What are the symptoms of blood clots in COVID-19 patients. How common are blood clots in hospitalized COVID-19 cases. What causes blood clots to form in coronavirus patients. Why is COVID-19 considered a vascular disease as well as a respiratory illness.

The Prevalence of Blood Clots in COVID-19 Patients

Recent global studies have shed light on the alarming frequency of blood clot formation in patients hospitalized with COVID-19. Deep vein thrombosis (DVT), a condition where blood clots form in deep veins, occurs in 14-28% of these patients. Arterial thrombosis, involving clots in arteries, affects 2-5% of cases.

Dr. Ambarish Satwik, a vascular and endovascular surgeon at Sir Ganga Ram Hospital in Delhi, reports encountering five to six such cases per week on average, with recent weeks seeing daily occurrences of these complications. This data underscores the significant vascular impact of COVID-19, extending beyond its well-known respiratory effects.

Risk Factors for Blood Clots in COVID-19

• Type-2 Diabetes Mellitus
• Advanced age
• Obesity
• Severe COVID-19 infection

Dr. Amrish Kumar, a consultant in the cardio-thoracic vascular department at Aakash Healthcare, notes that patients with conditions like type-2 Diabetes Mellitus are particularly susceptible to blood clot formation, though the exact incidence remains undetermined.

Understanding Deep Vein Thrombosis and Arterial Thrombosis

Deep Vein Thrombosis (DVT) is a serious condition characterized by blood clot formation in veins located deep within the body. Arterial thrombosis, on the other hand, involves clot development in arteries. But what’s the difference between veins and arteries?

• Arteries: Carry oxygen-rich blood from the heart to the body
• Veins: Transport blood low in oxygen from the body back to the heart

Understanding this distinction is crucial in comprehending the varied impacts of COVID-19 on the circulatory system.

The COVID-Clot Connection: A Closer Look

Dr. Satwik recently highlighted the COVID-clot connection in a tweet, sharing an image of a blood clot extracted from the lower limb arteries of a COVID-19 patient. This visual evidence underscores the severity of vascular complications in some coronavirus cases.

The incidence of heart attacks, strokes, or limb loss due to arterial clots in COVID-19 patients ranges from 2% to 5%. In the case shared by Dr. Satwik, the patient faced an acute circulatory cut-off due to clots, threatening limb viability. Through surgical intervention, the clots were successfully removed, preventing potential gangrene and amputation.

Increased Risk of Thromboembolism in COVID-19

A Lancet paper published in November 2020 highlighted the increased association between COVID-19 and the risk of thromboembolism (TE), which involves obstruction of blood vessels by blood clots. The study concluded that TE rates in COVID-19 patients are high and linked to a higher risk of mortality.

COVID-19: Beyond Respiratory Illness

Initially perceived as typical viral pneumonia, severe cases of acute COVID-19 were likened to acute respiratory distress syndrome (ARDS), leading to respiratory failure. However, autopsies on COVID-19 patients revealed a more complex picture.

Dr. Satwik explains that in addition to lung damage, researchers discovered clots in the microcirculation of the lungs. This finding led to a paradigm shift in understanding COVID-19 as a disease that affects blood vessels as much as the lungs.

The Mechanism of Clot Formation in COVID-19

In COVID-19 patients, blood vessel injury triggers the production of a protein that attracts platelets and other clotting factors, leading to clot formation. Dr. Kumar notes that approximately 20-30% of hospitalized COVID-19 patients develop this complication.

These clots can form anywhere in the body due to the ubiquity of blood vessels. While some clots occupy large blood vessels and become macroscopic, diffused microscopic clots in microcirculation across various organs are also observed.

Comparative Risk of Blood Clots: COVID-19 vs. Normal Conditions

A University of Oxford study published in April 2021 revealed that the risk of rare blood clotting following COVID-19 is approximately 100 times greater than normal. The research focused on cerebral venous thrombosis (CVT), a blood clot in a cerebral vein in the brain.

Key findings from the Oxford study include:

• CVT is more common after COVID-19 than in comparison groups
• 30% of CVT cases occurred in individuals under 30 years old
• The study covered 500,000 COVID-19 patients
• The risk of CVT was estimated at 39 in a million

Maxime Taquet, one of the study’s authors, emphasized the clear link between COVID-19 and CVT, as well as portal vein thrombosis (a clotting disorder of the liver), urging attention to these findings.

The Mechanism Behind COVID-19 Induced Blood Clots

Dr. Satwik explains that the SARS-CoV-2 virus attaches itself to the inner lining of the lung, adjacent to the air sacs. This proximity to blood vessels allows the virus to directly affect the vascular system, potentially triggering the clotting cascade.

The virus’s interaction with blood vessels can lead to various complications:

• Endothelial dysfunction
• Inflammation of blood vessel walls
• Activation of coagulation pathways
• Disruption of normal blood flow

These factors collectively contribute to the increased risk of blood clot formation in COVID-19 patients.

Recognizing and Managing Blood Clot Risks in COVID-19

Given the elevated risk of blood clots in COVID-19 patients, healthcare providers must remain vigilant for signs of thrombotic complications. Early recognition and appropriate management are crucial for improving patient outcomes.

Signs and Symptoms of Blood Clots

• Swelling in the affected limb
• Pain or tenderness
• Redness or discoloration of the skin
• Warmth in the affected area
• Sudden shortness of breath (if clot travels to lungs)
• Chest pain
• Rapid heartbeat

Patients exhibiting these symptoms should seek immediate medical attention, especially if they have a history of COVID-19 infection.

Preventive Measures and Treatment Options

Healthcare providers may consider the following approaches to manage blood clot risks in COVID-19 patients:

1. Anticoagulation therapy for high-risk patients
2. Early mobilization when possible
3. Compression stockings for bedridden patients
4. Regular monitoring of coagulation parameters
5. Prompt intervention for suspected thrombotic events

The choice of treatment depends on individual patient factors, severity of infection, and overall clinical picture.

Long-term Implications of COVID-19 Related Blood Clots

While the acute phase of COVID-19 poses significant risks for blood clot formation, the long-term implications of these vascular complications are still being studied. Researchers are investigating potential long-lasting effects on cardiovascular health and overall well-being.

Areas of Ongoing Research

• Long-term cardiovascular risks in COVID-19 survivors
• Optimal duration of anticoagulation therapy post-infection
• Impact on organ function due to microvascular damage
• Potential for chronic thromboembolic conditions

As our understanding of COVID-19’s long-term effects evolves, healthcare strategies may need to adapt to address these potential chronic complications.

Global Efforts to Combat COVID-19 Related Thrombosis

The recognition of COVID-19 as a vascular disease has spurred global research efforts and clinical trials aimed at better understanding and managing thrombotic complications. International collaborations are underway to develop optimal treatment protocols and preventive strategies.

Key Areas of Focus

• Development of targeted anticoagulation therapies
• Identification of early biomarkers for thrombosis risk
• Refinement of imaging techniques for detecting micro-clots
• Investigation of novel anti-inflammatory approaches

These collaborative efforts aim to reduce the morbidity and mortality associated with COVID-19 related blood clots, potentially improving overall patient outcomes.

As research progresses, it becomes increasingly clear that addressing the vascular complications of COVID-19 is crucial for comprehensive patient care. The medical community continues to adapt its approach, emphasizing the importance of a multidisciplinary strategy in managing this complex disease.

The evolving understanding of COVID-19’s impact on the vascular system underscores the need for continued vigilance, research, and adaptation of treatment protocols. As we navigate this pandemic, the insights gained from studying its thrombotic complications may have far-reaching implications for our understanding of viral infections and their systemic effects on the human body.

Covid-19 not just lung disease, can also cause dangerous blood clots: Experts

Global studies have shown that the prevalence of blood clot formation known as deep vein thrombosis (DVT) in hospitalised COVID-19 patients is 14-28 per cent and is a lower 2-5 per cent for arterial thrombosis.

The India experience is similar, said experts, stressing that the infection is about the blood vessels as much as about the lungs. “We are dealing with five-six such cases per week on average. This week it has been one a day of such complications,” said Dr Ambarish Satwik, vascular and endovascular surgeon at Delhi’s Sir Ganga Ram Hospital.

The prevalence of blood clot formation in COVID-19 is high in patients who have conditions such as type-2 Diabetes Mellitus, although the exact incidence remains unknown, added Dr Amrish Kumar, consultant, cardio-thoracic vascular department, Aakash Healthcare in southwest Delhi’s Dwarka locality.

While DVT is a serious condition that occurs when a blood clot forms in a vein located deep inside the body, arterial thrombosis is a clot that develops in an artery. Arteries are blood vessels that carry oxygen-rich blood away from the heart to the body, while veins carry blood low in oxygen from the body back to the heart.

Satwik drew attention to the Covid-clot connection in a tweet earlier this week in which he posted a picture of a blood clot cast taken out from the lower limb arteries of a COVID-19 patient. “What COVID clots look like. Covid produces blood clots. The incidence of heart attack, stroke, or limb loss due to an arterial clot in Covid varies from 2 per cent-5 per cent. We pried these out of the lower limb arteries of a Covid patient. We were able to save the limb,” Satwik said on May 5.

Explaining his tweet, which attracted a lot of attention and questions too, Satwik said the COVID-19 patient had an acute circulatory cut off because of the clots, and the limb was threatened. “So we had to physically do a surgical procedure and extract these clots, otherwise there would have been gangrene, and he would have ended up with an amputation.

We were successfully able to take the clots out and save the limb,” the surgeon explained. Authors of a Lancet paper published in November last year said studies suggested there is increased association between COVID-19 and the risk of thromboembolism (TE) or obstruction of a blood vessel by a blood clot. The authors of the paper concluded that TE rates of COVID-19 are high and associated with a higher risk of death.

“We have been understanding the pathophysiology of COVID-19 for over a year now. When it first hit China and the global west, it was thought that it was typical viral pneumonia. Severe cases of acute COVID were being labelled as similar to the acute respiratory distress syndrome (ARDS), which leads to respiratory failure,” Satwik noted.

However, a series of autopsies on COVID patients and their lungs revealed that what the doctors were seeing was not typical ARDS. “…in addition to that, they were finding clots in the microcirculation of the lungs. So it was then kind of understood that COVID is as much a disease of blood vessels as much it’s a disease of the lungs,” Satwik added. In a COVID-19 patient, when blood vessels are injured, they produce a protein that attracts platelets and other clotting factors that come together to form a clot, Kumar added.

“Studies have shown that around 20 to 30 per cent of hospitalised COVID-19 patients have developed this complication,” he told PTI. Because blood vessels are everywhere on the body, these clots could form anywhere, Satwik said. Some of these clots occupy big blood vessels and become macroscopic blood clots. “But otherwise we are seeing diffused microscopic clots in microcirculation in various organs,” he noted.

According to a University of Oxford study published in April, the risk of rare blood clotting following COVID-19 is around 100 times greater than normal. The research found that the rare blood clotting known as cerebral venous thrombosis (CVT) — a blood clot of a cerebral vein in the brain — is more common after COVID-19 than in any of the comparison groups, with 30 per cent of these cases occurring in the under 30s.

The study covered 500,000 COVID-19 patients. The risk would be 39 in a million, according to its finding.

“The signals that COVID-19 is linked to CVT, as well as portal vein thrombosis a clotting disorder of the liver is clear, and one we should take note of,” said Oxford’s Maxime Taquet, one of the authors of the study. Explaining how the virus causes blood clots in COVID-19 patients, Satwik said the virus is known to attach itself to the inner lining of the lung, and right next to these air sacs are very thin blood vessels or capillaries.

“The virus invades these blood vessels and starts affecting the inner lining of these blood vessels which produces a dysfunction within the blood vessels which produces these clots,” the surgeon said. As a result, he said, some clinicians were using blood thinners as part of the treatment and getting success. “What we have understood is these micro clots need immediate retrieval in order to save the limbs,” Satwik added.

He also said it is very difficult to know the prevalence of clots in the entire population infected with COVID. Although it is difficult to determine the vulnerability of COVID-19, individuals with existing cardiovascular morbidities are the ones who will suffer thrombotic complications, Satwik said.

According to Kumar, in COVID-19 patients, the clots seem to form in the tiny vessels of the lungs rather than the major vessels, adding that clots in the lungs usually happen in the case of typical strokes or heart attacks or deep vein thrombosis. “Risk of COVID-19 patients associated with blood clots are stroke (clot in the cerebral artery), clots in the lungs, heart attack, deep vein thrombosis, and thrombosis in both upper and lower limb arteries. Stroke can cause paralysis, but we have not seen any such so far in our hospital,” Kumar added.

