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Saturday, November 19, 2016

5.5 Million Clicks on This Blog

I just realized that we are now over 5.5 million views on this blog. That's pretty impressive, at least I think so. For a blog that I started on October 13, 2007, just so I could have something to do while working the night shift, that's pretty good.

Here we are, nine years later. I knew that I was going to focus on respiratory, but I had no idea what specific topics I was going to cover. I had no idea that this blog would take off the way it did, and the other opportunities that would transpire as a direct result of this blog.

I wrote my first post about a Beeper. How stupid! Much of my earlier writings were poorly written. Still, I was dedicated to it and would end up publishing at least one post every day for the first five years.

About a year after I started this blog, I received an email from a publisher at healthcentral.com. She wrote: "I love your blog. I especially love your humor. I love the way you write about 'stupid doctor orders,' and 'Bronchodilator reform.' We would love to have someone like you writing for us. We are willing to pay."

Of course, when you get emails like this, your first quest is to make sure it's real and not spam. This would spawn a writing career at healthcentral.com for the next seven years, and now at asthma.net and copd.net.

I have not been writing so much for this blog in recent years. This is not because I don't want to, more so that I now work day shift, have two more kids than I had back then, and don't have as much time for telling the truth about the respiratory therapy profession.

I would like to thank everyone who comes around here once in a while to see if there's anything new. I thank all those who have come here in the past. I thank all those of you who have written me emails or written comments such as, "I love your blog." It motivates me.

I will probably take a break for a while, but chances are pretty good I will keep this blog going. If you have questions, I will continue to answer them. In the meantime, I just want to say, "Thank YOU!!!" Thank you for making this blog such a success. The RT Cave is still the most popular respiratory therapy blog on the Internet, and that's all because of YOU. Thanks!

Monday, October 17, 2016

Debunking The Hypoxic Drive Theoery: The Truth About The Affects Of Oxygen On COPD

Originally published January 6, 2016.

I was recently interviewed by Rebecca Knutsen, a staff writer working for Advance for Respiratory Therapists.  She said she was working on a brief article that explores when to administer oxygen to hypoxemic patients with chronic obstructive pulmonary disorder.

The following are her questions followed by my answers.  

1.  Please describe hypoxic and hypercapnic drive:

Hypercapnic Drive: The central chemoreceptors on the medulla monitors the partial pressure of arterial CO2 (PaCO2). A normal PaCO2 level is 35-45 mmHG. When PaCO2 is high (>45 mmHg) a signal is sent to the medulla oblongata at the base of the brain to speed up breathing in order to blow off excess PaCO2. When PaCO2 levels are low (<35 mmHg) a signal is sent to the medulla oblongata at the base of the brain to decrease breathing in order to allow PaCO2 to accumulate. This is the main drive to breathe.

Hypoxic Drive: The peripheral chemoreceptors located at the bifurcations of the aortic arteries and the aortic arch monitor partial pressure of arterial oxygen (PaO2). This drive only becomes active when the PaO2 is less than 60 mmHg. This hypoxic response is far slower than signals sent by central chemoreceptors, and therefore the hypoxic drive has only a minor role in breathing.

2.  What tests does your organization use and what do they measure?

ABG: This is a blood draw from the radial, brachial or femoral artery that measures PaO2, PaCO2 and arterial pH.

Pulse oximeter: It’s a noninvasive device that slips over a finger, toe, or ear lobe. It determines the SpO2, which is an estimation of hemoglobin in the blood that are saturated with oxygen. This percentage can be used to estimate PO2. Generally, an SpO2 of 90 indicates the PO2 is about 60.

End Tidal CO2 Monitor: It’s a noninvasive device that can be connected to special nasal cannulas or endotracheal tubes. It determines the ETCO2, which is an estimation of the amount of CO2 exhaled. This percentage can be used to estimate PaCO2. In a person with healthy lungs, the EtCO2 is about 2-5 mmHg less than PaCO2.

3.  When is it recommended to administer oxygen to hypoxemic patients with COPD? 

Most medical experts now recommend administering the lowest amount of oxygen needed to maintain an SpO2 of 88-92%, or as directed by a physician.

