FLUID AND ELECTROLYTES

By Dr.Subash Arun

Fluids

Important definitions to understand body homeostasis: Osmolality(m):-no. of osmotically active particles per kg water/solvent(mOsm /kg ). 2*[Na] +[glucose]/18 +[BUN]/2.8Osmolarity(M):-no.of osmotically active particles in 1 litre of water in solution.(mOsm/l)Effective osmolality(tonicity):-osmotic force that is mediating the shift of water between the ECF & ICF.It depends on size of the solute particle & membrane permeability Effective osmolality-2*[Na] +[glucose]/18Oncotic pressure:-total osmatic effect of a non - diffusible colloid.eg:AlbuminElectrical neutrality:-total electric charge of cations equals that of the anions eg:RTA with hyperchloremic metabolic acidosis

VARIATIONS IN FLUID CONTENTBODY FATBecause fat cells contain little water and lean tissue is rich in water, the more obese the person, the smaller the percentage of total body water compared with body weight.This is also true between sexes because females tend to have proportionally more body fat than males.There is also an increase in fat cells in older people

VARIATIONS IN FLUID CONTENTAGE

Fluid compartments:highlights1,TBW consists of ICF[30-40%] & ECF[20-25] and two minor compartments,trans cellular[TCF 2%] and slowly exchangeable compartments[SEF-10%].2,TCF-gi secretions,acqueous humor,synovial fluid etc.3,SEF-bones,cartilages etc.4,equilibrium b/w hydrostatic&oncotic forces regulate intra vascular volume.5,oncotic pressure via albumin-draws fluid into vessels.6,hydrostatic pressure via pumping action of heart-pushes fluid out of intra vascular space near arterial end of capillaries.7,overall,there is net movement of fluid out of IVS to ICS,which is returned again via lymphatics.

Osmolality:highlights1,osmotic equilibrium b/w ECF and ICF-movement of water.2,0smolality of ECF equals to ICF.3,285-295 mOsm/kg.4,plasma osmolality=2*[Na]+[glucose]/18+BUN/2.85,meas~ and calc~ osmolality are within 10mOsm/kg.6,ineffective osmoles-urea,ethanol.7,in hyperglycemia(DKA) water moves from ICF to ECF causing dilutional hyponatremia despite elevated osmolality. [Na]corrected=[Na]measured+1.6*([glucose]- 100mg/dl]/100.

Osmolal gap-diff b/w meas~ and calc~ osmolality >10mOsm/kg.It is due to unmeasured osmoles eg:ethanol,ethylene glycol,methanol,mannitol.Pseudohyponatremia-diff b/w meas~ and calc~. d/t elevated lipids and proteinswater content of serum decreases d/t displacement. it is conc.of Na+ in serum water(without solid component) that is physiological relevant. plasma osmolality is normal despite hyponatremia.

Regulation of osmolality & volume: water balance determines osmolality.

sodium balance determines intra vascular volume.

In case of volume depletion, it takes precedence over regulation of osmolality and retention of water contributes to maintainence of IV volume.

Changes as little as 1%elicit regulatory mechanisms.

Blood volume or BPVolume receptorAtria and great veinsHypothalamusPosterior pituitary glandOsmoreceptors in hypothalamusOsmolarityADHKidney tubulesH2O reabsorptionvascular volume and osmolarityNarcotics, Stress, Anesthetic agents, Heat, Nicotine, Antineoplastic agents, SurgeryANTIDIURETIC HORMONE REGULATION MECHANISMS

Juxtaglomerular cells-kidneySerum Sodium Blood volumeAngiotensin IKidney tubulesAngiotensin IIAdrenal CortexSodium resorption (H2O resorbed with sodium); Blood volumeAngiotensinogen in plasmaRENINAngiotensin-converting enzymeALDOSTERONEIntestine, sweat glands, Salivary glandsVia vasoconstriction of arterial smooth muscleALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM

AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY

NORMAL REQUIREMENTS OF FLUIDS &ELECTROLYTES:Normal requirement of water&electrolytes consist of amounts necessary to replace URINARY loss & IWL,provide water for metabolism.calculated on basis of :Body weight,body surface area metabolic rate. metabolic rate is most physiological-BMR,muscular activity,growth. Most accurate meathod via CALORIC method by Holiday and segar.-IWL and URINARY loss parallels energy metabolism. The IWL -40 to 60 ml per 100cal metabolised renal water loss-50 to 70 ml stool-5 to 10 ml per 100cal. water produced from metabolism(oxidation)- 20 ml. So net req of water is 100-110 ml for 100cal metabolised.

