- Email: [email protected]
THE LANGERHANS CELL
672
when
they first present to a respiratory clinic28). Correction of their nocturnal hypoxaemia may therefore prevent severe pulmonary hypertension and cor pulmonale, and also improve survival, as shown by the recent N.I.H.29and M.R.C.3° controlled trials of long-term low-dose oxygen in chronic bronchitis and emphysema, in both of which oxygen was given at night. However, in the N.I.H. trial oxygen given mainly at night (12 h in the 24 h day) did not prolong life as much as oxygen for 19-24 h in the 24 h day. Despite the well-known risk that oxygen therapy may increase CO2 retention in these patients during an exacerbation,31 no serious rise in PC02 was seen with long-term low-flow oxygen (possibly because PC02 was not measured during sleep). Such oxygen at night’ did cause temporary reversible acidosis in one moderately hypoxic "blue bloater" in whom the hypoxic drive to breathing was preserved,32 but the reduction in this drive observable in most such patients33 may protect them from a rise in PC02. GUILLEMINAULT et a1.34 have cautioned against ,nocturnal oxygen therapy in chronic bronchitis, for they describe doubling in the duration of apnoeic events in REM sleep with 1’5 or 3 1/min of oxygen given through nasal prongs in four such patients with day-time somnolence and sleep apnoea, only one being a "blue bloater". Conversely in eleven patients with mild hypoxaemia (mean P02 66 mm Hg) from chronic obstructive lung disease, but without serious C02 retention (mean PC02 44 mm Hg), 2 1/min of oxygen by nasal prongs for half the night increased the time spent asleep, and reduced oxygen desaturation, but had no effect on episodes of apnoea or hypopnoea, when compared with the other half of the night without oxygen.35 Arterial PC02 was measured in five of these patients, but did not rise more during episodes of disordered breathing when they breathed oxygen than in similar episodes when they breathed’air. Certainty as to the safety of nocturnal oxygen in these patients clearly requires more measurements, but the recent trials suggest that the treatment is safe, if the oxygen flow is kept low and provided that the patients are not in an acute exacerbation of respiratory acidosis.31 Studies of effective respiratory stimulants during sleep in "blue bloaters" are badly needed, with 28.
29
30.
Catterall JR, Douglas NJ, Calverley PMA, et al. Hypoventilation is common, but sleep apnea rare, in transient nocturnal hypoxemia of ’blue and bloated’ bronchitis. Am Rev Resp Dis 1981; 123: 113. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemia chronic obstructive lung disease. Ann Intern Med 1980; 93: 391-98. M.R.C. Working Party. Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981; i:
681-86. 31. Warren PM, Avery A, Millar JS, Flenley DC. Respiratory failure revisited: Exacerbations of chronic bronchitis 1960-1968 and 1970-1976. Lancet 1980; i: 467-74 32 Leitch AG, Clancy LJ, Leggett RJE, et al Arterial blood gas tensions, hydrogen ion, and electroencephalogram during sleep in patients with chronic ventilatory failure. Thorax 1976; 31: 730-35. 33. Flenley DC, Franklin DH, Millar JS. The hypoxic drive to breathing in chronic bronchitis and emphysema. Clin Sci 1970; 38: 503-18. 34. Guilleminault C, Cummiskey J, Motta J. Chronic obstructive airflow disease and sleep studies. Am Rev Resp Dis 1980; 122: 397-406. 35. Kearley R, Wynne JW, Block AJ, et al The effect of low flow oxygen on sleep disordered breathing and oxygen desaturation. Chest 1980; 78: 682-85.
