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Home , Hypercalcaemia, Hyponatremia

6.6 Fluids and Rebecca Lindstrom Sowman and Claudia Rueb

Key points ■■ Water is essential for survival and has many functions in the body. ■■ Regulation of body fluid is under tight homeostatic control; maintenance of is an important aspect of dietetic management. ■■ Disorders of and water balance are common in clinical practice, particularly as a result of surgery, trauma, disease and drug therapy. ■■ Managing fluids and electrolytes is complex and can be challenging; it requires extensive knowledge and experience, usually from a lead clinician.

Humans can survive for several weeks without food, Movement and regulation of fluids but cannot withstand water deprivation for more than A number of processes determine the movement of a few days. Water has many vital functions in the body, ­water and other substances between body fluid com­ including: partments. Cell membranes can be permeable, semi‐­ • As a solvent for ions and molecules. permeable or impermeable to certain molecules, and act • As a transport medium, especially for the excretion of as an effective barrier between the cell and interstitial osmotically active solutes such as and salts. fluid by controlling the exchange of solutes and water. • As a lubricant. The movement of water across semi‐permeable mem­ • In temperature regulation. branes is known as osmosis; water moves into an area of higher solute to achieve equilibrium. Body fluids Water is the most abundant body fluid and accounts for Intravascular Interstitial uid approximately 60% total body weight in men and 50% uid (plasma) in women. Lean body tissue has a high water content + of 75%, in contrast to 10% in adipose tissue. In obese + Na K patients, lean body weight should be used to determine K+ total body water (TBW). Na+ Albumin SECTION 6 Albumin Body fluid compartments + K+ Total body water has two main compartments: intracel­ K Na+ lular fluid (ICF, 67%) within the cells, and (ECF, 33%) outside the cells. Extracellular fluid is further subdivided into interstitial fluid, which includes ICF ECF (33%) ICF (67%) the fluid surrounding the cells and the fluid of the lym­ Extracellular uid Intracellular uid phatic system, and intravascular fluid, the fluid portion of the blood (plasma volume) (see Figure 6.6.1). Figure 6.6.1 Body fluid compartments

Manual of Dietetic Practice, Sixth Edition. Edited by Joan Gandy. © 2019 The British Dietetic Association. Published 2019 by John Wiley & Sons Ltd. Companion website: www.manualofdieteticpractice.com SECTION 6 (Na exception by formed pumping gradient oftheelectrical romolecules, (withthe toelectrolytes butimpermeable towater andlarge ispermeable The cellmembrane mac ­ Regulation of intracellularfluidcompartment retention (renin–angiotensin–aldosteronesystem). tex torelease aldosterone, causingsodiumand water angiotensin II, stimulatestheadrenal cor whichinturn fluid, andelectrolytes. of Thisresults intheproduction inregulatingbloodpressure,that isimportant body apparatus, withinthekidney juxtaglomerular astructure blood flow andincreasesthesecretionofreninfrom ECF volume. in blood pressure reduces renal A reduction The kidneys alsoplay asignificantroleincontrollingthe release andregulatesthekidneys’ ofurine. production The volume receptorstriggera pathway thataffects ADH ume receptorsinthelarge veins andatriumoftheheart. bysubsequently bloodpressure)canbedetected vol­ to normal. Altered ECF (changes in bloodvolume and late sodiumandwater loss, back andtheECFwillreturn ume. triggersadifferent pathwayThis inturn tostimu­ by increasing the ECF vol to normal osmolarity to return ­ passive reabsorptionofwater by thekidneys andallows (ADH) (). The presence of ADH leadsto the triggers thirstandthereleaseofantidiuretichormone intake