how many more additional patients will have angiographie studies per¬ formed solely on the basis of these re¬
ports.
Letters, if clearly marked "For Publication, will be published "
as
Burton A. Sandok, MD
permits and at
space
Mayo Clinic
the discretion of the editor. They should be typewritten triple-spaced, with five or fewer references, should not exceed two pages in length, and will be subject to editing. Letters
are
not
acknowledged.
The Medical
Expert Witness in
Malpractice Suits
To the Editor.\p=m-\Ihave just finished reading Dr Paul C. Bucy's article (232:1352, 1975) and find it well done.
that he was too cautious concerning the physician's duty to testify as an expert against another physician when the issue is malpractice. We proudly consider ourselves a nation of laws, and rightly so. The physician in our society has reasonably high privileges and with that come equally high duties. An injured party ordinarily cannot sustain an action for malpractice without having an ex-
However, it
seems
to
physician, agreeing with malpractice did occur. The injured party cannot legally subpoena an expert, since only witnesses to fact can be subpoenaed, ergo, his entire case may turn on his ability to secure pert, ie,
a
an expert sue of
for his cause, not
on
the is-
malpractice itself. In the past, a physician's refusal to testify was called "conspiracy of silence." Today, in the face of the horrible malpractice mess, physicians may again be forgetting their duties, in a spasm of disgust over the entire situ¬ ation. The desperate plaintiff, re¬
quired by law to present an expert, will then find himself limited to select from physicians described as "profes¬ sional witnesses." These "hired guns" or "ladies of the night" are readily ca¬ pable of saying almost anything if the price is right. I ask the solid body of sound physi¬ cians not to shirk their duty, because it will only worsen the malpractice situation. If a physician is asked to be an expert witness, he should re¬ view the facts of the case as dis¬ passionately as possible and should give the requesting attorney his opin¬ ion equally straightforwardly. If, for any personal reason, the physician chooses not to testify, he should try to help the attorney find a qualified wit¬ ness. If this obligation is met, we will by John
D. Archer,
help destroy that handful of physi¬ cians who survive as "professional witnesses," and increase the input
of unbiased medical information into the judicial system. Alan Rosenberg, MD New York
me
him that
Edited
Rochester, Minn
MD, Senior Editor.
Arcus Senilis and Carotid Disease
Editor.\p=m-\Baglaand Golden reported (233:450,1975) the case of a 52\x=req-\ year-old woman, without any sympTo the
cerebrovascular disease, who for treatment of a urinary tract infection and was noted to have a unilateral arcus senilis on the right and a modest reduction in retinal arterial pressure on the left. Evidently, because of a similar earlier toms of
was
hospitalized
report (226:676, 1973) suggesting that
unilateral arcus is a sign of contralateral carotid artery disease, the patient, who was diabetic and perhaps hypertensive with arteriosclerotic
heart disease, was subjected to the risks of aortocervical angiography. A 40% narrowing of the right common carotid artery at its origin and bilaterally normal internal carotid arteries were seen. The authors, however, conclude that the clinical ophthalmologic findings "may be a function of nonvisualized small-vessel disease." I would agree; the disease was certainly "nonvisualized." They further suggest that their case (of nonvisualized disease) "provides confirmation of the observation that unilateral arcus senilis is a sign of con¬ tralateral occlusive disease." (Are we now to equate small-vessel disease with carotid occlusive disease?) I would rather suggest that their ar¬ ticle provides testimony to refute the thesis that unilateral arcus senilis is a sign of clinically significant contralateral carotid occlusive disease. We are all eager to identify pa¬ tients who may be at risk for stroke; however, it seems doubtful that this particular observation, even if confir¬ mation ever does appear, will prove to be clinically relevant. One wonders
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 06/13/2015
Furosemide for High Altitude Pulmonary Edema To the Editor.\p=m-\Therecent reply to
a
question regarding first aid equipment and acclimatization in mountain climbing (232:657, 1975) merits comment. Dr Mason suggests that furosemide (Lasix) given in large doses orally and intravenously may have dramatic beneficial effect in the treatment of high altitude pulmonary edema (HAPE). A case is described in which 120 mg orally and 80 mg inresulting in a travenously were given, 4,000-ml diuresis in 6 1/2 hours, with allegedly beneficial results. Unfortunately, such anecdotal reports have led to the indiscriminate use of furosemide in the treatment of HAPE as well as for the prevention of mountain sickness. Recently, a climbing party leader requested information about giving furosemide to all members of his party to prevent mountain sickness! Dr Mason points out that drug prophylaxis has been
disappointing.
