- Email: [email protected]
Reduction of coma by quinine loading dose in falciparum cerebral malaria
896
haemorrhage within the abdominal cavity. Her history of travel to a malaria-endemic country suggested investigation for malaria as a cause of the splenic rupture. Blood (typed Fya-b-) taken from the femoral vein showed a 1-8% P ovale infection with rings, trophozoites, schizonts, and multiple invasion. No other species of plasmodium was seen. DNA analysis of the blood sample using the P falciparum-specific Pfmdrprimer confirmed the absence of P falciparum.’ Histological examination of the lungs, brain, and kidney showed no important abnormalities. The liver showed slight sinusoidal congestion with prominence of Kupffer cells containing malarial pigment. The spleen contained areas of focal haemorrhage and frank haemorrhage within the subcapsular space and loss of the capsule. Expansion of sinusoids with prominent phagocytosis of red cells and malarial pigment was seen. P ovale as the cause of imported malaria in the UK is increasing. For example, statistics provided by the malaria reference laboratory (London School of Hygiene and Tropical Medicine) show that imported P ovale has risen from 2 7 % of all cases in 1986 to 7’1 % in Number of cases of NHL-CNS number of cases of glioma.
expressed
as
percentage of
have facilitated diagnostic classification, it is unlikely, in view of the skills available in our neuropathology department, that these lesions were previously misdiagnosed. Nor can an age shift in the at-risk population be the whole explanation.3 An increase in the frequency of NHL-CNS has also been recently noted elsewhere in the UK (Glasgow,4 Leeds5) and in the USA (Boston2). The rising frequency of NHL-CNS has implications for aetiology, epidemiology, and management. A diagnosis of NHLCNS is not encoded in the International Classification of Diseases 9th edition. Accurate national statistics are therefore very difficult to obtain from the Scottish Cancer Register or the Information and Statistics Division of the Scottish Health Service (J. A. Clarke, personnal communication). We therefore recommend the initiation of a national tumour register for NHL-CNS.
Department of Clinical Neurosciences, Western General Hospital, Edinburgh EH4 2XU, UK
MICHAEL G. O’SULLIVAN IAN R. WHITTLE ANNA GREGOR JAMES W. IRONSIDE
TL, Britt RH, Colby TV. Primary lymphoma of the central nervous system: clinicopathological study of experience at Stanford. J Neurosurg 1984; 60: 94-103. 2. Hochberg FH, Miller DC. Primary central nervous system lymphoma. J Neurosurg 1988; 68: 835-53. 3. Baumgartner JE, Rachlin JR, Beckstead JH, et al. Primary central nervous system lymphoma: natural history and response to radiation therapy in 55 patients with 1990; 73: 206-11. acquired immunodeficiency syndrome. Neurosurg J 4. Adams JH, Howatson AG. Cerebral lymphomas: a review of 70 cases. J Clin Pathol 1990; 43: 544-47. 5. Murphy JK, O’Brien CJ, Ironside JW. Morphologic and immunophenotypic characterisation of primary brain lymphomas using paraffin-embedded tissue. Histopathology 1989; 15: 449-60. 1. Helle
Spontaneous splenic rupture due to Plasmodium ovale malaria SiR,—Splenomegaly is characteristic of malaria, irrespective of the infecting species of plasmodium. In acute infections the spleen may enlarge to 500 g, and during repeated attacks can double this size. However, non-traumatic or spontaneous splenic rupture is P vivax has been the species in the few reported cases, the explanation being a rapid splenic enlargement during the acute stage, and therefore a greater risk of splenic rupture in P vivax malaria. We report what is, as far as we are aware, the first case of fatal splenic rupture due to infection with P ovale in the UK. A 51-year-old West-Indian woman, a long-time resident in the UK, took a nineteen day holiday to Ghana after the necessary vaccinations at a central London clinic. She was not advised to take antimalarial prophylactic drugs. Five days after her return she felt unwell and a week after this visited her doctor because of fever and headache and was prescribed pain killers. The following day she was found dead in bed. Necropsy done three hours later revealed no evidence of injury either superficially to the skin overlying the spleen or on deep dissection. On internal examination, the only major abnormality was a ruptured spleen with widespread rare.