4.  Why is hypoxic drive so controversial? 

The hypoxic drive is not controversial, it’s the hypoxic drive theory that’s controversial. To understand why it is so controversial it’s important to understand a little of the history of it. 

Back in the late 1940s and 50s, when oxygen first started to be used for patients with chronic obstructive pulmonary disease, it was observed that some of them became lethargic or lapsed into a coma after receiving high levels of oxygen.

Initial studies showed a decrease in ventilation in 26 of 35 patients with COPD given oxygen therapy, with a rise in CO2 and a fall in pH. A further study showed that stopping and starting oxygen therapy led to a fall and rise in CO2 respectively.

The concern became so great that in the 1950s a study was performed that ultimately lead Dr. EJM Campbell to give a lecture to pulmonologists in 1960 about the dangers of giving too much oxygen to COPD patients. It was this lecture that forever linked hypoxic drive with COPD, and gave birth to the hypoxic drive theory.

What is the hypoxic drive theory? The hypoxic drive theory states that some patients with COPD develop chronically elevated arterial CO2 levels, and so their hypercapnic drive becomes blunted, so they use their hypoxic drive to breathe instead. 

Therefore, giving high amounts of oxygen to these patients may blunt the hypoxic drive as well, thus completely blunting their drive to breathe. This may cause PaCO2 levels to rise to critical levels, resulting in narcosis and possible death. For this reason, COPD patients with suspected CO2 retention are limited to 2-3 lpm by nasal cannula, or 40% by venturi mask.

What’s wrong with this theory? The problem with this theory is that it’s a myth concocted on incomplete evidence. The study cited by Campbell included only four patients with COPD, and later studies failed to validate this theory. Yet it has continued to be a gold standard theory when dealing with COPD patients.

Under the guise of this theory, many patients who desperately need higher levels of supplemental oxygen to survive are deprived of it. Plus, as many respiratory therapists, nurses, and physicians have observed, when these patients are given the oxygen they need, rarely does this lead to complications.

When these patients go into respiratory failure, it’s going to happen regardless of how much oxygen they receive. And while higher levels of oxygen may cause CO2 to rise, it’s not due to oxygen blunting their hypoxic drive, which the hypoxic drive theory postulates, it’s due to either the Haldane effect or V/Q mismatching.

The Haldane effect: This was postulated by John Haldane, a pioneer in oxygen therapy. He proved that the Deoxygenation of arterial blood increases its ability to carry carbon dioxide. In other words, as fewer oxygen molecules are attaching to hemoglobin, more CO2 are attaching to hemoglobin.

Oxygen is more soluble in water and therefore has a higher affinity for hemoglobin, so if you increase oxygen in the blood, CO2 molecules are forced off hemoglobin and oxygen takes its place. This causes an increase PaCO2.

Add into this the fact that patients with COPD have limited reserves to increase their respiratory rate to blow off excessive CO2. Also add into this that many COPD patients already have an elevated hemoglobin levels, and so these patients are going to have lots of extra arterial CO2 molecules.

Out of respect for this theory, COPD patients should be maintained on the lowest level of oxygen required to maintain an oxygen saturation between 88-92%.

The Haldane effect was proven by a study described in 1996 in Critical Care Medicine, "Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease."

V/Q Mismatching: The air passages of COPD lungs become narrow due to remodeling, increased mucus production, and bronchospasm. Where this occurs the lungs are perfused but poorly ventilated. CO2 returning to these areas remain in arterial bloodstream, thus causing PaCO2 to rise.

Add into this that when alveoli are poorly ventilated the vasculature around them will constrict so oxygen goes to alveoli that are ventilated well. This is how these patients make efficient use of their diseased lungs.

Now add 100% oxygen and you screw up this naturally occurring phenomenon. Now the vasculature around that non-ventilating alveoli dilates, and this causes blood to be sent to the non functioning alveoli. Now you have even greater V/Q mismatching and more CO2 that doesn't get out of arterial blood. The end result is an increase in PaCO2.

