加護病房查房日誌(ICU notes)20170828
因為老師開始有日本的朋友,我應該要試著用英文寫一些東西(其實依該寫日文比較好,只是老師不會日文)。
(Due to Nippon friends, I should try to teach by English.)
今天來分享一個新的資訊,大家應該都知道angiotensin receptor blocker或是angiotensin-coenzyme inhibitors對吧?可以用來降血壓。但是今天要講的是angiotensin II,用來治療休克的血管收素劑。
(I will share a new study, you should know about angiotensin receptor blocker or angiotensin-coenzyme inhibitors, which can lower blood pressure. However, I will talk about angiotensin II as vasopressor for shock.)
有個隨機的臨床試驗研究angiotensin II的安全性和效果,作為血管收縮劑用在休克病人身上,大多是敗血性休克
(A randomized trial investigated the safety and efficacy of angiotensin II as a vasopressor agent for patients with vasodilatory (mostly septic) shock)
文獻來源(references): N Engl J Med. 2017;377(5):419. Epub 2017 May 21.
針對使用高劑量norepinephrine的病人,此研究比較加上angiotensin或安慰組。
(For patients receiving high-dose norepinephrine, the trial compared the addition of angiotensin or placebo.)
在並用angiotensin II這組的平均動脈壓比較高。
(The increase in mean arterial pressure (MAP) was greater in the angiotensin II group.)
此外,在angiotensin II這組的norepinephrine用量也比較少,而且在兩組的嚴重副作用並沒有差別。
(As well, less norepinephrine was required in the angiotensin II group and there was no difference in serious adverse events between the groups.)
不過在uptodate中提到,這樣的結果雖然振奮人心,但仍需要更多的研究來決定該藥品的角色。
(These results are encouraging, but further trials are indicated to determine the role of angiotensin II for the treatment of vasodilatory shock.)
ps: 我覺得九州大學找原文全文的功能不只比醫院好,也都比北醫快。
(ps: I think the speed of finding the full test is shorter than my hospital and tmu.)
同時也有10000部Youtube影片,追蹤數超過2,910的網紅コバにゃんチャンネル,也在其Youtube影片中提到,...
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加護病房查房日誌20170220
最近有同學在問sepsis,那我們就來複習一下吧。這個課程會分個幾天上喔。
首先,Sepsis是一種因感染而導致的發炎反應。比較常見的菌種是Gram positive bacteria。可能是某個器官的感染或是菌血症,甚至導致多重器官衰竭和死亡。
2016年the Society of Critical Care Medicine and European Society of Intensive Care Medicine (SCCM/EISCM)有對sepsis and septic shock有新的定義:
1. 敗血症(Sepsis)定義為因感染造成的宿主反應,導致致死性的器官衰竭。現在器官衰竭則由sequential (sepsis-related) organ failure assessment (SOFA) score超過兩分以上定義。原本的The systemic inflammatory response syndrome (SIRS) criteria 已經不再使用。SOFA score的算法可以看此網址: http://clincalc.com/IcuMortality/SOFA.aspx
2. 敗血性休克(Septic shock)定義為有敗血症,且有循環,細胞和代謝性不正常,經過適當的fluid resuscitation後,還需要血管升壓劑才能達到平均動脈壓(a mean arterial pressure (MAP)) ≥65 mmHg和 a lactate >2 mmol/L (>18 mg/dL).而且此情況會比單獨有敗血症的死亡率來的高。
3. 敗血症的危險因子包括: 住在ICU,院內感染,菌血症,老年人,免疫抑制,之前曾經住院,尤其是因為感染住院,社區型肺炎。
4. 懷疑或確定敗血症的病人,通常會有低血壓,心跳變快,發燒和白血球增生的情況。在嚴重一點,可能有休克的徵兆,如皮膚冷汗發酣,器官失能,如: 寡尿,急性腎衰竭,心志受到影響。
5. 死亡率很高,但這幾年因為醫療的進步有下降的趨勢,約10-52 %,越嚴重死亡率越高,若病人燒不起來,嗜中性球低下,年齡大於40歲,有AIDS,肝衰竭等共病症,不適當的抗生素都有可能預後較差。
mean arterial pressure 在 臨床筆記 Facebook 的最讚貼文
Post-resuscitation care: ERC–ESICM guidelines 2015 - EDITORIAL
The ERC-ESICM guidelines on post-resuscitation care are intended to be practical and more didactic, i.e. they tell the clinician exactly what to do. They cover the whole post-cardiac arrest patient pathway and include elements of pre-hospital care, in-hospital treatment and finally rehabilitation.
