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A case of haematemesis of bilharzial origin
574 TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE.
Vol. 49.
No. 6.
November, 1955.
A CASE OF HAEMATEMESIS
OF BILHARZIAL
ORIGIN
BY I. R . M I L N E
M.D. AND W .
J. E. D A R L I N G , M.B., D.T.M. •
H.
Salisbury, Southern Rhodesia. Clinical history. A E u r o p e a n girl, aged'4½ years, h a d b e e n o u t of sorts for a week. She h a d a t t e n d e d a c h i l d r e n ' s p a r t y o n 18th J u n e , 1954. O n the following day, 19th J u n e , she was listless a n d her m o t h e r k e p t h e r i n bed, t h i n k i n g t h a t the child h a d a b i l i o u s attack. O n this day t h e r e was n o rise of t e m p e r a t u r e a n d t h e bowels h a d o p e n e d . O n the m o r n i n g of 20th J u n e , t h e r e was v o m i t i n g - bile s t a i n e d a n d w a t e r y - a n d at 3 p.m. t h e r e was a f u r t h e r v o m i t w h i c h t h e m o t h e r t h o u g h t c o n t a i n e d blood. A t 5 p.m. m e d i c a l advice was s o u g h t for the first time. On examination the child was seen to have a good colour, T. 97.4°F., P. 110, and Resp. 24. She was not restless but complained of vague discomfort in the upper abdomen. T h e vomit at 3 p.m. had been k e p t - this appeared to be about 2 oz. in amount. It was dark brown and had the appearance of acid digested blood plus mucus threads. A rapid examination of the abdomen revealed no rigidity but there was fullness in the right hypochondrium. At 9 p.m. the child awakened, had a violent bout of vomiting and was re-examined at 9.30 p.m. Temperature was now 102 F., P. 140 and a marked degree of pallor was noted. The vomit was typical of a haematemesis with 2 - 3 oz. blood and blood clot. This specimen was retained for laboratory examination. Next morning, 21st June, the child looked very ill. There had been further vomiting and little urine had been voided in the last 24 hours. The child was admitted to St. Anne's Hospital that afternoon.
Examination now revealed very marked pallor. Temperature was 102°F., and pulse rate 140. No abnormality was detected on clinical examination of the respiratory or circulatory systems. On abdominal examination the liver was found to be tense and tender with the lower margin almost down to the level of the umbilicus. The spleen was also palpable. D i a g n o s i s at this stage was n o w c o n s i d e r e d to b e e n l a r g e m e n t of the liver due to portal congestion a n d r u p t u r e of varices r e s u l t i n g i n haematemesis. T h e cause of this was still undecided.
Laboratory investigations. (1) Both specimens vomit : Acid in reaction, R.B.C. + + and W.B.C. + + . ova found.
No schistosome
(2) Urine (21.VI.54) : Ova of S. haematobium + + + ; R.B.C. + + + ; leucocytes + + + . reaction acid ; S.G. 1024 ; no sugar ; albumin, faint trace. (3) Blood count (21.VI.54) : R.B.C. 3,680,000 per c.mm.; Hb. 59 per cent.; colour index 0.8 ; Total W.B.C., 17,700 per c.mm. Differential W.B.C. : Neutrophils 80 per cent. ; lymphocytes 13 per cent. ; monocytes 7 per cent. ; eosinophils nil. (4)
B.S.R. w 30 m.m. in 1st hour.
(5)
Cercarial skin test was positive.
I . R. M I L N E A N D W .
