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PERITONITIS CAUSED BY SLIME-PRODUCING COAGULASE NEGATIVE STAPHYLOCOCCI IN CONTINUOUS AMBULATORY PERITONEAL DIALYSIS
42 is whether or not these patients had an objectively discernible oedema in the parts of the body mentioned above at the time of onset of their complaints. The patients did not have "excessive bodily concern" at the time of interview. Replies to that section of the questionnaire might have been different before diuretic treatment
began. I suggest that these patients began with an awareness of that "fudging" of their physical attributes which is so characteristic of women (and less so men) as they pass from the "sharpness of feature" of youth to the roundness of physique of middle-age. This fudging affects the face, the breasts, the fingers, the waist, and to some extent the ankles. It might well be that these changes are first discerned subjectively as "swelling". This leads to some attempt to reshape the features. The various remedies available-crash dieting, purgation, diuretics-all perturb sodium homoeostasis. The remedies are used irregularly so that the induced disturbance of sodium homoeostasis and secondary water retention is variable in degree, even periodic or cyclical. Once started, the process can become aggravated by further dietary, diuretic, and purgation abuses. Idiopathic oedema could well be a social disease indirectly caused by the value apportioned in our society to women according to their shape. The main advantage of this pathogenesis, for which I claim no originality, is the therapy that follows. Pelosi’s hypothesis leads to the use of diuretics until the supposed underlying
neuroendocrine condition is resolved. If de Wardener’sl view is accepted, the patient can be handled sympathetically and given encouragement to avoid those remedies which exaggerate changes in salt and water homoeostasis. Diuretics should only be used for short-term symptomatic relief and in steadily decreasing dosage. The supposed underlying neuroendocrine abnormality remains obscure. The natural history of spontaneous remission usually after the menopause would fit in with a realisation by the patient that further changes are unavoidable with increasing age. Department of Medicine, Ninewells Hospital and Medical School,
W. K. STEWART
Dundee DD1 9SY 1. de Wardener HE.
Idiopathic
edema: Role of diuretic abuse.
Kidney
Int
1981;
19:
881-92.
PERITONITIS CAUSED BY SLIME-PRODUCING COAGULASE NEGATIVE STAPHYLOCOCCI IN CONTINUOUS AMBULATORY PERITONEAL
DIALYSIS
SIR,-Peritonitis is the major serious complication of continuous ambulatory peritoneal dialysis (CAPD).1 Coagulase negative staphylococci are the most common organism cultured from peritoneal dialysis effluents.2 Not all isolates of coagulase negative staphylococci cause clinically significant infections as defined by a white cell count above 100 cells/11, cloudy dialysis fluid, abdominal pain, and fever. A simple method to distinguish true pathogens from simple contaminants would be useful. Some strains of coagulase negative staphylococci produce a polysaccharide extracellular slime.3 This slime may be important in bacterial adherence to foreign bodies and may therefore increase the virulence of the organism. We studied the ability of coagulase negative staphylococci isolated from CAPD effluent to produce slime. 26 coagulase negative staphylococci were isolated from 22 of 140 patients on CAPD at the Queen Elizabeth Hospital during January to June, 1986. Isolates were examined for slime production as described by Christensen et all17 of 19 isolates from patients with clinically significant infections produced slime compared with 2 of 7 ISOLATES OF COAGULASE NEGATIVE STAPHYLOCOCCI IN CAPD EFFLUENTS FROM 22 PATIENTS I
isolates from patients who did not develop a clinical peritonitis (table). All 4 patients who required catheter removal because of a persistent antibiotic-resistant peritonitis had an infection with a
slime-producing organism. In-vitro studies have demonstrated increased adherence of slime-producing staphylococci to prosthetic devices,3afeature which may make the organism more difficult to eradicate.’ Our data show that the test for slime, production in coagulase negative staphylococcal peritonitis is a useful additional method for distinguishing contamination from clinically significant infections in CAPD. Also, catheter removal is more likely in slime-producing, coagulase negative staphylococcal infections, and a positive test may therefore provide an early indicator of severe infections, which are more difficult to eradicate with antibiotic therapy alone. Departments of Nephrology and Microbiology, Queen Elizabeth Hospital, Birmingham B15 2TH
M. BEAMAN L. SOLARO
D. ADU J. MICHAEL
J, Oreopoulos DG, Lio TT, Matthews R, De Veber GA. Management of peritonitis and bowel perforation during chronic peritoneal dialysis. Nephron 1976;
1. Rubin
16: 220-25. 2. Gruer LD, Turney JH, Curley J, Michael J, Adu D. Vancomycin and tobramycin in the treatment of CAPD peritonitis. Nephron 1985; 41: 279-82. 3. Christensen GD, Simpson WA, Bisno AL, Beachey EH. Adherence of slimeproducing strains of Staphylococcus epidermidis to smooth surfaces. Infect Immunol 1982; 37: 318-26. 4. Davenport DS, Massanari RM, Pfaller MA, Bale MJ, Streed SA, Hierholzer WJ. Usefulness of a test for slime production as a marker for clinically significant infections with coagulase negative staphylococci. J Infect Dis 1986; 153: 332-39.
