Harries, JR

Lawes, WE

English

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South Ahicau Medical Journal Suid-Afrikaanse Tydskrif vir GeneeskundeCape Town, 15 July 1961 Volume 35 No. 28 Deel 35 Kaapstad, 15 Julie 1961THE USE OF LIGHT HYPOTHERMIA I ACUTE LIFE-THREATENI GPOLIOMYELITISJ. R. IiARRlFS, M.D., M.R.C.P., Physician, and W. E. !.AWES, EF.A.R.C.S., Anaesthetist, King Ceorge VIHospital, NairobiIn the past few years the use of hypothermia has increasedin the treatment of various conditions, as distinct from itsuse during surgical operations. As far as we are awarethere have been no published reports from British sourcesof the use or' this technique in acute poliomyelitis, thoughMiorner et aP successfully treated a case of poliomyelitiswith hyperpyrexia. Mihaly Janos2 suggested that cooling,if used early, may reduce the degree of residual paralysis.In some 12 patients so treated Janos3 ,4 considered that thereturn of muscle power in 9 was more rapid than wouldnormally ha~e been expected. Russell5 considered thathypothermia would be detrimental in acute bulbo-spinalpoliomyelitis, because of the adverse effect of the colditself OD nerve cells when in an already damaged condition.ROSS6 and G ray7 have demonstrated, on experimentalanimals, that severe hypothermia could only be maintainedfor a short period of time if a successful outcome was to beexpected. Knocker6 has presented .evidence which suggeststhat severe hypothermia causes considerable disturbance tothe liver and other intestinal organs, though Rosomoff9denies this. It would appear from current literature(Delorme10) that hypothermia may cause derangement inthe normal biochemical relationships in the body; the ma-jority of these derangements being apparently of unknownorigin. It may be assumed that hypothermia, possibly even'light' hypothermia, as defined by Delorme,lo is not withoutcertain inherent dangers when used over a period of somedays.Certain types of life-threatening poliomyelitis (Lassenll)carry a high mortality, and it was considered that, thcughhypothermia may be dangerous, the risks specific to certaincases of acute bulbo-spinal encephalitis were so great, andthe residual degree of paralysis in those surviving so appalling,that hypothermia was justified; firstly, as a means of savinglife and, secondly, as a possible means of reducing theresidual paralysis. -Lqssenll and Engstrom12 have both reported very highmortality rates in cases of acute bulbo-spinal polio-ence-phalitis with hyperpyrexia, and our past experiences havebeen similar.METHODSCooling was effected by a water bed under the patient.Iced water was run in by gravity. Shivering was preventedby giving intravenous promethazine, 25 mg., cWorpromazine,25 mg., and pethidine, 50 mg., which was repeated if shiver-ing recurred. In all cases, once the temperature had beenbrought down to the required level, a maintenance dosewas rarely required.It was found that, provided the whole of the' back wascooled, it was not necessary to apply cooling agents to theother parts ef the body. The time to reach the requiredtemperature was about 5 hour and was therefore slowerthan is usually convenient in an operating theatre.The water bed was emptied when the temperature haddropped to within 2° - 3°C. (}o - 5°E) of the required level,and iced water was again run in if the temperature showedsigns of rising. In order to control ventilation and electrolytebalances in the acute phase, daily blood amples were takenfor the estimations of pH., PaC02 , electrolytes, and PCV.The body temperature was taken with a low-reading ther-mometer in the rectum. Blood pressure, pulse rates, andtemperatures were taken half-hourly. 'One patient was cooled down to 27· 5°C. (81' 5°E) for24 hours. This patient died at the end of 4 hours when thetemperature had been allowed to rise slowly to 35°C. (95°E).Another 5 were cooled to 32° - 34°C. (89' 6° - 93· 2°F.) forperiods of 2 - 6 days. One was kept at this temperaturefor 18 days. Another patient was kept at 35· 5°C. (95' 9°F.)for 12 days. Six patients were maintained afterwards at anormal temperature for a week or 0 by keeping them onthe water bed filled with tap-water.The following are two illustrative case historie :Case 1European male, aged 24. Height 6 ft. Weight 12 t. Admittedon 18 May 1957 from a hospital 100 miJes away where inter-mittent positive-pressure respiration had been instituted on 17May 1957.On admission. Complete paralysis of aB limbs, intercostals,diaphragm, and pharyngeal muscles; and diplopia, internalstrabismus and nystagmus were present. Temp. 39· 5°C. (103°F.).Blood pressure 280/140 mm. Hg. Arterial CO. tension 39 mm. Hg.Progress. The temperature varied between 39· 5° - 40· 5°C.