- Email: [email protected]
PREVENTION AND MANAGEMENT OF CURLING'S ULCER
138
reaction between spermatozoa and cervical mucus has been studied in detail by KREMER and JAGER,22 who used a sperm-cervical mucus contact (SCMC) test. In the presence of antisperm antibodies, motility of the spermatozoa in the seminal plasma changed into quick shaking or jerking movements without progression in the cervical mucus-apparently owing to attachment of the sperm tails to glycoprotein micelles in the mucus. This happened even after heating of the mucus to 56 1 C for 30 minutes, so it was not complement dependant. The SCMC test was, however, only positive if the sperms were coated with IgA, and this depended on the presence of antibodies in the seminal plasma which did not always accompany antibodies (chiefly IgG) in the serum.23 The proportion of naturally subfertile men who have seminal plasma antibodies rises linearly once the serum titre exceeds 32, whereas after vasectomy few men acquire seminal plasma antibodies until the serum titre is very high-more than 256.24 On p. 117 Dr LINNET and colleagues report that, after reversal of vasectomy, antibodies which were formerly present only in serum can appear in seminal plasma and interfere with infertility. This observation supports the notion that in males the antibody must be present in the seminal plasma to interfere with fertility, and explains the relation between antibodies and impaired fertility after vasectomy reversal. The effects of antisperm antibodies are far less clearly defined in females than in males. Using the TSAT, FRANKLIN and DUKES" found evidence of spermagglutination in no less than 78% of women with unexplained infertility; but since 11% of pregnant women also gave a positive result the validity of these findings was very doubtful. In fact the false-positive results were due to a beta-spermagglutinin which is not an antibody but probably a steroid.25 This beta activity can now be absorbed so that true sperm antibody activity is unchanged.26 Cervical mucus is difficult to test but, after homogenisation with bromelin, higher titres have been recorded in the cervical mucus than in serum13—the reverse of the situation in males. These refinements in technique will probably do much to clarify the effects of antisperm antibodies in women; cervical mucus is likely to provide as much useful information in women as does seminal plasma in men. The coexistence of a normal sperm count and a persistently poor postcoital test in an infertile couple strongly suggests the existence of antisperm antibodies, and these are most commonly found in the
22. Kremer J, Jager S. The sperm-cervical mucus contact test. a preliminary report. Fertil Steril 1976; 27: 335-40. 23. Kremer J, Jager S, Kuiken J, Van Slochteren-Draaisma T. Recent advances in diagnosis and treatment of infertility due to antisperm antibodies. In: Cohen J, Hendry WF, eds. Spermatozoa, antibodies and infertility. Oxford: Blackwell, 1978: 117-27 24. Rümke P. Autoantigenicity of spermatozoa. In. Cohen J, Hendry WF, eds. Spermatozoa, antibodies and infertility. Oxford: Blackwell, 1978. 25. Boettcher B, Kay DJ. Fractionation of a human spermagglutinating serum. Nature 1969; 223: 737-38. 26. Ingerslev HJ, Hjort T. Spermagglutinating antibodies and beta-spermagglutinins in sera from infertile and fertile women. Fertil Steril 1979; 31: 496-502.
husband: in 30 such couples KREMER et al. 27 detected antibodies in 25 husbands and only 5 wives. The fertility of about one-third of patients with antisperm antibodies can be restored with corticosteroids, either in long-term low dose or cyclical high doses;28,29 results with artificial insemination with or without sperm
disappointing. Before the start of be quite sure, firstly, that the antisperm antibodies are really interfering with fertility; secondly, that the husband’s sperm count is as good as possible; and, thirdly, that the wife has patent tubes and the presence and timing of ovulation has been
washing
have been
treatment one must
established. PREVENTION AND MANAGEMENT OF CURLING’S ULCER ALMOST
everything about Curling’s
ulcer is
controver-
sial-definition,l -6 incidence,4,5clinical relevance,4,7
history,4,5 pathogenesis,8,9 prevention 5,6,1 0-l’
natural and manage-
ment.3,5-7,13,14 The best-run cohort studies, therefore, are open to biases,’and such biases can be hard to detect. To say whether test and control groups are truly comparable one needs a mass of information on clinical and prognostic factors; 16,17 yet, in some controlled trials, not all the factors known to influence development and outcome have been con; sidered even at design ’stage (much less stated in the analysis). For instance, Curling’s ulcer is commonly defined as an acute gastroduodenal lesion which arises during the "natural history" of severe thermal injury. 3,4 The time of onset can vary from a few hours4,18 to three weeks’,’ after the burn. Yet
27. Kremer
J, Jager S, Van Slochteren-Draaisma T. The "unexplained" poor postcoital Int J Fetil 1978; 23: 277-81. Shulman S, Harlin B, Davis P, Reyniak JV. Immune infertility and new approaches to test.