without added oxygen, for such drugs may well interfere with sleep. The new French drug almitrine, which can improve hypoxaemia and C02 retention in "blue bloaters" ,36 clearly merits such a trial in sleep. The effects of drugs on breathing during sleep, since they concern two of the more important human activities, deserve attention from both drug regulatory bodies and the pharmaceutical industry. or
THE LANGERHANS CELL OF the many subjects which reliably produce heated and inconclusive debate amongst dermatologists, the epidermal Langerhans cell takes the prize. Some new findings, made more than a hundred years after this dendritic cell was discovered by Paul.Langerhans,’ now bid fair to mitigate its contentious reputation. The Langerhans cell was originally thought to be either a sensory receptor cell or an effete melanocyte, and progress in its definition was greatly impeded by lack of methods for firm identification of the cells. This deficiency was rectified in 1961 by Birbeck, Breathnach, and Everall2 who described the ultrastructural features of the Langerhans cell and in particular identified a unique racquet-shaped organelle, the Birbeck granule. The Langerhans cell also occurs in dermis, mucous membranes, and lymphatic tissue. Its derivation from a bone marrow mesenchymal cell has now been convincingly demonstrated as a result of transplantation and chimaera studies by Tamaki and Katz.3 The disease histiocytosis X, which affects bone, lungs, and skin, is probably due to proliferation of the Langerhans cell4 and the possibility that the Langerhans cell is the target cell in mycosis fungoides is being explored.s The major new discoveries, however, centre on the involvement of Langerhans cells in immunological reactions, especially allergic contact dermatitis. Convincing evidence of an important role in allergic contact dermatitis was first provided by Silberberg,6 who noted the intimate apposition of Langerhans cells with mononuclear cells in positive patch test reactions. The appearances of the Langerhans cell were often suggestive of increased secretory activity. The next important development was the realisation that Langerhans cells, like mononuclear phagocytes, serve a pivotal role in sensitisation, by processing antigens before their presentation to immunocompetent lymphocytes. Langerhans cells behave as dendritic scavengers of foreign small-molecular material which has trespassed within the epidermis.’ This finding is of especial relevance to allergic contact dermatitis, which usually involves a cutaneous hypersensitivity reaction to simple low-molecular-weight substances. The analogy with mononuclear phagocytes was further strengthened 36. 1.
Symposium on gas exchange and ventilation perfusion ratios. Round table, Almitrine Bull Eur Physiopathol Resp 1980; 16: 195p-208p. Langerhans P. Uber die Nerven der menschlichen Haut. Virchows Arch 1868; 44:
325-37. 2. Birbeck MS, Breathnach AS, Everall JD. An electron microscopic study of basal melanocytes and high level clear cells (Langerhans cells) in vitiligo. J Invest Dermatol 1961; 37: 51-64. 3. Tamaki K, Katz SI. Ontogeny of Langerhans cells J Invest Dermatol 1980; 75: 12-13 4. Basset F, Turiaf MJ. Identification par la microscopie electronique de particles de nature probablement virale dans les lesions granulomateuses d’une histiocytose-X pulmonaire. CR Acad Sci Paris 1965; 261: 3701-03. 5. Mackie RM. Initial event in mycosis fungoides of the skin is viral infection of epidermal Langerhans cells. Lancet 1981; ii: 283-84. 6. Silberberg I. Apposition of mononuclear cells to Langerhans cells in contact allergic reactions. Acta Dermatovener 1973; 53: 1-12. 7. Shelley WB, Juhlin L. Langerhans cells form a reticuloepithelial trap for external contact antigens. Nature 1976; 261: 46-47
673
emerged that Langerhans cells were the only epidermal cells expressing Fc-IgG receptors, Creceptors, and Ia antigens and, moreover, that they could replace labearing macrophages as activators of antigen-specific when it
allogeneic T cells.8-11 Further confirmation of the central role of Langerhans cell was obtained when Streilein et al.11 showed that contact sensitivity could not be induced in the mouse if the shaved skin had previously been depleted of Langerhans cells by irradiation with ultraviolet B (290-320 nm). It should therefore have come as no great surprise when 8-methoxypsoralen/ultraviolet-A photochemotherapy proved to inhibit experimental allergic contact sensitisation in man. Strauss and his colleagues’3 found reduced or absent allergic contact sensitisation to dinitrochlorbenzene in 55 of 102