India on Friday saw a single-day rise of 4,14,188 COVID-19 infections and 3,915 fatalities, pushing the country’s tally of cases to 2,14,91,598 (21. 4 million/2.14 crore) and the death toll to 2,34,083.

This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed.

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Deep Vein Thrombosis Specialist – Bakersfield, CA: Heart Vascular and Leg Center: Vascular Specialist

What is deep vein thrombosis (DVT)?

A DVT is a blood clot that forms in a vein located deep in your body. Though they most often occur in the veins in the legs, DVTs may develop in any vein throughout the body. 

DVT is a potentially life-threatening condition. If the blood clot — a gelatinous clump of blood — dislodges from the vein, it may travel through your bloodstream to your lungs and cause a pulmonary embolism.  

What causes deep vein thrombosis?

You may develop DVT from any condition that affects the flow of blood through your veins. Common causes include:

• An injury that damages your veins
• Pressure on the veins from excess body weight
• Use of birth control pills or hormone therapy
• Smoking
• Standing or sitting for long periods
• Health conditions such as cancer or inflammatory bowel disease
• Having a catheter placed in the vein

Your risk of developing DVT increases if it runs in your family, or you are over the age of 50. 

What are deep vein thrombosis symptoms?

DVT may develop without causing noticeable signs and symptoms. However, if you’re experiencing the following, you may have DVT and should contact Heart Vascular and Leg Center immediately for an evaluation.

Symptoms of DVT include:

• Leg pain 
• Leg swelling
• Inflammation or tenderness at a specific spot in your leg
• Muscle cramping

You should go to the nearest emergency room if you suspect you may have a pulmonary embolism, which causes shortness of breath, chest pain, and lightheadedness.  

How is a deep vein thrombosis diagnosed?

Heart Vascular and Leg Center is a full-service cardiology and vascular care practice that uses advanced technology to diagnose a DVT. Your provider reviews your symptoms, medical history, and family history during your exam and evaluates your leg.

To confirm or rule out a DVT, your provider may perform various tests, such as a vascular ultrasound, blood test, CT scan, or MRI.

How is a deep vein thrombosis treated? 

The goal of your DVT treatment plan is to stop the blood clot from getting bigger and breaking free. Your treatment may include:

• Blood thinners
• Clot busters (medications that break up the blood clot)
• Compression stockings to improve blood flow
• Filters that prevent blood clots from reaching your lungs

Heart Vascular and Leg Center also performs thrombectomies, surgical procedures that remove the blood clot from your vein. 

For expert cardiology and vascular care from a practice that offers the most advanced tools and treatments in the country, contact Heart Vascular and Leg Center by phone or schedule an appointment online today.  

Symptoms of cerebral venous thrombosis

The Food and Drug Administration and Centers for Disease Control recommended on Tuesday that states temporarily halt using Johnson & Johnson’s Covid-19 vaccine due to “extremely rare” blood clotting disorders that occurred in six women who received the vaccine in the U.S.

For context, more than 6.8 million doses of the J&J vaccine have been administered in the United States to date.

Still, at least 25 states including Washington D.C. have paused distributing the J&J vaccine.

The pause is taken “out of an abundance of caution,” so that the healthcare system can prepare to identify, diagnose and treat the condition, according to the FDA.

But many who have received the single-dose vaccine or are set to receive it are wondering what it means for them or their loved ones.

Here’s what you need to know:

What is the clotting disorder

Six women, ages 18 to 48, developed rare cerebral venous sinus thrombosis, which are blood clots in combination with low levels of blood platelets. One of the recipients died and another is in critical condition.

Although the exact cause is unclear, experts believe that after some people get this type of vaccine, their body has an immune response that “leads to activation of the platelets and these extremely rare blood clots,” Dr. Peter Marks, director of the FDA Center for Biologics Evaluation and Research said in a joint media call Tuesday.

But remember, “This is a really rare event,” Dr. Anthony Fauci said during a White House press briefing on Tuesday. It typically occurs in somewhere between two and 14 people per million, Marks said.

Who should look for symptoms

So far, the side effect seems to appear within six to 13 days after vaccination. So those who got the vaccine in the last couple of weeks or days should be aware of any symptoms that arise, Dr. Anne Schuchat, principal deputy director of the CDC, said in a media call Tuesday.

But “for people who got the vaccine more than a month ago, their risk for them is very low, at this time,” she said.

The blood clots also all occurred in women under the age of 50, but the current group is too small to make generalizations about certain conditions or factors that would predispose people to the blood clots, Schuchat said. The Advisory Committee on Immunization Practices, the CDC committee that makes vaccine recommendations, is going to review the data and make recommendations.

J&J said in a statement that it is working closely with regulators to assess the data.

Side effects to watch for

The symptoms of this type of blood clot are very different from the mild flu-like symptoms that people experience a few days following vaccination: tiredness, headache, muscle pains, chills, fever and nausea.

So what is relevant?

“If you receive the vaccine and develop severe headache, abdominal pain, leg pain or shortness of breath, you should contact your health care provider and seek medical treatment,” Schuchat said. (Blood clots can travel through your blood stream and become lodged, cutting off blood flow to important organs like the brain, heart or lungs. )

Symptoms of a low platelet count include things like easy bruising, nose bleeding and gum bleeding. (The low platelets with this complication make a typical clot treatment, the blood thinner heparin, “a mistake in this situation,” Fauci said Tuesday, “because it could be dangerous.”)

As mentioned, timing also matters: The blood clots have typically “occurred at least about a week after vaccination, and not longer than three weeks after vaccination, with a median of about nine days after vaccination,” Marks said.

What to do if you have an appointment to get the J&J vaccine

The FDA is working with state and federal governments to ensure that people who were scheduled to get the J&J vaccine can be rescheduled to get the Pfizer or Moderna vaccines, Jeff Zients, White House Covid-19 response coordinator on the J&J vaccine, said in a statement Tuesday.

Depending upon where you were scheduled to get the vaccine, the pharmacy, supermarket or state health authority may notify you directly to let you know if your shot is canceled or rescheduled.

However, this is based on a recommendation not a mandate, so some states and individual healthcare providers may choose to still give out the vaccine.

“If an individual healthcare provider has a conversation with an individual patient, and they determined that benefit for that individual patient is appropriate, we’re not going to stop that provider from administering the vaccine because it could be right,” Marks said. (For instance, for many people the risk of getting Covid may be more problematic than the risk for such a rare complication.)

What this means for the country’s vaccination rollout

This story has been updated to include a statement from Johnson & Johnson.

COVID Toe, Blood Clots And More Possible Symptoms Of COVID-19

As the Centers for Disease Control and Prevention expands its list of possible symptoms for COVID-19, health providers have been reporting  other problems in patients with the virus. A pulmonologist explores possible causes.

The CDC initially listed cough, fever and shortness of breath as symptoms of the virus. 

But the agency has since added a second category of possible symptoms: 

• chills
• repeated shaking with chills
• muscle pain
• headache
• sore throat
• new loss of taste or smell.

Healthcare Providers Are Reporting Other Problems

In a letter in the New England Journal of Medicine, a team of doctors from Mount Sinai Health System in New York contends COVID-19 can cause blood clots that can lead to stroke and other health concerns.

Also, dermatologists have reported “COVID toes”or frostbite-like patches showing up on people’s toes. This harmless rash often went away on its own without treatment, but many of the same patients tested positive for COVID-19.

“One thing that has become exceedingly clear in taking care of COVID patients is it’s not simply a respiratory disease,” said Dr. John Hollingsworth II, a pulmonologist associated with Texas Health Harris Methodist Hospital Fort Worth. “It’s a systemic disease and really can affect all the organ systems depending on the severity of disease.”

INTERVEW HIGHLIGHTS:

COVID Toes

The skin is one of the largest organ systems in the body and with many systemic infections or diseases, we see manifestations in the skin. We’re seeing that with COVID-19 also, we see the changes in the distal extremities and toes. It’s been described in a number of reports where people get rashes across the torso, and this is very common in what we see with other diseases that involve the vasculature and have a vasculitis-like picture. So, this is very consistent with what we see with other viruses that you have dermatologic manifestations.

Blood Clots And Strokes Associated With COVID-19, As Well As Liver Failure

• The virus clearly can enter a number of different cell types in many different organ systems. In fact, when you look at organs like the neurologic tissue or in the kidney or even in blood cells, I mean it appears as though there are viral inclusions and entry of the virus into these cells. So it’s not entirely surprising that there are neurologic manifestations.
• Stroke, on the other hand, is a much more rare complication that has been described in a number of case reports. In our hospital, I’ve seen the same thing where people will present without other risk factors and present with stroke and also have COVID-19. There’s a lot of emerging evidence that COVID does cause a microvascular disease or microvascular thrombosis which can also cause the vascular changes as well as a hypercoagulable-like state where you can develop either stroke, pulmonary embolus or a blood clot in the legs.

So, How Does A Doctor Know Whether To Test For Or Suspect COVID-19?

This is becoming more and more difficult to discern who actually has COVID-19. Part of that depends on a prevalence of disease in the community. As the prevalence of disease increases, the suspicion that people have COVID actually has to go quite higher with a number of different symptoms. I think that’s in part the reason the CDC and the WHO (World Health Organization) have both very broad symptoms when they’re thinking about COVID-19.

How Should The Public React To All This?

• I think it boils down to controlling spread of disease, social distancing, hand-washing, not getting out into public when you’re sick. The rationale behind that is just buying time. So we have new therapies to treat patients effectively when they do end up in the hospital.
• I think it’s very confusing to people because there is so much information that comes out and some of that information is accurate, but some of that information is incomplete or even misinformation. So, I would really rely on experts in the field like Dr. Tony Fauci who give good sound advice about how to approach this disease moving forward.
• When approached in the hospital, I strongly encourage people to participate in those (clinical) trials because that’s really the way we move the market forward as a society to have new novel therapies that actually effectively treat patients once they have this infection.

RESOURCES:

Expanded List of Symptoms of Coronavirus

C.D.C. Adds New Symptoms to Its List of Possible Covid-19 Signs

Doctors Find Some Younger COVID-19 Patients Suffer Serious Strokes

‘Frostbite’ toes and other peculiar rashes may be signs of hidden coronavirus infection, especially in the young

How a Huge Blood Clot Took the Shape of a Lung Passage

On Tuesday, The New England Journal of Medicine tweeted the most recent addition to its photo series of the most visually arresting medical anomalies. The image is of a mysterious, branchlike structure that, posted elsewhere, would probably pass for a cherry-red chunk of some underground root system or a piece of bright reef coral. But this is no creature of the deep. It’s a completely intact, six-inch-wide clot of human blood in the exact shape of the right bronchial tree, one of the two key tubular networks that ferry air to and from the lungs. And it was coughed up in one piece.

The clot is beautiful, and it’s also kind of gross. The tweet received a slew of replies from those frightened that the photo showed an actual coughed-up lung, which is about as likely to happen as your brain falling out of your butt. But even the doctors who treated the 36-year-old man who produced the clot aren’t entirely sure how it could have emerged without breaking.

Read: Why fractals are so soothing

Georg Wieselthaler, a transplant and pulmonary surgeon at the University of California at San Francisco, says the unnamed patient was initially admitted to the intensive-care unit with aggressive end-stage heart failure. Wieselthaler quickly connected the patient’s struggling heart to a pump designed to help maximize blood flow through the body. But this type of ventricular-assist device comes with its own risks. “You have high turbulence inside the pumps, and that can cause clots to form inside,” Wieselthaler says. “So with all these patients, you have to give them anticoagulants to make the blood thinner and prevent clots from forming.”

These anticoagulants themselves can lead to trouble. In a healthy person, oxygen-starved blood leaving the heart travels an intricate network of capillaries through the lungs for an oxygenating pit stop by the airways. Usually, if small fissures occur in this network, the body’s clotting agents show up to slap some circulatory duct tape on them until they heal. But for someone taking anticoagulants, the body can’t efficiently patch things up if any part of this tight blood-vessel network is breached, and things can spiral out of control.

