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SURGERY B#4 L#3

Fluid and Electrolytes


Jonathan Joy Adora, MD, FPCS, FACS,FPALES, FPSGS Jan uary 22, 2016

TOPIC OUTLINE Body Fluid Compartment


I. Fluid and electrolyte
A. Osmolarity and Osmolality B. Potassium The 60-40-20 rule - remember this!
B. Regulation of Fluid and Electrolyte C. Calcium
Movement D. Phosphate 60 % of body weight is water
II. Fluid spacing E. Magnesium o 40% - intracellular fluid - largest proportion in skeletal muscle
III. Disturbance in Fluid Balance IV. Electrolyte Imbalance
A. Sodium o 20% -extracellular fluid: divided into interstitial and
Hello! We asked Dr. Adora as to how he will make questions for the exam and he said that he uses the intravascular fluid
textbook when making questions and since most of the content of the lecture are from the book, we opt
to include a handful of book trans. Plasma (5% of body weight) and interstitial fluid (15% of body
weight)
LEGEND Total body water (TBW) - 60% of body weight
From the Lecture/PPT Slides Intracellular fluid 2/3
From the audio recording of the lecturer Extracellular fluid 1/3
From the Book/Other Sources – (Schwartz)
o Interstitial fluid 75% of extracellular fluid
I. FLUID AND ELECTROLYTES o Intravascular fluid 25% extracellular fluid
This is a very important topic in surgery
Homeostasis
Provide transportation of nutrients to cells
Carry waste products away from cells (and eliminate them through
the kidneys, lungs, skin)
Provide environment for chemical reactions to occur (important
because they carry minerals, electrolytes which stimulate other
reactions inside the cell or inside the body)
Diseases, drugs (most common is your diuretic), therapy that
affect balance
Diseases that affect homeostasis - fever, malignancies

Body Fluid Composition


Water -majority of our body fluid ECF is measured using indicator dilution methods.
60% of body weight o by measuring distribution volumes of NaBr and radioactive sulfate
Carries nutrients and waste products Intracellular compartment- determined indirectly (TBW-ECG=ICF)
Concentration gradient between compartments maintained by ATP–
Part in metabolic reactions
driven Na-K pumps in cell membranes.
Solvent, lubricant
Plasma and interstitial fluid composition differs only slightly in ionic
Regulation of body temperature composition.
Maintains blood volume o The slightly higher protein content (organic anions) in plasma
Found in food/beverages (unfortunately not in alcohol which is results in a higher plasma cation composition relative to the
actually a diuretic) interstitial fluid, as explained by the Gibbs-Donnan equilibrium
Daily requirement: 2000-3000 mL/day (about 8-10 glass per day) equation.
If you have underlying disease such as those on mechanical o Proteins add to the osmolality of the plasma and contribute to the
ventilator, those with fever, inflection, you need a lot more than balance that determine fluid balance across the capillary
2000-3000 ml) endothelium.
Although the movement of ions and proteins between the various fluid
Total Body Water (TBW) compartments is restricted, water is freely diffusible.
Water is evenly distributed in all fluid compartments of the body
Water constitutes approximately 50% to 60% of total body weight.
o any additional volume of water little increase in the volume of
total body weight and total body water any one compartment
o relationship is constant
o reflection of body fat Distribution of Body Fluids
Lean tissues (muscle and solid organs) have higher water content than Pediatrics
fat and bone 80% of body weight-newborn body fluid is greater than in adult
o young, lean males- higher proportion of body weight as water than More susceptible to dehydration
elderly or obese Pronounced symptoms
Deuterium oxide and tritiated water-used in clinical research to During surgeries of pediatric patient, we usually compute for
measure TBW by indicator dilution methods. maximum allowable blood loss of fluid loss
Average young adult male, TBW = 60% of total body weight Aging
Average young adult female, TBW = 50% of total body weight Decreased percent body
o Females - higher percentage of adipose tissue and lower percentage fluid
of muscle mass in most. Increased adipose tissue
o Estimates of percentage of TBW should be adjusted downward with decreased muscle
approximately 10% to 20% for obese individuals and upward by 10% mass
for malnourished individuals. Decreased renal function
Newborns have approximately 80% of their total body weight comprised Diminished thirst perception
of water.
o But this decreases to approximately 65% by 1 year of age and Figure 1. Fluid Body
thereafter remains fairly constant. Composition

Fluid intake and Losses Major Solutes


Chemicals dissolved in body fluid, distribution affects fluid balance
Regulated by:
o Intake
o Output
o Acid base balance
o Hormones (ADH, aldosterone etc)
o Cell integrity (destruction of cells such as in trauma, surgery)
Cation - positively charged:
o Calcium
o Na+ - major extracellular cation; affects movement of water
+
o H -affects acidity or pH
+
o K -important for the heart

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Fluid and Electrolytes SURGERY I

Anions- negatively charged ions The concentration of electrolytes usually is expressed in terms of the
o Cl chemical combining activity, or equivalents.
o HCO3 Equivalent = atomic weight (g)/valence
o PO4 For univalent ions such as sodium, 1 mEq = 1 mmol.
Non Electrolyte solute For divalent ions such as magnesium, 1 mmol = 2 mEq.
o Proteins and glucose - important to know bec they usually o The number of milliequivalents of cations must be balanced by the
affects fluid movement in the body same number of milliequivalents of anions.
o Expression of molar equivalents alone does not allow a physiologic
comparison of solutes in a solution.
Movement of water across a cell membrane is dependent on osmosis.