psoriatic patients receiving photochemotherapy (PUVA), though the irritant response to DNCB was normal. Similar results were subsequently reported by Newcastle workers. 14
,
suppression is due to apparent depletion of the Langerhans cell network in the epidermis now receives support from Friedmann.ls He measured the population density of Langerhans cells in the clinically normal epidermis of 25 patients. Before PUVA treatment the mean population density of Langerhans cells was 713±60 SEM/mm2 epidermal surface area; after 7 treatments there were only 56±29/mmz remaining. Morphologically, the earliest change was loss of dendritic processes. Thus it seems that the impairment of DNCB sensitisation may be a result of subnormal antigen recognition and processing within the epidermis, although direct actions on T lymphocytes by ultraviolet cannot be excluded. The implications of these findings are wide. If mutagenic change in keratinocytes or melanocytes is a random event within the skin, then the existence of competent immunosurveillance within the skin becomes crucial. Prolonged exposure of the skin to ultraviolet, whether natural or artificial, could not only cause mutations in these cells but also exert a "pseudopromotor" action13 due to impaired recognition of foreign antigens, thus encouraging clonal outgrowth of malignant cells. Friedmann’s findings must reinforce anxiety about the longterm effects of prolonged exposure of skin to ultraviolet, including PUVA treatment for psoriasis. That this
THE LUNG IN BURNS THE term burn-lung Vietnam war of certain
syndrome was used during the extensively burned patients with
acute respiratory distress.’ Most of the burns had been sustained in the open, from flame-throwing weapons, bombs, or gasoline related explosions. The patients often died. 8
Stingl G, Wolff-Schreiner EC, Pichler WJ, Gschnait F, Knapp W, Wolff K. Epidermal Langerhans cells bear F and C3 receptors. Nature 1977; 268: 245-46. 9. Rowden G, Lewis MG, Sullivan AK. Ia antigen expression on human epidermal Langerhans cells. Nature 1977; 268: 247-48. 10. Klareskog L, Tjernlund UM, Forsum U, Peterson PA. Epidermal Langerhans cells express Ia antigens. Nature 1977; 268: 248-50. 11Stingl G, Katz SI, Green I, Shevach EM The functional role of Langerhans cells. J Invest Dermatol 1980; 74: 315-18. 12. Streilein JW, Toews GT, Gilliam JN, Bergstresser PR. Tolerance of hypersensitivity. to 2, 4, -dinitro-1-fluorobenzene: the role of Langerhans cell density within epidermis. J Invest Derm 1980; 74: 319-22. 13. Strauss GH, Greaves MW, Price M, Bridges BA, Hall-Smith P, Vella Briffa D. Inhibition of delayed hypersensitivity reactions in skin (DNCB test) by 8-methoxypsoralen photochemotherapy. Lancet 1980;ii 556-59. 14. Moss C, Fnedmann PS, Shuster S. Inhibition of delayed hypersensitivity skin reactions in patients on methoxypsoralen photochemotherapy. Lancer 1980; ii: 922. 15. Friedmann P. Disappearance of epidermal Langerhans cells during PUVA therapy. Br
J Dermatol 1981; 1 Getzen
105: 219-21
LC, Pollack EW Fatal respiratory distress in burned patients Surgery Gynecol Obstet 1981; 152: 741-44.
Inhalation of smoke did not seem to be a factor in the respiratory distress, whereas in peacetime, respiratory troubles arise particularly in people who have been trapped in burning buildings or confined spaces; the lung is damaged by smoke from burning furniture made with polyurethane and plastic foams.2-’ Carbon monoxide, nitric oxide, nitrogen peroxide, and hydrocyanic acid are among the substances under suspicion. Many causes of respiratory distress in burned patients have now been identified and it is doubtful whether the label of burn-lung syndrome needs to be preserved. This, indeed, is the message from a recent review of the causes of death in the Vietnam patients. Deaths from respiratory distress in the first forty-eight hours from the time of burning were due to overhydration or overloading with transfusion solution in patients who had coexisting renal failure. Later deaths were attributable to overhydration, pseudomonas sepsis, and aspiration pneumonia. The same report states that the use of colloids such as albumin, instead of crystalloid solutions, in the treatment of shock reduced the incidence of pulmonary oedema. In the U.K., human plasma protein fraction (mainly albumin) and the colloid dextran 110 are the main agents used for treatment of shock in the first forty-eight hours, and this may be why reports of burn lung are uncommon there. Pulmonary oedema due to overhydration should be recognised by clinical examination coupled with review of the fluid balance sheet. Bronchopneumonia and pulmonary sepsis also arise and are treated in the usual way. For relief of respiratory obstruction the use of endotracheal intubation instead of tracheostomy has considerably lessened mortality from pulmonary infection, particularly from Pseudomonas aeruginosa. 