Can you use expired asthma meds?

The following is from healthcentral.com/asthma.

"Is It OK to Use Expired Asthma Medicines?" (originally published 5/23/11)

You found your asthma medicine sitting at the bottom of your sock drawer and now you're wondering:  Can I still use it?  Is it safe?  Will it still work?  Is it okay to use expired asthma medicines?

Asthma medicine has a tendency to be expensive. One Advair Discus costs over $100 just for one month.  Even with good health insurance, I pay about $1 for each Singulair pill.  The cost of other asthma medicines can add up to.

If you're normal like me, you lose your inhalers.  I just opened three brand new Ventolin inhalers in the past week, and I already can't find two of them.  I did find one when I cleaned under the bed, yet it was dated January 2009.

While it's recommended every asthmatic have a rescue inhaler like Ventolin on hand at all times, and that we replace it every year, I know of many of you guys who have one yet it's done nothing but sit at the bottom of your sock drawer.  Now you're short of breathe and wondering, can I still use it?

More recently I received a question about how long Advair is good for.  This person had no insurance and wanted to know if it was safe to use an Advair that was opened but expired four months ago.  She also had one Advair that was expired but was never opened.

Are these medicines safe?  Would they still be effective if used?

When I was a kid I'd lose inhalers all the time.  If the one I was using ran out, and I for some reason didn't tell my mom I needed a new one, and I was having a raging asthma attack in the middle of the night, I'd rummage my room hoping to find a lost one.

Then I'd find one and take a puff.  If you've ever taking a hit off an expired Ventolin inhaler you'd know it, because it tastes like rotten mints.  Yet you wouldn't mind so much, because it still helped you get your breath back.

More recently I did some research to find out what the scientific evidence was regarding old and expired medicine.  I asked the pharmacist where I work, and he gave the old stand-by and political response, "It's good for up to a year."

Yet that didn't satisfy me.  So I continued my search for answers.  What I learned is that science has pretty much proven that no asthma medicine will harm you if you use it beyond its expiration date.

So in that sense you can feel okay about using expired medicines.  I mean, I'm proof expired asthma medicines don't kill.  If nothing else, I've proved that many times.

As far as potency, over time asthma medicines do become less potent, although they will still work better than using nothing.  In fact, most new medicines are good for two to three years from the day they are produced so long as they remain in the original packaging.

And considering a medicine may sit on the shelf of storerooms, trucks and then pharmacies, the expiration date is generally listed as one year as of your purchase date.

So you can see there really is no scientific reasoning for that expiration date.  The medicine might still be potent for some time.  So if your package is not opened, you should be able to use older medicine (within reason of course).

However, once the original container is opened for use or dispensing, the expiration date on the container no longer applies.  In fact, according to, this ABC News post, the expiration date of a medicine is actually just the predicted date at which the drug will lose 10 percent of its potency.

Once a medicine loses more than 10 percent of its potency it's no longer considered effective.  From that point on, it continues to lose more and more of it's potency.  Plus, if it's an an inhaler, it starts to taste nasty.

The expiration date also assumes you are storing the medicine at the recommended temperature and humidity.  Most medicine should be somewhere between 59 and 86 degrees F (15-30 degrees C) and away from light and moisture.  You'll have to check the package of your medicines to see the exact recommendations.

This means that asthma medicines should not be stored in the bathroom where
it will be exposed to high humidifiers during and after showers.  So I suppose the bathroom medicine cabinet’s not such a wise place to store your meds after all.

While most asthma drugs are not hazardous if used after their expiration dates, the efficacy of the medicine after that date can no longer be guaranteed.  Thus, if you are using an expired medicine you may not be getting the expected results.

So, should you use those expired asthma medicines?  At least now you can make an educated decision.

read more...

My Book: Trauma Informed Treatment: The Restorative Approach

My book, Trauma Informed Treatment: The Restorative Approach, is coming out this spring, published by NEARI press. Here is what Kay Saakvitne, PhD said about it: Dr. Saakvitne is the author of Risking Connection, Trauma and the Therapist, Transforming the Pain, and many other books, chapters and articles:

"Pat Wilcox conveys the accumulated wisdom of her years working with children too often overlooked by others in this remarkable and inspiring book. The Restorative Approach has the potential to radically change child mental health treatment (and parenting) for children with challenging behaviors and histories of trauma. Integrating current research on trauma and treatment with practicality, compassion, and ethics, Wilcox presents a compelling case for the Restorative Approach as a best practice in trauma-informed child treatment. The book is exceptional in its many detailed clinical examples of effective interventions making it immediately accessible and useful to all staff. Wilcox’s full exploration of all objections to the Restorative Approach convinces the reader of her complete understanding of the real conditions under which most child mental health settings function. Ultimately this book is inspirational; it offers hope for children, their families, and mental health professionals working with them. It should be required reading for all staff working with children in mental health systems. "

read more...

Trials and trivializations result in character and refined faith

We have all faced trials in our lives where we have said, "Why is this happening to me?"  Or we have said, "Why do I have to endure such pain or misery?"  Yet the challenges we face are never more than what we can handle, and they always make us a better person, even if we don't see it that way at the time.

Character, modesty, humility, wisdom and a refining of our faith are developed through the hardships we face during the course of our lives.  We may sometimes feel as though things could not get worse, or we may feel like things may never get better, yet there is always a way out.

"No testing has overtaken you that is not common to everyone.  God is faithful, and he will not let you be tested beyond your strength, but with the testing he will also provide the way out so that you may be able to endure it" (Corinthians 10:13)

Another great description of the hardships of man is Psalm 77 which was written by the philosopher Asaph.  He describes his cries in the night because something horrible has happened to his life.  He describes his terrible suffering.  We all can relate to Asaph in this Psalm because at some point in our life we all faced a challenge that seemed to be never ending.

We face death and the challenges of death.  We face disease and the challenges of disease not just of our selves but the other people in our lives.  We face failures, such as the inability to get a job or of losing a job.  Since we are presently in a recession, many of us are presently facing the economic hardships that come with a recession.

Asaph writes, "...and my soul refused to be comforted."  Here he is describing how many of us felt during our time of hardship, our time of need.  No matter what we did we couldn't think of anything that would comfort us.  No words of others were comforting.  It seemed you were doomed to live in the miserable world you saw that day.

I remember being in the asthma hospital when I was 15, and even though I was told it would only be for 6-8 weeks, it seemed to last forever.  And then when the 6-8 weeks was up, I was told I would need to stay at the hospital another 6-8 weeks or longer.  I felt trapped.  I felt there was no way out.  I felt that nothing was ever going to get better.  I was depressed. I felt God hated me and was punishing me.

Then in our distress we yearn for the good ole days, as Asaph writes, "I thought about the former days, the year of long ago; I remember my songs in the night."  When I was suffering back then, I remember thinking about what my parent's house looked like.  I remembered my mom's smile and my dad's stern hand.  I remembered playing with my brothers.  I kept thinking of what it would be like to return to those days.  Even though my asthma was bad, I was still happy.

Yet here I was trapped in this hospital where I didn't want to be.  However, I never gave up.  I remember every night after the counselors had us go to our rooms for the night with the lights out, I would crouch down by the little night light on the lower part of the wall and I would open my Bible.  I would pray first off that no one would open the door to come check on me, because I didn't want to get caught.  It's not that I was doing something wrong, it was more I didn't want to explain myself.  And, thankfully, of all the three months worth of days I did this, I never once was caught.

I prayed.  I said every prayer I knew of at the time.  My mom gave me some book marks with prayers on them, and even thought the prayers may not have been relevant to my situation, I prayed them anyway.  I remember one of the prayers was footprints in the sand, and another was the alcoholics creed (although I didn't know it was the alcoholics creed at the time).  It was "God, grant me the serenity to..."