Osmotic equilibrium
reached when water moves across a semipermeable membrane to
equalize the concentration
movement is determined by the concentration of the solutes on each side
of the membrane.

Osmotic pressure
measured in units of osmoles (osm) or milliosmoles (mOsm) that refer
to the actual number of osmotically active particles.
o Ex: 1 mmol of sodium chloride contributes to 2 mOsm (one from
sodium and one from chloride).
Principal determinants of osmolality- concentrations of sodium,
glucose, and urea (blood urea nitrogen, or BUN):
Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)
Osmolality of the intracellular and extracellular fluids = 290 and 310
mOsm in each compartment.

Cell membranes are permeable to water


Any change in osmotic pressure in one compartment is accompanied by
a redistribution of water until osmotic pressure between
compartments is equal.
o Ex: if ECF sodium concentration increases net movement of
water from the intracellular to the extracellular compartment.
o Conversely, if the ECF sodium concentration decreases, water will
move into the cells.
Although the intracellular fluid shares in losses that involve a change in
concentration or composition of the ECF, an isotonic change in
volume in either of the compartments is not accompanied by the net
movement of water as long as the ionic concentration remains the
same.
For practical clinical purposes, most significant gains and losses of body
fluid are directly from the extracellular compartment.
Take note!
B. Regulation of Fluid and Electrolyte Movement
Potassium cause Cardiac symptoms
while Sodium causes Neurologic symptoms Diffusion- movement of particles/substances dissolved in water
Filtration-movement of water, dependent on water pressure so
basically water pushing water towards a different compartment
Table1 . Normal Values of electrolytes (Memorize!) Active transport- Na/K pump-requires energy (ATP) moves
particles from low concentration to high concentration
Osmosis-movement of water

Normal Exchange of Fluid and Electrolytes


Average intake of 2000 mL of water per day
o approximately 75% from oral intake and the rest extracted from
solid foods.
It is important to know the normal values because you will use it in Daily water losses include 800 to 1200 mL in urine, 250 mL in stool, and
the computation of Anion gap, potassium deficit etc. 600 mL in insensible losses.
o Insensible losses of water occur through both the skin (75%) and
A. Osmolarity and Osmolality lungs (25%) and can be increased by such factors as fever,
Difference: Osmolality is per kg and Osmolarity is per Liter hypermetabolism, and hyperventilation.
Osmolality o Sensible water losses such as sweating or pathologic loss of
Indicates water balance of the body gastrointestinal (GI) fluids vary widely, but these include the loss of
Serum Osmolality is 285-295 mOsm/kg electrolytes as well as water
High- water deficit (concentrated)
Low is water excess (dilute)
Urine osmolality is 50-1200 mOSm/kg (ave 500-800 mOSm/kg)- it
is a good indicator of ADH/ vasopressin which affects sodium
concentration thus affecting movement of water across
compartment
Together (serum and urine osmolality) are used to determine what
is causing a sodium imbalance

Osmotic Pressure
The physiologic activity of electrolytes in solution depends on
o # of particles per unit volume (mmol/L)
o # of electric charges per unit volume (mEq/L)
o # of osmotically active ions per unit volume (mOsm/L)
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Fluid and Electrolytes SURGERY I

Kidneys must excrete a minimum of 500 to 800 mL of urine per day, Table 3. IV fluids concentration
regardless of the amount of oral intake To clear the products of
metabolism
The typical individual consumes 3 to 5 g of dietary salt per day, with
the balance maintained by the kidneys.
o With hyponatremia or hypovolemia, sodium excretion can be
reduced to as little as 1 mEq/d or maximized to as much as 5000
mEq/d to achieve balance except in people with salt-wasting
kidneys.
Sweat is hypotonic, and sweating usually results in only a small sodium
loss. When you infuse IV fluid to px, you have to know if its isotonic, hypo
GI losses are isotonic to slightly hypotonic and contribute little to net or hyper so you will know if it promotes water retention or water
gain or loss of free water when measured and appropriately replaced by excretion
isotonic salt solutions.
Plasma expanders- used when there is no ready blood products
Table 2. Regulation of Water Balance Ex: colloid, serum, protein, albumin

