Flluid and Elect

PLASMA OSMOLALITY AND TONICITY

The osmolality of the plasma (Posm) – sum of the osmolalities of the individual solutes in the plasma.

Most of the plasma osmoles are sodium salts, with lesser contributions from other ions, glucose, and urea. Under normal circumstances, the osmotic effect of the plasma ions can usually be estimated from two times the plasma sodium concentration.

plasma tonicity – refers to those solutes that affect the transcellular distribution of

water, which is normally represented by sodium salts and glucose but not urea. Under steady-state conditions, urea is an ineffective osmole, and therefore does not contribute to plasma tonicity.

fluids

Electrolyte Solutions forParenteral Extracellular fluid

– na142 cl103 k4 hco3-27 ca5 mg3 mosm280–310 Lactated Ringer's

– Na130 cl109 k4 hco3-28 ca3 mosm 273 0.9% Sodium chloride

– na154cl154 mosm   308 D50.45% Sodium chloride

– na 77 cl77   mosm 407 D5 W

      mosm 253 50 gr of glucose 3% Sodium chloride

– Na513 cl513  mosm  1026

fluids

The type of fluid administered depends on the patient's volume status and the type of concentration or compositional abnormality present.

Both lactated Ringer's and normal saline are considered isotonic and are useful in replacing gastrointestinal losses and extracellular volume deficits. Lactated Ringer's is slightly hypotonic in that it contains 130 mEq of sodium, which is balanced by 109 mEq of chloride and 28 mEq of lactate. Lactate is used rather than bicarbonate because it is more stable in intravenous fluids during storage. It is converted into bicarbonate in the liver following infusion, even in the face of hemorrhagic shock.

Recent evidence has suggested that resuscitation using lactated Ringer's may be deleterious because it activates the inflammatory response and induces apoptosis. The component that has been implicated is the D isomer of lactate, which unlike the D isomer is not a normal intermediary in mammalian metabolism. Traditionally, solutions contain a 50:50 mixture of the D and D isomer. In vitro studies show that only the D isomer does not activate neutrophils. 20

fluids

Sodium chloride is mildly hypertonic, containing 154 mEq of sodium that is balanced by 154 mEq of chloride. The high chloride concentration imposes a significant chloride load upon the kidneys and may lead to a hyperchloremic metabolic acidosis. It is an ideal solution, however, for correcting volume deficits associated with hyponatremia, hypochloremia, and metabolic alkalosis.

The less concentrated sodium solutions, such as 0.45% sodium chloride, are useful to replace ongoing gastrointestinal losses as well as for maintenance fluid therapy in the postoperative period. This solution provides sufficient free water for insensible losses and enough sodium to aid the kidneys in adjustment of serum sodium levels.

The addition of 5% dextrose (50 g of dextrose per liter) supplies 200 kcal/L, and it is always added to solutions containing less than 0.45% sodium chloride to maintain osmolality and thus prevent lysis of red blood cells that may occur with rapid infusion of hypotonic fluids.

The addition of potassium is useful once adequate renal function and urine output are established.

alternative solutions

Hypertonic saline solutions (3.5% and 5%) are used for correction of severe sodium deficits.

Hypertonic saline (7.5%) has been used as a treatment modality in patients with closed head injuries. It has been shown to increase cerebral perfusion and decrease intracranial pressure, thus decreasing brain edema.

Small-volume hypertonic saline, compared to large-volume isotonic saline, has also been shown to be an effective volume expander in models of hemorrhagic shock.

crystalloids

However, there also have been concerns of increased bleeding, as hypertonic saline is an arteriolar vasodilator.

Yet hypertonic saline may be no better than standard-of-care isotonic saline. however, patients with shock and a concomitant closed head injury did demonstrate benefit.

anti-inflammatory and immunomodulatory properties.

Colloids

Due to their molecular weight, they are confined to the intravascular space and their infusion results in more efficient plasma volume expansion. However, under conditions of severe hemorrhagic shock, capillary membrane permeability increases, permitting colloids to enter the interstitial space, which can worsen edema and impair tissue oxygenation. The theory that these high molecular weight agents "plug" capillary leaks that occur during neutrophil-mediated organ injury has not been established.

There are four major types of colloids available—albumin, dextrans, hetastarch, and gelatin.

Colloid solutions with smaller size particles and lower molecular weights exert a greater oncotic effect, but are retained within the circulation for a shorter period of time than larger and higher molecular weight colloids.

Albumin

(molecular weight 70,000) from pooled human plasma, then heat sterilized. 5% (osmolality 300 mOsm/L) or 25% (osmolality

1500 mOsm/L) solution. allergic reactions. renal failure and impair pulmonary function when

used for resuscitation of hemorrhagic shock.

