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Seminar ON FLUID AND ELECTROLYTE IMBALANCE

Fluid n Electrolyte Balance

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SeminarON

FLUID AND ELECTROLYTE IMBALANCE

INTRODUCTION

BODY FLUID CAMPARTMENT

MECHANISMS CONTROLLING FLUID AND ELECTROLYTE MOVEMENTDiffusionFaciliated diffusionOsmosisOsmotic pressureOsmolalityOsmolarityOsmotic movement of fluidHydrostatic pressureOncotic pressure

Diffusion

Osmotic movement of fluid

FLUID MOVEMENT IN CAPILLARIESFluid shifts1Shifts of plasma to interstitial fluidElevation of venous hydrostatic pressureDecrease in plasma oncotic pressureElevation of interstitial oncotic pressure2Shifts of interstitial fluid to plasma

FLUID MOVEMENT BETWEEN EXTRACELLUAR FLUID AND INTRACELLUAR FLUID

FLUID SPACING

REGULATION OF WATER BALANCE

1 Hypothalamic regulationCONT..2Pituitary Regulation3Adrenal Cortical Regulation4Renal regulation5Cardiac regulation6 Gastrointestinal regulation7 Insensible water loss

3Adrenal Cortical RegulationFactors affecting aldosterone secretion

Effects of stress on fluid and electrolyte balanceEffects of stress on fluid and electrolyte balance

Cardiac regulationFLUID IMBALANCEFluid deficit (hypovolemia)It occurs when loss of extracellular fluid volume exceeds the intake of fluid.Causesa. Reduced fluid intakeb. Fluid lossc. Sequestration of body fluidsClinical ManifestationsExtracellular Fluid DepletionSkin: poor turgorMouth: dry mucous membranesCardiovascular: postural hypotension (early), low blood pressure, tachycardia, increased respiration, decreased vein fillingWeight: loss Urine: low output, increased specific gravity

Assessment and diagnostic evaluationHealth history and physical examination to determine causeLaboratory data useful in evaluating fluid volume status include BUN. It will be elevated out of proposition to the serum creatinine level (a ratio greater than 20:1) Hematocrit level is greater than normalSerum electrolyte changes may also exist.potassium and sodium levels can be reduced hypokalemia ,hyponatremia or elevated hyperkalemia ,hypernatremia Urine specific gravity is increasedUrine osmolality is greater than 45omOsm/kg

Medical management Isotonic electrolyte solution is administered IV (lactated ringers solution or 0.9% sodium chloride)As soon as the patient becomes normotensive,a hypotonic ectrolyte solution (0.45% sodium chloride) is often used Nursing managementThe nurse monitors and measures fluid intake and output at least q 8 hours (sometimes hourlyDaily body weight (acute loss of 0.5 kg represents a fluid loss of approximately 500mlVital signs should be closely monitored (weak,rapid pulse and postural hypotension decrease temperature)Skin and tongue turgor should be monitored on a regular basisUrinary concentration

Fluid excess (hypervolemia)Fluid volume excess (FVE) refers to an isotonic expansion of the ECF caused by the abnormal retention of water and sodium CausesOverhyderationExcessive sodium intake Failure of renal or hormonal regulatory functionsClinical ManifestationsOverhydrationChanges in behavior: confusion, in coordination, convulsionsHyperventilationSudden weight gainWarm, moist skinIncreased intracranial pressure: slow bounding pulse with an increase in systolic and decrease in diastolic blood pressures Peripheral edema, usually not marked

Assessment and diagnostic evaluationHistory collection & Physical examination.Laboratory test include BUN and hematocrit levels decreased In chronic renal failure, both serum osmolality and sodium level Urine sodium is increased if the kidneys are attempting to excrete excess volume (hypervolemia occurs when aldosterone is chronically stimulated e.g. cirrhosis, heart failure, and nephrotic syndrome urine sodium levels, will not raise in these conditions.Chest X-ray may reveal pulmonary congestion.Medical managementPharmacologic therapyThiazide diuretics are used initially If these are not effective, loop diuretics (furosemide) are prescribed.

