- Email: [email protected]
HYPERTHERMIA IN HYPERBARIC ACTIVITIES
1303
symptoms to the bowel. We learned too that there are cofactors involved with the headaches. These are connected with posture and
breathing. Much criticism ofbiofeedback work is based on the comment that it is merely a placebo effect. In the psychosomatic diseases of which we have had most experience, a placebo effect does seem to be one of the components in achieving a good result. Instead of deriding this effect, we think that it should be encouraged, and we suggest that the placebo effect should be further studied-e.g., by following up suggestions that placebo analgesia is achieved by the release of en-
dorphin, Research
on
biofeedback should be extended
to
other diseases
(e.g., anxiety states) where drug therapy, though effective in some cases, may lead to addiction and often does not treat the underlying cause.
Department of Medical Electronics, St Bartholomews’s Hospital, London EC1A 7BF
B. W. WATSON A. WOOLLEY-HART
TETANY ASSOCIATED WITH CIS-PLATIN
SIR,-Tetany resulting from hypomagnesaemia and hypocalcaemia following cis-platin has been reported previously. We describe a further case which occurred without the concurrent administration of a diuretic. A 23-year-old man presented with unilateral gynaecomastia in October, 1979. He had a left para-aortic mass (confirmed by intravenous urography and computerised tomography of the abdomen) and a right epididymal mass. Chest X-ray showed multiple soft tissue densities throughout the lung fields. His human chorionic gonadotrophin (&bgr;- HCG) (3100 fg/1) and hydroxybutyrate dehydrogenase (2534 IU/1) were raised but the a-fetoprotein level was normal. He had been fit previously with no renal, endocrine, or
gastrointestinal abnormality. Testicular teratoma was diagnosed and combination chemotherapy was started with cis-platin 20 mg/m2i.v. and VP-16 100 mg/m2i.v. daily for five days, repeated every three weeks, and bleomycin 30 mg i.v. weekly. Before cis-platin, one litre of normal saline was infused in two hours, then 500 ml were given six hourly. Before therapy serum calcium, urea, and electrolytes, creatinine
clearance, and ward testing of the urine magnesium was not measured.
were
normal. Serum
After one course of therapy the epididymal mass had shrunk and biochemical markers fell. Because of persistent soft tissue densities on chest X-ray, vinblastine 0 - 1 mg/kg i.v. on days 1 and 2 was added to the three subsequent courses. LABORATORY FINDINGS IN PATIENT ON CIS-PLATIN
Nine days after the fourth course he was readmitted complaining of cramps of the hands and feet. Trousseau’s sign was positive but Chvostek’s sign was negative. Pedal spasm developed when he sat upright. He had mouth ulcers and fever (37-5°C). Investigation showed neutropenia, hypomagnesaemia (0 - 25 mmol/1 [0 6 mg/dl]), hypocalcaemia (corrected to serum albumin of 45 g/l= 1’ 93 mmol/1 [7 7 mg/dl]) and hypokalaemia (3-4 mmol/1). Intravenous magnesium sulphate, calcium gluconate, and potassium chloride were given. Intravenous cefuroxime was administered because of presumed infection. Urinary calcium and potassium were normal, urinary protein was less than 0 - 05 g/1 and there was no glycosuria.
was present (see table). Five weeks urinary magnesium returned to normal. Hypomagnesaemia was reported in 15 of 16 children, 8 with neuroblastoma and 8 with a variety of solid tumours, receiving treatment with cis-platin. 4 of the 16 (all with neuroblastoma) had tetany with low serum calcium levels. Urinary magnesium levels
However, magnesium wasting after admission
were not
The
measured.