If a patient with COPD is going to fail this is going to be the reason. If they need oxygen you give it to them, because doing otherwise will further compromise them. If they go into respiratory failure, you treat it with either noninvasive ventilation or mechanical ventilation.

V/Q Mismatching was proven via a study completed in 1980 and reported in American Review of Respiratory Disorders, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure,"

Conclusion: Modern evidence suggests that the hypercapnic drive is never completely blunted, and therefore even COPD patients with chronically elevated PaCO2 will not stop breathing in the presence of higher oxygen levels. There is such a thing as the hypoxic drive, but the hypoxic drive theory is a myth.

To read the final published version of my interview read "Oxygen and COPD: Debunking the hypoxic drive theory."

Further References:
RT Cave Facebook Page
Rick Frea's Facebook
RT Cave on Twitter
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Wednesday, July 6, 2016

Bronchiolitis: Everything you need to know

Bronchiolitis, otherwise known as Respiratory Syncycial Virus (RSV), is a condition common in children that have symptoms very similar to asthma, and is most common between November and April.

It's more common in children because their airways are smaller and more susceptible to narrowing. Usually it occurs within the first two years, with it's peak at 3-6 months.This condition presents nearly identical with asthma, and is often treated or misdiagnosed as such.

In fact, according to "Allergy and Asthma: Practical Diagnosis and Management," it is "clinically indistinguishable from bronchial asthma."Yet the course of treatment for bronchiolitis is different from that of asthma.

For instance, while corticosteroids and bronchodilators work great to reverse airway obstruction caused by asthma, these medicines do little for bronchiolitis (or RSV). So it's important to be able properly diagnose RSV from asthma.

According to Allergy and Asthma, "there are laboratory studies designed to identify viral antigens to pinpoint any of the six different viruses that can cause acute bronchiolitis." This test starts by the RN, RT or lab technician performing a nasal swab to retrieve cells from the nasal passage.

A viral swab won't rule out asthma, but it can rule in RSV so proper treatment can be
determined. Other viruses that might cause bronchiolitis are: Adenovirus, enterovirus, Influenza virus and Chlamydia pneumoniae.

So, technically speaking, RSV is common cause of bronchiolitis, and not a synonym for it. Yet the two are usually linked hand in hand.

We know that asthma is a disease that causes airway narrowing due to increased secretions and inflammation of the air passages in the lungs (bronchioles) due to exposure to asthma triggers. This results in bronchospasm that is reversible with time or, when more severe, bronchodilators such as Albuterol. Corticosteroids are used to treat the inflammation.

Bronchiolitis, on the other hand, is inflammation of the bronchioles due to a virus. (click here for a good picture of this). Narrowing of the airways can occur, resulting in air trapping and hypoxia.
Another complication of this is increased secretions. Bronchospasm is not a complicaiton of bronchiolitis, and therefore bronchodilators are of little use.

Bronchodilators are of little use for bronchiolitis because this medicine does not treat inflammation, it treats bronchospasm.

However, if asthma is suspected to be exacerbated by a virus (and viruses are the #1 cause of asthma exacerbations), bronchodilators should be ordered prn, or as needed.

I have heard of some doctors prescribing Atrovent for bronchiolitis. Our Pediatricians seldom use this, however our ER doctors do.

However, according to Glenn Campell, RRT and Respiratory Clinical Specialist at Children's Hospital in New Orleans, Atrovent should rarely be used to treat asthma and bronchiolitis because "it has been our experience that Iprotropium Bromide (Atrovent) will actually exacerbate the issue by possibly causing mucus plugs secondary to "thickening of secretions".

This, however, is also controversial.

Since there isn't much we can do to treat viruses, the main treatment is supportive measures.

Usually patients with this don't need to be admitted, and usually those admitted for it are obligate nose breathers and are dehydrated due to the child being unable or unwilling to take in fluids, such as refusing to breast feed, or refusing the bottle. So IV fluids is usually indicated.

Antibiotics usually are of little use unless a bacteria is the suspected cause (which is rare).

Otitis media may, however, be treated with antibiotics.

Studies show that bronchodilators should be tried, but if no improvement is observed these should be stopped.