Fluid req in relation to body weight:

Fluid req. based on body surface area: 1500ml per m2 per day. Na+ -50mEq per m2. k+ -30mEq /m2 cl- 30mEq/m2.

The req are met using N/5 saline in 5%dextrose with 1ml of 15 %KCL per 100 ml IVF. it provides 30mEq Na+ & 20 mEq k+ per litre of solution.

Fluid TypesFluids in the body generally arent found in pure formsIsotonic, hypotonic, and hypertonic typesDefined in terms of the amount of solute or dissolve substances in the solutionBalancing these fluids involves the shifting of fluid not the solute involved

Isotonic SolutionsNo net fluid shifts occur between isotonic solutions because the solution are equally concentratedEx. NSS or 0.9SS

Hypotonic SolutionsHas a lower solute concentration than another solutionFluid from the hypotonic solution would shift into the second solution until the two solutions had equal concentrationsEx. Half normal or 0.45%SS

Hypertonic SolutionsHas a higher solute concentration than another solutionFluid from the second solution would shift into the hypertonic solution until the two solutions had equal concentrationsEx. 3%NS

Fluid MovementsFluids and solutes constantly move within the body, which allows the body to maintain homeostasisFluids along with nutrients and waste products constantly shift within the bodys compartments from the cell to the interstitial spaces, to the blood vessels and back again

Fluid MovementsTypes of TransportA. Active transport B. Passive transportDiffusionOsmosisFiltration

FLUID DEFICIT/HYPOVOLEMIAMay occur as a result of:Reduced fluid intakeLoss of body fluidsSequestration (compartmentalizing) of body fluidsPathophysiology and Clinical Manifestations

DECREASED FLUID VOLUMEStimulation of thirst center in hypothalamusPerson complains of thirst ADH Secretion Water resorption Urine OutputRenin-Angiotensin-Aldosterone System Activation Sodium and Water Resorption Urine specific gravity

Pathophysiology and Clinical ManifestationsUNTREATED FLUID VOLUME DEFICITDepletion of fluids available BODY TEMPERATUREDry mucous membranesDifficulty with speechCells become unable to continue providing water to replace ECF lossesSigns of circulatory collapse blood pressure heart rate respiratory rateRestlessness and Apprehension

Hypovolemia InterventionMonitor fluid intake and outputChecked daily weight (a 1lb(0.45kg) weight loss equals a 500 ml fluid loss)Monitor hemodynamic values such as CVPMonitor results of laboratory studiesAssess level of consciousnessAdminister and monitor I.V. fluidsApply and adjust oxygen therapy as orderedIf patient is bleeding, apply direct continuous pressure to the area and elevate it if possibleAssess skin turgorAssess oral mucous membranesTurn the patient at least every 2 hours to prevent skin breakdown Encourage oral fluids

HypovolemiaWarning SignsCool pale skin over the arms and legsDecreased central venous pressureDelayed capillary refillDeterioration in mental status flat jugular veinsOrthostatic hypotensionTachycardiaUrine output initially more than 30ml/min, then dropping below 10ml/hourWeak or absent peripheral pulsesWeight loss

Composition of Different Intravenous Solution

IVFDextrose (g/L)Na (meq/L)Cl (meq/L)K (meq/L)Lactate (meq/L)D5 0.9% NaCl50154154D5 0.15% NaCl502525D5 0.3% NaCl505151D5 0.45% NaCl507777D5 IMB5025222023LRS0130109428NSS0154154D5LRS50130109428

Fluid Replacement TherapyISOTONIC SOLUTION

FactsExamplesUses-same osmolality as plasma (app. 275 to 295 mOsm/kg)-vascular space osmolality not altered by infusion-expand intracellular and extracellular space equally; degree of expansion correlates with amount of fluid infused-no solution-related shifting between ICF and ECF spaces-cells neither shrink nor swell with fluid movementDextrose 5% in water,

Normal Saline Solution,

Lactated Ringers SolutionFluid loss and dehydrationHypernatremia

Blood transfusion, fluid challenges, resuscitation, shock, metabolic alkalosis, hypercalcemia, hyponatremia

Acute blood loss, burns, dehydration, hypovolemia

Fluid Replacement Therapy HYPOTONIC SOLUTION

Fluid Replacement TherapyHYPERTONIC SOLUTION

FLUID EXCESS/HYPERVOLEMIAPsychiatric Disorders, SIADH, Certain head injuriesDietary Sodium IndiscretionRenal and endocrine disturbances, malignancies, adenomasOverhydrationExcessive Sodium IntakeFailure of renal or hormonal regulatory functionsFLUID VOLUME EXCESS/HYPERVOLEMIA