of hypomagnesaemia, hypocalcaemia, and hypokalaemia with tetany prompted another study2 which included a retrospective review of 37 adult patients treated with cis-platin. 21 patients acquired hypomagnesaemia whilst receiving cis-platin. Of these, 1 patient had muscle irritability, twitching, and a positive Chvostek sign and a further patient had carpopedal spasm. Serum magnesium and calcium levels were low. A further 8 had hypomagnesaemia after cis-platin was withdrawn and in 8 others magnesium levels remained normal. A prospective study of 7 patients treated with cis-platin found hypomagnesaemia and inappropriate urinary magnesium losses in 2. Hypomagnesaemia has not been associated with the use of bleomycin, VP-16, or cefuroxime. Both mannitol3 and frusemide4 may increase the renal excretion of magnesium and were administered to patients in the series described above, but were not used in our patient. We therefore attribute the hypomagnesaemia and renal magnesium wasting to cis-platin. The experience in our patient and the reports from other centres suggest that cis-platin may cause a renal tubular defect and magnesium wasting. The defect may be reversible with time. We suggest that serum magnesium and calcium levels be monitored in patients receiving cis-platin so that replacement therapy can be started promptly if need be. occurrence
I.C.R.F.
Department of Hackney Hospital,
Medical
R. STUART-HARRIS B. A. J. PONDER P. F. M. WRIGLEY
Oncology,
London E9
HYPERTHERMIA IN HYPERBARIC ACTIVITIES
SIR,-The dangers of hypothermia in diving are well recognised. However, the risk of irreversible hyperthermia is less well appreciated. During the past four years, six fatal cases of hyperthermia in
decompression chambers or submersible work chambers have come to our notice. Four were in tropical climates and two in temperate climates. On several occasions, in the U.K., one of us (J.D.K.) has experienced disturbing rises in chamber temperature on compression. Case1 A medical assistant and a doctor entered a recompression chamber to attend a diver with pulmonary barotrauma. They were compressed to 60 m (equivalent depth sea water) on a 23/77 mixture of ’Heliox’. The ambient temperature was approximately 35°C and humidity 85%. The medical assistant was an obese West African, 152 cm tall; the doctor was lean and 180 cm tall. The medical assistant remained lightly clothed, the doctor removed all his clothing, and drank copious quantities of fluid while the medical assistant declined to drink. After 26 min the medical assistant was so distressed that he entered the outer lock to decompress but he still drank nothing; he became increasingly distressed, and was observed picking at his clothes in a confused state, and when he left the chamber he collapsed. After about 15 min he was recompressed to 42 m at which time he was stuporose with an irregular, almost impalpable pulse of about 120/min and a respiratory rate of 50/min. He was given 500 ml 5% dextrose with 20 mg dexamethasone but he died some 5’/2 h later. At necropsy the body and tissues were noted to be very dry with no interstitial fluid. The sodium CSF was 174 mmol/1 1. Hayes FA, Green AA, Senzer N, Pratt CB. Tetany: a complication of cisdichlordiammineplatinum (II) therapy. Cancer Treat Rep 1979, 63: 547-48 2. Schilsky RL, Anderson T Hypomagnesemia and renal mangnesium wasting in patients receiving cis-platin. Ann Intern Med 1979, 90: 929-31. 3. Parfitt AM. The acute effects of mersalyl, chlorthiazide and mannitol on the renal excretion
of calcium and other
4 Duarte CG Effects
and
ions in man.
Clin Sci
1969;
of ethacrynic acid and furosemide on magnesium. Metabolism 1968; 17: 867-76
36: 267-82
urinary
calcium, phosphate
1304
(normal mean 127 in Naumann’s series’ and 131 in a personal series often cases [LM.C.]). There were no other gross abnormalities. .
Case 2 Three American divers made a shallow sports dive, using scuba gear in the Persian Gulf. One made an emergency ascent, after which he briefly lost consciousness. 90 min later he and a medical technician were recompressed to 30 m sea water equivalent in a two compartment chamber standing in the sun without external cooling. Ambient temperature was 48 - 3°C and humidity above 75%. During compression both men complained of the intense heat. The patient was lean while the technician had considerable subcutaneous fat. Both wore briefs only. The medical technician attended to the patient encouraging him to drink but not doing so himself. After about 1 h the technician became confused, irrational, and aggressive and lost all control, lying on the floor kicking and screaming. The patient had sufficiently recovered to examine the technician. Some 90 min after the recompression the technician died. The diver continued to improve and the chamber was cooled by the application of ice. Two days after the incident the empty chamber was again compressed at the same rate and to the same depth. The ambient weather conditions were similar. The temperature inside the chamber rose to65°C. A necropsy done locally did not establish the cause of death. The final temperature (T2) in a compression chamber is calculated from the equation:
Where
ratio of specific heat (approximately 1 - 4 in oxyhelium mix=maial temperature inabsolute; PI =mitial pressure; and
y = the
tures) ; Tl P2 = final pressure.