28.
treatment.
Fertil Steril 1978; 29: 309-13.
29.
Hendry WF, Stedronska J, Hughes L, Cameron KM, Pugh RCB. Steroid treatment of male subfertility caused by antisperm antibodies. Lancet 1979; ii: 498-500. 1. Menguy R. Acute gastric mucosal bleeding. Annu Rev Med 1972; 23: 297-312. 2. Goodman AA, Osborne MP. Stress ulcer. A definition, a discussion of other stressassociated upper gastrointestinal lesions, and an experimental model. Am J Surg 1973; 125: 461-63. 3.
4.
Stremple JF, Mon H, Lev R, Glass GBJ. The stress ulcer syndrome. In: Current problems in surgery Chicago: Year Book Medical Publishers, 1973: 1-64. Czaja AJ, Mc Alhany JC, Pruitt BA. Acute gastroduodenal disease after thermal injury. An endoscopic evaluation of incidence and natural history. N Bngl J Med 1974; 291: 925-29.
5. Muir IFK, Jones PF. Curling’s ulcer. a rare condition. Br J. Surg 1976; 63: 60-66 6. Schumpelick V, Horatz K, Schreiber HW. Das Stressulcus. Langenbacks Arch Chir
1977; 344: 141-55. 7. Editorial. Prevention or cure for stress-induced gastrointestinal bleeding? Br Med J 1980; 281: 631-32. 8 Silen W. New concepts of the gastric mucosal barrier. Am J Surg 1977; 133: 8-12. 9. Menguy R. The prophylaxis of stress ulceration. N Engl Med 1980; 302: 461-62 J
10. McElwee HP, Sirinek KR, Levine BA. Cimetidine affords protection equal to antacids in prevention of stress ulceration following thermal injury. Surgery 1979; 86: 620-26. 11. Solem LD, Strate RG, Fischer RP. Antacid therapy and nutritional supplementation in the prevention of Curling’s ulcer. Surg Gynecol Obstet 1979; 148: 367-70 12. Choctaw WT, Fujita C, Zawacki BE. Prevention of upper gastrointestinal bleedingin burn patients. Arch Surg 1980; 115: 1073-76. 13. Skillman JJ, Silen W. Stress ulceration in the acutely ill. Annu Rev Med 1976; 27: 9-22. 14. Hetzel D. Prevention or cure for stress-induced gastrointestinal bleeding? Br Med J 1980; 281: 1348-49. 15. Feinstein AR. Epidemiologic studies. In Epidemiologie und Arzneimittelsicherheit Berlin: Schering, 1977: 23-39. 16. Lorenz W, Fischer M, Rohde H, Troidl H, Reimann H-J, Ohmann Ch. Histamine and stress ulcer: new components in organizing a sequential trial on cimetidine prophylaxis in seriously ill patients and definition of a special group at risk (severe polytrauma). Klin Wschr 1980; 58: 653-65. 17. Fischer M, Lorenz W, Rohde H. The use of cimetidine in preventing clinically manifest stress ulcers in patients with severe polytrauma. In : Cimetidine(Tagamet). Amsterdam Excerpta Medica, 1980; 45-51 18. Lucas ChE, Sugawa Ch, Riddle J, Recter F, Rosenberg B, Walt AJ. Natural history and surgical dilemma of "stress" gastric bleeding. Arch Surg 1971; 102: 266-73.
