LETTERS
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at a cosr of ±R2 000 (exam fee plus inrercity air fare and accommodation) .
The College sers the paper and collecrs the fees but makes no effon actually to help the aspiring examinee.
The powers-thar-be should decide whar they wanr to achieve with this examination - do they wanr reaching hospital-type academic excellence, or do they want to improve the rural GP's knowledge of and enthusiasm for primary emergency care?
B. H. IIl'lEUWOUDT West Vaal Hospital Orkney, Tv!
I. Morris M. Emergency medicine in South Africa (Letter).S Afr Med] 1993; 83: 689.
Professor C.
J.
Mieny, Chainnan: Examjnations and Credentials CoDUDittee, College of Medicine of South Africa, comments: A few of the sratements in Dr Nieuwoudt's letter should be put in the correct context. He stares that only 9 candidates for the April 1993 Dip. P.E.c. examination were allowed to attend the oral examination, 'so few out of the hundreds of students attending the courses' ar Wits and Pretoria. The fact is that only 9 candi-dares entered the examination and all 9 were allowed to proceed to the oral examination; 4 passed.Secondly, he stares thar 'prospective candidates are duped by the "Scope and objectives" in the exam regula-tions', and then continues: 'Anyone under the impression that the Dip P.E.C. is just an advanced first-aid course is sadly mistaken!'
Indeed the Dip. P.E.C. is nothing of the son. It is a postgraduate diploma designed to foster continuing medical education and to raise standards of care in.emergency situa-tions. Surely we owe it to the public to ensure thar holders of diplomas of the College of Medicine of South Africa have complied with cenain standards!
In the most recent (October 1993) examination 15 can-didates wrote the examination; 13 were allowed to proceed to the oral and 11 passed, a pass rate of73%.
Dr Nieuwoudr's comments on the book The
Manage-ment of Emergenciesare not relevapr because the book is not prescribed by the College.
Notwithstanding the above, Dr Nieuwoudt expresses certain concerns that do need to be addressed by the College.
The requirements and syllabus for the exam should be clearly spelled out, while at the same time realising that emergency care is indeed a very wide subject and is nor easily defined in row.
The question of appropriate prescribed texts should be and will be reconsidered by the College.
Although it is true that well-structured practically orien-tated courses are desirable, it must be remembered that the courses in the Transvaal are run by the university depan-ments and nor by the College, and at the University of the Witwatersrand the course is not designed as training only for the Dip. P.E.C. but is for medical practitioners, ambu-lance personnel, nurses, etc.
Trick questions and/or second-guessing the examiner have never formed pan of the approach of the College, which prides itself on the quality, and in the sense of responsibility and fair play, of its examination panels.
The College welcomes any suggestions that may assist it in designing the scope and content of its diplomas.
Marked hypokalaemic rhabdomyolysis
due to purgative abuse
To the Editor: Purgative abuse is common and may result in hypokalaemia. Purgative abuse causing marked hypo-kalaemia, resulting in rhabdomyolysis, is most unusual.
We have recently had the opportunity to study a 60-year-old woman who init;ially presented with muscle pain and weakness, most suggestive of rhabdomyolysis. On
funher investigation she was found to have a serum potas-sium value of 1,6 J.1mol/l and a bicarbonate value of 38 J.1illol/l. Serum urea and creatinine values were normal. Muscle enzyme levels were markedly elevated, with a crea-tine kinase value of 14 700 UII. A collagen vascular screen was within normal limits. The calcium and magnesium values were slightly reduced. An ECG done at the time was compatible with the marked hypokalaemia.Itwas extreme-ly difficult to obtain a satisfactory history of purgative abuse, but we were finally able to esrablish that she had been raking 12 phenolphthalein-containing purgatives daily for the pasr 15 years. When this was stopped and the elec-trolyte values were corrected, both the serum porassium and the creatine kinase values returned to normal. Ar dis-charge from hospiral she was torally asympromatic. Unfortunarely she has been lost to follow-up, so we do nor know whether she has gone back to her bad old ways.