Since ECF becomes hypoosmolar, fluid moves into the cells to equalize the concentration on both sides of the cell membrane

Thus there, is an increase in intracellular fluidThe brain cells are particularly sensitive to the increase of intracellular water, the most common signs of hypoosmolar overhydration are changes in mental status. Confusion, ataxia, and convulsions may also occur.Other clinical manifestations include: hyperventilation, sudden weight gain, warm, moist skin, increased ICP: slow bounding pulse with an increase in systolic and decrease in diastolic pressue and peripheral edema, usually not marked

HypervolemiaEvaluating pitting edemaPress your fingertip firmly into the patients skin over a bony surface for a few seconds. Then note the depth of the imprint your finger leaves on the skinA slight imprint indicates +1 pitting edemaA deep imprint, with the skin slow to return to its original contour, indicates a +4 pitting edemaWhen the skin resists pressure and appears distended, the condition is called brawny edema, which causes the skin to swell so much that fluid cant be displaced

HypervolemiaDiagnostic Findings:Decreased hematocrit resulting from hemodilutionlow serum Na level(dilutional hyponatremia)Low serum K and BUN levels either due to hemodilution or higher levels may indicate renal failureLow oxygen levelAbnormal chest x-rayIndicates fluid accumulationMay reveal pulmonary edema or pleural effusions

HypervolemiaTreatmentNa and fluid intake restrictionDiuretics to promote excess fluid excretionMorphine and nitroglycerin (Nitro-Dur) for pulmonary edemaDilate blood vesselsReduce pulmonary congestion and amount of blood returning to the heartDigoxin for heart failureStrengthens cardiac contractions

HypervolemiaTreatmentSupportive measuresOxygen administrationBed restHemodialysis or continuous renal replacement therapy for renal dysfunction

Electrolytes

Which one is not a cation? A. Calcium B. Magnesium C. Phosphorous D. Sodium

Anions and CationsAnions

CationsBicarbonateChloridePhosphorousCalciumMagnesiumPotassiumSodium

WHAT DO ELECTROLYTES DO?

Controls and regulates volume of body fluids Its concentration is the major determinant of ECF volume Is the chief electrolyte of ECF Influence ICF VolumeParticipates in the generation and transmission of nerve impulses Is an essential electrolyte in the sodium-potassium pump RDA: 3mEq/kg/day Eliminated primarily by the kidneys, smaller in feces and perspiration Salt intake affects sodium concentrations Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosterone Normal value: 135-145 mEq/L

HYPONATREMIA1,Serum Na

HYPONATREMIA( Na

PATHOPHYSIOLOGY OF HYPONATREMIASodium loss from the intravascular compartmentDiffusion of water into the interstitial spacesSodium in the interstitial space is dilutedDecreased osmolarity of ECFWater moves into the cell as a result of sodium lossExtracellular compartment is depleted of waterCLINICAL SYMPTOMS

CLINICAL MANIFESTATIONS OF HYPONATREMIAMuscle WeaknessAPATHYPostural hypotensionNausea andAbdominal CrampsWeight LossClinical manifestations occur when serum Na is

Treatment of hyponatremia:1,treat hypotension,regard less of serum sodium(ns bolus,RL,5%albumin).In asymp cases with hypovolemia WHO ORS is given.2,in chronic hyponat~ correct deficit over 48-72hrs,rapid decline is ass.vt PONTINE myelinosis.3,rate of increase is 0.5mEq/hr(8-10mEq/l/day),in first 48 hrs correction should not exceed 15-20mEq/l.4,In acute and symptomatic cases-IV infusion of 3%NS @3-6 ml/kg over 10-15 min increase Na+ by 5-6mEq/l. it can be repeated if no improvement in symp.occurs.5,the dose of sodium req. is calculated by: Na deficit=0.6*(body weight)*[desired Na-observed Na]mEq/l

in SIADH hyponatremia,hypoosmolality,oliguria,mild expansion of fluid volume,urinary Na wasting. urine osmolality is HIGH. no edema. Rx:1,fluid restriction 2,3%NS if symptomatic 3,frusemide to increase free water clearence 4,lithium&demeclocycline is to be used cautiously.

