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1

In 0.9% NaCl, what is the concentration of Na & Cl? Why might they have different concentrations in plasma?

 

  • Na = 154 mEq/L
    • although higher than normal plasma Na concentration, it equals the aqueous phase of plasma (phase that is in osmotic equilibrium with the rest of body fluids)
  • Cl = 154 mEq/L
    • higher than normal plasma concentrations because 

 

It is the

2

Describe the composition of the following fluids in terms of sodium, potassium, chloride, lactate, acetate as well as the pH and osmolality

  • 0.9% NS
  • Lactated Ringer's 
  • 5% Albumin
  • Plasma-lyte

3

  • Sodium concentration in LR is ____ than that of blood. and is ___ mEq/L.
  • LR also contains ______, _______, and ______.
  • lactate = a _____ that is metabolized by the liver into _____.

  • Sodium concentration in LR is lower than that of blood. and is 130 mEq/L.
  • LR also contains K, Ca, and lactate.
  • lactate = a buffer that is metabolized by the liver into bicarbonate.

4

The concentration of sodium in balanced salt solutions (eg, Plasma-Lyte, Normosol) is ______ to that of blood.

  • For example, Plasma-Lyte's sodium concentration is ______ mEq/L. Plasma-Lyte also contains ______ and ______, as well as ______, a buffer that is converted to bicarbonate independent of the ______

The concentration of sodium in balanced salt solutions (eg, Plasma-Lyte, Normosol) is equivalent to that of blood.

  • For example, Plasma-Lyte's sodium concentration is 140 mEq/L. Plasma-Lyte also contains potassium and magnesium, as well as acetate, a buffer that is converted to bicarbonate independent of the liver

5

How does hyperchloremic metabolic acidosis occur with fluid therapy? How do you avoid this?

Large volume 0.9% sodium chloride resuscitation generates a hyperchloremic acidosis and renal vasoconstriction, both of which contribute to unpredictable water retention and electrolyte derangement

  • acidosis can be avoided with the use of a solution containing less chloride than 0.9% sodium chloride, such as LR (subphysiologic Na concentration --> hypoNa if in excess) or Plasma-Lyte (expensive).

6

Give 2 reasons why post-op hypoNa occurs in regards to fluid therapy?

ADH release due to surgical stress

  • During and after surgery, surgical stress results in the release of antidiuretic hormone. 
  • In normovolemic postsurgical patients, the administration of additional sodium (ie, 0.9% sodium chloride) can result in a paradoxical fall in sodium concentration because the sodium contained in these solutions is excreted in the urine, resulting in net retention of electrolyte-free water.
  • hyponatremia is commonly observed in postsurgical patients.

Administration of other crystalloid fluids

  • It can also occur if too much LR or a balanced salt solution is administered

 

 

7

Why might there be hypokalemia post-op?

Aldosterone is released in response to hypotension or hypovolemia

  • It acts in the kidney to retain sodium and waste potassium. The degree of this hormonal response for a particular patient or type of surgery is highly variable, as is the degree of associated electrolyte derangement.
  • Although intravascular volume is restored, potassium levels are unpredictably affected. This process is compounded by the administration of supernormal sodium doses with intravenous fluid therapy during and after surgery

8

What are the effects of transfusions on postoperative abnormalities and why?

  • The effects of transfusion on the development of postoperative electrolyte abnormalities depend upon the amount given, the clinical status of the patient, the temperature of the blood when it is transfused, and the duration of blood storage.
  • Hyperkalemia
    • As stored red blood cells age, they lyse, leaking potassium into the extracellular fluid. In this way, older banked blood tends to contain more extracellular potassium.
  • When citrate, a red blood cell additive, is administered, it may result in the chelation of serum electrolytes, resulting in hypokalemia, hypocalcemia, or hypomagnesemia.
  • Lactic acid
    • Banked red blood cells exist in an anaerobic environment, leading to the production and accumulation of lactic acid.
    • The transfusion of red blood cells provides an acid load of approximately 15 mEq per unit, the sum of the citric acid anticoagulant and red blood cell lactic acid production.
    • In the normal individual, the acid load of banked blood can be adequately accommodated by metabolic and respiratory mechanisms. However, when red blood cells are transfused rapidly or in a large volume, profound electrolyte derangement is often observed in conjunction with acid-base disorder. This is further exacerbated when the product is not warm.
  • Autologous blood transfusion: To a lesser extent, this also applies to autologous blood transfusion, which may be used during resuscitation in the trauma bay, intensive care unit, or operating room. Rapidly lost blood is collected, washed, and returned to the patient promptly. The washing process reduces the potassium and lactate content in the sample

