新冠日记 3.19.2020

继续每天五六个疑似病人。每天无数的邮件，无数的微信。也有很多社区的华人热心捐赠，把自己攒下来的口罩捐助出来给我们医护人员，送到家门口，充分感到了华人的友爱和团结。

昨天的一个病人确诊了，今天收到了感染科人的电话，问我有无防护，说我是低危险人群，让我每天测两次体温，一旦有上呼吸道感染症状就在家休息。

每天睡觉的时候和早上起来没有任何不舒服，下午回家以后就头疼脑涨胸口发闷。明显的是压力太大造成的紧张。每天晚上父母都一定要和我对话，确定我一切安好。

今天加州州长宣布全州“封城令”，并表示未来八周有可能全州2500万人感染。

为对抗快速传播新冠病毒，州长要求将USNS MERCY hospital ship停驻在洛杉矶港口，以帮助该地区的医疗体系免于流行病的影响。

今天给在另一个医院上班的朋友送了几个口罩，她回赠我消毒纸。我们自嘲，这个时代，LV, tiffiny 不再流行，最流行的是厕所纸和消毒液。

新冠 3.16.2020

休息了两个星期，终于还是要回去上班了， 大有风萧萧兮易水寒的悲壮。
已经知道会有一个病人是疑似，结果还有一个病人刚刚收住院，更象是COVID19的症状。
照顾这些病人的护士都是一对一了，我以为的保护隔离服原来就是平常用的黄色薄薄一层的隔离衣。N95 还有，可是头套，鞋套却不要求。
我还是戴上了所有的东西，双层手套，不用自己的听诊器。
今天下来不停的洗手，消毒手机，听诊器，洗手，擦电脑桌。

和同事聊天发牢骚，也和传染科医生讨论隔离的措施，为什么和中国的差别那么大。

这一通下来，深深的感觉到了防护的漏洞，越发觉得感染率的增加是不可避免的。上车脱掉白大褂，放进 塑料带消毒密封。换鞋，消毒密封。

回家换衣服，立刻洗澡。

明天开始决定去医院立刻换上医院的scrubs.

听说旧金山今天封城了。圣地亚哥今天确诊病例55。 中国医生同僚们开始讨论从中国统一买防护服保护自己。

新冠日记3.15.2020

今天放晴了。

又美美的睡了一个懒觉到自然醒。劳工出门采购了，不管如何计划新鲜的蔬菜水果还是不够，打来电话说两家长去的超市，面包冷冻食品都售罄。

看到华人网说道波士顿，想起来和波士顿一为做家庭医生的好友联系一下。她老公是Biogen公司的，现在全公司也都停业。所有学校都停课，也是一片恐慌中。

互相道个珍重之后挂了电话，心有萋萋然的感觉。

微信朋友圈继续调侃，继续恐慌，还有准备囤枪自卫的。

我下周开始上班，需要两周，不知到是不是应该在外面租个房子，防止把病毒带回家。医生圈也有一些朋友有同样的顾虑。

国内的家人开始担心我们了，弟弟发来很多紫外线灯的信息。我们昨天已经在亚麻讯下单。晚上要好好琢磨如何消毒我在医院上班物件的问题。

脸书上刚刚加入了COVID 19的讨论群，全是医护人员。

新冠日记3.12.2020

3。12。2020

一会太阳一会雨

继续宅在家

劳工开始 work from home

早上股市再次熔断，哀号一片。

大家都在脸书上要求停课，PUSD却坚持不停。

华夏中文学校决定这周停课。不知道以后如何。

今天谈到夏天的欧洲行估计要取消了。

刘倩娜已经取消了意大利之行。

新冠日记 3.13.2020

3.13.2020

今天继续阴雨

孩子们上学了，老公从昨天开始work from home。

今天收到了学区通知，从下周一开始休学三周。这个决定是所有圣地亚哥学区共同决定的。
微信群里看到很多照片，都是当地的商店人头攒动，排了长队，Vons 货架也开始空了，看来是老美开始恐慌存货的时候到了。

今天总统讲话，接受drive through test nationalwide.

今天：Trump Declares National Emergency as Virus Outbreak Worsens

加洲，华盛顿洲将在今天开始停止通航

美国今日确诊人数2068，死亡41。圣地亚哥无新的确诊。


今天单位的email:

Information Intensivist on the front line in Seattle

Edited by Roger Schechter, M.D. for format, punctuation and to translate some abbreviations. Also a few comments added.

• 21 pts and 11 deaths since 2/28. 

• Patients who are young (20s), fit, no comorbidities, critically ill-It does happen. 