16Hemodialysiscont.Nutritional therapyDietary restriction of sodium, an average daily diet not restricted in sodium contains 6-15g of salt ,where as low-sodium diets can range from a mild restriction to as little as 50g of sodium per day Nursing management the nurse measures intake and output at regular intervals to indentify excessive fluid retentionThe patient is weighed daily and acute weight gain is noted (0.9 kg) represents a gain of approximately 1L of fluidAssess breath sounds at regular intervals in at risk patients particularly when parenteral fluid is administeredThe nurse monitors the degree of edema in most dependent parts of body, such as feet and ankles in ambulatory patients and sacral region in bed ridden patientsThe degree of pitting edema is assessed, and the extent of peripheral edema is monitored by measuring circumference of the extremity with a tape marked in millimeters.

ELECTROLYTE IMBALANCE1.SodiumThe normal concentration of sodium in the blood is 135 to 145 mEq/L.

A.HyponatremiaHyponatremia refers to a serum sodium concentration less than 135 mEq/L.EtiologySodium lossGI losses: diarrhea, vomiting, fistuals, NG suctionRenal losses: diuretics, adrenal insufficiency, sodium wasting from renal diseaseSkin losses: burns, wound drainageWater gain (sodium dilution)SIADHCongestive heart failureExcessive hypotonic IV fluidsPrimary polydipsia

Clinical manifestation

Decreased ECF volume (sodium loss)Irritability, apprehension, confusionPostural hypotensionTachycardiaRapid,thready pulseDecrease CVPDecrease jugualar venous fillingNausea, vomitingDry mucous membraneWeight loss Tremors,seizures,comaNormal or increased ECF volume (water gain)Headache.lassitude.apathy,weakness,confusionNausea, vomitingWeight gainIncrease CVP,increase BPMuscle spasm seizures,coma

Diagnostic evaluationLab test to be performed,serum sodium level less than 135 mEq/L in SIADH it may be quite low, such as 100mEq/L or lessSerum osmolality is also decreased, except in azotemia or ingestion of toxinsUrinary sodium if cause is due to sodium loss value will be less than 20mEq/L and specific gravity is low,such as 1.002-1.004If the cause is SIDH urinary sodium is greater than 20mEq/L specific gravity is usually over 1.012

Medical ManagementSodium replacementAdministration of sodium by mouth, nasogastric tube, or the parentral route. lactated ringers solution or isotonic saline (0.9% sodium chloride) solution may be prescribed Water restrictionWhen neurologic symptoms are present, it may be necessary to administer small volume of a hypertonic sodium solution such as 3% or 5% sodium chloride

Nursing managementEarly detection and treatment of this disorder are necessary to prevent serious consequencesFor patient at risk the nurse monitor fluid intake and output as well as daily body weightsAbnormal loss of sodium or gain of water are notedGI manifestation, such as anorexia, nausea ,vomiting and abdominal cramping are also notedNurse must be particularly alert for CNS changes

HypernatremiaA serum sodium level above 145 mEq/L is termed hypernatremia. Hypernatremia may occur as a result of fluid deficit or sodium excess.EtiologyWater loss (sodium concentration)Increase insensible water loss or perspiration (high fever,heatstroke)Diabetes insipidusOsmotic dieresisSodium gainI V hypertonic NaCl I V sodium bicarbonateI V excessive isotonic NaClPrimary hyperaldosteronismSaltwater near drowing

Clinical manifestationDecreased ECF volume (water loss)Intense thirst, dry, swollen tongueRestlessness.agitation,twitchingSeiures,comaWeaknessPostural hypotension, decrease CVPWeight lossNormal or increased ECF volume (sodium gain)Intense thirstRestlessness, agitation, twitchingSeizures, comaFlushed skinWeight gainPeripheral and pulmonary edemaIncreased BP increased CVPDiagnostic evaluationIn hypenatremia, the serum sodium level exceeds 145mEq/L and serum osmolality exceeds 295mOsm/kg. The urine specific gravity and urine osmolality are increased as the kidney attempt to conserve water

