#because he has fluid on his lungs AND covid AND pneumonia | Explore Tumblr Posts and Blogs

thatblondeperson · 2 years

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So here’s the update.

My dad’s health has been in question for a while, but it’s taken a very very sharp turn. I’ve been waiting until the official diagnosis was given, and it has been confirmed to be a terminal lung disease called idiopathic pulmonary fibrosis.

Basically we think this started in 2020 when, pre-Covid, he had this viral infection that either exasperated existing minimal scarring in his lungs that had developed over time, or caused severe scarring in his lungs that has been progressing slowly, up until last year when it just escalated.

When he got the viral infection in 2020, they thought it was pneumonia, but that was a bust, and since it was viral, they said it would just heal on its own. he spent a night in the hospital, and then that was that. He developed a persistent cough after that and it was found that he had a lot of fluid buildup in his lungs. This would also go away in a couple of years, they said. It didn’t.

A couple years later, it starts getting worse. It had been stagnant for a while, but he took a road trip on Route 66 and there must have been something with the higher elevation he reached that once again exacerbated the scarring in his lungs, and accelerated his condition. We’re at a pretty low elevation here, so that makes sense. We started checking in with doctor’s who wanted him to do all these blood tests and it just wasn’t coming up with anything. he took another trip to Wisconsin for a family reunion and when he came back, he was NOT ok.

Pretty rapidly he became almost immobile. He couldn’t walk around the house without needing to rest. They started testing for COPD, they gave him an inhaler that did nothing, he wasn’t sleeping because his coughing had gotten so much worse, and it was awful. They set him up for a breathing exam and he was turned away because it would have been a heavy stress on him just to breathe into a machine for 30 minutes. The guy asked if anyone had looked into his AFib possibly causing issues with his lungs and all the fluid. At this point my mom and I were begging him to go to the ER and he wouldn’t. Finally started asking for a cardiology appt and it was so far out, that my dad agreed to check in, and he was pretty much immediately admitted to the hospital.

The main goal there needed up being monitoring his blood pressure, and getting the fluid out of his lungs. My dad ended up losing 20lbs in his visit and his appetite was already severely low before this. I’m not even gonna touch on the complications he had after a polyp removal because no one needs to know that, but he’d already been losing weight, and he was starting to look pretty scary skinny. But once the fluid had been mostly dried up and his blood pressure appeared stable, the doctor’s were still considering a pacemaker before deciding to let him out. Well. Before he left, his heart stopped for 4.5 seconds, and then we had the pacemaker put in.

He did get to come home right after that surgery, but a few days later he took a nasty fall that had me calling 911. One more night in the ER and we thought after that we were on the right track. I was taking time off to make sure he was OK before a trip I’d already paid for. We had him on Lasix to dry up the fluid in his lungs, and the pacemaker was keeping him from any other heart issues, besides the AFib of course. He was going to be put on oxygen, but they really thought they’d solved it so we had them take the stuff back. But he wasn’t getting better, and even after upping the Lasix dosage, he was still struggling.

He got some CT scans of his lungs done and we saw a pulmonologist who was shocked with how poor my dad’s condition was. His lungs were only working at about 35% capacity and the scarring...holy shit guys it was bad. He immediately had my dad go back on oxygen, but he was already recommending a lung transplant on this first visit. He figured it was IPF, but wanted to be sure. We’ve been doing lots of testing since then, even found very low risk prostate cancer during that time, but today in a 1hr and 40min appt, IPF was confirmed.

What does this mean? My dad is dying.

With IPF, you’re looking at a 3-5yr lifespan on average. There is no reversing it without a lung transplant. He’s already probably had it for 3 years now so...obviously that’s not good. We’re literally discussing assets now. The lung transplant is a possibility, but the soft cutoff is 70yo, and my dad is turning 69 this year. not to mention, lung transplants are a long wait, with the highest rejection rate of any other organ transplant, and the rest of your life the lungs have to be constantly monitored to prevent rejection. That’s a lot to put him through, if we even can put him through it.

Today we were given a LONG list of blood tests he needs to get, about 80 of them, and several other things he needs to book including another colonoscopy and a dental exam???? All to see if he qualifies to even get the lung transplant. But before he can even get the transplant or maybe get on the list, we need to do radiation therapy for that low risk prostate cancer I mentioned. That’s gotta be gone before he can get a transplant. And this is all to say that even if he gets on the list, will he even get lungs??? And if he does, do we want to put him through a month long recovery stay at a hospital an hour away from us? What if complications come up and he dies? Like...if we’ve got little time left, what do we do with it? Do we try to extend it at an incredibly high risk at my dad’s age? Or do we just let him live it out and try to make the best of it? I don’t know.

This has been an intense weight on me. I’m doing my best to keep myself distracted, and lord knows my meds are doing most of the heavy lifting here because I haven’t cried yet. I did take more time off when we first found out that he was terminal and went full escapist and churned out a fanfiction faster than I ever have in my life but HEY, that’s at least a somewhat healthy coping mechanism.

Maybe it’s just not settling in because even with the oxygen, he seems ok right now, and it’s hard to think about the reality that my dad is dying, even though I’m already considering the memorial service we’d have, as well as asking him which car he would like his 3D printed urn to be modeled after. And all with a straight face, and with jokes, because it isn’t happening right now. He’s not dying, he’s fine.

Except he is dying and the clock is ticking down faster than we expected.

Mom’s a wreck. We always knew she’d outlive dad, but just didn’t think it would happen so soon.

I don’t know what to do and yet I’ve been handling this like a pro. I’ve been an amazing help, a godsend my dad says.

But this is all just a lot and I don’t know what to do. At least Elton has been amazing company for my dad, and he’s been so mellow and hasn’t once tried to chew the oxygen tubes, which I was afraid of.

I just kinda wanna let it out, but idk really how. Someone take me to a rage room so I can just break a bunch of shit and scream for a while, please.

#personal #tmi #medical tw #death tw #dying tw #ipf #idiopathic pulmonary fibrosis #long post

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dellb1969 · 2 years

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The height of Covid, a time when I lost my father and eight months to the day my older brother. I didn’t write much about it on this page, just my family page. I chronicled the experience for family members and friends so they would know what the slow journey was like.

In a matter of weeks I would go through the process of finding my way through one the darkest periods of my life. My brothers death affected me profoundly, shook me to the core.

What I discovered in those moments were peace, love, gratitude and compassion.

My brother who brought God to me in my darkest hours of an abusive life is still my hero. He wasn’t a perfect human, but he was there when it counted, when it meant the most.

November 10, 2020

I see you big brother.

This morning I spent over an hour on the phone with the chaplain's office at the hospital making a request for Jr's last rites. My mother wanted him to at the very least be anointed with oil, they performed the entirety.

They asked that I share stories of Jr. so that they could know him better. I told them that he loves his wife, children and grandchildren. That Chelle was his light, she always has been his touchstone. I told them of our dad's passing this past Spring, his namesake and how he missed the funeral due to being where he was placed. I went over that my brother was a good man, but no angel and I wanted them to know why he was where he was and the fact that his addictions placed him there. I told them that he is my mother's favorite and he wanted so much to be home for her, to take care of her.

They asked that I share a story about him that I felt demonstrated his heart, his spirit. I told them that when we were little boys he was a student at Tekakwitha Children's Home during kindergarten and the first grade. Of how sometimes he would come home for weekends and he would come bouncing in the front door carrying his little suitcase. Jr. walked with a bounce. He opened his suitcase to give me and Lawren candy that he could buy with earned allowances at school.

I went on to tell them that when Sunday dinner time would approach brother would begin to get ready to head back to school, my little heart would have a sinking feeling. Because of our lives back then, sometimes he wouldn't have a ride back to school and so he would set out walking. He would walk down the gravel road carrying his suitcase and I'd cry while watching from the porch, all of the while he'd reassure me that it would be ok, 'I'll wave to you.'

Little by little he'd get further away and I would step higher on the porch to watch his bouncing steps grow smaller in the distance. He'd disappear over the hill and I'd stand on the highest rail to wait, watching for him to rise on the other side and when he did, he'd turn and wave.

Jr. has Covid-19 pneumonia, in the images of his lungs they cannot see them, they're fluid filled. This places his mortality rate at 5% chance of survival.

The nurse asked if I had an iPhone, 'I can FaceTime you while I am in there giving him his meds this afternoon', I quickly called Chelle, Mom and Jaimie Lynn to get messages to pass on to him. This broke my heart as I am certain it did theirs.

As soon as he came on the screen I said, 'There you are! That's my big brother. I love you, Jr.' I went on doing my best to smile and deliver the messages given to me. I told him of the love being sent through Facebook of family and friends. 'Can you hear them?'

I told him about talking with the priest and of sharing stories and I retold him the story of the little suitcase and it was then that I broke. I told him that it would be ok to go, Chelle wouldn't want him to suffer. He looked so peaceful laying there, I could see past the wires and hoses, I said, 'I see you big brother, I'm here.'

Fr. Kruger asked me where I thought Jr. was right now and I replied, 'He's on his journey, somewhere he is being comforted, talking to loved ones, talking to God, asking for forgiveness, in a place of redemption.' I told him I don't know how it is that I know this, but I feel it. He replied, 'Do you know what we in the priesthood call that place? The Thin Veil and that's exactly where he is. Do you see the back of your brother's head, he's walking away on his journey and when he's ready he'll turn to wave at you.'

So now, we wait…

#covid 19 #covid diaries #covid deaths #big brother #mourning #siblings

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ursa-mediocre · 3 years

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My dog died today, and it fucking sucks.

She’d had symptoms of a collapsing trachea for a while, mainly a weird cough when she got excited or if pressure was put on her neck. Around March she was due for a dental cleaning where they intubated her and I asked the vet if that’d be an issue but they didn’t seem worried about it so I went ahead with it. Afterwards she had a different sort of cough for a long enough time that I contacted the vet again and they said it was most likely irritation from being intubated that should clear up. I did make her an appointment when I called but it was for a couple weeks out and in between then the cough did get better to the point I considered cancelling it.

A week before her appointment she had what turned out to be an arthritis flair up and I took her to the Emergency Vet and so decided to keep the appointment at her vet. At the appointment the vet was more worried about the cough while I was more worried about the arthritis since the cough was sorta back to pre-intubation frequency. He prescribed a tapering course of prednisone which seemed to help both issues a lot but there wasn’t any discussion of follow up after the course was over. But during and a couple weeks after she was fine so I wasn’t too worried about it.

Then a few weeks ago she started coughing again, and it was sort of up and down. I wanted to wait and see if it’d improve when the weather did, because at this point I was feeling like every time I went to the vet freaked out about something I left feeling silly. Tuesday I finally made her an appointment, but they were booking out a month so it wasn’t until August 17th.

