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NEPHROLOGY-CASE REPORTCentral pontine and extrapontine myelinolysis secondary to fast correction of severe hyponatremia and hypokalemia in an alcoholic patientAhmad Ghaith Tarakji•Ahmad Raed Tarakji•Uzma ShaheenReceived:2May2011/Accepted:4November2012ÓSpringer Science+Business Media Dordrecht2012ObjectiveTo confirm the importance of slow correction of serum sodium and potassium by describing a case of a woman with chronic alcoholism and malnutrition who developed central pontine and extrapontine myelinol-ysis(CPM)after fast correction of severe hyponatre-mia and hypokalemia.Case reportA59-year-old white alcoholic female was transferred to ER by ambulance at04:52 a.m.for lethargy, disorientation,weakness,falls,and headache for few days.She was only drinking alcohol for few days but not eating.She had history of hypertension,and she was taking Lorazepam2mg thrice daily,Ramipril 2.5mg once daily and Hydrochlorothiazide12.5mg once daily.Her initial vital signs by paramedics revealed BP of124/56mmHg,pulse of75bpm,and temperature of36.7°C.Her weight was60kg,and her height was161cm.Her Glasgow Coma Scale was13/15.On examination,the patient was con-fused,only oriented to place and had slurred speech and multiple bruises of different ages.Her pupils were5mm,equal and reactive to light.No other significantfindings were found.Initial laboratory results are shown in Table1.Intravenousfluids were started asfirst line of1L of Normal Saline with40mEq of KCl at100mL/h and second line of250mL of Normal Saline with40mEq of KCl at50mL/h.Head CT scan was negative for acute hemorrhage,infarct,or edema.Thiamine 100mg IVP was given,and third IV line was then initiated with1L of Saline with40mEq of KCl at 100mL/h.Her blood pressure suddenly dropped to 82/44mmHg,so a bolus of Normal Saline500mL was given,and her blood pressure improved to 152/87mmHg within15min.She was transferred to ICU where she additionally received IV magnesium sulfate,oral potassium chloride,and oral sodium phosphate replacements.Serial blood chemistry tests were done,and IVfluid types and rates were adjusted accordingly.During thefirst day,she excreted a large amount of diluted urine which could be secondary to a quick decrease in serum vasopressin level when herA.G.TarakjiAleppo University,Aleppo,SyriaA.R.TarakjiDepartment of Medicine,Yarmouth Regional Hospital, Yarmouth,NS,CanadaA.R.Tarakji(&)Nephrology and Hypertension Maritime Clinic, Yarmouth Regional Hospital,60Vancouver Street, Suite405,Yarmouth,NS B5A2P5,Canadae-mail:dartmo@U.ShaheenDepartment of Diagnostic Imaging,Yarmouth Regional Hospital,Yarmouth,NS,Canada DOI10.1007/s11255-012-0329-3volume status had improved(Table2).Therefore,her serum sodium and potassium were corrected so fast over the next48h as in Fig.1.However,her serum phosphorus was corrected slowly over the next5days (Day2:0.18(nadir),Day3:0.35,Day4:0.76,and Day 5:1.20mmol/L).Over the next3days,she had improved with no alcohol withdrawal symptoms but she was still weak requiring physiotherapy.On8th hospital day,she started with slurred speech again with difficulty swallowing and drooling.MRI study of the brain was ordered,and thefindings were consistent with CPM as in Fig.2.She received continuous rehabili-tation and supportive care by interdisciplinary team with slow recovery and improvement.A repeat MRI study of the brain after3months showed a degree of improvement of the CPMfindings,and she was eventually discharged home after5months. DiscussionOur case is a typical one for CPM in an alcoholic mp and Yazdi[1]found that chronic alcoholism and correction of hyponatremia are com-mon with an incidence of39.4and21.5%,respec-tively,in442documented cases of CPM between1986 and2001.The literature suggests that‘‘increases of10–12mEq/L within24h and increases ofTable1Blood and urine tests resultsBloodTest(normal range)Result Test(normal range)ResultNa?(136–145mmol/L)100INR(0.8–1.3)0.9 K?(3.6–5.2mmol/L) 1.7CPK(21–215U/L)3,895 Cl-(98–107mmol/L)57Alb(35–47g/L)38 Total CO2(21–32mmol/L)29Etoh(0.0–0.0mmol/L)0.4 Urea(3.0–7.9mmol/L) 3.7TSH(0.465–4.680mIU/L)0.448 Creatinine(53–115l mol/L)40FT4(10.0–28.2pmol/L)14.4 Random glucose(3.9–6.0mmol/L) 5.2Osmolality(266–298mmol/Kg)200 Mg(0.74–0.99mmol/L)0.69Phos(0.81–1.58mmol/L)0.36 Ca(2.10–2.70mmol/L) 2.08Arterial blood gasPH(7.35–7.45)7.57PO2(83–108mmHg)63.5 PCO2(32–45mmHg)35.3O2sat(95.0–99.0%)95% Lactate(0.5–1.6mmol/L)0.8FIO2RA Urine(random sample)Specific gravity(\1.005–1.025) 1.015Osmolality(50–1,400mmol/Kg)416 PH(5–8.5) 6.5Na?(mmol/L)15 Protein(\0.1g/L)0.3K?