Medial managementTreatment consists of gradual lowering of the serum sodium level by the infusion of a hypotonic electrolyte solution (0.3% sodium chloride)isotonic nonsaline solution(dextrose 5% in water ) indicated when water need to be replaced without sodium and decreases cerebral deemaDiuretics also may be prescribed to treat the sodium gain.Desmopressin acetate may be prescribed to treat diabetes insipidus if it is the cause of hypernatremia

Nursing managementPreventing hypernatremiaIf fluid intake is inadequate the nurse consults with physician to plan alteranate route for intake, either by enteral feedings or by the parentral routeIf enteral feeding are used sufficient water should be administered to keep the serum sodium and BUN within normal limits For patient with diabetes insipidus, adequate water intake must be ensured .If the patient has a decreased level of consciousness or other disability interfering with adequate fluid intake, parentral fluid replacement therapy may be prescribedCorrecting hypernatremiaThe nurse monitors patients response to the fluids by reviewing serial sodium level and observing for changes in neurologic signsThere should be gradual decrease in serum sodium level(neurologic signs improve)

PotassiumThe normal concentration of potassium in the blood is 3.5 to 5.5 mEq/L.hypokalemiaA low level of serum potassium, less than 3.5 mEq/L, is known as hypokalemia.EtiologyPotassium lossGI losses: diarrhea, vomiting, fistuals, NG suctionRenal losses :diuretics, hyperaldosteronism, magnesium depletionSkin losses: diaphoresisDialysisShift of potassium into cellsIncreased insulin e.g. I Vdextrose load Alkalosis Tissue repairIncrease epinephrine e.g. stressLack of potassium intakeStarvationDiet low in potassiumFailure to include potassium in parentral fluids if NPO

Clinical manifestationFatigueMuscle weaknessLegs crampsNausea vomiting, ileussoft, flabby musclesWeak, irregular pulsepolyuriaHyperglycemiaelectrogram changesST segment depressionFlattened T wavePresence of U waveVentricular arrhythmias eg. PVCsBradycardiaEnhanced digitalis effectDiagnostic evaluationSerum potassium concentration is less than the lower limit of normalECG changesABG value associated with metabolic alkalosis24 hour urine potassium excretion test can be performed to distinguish between renal and extrarenal lossUrinary potassium excretion exceeding 205mEq/24 h with hypokalemia suggest that renal potassium loss in the cause

Medical managementIf hypokalemia cannot be prevented by conventional measures such as increased intake in the daily diet, it is treated with oral or IV replacement therapy Potassium loss must be corrected daily; administration of 40 to 80 mEq /day of potassium are adequate in the adult if there are no abnormal losses of potassiumFor patient at risk for hypokalemia, a diet containing sufficient potassium should be provided. Dietary intake of potassium in the average adult is 50 to 100 mEq /day. Food high in potassium includes fruits (especially raisins, bananas, apricots, and oranges), vegetables, legumes, whole grains, milk and meat.When dietary intake is inadequate, the physician may prescribe oral or IV supplements. Many salt substitute contain 50 to 60 mEq of potassium per teaspoon and may be sufficient to prevent hypokalemiaIV route is mandatory for patients with severe hypokalemia (e.g. serum level of 2mEq/L) by prescribing potassium acetate or potassium phosphateNursing managementPreventing hypokalemiaCorrecting hypokalemia

HyperkalemiaA serum potassium level greater than 5.5 mEq/L is termed hyperkalemia.EtiologyExcess potassium intakeExcessive or rapid parentral administrationPotassium-containing drugs ( e.g. potassium penicillin)Potassium containing salt substituteShift of potassium out of cellsAcidosisTissue catabolism (e.g. fever, sepsis, burns)Crush injury

Failure to eliminate potassiumRenal diseasePotassium-sparing diureticsAdrenal insufficiencyACE inhibitors