Laxative abuse is a cause of lower gastro-intestinal porassium loss that is often difficulr to diagnose.'Asin the case of surreptitious vomiting, it is often difficult to obtain a satisfactory history of such abuse. To complicate matters, patients usually complain of constipation and nor of diar-rhoea.
J.C. KALLMEYER
I. N.MACLEOD B.BHAGWAN
Chelmsford Medical Centre Durban
I. Schwartz WE, Redman AS. Metabolic and renal studiesinchronic potassium depletion resulting from overuse of laxatives. ] Clin
Invest1953; 32: 258.
Anticholinerge intoksikasiedelirium
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'n lewensbedreigende toestand
Aan die Redakteur: Anticholinerge intoksikasiedelirium in pasiente met psigiatriese steurings kan 'n diagnostiese dilemma skep wanneer dit onderskei moer word van 'n akure psigotiese afbraak, 'n psigoaktiewe subsrans ont-trekkingsdelirium en ander organiese breinsindrome.1
•3
Hierdie problematiese differensiele diagnose word deur die volgende gevalsbeskrywing weerspieel.
InJanuarie 1993 is 'n 25-jarige man mer paranoiede skisofrenie in Stikland-hospitaal opgeneem nadat die polisie horn gevind het waar hy naak en doelloos op 'n strand rondgedwaal her. Die pasient ly vir die afgelope 5 jaar aan skisofrenie en is 4 keer vanrevore in 'n hospiraal ogpeneem. InNovember 1992 is hy ontslaan op maandelikse doserings van flupentiksol dekanoaar 40 mg intramuskuler en orfe-nadrien 100 mg daagliks per mond.
Mer toelating was die pasienr baie rusreloos, sy bewus-syn was verrroebel en hy was nie georienteerd ten opsigre van tyd en plek nie·. Gehoor-, taktiele en visuele hallusi-nasies was reenwoordig. Die pasienr her formikasie geroon - hy her horn verbeel dar daar insekte onder sy vel rond-kruip en hy her denkbeeldige goggas en krappe wat op sy lyf geloop het probeer wegslaan. Sy konsentrasie en kort-rermyn geheue was ingekon. Gedagreprosesse was onsame-hangend met los assosiasies en daar was wane van agrer-volging teenwoordig.
Fisiese ondersoek het 'n rooi en warm gelaat geroon. Die pasienr se mond was droog, pupille was gedilareer en her swak op lig gereageer. Polsspoed was 120/min en bloed-druk140/80mmHg. Temperatuur was 37,6°C. 'n Growwe tremor van veral die voorarms was reenwoordig.
'n Spoed volbloedrelling, meum en elektroliere was nor-maal. Die pasient het onrken dat hy enige subsranse mis-bruik het en hy was nie bekend aan die hospitaal as 'n sub-sransmisbruiker nie. Die voorlopige differensiele diagnose van 'n subsrans-geinduseerde delirium of'n akute psigo-tiese afbraak is gemaak en die pasiem is mer bensodiasepien behandel.
Vier-en-twintig uur na roelating was die pasiem helder van bewussyn en ren volle georienteerd, en daar was geen
LE"rrERS
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BRIEWE
plasebofase, aangewend.Veneuse bloedvirdie bepaling van die konsenrrasies van plasma-~-endorfienasook -leusienenkefalien is volgens erkende materiaalinsamelingstegnieke uurliks tussen Q6hOO en 10hOO van proefpersone bekom" Hormoonkonsenrrasies is vervolgens volgens aanvaarde radio-immuun-essaiprose-dures gekwantifiseer"
Ten einde die effek van naloksoon op konsenrrasies van endogene opioiedevir die gespesifiseerde periode te eval-ueer, is kovariansie-analise (met aanvangskonsentrasies as kovariant, asook periode- en behandelingseffekte in ag genome) op die berekende area onder die tydkromme (ADC) uitgevoer.
