serum phosphorus level less than 2.0 mg/dL should be hospitalized for intravenous therapy to correct electrolyte deficiencies. Continuous telemetry may also be needed to monitor cardiopulmonary physiology.



Tx: Restrict dietary potassium, ensure adequate hydration, and use loop diuretics as necessary.

Severe hyperkalemia (>6.0 meq/L [6.0 mmol/L]) is associated with life-threatening cardiac dysrhythmias; patients with severe hyperkalemia require emergent hospitalization for medical management.

Stabilize (Cacl) Temporize (Insulin, NaHCO3, beta-agonist); decrease total body K+ (loop Diuretics, kayexylate, dialysis)

Calcium gluconate

Raises threshold for depolarization (myocardial membrane stabilization)

Sodium bicarbonate

Shifts potassium intracellularly.  Patients with severe kidney disease or hypervolemic states, such as CHF, may not tolerate alkalinization or the associated sodium load. Ideally, the serum bicarbonate and creatinine should be checked before intravenous sodium bicarbonate is administered.


Shifts potassium intracellularly.  In euglycemic patients, a combination of insulin (10U) and glucose (25g) is typically administered concomitantly to decrease the risk of hypoglycemia (can lower the serum potassium level by 0.5 to 1.0). In hyperglycemic patients insulin alone should be given.

β-Agonists (eg, inhaled albuterol)

Shifts potassium intracellularly.  Probably more effective than IV sodium bicarbonate. It

Measures to promote potassium loss from the body (Kayexalate, furosemide, or dialysis) take time to work.

Loop diuretics

Increases renal excretion of potassium.  Depending on the patient’s kidney function and volume status, may be considered, but they take hours to work and should not take the place of immediate therapy.

Sodium polystyrene sulfonate (kayexelate)

Ion exchange resin binding potassium in the gut; may be no more effective than laxatives and has been associated with intestinal necrosis; ; need good bowel function.  The delayed onset of action of this drug prevents this from being the best initial intervention.


Extracorporeal removal of potassium

.1 for every 10 mEq



  • Surreptitious vomiting 
    • Physical findings that are characteristic of surreptitious vomiting are scars/calluses on the dorsum of the hands, and dental erosions.  The dorsal scars result from repeated chemical/mechanical injury as the patient uses his/her hands to induce vomiting.  Dental erosions result due to increased exposure to gastric acid.  Surreptitious vomiting may also result in hypovolemia and hypochloremia, which in turn lead to a low urine chloride concentration.
  • Diuretic abuse (Potassium-wasting diuretics)
  • Bartter syndrome
  • Gitelman's syndrome 
    • Hypokalemia, alkalosis and normotension, but their urine chloride concentrations are high.
  • Diarrhea

Hx: In some patients, clinically significant hypokalemia can result, causing muscle weakness, arrhythmias, and EKG changes.  Other common side effects of beta-2 agonists include tremor, headache and palpitations.

Symptoms of hypokalemia depend on the severity of the imbalance, but can include weakness, fatigue, and muscle cramps.  Flaccid paralysis, hyporeflexia, tetany, rhabdomyolysis, and arrhythmias may occur with severe hypokalemia (serum concentration <2.5 mEq/L).  An ECG will show broad flat T waves, U waves, ST depression, and premature ventricular beats.  Atrial fibrillation, torsades de pointes, and ventricular fibrillation can occur. 

Beta-2 agonists like albuterol reduce serum potassium levels by driving potassium into cells.