III. DISTURBANCE IN FLUID BALANCE


Classification of Body Fluid Changes
Disorders in fluid balance may be classified into three general categories:
disturbances in (a) volume, (b) concentration, and (c) composition.
o Although each of these may occur simultaneously, each is a separate
entity with unique mechanisms demanding individual correction.
Isotonic gain or loss of salt solution results in extracellular volume
changes, with little impact on intracellular fluid volume.
If free water is added or lost from the ECF, water will pass between the
ECF and intracellular fluid until solute concentration or osmolarity is
equalized between the compartments.
Unlike with sodium, the concentration of most other ions in the ECF can
be altered without significant change in the total number of osmotically
active particles, producing only a compositional change.
For instance, doubling the serum potassium concentration will
profoundly alter myocardial function without significantly altering
volume or concentration of the fluid spaces.
A. Extracellular Fluid Deficit
Most common fluid disorder in surgical patients and can be either acute
or chronic.
o Acute volume deficit - associated with cardiovascular and central
nervous system signs
o Chronic deficit - display tissue signs, such as a decrease in skin
II. FLUID SPACING turgor and sunken eyes, in addition to cardiovascular and central
First spacing - normal nervous system signs
Second spacing – edema - including anasarca Laboratory examination may reveal an elevated blood urea nitrogen level
Third spacing- ascites, burn edema if the deficit is severe enough to reduce glomerular filtration and
o enclosed in a membrane you cant reuse the water inside hemoconcentration.
we do fasciotomy ecarotomy with patient with compartment Urine osmolality usually will be higher than serum osmolality, and urine
syndrome sodium will be low, typically <20 mEq/L.
Serum sodium concentration does not necessarily reflect volume status
and therefore may be high, normal, or low when a volume deficit is
present.
The most common cause of volume deficit in surgical patients is a loss of
GI fluids from nasogastric suction, vomiting, diarrhea, or
enterocutaneous fistula.

In addition, sequestration secondary to soft tissue injuries, burns, and


intra-abdominal processes such as peritonitis, obstruction, or prolonged
Figure 2. Isotonic, hypotonic and Hypertonic solutions surgery can also lead to massive volume deficits.

Isotonic-0.9 normal saline solution, so it doesn’t affect movement Symptoms


of water Elevated HR
Hypotonic solution have low substrate contents (minerals/ Low BP these 2 are symptoms of acute fluid loss
electrolyte content especially sodium) so water goes inside the Dry mouth thirst
cell Low urine output
o When infuse with hypotonic solution, cells usually expand or Confusion, lethargy
burst High Hct (not an indication of acute fluid loss because hct
Hypertonic- greater solutes the greater pull of water outside the level will rise if there isimbalance in rbc and plasma concen,
cell in acute fluid loss there is loss of both rbc and plasma
o Cells shrink however high hct- indication of chronic fluid loss), Hgh BUN,
Low Na, High osmolality

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Fluid and Electrolytes SURGERY I

What to do?
Fluids resuscitation
Normal saline or lactated ringers (avoid potassium until urine
output in increases)- if there is hemorrhage we give blood
products (1ml loss is to 1ml), tht’s the best but if not available
we use lactated ringers or plasma expanders though it does
not give hemoglobin it increases plasma volume
Medications for sources of fluid loss (for chronic extracellular
fluid deficit like enterocutaneus fistulas, diarrhea-
antidiarrheal, infection-antibiotics, fever- antipyretic
cvomiting- antiemesis )
Daily weight and strict Intake/output (weight loss or gain is the
best indication)
B. Extracellular Fluid Excess
May be iatrogenic or secondary to renal dysfunction, congestive heart
failure, or cirrhosis.
Both plasma and interstitial volumes usually are increased.
In fit patients, edema and hyperdynamic circulation are common and well
tolerated.
However, the elderly and patients with cardiac disease may quickly
develop congestive heart failure and pulmonary edema in response to
only a moderate volume excess.

Symptoms (primarily pulmonary and cardiovascular)