J. E. D A R L I N G
575
A diagnosis of Schistosoma haematobium infection, with portal congestion, was made. Treatment was commenced on the following day, 22nd June, with anthiomaline 0.5 c.c. given intramuscularly. Thereafter 1 c.c. was given daily until 29th June, when the patient was discharged from hospital. On 21st, 22nd and 23rd June she received systemic penicillin therapy to counter any possible secondary infection. By the time of discharge from hospital, liver and splenic enlargement had decreased considerably and the child looked well. Further treatment with anthiomaline, intramuscularly, was continued as an out-patient until 19th July, by which time a total of 21 c.c. had been given. On 1st August a urine specimen examined at Dr. G. V. Blaine's laboratory showed no ova and no cells. On 2nd August a clinical examination of the child revealed no abnormality of any of the systems, neither liver nor spleen being palpable. It is noteworthy that four specimens of stool examined between 21st June and 1st August showed no schistosome ova.
Associated history. In January, 1954, the family, consisting of mother, brother, aged 15 years, and two sisters, aged 13 years and 61- years, were camping at Mermaid's Pool, some 30 miles from Salisbury. This was the presumed source of infection. While the girl of 4~- years was in hospital, her sister, aged 61- years, was admitted for tonsillectomy. The operation was performed on 22nd June, and 4 hours after operation the child had a very severe haemorrhage from the left tonsillar fossa, which necessitated arrest by ligature under general anaesthesia. On investigation later, this child was found to be suffering from a urinary S. haematobium infection. Blood count was : R.B.C., 3,680,000 ; Hb. 59 per cent.; C.I., 0.8 ; W.B.C., 17,700. Differential : Neutrophils, 80 per cent. ; lymphocytes, 13 per cent. ; monocytes, 7 per cent. The urine contained ova of S. haematobium with R.B.C. + + and leucocytes ++. Unfortunately no further blood investigations were carried out in this case, but one wondered whether the active schistosome infection predisposed this patient to a severe postoperation haemorrhage. The other members of the family were examined, and the eldest sister, aged 13 years, and the brother aged 15 years, were also found to be suffering from schistosome infection. The mother was found to be free.
DISCUSSION
The case under review is deserving of record in view of the comparatively rare features met with : (1) Early age of the subject ; (2) haematemesis with portal congestion ; (3) much enlarged liver and spleen ; (4) hea W S. haematobium infestation. The clinical picture of the toxaemic stage in Southern Rhodesia is very variable (GELFAND, 1942 ; GELFANDand OSBOURNE, 1943). In the case under discussion the systems involved were the gastro-intestinal, reticulo-endothelial and renal. There was no evidence of symptoms or signs suggestive of miliary tuberculosis (RITCHKENand GEFLAND, 1954).
576
H A E M A ' r E M E S I S OF B I L H A R Z I A L O R I G I N
Summary of case.
Age : 4½ years. Presence of pyrexia. Symptomatology : haematemesis and toxic symptoms affecting the liver, portal circulation and renal systems. The weight since January, 1954, had been stationary. Urticarial eruption - - no history was given by the parent that a rash had appeared since January, 1954. Splenomegaly was present. Eosinophilia was not present in spite of the very heavy infection. Pathogenesis.
The mature female schistosomes with fully developed ova in the intestinal canal are found in the portal vein 4 - 6 weeks after the cercariae have pierced the skin or mucous membrane. Once the fully matured female has found her way via the mesenteric vessels to the small venules of the large intestine, ova depositions begin. It is interesting that in the case under review, no early toxaemic symptoms of an intense allergic reaction occurred, but the severe toxaemic symptoms developed 5 - 6 months after the presumed time of infection. Bilharzial hepat!c cirrhosis and s p l e n o m e g a l y - so-called Egyptian s p l e n o m e g a l y - are often important features of S. mansoni infection. When there is markedly increased portal pressure, the spleen may reach enormous dimensions. Haematemesis from ruptured varicose oesophageal veins is a dangerous complication (FAmLEY, 1950). In this case, the infecting agent was S. haematobium and not S. mansoni. REFERENCES FAIRLEY,N. HAMILTON(1950). Brit. Encl. med. Pract., 2, 476. GELFAND, lx~/[.(1942). Clin. Proc., 1, 247. OSBOURNE,H. S. (1943). Ibid., 2, 169. RITCHI~EN,J. & GELFAND, M. (1954). Brit. med. J., 1, 1419.