9

What are sources of post-op fluid losses?

Surgical diseases that result in abnormal bodily fluid losses can result in electrolyte disturbances.

  • Third-spacing fluid loss
    • Following surgery, approximately 2/3 two thirds of IV fluid extravasates into the extravascular space. This process is informally known as "third
      spacing" into the soft tissues, peritoneal cavity, or pleural cavity. As the patient recovers, the capillary
      leak resolves, and the fluid returns to the vascular space. Electrolyte deficits (hypoK, hypoMg, hypoCa, hypoP04) tend to follow this process in an unpredictable manner.
  • Gastrointestinal loss
    • Postoperative ileus or intestinal obstruction is commonly observed in surgical patients and may lead to vomiting that requires nasogastric drainage. The loss of a large volume of gastric fluid, which contains HCl acid, can lead to intravascular volume contraction, metabolic alkalosis, hypoCl, and hypoK. The loss of fluid volume stimulates aldosterone production, which promotes water retention and K wasting in the kidney. To produce more acid, the stomach pumps additional HCO3 into the serum. This excess HCO3 is excreted in the urine as an unabsorbed anion that obligates excretion of potassium to maintain electrolyte neutrality.
    • The pancreas generates a bicarbonate-rich fluid. When pancreatic fluid is lost externally, as with a
      pancreatico-cutaneous fistula following pancreatic injury (accidental or surgical), it generates a
      metabolic acidosis as well as secondary derangements in potassium
    • High-volume diarrhea, ostomy output, or enterocutaneous fistula drainage leads to unpredictable electrolyte derangements, including hypokalemia and hypomagnesemia.
  • Urinary loss
    • As the patient recovers from surgery, fluid returns to the vascular space and is evacuated by the kidneys. The mobilization of third-space fluid results in large-volume auto-diuresis, which is associated with potassium and magnesium wasting. Although there is no firm relationship that describes the volume of urine and expected level of electrolyte derangement, it is the author's experience that urinary outputs that exceed 30mL/kg/day during auto-diuresis are typically associated with deficits of potassium, magnesium, or phosphorus.
    • When auto-diuresis is associated with recovering renal dysfunction, such as that which resulted from an obstructing kidney stone or hypovolemia-induced acute kidney injury following hemorrhage, this electrolyte wasting can be exaggerated. 
    • Brain injury (accidental or surgical) can lead to diabetes insipidus (DI), syndrome of inappropriate ADH (SIADH), and cerebral salt wasting, which are associated with electrolyte derangements. 
    • Similarly, hyponatremia from disordered ADH production may be observed in liver failure patients awaiting transplantation. 
    • Following renal transplantation, allograft recovery often includes a phase of uncontrolled diuresis during which hypokalemia and hypomagnesemia commonly occur.
      • Similarly, when a native kidney obstruction is relieved (eg, laser lithotripsy for an obstructing ureteral stone), diuresis and electrolyte wasting may result.

10

Composition of GI losses per day [Review]

11

Brain injury and Na disturbance - Why?

Hyponatremia is more commonly observed in patients with traumatic or surgical brain trauma. In a study of neurosurgery patients, hyponatremia was observed in 10 and 50 percent of
patients, depending on the underlying condition
. Accidental and surgical trauma to the brain more commonly result in the production of ADH, which leads to inappropriate fluid retention and dilutional hyponatremia.

