A*******s
发帖数: 9638 | 1 一个病例动摇了我这么多年树立的信心。
我一直以为， 诊断疾病要的是证据。 没有证据，所有的猜测都是捕风捉影，所有的担
心都会成为事实，所以我强调证据， 证据是王道。
可是，下面这个病例让我感到无限的迷茫：
一个中年病人，ETOH abuse， 因为虚脱到ER时血钠是90多，补液， banana bag， 因
为担心CPM（ Central Pontine myelinolysis），补钠非常小心， 2天后出现了一次
seizure， 当时血钠是117，我开始看这个病人后， 就做了个MRI of brain， 结果是
正常。 5天后血钠133，病人也恢复到可以出院的状态。
一个星期后， 病人出现呼吸衰竭，肺炎，神志不清，血钠正常，重复的MRI证明是CPM。
我的疑虑是， CPM应该是在补钠第一天就发生了，为什么MRI两天后是正常的？ 病人也
慢慢好转， 1个星期后才又出现症状，MRI也出现了典型的病变。查了一下文献，MRI改
变是可以延迟的，但没人说得清为什么。
没有什么能比毫无作为更让人沮丧的了，到现在都不明白该怎么做才能预防这样的悲剧。
难道没看见的也得相信是真的？ |
L****n
发帖数: 12932 | 2 time to believe in God. He is going where God wants him to. |
A*******s
发帖数: 9638 | 3 He is not going anywhere now, he is in Lock-in.
I just feel frustrated, I knew it could happen, and I had a week to work on
it.
【在 L****n 的大作中提到】
: time to believe in God. He is going where God wants him to.
|
s********x
发帖数: 472 | 4 Very few things are absolute. Most of the time there are just probabilities.
So don't feel bad if you happen to pick a bad card.
CPM。
【在 A*******s 的大作中提到】
: 一个病例动摇了我这么多年树立的信心。
: 我一直以为， 诊断疾病要的是证据。 没有证据，所有的猜测都是捕风捉影，所有的担
: 心都会成为事实，所以我强调证据， 证据是王道。
: 可是，下面这个病例让我感到无限的迷茫：
: 一个中年病人，ETOH abuse， 因为虚脱到ER时血钠是90多，补液， banana bag， 因
: 为担心CPM（ Central Pontine myelinolysis），补钠非常小心， 2天后出现了一次
: seizure， 当时血钠是117，我开始看这个病人后， 就做了个MRI of brain， 结果是
: 正常。 5天后血钠133，病人也恢复到可以出院的状态。
: 一个星期后， 病人出现呼吸衰竭，肺炎，神志不清，血钠正常，重复的MRI证明是CPM。
: 我的疑虑是， CPM应该是在补钠第一天就发生了，为什么MRI两天后是正常的？ 病人也
|
A*******s
发帖数: 9638 | 5 看病需要理念和信心， 每天到医院进诊所面对的是各式各样的疑难杂症，没有这个理
念和信心是不可能坚持下来的。
我提这个case实在是太让人匪夷所思，尽管很多病现在无解，但都是我知道的。 这个
CPM我也是知道的，但这个病历让我感到教科书可能是错的。
probabilities.
【在 s********x 的大作中提到】
: Very few things are absolute. Most of the time there are just probabilities.
: So don't feel bad if you happen to pick a bad card.
:
: CPM。
|
s********o
发帖数: 3319 | 6 所以才要不停地做临床试验去拓展医学知识。
开始做住院医以后体会到 每个人的生命都是宝贵的，而这仅有的一次生命其实是极度
脆弱的。
【在 A*******s 的大作中提到】
: 看病需要理念和信心， 每天到医院进诊所面对的是各式各样的疑难杂症，没有这个理
: 念和信心是不可能坚持下来的。
: 我提这个case实在是太让人匪夷所思，尽管很多病现在无解，但都是我知道的。 这个
: CPM我也是知道的，但这个病历让我感到教科书可能是错的。
:
: probabilities.
