311
STEPWISE ANALYSIS IN 25 PATIENTS WHO DIED WHILE AWAITING CABS AND IN 50 MATCHED CONTROLS
OR
=
odds ratio, CI
=
confidence interval
compared with 50 controls who had CABS in the same year, matched for age, gender, type of surgery, and priority rating. A stepwise logistic regression of clinical, angiographic, and haemodynamic variables in all 75 patients identified six independent variables predictive for early death after assignment to a waiting list for CABS (table). We were surprised that the presence of unstable angina before angiography and/or severity of coronary artery disease were not the strongest predictors for early mortality; the functional characteristic of a positive exercise test with short duration proved a much stronger predictor. It was also noteworthy that the use of coumarins constituted an independent risk, unrelated to site of infarction and/or impaired left ventricular function. Furthermore impaired left-ventricular function, except that shown by cardiac enlargement on chest radiography, was not associated with early death whereas it is known to be associated with later mortality.3 Thus our results have shown that, even in the short-term while waiting for CABS, these characteristics are independent predictors of death. These indicators may contribute important additional information in the assessment of priorities for treatment in patients at high risk while waiting for CABS. Since our selection criteria were not much different from those Naylor and colleagues propose, one can expect similar findings from studies in which their scoring system is used. feel that their proposed sequence of major factors affecting urgency ranking should be reconsidered.
Therefore,
we
Departments of Cardiology and Cardiovascular Surgery, St Antonius Hospital Nieuwegein, 3435 CM Nieuwegein, Netherlands; and Department of Clinical Epidemiology, Erasmus University, Rotterdam
1.
MAARTEN J. SUTTORP J. HERRE KINGMA EGBERT M. KOOMEN JAN G. P. TIJGSSEN JO A. M. DEFAUW SJEF M. P. G. ERNST
Suttorp MJ, Kingma JH, Koomen EM, et al. Short term mortality in patients selected a case-control study. Am J Coll Cardiol 1990; 15: 116A (abstr). European Coronary Surgery Study Group. Long-term results of prospective randomized study of coronary artery bypass surgery in stable angina pectoris. Lancet 1982; ii: 1173-80. Passamani E, Davis KB, Gillespie MJ, Killip T. A randomized trial of coronary artery bypass surgery: survival of patients with a low ejection fraction. N Engl J Med 1985;
for coronary artery bypass surgery:
2.
3.
312: 1665-71.
Thrombolytic therapy in suspected myocardial infarction SiR,—The practice of starting thrombolysis immediately after the of symptoms of suspected acute myocardial infarction is gaining acceptance. This can lead to therapy beginning before the patient reaches hospital. We wish to add a note of caution. A 49-year-old man collapsed at work. An ambulance was called
onset
and he was taken to the emergency department of our hospital. There he complained of epigastric pain. The patient was alert (blood pressure 115/80 mm Hg, heart rate 95/min) and in severe pain which did not respond to oral nitroglycerine but was alleviated by intravenous nitroglycerine. An electocardiograph showed raised ST levels and high T waves in leads V2-V4 as well as some supraventricular premature beats and ventricular ectopic beats. Creatinine kinase, creatinine kinase-MB, glutamic oxaloacetic transaminase, and lactic dehydrogenase levels were normal. A myocardial infarction was suspected and thrombolytic therapy
discussed. To exclude cerebral haematoma following his collapse computed tomography was done, with normal results. After his transfer to the medical department (about 3 h after the incident) the patient’s enzymes were still normal; however, the red blood cell count was 3xx 10/1 and haemoglobin was 10-0 g/dl. Thrombolytic therapy was ruled out. The cause of the anaemia turned out to be a bleeding ulcer at the pylorus. Electroardiograph findings returned to normal after one day and there was no evidence of coronary heart disease. The patient, who had not had any previous gastric or duodenal complaints, recovered uneventfully on a standard anti-ulcer regimen. In our opinion it is not always easy, even for an experienced physician, to distinguish between myocardial infarction and other diseases with similar patterns of pain and clinical findings. If early thrombolytic therapy becomes standard practice we will have to expect a number of "mistreatments" with - possible fatal consequences. University Medical Clinic 1, A-1090 Vienna, Austria