Corticosteroids are also often used to treat this condition, however most studies show they have little to no effect on bronchial inflammation due to a virus.

However, some studies show that racemic epinepherine and dexamethasone have shown to be beneficial.

Still, most of the above therapies other than supportive measures remain controversial.

Supportive care may include oxygen and humidity, keeping the head upright, fluid intake (IV may be indicated), and constant monitoring of pulse oximetry to maintian an SpO2 between 91 and 94%.

One of the most effective therapies for bronchiolitis is simply clearing the airway of secretions, . A bulb syringe works nice, although in the hospital booger be gones work very well. Many times, if the SpO2 drops, suctioning alone will resolve the problem.

Nasal Steroid and Neosynephrine also work well to help keep the nasal passages open.For decreased sats and increased respiratory distress, suctioning should always be attempted before a breathing treatment, and many times suctioning alone will resolve the crisis. According to emedicine, the following are common symptoms of RSV:
  • Runny nose
  • Cough
  • Low grade fever
  • Increased work of breathing
  • Wheezing
  • Cyanosis
  • Grunting
  • Noisy breathing
  • Vomiting, especially post-tussive
  • Irritability
  • Poor feeding or anorexia
  • Increased Respiratory rate (50-60 breaths per minute)
  • Increased heart rate
  • Diffuse expiratory wheezing
  • Nasal flaring
  • Cyanosis
  • Inspiratory crackles
  • Ear infection (otitis media)
There is evidence that children who experience RSV are at an increased risk to develop asthma later in life. For more information, check out the following links:

National Guideline Clearinghouse: Guidelines for management of bronchiolitisRC Journal: Respiratory Care of Bronchiolitis Patients: A Proving Ground for Process ImprovementSeattlechildrens.org: Bronchiolitis

Everything RTs need to know about Sepsis

This post was originally published on January 29, 2008. It is part of the classics of the RT Cave collection. While some of this is outdated, most of it is not.

So, in our quest to become more well rounded therapists, we must now look into another common condition, a condition that is the leading cause of death in critical care units.

For starters, we need to know that is is the leading cause of death in critical care units. Of the 750,000 patients it effects every year, 250,000 will die. These statistics cannot, and are not, being ignored. Hospitals continue to work overtime to create guidelines to help caregivers both recognize and diagnose sepsis so those who have it can get the treatment they need. Likewise, efforts can be made to recognize who is at risk for developing sepsis so it can be prevented.

These statistics have gone pretty much unchanged since the early 1980s. So, even with modern knowledge and technology, hospitals have been unable to break this trend. Yet they are, as noted above, working overtime to do just that.

But there is another side of sepsis that we must look at, and this is the financial side. While the experts will tell you and me that they are working overtime to make changes that improve lives, the bottom line is usually money. And this is the case here as well. For instance, according to the MUST protocol (which is now outdated, and the link is outdated as well), cost estimates nationwide tend to scale into the $17 billion category. I'm not sure what the data is for each individual hospital, but I imagine it's a lot of money, most of which hospitals eat.

So, sepsis is expensive. Actually, we can probably go deeper than this, and say that Medicare probably forced hospitals to look at this. Now, many hospitals had already begun their own research into it, but the government seemed to force their hands, so to speak. I'm not blaming government here, I'm just saying, sepsis kills, it costs a lot of money, and efforts are ongoing to improve upon them.

So, with the hope that hospitals would create sepsis protocols (many are now well beyond a gamut of committee) of their own, the MUST protocol was created to be used as a guideline protocol. According to the protocol itself, most hospitals have not adapted it (although this has changed since the original publication of this article). but I do know that many hospitals are looking into creating their own sepsis protocols (most already have).

So, what is sepsis. It's caused by an injury. Your body is infected by a pathogen, most likely a bacteria. Your immune system recognizes this. T-cells identify them as harmful, and initiates an all out immune response. This ultimately causes cells in the infected area to leak their fluid, and this causes inflammation. This response is necessary to trap pathogens.