Either way I prayed, and I refined my faith.  Even though I felt trapped, I re-decided it was with a purpose -- to get my asthma better. Yet I was quickly realizing it was more than just asthma.  The challenges I endured at this place with the other kids and the counselors made me a better person overall.

Yes it was hard to see at that time, yet now looking back at it from the mind of the 40 year old me, I see that the challenges I endured at National Jewish Health/ National Asthma Center from January 1985 to July 1985 helped me develop a better character, humility and to become more modest.  Through my suffering, through the challenges that seemed to never want to end, I became a better person, and through my strength and desire not to lose faith, my faith grew to the size of a full blooming tree.

Asaph in his Psalm (versus 10-12) writes that in rediscovering ourselves we must remember all the good things that happened in the past, and all the good things going on in our lives today.  And Lord knows there are many good things going on in your life at all times, even though the hardships seem to overshadow the good things.

Yet I thought of the good.  I thought of how I have such great parents who gave me this opportunity to get my life in order, and my asthma better.  I have such good counselors and friends.  I had a good life overall, and when I got out of the hospital my life was going to be all the better.  Sometimes this was hard to do, yet as often as I was able I tried to think of all the good.

And the most remarkable thing about this entire event is that I did get out one day.  I remember my dad saying late in June of 1985, "Rick, you're coming home. I don't know exactly how I'm going to do it, but you're coming home.  I'm going to hang up now, but I want you to sit by the phone until I call back."

The funny thing was that we were only allowed 15 minutes on the phone, and my 15 minutes was up.  I was afraid my counselor would kick me out of the phone room so someone else could use it.  But for some rare reason (God perhaps) there was no one waiting behind me.  And my counselor wasn't being mean this day, and he allowed me to sit and wait for dad to call back.  My strength and prayer was answered.  The phone rang, "Rick, you're going home."

Another ironic thing is my faith came from inside me.  I didn't much read the Bible back then as I do now, what I knew of the Bible came from Catechism classes.  My faith came from my mom.  And I had never read Psalm 77 and even if I did I wouldn't have understood it anyway.

Facebook Twitter

read more...

Who is a Chronic CO2 retainer

I found a neat chart that shows the difference between chronic CO2 retainers and those with acute CO2 retention that is probably reversible:

Likely CO2 Retention

1.  Usually severely limited by breathlessness
2.  Cor pulmonale
3.  Polycythemia
4.  FEV1 less than 1 liter
5.  Home nebulizers
6.  Home oxygen
7.  Abnormal blood gases when well
8.  Admission blood gases show high CO2 and High HCO3 (example:  CO2 50, HCO3 32)
9.  Vital signs not different from normal
10.  Saturations not different from normal
11.  Reasonable air entry
12.  It's reasonable to maintain an SpO2 of 88-92%
13.  Disease generally complicated with either asthma or heart failure

Likely Ventilatory Failure

1.  Not usually limited by breathlessness
2. No signs of chronic hypoxemia
3.  FEV1 good
4.  Inhalers only at home
5.  Normal blood gases when well
6.  CO2 and HCO3 consistent with critical ill
7.  Critically ill
8.  Silent chest or feeble chest movement
9.  Dubious diagnosis of COPD
10.  Chest x-ray shows pulmonary edema or severe pneumonia
11.  It's reasonable to provide these patients with whatever oxygen they require to maintain adequate oxygenation

Studies show that of those COPD patients who present to the hospital in acute respiratory distress, about 50 percent have acute CO2 retention that is reversible with treatment, and about 50 percent are chronic CO2 retainers. 

Reference:

1. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusetts, page 24.  The authors also support the idea that the hypoxic drive theory is a hoax, and thus the reason for the explanation of CO2 retention. 

read more...

Times Reporter dies of asthma while on assignment

On Monday I was asked to write a post about a correspondent for the New York Times who died of an asthma attack while on assignment.  Because it dealt with the passing of a fellow asthmatic, it was among the most challenging things I've ever written.

The following was published at HealthCentral/asthma on Monday, Feb. 20, 2012:

"Prize Winning New York Times Correspondent Dies of Asthma"

Anthony Shadid was an asthmatic.  He carried his asthma medication with him.  He was also a Pulitzer Prize winning correspondent who risked everything to tell true life stories from dangerous regions of the Middle East.  He was shot once, arrested, and even abused.  Yet in the end what took his life wasn't the high risk job he loved, but his own asthma.

The New York Times reports that Shadid was in Syria gathering information for his current assignment, which "was fraught with dangers, not the least of which was discovery by the pro-government authorities in Syria."

He traveled at night to a mountainous border area between Syria and Turkey, and squeezed through a fence by pulling apart the wires.  Waiting on the other side were guides on horseback.  Yet there was a risk in doing that too for Shadid, because he was apparently allergic to horses.  That night he suffered an asthma attack.  He recovered with rest, the Times reports.

A week later Shadid was on his way out of Syria, was closing in on the Turkey border, when he came close to horses once again.  He became short of breath, leaned against a rock, and collapsed.  The apparent cause of death was asthma.

His coworkers confirm (click here) that he died doing what he loved most.  And this is the goal of any asthmatic, that we take our medicines as prescribed so we can live a normal, active life.  Shadid did just that, and the result was excellent reporting from the most dangerous part of the world. 

Bill Keller, Columnist and Former Executive Editor for the New York Times said "He went to places that were inaccessible and dangerous and miserable -- not as a daredevil or adrenaline junkie, not recklessly, often reluctantly, always with the most meticulous and careful planning -- but he knew you had to be there."

Asthma is sort of the same way.  It's "dangerous," even "miserable" at times.  Yet with meticulous and careful attention to your disease, by visiting with your doctor on a regular basis, by taking your medicine exactly as prescribed by your doctor, you can do the things you enjoy most in life. 

However small, there are still risks to having asthma.  The American Academy of Allergy, Asthma and Immunology (AAAI.org) notes that of the 300 million asthmatics in the world, 250,000 deaths are attributed to the disease each year.  That comes to less than a 0.83 percent chance of dying from asthma.

The risk is small, yet it's still there, always there. 

One of the scary things about asthma is it can go into hiding, and pretend not to be there.  Then it can creep up on you when you're least expecting it, and sometimes even strike quick. 

And it's for this reason we must always remember we have asthma, and do the best we can tocontrol it.  In this way we can live a normal life, and do the things we love, no matter how dangerous. 

read more...

Blood Gases: 4-5-6, 7,8,9 Rule

Your Question:  What is the 4-5-6, 7-8-9 rule?

My answer:  The idea for this rule is that by using the oxyhemoglobin dissociation curve you can estimate the patients PO2.  Basically you take the patient's SpO2 and subtract 30, such as follows:

SpO2               PO2

70%                 40

80%                 50

90%                 60

This is a good way of using a noninvasive pulse oximetry reading to "guestimate" that same patient's PO2 which is invasive to get by an arterial blood gas. 

read more...

The link between thunderstorms and asthma

The following is from healthcentral.com/asthma.

"Do thunderstorms cause asthma?"  (originally published on June 8, 2011)

A cool refreshing breeze redolent of rain is wafting over me as I write this.  The sky is overcast, and dark clouds are moving in; a distant rumble heard.  As I inhale I can feel a slight tightness deep within.

This reminds me of an article I read a few years ago that said most asthmatics have fewer symptoms during the summer months, yet this isn't so true during or after a thunderstorm.

The evidence showed there were an increased number of emergency room visits on days when there was a thunderstorm.