Today my family is having a memorial service for my uncle who died a few months ago, because his family wanted to bury him here but lived on the west coast. After the service the plan was to have people over our house, so we’ve also been preparing for that and have had people over the last two nights (she got lots of affection from my cousin’s kids which was nice).

Last night she was coughing really bad. I could hear her pacing in the hall, going back and forth between my parents’ room and my room. I’ve been giving her honey to try and help sooth her throat, and tried to get her to calm down, but it seemed like she couldn’t lay down without immediately having to stand up and cough.

Around 4 AM I took her to the emergency vet. I thought they’d just have to give her some sedatives or cough suppressants and maybe a prescription for steroids or anti-inflammatories. They put her on supplemental oxygen and said she’d probably have to stay the day to stabilize and then they’d take chest X-rays to see what was up and let me know.

So I got home around 5:30 and tried to sleep, and they called me around 2 hours later to tell me that she was still having trouble breathing, and they weren’t able to take X-rays yet but had done an ultrasound and found fluid in her lungs and asked me for permission to intubate and do CPR if necessary, which I’ve been asked about for other procedures so I consented not thinking they’d actually have to.

Then they called again an hour later and said that they had intubated her, lost her heartbeat, were performing CPR, and asked how quickly I could get there.

My mom drove me and when I got there they had gotten her heartbeat back but she wasn’t aware of anything. They took me to see her, and said that they weren’t sure if the fluid was from congestive heart failure, a blood clot, pneumonia, or irritation from the collapsing trachea, but that she’d probably need to go on a ventilator for any further treatment. We opted to try to get chest X-rays before deciding because she said that heart failure could possibly be treated. But when they went to do that they lost her heartbeat again so I had make the decision to let her go.

It was kind of funny when we got back to the room she was in because this tiny dog was surrounded by like a dozen women (one was standing on a chair?) and they had just gotten her heartbeat back again. But the vet had them unhook her from everything and took us to a room to sit with her. I held her wrapped up in a blanket like a baby. I couldn’t help but think that my own mother there with me had lost an actual baby and how unbearable that seems when my heart’s this broken over a dog.

I don’t know how long she was actually still alive while we sat there. There were a couple tiny coughs and noises when they first handed her to me but I don’t remember feeling her try to breath at all (she had had to be intubated after all, so she probably couldn’t). I told her I was sorry, because I was. I wish I had been a better medical advocate for her with her own vet, because not being able to go into the room with her through covid during appointments made it really difficult to know if they were seeing what I was seeing with her. I wish I had taken her in sooner. I wish I had known at 4:30, when she climbed into my lap as we pulled into the parking lot, that I should have said a proper goodbye then rather than immediately hand her over to the vet tech that came for her. I wish I had spent every moment I could have with her, giving her non stop attention. I told her that I loved her. I told her she was the best dog. The best Lola she could be.

I had to remember to call her previous owner, a girl that’s a few years younger than me. We had had visits every so often after I got Lola, but hadn’t in over a year because of covid. She texted me a few months ago saying that if it were possible she wanted to be with Lola when her time came. Part of the reason I wanted the X-rays was to get even a day or two so we could do proper goodbyes. But I had her talk on the phone with her instead, even though I knew she wasn’t really with us anymore.

I told her my plan was to have her cremated so she could have some of the ashes. We went over that with one of the vet techs, who helped set it up with a facility they partner with. She offered to take a paw print and I had had her make it with her paw that was missing a toe because that was uniquely Lola.

Lola hated people touching her paws. She never would’ve sat still in my lap for so long. She hated getting wet, she wouldn’t go for walks in the rain, and the top of her head was soaked in snot and tears. In her younger days if she caught me crying she’d try to lick up all my snot and get up my nose because she loved the taste of boogers. Her tongue was sticking out the whole time and turning blue before I finally stuck it back in her mouth.

I didn’t want to stop petting her. Her fur was so soft. Her little ears were so perfect and round from her last haircut. I don’t want to pet my dad’s dog because it feels like a betrayal. They walked her to the door with us, but wrapped her back up kind of clumsily so her back legs and tail flopped out and up like how she used to sleep when she was younger and it was hot. I used to grab them and call them her ‘lil chicken legs’.

I don’t want to think about where she is right now. Everyone there was very kind and respectful, I know the practicalities of body storage. I don’t actually want her to be cremated, but I also don’t want to bury her. I just want her to be here, I want to touch her fur and see her dumb foxy face. But I’m not about to fucking taxidermy my dog.

So now it’s about 2:30. My dog has been dead at least 5 hours. I hate it so far.

My dad and older brother were waiting outside when we got home. I put her paw print in the fridge until we can bake it. I went into the living room and saw her bed on the floor and had to go back outside for a minute. I poured out the water bowl I kept in my room for her. My family left for the memorial service, I tried to sleep more. Around 1:30 I got up and ate something for the first time today. There are people coming to the house soon to mourn an actual human.

I have to cancel her vet appointment. I have to cancel her CareClub and flea & tick medicine subscription. I have to clean her dishes, beds, toys, etc and figure out what to do with them. There are still treats in ‘her’ backpack, the one I would take with us hiking so she could ride in it when she got tired.

My family is very supportive, I have savings to cover whatever the final medical expenses will be. Lola was 14 (and 1/2!) and spoiled rotten. I hope she knows I loved her and did my best to take care of her. I hope she knows that’s why I took her to the hospital and wasn’t too scared there.

I’m not good at talking about my feelings. I just end up crying and I don’t like crying so I try to avoid it. I don’t really want or need anything other than for this not to have happened, which isn’t something anyone can provide. I think writing this all out has helped. But this happened today, and it fucking sucks.

#weeb problems #animal death #tw animal death #Lola girl

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amandaoftherosemire · 4 years

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My Unexpected Hiatus

Hey everybody! So I came back to tumblr after a surprise hiatus to find my notifications were insane and I’d missed so much. I have been terribly unreliable my whole life and the year from hell has not helped.

But the reason for my unannounced radio silence is that my husband spent some time in the hospital with pneumonia. It was thankfully not related to COVID but that didn’t mean it wasn’t awful. He was VERY sick with a strep infection and it got scary for a bit. We found that when pneumonia is really bad they call it “complicated pneumonia.” Like it’s a weird relationship on Facebook. Once they put in the chest tube to drain the massive amounts of fluid collapsing his lung, however, he rallied quickly and is doing well. He’s home now but still recovering, has to still go in every day for IV antibiotics, so I’m pretty focused on him.

I don’t yammer on about it because I know it’s boring to other people but you guys have to understand. I am stupid, head over heels, butt-crazy in love with my husband. He is 100% my favorite person in the entire world and I would be destroyed if something happened to him. I have not been okay while he’s been sick.

I wish I could say I’d been productive but I have not written anything in at least a month. I have some rough drafts of the first few chapters of a new Bucky series, so please stay tuned for that. And I have no doubt I will channel all this angst and terror into something since that seems to be my coping mechanism. 😉

For everyone who sticks with me through my seemingly inevitable flakery, thank you, I love you, I’m sorry. For my new followers, thank you! Please stick around, I will be back and more active when I can and there will be more stories, I promise. For everyone who has read, liked, reblogged and/or commented on anything I’ve written, THANK YOU! I haven’t had time to respond yet, but I read every single comment and loved every notification. You’re all amazing and make me feel so appreciated.

In the meantime, I can and will be responding to asks or messages, but I cannot promise more than that. I’ll be back and annoying as usual very soon.

#manda rambles #personal #update

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mcatmemoranda · 4 years

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Stuff I learned today in my pulmonology rotation:

The arrows in this CT scan show air bronchograms, which are areas where you can see the bronchioles clearly (black lines, which are the bronchioles that have air in them) because there is hyperdensity (white areas) around them. These are abnormal and indicate pneumonia or pulmonary edema. We have a pt today who had a spontaneous pneumothorax, which was treated with a pigtail and then a chest tube. He also has pneumonia.

From Wikipedia:

An air bronchogram is defined as a pattern of air-filled bronchi on a background of airless lung.

In pulmonary consolidations and infiltrates, air bronchograms are most commonly caused by pneumonia or pulmonary edema (especially with alveolar edema).

Other potential causes of consolidations or infiltrates with air bronchograms are:

Pulmonary edema Non-obstructive atelectasis Severe interstitial lung disease Pulmonary infarct Pulmonary hemorrhage Normal expiration

Ground glass opacities on CT are less dense than the hyperdensities you see in pneumonia; may be due to atypical bacteria.

From Wikipedia:

In radiology, ground glass opacity (GGO) is a nonspecific finding on radiographs and computed tomography (CT) scans. It consists of a hazy opacity that does not obscure the underlying bronchial structures or pulmonary vessels, and that indicates a partial filling of air spaces in the lungs by exudate or transudate, as well as interstitial thickening or partial collapse of lung alveoli.

The differential diagnosis of the many causes of GGO includes pulmonary edema, infections (including severe acute respiratory syndrome coronavirus 2 (COVID-19),[2] cytomegalovirus and Pneumocystis jirovecii pneumonia), various noninfectious interstitial lung diseases (such as hypersensitivity pneumonitis, Hamman-Rich syndrome), diffuse alveolar hemorrhage, cryptogenic organizing pneumonia, and pulmonary contusion.

Cryptogenic organizing pneumonia (COP), formerly known as bronchiolitis obliterans organizing pneumonia (BOOP), is an inflammation of the bronchioles (bronchiolitis) and surrounding tissue in the lungs. It is a form of idiopathic interstitial pneumonia.

It is often a complication of an existing chronic inflammatory disease such as rheumatoid arthritis, dermatomyositis, or it can be a side effect of certain medications such as amiodarone. COP was first described by Gary Epler in 1985.

The clinical features and radiological imaging resemble infectious pneumonia. However, diagnosis is suspected after there is no response to multiple antibiotics, and blood and sputum cultures are negative for organisms.

Hamman-Rich Syndrome = acute interstitial pneumonitis. Acute interstitial pneumonitis is a rare, severe lung disease that usually affects otherwise healthy individuals. There is no known cause or cure.

Acute interstitial pneumonitis is often categorized as both an interstitial lung disease and a form of acute respiratory distress syndrome (ARDS) but it is distinguished from the chronic forms of interstitial pneumonia such as idiopathic pulmonary fibrosis.

The most common symptoms of acute interstitial pneumonitis are highly productive cough with expectoration of thick mucus, fever, and difficulties breathing. These often occur over a period of one to two weeks before medical attention is sought. The presence of fluid means the person experiences a feeling similar to 'drowning'. Difficulties breathing can quickly progress to an inability to breathe without support (respiratory failure).

