I was working a day shift in the ER.  We were rather slow in the pediatric department, where I was assigned for the day, so I took the opportunity to go to another area to help a nurse draw blood from a patient described as a “difficult stick.”  Not long after, the experienced R.N. in the peds (pronounced peeds) department called me over our communication system.  “I need you back over here now,” she said in a firm, serious tone.  I knew it must be something important, so I went back there immediately.

As I entered the area, I saw a young, thin, white boy being wheeled on a stretcher from a regular room to the “trauma” or “code” pediatric room next door, where additional medical emergency equipment is located.  Our ER tech had the ambu (breathing) bag over the boy’s mouth, administering oxygen to him but not squeezing the transparent plastic part that looks like a football. This meant he was still breathing on his own.  Just as we entered the room, the boy went unconscious, becoming very pale, with blue lips.  These symptoms are signs of lack of blood flow, so as other co-workers began to join us, he was placed on a heart monitor and I briefly attempted to find a pulse.  The monitor showed an abnormal rhythm called ventricular tachycardia (V-tach) and I could not find a pulse, so I began CPR with chest compressions.  Stick-on defibrillation pads were placed on the boy, and the defibrillator was charged to 50 joules in preparation for electronic defibrillation of the heart.

The boy’s stunned parents were left outside as we concentrated on treating their son.  The doctor hit charge on the monitor, which emitted the sustained, high-pitched “woo” sound indicating the machine was charging.  He called “clear,” I stopped the compressions, and we all stepped back.  The boy was shocked and his body jerked upward.  I could see on the monitor that his V-tach had broken, and a more normal-looking rhythm appeared as I immediately moved in to resume compressions.  The boy immediately “pinked up,” the color returning to his face, neck, and entire body. (This is called ROSC, or return of spontaneous circulation.)  We stopped compressions and checked the monitor.  His heartbeat was normal.  He began moving his head slightly as well.  Over the next few minutes, the boy remained in a normal rhythm on the heart monitor, only slightly fast, and had normal blood pressure.  He had responded well to being defibrillated.

The V-tach, which looks like tall, thin mountain peaks on the monitor, was gone for now.  Those thin, continuous mountain peaks indicate that there is a serious malfunction of the heart’s electrical system, which is usually, but not always, accompanied by pulselessness.  This young boy had had the more lethal variety of V-tach, which does not produce a pulse and therefore quickly results in brain and organ death.  The electrical shock in defibrillation stops the whole electrical system briefly in hopes that when the electricity “comes back on,” it will go through the normal pathways again, producing a normal rhythm.

As I carefully examined this young man whom we had just brought back from the brink of death (by the grace of God), I noticed that he was only moaning and not making any purposeful eye contact.  We brought his parents back in and they hovered over him, stroking his head and trying to console him.  They were in a state of shock, fear, and confusion, asking for answers that, for the most part, we could not give— at least not yet.  We listened to his lungs, which were clear, and checked his oxygenation, which was also normal with the supplemental oxygen we were giving him. He was breathing on his own without any difficulty.

However, 15 minutes later he was still moaning, occasionally thrashing on the bed, and not speaking coherently.  His eyes were rolling around aimlessly.  At one point he was coherent enough to communicate to his mother that he could not see anything.  “Oh dear God,” I thought to myself, “was he deprived of oxygen to his brain to an extent that he has suffered brain damage?” This tall, thin, 11-year-old boy reminded me of my tall, thin, 12-year-old son.  The parents mentioned that he had recently had a growth spurt.

The nurse who received the patient had informed me that he was speaking normally on arrival, and that the reason he’d been brought in was that he had had a couple of unconscious episodes at home and his mother had discovered him sweating and “passed out” on the couch earlier that day.  She had called 911, but he had awakened on his own (probably a self-limiting episode of this abnormal cardiac rhythm).

Since his condition was critical,  the doctors decided that he should be transferred to the children’s hospital in the nearby major city. Soon that hospital was preparing to send their helicopter up to us, about a 15-minute flight. However, getting everyone (the pilot/ doctor/nurse/ paramedic) on the helicopter took longer, so we knew there would be a bit of a wait.