139
in one trial, by McElwee and others, 10 patients were accepted late as 48 h after the injury and the trial regimen (cimetidine versus antacids) lasted only ten days. Analysing this trial Lorenz et al. 16 have pointed to other possible pitfalls: experimentally, haemoconcentration is said to be important in the pathogenesis of stress ulcers after burns,19 yet this criterion was not mentioned; histamine induces gastrointestinal lesions in animals20 and human beings,21 and the early treatment of burns includes many drugs which can induce histamine release22 (e.g., analgesics, hypnotics, and resuscitation fluids)-again, information on this aspect is lacking. Lorenz singled out this trial, not for pillory, but because in quality it stands out from its predecessors. The conclusion-that cimetidine and antacids are equally effective-may be right or wrong because many of the known prognostic factors are not specified for the test and control groups. Apart from those already mentioned, relevant factors may include sepsis,23 coagulation disturbances, respiratory insufficiency, and even the treatment of respiratory insufficiency by positive end-expiratory pressure 24 or a-receptor blockade.25 In addition, a slight difference in severity of trauma favours the antacid group since 43% of the patients with antacids, but only 15% with cimetidine, are in the category with the smallest area burned (30-39% total body as
surface). There is
second reason why clinical trials have not been in very helpful the prevention and management of Curling’s ulcer. The endpoints in such trials have included: development oflesion identified by repeated endoscopy; 10 subclinical bleeding shown by radiolabelled erythrocytes or the ’Haemoccult’ test;26 clinically manifest bleeding with endoscopic confirmation of the lesions;16 clinically evident a
bleeding;3,11 clinically important bleeding;3and perforation (the catastrophic complication’°) or death.17 But the clinician who wants to know which regimen (applied or omitted) will prevent melaena, haematemesis, perforation, and death will be interested only in clinically manifest bleeding. Unfortunately there seems to have been only one controlled trial in which such an end-point was used and that dealt with severe polytrauma. 16,11 Workers who seek to persuade us of the relevance of endoscopic findings or tests of subclinical bleeding should seek a correlation between their data and the signs which are clinically obvious. In patients with severe trauma, including burns,2’ such a correlation was not found. Cimetidine,10 antacids,28 a high-nitrogen elemental diet,12 vigorous prophylaxis and therapy of infections by antibiotics,3 and the use of colloids instead of crystalloids dur19. Friesen SR. The
genesis of gastroduodenal ulcer following burns: An experimental study. Surgery 1950; 28: 123-58. 20. Büchner F, Molloy PS. Das echte peptische Geschwür der Ratte. Klin Wschr 1927; 6: 2193-96. 21 Katz D, Siegel HJ, Glass GBJ. Acute gastric mucosal lesions produced by augmented histamine test. Am J Digest Dis 1969; 14: 447-52. 22. Lorenz W, Doenicke A. Histamine release in clinical conditions. Mount Sinai J Med
1978; 45: 357-86. 23. Fumarola D Endotoxins and gastroduodenal ulceration after burns. Br Med J 1979; ii: 1142. 24. Beyer J, Schosser R, Conzen P, Funk W, Beckenlechner P, Messmer K. Regional blood flow m spanchnic organs during positive end expiratory pressure ventilation. Langenbeck’s Arch Chir Suppl Surg Forum 1980; 239-42 25. Mertz DP, Wick T, Thongbhoubesra T, Walloschek C. Über die akute Wirkung verschiedener pharmakologischer Substanzen auf die Säuresekretion an stimulierten menschlichen Magen. Klin Wschr 1970; 48: 821-22. 26. Priebe HJ, Skillman JJ, Bushnell LS, Long PC, Silen W. Antacid versus cimetidine in preventing acute gastrointestinal bleeding. N Engl J Med 1980; 302: 426-30. 27 Bowen JC, Fleming WH A prospective study of stress ulceration in Vietnam. South
28
Med J 1974, 67: 156-60. McAlhany JC, Czaja AJ, Pruitt
BA. Antacid control of
gastroduodenal disease after burns J Trauma 1976; 16:
complications 645-49.
