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Surgery 1.1 Dr. Rafael R.

Fluid and Electrolyte Management of the Surgical Patient Nov 5, 2013

OUTLINE Table 2. Total Body Water (TBW) as a Fraction of Total Body Weight
I. Water and Electrolyte Physiology Population Fraction (kg)
II. Composition of Fluid Compartments Infants 0.8
III. Body Fluid Changes Children 0.65
IV. Maintenance Water Requirements Adult Men 0.6
V. Maintenance Salt Requirements
Adult Women 0.5
VI. Perioperative Fluid Requirements
Elderly Men 0.5
VII. Disturbances in Fluid Balance
VIII. Disturbances of Sodium Homeostasis Elderly Women 0.45
IX. Disturbances of Potassium Homeostasis NOTE: Infants are prone to dehydration thus fluid resuscitation is more
X. Disturbances of Calcium Homeostasis aggressive. As they age, TBW increases. Exceptions are Obese and Elderly
XI. Disturbances of Magnesium subjects!
XII. Disturbances of Phosphorus  Obese:
o less TBW per unit of weight and a relatively expanded
WATER AND ELECTROLYTE PHYSIOLOGY ECV compared to ICV due to the relatively low water
Table 1. Functional Body Fluid Compartments content of adipose tissue
 Elderly:
% of TBW Volume of TBW Male (70Kg) Female (60Kg) o Body water composition is also altered in the elderly
such that by 80 years of age, TBW contributes only 50%
Extracellular Extracellular 14, 000 mL 10, 000 mL
of total body weight secondary to muscle atrophy (less
Volume 20% Volume
intracellular volume)!
Plasma 5% Plasma 3,500 mL 2,500 mL

Interstitial Interstitial 10,500 mL 7,500 mL Composition of Fluid Compartments

Fluid 15%

Intracellullar Intracellular 28,000 mL 20,000 mL

Volume 40% Volume

TOTAL 42,000 mL 30, 000 mL

NOTE: Do not forget to study this table! Some questions might be based
here. 
 The relationship between total body weight and total body water
(TBW) is relatively constant for an individual and is primarily a
reflection of BODY FAT!
 Lean tissues (muscle & solid organs) have higher water content
than fat and bone.
 Deuterium oxide and tritiated water: used to measure TBW
 50- 55% of weight in kg of females is water (↑% of adipost tissue;
↓% of muscle mass)
 60% in males is water
 Obese: minus 10-20% TBW; malnourished: plus 10% TBW Fig. 1. Normal chemical composition of the body fluid compartments
 TBW (total body water): 2/3 is in the ICV (intracellular volume),  ECF compartment:
whereas 1/3 of TBW is in the ECV (extracellular volume) Principal cation = Na
 ECV (20%): Plasma (5% of TBW) + Interstitial Fluid (15% of TBW) Principal anions = Cl and HCO3
 Interstitial Fluid (IF):  ICF compartment:
+ 2+
o Rapidly Equilibrating/ Intercellular- volume of IF that Cations = K and Mg
participates mostly in water exchange Anion = HPO4 and Proteins
o Slowly Equilibrating Fraction/Transcellular-  Concentration gradient is maintained by ATP-driven sodium-
cerebrospinal fluid, joint fluid, pleural fluid, peritoneal potassium pumps in the cell membranes.
fluid  The composition of plasma and interstitial fluid differs only slightly
 Intracellular water makes up approximately 40% of an individual's in ionic composition (plasma has higher protein content  higher
total body weight, with the largest proportion in the skeletal cation composition related to the interstitial fluid)
muscle mass > adipose tissue (hydrophobic; fat contains little  Proteins add to the osmolality of the plasma and contribute to the
water). If follows those leaner and younger individuals have higher balance of forces that determine fluid balance across the capillary
proportion of TBW compared to obese and elderly. endothelium.
 Red cell volume, approximately 2% to 3% of TBW, is part of the  Water is evenly distributed in all fluid compartments and freely
ICV; add the 5% of Plasma, therefore: diffusible in all fluid compartments in spite of the restricted
o Total blood volume is approximately 7% to 8% of total movement of ions and proteins between compartments.
body weight, or approximately 5L (4.9- 5.6L) in a 70-kg  Fluid compartments are separated by membranes that are freely
patient permeable to water. Protein and ion movements are restricted.

