FLUID AND ELECTROLYTE IMBALANCE

IntroductionPhysiologic homeostasis depends upon the normal fluid and electrolyte balance electrolyte imbalance is needed to be studied to promote the positive health outcomes. Positives outcomes are achieved through health promotion , health maintainance and health restoration strategies. Clearly water is not only responsible for body’s structure and function , it is also necessary for the maintainance of equilibrium and of life itself. Fluid and electrolyte imbalance commonly accompany illnesses. Severe imbalances may results in death. Such imbalances affect not only the acutely and chronically ill patients but also clients with faulty diets and those who take selected medications such as diuretics and gluccocorticoids preparations.So, every nurse must understand the process of fluid and electrolyte balance, identify clients at risk of imbalances , intervene as appropriate and evaluate the outcomes.

Fluids

Body fluid compartmentsThe two main fluid compartments in the body are:

1. Intracellular fluid i.e, ICF2. Extracellular fluid i.e,ECF1. Intracellular fluid - It is located within the cell , constitutes about 40% of

the body weight and 70% of the total water. The intracellular fluid provides the cell within the internal acqueous medium necessary for its chemical functions .

2. Extracellular fluid – It constitutes about 20% of the body weight and 30% of the total body weight .

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The extracellular fluid consist of interstitial fluid , intravasacular fluid , cerebrospinal fluid , intraocular fluid , synovial fluid , lymphatic fluid and secretions of gastrointestinal tract .

FUNCTIONS OF EXTRACELLULAR FLUID :

Transport nutrients , electrolytes , oxygen to cells and waste products for excretion .

Hydrolyzes food for digestive process . Regulates heat . Lubricates and cushions joints and membranes .

MECHANISM CONTROLLING FLUID AND ELECTROLYTE MOVEMENTMany different processes control the movement of fluid and electrolyte between the intracellular and extracellular spaces .

DIFFUSION : Diffusion is the movement of molecules from an area of higher concentration to an area of lower concentration .

FACILITATED DIFFUSION : In facilitated diffusion , one molecule moves from an area of higher concentration to an area of lower concentration with the help of some carrier . For example , glucose is transported into the cell with the help of insulin as a carrier molecule .

ACTIVE TRANSPORT : Active transport is a process in which molecules are moved from an area of lower concentration to an area of higher concentration and they require external energy for movement against the concentration gradient.

OSMOSIS : Osmosis is the flow of water between two compartments separated by a membrane permeable to water but not to solute. Osmosis requires no outside energy for movement. Water moves : from an area of low solute concentration to an area of higher concentration . from the compartment that is more diluted to side that is more concentrated.

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REGULATION OF FLUID ELECTROLYTE BALANCES

HYPOTHALAMIC REGULATION / THIRST

Water ingestion in the conscious client is regulated by the hypothalamus . The thirst mechanism is stimulated by hypotension and increased serum osmolality .A water deficit . Water ingestion will equal to water excretion in a client who has free accessible to water , a normal antidiuretic hormone ADH mechanism and a normal functioning .

DECREASED VOLUME OF INCREASED OSMOLALITY OF EXTR ACELLULAR FLUID EXTACELLULAR FLUID

STIMULATES OSMORECEPTORS DECREASED SALIVA IN HYPOTHALAMIC THIRST SECRETION CENTRE

DRY MOUTH

SENSATION OF THIRST

WATER ABSORBED FROM GI TRACT

INCREASED AMOUNT OF DECREASED OSMOLALITY OF EXTRACELLULAR FLUID EXTRACELLULAR FLUID

FIG. FACTOTS STIMULATING WATER INTAKE THROUGH THE THIRST MECHANISM

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RENIN – ANGIOTENSIN - ALDOSTERONE SYSTEM

The renin- angiotensin – aldosterone systemworks to maintain intravascular fluid balance and blood pressure .

