7

POTASSIUMBy H. BARRIE, M.D.

Medical Registrar, Epsom District Hospital

Comportment INTRACELLULAR EXTRACELLULAR

___Eq perHC0 u re

HCO3

H P04Electrolytes K

Nl CL

s04

gProtein

15 LitrsWater 30 Litres Ls

[4FI Plasma )FIG. i.-The distribution of water and electrolytes in the two compartments.

The subject of potassium metabolism, oftencoloured by forbidding biochemical jargon, hasdefeated many heroic attempts at comprehension.This article is intended as a clinical translation,both explanatory and descriptive, for the use ofthe average hospital practitioner seeking to masterthis difficult field of medicine.DistributionThe distribution of water and electrolytes in

the body will be more readily understood whenthe important concept of the body fluid com-partments has been grasped. The skeletonexcepted, water is distributed uniformly through-out the body, and of a total body water of 45 litres,30 litres are intracellular, and 15 litres are extracel-lular The plasma fraction constitutes one quarterof the extracellular compartment (3j litres)*.

*All figures quoted here apply to the average 70 kg.adult.

Electrolytes are not distributed uniformlythroughout the body. The intracellular electro-lytes are mainly potassium, magnesium andphosphate, whilst the extracellular electrolytesare mainly sodium, chloride and bicarbonate.Water and electrolytes constitute a finely

balanced system, each dependent upon the other.Thus changes in the amounts of body electrolyteresult in changes of fluid volume, and most ofthese changes are reflected by variations in theplasma concentrations.Having established potassium as but one member

of a group of electrolytes, it is necessary to focusupon it in rather more detail. Firstly it mustbe understood that there is no strict correlationbetween the concentrations in the intra- andextra- cellular fluids, although one can make thegeneralization that a sustained low serum level isusually associated with a low cellular level. Theaverage serum potassium is 5 mEq. per litre

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

8 POSTGRADUATE MEDICAL JOURNAL January 1954

(20 mg./Ioo ml.)*. On the other hand. the totalbody potassium is some 4,600 mEq. (I75 g.).Since the plasma (31 litres) constitutes a quarterof the extracellular compartment, it can be deducedthat of the 175 g. of body potassium only some 3 g.are extracellular. (See Fig. 2.) Although the greaterpart of the body's potassium is intracellular, itmust be made quite clear that the clinical mani-festations of potassium imbalance are related tovariations of the small extracellular fraction.Hence the well-known fact that the symptoms ofhypokalaemia are relieved by correction of theserum level although cellular repletion may notbe complete for several days. These observa-tions provide two important corollaries :-

I. The serum potassium level is no indicationof the body potassium in any acute condition.

2. The serum potassium level is directly relatedto the clinical state of the patient.Another important fact is that the potassium ion

is able to diffuse freely across the cell membraneand this property is believed to be due to thesmall size of the ion. Conversely the cell mem-brane is much less permeable to the more hydrated,and therefore larger, sodium ion, which is conse-quently confined to the extracellular fluid. There is

*A substance has a concentration of imEq./l. whenits equivalent weight in milligrammes is contained inI 1. (Eq. weight = atomic weight-valency). Thus

39X55 mEq. K'/I. = mgm./l. = 20 mgm./Ioo mts.

SODIUM POTASSIUM175 -G

Z Lc .

oss

i 50'G

Serum Level 325 -350 16 -22(per lOOmls) mgrms mcjrmsTotalBody 50 G 175 0Amount

Fs0. 2.-The distribution of sodium and potassium inthe two compartments. 98% of the bodypotassium is intracellular.

also some evidence in favour of an active cellmechanism for expelling sodium. It followsthen that the first of the above corollaries doesnot apply to sodium. Namely:The serum sodium level, when abnormal,

indicates body sodium. (Minor degrees of sodiumexcess or depletion are, of course, compensatedfor by changes in volume, the concentrationremaining normal.)Potassium BalanceThe balance of any substance should always be

considered in terms of gain and loss.Intake. Potassium is present in most foods,

the average intake from a normal diet varying from2 to 4 g. daily. Relatively large amounts can betaken by mouth provided that the urine flowis good.

Loss. Potassium leaves the body in the urineand in the alimentary secretions. The main loss,under normal circumstances, is via the kidneyand conservation occurs only to a limited extent.A profound knowledge ot renal physiology isunnecessary for a grasp of the following simpleprinciples :

(a) Decreased glomerular filtration causes potas-sium retention.