HYPERNATREMIAA serum sodium level above 150 mEq/L is termed hypernatremiaMay occur as a result of fluid deficit or sodium excessFrequently occurs with fluid imbalanceDevelops when an excess of sodium occurs without a proportional increase in body fluid or when water loss occurs without proportional loss of sodium.

PATHOPHYSIOLOGY OF HYPERNATREMIAIncreased Sodium concentration in ECFOsmolarity risesWater leaves the cell by osmosis and enters the the extracellular compartmentsDilution of fluids in ECFCells are water depletedSuppression of aldosterone secretionSodium is exreted in the urineCLINICAL SYMPTOMS

CLINICAL MANIFESTATIONSDry, sticky mucous membranesFirm, rubbery tissue turgorManic excitementTachycardiaDEATH

Clinical picture:1,movement of organic acids & H+ into ECF-M.Acidosis.

2,Hyperglycemia d/t low levels of insulin.

3,Hyperosmolality l/t shift of water from cells causing distention of cerebral vessels-SAH,SDH,ICH.

4,development of idiogenic osmoles in cells.

5,Doughy skin feel & reduced skin turgor.

6,irritable,lethargic

7,Seizures

Evaluation:1,history 2,urine osmolality3,urine Na+ in patients with D.I urine osmolality is

Treatment :1,treat hypotension irrespective of serum Na+.2,hypernatremic dehydration can be treated with ORS.3,twice the estimated deficit either with standard WHO ORS or ORS to water @2:1 over 12-24hrs.4,hypotonic infusates are used(N/4,N/5 NS ~40mEq/l)4,aim is to decrease serum Na by not> than 10-12mEq/l/day over 48hrs.(rate of drop-0.5mEq/l/hr).5,amount of fluid infused is calculated by: assess total body deficit assess fluid deficit/free water deficit=[observed Na-145]*4ml/kg*body weight. now Total body deficit free water deficit=solute fluid deficit(containing 80-100mEq/l Na).

In case of seizures during treatment infuse 3%NS 3-5ml/kg over 1-2 hrs.Renal replacememnt therapy is done for significnat hypernatremia[180-200 mEq/l] with renal failure.Hypocalcemia can occur rx by calcium gluconate.In D.I-increase oral intake of water avoid 5%dextrose d/t glycosuria and increased free water loss, isotonic fluids in case of shock, then administer fluids as calculated along with desmopressin.

Major cation of the ICF. Chief regulator of cellular enzyme activity and cellular water content.It is mostly in muscle and icf conc.is around 150mEq/l.Aldosterone and insulin maintain homeostasis. Aldosterone via distal expression of ROMK (secretory K+ channel)Insulin via increase in Na+-k+ -ATPase activity. Plays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue and cellular building; and maintenance of cellular metabolism and excitation,acid base balance. RDA: 2mEq/kg/day Sources: bananas, peaches, dates, apricots, oranges, melons and potatoes, meat, dairy product.Normal -3.5-5.5mEq/l

CAUSES AND EFFECTS OF HYPOKALEMIAKnown as a low level of serum potassium, less than 3.5 mEq/L Decreased Intake Food and Fluids as in starvationFailure to replace GI lossesIncreased Loss

AldosteroneGastrointestinal lossesPotassium-losing diureticsLoss from cells as in trauma, burnsShift of Potassium into Cells(No change in total body potassium)

HYPOKALEMIAGI TractAnorexia N&V Abdominal distention

CNSLethargy, Diminished deep-tendon reflexes, Confusion, Mental depressionMusclesWeakness, Flaccid paralysis, Weakness of respiratory muscles, Respiratory arrestCV SystemDecrease in standing BP, Dysrhythmias, ECG changes, Myocardial damage, Cardiac arrestKidneysCapacity to concentrate waste, water loss, thirst, kidney damage

Hypokalemia :highlights1,chronic hypokalemia is ass. with impairment of urinary conc. ability & urinary acidification d/t Interstitial nephritis. increase in ammonia formation in kidneys-alkaline urine with high ammonia content.2,ass with digoxin toxicity by increasing its binding to myocytes & increasing its action.3,Transtubular potas~ gradient[TTKG] is a measure of net K+ secretion in distal nephron. changes in urine osmolality that occur with water reabsorbtion in the CD. =K(urine)/K(serum)*serum osmolality/urine osmolalityIt cant be applied when urine osmol~ < serum osmol~.If TTKG4 significant renal loss.