DECREASED RENAL PERFUSION / GLOMERULAR FILTRATION RATE

RENIN PRODUCED BY KIDNEYS

ANGIOTENSINOGEN IS CONVERTED TO ANGIOTENSIN I WITH HELP OF RENIN

ANGIOTENSIN I IS CONVERTED TO ANGIOTENSIN II WITH THE HELP OF ACE IN LUNGS

ANGIOTENSIN II : increases thirst increases release of aldosterone increases blood pressure

ALDOSTERONE :

increases absorption of sodium ions increases absorption of water increases excretion of potassium increases excretion of hydrogen ions

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FIG . RENIN – ANGIOTENSIN – ALDOSTERONE MECHANISM

ANTIDIURETIC HORMONE – PITUITARY REGULATION

Antidiuretic hormone ADH , released by the posterior pituitary gland , regulates water excretion from the kidneys .

INCREASED SERUM OSMOLALITY MECHANICAL VENTILATION , DECREASED BLOOD PRESSURE ANAETHESIA , DRUGS , PAIN ,

INCREASE RELEASE AND PRODUCTION OF ANTIDIURETIC HORMONE [ADH]

ADH INCREASES DISTAL TUBULE PERMEABILITY TO REABSORPTION OF WATER

decreases urine output increases blood volume increases blood pressure decreases blood osmolality

FIG. ANTIDIURETIC HORMONE [ADH] RELEASE AND EFFECT

Two disorders of antidiuretic hormone [ADH] production illustrates the effect of ADH on water balance and urine output .

1. Diabetes Inspidus - due to deficient of ADH production 2. Syndrome of inappropriate antidiuretic hormone [SIAD] - due to excess

release of antidiuretic hormone .

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ADRENAL CORTICAL REGULATION

Extracellular fluid volume is maintained by a combination of hormonal influences . Hormones released by the adrenal cortex help regulate both water and electrolytes . Two groups of hormones secreted by the adrenal cortex are :

i. Glucocorticoids [Cortisol] – Inflammatory action and increase serum glucose level .

ii. Mineralocorticoids [Aldosterone] – Enhances sodium and potassium excretion . When sodium is reabsorbed , water follows as a result of osmotic changes .

Many body systems , including fluid and electrolyte balance , are affected by stress .

STRESS SIGNALS TO HYPOTHALAMUS

ANTERIOR PITUITARY POSTERIOR PITUITARY INCREASES SECRETION INCREASES SECRETION OF ACTH OF ANTIDIURETIC HORMONE

ADRENAL CORTEX - KIDNEYS INCREASES ALDOSTERONE INCREASES WATER INCREASES CORTISOL REABSORPTION

INCREASES SODIUM REABSORPTION

INCREASES POTASSIUM EXCRETION

FIG. EFFECT OF STRESS ON FLUID AND ELECTROLYTE BALANCE

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RENAL REGULATION – KIDNEYS

The primary organs for regulating fluid and electrolyte balance are the kidneys . They regulate the volume and osmolality of body fluids by controlling the excretionof water and electrolytes. The renal tubules are the main site of action for ADH and aldosterone .

As the filtrate [plasma] moves through renal tubules , selective reabsorption of water and electrolytes and secretion of electrolytes result in the production of urine that is generally different in composition and concentration than plasma [filtrate] . This helps to maintain normal plama osmolality , electrolyte balance , blood volume and acid-base balance .

Impaired kidney function may leads to edema , potassium and phosphorous retention , acidosis and other electrolyte imbalances .

ATRIAL NATRIURETIC PEPTIDE

CARDIAC ATRIA RELEASE ATRIAL NATRIURETIC FACTOR [ANF]

INHIBITS RENIN SECRETION

INCREASES URINARY EXCRETION OF SODIUM AND WATER

DECREASES BLOOD VOLUME AND CAUSES VASODILATION

GASTROINTESTINAL REGULATION

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Most of the body’s water is excreted by kidneys . A small amount of fluid is normally eliminated by the GI tract in faeces , but sometimes or usually diarrhoea and vomiting leads to fluid and electrolyte imbalances .