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 Sodium-containing fluids don’t only expand the intravascular

volume, it also expands the interstitial space by approximately  To restore blood volume using D5W which distributes
three times as much as the plasma (remember Na is the major evenly throughout TBW, it would be necessary to
ECF cation and remains associated with water!!!) administer 12L [(1L x 0.6)/0.05] OR [(1L x 42)/3.5] = 12
 Principal determinants of osmolality are the concentrations of where,
sodium, glucose and urea (blood urea nitrogen or BUN): 60% of 70kg = 42L (distribution volume of plain water)
5% of 70kg = 3.5L (normal plasma volume)
Calculated serum osmolality = 2 Na + (glucose/18) + (BUN/2.8)  To restore blood volume using crystalloids, 4L is needed
NORMAL: 290-310 mOsm (both intracellular and extracellular compartments) [(1L x 0.2)/0.05] OR [(1L x 14)/3.5] = 4
 Movement of fluids due to: where,
o Hydrostatic pressure: generated by the blood in the 20% of 70kg = 14L (distribution volume of crystalloids)
intravascular compartment 5% of 70kg = 3.5L (normal plasma volume)
o Osmotic pressure : equal to oncotic pressure; keeps the fluid  When using colloids, 1L is sufficient for the blood loss
intravascularly [(1L x 0.05)/0.05] OR [(1L x 3.5)/3.5] = 1
5% of 70kg = 3.5L (distribution volume of colloids)
Note: ECF compartment has higher protein content in plasma 5% of 70kg = 3.5L (normal plasma volume)
than interstitial fluid because it is effective circulating volume;  Therefore, the best solution to be used in acute situations
it is the one measured by blood pressure. is the colloids.

 Water is distributed evenly throughout all fluid compartments of

the body, so that a given volume of water increases the volume of Body Fluid Changes
any one compartment relatively little  A healthy person consumes an average of 2L of water per day,
 Distribution Volume of various crystalloid/colloid in Water – approximately 75% from oral intake and the rest extracted from
volume in which administered solution will dequilibrate over the solid foods.
short term and equilibrates into three fluid compartments  Daily water losses include 800 to 1200 mL in urine (principal
(plasma, interstitial fluid and intracellular volume) mechanism for maintaining water balance), 250 mL in stool, and
o Assume a 70-kg patient has suffered an acute blood loss 600 mL in insensible losses
of 1L (Goal: replace fluid loss) Table 3. Water exchange (60 – 80 kg Man)
 Remember: Average daily Minimal Maximal (mL)
o TBW is 42L (60% of 70 kg)wherein Extracellular Volume volume (mL) (mL)
(20% of 70 kg) is 14L (Plasma 3.5L and Interstitial Fluid H2O gain
o Blood loss is 1L located in the plasma fluid compartment
oral fluids 800 – 1, 500 0 1, 500 /h
o In clinical practice, there are three available solutions for
resuscitation solid foods 500 - 700 0 1, 500
 crystalloids are electrolyte containing wherein Na
+ Insensible:
+ water of 250 125 800
and K or electrolyte content approximates that of
the extracellular volume i.e. isotonic solutions such oxidation
as saline, NSS and lactated ringer solution water of solution 0 0 500
 colloid solutions are also electrolyte containing but H2O loss
differs to crystalloids in that colloids have higher urine 800 – 1,500 300 1,400 / h
molecular weight component (i.e. albumin, starch) intestinal 0 – 250 0 2, 500 / h
 plain water sweat 0 0 4, 000 / h
Insensible: 600 600 1, 500
What is the best solution to use to achieve goal?
lungs and skin
 TBW is the distribution volume for sodium-free water
 Insensible losses amount to 8 to 12ml / kg/ day and are divided
(D5W) – dextrose containing water; distributes evenly to all
into respiratory and cutaneous water loss
fluid compartment
 Insensible losses of water occur through both the skin (75%) and
 Extracellular volume (ECV) is the distribution volume for
lungs (25%), and can be increased by such factors as fever
crystalloid solution in which [Na+] approximates 140mEq/L
(increases water loss by 10% in every 1C rise above 37C),
 Plasma volume (PV) represents the distribution volume for hypermetabolism, and hyperventilation
most colloid solutions which is 5L.
 Respiratory insensitive water losses tend to be greater with
 Plain water=60%, crystalloid = 20%, colloid = 5% (volume inspiration of unhumidified air, as may occur with a
distribution) tracheostomy.
 The formula describing the effects of fluid infusion on PV  Kidneys MUST excrete a minimum of 500-800 mL of urine/day!
expansion is as follows: Maintenance Water Requirements
 Overall maintenance fluid requirements are dependent on weight
and are approximated using this table
Weight ml/kg/h ml/kg/day
First 10kg 4 100
Second 10kg 2 50
Each kilogram above 20kg 1 20