insodiumleadstoahigherECFosmolarity, which dependsonrenalexcretion. An increased controlling the retention or excretion of sodium. Sodium content, at andhomeostaticmechanisms aredirected The volume oftheECFiscontrolledby thesodium Regulation of extracellularfluidcompartment • • • tonicity, andismaintainedby thefollowing factors: effective osmoticpressureofasolutionisalsoknown as theosmoticpressure.ciple solutethatdetermines The pressure). containsoneprin­ Eachfluidcompartment the (themoresolutes, thegreateritsosmotic brane, of usedtoexpress theconcentration andisoften water mem­ isdrawn intoitthroughthesemi‐permeable Osmotic pressureofasolutionistheby which paramount. fluidosmolarityisthereforeMaintaining extracellular by canbeaffected swelling. inparticular and thebrain can beimpairedasaresult of thechangeincellvolume, ter willmove intothecells, and they swell. Cellfunction cells toshrink; withlow ECFsodium concentration, wa­ in water moving outofthecellsby osmosis, causing of theECF. willresult A highECFsodiumconcentration ume issensitive tochangesinthesodiumconcentration through active transport). This meansthattheICFvol­ teins) asthemainsolute. the osmoticpressureofasolutionwithcolloids(pro­ in maintainingoncoticpressure. Oncoticpressureis plasmaprotein space; albuministhemostimportant Plasma proteinsretainwater intheintravascular space. Sodium retainswater intheextracellular retainswater space. intheintracellular 372 + ) andpotassium(K + ) across the membrane ) acrossthemembrane ­ reflected in the sodiumconcentration. intheserum reflected try. Any disorders of sodium and water balance will be andurinebiochemis­ and interpretationofbothserum der needstobebasedonacarefulphysical examination therapy.drug any disor Appropriate treatmenttocorrect asaresultofsurgery,particularly trauma, diseaseand in clinical practice,balance are a common occurrence andwater Disorders ofsodium(andotherelectrolytes) Disorders of sodiumand water balance imbalancesmayelectrolyte occur. • • • intake andwater output, andisregulatedonthreelevels: Water homeostasisisdependentonthecontrolofwater Fluid balance highly concentrated urine will normally bepresent. urinewillnormally highly concentrated nous fluidor excessive loss. Thirstand oliguriawith dueto theinabilitytodrink,often inadequateintrave­ Water deficitusuallyresultsfromaninadequateintake, Water deficit sodium may stimulate thirst. mayand hypertension bepresent. Increasedserum leads toexpansion oftheECFvolume whereoedema losses suchasindiabetesmellitus. Sodiumretention large volumes of0.9%salinewheretherearehypotonic metabolic acidosisintheclinicalsetting;to correct or be theintravenous ofsodiumbicarbonate administration aldosteronism; anothercausecan orsecondary ­primary tokidney disease,renal sodiumretentionsecondary This canbetheresultofreducedsodiumexcretion, e.g. Sodium excess sodium chloride. treatedwithintravenousis normally infusionof0.9% effect.increase asacompensatory Sodiumdeficiency aswater sodium concentration lossmayin theserum sodium thatisimportant. There may belittlechange case ofasodiumdeficit, itisthetotal amountofECF renal failure, althoughICFlevels areunaffected. Inthe icit issevere, failureand thereisariskofcirculatory andtachycardia.ciated hypertension Ifthesodiumdef­ The resultisadecreaseintheECFvolume, with asso­ diabetic , ascitesandchronickidney disease. losses, e.g. diarrhoea, diuretictherapy, Addison’s disease, sodium deficitmay occurasaresultofgastrointestinal Sodium cannotbelostfromthebodywithoutwater. A Sodium deficit If any ofthesesystemsfailorbegintofail, fluidand sodium excretion andbloodpressure. Renin–angiotensin–aldosterone system – this regulates via ADH. lated Kidneys – sodium andwater excretion islargely regu­ duced andmostlyreabsorbedalongtheGItract. arepro­ andelectrolytes Gastrointestinal tract – fluids Section 6:Nutritionsupport ­ ­between