• USA has been past containment since January

• Currently, all of ICU is for critically ill COVID patients, 

• All of medsurg floors are for stable COVIDs and EOL care, half of PCU, half of ER. 

• New Respiratory symptom patients: Pulmonary Clinic offshoot is open

• CDC is no longer imposing home quarantine on providers who were wearing only droplet isolation PPE when intubating, suctioning, performing bronchoscopy, and in one case doing bloody neurosurgery. 

• Expect when it comes to your system you may initially have staff home-quarantined. Plan for this NOW. 

• Consider wearing airborne isolation PPE for aerosol-generating procedures in ANY patient in whom you suspect COVID, just to prevent the mass quarantines.

• We ran out of N95s (thanks, Costco hoarders) and are bleaching and re-using PAPRs, which is not accordingthe manufacturer's recommendation. 

• Not surprised about N95s as we use mostly CAPRs anyway, but still an issue.

• Terminal cleaning: (inc UV light) for ER COVID rooms are taking forever, Enviro Services is overwhelmed. This is bad since patients are stuck coughing in the waiting room. 

• Reccomend planning now for Enviro up-staffing, or having a plan for sick pts to wait in their cars (that is not legal here, sadly).

• CLINICAL INFO based on our cases and informationfrom CDC conference call today with other COVID providers in US:

o The Chinese data on 80% mildly ill, 14% hospital-ill, 6-8% critically ill are generally on the mark. Data very skewed by late and very limited testing, and the number of our elderly pts going to comfort care.  

o Being young & healthy (zero medical problems) does not rule out becoming vented or dead  

o Probably the time course to developing significant lower respiratory symptoms is about a week or longer (which also fits with timing of sick cases we started seeing here, after we all assumed it was endemic as of late Jan/early Feb). 

• Based on our hospitalized cases (including the not formally diagnosed ones who are obviously COVID) It is quite clinically unique:

o about 1/3 have mild lower respiratory symptoms requiring 1-5L O2 via NC.  

o 1/3 are sicker: Full Mask or NRB. 

o 1/3 tubed with ARDS. 

o Thus far, everyone is seeing: - Normal WBC. Almost always lymphopenia, occasionally poly-predominant but with Normal total WBC. Doesn't change, even 10 days in. 

o BAL lymphocytic despite blood lymphopenic (try not to bronch these pts; this data is from pre-testing time when we had several idiopathic ARDS cases) –

o Fevers, often high, may be intermittent; persistently febrile, often for >10d. It isn't the dexamethasone, it's the SARS2.

o Low Procalcitonin therefore not a useful measure for initial severe infection unless confused if bacterial sepsis or not, that may be useful to check initially and then again later to evaluatetrending if later concern for VAP etc.

o Elevated AST/ALT, sometimes alk phos. Usually in 70-100 range. No fulminant hepatitis. Notably, in our small sample, higher transaminitis at admit (150-200) correlates with clinical deterioration and progression to ARDS. (Editor’s note: This is likely a measure of other organ system effects of cytokine storm. Not only lungs are affected by “immune response overkill”.)

o LFTs typically begin to bump in 2nd week of clinical course. - mild AKI (Cr <2). Uncertain if direct viral effect, but notably SARS2 RNA fragments have been identified in liver, kidneys, heart, and blood. (Editor’s note: again appears to be a function of cytokine storm)

o Characteristic CXR always bilateral patchy or reticular infiltrates, sometimes perihilar despite normal Expiratory Flow and volume down at initial presentation. At time of presentation the radologic findings may be subtle, but always present, even in our patients on chronic high dose steroids. 

o NO effusions. CT is as expected, rarely mild mediastinal lymphadenopathy noted, occasionalsmall effusions late in course, which might be related to volume status/cap leak.

o Note - China is CT'ing everyone, even outpatients, as a primarily diagnostic modality. However, in US/Europe, CT is rare, since findings are nonspecific, would not change management, and the ENTIRE scanner and room have to terminal-cleaned, which is just impossible in a busy hospital. 

o For example 2 of our pts had CTs for idiopathic ARDS in the pre-test era; they looked like the CTs in the journal articles. Not more helpful than CXR. 

o When respiratory failure occurs, it is RAPID (likely 7-10d out from symptom onset, but rapid progression from hospital admit). 

o Common scenario for our pts is, admit 1L NC. Next 12hrs -> NPPV. Next 12-24hrs -> ventilated/rotoproned/Flolan therapy (Epoprostenol sodium). - Interestingly, despite some needing Flolan, the hypoxia is not as refractory as with H1N1. Quite different, and quite unique. Odd enough that you'd notice and say “how strange!”.