Rapid weight gain
Edema -usually in legs pitting or non pitting
High Bp, bounding pulses
Inc urine output
Jugular Vein distention
Crackles for
congestion
Dyspnea for
congestion Hypernatremia
Dec level of results from either a loss of free water or a gain of sodium in excess of
consciousness water.
Low hct, low BUN, Like hyponatremia, it can be associated with an increased, normal, or
High Na, low decreased extracellular volume (see Fig. 3-3).
osmolality
What to do? Hypervolemic hypernatremia
Diretics(ex: o caused either by iatrogenic administration of sodium-containing
furosemide, lasics) fluids, including sodium bicarbonate, or mineralocorticoid excess as
Fluid restriction seen in hyperaldosteronism, Cushing’s syndrome, and congenital
Sodium restriction adrenal hyperplasia.
Daily weight, strict I/O o Urine sodium concentration is typically >20 mEq/L, and urine
(Intake/output) osmolarity is >300 mOsm/L.
C. Volume Control
Normovolemic hypernatremia
Volume changes are sensed by both osmoreceptors and baroreceptors. o result from renal causes, including diabetes insipidus, diuretic use,
Osmoreceptors are specialized sensors that detect even small changes in and renal disease, or from nonrenal water loss from the GI tract or
fluid osmolality and drive changes in thirst and diuresis through the skin, although the same conditions can result in hypovolemic
kidneys. hypernatremia.
o For example, when plasma osmolality is increased: When hypovolemia is present, the urine sodium concentration is <20
Thirst is stimulated and water consumption increases, although mEq/L and urine osmolarity is <300 to 400 mOsm/L.
the exact cell mechanism is not known.
Hypothalamus is stimulated to secrete vasopressin, which Nonrenal water loss
increases water reabsorption in the kidneys. o occur secondary to relatively isotonic GI fluid losses such as that
Together, these two mechanisms return the plasma osmolality
caused by diarrhea, to hypotonic skin fluid losses such as loss due to
to normal. fever, or to losses via tracheotomies during hyperventilation.
Baroreceptors also modulate volume in response to changes in pressure o Thyrotoxicosis - cause water loss
and circulating volume through specialized pressure sensors located in o With nonrenal water loss, the urine sodium concentration is <15
the aortic arch and carotid sinuses. mEq/L and the urine osmolarity is >400 mOsm/L.
o Baroreceptor responses are both neural, through sympathetic and
parasympathetic pathways, and hormonal, through substances
Symptomatic hypernatremia
including renin-angiotensin, aldosterone, atrial natriuretic peptide,
o occurs only in patients with impaired thirst or restricted access to
and renal prostaglandins.
fluid, because thirst will result in increased water intake.
o The net result of alterations in renal sodium excretion and free water o Symptoms are rare until the serum sodium concentration exceeds
reabsorption is restoration of volume to the normal state.
160 mEq/L but, once present, are associated with significant
morbidity and mortality.
IV. ELECTROLYTE IMBALANCE o Because symptoms are related to hyperosmolarity, central nervous
A. Sodium system effects predominate
Changes in serum Na concentration are inversely proportional to TBW.
o abnormalities in TBW are reflected by abnormalities in serum Water shifts from the intracellular to the extracellular space in
response to a hyperosmolar extracellular space, cellular
sodium levels.
dehydration this can put traction on the cerebral vessels lead to
subarachnoid hemorrhage.
Central nervous system symptoms can range from restlessness and
irritability to seizures, coma, and death.
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Fluid and Electrolytes SURGERY I

The classic signs of hypovolemic hypernatremia, (tachycardia, Next, depletional versus dilutional causes of hyponatremia are evaluated.
orthostasis, and hypotension) may be present, as well as the unique In the absence of renal disease, depletion is associated with low urine
findings of dry, sticky mucous membranes. sodium levels (<20 mEq/L), whereas renal sodium wasting shows high
urine sodium levels (>20 mEq/L).
Causes o Dilutional causes of hyponatremia usually are associated with
Water loss or excess Na hypervolemic circulation. A normal volume status in the setting of
Decrease excretion hyponatremia should prompt an evaluation for a syndrome of
Increased intake inappropriate secretion of ADH.
Increased water loss-usually due to dilution, Na elevate if you
lose a lot of water Causes
Symptoms (F-R-I-E-D) Water excess
Fever Dilution
Restless Increased excrertion of Na
Increased fluid retention and BP Decreased intake
Edema (peripheral/pitting) Symptoms
Decreased urine output, dry mouth Confusion
What to do? Headace
Treat underlying cause Seizures
Diuretics-immediate treatment Abdominal cramps
Sodium restriction There are similarities in symptoms in hyper and hypo because it
Seizure precaution-in correcting sodium, reduce the sodium affects the brain
slowly What to do?
3% saline
Hyponatremia If caused by fluid excess will need fluid restriction