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o For the maintenance water requirement of a 70kg man, o Capillary leak may persist as long as 24hrs into the
first 20kg is equal to 1.5L and the remaining 50kg is postoperative period and should be considered as part of
multiplied by 20 (equal to 1L), therefore water ongoing losses in the immediate postoperative period.
requirement is 2.5L.  On-Going Fluid Losses
o Usually represent GI losses from stomas, tubes (ileostomy
Maintenance Salt Requirements or colostomy tubes, NGTs), drains, or fistulae (any
 Typically, an individual consumes 3-5 g (100 to 250 mEq/day) of abnormal communication between two epithelialized
dietary salt per day; balanced by salt losses in sweat, stool and structures common morbid fistula is presence of
urine. enterocutaneous fistula)
o In perioperative patients, maintenance of sodium is  The electrolyte composition of the output depends on the source
achieved with 1-2 mEq/kg/day of effluent (i.e. saliva, colonic juice, gastric juice, etc)
o So for a 70kg man, he would have a maintenance sodium
requirement of 70-140mEq/day Table 6. Electrolyte content of different organs
 Renal conservation of sodium is extraordinary and in some cases Source Volume (ml) Na Cl K HCO H
of profound volume depletion, urinary losses of sodium may be Stomach 1000-4200 20-120 130 10-15 - 30-100
less than 1 mEq/day due to aldosterone Duodenum 100-2000 110 115 15 10 -
 Normal potassium intake is approximately 40 to 120mEq/day, Ileum 1000-3000 80-150 60-100 10 30-50 -
approximately 10% to 15% of which is excreted as normal urinary
Colon 500-1700 120 90 25 45 -
o body potassium stores can be maintained with an intake of
Bile 500-1000 140 100 5 25 -
approximately 0.5 to 1.0mEq/kg/day
Pancreas 500-1000 140 30 5 115 -
Table 5. Electrolyte content of different solutions
Na K Cl Ca Lactate Glucose  Different effluent have different electrolyte component, thus the
Normal Saline (0.9% NSS) replacement fluid should be chosen to best approximate the
154 0 154 0 0 0
composition of the ongoing losses.
Dextrose 5% in water (D5W) 0 0 0 0 0 50
o Nasogastric losses are typically replaced by NSS + KCl;
D5W ½ NS 77 0 77 0 0 50 lactated ringer’s solution not used because of low/deficient
2/3 D5W, 1/3 NS 50 0 50 0 0 33 potassium content
Lactated Ringer’s 130 4 109 3 28 0 o Losses from a duodenal fistula may best be replaced using
 Although 0.9% saline is used frequently, the relatively high lactated Ringer’s solution because of bicarbonate content
concentration of chloride results in a hyperchloremic metabolic and also potassium content of hepatobiliary or duodenal
acidosis because of the inability of the renal tubule to excrete juice.
excess chloride. o Intractable vomiting, expect for hypochloremic,
 Lactated Ringer’s solution contains lactate which is converted to hyponatremic metabolic alkalosis. You can give NSS and KCl
bicarbonate via hepatic metabolism. This can buffer acid in cases  Lecture notes: For patients with gastric outlet obstruction (gastric
of shock, etc. However, this is contraindicated to patients with contents cannot go beyond the pylorus), the expected electrolyte
liver pathology! abnormality would be hyponatremic and hypochloremic, and
could also develop hypokalemia.
 “Perioperative” → first 12-24 hours after ongoing a surgical CLINICAL EVALUATION
procedure 1. Reassess the patient frequently to determine intravascular volume status
 Appropriate management of fluids and electrolytes in the a. Evaluation of heart rate, blood pressure, and most importantly, hourly
perioperative period requires a flexible yet systematic approach urine output (most reliable indicator of hydration status)
to ensure that fluid administration is appropriately tailored to the  In pediatric population, adequate hydration is indicated by
patient’s changing requirements. urination of a minimum of 1ml/kg/hr. In adult population,
o Requirements are based on: deficits, maintenance adequate hydration is indicated by urination of a minimum of
requirements, and any ongoing losses 0.5ml/kg/hr. Any values below is indicative of inadequate
 Deficits approximate intraoperative blood loss. Also includes fluid hydration
losses from evaporative or third space fluid sequestration.  Resting tachycardia (>90 beats/min) is assumed to be a common
o due to the shift of crystalloid from the intravascular space occurrence in hypovolemic patients, but tachycardia in the supine
to the interstitium, crystalloid should replace blood loss in position is absent in majority of patients with moderate to severe
a ratio of 3-4:1 blood loss (which is why heart rate is not reliable).
o Third Spacing: extensive dissection at the operative site  Hypotension in the supine position is also an insensitive marker of
induces a localized capillary leak, the result of which is blood loss (usually appears in the advanced stages of hypovolemia
extravasation of intravascular fluid into the interstitium - blood loss exceeds 30% of blood volume)
with edema formation (amount from fluid escape from b. Orthostatic Vital Signs
intravascular to interstitium).  A significant orthostatic change is defined as any of the ff: ↑ pulse
 Inguinal herniorrhaphy- loss of 4 ml/kg/h rate of at least 30 beats/min; ↓ systolic pressure > 20mmHg, or
 Aortic aneurysm repair- loss 8 ml/kg/h dizziness on standing
 Third Spacing can also be induced by presence of  Occurs because of pooling of blood going into lower extremities
infection, inflammation or burns (widening of about 7-8kgs that induces a shift in the heart rate and blood
endothelial spaces) pressure

