Fluid and Electrolytes

Blood, skin,

muscle

Skeleton

Fluid and Electrolytes- These are the liquid component of the human body that account for approximately

60% of the body weight of a typical adult.

Important functions

1. Maintenance of blood volume.

2. Cellular transport of vital substances such as oxygen and glucose.

3. Transport of cellular waste products to the lungs and kidneys for removal.

4. Lubrication and cushioning

5. Hydrolysis of food in the digestive system.

6. Reactant and medium for the chemical reactions in cells.

7. Maintenance of body temperature.

Factors that influence the amount of body fluid are as follows

Influencing Factor Parameter Amount

AgeOlder

Younger

GenderFemale

Male

Body fatAverage

Overweight

Amount of fluid in organs:

Fluid and electrolytes are found in body’s two different compartments:

> Intracellular – within the cell.

> Extracellular – outside the cell.

Approximately, two thirds of the fluid is in the intracellular

compartment and the remaining one third on the extracellular compartment.

Medical Surgical Nursing|

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Column1 Extracellular Fluid

The Intracellular Compartment

- It is primarily located in the skeletal mass.

- It comprises two thirds of the fluid since 70% of a cell is water.

The Extracellular Compartment

- this compartment is further subdivided into:

Interstitial fluid space

o It contains the fluid that surrounds the cell and totals about 11-12L in an

adult.

o It delivers materials as well as removal of body waste.

o It also plays a role in intercellular communication.

Intravascular fluid space

o This makes up the fluid within blood vessels. Approximately 3L of the

average 6L of blood volume is made up of plasma. The remaining 3L then

comprises the erythrocytes, leukocytes, and thrombocytes.

Transcellular fluid space

o This makes up 1% to 3% of body weight or approximately 1L of fluid. It

includes the following:

● Digestive fluid● Pericardial fluid● Pleural fluid● Synovial fluid● Lymphatic fluid● Intraocular fluid● Cerebrospinal fluid

o Large amount of fluid in this space can become sequestered. This event is

what we call “third spacing” . In this event, the fluid is not available for


exchange between compartments or spaces not because of fluid loss.

*Body fluid normally shifts between the two major compartments or spaces in an effort to maintain equilibrium between the spaces ultimately leading to homeostasis that is crucial for life.

Electrolyte Normal Range (mEq/L) FunctionsSodium (Na+)

Intravascular

142

Interstitial

146Intracellula

r

15

● Exerts an extracellular osmolality, thereby regulating movement of body fluids.

●Facilitates nerve impulses through active transport and the sodium-potassium pump

Potassium (K+)

5 5 150

●Maintains nervous impulse conduction in the heart

●Promotes skeletal muscle function

●Plays a small role in osmotic regulation

●Assists with acid-base regulation

Chloride (Cl-)

102 114 1

●Maintains electroneutrality by passively following the positively charged ions

● Helps regulate osmotic pressure differences between intracellular and extracellular fluid compartments

●Regulates body water balance with sodium

● Combines with H+ in gastric mucosal cells to make hydrochloric acid.

Calcium (Ca2+) 5 3 2

● Major structural component of bones and teeth

● Plays a role in blood coagulation

● Promotes muscle contraction and nervous impulse transmission

● Decreases neuromuscular irritability

Phosphorous (PO4+) 2 2 100

● A structural component of bones and teeth

● Helps maintain acid-base balance

● Energy production (ATP)

● Delivery of oxygen to tissues as a component of 2.3-DPG


Magnesium (Mg2+) 2 1 27

● Ensures the cross-membrane transport of sodium and potassium in the sodium-potassium pump

● Promotes neuromuscular excitability

● Plays role in heart contraction

● Facilitates transmission of central nervous system impulses

●Part of many enzymatic reactions for carbohydrate and protein metabolism

Regulation of Fluid Body CompartmentsFluid shifts from through the membrane from region of low solute concentration until

the solutions are of equal concentration. This diffusion of water caused by a fluid

concentration gradient is known as osmosis.

In osmosis, the magnitude of force depends on the number of particles dissolved in

the solutions, not on their weights. The number of dissolved particles contained in a unit of

fluid determines the osmolality of a solution which influences the movement of fluid

between the fluid compartments.

OSMOSIS. Movement of fluid from area of lower solute concentration to an area of higher

solute concentration with eventual equalization of the solute concentrations.

Osmolality expresses the concentration of a solution in terms of how strongly it can

attract water across a membrane. Expressed in osmoles (the amount of molecules/ions in

solution) or milliosmoles per kilogram (mOsm/kg) of the solution, plasma osmolality

averages 290 +/- 5 mOsm/kg.

Tonicity is the ability of all the solutes to cause an osmotic driving force that

promotes water movement from one compartment to another. It determines the normal

state of cellular hydration and cell size. Sodium, glucose, and mannitol do not readily cross

the cell membrane and are therefore effective osmoles affecting water movement.


osmotic pressurehydrostatic pressure

Three other terms are associated with osmosis:

● Osmotic pressure – is the amount of hydrostatic

pressure needed to stop the flow of water by osmosis. It

is primarily determined by the concentration of solutes.

● Oncotic pressure – is the osmotic pressure exerted by

proteins i.e. albumin.

● Osmotic dieresis – is the increase in urine output

caused by the excretion of substances such as glucose,

mannitol, or contrast agents in the urine.

Diffusion is the natural tendency of a substance to move

from an area of higher concentration to one lower concentration. It occurs through the

random movement of ions and molecules.

Examples of diffusion are the exchange of oxygen and carbon dioxide between the pulmonary capillaries and alveoli and the tendency of sodium to move from the ECF compartment, where the sodium concentration is high, to the ICF where the concentration is low.

Filtration

Hydrostatic pressure in the capillaries tends to filter fluid out of the intravascular

compartment into the interstitial fluid. Water and solute movement occurs from an area of

high concentration area to an area of low hydrostatic pressure. This allows the kidneys to

filter 180L of plasma per day.

Another example of filtration is the passage of water and electrolytes from the

arterial capillary bed to the interstitial fluid. In this instance, the hydrostatic pressure is

furnished by the pumping of the heart.

Sodium-Potassium Pump

Since sodium has a greater concentration in the ECF than that of the ICF, it tends to

enter the cell by diffusion. This tendency is offset by the sodium-potassium pump which is

located in the cell membrane and actively moves sodium from the cell into the ECF.

Conversely, the high intracellular concentration of potassium is maintained by

pumping potassium into the cell.


Normal Gains and Loses of Fluid and Electrolytes

A healthy normal person body fluids are constantly being lost and replaced. Water

and electrolytes are gained and lost in various ways and different routes.

Kidneys

This organ is responsible in excreting fluids in the form of urine and accounts for

approximately 1 to 2L in a typical adult. A general rule is that the output is approximately

1mL of urine per kilogram of body weight per hour (1mL/kg/h) in all age groups.

Skin

Sensible perspiration refers to visible water and electrolyte loss through the skin

(sweating). The chief solutes in sweat are sodium, chloride, and potassium. Actual sweat

losses can vary from 0 to 1000 mL or more every hour depending on the environmental

temperature. Continuous water loss by evaporation (approximately 600mL/day) occurs

through the skin as insensible perspiration, a non-visible form of water loss. Fever

greatly increases insensible water loss through the lungs and the skin, as does of the natural

skin barrier i.e. major burns.

Lungs

The lungs normally eliminate water vapor (insensible loss) at a rate of approximately

400mL every day. The loss is much greater with increased respiratory rate or depth, or in a

dry climate.

Gastrointestinal Tract

Eight liters of fluid circulates through the GI tract every 24 hours but has the usual

loss of only 100-200mL daily. This happens because the bulk of the fluid is normally

reabsorbed in the small intestine.

Approximate values of average gains and losses

Average Daily Intake and Output in an Adult

Intake (mL) Output (mL)


Oral Liquids 1200-1300 Urine 1500

Water in Food 1000 Stool 150-200

Metabolism 300 Insensibl

e

Lungs 300-350

Skin 500-600

Total 2500-2600 Total 2500-2600

Laboratory Tests for Evaluating Fluid Status

Osmolality

It is the concentration of fluid that affects the movement of water between fluid

compartments by osmosis. It also measures the solution’s ability to create osmotic pressure

and affect the movement of water. It is expressed as milliosmoles per kilogram of water

(mOsm/kg).

Osmolarity is another term that describes the concentration of solutions but osmolality is

more commonly used in clinical practice. It is expressed as milliosmoles per liter of solution

(mOsm/L)

Serum osmolality primarily reflects the concentration of sodium, although blood

urea nitrogen (BUN) and glucose play a major role in determining serum osmolality.

Plasma osmolality- it is useful to measure

this because plasma osmolality is the main

regulator of the release of antidiuretic

hormone (ADH), which plays a major role in

water regulation. Since sodium predominates

in the ECF, plasma osmolality can be estimated by bedside by doubling the serum sodium

level or by using the formula:

Na+ x 2 = Glucose + BUN 18 3 *approximate value of serum osmolality

Urine osmolality- determined by urea, creatinine, and uric acid. When measured with

osmolality, urine osmolality is the most reliable indicator of urine concentration.

Urine specific gravity- measures the kidneys’ ability to excrete or conserve water. The

specific gravity of urine of compared to the weight of distilled water, which has the specific

gravity of 1.000. Normal range for specific gravity is 1.010 to 1.025. Urine specific gravity

can be measured in two ways:

By placing a calibrated hydrometer or urinometer in a cylinder of approximately

20mL of urine.


Osmolality Normal Range

Serum/Plasma 275-300 mOsm/kg

Urine 250-900 mOsm/kg

By using refractometer or dipstick with a reagent for this purpose.

Specific gravity varies inversely with urine volume: normally, the larger the volume of the

urine, the lower the specific gravity. Specific gravity is a less reliable indicator of urine

concentration than that of the urine osmolality since increased glucose or protein can falsely

elevate specific gravity.

Factors Affecting Serum and Urine Osmolality

Fluid Increasing Osmolality Decreasing Osmolality

Serum

(275-300 mOsm/kg water)

● Severe dehydration

● Free water loss

● Diabetes insipidus

● Hypernatremia

● Hyperglycemia

● Stroke or head injury

● Renal tubular necrosis

● Consumption of methanol

● Fluid volume excess

● SIADH

● Renal failure

● Diuretic use

● Adrenal insufficiency

● Hyponatremia

● Overhydration

●Paraneoplastic syndrome

Urine

(250-900 mOsm/L water)

● Fluid volume deficit

● SIADH

● Congestive heart failure

● Acidosis

● Fluid volume excess

● Diabetes insipidus

● Hyponatremia

● Aldosteronism

● Pyelonephritis

Blood Urea Nitrogen (BUN)

It is the end product of the metabolism of protein (from both muscle and dietary

intake) by the liver.