1990. The reason is uncertain but may relate to an increase in Africans travelling to West Africa where the heaviest transmission of P ovale in sub-Saharan Africa takes place. Thus in the 2 years 1989-90, 69% of all cases of P ovale were imported from West African countries.2 The absolute requirement for visitors to malaria-endemic regions is that appropriate advice should be given about protection against mosquito bites and malaria chemoprophylaxis. Travellers should be made aware of the symptoms of malaria, and general practitioners the possibility of malaria in such a traveller. We thank Dr D. Warhurst for the DNA analysis.
Departments of Haematology and Forensic Medicine, London Hospital Medical London E1 2AD, UK
College,
CHRISTINE A. FACER D. ROUSE
1 Warhurst DC, Awad El Kanem FM, Miles MA. Simplified preparation of malarial blood samples for polymerase chain reaction. Lancet 1991; 337: 303-07. 2. Bradley DJ, Warhurst DC, Blaze M, Smith V. Malaria imported into the United Kingdom 1989 and 1990. Commun Dis Rep 1991; 1: R45.
Reduction of coma by quinine loading dose in falciparum cerebral malaria StR,—Increasing Plasmodium falciparum resistance to chloroquine and severity of cerebral malaria have become a major problem in Yaounde, Cameroon.’ On the basis of pharmacokinetic indices in cerebral malariaaquinine infusion regimen (8 mg of quinine base/kg body weight over 1 h followed by 8 mg of base/kg over 7 h, then 8 mg/kg over 8 h three times daily for 3 days) was randomly allocated to 10 patients; 10 others received a standard regimen used in Cameroon (8 mg of base/kg over 8 h, three times daily for 3 days). Thick blood films were obtained every 3 h for the first 12 h and every 12 h thereafter. They were stained with Giemsa and examined for parasites. All patients were African. They all had cerebral malaria and fulfilled the definition proposed by Warrell et al3-unrousable coma according to the Glasgow coma scale that was not attributable to other causes of encephalopathy, and P falciparum mono specific COMPARISON BETWEEN TREATMENT GROUPS ON ADMISSION AND AFTER START OF TREATMENT
*Non-parametnc Mann-Whitney U test corrected for ties. iv intravenous, NS not significant. =
=
897
2000 parasites/)il of whole blood).4 Both treatment respect to age, body temperature, severity, groups and duration of coma on admission (table). All patients recovered and were discharged 3 days after admission. No obvious harmful effect was observed. In the loading-dose group, there was a significant decrease in the duration of coma, and the parasite clearance times were reduced by an average of 25% (table). Davis et al5 recommended the use of an intravenous quinine loading dose as being a safe and effective treatment. We are unaware of other reports of controlled trials of the clinical efficacy of a quinine loading dose, and our preliminary findings show its effectiveness and good tolerance. Our results need to be confirmed but they indicate the usefulness of this simple regimen as a treatment for severe malaria, even in places where intensive-care facilities are not available.
