Ch 7.1: Fluids, Electrolytes Flashcards
Water
50-60% total body weight
TBW
Total body water
Function of weight, age, sex, relative amount of body fat (least hydrated)
TBW distribution:
- ICF (intracellular) = 2/3 of TBW
- ECF (extracellular) = 1/3 of TBW
- TCF (transcellular) = 3% of TBW
Why is ECF the most clinically important fluid department?
it contains intravascular and interstitial spaces
Major extracellular osmole holding water in the extracellular space
Sodium
Major intracellular osmole holding water within the cells
Potassium
Na-K-ATPase pumps
Maintenance of ECF/ICF compositions
Key role in regulating cell volume
D5W-IVF effect on ECF/ICF
Dextrose metabolized
Water distributed proportionally to all fluid compartments:
* ICF: 2/3 (667 mL)
* ECF: 1/3 (333 mL)
Within the ECF:
* Intravascular space: 25% (83 mL)
* Interstitial fluid: 75% (250 mL)
0.9% NaCl-IVF effect on ECF/ICF
0.9% NaCl is an isotonic saline
Distributed completely to ECF (sodium is major extracellular osmole)
* ICF: 0 mL
* ECF: 1000 mL
* 25% (250 mL) remains in intravascular space
* 75% (750 mL) - interstitial space
Which is more efficient at expanding the intravascular (plasma) space?
D5W or 0.9%-NaCl
Isotonic saline is 3x more efficient than 5% dextrose in water at expanding the intravascular space (plasma)
What effect does a hypertonic saline (3% NaCl) have?
Establishes osmotic gradient that results in movement of water out of the cells and into the ECF until osmotic equilibrium is obtained
Osmolality increases in both spaces:
* ECF – addition of NaCl
* ICF – water loss
Osmotic forces
determine the distribution of water between ICF and ECF spaces
Plasma oncotic and hydrostatic pressures
manage movement of fluid between plasma and interstitial fluid
Third spacing:
Caused by a disruption in oncotic and/or hydrostatic pressure → net flow of fluid from one compartment to another
Plasma-to-interstitial fluid shift → accumulation of excess fluid:
* Edema: interstitial space
* Effusion: potential fluid spaces
What can an acute reduction in blood volume cause?
During third-spacing
Can lead to severe volume depletion if not replaced
Third spacing in critical illness
- Capillary permeability increases → leakage of albumin from plasma to interstitial space → reduced plasma oncotic pressure
- Favors movement of fluid from intravascular → interstitial space
Third spacing can occur in the following scenarios:
- Intestinal obstruction
- Ileus
- Pleural effusions or ascites
- Severe acute pancreatitis
- Peritonitis
- Trauma
- Bleeding
- Obstruction of a major venous system
On average, healthy adults require _ _ _ mL/kg/d of fluid
30-40 mL/kg/d
Fluid losses - sensible vs insensible
- Sensible (easily measurable) losses from GI tract and kidneys account for most fluid loss
- Insensible losses from lungs/skin can contribute up to 1L/day
Additional fluid required in:
- Severe diarrhea or emesis
- Large draining wounds
- Excessive diaphoresis
- Constant drooling
- Paracentesis losses
- Persistent fevers
- Drains
- High gastric, fistula, and ostomy outputs
- Lactation
Strategies to measure outputs that may otherwise not be collectable:
- Weigh wound dressings before and after placement to determine losses from open wounds
- Excessive diaphoresis that soaks the bed is usually = 1 liter of fluid
Heart failure
- 20-25 mL/kg of estimated dry weight
- Should take into consideration edema, fatigue, SOB
- 2g sodium restriction (83 mEq/d)
**HF patients with significant overload should initially be treated with loop diuretics and sodium/fluid restrictions **
Maintenance Fluid Requirements
Weight and Age Based Formula
- 18-55 years: 35 mL/kg/day
- 56-75 years: 30 mL/kg/day
- > 75 years: 25 mL/kg/day
- Fluid-restricted adults: < 25 mL/kg/day
Based on 2023 NFM course
Maintenance Fluid Requirements
Energy based Formula
1 mL/kcal consumed or required
Not encouraged in >65 YOA
Based on 2023 NFM course
Maintenance Fluid Requirements
Holliday-Segar Formula
1500 mL for the first 20 kg of body weight, then ADD
- 20 mL/kg remaining kg of BW
Based on 2023 NFM course
Maintenance Fluid Requirements
Adjusted Holliday-Segar Formula
1500 mL for the first 20 kg of body weight, then ADD
- < 50 YOA: 20 mL/kg of remaining BW
- > 50 YOA: 15 mL/kg of remaining BW
Based on 2023 NFM course
Disorders of Fluid Balance - Disturbance of Volume
Hypervolemia
Volume overload
Excessive gain of fluid
Disorders of Fluid Balance - Disturbance of Volume
Hypovolemia & Causes
Volume depleton
Excessive fluid loss
- Often follows GI hemorrhage, vomiting, diarrhea, and diuresis
Disorders of Fluid Balance - Disturbance of Concentration
What is recognized by a change in serum sodium concentration and plasma osmolality?