Dextrans

glucose polymers produced by bacteria grown on sucrose media 40,000 (dextran 40) or 70,000 (dextran 70)

molecular-weight solutions. They lead to initial volume expansion due to their

osmotic effect, but are associated with alterations in blood viscosity.

Thus dextrans are used primarily to lower blood viscosity rather than as volume expanders.

Hydroxyethyl starch

Hetastarches are produced by the hydrolysis of insoluble amylopectin, followed by a varying number of substitutions of hydroxyl groups for carbon groups on glucose molecules.

The molecular weights can range from 1000 to 3,000,000. Hemostatic derangements have been related to decreases in

von Willebrand factor and factor VIII:c, and its use has been associated with postoperative bleeding in cardiac and neurosurgery patients.

Hetastarch also can induce renal dysfunction in patients with septic shock and in recipients of kidneys procured from brain-dead donors.

associated coagulopathy and hyperchloremic acidosis (due to its high chloride content).

Hextend

is a modified, balanced, high molecular weight hydroxyethyl starch that is suspended in a lactate-buffered solution, rather than in saline.

Hextend to a similar 6% hydroxyethyl starch in patients undergoing major abdominal surgery demonstrated no adverse effects on coagulation with Hextend other than the known effects of hemodilution.

Hextend has not been tested in massive resuscitation, and not all clinical studies show consistent results.

Gelatins

bovine collagen. The two major types are

– urea-linked gelatin and s– uccinylated gelatin (modified fluid gelatin,

Gelofusine).

Concentration Changes

Changes in serum sodium are inversely proportional to TBW. Therefore, abnormalities in TBW are reflected by abnormalities in serum sodium.

Signs and symptoms of hyponatremia are dependent upon the degree of hyponatremia and the rapidity with which it occurred. Clinical manifestations are primarily central nervous system in etiology and are related to cellular water intoxication and associated increases in intracranial pressure.

Hyponatremia

excess of extracellular water relative to sodium

There r 2 major pts for the evaluation of hyponat– plasma osmolarity ,excess of solute relative to

free water– Extracellular volumesodium depletion or dilution.

excess of solute relative to free water

untreated hyperglycemia or mannitol administration.

Glucose exerts an osmotic force in the extracellular compartment, causing a shift of water from the intracellular to the extracellular space and subsequent dilutional hyponatremia. Hyponatremia can therefore be seen when the effective osmotic pressure of the extracellular compartment is normal or even high. When evaluating hyponatremia in the presence of hyperglycemia, the corrected sodium concentration should be calculated: 1.6 na for each 100 hgt

Lastly, extreme elevations in plasma lipids and proteins can cause pseudohyponatremia, since there is no true decrease in extracellular sodium relative to water.

Dilutional hyponatremia

– excess extracellular water and therefore a high extracellular volume status. intentional (excessive oral water intake) Failure of systems iatrogenic (intravenous) excess free water administration Postoperative patients ,increased secretion of antidiuretic hormone,

which increases reabsorption of free water from the kidneys with subsequent volume expansion and hyponatremia.

– This is usually self-limiting in that both hyponatremia and volume expansion decrease antidiuretic hormone secretion.

Drugs(elderly++++)– antipsychotics – tricyclic antidepressants – angiotensin-converting enzyme inhibitors.

Physical signs of volume overload are usually absent and laboratory evaluation reveals hemodilution.

Depletional causes

decreased intake – low-sodium diet– enteral feeds that are typically low in sodium,

increased loss of sodium-containing fluids. – gastrointestinal losses (vomiting, prolonged nasogastric

suctioning, or diarrhea)– renal losses (diuretics or primary renal disease).

Depletional hyponatremia is often accompanied by extracellular volume deficit.

differentiate the etiology

First, exclude hyperosmolar causes (hyperglycemia or mannitol) and pseudohyponatremia.

Next, consider depletional versus dilutional causes of hyponatremia. Depletional causes are usually associated with dehydration.

– extrarenal as from gastrointestinal losses, urine sodium levels are usually low (<20 mEq/L),

– renal causes of sodium loss, urine sodium levels are usually high (>20 mEq/L).

Dilutional causes of hyponatremia are usually associated with a high effective circulating volume.

A normal volume status in the case of hyponatremia should prompt an evaluation for a syndrome of inappropriate secretion of antidiuretic hormone.

Clinical Manifestations

Central nervous system– Headache, confusion, hyper- or hypoactive deep tendon reflexes, seizures,

coma, increased intracranial pressure MusculoskeletalWeakness,

– fatigue, muscle cramps/twitching GastrointestinalAnorexia

– nausea, vomiting, watery diarrhea Cardiovascular

– Hypertension – bradycardia if significant increases in intracranial pressure

Tissue– Lacrimation, – Salivation

RenalOliguria

The cerebral adaptation permits patients with chronic hyponatremia to appear to be asymptomatic despite a plasma sodium concentration that is persistently as low as 115 to 120 meq/L.

treatment

Most cases of hyponatremia can be treated by free water restriction and, if severe, the administration of sodium. In patients with normal renal function, symptomatic hyponatremia does not occur until the serum sodium level is greater than or equal to 120 mEq/L.