The normal BUN is 10 to 20 mg/dL (3.6 to 7.2 mmol/L). The BUN level varies with

urine output.

Factors that increase BUN includes: Factors that decrease BUN

includes:

● Decreased renal function ● End-stage liver disease

● Gastrointestinal bleeding ● Low protein diet

● Dehydration ● Starvation

● Increased protein intake ● Conditions that expand fluid

volume

● Fever

● Sepsis

Creatinine

It is the end product of muscle metabolism. It is a better indicator of renal function

than BUN since it does not vary with protein intake and metabolic state. The concentration

however depends on lean body mass and therefore varies from person to person. The

normal serum creatinine is approximately 0.7 to 1.4 mg/dL (62 to 124 mmol/L) Creatinine

levels increase when renal function decreases.


Amino acid

Ammonia molecule

sUrea

Excretion through

urine

Hematocrit

It measures the volume percentage of red blood cells (erythrocytes) in whole blood

and normally ranges from 42% to 52% for males and 35% to 47% for females.

Urine Sodium Values

It changes with sodium intake and the status of fluid volume: as sodium intake

increases, excretion increases and as the circulating fluid volume decreases, sodium is

conserved.

Normal urine sodium levels range from 75 to 200 mEq/24 h (75 to 200 mmol/24 h).

A random specimen usually contains more than 40 mEq/L of sodium. Urine sodium levels

are used to assess volume status and are useful in the diagnosis of hyponatremia and acute

renal failure.

Homeostatic Mechanisms

Kidney Functions

The kidneys normally filter 170 L of plasma every day in adult while excreting only

1.5 L of urine. Major functions of the kidneys in maintaining normal fluid balance include

the following:

Regulation of the ECF volume and osmolality by selective retention and excretion

of body fluids.

Regulation of electrolyte levels in the ECF by selective retention of needed

substances and excretion of unneeded substances.

Regulation of pH of the ECF by retention of hydrogen ions.

Excretion of metabolic wastes and toxic substances.

*For geriatric patients, there may substantially reduced renal function therefore there may

be high-normal or minimally elevated creatinine levels.

Heart and Blood Vessel Functions

The pumping action of the heart circulates blood through the kidneys under sufficient

pressure to allow for urine formation. Failure of this pumping action interferes with renal

perfusion and thus with water and electrolyte regulation.

Lung Function

Through exhalation, the lungs remove approximately 300 mL of water daily in the

normal adult. Abnormal conditions, such as hyperpnea (abnormally deep respiration) or


Increase in hematocrit DehydrationPolycythemia

Decrease in hematocrit OverhydrationAnemia

continuous coughing increases fluid loss; mechanical ventilation with excessive moisture

decreases the loss.

Also, the lungs play a major role in maintaining acid-base balance.

Pituitary Functions

The hypothalamus manufactures ADH, which is stored in the posterior pituitary

gland and released as needed. ADH is sometimes called the water conserving hormone

because it causes the body to retain water.

Adrenal Functions

Aldosterone, a mineralocorticoid secreted by the zona glomerulosa of the adrenal

cortex, has a profound effect on fluid balance. Increased secretion of aldosterone causes

sodium retention and thus, water retention and potassium loss; conversely, decreased

secretion of aldosterone causes sodium and water loss and potassium retention.

Parathyroid Functions

This organ embedded in the thyroid gland, regulates calcium and phosphate balance

by means of the parathyroid gland (PTH). The PTH influences bone resorption, calcium

absorption from intestine, and calcium reabsorption from renal tubules.

Baroreceptors

These are small nerve cell receptors that detect changes in pressure within blood

vessels and transmit this information to the central nervous system.

Renin-Angiotensin-Aldosterone System

Aldosterone is a volume regulator and is also released as serum potassium increases, serum

sodium decreases, or adrenocorticotropic (ACTH) hormone increases.

Antidiuretic Hormone (ADH) and Thirst

ADH and thirst mechanism have important roles in maintaining sodium concentration

and oral intake of fluids. Oral intake is controlled by the thirst center located in the

hypothalamus. As serum concentration or osmolality increases or blood volume decreases,

neurons in the hypothalamus are stimulated by intracellular dehydration; thirst then occurs,

and the person increases her intake of oral fluids.

The absence or presence of ADH is the most significant factor in determining whether

the urine that is excreted is concentrated or dilute.


Decreased renal perfusion

Release of renin by the juxtaglomerular cell in the kidneys.

Converts angiotensinogen found in

the liver into ANGIOTENSIN I

ANGIOTENSIN II in the lungs

VASOCONSTRICTION

Activates SNS thereby releasing ALDOSTERONE

SNS stimulatio

n

Angiotensin II

stimulation

Increased

arterial pressur

e

Atrial Natriuretic Peptide (ANP) also called atrial natriuretic factor

It is a 28-amino-acid peptide that is synthesized, stored, and released by muscle cells

of the atria of the heart in response to several factors.

Osmoreceptors

Located on the surface of the

hypothalamus, it changes sodium

concentration. As osmotic pressure

increases, the neurons become

dehydrated and quickly release impulses

to the posterior pituitary which increases

the release of ADH. The ADH then travels

in the blood to the kidneys, where it alters

permeability to water causing increased

reabsorption of water and decreased urine

output. The retained water dilutes the ECF

and returns its concentration to normal.

Restoration of normal osmotic pressure

provides feedback to the osmoreceptors

to inhibit further ADH release.

Fluid Volume Disturbances

HYPOVOLEMIA

Also known as fluid volume deficit it occurs when loss of ECF volume exceeds the

intake of fluid. It occurs when water and electrolytes are lost in the same proportion as they

exist in normal body fluids, so that the ratio of serum electrolytes to water remains the

same.


It should not be confused with the term dehydration which refers to loss of water

alone, with increased serum sodium levels.

Third space fluid shifts or the movement of fluid from vascular system to other body

spaces also cause fluid volume deficit as in edema formation in burns or ascites with liver

dysfunction.

Clinical manifestations:

Acute weight loss Decreased skin turgor

Oliguria Cool, clammy skin related to peripheral

vasoconstriction

Postural hypertension Weak, rapid heart rate

Flattened neck veins Increased temperature

Thirst, anorexia, nausea, latitude Muscle weakness and cramps

Decreased central venous pressure Concentrated urine

Assessment and Diagnostic Findings:

Elevated BUN out of proportion to the serum creatinine (ratio greater than 20:1)

The cause can be identified through the patient’s health history and physical

examination

Increased hematocrit level since red blood cells become suspended in a

decreased plasma volume.

Electrolyte changes: sodium and potassium

● Hypokalemia occurs with GI and renal losses

● Hyperkalemia occurs with adrenal insufficiency

● Hyponatremia occurs with increased thirst and ADH release.

● Hypernatremia results from increased insensible losses and diabetes insipudus.

Urine specific gravity is increased in relation to the kidneys’ attempt to conserve

water and decreased with diabetes insipidus

Urine osmolality is greater than 450 mOsm/kg because the kidneys try to

compensate by conserving water.

Medical management


Hypovolemia

vomiting, diarrhea,

suctioning, sweating

decreased intake or inability to gain access to

water

diabetes insipidus, adrenal

insufficiency, osmotic diuresis, hemorrhage, and

coma

The ultimate goal is to replace the lost fluid and electrolyte and the health care

provider plans for the maintenance requirements of the patient. If the deficit is not very

severe, the oral route is preferred, provided that the patient can drink.

However, if the fluid losses are acute or severe, the intravenous route is required.

Isotonic Intravenous Fluids

Solution Common Use

0.9% NaCl (308 mOsm/L)

[Na+ 154 mEq/L] [Cl- 154mEq/L]

● Expands ECF; beneficial in providing fluid

replacement when sodium and chloride loss has

occurred.

● Not used for maintenance

D5W (252 mOsm/L)

[5% dextrose in water]

● Used when replacing water in hypernatremic

patients.

● Provides 170 calories

● Can lead to water intoxication and dilutional

hyponatremia

Lactated Ringer’s Solution (274

mOsm/L)

[Na 130 mEq/L, Cl 109 mEq/L, K 4

mEq/L,

Ca 3 mEq/L, lactate 28 mEq/L]

● Used for replacement of fluid because of multiple

electrolytes and isotonic expansion of blood

volume.

● Used commonly for GI losses

● Not given for more than 48 hours due to the

riosk of calcium depletion.

Dextran 70 [6% solution of

polysaccharide combined with saline

or dextrose or water]

● Expands blood volume

● Decreases blood viscosity

Hetastarch (310 mOsm/L) ● Used for rapid volume expansion

● May prolong bleeding time

Hypotonic Solutions

Solution Common use

0.45% NaCl (1/2 strength) (154

mOsm/L)

[1/2 normal saline, ½ water]

0.33% NaCl (1/3 strength) (103

mOsm/L)

[1/3 normal saline, 2/3 water]

● These are fluids that hydrate the cell and do not

provide calories.

● Useful in treating hypernatremia when it is

desired to replace water and sodium.

Hypertonic Solutions

Solutions Common Use

5% dextrose in 0.45% NaCl (406

mOsm/L)

● Promotes hydration and good for maintenance

50% dextrose in water (2525

mOsm/L)

● Used to treat hypoglycemia and nutritional

replacement

● Can cause osmotic dieresis

3% or 5% NaCl (grossly hypertonic) ● Used to treat SIADH


● Can cause increased intracranial pressure

Albumin (25%) [1500 mOsm/L]

given in 50 or 100 ml units

● Expands plasma volume and increases oncotic

pressure

● Use with caution in cardiac or renal patients

HYPERVOLEMIA

This refers to an isotonic expansion of the ECF caused by the abnormal retention of

water and sodium in approximately the same proportions in which they normally exist in the

ECF. It is always secondary to an increase in the total body sodium content, which, in turn,

leads to an increase in total body water. Since there is isotonic retention of body substances,

the serum sodium concentration remains essentially normal.