In Wieselthaler’s case, blood eventually broke out of his patient’s pulmonary network into the lower right lung, heading directly for the bronchial tree. After days of coughing up much smaller clots, Wieselthaler’s patient bore down on a longer, deeper cough and, relieved, spit out a large, oddly shaped clot, folded in on itself. Once Wieselthaler and his team carefully unfurled the bundle and laid it out, they found that the architecture of the airways had been retained so perfectly that they were able to identify it as the right bronchial tree based solely on the number of branches and their alignment.

“We were astonished,” Wieselthaler says. “It’s a curiosity you can’t imagine—I mean, this is very, very, very rare.”

It’s rare, but not entirely unprecedented. A case study that appeared in The Journal of the American Medical Association back in 1926 describes a 34-year-old woman who was admitted to Rochester Municipal Hospital with an airway infection and coughed out “a large piece of membrane”—a layer of cells and gunk collected by the infection—“which proved to be a cast of the trachea, both bronchi, and several bronchioles.” In September 2005, the European Journal of Cardio-Thoracic Surgery published a photo of a smaller bronchial-tree cast coughed up by a pregnant 25-year-old who had developed a disorder impairing her clotting agents. She recovered and was able to deliver a healthy infant. The woman with the airway infection, who was born before the diphtheria vaccine, was not as lucky.

Read: The doctors whose patients are already dead

The primarily pediatric condition plastic bronchitis, a lymphatic-flow disorder associated with various heart and lung diseases, causes a buildup of lymph fluid in the airways that becomes hard and rubbery, which many people cough up in a similarly pristine structure. And for asthmatics, mucus plugs can harden in the airways thanks to factors like bronchoconstriction and dehydration, making them ready to be coughed up during an asthma attack.

Still, for all these cases, only the mother-to-be coughed up a cast made of blood, the largest ever photographed until UCSF’s. Congealed blood is less sturdy and sticky than hardened lymph or mucus, so why didn’t the cast break apart?

Wieselthaler suspects the answer might involve fibrinogen, a protein component of blood plasma that essentially acts as the “glue” of a clot by trapping platelets to form a mass. The infection that Wieselthaler’s patient had, in addition to aggravating his heart failure, caused a higher-than-normal concentration of fibrinogen in his blood. It’s possible, Wieselthaler says, that the blood in his airways was unusually rubbery, capable of surviving the bumpy ride up the trachea unscathed.

Gavitt Woodard, a clinical fellow in UCSF’s thoracic-surgery department who helped Wieselthaler capture the photo, suggests that the size of the clot itself may have been what allowed the patient to cough it up. It’s possible that “because it was so large, he was able to generate enough force from an entire right side of his thorax to push this up and out,” she says. Were it broken up into smaller segments, “he might not have been able to generate the force.”

Wieselthaler says that although his patient felt instantly better after coughing up the clot, its size clearly indicated the severity of his situation. Wieselthaler and Woodard put the man on a breathing tube and were able to stop his bleeding with a more invasive procedure, but the numerous complications of his heart failure were already too severe. He died a week later.

It can feel boorish to admire a by-product of the complete breakdown of a human body. But the photo is captivating because the clot’s structure shows a part of every human body, a biological filigree anyone can appreciate as a part of themselves, too. That’s why Woodard and her mentor shared the photo in the first place: “Recognizing the beautiful anatomy of the human body is the main point of it,” she says.

What we know about the AstraZeneca vaccine and blood clots

The AstraZeneca COVID-19 vaccine has made headlines across the world for its potential links to a very rare, but serious, syndrome involving blood clotting and low platelet levels. Many people are understandably concerned: What’s causing these blood clots in the first place? How are they different to other types of blood clots? And why wasn’t this picked up during the vaccine’s clinical trials?

Here is what we know so far about the science behind blood clotting, our understanding of how it might be connected to the AstraZeneca vaccine, and how scientists and health authorities are investigating the risks.

What is blood clotting?

Blood clotting is a process your body uses to prevent bleeding. When a blood vessel is damaged—for example, if you cut yourself—blood cells called platelets rush to the site of the injury and clump together with proteins and other blood cells, forming a clot to plug the hole. This minimises further bleeding while your body starts repairing the damage.

Blood clots are formed as blood cells are held together with a protein mesh. Image adapted from: David Gregory & Debbie Marshall / Wellcome Collection; CC BY 4.0

However, sometimes a clot can form inside a vein or artery. This blocks the normal flow of blood in that part of the body and can cause serious harm, especially if it restricts blood flow to tissues or vital organs like the brain (such as in the case of stroke). There are lots of different reasons why problematic clotting might occur—some common causes include recent surgery and reduced mobility, genetic disorders that make blood more prone to clotting, or medications that affect certain hormones, such as the oral contraceptive pill. Even sitting still for a long time, like on a long international flight, can lead to clotting in the deep veins of the legs.

Blood clotting is a complex process, involving many different proteins and chemical messengers all interacting with each other in a series of reactions. Venous thromboembolism, an umbrella term for several common blood clotting diseases, is quite common, affecting roughly 17,000 Australians each year. While cases can vary in severity, many are treatable with medications such as heparin and other anti-clotting treatments.

Blood clots are a known complication of COVID-19 itself. One analysis found that 14.7 per cent of COVID-19 patients developed some form of blood clotting, often in places like the legs or lungs, where other blood clots are more commonly found.

What is ‘thrombosis with thrombocytopenia syndrome’ (TTS)?

Health authorities have noticed a rare pattern of symptoms that some people have experienced following an AstraZeneca vaccination. This collection of symptoms has been called ‘thrombosis with thrombocytopenia syndrome’, or TTS, and involves the formation of a blood clot (also called thrombosis), typically in uncommon places such as veins in the brain or abdomen, together with low levels of platelets in the blood (also called thrombocytopenia).

Although TTS is serious, it’s also very rare. The Australian Technical Advisory Group on Immunisation (ATAGI) estimates that out of every 100,000 people vaccinated with AstraZeneca, one or two people may experience TTS. The risk might be higher for people under 60, but any estimates of risks for specific age groups are still imprecise because there are so few cases to analyse.

The syndrome is similar to another rare condition called heparin-induced thrombocytopenia, which occurs when someone has an unusual immune reaction to heparin, a common anti-clotting medication. In these cases, heparin interacts with a protein found in blood platelets called platelet factor 4 (PF4). The immune system then mistakenly interprets this PF4-heparin combination as foreign and produces antibodies to attack it. This triggers a chain of events where platelets become ‘activated’, sticking together to form clots. The immune system keeps activating platelets, leading them to release proteins into the bloodstream that stimulate the clotting system to produce even more clots.

It is important to realise that most blood clots are not caused by immune processes.

Scientists think a similar reaction might be taking place caused by the AstraZeneca vaccine (or components of it) interacting with PF4 proteins and triggering an immune response. It is particularly challenging for scientists to study the way TTS works, because it is so rare.

It is important to realise that most blood clots are not caused by immune processes. This suggests that, for people who have experienced blood clots in the past, or have other risk factors that might increase their chances of developing a clot (such as taking the oral contraceptive pill), the AstraZeneca vaccine may not pose an extra risk, because the causes of the clotting are fundamentally different. Scientists and health authorities have not yet been able to confirm how AstraZeneca vaccine causes blood clots—there is still a lot that we simply don’t know.

However, we do know that even if someone becomes ill with TTS, doctors now have a better understanding of the condition. It’s much easier to diagnose and get the right treatment, so the chances of recovery are higher than they were before.

How are scientists and health authorities investigating the link?

Health authorities have seen enough cases of TTS taking place from 4 to 30 days following an AstraZeneca vaccine to say a link between the vaccine and the disease is likely.

The first signs of a possible link between the AstraZeneca vaccine and unusual blood clots appeared as vaccination programs were rolled out in several European countries. The European Medicines Agency (EMA) identified a pattern in their data (statisticians call this a ‘signal’) about unwanted health impacts following vaccination. The signal showed that a small number of people were developing serious and unusual blood clots in combination with low levels of platelets within a month of receiving the AstraZeneca vaccine. Countries like Germany, Norway and Spain made the decision to temporarily pause their vaccine rollouts so health authorities could investigate the problem before restarting the program.

A signal can only indicate that there may be a link between a vaccine and a side effect: it raises a flag for health authorities to show that further investigation might be needed. It cannot provide any information about why the side effect might occur, or whether some groups of people are at higher risk than others. A signal doesn’t always mean the vaccine directly causes that side effect. Answering these questions requires further investigation into what’s causing the problem and how it might (or might not be) linked to a vaccine, as has been done with the AstraZeneca vaccine and TTS.

Health authorities continue to monitor a vaccine’s safety as it is rolled out to the public. Image adapted from: CDC/Unsplash; CC0

The rarity of TTS is the main reason it was not detected during vaccine clinical trials. Clinical trials typically involve many thousands of people, not millions: if a side effect or complication only occurs for a few people out of a million, it may not happen for any of the participants in a clinical trial. This is why health authorities continue to monitor a vaccine’s safety as it is rolled out more widely so that very rare potential side effects can be identified and investigated.

Importantly, the overall number of reports of blood clots following vaccination is not a cause for concern. There will always be a chance that someone will develop a blood clot regardless of whether they’ve just received a vaccine or not—health authorities refer to this as the ‘background rate’ of a given symptom or disease. These more common cases of venous thromboembolism, which are not associated with low platelet levels, do not meet the criteria for TTS and are unlikely to be caused by the vaccine.

Even with the small risk of TTS associated with the AstraZeneca vaccine, it is still highly effective at preventing severe COVID-19. Health authorities must balance the risk associated with the vaccine against the significant benefits of vaccination in protecting individuals and the community against severe illness and death from COVID-19. All COVID-19 vaccines currently in use are valuable tools for controlling the spread of disease and limiting the serious complications that COVID-19 can cause.

This article is based on scientific evidence but is not medical advice. Please speak with your doctor for advice regarding your personal circumstances and vaccines for COVID-19.

Funded by the Australian Government Department of Health.

This article was produced by the Australian Academy of Science. It has been reviewed by the following experts: Professor Carola Vinuesa FAA FAHMS Co-Director, Centre for Personalised Immunology, John Curtin School of Medical Research, Australian National University; Professor Beng Chong Professor of Medicine (Conjoint), UNSW Sydney & Director of Haematology, NSW Health Pathology, The St George and Sutherland Hospitals; Professor Matthew Cook Director of Immunology, Canberra Hospital & Professor at John Curtin School of Medical Research, Australian National University; Dr Rod Lamberts Deputy Director, Australian National Centre for the Public Awareness of Science; Dr Ketaki Sharma Staff Specialist, National Centre for Immunisation Research and Surveillance & Conjoint Clinical Lecturer, Discipline of Child and Adolescent Health, University of Sydney. The writing of this article was supported by Academy staff: Emma Berthold and Dr Hayley Teasdale.

Focus on the Clinical Picture

Abstract

Acute pulmonary embolism (APE) is characterized by numerous clinical manifestations which are the result of a complex interplay between different organs; the symptoms are therefore various and part of a complex clinical picture. For this reason, it may not be easy to make an immediate diagnosis. This is a comprehensive review of the literature on all the various clinical pictures in order to help physicians to promptly recognize this clinical condition, remembering that our leading role as cardiologists depends on and is influenced by our knowledge and working methods.

Keywords: Pulmonary embolism, Sudden cardiac death, Syncope, Deep vein thrombosis

INTRODUCTION

Acute pulmonary embolism (APE) is the most serious clinical presentation of venous thrombo-embolism (VTE) with fatal pulmonary embolism (PE) being a common cause of sudden death (SD), usually resulting from a complication of deep venous thrombosis (DVT).