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2. Hematocrit  Hyponatremia can also be seen with an excess of solute relative to

 Usually not used because use of hematocrit to estimate blood loss is free water, such as with untreated hyperglycemia or mannitol
unreliable and inappropriate; decrease in hematocrit in the early (osmotic diuretic) administration.
hours after acute blood loss is usually the result of volume o Glucose exerts an osmotic force in the extracellular
resuscitation rather than ongoing blood loss compartment, causing a shift of water from the intracellular
3. Invasive Hemodynamic Measures to the extracellular space.
 CV catheters, pulmonary artery catheters (allow measurement of  Hypovolemic hyponatremia is a common presentation in the post
cardiac output and systemic oxygen transport) surgical patient (inc ADH), in decreased sodium intake, GI losses –
4. Acid-Base Parameters vomiting, lose bowel movements, chronic use of diuretics
 Provide information about the adequacy of tissue oxygenation;
arterial base deficit and arterial lactate concentration Table 7. Clinical Manifestations of Abnormalities in Hyponatremia


 ECV deficit is the most common fluid disorder in surgical patients
and can either be acute (CV or CNS signs) or chronic (CV, CNS +
decrease in skin turgor and sunken eyes).
 ECV excess may be iatrogenic or secondary to renal dysfunction,
congestive heart failure, or cirrhosis (hypoalbuminemia)
 Volume changes are sensed by:
o Osmoreceptors: drive changes in thirst and diuresis through
the kidneys
o Baroreceptors: through specialized pressure sensors located Treatment of ↓Na:
in the aortic arch and carotid sinuses; responses are both  Hypovolemic ↓Na: volume resuscitation with isotonic (normal
neural (sympathetic and parasympathetic pathways) and saline) fluids
hormonal (renin-angiotensin, aldosterone, atrial natriuretic  Euvolemic ↓Na: fluid restriction and careful monitoring of serum Na
peptide, renal prostaglandins) and volume status
o In severe cases, judicious use of 3% NS + Loop diuretics to
Disorders of Sodium Homeostasis increase serum Na by 0.5-1 mEq/hr
 Changes in serum Na concentration are inversely proportional to  Hypervolemic ↓Na: water restriction, with or without loop
TBW. diuretics
 Values in the range of 125-130 are rarely life-threatening.
 Occurs when there is an excess of extracellular water
relative to Na – either through Na depletion or dilution
 Serum Na: < 135 mEq/L  Dilutional Hyponatremia: results from extracellular water
 Severe hyponatremia: < 120mEq/L; associated with irreversible excess; high extracellular volume
neurologic complications o Causes: excessive oral water intake, iatrogenic IV
 Sodium deficit is estimated by: excess, increased secretion of anti-diuretic hormone,
Na deficit in mEq= (140 – serum Na) x 0.6 x (body weight in kg) drugs such as antipsychotics, tricyclic antidepressants,
 Hypertonic: occurs in the setting of hyperglycemia or elevated and ACEi
BUN, which induces a shift of water from ICV to the extracellular o Physical signs are usually absent; labs reveal
space. hemodilution.
o Each 100 mg/dL rise in serum glucose or 30 mg/dL rise in BUN  Depletional Hyponatremia: associated with ECF volume
correlates to a 1.5-2 mEq/L decrease in serum Na . deficit
 Isotonic: pseudohyponatremia o Causes: decrease intake or increased loss of Na -

o Extreme hyperlipidemia or hyperproteinemia containing fluid, GI losses, renal losses

o Largely artifact NO NEED TO CORRECT  Extreme elevations in plasma lipids and proteins can cause
 Hypotonic: most common pseudohyponatremia because there is no true decrease in