Inflammatory mediators are released into the blood stream and sent to the area of infection to cause inflammation. Ironically, sepsis is a pathological process caused by the widespread release of these inflammatory markers into the bloodstream, with or without an initiating infection. When these get to organs, they can injure them, even cause them to fail, resulting in death.

There's a little more to it that what I just described, although it's all a respiratory therapist needs to know.  The basic theory here is early recognition and early treatment can greatly diminish injury, and reduce the death rate from sepsis. This, in turn, can reduce healthcare costs.

(Although, ironically, the costs to individual hospitals rises considerably. This is especially true as they do many procedures automatically on anyone who meets criteria for the sepsis protocol. Medicare will usually be the only one who saves money,and that's usually all that matters.  But I digress.)

Here are the early signs of Sepsis:

A. Suspected Infection

B. Two of the following: Meeting two of these should trigger the sepsis protocol (editors note: This may have changed slightly since then).
  1. Temperature greater than 100.4, <96 .8="" li="">
  2. Fast heart rate, or greater than 90 beats per minute
  3. Fast respiratory rate, or greater than 20 breaths per minute, or a PaCO2 that is elevated above a person's baseline (for this reason, an ABG is usually included in the sepsis protocol. Likewise, a pH that is acidotic can be an early sign of organ failure)
  4. <32>High white blood cell count (greater than 12,000 or <4000>10% bands)
C. Systemic blood pressure <90>

D. Lactate greater than 4.0 or elevated LDH

E. Decreased platelets (watch for DIC)

F. Decreased PaO2, or a PaO2 below normal for that patient

G. Altered mental status not due to drugs may signify organ failure.

Here are the signs of Severe Sepsis:

A. Patient receiving antibiotics & needs Vasopressor (this is a dangerous sign).

B. Pt showing signs of organ failure in 2 + systems for <= 24 hrs.
<90>
C. Patient showing signs of Adult Respiratory Distress Syndrome, DIC, or Multi System Organ Failure.

There, that's pretty much all you need to know. These are all things you can learn from a quick assessment, which may entail talking to the patient or family members, talking with doctors and nurses, or simply by looking into the patient's chart. We at the RT Cave think it's always a good idea to look a the patient's laboratory results anyway, if time allows.

From there doctors and nurses use their magic potions to fix the patient. This may entail Activated Protein C, the only drug to show any efficacy in sepsis. It may also entail antibiotics and steroids. It may also include vasopressors to control blood pressure.

Central Venous Catheter administration may be indicated to adjust vasopressors, to monitor fluids, and to determine if a blood transfusion is indicated. These and other therapies may be prescribed just in case it might do something, which is often the issue with administering albuberol for sepsis and heart failure. So, you never know, albuterol might also be indicated for sepsis.

It's nice to know all this, although it comes secondary to whatever our job is at the time. The hardest part about treating patients is getting to the bottom of what's causing their symptoms, and you and I both know a breathing treatment with albuterol is often a top-line option. So, while you're standing there waiting for the treatment to get done, you can do some investigating for the true cause of that shortness of breath, or whatever symptoms you are treating.

Still, I have had times when the true diagnosis eludes even the best nurses and doctors, and in these cases it's nice to have a well rounded RT come into the scene and say, "Hey, maybe this is what the true cause is!"

Edited on July 5, 2016, by John Bottrell 

Everything RTs need to know about Sepsis

This post was originally published on January 29, 2008. It is part of the classics of the RT Cave collection. While some of this is outdated, most of it is not.

So, in our quest to become more well rounded therapists, we must now look into another common condition, a condition that is the leading cause of death in critical care units.

For starters, we need to know that is is the leading cause of death in critical care units. Of the 750,000 patients it effects every year, 250,000 will die. These statistics cannot, and are not, being ignored. Hospitals continue to work overtime to create guidelines to help caregivers both recognize and diagnose sepsis so those who have it can get the treatment they need. Likewise, efforts can be made to recognize who is at risk for developing sepsis so it can be prevented.

These statistics have gone pretty much unchanged since the early 1980s. So, even with modern knowledge and technology, hospitals have been unable to break this trend. Yet they are, as noted above, working overtime to do just that.

