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In the early part of 1922 seven cases of encephalitis lethargica were treated at the Apia Hospital, and, as these are the first cases to be recognized in Samoa, they appear worthy of being reported.

There are several points of interest in this minor “epidemic.” The first case was admitted to hospital on the 12th February, and the last case on the 20th April, a period of 10 weeks. The patients were drawn from different parts of the island of Upolu, and in no instances could any contact or other possibility of case infection be established. No cases were reported from Eastern Samoa; in fact the American authorities stopped all passenger traffic from Apia to Pago Pago. In all probability there were many more sufferers who were not brought to hospital, but a careful watch has revealed no fresh case since April.

The months February-April fall in the wet season, and, as a rule, are the most unpleasant months of the year; but during the period under review the weather was much better than the average. The amount of sickness at that time was not great. There had been an epidemic of mild measles in July-September, 1921, but this had died out before February, 1922, only sporadic cases being reported. Samoa suffered severely during the influenza epidemic of 1918, and there was another epidemic, not so severe as the first one, in 1920 when the Prince of Wales visited Apia. Since that time influenza has been of the ordinary mild type and never very prevalent.

In this series there were 5 males and 2 females, the ages ranging from 8 years and 30 years. None of the cases, with the exception of case 7, gave any history of illness preceding the onset of encephalitis lethargica. There were two deaths. Case 5, after a temporary improvement, became comatose and was finally removed by his friends to die at home shortly afterwards; case 6 died of acute heart failure, evidently due to involvement of the vagus. All the other cases made complete recoveries. Case 3 showed no sign of lethargy or paralysis, the predominant symptom being rhythmical clonic contractions of the abdominal muscles and of the limbs. Case 7 was very similar to case 3, but in addition he showed some lethargy, squint, ptosis and facial paralysis. The remainder of the cases gave a more typical picture with lethargy and more or less extensive paralysis.

The blood picture showed a moderate leucocytosis except in case 3, in which the white count was 21,100. All of the other cases had counts of from 8,200 to 14,300. Normally a Samoan has a relatively high white count, so that the leococytosis was moderate. The differential count showed some increase in the polymorphs.

The urine in all cases was normal. Lumbar puncture was not done in any case. In none of these cases was the temperature high.

Cases 1 and 2 had a slow pulse rate (between 60 and 70) which rose to the normal with the establishment of convalescence. Case 5 had also a slow pulse which, at one period, became irregular, showing coupling of beats. Later, as his condition became grave, the pulse rate increased and became regular. Case 6 had a pulse rate of from 60 to 70 until shortly before death.

The treatment adopted was the administration of hexamine by the mouth and the production of a fixation abscess by the injection of turpentine under the skin of the thigh. This was done in six cases with one death. Although it is unsound to dogmatise on such a small number of cases, I feel sure that the turpentine injections were of some use. In each instance improvement was noticed within 48 hours of the injection. Case 5, who died, showed a slight improvement after the injection but this was merely temporary. Case 3 was better for three days after the injection, but the symptoms returned with renewed vigour for several days; finally she made a complete recovery. In the other four cases the improvement was maintained without interruption. It was especially noticeable in cases 1,2, and 4; these patients were becoming more lethargic until the administration of turpentine, but 36 hours after a distinct improvement was noticed. Case 6 was not given an injection. The inconvenience of this treatment to the patient was not great, and I should certainly recommend it in every case of lethargic encephalitis.

Case1.—Samoan male; 13 years. Onset gradual; giddiness, squint, diplopia, drowsy. Parents volunteered the information that he was restless and sleepless at night, rambling about the house and talking irrationally. Admitted on the fourth day of the disease. Drowsy, slow cerebration, irritable if roused, twitching of hands and feet, ptosis, strabismus, and facial paralysis. The fundi were normal, ears normal, no rigidity of the neck muscles, no Kernig’s; urine negative; W. B. C. 14,000; polymorphs, 46 per cent. He became more lethargic until the sixth day of the disease, when he was given hexamine by the mouth and turpentine, m.8, subcutaneously. On the eighth day slight improvement was noticed and this continued without interruption. Slight facial paralysis was noted on the thirty-third day. He was remained in good health since.