If neurologic symptoms are present,– then 3% normal saline should be used to increase the sodium by no more

than 1 mEq/L per hour until the serum sodium level reaches 130 mEq/L or neurologic symptoms are improved.

asymptomatic hyponatremia should – increase the sodium level by no more than 0.5 mEq/L to a maximum

increase of 12 mEq/L per day, and even slower in chronic hyponatremia. The rapid correction of hyponatremia can lead to pontine myelinolysis,

– with seizures, weakness/paresis, akinetic movements, and unresponsiveness, and may result in permanent brain damage and death.

– Magnetic resonance imaging (MRI) may assist in the diagnosis.

Basic pts

Hgt and correction of na by 2.6 increase for each 100 above 100 hgt Replacement fluids

– 1L nss 154 meq na– 1amp nacl 68 meq na– 1L 3%nacl 513 meq na

Correction – 1meq/hr if sym– 0.5meq/hr if assympt– Max of 12 meq/day

Tbw= 0.5 or 0.6 * tbw and remember to subtract 0.1 if obese Tna deficit=tbw*(135-calc) Feeding status

Basic pts2

Total na deficit/replacement fluid= number of liters needed to correct the deficit

Total na deficit/correction speed= number of days to correct

Feeding status to see the amount of maintenance fluid to be used

Hypernatremia

Hypernatremia results from either a loss of free water or a gain of sodium in excess of water.

Like hyponatremia, it can be associated with an increased, normal, or decreased extracellular volume

Symptomatic hypernatremia usually results only in patients with impaired thirst or restricted access to fluid, as thirst will result in increased water intake.

Symptoms are rare until the serum sodium concentration exceeds 160 mEq/L but, once present, are associated with significant morbidity and mortality.

symptoms

hyperosmolarity, central nervous system effects predominate .Water shifts from the intracellular to the extracellular space in response to a hyperosmolar extracellular space, resulting in cellular dehydration.

This can put traction on the cerebral vessels and lead to subarachnoid hemorrhage.

The classic signs of hypovolemic hypernatremia (tachycardia, orthostasis, and hypotension)

symptoms2

Central nervous– systemRestlessness, lethargy, ataxia, irritability, tonic spasms, delirium,

seizures, coma Musculoskeletal

– Weakness Cardiovascular

– Tachycardia, hypotension, syncope Tissue

– Dry sticky mucous membranes, red swollen tongue, decreased saliva and tears

Renal– Oliguria

Metabolic– Fever

Hypervolemic hypernatremia

iatrogenic administration of sodium-containing fluids (including sodium bicarbonate)

mineralocorticoid excess – as seen in hyperaldosteronism, – Cushing's syndrome, and – congenital adrenal hyperplasia.

Urine sodium is typically greater than 20 mEq/L and urine osmolarity is greater than 300 mOsm/L

Normovolemic hypernatremia

renal – diabetes insipidus– diuretics– renal disease

nonrenal – gastrointestinal – skin

hypovolemic hypernatremia

Renal – diabetes insipidus– osmotic diuretics– adrenal failure– renal tubular diseases

The urine sodium concentration is less than 20 mEq/L and urine osmolarity is less than 300 to 400 mOsm/L.

Nonrenal water loss – gastrointestinal fluid losses such as diarrhea– skin fluid losses such as fever or tracheotomies. – thyrotoxicosis– hypertonic glucose solutions for peritoneal dialysis.

With nonrenal water loss, the urine sodium concentration is less than 15 mEq/L and the urine osmolarity is greater than 400 mOsm/L.

Treatment of hypernatremia

treatment of the associated water deficit. In hypovolemic patients, volume should be

restored with normal saline. Once adequate volume status has been achieved, the water deficit is replaced using a hypotonic fluid such as 5% dextrose, 5% dextrose in 1/4 normal saline, or enteral water.

The rate of fluid administered should be titrated to achieve a decrease in serum sodium of no more than 1 mEq/h and 12 mEq/d for treatment of acute hypernatremia. Even slower correction should be undertaken with chronic hypernatremia (0.7 mEq/L/h), as overly rapid correction can lead to cerebral edema and herniation.

The type of fluid depends on the severity and ease of correction.– Oral or enteral replacement is acceptable in most cases, – intravenous replacement with half- or quarter-normal saline can be used.

Caution should also be exercised when using 5% dextrose in water in order to avoid overly rapid correction.

