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21 Februarie 1953 S . A . T Y D S K R I F VIR G E N E E S K U N D E 153giftige uitwerkings wat deur n voorlob-ekstrak veroorsaakword, ooreenstem met die wat deur DCA-oor -doseri ngby die ro t veroorsaak word. Sy resul tate bek lemtoon dienoodsaaklikheid vir versigtigheid met di e wyse waarophierdie geneesmiddels by menslike terapie en kliniese navorsing verbind mag word. Hulle toon ook die noodsaaklikheid vir nadere studie deur die mediese professie vanhierdie belangrike ontwikkeling in endokrinologie, en dienoodsaaklikheid om die fisiologiese beginsels, wat betrokkeis as ons hierdie nuwe ondernemings met vertroue enveiligheid so u begin, te assimileer. n Uitstekende bydraetot hierdie studieveld is die simposium wa t tydens die 1952: ongres oa r Cor ti sone en ACTH gelewer is. Di t sal binnekort in h ie rdie y skrif verskyn.

administration of anterior pituitary extracts an d cortisone.Selyes observations, however, indicate that th e toxic effectsproduced by a n a nt eri or pituitary extract resemble thoseproduced by DC A over -dosage in the rat . Hi s results urgethe need f or c au ti on in the way in which these remediesmay be combined in human t herapy an d clinical research.They also indicate the need for close s tudy by the medicalprofession of this important development in endocrino ogy, and the need to assimilate the ph y iologicalprinciples involved if we are to embark on these newventures with confidence an d safety. Th e 1952 Congresssymposium on cortisone and A CT H ( to be published soonin this Journal will provide an excellent contribution tothis field of study.

PARALYTIC ILEUS DU E TO POTASSIUM DEPLETIOS. GRIEVE M.B., M.R.C.P.

Coronation Hospital JohannesburgDuring the past few years the potassium ion has assumeda place of extreme importance in electrolytic s tudies .Numerous symptoms an d signs have been attributed toeither hypokalaemia or hyperkalaemia. On e of the syndromes ascribed to hypokalaemia is the state of paralyticileus. This paper reports 2 cases of paralyt ic ileus, inwhich the etiological agent was thought to be hypokalaemia.Only 2 of the total body pot assium is present in theextracellular fluid,7 in a concentration of 18-22 mg. per100 C.c. (3.8-5.5 meq.). Th e remaining 98 is in the intracellular fluid, liver an d muscle cells an d here potassium isthe chief basic io n of th e cells. During normal cellcatabolism, potassium is released an d 2- 4 gm. of potassiumare excreted dai ly, 80 in the urine. Th e average dailyrequirements of the body are 4-8 gm. Exci tability an dother properties of muscle depend to some extent on therelative concentrations of potassium within an d without itsfibres. Potassium chloride solutions have a rapid anticurarizing effect.Darrow 3. 5 ha s discussed the symptoms an d signs ofhypokalaemia. When the serum potassium is below14 mg. pe r 100 C.c. of serum the following ma y be noted:

Apathy. lethargy and drowsiness.2. Anorexia and nausea.3. Weakness of skeletal muscle, twitching. first involving thelimbs and then the respiratory muscles, leading to dyspnoea anda shallow, infrequent, gasping respiration.1. 2 6 94. Intestinal distention and paralytic ileus due to atonyof smooth muscle.5. Cardiac abnormalities with characteristic electrocardiographic changes possibly due to a replacement of potassiumby sodium in the cardiac cells with resultant oedema. Thesechanges have been described by numerous authors and arebetter seen in the chest leads. They consist of a prolongedQT interval, flattening or inversion of the T waves,extrasystoles and A V Block.None of the above changes is specific, but ifhypokalaemia is present with an y of these symptoms,correction of such hypokalaemia is strongly indicated.Webster an d others 6. 9 state that hypokalaemia ma ycause an inhibition of intestinal musculature aggravating

an ileus established fro m so me o the r cause, or be the solecause of such an ileus.CASE 1

An Afr ican female aged 31 was admitted to hospi ta l on12 February 1952 in a state of kwashiorkor. loShe was mentally confused, bu t gave a h is tory of chronicalcoholism of some years' duration and stated that shehad been unable to eat or d ri nk a ny th in g d ur in g th e lastweek because of continuous vomiting.Examina tion showed evidence of gross malnutritionmainly of a pellagrinous type. Gros s oed ema of thes ac ru m a nd l ower limbs was pres ent an d the face, armsan d legs showed the characteristic scaling an d pigmentation. Th e tongue was small, fiery red in colour tenderan d showed too th indentation marks. Th e gums wereseptic an d the hair was coarse, bri tt le an d reddish brownin colour. Th e cardiovascular and respiratory systemswere normal, the blood pressure being 116/50 mm. Hg.There were well-marked neurit ic mani fes tat ions in th elower limbs, bu t the cranial nerves were normal. Examination of the abdomen revealed generalized tenderness bu tno distension was presen t an d pelvic examination wasnormal.