Case 2.—Samoan male; 12 years. Onset gradual with vomiting, fever, giddiness, headache, strabismus, drowsiness, twitching of hands and legs, irrational talking. Admitted on the fifteenth day. Drowsy, slow cerebration, facial paralysis, ptosis, strabismus, twitching of arms, legs and face. W. B. V 14,300; polymorphs 37 per cent. On the sixteenth day put on hexamine and turpentine, m.8, subcutaneously. Improvement noticed on the eighteenth day and this continued. W. B. C. rose to 29,700 after the injection, the polymorphs being now 54 per cent. On the twenty-fifth day there was a very slight facial paralysis. He was discharged well on the thirty-third day.

Case 3.—Samoan female; 30 years. Onset gradual with pain in the ride hand, later passing up to elbow and shoulder. On the seventh day clonic rhythmical spasms of the abdominal muscles. Admitted to hospital on the fourteenth day. There were no lethargic symptoms; clonic spasms of the abdominal muscles, and of the left leg. There was no hyperæsthesia. On the fifteenth day the W. B. C. was 21,000, the polymorphs being 81.5 per cent. On the sixteenth day the arms were also affected. She was given hexamine and turpentine, m.15, subcutaneously. On the seventeenth and eighteenth days she was better. W. B. C 26,800; polymorphs 77.5 per cent. On the nineteenth day the twitching was worse, the face muscles being also involved. Slept badly at night and talked incessantly in her sleep. On the twenty-second day there was some improvement. On the thirty-third she appeared well. She was discharged on the thirty-fourth day. In additional to the treatment mentioned she received morphia and veronal on several occasions, as her mental state was one of great anxiety.

Case 4.—Samoan, female; 11 years. Onset gradual with increasing drowsiness, squint, facial paralysis, and twitching of legs and arms. W. B. C. 11,400; polymorphs, 75 per cent. Admitted on fifth day, the symptoms being as detailed above. She vomited once on this day. On seventh day she seemed a little brighter. On the eighth day she was much more lethargic. Turpentine, m.15, was injected. On the ninth day she was brighter, and the symptoms cleared up rapidly from this date. On the fourteenth day a pemphigoid rash appeared on the body. She was discharged on the nineteenth day.

Case 5.—Samoan, male; 8 years. History of three weeks’ illness; abdominal pain, headache and fever. On the eighteenth day he vomited and complained of pain in the left chest. Admitted on the twenty-first day. There was some tenderness of the abdomen with slight distension. Some questionable signs at the left base. W. B. C. 11,500; polymorphs 73.5 per cent. On the twenty-third day he was given a second injection of m.10. On twenty-eighth day he was seemed far better but on the thirtieth day he was worse, passing urine involuntarily. On the thirty-first day he has right facial paralysis and twitching of the right hand and left side of face, and on the thirty-third day his condition was very bad; he was restless and noisy; pulse slow and irregular, and respirations of the Cheyne-Stokes type. He has also difficulty in swallowing. On the thirty-sixth day his condition was obviously hopless and he was taken home by his relatives. He died soon afterwards.

Case 6.—Samoan, male: 17 years. History of vomiting and diarrhœa five days before admission to hospital, but he had appeared well until sudden onset of illness. The day of admission, sixth day, he suddenly developed epileptiform convulsions. W. B. C., 9,100; polymorphs 72 per cent. On the seventh and eighth days he was very drowsy and could only be roused with difficulty; irritable squint noticed. On the ninth day he vomited without obvious cause. On the tenth day his general condition seemed better, but he was still vomiting. On the eleventh day a miliary rash appeared on the body; still vomiting. On the twelfth day his condition was good, but he was still vomiting. On the thirteenth day he suddenly developed symptoms of acute dilatation of the heart, and he died in less than an hour’s time.

Case 7.—Chinese male [sic]; 28 years. This man was admitted to hospital in January with symptoms of incipient beri-beri. Six weeks after admission he complained of severe headache, fever (101.6F.), and twitching of muscles of abdomen and legs. He had difficulty in passing urine. W. B. C. 8,200; polymorphs 69 per cent. Next day he had ptosis of left eyelid; doubtful squint; right facial paralysis. He was very drowsy and slow in answering questions. He was given hexamine and turpentine, m.20, subcutaneously. Three days after the injection—W. B. C. 15,900; polymorphs 89 per cent. He started to improve almost immediately and was recovered in a fortnight.

I have to thank Dr. Trail, C. M. O., for permission to publish these notes, Dr. Armstrong for the notes on case 7, Dr. Veitch in whose wards the Samoan cases were treated; and Mr. C. E. Berry who did all the blood counts.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

Nil.