A low serum sodium level occurs when there is an excess of extracellular Can’t be fixed by adding Na to the diet
water relative to sodium.
In most cases, hyponatremia is a consequence of either sodium depletion
or dilution. B. Potassium
Dilutional hyponatremia frequently results from excess extracellular Average dietary intake -50
water and therefore is associated with a high extracellular volume status. to 100 mEq/d
o Excessive oral water intake or iatrogenic intravenous (IV) excess Extracellular potassium is
free water administration can cause hyponatremia. maintained within a
Postoperative patients are particularly prone to increased secretion of narrow range, principally
antidiuretic hormone (ADH), which increases reabsorption of free water by renal excretion of
from the kidneys with subsequent volume expansion and hyponatremia. potassium, which can
o This is usually self-limiting in that both hyponatremia and volume range from 10 to 700
expansion decrease ADH secretion. mEq/d.
Additionally, a number of drugs can cause water retention and Although only 2% of the
subsequent hyponatremia, such as the antipsychotics and tricyclic total body potassium (4.5
antidepressants as well as angiotensin-converting enzyme inhibitors. mEq/L × 14 L = 63 mEq)
The elderly are particularly susceptible to drug-induced hyponatremia. is located within the
Physical signs of volume overload usually are absent, and laboratory extracellular compartment
evaluation reveals hemodilution. = critical to cardiac and
Depletional causes of hyponatremia are associated with either a neuromuscular function
decreased intake or increased loss of sodium-containing fluids. The intracellular and
A concomitant ECF volume deficit is common. extracellular distribution
o Causes include decreased sodium intake, such as consumption of a of potassium is influenced
low-sodium diet or use of enteral feeds, which are typically low in by a number of factors,
sodium; GI losses from vomiting, prolonged nasogastric suctioning, including surgical stress,
or diarrhea; and renal losses due to diuretic use or primary renal injury, acidosis, and tissue
disease. catabolism.
o Hyponatremia also can be seen with an excess of solute relative to Hyperkalemia
free water, such as with untreated hyperglycemia or mannitol
administration. serum potassium concentration above the normal range of 3.5 to 5.0
o Glucose exerts an osmotic force in the extracellular compartment mEq/L.
a shift of water from the intracellular to the extracellular space. It is caused by excessive potassium intake, increased release of potassium
Hyponatremia therefore can be seen when the effective osmotic pressure from cells, or impaired potassium excretion by the kidneys
of the extracellular compartment is normal or even high. Increased intake can be either from oral or IV supplementation, or from
o When hyponatremia in the presence of hyperglycemia is being red cell lysis after transfusion.
evaluated, the corrected sodium concentration should be calculated Hemolysis, rhabdomyolysis, and crush injuries can disrupt cell
as follows: membranes and release intracellular potassium into the ECF.
For every 100-mg/dL increment in plasma glucose above normal, the Acidosis and a rapid rise in extracellular osmolality from hyperglycemia
plasma sodium should decrease by 1.6 mEq/L or IV mannitol can raise serum potassium levels by causing a shift of
Lastly, extreme elevations in plasma lipids and proteins can cause potassium ions to the extracellular compartment.
pseudohyponatremia, because there is no true decrease in extracellular Because 98% of total body potassium is in the intracellular fluid
sodium relative to water. compartment, even small shifts of intracellular potassium out of the
Signs and symptoms of hyponatremia are dependent on the degree of intracellular fluid compartment can lead to a significant rise in
hyponatremia and the rapidity with which it occurred. extracellular potassium.
Clinical manifestations primarily have a central nervous system origin A number of medications can contribute to hyperkalemia, particularly in
and are related to cellular water intoxication and associated increases in the presence of renal insufficiency, including potassium-sparing
intracranial pressure. diuretics, angiotensin-converting enzyme inhibitors, and nonsteroidal
Oliguric renal failure also can be a rapid complication in the setting of anti-inflammatory drugs (NSAIDs).
severe hyponatremia. Spironolactone and angiotensin-converting enzyme inhibitors interfere
A systematic review of the etiology of hyponatremia should reveal its with aldosterone activity, inhibiting the normal renal mechanism of
cause in a given instance. potassium excretion.
o Hyperosmolar causes, including hyperglycemia or mannitol infusion Acute and chronic renal insufficiency also impairs potassium excretion.
and pseudohyponatremia, should be easily excluded. Symptoms of hyperkalemia are primarily GI, neuromuscular, and
cardiovascular
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Fluid and Electrolytes SURGERY I