Clinical manifestations

These stem from expansion of the ECF and include:

Edema

Distended neck veins

Crackles over the lung field

Tachycardia, increased blood pressure

Shortness of breath and wheezing

Increased weight

Assessment and Diagnostic Findings

Decreased BUN and hematocrit levels because of plasma dilution

If with renal problems:

o decreased serum osmolality and sodium level

o increased sodium level

Chest x-rays may reveal pulmonary congestion

Medical Management

Management will always be directed at the causes i.e. removing the offending

substance or drug as in excessive administration of sodium-containing fluids.

Symptomatic treatment consists of administering diuretics and restricting fluid and

sodium.

● Pharmacologic treatment

Diuretics- the choice of drug will be based on the following:

Severity of the hypervolemic state

Degree of impairment of renal function


Simple fluid overload

Diminished homeostatic functions

Excessive administration of table salts

Excessive administration of sodium-containing fluids

Potency of the diuretic

● Thiazide diuretics – block sodium reabsorption in the distal tube, where 5% to

10% of filtered sodium is reabsorbed. Eg. hydrochlorothiazide or metolazone.

● Loop diuretics – block sodium in the ascending limb of the loop of Henle, where

20%-30% of sodium is reabsorbed. Eg. furosemide, bumetanide, or torsemide

Usage of diuretics can also cause hypokalemia since potassium will also be

removed. Diuretics that act on the last distal tubule of the nephrons (eg.

Spirinolactone) will prevent hypokalemia. However, these kinds of diuretics can

cause hyperkalemia especially in patients with decreased renal function.

Hyponatremia occurs with diuresis due to increased release of ADH secondary to

reduction in circulating volume.

Hypomagnesemia occurs due to decreased reabsorption and increased excretion of

magnesium by the kidney.

● Hemodialysis

This modality will reinforce removal of excess sodium and fluid from the body.

● Nutritional Therapy

Dietary restriction of sodium

● A normal diet without sodium restriction commonly contains 6 to 15 g of

salt whereas a sodium-restricted diet can range from mild restriction to as

little as 250 mg of sodium.

● Half of ingested sodium is in the form of seasoning therefore, seasoning

substitute can

play a major role in decreasing sodium intake.

Water restriction

● Depending on water source, it may contain as little as 1 mg or more than

1500 mg per quart. Distilled water may be needed to use or if bottled water

will be used, the label must be carefully read because some of them have 0 to

1200 mg/L.

Protein intake may be increased in patients who:

● Are malnourished

● Have low serum protein levels in an effort to increase capillary oncotic

pressure and pull fluid out of the tissues into vessels for excretion by the

kidneys.

Nursing Management

Accurate measurement of intake and output

This should be done on a daily basis, taken at the same time and with the

same clothes the patient wears. A weight gain of 2.2 lb (1kg) is equivalent to a

gain of 1 L of fluid

Assessment of breath sounds

This should be done at regular intervals in an at risk patients, particularly if

parenteral fluid is being administered.

Assessment of edema


The nurse should assess to monitor for the degree of edema in the most

dependent parts of the body such as the feet and ankles in ambulatory patients

and the sacral region in patients confined to bed.

The degree of pitting edema is assessed and the extent of peripheral edema

is monitored by measuring the circumference of the extremity with a tape marked in

millimeters.

Preventing Fluid Volume Excess

● Adherence to sodium-restricted diet

● Avoiding over-the-counter drugs for they may contain sodium

Detecting and Controlling Fluid Volume Excess

● Regular rest periods may be beneficial because bed rest favors diuresis

of edema fluid. This should promote blood circulation and increase renal

perfusion since this will diminish venous pooling.

● Rate of parenteral fluid and patient’s response must be closely

monitored. If dyspnea or orthopnea is present, the patient is placed then to

semi-fowler’s position to promote lung expansion. The patient cold also be

turned at different positions at regular intervals.

Teaching Patients About Edema

Edema is a common manifestation of FVE and patients need to recognize its

symptoms and understand its importance.


INCREASED CAPILLARY PERMEABILITY (burns, allergic inflammation reaction)

Loss of plasma proteins

DECREASED CAPILLARY ONCOTIC PRESSURE INCREASED TISSUE ONCOTIC PRESSURE

EDEMA

Decreased transport of capillary filtered protein

LYMPH OBSTRUCTION

Decreased absorption of interstitial fluid

Decreased absorption of interstitial fluid

Fluid movement to tissues

Increased Na + H20 renal retention

Edema can be localized (in the ankle as in rheumatoid arthritis) or generalized (as

in cardiac and renal failure). A severe generalized edema is called anasarca. Pitting

Edema is so named because a pit forms after a finger is pressed in to the edematous area.

In pulmonary edema, the amount of fluid in the pulmonary interstitium and the alveoli

increases. The patient with pulmonary edema commonly complains of shortness of breath,

diaphoresis, increased respiratory rate, diaphoresis, and crackles and wheezing upon lung

auscultation.

Ascites is a form of edema in which fluid accumulates in the peritoneal cavity; it

results from nephritic syndrome, cirrhosis, and some malignant tumors. The patient

commonly reports shortness of breath, and a sense of pressure because of the

pressure on the diaphragm.

The goal of treatment is to preserve or restore the circulating intravascular fluid volume.

Signs and symptoms of hypervolemia and hypovolemia

Parameters Hypovolemia HypervolemiaSkin and

subcutaneous tissues

Dry, less elastic Warm, moist, pitting edema over bony prominences,

wrinkled skin from pressure of clothing

Face Sunken eyes (late symptom) Periorbital edema

Tongue Dry, coated (early symptom)Fissured (late symptom)

Moist

Saliva Thick, scanty Excessive, frothy

Thirst Present May not be significant

Temperature May be elevated May not be significant

Pulse Rapid, weak, thread Rapid

Respirations Rapid, shallow Rapid dyspnea, moist rales, cough

Blood pressure Low, orthostatic hypotension, small pulse pressure

Normal to high

Weight Loss Gain

Factors affecting water balance

Water Excess Water DeficiencyIntake Thirst Decreased thirst threshold

Increased osmolalityPotassium depletionHypercalcemiaFeverDry mucous membranes, poor oral hygiene, unmisted O2 administrationHypotension

Increased thirst thresholdDecreased osmolalityLack of accessPsychiatric disorders


Parenteral fluids Psychiatric disordersExcessive D5W

Deficient replacementOsmotic loadsHyperalimentationHyperglycemiaMannitolRadiographic contrast agents

Output Sweating High ambient temperatureHigh altitudeFever

Renal excretion Inappropriate ADH releaseAppropriate ADH releaseCongestive heart failureDecompensated cirrhosisVolume depletionAdrenal insufficiencyRenal salt wastingHemorrhageDiuretics, NSAIDs BurnsHypothyroidismRenal diseases

Excess excretionPotassium depletionHypercalcemiaLithium administrationDemeclocycline Methoxyflorane

source: 8th ed. Critical Care Nursing Morton et. al. pp. 656

Electrolyte Imbalances

SODIUM IMBALANCESSodium is regulated by ADH, thirst, and the renin-angiotensin-aldosterone system. It

is the primary regulator of ECF volume. A loss or gain of sodium is usually accompanied by a loss or gain of water.

Electrolyte Imbalance

Clinical manifestations Diagnostic test results

HYPONATREMIASodium deficit

● Muscle twitching

● Lethargy, confusion, seizures, and coma

● Hypotension and tachycardia

● Nausea and vomiting

● Oliguria or anuria

● Serum sodium <135 mEq/L

● Decreased urine specific gravity

● Decreased serum osmolality

● Urine sodium

● Increased RBC count

Contributing Factors

Loss of sodium, as in use of diuretics, loss of GI fluids, renal disease, and adrenal insufficiency.

Gain of water as in excessive administration of D5W and water supplements. Disease states associated with SIADH such as head trauma and oat-cell lung tumor Medications associated with water retention (oxytocin and certain tranquilizers) Hyperglycemia and heart failure

Medical Management

Sodium replacement


Careful administration of sodium by mouth, nasogastric tube, or parenteral

route. Serum sodium must not be increased by more than 12 mEq/L in 24

hours to avoid neurologic damage due to osmotic demyelination.

Water restriction

Hyponatremia is treated by restricting fluid to a total of 800 mL in 24 hours.

This is far safer than sodium administration and is usually effective but if

neurologic symptoms are present, administration of hypertonic solutions is

needed.

Nursing Management

The nurse monitors for the patient’s intake and output daily and measures the

patient’s weight on a daily basis as well.

The nurse should also watch out for central nervous system changes such as:

o Lethargy

o Confusion

o Muscle twitching

o Seizures

Watch out for GI symptoms such as

o Anorexia

o Nausea

o Vomiting

o Abdominal cramping



HYPERNATREMIA

Sodium excess

● Agitation, restlessness, fever, and decreased level of consciousness

● Hypertension, tachycardia, pitting edema, and excessive weight gain

● Thirst, increased viscosity of saliva, rough tongue

● Dyspnea, respiratory arrest, and death

● Serum sodium >145mEq/L

● Urine sodium <40 mEq/24h

● High serum osmolality

Contributing factors

Water deprivation

Diabetes insipidus

Heat stroke

Hyperventilation

Watery diarrhea

Burns, diaphoresis

Excess corticosteriod, sodium bicarbonate, and sodium chloride administration

Salt water near drowning

Medical Management


Gradual lowering of the serum sodium level by infusing hypotonic (0.3% NaCl)

electrolyte solution or an isotonic nonsaline (D5W) solution.

To decrease the risk for cerebral edema, hypotonic solution is used rather than

using D5W because a hypotonic solution allows a gradual reduction in the serum

sodium level.

Diuretics may also be prescribed to treat sodium excess.

As a general rule, the serum sodium level is reduced at a rate not faster than 0.5 to

1 mEq/L per hour to allow sufficient time for readjustment through diffusion across

fluid compartments.

Nursing Management

Alert the patient about using over-the-counter medications that have a high salt

content.

The nurse must also obtain medication history.

Note the patient’s thirst or elevated body temperature.

Monitor for behavioral changes such as restlessness, disorientation, and lethargy.

Monitor for the patient’s response if he is on parenteral fluids to manage the

condition.

POTASSIUM IMBALANCES

It is the major intracellular electrolyte and 98% of the body’s potassium is inside the

cell and the remaining 2% is in the ECF, this 2% is important in neuromuscular function.