- Overhydration - Gain of water alone
- Dehydration - Loss of water only
Disorders of Fluid Balance - Composition
Disturbance of Composition
Gain or loss of potassium, magnesium, calcium, phosphate, chloride, bicarbonate, or hydrogen ions
Electrolytes
Acute abnormality –
developed < 48 hours
Associated with symptoms requiring immediate treatment
* Ex: AMS with acute hyponatremia
Electrolytes
Chronic abnormality –
pt often asymptomatic
Patient may be harmed if disorder is corrected too rapidly
* Ex: chronic hyponatremia
What should you do if labs are inconsistent with trends?
Validate accuracy of specimen prior to treatment
Electrolyte above normal level – Potential treatments
- Consider removing electrolyte supplementation from IVF or PN
- Changing an enteral formulation containing the electrolytes to something else
- D/c’ing medications that could contribute to electrolyte disorder
- Manage acid-base abnormalities (e.g., metabolic acidosis)
- Inducing renal or GI elimination of the electrolyte
How should patients with volume overload receive electrolyte repletions?
Patients with volume overload should receive volume-restricted electrolyte replacement, or PO therapy when able
Electrolytes
Why does peripheral administration have limits for volume and rate of administration?
- Potassium/calcium especially
- Exceeding limits can → tissue damage and potential patient harm
Sodium
Sodium disorders are a result of:
Alterations in water balance
Sodium
Adequate intake of sodium is
_ _ _ mg (_ _ mEq)
daily
Adequate intake (AI) is 1500 mg (65 mEq) daily
Sodium
Clinically relevant hyponatremia:
Lab value & what do you do in response?
- Serum sodium <130 mEq/L
- Determine serum sodium concentration and volume status
Role of sodium in the body
- Major osmotic determinant in regulating ECF volume and water distribution in the body
- Determines membrane potential of cells
- Active transport of molecues across cell membranes (Na-K-ATPase pumps)
Sodium
When are clinical manifestations of hyponatremia more likely to occur?
Lab value
Na <125 mEq/L
Sodium
Hypertonic hyponatremia
- Serum osmolarity >295 mOsm/L
- Caused by presence of osmotically active substances other than sodium in the ECF
- Common causes: hyperglycemia, mannitol
Sodium
Formula to correct serum sodium in setting of hyperglycemia
Corrected Na = serum Na + 0.016 (serum glucose – 100)
Hypertonic hyponatremia
Sodium
Why do you not want to correct sodium too quickly?