(b) Decreased tubular reabsorption causespotassium depletion.

Loss also occurs from the gastro-intestinalfluid, and in this respect it is worth remenberingthat the gastric juice contains four times theconcentration of potassium to that of plasma.The practical applications of this will be consideredlater, but it should be apparent already that renaland gastrointestinal disorders are the basis ofpotassium imbalance.

RegulationBalance and regulation are not synonymous,

and therefore the whole story cannot be toldmerely in terms of input and output. There area number of factors, both known and unknown,which regulate potassium distribution, and thesemust now be considered.

I. Protein Metabolism. Potassium is the chiefcellular electrolyte and therefore tissue breakdownwill result in a release of the substance. Thismechanism has been postulated to account forsome of the manifestations of the crush syndrome.Similarly, raised serum potassium levels havebeen demonstrated shortly after myocardialinfarction (Wilhelm, 195I), and are held re-sponsible for the peaked or deep T waves of theelectrocardiogram.

2. Carbohydrate Metabolism. Potassium movesinto the cells whenever carbohydrate metabolismis stimulated. This is dependent upon the

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

January 1954 BARRIE: Potassium 9

mEq HoC

HCOHCO 3

B ci BB

u)Cl Cl

Protein oei Poein

Normal AlkalosisFIG. 3.-To show how loss of chloride from vomiting, as, for instance, in pyloric stenosis, leads to

a compensatory rise in extracellular bicarbonate and fall in sodium and potassium.

deposition of a cellular potassium-glycogen com-plex. Thus a fall in the serum potassium can beproduced, experimentally and clinically, by theadministration of glucose, insulin or adrenaline,and this principle is put to practical use in thetreatment of potassium intoxication. Unfortunate-ly it is also a contributing cause of the severedepletion that occurs in a patient who, treatedwith insulin and intravenous glucose, enters uponthe diuretic recovery phase of diabetic ketosis.It has also been suggested that the same factor isoperative in the rare condition known as FamilialPeriodic Paralysis, which is frequently pre-cipitated by a large carbohydrate meal.

3. Acid-Base Disorders. Mention has alreadybeen made of the small ion size which renderspotassium so freely diffusable across the cellmembrane. This exchange is therefore notsurprisingly activated by acid-base disturbance.The compensatory rise in serum bicarbonate andfall in sodium and potassium resulting fromalkalosis primarily due to loss of chloride is notdifficult to follow. (See Fig. 3.) However, theinverse relationship of the serum bicarbonate tointracellular potassium is somewhat more complex.For instance ingestion of lactate or bicarbonatecauses an increased excretion of potassium in theurine. Clinically the alkalosis of Cushing'ssyndrome will not respond to administration ofammonium chloride but will respond to potassium.The fact remains that a rise in serum bicarbonatetends to draw potassium out of the cells. Asimilar shift takes place in severe dehydration

when the osmotic pressure of the body fluids isincreased. A low potassium state can also besuperimposed upon acidosis when there is ageneral depletion of base, and it is thought bysome that the symptoms of potassium deficiencyare then potentiated.

4. Adrenal Cortex. The influence of the'salt and water' hormone of the adrenal cortexis of course well known. Desoxycorticosterone(DOCA) promotes retention of sodium andexcretion of potassium. The patient withAddison's disease has a high serum potassium anda low serum sodium level. In overtreatmentwith D CA, ACTH, or cortisone, or inCushing's syndrome, these levels are reversed.There is much talk at the present time of stress,and it is possible that the post-operative loss ofpotassium so frequently observed is in part dueto adrenal cortical hypersecretion. Evidence infavour of this mechanism is provided by the fallin the number of circulating eosinophyls followingsurgery, when the degree of the response isproportional to the severity of the operation(Coppinger and Goldner, 1950).Clinical Potassium DepletionThe function of potassium is in some way

concerned with nerve and muscle fibre excit-ability, and this accounts for the clinical featuresof potassium disturbance.The symptions of depletion are listlessness,

loss of appetite and muscular weakness. A moreadvanced state is marked by apathy, breathlessness