Substitution of pressures (in atmospheres) ing reveals the following final temperature:
If hyperthermia does develop the ambient temperature must be rapidly reduced, and the patient must be forced to drink or be given by intravenous infusion cooled dextrose saline (1 litre in the first hour, followed by 500 ml hourly, while keeping a watch for cir-
culatory overloading). Several heat disorders are recognised’ but only a few are relevant hyperbaric environment. These are: (a) Hypochloraemic (or salt deficiency) heat exhaustion, due to inadequate replacement of salt loss in a hot environment, leading to dehydration and reto
duced blood volume.22 (b) Water deficiency heat exhaustion ’ due to lack of drinking water in a hot environment. (c) Exercise induced heat exhaustion attributable to physical exertion in a hot environment with sweating without replenishing salt or water.
The morbid anatomical findings are non-specific, other than the lack of interstial fluid. However, biochemical examination of vitreous humor and CSF may give some indication of electrolyte disturbance at the time of death, and crypt epithelial degenerations of the small-intestinal mucosa (where this can be done) has been suggested as an indication of hyperthermia. Unlike hypothermia, hyperthermia is an irreversible and rapid process, and once protein coagulation of vital centres has occurred death is inevitable.
generalised
We thank Prof. M. M. R. Williams, department of nuclear engineering, Queen Mary College, London, for his advice on the thermodynamic aspects.
Phillips Petroleum Company Europe-Africa, Portland House, Stag Place, London SW1E5DA
R.A.F.COX
North Sea Medical Centre, Great Yarmouth
N.K.I.MCIVER
London Hyperbaric Medical Service
J.D.KING
Employment Medical Advisory Service
I.M.CALDER
regularly used in div-
This assumes no heat loss but emphasises the theoretical seriousof the hazard. The risk is greater where the ambient temperature is higher, and with oxyhelium the transfer of heat to the victim’s vital centres is more rapid that it is with air. If the relative humidity is more than 80% sweating ceases to be an effective cooling mechanism, and a person in a compression chamber at an ambient temperature of more than 37°C and a relative humidity above 80% can only absorb heat with a corresponding rise in his core temperature. The danger of hyperthermia seems greater for a fat person than for a thin one. Hyperthermia is most likely when compression is at normal rates (30 m/min) in high ambient temperatures, when compression is rapid (e.g., for emergency treatment of decompression sickness or air embolism) using oxyhelium at normal ambient temperatures, and when a heavy work load is undertaken in high temperatures and pressures. The symptoms and signs of impending hyperthermia are restlessness and anxiety, confusion, absence of sweating (hot and dry skin), and circulatory collapse. Prevention is most likely to be effective if the condition is considered at an early stage when copious fluids (at least 1 litre/h) should be given accompanied by, the shedding of all clothing and the sponging of skin with cold water. Compression when using oxyhelium should not exceed 1’ 5 atm/min. In tropical areas, compression chambers should not be insulated and should be located in an air-conditioned building or shaded from the sun and hosed down with cold water. All operators of compression chambers must be alerted to the danger of hyperthermia. In neither of the above cases did those on the outside of the chamber consider the possibility of heatstroke. ness
DIAGNOSIS OF ACUTE CHOLECYSTITIS
SIR,-Your Nov. 22 editorial emphasis the importance of attempting to confirm a clinical diagnosis of acute cholecystitis before elective cholecystectomy. Although anatomical methods of imaging, such as contrast radiology and grey scale ultrasound, may be helpful in establishing a diagnosis of acute cholecystitis, cholescintigraphy using technetium labelled radiopharmaceuticals is a more reliable diagnostic tool. 5,6 Hepatobiliary imaging with technetium-99m labelled HIDA (dimethyl acetanilide iminodiacetic acid) provides functional information regarding cystic duct patency and is both highly sensitive and specific in the diagnosis of acute cholecystitis.7,8 In addition cholescintigraphy improves diagnostic confidence and overall 9 management in the problem of undiagnosed abdominal pain.9 is a safe non-traumatic techninon-invasive, Cholescintigraphy que which can be done shortly after hospital admission to provide surgeons with a reliable means of confirming or refuting a diagnosis of cholecystitis prior to cholecystectomy. University Department of Medicine, Glasgow Royal Infirmary, Glasgow G4 0SF
WSS, Waterlow JC, Hudson MF. Desert climate: Physiological and clinical observations Lancet 1944; ii: 491-97 3. Adolph EF. Water metabolism. Ann Rev Physiol 1947; 9: 381-408. 4. Black DAK, McCance RA, Young WF. A study of dehydration by balance ex2. Ladell
periments. J Physiol (Lond) 1944; 102: 406-14. 5. Down RH, Arnold J, Goldin A, Watts JMcK, Benness G.
