This article describes the clinical course and management of a patient who developed hyperkalaemic acute renal failure due to a herbal medicine, Callilepsis laureola

Hitchcock, P.J.

Seedat, Y. K.

English

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832 S.-A. MEDIESE TYVSKRIF 31 Julie 1971Focal activity is found in both left frontal areas and onthe right side and it was noted that of the other 5 adultcases, 3 also had evidence of focal activity in a temporallobe. Further, it is suggested that the 18-Hz temporal acti-vity in the 3 cases described may be a stage of develop-ment, representing a higher harmonic of a diencephalic 6-Hz rhythm, which is also manifest as positive spikes.Finally, comparison of the age incidence of FSPSPS withanterior temporal spike foci reveals an astonishing rela-tionship; as the incidence of FSPSPS declines in early adultlife, so the incidence of temporal foci increases.'"I wish to thank Dr M. H. Webster, Secretary for Health.for permission to publish this paper: Dr A. P. Baker forpermission to study patients under his care and for his advice:and Mr 1. Newton for the electro-encephalographs.REFERENCESI. Ardrey, R. (1961): African Genesis. London: Coli ins.2. Baker, A. P. (1970): Rhodesia Science News, 7, 238.3. Black, D. A. K. (1970): Brit. Med. J., 2, 387.4. Cobb, W. A. in Hill, D. and Parr, G., eds. (1963): EleclroencepJwlo-graphy: A Symposium on its Various Aspec{s~ 2nd eel., p. 324. London:McDonald.5. Idem (1963): 01'. cit.,· p. 307.6. Dart, R. A. (1949): American Journal of Physical Anthropology,March 1949.7. Idem (1953): International Anthropological and Linguistic Review, I,4.8. Davis. D. R. (1966): All Introduction to Psychoparllology, 2nd ed.,p. 19. London: Oxford University Press.9. Demerdash, A., Eeg-Oloffson, O. and Petersen, I. (1968): Develop.Med. Child Neurol., 10, 309.10. Fish, F. (1962): Schizophrenia, pp. 64 - 76. Bristol: 1. Wright & Sons.11. Garneski, T. M. (1960): Electroenceph. Clin. Neurophysiol., 12, 505.12. Gibbs, E. L., Rich, C. L. and Gibbs, F. A. (1960): Ibid., 12, 265.13. Gibbs, F. A. and Gibbs, E. L. (1952): Arias of Eleclro-encepJwlo-graphy, \'01. 2, 1st ed., pp. 329 - 334. Cambridge. Mass.: AddisonWesley.14. Idem (1963): Ibid., IS, 533.15. Idem (1964): Alias of Eleclro-enceohalography, \'01. 3, 1st ed., pp. 57-61. Cambridge, Mass.: Addison Wesley.16. Idem (1964): 01'. cit.," p. 5.17. Glenn, C. G., Knuth, R. and Virgil, M. (1966): Dis. Ner\'. Syst., 27,662.18. Grey-Waiter, W. (1961): The Living Brain, p. 181. Harmondsworth:Penguin Books. .19. Gross, M. D. and Wilson, W. C. (1964): Arch. Gen. Psych,at., 11,20. ~~~ssman, C. (1963): Electroenceph. Clin. Neurophysiol., IS, 145.21. Hill, D. in Hill, D. and Parr, G., eds. (1963): Elecrroencephalography;A Symposium on its Various Aspeccs~ pp. 395 - 396. London:McDonald.22. Hona, T., Emura, H. and Kisa, S. (1965): Yonago Acta Med., 9, 245.23. Hughes, J. R., Schagenhauff, R. E. and Magross, M. (1965): Chn.europhysiol., 18, 7 I. . .24. Kiloh, L. G. and Osselton, J. W. (1961): C!Jlllcal Electroencephalo-graphy, 1st ed., p. 50. London: Bunerworth.25. KnOll, J. R. and Meder Mayer, E. (1963): Electroenceph. Clin. Neuro-physiol., 15, 145.26. Kozaezewska, W. and Kayanowska, J. (1962): Ibid., 14, 582.27. Little, S. C. (1963): Ibid., IS, 145.28. Magoun, H. W. (1963): The Waking Brain, 2nd ed., pp. 53 - 68.Springfield, Ill.: Charles C. Thomas.29. Metcalf, D. R. (1963): Electroenceph. Chn. europhysiol., 15, 145.30. Millen, F. J. (1963): Ibid.,31. Pichot, P. (1965): Proceedings of che Leeds SYlnpos;um 011 BehaviourDisorders. p. 3.32. Petersen, I. and Akesson, H. O. (1969): Acta genet. (Basel) , 18, 163.33. Rodin, E. A. (1964): Electroenceph. Chn. Neurophysiol., 17, 566.34. Rousseau, J. J. (1959): In Essays in Philosophy, pp. 35- - 64. NewYork:35. Sayed, Z. A., Lewis, S. A. and Brittain, R. P. (1969): Brit. J.Psychiat., lIS, I I