parasitaemia (>
were similar with
Intensive Care Unit, Hôpital Central de Yaoundé, Yaoundé
Medical Entomology and
Epidemiology Units, OCEAC/ORSTOM, BP288, Yaoundé, Cameroon Hôpital
Central de Yaoundé
J.-J. FARGIER F. J. LOUIS M. COT B. MAUBERT
C. HOUNSINOU
OCEAC/ORSTOM, Yaoundé
J.-P. LOUIS
Centre National de Référence pour la Chimiosensibilité du Paludisme, IMET, Paris, France
J. LE BRAS
Institut de Médecine Tropicale du Service de Santé des Armées, Marseille
J. E. TOUZE
1. Hengy C, Jambou R,
Eberle F, et al. Problèmes thérapeutiques poses par la chimiorésistance de P falciparum aux antimalariques à Yaoundé, Cameroun. Abstracts of the VII International Congress of Parasitology, Paris. Bull Soc Fr Parasitol 1990; 8 (suppl 1): 430. 2. White NJ, Looareesuwan S, Warrell DA, Warrell MJ, Bunnag D, Harinasuta T. Quinine pharmacokinetics and toxicity in cerebral and uncomplicated falciparum malaria. Am J Med 1982; 73: 564-72. 3. Warrell DA, Looareesuwan S, Warrell MJ, et al. Dexamethasone proves deleterious in cerebral malaria: a double blind trial in 100 comatose patients. N Engl J Med 1982; 306: 313-19 4. Warrell DA, Molyneux ME, Beales PF, eds. Severe and complicated malaria. Trans R Soc Trop Med Hyg 1990; 84 (suppl 2): 1-65. 5. Davis TME, Supanaranond W, Pukrittayakamee S, et al. A safe and effective consecutive-infusion regimen for rapid quinine loading in severe falciparum malaria. J Infect Dis 1990; 161: 1305-08.
Malaria, bednets, and mortality SIR,-Dr Velema (Sept 7, p 642) suggests alternative explanations for the large impact on childhood mortality associated with the introduction of insecticide-treated bednets reported by us (June 22, p 1499). He questions the importance of malaria as a cause of death in The Gambia. Velema accepts that insecticide-treated bednets may have prevented deaths caused by malaria. However, there was a further non-specific reduction in mortality, which we attributed to malaria acting as a risk factor for mortality due to other causes. This can be termed indirect mortality. Velema suggests that, rather than malaria being an indirect cause of death, the non-specific reduction in mortality might have resulted from weekly contact of children with village health workers (VHWs). In support of this he cites a study from Benin1 in which children seen by a VHW had a lower risk of dying in the next 6 months than children not seen. This non-specific protective effect of contact with a VHW could not be related to any particular curative or preventive measure. It may be that unprompted contact with health services is a marker of health awareness and of a protective health-conscious attitude, rather than a
childhood mortality is that, in addition to being a major direct cause of death, malaria is also an important factor in mortality due to other causes.
Institute de Parasitologia "Lopez Neyra", 18001 Granada, Spain; London School of Hygiene and Tropical Medicine, London, and Department of Zoology, University of Glasgow, UK
PEDRO L. ALONSO JOANNA R. M. ARMSTRONG STEVE W. LINDSAY
JP, Alihonou EM, Gandaho T, Hounye FH. Childhood mortality among of primary health care in a rural West African community. Int J Epidemiol 1991; 20: 474-79. 2. Greenwood BM, Greenwood AM, Bradley AK, et al. Comparison of two strategies for 1. Velema
users and non-users
control of malaria within a primary health care programme in The Gambia. Lancet 1988; i: 1121-27
Antithrombin III, blood loss, and transfusion requirements during liver transplantation SIR,-Severe intraoperative bleeding is one of the main problems during liver transplantation. Besides specific surgical or technical causes, it may be secondary to acquired haemostatic defects: hypoprothrombinaemia, haemodilution, thrombocytopenia, and primary or secondary hyperfibrinolysis. Between January, 1987, and December, 1990, 101 liver transplants were done at our institution, and the mean blood loss was 14 (SD 16) litres (1987-88), 5 (4) litres (1989), and 4 (3) litres (1990). During the first 22 transplants all patients were infused with antithrombin III (AT III), with the aim of maintaining levels above 80% activity, and were retrospectively divided into two groups according to the AT III value obtained throughout surgery (group A, more than 80%; group B, less