o May occur in the setting of hypovolemia, euvolemia, or extracellular
hypervolemia 
Na relative to water.
 Signs and symptoms primarily have a central nervous
system origin and are related to cellular water intoxication
and associated increases in intracranial pressure; they are
also dependent on the degree of hyponatremia and the
rapidity with which it occurred.

 Serum Na:> 145 mEq/L
 Invariably associated with HYPERTONIC STATES
o Hypovolemic ↑Na: vomiting, diarrhea and forced diuresis
o Euvolemic ↑Na: free water loss via lungs, skin or open
wounds or from Diabetes Insipidus
o Hypervolemic ↑Na: most often iatrogenically induced from
resuscitation with hypertonic fluids
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Table 8. Clinical Manifestations of Abnormalities in Hypernatremia Table 9. Etiologies of Hypokalemia

 Treatment: regardless of cause is free water replacement

H20 deficit (L) = 0.6 x (Wt. in kg) x (serum Na – 140)
st  Serum K: >5mEq/L
 Half of the water deficit should be given over the 1 24hrs, while
 Acute rises in K can cause fatal ventricular dysrhythmias.
the remainder given, over the next 24-48hrs.
+  Causes: renal failure, acidosis, insulin deficiency, rhabdomyolysis,
 Serum Na should not be reduced by more than 0.5 mEq/L/hr, to
cell lysis, drugs (succinylcholine, aldactone) and ischemia-
prevent cerebral swelling
reperfusion syndromes
 Pseudohyperkalemia - seen in red blood cell hemolysis in the
 Results from either a loss of free water or a gain of Na collecting tube, false elevation of potassium
 Hypervolemic ↑Na
o Caused by either iatrogenic administration of Na - Table 10. Etiologies of Hyperkalemia
containing fluids, including Na bicarbonate, or
o Urine sodium concentration is >20 mEq/L
o Urine osmolarity is >300 mOsm/L]
 Normovolemic ↑Na
o Result from renal causes, including diabetes insipidus,
diuretic use, and renal disease, or from nonrenal
water loss from the GI tract or skin
o Urine sodium concentration is <20 mEq/L
o Urine osmolarity is <300 to 400 mOsm/L]
 Symptoms occur only in patients with impaired thirst or
restricted access to fluid and only if serum Na
concentration exceeds 160 mEq/L
o CNS effects predominate (restlessness and irritability,  Treatment:
to seizures, coma, and death) o Remove all K-containing fluids.
o Obtain ECG and if with changes consistent with ↑K, use 10%
 [Classic signs of hypovolemic hypernatremia = tachycardia,
Ca gluconate IV to stabilize the cardiac membrane.
orthostasis, and hypotension]
o The most rapid (although temporary) treatment is to induce
transcellular shift of K into cells 1amp D50 + 10 ‘u’ of
Disorders of Potassium Homeostasis regular insulin
HYPOKALEMIA o Definitive Tx: eliminate K from the body
 Serum K: <3 mEq/L o Loop diuretics or, in the case of renal failure, hemodialysis
 Most often the result of abnormal losses (diarrhea, GI fistula, o Excretion in the stool is facilitated by POLYSTYRENE
urinary losses, acidosis), and not of inadequate intake SULFONATE (a Na-K exchange resin).
 Often accompanied by hypomagnesemia, thus correction of
magnesium is essential 
+ +
Caused by excessive K intake, increased release of K from
 IV potassium replacement should be performed slowly, with +
cells, or impaired K excretion by the kidneys
concentrations not exceeding >40 mEq/L. o Oral or IV supplementation
 When administering higher concentrations, do cardiac monitoring o Hemolysis, rhabdomyolysis, and crush injuries can
(it is a cardiac membrane irritant and may cause ventricular disrupt cell membranes and release intracellular K