Animal studies suggest that after return of spontaneous circulation (ROSC), hyperoxia may worsen neurological injury. Clinical data on neurological injury are conflicting but a recent study of air versus supplemental oxygen in ST-elevation myocardial infarction showed deleterious effects of oxygen treatment. As soon as arterial blood oxygen saturation can be monitored reliably, the ERC-ESICM recommendation is to titrate the inspired oxygen concentration to maintain the arterial blood oxygen saturation in the range of 94–98 %. As yet, there are no prospective data defining an optimal plasma carbon dioxide target in the post-cardiac arrest patient, and observational data are inconsistent. Until further data are available the recommendation is to aim for normocarbia.
If cardiac arrest has been caused by an acute coronary occlusion, achieving coronary reperfusion as soon as possible is a high priority. Emergent cardiac catheterisation laboratory evaluation (and immediate percutaneous coronary intervention (PCI) if required) should be performed in adult patients with ROSC after out-of-hospital cardiac arrest (OHCA) of suspected cardiac origin with ST-elevation (STE) on the ECG. This recommendation is relatively non-controversial; the management of those patients with a likely cardiac cause of their cardiac arrest but without STE on the ECG is less well defined. In general, it is reasonable to discuss and consider emergent cardiac catheterisation laboratory evaluation after ROSC in patients with the highest risk of a coronary cause for their cardiac arrest. The ERC-ESICM guidelines include recommendations on the timing of computed tomography (CT) scanning in relation to coronary catheterisation and these are summarised in a post-cardiac arrest algorithm.
The prevention of post-ROSC hyperthermia and the implementation of targeted temperature management (TTM) remains a strong recommendation in the ERC-ESICM guidelines. There is no international consensus on the precise target temperature—the current recommendation is to maintain a constant temperature in the range 32–36 °C for 24 h.
Predicting the final neurological outcome of those who remain comatose after resuscitation from cardiac arrest is problematic and it is now generally accepted that decisions about withdrawal of life-sustaining treatment (WLST) have been made far too early. The ERC and ESICM have already published guidelines on prognostication after cardiac arrest and these have been incorporated into the 2015 post-resuscitation care guidelines. The principles of prognostication are that it is generally delayed until at least 3 days after cardiac arrest and it is multimodal.
Many cardiac arrest survivors have cognitive and emotional problems long after hospital discharge. To date, there have been few structured programmes to rehabilitate these patients and this is a component of the patient pathway that can be improved considerably. The ERC-ESICM guidelines provide recommendations on the follow-up care for post-cardiac arrest patients.
Since 2010, considerable progress in clinical research has created important advances, making these post-resuscitation guidelines immediately applicable in many patients. However, there are still knowledge gaps, which require further investigation. Temperature management is probably the field in which most questions remain unsolved. Should we use a specific cooling technique? What is the best sedation strategy during cooling? Who are the best candidates for a lower target temperature target (32–34 °C)? Should we start cooling during transport to hospital? As early pneumonia is very frequent in cooled patients, should we give prophylactic antibiotics? Ongoing clinical studies might provide definitive conclusions in the very near future. The optimal management of post-resuscitation circulatory failure also remains controversial. Although some clinical data suggest 75 mmHg as a target for mean arterial pressure, this should be further investigated in prospective studies. The use of steroids during the post-resuscitation shock also requires further exploration. Brain injury is the cornerstone of outcome: new imaging and electrophysiological investigations will help to refine the neuroprognostication strategy that has been proposed. Finally, follow-up care for survivors is now recommended but we need high-level evidence for this rehabilitation phase.
While further science is awaited, we sincerely hope that these 2015 guidelines will help intensive care clinicians to treat their post-cardiac arrest patients.
http://bit.ly/1GJLsHZ
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