VOMITING AND THE MIGRATING MOTOR COMPLEX
SiR,—Abnormalities of postprandial gastric function, including diminished contractile amplitude,l delayed solid emptying,2 and tachygastria,3have been described in patients with unexplained nausea and vomiting. In most such patients, episodes of nausea and vomiting are related to mealtimes, the vomitus containing undigested food. We report here a case of unexplained nausea and vomiting in which symptoms also recurred regularly throughout periods of fasting, when the vomitus contained no food. A 54-year-old woman was referred for investigation of a 7-year history of persistent vomiting, which had started 2 weeks after hysterectomy. Episodes of vomiting preceded by nausea occurred throughout the day, most often after meals, but not at night. The patient did not complain of abdominal pain or symptoms of gastro-oesophageal reflux but there had been significant weight loss (from 69 kg to 55 kg). She had a history of Klippel-Trenaunay syndrome and cholecystectomy. Physical examination and chest X-ray were unremarkable. Haematological and biochemical profiles were normal. Barium meal and small bowel follow-through, upper gastrointestinal endoscopy, and a computerised tomographic brain scan were normal. Radionuclide studies demonstrated significant impairment of oesophageal transit and significant delay in gastric emptying of both solids and liquids. There had been no symptomatic improvement after metoclopramide or domperidone, but some improvement was noted after chlorpromazine. A thorough study of upper gastrointestinal motility was done. The patient fasted for 12 h and then a trans-nasal catheter was positioned fluoroscopically so that recording orifices were located in the gastric antrum and at two sites in the duodenum. After 3 h of recording the patient complained of nausea and she vomited. The bilestained vomitus consisted of accumulated gastric secretions and swallowed saliva. The vomiting coincided with onset of the gastric component of the migrating motor complex (MMC) which then propagated normally down the small intestine (figure). This pattern of vomiting, concurrent with the gastric component of the MMC, was repeated twice. A 540 kcal meal was then provided. Typical postprandial motor patterns were not established and, within 30 min of eating, the patient complained of nausea and vomited the meal. This postprandial episode of vomiting was again coincident with onset of the MMC in the stomach. Two further MMCs were then observed, each associated with vomiting.
began. I suggest that these patients began with an awareness of that "fudging" of their physical attributes which is so characteristic of women (and less so men) as they pass from the "sharpness of feature" of youth to the roundness of physique of middle-age. This fudging affects the face, the breasts, the fingers, the waist, and to some extent the ankles. It might well be that these changes are first discerned subjectively as "swelling". This leads to some attempt to reshape the features. The various remedies available-crash dieting, purgation, diuretics-all perturb sodium homoeostasis. The remedies are used irregularly so that the induced disturbance of sodium homoeostasis and secondary water retention is variable in degree, even periodic or cyclical. Once started, the process can become aggravated by further dietary, diuretic, and purgation abuses. Idiopathic oedema could well be a social disease indirectly caused by the value apportioned in our society to women according to their shape. The main advantage of this pathogenesis, for which I claim no originality, is the therapy that follows. Pelosi’s hypothesis leads to the use of diuretics until the supposed underlying
neuroendocrine condition is resolved. If de Wardener’sl view is accepted, the patient can be handled sympathetically and given encouragement to avoid those remedies which exaggerate changes in salt and water homoeostasis. Diuretics should only be used for short-term symptomatic relief and in steadily decreasing dosage. The supposed underlying neuroendocrine abnormality remains obscure. The natural history of spontaneous remission usually after the menopause would fit in with a realisation by the patient that further changes are unavoidable with increasing age. Department of Medicine, Ninewells Hospital and Medical School,
W. K. STEWART
Dundee DD1 9SY 1. de Wardener HE.
Idiopathic
edema: Role of diuretic abuse.
Kidney
Int
1981;
19:
881-92.