WOLFGANG BASE PETER SIOSTRZONEK
Hughes Day revisited SiR,—In the Wizard of Oz Dorothy exclaims: "Toto, I do not think in Kansas any more". Her statement is often used to reflect "future shock" when conditions around us change rapidly. Future
we are
shock for coronary care started in Kansas some twenty-five years ago when Hughes Day put together the first coronary care unit in a community hospital, thereby initiating more than two decades of coronary care. Progress has seemed to beget progress, as it does when one is focusing and spending the time on a problem. Cardiopulmonary resuscitation was the foundation for these advances. However, despite the excitement over thrombolysis we seem to be reaching a plateau or a point of diminishing return on our progress curve, because we lack ways to recruit the community. What we need is another Hughes Day to gear us up another notch-to complete the loop in the community just as has been done within hospitals over the past twenty-five years. Educating the community does not seem to be enough. What is lacking is the means to change the behaviour of the community and to re-programme society so that early cardiac care is linked to the
hospital. Thrombolytic therapy can only help those who come into the system early. Perhaps even more important is protection for those patients with prodromal symptoms. There are 6700 hospitals in the United States. Should not such hospitals serve as early cardiac care centres committed to educating the community about early cardiac care, introducing behavioural modification changes, and setting up user-friendly transport arrangements and check-up systems in hospital emergency rooms. Such a link between patients in need and hospitals with the means to provide early cardiac care could be the quantum leap required. Hughes Day was a clinician in a community hospital who brought logic and simplicity to bear in setting up the first coronary care unit. Quarter of a century ago, coronary care units developed overnight because that made sense. The same should apply to early cardiac care centres. Exacting standards of scientific proof may take years to meet, at the expense of human suffering. Paul Dudley White Coronary Care System, Saint Agnes Hospital, Baltimore, Maryland 21229, USA
RAYMOND D. BAHR
Oestrogens, arterial status, and postmenopausal women SIR,-Dr Bourne and colleagues (June 16, p 1470) report a coefficient of variation for measurement of uterine artery pulsatility index (PI), with transvaginal ultrasound in non-pregnant women. However, further data are required before conclusions about the arterial effects of transdermal oestradiol can be drawn from this uncontrolled study. Serum oestradiol concentrations should be measured, since these are highly variable following the application of ’Estraderm TTS’
312
In sheep, progesterone reverses the increase in uterine blood flow seen after oestradiol administration,and a similar effect may be expected with potent synthetic progestagens such as norethisterone. Norethisterone has a half-life of up to 12 h, hence a carry-over effect has to be considered. The stage in the treatment cycle at the time of observation may be critically important. The resolution of currently available ultrasound equipment does not allow accurate measurement of endometrium less than 1 mm thick; thus, the data presented cannot serve as a measure of compliance with treatment. Oestradiol may act via a genomic or classic oestrogen receptor mechanism to bring about changes in vessel wall distensibility by protein synthesis. These would be reflected in the PI, as demonstrated by Bourne et al. However, oestradiol is known to act as a vasodilator by mechanisms independent of the cytosol/nuclear oestradiol receptor3which may involve eosinophil migration into the uterus.4
patches.’
Department of Obstetrics and Gynaecology, St Mary’s Hospital Medical School, London W2 1PG, UK 1.
Stanczyk FZ, Shoupe D, Nunez V, et estradiol delivery in postmenopausal
R. W. STONES
al. A randomized comparison of nonoral Am J Obstet Gynecol 1988; 159:
women.
1540-46. 2. Resnik R, Brink GW, Plumer MH. The effect of progesterone on estrogen-induced uterine blood flow. Am J Obstet Gynecol 1977; 128: 251-54. 3. Penney LL, Frederick RJ, Parker GW. 17-&bgr;-estradiol stimulation of uterine blood flow in oophorectomized rabbits with complete inhibition of uterine RNA synthesis. Endocrinology 1981; 109: 1672-76. 4. Tchernitchin A, Roorijck J, Tchernitchin X, et al. Dramatic early increase in uterine eosinophils after oestrogen administration. Nature 1974; 248: 142-43.