Acute interstitial pneumonitis typically progresses rapidly, with hospitalization and mechanical ventilation often required only days to weeks after initial symptoms of cough, fever, and difficulties breathing develop.

Rapid progression from initial symptoms to respiratory failure is a key feature. An x-ray that shows ARDS is necessary for diagnosis (fluid in the small air sacs (alveoli) in both lungs). In addition, a biopsy of the lung that shows organizing diffuse alveolar damage is required for diagnosis. Other diagnostic tests are useful in excluding other similar conditions, but history, x-ray, and biopsy are essential. These other tests may include basic blood work, blood cultures, and bronchoalveolar lavage.

The clinical picture is similar to ARDS, but AIP differs from ARDS in that the cause for AIP is not known.

The chest tube is connected to a Pleur-evac. The first chamber will bubble if suction is on; it actively sucks air out of the pleural space. It tells you in centimeters of water how much suction is being applied. The pt I saw today had a little over 20 cm of H2O of suction. Normally, the visceral and parietal pleura have a small amount of fluid between them. In PTX, that space has air in it. The chest tube and Pleur-evac get air out of that space. The second chamber of the Pleur-evac will bubble as long as air is still in the pleural space. That's what happened with the pt from today. So he will need to keep the chest tube in until his PTX is better and no more air is coming into the pleural space.

I asked the attending to explain the pathophysiology of clubbing. I recall learning that it can be associated with heartor lung disease, but I don't know why it happens. She said that in chronic respiratory failure, hypoxia triggers fibroblasts that cause nail clubbing, but nobody really knows why. The second image shows clubbing. From Wikipedia:

Nail clubbing, also known as digital clubbing or clubbing, is a deformity of the finger or toe nails associated with a number of diseases, mostly of the heart and lungs. When it occurs together with joint effusions, joint pains, and abnormal skin and bone growth it is known as hypertrophic osteoarthropathy.

Clubbing is associated with lung cancer, lung infections, interstitial lung disease, cystic fibrosis, or cardiovascular disease. Clubbing may also run in families, and occur unassociated with other medical problems.

Clubbing is associated with Lung disease:

Lung cancer, mainly non-small-cell (54% of all cases), not seen frequently in small-cell lung cancer ( Heart disease:

Any disease featuring chronic hypoxia Congenital cyanotic heart disease (most common cardiac cause) Subacute bacterial endocarditis Atrial myxoma (benign tumor) Tetralogy of Fallot

It can apparently also occur in GI disease.

Gastrointestinal and hepatobiliary:

Malabsorption Crohn's disease and ulcerative colitis Cirrhosis, especially in primary biliary cirrhosis Hepatopulmonary syndrome, a complication of cirrhosis

Others:

Graves' disease (autoimmune hyperthyroidism) – in this case it is known as thyroid acropachy Familial and hereditary clubbing and "pseudoclubbing" (people of African descent often have what appears to be clubbing) Vascular anomalies of the affected arm such as an axillary artery aneurysm (in unilateral clubbing)

Nail clubbing is not specific to chronic obstructive pulmonary disease (COPD). Therefore, in patients with COPD and significant degrees of clubbing, a search for signs of bronchogenic carcinoma (or other causes of clubbing) might still be indicated.

A congenital form has also been recognized.

The exact cause for sporadic clubbing is unknown. Theories as to its cause include:

Vasodilation (i.e., distended blood vessels). Secretion of growth factors (e.g., platelet-derived growth factor and hepatocyte growth factor) from the lungs. Overproduction of prostaglandin E2 by other tissues. Increased entry of megakaryocytes into the systemic circulation. Under normal circumstances in healthy individuals, megakaryocytes that arise from the bone marrow are trapped in the pulmonary capillary bed and broken down before they enter the systemic circulation. It is thought that in disorders where there is right-to-left shunting or lung malignancy, the megakaryocytes can bypass the breakdown within the pulmonary circulation and enter the systemic circulation. They are then trapped within the capillary beds within the extremities, such as the digits, and release platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF). PDGF and VEGF have growth promoting properties and cause connective tissue hypertrophy and capillary permeability. This seems to be the theory the attending was explaining.

#air bronchograms #air bronchogram #bronchogram #CT #imaging #ground glass #ground glass opacity #pulmonology #chest tube #clubbing

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itsmunkychoi · 4 years

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Update on Noa

Day 3

So heres the deal with Noa. His whole life he’s had large tonsils and the doctors say hes probably always have been sickly because his immune system has been weak since hes had issues with his tonsils. He never had any swelling untill now and we are being advised to remove them in a few weeks once his health improves. So this is what is wrong with Noa. He has pneumonia scattered on both lungs (this is the second time this happened to him), he has strep throat again apparently (for like the second or third time now), he also has a lot of mucus and phlegm covering his air ways which is not helping him breath too well. His neck is swollen on both sides because his lymph nodes are swollen, his tonsils are swollen too which is why his whole neck and face is swollen as well. He was diagnosed with sleep apnea as well. They said his sleep apnea will be better once the tonsils come out. He cannot lie down on his back or he will suffocate so he needs to sleep in his sides. Hes been having fevers of 103 and is on iv fluids and a few different types of antibiotics to help fight all of these infections. He also got a shot to help with the strep because amoxicillin does nothing for him. Deinking and eating is difficult for him. Today is the first time that he actually picked at some of his food in over 3 days. So that is good. His swelling gets worse everyday so ENT keeps checking him to make sure that his tonsils havent smelled up anymore. Right now the tonsils are so enlarged that they’re almost touching which is why hes having a hard time breathing. Noa is also diagnosed with multi inflammatory syndrome.

#noa #sick #champ

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doctorletmebebrave · 4 years

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My grandpa has Covid-19.

I don't even really know how I feel about it. Not sad, just maybe...hollow? I hate to sound so extremely morbid and pessimistic but I'm just mentally preparing for his death. I knew back in March that if any of my grandparents got the virus that they'd probably die and I feel like I've been bearing that mental weight since then. He's like 94, so that automatically puts him at a very high risk.

That means that my (step)grandma has been exposed too. She's 104. That woman has lived through the Spanish Flu. She's not sick so far thankfully, but it doesn't matter because if my grandpa dies then she'll die too. They're incredibly dependent on each other, and she cries when he's gone for even an hour. If one of them goes, the other will follow.

My uncle is the one who took him to the hospital, so he's also exposed. He doesn't live in Wisconsin where my grandpa does (none of our family is there) so he's quarantined to a hotel room for two weeks. I hope he's okay too. He's not dumb though and I know he was super careful about masks and stuff. Even though it is terrible that my uncle has been exposed, I'm grateful that my grandpa didn't have to spend hours at the hospital alone while they were checking him out.

I probably shouldn't be so dismal. My grandpa is not super sick so far, they released him from the hospital and he only has a low fever. He is congested and they did find fluid in his lungs, but it was edema and not pneumonia. I shouldn't bury someone before their time, since elderly people can recover and while he isn't in great shape he could also be doing much much worse for his age. But I can't shake that feeling that it's finally the end of the line, because this virus lingers and gets worse and then better and then worse again and messes your whole body up along the way.

It breaks my heart a little that all of this is happening across the country for me, hundreds of miles of space between us. I wouldn't have been allowed in to see him anyway though, even if I could be there. But I think, will August 2019 be the last time I ever got to see them in person?

#long post i guess im just feeling sad and rambly #theyre so so so old so it's not like it's a surprise that they could die #i have honestly been wondering for years now if each visit would be the last #i have spent many happy days with them so it will be ok.#fingers crossed and prayers that he recovers though. but even if he doesn't #he lived a full and happy life to a very old age #and he is proud of me #and he is proud that i am following in his footsteps careerwise #personal #long post #covid 19

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warmtwinkie · 4 years

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When the coronavirus enters the human body, it uses microscopic spikes to attach itself to mucous cell membranes in the back of a person’s throat. Through those spikes, the virus’ genetic material enters the human cells, repurposing those cells in order to make more of the virus. The viral cells then make their way down the bronchial tubes, inflaming the mucous membranes in the lungs. With oxygen impaired, the lungs become a breeding ground for pneumonia, causing the lungs to fill with “fluid, pus and dead cells.”

If the lungs fill with enough fluid that not even a respirator will help, the patient will often die.

Those patients have it easy, however, according to a prominent resident of the White House. Throughout the national battle with COVID-19, President Donald Trump has maintained that he, not those being infected with the often-deadly virus, is the true victim of the pandemic.

In briefing after briefing, Trump has lashed out at the news media who have dared to question his uneven handling of the crisis. On Twitter Wednesday, the president accused the “LameStream Media” of being “the dominant force in trying to get me to keep our Country closed as long as possible in the hope that it will be detrimental to my election success.”

Last week, when NBC News’ Peter Alexander asked the president what he would say to American citizens who were feeling scared, Trump answered with “I say that you’re a terrible reporter. That’s what I say.”

On Sunday, Trump couldn’t even let go of his victimhood complex for a brief second when told which U.S. senators were concerned they had contracted the virus. When a reporter informed the president that Utah Sen. Mitt Romney had quarantined himself, a sardonic Trump cracked, “Romney’s in isolation? Gee, that’s too bad.” Romney, of course, was the single Republican senator who voted to convict Trump in the impeachment trial that ended, incredibly, less than two months ago.

Trump’s hour-and-a-half briefing on Sunday delved into bizarre, Fellini-esque territory when he went on a tangent about the personal toll it had taken on him to run for president. “It cost me billions of dollars to be president of the United States,” Trump said, after calling PBS reporter Yamiche Alcindor’s question about whether he has sold any stocks amid the outbreak a “nasty question.”

“I think it’s very tough for rich people to run for office,” the president told citizens anxious about losing their livelihoods in the face of a deadly pandemic.

Of course, Trump’s initial response to the crisis laid the blueprint for his future obfuscation and blundering of the facts. After claiming in late January that “we have it totally under control,” and that the virus was “one person coming in from China,” Trump quickly pivoted to accusing Democrats and the media of using COVID-19 as a “new hoax” to bring him down.

“They tried the impeachment hoax,” Trump told a rally in South Carolina on February 28. “That was on a perfect conversation. They tried anything. They tried it over and over. They’d been doing it since you got in. It’s all turning. They lost. It’s all turning. Think of it. Think of it. And this is their new hoax.”

When Washington Governor Jay Inslee was critical of Trump’s initial handling of the pandemic, Trump referred to Inslee as “a snake.”