In the United States PE affects about 500,000 to 600,000 people per year, with 200,000 to 300,000 deaths per year.¹⁾ PE is the third most frequent cardiovascular disease after acute myocardial infarction (AMI) and stroke, with an annual incidence of 1–2 per 1,000 people (100–200 per 100,000 inhabitants).^2),3)

In 2001, the number of VTE-related deaths was estimated at 543,454 per annum across Europe, more than double comparing with the number of combined deaths due to acquired immune deficiency syndrome (AIDS) (5,860), breast cancer (86,831), prostate cancer (63,636), and road accidents (53,599).^4),5),6) The correct annual number of VTE events is hard to obtain due to the difficult diagnosis based mostly on the following factors: 1) VTE is often clinically silent with the first sign of the disease being sudden fatal death (30–50% of cases)⁷⁾; 2) clinical presentation mimics the characteristics of several other conditions, resulting in mistaken diagnoses⁸⁾; 3) PE detection during autopsy is very difficult and requires close inspection of the pulmonary vascular tree in order to uncover small acute emboli or the residua of chronic thrombo-emboli⁹⁾; and 4) sensitivity and specificity of diagnostic tests for the disease remain weak.¹⁰⁾

PE risk factors include obesity, immobilization, cigarette use, cancer, surgery, trauma, pregnancy, oral contraceptives or hormone replacement therapies, and a prior history of PE or a known hype-coagulable disorder. However 30% of patients with PE have no detectable provoking factors and, as shown in the Emergency Medicine Pulmonary Embolism in the Real World Registry (EMPEROR), International Cooperative Pulmonary Embolism Registry (ICOPER), and Registro Informatizado de Enfermedad TromboEmbólica (RIETE) registries, the mean age of PE patients ranges from 56 to 66 years, with older people and females having mild prevalence.^{11),12),13),14)} Clinical presentation of PE varies from an asymptomatic small pulmonary embolus with low mortality to a massive PE resulting in failure of the right ventricular (RV) with shock, and/or death.¹⁵⁾

Many fatal pulmonary emboli remain unrecognised due to the lack of routine postmortem examinations leading to an underestimation of their incidence.^{16),17),18),19)} Prompt diagnosis of this potentially deadly disease is of utmost importance, therefore knowledge of the salient features associated with PE may enable physicians to make the diagnosis facilitating the following appropriate treatment strategy.

SYMPTOMS AND SIGNS OF PE

Pain can be related to local disturbances in pulmonary circulation, pleural involvement or impairment of coronary circulation. Central PE may produce typical angina also due to RV ischemia; while pleuritic chest pain can be the consequence of pleural irritation due to pulmonary infarction secondary to small distal pulmonary artery (PA) embolization.^20),21),22) Dyspnea has a multi-factorial origin, resulting from bronchospasm or vasospasm, disturbances in pulmonary circulation, immobility or diminished respiratory excursion of the diaphragm, atelectasia and/or pulmonary infarction, anoxia, or impairment of cardiac function. In patients with pre-existing heart failure or pulmonary disease, deteriorating dyspnea may be the only symptom indicative of PE. Anoxia is manifested clinically by cyanosis. Hyperbilirubinemia may occur when hepatic congestion co-exists. Dyspnea, chest pain, and cough are the most frequent symptoms of PE, while fever, tachycardia, abnormal pulmonary signs, and peripheral vascular collapse are the most common physical findings. Cyanosis, hemoptysis, syncope, and the various manifestations of acute cor pulmonale are less commonly observed.

CLINICAL PICTURES

PE is a prevalent and potentially life-threatening cardiovascular condition that may be difficult to diagnose due to a wide spectrum and often nonspecific manifestations (). Diagnosis of PE may therefore involve multiple specialties, including emergency medicine, cardiology, internal medicine, obstetrics and gynaecology, surgical services, and sometimes urgent interventional radiology. A number of medical centers across the United States, including Massachusetts General Hospital and Brigham and Women’s Hospital, have already founded multidisciplinary PE response teams in order to improve diagnosis and access to advanced therapies. Given this premise the purpose of this review was to focus on syndromes more than individual symptoms in patients in which APE can be suspected in order to develop a more comprehensive view of PE patients.

Table 1

Clinical presentation of PE

Clinical pictures of APE:

1. SD (sudden cardiac arrest; SCA)

2. Similar to acute respiratory distress syndrome (ARDS)

3. Typical respiratory failure (hypoxia and hypocapnia)

4. Asthmatic crisis-like syndrome

5. Fever syndrome with or without pseudopneumonia (with or without pleural effusion)

6. Acute right heart failure/shock/hypotension (often with epigastric pain)

7. Left heart failure (with pulmonary congestion)

8. Chest pain similar to pleuritic syndrome with or without haemoptysis (with or without effusion)

9. Similar to acute coronary syndrome (ACS) (with or without chest pain)

10. PE with paradoxic embolism (with corresponding clinical picture due to embolization site and resulting in: AMI, stroke, flank pain [due to acute splenic infarction or acute renal infarction], acute abdomen, and upper or lower extremity embolism. In all these paradoxical embolism conditions, the main symptom may be systemic or not)

11. Syncope

12. Complete atrioventricular (AV) block with idioventricular rhythm

13. Persistent or paroxysmal atrial fibrillation (AF), atrial flutter, atrial tachycardia, paroxysmal supraventricular tachycardia (PSVT)

14. DVT and silent PE

15. Platypnea-orthodeoxia

16. Abdominal pain without abdomen acute

17. Delirium

SD

SD is defined as unexpected natural death from a cardiac cause (coronary disease, hypertrophic cardiomyopathy, valvular disease, no structural abnormalities)²³⁾ or non-cardiac cause (respiratory, cerebral, drug overdose, exsanguination, metabolic, sepsis, near drowning hypothermia trauma)²⁴⁾ that occurs within a short time interval (generally within 1 hour of onset of symptoms) in patients with no prior potentially-fatal condition.^25),26),27). Most victims (>90%) have underlying cardiac abnormality.²⁸⁾ The most frequent cause of SD is coronary disease (80% of cases) with the risk of sudden cardiac death (SCD) being higher in men than in women and it increases with age due to the higher prevalence of coronary artery disease (CAD) in older individuals. Only a small percentage of patients show no structural abnormalities.^29),30) The incidence of SD in the United States is 1 person per 1,000/year with SD being the initial clinical manifestation in 25–30% of patients with PE, and it accounts for approximately 1.3% of the total deaths in western countries.^31),32) Seventy-five percent of SD cases include overweight/obese patients with 31% of these patients having history of psychiatric disorders in pharmacological treatment, supporting the recently-reported association between mental disorders and PE risk.^33),34),35) The percentage of clinically unsuspected PE causing in-hospital SD has been reported to be as high as 50% to 80%.^36),37) SD due to PE can occur in the presence of ACS, developing ventricular arrhythmia, or during non-shockable rhythm. Recently, Bougouin et al.³⁵⁾ showed in a large population-based registry that PE-related SCA is not rare, accounting for 3% of all SCA patients admitted in hospital alive. Moreover, this study highlighted that PE-related SCA should be suspected in cases of non-shockable rhythm, in women, and in those with prior thrombo-embolism.³⁸⁾ The cause of cardiac arrest is not easily recognized, especially when the initial rhythm is different from ventricular fibrillation; in the majority of cases, the mechanism of cardiac arrest in massive PE is pulseless electrical activity (PEA) (a syndrome characterized by the absence of a palpable pulse in an unconscious patient with organized electrical activity).

Similar to ARDS

Non-cardiogenic pulmonary edema or ARDS occurs in a wide variety of clinical settings, such as hypovolemic shock, major trauma, and septicemia; it was described as a complication of classic PE by Windebank and Moran in 1973, although in this instance no pulmonary capillary wedge pressures were obtained. In 1982, Adrian et al. documented PE in patients with pulmonary edema while performing right heart catheterisation that showed normal post-capillary pressure, therefore excluding left ventricular (LV) failure as a cause of the pulmonary edema; moreover, the finding of pulmonary edema confined to unobstructed portions of the pulmonary capillary bed confirmed the diagnosis.

It has been proposed that the release of vasoactive substances from clots may lead directly to increased capillary permeability or to venous constriction and increased capillary hydrostatic pressure; in addition, it is possible that fibrin micro-emboli may injure pulmonary capillaries. All these possibilities may, of course, produce edema downstream of the obstruction. Another mechanism proposed has been a mal-distribution of blood flow causing some areas of a lung to be over-perfused, resulting in interstitial and alveolar edema.³⁹⁾

Typical respiratory failure (hypoxia and hypocapnia)

In blood gas analysis, hypoxemia is considered a typical finding of APE, but up to 40% of these patients have normal arterial oxygen saturation and 20% have a normal alveolar-arterial oxygen gradient.^40),41) However, when hypoxemia is present during PE dyspnea is the first symptom of respiratory failure as a consequence of hemodynamic disturbances. Hemodynamic disturbance includes low cardiac output resulting in desaturation of the mixed venous blood flow that together with areas of reduced flow (due to obstructed vessels) and areas in which flow is increased lead to ventilation-perfusion mismatch. In about one-third of patients’ severe hypoxemia can be detected when right-to-left shunt (through a patent foramen oval [PFO]) is present. This is caused by an inverted pressure gradient between the right atrium and left atrium; in these clinical pictures hypocapnia is also often present. The chest X-ray is frequently abnormal, and although findings are usually non-specific in PE, they are useful for excluding other causes of dyspnea or chest pain.

The classic presentation of APE may be difficult or impossible to recognize in critically ill patients with respiratory failure. Symptoms are difficult to obtain and assess in patients who are intubated and receiving therapy with mechanical ventilation. In patients previously diagnosed with chronic obstructive pulmonary disease (COPD), the usual clinical manifestations of pulmonary emboli (symptoms, signs, chest X-ray film, electrocardiogram (ECG), and changes in arterial blood gas levels) are frequently already present due to the severe underlying pulmonary disease, and any superimposed manifestations of pulmonary emboli may not be evident. In this group, the ventilation/perfusion lung scan correlated poorly with pulmonary angiographic results and during examination at autopsy, the scan was generally insufficient to rule in or rule out pulmonary emboli. Currently, pulmonary angiography remains the only reliable technique to confirm or exclude PE.⁴²⁾

Asthmatic crisis (bronchial asthma-like symptoms induced by PE)

PE is known to induce symptoms such as bronchial asthma therefore diagnosis of PE may be difficult if a previous history of asthma is present.^43),69) However the mechanism behind bronchoconstriction in PE is not fully understood. It has been suggested that pharmacologically-active substances may be released at thrombo-embolic sites, leading to the excitation of specific chemoreflexes. Such agents include acetylcholine, histamine, serotonin, and the plasma kinins, all of which have bronchoconstrictor properties,^11),12) suggesting that bronchoconstriction occurring with pulmonary emboli may be related to the presence of a substance whose activity or release is blocked by heparin, as evidence of bronchoconstriction in selected patients appears to represent an objective and sensitive, although nonspecific, index of PE.^44),45),46) As discussed above, there is a broad differential diagnosis for chronic asthma. In adults, acute severe asthma is almost invariably associated with a diagnosis of chronic asthma. However, in PE, the onset of symptoms (principally breathlessness) varies from very acute (minutes) with a clear precipitant to more sluggish (days) with no clear trigger. Signs consistent with acute severe asthma include difficulty completing sentences, tachycardia, tachypnoea, and a widespread polyphonic wheeze with oxygenation often preserved, however older patients or those with more chronic disease baseline blood gas may be abnormal and this should always be considered. In order to make a differential diagnosis, routine investigations should include appropriate blood tests, 12-lead ECG, and chest X-ray to assess the presence and/or absence of an additional acute pathology (e.g. lobar pneumonia, pneumothorax) moreover an echocardiography could be performed in order to assess RV shape and function.⁴⁷⁾

Fever syndrome with or without pseudopneumonia (with or without pleural effusion)

PE may be accompanied by fever and show evidence of pulmonary infiltrates at X-ray; in this case differential diagnosis from other diseases such as pneumonia is mandatory. The clinical features of pneumonia and PE are very different. PE has a more sudden onset, and the dyspnea is more prominent than cough and sputum. In addition, dyspnea-related PE has no radiological features and is not responsive to antibiotics with fever being a later phenomenon of the disease. Pneumonia, on the other hand, has a progressive onset with a more prominent cough, sputum, and fever that appears earlier. Usually chest pain is present in PE. Attention should be paid to young patients without obvious features of PE, and differentiation between pneumonia and PE should be carefully conducted in order to ensure timely diagnosis and appropriate treatment.⁴⁸⁾

Acute right heart failure/shock/hypotension (often with epigastric pain)

Right heart function and a hemodynamic picture play a key role in PE patient classification. The presence of hypotension is the most significant predictor of poor outcome, and defines patients with massive PE or high-risk PE. Normotensive patients with evidence of RV dysfunction, assessed by echocardiography, define the sub-massive category and are patients at intermediate risk of poor outcome.⁴⁹⁾ Shock or hypotension are present in 5–10% of PE patients with patients with myocardial injury or shock index (heart rate/systolic blood pressure [mmHg]) is >1 having the worst prognosis in which a rapid diagnosis and treatment are mandatory.^50),51) A physical examination of these patients is extremely important: the jugular venous pulse is often elevated with a prominent V wave, a parasternal RV heave may be palpable. On auscultation, a tricuspidalic murmur with increased S2, and a right-sided S4 (in up to 25% of patients) may be present. In patients with RV failure, the ECG may show sinus tachycardia, signs of RV strain, re-polarization abnormalities, or ischemia including a complete or incomplete right bundle branch block with a right axis deviation (>90°) or S1Q3T3 pattern; other ECG features could be Qr in lead V1, ST elevation in V1, or pre-cordial T-wave inversions. T-wave inversions in the pre-cordial leads seems to correlate with both the severity of the PE and the presence of RV dysfunction with normalization being a sign of favorable outcome. Increased mortality has been shown in patients with AF, a low QRS voltage and premature ventricular contractions all reflecting the degree of RV failure and hemodynamic compromise.^52),53)