water andsodium, extracellular wherewater isanimbalance The maincauseofhyponatraemia Diagnosis and management agitation, andseizures. sodium level <125 ache and confusion. Severe (serum hyponatraemia sodium 125–129 (serum Clinical manifestations hyponatraemia ofmoderate Symptoms tonic intravenous fluidsandsurgery. body weight, thiazideandthiazide‐like , hypo­ <135 sodiumlevel isdefinedasaserum Hyponatraemia of Hyponatraemia Sodium (Na Sodium oedema canoccur; isusuallypresent. hyponatraemia impaired excretion. Ifsevere, overhydration cerebral and ure) orexcessive water intake, usuallyinassociationwith e.g. inappropriate(increased ADH secretionorrenalfail­ This isusuallycausedby eitherimpairedwater excretion, Water excess usually present. of asimilarvolume ofisotonicfluid; is hypernatraemia ontheECFvolumeThere islesseffect thanfromtheloss 6.6 losses such as diarrhoea or .losses suchasdiarrhoea sodium intake, unlesstherearesignificant extrarenal kidneys. sodiumlevels Urinary dietary usuallyreflect via sweat and faeces; themajorityisexcreted viathe day (138 The average sodiumintake inthe UKis8.1 dietary controls thevolume fluidinthebody. oftheextracellular Hypovolaemia hyponatraemia States ofhypotonic Table 6.6.1 SIADH, syndrome ofinappropriate secretion ofantidiuretic hormone. Hypervolaemia Euvolaemia mmol/L. includeincreasingage, Riskfactors lower Fluids and electrolytes mmol/day). A smallamountofsodiumislost + ) is the principal extracellular cationand ) istheprincipalextracellular Hypotonic hyponatraemia mmol/L) isassociatedwithvomiting, mmol/L) canbenausea, head­ sodium Loss ofwaterand and/or sodium Changes inwater and water Increase insodium Increase inwater g/ mlk H 4.1 =287mmol/kg • • tomatic hyponatraemia, theuseofhypertonic underlying causeaswell water. asrestricting Insymp­ mic ­ Treating patientswitheuvolaemic andhypervolae­ Management of hypotonichyponatraemia itself.hyponatraemia This focuses thanthe ontheunderlyingdisorderrather Management of non‐hypotonichyponatraemia (see Table 6.6.1).respectively) laemic, euvolaemic andhypervolaemic hyponatraemia, orincreasedexisting sodiumstores(i.e.normal hypovo­ siae a 2 ×(Na as estimated measurement isnotavailable, osmolalitycanbe serum is usedasafirststeptocategorise hyponatraemia. Ifa sodium, chloride, bicarbonate, proteinandglucose, and oftheblood,the liquidcomponent(serum) including tonicity) describestheamountofchemicalsdissolved in aetiology ofhyponatraemia. osmolality(serum Serum condition successfully, itishelpfultounderstandthe is inexcess asopposedtosodium. Inordertotreatthis • slightly.but reference vary ranges Normal serum osmolalityis275–290 serum Normal Hypotonic hyponatraemia canoccur withdecreased,Hypotonic hyponatraemia Hyponatraemia canbeclassifiedas: Hyponatraemia o eape 2 ×(Na example For ◦ ◦ ◦ kg H Hypotonic hyponatraemia: osmolality<275 serum kg H Isotonic hyponatraemia: osmolality275–290 serum kg H hyponatraemia: osmolality>290 serum Hypertonic ◦ ◦ ◦ hyperproteinaemia. tonicity, serum Normal caused by hyperlipidaemia, tonicity,High serum e.g. hyperglycaemia. Low tonicity. serum hyponatraemia successfullymeanseliminatingthe hyponatraemia 2 2 2 O. O. O. • • Extrarenal: urinarysodium <20 • • Renal: urinarysodium>20 Underlying cause • Urinary sodium<20 • Urinary sodium>20 SIADH, post‐operativestate , Excessive sweating,bloodloss Gastrointestinal losses Ketonuria, diuretics, salt‐wastingnephropathy cardiac failure, livercirrhosis, ) Disorders associatedwithoedema(e.g.congestive Renal failure + 2 +K O. + 136 +K + lcs (mmol/L). ) +ureaglucose mmol/L mmol/L + mmol/L +glucose 5.0 4.2) +urea mmol/L mmol/kg H mmol/ mmol/ mmol/ 373 2 O, O, ­ ­