PATHOPHYSIOLOGY OF HYPOKALEMIA= Action PotentialNerve and Muscle ActivityLow Extracellular K+Increase in resting membrane potentialThe cell becomes less excitable

Sodium is retained in the body through resorption by the kidney tubulesPotassium is excretedAldosterone is secretedUse of certain diuretics such as thiazides and furosemide, and corticosteroidsIncreased urinary outputLoss of potassium in urine

TREATMENT:1,determine cause2,ass. with acidosis or alkalosis3,if it is ass. with hypertension/normal Bp.4,correct deficit over 24hrs.5,stop on going losses-K+sparing diuretics,volume restoration with NS,correct HYPOMAGNESEMIA.6,deficit replacement-oral route,2-4mEq/kg/d(max.120-240) in 3 divided doses.7,in acidosis use K+citrate or acetate.8,in c/o severe hypoK(

HYPERKALEMIA:highlights1,sr.K+>5.5mEq/l,MC ass. With renal insuffiency,acidosis.

2,sudden rapid onset of hyperK+ results in cardiac arrythymias.

3,factitious hyperK+standing sample,squeezing of extremities during phlebotomy,thrombocytosis/leucocytosis.4,true hyperK+increased intake,extra cellular shift,decreased excretion.

CAUSES AND EFFECTS OF HYPERKALEMIASerum potassium level greater than 5.5 mEq/LExcess IntakeDietary intake of excess of kidneys ability to excrete; Excess parenteral administrationDecreased Loss

Potassium-sparing diuretics; Renal failure; Adrenal insufficiencyShift of Potassium out of the CellsExtensive injuries, crushing injuries, metabolic acidosis

HYPERKALEMIAGI TractN&V Diarrhea, Colic

CNSNumbness, paresthesiasMusclesEarly: irritabilityLate: weakness leading to flaccid paralysisCV SystemConduction disturbance, ventricular fibrillation, Cardiac ArrestKidneysOliguria leading to anuria

Treatment:

Most abundant electrolyte in the body. 99% in bones and teeth Close link between calcium and phosphorus. High PO4, Low Ca Necessary for nerve impulse transmission and blood clotting and is also a catalyst for muscle contraction and other cellular activities Needed for Vitamin B12 absorption and use Necessary for strong bones and teeth and thickness and strength of cell membranes RDA: 1g for adults. Higher for children and pregnant and lactating women according to body weight, older people, esp. post-menopausal Found in milk, cheese, and dried beans; some in meat and vegetables Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and perspiration Normal value 8.5 10.5 mg/dl

HYPOCALCEMIA(sr,Ca

PATHOPHYSIOLOGY OF HYPOCALCEMIACalcium ions are thought to line the pores of cell membranes, especially neuronsCalcium and Sodium repel each otherWhen serum calcium levels are low, this blocking effect is minimizedWhen Sodium moves more easily into the cell, depolarization takes place more easilyThis results in increased excitability of the nervous system leading to muscle spasm, tingling sensations, and if severe, convulsions and tetanySkeletal, smooth, and cardiac muscle functions are all affected by overstimulationSodiumCalcium

CLINICAL MANIFESTATIONS OF HYPOCALCEMIA

COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, FINGERTIPS OR TOES

PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOW.LARYNGOSPASMSEIZURESPROLONGED QTc INTERVALDPERESSION,PSYCHOSISINTRA CRANIAL HYPERTENSION

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

TREATMENT:1,tetany,laryngospasm,seizures are treated by 2ml/kg of 10%calcium gluconate IV.2,initial IV bolus are given every 6th hrly.

3,10%calcium gluconate(9.8 mg elemental Ca+2/ml)

4,10%calcium chloride (27 mg/ml)

5,oral therapy with 40-80 mg/kg/day.

6,correct hypomagnesemia

7,correct hypo Ca+2 first when ass.with acidosis.

HYPERCALCEMIA: Serum concentration > 11mg/dLCauses and EffectsLoss from bonesImmobilization, Carcinoma with bone metastases, Multiple myelomaExcess Intake

Calcium diet (esp. milk)Antacids containing calciumIncrease in factors Causing Mobilization from bonePTH, Vitamin D, steroid therapyHYPERCALCEMIAKidneysStonesKidney DamageCNSDeep-tendon reflexesLethargyComaBonesBone painOsteoporosisFracturesMusclesMuscle fatigue, hypotonia GI motilityCV SystemDepressed activityDysrhythmiasReduced QTcCardiac Arrest

HOW IT HAPPENSHYPERCALCEMIADEPRESSED NERVE AND MUSCLE ACTIVITYDEEP TENDON REFLEXES MAY BE DECREASED OR ABSENT

MYOCARDIAL FUNCTION IS ALTERED

CLINICAL MANIFESTATIONS OF HYPERCALCEMIADecreased GI MotilityCardiac DysrhythmiasConstipationNauseaMental status changes: lethargy, confusion, memory loss

CLINICAL MANIFESTATIONS OF HYPERCALCEMIAImmobilizationBone DemineralizationCalcium accumulates in the ECF and passes through the kidneysCa PrecipitationCalcium Stones

TREATMENT:1,Hydration and urinary excretion.