It should be pointed out that there is insufficient evidence from appropriately conducted clinical studies that furosemide is indicated in the treatment of HAPE or acute mountain sickness. High altitude pulmonary edema is not due to cardiac failure. In severe cases, hypotension, a low car¬ diac output, hemoconcentration, and a shock-like state are present.' Fur¬ ther reduction of plasma volume by diuretics in such situations is more likely to aggravate hypotension. In many instances, HAPE can be treated by bed rest alone; hence, im¬ provement after the administration of furosemide cannot be attributed to the diuretic.2 Furosemide does not prevent acute mountain sickness, and in recent studies, this diuretic pro¬ duced hypovolemia, postural hypoten¬ sion, and syncope in subjects at 3,780 m.3 Persons with HAPE should be treated by prompt removal to a lower altitude, bed rest, and oxygen. Diure¬ sis induced by the use of furosemide may result in severe weakness that may make evacuation to a lower alti¬ tude on foot difficult. In addition, un¬ due confidence in diuretics may result
in failure to promptly institute bed rest therapy, to delay the use of oxy¬ gen, and to remove the patient to a
lower altitude, all of which have been clearly demonstrated to be of value in the treatment of HAPE. Herbert N. Hultgren, MD Chairman, Medical Committee American
Alpine Club
Palo Alto, Calif 1.
Hultgren H, Lopez C, Lundberg E, et al: Physiologic
studies of pulmonary edema at high altitude. Circulation
29:393-408, 1964.
2. Marticorena E, Hultgren H: Treatment of high altitude pulmonary edema by bed rest alone, abstracted. Circulation 34(suppl 3):163-164, 1966. 3. Hultgren H, Billisoly J, Fails H, et al: Plasma volume changes during acute exposure to high altitude, abstracted. Clin Res 21:224, 1973.
Shower Hazard? To the Editor.\p=m-\Anew product called
"Shower Massage" is now on the market and receiving considerable adver-
tising promotion. Having purchased a unit, I found it to be quite delightful
and effective. I also found, however, that when the unit is turned to the massage setting, it does indeed massage\p=m-\especially the carotid sinus. A very high\x=req-\ intensity, pulsating water stream is delivered. In my own case, this stream was capable of considerably slowing my sinus mechanism. This could be reproduced at will. I would be concerned about the potential hazard of this device, especially in patients with sensitive carotid sinus mechanisms or cardiac arrhythmias. Syncope in a shower might prove disastrous. In older patients, massage of a partially occluded carotid artery might well result in a cerebrovascular accident. I suggest that the cardiac effect of the water massage could be easily studied by electrocardiographic monitoring of volunteer subjects in the shower. If it is indeed demonstrated that significant changes in cardiac rhythm occur, then a suitable warning should accompany the sale of the product. In any event, I would certainly ad¬ vise elderly patients against direct¬ ing the massage stream to the neck area. Sidney Richman, MD
Bloomfield, Conn
Softened Water To the Editor.\p=m-\Dr Shaper (230:130, 1974) has succinctly summarized the series of statistical studies relating
soft water and fatal heart attacks and strokes. Some of his conclusions may be erroneous in that no
naturally
distinction is made between naturally soft water and water softened by a home appliance. Naturally soft water is most often relatively acidic and has a low dissolved-solids content.1 The studies summarized by Shaper generally show that such water supplied to a community may render it susceptible to higher incidence of fatal heart attacks and strokes. Softened water, however, is more like the naturally hard water from which it is made, generally low in acidity, with relatively large quantities of dissolved solids.1 Softened water differs from the original supply in its substitution of sodium ions for virtually all calcium, magnesium, and other heavy metals. The average adult derives in excess of 90% of total daily intake of both sodium and calcium from food2 and the remainder from water. About 60% of magnesium comes from food. It is logical to conclude that the hardness of drinking water should not affect susceptibility to fatal heart attacks and that the real culprit is one of the trace constituents of water that may be associated with hardness only in a