Comparison of Accuracy of glutamate scanning with oral cholecystography and ultrasonography in diagnosis of acute cholecystitis. Lancet 1979, ii: 1094-97. 6.Weissmann HS, Frank M, Rosenblatt R, Goldman M, Freeman LM. Cholescintigraphy, ultrasonography and computerized tomography in the evaluation of biliary tract disorders. Sem Nucl Med 1979; 9: 22-35. 7 Weissmann HS, Frank MS, Bernstein LH, Freeman LM. Rapid and accurate diagnosis of acute cholecystitis with 99mTc-HIDA cholescinitigraphy.Am J Radiol 1979;
99mTc-pyridoxylidene
132: 523-28. 8
O’Callaghan JD, Verow PW, Hopton D, Craven JL. The diagnosis of acute gallbladder disease by technetium-99m-Labelled HIDA hepatobiliary scanning. Br J Surg 1980; 67: 805-08.
JE, Fink-Bennett DM, Thrall JH, Resinger WW, Calderon HC, Mirkes SH, Shah PK. Efficacy of hepatobiliary imaging in acute abdominal pain. J Nucl Med 1980; 21: 919-24.
9. Freitas
1. Naumann HN. 98: 16-19.
Cerebro-spinal fluid electrolytes after death. Proc Soc Biol Med 1958;
D. W. M. PEARSON H. W. GRAY
symptoms to the bowel. We learned too that there are cofactors involved with the headaches. These are connected with posture and
breathing. Much criticism ofbiofeedback work is based on the comment that it is merely a placebo effect. In the psychosomatic diseases of which we have had most experience, a placebo effect does seem to be one of the components in achieving a good result. Instead of deriding this effect, we think that it should be encouraged, and we suggest that the placebo effect should be further studied-e.g., by following up suggestions that placebo analgesia is achieved by the release of en-
dorphin, Research
on
biofeedback should be extended
to
other diseases
(e.g., anxiety states) where drug therapy, though effective in some cases, may lead to addiction and often does not treat the underlying cause.
Department of Medical Electronics, St Bartholomews’s Hospital, London EC1A 7BF
B. W. WATSON A. WOOLLEY-HART
TETANY ASSOCIATED WITH CIS-PLATIN
SIR,-Tetany resulting from hypomagnesaemia and hypocalcaemia following cis-platin has been reported previously. We describe a further case which occurred without the concurrent administration of a diuretic. A 23-year-old man presented with unilateral gynaecomastia in October, 1979. He had a left para-aortic mass (confirmed by intravenous urography and computerised tomography of the abdomen) and a right epididymal mass. Chest X-ray showed multiple soft tissue densities throughout the lung fields. His human chorionic gonadotrophin (&bgr;- HCG) (3100 fg/1) and hydroxybutyrate dehydrogenase (2534 IU/1) were raised but the a-fetoprotein level was normal. He had been fit previously with no renal, endocrine, or
gastrointestinal abnormality. Testicular teratoma was diagnosed and combination chemotherapy was started with cis-platin 20 mg/m2i.v. and VP-16 100 mg/m2i.v. daily for five days, repeated every three weeks, and bleomycin 30 mg i.v. weekly. Before cis-platin, one litre of normal saline was infused in two hours, then 500 ml were given six hourly. Before therapy serum calcium, urea, and electrolytes, creatinine
clearance, and ward testing of the urine magnesium was not measured.