(103° - 105°F.) for the next 5 days. The patient was cooled onthe sixth day after admission to 31 ° - 34· 5°C. ( 8° - 94°F.). Thiswas continued for the next 6 days, and thereafter the temperaturewas maintained at 36· 7°C. (98°F.) for a further 2 weeks. Thehypertension was controlled during the cooling period with 'an 0-lysen' and 'mecamylamine'. Swallowing returned on 10 September1957, i.e. 4 months after the onset of the disease.Case 2European female, aged 20. Height 5 ft. 6 inches. Weight 10 st.Admitted on 30 August 1957 on the third day of the illness.On admission. Temp. 39· 5°C. (1 03· 2°F.). Stiffness of neckand back, considerable agitation, and weakness of biceps onboth sides and of tbeabdorninal muscles were present. Vital capacity1,900 m1. Vomiting persistent. Respiration became paradoxicaJsoon after admission, Cooling was begun on the day of admissionand w~ maintained at 31° - 34· 5°C. ( ° - 94°F.) for 5 daysfrom the second day after admission.Progress. During the subsequent course of the illness her vitalcapacity fell to 500 m1. and necessitated artificial ventiJation in atank. She then developed ocular motor palsies, facial paralysis,and bulbar paralysis necessitating tracheotomy and intermittentpositive-pressure respiration. She was comatose for 24 hours atthis juncture. Four day after cessation of cooling, she developedacute dilatation of the stomach. Some 4 months later she was-5733574 S.A. MEDICAL JOURNAL 15 July 1961fio~ to the United Kingdom. At this time both her legs wereqwte powerful, but the arms were severely paralysed with move-ments present only in the fingers, and she had no measurablevital capacity.RESULTSOf the 9 patients treated by cooling 3 died. The 3 deathsoccurred among the 8 who had bulbo-spinal paralysis andwho were treated with intermittent positive-pressure respira-tion. The ninth patient was treated in a tank respirator.Three patients showed hyperpyrexia, with sustainedtemperatures or rising temperatures above 40°C. (I04°E)and lasting from 3 to 10 days after the onset of paralysis,and this was also associated with hypotension or hyper-tension. The remaining 6 patients all had temperaturesabove 39°C. (I02°F.) and tbis was associated with hyper-tension, paralytic ileus, and pulmonary thrombosis in 1,acute dilatation of stomach, and coma in 2, and hypotensionin 1. The mortality rate for these complications, as given byLassen,13 is shock 65 %, hyperpyrexia 91 % and hypertension42%. . 'All 3 of our patients showing hyperpyrexia survived,whereas previously all our adult patients with hyperpyrexiahad died. It is perhaps of significance that all 3 patientsin tills series who died were inadvertently allowed to coolbelow 31°C. (88°F.) for short periods, and certainly 1 whodied was allowed to cool too low to 26· 1°C. (79°F.), and1 other patient was cooled for too long-18 days. Of the 6who survived only 2 ever reached these figures.ECG ChangesTwenty-four electrocardiograms were taken in 7 patientswhose temperatures varied between 30° and 35°C. (86°-95°F.). All showed a prolonged QT interval. Two showeda partial right bundle-branch block and 2 showed occasionalectopic beats. Large wide P waves and marked clockwiserotation of a vertical heart was observed in 1 of the patientsshowing partial right bundle-branch block, and the changeswere present at 34·3°C. (93·7°F.) and reverted to normalwhen the temperature reached 37°C. (98' 6°F.). The otherpatient with partial right bundle-branch block, whosetemperature had risen to 36·4°C. (97' 5°E), showed deepS waves in Lead I, deep Q waves in Lead m, plus a secondaryR wave in VR with a clockwise rotation of a vertical heart.This patient died of an auricular thrombus extending intothe right ventricle and both pulmonary arteries. Dundeeet 01. 14 recorded a patient dying of pulmonary embolism13 days after freezing.An injury-potential was seen in 2 cases, one at 30°C.