Vir die 4-uurperiode was die gemiddeldeplasma-~ endorfienkonsenrrasie (ADC) met plasebolOediening 25% (95% venrouensinterval: 16% - 33%) hoeras met nalok-soontoediening. Die gemiddelde plasmaleusienenke-falienkonsentrasie (ADC) met naloksoontoediening was egter slegs 8% (95% venrouensinterval: -4% - 21 %) hoer as met plasebolOediening (TabelI).
Dit die resultatewildit voorkom asof naloksoomoedien-ingplasma-~-endorfienkonsenrrasiesstatisties beduidend asook fisiologies relevant veT/aagsonder om leusienen-kefalienkonsentrasies betekenisvol te beinvloed.
Beta-endorfien is ekwipotem met betrekking tot verplas-ing van mu- en delta-reseptoragoniste, dog venoon min effek op biochemiese assosiasies met kappa-reseplOre .... Leusienenkefalien het gering groter affiniteitvirdelta- asvir
mu-reseplOre, terwyl dit by kappa-reseplOre bykans lOtaal inen voorkom.s-7
Die dosisafhanklike werkingswyse van naloksoon in ag genome, sou verwag kon word dat naloksoon (0,4 mg inrra-veneus as enkeldosering) by uitstek met mu-reseplOre sou interreageer. Resultate toon aan dat naloksoon 'n afname in ~ndorfiensekresietot gevolg het. 'n Moontlike verklaring virhierdie tendens is dat naloksoon deur mu-reseptor-blokkade regulerende negatiewe terugvoermeganismes aktiveer/potensieer.
Resultate lOon verder ook aan dat naloksoomoediening nie 'n beduidende effek op leusienenkefaliensekresie uit-oefen nie. 'n Waarskynlike verklaringvirhierdie verskynsel is dat die aangewende dosis van naloksoon te laag was om merkbare effek op delta-reseplOre uit te oefen.
1. Dilsaver SC. Anrimuscarinic agents as substance of abuse: a review. JCIin PsycJwphannacol1988;8: 14-22.
2. Gelenberg AI. Use and abuse of anticholinergicdrugsin psychiatIy. JCIinPsychiatry1984; 6: 148-1 ?5.
3. McEvoyJP.Theclinical use of anticholinergic drugs as rreaunent fot extrapyramidal side-effecrs of neurolepticdrugs.J Clin Psycho-pharmaco11983;3: 288-302.
4. JohnsonAL,HollisterLE,Berger PA. The anticholinergic intoxica-tion syndrome:diagnosisand treaunent.JClin Psychiatry1981; 42: 313-317.
F.J.lWGO I.J. E1DELMAN Depanement Psigiarrie Universiteit van Stellenbosch en Tygerberg-hospitaal
Tygerberg,KP
Basale sekresie van endogene opioiede
na intraveneuse naloksoon
visuele of taktiele hallusinasies nie. Die pasiem het beken dat hy ongeveer 40 orfenadrientablene (50 mg) geneem het op aandrang van 'n kennis wat ook 'n skisofreen is met ruimervaringin die misbruik van psigoaktiewe substanse.
Die finale diagnose was anticholinerge intoksikasie-delirium in 'n pasient met paranoiede skisofrenie. Die volledige konstellasie van simptomatologie in die anti-cholinerge inlOksikasiesindroom is soos volg: disorientasie, onsamehangendheid, hallusinasies, wane, abnormale psigo-molOriese verskynsels, fluktuerende bewussynsvlak, gedila-teerde nie-reaktiewe pupille, dowwe visie, warm en droe vel, rooi gelaat,droe mond en keel, probleme om te sluk, onwelriekende asem, verminderde dermkianke, urinere retensie, tagikardie, hipertensie, tagipnee, koors en koma"
Anticholinerge middels word algemeen voorgeskryf in psigiatrievirekstrapiramidale newe-effekte van neuro-leptika.' Dit word moontlik algemeen misbruik as 'n euforiant, en die neem van groot hoeveelhede kan 'n deliri-um presipiteer wat SotllS beskryf word as 'n 'psigedeliese' ondervinding! Anticholinerge intoksikasiedelirium is 'n lewensbedreigende toestand en die diagnose moet altyd oorweeg word in pasiente wat anticholinergika gebruik en wat 'n deliriumbeeld ontwikkel.