Frequent neurologic evaluation as well as frequent evaluation of serum sodium levels also should be performed

60 mL/h plus 1 mL/kg per hour for any increment of weight

over 20 kg, to a maximum of 120 mL/h (total daily fluid intake

3000 mL). Thus, an individual who weighs 45 kg would receive

40 mL/h (10 x 4 mL/h) plus 20 mL/h (10 x 2 mL/h) plus 25 mL/h (25 x 1 mL/h) = 85 mL/h.

WATER DEFICIT

                                        plasma [Na+]   Water deficit   =   CBW  x   (—————————    -    1)                                               140

CBW refers to estimated current body water. The total body water is normally about 60 and 50 percent of lean body weight in younger men and women, respectively, and is somewhat lower in the elderly (about 50 and 45 percent in men and women, respectively) [2].

use values about 10 percent lower (50 and 40 percent) in hypernatremic patients who are water-depleted.

cont

Thus, in a 60 kg woman with a plasma sodium concentration of 168 meq/L, total body water is about 40 percent of body weight and the water deficit can be approximated from:

  Water deficit   =   0.4  x  60  ([168/140]  -  1)                         =   4.8 liters to be corrected at a max rate of 12

meq /day decrease in serum na

This formula estimates the amount of positive water balance required to return the plasma sodium concentration to 140 meq/L. Then, when calculating the amount of free water to give (either intravenously, as dextrose in water, or orally if the patient is able to drink), insensible losses and some part of urine and gastrointestinal losses must be added to the calculation.

APPLICATION TO THE PATIENT

The 28 meq/L rise in the plasma sodium concentration should be corrected over 56 h, which involves the administration of 4.8 L of free water (usually intravenously, as dextrose in water) at a rate of approximately 80 mL/h.

As mentioned above, however, the water deficit estimates the positive water balance that must be achieved; thus, continuing free water losses must also be replaced, such as insensible losses (about 30 to 40 mL/h) and any continued dilute urinary or gastrointestinal losses.

"Dilute" refers to a sodium plus potassium concentration in the fluid lost that is lower than that in the plasma. Thus, the excretion of 100 mL/h of urine with a sodium plus potassium concentration half that of the plasma is equivalent to losing 50 mL/h of free water.

Potassium Abnormalities

The average dietary intake of potassium is approximately 50 to 100 mEq/d, which in the absence of hypokalemia is excreted primarily in the urine.

Extracellular potassium is maintained within a narrow range, principally by renal excretion of potassium, which can range from 10 to 700 mEq/d.

Although only 2% of the total body potassium (4.5 mEq/L x 14 L = 63 mEq) is located within the extracellular compartment, this small amount is critical to cardiac and neuromuscular function; thus even minor changes can have major effects on cardiac activity. The intracellular and extracellular distribution of potassium is influenced by surgical stress, injury, acidosis, and tissue catabolism.

Hyperkalemia

above the normal range of 3.5 to 5.0 mEq/L. excessive potassium intake , increased release of potassium from cells, or impaired excretion by the kidneys (Table

2-4). 5..

Increased intake

oral or intravenous supplementation blood transfusions

increased release from cells

Hemolysis rhabdomyolysis crush injuries gastrointestinal hemorrhage Acidosis rapid increase of extracellular osmolality

(hyperglycemia or mannitol administration) – Since the majority of total body potassium is intracellular,

even small shifts of intracellular potassium out of the intracellular fluid compartment can lead to a significant rise in extracellular potassium

Impaired potassium excretion

medications particularly in the presence of renal insufficiency

potassium-sparing diuretics angiotensin-converting enzyme inhibitors nonsteroidal anti-inflammatories renal insufficiency renal failure.

Symptoms of hyperkalemia

gastrointestinal – nausea, vomiting, intestinal colic, and diarrhea;

neuromuscular– range from weakness to ascending paralysis to

respiratory failure

Cardiovascular,– range from electrocardiogram (ECG) changes to

cardiac arrhythmias and arrest.

ECG changes that may be seen with hyperkalemia include:

Peaked T waves (early change) Flattened P wave Prolonged PR interval (first-degree block) Widened QRS complex Sine wave formation , no p & very wide qrs Ventricular fibrillation

treatment

Potassium removal  –  Kayexalate  

  Oral administration is 15–30 g in 50–100 mL of 20% sorbitol     Rectal administration is 50 g in 200 mL 20% sorbitol 

–  Dialysis ,should be considered when conservative measures fail. Shift potassium   

