What Is Ketamine?

Ketamine, often referred to on the street as “Special K” or “Vitamin K,” is a dissociative anesthetic originally developed for use in both veterinary and human medicine, especially dentistry. It stands out due to its ability to induce a trance-like state, where the patient remains aware of their surroundings but detached from their senses and consciousness.

First synthesized in 1962, Ketamine gained prominence during the Vietnam War in the 1970s. Its minimal depressive effects on the respiratory and circulatory systems made it an invaluable tool in battlefield medicine, as it did not require intensive monitoring of medical professionals not readily available. Unlike general anesthetics that render patients completely unconscious, Ketamine induces a state of dissociation where the mind and body appear disconnected.

Its chemical structure is most closely related to Phencyclidine (PCP) and was used as a starting point for the synthesizing of Ketamine. Due to its unique effects, Ketamine serves as an effective anesthetic and has become a focal point for discussions around both its therapeutic potential and its risks for abuse.

 

Recreational Use: A Dangerous Allure

Despite its medical utility, Ketamine has also become a drug of abuse. The rise of recreational Ketamine use began in the early 2000s, particularly within the rave and club culture. Dosages at a sub-anesthetic level will not cause complete dissociation, and the effects are often reported by users as “dreamlike” and often combine it with MDMA (Ecstasy) to heighten its effects.

However, recreational dosing can be perilous. High doses can lead to a “K-hole,” where users experience near-anesthetic states, losing awareness of their surroundings and themselves. This detachment significantly increases the risk of injury or fatal accidents.

Ketamine is typically manufactured as a liquid for medical use but is often dehydrated into a white crystalline powder for recreational purposes. The powder is commonly snorted or rehydrated for injection, posing additional risks of contamination and infection.

 

Ketamine’s Role in Mental Health Treatment

Over the past two decades, Ketamine has emerged as a potential breakthrough in mental health treatment. Its rapid effects on conditions such as depression, anxiety, and post-traumatic stress disorder (PTSD) have captivated researchers and clinicians. Unlike traditional antidepressants, which can take weeks to show results, Ketamine has demonstrated positive effects within hours or days.

Though the precise mechanisms by which Ketamine operates remain unclear, it is believed to interact with glutamate receptors in the brain, promoting neural plasticity and creating new pathways. However, Ketamine treatment is not a simple take-home solution. It requires a controlled clinical setting to ensure safety and efficacy, given its potential for abuse.

This promising application comes with caveats. The long-term effects of Ketamine use, even in therapeutic contexts, are not yet fully understood. As such, its administration remains carefully regulated, often as part of a broader mental health treatment plan.

 

The Risks of Ketamine Abuse

Ketamine abuse continues to pose significant public health challenges. Overdose deaths, like the tragic case of actor Matthew Perry, highlight the drug’s dangers. Misuse can lead to severe psychological and physical consequences, including hallucinations, memory loss, and urinary tract problems—commonly referred to as “Ketamine bladder syndrome.”

Furthermore, self-administering Ketamine outside of professional guidance carries the risk of contaminated or mislabeled products, exacerbating its hazards. The line between therapeutic use and abuse can blur, particularly when patients self-medicate without adequate oversight.

 

Moving Forward: Education and Regulation

As Ketamine’s therapeutic potential gains attention, so too must the focus on its risks. Education around safe usage, the dangers of recreational use, and the importance of proper medical oversight is critical. Policymakers must also address the regulatory gaps that allow for illicit production and distribution.

Collaboration among healthcare providers, law enforcement, and community organizations is essential to strike a balance between leveraging Ketamine’s benefits and mitigating its risks. This includes expanding access to safe, clinical Ketamine treatments while cracking down on illegal distribution channels.