“Let me just tell you, we have a lot of problems with the governor and the governor of Washington,” Trump said of Inslee, who, at the beginning of the outbreak was seeing his residents die at a faster rate than anywhere in the country. “That’s where you have many of your problems, OK?” Trump said, ignoring the fact that Washington residents were, in fact, constituents of his, as well.

At the same March 7 press conference, Trump suggested he has a natural affinity for science because he had an uncle who once taught at MIT and helped pioneer the use of radiation to treat cancer.

“Every one of these doctors said, ‘How do you know so much about this?’” Trump told the reporters gathered. “Maybe I have a natural ability. Maybe I should have done that instead of running for president.”

Clearly, when Trump sees any issue, he only sees himself and thinks only of how it affects his legacy. It is why, as he has begun to hold more frequent briefings, members of his Coronavirus Task Force must always shower him with ego-salvaging praise. Despite the fact that in each new press briefing the president seems more petulant than the last, Dr. Fauci and Dr. Birx continue to show grace and appease his constant neediness.

This is the president of the United States speaking in the White House briefing room during a pandemic and shortage of medical supplies, right after the 500th American died from the virus.

At the same time Trump is asking citizens to trust their government to respond to the coronavirus outbreak, he is trying to convince Americans that the government is untrustworthy. At the same time Trump needs to use the media to dispense accurate information about what his administration is doing to keep people safe, he is urging the public to not trust the media.

And while he continues to believe he is the victim of this pandemic, it is becoming increasingly clear that he is, himself, a virus.

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nfl2sevensummits · 4 years

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Andrew Hughes has been chasing mountains around the world in his attempt to climb the Seven Summits. Despite being pushed back on a few of his climbs, he continues to show his resiliency by coming back, not giving up and staying the course

169: Andrew Hughes: Mountain Climber, Explorer, Writer, and Speaker talks about overcoming the loss of his marriage and a complete career shift away from law towards focusing on his passion for the outdoors.

Andrew Hughes

What was the whole idea behind the 5683 steps personal training challenge that Andrew Hughes did after the pandemic? “Like you, we were both supposed to be in Nepal this last season climbing, and when that all of a sudden changed because the world changed around us, it became, I think, important to find a way to still kind of pursue some kind of training, and a lot of training is limited based upon the state. I’m a homeowner in Washington, and the ability to stay within my little neighborhood, I explored every little park I could do by walking around with a weighted pack on. At a certain point in time I realised I needed something more to train to.”

On this episode of Finding Your Summit Podcast, we talk with Andrew Hughes, Mountain Climber, Explorer, Writer, and Speaker. Like Mark Pattison, Andrew Hughes was also all set to travel to Mount Everest until the COVID-19 pandemic disrupted the world. Andrew talks about the adversity that he overcame. “I studied, going to law school and getting multiple degrees from good institutions in London and Seattle. I practiced law. I ran for Congress. I got married. I thought I had, kind of the perfect ensemble of things you are supposed to have to be content and to be satisfied, it just wasn’t there. There was something missing, and when those things started crumbling even further around me, I realised I had built a foundation of my happiness on the wrong things.”

What You Will Learn:

What was the life-changing situation that pushed Andrew out of his old life and towards his new one? “Towards the tail end of my marriage falling apart and all my political things kind of falling apart as well, I climbed a mountain, and there was something about living in that discomfort and that growth that came from it that just drew me back to wanting to do more and more of it. It was this movement through meditation, this healing. It was almost this sermon, you want to be told over and over again, and the more you went back to it, the more you learned. When things actually fell apart I made a choice to restructure my life, find ways to create enough income where I could do the things that were meaningful to me, but maybe didn’t reconcile externally with what people saw as success.”

How do the mountains factor into Andrew Hughes’ life? “We always look at maybe a marriage, or a promotion, or a career, or a job as the peak of where we want to go to, and we forget that the mountain is involving much more than that. So, you flatten the mountain, and then you just see actually how far the journey is, and it always goes beyond the summit. There is always going to be future summits we have to reach for, and so, maintaining enough energy and perspective of where we really want to get to, and not just the summit is most important.”

When did climbing become the missing link that reconnected Andrew Hughes with his goals and desires for fulfillment? “I ran for U.S. Congress in 2012, and climbed, and lost. I came third out of seven in my field, and about a year later my marriage started falling apart at the time, and I climbed Rainier in 2014 and I was so excited about it. I came back down and signed up for a six-day course at the north Cascades with Alpine Ascends, and I got back from that, and my ex-wife at the time was moving out of the house. So, it was a very clear delineation between my path towards the outdoors and my path in that relationship.”

What talks about happened when he got high-altitude pulmonary edema. “High-Altitude Pulmonary Edema is one of the two things you really don’t want to get. Altitude Cerebral Edema and pulmonary edema. Essentially, pulmonary edema is your lungs begin to fill with fluid and you begin to drown to death on the mountain. Your oxigen can’t go through and reach the rest of your body as your lungs fill up. I was helicoptered off. I was staying by myself at the base of the mountain. I kind of had to reassess over the next few weeks whether this was something I was even able to do.”

What are some of the exciting elevated heights that mountain climbing has taken Andrew Hughes to? “I just got back from Antartica where I did three different expeditions tied together. I did several in January. I’ve been able to climb six of the seven highest volcanoes in the world and the highest mountains, to hopefully finishing that off in the next year.”

Antarctica Trifecta

Andrew Hughes talks about climbing astonishing summits in Antarctica. “We flew in. We were a little bit delayed. It was after the Chilean Airforce aircraft had crashed. So they actually grounded all flights in. We were first trying to get in and then we eventually got in and we hit the ground running once we did. We flew out. Luckily, we were one of the only places to get out to the 89th degree with all of our skis and sleds and small expedition team. They dropped us off at the 89th degree and there is absolutely nothing around you, and you’ve got your compass and your sled and your teammates, and you just start heading towards what you hope is the South Pole, and we got there within about six days.”

The Everest and Lhotse

During this episode of Finding Your Summit Podcast, Andrew Hughes also expresses his initial plans to take on climbing both Everest and Lhotse before COVID-19 put those plans on pause. “I was actually on Everest last year with Adventure Consultants and was on our summit push coming out of Camp 2, and had this horrific cough all of a sudden come up that turned out to be pneumonia. So I was evacked off. I was in my tent actually the night my team was summiting and I could hear them on the walkie-talkies stuck in Camp 2. I walked away from it and realised that I definitely wanted to come back.”

Links to Additional Resources:

Mark Pattison: markpattisonnfl.com

Emilia’s Everest - The Lhotse Challenge: https://www.markpattisonnfl.com/philanthropy/

Andrew Hughes website: AndrewIHughes.com

Andrew Hughes Instagram: Instagram

Check out this episode!

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xtruss · 4 years

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Covid-19 Patients Sharing Ventilators Is Possible—But Not Ideal

The science of coventilation for coronavirus cases illustrates a complicated dilemma.

— By Alissa Greenberg | Tuesday May 12, 2020 | NOVA

Less-invasive ventilators use a mask rather than a tube inserted into the patient's throat.

On March 20, as severe cases of COVID-19 spiked in northern Italy, emergency medicine doctor Marco Garrone paused during a chaotic shift to tweet a photo: two patients, next to each other in hospital beds, with arcs of tubing connecting them to the same ventilator. “This is what we are down to,” he wrote. “Splitting ventilators, and facing serious dilemmas like choosing who will be actually ventilated when everybody should Take This Seriously”

A month later, as caseloads skyrocketed across the pond in New York City, Columbia Presbyterian Hospital hurried to draft protocols for ventilator sharing. And around the same time, an emergency medicine doctor in Michigan named Charlene Babcock posted a YouTube tutorial featuring step-by-step directions on how to modify a ventilator so it can accommodate multiple patients. That video racked up nearly a million views in the ensuing weeks.

“Here’s my disclaimer,” Babcock says to the camera. “This is off-label use of the ventilator.” But, she adds, extreme circumstances may call for measures that otherwise would be deemed too risky. “If it was me, and I had four patients—and they all needed intubation, and I only had one ventilator—I would simply have a shared discussion with all four families and say: ‘I can pick one to live, or we can try to have all four live.’”

The appearance of ventilator sharing (or “coventilating”) this spring in places where the novel coronavirus has hit the most severely prompts a number of questions: How does a ventilator work? Why is it possible for more than one patient to use a ventilator at once? And if it’s possible, why aren’t more doctors in hard-hit areas doing it? Good news: This is the first in a NOVA series answering burning coronavirus questions just like these.

How Do Ventilators Work?

Treating a patient in extreme respiratory distress is “like staring out the window and seeing people free fall,” says Albert Kwon, an anesthesiologist at New York Medical College. Doctors don’t know how long their patients have been “falling” or how long they’ll continue to fall without intervention; they must make an on-the-spot assessment about whether a parachute is necessary.

In that case, they can choose from several options, ranging from less to more invasive. All ventilators provide oxygen and promote its absorption in the bloodstream while also helping rid the body of the resulting carbon dioxide. The ones you’ve probably heard the most about during the COVID-19 pandemic provide a stream of air into the lungs via a tube inserted into a patient’s throat.

This stream of air exerts positive pressure, which is the opposite of how breathing usually works. When we breathe in on our own, our diaphragm muscles move down in our chests, increasing available space and creating an area of negative pressure that causes air to rush in. (There is one ventilator that works on negative pressure, which you’ve probably heard of: the iron lung.)

High-magnification images show the surface of alveoli in healthy mouse lungs (left) and lungs with ventilator-induced damage (right). Image Credit: Kate Hamlington Smith, University of Colorado School of Medicine

One reason COVID-19 patients need to use ventilators is because their lungs become so stiff that the diaphragm isn’t strong enough to complete its normal movement, causing breathing to slow or stop. Ventilation also keeps the lungs inflated while they heal. That’s important because inflamed capillaries in sick lungs can leak a protein-rich fluid, increasing surface tension in the liquid that normally coats the lungs and making them vulnerable to collapse.

But even healthy lungs are at risk during this process, because their tissues are not usually subject to positive pressure. That means that getting pressure levels wrong during ventilation can be dangerous. Too low, and a patient doesn’t get enough oxygen. Too high, and the lungs can become overinflated, causing their tissue to tear.

At first glance, the ventilator used in the most severe COVID-19 cases looks fairly simple: a tube that goes down the patient’s throat, two hoses that connect the tube to the machine itself (one for pushing air into the lungs and one for bringing carbon dioxide back out of the body); seals, valves, and filters to keep gases moving in the right direction; and a central case. But inside that case lives a much more complicated device, replete with pressure, flow, and oxygen sensors, and sets of circuitry and alarms associated with each element. A standard hospital ventilator has 1,500 parts, features several layers of fail-safes, and can cost around $30,000.