Clinical manifestationIrritabilityAnxietyAbdominal cramping,diarrheaWeakness of lower extremitiesParesthesiasIrregular pulseCardiac standstill if hyperkalemia sudden or severeElectrogram changesTall,peaked T waveProlonged PR intervalST depressionLoss of P wave Widening QRSVentricular fibrillationVentricular stand stillDiagnostic evaluationSerum potassium level and ECG changesABG analysis may reveal metabolic acidosisMedical managementRestriction of potassium and potassium containing medication should be donePrevention of hyperkalemia by the administration, either orally or by retention enema, of cation exchange resins (eg kayexalate)Cation exchange resins cannot be used if patient has a paralytic ileusEmergency pharmacological therapyWhen serum potassium levels are dangerously elevated, it may be necessary to administer IV calcium gluconate. Within minute after administration, calcium antagonizes the action of hyperkalemia on the heart. It does not reduce potassium level it antagonizes the adverse cardiac conduction abnormalitiesMonitoring BP is essential to detect hypotension which may result from the rapid IV administration of calcium gluconate, IV administration of sodium bicarbonate may be necessary to alkanize the plasma and cause temporary shift of potassium into cells, and if furnish sodium to antagonize the cardiac effect of potassium.IV administration of regular insulin and a hypertonic dextrose solution causes a temporary shift of potassium into cells and its action begin within 30 mts and lasts for several hoursBeta -2 agonists also move potassium into the cells and be used in the absence of cardiac diseases

Nursing management

Preventing hyperkalemiaEncourage the patients who are at risk to adhere to the prescribed potassium restriction.eg coffee, cocoa, tea dried fruits Correcting hyperkalemiaNurse should closely monitor the solution and rate of administration. When potassium is added to parental solutions, the potassium mixed with the fluid by converting the bottle several times

CalciumThe normal total serum calcium level is 8.5 to 10 mg/dl. This includes the non-ionized (bound to albumin and in combination with citrate or phosphate) and ionized (metabolically active) calcium.HypocalcemiaHypocalcemia is defined as a total serum calcium concentration of less than 8.5 mg/dl or an ionized calcium concentration of less than 4 mg/dl.EtiologyDecreased total calciumChronic renal failureElevated phosphorousPrimary hypothyroidismVitamin D deficiencyMagnesium deficiencyAcute pancreatitis Loop diureticsChronic alcoholismDiarrheaDecrease serum albumin (patient is usally asymptomatic due to normal ionized calcium level)Decreased ionized calciumAlkalosisExcess administration of citrated blood

Clinical manifestationEasy fatigabilityDepression, anxiety, confusionNumbness and tingling in extremities and region around mouthHyperreflexia,muscle crampsChvosteks signTrousseaus signLargneal spasmTetany, seizuresElectrocardiogram changesElongation of ST segmentProlonged QT intervalVentricular tachycardia

Diagnostic evaluationWhen evaluating serum calcium levels, one must consider several variables, such as serum albumin level and arterial pHFor every decrease in serum albumin of 1g/dl below 4g/dl, the total serum calcium level is underestimated by approximately 0.8 mg/dl .there is a method to calculate the corrected serum calcium levelMeasured total serum calcium level mg/dl + o.8 * (4.0measured albumin level g/dl =corrected total serum calcium levelWhen the arterial Ph increases (alkalosis), more calcium becomes bound to protein as a result ionized portion decreasesAcidosis has the opposite effectPTH level decreased in hypothyroidism.Magnesium and phosphorus levels need to be assessed to identify possible causes of decreased calcium

Medical managementAcute symptomatic hypocalcemia is to be treated with IV administration of calcium. parenteral calcium salt include calcium gluconate - it is not used often because it is more irritating and can cause sloughing of tissue if it infiltrate calcium chloride-produces a higher ionized calcium than gluconate and caicium gluceptate.Too rapid IV administration of calcium causes cardiac arrest, preceded by bradycardia.IV calcium should be diluted in D5W and given as slow bolus or slow infusion, site must be observed for any evidence of infiltrationVitamin D therapy may be instituted to increase calcium absorption from GI tract .aluminum hydroxide, calcium acetate or calcium carbonate antacids may be prescribed to decrease elevated phosphorous levels before treating hypocalcemia for the patient with CRF Increasing dietary intake of calcium to at least 1000 to 1500 mg/day in adult is recommended (e.g. milk products, green leafy vegetables) Nursing managementSeizure precautions are initiated when hypocalcemia is severe Status of airway is closely monitored because laryngeal stridor can occur People at risk for osteoporosis are instructed about the need for adequate dietary calcium intakeTeaching topics may involve discussion of medication such as alendronate and calcitonin to reduce the rate of bone loss Teaching also address strategies to reduce risk of falls