than 80%). Group A had a significantly lower blood loss than group B (p :::; 0.05).1 Harper et al2 suggested AT III supplementation during the anhepatic phase and early after reperfusion to maintain values above 70% activity to control clotting activation and secondary fibrinolysis.2 These data were the rationale for a prospective randomised study in cirrhosis. From January, 1989, to April, 1990,29 patients with postnecrotic cirrhosis (Child score B and C) having liver transplantation were randomised to receive (13 patients) AT III supplementation or no supplementation (16 patients) (AT III activity was below 50% in both groups). The groups were similar in age, sex, preoperative Child score, and basal haemostatic indices. AT III (’Thrombhibin’, Immuno, Italy) was given by bolus infusion before the induction of anaesthesia. The dose was calculated to obtain a preoperative level of 100% (AT IIIunit= [100- plasma activity value]/kg bodyweight). Thereafter, 1000 IU/h were given by continuous infusion throughout surgery. Prothrombin; thrombin and reptilase times; activated partial thromboplastin time; platelet count; fibrinogen; AT III; plasminogen; &agr;2-antiplasmin; total (TDP), fibrinogen (FgDP), and fibrin (FbDP) degradation products; thrombin-antithrombin and complexes (TAT); COAGULATION INDICES, BLOOD LOSS, TRANSFUSION NEEDS, AND OPERATION TIME IN PATIENTS RECEIVING AT III AND CONTROLS
protective measure per se. In The Gambia, VHWs have few resources to exercise any direct
curative action: their role in preventive medicine and health education is negligible. As we reported in our paper, the comparison of mortality rates in villages with and without the presence of a simple, village-based primary health care programme suggests that this scheme does not significantly reduce child mortality in The Gambia. A similar conclusion was drawn in a previous study.2 We feel that the most likely explanation for the large reduction in
Mean (SD) values are shown TAT < ttg/mL FgDP<0.5 5)ig/ml, FbDP< 0.5 pg/ml. Normal values: AT 111>80%, CLI=clot lysis mdex, PRC=packed red cells, FFP=fresh frozen plasma,
PLT = platelets *p < 0,001. tp 00001, Mann Whitney test.
haemorrhage within the abdominal cavity. Her history of travel to a malaria-endemic country suggested investigation for malaria as a cause of the splenic rupture. Blood (typed Fya-b-) taken from the femoral vein showed a 1-8% P ovale infection with rings, trophozoites, schizonts, and multiple invasion. No other species of plasmodium was seen. DNA analysis of the blood sample using the P falciparum-specific Pfmdrprimer confirmed the absence of P falciparum.’ Histological examination of the lungs, brain, and kidney showed no important abnormalities. The liver showed slight sinusoidal congestion with prominence of Kupffer cells containing malarial pigment. The spleen contained areas of focal haemorrhage and frank haemorrhage within the subcapsular space and loss of the capsule. Expansion of sinusoids with prominent phagocytosis of red cells and malarial pigment was seen. P ovale as the cause of imported malaria in the UK is increasing. For example, statistics provided by the malaria reference laboratory (London School of Hygiene and Tropical Medicine) show that imported P ovale has risen from 2 7 % of all cases in 1986 to 7’1 % in Number of cases of NHL-CNS number of cases of glioma.
expressed
as
percentage of
have facilitated diagnostic classification, it is unlikely, in view of the skills available in our neuropathology department, that these lesions were previously misdiagnosed. Nor can an age shift in the at-risk population be the whole explanation.3 An increase in the frequency of NHL-CNS has also been recently noted elsewhere in the UK (Glasgow,4 Leeds5) and in the USA (Boston2). The rising frequency of NHL-CNS has implications for aetiology, epidemiology, and management. A diagnosis of NHLCNS is not encoded in the International Classification of Diseases 9th edition. Accurate national statistics are therefore very difficult to obtain from the Scottish Cancer Register or the Information and Statistics Division of the Scottish Health Service (J. A. Clarke, personnal communication). We therefore recommend the initiation of a national tumour register for NHL-CNS.