 

Detecting Ketamine Abuse: The Role of Drug Testing

Given Ketamine’s dual role as a life-saving anesthetic and a drug of abuse, the need for effective detection methods is paramount. Drug testing serves multiple purposes, from monitoring individuals in treatment programs to ensuring safety in workplaces or legal contexts. National Test Systems offers various urine testing options to detect Ketamine use. These include single-panel dip tests, which are also useful for surface or powder testing, and multi-panel test cups for broader drug screening. Such tools are essential for identifying illicit use and ensuring appropriate intervention.

 

Final Thoughts

Ketamine stands at a fascinating intersection of medicine, mental health, and public safety. Its ability to revolutionize mental health treatment is undeniable, yet the dangers of abuse cannot be ignored. By promoting awareness, supporting research, and maintaining vigilant oversight, we can harness Ketamine’s potential responsibly and effectively.

In recent years, a new substance has quietly infiltrated gas stations, smoke shops, and convenience stores across the United States, contributing to the growing problem of “gas station dope.” Known by names like Zaza (Zaza Red, Zaza White) and Tianaa (Tianaa White, Green, Red), this substance, Tianeptine, has evolved from a little-known antidepressant into a drug of concern, responsible for an increasing number of poisonings, addiction cases, and even deaths. Originally developed in the 1960s by the French Society for Medical Research, Tianeptine has slipped through the cracks of federal regulation in the U.S. Its opioid-like effects, especially at high doses, have made it a popular but dangerous drug for recreational use, leading to a troubling spike in poisonings and other serious health consequences. We touched briefly on Tianeptine in our Gas Station Dope webinar, but as we are hearing more and more about its misuse from our clients, we felt it needed its own spotlight. This blog will dive into the history, pharmacology, dangers, and public health concerns of Tianeptine misuse, as well as the ongoing legislative responses to control its spread.

 

What is Tianeptine?

Tianeptine is classified as an atypical tricyclic antidepressant. While it shares some molecular similarities with traditional tricyclic antidepressants (its three-ring structure gives it the name “tricyclic”), it has an atypical mechanism of action. One of the most significant factors that makes Tianeptine stand out is its mild μ-opioid agonist properties, meaning it binds to opioid receptors in the brain, leading to mood-elevating and pain-relieving effects, not unlike opioids.

In therapeutic doses, Tianeptine’s antidepressant properties have been used in various countries to treat depression and anxiety disorders. However, at high doses, it acts more like an opioid, which significantly increases the risk of addiction, overdose, and death. Because of this, recreational use of Tianeptine has become a growing public health threat, particularly in regions where it is easily accessible and largely unregulated.

 

Historical Context

The earliest recorded instances of Tianeptine misuse date back to 1989 in Europe, particularly in France. Since then, its misuse has slowly increased, with its effects becoming more widely recognized and documented. Despite early warnings, the drug’s reputation as a relatively safe antidepressant in other parts of the world shielded it from regulatory scrutiny in the U.S. until more recently.

 

The Opioid Crisis Connection

The opioid crisis has made Americans more aware of the dangers of opioid addiction. Yet, many are unaware that substances like Tianeptine, legally sold under names like Zaza and Tianaa, are part of the problem. The CDC reported an alarming increase in Tianeptine-related poisonings, from 11 cases between 2000 and 2013 to 151 cases in 2020 alone *figure 1. The fact that it can be purchased in gas stations, often without any age restrictions or warnings, makes it a hidden danger.

 

Health Risks of Tianeptine Misuse

While Tianeptine is marketed as a dietary supplement in the U.S., consumers are often unaware of the potential dangers of misuse. At higher-than-recommended doses, it exhibits opioid-like effects—leading to euphoria, sedation, and a reduction in pain. This has made it attractive to those seeking an opioid-like experience without the perceived stigma or legality issues associated with traditional opioids.