secondary way.3 The epidemiologic studies summa¬ rized by Shaper have consistently compared naturally soft water with naturally hard water. There is no evi¬
dence that softened water can be im¬ plicated. Indeed, a study in 1971 com¬ paring naturally hard water with softened water demonstrated the re¬ verse relationship, namely, that per¬ sons using softened water suffered fatal heart attacks at a lesser rate.4 Some of the workers in the field be¬ lieve that the higher acidity of natu¬ rally soft water, compared with that of naturally hard water, leaches cad¬ mium from galvanized water pip¬ ing. M Cadmium in very small quan¬ tities has been shown to cause high blood pressure and cardiovascular dis¬ ease in test animals.5 If so, water softened in the home is not likely to be related to fatal heart attacks any more than the original hard water supply from which it is generated. A recent study (Med World News, October 1974, p 45) appears to lend further support to such a conclusion. The death rates of matched groups in Kansas City, Mo, and Kansas City, Kan, were compared. The two com¬ munities use the same water source, the Missouri River, but the Missouri city softens its water municipally. The rate of deaths from heart disease
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 06/13/2015
is 50% higher in the Kansas city, which serves its residents the harder water. The cadmium content of the Kansas community water supplied at the tap is three times that of the Mis¬ souri city and the blood of the Kansas group contained 13 times as much cadmium. The Kansas test group had significantly higher average blood pressure as well. (Municipal and do¬ mestic softening processes are known to remove cadmium and other toxic heavy metal ions that may be present in the water supply.) Two recent communications serve to further point out the confusion that exists among the many epidemiologic studies that have been re¬ ported. Three matched communities in California (Reseda, Burbank, and Downey)6 with widely varying hard¬ ness of the water supply were com¬ pared. The authors conclude that no consistent association exists between deaths from heart disease and the de¬ gree of water hardness. A similar comparison of groups in Melbourne and Brisbane, Australia,7 also yielded no consistent association. The existing data hardly warrant the strong conclusions of Dr Shaper and certainly do not implicate soft¬ ened water. However, should the con¬ sumer prefer, a hard-water line can be provided to a kitchen or bathroom tap for drinking purposes without the need to forego the benefits of soft¬ ened water. Bert Keilin, PhD, Executive Director Pacific Water Conditioning Association Irvine, Calif 1. Schroeder HA, Kraemer LA: Cardiovascular mortality, municipal water, and corrosion. Arch Environ Health 28:303-311, 1974.
2. Mickelsen 0: The nutritional and health implications of water. Proc Int Water Quality Symposium 5:35\x=req-\ 37, 1970. 3. Anderson T: Can water cause heart disease? Proc
Int Water
Quality Symposium 6:28-32,
1972.
4. Comstock GW: Fatal arteriosclerotic heart
disease, home, and socioeconomic characteristics. Am J Epidemiol 94:1-10, 1971. 5. Schroeder HA: Cadmium hypertension in rats. J Chronic Dis 18:647-656, 1965. 6. Allwright SA, Coulson A, Detels R, et al: Mortality and water hardness. Lancet 2:860-864, 1974. water hardness at
7.
Myers
D:
1:398-399, 1975.
Mortality
and water hardness. Lancet
Reply.\p=m-\Thepurpose of the short review was to indicate that we now have reasonable evidence that there is an important association between the softness and hardness of drinking water and death rates from cardiovascular disease. It is not unexpected that the manufacturers of water-softening equipment should be concerned about this association. I emphasized that we "are, however, very far from knowing what specific factors are involved or how they work." Whether In
ports.