So many asthmatics complained of asthma symptoms after thunderstorms this prompted the powers that be to pay lots of money to study this matter.

I read it first at COPD News of the Day in her post, "Weather and COPD -- thunderstorms linked to asthma attacks."  She wrote about a study completed in the southern states by researchers at the University of Georgia and Emory University.

The study, which you can read more about here at Science Daily, examined 10 million emergency room visits for asthma in hospitals around Atlanta from 1993 to 2004, and concluded there was a three percent increase in asthma visits on the day after a thunderstorm.

Experts surmise this may be because rain causes pollen grains to rupture causing minute particles that can be inhaled.  If it's windy (I can still feel the breeze) these particles can waft right up your nares and into your lungs.

And of course we know what happens from there.  If you're allergic to pollen, inflammation in your sensitized lungs increases, and you feel tight -- like I do now.

Another study reported here at Medescapes.com was done in 2003 in the United Kingdom and showed emergency rooms visits for asthma exacerbations increased 8.6-10 percent the day after a thunderstorm.

This study showed an increase in fungal spores by 50 percent, and determined this might be a possible cause of increased thunderstorm related asthma.

I observed rain as an asthma trigger years ago, yet I figured it was due to a change in barometric pressure or increased humidity.  Yet the theories noted above make sense too.

The experts may continue to debate the cause for some time, yet it does appear that thunderstorms can indeed trigger asthma.

Of course we could shut our windows and hide in a bubble somewhere like my 2-year-old daughter would like done.  She's now grasping my leg and saying, "Daddy, I'm scared!".

Yet then we'd miss out on a good thunderstorm, and the cool, refreshing breeze it provides.

read more...

Taking Care of Mercedes and her Mother- a Cautionary Tale

Mercedes is ten years old. Her developing brain was affected in utero by medications that her mother was taking. She experienced neglect and domestic violence while growing up. She has been in several placements and received various episodes of treatment. `Her mother, Maria, who also has three other children, has remained committed to her and has been involved in her care. Mercedes was placed in residential treatment, and she and her mother were working on reconnecting. Meanwhile Maria is trying to manage her job as a cleaning woman, caring for her three children at home, and taking some courses to become as nurse’s aide. This is a dream she has had for a long time and she is excited to be making progress.

In the program, Mercedes was one of the more difficult residents. She quickly became extremely agitated when her needs were not met immediately, and was often severely violent with both staff and other residents. The program was helping her by having a single staff assigned to her. Whenever that staff saw early signs of dysregulation they would help Mercedes use sensory interventions, physical activity and distraction to avoid a major episode. Mercedes was also on several medications. In therapy Mercedes and her therapist would go for walks, complete puzzles, use art, and clap with music to give Mercedes experiences of regulation in the presence of a positive adult and to build and regulate her lower brain. Mercedes does want to learn how to stay calm, and she feels bad afterwards when she hurts someone. Her mother Maria was attending regular family therapy and taking Mercedes on short visits. The focus of these was to support Maria and Mercedes in having some enjoyment and positive experiences together to rebuild their bond. This combination of intensive treatment was beginning to work, and Mercedes was now occasionally noticing her own beginning distress and herself asking to use her crisis kit. She and her mother were just starting to practice some skills she could use at home.

However, the current thinking in child welfare is that youth under 12 should not be in residential treatment. So, Mercedes was discharged home, and many supports were arranged for the family. Since then, she has been unremittingly violent, beating up her siblings and sending a child in one of her programs to the hospital. Maria has arranged for the siblings to stay at her mother’s for the weekends so that Mercedes won’t hurt them. Maria herself is exhausted and hopeless. She has had to drop one of her courses and is finding it difficult to complete her work in the one she continued.

What went wrong?

I have to warn you here that my understanding of what is needed to help has become somewhat radical, as you will see through my comments.

First, as Mercedes left the program, her mother stopped her medications. She did so because she believed that her pediatrician had told her that these medications might lead to diabetes. Maria’s own mother has diabetes, and Maria has seen firsthand the problems it causes. She doesn’t want this for her daughter. Maria explained to the unit psychiatrist that she planned to do this, but he did not alert anyone.

Maria and Mercedes were given generous help as Mercedes was discharged home. They were given an in-home team of a therapist with behavioral training, a parent aide and a psychiatrist; Mercedes was enrolled in a therapeutic after school program with a therapist, family therapy and a psychiatrist; and Mercedes attended a special ed out of district school with special ed teachers, a therapist and the possibility of a psychiatrist. Yet all this help wasn’t enough.

So, a ten-year-old child who cannot utilize verbal therapy now has three therapists. These therapists have different theoretical understandings and have not spoken with each other. Furthermore, Maria is expected to cooperate with the in home team and have family meetings with them. They are suggesting that she create a sticker chart through which Mercedes could earn little toys by not being violent. Maria created one with the therapist, but she usually forgets to fill it out. If she does fill it out and does not give Mercedes one of her points, Mercedes becomes furious and another rageful episode is triggered. So when she remembers it at all Maria usually gives Mercedes all her points. Maria feels bad about this- it feels like just one more way she has failed Mercedes and been a bad mother, as she thinks she has been all of Mercedes’s life.

Maria is also expected to attend family therapy at the after school program. Well, at least this sometimes includes a meal. But in the therapy she usually hears a long description of what Mercedes has done wrong that week. Maria feels awful that her daughter sent a child to the hospital. But she has no idea what she is supposed to do about it. She can feel it coming that this program is going to kick Mercedes out, and then what is she supposed to do in the afternoons? She can’t quit her job but knows Mercedes cannot be left alone with her siblings.

And school… that’s just another place that calls her with stories of Mercedes horrible behavior. All these people tend to blend in her mind anyway and she can’t usually remember their faces.

So what would be better?

Prior to Mercedes discharge there should be a meeting of all the service providers. In this meeting, it would be flagged that mother is against medication. The providers would decide which psychiatrist will take over the case. That psychiatrist will meet with Maria and respectfully explore her concerns about diabetes. The truth about any connection of the medications with diabetes will be explored, and a plan will be created that does not involve Mercedes going off all meds just as she makes a major transition.

The therapists will decide just what each of their roles is, with both Mercedes and mom. What treatment will be most helpful for mom? How can we avoid overstressing her with demands that she attend various meetings?

Equally important, the team will agree on their approach to Mercedes. Preferably they will all agree on a single message that all team members can use in their work, such as, we are working on ways to calm yourself down when you are upset so that you stay safe and don’t huts anyone else.

I do not think sticker charts are any help at all in this situation. If Mercedes knew how to act better she would. Instead, the in home team can be very valuable in helping Mercedes practice her calming strategies in the real life situation. Ideally, one of the therapists will make a chart with Mercedes about things that help her stay calm. This chart will be shared with all team members and they will all use it. Mercedes will have tools, such as a sensory kit, in all parts of her life and the same help from all her providers to use it when she starts feeling agitated.

Mercedes has a very troubled relationship with her three siblings. She is very angry that they got to stay with their mother while she has been out of the home. Plus those siblings have their own problems and often say and do things they know will agitate her. Here too is an important role for the in home team. They can do activities with Mercedes and her siblings, perhaps one at a time, and be there to avert arguments and violence. The activities should be short at first and very pleasurable to help build a bond between these children.

Let’s ask Maria what would really help her. Maybe some community activities could be found for the other 3 kids so that Mercedes and Maria have time together. Maybe Maria needs some time on her own to do her school work- can the in home aide take care of all the kids for an hour or two, using that time to work on their connection?

One therapist could start an email list or list serve so the each provider writes about what happened in their segment every day and all the providers read it. This will help create a cohesive team. It would be especially important to share all positive events and successes.