arrhythmia) because measured extracellular K represents only a into the ECF.

small proportion of total body K, small changes in serum o Acidosis and a rapid rise in extracellular osmolality
concentrations lead to significant alterations in body functions. from hyperglycemia or IV mannitol can raise causes a
 More common than hyperkalemia +
shift of K ions to the extracellular compartment
 May be caused by inadequate potassium intake; excessive renal o Drugs:
K -sparing diuretics (spironolactone),
potassium excretion; potassium loss in pathologic GI secretions, or angiotensin-converting enzyme inhibitors, and NSAIDs
intracellular shifts from metabolic alkalosis or insulin therapy, and  Symptoms are primarily GI, neuromuscular, and
drugs cardiovascular.
 Symptoms are primarily related to failure of normal contractility of  Hyperkalemia: used for lethal injection and coronary
GI smooth muscle, skeletal muscle, and cardiac muscle bypass surgery (to stop the heart during surgery because
you cannot do the procedure with the heart beating).

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 Calcium(8.5- 10.5meq/L) GI Anorexia, Nausea, vomiting, abdominal pain
o Most abundant electrolyte in the human body, 99% found in bone Neuromuscular Weakness, confusion, coma, bone pain
o Plasma Ca is divided into: CV Hypertension, arrhythmia, polyuria
 Free ionized form (50%): most useful laboratory value, Renal Polydipsia
physiologically active  Treatment:
 Complexed to phosphate and other anions (10%) o Rapid correction: saline infusion to expand intravascular volume, IV
 Protein-bound form (40%): biologically inactive Furosemide (40- 80mg) to induce calciuresis
o Calcitonin: inhibits bone resorption and decreases renal tubular
HYPOCALCEMIA reabsorption of Ca
 Serum Ca:<8.5mg/dL, or ionized level < 4.5mg/dL o Corticosteroids: inhibit action of Vit D
 Causes include intracellular shifts caused by infusion of large volumes of o In patients with hypercalcemic crisis, BISPHOSPHONATES are given to
resuscitation fluids, magnesium depletion, pancreatitis, post-thyroid/ inhibit bone resorption.
parathyroid surgery
From 2015-A Trans:
 Also, from rapid transfusion of blood products due to the citrate load
(CHELATION)  Usual causes: primary hyperparathyroidism, malignancy or
metastasis in bone, secretion of parathyroid hormone-related
 Clinical manifestations of HYPOCALCEMIA:
o ECG changes: prolonged QT interval, T-wave inversion, heart block,
and ventricular fibrillation  Symptoms: neurologic impairment, musculoskeletal weakness
and pain, renal dysfunction, GI symptoms, and cardiac
System HYPOCalcemia
symptoms such as hypertension and arrhythmia
GI -
Neuromuscular Hyperactive reflexes (Chvostek’s and Trousseau’s sign), DISTURBANCES OF MAGNESIUM HOMEOSTASIS
paresthesia, carpopedal spasm, seizures  Magnesium (1.6- 2.8mg/dL)
CV Heart Failure o Plays an important role in energy metabolism, protein synthesis and
 Treatment: cell division
o Aimed at treating the underlying cause o Intimately involved in the regulation of calcium movement across
o Replacement should be given to symptomatic patients, and those with muscle membranes
serum Ca <7mg/dL, or ionized Ca <3mg/dL
o Ca gluconate- contains 9mg of elemental Ca per mL HYPOMAGNESEMIA
o Ca chloride- contains 27mg/mL  Serum Mg:< 1.6mg/dL
o All patients should have ECG monitoring, as bradycardia and  Occurs due to poor dietary intake, diuretic treatment, abnormal gut losses
hypotension are relatively common sequelae (biliary or small bowel fistulae and massive diarrhea) and alcoholism
 Often accompanied by K depletion thus hypokalemia is refractory to K
 Causes: pancreatitis, massive soft tissue infections such as replacement alone
necrotizing fasciitis, renal failure, pancreatic and small bowel  Treatment:
fistulas, hypoparathyroidism, toxic shock syndrome, o MAGNESIUM SO4 (1g=8mEq), can be given in patients with pre-
abnormalities in magnesium levels, and tumor lysis syndrome eclampsia
 Malignancies associated with increased osteoclastic o Infusion should not exceed 2g/hr or 16mEq/hr to avoid hypotension
activity, such as breast and prostate cancer, can lead to o In life threatening arrhythmias, Magnesium Sulfate may be given as a
hypocalcemia from increased bone formation. bolus of 1-2g IV over 5 minutes
 Asymptomatic hypocalcemia may occur when
hypoproteinemia results in a normal ionized calcium level] HYPERMAGNESEMIA
 In general, neuromuscular and cardiac symptoms do not  Serum Mg:>2.8mg/dL
occur until the ionized fraction falls below 2.5 mg/dL.  Usually iatrogenic, a result of administration of antacids or laxatives
 Clinical findings: paresthesias of the face and extremities,  Other causes: renal insufficiency and massive hemolysis
muscle cramps, carpopedal spasm, stridor, tetany, seizures,  Treatment:
hyperreflexia, positive Chvostek’s sign, positive Trosseau’s o In life-threatening magnesium excess (>12mg/dL) IV Ca gluconate to
sign reverse cardiac effects, hydration with NS + IV Furosemide;
 Complications: decreased cardiac contractility and heart hemodialysis