12

Electrolyte abnormalities due to tissue injury/ischemia and reperfusion. Describe situations where this may occur and what the resulting abnormalities would be

 

Mechanical tissue destruction and ischemia induced
tissue injury can cause tissue necrosis and cell lysis.

  • The resulting cell injury may lead to the release of intracellular potassium into the bloodstream, causing profound hyperkalemia. With muscle injury, myoglobin is released into the circulation and can be nephrotoxic, further impairing potassium excretion. Phosphate released from cells leads to hyperphosphatemia and may also lead to calcium scavenging and hypocalcemia. When associated with significant muscle injury, these electrolyte disturbances are referred to collectively as part of a syndrome termed rhabdomyolysis.

Surgical trauma (ie, planned muscle division) results in muscle injury.

  • Surgical patients can also experience muscle compression injury if improperly positioned in the operating room or if subjected to a prolonged period of immobility. Patient positioning may also promote muscle ischemia by interrupting anatomic blood flow (eg, stirrups) or by compression (eg, pressure from security belts when patient is rotated into a lateral position). Generally, positions maintained for under two hours are unlikely to cause significant injury. However, patient factors, particularly obesity, may contribute to increased pressure, thereby leading to unanticipated muscle injury during shorter procedures, which has been demonstrated in a number of surgical populations

Ablative or embolic procedures, such as for liver tumors, also result in acute tissue ischemia.

  • With tumor ablation, rarely, tumor lysis syndrome may be observed. Tumor lysis syndrome is well described in case reports in patients who undergo transarterial chemoembolization of large liver tumors, although "large" is not well defined. In these cases, hyperkalemia, hyperphosphatemia, and hypocalcemia may be observed.

13

Refeeding syndrome - what electrolyte deficiencies are associated with this?

 

  • As malnourished patients recover from surgery and resume dietary intake, they are at risk for refeeding syndrome, a collection of electrolyte derangements associated with a massive intracellular shift of electrolytes. Hypophosphatemia is commonly observed as extracellular phosphate is rapidly taken into the cells to generate ATP.
  • Hypokalemia and hypocalcemia are also commonly observed. Malnourished patients should be closely monitored for clinical and laboratory evidence of refeeding syndrome when their nutritional intake is resumed.

14

Acid-bace imbalances in postop setting: Describe scenarios to the following disorders and explain how they affect electrolytes?

  • metabolic acidosis
  • metabolic alkalosis
  • respiratory acidosis
  • respiratory alkalosis

 

Acid-bace imbalances in postop setting: Describe scenarios to the following disorders and explain how they affect electrolytes?

  • metabolic acidosis
    • large-volume blood loss and under-resuscitation. The commonly observed scenario is the patient with hemorrhagic shock from large surgical blood
      loss, which leads to reduced end-organ perfusion and lactic acidosis. This generates a "gap"
      acidosis. Conversely, a patient who undergoes a large volume of 0.9% sodium chloride infusion. may experience hyperchloremic acidosis associated with the large chloride load. This generates
      a "non-gap" acidosis. Both of these types of acidosis lead to hyperkalemia.
  • metabolic alkalosis
    • This commonly results from volume contraction combined with gastric fluid loss in the postoperative patient. The classic scenario is the patient with a bowel obstruction who undergoes laparotomy, during/after which aggressive third-spacing of fluid into the peritoneal cavity and intestinal lumen leads to volume contraction. Emesis and nasogastric tube
      decompression lead to further large-volume loss of HCl. As the stomach produces more HCl to replace this loss, it delivers HCO3 into the serum. In this
      manner, volume contraction and HCl loss generate a hypochloremic hypokalemic metabolic
      alkalosis
      . There is a very small amount of potassium in gastric fluid that is directly lost during
      vomiting and gastric tube decompression as well.
  • respiratory acidosis
    • The typical scenario is the postoperative patient who receives excessive narcotic pain medication, which results in narcotic-induced respiratory depression, hypoventilation, hypercapnia, and subsequent respiratory acidosis and hyperkalemia.
  • respiratory alkalosis
    • may develop following thoracic surgery or upper abdominal surgery in the patient who experiences severe incisional pain. To limit the pain, the patient takes quick shallow breaths, which leads to hypocarbia, respiratory alkalosis, and hypokalemia.