2 HypercalcaemiaHypercalcemia refers to a total serum calcium concentration greater than lOmg/dl.

EtiologyIncreased total calciumMultiple myelomaOther malignancyProlonged immobilizationHyperparathyroidismVitamin D overdoseThiazide diuretics

Increased ionized calciumAcidosis

Clinical manifestationLethargy,weaknessDepressed reflexesDecreased memoryConfusion, personality changes, psychosisAnorexia, nausea vomitingBone pain, fracturesPolyuria, dehydrationNephrolithiasisStupor, comaElectrocardiogram changesShortened ST segmentShortened QT intervalVentricular arrhythmiasIncreased digitalis effect

Dignostic evaluationAnalysis of serum calcium-more than normalECG-shortening of QT interval and ST segment, PR interval prolonged double-antibody PTH test done to differentiate between hyperparathyroidism and malignancy a cause of hypercalcemiaX-rays- presence of osteoporosisSulkowitch urine test-amount of calcium in urineMedical managementPharmacologic therapyGeneral measures include administering fluids to dilute serum calcium and promote its excretion by the kidneys, mobilizing the patient, and restricting dietary calcium intake.IV administration of 0.9% sodium chloride solution temporarily dilute the serum calcium level and increases urinary calcium excretion by inhibiting tubular reabsorption of calcium.Administering IV phosphate can cause reciprocal drop in serum calciumFurosemide is often used in conjunction with administration of a saline solution (causes diueresis and increases calcium excretionCalcitonin can be used to lower the serum calcium level and is useful for patients with heart disease or renal failureCorticosteroids may be used to decrease bone turnover and tubular reabsorption for patients with sarcoidosis, myelomasBiphosphonates inhibit osteoclast acitivityMithramycin, a cytotoxic antibiotic, inhibits bone resorption and thus lowers the serum calcium level.

Nursing managementMonitor for hypocalcaemia in patients at risk. Intervention such as increasing patient mobility and encouraging fluids can help prevent hypocalcaemia, or at least minimize its severityPatients are encouraged to drink 3 to 4 quarts of fluid dailyAdequate fiber should be provided in the diet to offset the tendency for constipationSafety precautions are taken if patient has mental symptomNurse monitor for ECG changes

MagnesiumThe normal serum magnesium level is 1.5 to 2.5 mEq/L. HypomagncsemiaHypomagnesemia is a serum magnesium level of less than 1.5 mEq/L.

EtiologyDiarrheaVomitingChronic alcoholismImpaired GI absorptionMalsorption syndromeProlonged malnutrition large ueine outputNG suctionPoorly controlled diabetes mellitusHyperaldosteronism

Clinical manifestationMental changes: agitation,depression,confusionCNS: convulsions,parathesis,tremor,ataxiaMuscles: cramps,spasticity,tetanyCVS: tachycardia, hypotension,dysrhythmiasDiagnostic evaluationLaboratory analysis of serum magnesium is less than normalHypomagnesmia associated with hypokalemia and hypocalcemia25% of magnesium is protein bound, principally to albumin. A decrease in serum albumin level can, therefore, reduce the measured total magnesium concentration: but it does not reduce the ionized plasma magnesium concentration.ECG evaluations reflect magnesium, calcium, and potassium deficiencies. tachydysrhythmias, prolonged PR and QT interval, ST segment depression, flattened T waves and a prominent U waveUrinary magnesium levels may be helpful in identifying causes Two newer techniques (nuclear magnetic resonance spectroscopy and the ion selective electrode) are sensitive and direct means to measure ionized serum magnesium levels