Radiography of the chest showed no abnormality an d ablood c ou nt g av e a haemoglobin of 10.1 gm. with a normaltot al and differential white count . No eosinophils wereseen on a wet preparation. A blood Wassermann tes t wasstrongly positive an d examination of the cerebrospinal fluidwas normal in every respect. Th e liver function testsshowed a marked degree of hepato-cellular damage.D urin g the fol lowing 2 d ay s t he ra py consisted of

ward diet an d parenteral vitamins. There was no vomitingbu t the patient ha d 2 large, loose s too ls daily. Examination of these stools showed th e presence of ascaris ova,bu t culture was negative.On 15 February the pa tie nt c ompla ined of severe,generalized abdominal pain an d was vomiting. She hadha d no bowel act ion in the last 18 hours an d examination

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154 S.A. M E D I C A L J O U R N A L 21 February 1953showed her abdomen to be markedly distended, withgeneralized tenderness and guarding. X- ray films of herabdomen revealed grossly dilated loops of small bowel withnumerous fluid levels. The biochemistry at this stage wasas follows:

Potassium: 13.4 mg. per 100 c.c. (3.4 meq. .Sodium: 320 mg. per 100 c.c. (139 meq. .Chloride (as laC ): 440 mg. per 100 c.c. (75 meq. .Sugar: 69 mg. per 100 c.c.Serum albumin: 1.6 gm. per 100 c.c.Serum globulin: 4.2 gm. per 100 c.c.CO,-combining power: 69 vols. 31 meq. .An elec trocardiogram at this stage showed small complexes with isoelectric T waves in practically all the leads.An U wave was prominent in all the chest leads. 0 otherabnormali ty was noted. A diagnosis of paralytic ileus wasmade and hypokalaemia was thought to be the cause.Malnutri tion, d iarrhoea and vomiting were thought to bethe etiological factors in the product ion of hypokalaemia.The patient was accordingly given 2 gm. of potassiumchloride in 100 C.c. of milk orally at 2-hourly intervals until16 gm. had been given. Serum potassium levels before andafte r were 13.7 and 16.5 mg. per 100 C.c. of serumrespectively. Serial elect rocardiography showed a rise inthe ST segment and the T wave above the isoelectric lineand the disappearance of the U wave. At the end of

24 hours the patient was much improved and theabdominal distension and tenderness was considerablyreduced. A further 20 gm. of potassium chloride was givenby mouth during the next 48 hours and, at the end of thistime, the patient had no complaints and her abdomenpresented normal features on examination. Dailyradiography showed a corresponding improvement. On20 February the biochemistry was as follows:Potassium: 21 mg. per 100 c.c. (5.4 meq.).Sodium: 325 mg. per 100 C.c. (141 meq. .Chloride (NaCl): 560 mg. per 100 C.c. (95 meq. .CO,-combining power: 54 vols. (24.5 meq.).

The patient was given a total of 36 gm. of potassiumchloride orally; no other therapy or medication was used.CASE 2

An elderly African female, aged approximately 60 years,was admitted to hospital on 23 February 1952. She wasmentally confused, but complained of pain in both renalangles, diarrhoea and vomiting of about one month'sduration.Examination showed a markedly emaciated, dehydrated,

elderly female. The cardiovascular and respiratorysystems were normal, the blood pressure being 100/60 mm.Hg. There was marked tenderness in both renal anglesand over the bladder, otherwise no abnormality was foundin the abdomen.Chronic pyelo-nephritis was diagnosed and confirmed oncystoscopy, both kidneys being hydronephrotic. A stricturewas foun d in the pelvis of the right kidney. ol wascultured from both pelves and this organism was no tsensitive to any antibiotic. In spite of this findingstreptomycin, penicillin and gantris in were given in largedoses. Th e patient was also treated with intravenous fluidsand an attempt was made to restore her electrolyticbalance to normal.