were
normal. Serum
After one course of therapy the epididymal mass had shrunk and biochemical markers fell. Because of persistent soft tissue densities on chest X-ray, vinblastine 0 - 1 mg/kg i.v. on days 1 and 2 was added to the three subsequent courses. LABORATORY FINDINGS IN PATIENT ON CIS-PLATIN
Nine days after the fourth course he was readmitted complaining of cramps of the hands and feet. Trousseau’s sign was positive but Chvostek’s sign was negative. Pedal spasm developed when he sat upright. He had mouth ulcers and fever (37-5°C). Investigation showed neutropenia, hypomagnesaemia (0 - 25 mmol/1 [0 6 mg/dl]), hypocalcaemia (corrected to serum albumin of 45 g/l= 1’ 93 mmol/1 [7 7 mg/dl]) and hypokalaemia (3-4 mmol/1). Intravenous magnesium sulphate, calcium gluconate, and potassium chloride were given. Intravenous cefuroxime was administered because of presumed infection. Urinary calcium and potassium were normal, urinary protein was less than 0 - 05 g/1 and there was no glycosuria.
was present (see table). Five weeks urinary magnesium returned to normal. Hypomagnesaemia was reported in 15 of 16 children, 8 with neuroblastoma and 8 with a variety of solid tumours, receiving treatment with cis-platin. 4 of the 16 (all with neuroblastoma) had tetany with low serum calcium levels. Urinary magnesium levels
However, magnesium wasting after admission
were not
The
measured.
of hypomagnesaemia, hypocalcaemia, and hypokalaemia with tetany prompted another study2 which included a retrospective review of 37 adult patients treated with cis-platin. 21 patients acquired hypomagnesaemia whilst receiving cis-platin. Of these, 1 patient had muscle irritability, twitching, and a positive Chvostek sign and a further patient had carpopedal spasm. Serum magnesium and calcium levels were low. A further 8 had hypomagnesaemia after cis-platin was withdrawn and in 8 others magnesium levels remained normal. A prospective study of 7 patients treated with cis-platin found hypomagnesaemia and inappropriate urinary magnesium losses in 2. Hypomagnesaemia has not been associated with the use of bleomycin, VP-16, or cefuroxime. Both mannitol3 and frusemide4 may increase the renal excretion of magnesium and were administered to patients in the series described above, but were not used in our patient. We therefore attribute the hypomagnesaemia and renal magnesium wasting to cis-platin. The experience in our patient and the reports from other centres suggest that cis-platin may cause a renal tubular defect and magnesium wasting. The defect may be reversible with time. We suggest that serum magnesium and calcium levels be monitored in patients receiving cis-platin so that replacement therapy can be started promptly if need be. occurrence
I.C.R.F.
Department of Hackney Hospital,
Medical
R. STUART-HARRIS B. A. J. PONDER P. F. M. WRIGLEY
Oncology,
London E9
HYPERTHERMIA IN HYPERBARIC ACTIVITIES
SIR,-The dangers of hypothermia in diving are well recognised. However, the risk of irreversible hyperthermia is less well appreciated. During the past four years, six fatal cases of hyperthermia in
decompression chambers or submersible work chambers have come to our notice. Four were in tropical climates and two in temperate climates. On several occasions, in the U.K., one of us (J.D.K.) has experienced disturbing rises in chamber temperature on compression. Case1 A medical assistant and a doctor entered a recompression chamber to attend a diver with pulmonary barotrauma. They were compressed to 60 m (equivalent depth sea water) on a 23/77 mixture of ’Heliox’. The ambient temperature was approximately 35°C and humidity 85%. The medical assistant was an obese West African, 152 cm tall; the doctor was lean and 180 cm tall. The medical assistant remained lightly clothed, the doctor removed all his clothing, and drank copious quantities of fluid while the medical assistant declined to drink. After 26 min the medical assistant was so distressed that he entered the outer lock to decompress but he still drank nothing; he became increasingly distressed, and was observed picking at his clothes in a confused state, and when he left the chamber he collapsed. After about 15 min he was recompressed to 42 m at which time he was stuporose with an irregular, almost impalpable pulse of about 120/min and a respiratory rate of 50/min. He was given 500 ml 5% dextrose with 20 mg dexamethasone but he died some 5’/2 h later. At necropsy the body and tissues were noted to be very dry with no interstitial fluid. The sodium CSF was 174 mmol/1 1. Hayes FA, Green AA, Senzer N, Pratt CB. Tetany: a complication of cisdichlordiammineplatinum (II) therapy. Cancer Treat Rep 1979, 63: 547-48 2. Schilsky RL, Anderson T Hypomagnesemia and renal mangnesium wasting in patients receiving cis-platin. Ann Intern Med 1979, 90: 929-31. 3. Parfitt AM. The acute effects of mersalyl, chlorthiazide and mannitol on the renal excretion
of calcium and other
4 Duarte CG Effects
and
ions in man.