To prevent osmotic demyelination
Target rate of sodium correction for hyponatremia should not exceed
* Acute: 10-12 mEq/L/d
* Chronic/unknown duration: 6-8 mEq/L/d
Sodium
Isotonic hyponatremia
- Serum osmolarity in normal range: 280-295 mOsm/L
- Rarely observed with recent advances in lab analysis
- Fraction of serum that is composed of water is reduced = excess of plasma proteins or lipids
- Isotonic infusions: dextrose, mannitol
Sodium
What is pseudohyponatremia caused by?
hypertriglyceridemia; hyperproteinemia
Sodium
Hypotonic hyponatremia:
- serum osmolarity <280 mOsm/L
- Requires detailed assessment of volume status and urine sodium osmolality
- Check urine osmolality: >100 mOsm/kg = inappropriate renal dilution
Sodium
Hypovolemic hypotonic hyponatremia
Include sodium / TBW
↓↓ total body Na; ↓ TBW
* Patients lose more sodium in relation to water
* Critical to identify source of fluid loss
* Urine osmolality > serum osmolality = concentrated urine + body’s attempt to retain fluid
Sodium
What can cause hypovolemic hypotonic hyponatremia?
Cerebral salt wasting 2/2 SAH can → hypovolemic hyponatremia
Extrarenal losses:
Diarrhea, GI fistula output, excessive sweating, burns, open wounds, and fluid drains (peritoneal, pleural, biliary, or pancreatic)
Renal losses:
Diuretics, osmosis diuresis,
Sodium
Hypovolemic state:
Determine ECF volume & treatment
- ECF volume status: Tachycardia, low BP, poor skin turgor
- Treatment: isotonic fluids to expand ECF volume
Sodium
Euvolemic hypotonic hyponatremia
Include sodium / TBW
+/= total body Na; ↑ TBW
- Urine osmolality > serum osmolality & Urine Na+ > 20 mEq/L
- Indicates kidneys are inappropriately concentrating urine (would be dark urine)
- Volume status is adequate
- Urine osmolality > serum osmolality AND urine Na >20 = kidneys inappropriately concentrating urine
Sodium
What can cause euvolemic hypotonic hyponatremia?
Commonly associated with SIADH
- Hypothyroidism
- Drug-induced
Sodium
Euvolemic state
Determine ECF volume & treatment
- ECF volume status: Normal pulse, BP, skin turgor; no edema
- Treatment (additional causes): correct the underlying disorder + fluid restriction
SIADH
* Fluid restriction 500-1000 mL/d
* Concentrate PN
* Ensure at least isotonic fluids (PN concentration = 154 mEq Na/L)
* NaCl tablets
* Urea
* Vaptan
Deficiency
* Glucocorticoids
Hypothyroid
* Thyroid hormone replacement
Sodium
Hypervolemic hypotonic hyponatremia
Include sodium / TBW
↑ total body Na; ↑↑ TBW
* Pts have some element of end-organ damage (renal failure, hepatic failure w/ ascites, HF)
→ fluid retention or third spacing
* Patients retain more water > sodium
Sodium
Hypervolemic state
Determine ECF volume & treatment
- ECF volume status: Edema
- Treatment: fluid and sodium restrictions; concentrate PN, diuretics, vaptans
Sodium
SIADH
Cause, what happens, what contributes to it, what does pt present w/?