Acute compartment syndrome secondary to theophylline overdose SIR,-We describe
a patient who had an acute compartment after an overdose with aminophylline-a complication which has not been previously reported. A 41-year-old woman was admitted 12 hours after taking an unknown number of aminophylline slow-release 225 mg tablets. She was alert with a sinus tachycardia of 110 beats per minute. Abnormal laboratory findings included hypokalaemia (2-3 mmol/1), hypocalcaemia (total calcium 1-83 mmol/1, albumin 43 g/1), and neutrophilia (26-5 x 106/1). Theophylline concentration was 165 mg/1 (therapeutic range 10-20 mg/1). Immediate treatment with oral activated charcoal and magnesium sulphate was instituted, together with intravenous potassium and calcium chloride. Episodes of supraventricular tachycardia occurred, necessitating treatment with intravenous atenolol and cardioversion. She had grand mal seizures which continued, together with intense muscle spasms, despite diazepam and propofol sedation. Oliguric renal failure developed with pigmented urinary casts and a creatine kinase of over 144 000 IU/1. 40 hours after ingestion there was a secondary rise in theophylline (figure) associated with further seizures and profound hypotension. Charcoal haemoperfusion resulted in rapid haemodynamic improvement and a halving of theophylline concentrations. Her calves were swollen and tight and the skin overlying her anterior tibial compartments was discoloured, raising the possibility of acute compartment syndrome. The compartment pressures were measured with the slit catheter technique’ which confirmed compartmental hypertension (right anterior 48 mm Hg, left anterior 65 mm Hg, right deep posterior 17 mm Hg, and left deep posterior 10 mm Hg; normal below 10 mm Hg). The patient had immediate surgical exploration of both lower limbs through two longitudinal incisions. Although the anterior tibial and peroneal muscle groups of both legs were of questionable viability there was no obvious muscle necrosis and the tissues were left for 24 h to allow full recovery if possible. Subsequent exploration, however, revealed complete muscle necrosis in the anterior compartments, and the muscles were radically excised. She made a good recovery, remained dialysis dependent until 25 days after admission, and, despite the absence of anterior tibial and peroneal muscle groups in both legs, could walk with the aid of sticks. Acute compartment syndrome is an important, but uncommon, clinical entity.2,3 If missed, it can lead to substantial morbidity and in
syndrome
0
I 0
.
I
20 0
.
1
40
.
I
.
60
1
80
.
I
.
I
.
I
.
I
100 120 140 1600
Time after overdose
(hours)
Hourly theophylline concentrations after overdose. severe cases amputation of the affected limbs.’ Causes include fractures, soft tissue injuries, prolonged limb compression, and arterial injuries. Although compartment syndrome after drug overdose with barbiturates and opiates has been described,5,6 it has not been reported following theophylline overdose. Mechanisms include pressure necrosis due to prolonged limb compression,’ uncontrolled muscular activity due to seizures, and possibly a direct myotoxic event.5,6 In our patient the compartmental damage was bilateral and the patient lay in bed at home after the overdose, making pressure necrosis unlikely. The fitting was exacerbated by hypocalcaemia, a recognised feature of rhabdomyolysis-induced renal failure.8 We conclude that theophylline is a myotoxic drug, and that an acute compartment syndrome can, rarely, complicate its overdosage. Furthermore, compartmental pressure monitoring is an important clinical investigation and should be mandatory in suspected cases of acute compartment syndrome, especially in the
unconscious patient. We thank Mr W. W. Barrie, Dr J. permission to report this patient.