But there is another side of sepsis that we must look at, and this is the financial side. While the experts will tell you and me that they are working overtime to make changes that improve lives, the bottom line is usually money. And this is the case here as well. For instance, according to the MUST protocol (which is now outdated, and the link is outdated as well), cost estimates nationwide tend to scale into the $17 billion category. I'm not sure what the data is for each individual hospital, but I imagine it's a lot of money, most of which hospitals eat.

So, sepsis is expensive. Actually, we can probably go deeper than this, and say that Medicare probably forced hospitals to look at this. Now, many hospitals had already begun their own research into it, but the government seemed to force their hands, so to speak. I'm not blaming government here, I'm just saying, sepsis kills, it costs a lot of money, and efforts are ongoing to improve upon them.

So, with the hope that hospitals would create sepsis protocols (many are now well beyond a gamut of committee) of their own, the MUST protocol was created to be used as a guideline protocol. According to the protocol itself, most hospitals have not adapted it (although this has changed since the original publication of this article). but I do know that many hospitals are looking into creating their own sepsis protocols (most already have).

So, what is sepsis. It's caused by an injury. Your body is infected by a pathogen, most likely a bacteria. Your immune system recognizes this. T-cells identify them as harmful, and initiates an all out immune response. This ultimately causes cells in the infected area to leak their fluid, and this causes inflammation. This response is necessary to trap pathogens.

Inflammatory mediators are released into the blood stream and sent to the area of infection to cause inflammation. Ironically, sepsis is a pathological process caused by the widespread release of these inflammatory markers into the bloodstream, with or without an initiating infection. When these get to organs, they can injure them, even cause them to fail, resulting in death.

There's a little more to it that what I just described, although it's all a respiratory therapist needs to know.  The basic theory here is early recognition and early treatment can greatly diminish injury, and reduce the death rate from sepsis. This, in turn, can reduce healthcare costs.

(Although, ironically, the costs to individual hospitals rises considerably. This is especially true as they do many procedures automatically on anyone who meets criteria for the sepsis protocol. Medicare will usually be the only one who saves money,and that's usually all that matters.  But I digress.)

Here are the early signs of Sepsis:

A. Suspected Infection

B. Two of the following: Meeting two of these should trigger the sepsis protocol (editors note: This may have changed slightly since then).
  1. Temperature greater than 100.4, <96 .8="" li="">
  2. Fast heart rate, or greater than 90 beats per minute
  3. Fast respiratory rate, or greater than 20 breaths per minute, or a PaCO2 that is elevated above a person's baseline (for this reason, an ABG is usually included in the sepsis protocol. Likewise, a pH that is acidotic can be an early sign of organ failure)
  4. <32>High white blood cell count (greater than 12,000 or <4000>10% bands)
C. Systemic blood pressure <90>

D. Lactate greater than 4.0 or elevated LDH

E. Decreased platelets (watch for DIC)

F. Decreased PaO2, or a PaO2 below normal for that patient

G. Altered mental status not due to drugs may signify organ failure.

Here are the signs of Severe Sepsis:

A. Patient receiving antibiotics & needs Vasopressor (this is a dangerous sign).

B. Pt showing signs of organ failure in 2 + systems for <= 24 hrs.
<90>
C. Patient showing signs of Adult Respiratory Distress Syndrome, DIC, or Multi System Organ Failure.

There, that's pretty much all you need to know. These are all things you can learn from a quick assessment, which may entail talking to the patient or family members, talking with doctors and nurses, or simply by looking into the patient's chart. We at the RT Cave think it's always a good idea to look a the patient's laboratory results anyway, if time allows.

From there doctors and nurses use their magic potions to fix the patient. This may entail Activated Protein C, the only drug to show any efficacy in sepsis. It may also entail antibiotics and steroids. It may also include vasopressors to control blood pressure.

Central Venous Catheter administration may be indicated to adjust vasopressors, to monitor fluids, and to determine if a blood transfusion is indicated. These and other therapies may be prescribed just in case it might do something, which is often the issue with administering albuberol for sepsis and heart failure. So, you never know, albuterol might also be indicated for sepsis.