HYPOKALEMIAPotassium deficit

● Dizziness, hypotension, dysrhythmias, ECG changes, and cardiac arrest

● Nausea, vomiting, anorexia, diarrhea, decreased peristalsis, and abdominal distension

● Muscle weakness, fatigue, and leg cramps

● Serum potassium <3.5mEq/L

● Coexisting low serum calcium and magnesium levels not responsive to treatment for hypokalemia usually suggest hypomagnesemia

● Metabolic alkalosis

● ECG changes, including flattened T waves, elevated U waves, depressed ST segment


Diarrhea


Vomiting

Gastric suction

Corticosteriod administration, diuretic administration

Bulimia, starvation

Alkalosis

Digoxin toxicity

Medical Management

Oral or intravenous replacement therapy.

Administration of 40 to 80 mEq/L of potassium is adequate in an adult without

abnormal losses.

Foods high in potassium such as fruits and vegetable, legumes, whole grains, milk,

and meat should be recommended.

IV route for replacement is mandatory if the deficit is severe (2 mEq/L)

Nursing Management

Watch out for fatigue, anorexia, muscle weakness, decreased bowel motility,

paresthesias, and dysrhythmias.

Closely monitor patients who are taking digitalis for they are prone for digitalis

toxicity.

NEVER ADMINISTER POTASSIUM BY IV PUSH.

Potassium should be administered only after adequate urine flow has been

established.

Look closely for ECG changes (flat T wave or a prominent U wave)

Renal function should be monitored through BUN and creatinine levels and urine

output.

Great care should be taken when administering potassium most especially in older

adults, who have lower lean mass and total body potassium levels and therefore

lower potassium levels.

Remember that loss of renal function declines with advancing years so potassium

may be retained more readily in older adult than in younger people.



HYPERKALEMIAPotassium excess

● Tachycardia changing to bradycardia, ECG changes, and cardiac arrest

● Nausea, vomiting, and abdominal cramps

● Muscle weakness and flaccid paralysis

● Serum potassium >5mEq/L

● Metabolic acidosis

● ECG changes, including tented and elevated T waves, widened QRS complex, prolonged PR interval, flattened or absent P waves, depressed ST segment



Oliguric renal failure Use of potassium sparing diuretics Metabolic acidosis Crush injury Burns Rapid IV administration of potassium

Medical Management

An immediate ECG should be obtained. Shortened repolarization and peaked T

waves are seen initially.

Do a repeat serum potassium level from a vein without an IV infusing potassium.

In non-acute situations, potassium restricted diet is advised and removal of

potassium-containing medications.

Prevention of hyperkalemia can be achieved by administration either orally or

through retention enema of cation exchange resins (i.e. Kayexalate) however this

medication is contraindicated for patients with paralytic ileus because

intestinal perforation can occur.

If K levels are dangerously elevated, it may be necessary to administer IV calcium

gluconate. This drug will not reduce the serum potassium but will antagonize

adverse cardiac conduction abnormalities. Be aware that calcium gluconate is not

interchangeable with calcium chloride because calcium gluconate has 4.5 mEq

of calcium and calcium chloride has 13.6 mEq/L of calcium.

IV administration of sodium bicarbonate may be necessary to alkalinize the

plasma and cause a temporary shift of potassium into the cells.

The use of beta-2 antagonists such as albuterol shows an evidence of highly

effective decreasing of potassium but remains controversial because they can cause

tachycardia and chest discomforts.

If hyperkalemic condition is transient, actual removal of potassium is necessary. This

could be done by using cation exchange resins, peritoneal dialysis, hemodialysis, or

other forms of renal replacement therapy.

IV administration of insulin and a hypertonic dextrose solution causes a

temporary shift of potassium into the cells. Diuretics can also be used to excrete

potassium.

Nursing management

Early identification of hyperkalemia in patients at risk should be done i.e. those with

renal failure.

The nurse then observes for signs of muscle weakness and dysrhythmias. Also,

observe for signs of paresthesias and GI disturbances such as nausea and

intestinal colic are noted.

To avoid erroneous reports of high serum potassium levels, observe the following

when withdrawing the blood:


Avoid prolonged use of a tourniquet

Warn the patient not to exercise the extremity before the blood is

drawn.

Do not take the blood sample at the extremity where potassium is

administered.

Deliver the blood sample as soon as possible to prevent hemolysis.

Reinforce potassium-restricted diet. The following foods should be avoided:

Fruits and vegetables

Legumes

Whole-grain breads

Meat

Milk and eggs

Coffee, tea, and cocoa

Conversely, the following foods can be prescribed for they have minimal potassium

content:

Butter and margarine

Cranberry juice or sauce

Ginger ale

Gumdrops or jellybeans

Hard candy

Root beer

Sugar and honey

Great care should be taken when administering potassium, paying close attention to

the solution’s concentration and rate of administration.

Remember that potassium is always incorporated to the IV solution and then

mixed with the fluid by inverting the bottle several times.

Remember not to add the potassium in a hanging bottle because potassium might

be administered as a bolus.

CALCIUM IMBALANCES

More than 99% of the body’s calcium is located in the skeletal system; calcium is a

major component of bones and teeth. About 1% of skeletal calcium is rapidly exchangeable

with blood calcium, and the rest is more stable and only slowly exchanged. Calcium plays a


major role in transmitting nerve impulses and helps regulate muscle contraction and

relaxation, including cardiac muscle.



HYPOCALCEMIACalcium deficit

● Anxiety, irritability, twitching around the mouth, laryngospasm, seizure, positive Chvostek’s sign and Trousseau’s sign

● Hypotension and dysrhythmias due to decreased calcium influx

● Tetany

● Serum calcium <8.5mg/dL

● Low platelet count

● ECG changes: lengthened QT interval, prolonged ST segment, arrhythmias

● Possible changes in serum protein levels


Hypoparathyroidism that may follow thyroid surgery or radical neck dissection.

Malabsorption, Vitamin D deficiency, alkalosis

Pancreatitis

Massive subcutaneous infection

Generalized peritonitis

Massive transfusion of citrated blood

Chronic diarrhea

Decreased parathyroid hormone

Diuretic phase of renal failure

Burns

Medical Management

Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment

with IV administration of calcium. Parenteral administration of calcium salts

include the following:

o Calcium gluconate, calcium chloride, calcium gluceptate

Although calcium chloride has significantly more ionized calcium level,

I is not commonly used because it is more irritating and can cause

sloughing of tissue if it infiltrates.

Administer calcium diluted in D5W solution and given as slow IV bolus of slow IV

infusion. It should not be given with 0.9% sodium chloride because it increases renal

calcium loss.

Vitamin D therapy may be instituted to increase calcium absorption.

Aluminum hydroxide, calcium acetate, or calcium carbonate antacids may be

prescribed to decrease elevated phosphorous levels before treating hypocalcemia in

patients with chronic renal failure.


Nursing Management

Calcium can cause postural hypotension therefore; the patient must be kept in

bed.

Observe the patient for signs of digitalis toxicity because calcium ions exert a

similar effect to that of the digitalis.

Also, the nurse must closely observe the rate of administration because too rapid IV

administration can cause cardiac arrest.

The nurse must also clarify with the physician about which calcium salt should be

administered since calcium gluconate yields 4.5 mEq/L of calcium while

calcium chloride yields 13.6 mEq/L.

Seizure precautions must be initiated and status of the airway is given paid

more attention. Safety precaution is also observed because patient may experience

confusion.

Recommend taking foods that are high in calcium to at least 1000-1500 md/day:

o Milk products

o Green, leafy vegetables

o Canned salmons or sardines

o Fresh oysters

The nurse must also advise the patient in taking in calcium supplements if calcium

cannot be well supplied by the patient’s diet. These supplements must be taken in

divided doses with meals.

Warn the patient about alcohol and caffeine intake because these can decrease

calcium absorption, and smoking increases urinary calcium excretion.

The patient is also cautioned about the overuse of laxatives and antacids that

contain phosphorus because their use decreases calcium absorption.



HYPERCALCEMIACalcium excess

● Drowsiness, lethargy, headaches, irritability, confusion, depression, or apathy

● Weakness and muscle flaccidity

● Bone pain and pathological fractures

● Heart block

● Anorexia, nausea, vomiting, constipation, and dehydration● Flank pain

● Serum calcium >10.5mg/dL

● ECG changes: sign of heart block and shortened QT interval

● Azotemia

● Decreased parathyroid hormone level


Hyperparathyroidism, malignant neoplastic disease

Prolonged immobilization

Overuse of calcium supplements or Vitamin D excess


Oliguric phase of renal failure

Thiazide diuretic use

Increased parathyroid hormone, digoxin toxicity

Medical Management

Therapeutic aims in hypercalcemia include decreasing the calcium serum level

Reversing the process causing hypercalcemia

Treating the underlying cause includes:

o Chemotherapy for a malignancy

o Parathyroidectomy for hyperparathyroidism

IV administration of 0.9% sodium chloride solution to temporarily dilute the serum

calcium level and increases urinary calcium excretion by inhibiting tubular

reabsorption of calcium.

Administration of IV phosphate can cause a reciprocal drop in serum calcium

Furosemide is often used in conjunction with administration of saline solution to

cause diuresis increasing calcium excretion.

Calcitonin is often used to lower calcium levels for patients with heart disease or

renal failure who cannot tolerate large amounts of sodium. It reduces bone

resorption, increasing depositing of calcium and phosphorous in the bones and

increases urinary excretion of calcium and phosphorous.

Nursing Management

Remember to do skin allergy testing before administration of calcitonin and must be

administered intramuscularly rather than subcutaneously because patients with

hypercalcemia have poor perfusion in the SQ.

Encourage mobilization and increasing fluid intake. Fluids with sodium are

encouraged unless contraindicated because sodium favors calcium excretion. The

patient is advised to take 3 to 4 quarts of fluids.

Adequate fiber should be provided in the diet to offset a tendency of constipation.

The patient and the family are informed that there may be some mental changes

and can be reversed with the treatment.


MAGNESIUM IMBALANCESMagnesium is the second most abundant electrolyte in the intracellular compartment

after potassium. It acts as an activator for many intracellular enzyme systems and plays a

role in both carbohydrate and protein metabolism. Magnesium produces its sedative effect

at the neuromuscular junction, probably by inhibiting the release of the neurotransmitter

acetylcholine.



