64
Role of local anaesthetics in urethral strictures after transurethral surgery
DETAILS OF 11 PATIENTS WITH CEREBRAL OEDEMA AND OF 20 CONTROLS
SIR,-Epidemics of urethral strictures after transurethral resection of the prostate have been reported.’ In some instances rubber catheters have been identified as the cause of this complication.2,3 In the past two years, urologists in Italy have noted a sudden increase in the incidence of urethral strictures after surgery. At this hospital the number of strictures increased sharply during 1988: Year 1984 1985 1986 1987 1988
Procedures 132 101 140 140 129
Number of strictures 3 (2.27) 4 (3.96) 5 (3.57) 3 (2.14) 25 (19.38)
(%)
After an evaluation of possible aetiological agents, the only common causative factor we could identify was a change in the composition of the lubricant gel. Investigation revealed that the concentration of tetracaine chlorhydrate, used as an anaesthetic agent, in the gel had been changed from 0.1to 3% in this time period. To investigate the coincidence in rise in urethral strictures and the variation in concentration of this ester-like local anaesthetic, a prospective randomised clinical study has been initiated. Patients undergoing transurethral surgery of the prostate in nineteen Italian institutions are being randomised to either tetracaine chlorhydrate 3%, lignocaine chlorhydrate 1%, or pure lubricant gel devoid of anaesthetic agent. While the results of this study are awaited, we wish to draw attention to our impression that high doses of ester-like, topical local anaesthetics may harm the urethral mucosa.4-6 Urology Department, C T.O. Hospital, Rome, Italy
VITO PANSADORO
*From admission to return to normal. tCorrected for
high glucose.
admission (p < 0-001) and decrease of serum osmolality (p < 0001) best predicted cerebral oedema (odds ratios 1.66 and 1796,
respectively). The long duration of hypertonicity before admission could result in an increase in brain volume.2 The initial brain volume and the fall in osmolality may be the most important factors in the development of clinical cerebral oedema. The recorded fall in serum osmolality in the patient group could account for an 11 ’4% increase in brain volume, whereas in the controls, an increase of only 5% would be expected. This difference of 6-4% increase in brain volume could be responsible for the presence of symptoms. Since serum osmolality is determined by serum glucose and sodium concentrations and affected by water loading, one can speculate that in some patients the role of one factor may be more important than that of others, whereas in some patients several factors could be
contributory. 1.
Syme RRA. Epidemic of acute urethral stricture after prostate surgery. Lancet 1982; ii:
925. 2. Hammarsten J. Urethral strictures following transurethral resection of the prostate. The role of catheter. BrJ Urol 1989; 63: 397. 3. Talja M. Toxic catheters and diminished urethral blood circulation in the induction of urethral strictures. Eur Urol 1986; 12: 340. 4. Aldrete JA. Allergy to local anesthetics. JAMA 1969; 207: 356. 5. Charlton JE. Systemic toxicity of local anaesthetics. In. Trauma, stress and immunity in anaesthesia and surgery. London: Butterworth, 1982. 6. Adriam J. Fatalities following topical application of local anesthethics to mucous
membranes. JAMA 1956; 17: 1527.
Cerebral oedema in diabetic ketoacidosis in children SIR,—The frequency of cerebral oedema in diabetic ketoacidosis has been estimated as 1%, the pathogenesis has not been established, and there is no consensus on treatment. The outcome in patients with cerebral oedema is poor (60-80% mortality, 13-26% impaired, and only 7-14% normal).l At the Children’s Hospital of Columbus 1006 episodes of ketoacidosis have been recorded during the past 14 years. Data for 11 patients with cerebral oedema were compared with those for 20 random controls with ketoacidosis without this condition. Seventy variables were analysed by stepwise multiple logistic regression (BMDP). Grouped data are expressed as mean and SEM. Differences between groups were evaluated with the unpaired t-test.