The keys to the intervention being successful and to Mercedes being able to stay home are:

• Coordination, communication clear roles and a mutually agreed approach among the team

• Medication management that is respectful towards mother and addresses her concerns

• Listening to the family and doing what actually helps them instead of what further overwhelms and demoralizes them

• Physically based activities for Mercedes in which the experiences and practices bodily regulation

• An emphasis on activities that increase fun, connection and joy between the family members.

It is not just the quantity of help that we give people that ensures success. It is the well planned, respectful and coordinated help.

And wouldn’t it be great to discover that Mercedes had been able to stay home and that she was calmer a year later?

read more...

Hospital Cafeteria

You'd think being a hospital that the cafeteria would serve something healthy.  People will say that you can have a salad, but there's two problems with salads:  1) they don't fill you up, and 2) salads require salad dressing and even the fat free stuff either tastes like crap or has too many cards.  So salad's off the table.

So then there's the sandwich stuff.  Well, the tuna fish I'm sure is made from high fat salad dressing, and so too are the noodles and coleslaw.  And a sandwich is like eating a bowl of cereal in the morning:  it doesn't fill you up either.  Or at least it doesn't fill me up.  

I like a meal.  And when you have to choose between 10 grams of fat lasagna and a Cuban sandwich, you have no choice but to go with the fail safe lasagna.  You can't screw up lasagna.  It tasted fine.  The taste is hardly ever the problem.  It's the 10 grams of fat.  And that's before the garlic bread I gave away.  

The Cuban sandwich was another story.  I Googled it before I went down.  Now, if you have to Google something on the menu, chances are you won't like it.  If you don't know what it is, it ain't good.  And it sure didn't look good.  Plus the average Cuban has about 30 grams of fat.  Nope.  Not for this guy.

So where's the healthy option?  There ain't none.  So that's why I usually take my own food to work.  Yet still, you'd think considering this is a hospital there'd be healthy choices.  But that's not the case one bit.  

The funny thing is, on the hospital website it talks about how healthy the menu food is.  It even mentions 10 and 30 grams of fat.  Ten grams of fat in a meal once in a while isn't terrible, yet I don't consider 10 grams of fat in one sitting every day every meal a good thing.  

To me, 5 grams of fat, even 8 is fine.  But 10 and 30?   Where's the healthy option?  Who defines healthy these days.  If this is the kind of options they serve in public schools, no wonder we've turned into a fat nation.  

The problem is sometimes there's nothing to take to work.  Then what do you do?  You have no choice but to eat cafeteria food, regardless of how unhealthy and yucky it is.  Same think with school meals.

My friends say I'm picky.  Yet that's not true at all.  I can eat most food.  I just prefer to eat unhealthy food when I'm on a vacation with my wife or doing something fun outside work, or when I go to McDonalds.  When I eat something unhealthy I want the food to be fun and tasty and not at work (with a few exceptions of course.)

read more...

Hypoxic Drive Theory: A history of the myth

It's frustrating to watch a patient gasp for air.  Even worse, it's painful to watch a patient gasp for air because his doctor refuses to allow him much needed supplemental oxygen based on a 50-year-old medical myth:  the hypoxic drive theory.

The theory postulates that giving a patient with chronic (it's always there) carbon dioxide (CO2) retention, such as occurs in 50 percent of chronic obstructive pulmonary disease (COPD) patients who present with respiratory distress, will cause their CO2 to rise, breathing to slow down, and ultimately knock out their drive to breathe and cause respiratory acidosis and ultimately death.

The problem is the theory doesn't hold water with real world experience.  Of hundreds of thousands of patients we RTs take care of on a daily basis and place on supplemental oxygen (even as much as 100 percent oxygen), we see very few stop breathing. I give all my breathing treatments with oxygen, and no patient ever stopped breathing during a treatment.

If a patient suffering from an acute exacerbation of COPD is going to stop breathing, it's going to happen whether he receives oxygen or not due to exhaustion.  We've known this for years, but we lacked proof.

Now we have proof, because in 1987 the hypoxic drive theory was disproved. (1) The problem was that this proof came after the hypoxic drive theory had already become ingrained in the minds of prominent and well respected physicians around the world.  Despite evidence to the contrary, generation after generation of physicians have been educated about the hypoxic drive theory.  The theory, thus, has become a fact.

The result is needless suffering by many COPD patients and in some cases an untimely death.  The agony of watching patient's suffer due to a myth, or hoax as some call it, has driven many RTs to an early retirement.

So, what is the hypoxic drive theory anyway?

The main drive to breath comes from neurons in the medulla oblongata at the base of the brain.  These neurons receive signals from central chemoreceptors on the medulla and peripheral chemoreceptors located in the bifurcations of the aortic arteries and the aortic arch. 

Respiratory rate is adjusted to maintain a normal acid base balance (pH) throughout the body.  The majority of the times, the central chemo receptors send signals to the brain that control breathing. They monitor carbon dioxide (CO2) levels.  When CO2 levels are high a signal is sent to speed up the drive to breathe to blow off the excess CO2.  In this way, CO2 is our main drive to breathe.

The peripheral chemo receptors send a signal to breathe when the partial pressure of oxygen in the arteries (PaO2) is less than 60. This is referred to as the hypoxic drive.  This hypoxic response is far slower than signals sent by central chemoreceptors, and therefore the hypoxic drive has only a minor role in breathing. 
In COPD patients, chronic airway obstruction due to bronchospasm and increased mucus secretion blocks air passages, and as a result many alveoli become ineffective at ventilating (CO2 cannot get out and oxygen cannot get in).  For these patients, this results in a chronically elevated CO2, such as greater than 50), and lowered oxygen level (PO2), such as less than 60. (2)

As CO2 rises, bicarbonate (HCO3) falls in order to compensate and prevent acidosis (a drop in pH, or a pH less than 7.35).  The result here is that many of these patients normally live with something like a PaCO2 of 50 and a PaO2 of 50 and a Bicarb of 30.  The hypoxic drive theory has it that the high CO2 may make the chemoreceptors tolerant of the high CO2 and thus CO2 ceases to be that person's drive to breath.  These patients are your prototypical CO2 retainers. They hypoxic drive theory, thus, states that many of them are hypoxic drive breathers. 

The hypoxic drive theory is taught in medical schools, and it's recommended that any COPD patient who is a CO2 retainer could be a hypoxic drive breather.  If you give them too much oxygen, enough to drive their PO2 above 70, you will be blunting their hypoxic drive to breathe, their respirations will slow, their CO2 will rise, acidosis will occur they will become lethargic, and ultimately they will stop breathing.  Yet evidence suggestsa "reduction in hypoxic ventilatory drive may not be the sole mechanism causing increasing hypercapnia in (COPD patients)." (3)

I polled over 60 nursing students over the past couple years and close to 100 percent of them believed that all COPD patients were hypoxic drive breathers who shouldn't be overly oxygenated.  Most doctors I work with believe a CO2 greater than 40 signifies a hypoxic drive breather. 

The truth is that less than 25 percent of chronic CO2 retainers use the hypoxic drive to breathe, (4) and it's not as significant as once believed. Of patients who present to hospitals in respiratory distress, half will have reversible CO2 retention, and half will be chronic CO2 retainers.  (5)

So how did this theory become so engrained in the minds of physicians?

It must be noted here I have much admiration and respect for the medical community.  They do things I couldn't comprehend doing myself -- such as cutting people open and stitching.  Often I think it's better to be a respiratory therapist because, while we're a part of the critical thinking team, the final decision lies in the hands of the physician.