– Glucose 1 ampule of D50 and regular insulin 5–10 units intravenous   

– Bicarbonate 1 ampule intravenous Counteract cardiac effects   

– Calcium gluconate 5–10 mL of 10% solution

Hypokalemia

Hypokalemia is more commonly seen in the surgical patient. It may be caused by

inadequate intake – dietary,– potassium-free intravenous fluids – total parenteral nutrition with inadequate potassium replacement

excessive renal excretion – hyperaldosteronism, – medications such as diuretics that increase potassium excretion – drugs such as penicillin that promote renal tubular loss of

potassium

Causes 2

loss in gastrointestinal secretions– stool or – renal potassium loss from vomiting– high nasogastric output

intracellular shifts (as seen with metabolic alkalosis or insulin therapy)

– The change in potassium associated with alkalosis can be calculated by the following formula:0.3 meq for each 0.1 ph unit rise

Additionally, drugs such as amphotericin, aminoglycosides, foscarnet, cisplatin, and ifosfamide that induce magnesium depletion will cause renal potassium wastage

The symptoms of hypokalemia

gastrointestinal,– ileus, constipation, weakness, fatigue,

neuromuscular,– diminished tendon reflexes, paralysis

cardiac – cardiac arrest (pulseless electrical activity or asystole). – ECG changes suggestive of hypokalemia include:

U waves T-wave flattening ST-segment changes Arrhythmias (especially if patient is taking digitalis)

treatment

Caution should be exercised when oliguria or impaired renal function is coexistent.

Serum potassium level <4.0  – Asymptomatic, tolerating enteral nutrition: KC1 40 mEq per enteral access

x 1 dose 

–  Asymptomatic, not tolerating enteral nutrition: KCl 20 mEq IV q2h x 2 doses 

–  Symptomatic: KCl 20 mEq IV q1h x 4 doses  Recheck potassium level 2 hours after end of infusion; if <3.5 mEq/L and asymptomatic, replace as per above protocol

10 to 20 meq/h, and maximal concentration of 100 to 200 meq/L A loss of 4 to 3, is roughly 200to300 meq of total body stores

Magnesium Abnormalities

found primarily in the intracellular compartment, in the extracellular space, one third is bound to

serum albumin. Therefore the plasma level of magnesium may be a poor indicator of total body stores in the presence of hypoalbuminemia.

Magnesium should be replaced until levels are in the upper limit of normal..

hypermag rare but can be seen with

– impaired renal function – excess intake in the form of

total parenteral nutrition or magnesium-containing laxatives and antacids.

Symptoms may be gastrointestinal (nausea and vomiting), neuromuscular (weakness, lethargy, and decreased reflexes), or cardiovascular (hypotension and arrest). ECG changes are similar to those seen with hyperkalemia and include:

Increased PR interval Widened QRS complex Elevated T waves

Hypermagnesemiacorrection

withhold exogenous sources of magnesium, correct volume deficit,

correct acidosis if present. To manage acute symptoms, calcium

chloride (5 to 10 mL) should be administered to antagonize the cardiovascular effects.

If elevated levels or symptoms persist, dialysis is indicated

hypomag

particularly in the ICU. The kidney is primarily responsible for

magnesium homeostasis through regulation by calcium/magnesium receptors on renal tubular cells that sense serum magnesium levels.

etiologies

poor intake (starvation, alcoholism, prolonged use of intravenous fluids, and total parenteral nutrition with inadequate supplementation of magnesium),

increased renal excretion (alcohol, most diuretics, and amphotericin B)

gastrointestinal losses (diarrhea) malabsorption acute pancreatitis diabetic ketoacidosis primary aldosteronism.

Symptoms of mag dep

Magnesium depletion is characterized by neuromuscular and central nervous system hyperactivity, and symptoms are similar to those of calcium deficiency, including hyperactive reflexes, muscle tremors, and tetany with a positive Chvostek's sign .Severe deficiencies can lead to delirium and seizures. A number of ECG changes can also occur and include:

Prolonged QT and PR intervals ST-segment depression Flattening or inversion of P waves Torsades de pointes Arrhythmias

Correction1

– Magnesium level 1.0–1.8 mEq/L:   Magnesium sulfate 0.5 mEq/kg in normal saline

250 mL infused IV over 24 h x 3 days  Recheck magnesium level in 3 days

correction2

– Magnesium level <1.0 mEq/L:   Magnesium sulfate 1 mEq/kg in normal saline

250 mL infused IV over 24 h x 1 day, then 0.5 mEq/kg in normal saline 250 mL infused IV over 24 h x 2 days  Recheck magnesium level in 3 days

If patient has gastric access and needs a bowel regimen:  Milk of magnesia 15 mL (approximately 49 mEq magnesium) q24h per gastric tube; hold for diarrhea

Phosphorus Abnormalities

Phosphorus is the primary intracellular abundant in metabolically active cells. Phosphorus is responsible for maintaining

energy production in the form of glycolysis or high-energy phosphate products such as adenosine triphosphate (ATP)

tightly controlled by renal excretion.

