电解质异常病患之常规检查

1、電解質異常病患之常規檢查發現電解質異常時，除非危及生命現象，請勿先行治療或施打點滴，應暫停急診所開立之點 滴,因為會干擾診斷,等病史問完,spot urine及24hr urine收集完成後再開始分析治療 PriKiwd to* Proceed tmHow Churl 2Flow Chart 3Fluw Chart 1. Initial steps in the patient with a very low P.Refere nee: Groe neveld JH QJM. 2005;98:305-316.病史請確認以下情形並且詳述於present illness and past hist

2、ory? 有無嘔吐、下痢、水分攝取缺乏(Rece nt GI in take history)大量出汗、排尿過量等情形？?有無意識障礙？? 有無腎臟、胃腸、荷爾蒙異常(adrenal, thyroid and pituitary disease)心衰竭、肝硬化等 系統性疾病病史？? 有無 DM, HTN, Lung, brain , autoimmune disease?請詳問 recent drug history懷疑病人有脫水現象請測Spot urine Na, Osm, CrBlood: CBC(HCT), BUN/Cr, Osm, NaFeNaUrine amountPE: skin

3、turger, tongue, axillary moisture,三態血壓,pulse rate治療Order請開Body weight qdUrine amount qdAbdominal echo 19001X, 放射科執行 ; 看腎臟有無異常如 nephrocalcinosisBlood 請 check:Na, K, Cl, Mg, Ca, Uric acid, P,BUN, Cr, Glu, HgBAlb, Total protein, Osm,ABG 包含 pH, HCO3Renin, cortisol, aldosterone, thyroid functionSpot Urin

4、e 應在急診入院後且治療前 , 盡快完成檢查 Na, K, Cr, Osm, Ca, urine acid, P, Cl, MgUrine ABG:目的要算厶U-BPC02normal >20,檢查 distal tubule 是否正常24hr Urine Spot urine收完馬上囑主護開始收 24hr urine,不要等到次日再開始Na, K, Cr, 0sm, Ca, urine acid, P, Cl, Mg於病歷上記載上述所有檢查結果 . 並且計載以下計算結果Fe(Na, Ca, uric acid, Mg, P, HC03)U/P Na例如 Fe Na = x 100%U/

5、P CrU/P KTTKG= U/P 0smU k, Ucr 使用spot urine結果計算即可Blood anion gap = Na -Cl -HCO3Urine anion gap = Na + K -Cl 使用 spot urine 計算即可Calculated osm; Osmolality gap假设懷疑pituitary function異常，請測TSH, ACTH, LH/FSH, GH, PRL, ADHPituitary MRIGonad function 也要一起測,17-estradiol, testosterone相關教科書資料表格或本講義有關流程圖請列印貼病歷供查

6、房時討論最後請先思考疾病可能原因，再與主治醫師討論假设為鉀離子疾病，請練習快速診斷法：使用spot urine K/Cr, TTKG以及EKG,在24hrs urine尚未收集前就快速診斷到底低血鉀是 因 intracellular shift 或 K deficit (loss)Spot Urine K/Cr:In tracellular shift large K deficitPoiassiurrbcreatimne itio, mmofnmol1.3 ±0.14.l±Q.2tRefere nee: Lin SH, Arch In tern Med, 2004; 16

7、4, 1561-1566PS:請注意urine K與serum Cr單位，需先換算為mmolSerum Cr 1mg/dl = 88 卩 mo/L =0.088 mmol/L假设懷疑是 Thyroitoxicosis 請務必檢視 EKG: Relatively rapid heart rate, high QRS voltage, and first-degree AV blockare importa nt clues suggest ing TPP in patie nts who prese nt with hypokalemia and paralysis. Hsu et al. El