INSENSIBLE WATER LOSS

INSENSIBLE WATER LOSS: which is invisible vapourization from the lungs and skin , assists in regulating body temperature .Normally about 900ml per day is lost .

SENSIBLE WATER LOSS: excess sweating / sensible perspiration caused by fever or high environmental temperature may lead to large loss of water and electrolyte .

FLUID IMBALANCES

EXTRACELLULAR FLUID VOLUME DEFICIT

DEFINITION : Extrcellular fluid volume deficit is commonly called dehydration or decrease in intravascular and interstitial fluid .

CAUSES :

Lack of fluid intake due tp impaired thirst mechanism . Excessive fluid output through diaphoresis , GI suction , blood loss , burns ,

deceased antidiuretic hormone . Alteration in any of the regulators of fluid balances . Stimulants result in increased Renin-Angiotensin-Aldosterone response that

causes sodium retention .

CLINICAL FEATURES :

Loss of body weight . Changes in intake and output i.e, thirst and urine output decreases .

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Changes in vital signs : systolic blood pressure decreases , weak pulse , CVP decreases , pulmonary capillary wedge pressure decreases , heart rate increases ,

flat jugular vein . Mouth mucous membrane becomes dry . Sunken eyes . Cracked lips . Furrows on tongue . Tenting of skin [decreasedskin turgor] . Muscle weakness . Decreased and hard faeces . Hallucinations and confusion .

DIAGNOSTIC EVALUATION :

Hypernatremia Osmolality : > 295 mOsm/kg Plasma sodium : > 145 mEq/L BUN : > 25mg/dl Plasma glucose : > 120 mg/dl Hematocrit : .55%

MANAGEMENT

1. ORAL REHYDRATION – Oral glucose replacement solution are palatable , a good source of fluid , glucose and electrolytes and even they are absorbed quickly.

2. INTRAVENOUS REHYDRATION –Intravenous fluids are used for replacement . The volume of fluid is calculated on basis of client’s weight and other factors.

Isotonic ECFVD is treated with isotonic solution . Hypertonic ECFVD is treated with hypotonic solution . Hypotonic ECFVD is treated with hypertonic solution .

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3. Monitoring for complications of fluid restoration – A client with severe ECFVD is accompanied by severe heart , pulmonary , liver or kidney disease cannot tolerate large volume of fluid or sodium without the risk for developmemt of heart failure . For unstable client , monitors are used to detect increasing pressure from fluid . If deficit has existedfor more than 24hrs , it is dangerous to correct this deficit too rapidly . Urine output , body weight and laboratory volumes of sodium , osmolality , BUN and potassium are monitored closely .

4. Correction of underlying problem : Antiemetics Antidiarrhoeals Antibiotics Antipyretics

NURSING MANAGEMENT

1. Deficit fluid volume Restore oral fluid intake . Restore fluid by intravenous . Reduce risk of deficit fluid volume . Control of underlying problems . Monitor for complications .

2. Impaired oral mucous membrane Oral care regularly 2-4 hourly . Apply lip moisturizer. Rinse client’s mouth every 1-2 hourly . Examine client’s mouth with penlight for debris .

3. Risk for injury Provide safety through step progression position change . Place alarm monitors on client’s bedside . Restraints sometimes may be needed .

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EXTRACELLULAR FLUID VOLUME EXCESS

DEFINITION : Extarcellular fluid volume excess is a fluid overload or overhydration.

CAUSES :

Compromised regulation of fluid movement and excretion , example – Hypothtroidism , Renal disorder , Decreased plasma protein .

Excessive ingestion of fluids or foods containing sodium , example – Excessive amount of saline intravenous , Ingestion of high sodium food , Excessive use of enema with sodium .

Increased ADH and aldosterone , example – Certain barbiturates , narcotics , Cushing syndrome , Glucocortiods , SIADH .