Letters, if clearly marked "For Publication, will be published "
as
Burton A. Sandok, MD
permits and at
space
Mayo Clinic
the discretion of the editor. They should be typewritten triple-spaced, with five or fewer references, should not exceed two pages in length, and will be subject to editing. Letters
are
not
acknowledged.
The Medical
Expert Witness in
Malpractice Suits
To the Editor.\p=m-\Ihave just finished reading Dr Paul C. Bucy's article (232:1352, 1975) and find it well done.
that he was too cautious concerning the physician's duty to testify as an expert against another physician when the issue is malpractice. We proudly consider ourselves a nation of laws, and rightly so. The physician in our society has reasonably high privileges and with that come equally high duties. An injured party ordinarily cannot sustain an action for malpractice without having an ex-
However, it
seems
to
physician, agreeing with malpractice did occur. The injured party cannot legally subpoena an expert, since only witnesses to fact can be subpoenaed, ergo, his entire case may turn on his ability to secure pert, ie,
a
an expert sue of
for his cause, not
on
the is-
malpractice itself. In the past, a physician's refusal to testify was called "conspiracy of silence." Today, in the face of the horrible malpractice mess, physicians may again be forgetting their duties, in a spasm of disgust over the entire situ¬ ation. The desperate plaintiff, re¬
quired by law to present an expert, will then find himself limited to select from physicians described as "profes¬ sional witnesses." These "hired guns" or "ladies of the night" are readily ca¬ pable of saying almost anything if the price is right. I ask the solid body of sound physi¬ cians not to shirk their duty, because it will only worsen the malpractice situation. If a physician is asked to be an expert witness, he should re¬ view the facts of the case as dis¬ passionately as possible and should give the requesting attorney his opin¬ ion equally straightforwardly. If, for any personal reason, the physician chooses not to testify, he should try to help the attorney find a qualified wit¬ ness. If this obligation is met, we will by John
D. Archer,
help destroy that handful of physi¬ cians who survive as "professional witnesses," and increase the input
of unbiased medical information into the judicial system. Alan Rosenberg, MD New York
me
him that
Edited
Rochester, Minn
MD, Senior Editor.
Arcus Senilis and Carotid Disease
Editor.\p=m-\Baglaand Golden reported (233:450,1975) the case of a 52\x=req-\ year-old woman, without any sympTo the
cerebrovascular disease, who for treatment of a urinary tract infection and was noted to have a unilateral arcus senilis on the right and a modest reduction in retinal arterial pressure on the left. Evidently, because of a similar earlier toms of
was
hospitalized
report (226:676, 1973) suggesting that
unilateral arcus is a sign of contralateral carotid artery disease, the patient, who was diabetic and perhaps hypertensive with arteriosclerotic
heart disease, was subjected to the risks of aortocervical angiography. A 40% narrowing of the right common carotid artery at its origin and bilaterally normal internal carotid arteries were seen. The authors, however, conclude that the clinical ophthalmologic findings "may be a function of nonvisualized small-vessel disease." I would agree; the disease was certainly "nonvisualized." They further suggest that their case (of nonvisualized disease) "provides confirmation of the observation that unilateral arcus senilis is a sign of con¬ tralateral occlusive disease." (Are we now to equate small-vessel disease with carotid occlusive disease?) I would rather suggest that their ar¬ ticle provides testimony to refute the thesis that unilateral arcus senilis is a sign of clinically significant contralateral carotid occlusive disease. We are all eager to identify pa¬ tients who may be at risk for stroke; however, it seems doubtful that this particular observation, even if confir¬ mation ever does appear, will prove to be clinically relevant. One wonders
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 06/13/2015
Furosemide for High Altitude Pulmonary Edema To the Editor.\p=m-\Therecent reply to
a
question regarding first aid equipment and acclimatization in mountain climbing (232:657, 1975) merits comment. Dr Mason suggests that furosemide (Lasix) given in large doses orally and intravenously may have dramatic beneficial effect in the treatment of high altitude pulmonary edema (HAPE). A case is described in which 120 mg orally and 80 mg inresulting in a travenously were given, 4,000-ml diuresis in 6 1/2 hours, with allegedly beneficial results. Unfortunately, such anecdotal reports have led to the indiscriminate use of furosemide in the treatment of HAPE as well as for the prevention of mountain sickness. Recently, a climbing party leader requested information about giving furosemide to all members of his party to prevent mountain sickness! Dr Mason points out that drug prophylaxis has been
disappointing.