During the following 10 days her general state appearedto improve and the urinary infection seemed to settle.

Repeated cystoscopy showed no real change although theurine from each pelvis was now sterile. On 5 March,11 days after admission, the patient was found to be complaining of severe abdominal pain an d to be vomitingfrequently. Examination showed her abdomen to beextremely tender and distended with marked generalizedguarding. An X ray showed dis tended loops of smallbowel with numerous fluid levels suggesting a paralyticileus.A blood count at this stage was normal apart from ahaemoglobin of 11.3 gm., and the biochemistry was asfollows:Potassium: 10.9 mg. per 100 c.c. (2.7 meq.).Sodium: 300 mg. per 100 c.C. (130 meq.).Chloride: 485 mg. per 100 C.c. (83 meq.).Urea: 13 mg. per 100 c.c.Sugar: 121 mg. per 100 c.c.CO -combining power: 44 vols. (20 meq.).Serum albumin: 1.2 gm. per 100 c.e.Serum globulin: 2.8 gm. per 100 c.c.An electrocardiogram at this stage showed normalrhythm, small complexes in all leads, ST segmentsdepressed below the isoelectric line in leads VI and V2 andT waves isoelectric in all leads.Hypokalaemia was thought to be the cause of theparalytic ileus and potassium chloride was given intravenously in a 5 dextrose in norm al saline mixture. Atotal of 36 gm. of potassium chloride in 4,000 c.C.. ofglucose in saline was given in 72 hours. At the end ofthis time, the serum potassium was 13.8 mg. pe r 100 c.c.The patient was now considerably improved, the abdominaldistension was much less and t he abdominal tendernesswas minimal. Serial radiography had confirmed iheimprovement. The pat ient was now given ora l potassiumchloride as there was no further vomiting an d after afurther 3 days there was no signs of ileus, the abdomenbeing scaphoid and not tender. Serial electrocardiographyshowed a rise in the T waves to a level of 2 mm. abovethe isoelectric line. The biochemistry on 11 March was asfollows:Potassium: 16.8 mg. per 100 e.e. (4.3 meq.).Sodium: 310 mg. per 100 c.C. (134.7 meq.).Chloride: 485 mg. per 100 e.e. (83 meq.).Urea: 24 mg. per 100 c.e.CO,-combining power: 48 vols. 21 meq.).This pat ient received 36 gm. int ravenously and 36 gm.orally of potassium chloride over 6 days. .

Later this patient deteriorated an d died on 28 March1952. Autopsy confirmed the diagnosis of chronic pyelonephr it is and revealed no abnormality in the bowel.

DISCUSSIONDarrow and his co-workers 3. 5 demonstrated bothexperimentally and clinically the co-existence of intracellular potassium deficiency, metabolic acidosis andhypochloraemia. This state occurs in the presence ofnormal renal function when the re is loss of a single ionsuch as chloride or potassium. Numerous authors 2 6 8have stressed the importance of hypochloraemia, whichdoes no t respond to the usual therapy being associatedwith hypokalaemia. This applies particularly to postoperative states. Th e first case described exemplifies thisbiochemical state well. She was admitted in a state ofgross malnutri tion, deficient in chloride and potassium,but not sodium, and her CO combining power gave a

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21 Februarie 1953 S.A. TYDSKRIF VIR GENEESKUNDE 155high reading. The paralytic ileus responded extremelywell to treatment with oral potassium in spite of t he fac tthat her intestinal mucosal absorption might have beendeficient and in t he p resence of some degree of vomitingand diarrhoea.Th e second case, although showing hypochloraemia and

hypokalaemia, was acidotic with a normal sodium value inher blood. The p robable reason fo r this was the renaldamage present , although no retention of urea or othersubstances occurred until the final stages of the disease.In this case the paralytic ileus responded well to intravenoUs therapy with potassium chloride although anxietywas fel t at the time of giving such intravenous therapy inthe presence of gross kidney damage.In the t reatment of hypokalaemia, Eliel and others 6 7have recommended that potassium chloride should begiven orally in doses 6-18 gm. daily. No untoward effectshould occur , provided renal function is normal. Mosto f the potas sium is excreted in 3 or 4 hou rs , a s potas siumis also a good diuretic. The mixture is conveniently givenin a glass of milk or orange juice.Eliel 6 recommends that 6 gm. of potassium chloride begiven in each litre of g lucose in normal saline or simplynormal saline. Darrow 3_5 stated that 0.26 gm. of potassium chlor ide per kg. body weight is safe if injected slowlyintravenously over a period of 8 hours. Thus 18 gm. maybe given to a patient weighing 70 kg. In the second casedescribed here 9 gm. of pot as si um chlor ide were added toeach vacolitre with correction of the potass ium deficit andno toxic effects.