6,7 Prolonged intubation, however, has its own problems of tracheal and laryngeal ulceration, and the lesions may be a source of infection. Prolonged central intravenous catheterisation can also result in multiple lung abscesses when septic emboli arise from the catheter tip.8 Aspiration pneumonia has also occurred, even in patients having nasogastric suction. There seems no way of reliably detecting and monitoring the type of patient who will get this complication, which is often fatal. Pulmonary thromboembolism can be prevented by prophylactic anticoagulant therapy, but this is usually restricted to patients with burns of less than 15% of body surface, because of the danger of haemorrhage from gastric erosions and Curling’s ulcers in those with larger burns. The traditional sign of pulmonary oedema is the rale, which points to excess water in the airways. This, however, is a late sign and we really want to know when passage of water across the pulmonary capillary endothelium becomes abnormally large or when the alveolar capillary barrier is beginning to fail or when lymphatic drainage is obstructed. The basal pulmonary extravascular water has usually increased between threefold and fivefold - before clinical signs are detected.9 Electron microscopy, biochemical studies of the -
2 Matter P, Barclay TR, Konickova Z Research in burns. Bern: Hans Huber Publishing, 1971 427. 3. Vivori E, Cudmore RE. Management of airway complications of burns. Br Med J 1977, ii 1462-64 4. Kimmerle G. Combust Toxicol 1974, 1: 4. 5 Wooley WD Br Polymer J 1971; 3: 186. 6 Eckhauser FE, Bellote J, Burke JF, Quinby WC. Tracheostomy complicating massive burn injury; a plea for conservation Am J Surg 1974, 127: 418 7. Maylan JA, West JT, Nash G Tracheostomy in thermally injured patients Am Surg 1972; 38: 119. 8 Cason JS. The treatment of burns. London- Chapman and Hall, 1981. 9 Morgan A, Collins JJ, Griswold AB A system for measurement of pulmonary extravascular water in the I.C U In: Computers in cardiology Long Beach: Institute of Electrical and Electronic Engineers, 1975: 201.
when
they first present to a respiratory clinic28). Correction of their nocturnal hypoxaemia may therefore prevent severe pulmonary hypertension and cor pulmonale, and also improve survival, as shown by the recent N.I.H.29and M.R.C.3° controlled trials of long-term low-dose oxygen in chronic bronchitis and emphysema, in both of which oxygen was given at night. However, in the N.I.H. trial oxygen given mainly at night (12 h in the 24 h day) did not prolong life as much as oxygen for 19-24 h in the 24 h day. Despite the well-known risk that oxygen therapy may increase CO2 retention in these patients during an exacerbation,31 no serious rise in PC02 was seen with long-term low-flow oxygen (possibly because PC02 was not measured during sleep). Such oxygen at night’ did cause temporary reversible acidosis in one moderately hypoxic "blue bloater" in whom the hypoxic drive to breathing was preserved,32 but the reduction in this drive observable in most such patients33 may protect them from a rise in PC02. GUILLEMINAULT et a1.34 have cautioned against ,nocturnal oxygen therapy in chronic bronchitis, for they describe doubling in the duration of apnoeic events in REM sleep with 1’5 or 3 1/min of oxygen given through nasal prongs in four such patients with day-time somnolence and sleep apnoea, only one being a "blue bloater". Conversely in eleven patients with mild hypoxaemia (mean P02 66 mm Hg) from chronic obstructive lung disease, but without serious C02 retention (mean PC02 44 mm Hg), 2 1/min of oxygen by nasal prongs for half the night increased the time spent asleep, and reduced oxygen desaturation, but had no effect on episodes of apnoea or hypopnoea, when compared with the other half of the night without oxygen.35 Arterial PC02 was measured in five of these patients, but did not rise more during episodes of disordered breathing when they breathed oxygen than in similar episodes when they breathed’air. Certainty as to the safety of nocturnal oxygen in these patients clearly requires more measurements, but the recent trials suggest that the treatment is safe, if the oxygen flow is kept low and provided that the patients are not in an acute exacerbation of respiratory acidosis.31 Studies of effective respiratory stimulants during sleep in "blue bloaters" are badly needed, with 28.