IS.36. Silverman, D. (1964): Electroenceph. Clin. Neurophysiol., 16, 395.37. Idem (1967): Ibid., 23, 207.38. Slater, E. and Roth, M. (1969): Clinical Psychiatry, 3rd ed., p. 157.London: Bailliere, Tindall & Cox.39. Small, J. G. (1968): Electroenceph. CIin.. europhysiol., 24, 561.40. Small, J. G., Sharpley, P. and Small, I. F. (1968): Arch. Gen.Psychiat., 18, 232.41. Small, J. G. and Small, 1. F. (1964): Ibid., 11, 645.42. Stehle, H. C. (1960): Electro-enceph. Chn. Neurophysiol., 12, 265.43. Sutherland, J. B. and Tait, H. (1969): The Epilepsies, p. 3. London:Williams & Wilkins.44. Thomas, J. E. and Klass, D. W. (1968): Neurology (Minneap.), 18,587.45. Tsuzuki, H. (1967): Folia Psychiat. Neurol. Jap., 21, 181.46. Walker, A. E. and Marshall, C. (1963): Electroenceph. Clin. Neuro-physiol., IS, 145.47. Whitehouse, D., Pappas, J. A., Escala, P. H. and Livingston, S.(1967): New Engl. J. Med., 276, 23.48. Wiener, J. M., Delano, J. G. and Klass, D. W. (1966): Arch. Gen.Psychiat., IS, 144.49. Williams. D. (1966): Brit. Med. J., I, 1439.50. Idem (1969): Brain, 92, 503.51. Zitrin, C., Greenberg, I. M. and Steiner, F. (1963): Arch. Gen.Psychiat., 9, 559.Acute Renal Failure from Callilepsis laureola*Y. K. SEEDAT, M.D., M.R.e.p. (LOND.), F.e.p. (S.A.) AND P. J. HITCHCOCK, M.B., B.CH., F.e.p. (S.A.),Department of Medicine, University of Natal and King Edward VIII Hospital, DurbanSUMMARYThis article describes the clinical course and managementof a patient who developed hyperkalaemic acute renalfailure due to a herbal medicine, Callilepsis laureola.S. Air. Med. J., 45,832 (1971).Acute renal failure due to herbal medicine among Bantupatients is not uncommon. In many of the patients ahistory of herbal ingestion is not forthcoming except ondirect questioning; even if a history is obtained it is diffi-cult to ascertain whether the herbal medicine is responsibleas the patient could have taken herbal "medicine for"Date received: 31 March 1971.symptoms of uraemia once acute renal failure had de-veloped. This report describes a patient who presentedwith features of hyperkalaemia due to acute renal failure.A Bantu male, aged 42 years, presented with symptoms ofpain in both loins and the epigastrium and passage ofdiarrhoea with blood and pus. He was tentatively diagnosedas a case of amoebic dysentery with amoebic liver abscessand the possibility of pyelitis was entertained; because ofthe likelihood of pyelitis he was inadvertently treated bythe resident medical officer with tetracycline 250 mg q.i.d.and potassium citrate 15 ml t.i.d. for 4 days (84 mEqpotassium daily). Four days after admission he was foundto be completely paralysed with no sensory loss; theextremities were cold and clammy and there was brady-cardia with a poor pulse volume. He was anuric with aurine volume of less than lOO ml in 24 hours. An electro-31 July 1971 S.A. MEDICAL JOURNAL 833Herbal medicine is not an uncommon cause of acute renalfailure in the Bantu and this should be considered in allcases presenting. with acute renal failure. This case reportraises some interesting facts for discussion.Callilepsis laureola ('impila.), the cause of the acuterenal failure in our patient, is a known poison. Zulus takea decoction of the root as a vermifuge and the infusion asa purgative. A paste of the root i~ used to kill maggots incattle.' Maberley' records that the root gathered in' winteris a cough remedy and that he has found that the activeprinciple, which is a resin, is useful in the treatment ofwhooping-cough. 