CLINICAL FEATURES :

Cough , Dypnea , Crackles , can be ausculcated over the lung area . Pallor , Cyanosis , Deceased tissue perfusion , Increased carbon dioxide

blood gases abnormalities . Systematic venous engorgement Jugular vein distension . Peripheral vein filling time greater than 5 seconds . Bounding pulse . Elevated blood pressure . Increased right atrial CVP and PCWP .

DIAGNOSTIC EVALUATION :

Plasma osmolality : < 275 mOsm/kg Plasma sodium : < 135 mEq/L Hematocrit : < 45% Specific gravity : < 1.010 BUN : < 8 mg/dl

MANAGEMENT :

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Restriction of sodium and fluids : Because sodium retains water , sodium intake is commonly restricted especially in those clients with renal or heart failure .

Promoting urine output : Mild diuretics and digitalis promote fluid loss and diuretics also causes excretion of magnesium and potassium loss in urine .

NURSING MANAGEMENT :

1. Excess fluid volume Reduce sodium and fluid intake . Mobilize fluid electrolye imbalances . Reduce complications like digitalis toxic effects , cerebral.

INTRACELLULAR FLUID VOLUME DEFICIT

DEFINITION : Intracellular fluid volume deficit is decrease in fluid within the cells.

CAUSES :

Excessive fluid loss . Insufficient fluid intake . Failure of regulatory mechanism . Loss of GI fluid from vomitting , diarrohea , gastrointestinal suctioning ,

intestinal fistula and intestinal drainage . Haemorrhage . Chronic abuse of laxatives and enemas . Water and sodium losses during sweating from exercise or increased

environmental temperature . Excessive renal losses of water and sodium from diuretic therapy .

CLINICAL FEATURES :

Dry and sticky mucous membrane . Decreased urine output . Anxiety and confusion .

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Diminished skin turgor . Dry , pale and cool extremities . Orthostatic hypotension . Decrease capillary refill . Increase body temperature . Weight loss . Thirst .

DIAGNOSTIC EVALUATION :

Serum electrolyte : sodium increases and potassium decreases . Serum osmolality : osmolality is high . Hematocrit : high . Urine specific gravity : high . Central venous pressure : low .

MANGEMENT :

1. Oral rehydration : It is the safest and most effective treatment for fluid volume deficit in alert clients who are able to take oral fluids . Adults requires minimum of approximately 30ml per kg body weight for maintainence .

2. Intravenous therapy : When fluid deficit is severe or client is unable to ingest fluid , the intravenous route is used to administer replacement fluid. Isotonic : 5% dextrose in water D5W . 0.9% sodium chloride . 5% dextrose and 0.45% sodium chloride . Ringer’s solution . Lactated ringer’s solution .Hypertonic : 10% dextrose in water . 20% dextrose in water . 50% dextrose in water . 3% sodium chloride . Hypotonic : 0.45% sodium chloride .

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3. Fluid challenge : A fluid challenge , the rapid administration of a designated amount of intravenous fluid may be performed to evaluate fluid volume when urine output is low and cardiac or renal functioning is questionable .

NURSING MANAGEMENT :

1. Deficit fluid volume . Assess intake and output regularly . Monitor fluid balances regularly . Assess vital signs , CVP , peripheral pulse . Weight the client daily . Adminster intravenous fluids . Monitor laboratory values : electrolytes , serum osmolality , BUN and

hematocrit .2. Ineffective tissue perfusion .

Monitor changes in level of consciousness . Monitor serum creatinine , BUN , cardiac enzymes . Change position 2 hourly .

3. Risk for injury . Keep side rails of bed up .

Slowly raise the client from supine to sitting then to standing position.

INTRACELLULAR FLUID VOLUME EXCESS

DEFINITION : When sodium and water are retained within the cells i.e, known as intracellular fluid volume excess .

CAUSES :

Fluid overload i.e, water and sodium retention . Administration of excessive amount of hypo-osmolar intravenous fluid .