29
30.
Catterall JR, Douglas NJ, Calverley PMA, et al. Hypoventilation is common, but sleep apnea rare, in transient nocturnal hypoxemia of ’blue and bloated’ bronchitis. Am Rev Resp Dis 1981; 123: 113. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemia chronic obstructive lung disease. Ann Intern Med 1980; 93: 391-98. M.R.C. Working Party. Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981; i:
681-86. 31. Warren PM, Avery A, Millar JS, Flenley DC. Respiratory failure revisited: Exacerbations of chronic bronchitis 1960-1968 and 1970-1976. Lancet 1980; i: 467-74 32 Leitch AG, Clancy LJ, Leggett RJE, et al Arterial blood gas tensions, hydrogen ion, and electroencephalogram during sleep in patients with chronic ventilatory failure. Thorax 1976; 31: 730-35. 33. Flenley DC, Franklin DH, Millar JS. The hypoxic drive to breathing in chronic bronchitis and emphysema. Clin Sci 1970; 38: 503-18. 34. Guilleminault C, Cummiskey J, Motta J. Chronic obstructive airflow disease and sleep studies. Am Rev Resp Dis 1980; 122: 397-406. 35. Kearley R, Wynne JW, Block AJ, et al The effect of low flow oxygen on sleep disordered breathing and oxygen desaturation. Chest 1980; 78: 682-85.
without added oxygen, for such drugs may well interfere with sleep. The new French drug almitrine, which can improve hypoxaemia and C02 retention in "blue bloaters" ,36 clearly merits such a trial in sleep. The effects of drugs on breathing during sleep, since they concern two of the more important human activities, deserve attention from both drug regulatory bodies and the pharmaceutical industry. or
THE LANGERHANS CELL OF the many subjects which reliably produce heated and inconclusive debate amongst dermatologists, the epidermal Langerhans cell takes the prize. Some new findings, made more than a hundred years after this dendritic cell was discovered by Paul.Langerhans,’ now bid fair to mitigate its contentious reputation. The Langerhans cell was originally thought to be either a sensory receptor cell or an effete melanocyte, and progress in its definition was greatly impeded by lack of methods for firm identification of the cells. This deficiency was rectified in 1961 by Birbeck, Breathnach, and Everall2 who described the ultrastructural features of the Langerhans cell and in particular identified a unique racquet-shaped organelle, the Birbeck granule. The Langerhans cell also occurs in dermis, mucous membranes, and lymphatic tissue. Its derivation from a bone marrow mesenchymal cell has now been convincingly demonstrated as a result of transplantation and chimaera studies by Tamaki and Katz.3 The disease histiocytosis X, which affects bone, lungs, and skin, is probably due to proliferation of the Langerhans cell4 and the possibility that the Langerhans cell is the target cell in mycosis fungoides is being explored.s The major new discoveries, however, centre on the involvement of Langerhans cells in immunological reactions, especially allergic contact dermatitis. Convincing evidence of an important role in allergic contact dermatitis was first provided by Silberberg,6 who noted the intimate apposition of Langerhans cells with mononuclear cells in positive patch test reactions. The appearances of the Langerhans cell were often suggestive of increased secretory activity. The next important development was the realisation that Langerhans cells, like mononuclear phagocytes, serve a pivotal role in sensitisation, by processing antigens before their presentation to immunocompetent lymphocytes. Langerhans cells behave as dendritic scavengers of foreign small-molecular material which has trespassed within the epidermis.’ This finding is of especial relevance to allergic contact dermatitis, which usually involves a cutaneous hypersensitivity reaction to simple low-molecular-weight substances. The analogy with mononuclear phagocytes was further strengthened 36. 1.