It should be pointed out that there is insufficient evidence from appropriately conducted clinical studies that furosemide is indicated in the treatment of HAPE or acute mountain sickness. High altitude pulmonary edema is not due to cardiac failure. In severe cases, hypotension, a low car¬ diac output, hemoconcentration, and a shock-like state are present.' Fur¬ ther reduction of plasma volume by diuretics in such situations is more likely to aggravate hypotension. In many instances, HAPE can be treated by bed rest alone; hence, im¬ provement after the administration of furosemide cannot be attributed to the diuretic.2 Furosemide does not prevent acute mountain sickness, and in recent studies, this diuretic pro¬ duced hypovolemia, postural hypoten¬ sion, and syncope in subjects at 3,780 m.3 Persons with HAPE should be treated by prompt removal to a lower altitude, bed rest, and oxygen. Diure¬ sis induced by the use of furosemide may result in severe weakness that may make evacuation to a lower alti¬ tude on foot difficult. In addition, un¬ due confidence in diuretics may result
in failure to promptly institute bed rest therapy, to delay the use of oxy¬ gen, and to remove the patient to a
lower altitude, all of which have been clearly demonstrated to be of value in the treatment of HAPE. Herbert N. Hultgren, MD Chairman, Medical Committee American
Alpine Club
Palo Alto, Calif 1.
Hultgren H, Lopez C, Lundberg E, et al: Physiologic
studies of pulmonary edema at high altitude. Circulation
29:393-408, 1964.
2. Marticorena E, Hultgren H: Treatment of high altitude pulmonary edema by bed rest alone, abstracted. Circulation 34(suppl 3):163-164, 1966. 3. Hultgren H, Billisoly J, Fails H, et al: Plasma volume changes during acute exposure to high altitude, abstracted. Clin Res 21:224, 1973.
Shower Hazard? To the Editor.\p=m-\Anew product called
"Shower Massage" is now on the market and receiving considerable adver-
tising promotion. Having purchased a unit, I found it to be quite delightful
and effective. I also found, however, that when the unit is turned to the massage setting, it does indeed massage\p=m-\especially the carotid sinus. A very high\x=req-\ intensity, pulsating water stream is delivered. In my own case, this stream was capable of considerably slowing my sinus mechanism. This could be reproduced at will. I would be concerned about the potential hazard of this device, especially in patients with sensitive carotid sinus mechanisms or cardiac arrhythmias. Syncope in a shower might prove disastrous. In older patients, massage of a partially occluded carotid artery might well result in a cerebrovascular accident. I suggest that the cardiac effect of the water massage could be easily studied by electrocardiographic monitoring of volunteer subjects in the shower. If it is indeed demonstrated that significant changes in cardiac rhythm occur, then a suitable warning should accompany the sale of the product. In any event, I would certainly ad¬ vise elderly patients against direct¬ ing the massage stream to the neck area. Sidney Richman, MD
Bloomfield, Conn
Softened Water To the Editor.\p=m-\Dr Shaper (230:130, 1974) has succinctly summarized the series of statistical studies relating
soft water and fatal heart attacks and strokes. Some of his conclusions may be erroneous in that no
naturally
distinction is made between naturally soft water and water softened by a home appliance. Naturally soft water is most often relatively acidic and has a low dissolved-solids content.1 The studies summarized by Shaper generally show that such water supplied to a community may render it susceptible to higher incidence of fatal heart attacks and strokes. Softened water, however, is more like the naturally hard water from which it is made, generally low in acidity, with relatively large quantities of dissolved solids.1 Softened water differs from the original supply in its substitution of sodium ions for virtually all calcium, magnesium, and other heavy metals. The average adult derives in excess of 90% of total daily intake of both sodium and calcium from food2 and the remainder from water. About 60% of magnesium comes from food. It is logical to conclude that the hardness of drinking water should not affect susceptibility to fatal heart attacks and that the real culprit is one of the trace constituents of water that may be associated with hardness only in a
