之前寫過一篇關於索命麻醉的文章
有興趣的讀友可以翻出來再看一次
https://www.facebook.com/309451919769378/posts/316504692397434?sfns=mo
今天來談談 【肌肉鬆弛劑】
肌肉鬆弛劑,又是一個『中文誤我』的故事。
本文這裡講得肌肉鬆弛劑,指的是【阻斷肌肉神經傳導的藥物。】#Neuromuscular #blockade
也就是上一篇文章裡面講到,讓病人 #不動 的藥物。
跟你腰酸背痛,醫師開給你吃的【肌肉鬆弛劑】完全是兩回事。
#skeletal #muscle #relaxants
跟醫美診所打在你臉上,說是讓你臉部的肌肉放鬆,然後消除你原本可以夾死蒼蠅的皺紋的【肉毒桿菌】也是兩回事。
#botulinum #toxin
以英文來看,你完全不會弄錯。
但中文都翻譯成『肌肉鬆弛劑』,是不是就很容易被不知情的人混淆了呢?
不知道各位讀友是否還有人記得,2002年的新聞:
北城婦幼醫院的護士黃xx,因為將肌肉鬆弛劑當成B型肝炎疫苗,為新生兒施打,因此造成六女一男共七名新生兒生命垂危的不幸事件。
事實上,此類的肌肉鬆弛劑就是作用在神經與肌肉相交接處,讓要求肌肉收縮的神經訊號無法傳遞,達成讓全身的骨骼肌都無法收縮的藥理效果。(#如手繪圖一)
此類藥物起源於南美洲土著的 #箭毒(curare),最初的作用是塗在箭尖,中箭者意識清醒,也能感受到痛苦,但全身肌肉無力,全身都不能動麻痺而死!因為中了箭毒,你連呼吸的肌肉都不能收縮,所以你會活活不能呼吸窒息而死,後來這類藥物被廣泛用在手術上,也就是現今我們手術中會使用的 #肌肉鬆弛劑 (由英文來看,稱之為神經肌肉阻斷劑更合適)
(小編按:所以每個麻醉醫師都是 #用毒高手?)
至於口服的肌肉鬆弛劑呢?
阿婆腰痠背痛,抱小孩的媽媽手臂痠痛,運動員運動傷害肌肉拉傷,醫師很常開的口服的肌肉鬆弛劑,大概都歸類於這一類。
比如說 #Baclofen 是抑制腦和脊髓突觸的傳導,減少肌肉過度的收縮。常用在中風病人的肢體攣縮,可能會有一點輕微的嗜睡。
#Mephenoxalone 是最常見口服的肌肉鬆弛劑,可以抑制神經衝動的傳導,而達到緩解骨骼肌筋攣造成的肌肉疼痛,經由神經系統作用來產生肌肉鬆弛的效果。可以用來治療腰痛,落枕的脖子痛,過度使用造成的肌肉痛,肌肉僵硬。
以上這些口服的藥物是用來緩解肌肉收縮,或是減少肌肉的收縮,使肌肉放鬆。而針劑的箭毒類的肌肉神經阻斷劑,是造成肌肉的麻痺,而讓肌肉完全不能收縮,以便手術。 這是完全不同的藥物
但...但...但... 別懷疑~
真的會有 強克!崔西!卡比琪!的垃圾醫生,分不清楚這兩類藥的差別。
註:#junk #trash #garbage
醫師執照也不知道是去 #波蘭 買的,還是拿雞腿去換的。
這樣都敢學人家當醫生,也不知道勇氣是不是梁靜茹給的。
講兩個恐怖故事好了~
故事一:
有個診所的醫師,因為診所護理師腰痠背痛,因為診所沒有口服的肌肉鬆弛劑,所以好心的拿手術用的“肌肉鬆弛劑”幫護理師來一針~
然後呢?
護理師就沒有然後了~嗯,中了箭毒麻痺而死的故事,寫出來大概不是PG13,已經分類為R級了。
崔西卡比琪醫師呢?和解就把事件壓下來了~所以 #沒上新聞。
#不自殺聲明
#不要查我水表
故事二:
某個中部很鄉下的小醫院。
骨科手術,病患下肢骨折,被施打半身麻醉。
(有在發漏粉專的各位麻的法課友應該就知道,半身麻醉是從脊椎骨縫打針,只有麻醉下半身。而病人的上半身是清醒的,還會講話會聊天會呼吸~)
骨科醫:病人腳還在用力,還會踢我。
麻醫:心裏OS(蛤?都從脊椎阻斷傳導了...怎麼可能用力)
骨科醫:你技術這麼爛,有麻跟沒麻差不多!