At least five of us staff members stayed at the boy’s bedside, riveted with concern for this child.  More frequent PVCs (a possible precursor to that more serious problem) began to show up on the heart monitor, and then short runs of V-tach also occurred.  This all indicated potential trouble.  We called the doctor into the room just in time for a sustained V-tach to appear.  The boy’s body went limp and lifeless again, and again I performed chest compressions until the defibrillator could be charged and discharged.  He again responded well to one shock at 50 joules.  We tried giving him an emergency anti-arrhythmic drug called Amiodarone at a dose appropriate for a child, but for a third time, he went into this lethal dysrhythmia.  Thankfully, for a third time, he was shocked back from the brink of death.

We then tried another drug called Lidocaine, an older drug for this type of problem, and it may have been what helped stave off any further episodes until the team arrived from the children’s hospital.  Also thankfully, the boy’s vision returned after about 45 minutes, and as he left to go on the helicopter he was speaking normally to his mother.  During the wait for the children’s hospital team, we had performed an echocardiogram, which is an ultrasound that shows the general size and function of the heart.  His was perfectly normal, which ruled out a possible cause for his symptoms such as cardiomyopathy (enlarged heart) or valve disease, which could potentially trigger these types of lethal dysrhythmias.

This episode was one of the top five intense moments I have had in my more than 20 years of nursing.  Every “code” is intense, but caring for children in life-threatening situations is the most stressful for me and most nurses.  While we were treating this child, we sought to determine the cause of his problem.  Was he dehydrated?  No.  Were his electrolytes (potassium, magnesium, sodium) abnormal?  No.  Did he have any heart defects?  No.  Any other serious medical problems?  No.  Could he have ingested any drugs?  No…. except he did take one drug prescribed for his ADHD.  The drug is a central nervous system stimulant that has been known to cause sudden cardiac death.  There is a warning from the FDA about the increased risk of death from this type of drug if you have a known heart problem.

I later mentioned this case and the boy’s use of that particular stimulant to our staff psychiatrist.  He said, “That is probably what did it.”  (He is exceptionally candid about the negative effects of these drugs on kids).  However, our ER doctor was in some denial about this as a possible cause.  I did mention to the boy’s mother that the drug could cause this problem, so hopefully he will not be put back on it.  She voluntarily suggested that not taking it would be best for him.  I also talked to our ER pharmacist about the incident, and he, too, agreed it was probably the CNS stimulant that caused the problem, and the data source he checked confirmed that this particular drug has been linked to these lethal heart dysrhythmias.  What many people don’t realize is that these drugs are amphetamines, or derivatives of them, commonly known on the street as Speed.

However, the pharmacist also said that since we hospital staff had not administered the drug to the boy that day, we were not the appropriate ones to fill out a medication adverse-reaction report.  He suggested that I go online and file a report at FDA Medwatch, which I did, indicating in the section provided that I was a health care provider.  At the end of the submission, a pop-up appeared, stating that my report “has been submitted to a database.”  That was not very reassuring.  I felt like I had thrown a stone into a large reservoir never to be seen again.  There was also an option to be contacted by the manufacturer, and it said that by choosing “no,” I might be impeding their ability to monitor possible future adverse reactions.  I have a hard time believing that they are seriously motivated to learn about adverse reactions to profitable drugs. This warning also reminded me of the FDA’s practice of relying on drug companies themselves to monitor and report adverse reactions to their drugs to the agency.  I wondered what effect self-reporting might have on sales.

I also wondered how many times something like this had occurred and not been reported?  I am sure it must be in the thousands, or tens of thousands.  If I had not gone out of my way to make a report to the FDA, it would never have been done, and even so, it is doubtful that my report will be acted upon.  I think most people are under the impression that there is a more established method for monitoring and reporting adverse reactions to these types of drugs.  There isn’t.

As I mentioned, the ER doctor was in denial about the ADHD med being the most likely cause of this child’s nearly dying, even though both the pharmacist and staff psychiatrist (who have more specific training in this area) thought that it was.  This is a very disturbing reality.  In any other situation where there had been an accidental or intentional ingestion of Speed, there would have been no doubt that it was the cause of the problem.  However, as many of us are aware and Robert Whitaker has insightfully pointed out, there is a cloud of delusion and collusion that hangs over the otherwise brilliant minds of many in the medical profession, and in society as a whole.  My hope and prayer is that this dramatic look at a negative effect of this class of drugs will help you understand that, in my professional assessment, the risks of these drugs outweigh their benefits.

 

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Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.





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