0 reference could be found by us ofthe value of 'impila' in the treatment of impotence asoccurred in our patient.The management of hyperkalaemia in acute renalfailure is a medical emergency as it is a common causeof sudden death. Because of the electrocardiographicfeatures of hyperkalaemia and the clinical picture ofmuscular paralysis from hyperkalaemia, our patient wastided over the immediate period with calcium gluconate,sodium bicarbonate intravenously and soluble insulin withintravenous dextrose until the effect of peritoneal dialysisin lowering the serum potassium was obtained. This patientwas inadvertently given potassium citrate before it wasrealized that he was oliguric. This strongly illustrates thepoint that sodium citrate is a very much safer (and just aseffective) urinary alkinizer. It is likely that in our patientthe inadvertent use of potassium citrate precipitated thehyperkalaemic manifestations. The use of tetracycline aswas done in our case is to be condemned in oliguric states,as tetracycline has an anti-anabolic factor· and may havea direct toxic effect on an already vulnerable kidney,"We wish to thank Dr H. R. J. Wannenburg, 1edical Superin-tendent of King Edward VIII Hospital. for permission topublish.REFERENCES1. Wrong, 0 .. and Davies, H. E. F. (1959): Quart. J. Med., 28. 259.2. Watt, J. M. and Breyer-Brandwijk, M. 1. (1932): The Medicinal andPoisonous Plants 0/ Southern Africa, 1st ed.. p. 194. Edinburgh:E. & S. Livingstone.3. Maberley, 1. (1905): Report of a Joint Meeting of the British andSouth African Associations for the Advancement of Science, 3, 340.4. Shils, M. E. (1963): Ann. Intern. Med .. 58, 389.5. Edwards, O. M., Huskisson, E. C. and Taylor, R. T. (1970): Brit.Med. 1., I, 26.DISCUSSIONsedimentation rate was 4 mm/hour; serum cholesterol was220 mg/ 100 ml; the amoebic gel diffusion test was negative;retrograde pyelography excluded postrenal obstruction andshowed the kidneys to be of normal size. Urine urea was56 mg/lOO ml, urinary sodium 62 mEq/litre, and urinarypotassium 100 mEq/litre; blood sugar 118 mg/lOO ml,serum bilirubin 0·7 mg/lOO ml, direct Van den Berghnegative, total protein 7· I g/ lOO ml, serum albumin 2·1 g/lOO ml, serum globulin 5·0 g/ 100 ml, serum alkaline phos-phatase 12 KA units; serum glutamic oxaloacetic trans-aminase 46 units/ml (normal 9 - 40 units/ml), serum glu-tamic pyruvate transaminase 5 units/ml (normal 5 - 35units / ml) and serum lactic dehydrogenase 587/ per ml(normal 100 - 500 units/ml). An ammonium chlorideassay according to the short test of Wrong and Davies'showed that the acidification power of the kidney wasnormal in that the urinary pH was 4·65 when the pH ofthe blood was 7·.3.21ft AFTER START OFPERllONEAL DIALYSISn:r~:::--t':~.~.1(~0.'r.;·:i~· i~jc-,-~...: i I· ; ,.\: i ! '.' i ~_:_,_.__:...ti; ,.\i :~~~AI\_.L_... ~Fig. 1. Seriai eiectrocardiograms of the patient showingchanges reverting from hyperkalaemia to a normal state.On recovery, direct questioning gave a history of hishaving visited a witch-doctor for impotence; he wasprescribed a herbal medicine 'impila', which he tookorally after it was boiled in water. The patient did notfollow the instructions of the witch-doctor in preparingthe herbal medicine. He placed the infusion into onebottle instead of diluting it to fill 8, and thus the dose wasat least 8 times greater than prescribed.The urine contained albumin 2, sugar 1, pus cells I andamorphous debris 1. The blood count showed haemoglobin16·5 g/100 ml, white cell count II OOO/mm'. ErythrocyteSERIAL REC~ON:;S OF V2cardiogram showed gross widening of the QRS complex,tall T waves, no P waves and bradycardia (Fig. I), whichwere features of hyperkalaemia. He was immediatelytreated with 20 ml of 10% calcium gluconate intravenously,40 ml of 4% sodium bicarbonate and 20 units soluble in-sulin with 50 g dextrose intravenously. This was followedwith peritoneal dialysis over 48 hours, as the patient hada serum potassium of 8 mEq/litre and blood urea of 310mg/100 m!. Twenty-four hours later the serum potassiumwas 5 mEq/litre and the electrocardiogram was normal(Fig. 1).11

Acute Renal Failure from Callilepsis laureola

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Acute Renal Failure from Callilepsis laureola

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