Hyperphosphatemia

Most cases of hyperphosphatemia are asymptomatic, but significant hyperphosphatemia can lead to metastatic soft tissue calcium-phosphorus complexes.

decreased urinary excretion

impaired renal function. Hypoparathyroidism hyperthyroidism also can decrease urinary

excretion of phosphorus and thus lead to hyperphosphatemia.

Increased release of endogenous phosphorus ,increased production of phosphorus.

cell destruction rhabdomyolysis tumor lysis syndrome hemolysis sepsis severe hypothermia malignant hyperthermia

increased intake

Excessive phosphate administration (phosphorus-containing laxatives) may also lead to elevated phosphate levels.

Hyperphosphatemiacorrection

Phosphate binders such as sucralfate or aluminum-containing antacids can be used to lower serum phosphorus levels.

Calcium acetate tablets are also useful when hypocalcemia is simultaneously present.

Dialysis is usually reserved for patients with renal failure

Hypophosphatemia

Hypophosphatemia can be due to a decrease in phosphorus intake, an intracellular shift of phosphorus, or an increase in phosphorus excretion.

Clinical manifestations of hypophosphatemia are usually absent until levels fall significantly. In general, symptoms are related to adverse effects on the oxygen availability of tissue and to a decrease in high-energy phosphates and can be manifested as cardiac dysfunction or muscle weakness.

Decreased intake

can occur with malnutrition or if decreased gastrointestinal absorption is present (malabsorption or phosphate binders).

intracellular shift

Most cases respiratory alkalosis, insulin therapy refeeding syndrome hungry bone syndrome.

Hypophoscorrection

–  Phosphate level 1.0–2.5 mg/dL:   Tolerating enteral nutrition: Neutra-Phos 2

packets q6h per gastric tube or feeding tube   No enteral nutrition: KPHO4 or NaPO4 0.15

mmol/kg IV over 6 h x 1 dose   Recheck phosphate level in 3 days

– Phosphate level <1.0 mg/dL:   KPHO4 or NaPO4 0.25 mmol/kg over 6 h x 1

dose 

1 amp napo4 10.44 mmol

Phosphorus repletion protocol

Calcium Abnormalities

The vast majority of the body's calcium is contained within the bone matrix with only less than 1% found in the extracellular fluid.

Serum calcium is distributed among three forms: protein-bound (40%), complexed to phosphate and other anions (10%), and ionized (50%).

It is the ionized fraction that is responsible for neuromuscular stability and can be measured directly.

When measuring total serum calcium levels, the albumin concentration must be taken into consideration:0.8 cal \ for a 1 alb\

Unlike changes in albumin, changes in pH will affect the ionized calcium concentration. Acidosis decreases protein binding, thereby increasing the ionized fraction of calcium.

Hypercalcemia

serum calcium level above the normal range of 8.5 to 10.5 mEq/L, or an increase in the ionized calcium level above 4.2 to 4.8 mg/dL. Primary hyperparathyroidism in the outpatient setting and malignancy (associated bony metastasis or due to secretion of parathyroid hormone–related protein) in hospitalized patients account for most cases of symptomatic hypercalcemia.

Symptoms of hypercalcemia

which vary with the degree of severity, neurologic (depression, confusion, stupor, or coma), musculoskeletal (weakness and back and extremity

pain), renal (polyuria and polydipsia as kidneys lose their

ability to concentrate), gastrointestinal (anorexia, nausea, vomiting,

constipation, abdominal pain, and weight loss). Cardiac symptoms also are present and can include

hypertension, cardiac arrhythmias, and a worsening of digitalis toxicity.

ECG changes of hypercalcemia include:

Shortened QT interval Prolonged PR and QRS intervals Increased QRS voltage T-wave flattening and widening AV block (can progress to complete heart

block, then cardiac arrest with severe hypercalcemia)

Hypercalcemiacorrect

Treatment is required when hypercalcemia is symptomatic, which usually occurs when the serum level exceeds 12 mg/dL.

The initial treatment is aimed at repleting the associated volume deficit then inducing a brisk diuresis with normal saline.

Treatment of hypercalcemia associated with malignancies

Hypocalcemia

Hypocalcemia is defined as a serum calcium level below the normal range of 8.5 to 10.5 mEq/L, or a decrease in the ionized calcium level below the range of 4.2 to 4.8 mg/dL.

Hypocalcemia rarely results from decreased intake, as bone reabsorption can maintain normal levels for prolonged periods of time

The etiologies of hypocalcemia

pancreatitis, massive soft tissue infections such as necrotizing

fasciitis, renal failure, pancreatic and small bowel fistulas, Hypoparathyroidism toxic shock syndrome abnormalities in magnesium, tumor lysis syndrome.

etio

removal of a parathyroid adenoma as atrophy of the remaining glands and avid bone uptake of calcium occurs.