HYPOMAGNESEMIAMagnesium deficit

● Nearly always co-exists with hypokalemia and hypocalcemia

● Hyperirritability, tetany, leg and foot cramps, positive Chvostek’s sign and Trousseau’s sign, confusion, delusions, and seizures

● Dysrhythmias, vasodilation, and hypotension

● Serum magnesium <1.5mEq/L

● Coexisting low serum potassium and calcium levels


Hyperparathyroidism, hyperaldosteronism

Chronic alcoholism

Diuretic phase of renal failure

Malabsorption

Diabetic ketoacidosis

Refeeding after starvation, parenteral nutrition

Chronic use of laxative, diarrhea

Acute myocardial infarction, heart failure

Decreased serum potassium and calcium

Pharmacologic agents (gentamicin, cisplatin, cyclosporine)

Medical Management

Mild magnesium deficiency can be corrected by diet alone. The following foods are

principal dietary sources of magnesium:

o Green leafy vegetables

o Nuts, seeds, legumes, whole grains, and seafood

o Peanut butter and cocoa

Magnesium salts can be administered orally in an oxide or gluconate form to replace

continuous excessive losses. Magnesium sulfate is the most commonly used

magnesium salt.

Nursing Management


Patients receiving IV magnesium should be monitored not to exceed 150 mg/min or

67 mEq/L over 8 hours.

Vital signs must be monitored accurately to identify changes in cardiac rhythm,

hypotension, and respiratory distress.

Monitoring of the patient’s urine output before and after magnesium administration;

physician is notified if the urine output is less than 100 mL over 4 hours

Calcium gluconate must be readily available to treat possible hypocalcemic tetany or

hypomagnesmia

Seizure precaution is instituted

The ability to swallow should be assessed with water before administering oral

medications or food to the patient.

The nurse also assesses neuromuscular irritability by grading deep tendon reflexes.

For patients experiencing hypomagnesemia from abuse of alcohol, the nurse

provides teaching, counseling, support, and possible referral to alcohol abstinence

programs.



HYPERMAGNESEMIAMagnesium excess

● Uncommon, caused by decreased renal excretion (renal failure) or increased intake of magnesium

● Diminished reflexes, muscle weakness to flaccid paralysis

● Respiratory distress

● Heart block, bradycardia

● Hypotension

● Serum magnesium >2.5mEg/L

● Coexisting elevated potassium and calcium levels


Oliguric phase of renal failure

Adrenal insufficiency

Excessive IV magnesium administration

Diabetic ketoacidosis

Hypothyroidism

Medical Management

This can be prevented by avoiding the administration of magnesium to patients with

renal failure.

In emergency situations such as respiratory distress or defective cardiac

conduction, ventilator support and IV calcium gluconate are indicated. IV calcium

gluconate will antagonize the effect of magnesium in the cardiovascular and

neuromuscular systems.


Hemodialysis with magnesium-free dialysate can reduce the serum magnesium to a

safe level within hours.

Administration of loop diuretics and sodium chloride or Lactated Ringer’s solution

enhances magnesium excretion in patients with adequate renal function.

Nursing Management

The nurse monitors for hypotension and shallow respirations as well as decreased

patellar reflexes and diminished level of consciousness.

Caution is essential when taking over-the-counter drugs that may contain

magnesium.

PHOSPHOROUS IMBALANCESIt is essential to the function of muscle and red blood cells, the formation of

adenosine triphosphate (ATP) and of 2,3-diphosphoglycerate which facilitates release of

oxygen from hemoglobin, and the maintenance of acid-base balance, as well as to the

nervous system and the intermediary metabolism of carbohydrate, protein, and fat.

Electrolyte Imbalance Clinical manifestations Diagnostic test results

HYPOPHOSPHATEMIAPhosphorous deficit

● Muscle weakness, tremor, and paresthesia

● Peripheral hypoxia

● Serum phosphate <2.5mg/dL

● Urine phosphate >1.3g/24h


Refeeding after starvation

Alcohol withdrawal

Diabetic ketoacidosis, respiratory alkalosis

Decreased magnesium and potassium, vitamin D deficiency

Vomiting, diarrhea

Hyperparathyroidism

Burns, acid-base disorders

Diuretic and antacid use

Medical Management

Adequate amounts of phosphate should be added to parenteral solutions, and

attention should be paid to the phosphorous levels in enteral feeding solutions.

Aggressive IV phosphorous correction is usually limited to patients whose serum

phosphorous levels decrease to less than 1 mg/dL and whose GI tract is not

functioning.

The rate of phosphorous administration should not exceed 10 mEq/h.


Nursing Management

IV site where phosphorous is being administered should be monitored for sloughing

off and necrosis that can possibly occur alongside infiltration.

Be aware of the dangers of IV phosphorous that include tetany from hypocalcemia

and calcifications in tissues (blood vessels, heart, lung, kidneys, eyes) from

hyperphosphatemia.

Give attention to preventing infection because hypophosphatemia may alter

granulocytes.

For mild hypophosphatemia, dietary replacement should be enough:

o Milk and milk products

o Organ meats

o Nuts and whole grains

o Fish and poultry

With moderate hypophosphatemia, supplements such as:

o Neutra-Phos capsules (240 mg phosphorous/capsule)

o Fleet’s phosphorous soda (815 mg phosphorous/5 mL)


HYPERPHOSPHATEMIAPhosphorous excess

● Usually asymptomatic unless leading to hypocalcemia then evidenced by tetany and seizures

● Serum phosphate >4.5mg/dL

● Serum calcium <9mg/dL

● Urine phosphorous <0.9g/24h


Acute and chronic renal failure

Excessive intake of phosphorous

Vitamin D excess

Respiratory Acidosis

Hypoparathyroidism

Volume depletion

Leukemia/lymphoma treated with cytotoxic agents

Increased tissue breakdown

Rhabdomyolysis

Medical Management

Treatment is directed at the underlying disease.

Vitamin D preparations such as calcitrol which is available in both oral (Rocatrol) and

parenteral (Calcijex)

IV administration of calcitrol does not increase serum calcium unless its dose is

excessive, thus permitting more aggressive treatment of hyperphosphatemia with

calcium-binding antacids, phosphate-binding gels or antacids.


Forced diuresis with a loop diuretic, volume depletion with saline, and dialysis.

Surgery may be indicated for removal of large calcium-phosphorous deposits.

Nursing Management

Advise the patient to avoid phosphorous-rich foods such as:

o hard cheese

o nuts, whole grain cereals

o dried fruits and dried vegetables

o meat and kidneys

o sardines

o sweetbreads and foods made with milk

When appropriate, advise the patient to avoid phosphate containing substances such

as

o Laxatives

o Enemas

The nurse also monitors for signs of impending hypocalcemia and to monitor

changes in urine output.

CHLORIDE IMBALANCESIt is contained in gastric and pancreatic juices, sweat, bile, and saliva. Sodium and

chloride in water make up the composition of the ECF and assist in determining osmotic

pressure. The serum level of chloride reflects a change in dilution and concentration of the

ECF and does so in direct proportion to the sodium concentration.



HYPOCHLOREMIAChlorine deficit

● Muscle hypertonicity and tetany

● Shallow, depressed breathing

● Usually associated with hyponatremia and its characteristic symptoms, such as muscle weakness, and twitching

● Serum chloride <98mEq/L

● Serum pH >7.45 (supportive value)

● Serum CO2 >32 mEq/L (supportive value)


Addison’s disease

Reduced chloride intake or malabsorption

Untreated diabetic ketoacidosis, metabolic alkalosis, overuse of bicarbonate

Excessive sweating, diarrhea

Vomiting, gastric suctioning

Sodium and potassium deficiency


Loop, osmotic, thiazide diuretic

Rapid removal of ascitic fluid with high sodium content

Intravenous fluids that lack chloride (dextrose and water)

Draining fistulas and ileostomies

Heart failure, cystic fibrosis

Medical Management

Treatment involves correcting the cause of hypochloremia and the contributing

electrolyte and acid-base imbalances.

Normal saline (0.9%) and half strength (0.45%) solution is administered to replace

chloride.

Reevaluate whether the patient receiving diuretic should be discontinued or

changed.

Ammonium chloride may be prescribed to treat metabolic alkalosis depending on

patient’s weight and serum chloride level. Use in caution with patients with impaired

liver or renal fxn.

Nursing Management

Foods high in chloride should be given:

o Tomato juice

o Eggs, cheese, and milk

o Salty broth, canned vegetables, and processed meats

Water without electrolytes should be avoided because it excretes large amount of

chloride.

Monitor for the patient’s intake and output; ABGs as well as consciousness and

muscle strength.

Monitor patient’s vital signs and respiratory assessment is frequently carried out.


HYPERCHLOREMIAChlorine excess

● Deep, rapid breathing

● Weakness

● Diminished cognitive ability, possibly leading to coma

● Serum chloride >108mEq/L

● Serum pH <7.35,

● Serum CO2 < 22 mEq/L(supportive values)


Excessive sodium chloride infusions with water loss; hypernatremia

Head injury

Renal failure

Corticosteroid use

Dehydration; severe diarrhea (loss of bicarbonate)

Respiratory alkalosis

Administration of diuretics, overdose of salicylates


Kayexalate, acetazolamide, phenylbutazone

Ammonium chloride use

Hyperparathyroidism, metabolic acidosis

Medical Management

Directed at correcting the underlying cause and restoring electrolyte, fluid, and acid-

base balance are essential.

Hypotonic IV solutions may be given to restore balance.

o Lactated Ringer’s solution may be prescribed to convert lactate to

bicarbonate in the liver ultimately increasing bicarbonate and corrects the

acidosis.

IV sodium bicarbonate may be administered to increase bicarbonate levels. This will

lead to the renal excretion of chloride ions as bicarbonate and chloride compete for

combination with sodium.

Diuretics may be prescribed as well.

Sodium, chloride, and fluids are restricted.

Nursing Management

Monitoring of vital signs and arterial blood gas values.

Measuring patient’s intake and output.

Assessment findings related to respiratory, neurologic, and cardiac systems are

documented and observed for any changes that should be communicated with the

physician.

The nurse teaches the patient about the diet that should be followed to manage

hyperchloremia and maintain adequate hydration.

ACID-BASE IMBALANCESAlterations in acid-base balance can affect cellular metabolism and enzymatic

processes.

Acids and Bases

Acids are substances that give up a hydrogen ion. Hydrochloric acid, as a common

acid, can separate into hydrogen and chloride. Bases are substances that accept a

hydrogen ion. Bicarbonate (HCO3) as a common base then can accept a hydrogen ion to

form carbonic acid (H2CO3), a weak acid.

In acid-base balance and regulation, the weak acid carbonic acid and the base

bicarbonate plays are the most important. While carbonic acid plays a major role in acid-


base balance, it is hardly measured because it dissolves in the plasma to form carbon

dioxide (CO2) and water (H2O).