Yet while I respect and admire them, I also understand the medical profession is notorious for being proud, dogmatic, and slow to accept new ideas. Take 1543 as an example.  In medical school an assistant would dissect a human corpse while the professor read from Galen.  Andreas Vesalius observed that what was being read was different from what he was seeing.

For example, Galen's writings described the sternum as having eight parts, yet the human sternum being dissected had only three parts.  Later, when Vesalius was dissecting an ape, he learned it was the ape that had an eight part sternum.  Galen had made his writings based on dissections of apes.  This made sense considering in Galen's day it was illegal to dissect a human corpse.

In the 16th century artists like Michelangelo knew more about the human anatomy than physicians, so Vesalius hired Johannes Oporinus to draw accurate pictures of human anatomy, and Vesalius published the first ever book on human anatomy De humani corpus.

Yet Galen could nary be wrong, and Vesalius was laughed out of town.  Of course he is now considered the father of human anatomy.

In 1816 Rene Laennec invented the stethoscope, and instead of the medical community adapting his invention to improve their diagnostic skills, he was immediately mocked.  Doctors didn't think they should have to carry such frivolous equipment with them.

In 1847 Ignaz Semmelweis observed that moms whose babies were delivered by medical students were far more likely to die of child bed fever compared to moms whose babies were delivered by midwives.

Semmelweis proved the midwives were cleaner because the midwives washed their hands between patient procedures. Semmelweis made it mandatory for doctors to wash their hands in chlorinated lime solutions just like the midwives did.  In the months that followed moms dying of child bed fever plummeted.  Yet Semmelweis was hated and treated like a nut.

How dare he tell the well established medical community what to do?  You see, back then medical status was determined by how much blood you had on your hands and apron.  Since Semmelweis could offer no scientific proof why hand washing did any good, Semmelweis was laughed out of town.  (6)

Oxygen was discovered in 1777 by Joseph Priestley.  In 1922 John Haldane wrote about his own research on oxygen in "The Therapeutic Administration of Oxygen."  Soon thereafter oxygen tanks became more and more common at the patient bedside, and ultimately oxygen was piped into the walls of hospitals.  Among the patients administered oxygen was COPD patients.  (7)

It was soon observed that oxygen made these patient's CO2 rise, and some of these patients lost their drive to breathe.  In 1949 a case was documented where a man with emphysema "lapsed into a coma after receiving oxygen therapy but rapidly recovered after the oxygen was removed," according to Nicola Cooper, Kirsty Forrest, Paul Cramp in their 2006 textbook, "Essential guide to acute care." 

The text also explains that "in 1954 a decrease in ventilation in 26 out of 35 patients with COPD given oxygen therapy, with a rise in PaCO2 and a fall in pH.  No patient with a normal baseline PO2 showed these changes.  In a further study it was showed that stopping and starting oxygen therapy led to a fall and rise of PaCO2, respectively."  (8)

The concern became so great that in the 1950s a study was done 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.  (9)

Yet instead of a scientific theory being treated as a scientific theory it was treated as scientific fact, and this began the accepted practice of keeping patients in much need of supplemental oxygen hypoxic.  The medical profession decided the hypoxic drive theory sounded good so it must be good. The Hypoxic Drive Theory thus became the law of COPD land.  Any evidence to the contrary would be rejected.  

Of interest here is that the study Campbell referred to in his lecture consisted of only four COPD patients.  Because the hypoxic drive theory provided the first best example of why a COPD patient might stop breathing in the presence of oxygen, the theory has been taught from one generation to the next.  Despite scientific evidence, it has become the gold standard when treating COPD patients. (10)

So you can see how the medical profession has a long history of being relentless when it comes to holding on to antiquated ideas and adapting newer and better methods.  So it only makes sense that a theory concocted in 1960 and taught in medical schools would be a tough theory to let go of.

So where's the evidence the hypoxic drive theory is a myth?

Ironically, there has never been a real scientific study done to prove the hypoxic drive theory.  There have been several studies performed whereby researchers concluded the rise in CO2 in the presence of oxygen was caused by the hypoxic drive being knocked out, but this conclusion was not based on scientific evidence.

On the contrary, there are many studies that disprove the theory.

In 1989 Greggory A. Schmidt M.D. and Jesse B. Hall M.D. wrote an article, "Oxygen Therapy and Hypoxic Drive to Breath:  Is There Danger in the patient with COPD?" that was published in Critical Care Digest (1989, 8:52-53) questioning the popular hypoxic drive theory.  Schmidt and Hall reported that little science was used in coming up with this theory.  No COPD patients were given oxygen and had their ventilations simultaneously measured.  (11)

In fact, they report that in one study COPD patients were given oxygen and they found that "the rise in CO2 could not be accounted for by hypoventilation."

Likewise, a follow up study determined that supplemental oxygen to COPD patients caused decreased ventilation in some, unchanged ventilation in some, and normal ventilation in some. They wrote that "The commonest pattern was of early hypoventilation followed by a return to baseline.

Schmidt and Hall "attributed the rise in CO2 to an increase in the dead space to tidal volume ratio (also referred to as ventilation/ perfusion mismatching) consequent to oxygen therapy, though the mechanism for this change is unclear."

In another study, 22 COPD patients were given 100% oxygen and ventilations fell by an average of 20% for those who were CO2 retainers, yet the cause was determined not to be due to ventilation/ perfusion mismatching, "not just a failure of ventilatory response to the increase in PaCO2."  (12) 

Another study showed that oxygen induced hypercarbia was not caused by knocking out the drive to breathe.  In stable patients with COPD given 100% oxygen over a period of 15 minutes, oxygen saturations increased by about 7.6% and PaCO2 rose by about 6.6 mmgH, while minute ventilation was unchanged in all those studied. (13)

Yet all these and other studies came too late.  The gold standard of COPD care had already been ingrained into the medical profession.  Disproving it, even with science, may be next to impossible.

So what is the true effect of oxygen on COPD patients?

Since 1960, several studies have demonstrated what really happens when CO2 retainers are exposed to supplemental oxygen.  The best explanation comes from John Haldane himself in what is now referred to as the Haldane Effect, and another process we refer to as ventilation/ perfusion (V/Q) mismatching.

1.  The Haldane effect:   CO2 attaches to unsaturated hemoglobin molecules. Oxygen is more soluble in water and therefore has a higher affinity for hemoglobin, so if you increase oxygen in the blood by supplemental oxygen, CO2 molecules are forced off hemoglobin and oxygen takes its place.  This causes an increase in CO2 in the blood, or an increased PaCO2.

Most people would simply increase their respiratory rate and blow off this CO2.  Yet COPD retainers who are in respiratory distress may not have the capacity to increase their respiratory rate, so their respiratory rate remains the same.  This causes their PaCO2 to rise.

Now consider that this patient may have an elevated hemoglobin level after years of oxygen deprivation, and you're going to have lots of extra CO2 molecules roaming around the blood stream.  This may be on top the patient's already elevated CO2 retention.

All these CO2 molecules are transported back to the lungs for ventilation to take place.  Yet because many alveoli are poorly ventilated, and because the patient's ability to increase ventilations is tapped out, PaCO2 levels will rise.

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." (14)

2.  VQ mismatching:  COPD results in poorly ventilated alveoli due to bronchospasm and mucus plugs.  When an alveoli is poorly ventilated the vasculature around it will constrict so oxygen goes to alveoli that are ventilated well.  This is how that patient's body has made efficient use of his 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 the blood. 

This theory 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," (15)

How should COPD patients be managed?

The evidence suggests that supplemental oxygen may increase CO2 levels in some COPD patients, particularly those who are CO2 retainers.  While it is rare, it is still something that should weigh on the minds of medical professionals taking care of these patients.