NZMJ, 1922, pp.267-271

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

In the early part of 1922 seven cases of encephalitis lethargica were treated at the Apia Hospital, and, as these are the first cases to be recognized in Samoa, they appear worthy of being reported.

There are several points of interest in this minor “epidemic.” The first case was admitted to hospital on the 12th February, and the last case on the 20th April, a period of 10 weeks. The patients were drawn from different parts of the island of Upolu, and in no instances could any contact or other possibility of case infection be established. No cases were reported from Eastern Samoa; in fact the American authorities stopped all passenger traffic from Apia to Pago Pago. In all probability there were many more sufferers who were not brought to hospital, but a careful watch has revealed no fresh case since April.

The months February-April fall in the wet season, and, as a rule, are the most unpleasant months of the year; but during the period under review the weather was much better than the average. The amount of sickness at that time was not great. There had been an epidemic of mild measles in July-September, 1921, but this had died out before February, 1922, only sporadic cases being reported. Samoa suffered severely during the influenza epidemic of 1918, and there was another epidemic, not so severe as the first one, in 1920 when the Prince of Wales visited Apia. Since that time influenza has been of the ordinary mild type and never very prevalent.

In this series there were 5 males and 2 females, the ages ranging from 8 years and 30 years. None of the cases, with the exception of case 7, gave any history of illness preceding the onset of encephalitis lethargica. There were two deaths. Case 5, after a temporary improvement, became comatose and was finally removed by his friends to die at home shortly afterwards; case 6 died of acute heart failure, evidently due to involvement of the vagus. All the other cases made complete recoveries. Case 3 showed no sign of lethargy or paralysis, the predominant symptom being rhythmical clonic contractions of the abdominal muscles and of the limbs. Case 7 was very similar to case 3, but in addition he showed some lethargy, squint, ptosis and facial paralysis. The remainder of the cases gave a more typical picture with lethargy and more or less extensive paralysis.

The blood picture showed a moderate leucocytosis except in case 3, in which the white count was 21,100. All of the other cases had counts of from 8,200 to 14,300. Normally a Samoan has a relatively high white count, so that the leococytosis was moderate. The differential count showed some increase in the polymorphs.

The urine in all cases was normal. Lumbar puncture was not done in any case. In none of these cases was the temperature high.

Cases 1 and 2 had a slow pulse rate (between 60 and 70) which rose to the normal with the establishment of convalescence. Case 5 had also a slow pulse which, at one period, became irregular, showing coupling of beats. Later, as his condition became grave, the pulse rate increased and became regular. Case 6 had a pulse rate of from 60 to 70 until shortly before death.

The treatment adopted was the administration of hexamine by the mouth and the production of a fixation abscess by the injection of turpentine under the skin of the thigh. This was done in six cases with one death. Although it is unsound to dogmatise on such a small number of cases, I feel sure that the turpentine injections were of some use. In each instance improvement was noticed within 48 hours of the injection. Case 5, who died, showed a slight improvement after the injection but this was merely temporary. Case 3 was better for three days after the injection, but the symptoms returned with renewed vigour for several days; finally she made a complete recovery. In the other four cases the improvement was maintained without interruption. It was especially noticeable in cases 1,2, and 4; these patients were becoming more lethargic until the administration of turpentine, but 36 hours after a distinct improvement was noticed. Case 6 was not given an injection. The inconvenience of this treatment to the patient was not great, and I should certainly recommend it in every case of lethargic encephalitis.

Case1.—Samoan male; 13 years. Onset gradual; giddiness, squint, diplopia, drowsy. Parents volunteered the information that he was restless and sleepless at night, rambling about the house and talking irrationally. Admitted on the fourth day of the disease. Drowsy, slow cerebration, irritable if roused, twitching of hands and feet, ptosis, strabismus, and facial paralysis. The fundi were normal, ears normal, no rigidity of the neck muscles, no Kernig’s; urine negative; W. B. C. 14,000; polymorphs, 46 per cent. He became more lethargic until the sixth day of the disease, when he was given hexamine by the mouth and turpentine, m.8, subcutaneously. On the eighth day slight improvement was noticed and this continued without interruption. Slight facial paralysis was noted on the thirty-third day. He was remained in good health since.

