fluid and electrolyte imbalance

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Name: laxmi thapa & ravisha pokhrel B.sc nursing 3 rd year College of medical sciences, bharatpur

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Page 1: fluid and electrolyte imbalance

Name: laxmi thapa & ravisha pokhrel

B.sc nursing 3rd yearCollege of medical

sciences, bharatpur

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Help maintain body temperature and cell shape Helps transport nutrients gases and wastes

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The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each 24 hours. Ave= 2500 mL

Normally INTAKE = OUTPUTFLUID IMBALANCEFLUID IMBALANCE

• Changes in ECF volume = alterations in sodium balance• Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity• Fluid excess or deficit = loss of fluid balance• As with all clinical problems, the same pathophysiologic change is not of

equal significance to all people• For example, consider two persons who have the same viral syndrome with

associated nausea and vomiting

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It is an abnormally decreased or increased fluid volume or rapid shift from one compartment of body fluid to anotherHypovolemiaHypervolemia

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• May occur as a result of:May occur as a result of:• Reduced fluid intakeReduced fluid intake• Loss of body fluidsLoss of body fluids• Sequestration (compartmentalizing) of Sequestration (compartmentalizing) of

body fluidsbody fluids PathophysiologyPathophysiology

DECREASED FLUID VOLUMEDECREASED FLUID VOLUME

Stimulation of Stimulation of thirst center in thirst center in hypothalamushypothalamus

Person complains of Person complains of thirstthirst

↑ ↑ ADH SecretionADH Secretion

↑ ↑ Water resorptionWater resorption

↓ ↓ Urine OutputUrine Output

Renin-Angiotensin-Renin-Angiotensin-Aldosterone System Aldosterone System

ActivationActivation

↑ ↑ Sodium and Sodium and Water ResorptionWater Resorption

↑ ↑ Urine specific gravity except Urine specific gravity except with osmotic diuresiswith osmotic diuresis

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acute weight lossOliguriaLow bpSunken eyesDizzinessWeaknessDecreased skin turgorConcentrated urine

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• Fluid Management• Oral rehydration therapy – Solutions

containing glucose and electrolytes. E.g., Pedialyte, Rehydralyte.

• IV therapy – Type of fluid ordered depends on the type of dehydration and the clients cardiovascular status.

• Diet therapy – Mild to moderate dehydration. Correct with oral fluid replacement.

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Monitor & measures fluids at least every 8 hours and sometimes hourly

Monitor daily body weightMonitor vital signsObserve for weak, rapid pulse and

orthostatic hypotensionMonitor urine concentration by

measuring urine specific gravityAssess degree of oral and mucous

membrane moisture

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To prevent hypovolemia, the nurse identifies patient at risk and takes measures to minimize fluid loss. For ex: the patient has diarrhoea, measures should be implemented to control diarrhoea and replacement fluid administered. This includes antidiarrheal medication and small volume of oral fluids at frequent intervals

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It refers to an isotonic expansion of the ECF caused by abnormal retention of water and sodium in approximately the same proportion in which they normally exist in the ECF.

It is most often secondary to an increase in total body water.

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Common Causes:Congestive Heart FailureEarly renal failureIV therapyExcessive sodium ingestionSIADHCorticosteroid

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Signs/SymptomsIncreased BPWeight gainBounding pulseVenous distentionPulmonary edema

DyspneaOrthopnea (diff. breathing when

supine)crackles

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Pharmacological therapyDiuretics such as thiazide diuretics and

loop diureticsThiazide diuretics: hydrochlorothiazideLoop diuretics: furosemide, torsemidePotassium supplement

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I/O chart at regular intervals to identify excessive fluid retention

Breath sound are assessed at regular intervals in at risk patient particularly if parenteral fluid are being administered

Monitor the degree of edema in most dependent parts of body such as feet & ankles

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If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Haemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid base balance and to remove sodium and fluid. Continuous renal replacement therapy may also be required

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IF it is important to detect FVE before the condition become severe. Intervention include promoting rest, restricting sodium intake , monitoring parenteral fluid therapy and administering appropriate medications

Regular rest periods may be beneficial because bed rest favours diuresis of fluid