secondary way.3 The epidemiologic studies summa¬ rized by Shaper have consistently compared naturally soft water with naturally hard water. There is no evi¬
dence that softened water can be im¬ plicated. Indeed, a study in 1971 com¬ paring naturally hard water with softened water demonstrated the re¬ verse relationship, namely, that per¬ sons using softened water suffered fatal heart attacks at a lesser rate.4 Some of the workers in the field be¬ lieve that the higher acidity of natu¬ rally soft water, compared with that of naturally hard water, leaches cad¬ mium from galvanized water pip¬ ing. M Cadmium in very small quan¬ tities has been shown to cause high blood pressure and cardiovascular dis¬ ease in test animals.5 If so, water softened in the home is not likely to be related to fatal heart attacks any more than the original hard water supply from which it is generated. A recent study (Med World News, October 1974, p 45) appears to lend further support to such a conclusion. The death rates of matched groups in Kansas City, Mo, and Kansas City, Kan, were compared. The two com¬ munities use the same water source, the Missouri River, but the Missouri city softens its water municipally. The rate of deaths from heart disease
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 06/13/2015
is 50% higher in the Kansas city, which serves its residents the harder water. The cadmium content of the Kansas community water supplied at the tap is three times that of the Mis¬ souri city and the blood of the Kansas group contained 13 times as much cadmium. The Kansas test group had significantly higher average blood pressure as well. (Municipal and do¬ mestic softening processes are known to remove cadmium and other toxic heavy metal ions that may be present in the water supply.) Two recent communications serve to further point out the confusion that exists among the many epidemiologic studies that have been re¬ ported. Three matched communities in California (Reseda, Burbank, and Downey)6 with widely varying hard¬ ness of the water supply were com¬ pared. The authors conclude that no consistent association exists between deaths from heart disease and the de¬ gree of water hardness. A similar comparison of groups in Melbourne and Brisbane, Australia,7 also yielded no consistent association. The existing data hardly warrant the strong conclusions of Dr Shaper and certainly do not implicate soft¬ ened water. However, should the con¬ sumer prefer, a hard-water line can be provided to a kitchen or bathroom tap for drinking purposes without the need to forego the benefits of soft¬ ened water. Bert Keilin, PhD, Executive Director Pacific Water Conditioning Association Irvine, Calif 1. Schroeder HA, Kraemer LA: Cardiovascular mortality, municipal water, and corrosion. Arch Environ Health 28:303-311, 1974.
2. Mickelsen 0: The nutritional and health implications of water. Proc Int Water Quality Symposium 5:35\x=req-\ 37, 1970. 3. Anderson T: Can water cause heart disease? Proc
Int Water
Quality Symposium 6:28-32,
1972.
4. Comstock GW: Fatal arteriosclerotic heart
disease, home, and socioeconomic characteristics. Am J Epidemiol 94:1-10, 1971. 5. Schroeder HA: Cadmium hypertension in rats. J Chronic Dis 18:647-656, 1965. 6. Allwright SA, Coulson A, Detels R, et al: Mortality and water hardness. Lancet 2:860-864, 1974. water hardness at
7.
Myers
D:
1:398-399, 1975.
Mortality
and water hardness. Lancet
Reply.\p=m-\Thepurpose of the short review was to indicate that we now have reasonable evidence that there is an important association between the softness and hardness of drinking water and death rates from cardiovascular disease. It is not unexpected that the manufacturers of water-softening equipment should be concerned about this association. I emphasized that we "are, however, very far from knowing what specific factors are involved or how they work." Whether In