Since carbon dioxide is in balance with carbonic acid and is easier to measure, it is

then expressed as a component in the acid-base balance. Carbon dioxide is referred to as

PCO2 when discussing acid-base balance because the ‘P’ represents partial pressure of

carbon dioxide. PaCO2 is used to refer to carbon dioxide in the arterial blood.

Carbon dioxide is a volatile acid because it is eliminated by the lungs and is

generated by the metabolism of food.

The base bicarbonate is added to the body in small amounts from dietary intake. The

gain of bicarbonate is offset by the normal loss of it through the stool. It plays a major role in

acid-base balance since it accepts hydrogen ion to neutralize acids.

The acid-base ratio is 1:20 where there is one part acid for every 20 parts base.

If this ratio is altered, derangement occurs in the acid-base environment.

pH

Acidity or alkalinity of body fluids is expressed in terms of the concentration of

hydrogen ions. The normal concentration of hydrogen ions has a very narrow range and is

small that makes it difficult to work with clinical setting so the concentration of hydrogen

ions is expressed as pH.

The pH has an inverse relationship to hydrogen ion concentration therefore;

The more hydrogen ions present, the lower the pH (acidic)

The fewer hydrogen ions present, the higher the pH (alkaline)


Physiology

The normal acid-base environment is achieved by and maintained by three primary

mechanisms:

Chemical buffering (neutralizing) by intracellular and extracellular buffers.

Respiratory control of carbon dioxide via changes in rate and depth of respirations.

Renal regulation of bicarbonate concentration and secretion of hydrogen.

Mechanism of Regulating Acid-Base Balance

Action Time Effect

Chemical buffers in cells and extracellular fluidInstantaneous

Combine with the acids and bases added to

system to prevent marked changes in pH.

Respiratory SystemMinutes to hours

Controls carbon dioxide concentration in ECF

by changes in rate and depth of respiration.

KidneysHours to days

Increases or decreases quantity of sodium

bicarbonate in ECF.

Combines bicarbonate or hydrogen with

other substances and excretes them in urine.

Chemical Buffers

The presence of chemical buffers in body fluids and tissue allows the pH to remain in

narrow range so that the pH is not greatly altered. This does not change the absolute

number of hydrogen ions liberated by a strong acid or removed by a strong base but lessens

the effect of acid and base. The primary chemical buffers include:

Bicarbonate buffers

o This is the most important buffer in the plasma and interstitial fluid and is

responsible for 80% of buffering in extracellular fluid. It buffers by accepting a

hydrogen ion and forming the weak acid carbonic acid.

Bicarbonate can be depleted quickly when buffering large acid loads but in the short

term it is effective in maintaining a life-sustaining pH.

Intracellular buffers

o It plays an important role in maintaining acid-base balance since it accounts for

approximately 75% of all chemical buffering that takes place inside the cells.

Hemoglobin is the most plentiful and powerful protein buffer, since red blood cells

provide almost 70% of all buffering in the blood.


Bicarbonate

Hydrogen ion

Carbonic acid

Phosphate buffers

o It is present in tubular fluid in the kidney aside from its role in intracellular

buffering. Phosphate buffers enable the kidney to increase excretion of hydrogen

ions in the urine. Without the phosphate buffers, the urine would quickly become

very acidic.

Bone buffers

o Bone carbonate contributes to maintaining the acid-base balance by buffering up

to 40% of an acute acid load. In the presence of a chronic acidic load as in chronic

renal failure, the bone buffers play an even greater role.

Respiratory Regulation

The role of the lungs in acid-base balance involves the regulation of carbon dioxide.

The rate and depth of alveolar ventilation determines how much carbon dioxide is

eliminated or retained. Normally, the amount of carbon dioxide eliminated equals the

amount produced by metabolic processes. When this balance is not maintained there will be

two conditions may occur:

Respiratory acidosis

o Retention of the volatile acid carbon dioxide or too little carbon dioxide eliminated

for amount produced.

Respiratory alkalosis

o Loss of the volatile acid carbon dioxide or too much carbon dioxide eliminated for

amount produced.

Respiratory compensation does occur with metabolic disturbances but since the

lungs are only able to eliminate volatile acids, compensation is limited when a fixed acid

load occurs. Maximal respiratory compensation can take up to 12 to 24 hours.

Renal Regulation

Renal regulation prevents progressive metabolic acidosis as bicarbonate buffers are

used up. Normally functioning kidneys does this by resorption and regeneration of

bicarbonate and excretion of hydrogen ions.

Regeneration of bicarbonate is done when hydrogen is secreted in the tubular fluid

and then combines with bicarbonate and forms carbonic acid which separates into carbon

dioxide and water. The water part is excreted and the carbon dioxide is resorbed converted

back to bicarbonate thus replacing the bicarbonate lost to buffering. In the presence of

alkalosis, less bicarbonate is generated because fewer hydrogen ions are secreted.

Conversely in acidosis, increased amount of bicarbonate is generated because of the

increased hydrogen ion secretion.

The kidneys help maintain a 1:20 ratio of acids to bases by excreting excess

hydrogen ions depending on pH. Renal compensation for respiratory acidosis or alkalosis

returns the pH to near normal. It is much more effective for respiratory disturbances than

respiratory compensation is for metabolic disorders. However, the initial renal compensation

response takes up to 24 hours with a maximal response taking 3 to 4 days.


Arterial Blood Gases

Arterial blood provides valuable information about the acid-base status because

venous blood is not suitable for assessment of oxygen tension and pH. The nurse draws

arterial blood without exposure to air in a heparinized syringe using the appropriate artery

(radial, brachial, or femoral).

ABG analysis is the measurement of the following parameters:

pH

o The direct reflection of hydrogen ions and thus the acid/base ratio. This signals

the severity of the disorder. The perfect pH is 7.40 with the range of 7.35-7.45.

A normal pH may exist in the following conditions:

mixed acid-base disturbance

when the compensation has returned the pH to normal or near normal

PaCO2

o This reflects the alveolar function.

Hypercapnia (PaCO2 greater than 45 mmHg) signals alveolar

hypoventilation and respiratory acidosis or compensation for metabolic

alkalosis.

Hypocapnia (PaCO2 less than 35 mmHg) results from alveolar

hyperventilation causing respiratory alkalosis or compensation for

metabolic acidosis.

Bicarbonate

o As a major component of bases, bicarbonate is calculated from the pH and

PaCO2. Its normal values are 22 to 26 mEq/L.

Serum Electrolytes

Electrolytes are affected by the acid-base status. Acute changes in pH are

accompanied by changes in serum potassium concentration:

In acidemia, potassium shifts out of the cells and excess hydrogen moves into the

cell to be buffered.

In alkalemia, potassium goes into the cells and hydrogen moves out of the cells to

be buffered.

Electrolyte values are necessary to calculate anion gap which is the difference

between measured cations (sodium and potassium) and measured anions (chloride and

bicarbonate). Because potassium has a low value (3.5-5.0 mEq/L), it is not used in

calculating anion gap:

Anion gap= Na – (Cl + HCO3)

The normal anion gap is 12 +- 2. A gap greater than 14 usually indicates the

presence of unmeasured anions such as the organic acids lactate or ketoacids.

Albumin is a measurable anion and important buffer that can affect anion gap when

decreased.


ACID-BASE DISTURBANCESDisturbances of acid-base balance can be metabolic or respiratory in origin and

can cause either an acidosis or alkalosis. These imbalances are also classified as acute

or chronic. It is important to note that more than one condition can occur at the same time.

The only two disorders that cannot occur simultaneously are respiratory acidosis and

respiratory alkalosis.

Respiratory Acidosis

Whether acute or chronic, it is the result of alveolar hypoventilation and results in

hypercapnia. This condition has partial pressure of carbon dioxide (PaCO2) greater than 45

mmHg. The degree to which the increased PaCO2 alters the pH depends on how rapidly the

increase occurs and the body’s ability to compensate with the blood buffer system and renal

regulation. Because of the limitations of blood buffer system and the delay in renal

regulation, a rapid decrease in pH is usually seen in acute increases in PaCO2.

Clinical manifestations:

● Dyspnea ● Tachypnea

● Restlessness ● Confusion

● Diaphoresis

In severe cases:

● Lethargy ● Ventricular dysrhythmias

● Cyanosis ● Coma

● Dilated conjunctival and facial blood vessels

Common causes:

o Depression of the respiratory center by drugs, cerebral injury or disease,

sudden cardiac arrest.

o Structural abnormalities as in flail chest

o Neuromuscular abnormalities as in hypokalemia

o Systemic Problems as in acute respiratory distress syndrome

o High carbohydrate diet

o Airway obstruction and lung disorders

o With acute lung disorders, hypoxemia occurs before hypercapnia

Medical Management:

o Patients may require suctioning to ensure open airway and chest

physiotherapy may be ordered.

o If PaCO2 is greater than 50 to 60 mmHg, the patient may require intubation

and mechanical ventilation.

o In patients with chronic respiratory acidosis, treatment with supplemental

oxygen must be approached cautiously. It is usually administered at 1 to 3

L/min, with careful ongoing monitoring.

o Antibiotics are prescribed if infection is causing or contributing to respiratory

acidosis.


Nursing Management:

o Health history, assess for the following:

Length of time since onset of symptoms

Presence of dyspnea

Complaints of anxiety or restlessness

Changes in level of consciousness-confusion or lethargy

o Physical examination:

Increased heart rate and respiratory rate

Signs of diaphoresis

Asterixis

Dilated conjunctival and facial blood vessels

Ventricular dysrhythmias

Cyanosis (late sign)

o Patient’s airway is maintained by encouraging coughing.

o For patients under mech-vent, the nurse monitors for the settings and checks

for the patency of the tubes.

o Monitoring of the bowel sounds and abdominal distention is necessary to

prevent a decrease in diaphragmatic movement secondary to abdominal

pressure, which may further compromise respiratory status.

o The semi-fowler’s position allows for expansion of the chest wall and is

appropriate for most patients.

o For mechanically ventilated patients with unilateral lung disease, a side lying

position would be best so that it increases perfusion to the dependent (down

side) healthy lung and increases ventilation to the diseased upper lung.

o Prone position often benefits patients with ARDS because it improves

ventilation/perfusion mismatch.

Respiratory Alkalosis

This is the result of hyperventilation leading to hypocapnia (PaCO2 less than 40

mmHg). The acute decrease in PCO2 causes a mild but rapid decrease in serum bicarbonate,

occurring within 10 minutes and reaching a constant state in approximately 10 minutes.