Sodium and fluid restriction should be instituted as indicated

Fowlers position should be maintain to promote lung expansion

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• Controls and regulates volume of body fluidsControls and regulates volume of body fluids

• Its concentration is the major determinant of ECF volumeIts concentration is the major determinant of ECF volume

•Participates in the generation and transmission of nerve Participates in the generation and transmission of nerve impulsesimpulses

• Eliminated primarily by the kidneys, smaller in feces Eliminated primarily by the kidneys, smaller in feces

• Salt intake affects sodium concentrationsSalt intake affects sodium concentrations

• Sodium is conserved through reabsorption in the kidneys, a Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosteroneprocess stimulated by aldosterone

• Normal value: 135-145 mEq/LNormal value: 135-145 mEq/L

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Refers to the serum sodium concentration less than 135 mEq/L

Common with thiazide diuretic use, but may also be seen with loop and potassium-sparing diuretics as well

Occurs with marked sodium restriction, vomiting and diarrhea, SIADH, etc. The etiology may be mulfactorial

May also occur postop due to temporary alteration in hypothalamic function, loss of GI fluids by vomiting or suction, or hydration with nonelectrolyte solutions

Postoperative hyponatremia is a more serious complication in premenopausal women. The reasons behind this is unknown

Therefore monitoring serum levels is critical and careful assessment for symptoms of hyponatremia is important for all postoperative patients

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Sodium loss from the intravascular compartmentSodium loss from the intravascular compartment

Diffusion of water into the interstitial spacesDiffusion of water into the interstitial spaces

Sodium in the interstitial space is dilutedSodium in the interstitial space is diluted

Decreased osmolarity of ECFDecreased osmolarity of ECF

Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss

Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss

Extracellular compartment is depleted of waterExtracellular compartment is depleted of water

CLINICAL SYMPTOMSCLINICAL SYMPTOMS

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Muscle Weakne

ss

APATHY

Postural hypoten

sion

Nausea andAbdomi

nal Cramps

Weight Loss

In severe hyponatremia: mental confusion, delirium, shock and comaIn severe hyponatremia: mental confusion, delirium, shock and coma

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Contributing FactorsExcessive diaphoresisWound DrainageNPOCHFLow salt dietRenal DiseaseDiuretics

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Assessment findings: Neuro - Generalized skeletal muscle weakness.

Headache / personality changes.Resp.- Shallow respirationsCV - Cardiac changes depend on fluid volumeGI – Increased GI motility, Nausea, Diarrhea

(explosive)GU - Increased urine output

Plasma osmolality:2Na + glucose/18 + BUN/2.8

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Interventions/TreatmentRestore Na levels to normal and prevent

further decreases in Na.Drug Therapy –

(FVD) - IV therapy to restore both fluid and Na. If severe may see 2-3% saline.

(FVE) – Administer osmotic diuretic (Mannitol) to excrete the water rather than the sodium.

Increase oral sodium intake and restrict oral fluid intake.

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• A serum sodium level above 145 mEq/L is A serum sodium level above 145 mEq/L is termed hypernatremiatermed hypernatremia

• May occur as a result of fluid deficit or May occur as a result of fluid deficit or sodium excesssodium excess

• Frequently occurs with fluid imbalanceFrequently occurs with fluid imbalance• Develops when an excess of sodium occurs Develops when an excess of sodium occurs

without a proportional increase in body without a proportional increase in body fluid or when water loss occurs without fluid or when water loss occurs without proportional loss of sodiumproportional loss of sodium

• Risk Factors: excess dietary or parenteral Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes sodium intake, watery diarrhea, diabetes insipidus, damage to thirst center, too insipidus, damage to thirst center, too young, too old, those with physical or young, too old, those with physical or mental status compromise, and people with mental status compromise, and people with hypothalamic dysfunctionhypothalamic dysfunction

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Increased Sodium concentration in ECFIncreased Sodium concentration in ECF

Osmolarity risesOsmolarity rises

Water leaves the cell by osmosis and enters Water leaves the cell by osmosis and enters the the extracellular compartmentsthe the extracellular compartments

Dilution of fluids in ECFDilution of fluids in ECF Cells are water depletedCells are water depleted

Suppression of aldosterone Suppression of aldosterone secretionsecretion

Sodium is exreted in the Sodium is exreted in the urineurine

CLINICAL SYMPTOMSCLINICAL SYMPTOMS

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Dry, sticky Dry, sticky mucous mucous

membranesmembranes

Firm, rubbery Firm, rubbery tissue turgortissue turgor

Manic Manic excitementexcitement

TachycardiaTachycardiaDEATHDEATH

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Assessment findings: Neuro - Spontaneous muscle twitches.