It's nice to know all this, although it comes secondary to whatever our job is at the time. The hardest part about treating patients is getting to the bottom of what's causing their symptoms, and you and I both know a breathing treatment with albuterol is often a top-line option. So, while you're standing there waiting for the treatment to get done, you can do some investigating for the true cause of that shortness of breath, or whatever symptoms you are treating.

Still, I have had times when the true diagnosis eludes even the best nurses and doctors, and in these cases it's nice to have a well rounded RT come into the scene and say, "Hey, maybe this is what the true cause is!"

Edited on July 5, 2016, by John Bottrell 

Tuesday, July 5, 2016

What is Disseminated Intravascular Coagulation (DIC)?

Classics of the RT Cave. This post was originally published March 18, 2008.

First off, I worked a bunch of years in the hospital setting before I had a clue what DIC was. I had observed the symptoms many times. I remember many patients, most of them on ventilators, who seemed to be seeping fluid from their pores. Yet I heeded this condition little attention, mainly because I was a newer RT who was intently focused on getting my own work done.

Then one day I remember one of our senior therapists told me in report she told the nurses to keep a particular close watch on this trauma patient because he was at high risk for DIC and ARDS. It later turned out she was right, and the patient developed both ARDS and DIC. So, it did not pass me by how this senior was correct in her prediction. I was curious to know what she knew.

So I asked her, and she said, "Do some research on DIC, and then get back to me. Do a Google search." She paused, then added, "I think that all therapists coming out of school should focus on doing their jobs and doing them well. However, there comes a time when you should take a look at the other aspects of the healthcare industry, and in this way become well rounded therapists. I say this because well rounded therapists are better team players. While nurses are busy looking in one direction, you can say, "Hey, look here!"

So, that said, here is what I learned about DIC. Here is how you can predict what patients might develop DIC.

First of all, DIC is an acronym for Disseminated Intravascular Coagulation. It is almost always a secondary disease, or a consequence of other diseases, disease conditions, or circumstances. In our patient, it was secondary to trauma.

DIC is a condition, more so than a disease. It is a process that occurs when the proteins in the bloodstream that normally cause clotting in an injured area overreact, form tiny clots all over the body. Then, clotting factors now exhausted, this causes the patient to bleed abnormally. Bleeding occurs from nearly every orifice, including skin pores, the anus, etc. It just leaks out. It's kind of gross. You better wear gloves when you touch such a person (well, you should always wear gloves, but int his case you'll definitely want to).

When you do an ABG, for example, you might hold the site for the recommended five minutes and the patient still doesn't stop bleeding. Usually, when this happens, the RN will have to wrap gauze around the puncture site and bind tape around the patients arm to act like a tourniquet. I've seen this done on many occasions.

Technically speaking, on these patients, a doctor will want to limit the number of blood draws (ABGs included), because of the complications of bleeding. Another thing for us therapists to remember is to be very careful when suctioning. Ideally (and I think this should be standard procedure anyway), the catheter should not be advanced all the way to the corina so as not to puncture it and cause it to bleed.

In severe cases, the patient will seep ooze right out of the pores on his skin. This can be quite disgusting. This is what I described above. But I've seen it quite a few times already. I will probably see it more times in the future. If you work in the critical care or emergency settings, you will see it too.

DIC can also cause sudden bruising, clotting, and, as I described, bleeding from multiply parts of the body, and can lead to severe bleeding, stroke, and lack of blood flow to arms, legs and organs. So, it's not good.

That said, how do you know who is at risk. Here is a list of who to watch.
  1. Infection in blood (Sepsis)
  2. Severe tissue injury, as in burns, trauma (particularly trauma to the head and brain)
  3. Recent surgery or anesthesia
  4. Reaction to transfusions
  5. Labor and delivery problems
  6. Liver disease
Trauma patients not only are at risk for getting DIC, but also ARDS and Sepsis. And sepsis in itself is primary cause of DIC in the hospital setting. And, if that wasn't enough, DIC may lead to acute renal failure and, ultimately, to multiple organ failure -- including the lungs.