The hemodynamic response to an APE depends on many factors, such as physiologic reaction to the vasoreactive substances released, the cardiopulmonary status of the patient at baseline and the size of the embolus and degree of pulmonary vasculature obstruction.⁵⁴⁾ A pulmonary vascular obstruction of >30% has been shown to correlate with the presence of RV dysfunction on echocardiographic examination.⁵⁵⁾

Signs of RV dysfunction with dilation on the transthoracic echocardiogram (TTE) include: 1) a ratio of RV to LV end-diastolic diameter >1 in the apical four chamber view, or 2) an RV end diastolic diameter >30 mm and/or loss of inspiratory collapse of the inferior vena cava. In contrast to the global hypokinesis seen in PAH patients with RV failure, PE patients may exhibit sparing of the RV apex with hypokinesis of the RV free wall and base; a finding termed the “McConnell sign.” The McConnell sign has been shown to have a specificity of 94% and sensitivity of 77% for diagnosing PE⁵⁶⁾ echocardiographic examination can help in suggesting the presence of preexisting cardiopulmonary disease, such as chronic PAH.⁵⁷⁾

Left heart failure with possible pulmonary congestion

Cariogenic pulmonary edema in PE patients may be due to⁷⁸⁾: 1) Occlusion of PA branch causing increased flow in the other branches causing high lung capillary pressure; and 2) compression of LV by dilated RV

Although the first scenario can be promptly diagnosed, PE in patients with pulmonary edema due to compression of LV by dilated RV can be difficult. In fact, this category of patients has a complicated clinical picture that may be impossible to solve on the basis of clinical presentation alone and without the help of technology such as echocardiography; in general, they have long standing dyspnea, bilateral pulmonary congestion at the physical examination with a dilated RV at echocardiographic examination, leading to left ventricle compression.^58),59)

Chest pain similar to pleuritic syndrome with or without hemoptysis (with or without effusion)

Chest pain pleuritic syndrome describes a scenario involving pulmonary infiltration and chest pain, where pain is correlated to breathing and to position; this clinical presentation is evidence of pulmonary infarction.^60),61) with small distal emboli creating areas of alveolar hemorrhage, without hemodynamic relevance, resulting in hemoptysis, pleuritis, and pleural effusion which is usually mild.⁶¹⁾

Similar to ACS (with or without chest pain)

Similar to left main disease

In some cases, a massive PE may mimic ACS, with chest pain, hypotension, tachycardia, hypoxia; ECG with ST elevation in leads augmented vector right (aVR) and V1 with ST depression in I, augmented vector left (aVL), and V4–6 with coronary angiography revealing non-obstructive coronary arteries.⁶²⁾ The “neglected” lead aVR overlooks the LV cavity and gives specific information regarding the RV infundibulum and basal interventricular septum. Therefore, in massive APE the ST elevations in lead aVR is frequently seen, and is associated with an overall worse prognosis. Possible reasons for the finding of ST elevations in aVR and V1 and diffuse ST depressions in the lateral leads in massive APE may be related to diffuse subendocardial ischemia, due to poor LV inflow and subsequent poor coronary blood flow as well as acute RV overload and possible RV infarct. Recognizing this pattern is extremely important in patients with acute massive PE, due to the need for prompt diagnosis and following appropriate therapy.^63),64)

Similar to anterior interventricular coronary disease

1) Pseudo-anterior-non-ST-segment elevation myocardial infarction (STEMI)

In patients with severe APE, a negative T wave was often observed in precordial leads (leads V1–4). However, this finding is also found in ACS due to left anterior descending CAD. Prompt differentiation between the 2 diseases is crucial for the selection of appropriate treatment. In patients with APE and ACS who have negative T wave in leads V1–4, peak negative T wave in leads V1–2 simply but accurately differentiates APE from ACS. In APE, anterior negative T is the consequence of an enlargement of the RV and may also be a sign of RV ischemia given the fact that leads V1 and V2 face the anterior region of the RV. In addition, negative T waves in leads III are very common given the fact that lead III faces the inferior region of the RV.⁶⁵⁾ Negative T waves are also found on ECG at presentation in an appreciable number of patients with left main disease that have similar ECG findings, however in this category of patients, negative T waves are more broadly distributed around lead aVR in the limb leads and the precordial leads, with the exception of lead V1.⁶⁶⁾

2) Pseudo antero-septal STEMI

ECG abnormalities are seen in 70–80% of patients with APE. Many cases of APE with ST elevation V1–V3/V4 have been described in literature.^67),68) It is quite challenging to differentiate APE from anterior STEMI mainly due to fatal outcomes if STEMI is not diagnosed. However, when clinical presentation is more suggestive of APE, and ECG features are not classic for STEMI (e.g. absence of reciprocal ST deviation), prompt referral to pulmonary angiography computed tomography (CT) and timely delivery of good resolution images should be performed to expedite diagnosis in this specific instance; in this case a bedside echocardiogram looking for regional wall-motion abnormalities and evidence of RV dilation may also be useful.⁷⁰⁾ However when the clinical picture is not so clear, It become very difficult to differentiate APE with ST elevation from anterior STEMI. Several mechanisms for the development of ST-segment elevation in APE have been proposed: the development of RV transmural ischemia and infarction; with RV dilation and failure, in this picture RV is unable to generate enough systolic pressure to overcome the acute increase in after-load, leading to increased RV oxygen demand and a significant reduction of pulmonary perfusion. This, together with leftward shift of the interventricular septum, will reduce the LV preload; and the subsequent cardiac output and coronary flow; in addition hypoxia can cause severe RV transmural ischemia leading to ST-segment elevation in leads V1–V3/V4.^71),72),73) Numerous studies of submissive and massive PE with these clinical features and no occlusive CAD have been reported.^74),75) Another explanation for ST-segment elevation in leads V1–V3/V4 in APE is paradoxical coronary embolism through an atrial septal defect or PFO (which has a prevalence of 25–35% in autopsy series) in the setting of a sudden rise of right heart pressure, creating a right-to-left shunt.^76),77),78) This suggests that initial presentation with STEMI may mask a concomitant APE and prompt recognition and treatment of both pathologies is of great importance; in fact patients with paradoxical coronary embolism may not have underlying atherosclerosis, and thrombus aspiration may be the treatment of choice.

PE with paradoxical embolism (clinical picture depending on site of embolization)

PE with paradoxical embolism refers to the clinical phenomenon of thromboembolism originating in the venous vasculature and travelling through an intracardiac or pulmonary shunt into the systemic circulation.

Pulmonary hypertension and massive or sub-massive PE are the high-risk factors for paradoxical peripheral arterial embolism. PFO is the most common intracardiac shunt. The prevalence of a PFO appears to decrease with increasing age, with an incidence of 34% during the first 3 decades, 25% during the third to seventh decade, and <20% among octogenarians.⁷⁹⁾ Under physiological conditions, a pressure gradient is maintained between the left and the right atrium which results in passive closure of the PFO. In the case of increased right atrial pressure exceeding left atrial pressure, as observed at the end of Valsalva maneuvers (such as coughing, sneezing, squatting, defecation, and micturition), a transient right to left shunt may occur which may lead to presence of thrombi into the systemic circulation. A permanent increase in right-sided cardiac pressure, as observed after PE or other causes of pulmonary arterial hypertension, may result in a significant or possibly permanent right to left inter-atrial shunt, increasing the risk of paradoxical embolism.

Additional anatomical variations are also associated with PFO:

• The Eustakian valve is an embrionic remnant of the right valve of the sinus venous that in utero directs oxygenated venous blood from the inferior vena cava to the foramen ovale. The Eustakian valve gradually disappears after delivery in the majority of individuals, however residual prominent may direct venous blood to the fossa ovalis and cause significant right to left shunt in some individuals. PFO and residual prominent Eustakian valve are found to coexist (approximately 70% of cases), especially in patients with paradoxical embolism.⁸⁰⁾

• The Chiari network, observed in 2–4% of the general population, is another embrionic remnant of the right valve of the sinus venous (in the right atrium) that results from incomplete re-absorption during embryonic heart development. It is frequently associated with PFO, right to left shunt, or an atrial septal aneurysm (ASA), all of which facilitate paradoxical embolism.

All intracardiac communication, including ventricular septal defects, have a certain risk for paradoxical embolism. By contrast patients with pulmonary arteriovenous malformations have a permanent right to left shunt, permitting the passage of thrombi or septic emboli into the systemic circulation.⁸¹⁾

The clinical picture resulting from intracardiac communication depends on the embolisation site, and can be associated with the following:

• AMI (STEMI): Paradoxical embolism through a PFO is the most likely cause of AMI, occurring in approximately 5/1,000 patients. While this is quite a low rate, the incidence is still high enough to warrant clinical attention especially in younger patients or in the case of RV infarction.^82),83),84)

• Stroke: Cerebro-vascular accidents constitute the most frequent relevant clinical manifestations of presumed paradoxical embolism. The cause of stroke remains unidentified by routine diagnostic testing in about 40% of patients, known as the so-called cryptogenic stroke.⁸⁵⁾ PFO is increased more than 2-fold among patients with cryptogenic stroke compared with patients with conventional causes of stroke.

• Flank pain (due to acute renal infarction, flank pain with hematuria)⁸⁶⁾

• Acute mesenteric ischemia (acute abdomen)⁸⁷⁾

• Lower extremity embolism: cold and pulseless extremities secondary to peripheral arterial occlusion.⁸⁸⁾ Surgical thromboembolectomy efficiently reduces mortality rate compared to conservative management with thrombolysis or anticoagulation. Pulmonary hypertension and massive or sub-massive PE are the high-risk factors for paradoxical peripheral arterial embolism. For secondary prevention of paradoxical peripheral arterial embolism, combined medical therapy can result in a significant reduction of the risk of recurrent embolic events or death.^89),90)

These cases demonstrate the high index of possible paradoxical emboli due to concurrent arterial and venous embolism. A correct and prompt diagnosis is extremely important and the use of echocardiographic examinations and more sensitive trans-esophageal echocardiography and transcranial doppler (TCD) sonography have a key role⁹¹⁾ in the detection of a right to left shunt regardless of its location.

Syncope

Syncope is defined as a transient loss of consciousness attributable to global cerebral hypoperfusion, further characterized by rapid onset, brevity, and spontaneous recovery. It is a common reason for arrival at the emergency department (ED), accounting for approximately 1% of attendances. In the United States, 30–40% of such patients are subsequently admitted for further investigation. The prevalence of PE among patients hospitalized for syncope is not well-documented however recent studies by Duplyakov et al.⁶⁶⁾ and the German register, Management Strategy and Prognosis of Pulmonary Embolism Registry (MAPPET) showed that the rate of syncope in patients with high-risk PE was 29.9% and 35% respectively.

Three possible mechanisms of syncope in patients with PE have been proposed:

• Syncope may be caused by thrombosis of more than 50% of the lung arterial system, which leads to a sidecrease gnicifcant decrese of cardiac output, followed by arterial hypotension and reduction of cerebral blood flow.

• A second mechanism causing syncope may be the activation of the vasovagal reflex. In 1867, von Bezold proposed the theory of cardiac depressor reflex, which was later completed by Jarisch. The essential point of the Bezold-Jarisch reflex is an activation of mechanoreceptors located in the left ventricle. In acute pulmonary thrombo-embolism, when an embolus lodges in a large branch of the PA, it may trigger a hyper-adrenergic state, resulting in an increase in the LV contractility with restriction of the diastolic filling. This could stimulate the ventricular mechanoreceptors (type C afferent fibers) involved in the Bezold-Jarisch reflex and lead to an increase in the efferent vagal response, causing a decrease in heart rate, a delay in AV conduction and a decrease in sympathetic tonus, resulting in peripheral vasodilation, and finally syncope.