Department of Clinical Neurosciences, Western General Hospital, Edinburgh EH4 2XU, UK
MICHAEL G. O’SULLIVAN IAN R. WHITTLE ANNA GREGOR JAMES W. IRONSIDE
TL, Britt RH, Colby TV. Primary lymphoma of the central nervous system: clinicopathological study of experience at Stanford. J Neurosurg 1984; 60: 94-103. 2. Hochberg FH, Miller DC. Primary central nervous system lymphoma. J Neurosurg 1988; 68: 835-53. 3. Baumgartner JE, Rachlin JR, Beckstead JH, et al. Primary central nervous system lymphoma: natural history and response to radiation therapy in 55 patients with 1990; 73: 206-11. acquired immunodeficiency syndrome. Neurosurg J 4. Adams JH, Howatson AG. Cerebral lymphomas: a review of 70 cases. J Clin Pathol 1990; 43: 544-47. 5. Murphy JK, O’Brien CJ, Ironside JW. Morphologic and immunophenotypic characterisation of primary brain lymphomas using paraffin-embedded tissue. Histopathology 1989; 15: 449-60. 1. Helle
Spontaneous splenic rupture due to Plasmodium ovale malaria SiR,—Splenomegaly is characteristic of malaria, irrespective of the infecting species of plasmodium. In acute infections the spleen may enlarge to 500 g, and during repeated attacks can double this size. However, non-traumatic or spontaneous splenic rupture is P vivax has been the species in the few reported cases, the explanation being a rapid splenic enlargement during the acute stage, and therefore a greater risk of splenic rupture in P vivax malaria. We report what is, as far as we are aware, the first case of fatal splenic rupture due to infection with P ovale in the UK. A 51-year-old West-Indian woman, a long-time resident in the UK, took a nineteen day holiday to Ghana after the necessary vaccinations at a central London clinic. She was not advised to take antimalarial prophylactic drugs. Five days after her return she felt unwell and a week after this visited her doctor because of fever and headache and was prescribed pain killers. The following day she was found dead in bed. Necropsy done three hours later revealed no evidence of injury either superficially to the skin overlying the spleen or on deep dissection. On internal examination, the only major abnormality was a ruptured spleen with widespread rare.
1990. The reason is uncertain but may relate to an increase in Africans travelling to West Africa where the heaviest transmission of P ovale in sub-Saharan Africa takes place. Thus in the 2 years 1989-90, 69% of all cases of P ovale were imported from West African countries.2 The absolute requirement for visitors to malaria-endemic regions is that appropriate advice should be given about protection against mosquito bites and malaria chemoprophylaxis. Travellers should be made aware of the symptoms of malaria, and general practitioners the possibility of malaria in such a traveller. We thank Dr D. Warhurst for the DNA analysis.
Departments of Haematology and Forensic Medicine, London Hospital Medical London E1 2AD, UK
College,
CHRISTINE A. FACER D. ROUSE
1 Warhurst DC, Awad El Kanem FM, Miles MA. Simplified preparation of malarial blood samples for polymerase chain reaction. Lancet 1991; 337: 303-07. 2. Bradley DJ, Warhurst DC, Blaze M, Smith V. Malaria imported into the United Kingdom 1989 and 1990. Commun Dis Rep 1991; 1: R45.