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Aandie Redakteur: Dit is bekend dat sekresie van endo-gene opioiede (p-endorfien/leusienenkefalien) deur biolo-giese negatiewe terugvoermeganismes, eksogene faktore asook farmakologiese agense gemoduleer word.',2 Nalok-soon is 'n suiwer opioiedreseptQrantagonis watvirverskeie kliniese indikasies, as 'n bolusdosis of altematief as 'n kon-stante infuus, inrraveneus toegedien word.3Die middel is
konwerkend (1 - 4 uur). Dit oefen 'n onbevredigende effek lit indien oraal lOegedien.3
Alhoewel naloksoon in terapeutiese doserings (0,4 -2,0 mg vir volwassenes) oorwegend affiniteit vir mu-opioiedreseptore venoon, tree dit in hoer doserings ook kompeterend antagonisties by delta- en kappa-reseplOre
Op.3
Die doel van die smdie was om die effek van 'n enkel-dosering naloksoon (0,4 mg intraveneus) op die basale sekresie van ~-endorfienasook leusienenkefalienvir 'n periode van 4 uur te evalueer.
Vir die doel is gesonde mans as proefpersone in 'n enkeldosering, gerandomiseerde oorkruisstudie met 'n
E.H.DEWET R.SCHALL
J.M. C. OOSTHUIZEN
Depanemenre Geneeskundige Fisiologie en Fannakologie Universiteitvandie Oranje-Vrysraat
Bloemfonrein
1. Hughes I. Biogenesis, release and activation of enkephalins and dynorphins.Br Med BuIl1983;39(1): 17-24.
2. Imura H. ACTH and related peptides: molecular biology, bio-chemistIy and regulation of secretion. Clin EndocrinolMetab 1985;
14: 845-866.
3. WayWL,Way EL. Opioid analgesics and antagonists.In: Karzung BG, ed.Basic and Clinical Pharmacology.Los Altos, Calif.: Appleron
&Lange, 1989: 380.
4. De Wet EH. Normale en gewysigde sirkasiese sekresieparronevir
endogene opiolede in die mens. M.D.-proefskrif, Universiteit van die OVS, Bloemfonrein, 1991.
5. Yaskh TL Opioid recepror systems and the endorphins: a review of their spinal organization.JNeuroSU16' 1987; 67: 157-176.
6. Paterson SI, RobsonLE,Kosterlirz HW. Classification of opioid receprors.BrMed BuIl1983;39: 31-36.
7. Schiller PW, Wilkes BC. Conformational analysis of cyclic opioid peptide analogs.NIDA ResMonogr1988; 87: 60-73.
TASELI.
Gemiddelde plasma-!3-endorfienkonsentrasies en plasmaleusienenkefalienkonsentrasies (gemiddeld
±
SA) in11 gesonde mans Tyd Plasma-!3-endorfienkonsentrasies (fmoVml) Plasebo Naloksoon Plasmaleusienenkefalienkonsentrasies (fmoVml) Plasebo Naloksoon 06hOO 07hOO 08hOO 09hOO 10hOOAUC (6hOO-10hOO) (fmoVh/ml)
7,09 ± 1,45 6,64 ± 1,21 10,36± 1,75 9,27 ± 1,95 7,00 ± 1,61 33,32± 3,08 7,55 ± 1,63 5,73 ± 1,01 5,82±1,17 7,45 ± 2,25 7,18 ± 2,18 26,36 ± 5,20 18,27 ± 5,62 13,55 ± 3,86 9,73 ± 3,13 9,91 ± 3,08 7,00 ± 1,67 45,82 ± 9,69 19,64 ± 4,52 14,82 ± 3,74 10,73 ± 2,83 11,73±3,47 7,09 ± 1,92 50,64± 8,69