8、ectrocardiographic mani festati ons in patie nts with thyrotoxic periodic paralysis. Am J Med Sci. 2003;326:128-32*TFP(Cbsv d FPP orSPP (Chw 2)* Loh inlHke Non-renal K* loss Furrntrviwl K*How Chart Z Approach to the patient with low K# excretion.Refere nee: Groe neveld JH QJM. 2005;98:305-316.* Hipp

9、urk ucidusk Diurrhotii Hih HldiiNlvrunr IHu reties Carlijil likv kilduMerun v I皿|H、pr ENaC Ipmpm* Cb-SR wcvpkd(Cam 6) DCT t| pe Thiazide Vumhin(Chm 4 & 5> EHttiil RTA withH*srcrt'1km(Case 3)Flow Chari 3* Approach to the patierrt with high K亠 excretion.Refere nee: Groe neveld JH QJM. 2005;

10、98:305-316.DedinitionsHypokalemic periodic paralysis(HPP): shift of K into cells,(有 4 個 elements)1. Positive family history, clinically recurrent, hyperthyroidism,2. Abse nee of in take of age nts caus ing in tracellular K shift3. The patients require < 1.5mmol/kg KCL to return to normal K4. No a

11、cid-base disorderNon-hypokalemic periodic paralysiSN on-HPP): due to a large deficit of K1. > 3 mmol/kg of K to correct plasma K2. If acid-base disorder is presentfehla 1. Paiieni Characteristics and Final DiagnosisPatient GroupNo. olPlIlBMl咖, Mean ± SO, yMale-FemaleHypckaiemi: periadic para

12、lysis (n 30"IbyrolDMic periodic paralysii2028 ±BSpa rad ic periodic paralysis£±78:1Familial periodic paralyslis1ig1:0on-hypo Kalemie perkwlic paralysis in 13)Fiimary aldoroni&m1341:0Git&lnfun syndromeA24 ±23：1Liconice ingeuinn1721：CDirtai renaJ tubuln acidosis531

13、77; 232jFajioonl syndrome ritih proximsl renal iubylar iBCidOSiB1421：0Profound 帼it诫1471:0>blft 扎 Bitthftirtlcal Study RbsuIIs on AdmlUlOn in Palisnt GrOupt*StudyReFerencg Rai|BHvPQkalemlc Ftrhidlc PinlysitNon-Hypokilemii; Peniodlc ParalplsPlasmap«7 35-7.457.3& £ 0.037.39 ±0.12S

14、adiurn. minolt135 寸 42142 ±2141 ±3Fnbs&iuri, mrrol-'_2.0 ±0.31.9 ± 02hldrid mmol/L»10610619l05i6Bicafti Diiat mmol-l.24Q11.625.0 ± 8.8Rnsphite, mmol/L0>1 50«±02hgfiesium. mirDl.tC.7'1.0n.e±c.i0.7 ±0.2(Su 训镐 mtTiML*0莎3.2 ± 0 97.7 &

15、#177;1.3Urea nifrogn,3.0-7 .Q6.1 tl.BtCrBafjnine, mmol/La 06-0.10a .OB ± D OEO.OS±O.D2tUrinePotassium, mmol/LNAZI5±4fCr&aliininB, mmol几NA.6.8 e 2.83.7±1.2：Lriw QsmDlaliV. rOsm/RjNA5=0 11653Q3±105tbrine osmglallty-tnatinliH rauo, mOsm mrrolNA飆±2D10G±1BPntassium-

16、ereaiinifie fitlDr intnormiriolNA1±0.1Qi ±0.24Transtubyldi poU5ium DOncfntRftion gradientNA2.1 i D.5o- B 6 4 2 lualpswElslunuoo Ea黑 £5是=_su2Refere nee: Lin SH, Arch In tern Med, 2004; 164, 1561-1566 bypcaiimc Per Wk Pa misOhon-HypoMtamicPr ii zc Parif.'iis0123P asTia Fjli弱im Concs