B

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

POSTGRADUATE MEDICAL JOURNAL January I954

and frank flaccid paralysis. The findings includediminished or absent reflexes, rapid shallowrespirations and abdominal distension from musclehypotonia. The latter affects not only voluntarybut also smooth muscle. Indeed, paralytic ileusmay supervene ; it can be caused by, or may bethe cause of, a low potassium state. Cardiacchanges have also been described and theseinclude elevation of the systemic venous pressure,increased pulse pressure, dilation of the heart,functional systolic murmur and cardiac failure.The diagnosis is supported by typical electro-cardiographic changes which are said to appearwhen the serum potassium level is less than3.5mEq. per litre (I3.6 mg./Ioo ml.), but serialtracings invariably show a gradual developmentof these abnormalities at more moderate levels.Final proof is obtained by the estimation of theserum concentration.Before listing the causes of potassium depletion,

emphasis must once again be placed on thephysiological principles considered earlier. Ifone remembers that loss of cell fluid means lossof potassium, and that this loss is either from theurine or in the gastro-intestinal secretions, thena simple classification immediately suggests itself:

Cell Fluid Loss = Potassium Loss

Diarrhoea and vomiting; pyloricstenosis; gastric suction; in-

Primary testinal obstruction; paralyticAlimentary ileus; steatorrhoea; ulcerativeLoss colitis; ion exchange resins;

?PAS therapy.Diuretic recovery phase of acute

Primary tubular necrosis; post-opera-Renal tively; chronic nephritis (someLoss cases), renal acidosis (nephro-

calcinosis); aminoaciduria, e.g.Fanconi's syndrome.

Diabetic ketosis; alkalosis; waterMetabolic deprivation; familial periodic(combined loss) paralysis; overdosage with

DOCA, ACTH or cortisone;Cushing's syndrome; stress.

Perhaps the commonest example, always to befound in every surgical ward, is the post-operativepatient on gastric suction and intravenous glucose-saline,-the familiar 'suck and drip.'

It has been shown conclusively that the first post-operative week is marked by retention of sodium chlorideand water and by an increased excretion of nitrogen andpotassium. The estimation of the urinary chlorides inthis period is valueless because it provides an inevitablylow result in spite of a normal or raised serum level.These changes are independent of intake and follow anymajor surgical procedure, including orthopaedic opera-

tions and road accidents. The explanation is still notclear, but is likely to be related to compensatorymechanisms consequent upon increased tissue break-down, or the formation of an inflammatory exudate.(Wilkinson et al., I949 and I950.)

Firstly, therefore, some degree of negativepotassium balance is inevitable and large volumesof fluid, by raising the urinary output, willaggravate this tendency. Secondly, there is notonly a total absence of potassium intake, but,through suction, the electrolyte is being activelyremoved from the stomach where it is presentin four times the plasma concentration. Thirdly,suction has a double disadvantage because itresults in alkalosis which in itself causes a fallin the serum potassium level. Intravenousglucose is a fourth factor for, as already explained,stimulation of carbohydrate metabolism carriespotassium out of the extracellular fluid into thecells. Finally, any surgical approach is likely tobe attended by a considerable degree of stress andsubsequent adrenal cortical hyperactivity.

Illustrative Case History. Mrs. D.M., aged 54,was operated on for the relief of acute intestinalobstruction. A piece of strangulated small bowelhad to be freed from an intraperitoneal adhesion,and it was found necessary to employ post-operative suction and intravenous glucose-saline.Her recovery failed to reach expectations, and bythe 6th day after operation she was weak, hypo-tonic, all reflexes were diminished and the anklejerks were totally absent. Her chart showed anoutput of 2,000 ml. from suction in the previous24 hours, alone representing a loss of some40 mEq. of potassium. The serum potassium was3.5 mEq./l. and the alkali reserve 35 mEq./l. (78.6vol. CO,/ioo ml.). The electrocardiogram isshown in Fig. 4. She was given intravenouspotassium in the form of Cell Repair Solution(vide infra), go, 60 and 45 mEq. K' in the first,second and third 24 hour periods respectively.The serum potassium rose to 4.5 mEq./l. on thesecond day and to 5.2 mEq./l. on the third. Hercondition steadily improved and, from then on,she made an uneventful recovery.The medical counterpart of all this is to be

found in the patient recovering from diabeticcoma. He too has intravenous glucose and oralstarvation, and as a result potassium depletionis a well-recognised complication in the diureticrecovery phase.By way of interest, mention might be made of

the curious relative mildness of tetany in steator-rhea when the serum calcium level is known tobe low. This is now believed to be due to anassociated hypokalaemia. In such cases tetanyhas been precipitated by administration of potas-sium (Engel et al., 1949).