|
d**o
发帖数: 618 | 7 老大好象前几天刚安慰过一个处理CPM失败的同事？这一定是有天意、、
其实回头一想，你肯定也见过不少按理必死结果活得好好的，完全无法解释的病人，对
吧？白天路走多了也总会遇到神，临床就是这样时不时有点奇迹才有意思。
再说，我觉得MRI改变延迟是完全可以理解的，毕竟MRI看的是毫米量级的东西，可能
CPM在细胞层面上已经把myelin sheath剥离了，但剥下来的myelin被运走/降解得很慢
，T1/T2就没有改变。 |
A*******s
发帖数: 9638 | 8 我喜欢白天路走多了也总会遇到神， lol
问题的关键是这个病人恢复到出院的程度，你能想象myelin被破环了还能出院？
我个人觉得不是那么简单，或者这个CPM与Sodium根本没有关系。
【在 d**o 的大作中提到】
: 老大好象前几天刚安慰过一个处理CPM失败的同事？这一定是有天意、、
: 其实回头一想，你肯定也见过不少按理必死结果活得好好的，完全无法解释的病人，对
: 吧？白天路走多了也总会遇到神，临床就是这样时不时有点奇迹才有意思。
: 再说，我觉得MRI改变延迟是完全可以理解的，毕竟MRI看的是毫米量级的东西，可能
: CPM在细胞层面上已经把myelin sheath剥离了，但剥下来的myelin被运走/降解得很慢
: ，T1/T2就没有改变。
|
s****q
发帖数: 117 | |
s****q
发帖数: 117 | |
|
|
d**o
发帖数: 618 | 11 hmm, 对哦。要是出院时也做了MRI证据链就完整了。现有信息，是否可以假设
当初有轻度的myelin injury，MRI negative but still caused seizure, no
permanent lesion in pontine, but that site still very vulnerable when he was
discharged, 然后他出院以后不知道这个星期里又做了啥伤神经的事，也许又酗酒？
【在 A*******s 的大作中提到】
: 我喜欢白天路走多了也总会遇到神， lol
: 问题的关键是这个病人恢复到出院的程度，你能想象myelin被破环了还能出院？
: 我个人觉得不是那么简单，或者这个CPM与Sodium根本没有关系。
|
m******n
发帖数: 14 | 12 是不是是MRI的现象是CPM的result， 而不是cause。 由于已经有了CPM， 在发展中，
是MRI看不出来。是不是给有其他的生物证据来判断有没有CPM？ |
k********n
发帖数: 756 | 13 May require DWI for early diagnosis? |
s*******w
发帖数: 1879 | |
g*****d
发帖数: 991 | 15 Medicine is complicated and human is more complicated.
We, doctors, only know the piece of the corner iceberg, but we try to act
like a God. Too much pressure on doctor.
Are you sure CPM is 100% from sodium correction or not just from etoh abuse
or something else?
CPM。
【在 A*******s 的大作中提到】
: 一个病例动摇了我这么多年树立的信心。
: 我一直以为， 诊断疾病要的是证据。 没有证据，所有的猜测都是捕风捉影，所有的担
: 心都会成为事实，所以我强调证据， 证据是王道。
: 可是，下面这个病例让我感到无限的迷茫：
: 一个中年病人，ETOH abuse， 因为虚脱到ER时血钠是90多，补液， banana bag， 因
: 为担心CPM（ Central Pontine myelinolysis），补钠非常小心， 2天后出现了一次
: seizure， 当时血钠是117，我开始看这个病人后， 就做了个MRI of brain， 结果是
: 正常。 5天后血钠133，病人也恢复到可以出院的状态。
: 一个星期后， 病人出现呼吸衰竭，肺炎，神志不清，血钠正常，重复的MRI证明是CPM。
: 我的疑虑是， CPM应该是在补钠第一天就发生了，为什么MRI两天后是正常的？ 病人也
|
A*******s
发帖数: 9638 | 16 Order a test when patient is getting better? No wonder medicare cost is so
high these days. :)
The patient did not go back to drink.
was
【在 d**o 的大作中提到】
: hmm, 对哦。要是出院时也做了MRI证据链就完整了。现有信息，是否可以假设
: 当初有轻度的myelin injury，MRI negative but still caused seizure, no
: permanent lesion in pontine, but that site still very vulnerable when he was
: discharged, 然后他出院以后不知道这个星期里又做了啥伤神经的事，也许又酗酒？
|
A*******s
发帖数: 9638 | 17 To my knowledge, MRI is the only tool for CPM.