Irregular contractions. Skeletal muscle wkness. Diminished deep tendon reflexes

Resp. – Pulmonary edemaCV – Diminished CO. HR and BP depend

on vascular volume. GU – Dec. urine output. Inc. specific

gravity Skin – Dry, flaky skin. Edema r/t

fluid volume changes.

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Interventions/TreatmentDrug therapy Lowering of serum sodium level by

infusion of hypotonic electrolyte solutionDiuretics also may be prescribed to treat

sodium gainDesmopressin acetate to treat diabetes

insipidus if it is cause of hypernatremiaDiet therapy

Mild – Ensure water intake

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The nurse should assess for abnormal looses of water or low water intake and for large gains of sodium as might occur with ingestion of OTC medication that have high sodium content

The nurse should obtain a medication history, because some prescription medications have a high sodium content

The nurse also notes the patients thirst or elevated body temperature and evaluates it in relation to other clinical sign and symptoms

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The more K, the less Na. The less K, the more NaThe more K, the less Na. The less K, the more Na

• Plays a vital role in such processes such as transmission of Plays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal, electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; and intestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism and cellular building; and maintenance of cellular metabolism and excitationexcitation

• Assists in regulation of acid-base balance by cellular Assists in regulation of acid-base balance by cellular exchange with Hexchange with H

•Sources: bananas, peaches, kiwi, figs, dates, apricots, Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy productsdairy products

•Normal value: 3.5 – 5 mEq/LNormal value: 3.5 – 5 mEq/L

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Serum level is below 3.5 meq/l (3.5 mmol/L) usually indicates a deficit in potassium store

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= Action Potential= Action Potential

Nerve and Muscle ActivityNerve and Muscle Activity

Low Low Extracellular Extracellular

K+K+

Increase in Increase in resting resting

membrane membrane potentialpotential

The cell The cell becomes less becomes less

excitableexcitable

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Sodium is retained in the body through resorption by the Sodium is retained in the body through resorption by the kidney tubuleskidney tubules

Potassium is excretedPotassium is excreted

Aldosterone is secretedAldosterone is secreted

Use of certain diuretics such as thiazides and furosemide, and corticosteroidsUse of certain diuretics such as thiazides and furosemide, and corticosteroids

Increased urinary outputIncreased urinary output

Loss of potassium in urineLoss of potassium in urine

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Administration od 40- 80 meq/day of potassium is adequate in adult if there are no abnormal losses of potassium

Dietary intake of potassium in average adult is 50-100meq/day

When dietary intake is inadequate for any reason, oral or IV potassium supplements may be prescribed

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The nurse needs to monitor for its early presence in patients at risk

Fatigue, anorexia, muscle weakness, decreased bowel motility, paraesthesia and dysrhythmias are signal that warrant assessing the serum potasium concentration

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InterventionsAssess and identify those at riskEncourage potassium-rich foodsK+ replacement (IV or PO)Monitor lab valuesD/c potassium-wasting diureticsTreat underlying cause

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Serum potassium level greater than 5meq/L

Less common than hypokalaemia , but it is usually dangerous

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Contributing factors: Increase in K+ intakeRenal failureK+ sparing diureticsShift of K+ out of the cells

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In non acute situations, restriction of dietary potassium and potassium containing medications may correct the imbalance

Administration either orally or by retention enema of cation exchange resins

EMERGENCY PHARMACOLOGIC THERAPYEMERGENCY PHARMACOLOGIC THERAPY If serum potassium level are dangerously

elevated, it may be necessary to adm. IV calcium gluconate

Monitor blood pressure

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Patients at risk for potassium excess need to be identified and closely monitored for signs of hyperkalemia

Nurse should monitor I/O and observe for signs of muscle weakness and dysrythmias

Serum potassium level as well as BUN , creatinine, glucose & arterial blood gas values are monitored for patient at risk for developing hyperkalemia