from
acute
ing the shock phasehave all been recommended for the prevention of Curling’s ulcer. When the lesion shows itself clinically, with haemorrhage or perforation, the recommendations vary from cimetidine and antacids to laser coagulation and total gastrectomy. 3,S,6,7,14 In deciding what to do the clinician still has to rely heavily on personal experience, clinical impression, and faith. COAGULASE-NEGATIVE STAPHYLOCOCCI THE coagulase test-one of the more memorable features of
undergraduate microbiology-enables Staphylococcus aureus (coagulase positive) to be readily identified in the laboratory. The coagulase-negative staphylococci are more variably classified, but by Baird-Parker’s method are divided into Staph. saprophyticus and Staph. epidermidis.Staph. saprophyticus is usually regarded as non-pathogenic, being commonly found in air, soil, and dust, though some strains cause urinary tract infections in children2 and young women.3 Staph. epidermidis has long been regarded as a harmless commensal of man, the prevalence on skin being 85-100%, in nose, mouth, and nasopharynx 90%, and in vagina and uterine cervix 35-80%.4 This organism does, however, have pathogenic potential after insertion of surgical prostheses. Staph. epidermidis is an uncommon cause of subacute bacterial endocarditis, accounting for only 2-6% of cases. Diagnosis is often difficult because blood cultures may only intermittently be positive. The organism is a common contaminant of clinical specimens and làboratory cultures, and it tends to be dismissed as clinically irrelevant. But in patients with a prosthetic heart valve, Staph. epidermidis is the most frequent cause of endocarditis, accounting for 27% of earlyonset cases and 10% of late-onset cases. Here even a single positive blood culture among many negatives is not to be ignored and additional cultures should be set up. Some workers have tested by immunofluorescence for Staph. epidermidis antibodies in the patient’s serum as an indicator of genuine infection.5 Staph. epidermidis is also found in 14% of infections in peripheral vascular grafts.6 This is a serious in survivors it often complication carrying a high mortality; results in loss of both graft and limb.7 60-95% of infections involving cerebrospinal fluid (CSF) shunts are caused by Staph. epidermidis.8 The infection may be overt, with pyrexia in the early postoperative period, or it may show itself later and more insidiously as low-grade fever with anorexia, lethargy, and perhaps signs of raised intracranial pressure. The organism can usually be isolated from cultures of blood, CSF, and the wound site. Again, antibodies to Staph. epidermidis may be useful pointers when cultures are difficult to interpret. After total hip replacement Staph. epidermidis is second only to Staph. aureus as a cause of sepsis. The organisms 1. Baird-Parker AC The basis for the present classification of staphylococci and micrococci Ann NY Acad Sci 1974; 236: 7-14 2 Hermansson G, Bollgren I, Bergstrom T, Winberg J Coagulate-negative staphylococci as a cause of symptomatic urinary infections in children J Pediat 1974; 84: 807-10 3. Sellin M, Cooke DI, Gillespie WA, Sylvester DGH, Anderson JD Micrococcal urinary tract infections in young women Lancet 1975; ii: 570-72 4 Youmans GP, Paterson PY, Sommers HM The biologic and clinical basis of infectious diseases. Philadelphia W B Saunders, 1980: 83-92 5. Bayston R. Serological investigation in children with colonised Spitz-Holter valves J Clin Path 1972; 1072: 718-20. 6. Keighley MRB, Burdon DW. Antimicrobial prophylaxis in surgery Tunbridge Wells: Pitman Medical, 1979: 140-41. 7. Conn JH, Hardy JD, Chavez CM, Fain WR Infected arterial grafts, experience in 22 cases with emphasis on unusual bacteria and technics Ann Surg 1970; 171: 704-14. 8. Schoenbaum SC, Gardner P, Shillito J. Infections in cerebrospinal fluid shunts: Epidemiology, clinical manifestations and therapy J Infect Dis 1975, 131: 543-52