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

Janztarv I1954 BARRIE: Potassium iI

...................

.........

8Ag+.

····'·:··:i.··::t7.:(:wg

FIG. 4.-Case I. The first tracing (serum potassium = 3.5 mEq./l.) shows inversion of theT wave, depression of the ST segment and prominence of the U wave. The subsequenttracings show the gradual reversion to normal with treatment.

Another important cause of potassium depletionis gastro-enteritis in infants and the pioneer workof Darrow and his associates has contributedlargely to our present knowledge in this respect.

Illustrative Case History. A five months oldmarasmic and dehydrated infant, suffering fromdiarrhoea and vomiting possibly secondary to aB. proteus urinary infection, was rehydrated withsubcutaneous and intravenous glucose and salineinfusions. Potassium depletion became evidenton the third day of intravenous therapy. Hislimbs were hypotonic, his cry feeble, his abdomendistended and he could barely take a four drachmfeed. An X-ray film of his abdomen showedfluid levels (Fig. 5), the electrocardiogram wasabnormal (Fig. 6), and the serum potassium was2.8 mEq./l. (iI.img./ioomg.) He was givenone litre of Butler's solution (containing 15 mEq.K') intravenously slowly over the next 48 hours,and then oral potassium chloride 0.5 G. b.d. for afurther three days. Only four hours afterbeginning potassium therapy he took a ten drachmfeed readily, and by the fourth day was takingfive ounce feeds. His ileus had then disappearedand the electrocardiogram returned to normal.He appeared to make a complete recovery, butunfortunately succumbed to a second attack ofsevere gastro-enteritis two weeks later.

Clinical Potassium IntoxicationApart from paraesthesiae and irregularities of

cardiac rhythm, potassium intoxication is relativelysymptomless, but this silence is sinister for it mayend in sudden death. Clinical suspicion of thecondition is justifiable when a patient with therequisite circumstances for potassium retentiondevelops sudden cold grey pallor with peripheralcirculatory collapse, hypotension, indistinct heartsounds and bradycardia or rhythm irregularity.Mental confusion may be evident and numbnessand tingling in the limbs are said to be constantfeatures. Patients dying in uraemia may show aterminal rapidly ascending flaccid paralysis.Since death is due to ventricular standstill itfollows that the electrocardiographic changesare of greater clinical significance than the actualserum potassium level. Whilst a fatal issue maybe expected when the level exceeds 9 mEq./l.(35 mg./iooml.), the electrocardiogram beginsto record changes at about 7.5 mEq./l. (approx.3omg./Ioo ml.).

Potassium retention occurs in oliguric or anuricuraemia of renal or pre-renal causation. Araised serum potassium is present in Addison'sdisease but seldom reaches toxic levels. A danger-ous rise is generally due to a combination ofcircumstances which include defective renalfunction, increased tissue breakdown in grossinfections, and misguided potassium admin-istration.By now it will have become apparent that the

clinical manifestations of potassium disturbance

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

2POSTGRADUATIE MEDICAL JOURNAL January 1954

:s -.··W:

FIG. 5.-Case 2. Paralytic ileus due to potassium depletion. The first X-ray shows distended bowel with numerousfluid levels. The second filmrn, taken three days later after treatment, shows complete return to normal.

R~i~iJ~U~.,~~~~.~~~:.~ . ., ', ,·-;*.;-"~-r·~ ~.:'';·:', ~ ~'~~="

?MA>,..FIG. 6.-Case 2. The first tracing shows flat T waves and prominent U waves. The increasing

distortion of the tracings from interference as the serum potassium rises is striking testimonyof the infant's change from a state of weakness to one of lively resistance.

are due to abnormally high or low extracellularlevels. Therefore, even though the serum levelis a rather unreliable guide to the state of cellularpotassium, it is nevertheless a vital guide in themanagement of a case. It is perhaps insufficientlyrealised that the biochemical estimation involves.a prolonged series of reactions and precipitations-in fact, almost half a day's work for one technician.Hence, its repeated request inevitably results inconsiderable ill-feeling between pathologist andclinician. Moreover, the time lag is often toogreat for the acute emergencies necessitating thisinvestigation. Flame photometry is now super-seding biochemical estimation on account of itsspeed and simple technique, but the apparatusis not generally available as yet.