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InterventionsNeed to restore normal K+ balance:Eliminate K+ administrationInc. K+ excretion

LasixKayexalate (Polystyrene sulfonate)

Infuse glucose and insulinCardiac Monitoring

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HYPOCHLOREMIA is a serum chloride level below 97meq/L (97mmol/L)

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Irritability Tremors Muscle cramps Hyperactive deep tendon reflexes Slow shallow respiration Coma seizures

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Correcting the cause of hypochloremia and contributing electrolytes and acid-base imbalances

Normal saline (0.9% sodium chloride) or half strength saline(0.45% sodium chloride) solution is administered by IV to replace the chloride

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Monitor the patient I/O, arterial blood gas values and serum electrolyte levels

Changes in pts level of consciousness, muscle strength and movement and reported to the physician promptly

Vital signs are monitored and respiratory assessment is carried out frequently

Educate the pt about food with high chloride content which include tomato juice, banana, eggs, cheese etc

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Serum level of chloride exceeds 107 meq/L

Hypernatremia, bicarbonate loss and metabolic acidosis can occur with high chloride levels

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TachypneaWeaknessLethargyDeep and rapid respirationHypertensionDimnished cognitive ability If untreated it leads to:If untreated it leads to: Decrease in cardiac output, Decrease in cardiac output,

dysrhythmias and comadysrhythmias and coma

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Correcting the cause of underlying cause of hyperchloremia and restoring electrolyte fluid and acid base balance are essential

Hypotonic IV solution may be administered to restore balance

Lactated ringers solution may be prescribed to convert lactate to bicarbonate in liver

Diuretics may be administered to eliminate chloride as well

Sodium chloride and fluid are restricted

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Monitoring vital sign , arterial blood gas values and I/O is important to assess the patients status and the effectiveness of treatment

Assessment findings related to respiratory, neurologic and cardiac systems are documented and changes are discussed with physician

Educate about the diet

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More than 90% of body’s calcium is located in the skeletal system

The normal total serum calcium level is 8.6-10.2 mg/dl (2.2 to 2.6 mmol/L)

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The serum calcium value lower than 8.6mg/dl

Occurs in variety of clinical situation Older people and those with disabilities,

who spend on increased amount of time in bed have an increased risk of hypocalcaemia because bed rest increases bone resorption

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Contributing factors:Dec. oral intakeLactose intoleranceDec. Vitamin D intakeEnd stage renal diseaseDiarrhea

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Contributing factors (cont’d):Acute pancreatitisHyperphosphatemiaImmobilityRemoval or destruction of parathyroid gland

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Numbness Tingling of finger, toes and circumoral

region Anxiety Hyperactive deep tendon reflex Bronchospasm diarrhoea

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Assessment findings: Neuro –Irritable muscle twitches.

Positive Trousseau’s sign. Positive Chvostek’s sign.

Resp. – Resp. failure d/t muscle tetany.CV – Dec. HR., dec. BP, diminished

peripheral pulsesGI – Inc. motility. Inc. BS. Diarrhea

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Interventions/TreatmentDrug Therapy

Calcium supplements Vitamin D

Diet Therapy High calcium diet

Prevention of Injury Seizure precautions

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Status of airway is clearly monitored Safety precaution to be taken if

confusion is present Educate the patient about

hypocalcemia, and calcium containing foods like milk, yogurt, cheese, sea fruit, legumes, fruits

Avoid overuse of laxatives and antacids

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serum calcium value greater than 10.2 mg/dl

It is a dangerous imbalance when severe infact, hypercalcemic crisis has a mortality rate as high as 50% if not treated promptly

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Contributing factors:Excessive calcium intakeExcessive vitamin D intakeRenal failureHyperparathyroidismMalignancyHyperthyroidism

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Muscular weakness Constipation Anorexia Nausea & vomiting Dehydration Hypoactive deep tendon reflexes Calcium stones

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Assessment findings:Neuro – Disorientation, lethargy, coma, profound

muscle weaknessResp. – Ineffective resp. movementCV - Inc. HR, Inc. BP. , Bounding peripheral pulses,