reaction between spermatozoa and cervical mucus has been studied in detail by KREMER and JAGER,22 who used a sperm-cervical mucus contact (SCMC) test. In the presence of antisperm antibodies, motility of the spermatozoa in the seminal plasma changed into quick shaking or jerking movements without progression in the cervical mucus-apparently owing to attachment of the sperm tails to glycoprotein micelles in the mucus. This happened even after heating of the mucus to 56 1 C for 30 minutes, so it was not complement dependant. The SCMC test was, however, only positive if the sperms were coated with IgA, and this depended on the presence of antibodies in the seminal plasma which did not always accompany antibodies (chiefly IgG) in the serum.23 The proportion of naturally subfertile men who have seminal plasma antibodies rises linearly once the serum titre exceeds 32, whereas after vasectomy few men acquire seminal plasma antibodies until the serum titre is very high-more than 256.24 On p. 117 Dr LINNET and colleagues report that, after reversal of vasectomy, antibodies which were formerly present only in serum can appear in seminal plasma and interfere with infertility. This observation supports the notion that in males the antibody must be present in the seminal plasma to interfere with fertility, and explains the relation between antibodies and impaired fertility after vasectomy reversal. The effects of antisperm antibodies are far less clearly defined in females than in males. Using the TSAT, FRANKLIN and DUKES" found evidence of spermagglutination in no less than 78% of women with unexplained infertility; but since 11% of pregnant women also gave a positive result the validity of these findings was very doubtful. In fact the false-positive results were due to a beta-spermagglutinin which is not an antibody but probably a steroid.25 This beta activity can now be absorbed so that true sperm antibody activity is unchanged.26 Cervical mucus is difficult to test but, after homogenisation with bromelin, higher titres have been recorded in the cervical mucus than in serum13—the reverse of the situation in males. These refinements in technique will probably do much to clarify the effects of antisperm antibodies in women; cervical mucus is likely to provide as much useful information in women as does seminal plasma in men. The coexistence of a normal sperm count and a persistently poor postcoital test in an infertile couple strongly suggests the existence of antisperm antibodies, and these are most commonly found in the
22. Kremer J, Jager S. The sperm-cervical mucus contact test. a preliminary report. Fertil Steril 1976; 27: 335-40. 23. Kremer J, Jager S, Kuiken J, Van Slochteren-Draaisma T. Recent advances in diagnosis and treatment of infertility due to antisperm antibodies. In: Cohen J, Hendry WF, eds. Spermatozoa, antibodies and infertility. Oxford: Blackwell, 1978: 117-27 24. Rümke P. Autoantigenicity of spermatozoa. In. Cohen J, Hendry WF, eds. Spermatozoa, antibodies and infertility. Oxford: Blackwell, 1978. 25. Boettcher B, Kay DJ. Fractionation of a human spermagglutinating serum. Nature 1969; 223: 737-38. 26. Ingerslev HJ, Hjort T. Spermagglutinating antibodies and beta-spermagglutinins in sera from infertile and fertile women. Fertil Steril 1979; 31: 496-502.
husband: in 30 such couples KREMER et al. 27 detected antibodies in 25 husbands and only 5 wives. The fertility of about one-third of patients with antisperm antibodies can be restored with corticosteroids, either in long-term low dose or cyclical high doses;28,29 results with artificial insemination with or without sperm
disappointing. Before the start of be quite sure, firstly, that the antisperm antibodies are really interfering with fertility; secondly, that the husband’s sperm count is as good as possible; and, thirdly, that the wife has patent tubes and the presence and timing of ovulation has been
washing
have been
treatment one must
established. PREVENTION AND MANAGEMENT OF CURLING’S ULCER ALMOST
everything about Curling’s
ulcer is
controver-
sial-definition,l -6 incidence,4,5clinical relevance,4,7
history,4,5 pathogenesis,8,9 prevention 5,6,1 0-l’
natural and manage-
ment.3,5-7,13,14 The best-run cohort studies, therefore, are open to biases,’and such biases can be hard to detect. To say whether test and control groups are truly comparable one needs a mass of information on clinical and prognostic factors; 16,17 yet, in some controlled trials, not all the factors known to influence development and outcome have been con; sidered even at design ’stage (much less stated in the analysis). For instance, Curling’s ulcer is commonly defined as an acute gastroduodenal lesion which arises during the "natural history" of severe thermal injury. 3,4 The time of onset can vary from a few hours4,18 to three weeks’,’ after the burn. Yet
27. Kremer
J, Jager S, Van Slochteren-Draaisma T. The "unexplained" poor postcoital Int J Fetil 1978; 23: 277-81. Shulman S, Harlin B, Davis P, Reyniak JV. Immune infertility and new approaches to test.