It was about this time I started to understand the point my senior therapist was trying to make about being a well rounded therapist. This is why it's a good idea to go through and review the charts of all your patients, particularly the laboratory results. Yes, we can learn a lot from lab results. The following are some lab results that might show DIC:
  1. PTT: Again, I'm no expert here. However, according to Medline Plus, this is a test to determine how long it takes for the blood to clot. If a patient is on a blood thinner like Coumadin, the PTT may be therapeutically high. A high PTT is anything greater than 33, and greater than 60 is considered critical, and may be indicative of DIC.
  2. PT: Same as PTT, except for the high value is greater than 12.7 and greater than 40 is critical
  3. D-Dimer: Greater than 500 may be indicative of acute bleed, but can also indicative of pulmonary embolism and DVT.
  4. Platelets: A normal platelet count is 150,000 to 400,000. This is what is needed in order for normal clotting to occur. A low value will be 150,000, meaning abnormal bleeding may occur, and below 50,000 can mean a simple bump can cause bleeding. <80>
  5. INR: Greater than 1.2 is considered high, but greater than 6 is critical. This is indicative of DIC or acute bleed.
Now, keep in mind these critical values will vary from hospital to hospital, but at least this gives you an idea of what critical is, and what the labs of a patient in DIC might look like.

Also, you should know that there is a lot more involved in the DIC process than what I describe here, but this is pretty much all that a well rounded respiratory therapist needs to know.  Now, see if you can put this wisdom to good use and impress someone the next time you find one of these patients.

Edited on July 5, 2016, by John Bottrell

Friday, July 1, 2016

The RT Cave Blogosphere

So I need to make a few comments about this blog. First, as you may have observed, there are no longer ads on it. This is because Goodle Adsense fired me. They will not tell me what I did, which is unfortunate.

I was actually getting to the point I was making about $100 every 2-3 months, so it's not like I was getting rich off ads. And I wrote on this blog many years before I ever put ads on here, so it's not like I need the money as an incentive to write.

Still, I am also at a point in my life where I was seriously considering donating what I made on this blog to some respiratory charity. But that idea is gone now. It's not a big deal, but it still kind of stinks.

So that pretty much means this entire blog is a charity.

Another change made here is that I will no longer submit posts on this blog about myself. I actually made this change quite a few years ago, and some of you have already discovered by asthma blog, "Hardluck Asthma."

I actually started writing the history of asthma on Hardluck Asthma, before writing about the history on this blog. Then I decided to just make a new blog called, "Asthma History."

For the record, asthma was once an umbrella term for all that is short of breath, so every lung disease is covered there, not just asthma as we now know it. So, if your'e interested in a history, check out my history blog.

If you are interested in politics, you can check out my political blog. Actually, it's not so much a political blog, mainly a place I can write about things other than respiratory therapy, other than me, other than medical. So you can find me over at "Articulating Ideas."

Now, if you read my political blog, keep in mind I have an opinion. It's actually a place I can share ideas I have with my kids, if they so care to read what I write. Perhaps in the future they might get interested. Although, in all due fairness, I don't even think they know it exists because I don't talk about it much.

And, as is true on all my blogs, I am not politically correct. So, if you go over there, be nice. You can be honest, but be nice.

And, as is the case with this blog, there are no ads on my other blogs either. So, they are all charities.

That said, I also do blogging where I get paid. From 2008 to 2016 I was an asthma and COPD expert over at healthcentral.com. Some of those posts I republished here (come to think of it, maybe that's what Adsense didn't like).

Beginning this year I am an asthma and COPD expert at COPD.net and Asthma.net. These posts will not be republished here, per my contract. So, if you want to read them, you'll have to go there, or follow me on Facebook or Twitter. Or, you can like COPDdotnet on Facebook and Asthmadotnet on Facebook.

So you can find me all over the place. And that should explain why this blog has been less active of late. Still, I will post here from time to time, and I will link to it at the Respiratory Therapy Cave Fakebook page and on RT Cave on Twitter. So, you can follow me and I'll keep you posted.

Anyway, hope you are all doing well.