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Client’s continuously receiving 5% dextrose in water. Impaired homeostasis mechanism . Stress condition causes increase in release of ADH and aldosterone . Psychiatric disorders like schizophrenia .

CLINICAL FEATURES :

Peripheral or generalized oedema . Increase in total body water causes weight gain . Circulatory overload causes –

Full , bounding pulse . Distended neck and peripheral vein . Increased CVP . Cough , dyspnoea , orthopenea . Moist crackles in lungs . Pulmonary edema if severe ICFVE . Increased urine output . Ascites .

Altered mental status and anxiety . Confusion and unknown fear .

DIAGNOSTIC EVALUATION

Plasma sodium : < 125mgEq/L Hematocrit : decreases

MANAGEMENT :

1. Medication : Diuretics are commonly used to treat fluid volume excess . They inhibit sodium and water reabsorption , increasing urine output . LOOP DIURETICS :Furosemide [Lasix] .THIAZIDE LIKE DIURETICS : Chlorothiazide [Diuril] .POTASSIUM SPARING DIURETICS : Spironolactone [Aldactone] .

2. Fluid Management : Fluid intake may be restricted to client having fluid volume excess . The amount of fluid allowed per day is prescribed by

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primary care provider . All fluid must be calculated , including meals and thatis used to administer medication orally or intravenously .

3. Dietary management : Because sodium retention is a primary cause of fluid volume excess , so sodium restriction diet is often prescribed .

NURSING MANAGEMENT :

1. Excess fluid volume Assess vital signs , heart sounds , CVP , and volume of peripheral

arteries . Assess for the presence of edema . Obtain weight daily at same time of day . Provide oral hygiene 2hourly . Teach client about sodium restricted diet . Report significant changes in serum electrolytes . Administer oral fluids cautiously , adhering to any prescribed fluid

retention . Administer diuretics as prescribed .

2. Risk for impaired skin integrity Assess skin in pressure area and over bony prominences . Change position of client 2 hourly . Provide alterating pressure mattress , foot cradle , heel protectors

, to reduce pressure on tissues .3. Risk for impaired gas exchange

Ausculcate lungs for presence of wheezes and crackles . Place in fowler’s position if having dysponea or orthopenea . Monitor oxygen saturation level and ABG’s . Administer oxygen as indicated . Ausculcate heart for extra heart sounds .

EXTRACELLULAR FLUID VOLUME SHIFT [ THIRST SPACING ]

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DEFINITION : Extracellular fluid volume shift is a change in the location of Extracellular fluid between intravascular and interstitial space .

Fluids shifts are of types :

1. Vascular fluid shifts to interstitial space .2. Interstitial fluid shift to vascular space .

Fluid that shifts into interstitial space and remains there is known as third spacing.

Common sites for third spacing are :

Pleural cavity . Peritoneal cavity . Pericardial sac .

ETIOLOGY :

Increased hyrostatic pressure . Increased capillary permeability . Decreased serum protein level . Obstruction of venous portion of capillary or non functional lymphatic

drainage system . Pathologic process that triggers the inflammatory process . Decreased protein intake production , storage or increased loss in PEM and

liver or kidneys . Altered lymphatic function / Venous thrombosis impairs fluid return to

right atrium , thus producingfluid shifting . Peritoneal cavity – impaired protein synthesis , decreased colloidal osmotic

pressure .

CLINICAL FEATURES :

Pallor , cold limbs , weak and rapid pulse . Hypotension , oliguria , decreased level of consciousness . Bounding pulse . Engorgement of peripheral and jugular vein .

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DIAGNOSTIC EVALUATION :

Serum sodium : increased . BUN : increased . Urine specific gravity : increased .

MANAGEMENT

Replace fluid : Intravenous fluid administration to replace intravascular volume . Albumin given to replace protein loss from trauma . Fluids are titrated to maintain adequate blood pressure , CVP , PCWP,

urine output . Stabilize other problems :

Intravenous antibiotics are given to prevent sepsis . Vasodilators are given to maintain blood pressure . Steroids are given for inflammatory disorders .