28.
treatment.
Fertil Steril 1978; 29: 309-13.
29.
Hendry WF, Stedronska J, Hughes L, Cameron KM, Pugh RCB. Steroid treatment of male subfertility caused by antisperm antibodies. Lancet 1979; ii: 498-500. 1. Menguy R. Acute gastric mucosal bleeding. Annu Rev Med 1972; 23: 297-312. 2. Goodman AA, Osborne MP. Stress ulcer. A definition, a discussion of other stressassociated upper gastrointestinal lesions, and an experimental model. Am J Surg 1973; 125: 461-63. 3.
4.
Stremple JF, Mon H, Lev R, Glass GBJ. The stress ulcer syndrome. In: Current problems in surgery Chicago: Year Book Medical Publishers, 1973: 1-64. Czaja AJ, Mc Alhany JC, Pruitt BA. Acute gastroduodenal disease after thermal injury. An endoscopic evaluation of incidence and natural history. N Bngl J Med 1974; 291: 925-29.
5. Muir IFK, Jones PF. Curling’s ulcer. a rare condition. Br J. Surg 1976; 63: 60-66 6. Schumpelick V, Horatz K, Schreiber HW. Das Stressulcus. Langenbacks Arch Chir
1977; 344: 141-55. 7. Editorial. Prevention or cure for stress-induced gastrointestinal bleeding? Br Med J 1980; 281: 631-32. 8 Silen W. New concepts of the gastric mucosal barrier. Am J Surg 1977; 133: 8-12. 9. Menguy R. The prophylaxis of stress ulceration. N Engl Med 1980; 302: 461-62 J
10. McElwee HP, Sirinek KR, Levine BA. Cimetidine affords protection equal to antacids in prevention of stress ulceration following thermal injury. Surgery 1979; 86: 620-26. 11. Solem LD, Strate RG, Fischer RP. Antacid therapy and nutritional supplementation in the prevention of Curling’s ulcer. Surg Gynecol Obstet 1979; 148: 367-70 12. Choctaw WT, Fujita C, Zawacki BE. Prevention of upper gastrointestinal bleedingin burn patients. Arch Surg 1980; 115: 1073-76. 13. Skillman JJ, Silen W. Stress ulceration in the acutely ill. Annu Rev Med 1976; 27: 9-22. 14. Hetzel D. Prevention or cure for stress-induced gastrointestinal bleeding? Br Med J 1980; 281: 1348-49. 15. Feinstein AR. Epidemiologic studies. In Epidemiologie und Arzneimittelsicherheit Berlin: Schering, 1977: 23-39. 16. Lorenz W, Fischer M, Rohde H, Troidl H, Reimann H-J, Ohmann Ch. Histamine and stress ulcer: new components in organizing a sequential trial on cimetidine prophylaxis in seriously ill patients and definition of a special group at risk (severe polytrauma). Klin Wschr 1980; 58: 653-65. 17. Fischer M, Lorenz W, Rohde H. The use of cimetidine in preventing clinically manifest stress ulcers in patients with severe polytrauma. In : Cimetidine(Tagamet). Amsterdam Excerpta Medica, 1980; 45-51 18. Lucas ChE, Sugawa Ch, Riddle J, Recter F, Rosenberg B, Walt AJ. Natural history and surgical dilemma of "stress" gastric bleeding. Arch Surg 1971; 102: 266-73.