Respiratory alkalosis that persists beyond 6 hours is classified as chronic and renal

compensatory changes can cause further decrease in bicarbonate concentration and an

increase in pH toward normal levels.

Clinical Manifestations:

● Anxiety ● Lightheadedness

● Paresthesias ● Circumoral numbness

Common causes:

o Most commonly associated with hyperventilation related to anxiety.

o Occurs with pain, gram negative sepsis, high altitude sickness, and some

pulmonary disorders with or without coexisting hypoxemia.


o Salicylate overdose and intracerebral trauma that exert direct stimulation on

the respiratory center leading to hyperventilation.

Medical Management:

o Treatment aims at correcting underlying disorder

o The physician may order tranquilizers to treat anxiety-induced respiratory

alkalosis. If symptoms are severe, rebreathing into a paper bag or an oxygen

mask with a carbon dioxide reservoir may be useful.

o Pulse oximetry may be used to assess oxygenation before and during

treatment.

o Adequate pain management is important if the condition is caused by the

patient’s response to pain.

o If hypoxemia is the cause, oxygen therapy may be necessary

Nursing Management:


Length of time since the onset of symptoms

Complaints of pain or anxiety

Complaints of shortness of breath, dyspnea, lightheadedness

Presence of paresthesias or circumoral numbness

History of asthma, other pulmonary disorders, and central nervous

system trauma and related information.

o Physical examination, assess for the following:

Increased heart rate and depth of respiration

Confusion

Tetany, syncope, and seizures

Cardiac dysrhythmias and ST-T waves

o The nurse should assess for degree of anxiety and offer to stay with the

patient.

o Encourage the patient to have a normal breathing pattern by pacing the

client’s breathing or having the patient mimic the nurse’s breathing pattern.

o It may also help to have the patient rebreathe into a paper bag or oxygen

mask with an attached carbon dioxide reservoir.

o Monitor and check the patient’s pulse oximetry.

Metabolic Acidosis

This condition occurs when there is a primary decrease in serum bicarbonate

concentration (to less than 22 mEq/L)


● Hypotension ● Tachypnea

● Fruity breath ● Cold, clammy skin

● Nausea, vomiting ● Diarrhea

● Confusion

In severe cases:

● Kussmaul’s respirations ● Flushed, warm, dry skin


● Dysrhythmias ● Stupor

● Coma

Common causes:

o Loss of Bicarbonate:

Gastrointestinal: Diarrhea, biliary and pancreatic drainage

Renal: Renal tubular acidosis type 2

Acetazolamide

o Excess Acid Production:

Ketoacidosis, diabetes, alcohol-induced starvation

Lactic acidosis, rhabdomyolysis

o Excess Acid Ingestion:

Salicylates, methamphetamine

Cocaine

3,4-methylenedioxymethamphetamine (Ecstasy)

Medical Management:

o Directed at underlying disease

o In DKA, fluid and insulin are required

o In alcohol-related ketosis, glucose and saline are necessary

o Acute and renal failure would need hemodialysis or peritoneal dialysis to

restore acid-base balance

o Administration of sodium bicarbonate may be given in severe cases but

should be use in caution to patients with congestive heart failure or

pulmonary edema

Nursing Management:



History of headache, anorexia, nausea, vomiting, and diarrhea

Polyuria, Polydipsia


Hypotension

Tachypnea or Kussmaul’s respirations

Cold, clammy skin progressing to flushed, warm, and dry skin

Fruity breath

Changes in level of consciousness

Ventricular dysrhyhtmias

Metabolic Alkalosis

This condition occurs when there is excess serum bicarbonate from either a gain of

bicarbonate or loss of hydrogen, resulting in increase in pH.


● Muscle weakness ● Hyporeflexia

● Polyuria or polydipsia ● Cardiac rhythm disturbance

In severe cases:


● Neuromuscular irritability ● Apathy

● Confusion ● Stupor

Common causes:

o Gastrointestinal

Vomiting

Nasogastric suctioning

o Renal

Diuretics (especially thiazides)

Mineralcorticoid excess

Post chronic hypercapnia

Hypercalcemia, hypoparathyroidism

o Hydrogen ion shift into cells

Hypokalemia

Carbohydrate refeeding after starvation

o Bicarbonate retention

Administration or ingestion of bicarbonate

Massive blood transfusion

o Contraction alkalosis

Diuretics

Cystic fibrosis

Medical Management:

o Mild to moderate metabolic alkalosis does not usually require specific

therapeutic intervention and treatment is directed at correcting the

underlying disorder.

o Testing urine electrolyte before beginning treatment is necessary to

differentiate the cause of alkalosis.

o Hypokalemia often occurs and is responsible for symptoms of muscle

weakness and cardiac rhythm disturbances.

o Serum potassium may be given either orally or IV K salts to treat hypokalemia

o Isotonic saline infusion may be prescribed to correct volume deficits related

to metabolic alkalosis caused by diuretics or loss of gastric secretions.

o Acetazolamide (Diamox) may be used in patients with congestive heart

failure who cannot tolerate rapid volume expansion. This drug can cause

large losses of potassium and bicarbonate; therefore, potassium

supplementation may be necessary before starting the treatment.

Nursing Management:



History of vomiting, nasogastric suctioning, bulimia, diuretic use, or

abuse

Presence of muscle weakness

History of polydipsia and polyuria



Postural hypotension

Neuromuscular excitability associated with tetany

Changes in level of consciousness

o The nurse must monitor the electrocardiogram for the presence of

dysrhythmias.

o The nurse assesses for apical and radial pulses simultaneously to detect pulse

deficit.

Catheters

In medicine, a catheter is a tube that can be inserted into a body cavity, duct, or

vessel. Catheters thereby allow:

Drainage

Administration of fluids or gases

Access by surgical instruments.

The process of inserting a catheter is catheterization.

In urinary catheterization, or "cathing" for short, a plastic tube known as a urinary catheter

that is gently slid into a patient's bladder via his or her urethra. Catheterization allows the

patient's urine to drain freely from the bladder for collection, or to inject liquids used for

treatment or diagnosis of bladder conditions. The procedure of catheterization will usually be

done by a clinician, often a nurse, although self-catheterization is possible as well.

Indications for urinary catheterizations:

Intermittent catheterization

Collection of sterile urine sample.

Provide relief of discomfort from bladder distention.

Decompression of the bladder.

Measure residual urine.

Management of patients with spinal cord injury, neuromuscular degeneration, or

incompetent bladders.

Short-term indwelling catheterization

Post surgery and in critically ill patients to monitor urinary output.

Surgical procedures involving pelvic or abdominal surgery repair of the bladder,

urethra, and surrounding structures.

Urinary obstruction (e.g. enlarged prostate), acute urinary retention

Prevention of urethral obstruction from blood clots with continuous or intermittent

bladder irrigations

Instillation of medication into the bladder.

Long-term indwelling catheterization

Refractory bladder outlet obstruction and neurogenic bladder with urinary retention.

Prolonged and chronic urinary retention.

To promote healing of perineal ulcers where urine may cause further skin breakdown.

Contraindications


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Foley catheters are contraindicated in the presence of urethral trauma. Urethral

injuries may occur in patients with multisystem injuries and pelvic factures, as well as

straddle impacts. If this is suspected, one must perform a genital and rectal exam

first. If one finds blood at the meatus of the urethra, a scrotal hematoma, a pelvic

fracture, or a high riding prostate then a high suspicion of urethral tear is present.

One must then perform retrograde urethrography (injecting 20 cc of contrast into the

urethra).

Risks associated with catheterization include:

Urethral trauma and bleeding from inappropriate catheter size or use of

force.

Urinary tract infections related to poor sterile technique or long-term

catheterization.

Bladder spasms and pain

Choosing the appropriate catheter depends on

The size of the patient’s urethral canal

The expected duration of catheterization (e.g. intermittent or indwelling)

Knowledge of any allergies to latex or plastic.

The indications for catheterizing the patient (i.e. clot retention, child, bladder

instillation).

Catheters come in several basic designs

A Foley catheter (indwelling urinary catheter)is retained by means of a balloon at

the tip which is inflated with sterile water. The balloons typically come in two

different sizes: 5 cc and 30 cc. They are commonly made in silicone rubber or natural

rubber.

A Robinson catheter is a flexible catheter used for short term drainage of urine.

Unlike the Foley catheter, it has no balloon on its tip and therefore cannot stay in

place unaided.

A Coudé catheter is designed with a curved tip that makes it easier to pass through

the curvature of the prostatic urethra.

A hematuria (or haematuria) catheter is a type of Foley catheter used for Post-TURP

hemostasis. This is useful following endoscopic surgical procedures or in the case of

gross hematuria. There are both 2-way and 3-way hematuria catheters (double and

triple lumen).[1]

An external Texas or condom catheter is used for incontinent males and carries a

lower risk of infection than an indwelling catheter

Catheter diameters are sized by the French catheter scale (F). The most common

sizes are 10 F (3.3mm) to 28 F (9.3mm). The clinician selects a size large enough to allow

free flow of urine, and large enough to control leakage of urine around the catheter. A larger

size can become necessary when the urine is thick, bloody or contains large amounts of


http://en.wikipedia.org/wiki/French_catheter_scale

sediment. Larger catheters, however, are more likely to cause damage to the urethra. Some

people develop allergies or sensitivities to latex after long-term latex catheter use making it

necessary to use silicone or Teflon types. Silver alloy coated urinary catheters may reduce

infections. Types:

Straight-single use catheters

Have a single lumen with a small 1¼ cm opening.2-way Foley catheters (retention catheters)

Have an inflatable balloon that encircles the tip near the lumen or opening of the catheter.

Curved or Coude

Catheters have a rounded curved tip (elbowed) used in older male patients

with enlarged prostates which partially obstruct the urethra.

3-way Foley catheter


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Often called retention catheter, they have 2 or 3 lumens that encircle the

body of the catheter. One lumen drains the urine through the catheter into a

collection bag. The second lumen holds the sterile water when the catheter

is inflated and is also used to deflate the balloon. The third lumen maybe

used to instill medications into the bladder or provide a route for continuous

bladder irrigation.

Pediatric catheterization:

Size- 5, 6, 8, 10Fr. or smaller depending on the size of the urethra and age

of child.

Rarely are catheters left indwelling, typically they are intermittent and are

used to obtain sterile urine sample to rule-out infection.