- A disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (ADH)
- If water intake exceeds the reduced urine output, the ensuing water retention leads to the development of hyponatremia
- ADH: increases water reabsorption by the kidney
- Retain water (hypotonic hyponatremia); low UOP
- Presents with excessive thirst
SIADH essential diagnostic criteria:
Includes lab value
- Serum osmolality = < 275 mOsm/kg
- Urine osmolality = double to serum osmolality
- Urine sodium = >20
- No adrenal, thyroid, pituitary or renal insufficiency
- No recent diuretic use
SIADH causes
Respiratory (small cell lung cancer, pneumonia, abscess, tuberculosis)
Neurologic (tumors, trauma, meningitis, abscess, subarachnoid hemorrhage, pain, anxiety, nausea)
Medications
* Anticancer agents: cyclophosphamide, ifosfamide, vincristine, cisplatin, carboplatin
* Anticonvulsants: carbamazepine, oxcarbazepine
* Antidepressants: SSRIs, TCADs, MAOI, venlafaxine
* Antidiabetic agent: chlorpropamide
* Antipsychotics: phenothiazines, haloperidol
* Miscellaneous: opiates, 3,4-methylenedioxy-methamphetamine, NSAIDs
* Vasopressin analogs: desmopressin, oxytocin, terlipressin, vasopressin
Sodium
Hypernatremia - levels > _ _ _ mEq/L are associated with a significant increase in mortality
Levels >160 mEq/L associated with a significant increase in mortality
Sodium
Symptoms of hypernatremia
- Lethargy
- Twitching
- Weakness
- Seizures
- Confusion
- Coma
- Restlessness
- Death
- Irritability
Sodium
How to address hypernatremia:
- Assess volume status
- Correct water deficit: administer 50% within first 24 hours, remainder over next 24-48 hours
- Limit serum Na correction to 8-10 mEq or mmol / Liter per day → prevention of cerebral edema
Sodium
Equation for free water deficit
Water deficit (L) = TBW x [(serum Na – 140)/ 140]
TBW =
* 0.6 x weight (males)
* 0.5 x weight (females)
Sodium
Hypovolemic hypernatremia & causes
↓ Na / ↓↓ water
- Above normal serum osmolality
Causes:
* Osmotic or solute diuresis
* Post-obstructive diuresis
* Vomiting
* Diarrhea or excess laxative use
* High insensible losses
Sodium
Hypovolemic hypernatremia - treatment
- Replace free water deficit (oral water, enteral water flushes, dextrose 5% in water, 0.45% NaCl, addition of sterile water to PN)
- Insulin (hyperglycemia)
- Amino acid dose reduction (solute diuresis)
Sodium
Euvolemic hypernatremia & causes
WNL Na / ↓ water
Water losses exceed sodium losses
Common causes:
* Central diabetes insipidus → impairment of ADH secretion
—- DI also presents with extreme thirst like SIADH; polydipsia
* Nephrogenic DI → kidneys cannot respond to ADH circulating in serum
—- Hypercalcemia, hypokalemia, amphotericin B, cidofovir, foscarnet, demeclocycline, lithium
Sodium
Euvolemic hypernatremia- treatment
- Desmopressin (central diabetes insipidus)
- Remove offending agent, potassium replacement, thiazide diuretics, Na restriction (nephrogenic diabetes insipidus)
Sodium
Hypervolemic hypernatremia
& causes
↑↑ Na / ↑ water
Common causes:
* Hypertonic saline or Na bicarbonate infusions
* Hyperaldosteronism
Sodium
Hypervolemic hypernatremia - treatment
- Loop diuretic
- Hypotonic fluids (Na overload)
- Spironolactone/adrenalectomy (hyperaldosteronism)
What is the role of potassium in the body?
- Critical role in cell metabolism (protein and glycogen synthesis)
- Also maintains resting membrane potential with ratio between ECF and cell
What is the most important component in daily regulation of potassium balance?
Na-K-ATPase pump
impacts plasma potassium concentration
Additional impacts on potassium distribution:
- Insulin and catecholamines;
- exercise,
- extracellular pH,
- cellular breakdown
Symptoms of hypokalemia:
mild, mod, severe
- Mild depletion (3.0-3.5) → asymptomatic
- Lower serum levels → nonspecific sx: generalized weakness, lethargy, constipation
- Severe deficiency/consequences → muscle necrosis, ascending paralysis, arrhythmias, and death
What is hypokalemia often the result of?
Abnormal losses via urine or stool
What are two additional causes of hypokalemia?
- Can develop from transcellular shift of potassium from ECF → cells,
- Inadequate PO intakes
What are potential causes of transcellular shifts of potassium into the cells?