Departments of Surgery, and Nephrology, Leicester General Hospital, Leicester LE5 4PW, UK
1. Barnes
Feehally,
and Dr
J. Walls for their
DAVID M. LLOYD SIMON P. K. PAYNE CHARLES R. V. TOMSON MICHAEL R. BARNES MICHAEL
J. ALLEN
MR, Gibson MJ, Scott J, Bentley S, Allen MJ. A technique for the long term
measurement of
intra-compartmental pressure in the lower leg. J Biomed Eng 1985, 7: 35-39. 2. MacDonald JB, Jones HM, Cowan RA. Rhabdomyolysis and acute renal failure after theophylline overdose. Lancet 1985; i: 932-33. 3. Rumpf KW, Wagner H, Cnee CP, et al. Rhabdomyolysis after theophylline overdose. Lancet 1985; i: 1451-52. 4. Mubarak SJ, Hargens AR, eds. Compartment syndromes and Volkmann’s contracture. Monographs in clinical orthopaedics, vol III. London W B Saunders, 1981: 205. 5. Richter RW, Challener YB, Pearson J, Kagen LJ, Hamilton LL, Ramsey WH. Acute myoglobinuria associated with heroin addiction. JAMA 1971; 216: 1172-76 6. Perin AS, Rowland LP, Fraser DW Drugs, coma and myoglobinuria. Arch Neurol 1972; 26: 336-43. 7. Owen CA, Mubarak SJ, Hargens AR, Rutherford L, Garetto LP, Akeson WH Intramuscular pressures with limb compression: clarification of the pathogenesis of the drug induced muscle compartment syndrome N Engl J Med 1979; 300: 1169-72. 8. Knochel, JP. Rhabdomyolysis and myoglobinuria. In: Suki WN, Eknoyan G, eds The kidney m systemic disease. New York: John Wiley, 1981: 263.
In-vitro
production of TNF-&agr; in blood samples
SIR,-In a study of tumour necrosis factor (TNF-a) and openheart surgery blood was taken during bypass when the patient is anticoagulated with heparin, and for this reason all non-bypass samples, including preoperative and postoperative samples, were also taken into plastic tubes with heparin. The sandwich ELISA’ made use of rabbit polyclonal and mouse monoclonal antibodies to recombinant TNF-a and avidin-biotin-peroxidase complex detection. TNF-a in phosphate-buffered saline containing 2%
STEPWISE ANALYSIS IN 25 PATIENTS WHO DIED WHILE AWAITING CABS AND IN 50 MATCHED CONTROLS
OR
=
odds ratio, CI
=
confidence interval
compared with 50 controls who had CABS in the same year, matched for age, gender, type of surgery, and priority rating. A stepwise logistic regression of clinical, angiographic, and haemodynamic variables in all 75 patients identified six independent variables predictive for early death after assignment to a waiting list for CABS (table). We were surprised that the presence of unstable angina before angiography and/or severity of coronary artery disease were not the strongest predictors for early mortality; the functional characteristic of a positive exercise test with short duration proved a much stronger predictor. It was also noteworthy that the use of coumarins constituted an independent risk, unrelated to site of infarction and/or impaired left ventricular function. Furthermore impaired left-ventricular function, except that shown by cardiac enlargement on chest radiography, was not associated with early death whereas it is known to be associated with later mortality.3 Thus our results have shown that, even in the short-term while waiting for CABS, these characteristics are independent predictors of death. These indicators may contribute important additional information in the assessment of priorities for treatment in patients at high risk while waiting for CABS. Since our selection criteria were not much different from those Naylor and colleagues propose, one can expect similar findings from studies in which their scoring system is used. feel that their proposed sequence of major factors affecting urgency ranking should be reconsidered.
Therefore,
we
Departments of Cardiology and Cardiovascular Surgery, St Antonius Hospital Nieuwegein, 3435 CM Nieuwegein, Netherlands; and Department of Clinical Epidemiology, Erasmus University, Rotterdam
1.
MAARTEN J. SUTTORP J. HERRE KINGMA EGBERT M. KOOMEN JAN G. P. TIJGSSEN JO A. M. DEFAUW SJEF M. P. G. ERNST
Suttorp MJ, Kingma JH, Koomen EM, et al. Short term mortality in patients selected a case-control study. Am J Coll Cardiol 1990; 15: 116A (abstr). European Coronary Surgery Study Group. Long-term results of prospective randomized study of coronary artery bypass surgery in stable angina pectoris. Lancet 1982; ii: 1173-80. Passamani E, Davis KB, Gillespie MJ, Killip T. A randomized trial of coronary artery bypass surgery: survival of patients with a low ejection fraction. N Engl J Med 1985;
for coronary artery bypass surgery:
2.