SECTION 6 SECTION 6 and 0.45%NaCl), sodiumlevels andserum shouldnotbe nously. Infusatesshouldbe hypotonic (e.g. 5%glucose access available, fluidsshouldbeadministeredintrave ­ viaafeeding orenterally tube.orally Ifthereisnoenteral thelackofwater.correcting fully meanseliminatingtheunderlyingcauseaswell as mia (see Table 6.6.2). Treating success­ hypernatraemia ­ it ishelpfultounderstandtheaetiologyofhypernatrae respectively). Inordertotreatthisconditionsuccessfully, mic, euvolaemic and hypervolaemic hypernatraemia, orincreasedtotalbodysodium(i.e.normal hypovolae­ of sodium. canoccurwithdecreased, Hypernatraemia ween water andsodium, extracellular withanexcess isanimbalancebet­ The maincauseofhypernatraemia Diagnosis and management , seizuresand . >160 ing, whilesevere sodiumlevel (serum hypernatraemia sive thirst, , insomnia and muscletwitch­ sodium of151–160 (serum Clinical manifestations hypernatraemia ofmoderate Symptoms altered cognitive ormentalstatus. function This includesinfants, theelderlyandpatientswith recognise thirst, orthosewithreducedaccessto­ sodiumlevelserum arethosewithadecreasedabilityto >145 sodiumlevel isdefinedasaserum Hypernatraemia of Hypernatraemia prevent irreversible damage. brain levels shouldnotexceed 8–10 isotonic saline(0.9%NaCl). sodium ofserum Correction canbetreatedsuccessfullywith laemic hyponatraemia fluid extracellular volume. Mostpatientswith hypovo­ in combinationtolimittreatment‐inducedexpansion of increaseinsodium,tory used andfurosemideisoften (e.g. toachieve 3%NaCl)may benecessary asatisfac­ Hypervolaemia Euvolaemia Hypovolaemia States ofhypernatraemia Table 6.6.2 When replacingwater, fluidsshouldideallybegiven 374 mmol/L) isassociatedwithalteredmentalstatus, mmol/L. Patients atriskofdeveloping anelevated Identifying causeand managementof hypernatraemia mmol/L) includeexces­ Increase insodium Loss ofwater Loss ofwaterandsodium Changes inwaterand/orsodium mmol/L per24hoursto water. • mia. Itscausesinclude: intake istherefore thesolecausefor rarely hypokalae­ can significantlyreducepotassium excretion; insufficient <3.5 potassiumlevel definedasaserum It isgenerally of mia, whichmay occurwithor withoutpotassiumloss. ofclinical conditionscanresultinhypokalae­ A range Hypokalaemia Potassium (K Potassium • oedema andconvulsions. by >10 corrected cardiac . can therefore andpotentiallyfatal causemuscleparalysis function.cle andneural Bothhypo‐ andhyperkalaemia potential,membrane mus­ whichisessentialfor normal oftheresting and inthecellsismaindeterminant fluids intheextracellular the potassiumconcentrations cells inexchange for two potassiumions. of The ratio of thetwo cations by pumpingthreesodiumionsoutof maintainsthedifference indistribution membrane cell lar ­ tosodium,in contrast ­ whichisthemajorextracellu ◦ ◦ ◦ ◦ ◦ ◦ ◦ Hypokalaemia withoutpotassiumloss: Hypokalaemia withpotassiumloss: ◦ ◦ ◦ ◦ ◦ ◦ ◦ cation. The sodium–potassium ATPase pumpinthe dosis (DKA)ornonketotic hyperglycaemia). noticeable duringthetreatmentofdiabeticketoaci­ Excess alcohol. Gastrointestinal loss – vomiting, diarrhoea, laxatives. ofthesodium–potassium activity ATPase pump). intocellsby increasingthe regulate potassiumentry Elevated beta2‐adrenergic (catecholamines activity Refeeding syndrome. blastic anaemia). Increased cellularuptake (e.g. treatmentofmegalo­ Insulin excess (drives K Alkalosis (resultsinthemovement ofK exchange for anequimolarnumberofH mmol/L. In case of potassium depletion, the kidney Excess administration ofsodium‐containingIVfluids Primary hyperaldosteronism Cushing’s syndrome Diabetes insipidus • • • Extrarenal: <20 • • Renal: >20 Underlying cause Burns Excessive sweating,fever Gastrointestinal losses Diuretics Renal failure + ) is the principal intracellular cation ) istheprincipalintracellular mmol/L urinarysodium mmol/L per24hourstoavoid cerebral mmol/L urinarysodium Section 6:Nutritionsupport + intocells, may bemore + intocellsin + ). • • However, includes: treatmentgenerally limited evidence toguidetreatment, varies. andpractice potassium.cardium