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10 Articles in Volume 17, Issue #5
Cross-Linked Hyaluronic Acid Injection for Neuropathic Pain
Discussing Migraine: What to Try When Nothing Is Working
IV Propofol for Treatment of Chronic Intractable Cluster Headache: A Case Series
Letters to the Editor: Rapid Opioid Metabolizer, Intractable Pain, Adrenal Suppression, Traumatic Brain Injury
Migraine Treatment: What’s Old, What’s New
Schizophrenia Spectrum and Chronic Pain: Is Pain Insensitivity a Myth?
Spinal Fluid Flow and Pain Management
Step-by-Step Technique for Targeting Superficial Radial Nerve Pain
The Primary Care Provider’s Role in Diagnosing and Treating Rheumatoid Arthritis
What is the appropriate use of phone texting between physicians and patients?

Letters to the Editor: Rapid Opioid Metabolizer, Intractable Pain, Adrenal Suppression, Traumatic Brain Injury

June 2017
Page 1 of 3

Rapid Opioid Metabolizer

In January 2015, I was working in the emergency room when a young lady presented with signs and symptoms consistent with ureterolithiasis. In addition to standard treatment (tamsulosin, ketorolac, pyridium) and intravenous (IV) fluids, I prescribed the usual amount of hydromorphone (Dilaudid). I generally start with a 0.5 mg IV push; this dosage of medication did nothing to reduce the patient’s pain, and over the next 90 minutes, I slowly increased the dosage of IV hydromorphone to 2 mg.


On questioning the patient, she mentioned having a prior experience with severe pain that required high doses of opioid medication to control the pain.

Although the CT scan offered no evidence of a kidney stone, a prior history of having passed stones and her present signs and symptoms (hematuria on urinalysis) suggested that she had a stone despite the lack of confirmation on CT, which does happen. Because we could not get the pain under control, she was admitted to our small rural hospital and put on telemetry and oximetry.

Over the next 24 hours, the patient received 2 mg of hydromorphone every 2 hours; yet, her pain level never dropped below 6 to 7 out of 10 (based on a numeric pain scale). When prompted, she stated that while she was getting some relief it wasn’t sufficient to relax or rest. In response, I increased the delivery of hydromorphone to 2 mg every 1-1/2 hours and that brought her pain level down to about a 5 out of 10, permitting the patient to rest.

However, the patient stated that she could not sleep due to the noise from the cardiac monitor and the oximeter, and she removed them herself. The experienced nurse who was on duty did not call me. If she had, I would have informed the patient that unless she permitted the medical monitoring, she would have to seek care elsewhere.

When I was finally called at 4:30 AM the patient was found unresponsive with shallow breathing. The nurse stated that the patient responded to a sternal rub briefly and had been checking on her every half hour. Retrospectively, the patient had a stone that was passed during hypersedation.

The reason for my inquiry is that I had to use 4 single use vials of naloxone (Narcan) to wake her up. She had difficulty with short-term memory for several weeks. An MRI ordered 7 days after the event did not show evidence of acute cerebral anoxia.

Now, a full year later, the patient stated that she is still having problems with her short-term memory. The patient is suing the hospital for $10 million. It is evident that she is a rapid opioid metabolizer.

In looking for support for our case, I came across an article on genetic testing from the May 2016 issue of Practical Pain Management (PPM).1 Are there any other articles that might lend support to our pain care?

I feel that I gave this patient the best care possible, and now I feel betrayed for doing what I could to meet her pain needs.

(Doctor, Name Withheld)

Dear Doctor,

Your situation in which a patient is attempting to sue you and your hospital raises more than one ramification for pain practitioners. First, any patient who refused telemetry and oximetry when acutely ill and against medical advice, in my opinion, would lose all liability rights.

Clinically, the genetic factors with regard to this patient are significant. This patient has a history of kidney stones, which is a genetic disease. Given that she was a rapid metabolizer on cytochrome P450 testing offers further evidence of genetic variations. A patient with a known genetic propensity to stone formation and/or presentation of other intermittent pain-related disease, such as sickle cell anemia or porphyria, and who presented in acute pain would bring an extra risk of aberrant drug metabolism.  

Hydromorphone would be an excellent choice in these pain patients, since it doesn’t utilize the cytochrome P450 system for metabolism. In addition, it is very short-acting, so the every 2-hour dosage you administered would be most appropriate, and in a typical patient, would not accumulate or cause a toxic reaction.

In this case, your patient may have a genetic variation in her mu opioid receptor binding capacity and/or hydromorphone degradation capacity. Unfortunately, genetic testing to determine the presence of genetic variations is only in the formative stages.

Since you detected the hydromorphone accumulation problem and corrected it with naloxone, your patient should be grateful. Her complaint of any injury can only be a guess on her part, and her claim is not provable, as she would have required mental testing before and after the supposed offending event to demonstrate any clinically relevant decline.

Forest Tennant, MD, DrPH

Clinical Advances In Pain Care

I was pleased to see your attention to Ehlers-Danlos syndrome (EDS) and ankylosing spondylitis (AS) with regard to Elvis Presley and Howard Hughes,2-4 but I am concerned that “making a diagnosis does not a cure make.”

As you mentioned, Elvis and Howard Hughes both had at least 1 significant head trauma.2 Additionally, creative individuals like these 2 famous men exhibit greater facility (via altered dopaminergic signaling) in which they moved in and out of REM-like states, which built new cognitive associations that most typical patients may not achieve. In addition, these super-achievers had an ability to subsume normal “stop” signals in their sense of mission (known as passion for the rest of us).

Understanding these distinctions, it would be constructive to mention that amyloid is a structural repair protein, meaning there had to be structural damage, and that autoimmunity (as observed in multiple sclerosis [MS] and similar conditions) would be considered a secondary or tertiary consequence of a prior injury.

This knowledge puts us in a position to look with less bias at the [unpublished] practice of Brendan Stack, DDS, who treats dystonia, and David Williams, DDS, who dissected cadavers of patients with MS, adrenoleukodystrophy, Parkinson’s, and Alzheimer’s diseases.5 In these conditions, hypermobile temporal bone structures, as well as abnormal skull flexion, have been reported in people with MS—a test I replicated.

We have a better foundation to move beyond diagnosis and palliation to slow or arrest the progression of these diseases. For over 25 years, some doctors of osteopathy, doctors of chiropractic, physical therapists, dentists, and myofunctional (breathing) therapists have met and collaborated in treating small numbers of similar cases employing the ALF (advanced lightwire functional) appliance.6

Last updated on: June 15, 2017
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Migraine Treatment: What’s Old, What’s New

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