【在 m******n 的大作中提到】
: 是不是是MRI的现象是CPM的result， 而不是cause。 由于已经有了CPM， 在发展中，
: 是MRI看不出来。是不是给有其他的生物证据来判断有没有CPM？
|
A*******s
发帖数: 9638 | 18 All MRIs include DWI. The first one was normal, the sencod showed changes
consistent with acute infarct except bilateral irregular distribution. The
third one extended to basal ganglion with negative DWI.
【在 k********n 的大作中提到】
: May require DWI for early diagnosis?
|
A*******s
发帖数: 9638 | 19 Impossible
【在 s*******w 的大作中提到】
: 就没可能当初mri的诊断其实是错的？
|
A*******s
发帖数: 9638 | 20 What else could be other than sodium theory?
I agree we only know the tip of a iceberg on CPM.
abuse
【在 g*****d 的大作中提到】
: Medicine is complicated and human is more complicated.
: We, doctors, only know the piece of the corner iceberg, but we try to act
: like a God. Too much pressure on doctor.
: Are you sure CPM is 100% from sodium correction or not just from etoh abuse
: or something else?
:
: CPM。
|
|
|
k********n
发帖数: 756 | 21 It would be interesting to know when the second MRI was done and where the
DWI signal were. I suspect that DWI changes were the early sign of CPM on
MRI. I remember that CPM classically has two phases (improve and 5-7 days
later deteriorate) and presents exactly like this case.
【在 A*******s 的大作中提到】
: All MRIs include DWI. The first one was normal, the sencod showed changes
: consistent with acute infarct except bilateral irregular distribution. The
: third one extended to basal ganglion with negative DWI.
|
b******a
发帖数: 704 | 22 I guess alcohol abuse is the key here. The theroy of rapid correction of
hyponatraemia was based on normal patient population.
"Although less common, CPM may also present in patients
with a history of chronic alcoholism or other conditions related to
decreased liver function. In these cases, the condition is often unrelated
to correction of sodium or electrolyte imbalance."
Here is a case with some interesting discussion about the biphase
presentation of CPM in alcoholic or liver decompsated patient.
http://www.annalsofhepatology.com/PDF/vol5n4/Hp064-11.pdf
CPM。
【在 A*******s 的大作中提到】
: 一个病例动摇了我这么多年树立的信心。
: 我一直以为， 诊断疾病要的是证据。 没有证据，所有的猜测都是捕风捉影，所有的担
: 心都会成为事实，所以我强调证据， 证据是王道。
: 可是，下面这个病例让我感到无限的迷茫：
: 一个中年病人，ETOH abuse， 因为虚脱到ER时血钠是90多，补液， banana bag， 因
: 为担心CPM（ Central Pontine myelinolysis），补钠非常小心， 2天后出现了一次
: seizure， 当时血钠是117，我开始看这个病人后， 就做了个MRI of brain， 结果是
: 正常。 5天后血钠133，病人也恢复到可以出院的状态。
: 一个星期后， 病人出现呼吸衰竭，肺炎，神志不清，血钠正常，重复的MRI证明是CPM。
: 我的疑虑是， CPM应该是在补钠第一天就发生了，为什么MRI两天后是正常的？ 病人也
|
a**********2
发帖数: 3726 | 23 Well said. Every life is valuable. Sometimes an extra piece of work or extra
words can change a patient's life.
Not being a political discussion, I am very frustrated about the arguments
in other forums that tries to deprive some people of getting medicare or
medicaid. EVERY life is valuable, regardless of black or white, legal or
illegal.
【在 s********o 的大作中提到】
: 所以才要不停地做临床试验去拓展医学知识。
: 开始做住院医以后体会到 每个人的生命都是宝贵的，而这仅有的一次生命其实是极度
: 脆弱的。
|
A*******s
发帖数: 9638 | 24 2nd MRI was done 1 wk after the first MRI. DWI signal is right at the
central ponine.
【在 k********n 的大作中提到】
: It would be interesting to know when the second MRI was done and where the
: DWI signal were. I suspect that DWI changes were the early sign of CPM on
: MRI. I remember that CPM classically has two phases (improve and 5-7 days
: later deteriorate) and presents exactly like this case.
|
A*******s
发帖数: 9638 | 25 I concur. I wonder if any nutritional deficiency 2nd to ETOH abuse is the
culprit for CPM. Thiamine deficiency, for instance, in Alcoholics causes
Wernicke's encephalopathy but this patient did not have wernicke's lesions
in the brain, thanks to banana bags.