Symposium on gas exchange and ventilation perfusion ratios. Round table, Almitrine Bull Eur Physiopathol Resp 1980; 16: 195p-208p. Langerhans P. Uber die Nerven der menschlichen Haut. Virchows Arch 1868; 44:
325-37. 2. Birbeck MS, Breathnach AS, Everall JD. An electron microscopic study of basal melanocytes and high level clear cells (Langerhans cells) in vitiligo. J Invest Dermatol 1961; 37: 51-64. 3. Tamaki K, Katz SI. Ontogeny of Langerhans cells J Invest Dermatol 1980; 75: 12-13 4. Basset F, Turiaf MJ. Identification par la microscopie electronique de particles de nature probablement virale dans les lesions granulomateuses d’une histiocytose-X pulmonaire. CR Acad Sci Paris 1965; 261: 3701-03. 5. Mackie RM. Initial event in mycosis fungoides of the skin is viral infection of epidermal Langerhans cells. Lancet 1981; ii: 283-84. 6. Silberberg I. Apposition of mononuclear cells to Langerhans cells in contact allergic reactions. Acta Dermatovener 1973; 53: 1-12. 7. Shelley WB, Juhlin L. Langerhans cells form a reticuloepithelial trap for external contact antigens. Nature 1976; 261: 46-47
673
emerged that Langerhans cells were the only epidermal cells expressing Fc-IgG receptors, Creceptors, and Ia antigens and, moreover, that they could replace labearing macrophages as activators of antigen-specific when it
allogeneic T cells.8-11 Further confirmation of the central role of Langerhans cell was obtained when Streilein et al.11 showed that contact sensitivity could not be induced in the mouse if the shaved skin had previously been depleted of Langerhans cells by irradiation with ultraviolet B (290-320 nm). It should therefore have come as no great surprise when 8-methoxypsoralen/ultraviolet-A photochemotherapy proved to inhibit experimental allergic contact sensitisation in man. Strauss and his colleagues’3 found reduced or absent allergic contact sensitisation to dinitrochlorbenzene in 55 of 102
psoriatic patients receiving photochemotherapy (PUVA), though the irritant response to DNCB was normal. Similar results were subsequently reported by Newcastle workers. 14
,
suppression is due to apparent depletion of the Langerhans cell network in the epidermis now receives support from Friedmann.ls He measured the population density of Langerhans cells in the clinically normal epidermis of 25 patients. Before PUVA treatment the mean population density of Langerhans cells was 713±60 SEM/mm2 epidermal surface area; after 7 treatments there were only 56±29/mmz remaining. Morphologically, the earliest change was loss of dendritic processes. Thus it seems that the impairment of DNCB sensitisation may be a result of subnormal antigen recognition and processing within the epidermis, although direct actions on T lymphocytes by ultraviolet cannot be excluded. The implications of these findings are wide. If mutagenic change in keratinocytes or melanocytes is a random event within the skin, then the existence of competent immunosurveillance within the skin becomes crucial. Prolonged exposure of the skin to ultraviolet, whether natural or artificial, could not only cause mutations in these cells but also exert a "pseudopromotor" action13 due to impaired recognition of foreign antigens, thus encouraging clonal outgrowth of malignant cells. Friedmann’s findings must reinforce anxiety about the longterm effects of prolonged exposure of skin to ultraviolet, including PUVA treatment for psoriasis. That this
THE LUNG IN BURNS THE term burn-lung Vietnam war of certain
syndrome was used during the extensively burned patients with
acute respiratory distress.’ Most of the burns had been sustained in the open, from flame-throwing weapons, bombs, or gasoline related explosions. The patients often died. 8
Stingl G, Wolff-Schreiner EC, Pichler WJ, Gschnait F, Knapp W, Wolff K. Epidermal Langerhans cells bear F and C3 receptors. Nature 1977; 268: 245-46. 9. Rowden G, Lewis MG, Sullivan AK. Ia antigen expression on human epidermal Langerhans cells. Nature 1977; 268: 247-48. 10. Klareskog L, Tjernlund UM, Forsum U, Peterson PA. Epidermal Langerhans cells express Ia antigens. Nature 1977; 268: 248-50. 11Stingl G, Katz SI, Green I, Shevach EM The functional role of Langerhans cells. J Invest Dermatol 1980; 74: 315-18. 12. Streilein JW, Toews GT, Gilliam JN, Bergstresser PR. Tolerance of hypersensitivity. to 2, 4, -dinitro-1-fluorobenzene: the role of Langerhans cell density within epidermis. J Invest Derm 1980; 74: 319-22. 13. Strauss GH, Greaves MW, Price M, Bridges BA, Hall-Smith P, Vella Briffa D. Inhibition of delayed hypersensitivity reactions in skin (DNCB test) by 8-methoxypsoralen photochemotherapy. Lancet 1980;ii 556-59. 14. Moss C, Fnedmann PS, Shuster S. Inhibition of delayed hypersensitivity skin reactions in patients on methoxypsoralen photochemotherapy. Lancer 1980; ii: 922. 15. Friedmann P. Disappearance of epidermal Langerhans cells during PUVA therapy. Br
J Dermatol 1981; 1 Getzen
105: 219-21
LC, Pollack EW Fatal respiratory distress in burned patients Surgery Gynecol Obstet 1981; 152: 741-44.