o GI symptoms - nausea, vomiting, intestinal colic, and diarrhea. Increase digoxin toxicity
o Neuromuscular symptoms - range from weakness to ascending Diuresis
paralysis to respiratory failure.
o Early cardiovascular signs may be apparent from electrocardiogram What to do?
(ECG) changes and eventually lead to hemodynamic symptoms of Cardiac monitor
arrhythmia and cardiac arrest. Increased intake -unlike Na, you can give supplements orally
ECG changes that may be seen with hyperkalemia include high peaked T or K rich food
waves (early), widened QRS complex, flattened P wave, prolonged PR Watch digoxin toxicity
interval (first-degree block), sine wave formation, and ventricular Potassium IV (only if good urine output- normal 500-600 ml
fibrillation. per day or 30cc/ hour for px with catheter)
Spironolactone
Causes Treat constipation
Kidney failure,
Increased intake C. Calcium
Cell destruct The vast majority of the body’s calcium is contained within the bone
Acidosis matrix, with <1% found in the ECF.
Hypoxia Serum calcium is distributed among three forms: protein found (40%),
Exercise complexed to phosphate and other anions (10%), and ionized (50%).
Catabolic state It is the ionized fraction that is responsible for neuromuscular stability
Use of potassium diuretics-spironolactone and can be measured directly.
Symptoms (M-U-R-D-E-R) -pertains to heart When total serum calcium levels are measured, the albumin
Muscle weakness concentration must be taken into consideration:
Urine oliguria, anuria Adjust total serum calcium down by 0.8 mg/dL for every 1 g/dL
Respiratory distress decrease in albumin.
Decreased cardiac contractility Unlike changes in albumin, changes in pH will affect the ionized
ECG changes calcium concentration.
Reflexes, hyperreflexia or areflexia Acidosis decreases protein binding, thereby increasing the ionized
What to do? fraction of calcium.
Cardiac monitor Daily calcium intake is 1 to 3 g/d.
Kayexalate, calcium gluconate or glucose + insulin (insulin Most of this is excreted via the bowel, with urinary excretion relatively
increases potassium uptake in cells; give glucose because low.
insulin promotes hypoglycemia Total body calcium balance is under complex hormonal control, but
Lasix if kidneys are functioning disturbances in metabolism are relatively long term and less important
Potassium retriction in the acute surgical setting.
Dialysis if severe
Hypercalcemia
Hypokalemia serum calcium level above the normal range of 8.5 to 10.5 mEq/L or an
much more common than hyperkalemia in the surgical patient. increase in the ionized calcium level above 4.2 to 4.8 mg/dL.
It may be caused by inadequate potassium intake; excessive renal Primary hyperparathyroidism in the outpatient setting and malignancy
potassium excretion; potassium loss in pathologic GI secretions, such in hospitalized patients, from either bony metastasis or secretion of
as with diarrhea, fistulas, vomiting, or high nasogastric output; or parathyroid hormone–related protein, account for most cases of
intracellular shifts from metabolic alkalosis or insulin therapy. symptomatic hypercalcemia.
The change in potassium associated with alkalosis can be calculated by Symptoms of hypercalcemia, which vary with the degree of severity,
the following formula: Potassium decreases by 0.3 mEq/L for every include neurologic impairment, musculoskeletal weakness and pain,
0.1 increase in pH above normal. renal dysfunction, and GI symptoms of nausea, vomiting, and
Additionally, drugs such as amphotericin, aminoglycosides, cisplatin, abdominal pain.
and ifosfamide that induce magnesium depletion cause renal o Cardiac symptoms can be manifest as hypertension, cardiac
potassium wastage. arrhythmias, and a worsening of digitalis toxicity.
In cases in which potassium deficiency is due to magnesium depletion, ECG changes in hypercalcemia include shortened QT interval, prolonged
potassium repletion is difficult unless hypomagnesemia is first PR and QRS intervals, increased QRS voltage, T-wave flattening and
corrected. widening, and atrioventricular block (which can progress to complete
The symptoms of hypokalemia like those of hyperkalemia, are primarily heart block and cardiac arrest).
related to failure of normal contractility of GI smooth muscle, skeletal
muscle, and cardiac muscle. Causes
Findings may include ileus, constipation, weakness, fatigue, diminished Hyperparathoid
tendon reflexes, paralysis, and cardiac arrest. In the setting of ECF Vitamin D excess
depletion, symptoms may be masked initially and then worsened by Prolonged immobilization
further dilution during volume repletion. Renal failure
ECG changes suggestive of hypokalemia include U waves, T-wave Malignancies
flattening, ST-segment changes, and arrhythmias (with digitalis Symptoms
therapy). Lethargy
Confusion
Causes Prone to fratures
Vomiting Increase clotting itme (DVT)
Nasogastric tube losses Depressed reflexes
Diarrhea Kidney stones
Medications- Lasix, diuretics What to do?
Metabolic alkalosis Lasix
Rapid cell building Hydration with normal saline
Symptoms Increased oral fluid intake
Dysrhythmia
Weakness, paralysis Hypocalcemia
Nausea a/ vomiting serum calcium level below 8.5 mEq/L or a decrease in the ionized
Paralytic ileus-important in abdominal surgeons when bowel calcium level below 4.2 mg/dL.
+
fxn does not return to normal-check K levels and correct by The causes of hypocalcemia include pancreatitis, massive soft tissue
giving potassium rich food infections such as necrotizing fasciitis, renal failure, pancreatic and
Constipation
Low BP , weak pulse
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Fluid and Electrolytes SURGERY I