 

Signs of Tianeptine Overdose

Some of the most serious consequences of Tianeptine misuse include:

• Agitation and confusion
• Severe drowsiness and lethargy
• Sweating and rapid heartbeat
• High blood pressure
• Nausea and vomiting
• Slowed or stopped breathing (respiratory depression)
• Coma or death

Due to its opioid properties, Tianeptine overdose can look similar to opioid overdose, with the risk of respiratory failure being especially high. Unfortunately, public awareness about these risks is low, partly because the drug is often marketed as a “supplement” or “natural remedy.”

 

*figure 1

 

Legal and Regulatory Status

Despite the dangers, Tianeptine is not classified as a controlled substance at the federal level in the U.S. This means that in most states, it can still be legally sold in gas stations and other retail outlets. However, the FDA has ruled that it is unlawful for use in dietary supplements or food products, though enforcement of this ruling remains inconsistent.

Several states have taken their own steps to ban or restrict the sale of Tianeptine. These include:

• Michigan (2018)
• Alabama (2021)
• Tennessee (2022)
• Ohio (2022)
• Kentucky (2023)
• Florida (2023)
• Georgia (2024)

Some states, such as Indiana, are considering similar legislation, though no official law has been passed as of this writing. In states where Tianeptine has been banned, the black market has stepped in to fill the demand, with the drug now being trafficked illicitly. This mirrors patterns seen in the opioid crisis, where restrictions on legal access have led to a surge in illicit drug markets.

 

The Way Forward: Public Health Implications and Solutions

The rise of Tianeptine misuse is a clear example of the dangers posed by unregulated substances sold in seemingly harmless locations like gas stations. To address this issue, education and awareness are crucial. Both the general public and healthcare professionals need to be better informed about the risks associated with Tianeptine and other so-called “gas station drugs.” Additionally, policy measures at both the state and federal levels are needed to regulate the sale and distribution of Tianeptine. This could involve tighter controls on the sale of products containing the substance, as well as increased enforcement of existing FDA rules prohibiting its use in dietary supplements. Finally, international cooperation may be necessary to combat the global nature of Tianeptine misuse. As the drug continues to be prescribed in some countries, efforts to prevent its diversion into the U.S. market will require collaboration across borders.

 

Detection and Testing

One of the challenges in combatting Tianeptine misuse has been the difficulty in detecting the drug in standard drug tests. Until recently, most drug testing panels did not include Tianeptine. However, recent advances have led to the development of instant urine drug tests specifically designed to detect Tianeptine.

These tests are currently available as single-panel strip tests, but they have not yet been incorporated into more comprehensive multi-panel tests. This means that individuals who misuse Tianeptine can still pass many standard drug tests, complicating efforts to monitor its use in populations at risk.

We always get a lot of interesting questions from our clients. Sometimes these questions lead to meaningful and educational conversations or will even spark the next topic for one of our webinars. Sometimes, we get questions about something as simple as an excuse from one of your donors explaining as to why they might have had positive results on their drug test. Regardless, there is no such thing as a bad question and as a part of our core values here at National Test Systems, we encourage always asking why or how. Drug testing often encounters a myriad of excuses from individuals attempting to explain or justify why their results came back positive. These excuses can range from somewhat plausible to downright amusing. Still, I believe these are worth addressing, not only to be safe but, to know whether or not someone’s explanation is warranted and based on fact, or if they are just trying to pull one over on you.  If nothing else, I hope that this can shed a little light on certain myths, true or not, but most importantly the facts about excuses a donor may come up with.

The following entries all have come from actual questions I have received from clients over the years.

 

Myths VS Facts

1. Second-Hand Marijuana Smoke Causes Positive THC Results

CLAIM: “I went to a concert where people were smoking weed; that must be why my test was positive for THC.”

FALSE: To test positive for THC, a significant amount of the substance must be consumed in a direct manner, meaning to be inhaled or digested directly. Even in an environment, such as small room, with heavy second-hand smoke, the exposure most likely would not be sufficient to produce a detectable amount of THC metabolites in the body. Generally, the rule of thumb is that the individual would have had felt the effects of THC in order to have the amount needed in their system to test positive, but merely being present in a smoke filled environment would not cause a positive test result.