Positive Homan’s sign. Late Phase – Bradycardia, Cardiac arrestGI – Dec. motility. Dec. BS. ConstipationGU – Inc. urine output. Formation of renal calculi

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Interventions/TreatmentEliminate calcium administrationDrug Therapy Isotonic NaCL (Inc. the excretion of Ca)DiureticsCalcium reabsorption inhibitors

(Phosphorus)Cardiac Monitoring

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Increasing patient mobility and encouraging fluids

Encourage to drink 2.8 to 3.8L of fluid daily

Adequate fiber in diet is encouraged Safety precaution are implemented

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It is indicated by value below 2.5 mg/dl

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Contributing Factors:MalnutritionStarvationHypercalcemiaRenal failureUncontrolled DM

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Paresthesia Muscle weakness Bone pain & tenderness Chest pain Confusion Cardiomyopathy Seizures Tissue hypoxia

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Assessment findings: on lab analysis, serum phosphate level is less than 2.5 mg/L

Serum magnesium may be decreased due to increased urinary excretion of magnesium

X-ray may show skeletal changes of rickets

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MANAGEMENTTreat underlying causeOral replacement with vit. D IV phosphorus (Severe)Serum phosphate level should be closely

monitoredDiet therapy

Foods high in oral phosphate

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Identify the patient at risk for hypophosphatemia

Close monitoring of patient Vital signs and monitor serum

phosphorous level Check the level of consciousness Health education

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Serum phosphorus level that exceeds 4.5mg/dl (1.45 mmol/L)

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Tetany Tachycardia Anorexia Nausea & vomiting Muscle weakness Hyperactive reflexes

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Administration of vit.D such as calcitriol which is available both oral ( Rocaltrol) & parenteral ( Calajex, paricalcitol forms)

Calcium binding antacids Administration of amphojel with meals Restriction of dietary phosphate, forced

diuresis with loop diuretics volume replacement with saline

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Surgery may be indicated for removal of large calcium and phosphorus deposits

Dialysis may also lower phosphorus

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The nurse monitor patient at risk for hyperphosphatemia

If low phosphorus diet is prescribed, patient is instructed to avoid phosphorus rich food such as hard cheese, cream, nuts, meats etc

Nurse instruct patient to avoid phosphate containing laxatives and enemas

Monitoring for chnages in urine output

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HYPOMAGNESEMIAHYPOMAGNESEMIA Refers to below normal serum Refers to below normal serum

magnesium concentration 1.3mg/dl magnesium concentration 1.3mg/dl (0.62 mmol/L)(0.62 mmol/L)

It is frequently associated with It is frequently associated with hypokalemiahypokalemia

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Contributing factors:MalnutritionStarvationDiureticsAminoglcoside antibioticsHyperglycemia Insulin administration

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Neuromuscular irritability Mood changes Anorexia Vomiting Increased bp Increased deep tendon reflex insomnia

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Assessment findings:*Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia. Seizures*CV – ECG changes. Dysrhythmias. HTN*Resp. – Shallow resp.*GI – Dec. motility. Anorexia. Nausea

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Mild magnesium deficiency can be corrected by diet alone

Magnesium salt can be administered orally in an oxide or gluonate form

Vital signs must be assessed frequently Calcium gluconate must be readily

available to treat IV.mgso4

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Observe for its sign and symptom Safety precaution are institued Due to dysphagia, patient should be

screened Health education

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Serum magnesium level higher than 2.3 mg/dl

It is a rare electrolyte abnormality because kidney efficiently excrete magnesium

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Contributing factors: Increased Mag intakeDecreased renal excretion

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Flushing Hypotension Muscle weakness Drowsiness Depressed respiration Cardiac arrest diaphoresis

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Assessment findings:serum magnesium level is greater than 2.3mg/dlcreatinine clearance decreases to less than 3.0ml/min

ECG finding: prolonged PR interval : tall T waves : widened QRS

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Administration of magnesium Ventilatory support IV calcium gluconate Administration of loop diuretics and

sodium chloride Administration of lactated ringers IV

solution

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Risk for hypermagnesemia are identified and assessed

Monitor vital signs, noting hypotension and shallow respiration

Observe for decreased deep tendon reflex and changes in level of consciousness

Caution is essential when preparing and medicating magnesium containing fluid parenterally

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