(86°F.) and the other at 32· 8°C. (91' 2°E). The injury-potential was well marked in the former, and was associatedwith a respiratory and metabolic acidosis, pH 7·28, andPaC02 51· 8 mm. Hg. The latter patient also had a moderatedegree of respiratory acidosis, pH 7'37, and PaCO. 49·7mm. Hg. -Pulse RatesAll patients showed considerable tachycardia in thepyrexial phase, i.e. 100 - 160 (mean 134). With one exceptionall pul e rates slowed on cooling, the mean degree of fallbeing 40 per min.DISCUSSIOWe have used light hypothermia in 9 patients. Of these3 died, 1 on the 6th, 1 on the 9th, and 1 on the 26th day of~l1ness. In the prolonged cooling, which may be necessaryill the treatment of acute life-threatening poliomyelitis thereis difficulty in defining certain fundamental points, i.e: whento .cool, the degree of cooling, the duration of cooling,which cases to cool, and whether the cooling should beconsistently to the same degree. Reference to the literaturegives little help in solving these problems, and our criteriawere therefore understandably somewhat empirical.On theoretical grounds, from the evidence presented byRosomoff,9 it might appear that the reduction in oxygenconsumption and metabolism, the reduction in volume ofthe bram (and presumably the spinal cord), and possiblyan effect on the virus itself would justify the use of thistechnique.Although 4 of the cooled patients showed a considerableprolongation of the time during which paralysis was spread-ing, we do not consider that there was any startling evidencethat hypothermia in any way reduced the degree of paralysisin the acute phase. We feel that the numbers are far toosmall to say whether hypothermia reduced the degree ofresidual paralysis. Certainly in our cases the evidence wasnot strong enough to be convincing.It is considered that severely ill patients with acute life-threatening poliomyelitis should not be cooled below 32· 2°C.(90°F.). No useful purpose seems to be served in prolongingcooling for more than 5 or 6 days. Cases of hyperpyrexiain adults should be cooled. We are unable to comment onthe questions when to cool and whether the cooling shouldconsistently be to the same degree.Degree of fall of temperature. Fall of temperature variedfrom 3.3° to 11°C. (6° - 20°F.). Times taken to reach thelowest temperatures were 4 - 18 hours.In only 1 patient was the degree of 'after drop' alarming.In this case the cooling mass was withdrawn at 37· 2°C.(99°P.) and thereafter the temperature fell another 7·2°C.(BOE), i.e. to 30°C. (86°F.) during the next 3-;- hours. Thispatient was an overweight male-height 6 ft., weight 16-;-stone.SUMMARYThe use of light hypothermia is described in 9 cases of life-threatening bulbo-spinal poliomyelitis; of these 3 died. Thereasons for using this technique and some of the difficultiesencountered in planning the application of hypothermia arebriefly described.It is considered that hypothermia reduced the mortalityrate in severe bulbo-spinal paralysis.There was little evidence that the degree of residual paralysiswas reduced.We should like to thank the staff of the Medical ResearchLaboratory and the Administrative and Nursing Staff of KingGeorge VI Hospital for their invaluable assistance given to uswhen this work was being carried out.REFERE 'CESI. Miorner, G., Hacger, K. and Ryd, H. (l955): Lancet, 2, 593.2. Janos. M.: Personal communication.3. Idem (l956): Orv. Hetil .• 716.4. Idem (1956): Ibid., 719.5. Russell, W. R. (1955): Lancet, I, 457.6. Ross, D. N. (1956): Proe. Roy. Soc. Med., 49, 365.7. Gray, T. C. (1957): Lancet, I, 383.8. Knocker, P. (1955): Ibid., 2, 837.9. Rosomoff, H. L. (1956): Proc. Roy. Soc. Med., 49, 545.10. Delorme, E. J. (l956): Ibid., 49, 368.11. Lassen, H. C. (1955): \YId Hlth Org. teehn. Rep. Ser., Poliomyelitis, p. 177.12. EngslTom, G. G. (1954): Brit. Med. J., 2, 666.13. Lassen, H. C. (19.58).: International Poliomyelitis Congress. 4th Conference,p. 72. London: LtppUleott.14. Dundee, J. W., Cecil Gray, T., Mesham, P. R. and Scott W. E. B. (1953):Brit. Med. J., 2, 1237. '

THE USE OF LIGHT HYPOTHERMIA IN ACUTE LIFE-THREATENING POLIOMYELITIS

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THE USE OF LIGHT HYPOTHERMIA IN ACUTE LIFE-THREATENING POLIOMYELITIS

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