15

Explain the shifts in intra and extracellular K with the changes in pH.

In the acute setting, mild changes in serum pH are managed at the cellular level through Na-H exchange, Na-HCO cotransport, Na-organic anion cotransport, and Na-K-ATPase on cell membranes. The shift of potassium into cells is due to altered Na-K-ATPase activity, which is influenced by a variety of factors that are related to the stress response to surgery, including aldosterone secretion and adrenergic stimulation

In states of acid production (eg, lactic acidosis during hemorrhagic shock), we observe a rise in serum acid, a fall in serum pH, and hyperkalemia. Conversely, a drop in serum acid leads to hypokalemia, with H shifting out of cells and K shifting into cells. It is important to note that lactic acidosis does not directly cause a shift of potassium out of the cells, but the associated tissue ischemia and acute kidney injury often results in hyperkalemia

16

List some medical therapies in surgical patients that can cause electrolyte disturbances

 

  • Calcineurin inhibitors (eg, for solid-organ transplant recipients) cause hyperkalemia
  • Potassium-wasting diuretics (eg, for heart failure patients) cause hypokalemia.
  • Laxatives and enemas (eg, for patients with postoperative constipation) result in hypokalemia and hyponatremia.
  • Glucocorticoids (eg, treatment of Crohn colitis) result in hypokalemia.
  • Heated intraperitoneal chemotherapy (HIPEC; eg, for peritoneal carcinomatosis) is associated with hyponatremia 
  • Succinylcholine administration during surgery can lead to hyperkalemia, particularly in patients with renal failure or crush injury, in whom hyperkalemia may persist and can be life threatening.

17

Which patients should have daily electrolyte monitoring post-op

  • Continuous intravenous fluid administration
  • Blood transfusion
  • Fluid resuscitation (eg, fluid boluses for hypovolemia)
  • Major organ dysfunction (cardiac, renal, hepatic)
  • Head injury (eg, traumatic brain injury, neurosurgery)
  • Continuous bladder irrigation
  • Abnormal bodily fluid losses (eg, large-volume pancreatic fistula, high-output ostomy, gastric tube
  • evacuation therapy)
  • Large surface area wounds (eg, burn)
  • Rhabdomyolysis
  • Ileus
  • Parenteral nutrition
  • Pancreatitis

18

How do you treat hyponatremia?

How fast should you raise sodium?

What is the greatest risk for osmotic demyelination syndrome?

  • For most cases of mild hyponatremia following surgery, use of intravenous (IV) fluid that delivers more sodium (eg, 0.9% sodium chloride instead of 0.45% sodium chloride or Lactated Ringer's [LR] solution) is effective in preventing complications of hyponatremia.
  • As with the treatment of hyponatremia in medical patients, the serum sodium should be raised by no more than 8 mEq/L in a 24 hour period to avoid osmotic demyelination syndrome (ODS).
    • hyponatremia may be poorly tolerated in patients with head trauma or following neurosurgery, and correction by 4 to 6 mEq/L within a few hours may be necessary.
  • The risk of ODS is greatest in patients with a serum sodium of 120 mEq/L or less whose serum sodium has been low for 48 hours

19

Why might enteral replacements be poorly tolerated in postop patients?

  • Potassium
  • Magnesium
  • Calcium
  • Phosphate

  • Potassium – Nausea, vomiting, abdominal pain.
  • Magnesium – Laxative-like effects, poor bioavailability.
  • Calcium – Tastes like chalk, constipation, nausea.
  • Phosphate – Typically a mix of sodium phosphate and potassium phosphate; nausea, vomiting, diarrhea, abdominal pain.

20

  • How much should enteral potassium raise the serum level by? e.g. 20 mEq of KCl
  • How long should you wait before re-checking serum K levels following replacement?
  • Are there differences between enteric or IV replacement K?