Reduction of coma by quinine loading dose in falciparum cerebral malaria StR,—Increasing Plasmodium falciparum resistance to chloroquine and severity of cerebral malaria have become a major problem in Yaounde, Cameroon.’ On the basis of pharmacokinetic indices in cerebral malariaaquinine infusion regimen (8 mg of quinine base/kg body weight over 1 h followed by 8 mg of base/kg over 7 h, then 8 mg/kg over 8 h three times daily for 3 days) was randomly allocated to 10 patients; 10 others received a standard regimen used in Cameroon (8 mg of base/kg over 8 h, three times daily for 3 days). Thick blood films were obtained every 3 h for the first 12 h and every 12 h thereafter. They were stained with Giemsa and examined for parasites. All patients were African. They all had cerebral malaria and fulfilled the definition proposed by Warrell et al3-unrousable coma according to the Glasgow coma scale that was not attributable to other causes of encephalopathy, and P falciparum mono specific COMPARISON BETWEEN TREATMENT GROUPS ON ADMISSION AND AFTER START OF TREATMENT
*Non-parametnc Mann-Whitney U test corrected for ties. iv intravenous, NS not significant. =
=
897
2000 parasites/)il of whole blood).4 Both treatment respect to age, body temperature, severity, groups and duration of coma on admission (table). All patients recovered and were discharged 3 days after admission. No obvious harmful effect was observed. In the loading-dose group, there was a significant decrease in the duration of coma, and the parasite clearance times were reduced by an average of 25% (table). Davis et al5 recommended the use of an intravenous quinine loading dose as being a safe and effective treatment. We are unaware of other reports of controlled trials of the clinical efficacy of a quinine loading dose, and our preliminary findings show its effectiveness and good tolerance. Our results need to be confirmed but they indicate the usefulness of this simple regimen as a treatment for severe malaria, even in places where intensive-care facilities are not available.
parasitaemia (>
were similar with
Intensive Care Unit, Hôpital Central de Yaoundé, Yaoundé
Medical Entomology and
Epidemiology Units, OCEAC/ORSTOM, BP288, Yaoundé, Cameroon Hôpital
Central de Yaoundé
J.-J. FARGIER F. J. LOUIS M. COT B. MAUBERT
C. HOUNSINOU
OCEAC/ORSTOM, Yaoundé
J.-P. LOUIS
Centre National de Référence pour la Chimiosensibilité du Paludisme, IMET, Paris, France
J. LE BRAS
Institut de Médecine Tropicale du Service de Santé des Armées, Marseille
J. E. TOUZE
1. Hengy C, Jambou R,
Eberle F, et al. Problèmes thérapeutiques poses par la chimiorésistance de P falciparum aux antimalariques à Yaoundé, Cameroun. Abstracts of the VII International Congress of Parasitology, Paris. Bull Soc Fr Parasitol 1990; 8 (suppl 1): 430. 2. White NJ, Looareesuwan S, Warrell DA, Warrell MJ, Bunnag D, Harinasuta T. Quinine pharmacokinetics and toxicity in cerebral and uncomplicated falciparum malaria. Am J Med 1982; 73: 564-72. 3. Warrell DA, Looareesuwan S, Warrell MJ, et al. Dexamethasone proves deleterious in cerebral malaria: a double blind trial in 100 comatose patients. N Engl J Med 1982; 306: 313-19 4. Warrell DA, Molyneux ME, Beales PF, eds. Severe and complicated malaria. Trans R Soc Trop Med Hyg 1990; 84 (suppl 2): 1-65. 5. Davis TME, Supanaranond W, Pukrittayakamee S, et al. A safe and effective consecutive-infusion regimen for rapid quinine loading in severe falciparum malaria. J Infect Dis 1990; 161: 1305-08.
Malaria, bednets, and mortality SIR,-Dr Velema (Sept 7, p 642) suggests alternative explanations for the large impact on childhood mortality associated with the introduction of insecticide-treated bednets reported by us (June 22, p 1499). He questions the importance of malaria as a cause of death in The Gambia. Velema accepts that insecticide-treated bednets may have prevented deaths caused by malaria. However, there was a further non-specific reduction in mortality, which we attributed to malaria acting as a risk factor for mortality due to other causes. This can be termed indirect mortality. Velema suggests that, rather than malaria being an indirect cause of death, the non-specific reduction in mortality might have resulted from weekly contact of children with village health workers (VHWs). In support of this he cites a study from Benin1 in which children seen by a VHW had a lower risk of dying in the next 6 months than children not seen. This non-specific protective effect of contact with a VHW could not be related to any particular curative or preventive measure. It may be that unprompted contact with health services is a marker of health awareness and of a protective health-conscious attitude, rather than a
childhood mortality is that, in addition to being a major direct cause of death, malaria is also an important factor in mortality due to other causes.
