760
OUTCOME OF MECHANICAL VENTILATION
theory suggests that afferent impulses
go from a focus of lung disease to the brainstem to initiate vasodilatation in the nail bed and peripheral limb tissue; the hormonal theory invokes a tumourderived hormone acting on the distal limb tissue; and the shunt theory suggests that a substance normally degraded on passage through the lungs passes via arteriovenous shunts to affect the limb tissue. None of these theories can explain fmger clubbing in IBD and trichuris colitis. It has been shown that serum tumour necrosis factor ex (TNFêf.) is raised in patients with CF,3 IBD/* trichuris colitis (MacDonald TT, Cooper ES, unpublished), and other parasitic infections.S These findings may explain some of the signs of these chronic inflammatory illnesses, such as cachexia and growth retardation in children. High serum concentrations of TNFa have also been found in cachectic cancer patients.6 Severe chronic heart failure leads to cachexia and growth failure, an unexplained observation until Levine and colleagues7 reported that serum concentrations of TNFêf. are raised in this condition. The association of finger clubbing with raised TNFa in an otherwise disparate collection of diseases offers a new explanation. TNFa has many properties, including endothelial cell activation and promotion of angiogenesis, which make it a good candidate for a pathogenetic role in clubbing. Studies on the role of TNFx in clubbing will need to measure serum concentrations of TNFêf. in children with congenital cyanotic heart disease, and in patients with chronic lung infections and chronic liver disease.
Department of Paediatric Gastroenterology, St Bartholomew’s Hospital, London EC1A 7BE, UK
CHRISTIAN P. BRAEGGER CHRISTOPHER J. CORRIGAN THOMAS T. MACDONALD
1. Cooper ES, Bundy DAP. Trichiuris is not trivial. Parasitol Today 1988; 4: 301-06. 2. Seaton A, Seaton D, Leitch AG. Clubbing and hypertrophic osteoarthropathy. In: Crofton and Douglas’s respiratory diseases. Oxford: Blackwell, 1989: 113-15. 3. Suter S, Schaad UB, Roux-Lombard P, Girardin E, Grau G, Dayer JM. Relation between tumor necrosis factor-alpha and granulocyte elastase-alpha 1-proteinase inhibitor complexes in the plasma of patients with cystic fibrosis. Am Rev Respir Dis 1989; 140: 1640-44. 4. MacDonald TT, Hutchings P, Choy MY, Murch S, Cooke A. Tumor necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine. Clin Exp Immunol 1990; 81: 351-55 5. Scuderi P, Sterling KE, Lam KS, et al. Raised serum levels of tumour necrosis factor in parasitic infections. Lancet 1986; ii: 1364-65. 6. Balkwill F, Osborne R, Burke F, et al. Evidence for tumour necrosis factor/cachectin production in cancer. Lancet 1987; ii: 1229-32. 7. Levine B, Kalman J, Mayer L, Howard MF, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med 1990; 323: 236-41.
ECMO and outcome of mechanical ventilation in infants of birthweight
over 2 kg SIR,-Extracorporeal membrane oxygenation (ECMO) has been introduced in North America for the management of newborn babies with severe respiratory failure. Among 715 infants with a predicted mortality of 80%, the survival rate was 81% when ECMO was used.l Most survivors seem to function normally, in one series2 only 17% had moderate to severe neurological dysfunction. ECMO is, however, associated with important complications, and this morbidity will be reduced if individual centres look after large numbers of patients and thus acquire adequate experience. Yet a Lancet editoria 13 has suggested that in the UK there may be very few infants who would benefit from ECMO. King’s College Hospital (KCH) provides more than a third of the intensive-care cots for ventilation in the South-East Thames region (birth rate 55 000 yearly); thus review of the numbers of and outcome in infants ventilated at KCH who were suitable for ECMO in respect of maturity and birthweight would give a realistic indication of the need for this technique. In 16 months 235 infants were ventilated at KCH; only 38 weighed over 2.0 kg at birth and were 34 weeks’ or more gestational age (table). 12 of the 38 infants had an alveolar arterial O2 difference (AaD02) of over 620 mm Hg, which if maintained for 12 h correlates well with a predicted mortality of 80 % or greater. 6 of the 12 died (4 with severe congenital abnormalities) and 2 survivors are
TTN
=
transient
tachypnoea of the newborn.