Based on this evidence, Schmidt and Hall recommended that these patients be maintained on as little oxygen as possible to maintain an adequate oxygen saturation which most physicians would agree should be about 88-92 percent.  Many modern textbooks, including Textbook of Canadian Medical-Surgical Nursing, support this view. (16)

Yet Schmidt and Hall also note that oxygen is essential to sustaining life, and preventing such patients from receiving adequate oxygenation due to an unproven theory may be detrimental to the patient, and may even result in death.  For this reason, they recommend these patients be monitored and treated based on clinical assessment and work of breathing "rather than by arbitrary laboratory values."

Most studies show that in the absence of respiratory distress a COPD patient's CO2 may rise slightly in the presence of supplemental oxygen, yet will not cause the patient to stop breathing.  There have been many times I've had a CO2 retainer on 100% oxygen to maintain a hemoglobin saturation of 90 percent and I have rarely seen such a patient stop breathing.  In fact, in 17 years I've seen only one stop breathing.

The general idea in treating these patients is that if their ventilations decrease it's going to occur whether in the presence of oxygen or not.  If the patient's drive to breath is tapped, and CO2 levels rise to critical levels, the best treatment is to support the patient's ventilations with either non-invasive BiPAP or invasive ventilator.

What can we conclude here?


I personally think, as Schmidt and Hall suggest, that oxygen levels of COPD patients should be kept as low as possible in order to maintain adequate oxygenation, which should be an SpO2 of 88-92 percent and a PO2 of about 55-65 or somewhere in that area.  Chris Moulton and David W. Yates in their 2006 book "Lecture notes:  Emergency Medicine" recommend setting a goal "to raise the PaO2 above 50 mmHg without worsening the acidosis."  (17)

 If a patient's oxygen levels drop to critical levels, increasing supplemental oxygen should be an option.  This is common sense because without oxygen the body cannot function, the person may suffer an anoxic brain injury, and, if no oxygen is forthcoming, the person will die. 

If that patient's CO2 levels increase to critical levels while the oxygen saturation is acceptable and that patient shows signs of impending respiratory failure, the oxygen should be lowered first.  If this doesn't resolve the problem then ventilatory support (BiPAP or ventilator) would be the obvious next option.  

However, a trial on a higher oxygen level may sometimes be appropriate.  If the patient tolerates this higher oxygen level (say 100 percent) and the oxygen saturation remains in the 90 percent range, then the patient should remain on this oxygen level and weaned off it as his condition improves to maintain adequate oxygenation (SpO2 of 88-92 percent).

Yet if you have a chronic COPD retainer in the emergency room on 100% oxygen for over two hours to maintain an SpO2 of 86 percent, and as soon as that patient is admitted to a room the attending physician insists that you lower the oxygen immediately, you will have no choice but to comply.

Could the patient's family then sue because the patient died of doctor induced hypoxemia?  While they could, the hypoxic drive theory is so well ingrained by the medical community that use of it would most certainly hold up in a court of law.  So even though you don't support it, you must comply with the physician's order.

Surely the medical profession is loved and respected by most of us, yet that's not to say the profession is flawless. Even in the absence of scientific evidence many doctors will continue to worship the hypoxic drive theory (or myth/ hoax if you will) and prevent patients from receiving adequate oxygen levels.

It's been over 50 years that the hypoxic drive theory has been taught, and it may take 50 more to phase out the myth of the hypoxic drive theory.  So the moments of frustration will continue.  As RTs, we will have no choice but to comply with physician orders.

Yet, most important, we must continue to educate ourselves, challenge physicians, and encourage science. We must learn and teach facts.  We must continue this discussion here in the arena of ideas.

For further reading check out my post: The Hypoxic Drive:  Reality or Hoax.

References:

1. Schmidt, Greggory A., Jesse B. Hall M.D "Oxygen Therapy and Hypoxic Drive to Breath:  Is There Danger in the patient with COPD?" Critical Care Digest, 1989, 8, pages 52-53
2. Wilkins, Robert L, James K. Stoller, ed. "Egan's Fundamentals of Respiratory Care," 2009, pages 309-310
3. Caruana-Montaldo, Brendan, et al, "The Control of Breathing in Clinical Practice," Chest, 2000, 117, pages 205-225 (This article also provides a good review of the central and peripheral chemoreceptors and the drive to breathe)
4. Wojciechowski, William V., "Entry Level Exam Review for Respiratory Care:  Guidelines for success," 3rd edition, 2011, U.S., page 487?
5. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24
6. Tines, John Hudson, "Exploring the History of Medicine," 1999, great read for obtaining a pithy history of medicine
7. Glover, Dennis W. , "History of Respiratory therapy," 2010, page 94, great read for obtaining a pithy history of respiratory therapy
8. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24
9. Campbell, E.J.MRespiratory Failure,"  The British Medical Journal,  June 1965, 1451-1460 (article provided by link)
10. Reference not yet published.   Yes, I have privelidge to esoteric wisdom.  Will post when available. 
11. Schmidt, op cit, pages 52-53
12. Robinson, Tracey D., et al, "The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnia during Acute Exacerbations of Chronic Obstructive Pulmonary Disease," American Journal of Respiratory adn Critical Care Medicine, 2000, volume 161, pages 1524-1529
13. Dick, C.R., et al, "O2-induced change in ventilation and ventilatory drive in COPD," American Journal of Respiratory and Critical Care Medicine," volume 155, no. 2, Feb., 1997, pages 609-614
14. Hanson, et all, "Causes of hypercapnia with Oxygen Therapy in patients with Chronic Obstructive Pulmonary Disease," Critical Care medicine, 1996, volume 24, pages 23-28 (abstract available by link)  Source #3 above also indicates support for this theory (Caruano-Montaldo, ibid, page 218), and reference # 12 (Robinson, ibid, page 1527), and #13 (Dick, C.R., ibid)
15. Aubier, M, et al, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure", American Review of Respiratory Diseases,  1980, Volume 122, pages 747-754 (abstract available by link) Source #3 above also indicates support for this theory (Caruano-Montaldo, ibid, page 218)
16. Day, Rene A, Beverly Williams, Brunner and Suddarth's Textbook of Canadian Medical-Surgical Nursing, 2009, page 654.  Source #8 above also supports the veiw that the hypoxic drive is not responsible for hypercarbia in COPD patients given too much oxygen, and likewise supports the Haldane and V/Q mismatching theories (Cooper, op cit, page 24)
17. Moulton, Chris, David W. Yates, "Lecture notes:  Emergency Medicine," 3rd ed., 2006, pages 215-16

I would like to give special thanks to Jeffrey Whitnack, RRT,  for his speech to the 22nd Annual Tahoe Odysey Conference, "The death of the hypoxic drive theory."  He provided me with most of the above references and covered much of the same material, although much better than I ever could.  I'd provide a link to his web page, but I see it's been taken down.  I would also like to thank my un-named reference of whom I cannot currently acknowledge knowing.

read more...

Do high fat foods cause asthma?

The following post was originally published at HealthCentral/asthma on 5/16/2011:

"Do high fat foods trigger asthma?"

American's love Big Macs, Whoppers, French fries, onion rings and deep fried chicken.  These are convenient foods that are simply delicious.  Yet the old saying goes, "If it tastes good, it's probably not good for you."

Now we already knew such high-fat foods are bad for your heart.  Yet new evidence suggests they may also be bad for your lungs.

A study completed by Australian researchers in 2010 tested asthmatics before and after eating a meal, and determined that lung function was worse after eating a high-fat meal.

If that wasn't bad enough, the study also concluded that high-fat foods also made it so asthma rescue medicine (like Albuterol) worked less well.