o Thus far many are dying of cardiac arrest rather than inability to ventilate/oxygenate. - Given the inevitable rapid progression to ETT once respiratory decompensation begins, we and other hospitals, including Wuhan, are doing early intubation. Facemask is fine, but if the patient needs HFNC or NPPV just tube them electively. They definitely will need a tube anyway, & no point risking the aerosols.

o There does not appear to be MOSF (Multi-Organ System Failure). There's the mild AST/ALT elevation, maybe a small Creatnine bump, but no florid failure. except Cardiomyopathy. 

o Multiple pts here have had normal Ejection Fraction on formal Echo or POCUS at time of admit (or in a couple of cases Ejection Fraction40ish, chronically). Also Normal Troponin from ED. Then they get the horrible respiratory failure, without sepsis or shock. Then they turn the corner, off Flolan, supined, ventilator weaning, looking good, never any pressor requirement. Then over 12 hrs, newly cold, clamped, multiple-pressor shock that looks cardiogenic, EF 10% or less, then either VT->VF-> dead or PEA-> asystole in less than a day. Needless to say this is awful for families who had started to have hope. - We have actually had more asystole than VT, other facilities report more VT/VF, but same time course, a few days or a week after admit, and around the time they're turning the corner. This occurs on med-surg pts too; one today who is elderly and chronically ill but baseline EF preserved, newly hypotensive overnight, EF<10. Already no escalation has since died. So presumably there is a viral CM aspect, which presents later in the course of disease. - of note, no WMAs (wall motion abnormalities) on Echo, RV preserved, Troponins don't elevate. Could be unrelated, but I've never seen anything like it before, especially in a patient who had been Hemodynamically stable without sepsis. (Editor’s note: This is likely NOT a direct viral cardiomyopathy, but instead may reflect the inflammatory response of Cytokine Storm. It would be useful to have post-mortem biopsy results on these patients, including immunofluorescent studies. Presumably this has been performed and should be in the public medical domain) 

• Treatment –

o Remdesivir might work, some hospitals have seen improvement with it quite rapidly, marked improvement in 1-3 days. ARDS trajectory is impressive with it: pts improve much more rapidly than expected in usual ARDS.

o Recommended course is 10d, but due to scarcity all hospitals have stopped it when patientclinically out of the woods - none have continued >5d. It might cause LFT rise, but interestingly seems to rise (200s-ish) for a day or 2 after starting then rapidly back to normal – suggesting it is not a primary toxic hepatitis.

o Unfortunately, the Gilead compassionate use and trial programs require AST/ALT <5x normal, which is pretty much almost no actual COVID pts. Also CrCl>30 is required for the protocol, which is fine. 

o The CDC is working with Gilead to get LFT requirement changed now that we know this is a mild viral hepatitis. (Editor’s Note: This is likely not a mild viral hepatitis, but instead is immune mediated. I doubt the virus is infecting the liver)

o Currently the Gilead trial is wrapping up, NIH trial still enrolling, some new trial soon to begin can't remember where.

o Steroids are up in the air. In China usual clinical practice for all ARDS is high dose methylprednisolone. Thus, ALL of their patientshave had high dose methylprednisolone. Some question whether this practice increases mortality.

o It is likely that it increases secondary VAP/HAP. China has had a high rate of drug resistant Gram Negative Rod HAP/VAP and fungal pneumonia in these patients, with resulting increased mortality. 

o We have seen none, even in the earlier pts who were vented for >10d before being bronchoscoped (prior to test availability, again it is not a great idea to bronchoscope these pts now).

o Unclear whether VAP-prevention strategies are also different in China, but one wouldn't think so.

o Hong Kong is currently running an uncontrolled trial of Hydrocortisone 100 mg IV Q8.

o The general consensus in US among doctors who have cared for COVID pts is that steroids will do more harm than good, unless needed for other indications.

o Many of our pts have COPD on Inhaled Corticosteroid Therapy. Current consensus at Evergreen (Presumably Evergreen Medical Center, Kirkland), after some observation & some clinical judgment, is to stop Inhaled Corticosteroids if able, based on known data with other viral pneumonias and increased susceptibility to HAP. Thus far pts are tolerating that, no major issues ventilating them that can't be managed with vent changes. We also have quite a few on AE-COPD/asthma doses of methylprednisolone, so will be interesting to see how they do.

心肌炎看起来是致死的原因之一，我在amazon 上买了两瓶辅酶Q.万一家人有轻微感染，可以每天一颗保护心肌。