Medical managementMild magnesium deficiency can be corrected by diet alone. principal dietary sources of magnesium are green leafy vegetables, nuts ,legumes seafood ,butterWhen necessary, magnesium salts can be administered orally to replace continuous excessive losses.Patient receiving parenteral nutrition require magnesium in the IV solution to prevent hypomagnesmiaIV administration of magnesium sulfate must be given by an infusion pump and at a rate not to exceed 150mg/mt, a bolus dose given too rapidly can produce cardiac arrest.Vital signs must be assessed frequently to detect changes in cardiac rate or rhythm, hypotension, and respiratory distressMonitoring urine output is essential before, during, and after administration if urine decreases to less than 100ml over 4 hours should be notifiedCalcium gluconate must be readily available to treat hypocalcemic tetany or hypermagnesiumNursing managementPatient receiving digitalis is monitored closely because a deficit of magnesium can predispose them to digitalis toxicity.Safety precautions are institutedDysphagia may occur in magnesium depleted patients, the ability to swallow should be tested with water before oral administration of food or medicationThe nurse can instruct the patient about the need to consume magnesium rich foods

HypermagnesemiaHypermagnesemia is a serum magnesium level greater than 2.5 mEq/L.EtiologyRenal failure (especially if patient is given magnesium products)Excessive administration of magnesium for treatment of eclampsiaAdrenal insufficiency

Clinical manifestationDrowsy and lethargicRespiratory arrestLoss of deep tendon reflexesHypotension, flushing,Diagnostic evaluationLaboratory analysis of serum magnesium level is greater than normalECG changes may reveal a prolonged PR interval, tall T waves, and a widened QRS, prolonged QT intervals and artrioventricular blocks

Medical managementHypermagnesemia can be prevented by avoiding the administration of magnesium to patients with renal failure and by careful monitoring seriously ill patients who are receiving magnesium saltsIn patient with hypermagnesemia, all parenteral and oral magnesium salts are discontinuedIn emergencies, such as respiratory depression or defective conduction, ventilator support and IV calcium are indicatedHemodialysis with a magnesium- free dialysate can reduce magnesium to a safe level within hoursLoop diurectics and 0.45% sodium chloride solution enhance magnesium excretion in patients with adequate renal failureIV calcium gluconate antagonizes the neuromuscular effects of magnesiumNursing managementPatient at risk are identified and assessedThe nurse monitors the vital signs, noting hypotension and shallow respirationsNurse observes decrease patellar reflexes and changes in the level of consciousness Phosphate Hypophosphatemia is a serum phosphorous level of less than 2.5 mEq/L.

Etiology Malabsorption syndromeNutritional recovery syndromeGlucose administrationTotal parenteral nutritionAlcholol withdrawlPhosphate-binding atacidsRecovery from diabetic ketoacidosisRespiratory alkalosis

Clinical manifestation CNS dysfunction (confusion, coma)RhabdmyolysisRenal tubular wasting of magnesium, calcium, bicarbonateCardiac problem(arrthythmias, decreased stroke volume)Muscle weakness, including respiratory muscle weakness and difficult weaningOsteomalaciaDiagnostic evaluationPTH levels are increased in hyperparathyroidismSerum magnesium may decrease due to urinary increased excretion of magnesiumALP is increased with osteoblastic activityX-rays may show skeletal changes of osteomalacia or rickets

Medical managementphosphorous should be added to parentral solutionAggressive IV phosphorous correction is usually limited to patients whose serum phosphorous level fall below 1 mg/dl and whose GI tract is not functioninig and the rate should not exceed 10mEq/h

Nursing management malnourished patients receiving parenteral nutrition are at risk when calories are introduced too aggressively.Careful attention is given to prevent infectionHyperphosphatemia Hypophosphatemia is a serum phosphorous level of more than 4.5 mEq/L.Etiology Renal failureChemotherapeutic agentsEnemas containing phosphorous(fleet enema)Excessive ingestion of milk,phosphate- containing laxativesHypoparathyroidism

Clinical manifestationMuscle problems, tetanyDeposition of calcium-phosphate precipitates in skin, soft tissue, cornea, viscera, blood vesselsDiagnostic evaluationLaboratory analysis of serum phosphorousSerum phosphorous levels are normally higher in children, because of high rate skeletal growthX-ray studies may show skeletal changes with abnormal bone developmentPTH levels are decreased in hypoparathyroidismBUN and creatinine levels are used to assess renal function