“The number of safeties that have to be on a medical device like this is amazing,” says Nevan Hanumara, a research scientist in MIT’s Precision Engineering Research Group. “This is second only to aerospace.”

A medical ventilator.

Why Isn’t Ventilator Sharing More Common?

Ventilators have such complicated inner workings in part because ventilation is much more involved than just turning on a hose. The process requires doctors to consider myriad disease factors and patient measurements, making it almost an art rather than a science. "Tidal volume," for example, refers to the amount of air in each breath, "resistance" to the ease with which air moves through the lungs, and "compliance" to how stiff or flexible the lung tissue itself is. Clinicians can also adjust how fast patients breathe and regulate air pressure at each stage of those breaths.

All this means that while setting up coventilation is relatively simple—in her YouTube video, Babcock simply uses a cheap plastic adaptor to make space for more hoses—that doesn’t necessarily mean it’s safe. The first problem, Hanumara points out, is that coventilating requires using the same pressure with two very different sets of lungs. The healthier lungs receive more air because they inflate more easily, while the sicker, less flexible lungs won’t get as much.

Secondly, he adds, sensors calibrated for one person’s measurements may not work for two, meaning the appropriate alarms might not be triggered if there is an emergency. Some COVID-19 patients, for example, experience sudden, catastrophic changes in their lung health; without alarms, it’s much more difficult to catch these changes in time. And finally there’s the matter of cross-contamination. Although two coronavirus patients sharing a ventilator can’t give each other their infections, they might still swap pneumonia microbes, or even tuberculosis.

Given these risks, research on coventilation has divided the respiratory care community. Among the more recent studies, Assistant Director of Research at SUNY Downstate Department of Emergency Medicine Lorenzo Paladino successfully coventilated four sheep for 12 hours in 2008. (Garrone, the Italian doctor, looked to that study when setting up his coventilated patients in March.) Paladino and his coauthors chose sheep for their study because adults have similar respiratory physiology and weight as humans, and aimed for 12 hours because emergency protocols allow for delivery of equipment from the Strategic National Stockpile anywhere in the continental US within that time.

The study was prompted by the 2001 anthrax attacks and 2003 SARS outbreak, Paladino says, and was meant to provide a stopgap “bridge” measure for emergency physicians with inadequate supplies waiting for backup in a disaster situation—not to replace single ventilation in the long term. Before COVID-19, the technique was most famously used after the 2017 Las Vegas concert shooting, when a single ER saw a huge surge of gunshot patients and coventilated them to keep them alive while they waited for surgery.

Paladino compares the technique to a life vest. “We don’t condone crossing the Atlantic in a life vest,” he says. “But if I’m in the middle of the Atlantic, I would rather have a life vest than not. And I would hope that a boat is coming to pick me up soon.”

The Future of Coventilation

Not every patient is a good candidate for coventilating, Paladino stresses. Patients with active asthma should be excluded, as should those who tend to “fight” the ventilator, trying to draw a breath when the machine is expelling air, or vice versa. But even with these caveats in place, in the wake of the COVID-19 pandemic, six major organizations—including heavyweights like the Society of Critical Care Medicine and the American Society of Anesthesiologists—have made statements against coventilating, judging it too risky and ethically questionable to be worth considering. “There’s a very legitimate concern that instead of saving two people, you just highly increased the risk of mortality for two people,” says Bradford Smith, a biomedical engineer at the University of Colorado Anschutz Medical Campus.

These serious risks point to the urgency of the recent situations in Italy and New York that have led doctors to try coventilation. Smith, who recently published a “preprint” (a not-yet-peer-reviewed preliminary study) suggesting an algorithm to match patients for safer coventilation, runs down the list of options he would try before resorting to the technique: fixing old, broken ventilators; using available machines normally used for surgical anesthesia; attaching endotracheal tubes to similar but less-invasive machines used for sleep apnea. “This is so rife with problems that the first time I heard about it, I thought, 'This is the stupidest thing I’ve ever heard,’” Smith says. “But people are taking steps to mitigate all those issues.”

Coventilating practitioners can use filters between patients to help prevent cross-contamination, for example. And protocols drawn up by Columbia Presbyterian and the Department of Health and Human Services (HHS) this spring suggest workarounds to allow for some adjustment of ventilator settings, better monitoring of both patients, and use of some built-in alarms.

As in Paladino’s case, most research on coventilation stems from a drive to prepare for the worst. Smith says he was initially inspired to work on his algorithms because he was afraid he would have to use them. (“With the news coming out of Italy, I was on these chain emails of critical care physicians, and things sounded pretty dire,” he says.) And the fact that HHS thought it necessary to convene a taskforce in Washington D.C.—which included Paladino and Babcock—to produce coventilation guidelines for future use speaks to the severity of both the pandemic and predictions for global health over the next two years.

Smith hasn’t had to use his algorithms, but he fears fall flu season may provide another opportunity. He also wonders if they may be of use in other places around the world where ventilator supplies are meager, to give physicians and respiratory therapists valuable context about how different types of patients may react to coventilation.

“This is not how nations, or even states, deal with a ventilator problem,” Paladino says. Instead, he sees coventilation playing an important role for communities that are rural or isolated, or lack access to medical care. Imagine a small hospital that owns just three ventilators and then receives six desperately sick COVID-19 patients in one night. Then what? “One night you see a spike, and you ask for help from the neighbors,” he says. In the meantime, coventilating just might keep those patients alive.

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yourreddancer · 4 years

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The Infection That’s Silently Killing Coronavirus Patients

Opinion

The Infection That’s Silently Killing Coronavirus Patients

This is what I learned during 10 days of treating Covid pneumonia at Bellevue Hospital.

By Richard Levitan

Dr. Levitan is an emergency doctor.

· April 20, 2020

I have been practicing emergency medicine for 30 years. In 1994 I invented an imaging system for teaching intubation, the procedure of inserting breathing tubes. This led me to perform research into this procedure, and subsequently teach airway procedure courses to physicians worldwide for the last two decades.

So at the end of March, as a crush of Covid-19 patients began overwhelming hospitals in New York City, I volunteered to spend 10 days at Bellevue, helping at the hospital where I trained. Over those days, I realized that we are not detecting the deadly pneumonia the virus causes early enough and that we could be doing more to keep patients off ventilators — and alive.

On the long drive to New York from my home in New Hampshire, I called my friend Nick Caputo, an emergency physician in the Bronx, who was already in the thick of it. I wanted to know what I was facing, how to stay safe and about his insights into airway management with this disease. “Rich,” he said, “it’s like nothing I’ve ever seen before.”

He was right. Pneumonia caused by the coronavirus has had a stunning impact on the city’s hospital system. Normally an E.R. has a mix of patients with conditions ranging from the serious, such as heart attacks, strokes and traumatic injuries, to the nonlife-threatening, such as minor lacerations, intoxication, orthopedic injuries and migraine headaches.

During my recent time at Bellevue, though, almost all the E.R. patients had Covid pneumonia. Within the first hour of my first shift I inserted breathing tubes into two patients.

Even patients without respiratory complaints had Covid pneumonia. The patient stabbed in the shoulder, whom we X-rayed because we worried he had a collapsed lung, actually had Covid pneumonia. In patients on whom we did CT scans because they were injured in falls, we coincidentally found Covid pneumonia. Elderly patients who had passed out for unknown reasons and a number of diabetic patients were found to have it.

And here is what really surprised us: These patients did not report any sensation of breathing problems, even though their chest X-rays showed diffuse pneumonia and their oxygen was below normal. How could this be?

We are just beginning to recognize that Covid pneumonia initially causes a form of oxygen deprivation we call “silent hypoxia” — “silent” because of its insidious, hard-to-detect nature.

Pneumonia is an infection of the lungs in which the air sacs fill with fluid or pus. Normally, patients develop chest discomfort, pain with breathing and other breathing problems. But when Covid pneumonia first strikes, patients don’t feel short of breath, even as their oxygen levels fall. And by the time they do, they have alarmingly low oxygen levels and moderate-to-severe pneumonia (as seen on chest X-rays). Normal oxygen saturation for most persons at sea level is 94 percent to 100 percent; Covid pneumonia patients I saw had oxygen saturations as low as 50 percent.

To my amazement, most patients I saw said they had been sick for a week or so with fever, cough, upset stomach and fatigue, but they only became short of breath the day they came to the hospital. Their pneumonia had clearly been going on for days, but by the time they felt they had to go to the hospital, they were often already in critical condition.

In emergency departments we insert breathing tubes in critically ill patients for a variety of reasons. In my 30 years of practice, however, most patients requiring emergency intubation are in shock, have altered mental status or are grunting to breathe. Patients requiring intubation because of acute hypoxia are often unconscious or using every muscle they can to take a breath. They are in extreme duress. Covid pneumonia cases are very different.

A vast majority of Covid pneumonia patients I met had remarkably low oxygen saturations at triage — seemingly incompatible with life — but they were using their cellphones as we put them on monitors. Although breathing fast, they had relatively minimal apparent distress, despite dangerously low oxygen levels and terrible pneumonia on chest X-rays.

We are only just beginning to understand why this is so. The coronavirus attacks lung cells that make surfactant. This substance helps keep the air sacs in the lungs stay open between breaths and is critical to normal lung function. As the inflammation from Covid pneumonia starts, it causes the air sacs to collapse, and oxygen levels fall. Yet the lungs initially remain “compliant,” not yet stiff or heavy with fluid. This means patients can still expel carbon dioxide — and without a buildup of carbon dioxide, patients do not feel short of breath.

Share Your Stories From the Front Lines We want to hear from doctors, nurses and health care workers around the world.

Patients compensate for the low oxygen in their blood by breathing faster and deeper — and this happens without their realizing it. This silent hypoxia, and the patient’s physiological response to it, causes even more inflammation and more air sacs to collapse, and the pneumonia worsens until their oxygen levels plummet. In effect, the patient is injuring their own lungs by breathing harder and harder. Twenty percent of Covid pneumonia patients then go on to a second and deadlier phase of lung injury. Fluid builds up and the lungs become stiff, carbon dioxide rises, and patients develop acute respiratory failure.

By the time patients have noticeable trouble breathing and present to the hospital with dangerously low oxygen levels, many will ultimately require a ventilator.

Silent hypoxia progressing rapidly to respiratory failure explains cases of Covid-19 patients dying suddenly after not feeling short of breath. (It appears that most Covid-19 patients experience relatively mild symptoms and get over the illness in a week or two without treatment.)