andincreaseintracellular There is In acutehyperkalaemia, themyo theaimistoprotect ­ Management • • include: renalinsufficiency.concurrent Causesof hyperkalaemia ure. involves hyperkalaemia generally Dietary‐induced of clinical settings, but is usually aresult of renalfail­ without ECGchanges. Hyperkalaemiaoccursinavariety given potassium is≥6.5 iftheserum guidelines recommendthatemergency treatmentbe The thresholdfor emergency treatmentvaries, butmost Acute, severe hyperkalaemia requiresurgent treatment. Hyperkalaemia manner toreducetheriskofhyperkalaemia. intravenously aspotassiumchloride(KCl) inacontrolled vomiting and diarrhoea. Potassium administered isoften may result in gastrointestinal side effects, e.g. , hypokalaemia, be given potassium can often orally, but pokalaemia hasbeenaddressed. Inmildtomoderate clinical situation, andifthecauseofhy renalfunction ­ required dependsontheseverity ofhypokalaemia, to beidentifiedandtreated. Theamountofpotassium potassium toasafe level andfor theunderlyingcause serum The immediategoaloftreatmentistoraise Management 6.6 ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ potassium . Intravenous insulin–glucose infusiontoreduceserum againstmyocardial protect temporarily excitability. Intravenous calciumsalt(gluconate orchloride)to potassiumexcretion:Reduced urinary Increased potassiumreleasefromcells: ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ sparing diuretics(e.g. ). drugs, heparinandpotassium‐ anti‐inflammatory drugs,Certain e.g. angiotensininhibitors, non‐steroidal Addison’s adrenalinsufficiency). disease(primary . Acute andchronickidney disease. Hyperkalaemic periodicparalysis. suxamethonium). related (e.g.Drug betablockers, and suchasstatins, etc.). relating toseizures, ischaemia, exercise, or trauma of muscle damage (recent history Catabolic states, e.g. tumourlysissyndromeand K e.g. releaseofintracellular Pseudohyperkalaemia, Metabolic acidosis. caemic state. hyperosmolarInsulin deficiency – DKA, /hypergly ­ of liquorice. kaemia, hypomagnesaemia, , excess intake renal tubular acidosis, diuretics, corticosteroids, leu­ aldosteronism, type 1 and 2 loss – primary Urinary + duringphlebotomy. Fluids and electrolytes mmol/L withor (Ca Calcium include: .nancy andprimary Othercauses The mostcommon causesofhypercalcaemia are malig­ through calciumandvitamin Dsupplementation. is designedtoincreaseintestinal calciumabsorption ifpresent.corrected Inchronic hypocalcaemia, treatment secretion)oralkalosisshouldbe hormone parathyroid early aspossible. Magnesiumdeficiency (whichreduces the underlyingcauseandcommencespecifictreatment as , butitisalsoessentialtodetermine Acute treatedwithintravenous hypocalcaemia isnormally Management • • • • • • • • • • Causes ofhypocalcaemia include: Hypocalcaemia potentially life threatening, requiringurgent treatment. loss. Severe hypocalcaemia andhypercalcaemia areboth excess they arenotasignificantcontributortocalcium late inhibitcalciumabsorption, butunless consumedin levels. Fibre, ingeneral, andoxa andthebindersphytate ­ mia, calciumlevels serum for albumin must becorrected making adiagnosisofhypercalcaemia orhypocalcae­ ised calciumisphysiologically active. Therefore, before calcium isboundtoprotein, andtheremaining freeion­ the expense ofboneloss. About halfofthetotalserum is inadequate, bloodcalciumremainsnormal, butat homeostatic control; hence, even whencalciumintake ity of the nervous system. calcium is under tight Serum isrelatedtotheexcitabilplasma calciumconcentrations ­ and enzymeactivity. ofaltered The mostsignificanteffect function, release, hormone myocardial contractibility cation andhasvitalrolesinregulatingneuromuscular may benecessary. , peritonealdialysisandkidney transplantation, potassium. Renal replacementtherapy, suchashaemo­ of restriction diuretics (where appropriate)and dietary mia isusuallymanagedby usingcation‐bindingresins, should bediscontinuedifpossible. Chronichyperkalae­ Any prescribed drugs exacerbatingAny hyperkalaemia prescribeddrugs ◦ ◦ Refeeding syndrome. Rhabdomyolysis. (e.g.Drugs ). Critical illness. Large‐volume bloodtransfusions. Hyperphosphataemia. Ddeficiency. Acute . bonesyndrome(postparathyroidectomy). Hungry (PTH). Low hormone parathyroid ◦ ◦ Hypomagnesaemia. Hypoparathyroidism. 2+ ) isthebody’s mostabundantdivalent 375