麻醫:心裏OS(沒麻病人早就哇哇大叫痛了,阿婆醒著卻什麼話都沒說,就你話最多,可以不要尿不準怪馬桶歪嗎?)
骨科醫:不管啦,你給我打 #肌肉鬆弛劑。
麻醫:心裏OS(!!!要病人中箭毒清醒著麻痺而死???!!!)
你以為故事結束嗎?
麻醫拿出一支空針,從點滴裡抽了一點生理食鹽水,再加回去點滴。
麻醫:我幫你的病人加了肌肉鬆弛劑了~
骨科醫:就你嘴硬,早點加不就好了嗎?你看病人現在都鬆了,讓我好開多了!叫你早點加就不加,浪費大家時間....(以下省略一萬字)
嗯,據說那個骨科醫師到現在還依此為要求,要麻到他的手術的麻醉醫師都要幫他半身麻醉的病人打肌肉鬆弛劑。
#你以為我會承認那個麻醫是我嗎?
最後來聊聊下面的新聞,『術中清醒』
#麻,就是不痛。要給予病人適當的止痛藥物。(讓病人不痛)
#醉,就是不醒。要給予病人足量的鎮靜藥物。(讓病人睡著)
再加上 #肌肉鬆弛劑, 讓病人不動。
【不痛、不醒、不動,就是全身麻醉】
請參見《手繪圖二》
全身麻醉,麻的是你的腦,所以會讓你失去意識。如果讓你失去意識 #不醒 的藥物不夠,但 又給了你 #不動 的肌肉鬆弛劑,那索命麻醉的劇情,就會在你身上活活上演了。
下面的新聞就是個例子。
新聞:
意識清楚的狀態下「肚皮被醫師割開」病婦麻醉失敗,小手術變終生夢魘
https://www.ettoday.net/dalemon/post/42308
#本文歡迎轉載
#轉載請保留出處
同時也有1部Youtube影片,追蹤數超過83萬的網紅serpentza,也在其Youtube影片中提到,I cut myself on a rusty knife in China and had to get a Tetanus shot! So how does it work and is it really only $2? Tetanus, also known as lockjaw, i...
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Herbal #tea are popular beverage choices when it comes to #relax and #unwind. 😴
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@sleepywinkscom Day is the 1st part of REBALANCE - their proprietary #herbal blend with #chamomile, genmaicha, and #lemon balm. It combats #lifestyle-related #stress and anxiety, calms you down, and allows your body to naturally regulate its #sleep cycle.
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@sleepywinkscom Night is the 2nd part of REBALANCE - ingredients found in it (chamomile, #rooibos, valerian root) all act as mild sedatives and relaxants, naturally inducing restorative sleep. Taken before going to bed.
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ARDS
Do we need ARDS? This is a good question, isn’t it?
by Jean-Louis Vincent, Carlos Santacruz
After all, once we’ve made a diagnosis of ARDS (acute respiratory distress syndrome), what do we actually do with it? Does it really change the way we treat these patients? In Berlin, we revisited the criteria for ARDS diagnosis [1], but was this a major advance? Some years ago, one would have claimed that a diagnosis of ARDS indicated that a protective ventilation strategy using small tidal volumes was needed. However, we have now learned that this strategy is also of use in patients at risk of ARDS, and, even more, that it should be used in all ventilated patients, even for short periods of time during surgery [2]. Hence, because we also need to apply some positive end-expiratory pressure (PEEP) in severe hypoxemia, identification of ARDS does not mean different ventilator settings. Profound sedation, even with muscle relaxants, may be needed in all forms of severe respiratory failure, to improve tolerance to extreme respiratory conditions. Likewise, we have not been able to develop any specific pharmacologic intervention for ARDS. Admittedly, one could argue that the label ‘ARDS’ is merely a marker of severity, highlighting a need for special care and attention, but this is also the case for other causes of severe hypoxemia.