Institute de Parasitologia "Lopez Neyra", 18001 Granada, Spain; London School of Hygiene and Tropical Medicine, London, and Department of Zoology, University of Glasgow, UK
PEDRO L. ALONSO JOANNA R. M. ARMSTRONG STEVE W. LINDSAY
JP, Alihonou EM, Gandaho T, Hounye FH. Childhood mortality among of primary health care in a rural West African community. Int J Epidemiol 1991; 20: 474-79. 2. Greenwood BM, Greenwood AM, Bradley AK, et al. Comparison of two strategies for 1. Velema
users and non-users
control of malaria within a primary health care programme in The Gambia. Lancet 1988; i: 1121-27
Antithrombin III, blood loss, and transfusion requirements during liver transplantation SIR,-Severe intraoperative bleeding is one of the main problems during liver transplantation. Besides specific surgical or technical causes, it may be secondary to acquired haemostatic defects: hypoprothrombinaemia, haemodilution, thrombocytopenia, and primary or secondary hyperfibrinolysis. Between January, 1987, and December, 1990, 101 liver transplants were done at our institution, and the mean blood loss was 14 (SD 16) litres (1987-88), 5 (4) litres (1989), and 4 (3) litres (1990). During the first 22 transplants all patients were infused with antithrombin III (AT III), with the aim of maintaining levels above 80% activity, and were retrospectively divided into two groups according to the AT III value obtained throughout surgery (group A, more than 80%; group B, less than 80%). Group A had a significantly lower blood loss than group B (p :::; 0.05).1 Harper et al2 suggested AT III supplementation during the anhepatic phase and early after reperfusion to maintain values above 70% activity to control clotting activation and secondary fibrinolysis.2 These data were the rationale for a prospective randomised study in cirrhosis. From January, 1989, to April, 1990,29 patients with postnecrotic cirrhosis (Child score B and C) having liver transplantation were randomised to receive (13 patients) AT III supplementation or no supplementation (16 patients) (AT III activity was below 50% in both groups). The groups were similar in age, sex, preoperative Child score, and basal haemostatic indices. AT III (’Thrombhibin’, Immuno, Italy) was given by bolus infusion before the induction of anaesthesia. The dose was calculated to obtain a preoperative level of 100% (AT IIIunit= [100- plasma activity value]/kg bodyweight). Thereafter, 1000 IU/h were given by continuous infusion throughout surgery. Prothrombin; thrombin and reptilase times; activated partial thromboplastin time; platelet count; fibrinogen; AT III; plasminogen; &agr;2-antiplasmin; total (TDP), fibrinogen (FgDP), and fibrin (FbDP) degradation products; thrombin-antithrombin and complexes (TAT); COAGULATION INDICES, BLOOD LOSS, TRANSFUSION NEEDS, AND OPERATION TIME IN PATIENTS RECEIVING AT III AND CONTROLS
protective measure per se. In The Gambia, VHWs have few resources to exercise any direct
curative action: their role in preventive medicine and health education is negligible. As we reported in our paper, the comparison of mortality rates in villages with and without the presence of a simple, village-based primary health care programme suggests that this scheme does not significantly reduce child mortality in The Gambia. A similar conclusion was drawn in a previous study.2 We feel that the most likely explanation for the large reduction in
Mean (SD) values are shown TAT < ttg/mL FgDP<0.5 5)ig/ml, FbDP< 0.5 pg/ml. Normal values: AT 111>80%, CLI=clot lysis mdex, PRC=packed red cells, FFP=fresh frozen plasma,
PLT = platelets *p < 0,001. tp 00001, Mann Whitney test.