139
in one trial, by McElwee and others, 10 patients were accepted late as 48 h after the injury and the trial regimen (cimetidine versus antacids) lasted only ten days. Analysing this trial Lorenz et al. 16 have pointed to other possible pitfalls: experimentally, haemoconcentration is said to be important in the pathogenesis of stress ulcers after burns,19 yet this criterion was not mentioned; histamine induces gastrointestinal lesions in animals20 and human beings,21 and the early treatment of burns includes many drugs which can induce histamine release22 (e.g., analgesics, hypnotics, and resuscitation fluids)-again, information on this aspect is lacking. Lorenz singled out this trial, not for pillory, but because in quality it stands out from its predecessors. The conclusion-that cimetidine and antacids are equally effective-may be right or wrong because many of the known prognostic factors are not specified for the test and control groups. Apart from those already mentioned, relevant factors may include sepsis,23 coagulation disturbances, respiratory insufficiency, and even the treatment of respiratory insufficiency by positive end-expiratory pressure 24 or a-receptor blockade.25 In addition, a slight difference in severity of trauma favours the antacid group since 43% of the patients with antacids, but only 15% with cimetidine, are in the category with the smallest area burned (30-39% total body as
surface). There is
second reason why clinical trials have not been in very helpful the prevention and management of Curling’s ulcer. The endpoints in such trials have included: development oflesion identified by repeated endoscopy; 10 subclinical bleeding shown by radiolabelled erythrocytes or the ’Haemoccult’ test;26 clinically manifest bleeding with endoscopic confirmation of the lesions;16 clinically evident a
bleeding;3,11 clinically important bleeding;3and perforation (the catastrophic complication’°) or death.17 But the clinician who wants to know which regimen (applied or omitted) will prevent melaena, haematemesis, perforation, and death will be interested only in clinically manifest bleeding. Unfortunately there seems to have been only one controlled trial in which such an end-point was used and that dealt with severe polytrauma. 16,11 Workers who seek to persuade us of the relevance of endoscopic findings or tests of subclinical bleeding should seek a correlation between their data and the signs which are clinically obvious. In patients with severe trauma, including burns,2’ such a correlation was not found. Cimetidine,10 antacids,28 a high-nitrogen elemental diet,12 vigorous prophylaxis and therapy of infections by antibiotics,3 and the use of colloids instead of crystalloids dur19. Friesen SR. The
genesis of gastroduodenal ulcer following burns: An experimental study. Surgery 1950; 28: 123-58. 20. Büchner F, Molloy PS. Das echte peptische Geschwür der Ratte. Klin Wschr 1927; 6: 2193-96. 21 Katz D, Siegel HJ, Glass GBJ. Acute gastric mucosal lesions produced by augmented histamine test. Am J Digest Dis 1969; 14: 447-52. 22. Lorenz W, Doenicke A. Histamine release in clinical conditions. Mount Sinai J Med
1978; 45: 357-86. 23. Fumarola D Endotoxins and gastroduodenal ulceration after burns. Br Med J 1979; ii: 1142. 24. Beyer J, Schosser R, Conzen P, Funk W, Beckenlechner P, Messmer K. Regional blood flow m spanchnic organs during positive end expiratory pressure ventilation. Langenbeck’s Arch Chir Suppl Surg Forum 1980; 239-42 25. Mertz DP, Wick T, Thongbhoubesra T, Walloschek C. Über die akute Wirkung verschiedener pharmakologischer Substanzen auf die Säuresekretion an stimulierten menschlichen Magen. Klin Wschr 1970; 48: 821-22. 26. Priebe HJ, Skillman JJ, Bushnell LS, Long PC, Silen W. Antacid versus cimetidine in preventing acute gastrointestinal bleeding. N Engl J Med 1980; 302: 426-30. 27 Bowen JC, Fleming WH A prospective study of stress ulceration in Vietnam. South
28
Med J 1974, 67: 156-60. McAlhany JC, Czaja AJ, Pruitt
BA. Antacid control of
gastroduodenal disease after burns J Trauma 1976; 16:
complications 645-49.