3.
312: 1665-71.
Thrombolytic therapy in suspected myocardial infarction SiR,—The practice of starting thrombolysis immediately after the of symptoms of suspected acute myocardial infarction is gaining acceptance. This can lead to therapy beginning before the patient reaches hospital. We wish to add a note of caution. A 49-year-old man collapsed at work. An ambulance was called
onset
and he was taken to the emergency department of our hospital. There he complained of epigastric pain. The patient was alert (blood pressure 115/80 mm Hg, heart rate 95/min) and in severe pain which did not respond to oral nitroglycerine but was alleviated by intravenous nitroglycerine. An electocardiograph showed raised ST levels and high T waves in leads V2-V4 as well as some supraventricular premature beats and ventricular ectopic beats. Creatinine kinase, creatinine kinase-MB, glutamic oxaloacetic transaminase, and lactic dehydrogenase levels were normal. A myocardial infarction was suspected and thrombolytic therapy
discussed. To exclude cerebral haematoma following his collapse computed tomography was done, with normal results. After his transfer to the medical department (about 3 h after the incident) the patient’s enzymes were still normal; however, the red blood cell count was 3xx 10/1 and haemoglobin was 10-0 g/dl. Thrombolytic therapy was ruled out. The cause of the anaemia turned out to be a bleeding ulcer at the pylorus. Electroardiograph findings returned to normal after one day and there was no evidence of coronary heart disease. The patient, who had not had any previous gastric or duodenal complaints, recovered uneventfully on a standard anti-ulcer regimen. In our opinion it is not always easy, even for an experienced physician, to distinguish between myocardial infarction and other diseases with similar patterns of pain and clinical findings. If early thrombolytic therapy becomes standard practice we will have to expect a number of "mistreatments" with - possible fatal consequences. University Medical Clinic 1, A-1090 Vienna, Austria
WOLFGANG BASE PETER SIOSTRZONEK
Hughes Day revisited SiR,—In the Wizard of Oz Dorothy exclaims: "Toto, I do not think in Kansas any more". Her statement is often used to reflect "future shock" when conditions around us change rapidly. Future
we are
shock for coronary care started in Kansas some twenty-five years ago when Hughes Day put together the first coronary care unit in a community hospital, thereby initiating more than two decades of coronary care. Progress has seemed to beget progress, as it does when one is focusing and spending the time on a problem. Cardiopulmonary resuscitation was the foundation for these advances. However, despite the excitement over thrombolysis we seem to be reaching a plateau or a point of diminishing return on our progress curve, because we lack ways to recruit the community. What we need is another Hughes Day to gear us up another notch-to complete the loop in the community just as has been done within hospitals over the past twenty-five years. Educating the community does not seem to be enough. What is lacking is the means to change the behaviour of the community and to re-programme society so that early cardiac care is linked to the
hospital. Thrombolytic therapy can only help those who come into the system early. Perhaps even more important is protection for those patients with prodromal symptoms. There are 6700 hospitals in the United States. Should not such hospitals serve as early cardiac care centres committed to educating the community about early cardiac care, introducing behavioural modification changes, and setting up user-friendly transport arrangements and check-up systems in hospital emergency rooms. Such a link between patients in need and hospitals with the means to provide early cardiac care could be the quantum leap required. Hughes Day was a clinician in a community hospital who brought logic and simplicity to bear in setting up the first coronary care unit. Quarter of a century ago, coronary care units developed overnight because that made sense. The same should apply to early cardiac care centres. Exacting standards of scientific proof may take years to meet, at the expense of human suffering. Paul Dudley White Coronary Care System, Saint Agnes Hospital, Baltimore, Maryland 21229, USA
RAYMOND D. BAHR
Oestrogens, arterial status, and postmenopausal women SIR,-Dr Bourne and colleagues (June 16, p 1470) report a coefficient of variation for measurement of uterine artery pulsatility index (PI), with transvaginal ultrasound in non-pregnant women. However, further data are required before conclusions about the arterial effects of transdermal oestradiol can be drawn from this uncontrolled study. Serum oestradiol concentrations should be measured, since these are highly variable following the application of ’Estraderm TTS’