Case 2.—Samoan male; 12 years. Onset gradual with vomiting, fever, giddiness, headache, strabismus, drowsiness, twitching of hands and legs, irrational talking. Admitted on the fifteenth day. Drowsy, slow cerebration, facial paralysis, ptosis, strabismus, twitching of arms, legs and face. W. B. V 14,300; polymorphs 37 per cent. On the sixteenth day put on hexamine and turpentine, m.8, subcutaneously. Improvement noticed on the eighteenth day and this continued. W. B. C. rose to 29,700 after the injection, the polymorphs being now 54 per cent. On the twenty-fifth day there was a very slight facial paralysis. He was discharged well on the thirty-third day.

Case 3.—Samoan female; 30 years. Onset gradual with pain in the ride hand, later passing up to elbow and shoulder. On the seventh day clonic rhythmical spasms of the abdominal muscles. Admitted to hospital on the fourteenth day. There were no lethargic symptoms; clonic spasms of the abdominal muscles, and of the left leg. There was no hyperæsthesia. On the fifteenth day the W. B. C. was 21,000, the polymorphs being 81.5 per cent. On the sixteenth day the arms were also affected. She was given hexamine and turpentine, m.15, subcutaneously. On the seventeenth and eighteenth days she was better. W. B. C 26,800; polymorphs 77.5 per cent. On the nineteenth day the twitching was worse, the face muscles being also involved. Slept badly at night and talked incessantly in her sleep. On the twenty-second day there was some improvement. On the thirty-third she appeared well. She was discharged on the thirty-fourth day. In additional to the treatment mentioned she received morphia and veronal on several occasions, as her mental state was one of great anxiety.

Case 4.—Samoan, female; 11 years. Onset gradual with increasing drowsiness, squint, facial paralysis, and twitching of legs and arms. W. B. C. 11,400; polymorphs, 75 per cent. Admitted on fifth day, the symptoms being as detailed above. She vomited once on this day. On seventh day she seemed a little brighter. On the eighth day she was much more lethargic. Turpentine, m.15, was injected. On the ninth day she was brighter, and the symptoms cleared up rapidly from this date. On the fourteenth day a pemphigoid rash appeared on the body. She was discharged on the nineteenth day.

Case 5.—Samoan, male; 8 years. History of three weeks’ illness; abdominal pain, headache and fever. On the eighteenth day he vomited and complained of pain in the left chest. Admitted on the twenty-first day. There was some tenderness of the abdomen with slight distension. Some questionable signs at the left base. W. B. C. 11,500; polymorphs 73.5 per cent. On the twenty-third day he was given a second injection of m.10. On twenty-eighth day he was seemed far better but on the thirtieth day he was worse, passing urine involuntarily. On the thirty-first day he has right facial paralysis and twitching of the right hand and left side of face, and on the thirty-third day his condition was very bad; he was restless and noisy; pulse slow and irregular, and respirations of the Cheyne-Stokes type. He has also difficulty in swallowing. On the thirty-sixth day his condition was obviously hopless and he was taken home by his relatives. He died soon afterwards.

Case 6.—Samoan, male: 17 years. History of vomiting and diarrhœa five days before admission to hospital, but he had appeared well until sudden onset of illness. The day of admission, sixth day, he suddenly developed epileptiform convulsions. W. B. C., 9,100; polymorphs 72 per cent. On the seventh and eighth days he was very drowsy and could only be roused with difficulty; irritable squint noticed. On the ninth day he vomited without obvious cause. On the tenth day his general condition seemed better, but he was still vomiting. On the eleventh day a miliary rash appeared on the body; still vomiting. On the twelfth day his condition was good, but he was still vomiting. On the thirteenth day he suddenly developed symptoms of acute dilatation of the heart, and he died in less than an hour’s time.

Case 7.—Chinese male [sic]; 28 years. This man was admitted to hospital in January with symptoms of incipient beri-beri. Six weeks after admission he complained of severe headache, fever (101.6F.), and twitching of muscles of abdomen and legs. He had difficulty in passing urine. W. B. C. 8,200; polymorphs 69 per cent. Next day he had ptosis of left eyelid; doubtful squint; right facial paralysis. He was very drowsy and slow in answering questions. He was given hexamine and turpentine, m.20, subcutaneously. Three days after the injection—W. B. C. 15,900; polymorphs 89 per cent. He started to improve almost immediately and was recovered in a fortnight.

I have to thank Dr. Trail, C. M. O., for permission to publish these notes, Dr. Armstrong for the notes on case 7, Dr. Veitch in whose wards the Samoan cases were treated; and Mr. C. E. Berry who did all the blood counts.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

Nil.