- Metabolic alkalosis
- Increases in insulin and catecholamines (epi, norepi)
Potassium
What are potential causes of extracellular shift
- glucagon
- metabolic acidosis
- aldosterone (allows renal elimination)
Drug-induced hypokalemia - Increased renal potassium loss
Diuretics
* Acetazolamide (glaucoma tx)
* Thiazides (↑ excretion of Na/Cl; Increased reabsorption of calcium)
* Indapamide
* Metolazone (inhibits resorption of sodium and chloride in the proximal convoluted tubule)
* Bumetanide (loop; decreased reabsorption of Ca2+ and Mg2+)
* Furosemide (loop)
* Torsemide (loop)
Fludrocortisone
Hydrocortisone
Drugs associated with magnesium depletion:
* Aminoglycosides (antibiotics)
* Cisplatin (chemotherapy)
* Foscarnet (antiviral)
* Amphotericin B (antifungal)
* Posaconazole (antifungal; used in weakened immune states)
Drug-induced hypokalemia - Excess potassium loss in stool
- Patiromer (binds with potassium in the gut)
- Phenolphthalein (laxative; increased fecal sodium/potassium loss)
- Sodium polystyrene sulfonate (kayexelate, same as patiromer)
- Sorbitol
Drug-induced hypokalemia - Potassium shift from ECF to ICF
Beta-2 adrenergic agonists (respiratory dz: asthma, copd)
* Epinephrine
* Albuterol
* Terbutaline
* Pirbuterol
* Salmeterol
* Isoproterenol
* Ephedrine
* Pseudoephedrine
Theophylline (Bronchodilator)
Caffeine
Verapamil intoxication (calcium channel blocker)
Insulin (all types)
Generalized causes of losses
body systems
- Kidney losses- diuretics, hyperaldosteronism, amphotericin, aminoglycosides
- GI tract losses
- –Diarrhea (10 mEq/L)
- –Emesis / NG losses (up to 50 mEq/L)
- Skin losses – burns, strenuous exercise on hot humid day
- Altered distribution – alkalosis, catecholamine surge, excessive insulin
- Dietary – inadequate intake, large volumes of IV saline, pica
Liquid and slow release potassium supplementation
At what rate of potassium infusion…
1) does a patient require cardiac monitoring
2) should a central line be used, and why?
If infusion >10 mEq/h → continuous cardiac monitoring required
* CVC to avoid phlebitis and burning
Empiric potassium dose in PN for normal renal function and impaired renal function?
- Empiric potassium dose in PN: 1-2 mEq/kg/day
- 10 mEq of K intravenously increases serum K by ~0.1 mEq/L
- Decrease dose by 50% in renal impairment
What type of solutions do you want to avoid in hypokalemia when repleting?
Avoid dextrose solutions; can worsen hypokalemia 2/2 insulin stimulation → ITC shift
What electrolyte can cause refractory hypokalemia?
Hypomagnesemia
Can result in refractory hypokalemia 2/2 accelerated renal potassium loss or impairment of Na-K-ATPase pump activity
Clinical manifestations of hyperkalemia:
- changes in neuromuscular and cardiac function
- Muscle weakness, paralysis
- ECG changes
- Arrhythmias
In hyperkalemia, pts are often asymptomatic until >_ _ _ mEq/L
> 5.5 mEq/L
Etiology of hyperkalemia
- Traumatic blood draw – hemolyzed specimen
- Excessive intake – usually IV administration
- Altered distribution – acidosis, succinylcholine
- Massive cellular breakdown – intravascular hemolysis, burns, crush injuries, tumor lysis syndrome
Impaired renal excretion ** most often occurs in CKD **
* AKI, CKD 4/5
* ACEI, ARBs, K-sparing diuretics, aldosterone antagonists, NSAIDs, trimethoprim, tacrolimus
Meds:
Treatment of hyperkalemia (>6) or changes in ECG:
Stabilize myocardium
Calcium gluconate
Does NOT remove potassium
Meds:
Treatment of hyperkalemia (>6) or changes in ECG:
Shift potassium intracellularly
- Insulin +/- 50% dextrose
- Sodium bicarb
- Albuterol
Meds:
Treatment of hyperkalemia (>6) or changes in ECG:
Remove potassium
- Furosemide
- Sodium polystyrene sulfonate
- Patiromer (not for acute use)
- Sodium zirconium cyclosilicate (not for acute use)
- HD
Where is Magnesium found?
Mostly found in ICF (second most abundant intracellular cation)
Where is Magnesium absorbed?