• A third possible explanation is heart arrhythmias and conduction disturbances due to RV overload.

A history of syncope in patients with suspected PE should be considered as a possible criterion for the high risk of fatal complications during an in-hospital period.

Complete AV block with idioventricular rhythm

Complete AV block with idioventricular rhythm can be the initial manifestation of an APE sometimes together with syncope.

In the presence of syncope during pulmonary thromboembolism due to massive embolism and Bezold-Jarisch reflex (as previously mentioned), various degrees of AV block may occur. However, complete AV block is possible in the presence of preexisting complete left bundle-branch block. In fact, in this subset of patients, complete AV-block is known to be due to the development of acute right bundle-branch block, resulting in syncope. The development of right bundle-branch block is linked to its anatomic position; in fact, the right branch of the His bundle is particularly exposed due to its superficial sub-endocardial trajectory on the RV face of the septum, and it is therefore very sensitive to a sudden distension of the right cavities.

Persistent or paroxysm AF, atrial flutter, atrial tachycardia, PSVT

PE is often under-diagnosed for a long time because of its atypical symptoms, and the diagnosis is made only when the clinical picture is complicated by the onset of an arrhythmia that forces the patient to go to hospital. In this case the physician finds himself faced with an arrhythmia that is the consequence of another problem that may be unrecognized,⁹²⁾ which is the case with AF, atrial flutter, atrial tachycardia, and PSVT.

DVT and silent PE

In PE patients, clinical signs and symptoms suggesting thrombophlebitis are present in 32% of cases. However, DVT is present in 79% of cases, and if it is not present, it could mean that it has already embolized. In most patients with DVT, the clots are localized proximally with 40–50% of cases having a more complex clinical picture in which PE is present, but very often silent. Silent PE is frequent in the post-surgery phase, above all in patients without prophylaxis. APE develops 3–7 days after DVT and in 10% of cases can be fatal within 1 hour of the onset of symptoms.⁹³⁾

Platypnea-orthodeoxia

Platypnea-orthodeoxia is a syndrome of dyspnea and hypoxia in an upright posture (desaturation SO₂), relieved by recumbence. Platypnea-orthodeoxia is also associated with PFOs with and without PE and with or without paradoxical embolism. Two conditions must coexist to cause this syndrome: an anatomical component in the form of an interatrial communication, and a functional component that produces a deformity in the atrial septum resulting in a redirection of shunt flow with the assumption of an upright posture. The former may be an atrial septal defect, a PFO, or a fenestrated ASA. The latter may be cardiac, such as pericardial effusion or constrictive pericarditis; pulmonary, such as emphysema, arteriovenous malformation, pneumonectomy, or amiodarone toxicity; abdominal, such as cirrhosis or ileus; or vascular, such as aortic aneurysm or elongation. Platypnea-orthodeoxia could be explained on the basis of positional modification of abnormal shunting. The upright position could stretch the interatrial communication (a PFO, atrial septal defect or a fenestrated ASA) allowing more streaming of venous blood from the inferior vena cava through the defect, whether or not a persistent Eustachian valve coexists. In the case of a PFO, the occurrence of PE creates higher left atrial pressure that may be one of the elements to explain the shunt and the platypnea orthodeoxia.⁹⁴⁾

Abdominal pain without acute abdomen

It is well known that a number of patients affected by hemodynamic stable PE are admitted to the ED presenting chest pain without further symptoms of PE, but in a few cases, the presenting symptoms are even more unusual: in fact, 2 cases of PE in young men evaluated in the ED for acute pain in the upper abdomen and showing basal pulmonary abnormalities consistent with PE⁹²⁾ have been described in litetrature.

Delirium

Delirium, an acute confusional state, is a common, complex medical disorder associated with substantial morbidity and mortality among patients of 65 years and older. This potentially reversible cognitive disturbance is increasingly recognized as a sign of serious underlying illness. Hypoxia is a well-known precipitating factor for delirium and that PE is a common cause of hypoxia.

Therefore delirium may complicate PE in patients with other evidence of the disease. Delirium in the elderly should be regarded as an atypical presentation of PE related to the hypoxemia picture, acute ventricular impairment, hypotension, and/or paradoxical embolism that could explain this “lung-brain connection,” but the full mechanisms remain unknown.^93),95)

90,000 Patients – From varicose veins to thrombosis – just one step: 5 important questions about the causes and danger of varicose veins – No varicose veins, laser surgery clinic in Yekaterinburg, laser treatment of varicose veins Yekaterinburg, removal of spider veins, a phlebologist’s appointment in Yekaterinburg, a vascular surgeon’s appointment, treatment of varicose veins on legs, sclerotherapy

How to understand when to run to the hospital, and what will happen if you do not receive treatment

It is necessary and possible to treat varicose veins before it’s too late

Photo: “No varicose veins”

Today it is difficult to meet a person, who never felt heaviness in the legs or did not notice the scattering of spider veins on the body.But, as a rule, no one thinks about the serious consequences of this familiar to many symptoms. For example, to the formation of a blood clot, which at any time can come off the vessel wall and lead to a sad outcome.

Therefore, Thrombosis Day is celebrated all over the world in October to remind people once again how insidious and dangerous this disease can be.

According to the latest medical research, adult patients with varicose veins are five times more likely to develop deep vein thrombosis.Surgeon-phlebologist of the “No varicose veins” clinic for laser surgery Hrant Ambaryan answered the most popular questions about the treatment and prevention of varicose veins and how to prevent thrombosis.

Why are varicose veins dangerous?

Varicose veins are a disease accompanied by a thinning of the venous wall and an increase in the lumen of the veins. Because of varicose veins, the risk of blood clots increases, skin diseases appear – itching, burning, eczema and even venous ulcers, that is, painful deep defects of the skin and fatty tissue.Bleeding may even occur because the dilated, thinned vessel wall is easily damaged.

– If treatment is not started on time, irreversible consequences will occur, including death, – says Dr. Ambaryan.

Photo: “No varicose veins”

Why does varicose veins appear?

The main reasons are a sedentary lifestyle or, conversely, heavy physical exertion of a constant nature.

– Drivers and office employees spend a lot of time in a sitting position, while loaders, hairdressers, salesmen, factory workers, on the contrary, work on their feet all day.Both have a bad effect on the health of blood vessels, ”says Hrant Ambaryan. – In addition, varicose veins are more common in women, partly to blame for high heels and heavy bags. And, of course, you should always take into account bad habits – smoking, alcohol, unhealthy diet.

Therefore, it is very important to regularly exercise without lifting weights, give up fatty and smoked foods, fast food, excessive sweets, soda, strong tea and coffee, and alcohol.Avoid wearing clothes that are too tight or uncomfortable high-heeled shoes. While resting in a horizontal position, the legs should be kept slightly higher than the body. And, of course, get rid of excess weight and all addictions, especially tobacco.

How to understand that varicose veins have begun?

If at the end of the day there is a feeling of heaviness in the legs, buzzing, tingling, numbness, burning, edema occur, even just a trace of an elastic band of socks – this already indicates a violation of the exchange of fluid between tissues and blood vessels.Spider veins, discoloration of some areas of the skin, noticeable outlines of large blue veins, cramps that occur during the daytime when walking or while resting – all these are reasons for an immediate visit to the doctor. And for preventive purposes, a phlebologist should be visited once a year.

Photo: ru. depositphotos.com

What happens if varicose veins are not treated?

Most people with the above symptoms do not attach much importance to them.

– When varicose veins appear on the legs, patients believe that it can be cured at any time, and postpone the visit to the doctor, says Dr. Ambaryan.- This is a very big mistake, since varicose veins and its consequences lead to serious complications and even death. For example, venous thrombosis may develop. In 80% of cases, this happens gradually and secretly.

Often, the disease is diagnosed even with the development of life-threatening complications. So, one patient of the clinic “No varicose veins” came for examination when she already had an advanced stage of varicose veins. She ignored him for years. Doctors conducted an examination, did an ultrasound scan and noticed a blood clot.The patient was sent by ambulance to the hospital, where the blood clot was removed on time. If the woman continued to delay with the appeal, everything could end in disaster.

How are varicose veins diagnosed and treated now?

The gold standard for the diagnosis of varicose veins is ultrasound, Doppler and angiography. These methods show the speed of blood flow and help determine its violation in individual vessels. Most often, this is enough for the doctor to make an accurate diagnosis.

At the moment, there are three ways to treat varicose veins.The conservative method is suitable for patients with the initial stages of the disease: it does not reverse the pathological process, but helps to partially eliminate the symptoms of the disease. Minimally invasive treatment – sclerotherapy and percutaneous laser coagulation – is used in the first and second stages of varicose veins. These methods are on the border between surgical and drug treatments.

The most effective outpatient methods for treating varicose veins in the middle and late stages are combined phlebectomy, endovasal laser coagulation and radiofrequency ablation of the great or small saphenous veins.

“Of course, it’s better not to bring the situation to the operative intervention, so you need to listen carefully to your body and be examined in time,” Hrant Ambaryan summed up.

90 000 The risk of thrombosis was recognized as a rare side effect of the AstraZeneca vaccine :: Society :: RBC

The European regulator acknowledged that the risk of blood clots in those who received the vaccine from AstraZeneca is, but called it negligible

Photo: Claudia Alba / Global Look Press

The possibility of blood clots should be listed as one of the very rare side effects of the Vaxzevria vaccine developed by the Anglo-Swedish company AstraZeneca to protect against COVID-19 coronavirus infection.The corresponding decision was made by the Safety Committee of the European Medicines Agency (EMA).

The EMA reports that blood clots, including in the venous sinuses of the brain, are extremely rare, and the overall benefit of the vaccine in preventing COVID-19 infection is much greater than the risk of side effects.

“The EMA confirms that the overall benefit-risk ratio remains positive,” the message says.

According to the EMA, as of April 4, there were 222 cases of thrombosis in the European database, while about 34 million people were vaccinated with the AstraZeneca vaccine in the UK and the rest of Europe. In most cases, blood clots form within two weeks of the first dose of vaccine in women under 60 years of age. However, the EMA cannot name specific risk factors yet.

In this regard, the agency urged physicians to closely monitor the occurrence of signs of thromboembolism and thrombocytopenia in patients.

90,000 Coronavirus vaccinations: Seven people in Britain have died of thrombosis following the AstraZeneca vaccine

• James Gallagher
• BBC Science and Health Correspondent

April 3, 2021

Photo Credit, EPA

90,097 Seven UK residents who were vaccinated against the coronavirus with a vaccine produced by the University of Oxford and the AstraZeneca company died from thrombosis, which arose under atypical circumstances.These data BBC confirmed the British Medicines Control Agency (MHRA). At the same time, there is still no exact data on whether these diagnoses were directly related to vaccination, or became a coincidence.

A total of 30 of the 18 million Britons who received AstraZeneca as of 24 March affected thrombosis.

The British regulator insists that the benefits of vaccination outweigh any risks. The same conclusions are drawn by the World Health Organization and the European Medicines Agency.

“Patient safety remains our top priority,” said a spokesman for AstraZeneca. However, due to concerns about the safety of the vaccine, authorities in several other countries around the world, including Germany, France, the Netherlands and Canada, have decided to vaccinate with this drug only the elderly.

On Friday, the MHRA published data according to which 22 cases of sinus thrombosis of the dura mater (TSTMO) were found among the vaccinated, a rare diagnosis in which blood clots form in the brain.At the same time, a low level of platelets was noted in the blood of these people – elements that, among other things, contribute to the occurrence of thrombosis.

The British regulator also found eight more cases in which patients had other problems associated with thrombosis, but the platelet count also remained low.

Suspicious

The MHRA confirmed in an email sent to the BBC that “seven people [out of 30] have unfortunately died”.

“The benefits of preventing Covid-19 infection and its consequences still outweigh any risks and residents should continue to vaccinate when they receive invitations,” said MHRA head June Rein.

Photo by PA Media

In the meantime, experts continue to study whether the AstraZeneca vaccine can cause such thrombosis, which is usually extremely rare. This week, the European Medicines Agency said it was “not proven, but possible.”

There are two reasons for suspicion.

First, it is the unusual nature of thrombi: they occur when the level of platelets and specific antibodies associated with certain types of thrombosis is low.

“This increases the likelihood that this vaccine could be the causative agent of these rare and unusual cases of sinus thrombosis of the dura mater (DSTM). Although we do not know for sure at the moment, therefore urgent research is needed,” the BBC said. si Professor David Werring of the Institute of Neurology, University College London.