Hungry bone syndrome can develop postoperatively in secondary or tertiary hyperparathyroidism as bone is being rapidly remineralized, requiring high-dose calcium supplementation.

malignancies associated with increased osteoclastic activity such as breast and prostate cancer can lead to hypocalcemia from increased bone formation.

Calcium precipitation with organic anions is such as that seen with

hyperphosphatemia (tumor lysis syndrome or rhabdomyolysis)

pancreatitis (chelation with free fatty acids) massive blood transfusion (citrate)

symptoms

Asymptomatic hypocalcemia may occur with hypoproteinemia (normal ionized calcium), but symptoms can develop with alkalosis (decreased ionized calcium). In general, symptoms do not occur until the ionized fraction falls below 2.5 mg/dL, and are neuromuscular and cardiac in origin (see Table 2-5), including paresthesias of the face and extremities, muscle cramps, carpopedal spasm, stridor, tetany, and seizures.

Hyperreflexia positive Chvostek's sign (spasm resulting from

tapping over the facial nerve) Trousseau's sign (spasm resulting from pressure

applied to the nerves and vessels of the upper extremity, as when obtaining a blood pressure)

Decreased cardiac contractility and heart failure can also accompany hypocalcemia

ECG changes:

Prolonged QT interval T-wave inversion Heart blocks Ventricular fibrillation

Calcium correction

Normalized calcium level <4.0 mg/dL: 

–  With gastric access and tolerating enteral nutrition:

Calcium carbonate suspension 1250 mg/5 mL q6h per gastric access; recheck ionized calcium level in 3 days 

–  Without gastric access or not tolerating enteral nutrition:

Calcium gluconate 2 g IV over 1 h x 1 dose; recheck ionized calcium level in 3 days

Sodium bicarbs, how to use it

Cardiac arrest:

I.V.:

Initial: 1 mEq/kg/dose one time;

maintenance: 0.5 mEq/kg/dose every 10 minutes or as indicated by arterial blood gases

  Note: Routine use of NaHCO3 is not recommended and should be given only after adequate alveolar ventilation has been established and effective cardiac compressions are provided

Metabolic acidosis: I.V.: Dosage should be based on the following formula if blood gases and pH measurements are available:

  HCO3-(mEq) = 0.2 x weight (kg) x base deficit (mEq/L)

 Administer 1/2 dose initially, then remaining 1/2 dose over the next 24 hours; monitor pH, serum HCO3-, and clinical status

Note: If acid-base status is not available: 2-5 mEq/kg I.V. infusion over 4-8 hours; subsequent doses should be based on patient's acid-base status

Hyperkalemia: I.V.: 1 mEq/kg over 5 minutes

Chronic renal failure: Oral: Initiate when plasma HCO3- <15 mEq/L Start with 20-36 mEq/day in divided doses, titrate to bicarbonate level of 18-20 mEq/L

Renal tubular acidosis: Oral:   Distal: 0.5-2 mEq/kg/day in 4-5 divided doses   Proximal: Initial: 5-10 mEq/kg/day; maintenance: Increase as

required to maintain serum bicarbonate in the normal range

Urine alkalinization: Oral: Initial: 48 mEq (4 g), then 12-24 mEq (1-2 g) every 4 hours; dose should be titrated to desired urinary pH; doses up to 16 g/day (200 mEq) in patients <60 years and 8 g (100 mEq) in patients >60 years

For I.V. administration to infants, use the 0.5 mEq/mL solution or dilute the 1 mEq/mL solution 1:1 with sterile water; for direct I.V. infusion in emergencies, administer slowly (maximum rate in infants: 10 mEq/minute); for infusion, dilute to a maximum concentration of 0.5 mEq/mL in dextrose solution and infuse over 2 hours (maximum rate of administration: 1 mEq/kg/hour)

Antacid: Oral: 325 mg to 2 g 1-4 times/day

Prevention of contrast-induced nephropathy (unlabeled use): I.V. infusion: 154 mEq/L sodium bicarbonate in D5W solution: 3 mL/kg/hour for 1 hour immediately before contrast injection, then 1mL/kg/hour during contrast exposure and for 6 hours after procedure

calculation of bicarbonate deficit

  Assuming that respiratory function is normal, attainment of a pH of 7.20 usually requires raising the plasma bicarbonate to 10 to 12 meq/L [24] . The quantity of bicarbonate required can be estimated from the bicarbonate deficit:

    HCO3 deficit    =    HCO3 space   x   HCO3 deficit per liter

The apparent bicarbonate space is a reflection of total body buffering capacity, which includes extracellular bicarbonate, intracellular proteins, and bone carbonate [27,28] . At a normal to moderately reduced plasma bicarbonate concentration, excess hydrogen ions are buffered proportionately through the total body water and the apparent bicarbonate space is approximately 55 percent of lean body weight.