Cerebral oedema developed in 7 (0-7%) of our patients. The frequency was, however, higher in patients with new onset diabetes (3-3%, 5 of 151 ketoacidosis episodes) than in known patients (0-23%, p
Role of local anaesthetics in urethral strictures after transurethral surgery
DETAILS OF 11 PATIENTS WITH CEREBRAL OEDEMA AND OF 20 CONTROLS
SIR,-Epidemics of urethral strictures after transurethral resection of the prostate have been reported.’ In some instances rubber catheters have been identified as the cause of this complication.2,3 In the past two years, urologists in Italy have noted a sudden increase in the incidence of urethral strictures after surgery. At this hospital the number of strictures increased sharply during 1988: Year 1984 1985 1986 1987 1988
Procedures 132 101 140 140 129
Number of strictures 3 (2.27) 4 (3.96) 5 (3.57) 3 (2.14) 25 (19.38)
(%)
After an evaluation of possible aetiological agents, the only common causative factor we could identify was a change in the composition of the lubricant gel. Investigation revealed that the concentration of tetracaine chlorhydrate, used as an anaesthetic agent, in the gel had been changed from 0.1to 3% in this time period. To investigate the coincidence in rise in urethral strictures and the variation in concentration of this ester-like local anaesthetic, a prospective randomised clinical study has been initiated. Patients undergoing transurethral surgery of the prostate in nineteen Italian institutions are being randomised to either tetracaine chlorhydrate 3%, lignocaine chlorhydrate 1%, or pure lubricant gel devoid of anaesthetic agent. While the results of this study are awaited, we wish to draw attention to our impression that high doses of ester-like, topical local anaesthetics may harm the urethral mucosa.4-6 Urology Department, C T.O. Hospital, Rome, Italy
VITO PANSADORO
*From admission to return to normal. tCorrected for
high glucose.
admission (p < 0-001) and decrease of serum osmolality (p < 0001) best predicted cerebral oedema (odds ratios 1.66 and 1796,
respectively). The long duration of hypertonicity before admission could result in an increase in brain volume.2 The initial brain volume and the fall in osmolality may be the most important factors in the development of clinical cerebral oedema. The recorded fall in serum osmolality in the patient group could account for an 11 ’4% increase in brain volume, whereas in the controls, an increase of only 5% would be expected. This difference of 6-4% increase in brain volume could be responsible for the presence of symptoms. Since serum osmolality is determined by serum glucose and sodium concentrations and affected by water loading, one can speculate that in some patients the role of one factor may be more important than that of others, whereas in some patients several factors could be
contributory. 1.
Syme RRA. Epidemic of acute urethral stricture after prostate surgery. Lancet 1982; ii:
925. 2. Hammarsten J. Urethral strictures following transurethral resection of the prostate. The role of catheter. BrJ Urol 1989; 63: 397. 3. Talja M. Toxic catheters and diminished urethral blood circulation in the induction of urethral strictures. Eur Urol 1986; 12: 340. 4. Aldrete JA. Allergy to local anesthetics. JAMA 1969; 207: 356. 5. Charlton JE. Systemic toxicity of local anaesthetics. In. Trauma, stress and immunity in anaesthesia and surgery. London: Butterworth, 1982. 6. Adriam J. Fatalities following topical application of local anesthethics to mucous
membranes. JAMA 1956; 17: 1527.
Cerebral oedema in diabetic ketoacidosis in children SIR,—The frequency of cerebral oedema in diabetic ketoacidosis has been estimated as 1%, the pathogenesis has not been established, and there is no consensus on treatment. The outcome in patients with cerebral oedema is poor (60-80% mortality, 13-26% impaired, and only 7-14% normal).l At the Children’s Hospital of Columbus 1006 episodes of ketoacidosis have been recorded during the past 14 years. Data for 11 patients with cerebral oedema were compared with those for 20 random controls with ketoacidosis without this condition. Seventy variables were analysed by stepwise multiple logistic regression (BMDP). Grouped data are expressed as mean and SEM. Differences between groups were evaluated with the unpaired t-test.
Cerebral oedema developed in 7 (0-7%) of our patients. The frequency was, however, higher in patients with new onset diabetes (3-3%, 5 of 151 ketoacidosis episodes) than in known patients (0-23%, p