from
acute
ing the shock phasehave all been recommended for the prevention of Curling’s ulcer. When the lesion shows itself clinically, with haemorrhage or perforation, the recommendations vary from cimetidine and antacids to laser coagulation and total gastrectomy. 3,S,6,7,14 In deciding what to do the clinician still has to rely heavily on personal experience, clinical impression, and faith. COAGULASE-NEGATIVE STAPHYLOCOCCI THE coagulase test-one of the more memorable features of
undergraduate microbiology-enables Staphylococcus aureus (coagulase positive) to be readily identified in the laboratory. The coagulase-negative staphylococci are more variably classified, but by Baird-Parker’s method are divided into Staph. saprophyticus and Staph. epidermidis.Staph. saprophyticus is usually regarded as non-pathogenic, being commonly found in air, soil, and dust, though some strains cause urinary tract infections in children2 and young women.3 Staph. epidermidis has long been regarded as a harmless commensal of man, the prevalence on skin being 85-100%, in nose, mouth, and nasopharynx 90%, and in vagina and uterine cervix 35-80%.4 This organism does, however, have pathogenic potential after insertion of surgical prostheses. Staph. epidermidis is an uncommon cause of subacute bacterial endocarditis, accounting for only 2-6% of cases. Diagnosis is often difficult because blood cultures may only intermittently be positive. The organism is a common contaminant of clinical specimens and làboratory cultures, and it tends to be dismissed as clinically irrelevant. But in patients with a prosthetic heart valve, Staph. epidermidis is the most frequent cause of endocarditis, accounting for 27% of earlyonset cases and 10% of late-onset cases. Here even a single positive blood culture among many negatives is not to be ignored and additional cultures should be set up. Some workers have tested by immunofluorescence for Staph. epidermidis antibodies in the patient’s serum as an indicator of genuine infection.5 Staph. epidermidis is also found in 14% of infections in peripheral vascular grafts.6 This is a serious in survivors it often complication carrying a high mortality; results in loss of both graft and limb.7 60-95% of infections involving cerebrospinal fluid (CSF) shunts are caused by Staph. epidermidis.8 The infection may be overt, with pyrexia in the early postoperative period, or it may show itself later and more insidiously as low-grade fever with anorexia, lethargy, and perhaps signs of raised intracranial pressure. The organism can usually be isolated from cultures of blood, CSF, and the wound site. Again, antibodies to Staph. epidermidis may be useful pointers when cultures are difficult to interpret. After total hip replacement Staph. epidermidis is second only to Staph. aureus as a cause of sepsis. The organisms 1. Baird-Parker AC The basis for the present classification of staphylococci and micrococci Ann NY Acad Sci 1974; 236: 7-14 2 Hermansson G, Bollgren I, Bergstrom T, Winberg J Coagulate-negative staphylococci as a cause of symptomatic urinary infections in children J Pediat 1974; 84: 807-10 3. Sellin M, Cooke DI, Gillespie WA, Sylvester DGH, Anderson JD Micrococcal urinary tract infections in young women Lancet 1975; ii: 570-72 4 Youmans GP, Paterson PY, Sommers HM The biologic and clinical basis of infectious diseases. Philadelphia W B Saunders, 1980: 83-92 5. Bayston R. Serological investigation in children with colonised Spitz-Holter valves J Clin Path 1972; 1072: 718-20. 6. Keighley MRB, Burdon DW. Antimicrobial prophylaxis in surgery Tunbridge Wells: Pitman Medical, 1979: 140-41. 7. Conn JH, Hardy JD, Chavez CM, Fain WR Infected arterial grafts, experience in 22 cases with emphasis on unusual bacteria and technics Ann Surg 1970; 171: 704-14. 8. Schoenbaum SC, Gardner P, Shillito J. Infections in cerebrospinal fluid shunts: Epidemiology, clinical manifestations and therapy J Infect Dis 1975, 131: 543-52