small bowel fistulas, hypoparathyroidism, toxic shock syndrome, rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, severe
abnormalities in magnesium levels, and tumor lysis syndrome. hypothermia, and malignant hyperthermia.
Excessive phosphate administration from IV hyperalimentation solutions
Transient hypocalcemia or phosphorus containing laxatives may also lead to elevated phosphate
o occurs after removal of a parathyroid adenoma due to atrophy of the levels.
remaining glands and avid bone remineralization, and sometimes Most cases of hyperphosphatemia are asymptomatic
requires high-dose calcium supplementation. Significant prolonged hyperphosphatemia metastatic deposition of soft
Additionally, malignancies associated with increased osteoblastic tissue calcium-phosphorus complexes
activity, such as breast and prostate cancer, can lead to hypocalcemia
from increased bone formation. Causes
Calcium precipitation with organic anions is also a cause of Renal failure
hypocalcemia and may occur during hyperphosphatemia from tumor Tumor lysis syndrome
lysis syndrome or rhabdomyolysis. Hypoparathyroidism
Pancreatitis may sequester calcium via chelation with free fatty acids. Laxatives or enemas containing phosphate
Massive blood transfusion with citrate binding is another mechanism. Symptoms
Hypocalcemia rarely results solely from decreased intake, because Calcium deposits in joinys, skins, kidneys -because of
bone reabsorption can maintain normal levels for prolonged increased in calcium resorption from the bone
periods. Hypocalcemia
Tetany
Asymptomatic hypocalcemia Neuromascular irritability
o occur when hypoproteinemia results in a normal ionized calcium What to do?
level. Treat the hypocalcemia
Conversely, symptoms can develop with a normal serum calcium level
during alkalosis, which decreases ionized calcium. Hypophosphotemia
In general, neuromuscular and cardiac symptoms do not occur until the due to a decrease in phosphorus intake, an intracellular shift of
ionized fraction falls below 2.5 mg/dL
phosphorus, or an increase in phosphorus excretion.
Clinical findings may include paresthesias of the face and extremities, Decreased GI uptake due to malabsorption or administration of phosphate
muscle cramps, carpopedal spasm, stridor, tetany, and seizures.
binders and decreased dietary intake from malnutrition are causes of
Patients will demonstrate hyperreflexia and may exhibit positive chronic hypophosphatemia.
Chvostek’s sign (spasm resulting from tapping over the facial nerve)
Most acute cases are due to an intracellular shift of phosphorus in
and Trousseau’s sign (spasm resulting from pressure applied to the
association with respiratory alkalosis, insulin therapy, refeeding
nerves and vessels of the upper extremity with a blood pressure cuff or
syndrome, and hungry bone syndrome.
tourniquet).
Clinical manifestations of hypophosphatemia usually are absent until
Hypocalcemia decreased cardiac contractility and heart failure.
levels fall significantly.
ECG changes of hypocalcemia include prolonged QT interval, T-wave
In general, symptoms are related to adverse effects on the oxygen
inversion, heart block, and ventricular fibrillation
availability of tissue and to a decrease in high-energy phosphates, and
can be manifested as cardiac dysfunction or muscle weakness.
Causes
Hypoparathyroidism -hypcalcemia is seen in patients who Causes
undergone complete thyroidectomy due to possible
Malabsorption syndormes
devascularization or excision of parathyroid
Diarrhea
Malabsorption
Deficient serum albumin Excessive use of antacids
Increased serum Ph Hyperparathyroidism
Lack of Vitamin D because Vit Anemias
Chronic Renal failure Bleeding disorder
Symptoms Symptoms
Increased neuromuscular stimulation Impaired neurologic functions
Muscle spasms, cramps Anorexia
Chvostek sign - tap facial nerve there is hyperstimulation Osteomalacia
causing twitching What to do?
Trousseau sign -place tourniquet wait for 5 min, there isrolling Oral supplements
of wrist but very uncomfortable for px Decreased calcium intake because PO4 is inversely related to
Arrhythmias Ca intake
Intestinal cramping
What to do E. Magnesium
Give oral or IV supplements with Vit D (cant give oral calcium fourth most common mineral in the body
without Vit D because it is important for absorption) found primarily in the intracellular compartments.
Approximately one half of the total body content of 2000 mEq is
D. Phosphate incorporated in bone and is slowly exchangeable.
Primary intracellular divalent anion Of the fraction found in the extracellular space, one third is bound to
Abundant in metabolically active cells. serum albumin.
involved in energy production during glycolysis o Therefore, the plasma level of magnesium may be a poor indicator
found in high-energy phosphate products such as adenosine triphosphate. of total body stores in the presence of hypoalbuminemia.
Serum phosphate levels are tightly controlled by renal excretion.
Magnesium should be replaced until levels are in the upper limit of
Hyperphosphotemia normal.
due to decreased urinary excretion, increased intake, or endogenous Normal dietary intake is approximately 20 mEq/d
mobilization of phosphorus. excreted in both the feces and urine.
Most cases of hyperphosphatemia are seen in patients with impaired renal The kidneys have a remarkable ability to conserve magnesium, with renal
function. excretion <1 mEq/d during magnesium deficiency.