Scientists aren't sure why this is, yet there are theories.  One theory suggests that your asthmatic immune system might recognize saturated fat as an enemy and promptly acts to rid it from your system.

This response results in an increase in markers of inflammation such as leukotrienes and hystamine, and these increase inflammation in your respiratory tract.  This causes muscles lining your air passages to constrict, and thus an asthma attack is the result.

Perhaps due to the increased inflammation, asthmatics who used their rescue medicine after eating a high-fat meal did not get as much relief as those who ate low-fat meals.   Likewise, lung function improved less in subjects who used their rescue medicine after eating high-fat meals.

Obviously asthma rates have increased incrementally in the U.S. and other western nations over the past 20 years.  This new theory suggests one of the factors might be the high-fat foods we put into our bodies.

I've also read other studies that suggest that if you're exposed to something that triggers inflammation in your lungs, and exposed to it often enough, the inflammation may become permanent.  Thus, asthma is developed.

It's studies like this that remind us that the way we eat may determine the lives we live.  If you want to prevent asthma, or prevent an asthma flare, it may be a good idea to eat a healthy diet.

Does that mean we asthmatics should never eat great tasting, convenient and high-fat foods?  Absolutely not.  Yet it's good to know the facts, and it's good to know what foods might not be good for us.
Facebook
Twitter

read more...

I'm infested with RATS

My wife believes I'm having a midlife crisis, although I believe I'm not.  I'm just to the point I hate going to work because of all the BS procedures we have to do.  I guess you can say I'm infested with RATS.  If even half of what I did that related to my job benefited someone I'd be happy, yet less than 10 percent of what we do is of relevance.

I used to say 20 percent of what we do that pertains to our job is useful, yet thanks to Obamacare I've lowered that number to 10 percent.  Since the passage of Obamacare our hospital has opted to hire 30 more administrative staffers -- instead of more nurses -- to make sure the hospital is adequately reimbursed by the government.

The result here is more work for us respiratory therapists.

Yet I was sure to explain to my wife it's not every day I dread going to work, it's only the days when I know I'm going to have to do fake RT work.  If it's going to be slow I look forward to those days because then I can find my own work to do, such as blogging.  I find this to be much more useful than blowing the white mist of Albuterol past the faces of people with normal lungs, or doing 300 EKGs just because of an order set.

More recently I told a doctor that even though this patient was short of breath he has good air movement, which means his lung muscles are relaxed and his air passages dilated like yours and mine.  That means the Ventolin molecules we're sending down there are bouncing off the beta receptors and coming back out for you and me to inhale.

I know that sounds frivolous, yet that's the kind of humor we RTs have to create to maintain our livelihoods.  As you know from these posts, humor is one of the main therapies of fighting off  RATS.

Facebook
Twitter

read more...

Signs of asthma attack in infants

The following is from healthcentral.com/asthma.

"What are signs of asthma attack in infants?"

Although it's difficult to diagnose, kids can get asthma too.  Since infants can't communicate they are having trouble breathing, it's up to you to spot an attack and know what to do about it.

The most common signs of asthma in infants are:

• Coughing, especially at night: This is actually a classic sign of asthma.  It's often the only sign.
• Night time wakenings: May be due to coughing and/or chest tightness
• Wheezing: May be audible or silent

The following are signs your child's asthma might be getting worse, and immediate attention is necessary:

• Rapid respiratory rate: Breathing is faster than normal
• Trouble feeding:  Or lack of desire to eat
• Agitation/ crying: When babies can't breathe they get restless
• Retractions: One great way to tell babies are having trouble breathing is if his chest is being sucked in with each inspiration.
• Nasal flaring: This is the flaring out of the nares upon inspiration. It is done in an attempt to suck in extra air. A classic sign of air hunger in babies.
• Grunting on expiration: This is the baby's natural attempt to keep his lungs open. Another classic sign of air hunger.
• Cyanosis: This is the blue discoloration of skin caused by lack of oxygen to that area. Usually it's around the mouth, nose and fingertips. This is a sign the baby is not getting enough oxygen.

Your asthmatic may display one or a combination of any of the above signs.  Each child is unique, and this is why it's important for you to be vigilant to the specific signs your child displays.

Once diagnosed with asthma, you and your child's pediatrician will want to create an asthma action plan tailored just for your child.  This plan will help you monitor your child's asthma, and know what to do in the event you see the above signs.

Most asthma experts recommend all asthmatics have a rescue medicine called Albuterol or Xopenex on hand at all times.  These are bronchodilators.  They relax the muscles surrounding the air passages in your asthmatic child's lungs, and can rapidly make breathing easier.

This medicine can be given to your child using a nebulizer with a mask or an inhaler with a spacer and a mask.  While a nebulizer is the most common method, more recent studies actually show an inhaler is the best method to use.  However, the truly best method is whichever one your child accepts (to learn more click here).

Usually two puffs of the medicine are given if an inhaler is used.  These puffs should be spaced one to two minutes apart.  If a nebulizer is used, the treatment usually lasts about 10 minutes.

Of course this depends on the severity and control level of your child's asthma, yet if your child's need for his rescue medicine is greater than normal, then you should notify his pediatrician or take him to the emergency room.  Increased use of rescue medicine likewise a common sign of uncontrolled or worsening asthma.

If the signs of asthma go away after using the rescue medicine, you can simply monitor your child at home.  If the signs don't go away, you should call your child's doctor or take your child to a local emergency room.

Again, you should follow whatever guidelines written down when you and our child's doctor created an asthma action plan.

However, if your child is not yet diagnosed with asthma, you do not have an asthma action plan, and you observe any of the above signs, you should call your child's pediatrician or take him to the emergency room right away.

Since your infant doesn't have a voice, it's up to you to observe the signs of trouble breathing.  By being vigilant in this way you can make sure your child is always breathing easy, and you might even save his life.
>

read more...

Why do people die of asthma?

Your question:  Why do people die of asthma

 

My humble answer:  For most people, I'd guestimate about 90-99% percent, asthma is more annoying than something that kills.  Asthma is a disease that's reversible with either time or medicine, and can inflict poeple of any age at any time. You don't even need to have the asthma gene to get it.  Usually asthma doesn't become life threatening until it's mixed with other disease conditions, such as pneumonia, influenza, heart failure, kidney failure, etc.  Age can also be a factor here as well.  But, from my knowledge, asthma in and of itself has a very low death rate (less than 1% of asthmatics).  Smoking can also complicate asthma, as well as second hand smoke.  You haven't provided this information, so I'm just rattling off some possibilities here. 

Facebook
Twitter

read more...

Impressive link between Tylenol and asthma

This article was originally published on MyAsthmaCentral/Asthma January 17, 2012 with the headline "Does Tylenol Cause Asthma?"

Is it truly possible Tylenol (a.k.a. acetominophen) causes asthma?  The evidence seems to be pointing in that direction.

A stunning observation made by CNN Health was that asthma rates started to climb in 1980.  Coincidentally that was the same year aspirin was linked to Reyes Syndrome.

Also, that was the year Tylenol was first marketed as the pain reliever hospitals choose first.  You can see such a commercial  here.

Since 1980 asthma rates have risen dramatically.  The American Academy of Allergy Asthma and Immunology (aaaai.org) lists the following asthma statistics:

• Asthma rates in children under the age of 5 increased more than 160 percent from 1980 to 1994
• The prevalence of asthma increased 75 percent between 1980 and 1994

Coincidence?

Surely it's possible asthmatics simply have more pain than the average person.  It's also possible greater asthma wisdom has more patients being properly diagnosed.

Yet it's not just a few studies that link asthma to acetominophen, even our fellow asthma experts have observed the link and written about it.