Inhalation of smoke did not seem to be a factor in the respiratory distress, whereas in peacetime, respiratory troubles arise particularly in people who have been trapped in burning buildings or confined spaces; the lung is damaged by smoke from burning furniture made with polyurethane and plastic foams.2-’ Carbon monoxide, nitric oxide, nitrogen peroxide, and hydrocyanic acid are among the substances under suspicion. Many causes of respiratory distress in burned patients have now been identified and it is doubtful whether the label of burn-lung syndrome needs to be preserved. This, indeed, is the message from a recent review of the causes of death in the Vietnam patients. Deaths from respiratory distress in the first forty-eight hours from the time of burning were due to overhydration or overloading with transfusion solution in patients who had coexisting renal failure. Later deaths were attributable to overhydration, pseudomonas sepsis, and aspiration pneumonia. The same report states that the use of colloids such as albumin, instead of crystalloid solutions, in the treatment of shock reduced the incidence of pulmonary oedema. In the U.K., human plasma protein fraction (mainly albumin) and the colloid dextran 110 are the main agents used for treatment of shock in the first forty-eight hours, and this may be why reports of burn lung are uncommon there. Pulmonary oedema due to overhydration should be recognised by clinical examination coupled with review of the fluid balance sheet. Bronchopneumonia and pulmonary sepsis also arise and are treated in the usual way. For relief of respiratory obstruction the use of endotracheal intubation instead of tracheostomy has considerably lessened mortality from pulmonary infection, particularly from Pseudomonas aeruginosa. 6,7 Prolonged intubation, however, has its own problems of tracheal and laryngeal ulceration, and the lesions may be a source of infection. Prolonged central intravenous catheterisation can also result in multiple lung abscesses when septic emboli arise from the catheter tip.8 Aspiration pneumonia has also occurred, even in patients having nasogastric suction. There seems no way of reliably detecting and monitoring the type of patient who will get this complication, which is often fatal. Pulmonary thromboembolism can be prevented by prophylactic anticoagulant therapy, but this is usually restricted to patients with burns of less than 15% of body surface, because of the danger of haemorrhage from gastric erosions and Curling’s ulcers in those with larger burns. The traditional sign of pulmonary oedema is the rale, which points to excess water in the airways. This, however, is a late sign and we really want to know when passage of water across the pulmonary capillary endothelium becomes abnormally large or when the alveolar capillary barrier is beginning to fail or when lymphatic drainage is obstructed. The basal pulmonary extravascular water has usually increased between threefold and fivefold - before clinical signs are detected.9 Electron microscopy, biochemical studies of the -
2 Matter P, Barclay TR, Konickova Z Research in burns. Bern: Hans Huber Publishing, 1971 427. 3. Vivori E, Cudmore RE. Management of airway complications of burns. Br Med J 1977, ii 1462-64 4. Kimmerle G. Combust Toxicol 1974, 1: 4. 5 Wooley WD Br Polymer J 1971; 3: 186. 6 Eckhauser FE, Bellote J, Burke JF, Quinby WC. Tracheostomy complicating massive burn injury; a plea for conservation Am J Surg 1974, 127: 418 7. Maylan JA, West JT, Nash G Tracheostomy in thermally injured patients Am Surg 1972; 38: 119. 8 Cason JS. The treatment of burns. London- Chapman and Hall, 1981. 9 Morgan A, Collins JJ, Griswold AB A system for measurement of pulmonary extravascular water in the I.C U In: Computers in cardiology Long Beach: Institute of Electrical and Electronic Engineers, 1975: 201.