The second suspicious circumstance is the difference between the vaccines produced by AstraZeneca and Pfizer / BioNTech. In the case of the latter, in the UK, there were two cases of TSTMO in more than 10 million vaccinated – and in these patients the platelet count was not low.

However, experts are still not sure exactly how common this type of thrombosis is. Estimates range from two cases per million in a year to nearly 16 cases per million – and this is in the days before the Covid-19 pandemic. That being said, the coronavirus itself has been associated with an increased risk of thrombosis, and it may also cause an increase in the incidence of TSTMO.

90,096 In Germany, there are 31 known cases of TSTMO and nine deaths per 2.7 million people who received the vaccine, with the majority of diagnoses in middle-aged and young women.Data on the specific population groups affected by thrombosis in the UK has not been published, but it is assumed that this is a broader range of patients.

Test

All medications, from vaccines to paracetamol, can cause serious side effects. In one case in a million, routine flu shots are known to cause Guillain-Barré syndrome, a nerve disorder.

Therefore, in this case, the main question is whether the risk is justified?

Even if we assume that vaccines really were the cause of the disease, and this has not yet been proven, statistics indicate the likelihood of one death for every 2.5 million vaccinated.

Let’s compare this data with the proven threat of the coronavirus. If 2.5 million 60-year-old patients fall ill with Covid-19, about 50,000 of them will die. If the same number of 40-year-olds are infected, about 2,500 will die.

90,096 Experts continue to assess this balance between risks and benefits as new data become available and the vaccination program is expanded to younger people who are less at risk of dying from Covid-19.

Is there a connection?

As Professor Paul Hunter, a microbiologist at the University of East Anglia, told the BBC, there is growing evidence that thrombosis may indeed be related to AstraZeneca, but the benefits of vaccination still far outweigh the risks.

“Cases when foci of rare diseases occur completely by accident are known. But when such a focus is found in one country, and then it appears in another – as in the case of Germany, and now – with England, it seems to me that the probability of an accident the overlap here is very low, “says Hunter.

“Obviously, more research is needed, but it seems to me that now the evidence is starting to speak in favor of the fact that there is a causal relationship,” – says the expert.

However, health expert Professor Linda Bould of the University of Edinburgh told the BBC that thrombosis “rarely occurs” and “there is currently no reason to talk about a causal relationship. the vaccine produces these results. ”

She urged residents of the country to be vaccinated and added: “Covid itself significantly increases the risk of thrombosis, and it is possible that this may have to do with the reasons for what we are seeing.”

Scientists say they have found the cause of blood clots after vaccination with AstraZeneca. And it can be overcome | Hromadske TV

This is reported by The Wall Street Journal.

Scientists from the Norwegian University of Oslo claim that the cause of thrombosis in vaccinated patients was a strong immune response to the drug. In Norway, thrombosis was found in three women after vaccination, one of them died.

Professor Andre Holm then explained that specific antibodies to platelets were found in the woman’s blood, which caused thrombosis. “Nothing else [other than the vaccine] that the patients were taking could have produced such a strong immune response,” , he noted.

Scientists from the Greifswald University Hospital in Germany came to a similar conclusion. According to them, the AstraZeneca vaccine in rare cases can lead to the formation of antibodies that cause thrombosis.

“This complication will occur in a very, very small number of people. But if it happens, we now know how to treat such patients , ”Professor Andresa Grainacher said at a press conference.

German scientists propose to administer to patients who develop thrombosis after vaccination, immunoglobulin (intravenously) and anticoagulants – drugs that prevent blood clotting.

AstraZeneca and blood clots

In early March, a number of countries temporarily suspended the AstraZeneca vaccine following reports of possible side effects. However, not all countries decided so. For example, Austria has refused only a few batches of vaccines, but Belgium, Poland and the Czech Republic have indicated that they will continue to vaccinate AstraZeneca.

The World Health Organization and the European Medicines Agency (EMA) reported that no link has yet been found between vaccination with the coronavirus drug from AstraZeneca (including CoviShield) and health problems that arose after vaccination.

At the same time, the EMA noted that the connection between the AstraZeneca vaccine and the occurrence of blood clots is quite possible, but they added that it requires further research, so it cannot yet be unequivocally asserted.Since then, at least 10 European Union countries have decided to renew the use of AstraZeneca.

Special equipment against blood clots appeared in the reserve hospital at VDNKh

More than 200 pneumatic compressors were purchased for the intensive care unit of the reserve hospital in Pavilion 75 of VDNKh. The equipment will reduce the risk of venous thromboembolism in patients in intensive care.

“The presence in the hospital of such a life-saving resuscitation equipment, high-quality consumables and an implemented large-scale scheme for the delivery of oxygen with volumetric gasifiers once again confirms that the reserve hospital at VDNKh is equipped with all the necessary equipment that allows it to provide assistance to patients at the level of multidisciplinary hospitals,” he said Marat Magomedov, head of the intensive care unit at the reserve hospital at VDNKh.

The pneumatic compression device is a special leg cuff. The device simulates muscle contractions that occur in a person when walking or running. Wave-like movements from the bottom up, created by air pressure, help to improve lymph and blood flow, which prevents the formation of blood clots. Such devices prevent the development of fatal complications in patients who are being treated in intensive care and are forced to be motionless for a long time.

The reserve hospital at VDNKh has created a unique reanimation complex of 208 beds, equipped with expert-class breathing, monitoring and diagnostic equipment.Along with modern resuscitation equipment, a stationary computer tomograph Canon Aguilion Prime SP with 128 slices is installed in the block, endoscopic rooms are provided, there are two reception departments, there are water treatment rooms for hemodialysis and temporary storage of blood components.

Clinical diagnostic and microbiological laboratories are also functioning. Conditions for comfortable stay of patients have been created in the wards; beds are equipped with mattresses and other devices for the prevention of pressure sores.

In Moscow, patients with COVID-19 are admitted to five reserve hospitals opened in the Krylatskoye Ice Palace, Sokolniki Exhibition and Convention Center, Moskva Automobile Trade Center, Pavilion No. 75 at VDNKh and a hospital on the territory of the medical complex in Kommunarka. They are assigned to GKB No. 67, GKB named after F.I. Inozemtsev, S.S. Yudin and City Clinical Hospital No. 24. More than six thousand beds have been created in them.

Why are blood clots dangerous? – Articles

Thrombosis is so insidious that it may not be felt for a long time…

Thrombosis is so insidious that it may not make itself felt for a long time, and then lead to sad consequences. What is the nature of the blood clot, why these formations are so dangerous and how to identify them, said surgeon-phlebologist Andrei Maryasov.

– What is thrombosis?
– Thrombosis is the formation of dense masses of blood. They are able to block the vessels, move along them with the blood flow (for example, from the vessels of the lower extremities to the pulmonary artery) and can be fatal.

– Why do blood clots form?
– In order for the blood to clot and form a thrombus, 3 conditions must be met: violation of the integrity of the inner wall of the vessel, slowing down of blood flow and change in blood viscosity.
The prerequisites for this triad are different: taking hormonal drugs or hormonal imbalance, inactivity, some chronic diseases, injuries (for example, with prolonged wearing of plaster cast), extensive surgical interventions, varicose veins, and others.
By the way, studies have shown that varicose veins increase the risk of deep vein thrombosis of the lower extremities by 5 times. Also, statistics show that the vast majority (more than 90%) of thrombosis is associated with deep veins of the lower extremities. Blood clots formed in these vessels are able to migrate and move to the heart, pulmonary artery.

– How can you suspect you have a thrombosis?
– Some blood clots do not manifest themselves in any way, but in most cases, thrombosis is an acute condition.There is swelling of the extremity (if we are talking about deep vein thrombosis of the legs) and bursting pains, the temperature of the extremity decreases, and this condition requires an urgent call for an ambulance.
Superficial vein thrombosis is less dangerous and has pronounced symptoms: edema, redness, soreness in the vein projection. In this case, it is easier to diagnose and treatment can be started faster. With such symptoms, they turn to the surgeon, and urgently, otherwise the disease progresses and the thrombus can go into deep veins.

– Are there degrees of complexity of the disease, when will prevention help, when – medications, and when – only surgery?
– It depends on the blood clot itself. If it is floating, that is, there is an unattached element in the lumen of the vein, there is a high risk that it will come off, especially if it is more than 7 cm. In such cases, hospitalization and surgery are needed.
Thrombi of a small length, securely attached to the walls of the vessel, are treated with medication.But in order to identify the type of blood clot, it is imperative to undergo an examination, do an ultrasound or MRI of the vessels and start treatment.

– How long does a thrombus “mature” and why does it come off?
– It happens very quickly, blood coagulates in seconds. Blood clots tend to enlarge, so they can grow. And the separation occurs because the part of the thrombus that is not attached to the wall becomes too long and heavy.
A fresh blood clot is a soft, jelly-like structure, therefore, blood clots are most dangerous in the early days.Gradually, the formation becomes denser, becomes stronger, and the risk of a thrombus rupture decreases.

– Is the separation of a blood clot always fatal?
– Not always. Sudden death occurs if the blood clot is very large and, breaking off, it closes the entire lumen of the vessel. But small blood clots are also dangerous: they can, for example, block small pulmonary arteries and lead to partial death of a segment of the lung.

– There are many tips on the Internet on how to thin the blood.Some people advise drinking Aspirin. What blood thinning tips work and are universal?
– No drugs can be drunk without a doctor’s prescription, and even more so – to diagnose an increased blood clotting in oneself. Only a doctor can come to this conclusion after studying the patient’s coagulogram, and if a high blood viscosity is found, medications are prescribed if necessary.

Prevention of thrombosis is an active lifestyle, correct drinking regimen and wearing compression hosiery for people with chronic diseases (for example, varicose veins).

Still have questions? You can make an appointment with a phlebologist.

Treatment (removal) of thrombosis of hemorrhoids

What is acute external hemorrhoidal thrombosis (perianal venous thrombosis, acute external hemorrhoids)?

Acute thrombosis is a sudden-onset disease caused by the occurrence of blood clots in the venous plexuses of external hemorrhoids, which are located at the exit from the anal canal (Fig.1 and 2). Thrombosis is accompanied by swelling of the surrounding tissue, irritation of the skin and anal sphincter, which often leads to acute pain in the anal canal. Complicated thrombosis, as a rule, is accompanied by local necrosis of the skin over the thrombosed hemorrhoid and is accompanied at the beginning of its development by more vivid symptoms, however, after the onset of necrosis, painful sensations quickly subside if there is no thrombosis of nearby plexuses or edema or inflammation of the surrounding tissues does not develop.Sometimes, a small amount of blood is released through the resulting skin defect.

Fig. 1. Uncomplicated thrombosis of the external node

Fig. 2. Acute thrombosis of the external hemorrhoid with necrosis of the skin area above it.

What are external hemorrhoids? A bit of anatomy

External hemorrhoids (plexuses) are formations located under the skin at the border of the anal canal and perianal (around the anus) skin.They represent the venous plexus (Fig. 3). Usually they do not manifest themselves in any way, are not visible and are not defined by touch. As chronic progression worsens

internal hemorrhoids in the external changes occur, leading to their increase and loss of connection with the muscle ring of the anal canal. However, the most significant changes in the external nodes occur when a thrombus occurs in them.

Fig. 3. Diagram of the anal canal, at the exit from which external hemorrhoids are located (number 7 in the diagram).

How does acute external hemorrhoidal thrombosis manifest?

Patients with acute thrombosis of the external hemorrhoid complain of bulging, “bumps” (neoplasms) and / or pain of varying intensity in the anus. The size of the “bump” can be from several millimeters to several centimeters and is often accompanied by edema of the surrounding tissues (up to the entire circumference of the anal canal). In some patients, the disease proceeds without pain, but most of the pain is assessed as significant or intolerable.

To assess the degree of pain, a special visual analogue scale is used, in which you can independently determine the severity of pain. After all, this is the key point when choosing a treatment method. Surgical treatment will be most effective when the severity of pain is 7 or more points, while with pain up to 4 points, a conservative method of treatment can be considered optimal.

Fig. Visual analogue scale for assessing pain.