handicapped at follow-up. 5 of these 12 infants would have been ineligible for ECMO, because of their primary diagnosis; in addition the 2 with congenital diaphragmatic hernia who died had severe pulmonary hypoplasia. Thus in our cohort ECMO would have been appropriate in 5 infants-a requirement for ECMO ofI in 5000 births, which is not dissimilar to Field’s cited,s but unpublished, data. 3 of these 5 infants survived without problems and the remaining 2 died-a mortality of 40%, not the predicted 80%.4 Both infants who died deteriorated within 3 h and so did not truly fulfill the AaD02 criteria for ECMO ;4 it would probably have been technically impossible to stabilise them on an ECMO circuit within such a short time. Thus no infant in the 16 months examined would have benefited from ECMO. If selection criteria were relaxed, with abandonment of the AaD02 clause, 17 of the 38 mature ventilated infants would have been excluded from ECMO because of their primary diagnosis. 19 of the other 21 infants survived (survival rate 90%) and none had neurological impairment; thus it seems unlikely that ECMO would improve outcome in this group. It has been proposeds that between one and five units should be established in the UK to assess the potential impact of this technique. Our results emphasise that such a conclusion is premature. Before the introduction to the UK of this expensive technique with its associated morbidity, truly representative nationwide data are needed to accurately establish the numbers of infants who would benefit from ECMO. Department of Child Health, Regional Neonatal Intensive Care Centre, King’s College School of Medicine and Dentistry, London SE5 8RX, UK
A. GREENOUGH E. EMERY
1 Toomasian TM, Snedecor SM, Cornell RD. National experience with ECMO for newborn respiratory failure: data from 715 cases. University of Michigan, ECMO Data Registry, Department of Surgery and Biostatistics, 1986. 2. Bartlett RH, Gazzaniga AB, Toomasian JM. Extracorporeal membrane oxygenation in neonatal respiratory failure: 100 cases. Ann Surg 1986; 204: 23. 3 Editorial. Persistent fetal circulation and extracorporeal membrane oxygenation Lancet 1988; ii: 1289-91. 4. Krummer TM, Greenfield LK, Kirkpatrick BV. Alveolar-arterial oxygen gradients versus the neonatal pulmonary insufficiency index for prediction of mortality in ECMO candidates. J Pediatr Surg 1984; 19: 380. 5. Sosnowski AS, Bonser SJ, Field DJ, Graham TR, Firmin RK. Extracorporeal membrane oxygenation. Br Med J 1990, 301: 303-04.
CORRECTION How much of which antipsychotic? In this letter by DrP. Rowlands and Dr A. L. MacNeill (Aug 18, p 443) the table was reproduced mcorrecdy. Under the heading "depot medication", 2 x weekly and 4 x weekly should have read every 2 weeks and every 4 weeks, respectively.
OUTCOME OF MECHANICAL VENTILATION
theory suggests that afferent impulses
go from a focus of lung disease to the brainstem to initiate vasodilatation in the nail bed and peripheral limb tissue; the hormonal theory invokes a tumourderived hormone acting on the distal limb tissue; and the shunt theory suggests that a substance normally degraded on passage through the lungs passes via arteriovenous shunts to affect the limb tissue. None of these theories can explain fmger clubbing in IBD and trichuris colitis. It has been shown that serum tumour necrosis factor ex (TNFêf.) is raised in patients with CF,3 IBD/* trichuris colitis (MacDonald TT, Cooper ES, unpublished), and other parasitic infections.S These findings may explain some of the signs of these chronic inflammatory illnesses, such as cachexia and growth retardation in children. High serum concentrations of TNFa have also been found in cachectic cancer patients.6 Severe chronic heart failure leads to cachexia and growth failure, an unexplained observation until Levine and colleagues7 reported that serum concentrations of TNFêf. are raised in this condition. The association of finger clubbing with raised TNFa in an otherwise disparate collection of diseases offers a new explanation. TNFa has many properties, including endothelial cell activation and promotion of angiogenesis, which make it a good candidate for a pathogenetic role in clubbing. Studies on the role of TNFx in clubbing will need to measure serum concentrations of TNFêf. in children with congenital cyanotic heart disease, and in patients with chronic lung infections and chronic liver disease.
Department of Paediatric Gastroenterology, St Bartholomew’s Hospital, London EC1A 7BE, UK
CHRISTIAN P. BRAEGGER CHRISTOPHER J. CORRIGAN THOMAS T. MACDONALD
1. Cooper ES, Bundy DAP. Trichiuris is not trivial. Parasitol Today 1988; 4: 301-06. 2. Seaton A, Seaton D, Leitch AG. Clubbing and hypertrophic osteoarthropathy. In: Crofton and Douglas’s respiratory diseases. Oxford: Blackwell, 1989: 113-15. 3. Suter S, Schaad UB, Roux-Lombard P, Girardin E, Grau G, Dayer JM. Relation between tumor necrosis factor-alpha and granulocyte elastase-alpha 1-proteinase inhibitor complexes in the plasma of patients with cystic fibrosis. Am Rev Respir Dis 1989; 140: 1640-44. 4. MacDonald TT, Hutchings P, Choy MY, Murch S, Cooke A. Tumor necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine. Clin Exp Immunol 1990; 81: 351-55 5. Scuderi P, Sterling KE, Lam KS, et al. Raised serum levels of tumour necrosis factor in parasitic infections. Lancet 1986; ii: 1364-65. 6. Balkwill F, Osborne R, Burke F, et al. Evidence for tumour necrosis factor/cachectin production in cancer. Lancet 1987; ii: 1229-32. 7. Levine B, Kalman J, Mayer L, Howard MF, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med 1990; 323: 236-41.