 

2. Second-Hand Meth Smoke Causes Positive Results

CLAIM: “I am staying at someone else’s house, and they smoke a lot of meth; that must be why my test was positive for methamphetamine.”

FALSE: Similar to the THC myth, passive exposure to methamphetamine smoke is not enough to produce detectable levels of the drug in the body. It requires direct and substantial intake of the substance.

 

3. Drug Transfer Through Sexual Intercourse

CLAIM: “My significant other uses meth, and we had intercourse; that must be why my test was positive for methamphetamine.”

FALSE: While substances due flow through bodily fluids, there just would not be a significant enough amount in a person’s system, or bloodstream, to be transferred in such a scenario that would cause positive drug test result. Mucous membranes can absorb substances, but the concentration required to test positive far exceeds what would be transferred through intercourse.

 

4. Occupational Exposure to Alcohol

CLAIM: “I am a bartender, and I get alcohol on my skin and inhale the fumes all night; that must be why my test was positive for EtG (a marker for alcohol consumption).”

FALSE: Handling alcohol or inhaling its fumes is insufficient to elevate someone’s blood-alcohol levels to a detectable amount. To test positive, one would need to elevate their blood-alcohol level to excrete a detectable amount of the alcohol metabolite, EtG.

 

5. Mouthwash and Hand Sanitizer Use

CLAIM: “I gargle mouthwash/use hand sanitizer obsessively; that must be why my test is positive for EtG.”

FALSE: Although mouthwash and hand sanitizers do contain alcohol, the levels absorbed through gargling or skin contact are too low to result in a positive test for alcohol metabolites.

 

6. Nyquil and Alcohol

CLAIM: “I drank Nyquil because I have a cold; that must be why my test is positive for EtG.”

FALSE: Although Nyquil does in fact contain alcohol and could very well cause intoxication, the amount in which some one would need to consume in order to cause a positive result for EtG would have to be much more than the recommended amount and would not be normal for a person with a cold.

 

7. Nyquil, Sleep Aids and Methadone

CLAIM: “I drank Nyquil because I have a cold; that must be why my test is positive for methadone.”

TRUE: Nyquil contains doxylamine, which is known to cause false positive test results in all commercially available drug tests that screen for methadone. Doxylamine is also found in most sleep aids as well, such as Unisom, ZzQuil, and other over-the-counter medications.

.

7. Zantac and Methamphetamine

CLAIM: “I took Zantac for my acid reflux; that must be why my test is positive for methamphetamine.”

TRUE: Zantac (ranitidine), an over-the-counter medication used to treat acid reflux, heartburn, and other GI ailments, is known to have caused false positive results on all commercially available drug tests that screen for methamphetamine.

 

8. Poppy Seeds and Opiates

CLAIM: “I ate a poppy seed bagel; that must be why my test is positive for opiates.”

TRUE: Poppy seeds can contain trace amounts of codeine and morphine, enough to trigger a positive result for opiates. This is a well-documented phenomenon and a valid concern for those undergoing drug testing.

I have done some semi-scientific research on this, and my results can be found on this blog post. The short version is that poppy seeds do contain enough Codeine and/or Morphine to trigger a positive result, just from ingesting these foods. This is an exception to the rule mentioned above, in that one does not necessarily feel the effects of the Opiates in poppy seeds, even if there is a detectable amount in their urine.

Also important to note, is that ingestion of larger quantities of poppy seeds can and will cause Opiate intoxication.

 

9. Adulteration with Bleach or Visine

CLAIM: “I added bleach/Visine/oxidizing agents to my urine sample; that must be why my test was negative for THC.”

TRUE:  Bleach and other oxidizing agents can destroy THC molecules in urine, leading to a false negative result. This is a known and fairly common method of adulteration.

 

10. Gelatin Consumption and THC

CLAIM: “I drank Sure-Gel; that must be why my test was negative for THC.” 