CNN Health mentions a 2010 study of 320,000 teenagers in 50 countries where researchers concluded those who took acetominophen for at least one month were 2.5 times more likely to experience asthma symptoms.

The study showed that even those who took the medicine just once a year were 40 percent more likely to experience asthma, allergy and eczema symptoms.

A more recent study was published in the December 2010 issue of Pediatrics and you can read about it at USA Today.

The study found that kids between the ages of 6 and 7 who took Tylenol at least once a year and once a month had a 61 percent greater chance of developing asthma compared with kids who did not take any.

There have been studies linking moms who took acetominophen during their pregnancies with their children wheezing by age 3.

And another showed children given acetominophen for infection early in life had an increased incidence of asthma, allergies and rhinitis (nasal allergies) by age 7.

The Journal of Investigational Allergology & Clinical Imunology, published a 2008 article revealing the results of a study performed by the International Study of Asthma and Allergies in Children (ISAAC) that showed a "significant link" between acetaminophen and asthma.

According to this same article researchers believe acetominophen depletes your body of a protein called gluthione, especially in the liver.  According to American Healthcare Foundation (AHF), glutathione is a protein and an essential component of the immune system.  It's produced by cells throughout the body.

AHF describes that a low glutathione level has been linked to the "onset and progression of asthma."  Low levels have also been linked to the severity of an attack.  Studies have also linked inflamed cells with low levels of glutathione.

Since asthmatic airways always have a small degree of inflammation, and worsening of this inflammation may result in an asthma attack, this link seems rather significant.

Of course acetominophen is believed to be just  one of many things that deplete glutathione levels. According to the ISAAC article above, other things believed to deplete it include genetic factors, environmental factors and diet.

Despite the link, researchers still aren't convinced acetominophen causes asthma.  Likewise, the makers of Tylenol still claim their medicine is safe.  So you should expect to read more such studies in the coming years.

So should we stop giving our kids acetominophen products? You'll have to decide that for yourself.

Considering my asthma history, I'm not taking any chances giving my kids any acetominophen product, at least until the medicine gets scientifically cleared of any wrong

Facebook
Twitter

read more...

Hope versus desire

I wrote last Sunday about the need to teach about absolute truths and not worry about offending doctors and bosses in order to reform the medical field.  We must seek and teach the truth.  Yet since most of us know the truth hurts, we tend to turn a blind eye to it.  We've become apathetic enablers of the un-truth because that route is easiest. Instead we rely on HOPE!  We HOPE it will get better.

Yet hope is no way to lead the world into the future.  Hope will die with you.  It's good to have faith, yet hope will only lead a nation to destruction because those who hope are not doing.  Those who hope are dreaming of a better world.  Yet if there is one thing we should know as Americans is that dreams do not come true unless we act on them.

Even the Bible teaches that God helps those who help themselves.  Actually I think that's a quote made by some ancient philosopher and changed slightly by Ben Franklin when he wrote Poor Richard's Almanac, yet the idea has a certain truth to it.  The way to prosperity is through individual effort. 

Friedrich Nietzsche once wrote that,  "Hope is the worst of evils, for it prolongs the torments of man."  Hope never solved any problem.  Hope traps people right where they are, good or bad.  When you're hoping you are staying in your home, doing nothing, but thinking -- hoping.

There is no action with hope. There is action with desire.  Desire is when you want something and you go out and get it.  The founding fathers wanted freedom, and they gathered together, fearing death, and went out and sought and obtained freedom.  They didn't do it by sitting at home. They did it by grabbing a pen and a gun and seeking it.

Friedrich Nietzsche's, I think, meant that when you hope you see that something is wrong and you are dreaming of a better world or a better idea.  You are not happy, yet you see a world that is ideal to you and will make you happy. 

When you hope you are unhappy, incontent, miserable or not satisfied.  You are not happy.  Yet your torment continues because nothing is going to be done.  Hope never changes anything.

You can do the best for your child and then hope for the best.  You hope he makes the right decisions, and you hope that God helps him.  Yet God also says that He will help those who help themselves.  The parable of the talents told by Jesus through Matthew (25: 13-30) describes this well.
If you want something, you need to take risks.  God isn't going to help someone who buries his money.  You need to take risks.  There are risks in every thing we do, and nothing can remove the risk out of life.  It's a simple fact.  

So, even though you think there isn't much you can do once your child leaves the house, there is.  For one, you can continue to keep contact with him, and you can continue to set a good example.  You can continue to preach the truth, and you can continue to go to church or whatever good deeds you did when you were teaching your child. 

You must not sit around hoping.  Hope never did anything for anyone.  However, by making a good effort to teach your child, you made an effort.  Then, and only then, can you sit around hoping you made the best decisions and set the best examples.  Only then can you sit around hoping that God watches out for your child.

Hope, as used by most people, is an excuse for not trying.  It's good to have hope after you've made an effort, it's good to have hope after you desire something, yet it's not good just to sit around at your homes and hope things work out.  Because if that's all you're going to do nothing will ever change.

Desire, on the other hand, does change things.  Desire means you want something and you go out through hell or high water to seek what you are after.  Desire is action orientated.  Hope must come before and after desire and effort, but never should you rely on hope alone.  Hope is good, but not alone.

If you desire change in the medical field, for example, if you desire doctors to stop ordering needless breathing treatments, and you desire for the government and insurance companies to stop telling doctors what they have to order in order to get paid, then you have to make an effort. 

Desire should precede effort and hope should follow that.  Yet hope alone will not solve anything.  If you live on hope alone you will always wallow in misery. If you are an apathetic medical care worker because you're burned out because you think doctors are writing stupid orders, or because your hospital quality assurance or Keystone committee has created order sets, then you need to make an effort to seek and teach the absolute truth.  You must make the effort, and then you can hope for the best.

Another person can bring false hope.  Some people want you to feel like despots, to feel miserable, to feel apathetic, and then they want to to sit around hoping things will get better some day.  They want to trap you.  When you are trapped you'll feel there is nothing left but hope -- false hope.

Hope is an emotion.  Emotions don't solve problems.  You can feel sorry for someone, but hoping they make the right decisions isn't going to do any good.  Hope is the bottom feeling of people who think they don't matter in the greater scope of things.  Hope is the cry of those who think they have no control.  Quite frankly, most people don't like not mattering, so they hope.

So you want doctors to stop ordering stupid breathing treatments, or to quit believing in that stupid hypoxic drive hoax,  and so you hope that someday it gets better.  Yet what did you do to create change? 

The people who want to defeat us, the people who want to control us, want us to sit around hoping all day.  They want us to feel hopeless, apathetic, and then they have all the more power over us.  They want you to feel as though your life, your job, has no meaning. 

Heck, how many times have you heard an RT or RN say that 90% of what we do in the medical field has no reason?  Most of what we do wastes time or delays time.  That's what some people in power want.  They want you to hope so you have an excuse to sit around and do nothing but wine and complain.  They want you to feel empty.

Say you're playing a basketball game.  You can have hope that you win, but you can hope all you want because that alone won't bring about victory.  If you want to win you have to have desire, and you have to act on that desire with effort, and then you have to hope you gave it your best  as a team.

We must have family, faith, hope, love and charity.  Yet we must also have desire and we must also have effort.  To make the medical field better, to make the U.S. better, we must have hope, faith, charity, yet we must also have desire and effort. 

I'm not sitting around hoping things get better.  I'm not sitting around hoping the medical field gets better.  I'm not sitting around hoping doctors some day stop ordering stuff that's not scientifically proven to do anything.  I'm creating a better world.  I'm taking action.  I'm sitting here blogging.  What are you doing?


Facebook
 Twitter

read more...