(mmol/L)27 Glucose(\5.5mmol/L)Neg Cl-(mmol/L)64 Ketones(\0.5mmol/L) 3.9Urea(mmol/L)226Abnormal values in italicizedTable2Fluid balance in thefirst two days1st Day2nd DayTotalfluid intake5,010mL3,503mLPO850mL1,100mLIV NS?40mEq KCl/L2,329mL1,422mLIV NS?40mEq KCl/L590mL–IV NS?40mEq KCl/250mL250mL–IV D5W991mL981mLTotalfluid output4,830mL2,600mLAverage blood pressure111/64117/7318–25mEq/L within48h are sufficient to cause this syndrome’’[2]as happened with our patient.Recently,it has been recognized that correction of hypokalemia is similarly important as discussed by Berl and Rastegar[3]in their teaching case.Because sodium is mainly an extracellular cation and potas-sium is mainly an intracellular cation,loss of either one of these cations without water loss can lead to hypoosmolality.So,replacing serum potassium can play a significant role in correcting serum sodium as they showed with their calculation.Therefore,they recommended to modify the above rule as‘‘in chronic hyponatremia(duration[48h),the increase in serum sodium plus potassium levels should not exceed 12mEq/L in thefirst24h and18mEq/L in thefirst 48h’’[3].Even though that our patient had initially received Normal Saline(0.9%),instead of3%saline,then almost1L of5%dextrose in water(D5W) (Table2),her serum sodium was corrected quickly partially due to large urine output in thefirst day (almost5L).Unfortunately,repeated urine electro-lytes and osmolality measurements were not done serially to guide herfluid administration.However, she was not given Desmopressin as was recom-mended by Sterns and Hix[4].They stressed that ‘‘fear of osmotic demyelination does not justify therapeutic inaction(and)fear of complications from hyponatremic encephalopathy does not justify ther-apeutic excess’’[4].Our case is a good example of their strong recommendation that‘‘overcorrection of hyponatremia should be viewed as a medical emer-gency’’[4]since there is some animal evidence that intervening might decrease mortality[5].Furthermore,although it was corrected slowly in our case,severe hypophosphatemia probably contrib-uted to the development of CPM as suggested from cases report of CPM associated with isolated severely low serum phosphorus[6].Pontine myelinolysis usually affects corticobulbar fibers and corticospinal tracts causing dysarthria, dysphagia,andflaccid quadraparesis.Extrapontine involvement causes tremor and ataxia and can lead to movement disorders[7].It was reported that the initial lesions and the duration of these lesions on MRI do not correlate with severity of clinicalfindings or their improvement and the survival depends on the second-ary complications of this disease[8].ConclusionThis case is typical for central pontine and extrapon-tine myelinolysis secondary to rapid correction of serum sodium,potassium,and osmolality.Extreme caution with vigilance in correcting these serumcations together as suggested above is strongly recommended to avoid this disastrous,and sometimes fatal [9],complication.Conflict of interest The authors declare that they have no conflict of interest.Referencesmp C,Yazdi K (2002)Central pontine myelinolysis.Eur Neurol 47:3–102.Palmer BF,Sterns RH (2009)Fluid,electrolytes,and acid-base disturbances.Nephrol Self Assess Progr8:117–121Fig.2Head MRI.a Axial T2image shows central pontine hyperintensity with relative sparing ofcorticospinal tracts.b This lesion is hypointense on Sagittal T1-weighted image.c ,d On DWI axial images,restricted diffusion is noted at the periphery of this lesion and at the posterior and lateral aspects of thalami while the central part of this lesion is isointense on DWI sequence.e ,f No thalamic abnormality is present on FLAIR or T2-weighted sequences.This signifies that the central portion of this lesion has run a chronic course while the peripheral portion and thalamic components are acute3.Berl T,Rastegar A(2010)A patient with severe hyponatre-mia and hypokalemia:osmotic demyelination following potassium repletion.Am J Kid Dis55(4):742–7484.Sterns RH,Hix JK(2009)Overcorrection of hyponatremia isa medical emergency.Kidney Int76(6):587–5895.Gankam Kengne F,Soupart A,Pochet R,Brion JP,Decaux G(2009)Re-induction of hyponatremia after rapid overcor-rection of hyponatremia reduces mortality in rats.Kidney Int 76(6):614–6216.Michell AW,Burn DJ,Reading PJ(2003)Central pontinemyelinolysis temporally related to hypophosphataemia.J Neurol Neurosurg Psychiatry74:820–8267.Abbott R,Silber E,Felber J,Ekpo E(2005)Osmotic demy-elination syndrome.BMJ331:829–8308.Menger H,Jorg J(1999)Outcome of central pontine andextrapontine myelinolysis.J Neurol246:700–7059.Martin RJ(2004)Central pontine and extrapontine myeli-nolysis:the osmotic demyelination syndromes.J Neurol Neurosurg Psychiatry75(Suppl III):iii22–iii28。