312
In sheep, progesterone reverses the increase in uterine blood flow seen after oestradiol administration,and a similar effect may be expected with potent synthetic progestagens such as norethisterone. Norethisterone has a half-life of up to 12 h, hence a carry-over effect has to be considered. The stage in the treatment cycle at the time of observation may be critically important. The resolution of currently available ultrasound equipment does not allow accurate measurement of endometrium less than 1 mm thick; thus, the data presented cannot serve as a measure of compliance with treatment. Oestradiol may act via a genomic or classic oestrogen receptor mechanism to bring about changes in vessel wall distensibility by protein synthesis. These would be reflected in the PI, as demonstrated by Bourne et al. However, oestradiol is known to act as a vasodilator by mechanisms independent of the cytosol/nuclear oestradiol receptor3which may involve eosinophil migration into the uterus.4
patches.’
Department of Obstetrics and Gynaecology, St Mary’s Hospital Medical School, London W2 1PG, UK 1.
Stanczyk FZ, Shoupe D, Nunez V, et estradiol delivery in postmenopausal
R. W. STONES
al. A randomized comparison of nonoral Am J Obstet Gynecol 1988; 159:
women.
1540-46. 2. Resnik R, Brink GW, Plumer MH. The effect of progesterone on estrogen-induced uterine blood flow. Am J Obstet Gynecol 1977; 128: 251-54. 3. Penney LL, Frederick RJ, Parker GW. 17-&bgr;-estradiol stimulation of uterine blood flow in oophorectomized rabbits with complete inhibition of uterine RNA synthesis. Endocrinology 1981; 109: 1672-76. 4. Tchernitchin A, Roorijck J, Tchernitchin X, et al. Dramatic early increase in uterine eosinophils after oestrogen administration. Nature 1974; 248: 142-43.
Acute compartment syndrome secondary to theophylline overdose SIR,-We describe
a patient who had an acute compartment after an overdose with aminophylline-a complication which has not been previously reported. A 41-year-old woman was admitted 12 hours after taking an unknown number of aminophylline slow-release 225 mg tablets. She was alert with a sinus tachycardia of 110 beats per minute. Abnormal laboratory findings included hypokalaemia (2-3 mmol/1), hypocalcaemia (total calcium 1-83 mmol/1, albumin 43 g/1), and neutrophilia (26-5 x 106/1). Theophylline concentration was 165 mg/1 (therapeutic range 10-20 mg/1). Immediate treatment with oral activated charcoal and magnesium sulphate was instituted, together with intravenous potassium and calcium chloride. Episodes of supraventricular tachycardia occurred, necessitating treatment with intravenous atenolol and cardioversion. She had grand mal seizures which continued, together with intense muscle spasms, despite diazepam and propofol sedation. Oliguric renal failure developed with pigmented urinary casts and a creatine kinase of over 144 000 IU/1. 40 hours after ingestion there was a secondary rise in theophylline (figure) associated with further seizures and profound hypotension. Charcoal haemoperfusion resulted in rapid haemodynamic improvement and a halving of theophylline concentrations. Her calves were swollen and tight and the skin overlying her anterior tibial compartments was discoloured, raising the possibility of acute compartment syndrome. The compartment pressures were measured with the slit catheter technique’ which confirmed compartmental hypertension (right anterior 48 mm Hg, left anterior 65 mm Hg, right deep posterior 17 mm Hg, and left deep posterior 10 mm Hg; normal below 10 mm Hg). The patient had immediate surgical exploration of both lower limbs through two longitudinal incisions. Although the anterior tibial and peroneal muscle groups of both legs were of questionable viability there was no obvious muscle necrosis and the tissues were left for 24 h to allow full recovery if possible. Subsequent exploration, however, revealed complete muscle necrosis in the anterior compartments, and the muscles were radically excised. She made a good recovery, remained dialysis dependent until 25 days after admission, and, despite the absence of anterior tibial and peroneal muscle groups in both legs, could walk with the aid of sticks. Acute compartment syndrome is an important, but uncommon, clinical entity.2,3 If missed, it can lead to substantial morbidity and in
syndrome
0
I 0
.