NZMJ, 1922, pp.267-271

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

In the early part of 1922 seven cases of encephalitis lethargica were treated at the Apia Hospital, and, as these are the first cases to be recognized in Samoa, they appear worthy of being reported.

There are several points of interest in this minor “epidemic.” The first case was admitted to hospital on the 12th February, and the last case on the 20th April, a period of 10 weeks. The patients were drawn from different parts of the island of Upolu, and in no instances could any contact or other possibility of case infection be established. No cases were reported from Eastern Samoa; in fact the American authorities stopped all passenger traffic from Apia to Pago Pago. In all probability there were many more sufferers who were not brought to hospital, but a careful watch has revealed no fresh case since April.

The months February-April fall in the wet season, and, as a rule, are the most unpleasant months of the year; but during the period under review the weather was much better than the average. The amount of sickness at that time was not great. There had been an epidemic of mild measles in July-September, 1921, but this had died out before February, 1922, only sporadic cases being reported. Samoa suffered severely during the influenza epidemic of 1918, and there was another epidemic, not so severe as the first one, in 1920 when the Prince of Wales visited Apia. Since that time influenza has been of the ordinary mild type and never very prevalent.

In this series there were 5 males and 2 females, the ages ranging from 8 years and 30 years. None of the cases, with the exception of case 7, gave any history of illness preceding the onset of encephalitis lethargica. There were two deaths. Case 5, after a temporary improvement, became comatose and was finally removed by his friends to die at home shortly afterwards; case 6 died of acute heart failure, evidently due to involvement of the vagus. All the other cases made complete recoveries. Case 3 showed no sign of lethargy or paralysis, the predominant symptom being rhythmical clonic contractions of the abdominal muscles and of the limbs. Case 7 was very similar to case 3, but in addition he showed some lethargy, squint, ptosis and facial paralysis. The remainder of the cases gave a more typical picture with lethargy and more or less extensive paralysis.

The blood picture showed a moderate leucocytosis except in case 3, in which the white count was 21,100. All of the other cases had counts of from 8,200 to 14,300. Normally a Samoan has a relatively high white count, so that the leococytosis was moderate. The differential count showed some increase in the polymorphs.

The urine in all cases was normal. Lumbar puncture was not done in any case. In none of these cases was the temperature high.

Cases 1 and 2 had a slow pulse rate (between 60 and 70) which rose to the normal with the establishment of convalescence. Case 5 had also a slow pulse which, at one period, became irregular, showing coupling of beats. Later, as his condition became grave, the pulse rate increased and became regular. Case 6 had a pulse rate of from 60 to 70 until shortly before death.

The treatment adopted was the administration of hexamine by the mouth and the production of a fixation abscess by the injection of turpentine under the skin of the thigh. This was done in six cases with one death. Although it is unsound to dogmatise on such a small number of cases, I feel sure that the turpentine injections were of some use. In each instance improvement was noticed within 48 hours of the injection. Case 5, who died, showed a slight improvement after the injection but this was merely temporary. Case 3 was better for three days after the injection, but the symptoms returned with renewed vigour for several days; finally she made a complete recovery. In the other four cases the improvement was maintained without interruption. It was especially noticeable in cases 1,2, and 4; these patients were becoming more lethargic until the administration of turpentine, but 36 hours after a distinct improvement was noticed. Case 6 was not given an injection. The inconvenience of this treatment to the patient was not great, and I should certainly recommend it in every case of lethargic encephalitis.

Case1.—Samoan male; 13 years. Onset gradual; giddiness, squint, diplopia, drowsy. Parents volunteered the information that he was restless and sleepless at night, rambling about the house and talking irrationally. Admitted on the fourth day of the disease. Drowsy, slow cerebration, irritable if roused, twitching of hands and feet, ptosis, strabismus, and facial paralysis. The fundi were normal, ears normal, no rigidity of the neck muscles, no Kernig’s; urine negative; W. B. C. 14,000; polymorphs, 46 per cent. He became more lethargic until the sixth day of the disease, when he was given hexamine by the mouth and turpentine, m.8, subcutaneously. On the eighth day slight improvement was noticed and this continued without interruption. Slight facial paralysis was noted on the thirty-third day. He was remained in good health since.