Vol. 49.
No. 6.
November, 1955.
A CASE OF HAEMATEMESIS
OF BILHARZIAL
ORIGIN
BY I. R . M I L N E
M.D. AND W .
J. E. D A R L I N G , M.B., D.T.M. •
H.
Salisbury, Southern Rhodesia. Clinical history. A E u r o p e a n girl, aged'4½ years, h a d b e e n o u t of sorts for a week. She h a d a t t e n d e d a c h i l d r e n ' s p a r t y o n 18th J u n e , 1954. O n the following day, 19th J u n e , she was listless a n d her m o t h e r k e p t h e r i n bed, t h i n k i n g t h a t the child h a d a b i l i o u s attack. O n this day t h e r e was n o rise of t e m p e r a t u r e a n d t h e bowels h a d o p e n e d . O n the m o r n i n g of 20th J u n e , t h e r e was v o m i t i n g - bile s t a i n e d a n d w a t e r y - a n d at 3 p.m. t h e r e was a f u r t h e r v o m i t w h i c h t h e m o t h e r t h o u g h t c o n t a i n e d blood. A t 5 p.m. m e d i c a l advice was s o u g h t for the first time. On examination the child was seen to have a good colour, T. 97.4°F., P. 110, and Resp. 24. She was not restless but complained of vague discomfort in the upper abdomen. T h e vomit at 3 p.m. had been k e p t - this appeared to be about 2 oz. in amount. It was dark brown and had the appearance of acid digested blood plus mucus threads. A rapid examination of the abdomen revealed no rigidity but there was fullness in the right hypochondrium. At 9 p.m. the child awakened, had a violent bout of vomiting and was re-examined at 9.30 p.m. Temperature was now 102 F., P. 140 and a marked degree of pallor was noted. The vomit was typical of a haematemesis with 2 - 3 oz. blood and blood clot. This specimen was retained for laboratory examination. Next morning, 21st June, the child looked very ill. There had been further vomiting and little urine had been voided in the last 24 hours. The child was admitted to St. Anne's Hospital that afternoon.
Examination now revealed very marked pallor. Temperature was 102°F., and pulse rate 140. No abnormality was detected on clinical examination of the respiratory or circulatory systems. On abdominal examination the liver was found to be tense and tender with the lower margin almost down to the level of the umbilicus. The spleen was also palpable. D i a g n o s i s at this stage was n o w c o n s i d e r e d to b e e n l a r g e m e n t of the liver due to portal congestion a n d r u p t u r e of varices r e s u l t i n g i n haematemesis. T h e cause of this was still undecided.
Laboratory investigations. (1) Both specimens vomit : Acid in reaction, R.B.C. + + and W.B.C. + + . ova found.
No schistosome
(2) Urine (21.VI.54) : Ova of S. haematobium + + + ; R.B.C. + + + ; leucocytes + + + . reaction acid ; S.G. 1024 ; no sugar ; albumin, faint trace. (3) Blood count (21.VI.54) : R.B.C. 3,680,000 per c.mm.; Hb. 59 per cent.; colour index 0.8 ; Total W.B.C., 17,700 per c.mm. Differential W.B.C. : Neutrophils 80 per cent. ; lymphocytes 13 per cent. ; monocytes 7 per cent. ; eosinophils nil. (4)
B.S.R. w 30 m.m. in 1st hour.
(5)
Cercarial skin test was positive.
I . R. M I L N E A N D W .
J. E. D A R L I N G
575
A diagnosis of Schistosoma haematobium infection, with portal congestion, was made. Treatment was commenced on the following day, 22nd June, with anthiomaline 0.5 c.c. given intramuscularly. Thereafter 1 c.c. was given daily until 29th June, when the patient was discharged from hospital. On 21st, 22nd and 23rd June she received systemic penicillin therapy to counter any possible secondary infection. By the time of discharge from hospital, liver and splenic enlargement had decreased considerably and the child looked well. Further treatment with anthiomaline, intramuscularly, was continued as an out-patient until 19th July, by which time a total of 21 c.c. had been given. On 1st August a urine specimen examined at Dr. G. V. Blaine's laboratory showed no ova and no cells. On 2nd August a clinical examination of the child revealed no abnormality of any of the systems, neither liver nor spleen being palpable. It is noteworthy that four specimens of stool examined between 21st June and 1st August showed no schistosome ova.