【在 b******a 的大作中提到】
: I guess alcohol abuse is the key here. The theroy of rapid correction of
: hyponatraemia was based on normal patient population.
: "Although less common, CPM may also present in patients
: with a history of chronic alcoholism or other conditions related to
: decreased liver function. In these cases, the condition is often unrelated
: to correction of sodium or electrolyte imbalance."
: Here is a case with some interesting discussion about the biphase
: presentation of CPM in alcoholic or liver decompsated patient.
: http://www.annalsofhepatology.com/PDF/vol5n4/Hp064-11.pdf
:
|
k********n
发帖数: 756 | 26 So, those DWIs were suggestive of CPM but were still not early enough to
forecast the imminent CPM. Sad....
【在 A*******s 的大作中提到】
: 2nd MRI was done 1 wk after the first MRI. DWI signal is right at the
: central ponine.
|
A*******s
发帖数: 9638 | 27 I hope this case would remind everyone here of CPM before correcting the
hyponaltremia. If you have to use 3% Saline, do tell family about the risk.
For me, I would never use 3% saline. CPM with lock-in is even worse than
dying. |
b******a
发帖数: 704 | 28 Lampl, C. and K. Yazdi (2002). "Central pontine myelinolysis." Eur Neurol 47
(1): 3-10
The etiology and pathogenesis of this disorder are unclear and will be
discussed. Chronic alcoholism is still the most common underlying condition
of CPM patients. In the literature, 174 cases of CPM have been reported in
alcoholics since 1986, which is equivalent to an incidence of 39.4%.
Likewise, 95 cases of CPM following the correction of hyponatremia have been
documented since 1986 (21.5%). The role of hyponatremia and its correction
will be outlined in the discussion of the pathogenesis of CPM. The third
largest group of CPM cases are liver transplant patients (17.4%), with the
development of CPM being attributed to the immunosuppressive agent
cyclosporine in particular.
Depending on the involvement of other CNS structures, the clinical picture
can vary considerably. The large-scale introduction of magnetic resonance
imaging has increasingly facilitated the antemortem diagnosis of CPM,
although the radiological findings lag behind and do not necessarily
correlate with the clinical picture. As yet, there is no specific therapy of
choice. A number of therapeutic approaches have been tested and although
they have not been compared with regard to their rate of success, they have
all led to a substantial improvement in the prognosis of CPM.
Eur J Neurol. 2001 Mar;8(2):103-9.
A review of the causes of central pontine myelinosis: yet another apoptotic
illness?
how should CPM be prevented and treated?
We contend that patients at risk should be identified, metabolic stress
should be minimized, the supply of high energy compounds maximized and
antioxidants given. Patients at higher risk can be identified by their high
alcohol intake or by nutritional deficiency (especially if they have lost
weight). High doses of vitamins should be given on admission, particularly
thiamine to counteract subclinical deficiency and other compounds that act
as free radical scavengers, such as vitamin E and, to a lesser extent,
vitamin C. High-energy, readily metabolizable food, including glucose,
should also be given early on and continued for at least several weeks,
given that, as in our patient, clinical CPM may not occur until many days
after admission. If patients are unable to swallow these should be given
intravenously.
How should the hyponatraemia be corrected? Clearly, the mechanism
responsible for the hyponatraemia should be determined (SIADH, hypo-
adrenalism, salt-losing nephropathy, etc.) as this may need specific
attention. We suggest that if the sodium defect is large, any correction of
hyponatraemia should be performed exceptionally slowly over many weeks, to
minimize metabolic stress. As hyponatraemia in many patients resolves
spontaneously, albeit slowly, on a normal sodium content hospital diet, we
therefore recommend that (unless the situation is critical, such as with
seizures or substantial prerenal renal failure threatening acute tubular
necrosis, etc.) that a normal sodium content diet be given orally without
any added sodium, with the aim of correcting the hyponatraemia as slowly as
possible, maybe by no more than 2–3 mmol/day.
http://jnnp.bmj.com/content/74/6/820.1.full
http://www.nejm.org/doi/full/10.1056/NEJMicm066005
hyponaltremia. If you have to use 3% Saline, do tell family about the risk.
For me, I would never use 3% saline. CPM with lock-in is even worse than
【在 A*******s 的大作中提到】
: I hope this case would remind everyone here of CPM before correcting the
: hyponaltremia. If you have to use 3% Saline, do tell family about the risk.