A major reason this pandemic is straining our health system is the alarming severity of lung injury patients have when they arrive in emergency rooms. Covid-19 overwhelmingly kills through the lungs. And because so many patients are not going to the hospital until their pneumonia is already well advanced, many wind up on ventilators, causing shortages of the machines. And once on ventilators, many die.

Avoiding the use of a ventilator is a huge win for both patient and the health care system. The resources needed for patients on ventilators are staggering. Vented patients require multiple sedatives so that they don’t buck the vent or accidentally remove their breathing tubes; they need intravenous and arterial lines, IV medicines and IV pumps. In addition to a tube in the trachea, they have tubes in their stomach and bladder. Teams of people are required to move each patient, turning them on their stomach and then their back, twice a day to improve lung function.

There is a way we could identify more patients who have Covid pneumonia sooner and treat them more effectively — and it would not require waiting for a coronavirus test at a hospital or doctor’s office. It requires detecting silent hypoxia early through a common medical device that can be purchased without a prescription at most pharmacies: a pulse oximeter.

Pulse oximetry is no more complicated than using a thermometer. These small devices turn on with one button and are placed on a fingertip. In a few seconds, two numbers are displayed: oxygen saturation and pulse rate. Pulse oximeters are extremely reliable in detecting oxygenation problems and elevated heart rates.

Pulse oximeters helped save the lives of two emergency physicians I know, alerting them early on to the need for treatment. When they noticed their oxygen levels declining, both went to the hospital and recovered (though one waited longer and required more treatment). Detection of hypoxia, early treatment and close monitoring apparently also worked for Boris Johnson, the British prime minister.

Widespread pulse oximetry screening for Covid pneumonia — whether people check themselves on home devices or go to clinics or doctors’ offices — could provide an early warning system for the kinds of breathing problems associated with Covid pneumonia.

People using the devices at home would want to consult with their doctors to reduce the number of people who come to the E.R. unnecessarily because they misinterpret their device. There also may be some patients who have unrecognized chronic lung problems and have borderline or slightly low oxygen saturations unrelated to Covid-19.

All patients who have tested positive for the coronavirus should have pulse oximetry monitoring for two weeks, the period during which Covid pneumonia typically develops. All persons with cough, fatigue and fevers should also have pulse oximeter monitoring even if they have not had virus testing, or even if their swab test was negative, because those tests are only about 70 percent accurate. A vast majority of Americans who have been exposed to the virus don’t know it.

There are other things we can do as well to avoid immediately resorting to intubation and a ventilator. Patient positioning maneuvers (having patients lie on their stomach and sides) opens up the lower and posterior lungs most affected in Covid pneumonia. Oxygenation and positioning helped patients breathe easier and seemed to prevent progression of the disease in many cases. In a preliminary study by Dr. Caputo, this strategy helped keep three out of four patients with advanced Covid pneumonia from needing a ventilator in the first 24 hours.

To date, Covid-19 has killed more than 40,600 people nationwide — more than 10,000 in New York State alone. Oximeters are not 100 percent accurate, and they are not a panacea. There will be deaths and bad outcomes that are not preventable. We don’t fully understand why certain patients get so sick, or why some go on to develop multi-organ failure. Many elderly people, already weak with chronic illness, and those with underlying lung disease do very poorly with Covid pneumonia, despite aggressive treatment.

But we can do better. Right now, many emergency rooms are either being crushed by this one disease or waiting for it to hit. We must direct resources to identifying and treating the initial phase of Covid pneumonia earlier by screening for silent hypoxia.

It’s time to get ahead of this virus instead of chasing it.

Richard Levitan, an emergency physician in Littleton, N.H., is president of Airway Cam Technologies, a company that teaches courses in intubation and airway management.

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healthyworthyofficial · 5 years

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How does the coronavirus attack the human body ? .. NEW details !

The coronavirus could damage people's kidneys and send their immune systems 'haywire' as well as infecting the lungs, according to scientists. More than 90,000 people have now been infected with the disease, which is known to cause serious lung damage and deadly pneumonia. It does this by attaching to and reproducing in tissue inside the lungs, where it kills cells in the process of spreading. As the cells are killed they drop off the lungs' linings and build up in clumps inside the organs, making it hard to breathe and triggering further infections. The virus can also send the immune system into overdrive as it tries to fight off infection, triggering swelling which can lead to more breathing difficulties. If a severe infection takes hold it may move on to cause damage or dysfunction to the stomach, intestines, heart, liver and kidneys, and even provoke organ failure. Around 90,000 people around the world have been infected with the coronavirus since the beginning of January, and more than 3,000 patients have died. It comes as scientists today warned the coronavirus could become an infection that never goes away and causes seasonal outbreaks of illness, like flu.

Experts say the difficulty of containing the coronavirus is that so many patients have mild, cold-like symptoms and don't realise they have the infection – but it can quickly turn deadly

The coronavirus outbreak, which is teetering on the edge of becoming a global pandemic, has so far infected almost 90,000 people worldwide and killed more than 3,000 The coronavirus is officially a respiratory infection, meaning it affects the lungs and airways. Typical symptoms are a cough, trouble breathing and a fever. Among people who die from the infection – around 3.4 per cent of all patients, according to latest figures – most suffer from pneumonia, a lung infection which causes the airways to fill with fluid. Professor Mark Fielder, a biologist at Kingston University in London, said scientists have recently pinpointed the types of cells the virus appears to attack. He told Sky News that goblet cells and ciliated cells are the ones most affected by the coronavirus. They are responsible for keeping the inside of the lungs moist and clearing them of any debris like dust or bacteria. 'The problem we've got here is the virus infects these cells and starts to kill them,' Professor Fielder said. 'And as it kills them as part of its replication process, tissue falls into the lungs, and the lungs start to get blockages. And that blockage might mean that the patient develops pneumonia.' This could trigger pneumonia as the viruses and dead tissue clog up parts of the lungs and make them swell up, producing fluid which can block breathing. The immune system can also worsen the symptoms of COVID-19 by going 'haywire' and damaging healthy tissue in its attempts to stop the virus, Professor Fielder said. He told Sky: 'It can actually almost over attack, and become what we call hyperimmune, and set up a large attack which can then start to damage the healthy tissue underneath.' The coronavirus may also damage other internal organs as it takes hold in the body. Researchers have found signs that coronavirus patients have had damaged livers and kidneys, but there is little evidence to prove the virus caused it. Lung problems can reduce the amount of oxygen which circulates through the body, Dr James Cherry at the University of California, Los Angeles told Healthline, in turn starving organs like the kidneys of the oxygen they need to function properly. Organ failure is a serious health emergency and can kill if it's not repaired quickly. Dr Laura Evans, from the University of Washington, added that a 'good proportion' of people with severe coronavirus infections developed problems with other organs.

Coronavirus attaches to human cells by deceiving an enzyme which can make it 'fuse' to proteins inside the body and cause the infection

In little over a month more than 10,000 people have been tested for coronavirus in Britain, of which 36 came back positive Coronavirus explained: What are the chances I will die? How do I avoid it? Is it all a big fuss over nothing? World experts answer your questions CORONAVIRUS COULD BE 1,000 TIMES MORE INFECTIOUS THAN SARS The coronavirus could be up to 1,000 times more infectious than SARS because it plagues the body in the same way as HIV and Ebola, scientists warn. Experts initially presumed the spread of COVID-19 would follow the same trajectory as the SARS outbreak in 2002/3, because the viruses are almost identical genetically. SARS, or severe acute respiratory syndrome, infected 8,000 people worldwide and killed 774 people in a year in 2002. But in just two months the current coronavirus crisis has already hit around 90,000 and over 3,000 have succumbed to the illness. Nankai University researchers looked at the genome sequence of COVID-19 and found a section of mutated genes that did not exist in SARS. Instead the coronavirus has 'cleavage sites' similar to those in HIV and Ebola, which carry viral proteins that are dormant and have to be 'cut' to be activated. HIV and Ebola target an enzyme called furin, which is responsible for cutting and activating these proteins when they enter the body. The viruses trick furin so it activates them and causes a 'direct fusion' between the virus and the human cells. COVID-19 binds to cells in a similar way, the scientists found. 'This finding suggests may be significantly different from the SARS coronavirus in the infection pathway,' the scientists said in the paper. 'Compared to the SARS' way of entry, this binding method is "100 to 1,000 times" as efficient,' they wrote. The study was published on Chinaxiv.org, an online platform used by the Chinese Academy of Sciences. It’s hard not to feel a sense of impending doom when reading about the coronavirus infection that is rapidly sweeping the globe. Figures show it has killed more than 3,000 and infected almost 90,000 people in at least 65 countries. The majority of infections and deaths are in the Hubei province of China, where the never-before-seen virus emerged at the end of December. But in Italy, nearly 5,000miles (8,046km) from the source, cases have surged, forcing some northern towns – home to 55,000 people – into lockdown. Twelve Italians have died so far, and on Friday the first British fatality, a passenger aboard the Diamond Princess cruise liner quarantined in Japan, was reported. In the UK, of the more than 11,000 who have been tested for the virus, 36 have been diagnosed. No deaths on British soil have been recorded. Plans are in place to close schools, disrupt public transport and postpone major sports events, if the situation turns into a crisis. But for now, leading experts are urging the public to prepare and take measures to help prevent the spread of illness. The world wants to know what to do about it and so – from risks to the elderly or ill and how to self-quarantine, to what ordinary people can do to protect themselves – we asked some of the world’s leading experts for answers to the big coronavirus questions. How do you catch this virus? Covid-19 seems to spread much like flu, through coughs and sneezes. Once contracted, it lives and replicates in the tissues that line the airways. Secretions from these tissues – mucus and saliva – therefore also contain the virus. When an infected person coughs, sneezes, or simply talks, tiny droplets of moisture are expelled into the air, carrying the virus out of the body. Unless you are directly in the firing line, you should be safe. Droplets travel only up to 7ft.