PERITONITIS CAUSED BY SLIME-PRODUCING COAGULASE NEGATIVE STAPHYLOCOCCI IN CONTINUOUS AMBULATORY PERITONEAL
DIALYSIS
SIR,-Peritonitis is the major serious complication of continuous ambulatory peritoneal dialysis (CAPD).1 Coagulase negative staphylococci are the most common organism cultured from peritoneal dialysis effluents.2 Not all isolates of coagulase negative staphylococci cause clinically significant infections as defined by a white cell count above 100 cells/11, cloudy dialysis fluid, abdominal pain, and fever. A simple method to distinguish true pathogens from simple contaminants would be useful. Some strains of coagulase negative staphylococci produce a polysaccharide extracellular slime.3 This slime may be important in bacterial adherence to foreign bodies and may therefore increase the virulence of the organism. We studied the ability of coagulase negative staphylococci isolated from CAPD effluent to produce slime. 26 coagulase negative staphylococci were isolated from 22 of 140 patients on CAPD at the Queen Elizabeth Hospital during January to June, 1986. Isolates were examined for slime production as described by Christensen et all17 of 19 isolates from patients with clinically significant infections produced slime compared with 2 of 7 ISOLATES OF COAGULASE NEGATIVE STAPHYLOCOCCI IN CAPD EFFLUENTS FROM 22 PATIENTS I
isolates from patients who did not develop a clinical peritonitis (table). All 4 patients who required catheter removal because of a persistent antibiotic-resistant peritonitis had an infection with a
slime-producing organism. In-vitro studies have demonstrated increased adherence of slime-producing staphylococci to prosthetic devices,3afeature which may make the organism more difficult to eradicate.’ Our data show that the test for slime, production in coagulase negative staphylococcal peritonitis is a useful additional method for distinguishing contamination from clinically significant infections in CAPD. Also, catheter removal is more likely in slime-producing, coagulase negative staphylococcal infections, and a positive test may therefore provide an early indicator of severe infections, which are more difficult to eradicate with antibiotic therapy alone. Departments of Nephrology and Microbiology, Queen Elizabeth Hospital, Birmingham B15 2TH
M. BEAMAN L. SOLARO
D. ADU J. MICHAEL
J, Oreopoulos DG, Lio TT, Matthews R, De Veber GA. Management of peritonitis and bowel perforation during chronic peritoneal dialysis. Nephron 1976;
1. Rubin
16: 220-25. 2. Gruer LD, Turney JH, Curley J, Michael J, Adu D. Vancomycin and tobramycin in the treatment of CAPD peritonitis. Nephron 1985; 41: 279-82. 3. Christensen GD, Simpson WA, Bisno AL, Beachey EH. Adherence of slimeproducing strains of Staphylococcus epidermidis to smooth surfaces. Infect Immunol 1982; 37: 318-26. 4. Davenport DS, Massanari RM, Pfaller MA, Bale MJ, Streed SA, Hierholzer WJ. Usefulness of a test for slime production as a marker for clinically significant infections with coagulase negative staphylococci. J Infect Dis 1986; 153: 332-39.
VOMITING AND THE MIGRATING MOTOR COMPLEX
SiR,—Abnormalities of postprandial gastric function, including diminished contractile amplitude,l delayed solid emptying,2 and tachygastria,3have been described in patients with unexplained nausea and vomiting. In most such patients, episodes of nausea and vomiting are related to mealtimes, the vomitus containing undigested food. We report here a case of unexplained nausea and vomiting in which symptoms also recurred regularly throughout periods of fasting, when the vomitus contained no food. A 54-year-old woman was referred for investigation of a 7-year history of persistent vomiting, which had started 2 weeks after hysterectomy. Episodes of vomiting preceded by nausea occurred throughout the day, most often after meals, but not at night. The patient did not complain of abdominal pain or symptoms of gastro-oesophageal reflux but there had been significant weight loss (from 69 kg to 55 kg). She had a history of Klippel-Trenaunay syndrome and cholecystectomy. Physical examination and chest X-ray were unremarkable. Haematological and biochemical profiles were normal. Barium meal and small bowel follow-through, upper gastrointestinal endoscopy, and a computerised tomographic brain scan were normal. Radionuclide studies demonstrated significant impairment of oesophageal transit and significant delay in gastric emptying of both solids and liquids. There had been no symptomatic improvement after metoclopramide or domperidone, but some improvement was noted after chlorpromazine. A thorough study of upper gastrointestinal motility was done. The patient fasted for 12 h and then a trans-nasal catheter was positioned fluoroscopically so that recording orifices were located in the gastric antrum and at two sites in the duodenum. After 3 h of recording the patient complained of nausea and she vomited. The bilestained vomitus consisted of accumulated gastric secretions and swallowed saliva. The vomiting coincided with onset of the gastric component of the migrating motor complex (MMC) which then propagated normally down the small intestine (figure). This pattern of vomiting, concurrent with the gastric component of the MMC, was repeated twice. A 540 kcal meal was then provided. Typical postprandial motor patterns were not established and, within 30 min of eating, the patient complained of nausea and vomited the meal. This postprandial episode of vomiting was again coincident with onset of the MMC in the stomach. Two further MMCs were then observed, each associated with vomiting.