Monitor the followings regularly : Abdominal girth 8 hourly . Limb circumferences . Skin integrity to prevent skin breakdown of edematous area . Urine output 8 hourly . Plasma sodium , BUN and creatinine level .

ELECTROLYTES

Electrolytes are substances whose molecules dissociates or splits into ions when placed in water .

IONS : Ions are electrically charged particles .

CATIONS : Cations are positively charged particles . For example – Na+ , K+ etc .

ANIONS : Anions are negatively charged particles . For example – Cl- etc.

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NON-ELECTROLYTE : Non electrolyte are substances that do not dissociate into ions in solution .For example – Glucose and urea .

OSMOLALITY : A measure of the total substance [solute] concentration per kilogram of solvent .

OSMOLARITY : A measure of the total substance [solute] concentration per litre of the solvent .

SOLUTE : Substance that is dissolved in solvent .

SOLUTION : Homogenous mixture of solutes dissolved in a solvent .

SOLVENT : Substances that is capable of dissolving a solute .

MEASUREMENT OF ELECTROLYTES

Electrolytes can be measured by weight or combining power . The unit of weight

is milligram per deciliter [mg/dl] and combining power is miliequivalents per

litre [mEq/L] . Milliequivalents equals weight [in milligrams ] divided by atomic

weight and multiplied by the valence .

SODIUM IMBALANCES

Sodium is the most plentiful electrolyte in extracellular fluid [ECF]. Sodium is the

primary regulator of volume , osmolality and distribution of ECF .

Normal serum sodium : 135 – 145 mEq/L

EXTRACELLULAR EXTRACELLULAR EXPANSION

CONTRACTION

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VOLUME DEFICIT

RESULTING FROM:

VOLUME EXCESS RESULTING Water deficiency : Hypernatremia FROM :

Sodium deficiency : Hyponatremia Water excess : Hyponatremia

Isotonic ECF deficit : Normal sodium Sodium excess : Hypernatremia

Isotonic ECF excess : Normal sodium

FIG . DIFFERENTIAL ASSESSMENT OF EXTRACELLULAR FLUID VOLUME

HYPO-OSMOLAR HYPER-OSMOLAR IMBALANCE IMBALANCE

Na+Loss>water loss Na+ Gain>water gain

OSMOLAR ISOTONIC LOSS ISOTONIC GAIN OSMOLAR

BALANCE BALANCE

Water loss>Na+loss Water gain>Na+gain

HYPER-OSMOLAR HYPO-OSMOLAR

IMBALANCE BALANCE

FIG. ISOTONIC GAINS AND LOSSES AFFECT MAINLY THE EXTRACELLULAR FLUID COMPARTMENTS

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HYPONATRENMIA : When sodium levels are low , water is drawn into the cells of the body , causing them to swell.

HYPERNATREMIA : High levels of sodium in extracellular fluid , draw water out of body cells , causing them to shrink .

REGULATION OF SODIUM BALANCE IN THE BODY :

Kidneys are the primary regulator of sodium balance in the body . Mechanisms are :

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Renin – Angiotensin – A ldosterone System : Promotes the renal tubules to reabsorb sodium .

Antidiuretic hormone is released from posterior pituitary ADH promotes sodium and water reabsorption in the distal tubules of kidneys .

HYPONATREMIA

DEFINITION : Hyponatremia is a serum sodium level less than 135 mEq/dl . It may result from a loss of sodium from the body , but it may also be caused by water gain than dilute ECF .

ETIOLOGICAL FACTORS :

Inappropriate use of sodium free or hypotonic IV fluids after surgery or trauma .

Administration of fluids in patients with renal failure or psychiatric disorders .

SIADH will result in dilutional hyponatremia . Loss of sodium rich body fluid from GIT , kidneys or skin directly . Excessive hypotonic solutions .