Medical managementvitamin D preparation such as calcitol ( rocaltrol , in oral preparation) ,calcijiex ( for IV administration)Nursing managementWhen a low-phosphorous diet is prescribed, the patient is instructed to avoid phosphorous-rich foods such as hard cheese, creams, nuts, whole-grain, dried fruits, dried vegetablesThe nurse instruct patient to avoid phosphate containing substances such as laxatives and enemas that contain phosphateThe nurse also teaches the patient to recognize the signs of impeding hypocalcemia and to monitor for changes in urine output

Clinical managementAcid base and electrolyte imbalancesSigns and symptoms of hyponatremia, hpokalemia and metabolic acidosis may be notedHyperexicitability of muscles, tetany, hyperactive deep tendon reflexes, weakness, twitching, and muscle cramps Hypokalemia can cause hypochloremia, resulting cardiac dysrhythmias Hyponatremia can cause seizures and comaAssessment and diagnostic evaluationChloride, sodium and potassium are to be evaluatedABG analysis identifies acid-base balance (metabolic acidosis)Urine chloride level is also measured, decreases in hypochloremia

Medical management Normal saline (o.9% sodium chloride) or half strength saline (0.45 sodium chloride) solution is administered IV to replace the chloridePatients receiving diuretics (loop, osmotic, or thiazide) should discontinue these medications or change to another diureticAmmonium chloride, acidifying agents, may be prescribed to treat metabolic alkalosis; the dosage depends on the patients weight and serum chloride level. This agent is metabolized by the liver, and its effects last for about 3 daysNursing managementThe nurse monitors intake and output, arterial blood gas values, and serum electrolyte levels, as well as patient level of consciousness and muscle strength and movementVital signs are monitored and respiratory assessment is carried out frequentlyThe nurse teaches the patient about foods with high chloride content HyperchloremiaIt exists when the serum level exceeds 107 mEq/L (107 mmolHypernatremia, bicarbonate loss and metabolic acidosis can occur with high chloride levelHperchloremic metabolic acidosis is also known as normal anion gap acidosis.It is caused by the loss of bicarbonate ion via the kidney or GI tract with a corresponding increase in chloride ions. Chloride ion in the form of acidifying salts accumulates and acidosis occurs with a decrease in bicarbonate ions.Clinical managementSigns and symptoms of hyperchloremia are the same as those of metabolic acidosis, hypervolemia, and hypernatremiaTachypnea; weakness; lethargy; deep, rapid respirations; diminished cognitive ability; and hypertension occur If untreated, hyperchloremia can lead to decrease in cardiac output, dysrhythmias ,and coma,A high chloride level is accompanied by a high sodium level and fluid retention

Assessment and diagnostic evaluationSerum chloride level will be 108 mEq/L or greaterSerum sodium level will be greater than normal valueSerum pH is less than 7.35Serum bicarbonate level is less than 22 mEq/L There is a normal anion gap of 8-12 mEq/L (low anion gap may be attributed to hypoproteinnemia,while elevated anion gap due to metabolic acidosisUrine chloride excretion increases

Medical managementCorrecting underlying cause of hyperchloremia and restoring electrolyte, fluid, and acid base balance are essentialLactated ringers solution may be prescribed to convert lactate to bicarbonate in the liver, which will increase the base bicarbonate level and correct the acidosisSodium bicarbonate may be given IV to increase bicarbonate level, which leads to the renal excretion of chloride ions as bicarbonate and chloride compete for combination with sodiumDiuretics may be administered to eliminate chloride as well as sodium, fluids and chlorides are restrictedNursing managementMonitoring vital signs, ABG value, intake and output to assess the patient status and effectiveness of treatmentThe nurse teaches the patient about diet that to be followed.

NURSING MANAGEMENT FOR FLUID AND ELECTROLYTE IMBALANCE ASSESSMENTHealth HistoryPhysical ExaminationNURSING DIAGNOSESINTERVENTIONSIntake and Output MonitoringDaily WeightPromoting Oral IntakeTube FeedingParenteral FluidPatient/Family EducationEVALUATION

CONCLUSION

CONCLUSIONCONCLUSION60

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