  • 0.1 to 0.2 mEq for 20 mEq of KCL
  • at least 1 hour
  • Same absorption if normal intestinal function

21

Mg replacement

  • HypoMg must be corrected to faciliate ______ and _____ normalization
  • Why is oral Mg replacement not preferred in surgical patients?
  • How much do you need to raise Magnesium level by 0.4 mg/dL?
  • What are the replacements with mild-to-moderate vs. moderate-to-severe?
  • When should you dose reduce and by how much?
  • How long should you wait before re-checking Mg levels?

  • Hypomagnesemia needs to be corrected to facilitate normalization of hypokalemia and hypocalcemia.
  • Due to the laxative effect of oral magnesium and its variable bioavailability, oral magnesium is not routinely used to replace magnesium deficiencies in surgical patients.
  • For each 0.4 mg/dL below the target serum magnesium level, give magnesium sulfate 2 g (8 mmol) IV.
  • For mild-to-moderate hypomagnesemia (level is within 25 percent of the normal value), an initial dose of 2 to 4 g (8 to 16 mmol) IV is typically used. For moderate-to-severe hypomagnesemia (level below 75 percent of normal level), a total dose of 4 to 8 g (16 to 32 mmol) IV may be needed.
  • The dose should be reduced by 50 percent in patients with significant renal dysfunction
  • Due to gradual redistribution of magnesium to tissue following intravenous administration, levels are not repeated until 8 to 12 hours or more after the dose.

22

Ca replacement

  • How much calcium replacement do you need in order to raise calcium by 0.15 mg/dL?
  • Which calcium replacement is preferred and why?
  • How do you treat mild-to-moderate vs. moderate-to-severe hypocalcemia?
  • How soon do you repeat calcium levels?
  • When would you use oral calcium?

  • For each 0.15 mg/dL below the targeted ionized calcium level, administer 1 g (2.3 mmol) IV of calcium gluconate. We prefer measurement of ionized (ie, fraction unbound to plasma proteins) rather than total calcium (bound plus unbound) because it is a better indicator of functional calcium capacity in postoperative patients.
  • In most cases, acute hypocalcemia is treated with intravenous therapy, and calcium gluconate is the preferred form for nonemergency replacement. Concentrated calcium solutions (especially calcium chloride) are extremely caustic to tissues and should be administered in a central vein to avoid tissue extravasation.
  • For mild-to-moderate hypocalcemia (level is within 25 percent of the normal value), 1 or 2 grams (2.3 or 4.6 mmol) of IV calcium gluconate is typically given. The dose may be repeated after six hours based upon ionized calcium level. 
  • For severe (level below 75 percent of normal) or symptomatic hypocalcemia, calcium chloride, which provides three times the amount of elemental calcium per gram (as compared with calcium gluconate), is preferred. An initial dose of 1 g IV calcium chloride (6.8 mmol) or calcium gluconate 3 g (6.9 mmol) is given initially for symptomatic hypocalcemia and repeated as necessary. If greater than 4 g (9.2 mmol) of calcium gluconate is administered, consider repeating the serum ionized calcium level before administering further replacement therapy. 
  • Uncommonly, oral calcium is used in conjunction with intravenous calcium, such as in patients with hypocalcemia following parathyroidectomy; in such a case, standing oral calcium doses are titrated up slowly with as-needed doses of intravenous calcium until the serum calcium normalizes. These patients will often remain on calcium replacement therapy for a prolonged period of time, hence the oral route for therapy.

23

Phosphate replacement

  • How much phosphate IV should be given to raise 0.4 mg/dL of phosphate?
  • Which phosphate replacements are preferred?
  • How is mild-to-moderate hypophastemia treated?
  • How is symptomatic or severe hypophosphatemia treated?
  • Phosphate homeostasis is dependent on which organ?
  • When should you reduce phosphate replacement and by how much?
  • How should you deal with monitoring for serum PO4?
  • How do you adjust PO4 replacement when giving oral PO4 replacement? What do you need to be concerned about?