In children <2years of age a 5Fr. feeding tube can be used if a small

diameter catheter is not available.

Using feeding tubes can cause urethra trauma, a second pair of hands for

assistance is recommended for very young children.

Male catheterization:

16Fr. or 18Fr. catheter is typically used for most men, as they are more rigid

and often easier to insert past the prostate.

In males it is helpful to use a Urojet (syringe with lidocaine jelly) to minimize

the discomfort with the catheterizations.

Males who present with gross hematuria require 3-way Foley catheters with

the largest diameter that can be safely inserted. (22Fr., 24Fr.,)

Catheters should be attached to the inner upper thigh with a CathSecure.

This will minimize discomfort and prevent the catheter from being pulled

on/out.

When the foreskin is retracted for the purpose of catheterization remember

to return it back to its original place.

If resistance is met while inserting the catheter due care is used not to

damage the enlarged prostate. Never inflate the balloon until urine has been

visualized and is draining.

Female Catheterization:

12fr., 14Fr.or 16Fr. catheter is typically used.

Positioning is important to properly visualize the urethra in females.

If you are unable to visualize the urethra, raise pelvis with a pillow, blanket or

inverted bedpan.

If you insert catheter into the vagina leave it in place as a landmark and start

again with another sterile catheter.

Never inflated the balloon until you see urine.

If patient presents with gross hematuria a larger 3-way catheter needs to

inserted.


Combating infection

Everyday care of catheter and drainage bag is important to reduce the risk of infection.[7] Such precautions include:

Cleansing the urethral area (area where catheter exits body) and the catheter itself.

Disconnecting drainage bag from catheter only with clean hands

Disconnecting drainage bag as seldom as possible.

Keeping drainage bag connector as clean as possible and cleansing the drainage bag

periodically.

Use of a thin catheter where possible to reduce risk of harming the urethra during

insertion.

Drinking sufficient liquid to produce at least two liters of urine daily

Sexual activity is very high risk for urinary infections, especially for catheterized

women.

Recent developments in the field of the temporary prostatic stent have been viewed as a possible alternative to indwelling catheterization and the infections associated with their use

Prior to starting, explain to the patient what is going to happen and why they

need to be catheterized. Assess patients understanding and answer any questions

they may have. Collect supplies, it is helpful to bring a second catheter in case of

contamination of the first catheter. Clear off work space/ bedside table and begin to

position the patient. Raise the bed to an appropriate working height and position

yourself on the opposite side of you dominant hand. Keep in mind that it may be

necessary to obtain additional help with the catheterization.

Credits for urinary catheter: This web-based module was developed by Adam Szulewski based on content written by Lucy Rebelo for the Queen's University Faculty of Health Sciences Patient Simulation Lab.The module was created using exe : eLearning XHTML editor with support from Amy Allcock and the Queen's University School of Medicine MedTech Unit.

Nephrostomy tube

A small rubber tube that is placed through a hole in the skin and that extends

into the kidney. The tube allows direct drainage from the kidney. Often called a

percutaneous nephrostomy tube, the device attaches to a collection bag that

collects and measures urine output. The tube allows urine to bypass blocked or

damaged ureters in order to avoid the risk of infection or irreversible damage that

the backflow of urine causes for a patient with a blockage or leak.

Nephrostomy tube has several other functions, including the following:

To remove or dissolve renal calculi

To obtain direct access to the upper urinary tract for various endourologic procedures

To diagnose ureteral obstruction, filling defects, and anomalies via antegrade

radiography

To deliver chemotherapeutic agents to the renal collecting system


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To provide prophylaxis after resection for local chemotherapy in patients with tumors

of the renal pelvis.

Indications

Temporary urinary diversion associated with urinary obstruction secondary to calculi

Diversion of urine from the renal collecting system in an attempt to heal fistulas or

leaks resulting from traumatic or iatrogenic injury, malignant or inflammatory

fistulas, or hemorrhagic cystitis

Treatment of nondilated obstructive uropathy

Treatment of urinary tract obstruction related to pregnancy

Treatment of complications related to renal transplants

Access for interventions such as direct infusion of substances for dissolving stones;

chemotherapy; and antibiotic or antifungal therapy

Access for other procedures (eg, benign stricture dilatation, antegrade ureteral stent

placement, stone retrieval, pyeloureteroscopy, endopyelotomy)

Decompression of nephric or perinephric fluid collections (eg, abscesses, urinomas)

Contraindications

Bleeding diathesis (most commonly, uncontrollable coagulopathy)

Uncooperative patient

Severe hyperkalemia (>7 mEq/L) should be corrected with hemodialysis before the

procedure.

Preprocedural evaluation

Laboratory studies, including determination of prothrombin time (PT), activated partial

thromboplastin time (aPTT), platelet count, BUN and creatinine levels, hematocrit (Hct) and

hemoglobin (Hgb) levels, WBC count, and urinalysis and urine culture, are made.

Pertinent images (eg, sonograms, CT scans, intravenous urograms [IVUs], radionuclide

scintigrams) are reviewed to assess the location of the colon, liver, and spleen in

determining the approach.

Intravenous access is established and the patient is adequately hydrated.

Prophylactic antibiotics are administered 60 minutes before the procedure, especially if

pyonephrosis is suspected or if the obstruction is caused by a renal calculus. The use of

antibiotics is somewhat controversial; however, in patients with a known urinary tract

obstruction, antibiotics should be administered before the procedure (preferably 1 h before

puncture) and should be continued for at least 24 hours after the procedure. Antibiotics

should be chosen on the basis of urine culture results, if available. If the results are not

available, use of a broad-spectrum antibiotic is recommended.

The patient should receive nothing by mouth (NPO) for 4-8 hours before the procedure,

for conscious sedation precautions.

Some have advocated the placement of percutaneous nephrostomy tubes without

performing preprocedural coagulation studies, although the authors disagree with this

approach unless the situation is an absolute emergency. Because the kidney is highly


vascular, needle puncture and tract dilation in a patient with a coagulopathy could result in

massive hemorrhage.

Postprocedural management and follow-up

Postprocedural management and follow-up may include the following:

o Bedrest for 4 hours

o Return to the preprocedural diet

o Checking of vital signs every 30 minutes for 4 hours and then every shift

o Antibiotic therapy, if infection is identified or suspected

o Catheter flushing with 5 mL of bacteriostatic isotonic sodium chloride solution

and then aspiration every 6-12 hours

o Monitoring of urine output

Major complications with percutaneous nephrostomy tube placement include the following:

o Bleeding

o Sepsis

o Injury to an adjacent organ

Other major complications, though somewhat rare, have been reported to occur in as many

as 5% of patients. Complications of percutaneous nephrostomy may include the following:

o Massive hemorrhage requiring transfusion, surgery, or embolization (1-3%)

o Pneumothorax (<1%)

o Microscopic hematuria (common)

o Pain (common)

o Urine extravasation (<2%)

o Inability to remove the nephrostomy tube because of crystallization around

the tube site

o Death (0.2%)

o Sepsis (1.3%)

o Catheter dislodgement during the first month (<1%)

Suprapubic catheter

When placement of a urethral catheter is contraindicated or unsuccessful, percutaneous suprapubic urinary bladder catheterization is a commonly performed procedure to relieve urinary retention.1

This topic describes the Catheter over needle technique. The Seldinger technique is described in the Clinical Procedures topic Suprapubic Aspiration.

IndicationsSuprapubic catheterization is indicated (when transurethral catheterization is contraindicated or technically not possible) to relieve urinary retention due to the following conditions:

Urethral injuries

Urethral obstruction

Bladder neck masses

Benign prosthetic hypertrophy (BPH)


http://emedicine.medscape.com/article/437359-overview



Prostate cancer

Contraindications

Suprapubic catheterization is absolutely contraindicated in the absence of an easily

palpable or ultrasonographically localized distended urinary bladder.

Suprapubic catheterization is relatively contraindicated in the following situations:

o Coagulopathy (until the abnormality is corrected)

o Prior lower abdominal or pelvic surgery (potential bowel adherence to the

bladder or anterior abdominal wall; may recommend that a urologist perform

an open cystostomy)

o Pelvic cancer with or without pelvic radiation (increased risk of adhesions)

SP Catheter Care

It is very important to take good care of the suprapubic tube and drainage system.

They should be kept very clean. The bag should not be allowed to drag on the floor.

If the bag should accidentally be cut or begin to leak, it must be changed. An opening

anywhere along the entire system of tubing and bag will allow bacteria to enter. If these

would then reach your child's bladder, a urinary tract infection could result. It is not

acceptable to place the drainage bag in a plastic bag if it leaks.

Cleaning the Catheter

Follow the steps below to clean the area where the catheter enters the patient's body.

1. Wash your hands with soap and water.

2. Once a day, use a warm wet soapy wash cloth to clean the catheter and the skin

around it. Take care that you do not pull excessively on the catheter.

3. If there is any crustiness on the catheter that does not come off with soap and water,

you may use hydrogen peroxide on the catheter. Pour some hydrogen peroxide on a

cotton ball or gauze pad and wipe gently on the catheter.

4. Rinse the skin and catheter with plain water. Pat dry with a towel.

5. You may place a slit gauze dressing over the catheter site if you wish. It is not

required, but some people feel more comfortable doing so.

Bathing

While the patient has the SP catheter, he/she will need to take a sponge bath. Baths,

showers and swimming are not allowed.

Emptying the Bag

The large drainage bag must be emptied at least every 8 hours even if it is not full. If the

bag is small and fills quickly, it should be emptied when the bag is 2/3 full.

When emptying the bag, be careful not to touch the top of the spout to the container into

which it is being drained. Also, do not touch the top of the spout with your hands.



Changing the Bag

1. Wash your hands with soap and water.

2. Disconnect the tubing from the catheter. Insert the new drainage bag tubing into the

catheter.

3. If you are going to reuse the bag you just switched from, the connection site must be

covered with a sterile cap or gauze. The bag must be kept in a clean place.

Tips

Keep the drainage system below the level of the bladder so the urine does not back

up.

The leg bag will allow you to wear regular clothes and be free to play or work.

Remember that because it is small, it will need to be emptied often.

Be sure there are no kinks or bends in the tubing. Urine will not drain if this happens.

If the patient's drainage bag becomes dirty or foul-smelling, it needs to be changed.

If a hole is punctured in the bag or tubing, it also needs to be changed.

Make sure the patient drinks plenty of fluids. The urine should be light yellow and

clear.


Fluid and Electrolytes

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