Hypermagnesemia
Hypoparathyroidism or hyperthyroidism
o can decrease urinary excretion of phosphorus lead to rare but can be seen with severe renal insufficiency and parallel changes
hyperphosphatemia. in potassium excretion.
Increased release of endogenous phosphorus can be seen in association Magnesium-containing antacids and laxatives can produce toxic levels in
with any clinical condition that results in cell destruction, including patients with renal failure.

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Fluid and Electrolytes SURGERY I

Excess intake in conjunction with total parenteral nutrition (TPN), or QUIZ!


rarely massive trauma, thermal injury, and severe acidosis, may be 1. T/F. Women have higher total body water than men.
associated with symptomatic hypermagnesemia. 2. A 50 kg medical student who signed for the blood letting activity of Sagip
has a total body water of? Intracellular fluid? Extracellular fluid? Interstitial
Clinical examination may find nausea and vomiting; neuromuscular fluid? Intravascular fluid?
dysfunction with weakness, lethargy, and hyporeflexia; and impaired 3. Recite the magic 4 normal values of electrolytes.
cardiac conduction leading to hypotension and arrest. 4. This organ can stop RAAS upon detecting high blood volume
ECG changes are similar to those seen with hyperkalemia and include 5. A client with hypoparathyroidism complains of numbness and tingling in his
increased PR interval, widened QRS complex, and elevated T waves. fingers and around the mouth. What electrolyte imbalance?
A.Hyponatremia B. Hypocalcemia C.Hyperkalemia D. Hypermagnesemia
6. The doctor evaluates which of the following clients to be at risk for
Causes developing hypernatremia?
Renal failure A. 50-year-old with pneumonia, diaphoresis, and high fevers
Excessive intake of Mg containi antacids B.62-year-old with congestive heart failure taking loop diuretics
Adrenal insufficiency C.39-year-old with diarrhea and vomiting
Symptoms D.60-year-old with lung cancer and syndrome of inappropriate
antidiuretic hormone (SIADH)
Lethargy 7. A client is receiving an intravenous magnesium infusion to correct a serum
Nausea/vomiting level of 1.4 mEq/L. Which of the following assessments would alert you to
Loss of deep tendon reflex immediately stop the infusion?
Cardiac and respiratory stress A.Absent patellar reflex
What to do? B. Diarrhea
Increase fliud intake C.Premature ventricular contractions
D.Increase in blood pressure
May need dialysis if severe
8. The doctor should monitor for clinical manifestations of hypophosphatemia
Avoid magnesium containing drugs in which of the following clients?
A. A client with osteoporosis taking vitamin D and calcium supplements
Hypomagnesemia B. A client who is alcoholic receiving total parenteral nutrition
More important than hypermagnesium C. A client with chronic renal failure awaiting the first dialysis run
Magnesium depletion is a common problem in hospitalized patients, D. A client with hypoparathyroidism secondary to thyroid surgery
particularly in the critically ill. 9. The client diagnosed with diabetes insipidus weighed 180 pounds when
the daily weight was taken yesterday. This morning's weight is 175.6 pounds.
The kidney is primarily responsible for magnesium homeostasis through One liter of fluid weighs approximately 2.2 pounds. How much fluid has the
regulation by calcium/magnesium receptors on the renal tubular cells client lost (in milliliters)?
that respond to serum magnesium concentrations. A. 500 mL B. 1000 mL C. 2000 mL D. 4400 mL
Hypomagnesemia may result from alterations of intake, renal excretion,
and pathologic losses.
Poor intake may occur in cases of starvation, alcoholism, prolonged IV Answer:1) F. 2) 30, 20, 10, 7.5, 2.5. 3)K4-Cl104-Na140-pH7.4-CO240-
fluid therapy, and TPN with inadequate supplementation of magnesium. HCO324. 4) heart 5) B 6) A 7) A. 8) B. 9) B
Losses are seen in cases of increased renal excretion from alcohol abuse,
diuretic use, administration of amphotericin B, and primary Rationale:
5) Hypoparathyroidism can cause low serum calcium levels. Numbness and
aldosteronism, as well as GI losses from diarrhea, malabsorption, and tingling in extremities and in the circumoral area around the mouth are the
acute pancreatitis. hallmark signs of hypocalcemia. Normal calcium level is 9 to 11 mg/dl
The magnesium ion is essential for proper function of many enzyme 6) Diaphoresis and a high fever can lead to free water loss through the skin,
systems. resulting in hypernatremia. Loop diuretics are more likely to result in a
Depletion is characterized by neuromuscular and central nervous system hypovolemic hyponatremia. Diarrhea and vomiting cause both sodium and
hyperactivity. water losses. Clients with syndrome of inappropriate antidiuretic hormone
(SIADH) have hyponatremia, due to increased water reabsorption in the renal
Symptoms are similar to those of calcium deficiency, including
tubules.
hyperactive reflexes, muscle tremors, tetany, and positive Chvostek’s 7) An intravenous magnesium infusion may be used to treat a low serum
and Trousseau’s signs magnesium level. Normal serum magnesium is 5 to 2.5 mEq/L. Clinical
Severe deficiencies can lead to delirium and seizures. manifestations of hypermagnesemia are the result of depressed
A number of ECG changes also can occur and include prolonged QT and neuromuscular transmission. Absent reflexes indicate a magnesium level
PR intervals, ST-segment depression, flattening or inversion of P waves, around 7 mEq/L. Diarrhea and PVCs are not clinical manifestations of high
torsades de pointes, and arrhythmias. magnesium levels. Hypermagnesemia causes hypotension.
8) A client with osteoporosis taking vitamin and calcium supplements, a client
Hypomagnesemia is important not only because of its direct effects on with chronic renal failure awaiting dialysis, and a client with
the nervous system but also because it can produce hypocalcemia and hypoparathyroidism secondary to thyroid surgery are at risk for
lead to persistent hypokalemia. hyperphosphatemia. Alcoholics and clients receiving TPN are at risk for low
o When hypokalemia or hypocalcemia coexists with phosphorus levels, due to poor intestinal absorption and shifting of
hypomagnesemia, magnesium should be aggressively replaced to phosphorus into cells along with insulin and glucose.
assist in restoring potassium or calcium homeostasis. 9) 1L = 2.2 lbs = 1kg
Initial weight = 180 lbs Final weight = 175.6 lbs
= 180/2.2 = 175.6/2.2
Causes = 81.8 kg = 79.8 kg
Malabsorption TBW initial = 81.8*0.6 = 49.08 kg TBW final = 79.8*0.6 = 47.88 kg
Malnutrition Fluid loss = 49.08-47.88 = 1.2 kg or 1.2 L or 1200mL
Alcoholism
Loop diuretics
Renal tubular dysfunction
Symptoms-are more severe than hypermagnesemia
Convulsion
Tetany
Hypereactive reflexes
Increase heart rate
Insomnia
Dysarrythmia
Associated with low Ca+ and low K+
What to do?
Cardiac monitor
IV magnesium slow IV (Magnesium gluconate)
Oral supplements

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