A woman pictured with a medical mask covering her face. The only reason to wear a mask in public is if you think you are infected – to protect others (file photo)

Struggling: Pope Francis wipes his nose as he takes part in the penitential procession on Ash Wednesday in Rome, Italy, on February 26. He said yesterday he was only suffering from a cold But another risk comes when people cover their cough or sneeze with their hand and then touch something other people touch, such as a door knob or tap. Touch a contaminated surface, then touch your own mouth or nose, and the virus can be transmitted. The World Health Organisation (WHO) says the coronavirus can live on surfaces for several days. Günter Kampf of the University of Greifswald in Germany says such viruses can be killed by disinfectants such as alcohol or bleach – but many things we touch every day on transport or in public buildings are not frequently disinfected. If 14 per cent of those infected develop a severe disease and five per cent of them are critically ill, it could be a 'massive threat' according to an interview Dr Peter Openshaw, professor of experimental medicine at Imperial College London, gave The Times. 'It doesn't present like a common cold and the symptoms can range from completely unapparent to serious disease to going into intensive care. 'From what we have learnt so far, it seems that virus shedding - the transmission stage from infected persons - is going on relatively early during the course of infection. 'Tests can quite often become negative but then sometimes go positive again,' he said. According to Alistair Miles, head of epidemiological informatics, Wellcome Centre for Human Genetics, we should stop touching our faces. He told The Times: 'Stop touching your face. Especially stop touching your eyes, nose or mouth. 'Wash your hands often, especially before eating or touching food. 'While a mask seems like a good idea, there isn't a lot of good evidence that it can reliably prevent infection when worn by the public. But they are useful to put on a sick person to reduce their spreading of the virus.' He said: 'It looks unlikely this will be over quickly. It may be with us into next year and might eventually become a seasonal infection, returning each winter.' Could I die if I get it? It depends to some extent on how old you are. Covid-19 barely even causes symptoms in children, even babies, and in China is not known to have caused any deaths in under-tens. The main concern with children is that if they catch the virus they may pass it on to older at-risk individuals. This is why some headteachers have chosen to close schools, but this is not yet official policy. According to the most recent data from the China Centre for Disease Control, death rates are 0.2 to 0.4 per cent between the ages of ten and 50, but then start climbing.

Deep cleaning: A worker in a protective suit disinfects a tram car in Pyongyang, North Korea, on February 26. Symptoms of Covid-19 are a fever, a cough or trouble breathing You have a 1.3 per cent chance of dying from it in your 50s, a 3.6 per cent risk in your 60s, an eight per cent risk in your 70s, and a 14.8 per cent risk in your 80s. Risk climbs with age because older people more often have other diseases, such as cancer or conditions such as high blood pressure, diabetes or pulmonary disease, which worsen Covid-19. Professor Neil Ferguson, on the faculty of medicine at Imperial College London, told The Times: 'China seems to be suppressing transmission at the moment. In Italy we think there are many thousands of cases distributed across the country. In Iran there are tens of thousands, if not more. 'We calculated with an enormous amount of uncertainty that one per cent of those infected might die - with a fourfold margin of error in each direction. So a death rate of 0.25 per cent of cases would be similar to the 1957 and 1968 influenza pandemics while a four per cent rate would compare with the 1918 Spanish flu epidemic (with a death toll estimated at 40 million to 50 million). I have a horrible cold – could it be coronavirus? Symptoms of Covid-19 are not like those of a cold: it causes a fever, a cough and trouble breathing, not a runny nose or congestion. Most cases appear to be mild. If it’s mild, could I have the virus and not know it? The short answer is yes. Although at present only those who have been in contact with people known to be infected or who have been to a high-risk area (a full list of these locations comes later) should ask about being tested. Expert warnings about bats ignored for years This kind of virus was, until recently, found only in East Asian bats – and it doesn’t harm them. The virus is thought to have got to humans via bats sold in Chinese markets for food or traditional medicine, or via some other species also sold in the markets. Chinese scientists and some foreign colleagues have been warning for years that these bats were a risk. The first human cases were in December, in people with links to a wildlife market in the city of Wuhan: many worked there. After an initial attempt by local officials to hush up the outbreak, China launched a massive effort to contain the virus, shutting down Wuhan, which is bigger than London. In the Hubei province, where Wuhan is, case numbers now seem to be falling. But in a globalised economy with close trade and travel links, it was impossible to stop the virus getting out. It takes from two to 14 days after being infected by the virus to show symptoms – the average is five days. Chinese scientists say 80 per cent of all cases are quite mild. Some victims have barely any symptoms at all, so if you get sick you might not realise it’s Covid-19. Worryingly, it seems to be possible for people to spread it before they start showing symptoms – or even if they never do. Scientists at the Guangdong Centre for Disease Control and Prevention in China found one Covid-19 patient who showed no symptoms but had as much virus in his nose as people who had symptoms. In Germany, a woman with very mild symptoms – not enough to make her or anyone else suspicious – passed the virus to two people who shared a meeting room with her, who then passed it to two more people before they got symptoms. During the 2002 outbreak of severe acute respiratory syndrome, or SARS, it was discovered that people were infectious – with a high enough concentration of the virus in their fluids – only after they developed symptoms. This meant that isolating patients, to stop it spreading, was more straightforward. This time, ‘if people are infectious and spreading the virus before symptoms, then containment becomes much more difficult,’ warns Caroline Buckee of Harvard Medical School in the US. There have been these outbreaks before, like SARS, and we got through it. Do we really need to worry now? Experts have urged the public not to panic – however, people are being advised to stay informed. SARS infected more than 8,000 people and killed nearly 800 in 29 countries in less than a year. It went away because it spread poorly among people, and only after symptoms started.

Safe: Airport staff check the temperature of a passenger travelling from Milan, Italy, as part of the coronavirus screening procedure at the Debrecen airport in Hungary There was also a massive global campaign, led by the WHO, to isolate people who had been exposed. ‘It took a lot of hard work,’ says David Heymann of the London School of Hygiene and Tropical Medicine, who led that campaign at the WHO. ‘And we were lucky.’ SARS never invaded any developing countries which might have had trouble organising the surveillance and isolation required. This coronavirus spreads more readily, and has already infected more than ten times as many people, on all continents. But really, don’t more people die each year from falling down stairs than will be killed by coronavirus? More people do die in a year falling on stairs in the UK – 787 last year – than die of HIV, the virus that causes AIDS, which killed 428. Few would argue that HIV is trivial, or not something to avoid. At present, it is believed that one per cent of Covid-19 cases die. But this makes it as deadly as the 1918 ‘Spanish’ flu – one of the worst pandemics known, thought to have killed up to 50million worldwide. Should I wear a mask in public? No. Studies show they do not really protect you from being infected. Some think it makes you touch your face less, but others report it makes you do it more. The only reason to wear a mask in public is if you think you are infected – to protect others.

No risks: Commuters on a train in Milan, Italy, cover up completely. But studies show that wearing a face mask does not really protect you from being infected And, regardless, those who suspect they are infected are advised to stay at home and self-isolate (more on this later). Current advice from Public Health England is to wear one at home if you are caring for a sick person – and if you get sick, to stop you infecting others. The NHS may give you some if they tell you to self-quarantine. But don’t buy large quantities of masks. There is a global shortage and the close-fitting ‘respirator’ style ones, like N95 or FP2, which are similar to those worn by builders to protect them from toxic fumes, should be saved for the healthcare workers who will really need them. I think I’ve been exposed, but I feel fine. What should I do? Do not go to a clinic or the doctor’s without calling first. If you have the virus, you could infect more vulnerable people. The current official advice is this: if you have visited Hubei province in China in the past 14 days, or Iran, northern Italy and the Daegu and Cheongdo areas of South Korea since February 19, call NHS 111 – even if you do not have symptoms. You may well be asked to self-isolate for 14 days. If there is a risk that you may be infected, other family members or close contacts may also need to be contacted and questioned.

Stuck indoors: A guest wears a protective face mask as he stands by an open window at H10 Costa Adeje Palace, which is on lockdown over cases of cornoavirus, in Tenerife, Spain You should also contact the NHS on 111 if you have a cough, high temperature or are suffering shortness of breath and have been to other parts of mainland China or South Korea, Hong Kong, Japan, Macau, Malaysia, Singapore, Taiwan or Thailand in the past 14 days, or other parts of northern Italy (anywhere north of Pisa, Florence and Rimini), Cambodia, Laos, Myanmar or Vietnam since February 19. You should call the helpline if you think you may have been in close contact with someone who is infected. Even if you’ve been to a high-risk area, from what we know so far, if you don’t develop symptoms in 14 days, you don’t have the virus. This list may change, and the latest advice for England and Wales is on gov.uk. How do I isolate myself? Public Health England says stay home for 14 days. It means not going to work or school – employers and school heads should be informed. Do not go to public areas such as parks or shops and public transport or use taxis. Avoid having visitors, and ask friends, family or delivery services to get the shopping – and put it down outside, where you can pick it up.

Sweaty: Iran's Deputy Health Minister Iraj Harirchi wipes the swear off his face during a press conference in Tehran, before he confirmed being tested positive for coronavirus If you share a home with others, and they have not been advised to self-isolate, then stay in a separate, well-ventilated room. If you share a bathroom, use it after other people, use separate towels – and then clean it. If you share a kitchen, try not to use it when others do, eat in your room and wear a mask if others are there. Stopping you from infecting others is the one thing a surgical mask is good for. Public Health England advise that if a family returns from somewhere that requires quarantine when they get back, they can stay together and don’t have to be in separate rooms. Isn’t staying home for two weeks a bit extreme? Self-isolation for two weeks may be an unpleasant prospect. But it is absolutely vital, aimed at stopping the virus from getting loose and circulating generally, whereupon there will be far more cases, and it will be harder to protect the vulnerable, such as the elderly.