Pain is usually worse during bowel movements (bowel movement) and / or while sitting.The pain and swelling can be very severe, even unbearable for several days. The intensity of pain depends on the size of the blood clot and its location in relation to the muscles of the anal sphincter. In general, the manifestations of the disease can persist for several weeks, in exceptional cases even longer. Sometimes there is an independent evacuation of the thrombus from the hemorrhoid. This is preceded by necrosis (destruction) of the skin over the thrombus, and the thrombus “falls out” from the node. Outwardly, this is accompanied by the feeling of a “burst” ball, the release of a small amount of blood.Usually, after the evacuation of the thrombus, the pain sensations sharply decrease and the feeling of discomfort in the anus area gradually decreases. However, the necrosis of the mucous membrane over the thrombus does not always end with the evacuation of the thrombus, the necrosis can continue to spread to the hemorrhoid itself and the surrounding tissues, which is why this condition requires a specialist consultation. After the acute thrombosis has subsided, the patient most often has the so-called “cutaneous fringes” – excess skin where there was thrombosis.They do not require medical treatment, but they can cause cosmetic discomfort.

What causes acute thrombosis of the external hemorrhoid?

The cause of thrombosis is more often the overflow of the veins of the external hemorrhoidal plexus with blood, followed by a slowdown in blood flow in these vessels and the appearance of blood clots. Thrombosis against the background of venous congestion most often develops after a sharp or prolonged exertion. Lifting weights, straining for constipation or diarrhea, and childbirth are classic examples.Chronic stagnation of blood in the pelvic organs (which includes the anal canal) occurs with prolonged sitting, overweight, insufficient physical activity.

How to distinguish acute thrombosis of the external hemorrhoid from other diseases?

Usually, to diagnose acute thrombosis, it is enough to examine the patient and find out how the disease developed and what complaints are of concern. On examination, you can see an enlarged (sometimes up to several centimeters) knot located to the outside of the anus, possibly with a focus of necrosis in the center, often of a dark red color.When palpating (feeling) in the first few days, it is possible to clearly identify a thrombus in the node, when viewed at a later date, the thrombus is no longer so easy to determine, it begins to gradually “dissolve” and is partially replaced by scar tissue. External hemorrhoidal thrombosis must be distinguished from

infringement of a prolapsed internal hemorrhoid. In this situation, the internal hemorrhoidal node, normally located inside the anal canal, falls out, its legs are compressed, in which the vessels feeding it pass and the blood supply (ischemia) is disturbed, with the tissue of the node dying off (Fig.4 and 5). It is not difficult for a specialist to distinguish these conditions, but it is quite difficult for a patient to understand which node is causing him discomfort on his own. It is important to distinguish between these diseases, as their treatment varies considerably. When the internal hemorrhoid is infringed, as a rule, urgent surgical treatment is required.

Fig. 4. Restrained fallen out internal hemorrhoidal node with symptoms of tissue necrosis of the node.

Fig.5. A schematic representation of an infringement of an internal prolapsed hemorrhoid.

Acute (exacerbation of chronic) anal fissure – accompanied by the same pain syndrome as in thrombosis, but much more pronounced at the time of bowel movement. With this disease, there is a rupture of the mucous membrane of the anal canal. The appearance of an acute crack is often associated with a reflex “protective” spasm of the sphincter apparatus, which complicates wound healing. Conservative and surgical treatment of diseases is different.

Acute paraproctitis – similarity to acute thrombosis consists in the appearance of a mass in the anus, severe pain syndrome. Paraproctitis is an infectious and inflammatory disease with the formation of an abscess (abscess) in the pararectal region. The disease is accompanied by an increase in body temperature, general symptoms of intoxication. A mass in the anal canal is much larger and more painful than with thrombosis. There is often a discharge of pus on the skin or into the rectal lumen.An ultrasound examination is used for accurate diagnosis. The disease is extremely dangerous by the development of chronic purulent fistulas of the perianal region in the absence of adequate and timely treatment.

Should acute external hemorrhoidal thrombosis always be treated?

The choice of a method of treatment for this disease is one of the most controversial issues in general proctology. Like hemorrhoids, acute thrombosis does not turn into cancer, does not cause fatal complications, but can significantly affect the patient’s quality of life, often the pain syndrome is described as “unbearable”, with which it is “simply impossible to live.”

In our Clinic, a patient-oriented approach has been adopted to the choice of a method for treating acute thrombosis of external hemorrhoids: the doctor together with the patient determine how severe the symptoms are, how much the patient’s quality of life suffers, taking into account his employment and choose the method of treatment.

Acute thrombosis of the external hemorrhoid can be treated promptly (perform an operation), conservatively (take pills and use topically ointments and / or suppositories), or not at all, but choose a wait and see tactic.Research and practical experience show that surgical treatment allows you to get rid of the manifestations of the disease in a shorter time, conservative treatment is also allowed to get rid of the manifestations of the disease, but for a much longer time. The absence of any treatment also ends with recovery, the timing of which only slightly differs from the timing of intensive conservative treatment. The choice of the method of treatment is decisive in the choice of the patient and his assessment of the severity of the pain syndrome, therefore, the patient’s opinion is crucial for the choice of tactics.If the patient assesses the pain as unbearable, or he urgently needs to return to work, fly to another city or country, it is wiser to choose surgical treatment in the amount of removal of the hemorrhoidal node or evacuation of a blood clot from the node. Surgical treatment usually results in faster relief of unpleasant symptoms. If the pain syndrome allows the patient to fully live in this condition or the patient is not ready for surgery, it is possible to carry out conservative treatment aimed at reducing the pain syndrome and accelerating the process of organizing and resolving the thrombus.

How is acute external hemorrhoidal thrombosis treated?

Possibilities of surgical treatment

There are two main operations for the treatment of acute thrombosis of the external hemorrhoidal node: removal of the entire node or only a thrombus from it. The first operation is called economical (partial) hemorrhoidectomy (removal of only the external hemorrhoid), the second is thrombectomy. Both operations are effective from the point of view of eliminating the pain syndrome within 2-3 days after their completion, however, after the operation to evacuate a thrombus, a relapse (re-emergence of a thrombus) is more common.

Economical (partial) hemorrhoidectomy of a thrombosed node is a dissection of the skin around the node, its isolation and removal along with a thrombus. The operation can be performed under local anesthesia.

After removal of the hemorrhoid, a small wound surface is formed, which can cause pain, especially during bowel movements. But usually the pain is much less pronounced than in the presence of a thrombosed node, and only sometimes requires taking pill painkillers.

Thrombectomy is performed through an incision in the skin over the thrombus, after which the thrombus is removed and 1-2 sutures can be placed at the incision site. This intervention is almost always performed under local anesthesia.

Conservative treatment

Conservative treatment (tablets and local remedies – ointments and suppositories) is mainly aimed at relieving pain caused by a blood clot, reducing swelling and inflammation of the hemorrhoid, and normalizing the frequency and quality of stools.In pharmacies, there are a large number of drugs for the treatment of hemorrhoidal disease, but they are all approximately equal in effectiveness and can be used to treat acute thrombosis of the external hemorrhoid. Local remedies (ointments and suppositories) mainly have anesthetic, anti-inflammatory effect. Topical agents with an anticoagulant effect in the treatment of acute thrombosis are effective only for temporary prevention of the occurrence of new thrombi or, if the drug contains an anesthetic component, for pain relief.The tablets are also used to relieve pain (non-steroidal anti-inflammatory drugs, paracetamol) and to normalize venous blood flow in the pelvis (in the rectum), such as flavonoids. In addition, conservative treatment is carried out after surgery to eliminate possible postoperative symptoms. The conservative treatment regimen can only be determined by a specialist, and it is better to select a combination of drugs in each specific case, depending on the characteristics of each patient.

Do I need to prepare for surgery?

In most cases, it is possible to perform the operation on an outpatient basis under local anesthesia, i.e.That is, no hospitalization is required for treatment. However, it is still better for some patients to perform the operation in the operating room, for this you will need the standard tests and examinations necessary for hospitalization. No special bowel preparation is required for the operation.

What will happen after the operation?

Usually, patients feel a sharp relief after the operation and notice a decrease in pain syndrome (Fig. 6). Occasionally, continued minimal pain management is required.The main task of the patient in the postoperative period is stool normalization: soft stools cause much less painful sensations during bowel movement than dense ones. As a rule, patients return to their usual life 2-3 days after the operation, sometimes the very next day.

a)

b)

Fig. 6. View of the anus area before (a) and immediately after removal of the external hemorrhoid (b). Before the operation, the patient rated the pain level as 8 out of 10, immediately after the operation 4 out of 10.

Are there ways to prevent relapse / recurrence of the disease?

Prevention of recurrence of the disease is based on the exclusion of possible causes of thrombosis. Among them are tight stools, constipation or diarrhea, “reading in the toilet”, insufficient or, on the contrary, excessive physical activity (weightlifting, fitness), prolonged sedentary work. Unfortunately, there are no unambiguous methods for preventing the occurrence of acute thrombosis of the external hemorrhoid; we can only reduce the likelihood of its occurrence, but not completely exclude it.However, it should be noted that with conservative treatment, the likelihood of recurrence of the disease is higher than after the operation.

What should pregnant women and parturient women / women in labor with acute thrombosis do?

According to statistics, about a quarter of pregnant women and almost half of women in childbirth are faced with various manifestations of hemorrhoidal disease, the most painful of which is acute thrombosis. Usually, women in childbirth and especially pregnant women, in response to their complaints to the doctor, hear an offer to be patient.This approach is dictated by the fact that there are many contraindications to the use of the vast majority of drugs in pregnant women, and surgical intervention is regarded by the medical community as a factor that can provoke childbirth or stop breastfeeding. In practice, this means that regardless of the severity of the pain syndrome, sometimes very significant, women are forced to remain without any effective treatment. Pain due to thrombosis, in turn, can worsen the psychological state of pregnant or postpartum women and lead to undesirable consequences during childbirth (premature birth) or during breastfeeding (refusal to breastfeed).Our clinic is a supporter of a personalized approach to the treatment of acute thrombosis in these women. If acute thrombosis categorically interferes with the patient’s life, it should be actively treated using the entire arsenal of drugs used in ordinary patients, but taking into account the contraindications for drugs. In pregnant women in the II and III trimesters, it is possible to perform an operation to remove a thrombosed node (Fig. 7), as well as in postpartum women and women in labor (Fig. 8). During pregnancy, there are some restrictions on the drugs of local and general anesthesia that can be used.Specific medicines should be chosen jointly by both the coloproctologist and the obstetrician, so as not to harm the fetus or newborn. The specialists of our Clinic have experience in the treatment of both pregnant and postpartum women with manifestations of acute hemorrhoidal thrombosis with very good results, reviews of which our patients leave on our website as well.

a)

b)

Fig. 7. Acute thrombosis of the external hemorrhoid in a pregnant woman of 38 weeks.

Before surgery, pain syndrome was rated at 8 out of 10, immediately after surgery 3 out of 10.

a) appearance of a thrombosed external hemorrhoidal node with necrosis, b) appearance after removal of the thrombosed node.

a)

b)

Fig. 8. a) acute thrombosis of the external hemorrhoid with severe edema in the patient on the 5th day after childbirth, b) the patient’s condition on the 7th day after the operation. On the first day after the operation, the pain syndrome decreased from 9 to 4 out of 10.

You can read about the treatment of other manifestations of hemorrhoidal disease in pregnant women and women in childbirth in section Hemorrhoids in pregnant women .

What to do if you have undergone conservative treatment for thrombosis

The abundance of funds for the conservative treatment of thrombosis and often the physician’s disposition to use this technique leads to the fact that most thrombosis is treated conservatively. Patients come to our Clinic at different stages of the course of conservative therapy.Often this is a situation when conservative therapy was started immediately after the onset of a thrombus, there was some relief of the condition, pain syndrome decreased, but there remains a “bump” in the anus, some pain. Sometimes quite healthy people come who have experienced an episode of acute thrombosis several months or years ago and now they are worried about the presence of skin “fringes”, excess skin in the anus, which remain after the resolution of the acute condition. They can interfere with the quality of the hygiene of this area, affect the intimate life.What to do in this situation? And again, the main thing for the doctors of our Clinic will be the opinion of the patient. If you want to get rid of the manifestation of acute thrombosis, even if conservative treatment has already been carried out, a lot of time has passed – this can be done surgically.

Can thrombosis prophylaxis be carried out?

Unfortunately, there is no unequivocal recommendation, compliance with which would allow preventing thrombosis with a high probability. Stool normalization, “no library in the toilet”, refusal to engage in weightlifting – reduce the risk of acute thrombosis, but do not fully guarantee that thrombosis will not reappear in one of the external hemorrhoids.