SECTION 6 SECTION 6 • • • taemia, including: ofclinicalconditionscanresultinhypophospha­ A range Hypophosphataemia (PO Phosphate made totherelevant specialist. cause,depends ontheprimary shouldbe andareferral calcium repeated. Treatment of chronic hypercalcaemia stopped orreducedifappropriate, levels and serum of apy, contributing to hypercalcaemia should but be drugs discontinued ifpossible. exacerbating hypercalcaemiaprescribed drugs shouldbe trol insymptomaticormoresevere hypercalcaemia. Any of bisphosphonatesmay con­ berequiredfor long‐term hypovolaemia hasbeencorrected. Intravenous infusion they are sometimes used to treat hypercalcaemia once overload. The useofloopdiureticsiscontroversial, but ally nottheonlytreatment, anditmay leadtofluid calciumlevels;reducing theserum however, itisusu­ with intravenous fluids may be effective in slowly ECF depletion, andexpansion oftheECFcompartment Severe with occursinconjunction hypercalcaemia often Management • • • • • the renalacid–basebuffer system. lates oxygen delivery totissues. in Itisalsoimportant ofhaemoglobin the affinity for ­ integrityofcellmembranes.for the structural Itregulates anion andisessentialfor processesand allintracellular Mild hypercalcaemia may not require immediatether ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Decreased intestinal absorption: Increased renalexcretion Redistribution Chronic kidney disease. Adrenal insufficiency. . diseaseincludingtuberculosisand Granulomatous tion; thiazidediuretics; A). antacid, milk‐alkali syndrome, or intoxica­ related(e.g.Drug ; calciumco‐prescribedwith Prolonged immobilisation. 376 ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Hyperparathyroidism. Tubular disorders. Corticosteroids. Diuretics. Volume expansion. Metabolic acidosis. Recovery fromDKA. Refeeding syndrome. leukaemia). Rapid celluptake (e.g. bonesyndrome, hungry acute Catecholamines. Sepsis. Glucose/insulin therapy. alkalosis. Respiratory 4 3− ) isthebody’s mostabundant­ oxygen and thusregu­ trivalent ­ • • • • • Causes ofhyperphosphataemia include: Hyperphosphataemia safer; however, absorptioncanbeunpredictable. , supplementationis therefore andoral often ofphosphatecanleadtoextraskeletal administration toseveremoderate hypophosphataemia. Intravenous with Acute managementisusuallyonlynecessary Management • • include: absorption. Causesofhypomagnesaemia decrease its ­oxalates, and can bind the cation and ­absorbed, and othernutrientssuchasfibre, phytates, serum. magnesium is Only 30–50% of total dietary magnesium content, because only0.3%isfound in oftotalbody magnesiumisapoor predictor Serum Hypomagnesaemia Magnesium (Mg Magnesium phosphate binders. and oral disease, phosphaterestriction andistreatedwithdietary hyperphosphataemia isusuallyduetochronickidney ability ofthekidney toexcrete phosphateloads. Chronic ease, itisusuallyself‐resolving, owing tothecontinued nevertheless, kidney dis­ ormildtomoderate innormal volume expansion, phosphatebindersanddialysis; oral The treatmentofacutehyperphosphataemia includes Management ­reabsorption andexcretion. close homeostaticregulation, primarilythroughrenal and boneformation. Circulating magnesiumisunder relaxation, rhythm, heart nerve function, vascular tone RNA andDNA. and Itisessentialfor musclecontractions for thesynthesisofproteins, andisimportant reactions lular cation. in more than300 enzyme It is a co‐factor ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Increased intake: lysis syndrome, profound catabolicstress. rhabdomyolysis, haemolysis, chemotherapy, tumour Cell breakdown intoECF), (releaseofphosphorus e.g. Hypovolaemia. Hypoparathyroidism. Renal insufficiency. Gastrointestinal losses: Reduced intake (e.g. , ). ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Antacid abuse. Vomiting. andsteatorrhoea. diarrhoea Secretory Vitamin Ddeficiency. Phosphate‐binding agents. Malabsorption. Vitamin Dintoxication. Phosphate enemasandlaxatives. 2+ ­ ) isthesecondmostabundantintracel Section 6:Nutritionsupport prior toproviding magnesiumsupplementation. isrequired renal function should benotedthatsufficient times perday toreducetheirlaxative sideeffects. It magnesium supplementsindivideddosesthreetofour treatedbyMild hypomagnesaemia isoften givingoral losses.diarrhoea, electrolyte which leads tofurther ispoor,trointestinal tract andmagnesiumsaltscancause the urine. The absorptionofmagnesiumfromthegas­ to 50% of the infused magnesium will be excreted in above willreduceretention, range thenormal andup by plasmamagnesiumconcentrations; elevation abrupt essential astherenalreabsorptionthresholdisaffected slowly, over aperiodofhours. A slowofinfusionis rate administration. Intravenous repletionshouldbegiven • • include: Causes ofhypermagnesaemia Hypermagnesaemia phate (MgSO magnesium, exist. practices andvarying Magnesiumsul­ There arenouniversal guidelinesfor repletionof Management • • • • • • • • • 6.6 ◦ ◦ ◦ ◦ salts (e.g. antacids, laxatives andenemas). or Administration ofmagnesium‐containingdrugs Kidney disease – acute orchronic. Others bonesyndrome. Hungry Hyperaldosteronism. . Diabetes mellitus/DKA. Endocrine. amphotericin andaminoglycosides). rotoxins e.g. cyclosporine, cisplatin, pentamidine, (loopandthiazidediuretics,Drugs tacrolimus, neph­ Renal tubulardisorders. Renal losses. ◦ ◦ ◦ ◦ ECF expansion. Refeeding syndrome. . proton pumpinhibitors. ­fistulae, excessive use of laxatives, use of long‐term liac disease), bowel short syndrome, intestinal Vomiting, diarrhoea, malabsorption (e.g. IBD/coe­ Fluids and electrolytes 4 ) ismostcommonlyusedfor intravenous Viera AJ, Wouk N. (2015)Potassium disorders: and DU.Silverthorn (2016)HumanPhysiology, 7th edn. SanFrancisco: Rastergar A, SoleimaniM. (2001)Hypokalaemiaandhyperkalae ­ Palmer BF. (2015)Regulation ofpotassiumhomeostasis. Clin.J. Am. al.Minisola S, (2015) PepeThe diagnosisand J, PiemonteS, et Liamis G, MilionisHJ, ElisafM. (2010)‐inducedhypo­ Jahnen‐Dechent W, Ketteler M. (2012)Magnesiumbasics. Clin. Cooper MS, GittoesNJ. (2008)Diagnosisandmanagementofhypo­ Canada TW, TajchmanSK, TuckerAM, Assessment of hyponatraemia. (2018) Adrogué HJ, MadiasNE. N. (2000). Engl.J. Med. Adrogué HJ, MadiasNE. N. (2000). Engl.J. Med. Further reading Torrance. The editoracknowledges thepriorcontributionof Alan Acknowledgement of magnesium. calcium may begiven thecardiaceffects tocounteract necessary. Insevere hypermagnesaemia, intravenous this isassociatedwithrenaldisease, dialysismay be cause and then by removing excess magnesium. If Treatment isinitiallyby removing theunderlying Management • • . Am.Fam. Physician. 92(6): 488–495. Pearson. mia. Postgrad. Med.J. 77(914): 759–764. 10(6): 1050–1060. Soc. Nephrol. management ofhypercalcaemia. BMJ350: h2723. phosphatemia: a review. QJM103: 449–459. kidney J. 5: i3–i14. calcaemia. BMJ, 336(7656): 1298–1302. ASPEN. andAcid‐BaseFluids, Electrolytes, Handbook. Disorders Chicago: 2018. monograph/57/overview/aetiology.html. line]. Available athttp://bestpractice.bmj.com/best‐practice/ 342(20): 1493–1499. 342(21):1581–1589. Tissue breakdown – rhabdomyolysis, burns, DKA. tation given in error). Iatrogenic (e.g. highdosesofmagnesiumsupplemen­ (eds) (2015) et al. BMJ BestPractice [On­ Accessed 12October ASPEN. 377

SECTION 6