  • For each 0.4 mg/dL below normal, give 15 mmol of phosphate IV.
  • Sodium phosphate is preferred for intravenous phosphate administration. Potassium phosphate is an alternative, but it delivers 22 mEq potassium in a fixed ratio with each 15 mmol phosphate dose.
  • For mild-to-moderate hypophosphatemia (level within 25 percent of normal), 15 mmol of sodium phosphate IV is typically given.
  • In symptomatic or severe hypophosphatemia (level below 75 percent of normal), an initial dose of 30 mmol IV sodium phosphate is given.
  • Phosphate homeostasis is dependent upon kidney function
  • For patients with significant renal impairment (creatinine clearance [CrCl] <30 mL/minute), the phosphate dose should be reduced by 50 percent or more.
  • For moderate-to-severe derangement or during monitoring for refeeding syndrome, the serum phosphate level should be repeated two to four hours after the intravenous dose is completed. Individuals at risk for developing severe hypophosphatemia and refeeding syndrome (eg, malnourished, anorectic, alcoholic) require very close monitoring (ie, check serum phosphate level every 6 to 12 hours).
  • For patients with normal gut function, oral phosphate replacement (typically a mix of potassium phosphate-sodium phosphate) dose should be approximately tripled to equal the intravenous dose. As an example, 15 mmol intravenous sodium phosphate may be converted to oral therapy as 16 mmol oral potassium phosphate-sodium phosphate administered for three doses. Bioavailability of enteral phosphate supplementation is variable, and it can cause diarrhea. Commonly used enteral phosphate supplements include 250 mg (equivalent to 8 mmol) of phosphate per tablet. Weight-based dosing for enteral phosphate therapy is reviewed elsewhere.

24

K replacement rates

  • What rate is IV KCl given via peripheral IV? What are worries of quick infusion?
  • What rate is IV KCl give via central IV?
  • How much KCl can be given enterally? what's the concerns with large loads of administration?

 

K replacement

  • peripheral IV 
    • Potassium chloride may be given through a peripheral intravenous catheter at a rate of 10 to 20 mEq/hour in a low concentration (ie, 10 mEq per 100 mL) to minimize the caustic effects of potassium infusion on peripheral veins (ie, chemical thrombophlebitis) and to avoid transient severe hyperkalemia that can have serious consequences.
  • Central IV
    • In many institutions, central venous potassium infusion is limited to 20 mEq/hour to avoid inadvertent hyperkalemia. In emergency situations, 40 mEq/hour may be given centrally or peripherally (eg, through multiple lines). Potassium chloride infusions are available premixed in a minimum of 50 mL of nondextrose fluid.
  • Enteral
    • Conversely, as much as 80 mEq of liquid potassium chloride can be administered into the stomach at once, and it will be rapidly absorbed in most patients except those with abnormal gut function.
    • Caution is advised as this large quantity of potassium may induce vomiting and is often poorly tolerated. Instead, divided enteral doses of 20 mEq may be given several hours apart and are often better tolerated.

 

Ca replacement

  • In mild-to-moderate hypocalcemia, calcium replacement is typically given as 1 or 2 g (2.3 or 4.6 mmol) of IV calcium gluconate mixed in 50 mL of fluid and infused over 30 or 60 minutes through a peripheral or central venous catheter. The dose may be repeated as needed based on ionized serum calcium level.
  • In severe symptomatic hypocalcemia, 1 g (6.8 mmol) of calcium chloride or 3 g (6.9 mmol) of calcium gluconate diluted in 50 mL of fluid can be infused over 10 minutes to rapidly control symptoms; this dose is repeated as necessary.
  • Avoid rapid intravenous bolus of calcium, which can result in acute respiratory depression and asystole. Concentrated calcium solutions (especially calcium chloride) are extremely caustic to tissues and should be administered in a central vein to avoid extravasation.
  • Effective replacement of calcium in severe or symptomatic hypocalcemia may require administration of calcium as a continuous infusion following the initial IV dose(s).