Associated history. In January, 1954, the family, consisting of mother, brother, aged 15 years, and two sisters, aged 13 years and 61- years, were camping at Mermaid's Pool, some 30 miles from Salisbury. This was the presumed source of infection. While the girl of 4~- years was in hospital, her sister, aged 61- years, was admitted for tonsillectomy. The operation was performed on 22nd June, and 4 hours after operation the child had a very severe haemorrhage from the left tonsillar fossa, which necessitated arrest by ligature under general anaesthesia. On investigation later, this child was found to be suffering from a urinary S. haematobium infection. Blood count was : R.B.C., 3,680,000 ; Hb. 59 per cent.; C.I., 0.8 ; W.B.C., 17,700. Differential : Neutrophils, 80 per cent. ; lymphocytes, 13 per cent. ; monocytes, 7 per cent. The urine contained ova of S. haematobium with R.B.C. + + and leucocytes ++. Unfortunately no further blood investigations were carried out in this case, but one wondered whether the active schistosome infection predisposed this patient to a severe postoperation haemorrhage. The other members of the family were examined, and the eldest sister, aged 13 years, and the brother aged 15 years, were also found to be suffering from schistosome infection. The mother was found to be free.
DISCUSSION
The case under review is deserving of record in view of the comparatively rare features met with : (1) Early age of the subject ; (2) haematemesis with portal congestion ; (3) much enlarged liver and spleen ; (4) hea W S. haematobium infestation. The clinical picture of the toxaemic stage in Southern Rhodesia is very variable (GELFAND, 1942 ; GELFANDand OSBOURNE, 1943). In the case under discussion the systems involved were the gastro-intestinal, reticulo-endothelial and renal. There was no evidence of symptoms or signs suggestive of miliary tuberculosis (RITCHKENand GEFLAND, 1954).
576
H A E M A ' r E M E S I S OF B I L H A R Z I A L O R I G I N
Summary of case.
Age : 4½ years. Presence of pyrexia. Symptomatology : haematemesis and toxic symptoms affecting the liver, portal circulation and renal systems. The weight since January, 1954, had been stationary. Urticarial eruption - - no history was given by the parent that a rash had appeared since January, 1954. Splenomegaly was present. Eosinophilia was not present in spite of the very heavy infection. Pathogenesis.
The mature female schistosomes with fully developed ova in the intestinal canal are found in the portal vein 4 - 6 weeks after the cercariae have pierced the skin or mucous membrane. Once the fully matured female has found her way via the mesenteric vessels to the small venules of the large intestine, ova depositions begin. It is interesting that in the case under review, no early toxaemic symptoms of an intense allergic reaction occurred, but the severe toxaemic symptoms developed 5 - 6 months after the presumed time of infection. Bilharzial hepat!c cirrhosis and s p l e n o m e g a l y - so-called Egyptian s p l e n o m e g a l y - are often important features of S. mansoni infection. When there is markedly increased portal pressure, the spleen may reach enormous dimensions. Haematemesis from ruptured varicose oesophageal veins is a dangerous complication (FAmLEY, 1950). In this case, the infecting agent was S. haematobium and not S. mansoni. REFERENCES FAIRLEY,N. HAMILTON(1950). Brit. Encl. med. Pract., 2, 476. GELFAND, lx~/[.(1942). Clin. Proc., 1, 247. OSBOURNE,H. S. (1943). Ibid., 2, 169. RITCHI~EN,J. & GELFAND, M. (1954). Brit. med. J., 1, 1419.