A key issue is the notoriously heterogeneous nature of ARDS, as a result of the variety of associated diseases and also the underlying pathological alterations. Autopsy studies have revealed that many patients do not have the typical diffuse alveolar damage (DAD) pattern; in our experience, only 50 % of patients with a clinical diagnosis of ARDS who underwent autopsy had DAD [3]. In a very recent autopsy study, Lorente et al. [4] reported that DAD was associated with greater degrees of respiratory and general disease severity, and with a greater likelihood of death from shock. Kao et al. [5] reported that only 56 % of 101 patients with a clinical diagnosis of ARDS who underwent open lung biopsy had DAD; a pathological finding of DAD was associated with increased hospital mortality in these patients. Likewise, in 83 patients with ARDS who underwent open lung biopsy, Guerin et al. [6] reported that DAD, present in 58 % of these patients, was associated with more severe ARDS.
The risk is that, once a diagnosis of ARDS is made and the label attached, we may focus our attention on fine tuning mechanical ventilation and perhaps using prone positioning in severe cases (when practically feasible). We may think we have a diagnosis, so that the search for an underlying cause is neglected. Yet ARDS is not a specific disease and control of the cause is of paramount importance to maximize a patient’s chances of survival.
According to the standard criteria [1], a diagnosis of ARDS requires the presence of an identified risk factor. However, there are cases where the clinical presentation is identical, although there is no identified risk factor. Common causes of such ‘pseudo-ARDS’ cases were recently reviewed by Guerin et al. [7]. In a recent article in Intensive Care Medicine, Gibelin and colleagues [8] reviewed their experience at two large centers in Paris and found that 50 (7.5 %) of 665 patients labeled as ARDS in fact had ‘pseudo-ARDS’, because they did not have an identified risk factor. These patients in general had less severe acute illness and a slower progression of their respiratory failure. As expected, cancer, pulmonary fibrosis and vasculitis represented the majority of these cases, and this may explain the generally higher mortality rates in these patients. Importantly, some of these ‘pseudo-ARDS’ cases had potentially reversible conditions, and the use of corticosteroids may have been beneficial. Indeed, one could consider that corticosteroids were indicated in most, if not all, these patients, and were actually administered in 17/17 survivors and 25/33 non-survivors. The authors propose that this strategy should be studied prospectively, but we contend that the evidence in support of such an approach is already strong enough. In any case, a prospective study of these rare cases would hardly be feasible.
The key message is that we must always try to find a cause for severe acute respiratory failure. Indeed, this is a concept that can be generalized to any severe disease, and is also true for other syndromes, like sepsis, shock or coma. Even brain death needs to have a defined cause. Finding the underlying cause of the severe respiratory failure can not only help guide treatment but may also lead to earlier discontinuation of life support if a non-reversible, terminal condition is identified.
http://bit.ly/1SlGYxr
relaxants 在 serpentza Youtube 的最讚貼文
I cut myself on a rusty knife in China and had to get a Tetanus shot! So how does it work and is it really only $2?
Tetanus, also known as lockjaw, is an infection characterized by muscle spasms. In the most common type, the spasms begin in the jaw and then progress to the rest of the body. These spasms usually last a few minutes each time and occur frequently for three to four weeks. Spasms may be so severe that bone fractures may occur. Other symptoms may include fever, sweating, headache, trouble swallowing, high blood pressure, and a fast heart rate. Onset of symptoms is typically three to twenty-one days following infection. It may take months to recover. About 10% of those infected die.
Tetanus is caused by an infection with the bacterium Clostridium tetani, which is commonly found in soil, saliva, dust, and manure. The bacteria generally enter through a break in the skin such as a cut or puncture wound by a contaminated object. They produce toxins that interfere with muscle contractions, resulting in the typical symptoms. Diagnosis is based on the presenting signs and symptoms. The disease does not spread between people.
Infection can be prevented by proper immunization with the tetanus vaccine. In those who have a significant wound and less than three doses of the vaccine, both immunization and tetanus immune globulin are recommended. The wound should be cleaned and any dead tissue should be removed. In those who are infected tetanus immune globulin or, if it is not available, intravenous immunoglobulin (IVIG) is used. Muscle relaxants may be used to control spasms. Mechanical ventilation may be required if a person's breathing is affected.
Tetanus occurs in all parts of the world but is most frequent in hot and wet climates where the soil contains a lot of organic matter. In 2015 there were about 209,000 infections and about 59,000 deaths globally. This is down from 356,000 deaths in 1990. Description of the disease by Hippocrates exists from at least as far back as the 5th century BC. The cause of the disease was determined in 1884 by Antonio Carle and Giorgio Rattone at the University of Turin, with a vaccine being developed in 1924.
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