Distal jejunum and ileum
How is magnesium regulated/excreted?
Regulated by GI tract, kidney, and bone
What are some of magnesium’s functions?
- Enzyme cofactor: glucose metabolism, fatty acid synthesis and breakdown, and DNA and protein metabolism
- Maintenance of Na-K-ATPase pump / cell membrane action potential
- Neuromuscular transmission
- Cardiovascular tone
- Muscle contraction
Concomitant electrolyte abnormalities in hypomagnesemia:
Potassium and calcium
- Both refractory to treatment until magnesium deficit is corrected
How can hypomagnesemia impact insulin and glucose?
- May reduce insulin sensitivity and glucose cellular uptake
- Impair insulin secretion
- Reduce lipoprotein lipase
Etiology of hypomagnesemia:
- Poor PO intake
- Malabsorption or GI losses
- –Small bowel diseases, gastric bypass, alcoholism, laxatives, diarrhea
- Intracellular shift with insulin, refeeding, DKA, MI, hyperthyroidism
- Increased renal excretion
- CRRT
_ _ _ mEq of IV Mg increases serum Mg by _ _ _ mg/dL
8 mEq of Mg IV increases serum Mg by ~0.1 mg/dL
In healthy individuals
Parenteral IV Magnesium:
what is the max rate and why?
- Do not exceed 1 g/hr (8 mEq/h)
→ 50% of dose can be lost in urine - Adverse effects – phlebitis, injection site pain
How much should you reduce magnesium dosing in renal insufficiency?
Reduce empirical dose by 50% in renal impairment to avoid causing hypermagnesemia
What long term medication use may be associated with hypomagnesemia?
Long term PPI use may be associated with hypomagnesemia
- May not correct even with magnesium supplementation
- H2 blockers do not have this effect
Hypermagnesemia
Typically associated with renal dysfunction and Mg intake
Calcium is essential for;
- Normal muscle contraction
- Nerve function
- Blood coagulation
- Bone formation
Metabolically active form of calcium:
Iionized fraction of calcium
- Ionized calcium – most accurate method to assess calcium abnormalities
- Important in critical illness
How is calcium excreted?
Excess calcium is excreted in the urine
Calcium regulation:
* Vitamin D
* PTH
* Calcitonin
* Phosphorous
* pH
* Metabolic alkalosis
- Vitamin D (increases)
- Parathyroid hormone (increases)
- Calcitonin (decreases)
- Phosphorus (decreases ionized calcium level)
- pH (affects albumin binding)
- Metabolic alkalosis (decreases ionized calcium level)
Hypocalcemia occurrences:
Frequently occurs 2/2 hypoalbuminemia
Common in:
* Critically ill patients
* Sepsis
* Rhabdomyolysis
* Massive blood transfusions
How do massive blood transfusions affect calcium levels?
Xfusions 2/2 citrate preservative in blood bank binding with serum calcium
What is a side effect of PO calcium?
Constipation
Calcium chloride may cause:
Tissue necrosis if extravasation occurs
Management of hypocalcemia
- Correct hypomagnesemia if present (reduced parathyroid hormone)
- Hyperphosphatemia may require phos binders prior to calcium repletion to reduce the risk of soft tissue calcification
- Oral vitamin D therapy
- Parenteral calcium therapy
Causes of hypercalcemia:
acute vs chronic
- Acute > hypercalcemia of malignancy
- Chronic > primary hyperparathyroidism
Why does severe hypercalcemia (>14 mg/dL) require immediate treatment?
→ acute renal failure, obtundation, ventricular arrhythmias, coma, death
First step in treating hypercalcemia
Aggressive IV hydration – reverse volume depletion caused by hypercalcemia
Additional steps in treating hypercalcemia
- Calcitonin – rapid onset; tachyphylaxis ~ 48 hours
- HD – life threatening or in CKD
- Bisphosphonates – slower onset (4-10 days), longer duration / maintenance therapy
- Steroids – decreases calcitriol production and reduces intestinal calcium absorption
- Surgery (primary hyperparathyroidism)
Tachyphylaxis: acute, sudden decrease in response to a drug after admin
What medication is controversial in tx of hypercalcemia?