Phosphate replacement

  • Intravenous phosphate (in the form of sodium phosphate or potassium phosphate) is typically diluted in 250 mL of fluid and infused at a rate of 4 or 5 mmol/hour through a central or peripheral venous catheter. As an example, 30 mmol sodium phosphate may be administered  intravenously over six hours.
  • Slow infusion of phosphate is preferred to decrease the risk of injury due to calcium-phosphate precipitate, which can result in acute kidney failure.
  • In patients with severe hypophosphatemia and normal renal function, a maximum rate of 7.5 mmol/hour has been used.
  • Oral phosphate replacement is typically given in three or four divided doses through the day. Consider repeating the phosphate level after administering 45 or 60 mmol of oral phosphate (eg, with morning labs). Note that oral phosphate supplements include variable amounts of sodium and potassium. One commonly available phosphate tablet preparation (K-Phos Neutral) delivers 13 mEq sodium and 1.1 mEq potassium in a fixed ratio with 8 mmol of phosphate.

 

25

Mg replacement

 

Mg replacement

  • Magnesium sulfate is typically used for intravenous replacement therapy; 2 g (8 mmol) is mixed in 50 to 100 mL of fluid and infused over 30 to 60 minutes through a peripheral or central venous catheter, except in emergencies. In emergencies (eg, severe or symptomatic hypomagnesemia), 2 to 4 g (8 to 16 mmol) of magnesium sulfate diluted in 10 to 50 mL of sodium chloride can be given intravenously over 2 to 15 minutes.
  • For patients with significant renal impairment (nonemergency), a slower infusion rate (ie, .1 g/hour) has also been suggested to improve efficiency of replacement.

26

Ca replacement

  • How slow should you infuse for mild-to-moderate hypoCa?
  • How fast can you infuse for severe symptomatic hypoCa?
  • Why should you avoid rapid IV boluses of Ca?
  • What's the worry with concentrated Ca solutions?

Ca replacement

  • In mild-to-moderate hypocalcemia, calcium replacement is typically given as 1 or 2 g (2.3 or 4.6 mmol) of IV calcium gluconate mixed in 50 mL of fluid and infused over 30 or 60 minutes through a peripheral or central venous catheter. The dose may be repeated as needed based on ionized serum calcium level.
  • In severe symptomatic hypocalcemia, 1 g (6.8 mmol) of calcium chloride or 3 g (6.9 mmol) of calcium gluconate diluted in 50 mL of fluid can be infused over 10 minutes to rapidly control symptoms; this dose is repeated as necessary.
  • Avoid rapid intravenous bolus of calcium, which can result in acute respiratory depression and asystole. Concentrated calcium solutions (especially calcium chloride) are extremely caustic to tissues and should be administered in a central vein to avoid extravasation.
  • Effective replacement of calcium in severe or symptomatic hypocalcemia may require administration of calcium as a continuous infusion following the initial IV dose(s).

27

PO4 replacement

  • How quickly can you infuse sodium or potassium phosphate?
  • Why is slow infusion preferred?
  • Maximum rate of replacement in severe hypoPO4?

Phosphate replacement

  • Intravenous phosphate (in the form of sodium phosphate or potassium phosphate) is typically diluted in 250 mL of fluid and infused at a rate of 4 or 5 mmol/hour through a central or peripheral venous catheter. As an example, 30 mmol sodium phosphate may be administered  intravenously over six hours.
  • Slow infusion of phosphate is preferred to decrease the risk of injury due to calcium-phosphate precipitate, which can result in acute kidney failure.
  • In patients with severe hypophosphatemia and normal renal function, a maximum rate of 7.5 mmol/hour has been used.
  • Oral phosphate replacement is typically given in three or four divided doses through the day. Consider repeating the phosphate level after administering 45 or 60 mmol of oral phosphate (eg, with morning labs). Note that oral phosphate supplements include variable amounts of sodium and potassium. One commonly available phosphate tablet preparation (K-Phos Neutral) delivers 13 mEq sodium and 1.1 mEq potassium in a fixed ratio with 8 mmol of phosphate.