I
20 0
.
1
40
.
I
.
60
1
80
.
I
.
I
.
I
.
I
100 120 140 1600
Time after overdose
(hours)
Hourly theophylline concentrations after overdose. severe cases amputation of the affected limbs.’ Causes include fractures, soft tissue injuries, prolonged limb compression, and arterial injuries. Although compartment syndrome after drug overdose with barbiturates and opiates has been described,5,6 it has not been reported following theophylline overdose. Mechanisms include pressure necrosis due to prolonged limb compression,’ uncontrolled muscular activity due to seizures, and possibly a direct myotoxic event.5,6 In our patient the compartmental damage was bilateral and the patient lay in bed at home after the overdose, making pressure necrosis unlikely. The fitting was exacerbated by hypocalcaemia, a recognised feature of rhabdomyolysis-induced renal failure.8 We conclude that theophylline is a myotoxic drug, and that an acute compartment syndrome can, rarely, complicate its overdosage. Furthermore, compartmental pressure monitoring is an important clinical investigation and should be mandatory in suspected cases of acute compartment syndrome, especially in the
unconscious patient. We thank Mr W. W. Barrie, Dr J. permission to report this patient.
Departments of Surgery, and Nephrology, Leicester General Hospital, Leicester LE5 4PW, UK
1. Barnes
Feehally,
and Dr
J. Walls for their
DAVID M. LLOYD SIMON P. K. PAYNE CHARLES R. V. TOMSON MICHAEL R. BARNES MICHAEL
J. ALLEN
MR, Gibson MJ, Scott J, Bentley S, Allen MJ. A technique for the long term
measurement of
intra-compartmental pressure in the lower leg. J Biomed Eng 1985, 7: 35-39. 2. MacDonald JB, Jones HM, Cowan RA. Rhabdomyolysis and acute renal failure after theophylline overdose. Lancet 1985; i: 932-33. 3. Rumpf KW, Wagner H, Cnee CP, et al. Rhabdomyolysis after theophylline overdose. Lancet 1985; i: 1451-52. 4. Mubarak SJ, Hargens AR, eds. Compartment syndromes and Volkmann’s contracture. Monographs in clinical orthopaedics, vol III. London W B Saunders, 1981: 205. 5. Richter RW, Challener YB, Pearson J, Kagen LJ, Hamilton LL, Ramsey WH. Acute myoglobinuria associated with heroin addiction. JAMA 1971; 216: 1172-76 6. Perin AS, Rowland LP, Fraser DW Drugs, coma and myoglobinuria. Arch Neurol 1972; 26: 336-43. 7. Owen CA, Mubarak SJ, Hargens AR, Rutherford L, Garetto LP, Akeson WH Intramuscular pressures with limb compression: clarification of the pathogenesis of the drug induced muscle compartment syndrome N Engl J Med 1979; 300: 1169-72. 8. Knochel, JP. Rhabdomyolysis and myoglobinuria. In: Suki WN, Eknoyan G, eds The kidney m systemic disease. New York: John Wiley, 1981: 263.
In-vitro
production of TNF-&agr; in blood samples
SIR,-In a study of tumour necrosis factor (TNF-a) and openheart surgery blood was taken during bypass when the patient is anticoagulated with heparin, and for this reason all non-bypass samples, including preoperative and postoperative samples, were also taken into plastic tubes with heparin. The sandwich ELISA’ made use of rabbit polyclonal and mouse monoclonal antibodies to recombinant TNF-a and avidin-biotin-peroxidase complex detection. TNF-a in phosphate-buffered saline containing 2%