: For me, I would never use 3% saline. CPM with lock-in is even worse than
: dying.
|
A*******s
发帖数: 9638 | 29 A nice read and well summerized this thread. Thanks a million, bythesea.
47
condition
in
been
correction
【在 b******a 的大作中提到】
: Lampl, C. and K. Yazdi (2002). "Central pontine myelinolysis." Eur Neurol 47
: (1): 3-10
: The etiology and pathogenesis of this disorder are unclear and will be
: discussed. Chronic alcoholism is still the most common underlying condition
: of CPM patients. In the literature, 174 cases of CPM have been reported in
: alcoholics since 1986, which is equivalent to an incidence of 39.4%.
: Likewise, 95 cases of CPM following the correction of hyponatremia have been
: documented since 1986 (21.5%). The role of hyponatremia and its correction
: will be outlined in the discussion of the pathogenesis of CPM. The third
: largest group of CPM cases are liver transplant patients (17.4%), with the
|
s******v
发帖数: 477 | 30 老大请看：CPM can also happened in normonatremic alcoholic patients
http://tinyurl.com/coxkq47 |
|
|
s******v
发帖数: 477 | 31 老大请看：CPM can also happened in normonatremic alcoholic patients.
http://tinyurl.com/coxkq47 |
s******v
发帖数: 477 | 32 老大请看：CPM can also happened in normonatremic alcoholic patients.
http://tinyurl.com/coxkq47
【在 A*******s 的大作中提到】
: 一个病例动摇了我这么多年树立的信心。
: 我一直以为， 诊断疾病要的是证据。 没有证据，所有的猜测都是捕风捉影，所有的担
: 心都会成为事实，所以我强调证据， 证据是王道。
: 可是，下面这个病例让我感到无限的迷茫：
: 一个中年病人，ETOH abuse， 因为虚脱到ER时血钠是90多，补液， banana bag， 因
: 为担心CPM（ Central Pontine myelinolysis），补钠非常小心， 2天后出现了一次
: seizure， 当时血钠是117，我开始看这个病人后， 就做了个MRI of brain， 结果是
: 正常。 5天后血钠133，病人也恢复到可以出院的状态。
: 一个星期后， 病人出现呼吸衰竭，肺炎，神志不清，血钠正常，重复的MRI证明是CPM。
: 我的疑虑是， CPM应该是在补钠第一天就发生了，为什么MRI两天后是正常的？ 病人也
|
A*******s
发帖数: 9638 | 33 The MRI it displayed is not typical for CPM.
That is why a case study is not scientific.
【在 s******v 的大作中提到】
: 老大请看：CPM can also happened in normonatremic alcoholic patients.
: http://tinyurl.com/coxkq47
|
s******v
发帖数: 477 | 34 After read your post, I checked uptodate on CPM, here are what I learned
1) the three high risk of CMP: the level of sodium at the presentation,
duration of hyponatremia and the correction rate. Your patient was already
had two major risks before the treatment.
2)detection of CPM is MRI, however the MRI may not be positive for as long
as four weeks.
3)Even you give patient IV fluid carefully according to your calculation, it
is hard to predict speed of corrections because the mechanism of auto-
corrections.
4)In case overly rapid corretion the hyponatremia, relowing sodium level
maybe benificial. |
A*******s
发帖数: 9638 | 35 It is a good learning experience since such a topic is so common in our
daily practice.
For my case, I can buy the delayed MRI changes, but I can not accept a
delayed clinic presentation. Something is behind the CPM and Sodium may be
just the scapegoat.
it
【在 s******v 的大作中提到】
: After read your post, I checked uptodate on CPM, here are what I learned
: 1) the three high risk of CMP: the level of sodium at the presentation,
: duration of hyponatremia and the correction rate. Your patient was already
: had two major risks before the treatment.
: 2)detection of CPM is MRI, however the MRI may not be positive for as long
: as four weeks.
: 3)Even you give patient IV fluid carefully according to your calculation, it
: is hard to predict speed of corrections because the mechanism of auto-
: corrections.
: 4)In case overly rapid corretion the hyponatremia, relowing sodium level
|
s******v
发帖数: 477 | 36 CPM can happened in normanatremia alcoholic patient
http://tinyurl.com/c6y3gad |