 Ca > 10.4mg/dL or ionized Ca > 5.6mg/dL
 In hospitalized patients, MALIGNANCIES account for most cases
together comprise >90% of all cases
 Other causes include toxicity from drugs (thiazides, lithium, Vit A or D),
 Clinical manifestations of HYPERCALCEMIA
o ECG changes- shortened QT interval, prolonged PR and QRS intervals,
increased QRS voltage, T-wave flattening and widening, and
atrioventricular block (which can progress to complete heart block and
cardiac arrest)
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+  Neurologic patients
 Rare, but can be seen in renal insufficiency and changes in K
o Syndrome of Inappropriate Secretion of ADH (SIADH)
excretion  Not caused by osmotic or volume–related conditions
 Clinical manifestations: nausea and vomiting; neuromuscular  Goal: achieve net water balance; avoid volume depletion that
dysfunction with weakness, lethargy, and hyporeflexia; and compromises renal function
impaired cardiac conduction leading to hypotension and  Furosemide can induce free water loss
arrest] o Diabetes Insipidus
Hypomagnesemia  Increase in urine osmolality in response to a period of water
 Common problem in hospitalized and critically ill patients
 Mild: free water replacement
 May result from alterations of intake, renal excretion, and  More severe: vasopressin (5 units SQ)
pathologic losses o Cerebral Wasting
 Depletion is characterized by neuromuscular and CNS  Diagnosis of exclusion that occurs in patients with a cerebral lesion and
hyperactivity renal wasting of sodium and chloride with no other identifiable cause.
o Symptoms are similar to those of calcium deficiency  Hyponatremia is a secondary event (differentiating it from SIADH)
including hyperactive reflexes, muscle tremors, tetany, and  Malnourished patients: Refeeding syndrome
o Lethal condition that can occur with rapid and excessive feeding of patients
positive Chvostek's and Trousseau's signs
with severe malnutrition because of starvation, alcoholism, delayed enteral
o Severe deficiencies can lead to delirium and seizures] or parenteral support, anorexia nervosa, or massive weight loss in obese
 Hypomagnesemia is important not only because of its direct patients.
effects on the nervous system, but also because it can o Shift in metabolism from fat to carbohydrate stimulates insulin release 
produce hypocalcemia and lead to persistent hypokalemia. cellular uptake of phosphate, magnesium, potassium and calcium;
o Prevention: Slow institution of caloric repletion
HYPOPHOSPHATEMIA o Hyponatremia derives from breakdown of proteins, carbohydrate, and fats,
 intestinal uptake or  renal excretion and administered water.
 Treatment: o Hypocalcemia, hypermagnesemia, and hyperphosphatemia are common
o Phosphate replacement should be instituted when levels drop below (rememeber: ↑serum phosphate levels = ↓ serum calcium levels).
o Metabolic acidosis results from loss of ability to clear acid by-products.
 Cancer patients
o Na or K PO4 can be given in doses of 0.08- 0.24 mmol/kg over 4- 6 o Hypocalcemia: thyroidectomy/parathyroidectomy