Loop diuretics
- Enhance renal calcium excretion
- Requires vigilant monitoring to avoid further volume depletion
Phosphorous funtions:
- Essential part of nucleic acids, phospholipid membranes and nucleoproteins
- Key role in macronutrient metabolism
- Provides energy-rich bonds in ATP
- Bone and cell membrane composition
- Muscular function – especially myocardium and diaphragm
Primary causes of ITC shifts of phos
CHO and insulin, catecholamines, alkalosis
Release of Phos from cell → ECF:
cellular destruction, and acidosis
Hypophosphatemia symptoms:
Symptoms: neurologic, neuromuscular, cardiopulmonary, hematologic
Etiologies of hypophosphatemia
- Poor PO intake
- Critical illness
- Alcoholism
- Respiratory and metabolic alkalosis
- Poor absorption
- Phosphate binders, vitamin D deficiency, laxatives, diarrhea
- Increased renal excretion
- RRT
- Intracellular shifts
Why are dosing recommendations of phosphorous empirical?
Because serum phosphorous concentrations may not accurately reflect total body stores
Infusion rate shouldn’t exceed _ _ _ mmol/hr
Why?
Infusion rate shouldn’t exceed 7 mmol/hr
Faster infusion rates can cause thrombophlebitis and soft tissue calcium-phosphate deposition
Hyperphosphatemia
Rare, typically associated with renal dysfunction / CKD
Additional causes of hyperphosphatemia
- Endogenous release of phos into ECF from cellular destruction
- Massive trauma
- Cytotoxic agents - esp in tx of lymphomas and leukemias with large tumor burden
- Hypercatabolism
- Hemolysis
- Rhabdomyolysis
- Malignant hyperthermia
- Transcellular shifts of phos from ICF to ECF 2/2 respiratory or metabolic acidosis
Respiratory or Metabolic Acidosis + Phosphorous
Hyperphosphatemia
shifts of phos from ICF to ECF
Respiratory or Metabolic Alkalosis + Phosphorous
Hypophosphatemia
shifts of phos from ECF → cell
Treatment of hyperphosphatemia:
Reduced intake, phosphate binders
Gastric fluid loss replacement
0.45% NaCl (1/2 Normal Saline) + 10-20 mEq KCl/L
Stomach
mEq/L
sodium, chloride, potassium, bicarb
- Na: 60 mEq
- Cl: 130 mEq
- K: 15 mEq
- HCO3: 0 mEq
Duodenum
mEq/L
sodium, chloride, potassium, bicarb
- Na: 140 mEq
- Cl: 80 mEq
- K: 5 mEq
- HCO3: 0 mEq
Pancreas
mEq/L
sodium, chloride, potassium, bicarb
- Na: 140 mEq
- Cl: 75 mEq
- K: 5 mEq
- HCO3: 115 mEq
Bile
mEq/L
sodium, chloride, potassium, bicarb
- Na: 145 mEq
- Cl: 100 mEq
- K: 5 mEq
- HCO3: 35 mEq
Ileum
mEq/L
sodium, chloride, potassium, bicarb
- Na: 140 mEq
- Cl: 104 mEq
- K: 5 mEq
- HCO3: 30 mEq
Colon
mEq/L
sodium, chloride, potassium, bicarb
- Na: 60 mEq
- Cl: 40 mEq
- K: 30 mEq
- HCO3: 0 mEq
Small bowel fluid loss replacement
- Balanced crystalloid (e.g., Ringers Lactate, Plasmalyte)
- Bicarbonate or acetate-based customized fluid
- 0.9% NaCl (Normal Saline)
Rapid infusion of phosphate can result in tetany due to
ASPEN self assessment - PN
an abrupt decrease in serum calcium concentration
Thiazide diuretics
- act solely in the distal tubules
- do not interfere with urinary concentration and the ability of antidiuretic hormone to promote water retention
- use can cause hyponatremia in older patients