Clin Sci
1969;
of ethacrynic acid and furosemide on magnesium. Metabolism 1968; 17: 867-76
36: 267-82
urinary
calcium, phosphate
1304
(normal mean 127 in Naumann’s series’ and 131 in a personal series often cases [LM.C.]). There were no other gross abnormalities. .
Case 2 Three American divers made a shallow sports dive, using scuba gear in the Persian Gulf. One made an emergency ascent, after which he briefly lost consciousness. 90 min later he and a medical technician were recompressed to 30 m sea water equivalent in a two compartment chamber standing in the sun without external cooling. Ambient temperature was 48 - 3°C and humidity above 75%. During compression both men complained of the intense heat. The patient was lean while the technician had considerable subcutaneous fat. Both wore briefs only. The medical technician attended to the patient encouraging him to drink but not doing so himself. After about 1 h the technician became confused, irrational, and aggressive and lost all control, lying on the floor kicking and screaming. The patient had sufficiently recovered to examine the technician. Some 90 min after the recompression the technician died. The diver continued to improve and the chamber was cooled by the application of ice. Two days after the incident the empty chamber was again compressed at the same rate and to the same depth. The ambient weather conditions were similar. The temperature inside the chamber rose to65°C. A necropsy done locally did not establish the cause of death. The final temperature (T2) in a compression chamber is calculated from the equation:
Where
ratio of specific heat (approximately 1 - 4 in oxyhelium mix=maial temperature inabsolute; PI =mitial pressure; and
y = the
tures) ; Tl P2 = final pressure.
Substitution of pressures (in atmospheres) ing reveals the following final temperature:
If hyperthermia does develop the ambient temperature must be rapidly reduced, and the patient must be forced to drink or be given by intravenous infusion cooled dextrose saline (1 litre in the first hour, followed by 500 ml hourly, while keeping a watch for cir-
culatory overloading). Several heat disorders are recognised’ but only a few are relevant hyperbaric environment. These are: (a) Hypochloraemic (or salt deficiency) heat exhaustion, due to inadequate replacement of salt loss in a hot environment, leading to dehydration and reto
duced blood volume.22 (b) Water deficiency heat exhaustion ’ due to lack of drinking water in a hot environment. (c) Exercise induced heat exhaustion attributable to physical exertion in a hot environment with sweating without replenishing salt or water.
The morbid anatomical findings are non-specific, other than the lack of interstial fluid. However, biochemical examination of vitreous humor and CSF may give some indication of electrolyte disturbance at the time of death, and crypt epithelial degenerations of the small-intestinal mucosa (where this can be done) has been suggested as an indication of hyperthermia. Unlike hypothermia, hyperthermia is an irreversible and rapid process, and once protein coagulation of vital centres has occurred death is inevitable.
generalised
We thank Prof. M. M. R. Williams, department of nuclear engineering, Queen Mary College, London, for his advice on the thermodynamic aspects.