Hco3- deficit = tbw * 0.55 * bicarb deficit

However, the bicarbonate space rises in severe metabolic acidosis, since the fall in the plasma bicarbonate concentration means that there is an ever increasing contribution from the cells and bone, which have a virtually limitless supply of buffer. Thus, the bicarbonate space can reach 70 percent when the plasma bicarbonate concentration falls below 10 meq/L and may exceed 100 percent at levels below 5 meq/L [6] . The bicarbonate space at a given plasma bicarbonate concentration can be estimated from the following formula [28] :

  Bicarbonate space   =   [0.4  + (2.6  ÷  [HCO3])]  x  body weight (in kg)

If, for example, a patient with a lean body weight of 60 kg has a plasma bicarbonate concentration of 6 meq/L and the initial aim of therapy is to raise this value to 12 meq/L. The bicarbonate space is approximately 80 percent and 60 percent of body weight, respectively, at these two concentrations. Taking an average value of 70 percent:

    Bicarbonate deficit    =    0.7   x   60   x   (12   -   6)    =    252 meq

Cardiac arrest: I.V.: Initial: 1 mEq/kg/dose one time; maintenance: 0.5 mEq/kg/dose every 10 minutes or as indicated by arterial blood gases

  Routine use of NaHCO3is not recommended. May be considered in the setting of prolonged cardiac arrest only after adequate alveolar ventilation has been established and effective cardiac compressions. Note: In some cardiac arrest situations (eg, metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose), sodium bicarbonate may be beneficial.

Metabolic acidosis: I.V.: Dosage should be based on the following formula if blood gases and pH measurements are available:

  HCO3-(mEq) = 0.2 x weight (kg) x base deficit (mEq/L)   Administer 1/2 dose initially, then remaining 1/2 dose over the next 24 hours; monitor pH, serum HCO3-,

and clinical status   Note: If acid-base status is not available: 2-5 mEq/kg I.V. infusion over 4-8 hours; subsequent doses

should be based on patient's acid-base status

Hyperkalemia: I.V.: 50 mEq over 5 minutes (as appropriate, consider methods of enhancing potassium removal/excretion)

Chronic renal failure: Oral: Initiate when plasma HCO3- <15 mEq/L Start with 20-36 mEq/day in divided doses, titrate to bicarbonate level of 18-20 mEq/L

Renal tubular acidosis: Oral:   Distal: 0.5-2 mEq/kg/day in 4-5 divided

doses   Proximal: Initial: 5-10 mEq/kg/day;

maintenance: Increase as required to maintain serum bicarbonate in the normal range

Urine alkalinization: Oral: Initial: 48 mEq (4 g), then 12-24 mEq (1-2 g) every 4 hours; dose should be titrated to desired urinary pH; doses up to 16 g/day (200 mEq) in patients <60 years and 8 g (100 mEq) in patients >60 years

Antacid: Oral: 325 mg to 2 g 1-4 times/day

Prevention of contrast-induced nephropathy (unlabeled use): I.V. infusion: 154 mEq/L sodium bicarbonate in D5W solution: 3 mL/kg/hour for 1 hour immediately before contrast injection, then 1mL/kg/hour during contrast exposure and for 6 hours after procedure

To prepare solution, remove 154 mL from 1000 mL bag of D5W; replace with 154 mL of 8.4% sodium bicarbonate; resultant concentration is 154 mEq/L (Merten, 2004); more practically, institutions may remove 150 mL from 1000 mL bag of D5W and replace with 150 mL of 8.4% sodium bicarbonate; resultant concentration is 150

AG = Na+ - (Cl- + HCO3-) = 10 ± 2 mEq/L

each decline in albumin by 1 g/dL from normal (4.5 g/dL), anion gap decreases by 2.5 mEq/L

delta ag/delta hco3- ; agma 1.1 ---agma+ nagma ------1.2 agma+ malca

Na/cl ; 1.4

— In summary, strict recommendations that apply to all patients cannot easily be made. Assuming that the baseline AG is known or can be accurately estimated, the Δ /Δ ratio in an uncomplicated high AG metabolic acidosis should be between 1 and 2. A lower value (in which the Δ AG is less than expected from the Δ HCO3) reflects either urinary ketone losses (as in diabetic ketoacidosis), some cases of chronic kidney disease (in which tubular damage allows filtered anions to be excreted but limits the degree of hydrogen secretion) [14] , or a combined high and normal AG acidosis, as might occur if diarrhea were superimposed upon chronic kidney disease [1] .

On the other hand, a Δ /Δ ratio above 2 indicates the plasma HCO3 is higher than expected from the rise in the AG; this usually reflects a concurrent metabolic alkalosis, as with vomiting.