hours o Hungry bone syndrome  hypocalcemia following parathyroid surgery for
secondary or tertiary hyperparathyroidism (calcium is rapidly taken up by
HYPERPHOSPHATEMIA bones  hypocalcemia)
 Seen with impaired renal excretion, often associated with o Prostate and breast CA  ↑osteoblastic activity  hypocalcemia
hypocalcemia o Ifosfamide and cisplatin  hypomagnesemia
o Tumor lysis syndrome, bisphosphonates use  hyperphosphatemia
 Treatment: hydration + diuresis with acetazolamide
o Malignancy  hypercalcemia (bone destruction from metastasis)
 Phosphate binders: Al hydroxide will minimize intestinal absorption.  Saline volume expansion
 HD severe, refractory hyperphosphatemia –> dialysis  Loop diuretics
 Bisphosphonates (inhibit bone resorption)
 Calcitonin (tachyphylaxis is common)
Phosphorus Abnormalities
 Corticosteroids (may decrease tachyphylaxis)
 Phosphorus is the primary intracellular divalent anion and is  Dialysis (severe and refractory hypercalcemia)
abundant in metabolically active cells.
 Serum phosphate levels are tightly controlled by renal excretion.
Hyperphosphatemia SUMMARY
 Can be due to:  Proper management of fluid and electrolytes facilitates crucial
o Decreased urinary excretion: in cases of hypoparathyroidism or
homeostasis that allows cardiovascular perfusion, organ system
function, and cellular mechanisms to respond to surgical illness.
o Increased intake: IV or phosphorus-containing laxatives
o Endogenous mobilization of phosphorus – seen in any  Knowledge of the compartmentalization of body fluids forms the
condition that results in cell destruction] basis for understanding pathologic shifts in these fluid spaces in
 Usually asymptomatic but prolonged hyperphosphatemia can disease states.
lead to metastatic deposition of soft tissue calcium-phosphorus  Alterations in the concentration of serum sodium have profound
complexes. effects on cellular function due to water shifts between the
Hypophosphatemia intracellular and extracellular spaces.
 Can be due to:
o Decreased phosphorus intake: malabsorption or malnutrition Who is wise and understanding among you? By his good conduct let him show his
o Intracellular shift of phosphorus: in cases of respiratory works in meekness of wisdom. But if you have bitter jealousy and selfish ambition in
alkalosis, insulin therapy, refeeding syndrome and hungry bone your hearts, do not boast and be false to the truth. This is not the wisdom that
syndrome comes down from above, but is earthly, unspiritual and demonic. For where
o Increased excretion jealousy and selfish ambition exist, there will be disorder and every vile practice. But
 Usually asymptomatic until levels fall significantly, but in general the wisdom from above is first pure, then peaceable, gentle, open to reason, full of
symptoms are related to effects of O2 availability to tissue and mercy and good fruits, impartial and sincere.
decrease in high-energy phosphates (ATP) = cardiac dysfunction James 3:13-17
or muscle weakness.

Group 15 | Joan. Brief. Proceso. Marie. LanternQueen Edited by: JLP Page 7 of 7