Treatmenti. Potassium DepletionPotassium deserves to be regarded with the

same respect as any other dangerous drug.Before it is given to a patient, the practitionershould satisfy himself that its administration isclearly indicated on the clinical evidence alreadydescribed, and that the urinary output is adequate.Ideally each case should be controlled by estima-tion of the serum concentration and the electro-cardiogram, and in certain patients this is anabsolute necessity. 1 he routine treatment recom-mended is:

I. Control with serum level and/or E.C.G.2. Correct the causal condition.3. Replace the depleted electrolyte.

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

Yanuary 1954 BARRIE: Potassium 13

HYPOKALAEMIA YPERALAEM

Flat or inverted T wave.Depressed ST segment.Large U wave.High P wave.Prolonged QT interval.Ectopic beats.A-V block.

High-peaked T wave.Prolonged PR interval.Widening of QRS.P wave may disappear.RST ' saw-tooth ' pattern.Biphasic pattern.Ventricular arrest.

FIG. 7.-The electrocardiogram in potassium imbalance. The changes are listed as far as possiblein order of appearance. The above tracings have been specially selected for the gross abnor-malities which they illustrate, but it is important to appreciate that each person has an individualcombination of the various possible abnormalities and that there is no set tracing.

The corresponding serum potassium level of the first tracing, taken from a patientsuffering from a carcinoma of the pancreas with obstructive jaundice and profuse vomiting, was2.9 mEq/l.

Potassium repletion can be accomplished orally,subcutaneously or intravenously. Oral admin-istration is the method of choice, and the recom-mended dose is 5-10 g. of the chloride citrate,bicarbonate or phosphate daily, suitably diluted infruit juice or sweetened water.* The developmentor pre-existence of paralytic ileus establishes avicious circle which no amount of oral therapy canbreak. Thus it sometimes becomes necessary togive potassium intravenously with all the attendantrisks of a sudden rise to toxic levels. Thereforestrict control of dosage is necessary; in any casenot more than Ioo mEq. should ever be given inany 24 hours and not more than io mEq. in lessthan any one hour. Solutions should contain30 mEq./l. or less, and the urinary output shouldexceed 50 ml./hour.

It only remains now to consider the solution tobe employed. Owing to the fact that everyworker in this field has concocted his own solution,one is faced with a considerable choice in thisrespect. Perhaps the most popular misconceptionis that Hartmann's solution corrects potassiumdepletion. Hartmann's solution is only physio-logical in the sense that its electrolytes are presentin approximately the same concentration as inplasma. Thus, in order to replace the necessaryamount of potassium with Hartmann's solution,vast quantities of saline and water must also be

*These are adult doses. For the treatment in infantsthe reader is referred to the Medical Research CouncilMemorandum No. 26.

given, and this is clearly undesirable. Butler'srepair solution contains 15 mEq. K'/1.. whilstundiluted Darrow's solution contains 35 mEq.K'/l., and these are therefore more suitable.However, it is important not to lose sight of one'spurpose in treatment, because these cell repairsolutions contain other electrolytes, notably lac-tate, and are, therefore, best reserved for cases inwhich acidosis is prominent. Therefore, it isrecommended that intravenous potassium salts,when indicated, are given in one of two forms,each solution having the ideal concentration of30 mEq. K'/l:

(a) For potassium depletion per se : 2.2 G.of KCI in one litre of 5 per cent. glucose.

(b) For cellular depletion in general: CellRepair Solution. The following cell repairsolution was devised by Nabarro et al. (I952)on the basis of metabolic studies of electrolyteretention in recovery from diabetic ketosis, andcontains the major cellular electrolytes, potassium,magnesium and phosphate.

g.NaCI . .. .. .. 1.17K2HPO4 ..... 0.87KC1 . .. .. .. 1.49MgCl ....... 0.24Glucose .. .. .... 50Water .... . to I .

2. Potassium IntoxicationPotassium intoxication is a medical emergency.

Once again the principles of treatment are ;

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from

14 POSTGRADUATE MEDICAL JOURNAL January 1954

I. Control with serum level and E.C.G.2. Correct the causal condition.3. Reduce the toxic.level.This last stipulation is achieved by the intraven-

ous infusion of 50 g. of glucose with or withoutthe simultaneous injection of 50 units of insulin.Sodium and calcium are in part physiologicalantagonists to potassium and the additional use ofcalcium gluconate or saline is often recommended.When acute renal failure is present, the non-protein electrolyte-free regime devised by Bulland his colleagues should be employed. Inspecial centres more complicated forms of therapyare feasible and these include such measures asthe use of ion-exchange resins, peritoneal dialysisand the artificial kidney.