PATHOPHYSIOLOGY

Due to etilogical factors

Decreased osmolality of intracellular fluid

Cells swelled [water shift from ECF into intracellular fluid ]

Drops serum osmolality

Hyponatremia

CLINICAL FEATURES :

NEUROLOGIC MANIFESTATION : Cellular edema

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Headache , lethargy Irritability , confusion Personality changes Tremors , seizures , coma Hyperrflexia , muscle spasm Depression , dulled sensorium

MUSCULAR MANIFESTATIONS : Muscle cramps Weakness Fatigue

GASTROINTESTINAL MANIFESTATIONS : Anorexia Nausea , vomitting Weight loss Dry mucous membrane Abdominal cramping Diarrhoea

CARDIOVASCULAR MANIFESTATIONS : Postural hypotension Tachycardia Rapid , thready pulse Decreased CVP and jugular venous filling

DIAGNOSTIC EVALUATION :

Health history : Current manifestations Precipitating factors Chief complaints

Physical assessment : Head to toe examination for detecting the clinical features or any

abnormality in body functioning . Diagnostic tests :

Serum potassium : < 135 mEq/L .

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Serum osmolality : < 275 mOsm/kg . 24 hour urine specimen to evaluate sodium excretion .

MANAGEMENT

1. Medications : Sodium containing fluids are given . Fluids like Isotonic Ringer’s solution or Isotonic saline is

recommemded . Loop diuretics are given . Drugs related to sign and symptoms are given .

2. Fluid and dietary management If hyponatremia is mild , increase intake of sodium rich diet .

NURSING MANAGEMENT

1. Risk for imbalanced fluid volume Monitor intake and output . Weight daily . Use IV flow control devices . Explain and clear doubts of client and his family .

2. Risk for ineffective cerebral tissue perfusion Monitor serum electrolytes and serum osmolality . Assess neurological changes . Monitor mental status and orientation . Assess muscle strength and tone and deep tendon reflexes .

HYPERNATREMIA

DEFINITION : Hypernatremia is a serum sodium level greater than 145 mEq/L .

ETIOLOGICAL FACTORS :

Altered thirst . Inability to respond to thirst sensation or obtain water . Decreased synthesis of ADH from posterior pituitary gland .

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Excessive sweating. Diarrhea . Diabetes inspidus . Oral electrolyte solutions or hyperosmolar tube-feeding formulas . Excessive IV fluid such as normal saline , 3% or 5% sodium chloride , or

sodium bicarbonate . Primary hyperaldosteronism [hypersecretion of aldosterone ].

PATHOPHYSIOLOGY

Two regulatory mechanisms protect the body from hypernatremia :

i. Excess sodium in ECF stimulates the release of ADH , so more water is retained by the kidneys .

ii. Thirst mechanism is stimulated to increase the intake of water .

CLINICAL FEATURES

NEUROLOGICAL MANIFESTATIONS : Lethargy , weakness . Irritability . Seizures , coma and death . Altered mental status . Decreased level of consciousness . Muscle twitching .

Dry and sticky mucous membrane .

DIAGNOSTIC EVALUATION

Health history : Current manifestations . Precipitating factors . Chief complaints .

Physical assessment : Head to toe examination for detecting the clinical features or any

abnormality in body functioning .

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Diagnostic evaluation : Seum sodium : > 145mEq/L . Serum osmolality : > 295mOsm/kg . Water deprivation test is performed .

MANAGEMENT

MEDICATIONS :

Oral or intravenous water replacement . Hypotonic intravenous fluid[0.45% sodium chloride or 5% dextrose in

water ]. Diureticsgiven to increase sodium excretion.

NURSING MANGEMENT

1. Risk for injury Maintain fluid replacement . Monitor serum sodium and osmolality . Monitor neurologic functioning . Institute safety precautions as necessary. Make client oriented to time , place and person .

POTASSIUM IMBALANCES

Current NmoPAitory tor alancedimRCCCCCCN .

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