Case 2.—Samoan male; 12 years. Onset gradual with vomiting, fever, giddiness, headache, strabismus, drowsiness, twitching of hands and legs, irrational talking. Admitted on the fifteenth day. Drowsy, slow cerebration, facial paralysis, ptosis, strabismus, twitching of arms, legs and face. W. B. V 14,300; polymorphs 37 per cent. On the sixteenth day put on hexamine and turpentine, m.8, subcutaneously. Improvement noticed on the eighteenth day and this continued. W. B. C. rose to 29,700 after the injection, the polymorphs being now 54 per cent. On the twenty-fifth day there was a very slight facial paralysis. He was discharged well on the thirty-third day.

Case 3.—Samoan female; 30 years. Onset gradual with pain in the ride hand, later passing up to elbow and shoulder. On the seventh day clonic rhythmical spasms of the abdominal muscles. Admitted to hospital on the fourteenth day. There were no lethargic symptoms; clonic spasms of the abdominal muscles, and of the left leg. There was no hyperæsthesia. On the fifteenth day the W. B. C. was 21,000, the polymorphs being 81.5 per cent. On the sixteenth day the arms were also affected. She was given hexamine and turpentine, m.15, subcutaneously. On the seventeenth and eighteenth days she was better. W. B. C 26,800; polymorphs 77.5 per cent. On the nineteenth day the twitching was worse, the face muscles being also involved. Slept badly at night and talked incessantly in her sleep. On the twenty-second day there was some improvement. On the thirty-third she appeared well. She was discharged on the thirty-fourth day. In additional to the treatment mentioned she received morphia and veronal on several occasions, as her mental state was one of great anxiety.

Case 4.—Samoan, female; 11 years. Onset gradual with increasing drowsiness, squint, facial paralysis, and twitching of legs and arms. W. B. C. 11,400; polymorphs, 75 per cent. Admitted on fifth day, the symptoms being as detailed above. She vomited once on this day. On seventh day she seemed a little brighter. On the eighth day she was much more lethargic. Turpentine, m.15, was injected. On the ninth day she was brighter, and the symptoms cleared up rapidly from this date. On the fourteenth day a pemphigoid rash appeared on the body. She was discharged on the nineteenth day.

Case 5.—Samoan, male; 8 years. History of three weeks’ illness; abdominal pain, headache and fever. On the eighteenth day he vomited and complained of pain in the left chest. Admitted on the twenty-first day. There was some tenderness of the abdomen with slight distension. Some questionable signs at the left base. W. B. C. 11,500; polymorphs 73.5 per cent. On the twenty-third day he was given a second injection of m.10. On twenty-eighth day he was seemed far better but on the thirtieth day he was worse, passing urine involuntarily. On the thirty-first day he has right facial paralysis and twitching of the right hand and left side of face, and on the thirty-third day his condition was very bad; he was restless and noisy; pulse slow and irregular, and respirations of the Cheyne-Stokes type. He has also difficulty in swallowing. On the thirty-sixth day his condition was obviously hopless and he was taken home by his relatives. He died soon afterwards.

Case 6.—Samoan, male: 17 years. History of vomiting and diarrhœa five days before admission to hospital, but he had appeared well until sudden onset of illness. The day of admission, sixth day, he suddenly developed epileptiform convulsions. W. B. C., 9,100; polymorphs 72 per cent. On the seventh and eighth days he was very drowsy and could only be roused with difficulty; irritable squint noticed. On the ninth day he vomited without obvious cause. On the tenth day his general condition seemed better, but he was still vomiting. On the eleventh day a miliary rash appeared on the body; still vomiting. On the twelfth day his condition was good, but he was still vomiting. On the thirteenth day he suddenly developed symptoms of acute dilatation of the heart, and he died in less than an hour’s time.

Case 7.—Chinese male [sic]; 28 years. This man was admitted to hospital in January with symptoms of incipient beri-beri. Six weeks after admission he complained of severe headache, fever (101.6F.), and twitching of muscles of abdomen and legs. He had difficulty in passing urine. W. B. C. 8,200; polymorphs 69 per cent. Next day he had ptosis of left eyelid; doubtful squint; right facial paralysis. He was very drowsy and slow in answering questions. He was given hexamine and turpentine, m.20, subcutaneously. Three days after the injection—W. B. C. 15,900; polymorphs 89 per cent. He started to improve almost immediately and was recovered in a fortnight.

I have to thank Dr. Trail, C. M. O., for permission to publish these notes, Dr. Armstrong for the notes on case 7, Dr. Veitch in whose wards the Samoan cases were treated; and Mr. C. E. Berry who did all the blood counts.

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

Nil.

NZMJ, 1922, pp.267-271

Contact diana@nzma.org.nz
for the PDF of this article

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