17、niraton. tfif? !Fidure2. Transtubular potassium concentration gradients in tbs patient cohort.|f 1 HyfNMakemic PerParaksls&oOhtn-內 pcriaianilcPeriodic Paiatsj 5-°oOo! 3.° 8牛* 1 a.；r * Fasma Potassium ConcsTtrat on. tito/.Figura 3. Urine potassium-creatlrilnB ratios in ttie patient coho

18、rtRefere nee: Lin SH, Arch In tern Med, 2004; 164, 1561-1566Refere nee: Lin SH, Arch In tern Med, 2004; 164, 1561-1566HypokalemiaK* BMcretion rateAcld-bsss stateNormal Add-baseK- Shift、HPP、Bi numj Chlonquirtts、/Jadienergic： 科noni寸、Thecphlne? Caffeic、負Ik日 losis> Hypvilwfmli> Anaboictale> Hpt

19、rjidmtr gic： stateLow K* ecretjon raleAbnorrnll Aod-baseHigh K* excretion rateMetabolicaetdussMstatwlicalkaosis(-UAG, UO0)Blood pressuiet P rofomnd dljiivht* t Short b艸I syndromeiMaldbfrpt 冋n y VII OUS a den etna> Anorexianervofj> Chionic 3l®hQli5Hl、Remote 伽曲倚? Ex心出si诞seatingHigh> Tdue

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21、il ng 、Gastai cdnlnige h瀚卜 ortsble aibin Diarih«a h Lixriiot abuse、11 hydroxylaseAldosterone送otopieACTHdlefaentanalogue> CufhingRsj 17 s-hydroxylase汕MEsyndrome血忆朗t即、Caibnoxolone> Exo senateingestionhydro >x»fti5G de> boonoe mgjon 、Liddle's sndro me> DOC McrttlngtusmofLin

22、 SH Curr Medicinal、GS BS n Diurelicsdiuresisf Aminoglco sidef CispkjtinChem 2006Washi ngton Ma nual 32 editionHypokalaemia and paralysisK* excretion rate and acid baseLqw R+ exLTulion and normal acid baseHigh K cxcrclion mid ubnarnul acidAcid- base state?YhS |Hypcrth、roidism?Mctabulic acidosisMela b

23、n lieDistal RTA, usuallySiren'sTnlnciicJ Jirge dmrrhoeLi FrimaryaldoMemnni (tS nr BS DiureticsNOXI:* SPPYes, Lunik history FPPHypemc rnem i a Hyper nairaeinie HPPReferenee: Lin SH, Q J Med 2001； 94： 133-139Normal range以下三者代表 proximal tubule function 正常Fe Uric acid < 12% or 712Fe P <10Fe HC

24、O3 <5% normal; > 15% proximal RTAFeMg (>3%, ren al loss)Uk/Ucr (mmol/mmol) >1.5 ren al lossRenin sup ine 3-16 pg/mlupright 3-33 pg/mlAldostero ne 37.5-240 pg/ml以下代表 distal tubule function 正常 (U-B)PCO2 >20備註：對於每一位電解質病患(especially renal e- loss, RTA),除了判斷出腎原性以外,請 嘗試去判斷到底是 proximal tubul

25、e defect or distal tubule defectDaily urine Na 100-260 mEq/dayDaily urine K 25-100 mEq/dayDaily urine P 400-1300 mg/dayDaily urine uric acid 250-750 mg/daySIADH治療需限水，補充鹽水時只能用3% NaCI,因為normal saline會把serum Na越打越低Hypovolemic hyponatremia 治療算法(例：以 normal saline 1000cc=154 meq/L來治療；公式中 1 代表 TBW 增力卩 1 liter;男生 TBW=TBWx0.6;女生 TBW=TBWx0.5; PNa 代表血鈉; Na 代表經normal saline 1000cc治療後血鈉上升量)154 - PNa Na=TBW + 1 anion gap/ HCO3There is a 1:1 relati on ship betwee n the in crease in AG (AG) and the decrease in plasma bicarbo nate ( HCO3)<1 Comb