ECMO and outcome of mechanical ventilation in infants of birthweight
over 2 kg SIR,-Extracorporeal membrane oxygenation (ECMO) has been introduced in North America for the management of newborn babies with severe respiratory failure. Among 715 infants with a predicted mortality of 80%, the survival rate was 81% when ECMO was used.l Most survivors seem to function normally, in one series2 only 17% had moderate to severe neurological dysfunction. ECMO is, however, associated with important complications, and this morbidity will be reduced if individual centres look after large numbers of patients and thus acquire adequate experience. Yet a Lancet editoria 13 has suggested that in the UK there may be very few infants who would benefit from ECMO. King’s College Hospital (KCH) provides more than a third of the intensive-care cots for ventilation in the South-East Thames region (birth rate 55 000 yearly); thus review of the numbers of and outcome in infants ventilated at KCH who were suitable for ECMO in respect of maturity and birthweight would give a realistic indication of the need for this technique. In 16 months 235 infants were ventilated at KCH; only 38 weighed over 2.0 kg at birth and were 34 weeks’ or more gestational age (table). 12 of the 38 infants had an alveolar arterial O2 difference (AaD02) of over 620 mm Hg, which if maintained for 12 h correlates well with a predicted mortality of 80 % or greater. 6 of the 12 died (4 with severe congenital abnormalities) and 2 survivors are
TTN
=
transient
tachypnoea of the newborn.
handicapped at follow-up. 5 of these 12 infants would have been ineligible for ECMO, because of their primary diagnosis; in addition the 2 with congenital diaphragmatic hernia who died had severe pulmonary hypoplasia. Thus in our cohort ECMO would have been appropriate in 5 infants-a requirement for ECMO ofI in 5000 births, which is not dissimilar to Field’s cited,s but unpublished, data. 3 of these 5 infants survived without problems and the remaining 2 died-a mortality of 40%, not the predicted 80%.4 Both infants who died deteriorated within 3 h and so did not truly fulfill the AaD02 criteria for ECMO ;4 it would probably have been technically impossible to stabilise them on an ECMO circuit within such a short time. Thus no infant in the 16 months examined would have benefited from ECMO. If selection criteria were relaxed, with abandonment of the AaD02 clause, 17 of the 38 mature ventilated infants would have been excluded from ECMO because of their primary diagnosis. 19 of the other 21 infants survived (survival rate 90%) and none had neurological impairment; thus it seems unlikely that ECMO would improve outcome in this group. It has been proposeds that between one and five units should be established in the UK to assess the potential impact of this technique. Our results emphasise that such a conclusion is premature. Before the introduction to the UK of this expensive technique with its associated morbidity, truly representative nationwide data are needed to accurately establish the numbers of infants who would benefit from ECMO. Department of Child Health, Regional Neonatal Intensive Care Centre, King’s College School of Medicine and Dentistry, London SE5 8RX, UK
A. GREENOUGH E. EMERY
1 Toomasian TM, Snedecor SM, Cornell RD. National experience with ECMO for newborn respiratory failure: data from 715 cases. University of Michigan, ECMO Data Registry, Department of Surgery and Biostatistics, 1986. 2. Bartlett RH, Gazzaniga AB, Toomasian JM. Extracorporeal membrane oxygenation in neonatal respiratory failure: 100 cases. Ann Surg 1986; 204: 23. 3 Editorial. Persistent fetal circulation and extracorporeal membrane oxygenation Lancet 1988; ii: 1289-91. 4. Krummer TM, Greenfield LK, Kirkpatrick BV. Alveolar-arterial oxygen gradients versus the neonatal pulmonary insufficiency index for prediction of mortality in ECMO candidates. J Pediatr Surg 1984; 19: 380. 5. Sosnowski AS, Bonser SJ, Field DJ, Graham TR, Firmin RK. Extracorporeal membrane oxygenation. Br Med J 1990, 301: 303-04.
CORRECTION How much of which antipsychotic? In this letter by DrP. Rowlands and Dr A. L. MacNeill (Aug 18, p 443) the table was reproduced mcorrecdy. Under the heading "depot medication", 2 x weekly and 4 x weekly should have read every 2 weeks and every 4 weeks, respectively.