ConclusionIt is a sober reflection when one considers

that only a few years ago all that was known ofpotassium in clinical medicine could be writtenin a few lines. Now, if anything, the subject isover-emphasised. It is as well to maintain abalanced outlook, for it would be as unwise as it isunnecessary to prescribe potassium indiscrimin-ately to all cases in which depletion is likely toarise. ' The patient is as well as can be expected 'is a hospital stock phrase. It is when the patientis not as well as might be expected that the wisepractitioner looks for potassium imbalance.

AcknowledgmentsI wish to thank Dr. C. E. Dent for numerous

helpful suggestions, and Dr. H. K. Goadby andMr. Murray T. Pheils for allowing me publishdetails of patients under their care at St. Peter'sHospital, Chertsey. I am also indebted to Col.J. Lomer for invaluable assistance with thediagrams.

BIBLIOGRAPHYBLACK, D. A. K. (I953), 'Body fluid depletion,' Lancet, i, 353.BULL, G. M., JOELKES, A. M., LOWE, K. G., and EVANS, B.

(I949), ' The conservative treatment of anuric uraemia,' Ibid.,ii, 229.

BULL, G. M. (1952), 'Discussion on treatment of anuria,' Proc.Roy. Soc. Med., 45, 845.

CAYLEY, F. E. DE W. (1950), 'Potassium deficiency in PAStherapy,' Lancet, i, 447.

CONWAY, J., LEE, J., and SYKES, W. O. (I95I), 'Water andelectrolyte balance in disease,' Postgrad. Med. J., 27, 434.

COPPINGER, W. R., and GOLDNER, M. G. (I950), 'Theeosinophyl count after operation,' Surgery, 28, 75.

DARROW, D. C. (1950), 'The role of potassium in clinical dis-turbance of body water and electrolyte,' New Engl. J. Med.,242, 978, 1014.

ENGEL, F. L., MARTIN, S. P., and TAYLOR, H. (1949), ' Onthe relation of potassium to the neurological manifestations ofhypocalcaemic tetany,' Bull. Johns Hopkins Hosp., 84, 285.

GOVAN, C. D., and DARROW, D. C. (1946), 'The use of potas-sium chloride in the treatment of dehydration of diarrhoea ininfants,' J. Pediat., 28, 54I.

LUBRAN, M., and McALLEN, P. M. (I95I), 'Potassium de-ficiency in ulcerative colitis,' Quat. J. Med., 20, 221.

McALLEN, P. M. (I951), 'The E.C.G. associated with low levelsof potassium,' Brit. Heart J., 13, I59.

NABARRO, D. J. N., SPENCER, A. G., and STOWERS, J. M.(I952), ' The treatment of diabetic ketosis,' Lancet, i, 983.

SMART, G. A. (1952), 'Potassium," Progress in Clinical Medicine'(ed. Daley and Miller), Churchill; 2nd edition, p. II6.

WILHELM, S. K. (I95x),' Alteration in serum potassium andsodium in acute myocardial infarction,' Amer. J. Clin. Path.,21, 146.

WILKINSON, A. W., BILLING, B. H., NAGY, G., andSTEWART, C. P. (I949), ' Excretion of chloride and sodiumafter surgical operations,' Lancet, i, 640.

WILKINSON, A. W. et al. (I950), 'Excretion of potassium afterpartial gastre' tomy,' Ibid., ii, 135.

RUTHIN CASTLE,NORTH WALESA Clinic for the diagnosis and treatment of Internal Diseases (except Mental or Infectious Diseases). The

Clinic is provided with a staff of doctors, technicians and nurses.The surroundings are beautiful. The climate is mild. There is central heating throughout. The annual

rainfall is 30.5 inches, that is, less than the average for England.The Fees are inclusive and vary according to the room occupied.

For particulars apply to THE SECRETARY, Ruthin Castle, North Wales.Telegrams: Castle, Ruthin. Telephone: Ruthin 66

by copyright. on O

ctober 17, 2020 by guest. Protected

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.30.339.7 on 1 January 1954. D

ownloaded from