2,rapid lowering with isotonic NaCl solution.

3,Bisphosphonates(pamidronate,etidronate) have been used in treatment of hypercalcemia d/t Malignancy,immobilisation,hyper parathyroidism.

4,In renal failure peritoneal/hemo dialysis is used.

5,Cinacalcet (calcitonin like).

6,sub/total parathyroidectomy hyperPTH-reccurent renal stones or persistent sr.Ca+2 >12.5mg/dl.

Mostly found within body cells: LIVER and muscle tissues Second most important cation in the ICF, 2nd to K+ Functions: protein and DNA synthesis, DNA and RNA transcription, and translation of RNA, maintains normal intracellular levels of potassium,.helps maintain electric activity in nervous tissue membranes and muscle membranes.PTH secretion. RDA: about 18-30 mEq; children require larger amounts Sources: vegetables, nuts, fish, whole grains, peas, and beansVIT D and PTH enhance absorbtion. Absorbed in the intestines and excreted by the kidneys Plasma concentrations of magnesium range from 1.5 2.5 mEq/L, with about one third of that amount bound to plasma proteins

HYPOMAGNESEMIA: Serum level < 1.5 mEq/LUsually coexists with hypokalemia and less often with hypocalcemiaDecreased IntakeProlonged malnutrition, StarvationImpaired absorption from GI Tract

Malabsorption syndrome, Alcohol Withdrawal Syndrome, Hypercalcemia, Diarrhea, Draining gastrointestinal fistula ExcretionThiazides(Gitelman)ATN(recovery phase)HYPOMAGNESEMIAMental ChangesAgitation, Depression, ConfusionCNSConvulsions, Paresthesias, Tremor, AtaxiaSeizuresMusclesCramps, ,Spasticity, TetanyCV SystemTachycardia, Hypotension, DysrhythmiasHYPOKALEMIAMETABOLIC ACIDOSIS

PATHOPHYSIOLOGY OF HYPOMAGNESEMIALow serum magnesium levelIncreased acetylcholine releaseIncreased neuromuscular irritabilityIncreased sensitivity to acetylcholine at the myoneural junctionDiminished threshold of excitation for the motor nerveEnhancement of myofibril contraction

PATHOPHYSIOLOGY OF HYPOMAGNESEMIAMAGNESIUMINHIBITS TRANSPORT OF PTHDECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONEPOSSIBLE CALCIUM DEFICIT

CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIACONFUSIONDEPRESSIONCRAMPSTETANYCONVULSIONS

TREATMENT:1,in c/o severe hypo Mg+2slow infusion of MgSo4(50% solution) @dose of 25-50mg/kg(2.5-5.0mg/kg elemental Mg+2). repeated every six hours for a total of 2-3doses.

2,oral supplementation in asymp. Pts.

3,in pts with renal wasting Mg+2 sparing diuretics like spironolactone,amiloride.

HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/LSeldom develops in the presence of normal renal functionMay occur as a result of Mg replacementMay occur when MgSO4 is administered to prevent seizures resulting from eclampsiaCareful monitoring is imperative

PATHOPHYSIOLOGY

Renal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or absorption, etc.Accummulation of Mg in the bodyDiminishing of reflexes, drowsiness, lethargyMg Level RisesSevere Respiratory DepressionRESPIRATORY ARREST may occurAltered Electrical ConductionSlowed heart rate and AV BlockPeripheral vasodilationHypotension, flushing, and increased skin warmth

TREATMENT:1,In mild cases source is removed.

2,in severe cases IV Ca+2 gluconte directly antagonises the cardiac and neuromuscular effects.

3,dialysis in patients with renal impairment & serious cardiovascular effects.

THANK YOU

REFERENCES:1,Short Textbook of pediatrics,Suraj Gupte -11th edition.2,Nelson Textbook of Pediatrics-19th edition3,Principles of Pediatric & Neonatal Emergencies-3rd edition.4,GHAI,Essential Pediatrics-8th edition.

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