Dirty money: A bank clerk disinfects banknotes in the quarters of Suining Bank. China's central bank has ordered to disinfect cash and destroy cash received from hospitals Officials may also try to slow the spread of the virus by cancelling large gatherings and perhaps shutting down schools or transport. Apparently people with flu symptoms in some areas of the UK are being tested now. Why? Covid-19 is diagnosed by looking for the virus in samples taken from the nose or mouth. The UK has mostly tested people with risky travel or contact history. But Public Health England is now working with some hospitals and GP surgeries to test other patients, to see if the virus has already spread more widely. It's not snake flu, so what do we call it? Coronavirus seems to be what most people are calling the infection. But it’s not quite right – that’s the name of the family of viruses this thing belongs to. When looked at under a high-powered microscope, the virus is round with knobs on the outside that make it look like a little crown, hence ‘corona’. You’ve probably had one already: two coronaviruses cause common colds in people. Another coronavirus caused the disease SARS, which first emerged in 2002 in China, then died out within a few years. The official name for this infection is Covid-19, invented in February by the World Health Organisation from COrona VIrus Disease, and 2019, the year it emerged. At the same time the virus itself was named SARS-CoV-2 by a team of 17 virologists from six countries, who say it is actually the same species as the SARS virus. But a few small genetic differences mean it spreads much more readily among people than SARS did – which is why we haven’t been able to stop it as we did SARS. Fortunately, it is also only about a tenth as deadly as SARS. Some early reports called the virus ‘snake flu’ – a reference to early theories that it crossed into humans from snakes eaten as food. But it’s not flu, and the snake theory was quickly debunked. In eight hospitals, patients in intensive care with severe respiratory infections will be tested. In 100 GP surgeries, those coming in with milder flu-like symptoms – dry coughs, fever, shortness of breath – will be tested. As of Saturday, two cases had been found. What can I do to protect myself, and my family, if the virus starts spreading in the UK? ‘Think through how you will look after infected family members while avoiding infection yourself,’ says risk expert Peter Sandman. ‘Maybe get some plastic gloves in the case of caring for someone who is sick – perhaps a few disposable surgical masks to wear, for the same reason. Plan what to do for childcare if you or they are sick,’ he advises. Possibilities include making arrangements with neighbours or family to care for each other’s children if one or the other is sick – or see whether there are any emergency arrangements being organised in your community. When you are in public places, wash your hands often with soap, or at least alcohol-based hand cleaner, in case you’ve picked up the virus from some surface. If you must touch a public surface, don’t touch your face afterwards until you’ve washed. You can wear gloves, but don’t touch your face with those without taking them off first. Use a knuckle to push elevator buttons and a tissue to open doors and hold railings. Substitute an elbow bump for a handshake. Practise not touching your face when you are out in public, says Sandman. It’s hard, he admits, but not a bad skill to acquire. Sneeze or cough into a tissue (then bin it), or your elbow – as the old saying goes, it’s coughs and sneezes that spread diseases. I’ve read that there’s no vaccine for this virus. Will a flu jab protect me? Scientists are racing to come up with a vaccine or an antiviral drug for Covid-19, and some are now being tested, in record time. But there is currently no specific treatment, as it is an entirely new virus. Realistically, it’s not going to be available until next year.

A sunbather wears a face mask in the pool of H10 Costa Adeje Palace, which is on lockdown after cases of coronavirus were detected there, in Tenerife Coronaviruses are different from flu viruses, so the flu jab won’t offer protection. However, if you’re in a high-risk group for flu, and are eligible for a jab, it is advisable to have one. You don’t want complications of flu at a time when hospitals may be stretched by Covid-19 patients. I know people who have recently come back from holiday, and are now ill. Should they be self-quarantining? And if they aren’t, should I call the police or someone else? It is still flu season – other illnesses can be in circulation. The UK is advising self-quarantine only for people exposed to a known case, or who went to places where they might have encountered the virus. Check online for the current list of such places, and call the NHS, not the police, if you have doubts. My child’s school has been closed due to children there having come back from a high-risk area. Should we be self-isolating now? The school closed so you wouldn’t be exposed, and you will not have to self-quarantine.

People wearing protective face masks, following an outbreak of coronavirus, are seen in front of the giant Olympic rings at the waterfront area of Odaiba Marine Park in Tokyo, Japan Is it safe to travel at all right now? If you’re going somewhere with the same or lower levels of the virus than the UK, there seems little reason not to. In airports, rail terminals or other places where people with the virus may have been, take the precautions mentioned above. Don’t go close to places that have large or suspected outbreaks – this virus can spread fast. Check gov.uk for the latest travel advice. Dr Carmen Dolea, head of International Health Regulations Secretariat, World Health Organisation, told The Times: 'Aircraft cabins are absolutely not dangerous and travellers do not need to cancel their plans unless visiting restricted. 'The International Air Traffic Association (Iata) maintains an up-to-date list on its Travel Centre website. 'The best thing to do in aircraft cabins is to practise proper hand hygiene with alcohol-based rub or gels, and to use coughing etiquette. 'Make sure you cough and sneeze into your elbow, use a tissue and throw it in a bin.' I’ve read that the virus jumps from animal to humans. Could my dog be at risk? No. The WHO says there is no evidence of any involvement of cats or dogs with this virus. Last week’s reports about a dog in Hong Kong testing ‘weak positive’ for coronavirus were ‘incredibly irresponsible’, according to Jonathan Ball, Professor of Molecular Virology at the University of Nottingham. Experts say that the test probably picked up a bit of virus from contamination in the environment, not because the dog was infected. The coronavirus is thought to have come originally from East Asian fruit bats – so unless you have one of those for a pet, you’re OK. Even if you do have a bat, it will be fine – the virus doesn’t hurt them. Read the full article

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stephenmccull · 4 years

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As Threat of Valley Fever Grows Beyond the Southwest, Push Is On for Vaccine

One New Year’s Day, Rob Purdie woke up with a headache that wouldn’t quit. Vision problems, body aches and a slight fever followed. At the emergency room, the Bakersfield, California, resident was given antibiotics, which didn’t touch his symptoms. His headache turned into cluster headaches and the fatigue became worse.

“I was not really functional,” he said in a recent interview, recalling the beginning of his eight-year struggle with the mystery illness.

After five weeks, he ended up at Bakersfield’s Kern Medical, home to the Valley Fever Institute. A resident physician quickly realized the cause of the symptoms. A spinal fluid sample confirmed Purdie was suffering from valley fever, a fungal infection that occurs in the deserts of the Southwest, primarily Arizona and California. The infection had spread from his lungs into his brain, causing inflammation and headaches.

He was in and out of the hospital for a year with debilitating symptoms. There is no cure for valley fever; doctors use existing antifungal medications that often don’t relieve the symptoms. He tried three oral antifungal drugs and finally ended up with injections of amphotericin B — “salvage therapy,” meaning it is a drug of last resort — which he is still on, eight years later.

Purdie, 39, now works for the Valley Fever Institute, teaching others about the poorly understood disease. He still has no clue how he inhaled the spore that causes it. “I was probably out doing yardwork,” he said, “and took the wrong breath.”

Valley fever — coccidioidomycosis (“cocci” for short) is the scientific name — is an “orphan disease.” An orphan disease is defined in the U.S. as one affecting fewer than 200,000 people. Valley fever is diagnosed in the range of 10,000 to 15,000 cases a year in the U.S. with 160 fatalities, though both numbers are likely several times higher in reality because many cases are never identified. That’s why it’s often hard to attract attention to developing a vaccine.

In the 1980s, a promising vaccine candidate failed in clinical trials. There has been no other candidate for a vaccine until recently. Now, with mouse studies showing promise, there is a renewed push. Dr. John Galgiani, head of the University of Arizona’s Valley Fever Center for Excellence, is heading up vaccine research there and believes the vaccine shown to prevent valley fever in mice should be available for dogs, which also get infected in large numbers, as soon as next year. A veterinary vaccine company, Anivive, is developing it. “It’s very promising,” said Galgiani.

The same vaccine is in the early stage of development for humans, though it’s still years away.

In addition to Galgiani’s research, the National Institutes for Health’s National Institute for Allergy and Infectious Diseases is funding two other cocci vaccine research projects.

One drug, nikkomycin Z, has cured the disease in mice; experts believe it could do the same for humans. It’s being developed by the University of Arizona with funding from the National Institutes of Health, the Food and Drug Administration and other sources.

Valley fever is getting more attention for a few reasons. The number of cases has been increasing, and a study last year predicted it may spread north through the West as the climate warms. By 2095, five more states may be added to the list of 12 where the fungus now lives, growing its range in a swath across the West and into the Great Plains from Texas to Montana and North Dakota. The fungus is also found in Mexico and in Central and South America.

U.S. House Minority Leader Kevin McCarthy represents parts of California’s Central Valley, where cocci is prevalent. It’s a voting issue there and the Republican has made it a priority, bringing federal dollars to bear for research, surveillance and awareness.

The big problem with developing a vaccine is the relatively small market. The cost of studies to bring the drug to market, Galgiani estimated, is $50 million, while a federal study in 2000 pegged the cost of developing a vaccine at $360 million — though Galgiani believes it could be done for half that, still a hefty cost for a small group of patients.

“We don’t compete effectively against other investment opportunities,” he said.

Two types of the fungus Coccidioides cause valley fever. They dwell in desert soil between 2 inches and a foot deep and when disturbed become suspended in the air and are occasionally inhaled.

Cocci, sometimes called “desert rheumatism,” causes fever, cough, body aches, extreme exhaustion and difficulty breathing. There is no person-to-person spread.

Because the pneumonia-like symptoms are similar to those caused by the novel coronavirus, many cases of valley fever are likely being reported as COVID-19, Galgiani said, which means they are not getting treatment with antifungal medications that can temper symptoms if applied early on.

The infection can spur inflammation that “causes scarring and damage to parts of your nervous system,” Galgiani said. “Early diagnosis means less damage.”

Valley fever case numbers have grown substantially in the past five years, though they are down this year, perhaps because many doctors mistake the condition for COVID-19.

Most cases resolve on their own without treatment. Yet in 5% to 8% of diagnosed patients, the disease spreads to skin, bones and organs, and can be deadly. If it reaches the brain and spinal cord, as it did with Rob Purdie, it can cause meningitis, or swelling of the membranes. These patients, if they don’t die, may need antifungal treatments for life.

Blacks and Filipinos are four times more likely to have these serious effects than other demographic groups, according to Galgiani.

An epidemic devastated prisoners in the San Joaquin Valley, the southern section of California’s Central Valley, in the early and mid-2000s. Investigation showed the rate in two prisons — which had populations with higher numbers of minorities than the surrounding communities — was hundreds of times higher than in the surrounding area. Eventually, more than 30 prisoners died and many more had serious chronic infections.

The high season for infection is late summer and fall. Some 95% of the cases occur in the Central Valley and the Phoenix area. “They are in urban areas; you don’t have to be out on the desert to be infected,” Galgiani said.

Compounding the effects of valley fever is that it often goes undiagnosed. Even in Phoenix’s Maricopa County — where the fungus is endemic in the desert soil and 50% of the nation’s cases occur — it’s not on the radar screen of many doctors. Further complicating a diagnosis is that test results are often wrong and it may take two or three tests to identify the disease.

The lack of awareness of valley fever is one of the factors that led Purdie to take a job last year as outreach coordinator of the Valley Fever Institute. “There’s a lot of misinformation about it,” he said.

The vaccine that experts are banking on is called Delta CPS-1. It has proved very effective in mice in published studies and could be on the market as soon as next year for dogs. It’s estimated that 60,000 dogs contract valley fever every year in what’s known as the “Valley Fever Corridor” between Phoenix and Tucson, Arizona, and the numbers are probably similar for Bakersfield and other parts of the Central Valley. Symptoms in canines are similar to those in humans.

The same vaccine could one day prove effective in humans, though trials are years and many millions of dollars away. “It’s a great candidate for human immunization,” said Dr. Tom Monath, managing partner and chief scientific officer of Crozet BioPharma, which is working on the vaccine. “It’s hard to offer any promises, but it could take less than 10 years.”

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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