ANAEMrA T

In both ca se s s erial electrocardiography an d serumpotassium values were carried out . The use of th e electrocardiogram as a gui de t o such potassium therapy has beenemphasized. The return of flattened ST segments andT waves t o norma l indicates adequate therapy whereas theappearance of spiked T waves is thought to be the firstindication of potassium toxicity.4,6

SUMMARY1 Two cases ar e des cri bed i n which hypokalaemia is

thought to have been the etiologcal factor in the prod uction of paralytic ileus.2 The t reatment of these cases is discussed.3 The physiology of the potassium ion is brieflydiscussed.

I am grateful to Dr. V. D Gordon. superintendent of Coronation Hospital. for permission to pub lish this r epor t.

REFERE ICESI Black. D A K and Milne. M.D. (1952): Lancet, 1, 244.2 Brunsch. A (1948): Cancer, 1, 177.3 Darrow. D C (1945): J Paediat., 26, 519.4. Dar row, D. C (1946): J Paediat., 28, 515.5 Darrow, D C (1946): J Clin. Inves ., 26, 324.6 Eliel, L. P., Pear son, O H. and Rawson, R. W. (1950):New Eng. J. Med., 243, 472.7 Leonsins, A. J. (1951): S Afr. Med. J., 25, 127.8 Maddock. W. G. (1939): Am. J Surg. 46. 426-434.9 Webster. D. R., Hendrikson, W. and Currier , D. S. (1950):Ann. Surg.. 132, 777.10 Williams, C D (1933): Arch. Dis. Childh. , 8, 423.

OBSTETRrcsJAMES MILLER, M.B., CH-B. (CAPE), D.OBST.R.C.O.G., M.M.S.A., M.R.C.O.G.*

Port lizabethThe a im of this commentary is to show the differentiationbetween the physiological and the pathological anaemiasof t he p regnancy , with a classification of the l at te r basedon the aetiological factors . The preventive aspect, modernprinciples of t reatment and the effects of t he anaemia inobstetrics, ar e discussed.The tabulated results are based on personal observa

tions; th e wo rk was performed in two London hospitals.A pattern can be taken fo r subsequent work in thiscoun tr y on th e various social and rac ia l groups.Historical. Channing in 1842 reported 10 fatal cases anddrew a tt en ti on to a severe anaemia associated with pregnancy.In 1881, Willcocks descr ibed the physiological aspect ofanaemia in pregnancy.OsIer : 0 distinguished between Addison s anaemia and apernicious anaemia in pregnancy. He stated that whenrecovery occurred in the latter g roup, it was permanent , withfreedom from recurrence in later pregnancies.Subsequent l it erature shows the work of differentiating thesevere, and poss ib ly fatal anaemias, from the milder ones.which cause no more than vague symptoms and signs inpregnancy.

Whitby quotes t ha t in 1899, Hugouneng showed that t ofthe iron present in the foetus at term, was laid down during Late Depar tments of Obstetrics and Gynaecology. CentralMiddlesex Hospi ta l. London. N.W.IO, Paddington Hospi ta l,London, W.9.

the last 3 months of pregnancy, demonstrating the necessi tyof a ma ter na l diet rich in iron.Incidence. A survey 8 in t he Uni ted Kingdom revealedthat 7.5 of non-pregnant women had haemoglobin levelsbe low 80 .The Table I shows my survey on the haemoglobin esti

mation of 560 consecutive pregnant women, at their firstantenatal visit, irrespective of the dur at ion o f pregnancy.

TABLEHaemoglobin Haldane umber Percenrage

Over lOO 54 9.495-100 79 1490-94 151 2785-89 112 2080-84 104 18.675-79 32 5.770-74 14 2.365-69 7 1.260-64 4 .755-59 1 50-54 0 045-49 I .240-44 I

560 99.5