Phillips Petroleum Company Europe-Africa, Portland House, Stag Place, London SW1E5DA
R.A.F.COX
North Sea Medical Centre, Great Yarmouth
N.K.I.MCIVER
London Hyperbaric Medical Service
J.D.KING
Employment Medical Advisory Service
I.M.CALDER
regularly used in div-
This assumes no heat loss but emphasises the theoretical seriousof the hazard. The risk is greater where the ambient temperature is higher, and with oxyhelium the transfer of heat to the victim’s vital centres is more rapid that it is with air. If the relative humidity is more than 80% sweating ceases to be an effective cooling mechanism, and a person in a compression chamber at an ambient temperature of more than 37°C and a relative humidity above 80% can only absorb heat with a corresponding rise in his core temperature. The danger of hyperthermia seems greater for a fat person than for a thin one. Hyperthermia is most likely when compression is at normal rates (30 m/min) in high ambient temperatures, when compression is rapid (e.g., for emergency treatment of decompression sickness or air embolism) using oxyhelium at normal ambient temperatures, and when a heavy work load is undertaken in high temperatures and pressures. The symptoms and signs of impending hyperthermia are restlessness and anxiety, confusion, absence of sweating (hot and dry skin), and circulatory collapse. Prevention is most likely to be effective if the condition is considered at an early stage when copious fluids (at least 1 litre/h) should be given accompanied by, the shedding of all clothing and the sponging of skin with cold water. Compression when using oxyhelium should not exceed 1’ 5 atm/min. In tropical areas, compression chambers should not be insulated and should be located in an air-conditioned building or shaded from the sun and hosed down with cold water. All operators of compression chambers must be alerted to the danger of hyperthermia. In neither of the above cases did those on the outside of the chamber consider the possibility of heatstroke. ness
DIAGNOSIS OF ACUTE CHOLECYSTITIS
SIR,-Your Nov. 22 editorial emphasis the importance of attempting to confirm a clinical diagnosis of acute cholecystitis before elective cholecystectomy. Although anatomical methods of imaging, such as contrast radiology and grey scale ultrasound, may be helpful in establishing a diagnosis of acute cholecystitis, cholescintigraphy using technetium labelled radiopharmaceuticals is a more reliable diagnostic tool. 5,6 Hepatobiliary imaging with technetium-99m labelled HIDA (dimethyl acetanilide iminodiacetic acid) provides functional information regarding cystic duct patency and is both highly sensitive and specific in the diagnosis of acute cholecystitis.7,8 In addition cholescintigraphy improves diagnostic confidence and overall 9 management in the problem of undiagnosed abdominal pain.9 is a safe non-traumatic techninon-invasive, Cholescintigraphy que which can be done shortly after hospital admission to provide surgeons with a reliable means of confirming or refuting a diagnosis of cholecystitis prior to cholecystectomy. University Department of Medicine, Glasgow Royal Infirmary, Glasgow G4 0SF
WSS, Waterlow JC, Hudson MF. Desert climate: Physiological and clinical observations Lancet 1944; ii: 491-97 3. Adolph EF. Water metabolism. Ann Rev Physiol 1947; 9: 381-408. 4. Black DAK, McCance RA, Young WF. A study of dehydration by balance ex2. Ladell
periments. J Physiol (Lond) 1944; 102: 406-14. 5. Down RH, Arnold J, Goldin A, Watts JMcK, Benness G.
Comparison of Accuracy of glutamate scanning with oral cholecystography and ultrasonography in diagnosis of acute cholecystitis. Lancet 1979, ii: 1094-97. 6.Weissmann HS, Frank M, Rosenblatt R, Goldman M, Freeman LM. Cholescintigraphy, ultrasonography and computerized tomography in the evaluation of biliary tract disorders. Sem Nucl Med 1979; 9: 22-35. 7 Weissmann HS, Frank MS, Bernstein LH, Freeman LM. Rapid and accurate diagnosis of acute cholecystitis with 99mTc-HIDA cholescinitigraphy.Am J Radiol 1979;
99mTc-pyridoxylidene
132: 523-28. 8
O’Callaghan JD, Verow PW, Hopton D, Craven JL. The diagnosis of acute gallbladder disease by technetium-99m-Labelled HIDA hepatobiliary scanning. Br J Surg 1980; 67: 805-08.
JE, Fink-Bennett DM, Thrall JH, Resinger WW, Calderon HC, Mirkes SH, Shah PK. Efficacy of hepatobiliary imaging in acute abdominal pain. J Nucl Med 1980; 21: 919-24.
9. Freitas
1. Naumann HN. 98: 16-19.
Cerebro-spinal fluid electrolytes after death. Proc Soc Biol Med 1958;
D. W. M. PEARSON H. W. GRAY