FALSE: This is unfounded with no reliable evidence to support the claim that consuming gelatin products like Sure-Gel can affect THC test results. The body processes toxins through the kidneys and liver, carrying those toxins to the bladder, and consuming gelatin products to coat the bladder in an attempt to minimize levels of THC would have minimal impact on detection of these substances in urine.

 

Final Thoughts

Drug testing is a complex field with many myths circulating about what can and cannot cause a positive or negative result. Understanding the science behind these tests helps debunk these myths and ensures accurate interpretations of test results. While this showcased just a few “myths” or “excuses” surrounding this topic, it is important to note that there are many more examples of this and probably more yet to be seen or heard of. Donors will sometimes go to great lengths in order to adulterate or “justify” a drug test result and it is crucial for us to recognize these situations so that the best and most appropriate course of action can be taken.  

Share your experiences with us! Let us know if you have encountered any other interesting excuses or myths about drug testing. 

In recent months, the emergence of Medetomidine as a drug of concern has alarmed health professionals and law enforcement agencies across North America. Initially detected in Toronto in 2023, Medetomidine cases have now surged in the United States, particularly in Pennsylvania’s Philadelphia and Pittsburgh areas. The Center for Forensic Science Research & Education (CFSRE) has issued a public Alert due to the increasing instances of hospitalizations and overdose events linked to this potent veterinary tranquilizer.

 

Understanding Medetomidine

Medetomidine, sold under the brand name Domitor, is primarily approved for veterinary use on canines in the U.S. It belongs to a class of drugs known as alpha-2 adrenergic agonists, which also includes Romifidine and Detomidine. These substances share similar chemical structures and effects, including sedation, analgesia (pain relief), muscle relaxation, and anxiolysis (anxiety reduction). While these effects are beneficial in controlled veterinary settings, their misuse in humans poses significant health risks.

Medetomidine functions by stimulating alpha-2 adrenergic receptors in the central nervous system, leading to a decrease in the release of norepinephrine. This action results in sedation and analgesia. The drug’s potency and efficacy in animals have made it a valuable tool in veterinary medicine. However, these same properties make it particularly dangerous when used improperly in humans.

The rise of Medetomidine misuse began with the first signs observed in Toronto. Since then, the drug has spread to various parts of the U.S., with Pennsylvania being a primary hotspot. In April 2024, Philadelphia witnessed approximately 160 hospitalizations over just a few days, highlighting the drug’s rapid and dangerous impact. Additionally, Chicago has reported mass overdose events, indicating that the issue is not isolated and may soon affect broader regions.

Medetomidine is primarily being used as an additive to street opioids, including Fentanyl, and is also found in counterfeit pills. This trend is particularly concerning because the sedative properties of Medetomidine amplify the effects of opioids, increasing the risk of overdose. Similar to Xylazine, another veterinary tranquilizer misused in the illicit drug market, Medetomidine’s increased potency poses a severe threat to public health.

Reports from hospitals and emergency responders indicate a disturbing pattern of Medetomidine-related incidents. For instance, the surge in Philadelphia hospitalizations is attributed to the drug being mixed with other substances, leading to severe respiratory depression and unconsciousness. Emergency medical services in Chicago have also noted a rise in cases where individuals exhibit extreme sedation and unresponsiveness consistent with Medetomidine exposure.

 

Challenges in Detection and Treatment

One of the critical challenges in addressing Medetomidine abuse is the lack of effective detection and treatment options. Although it shares similarities with Xylazine, there is currently no instant drug test specifically for Medetomidine. This limitation hampers timely identification and intervention in overdose cases. Furthermore, because Medetomidine is not an opioid, the commonly used overdose reversal drug Narcan (Naloxone) is ineffective against it, complicating emergency response efforts.

Currently, Medetomidine can be detected using advanced laboratory techniques, but these are not readily available in emergency settings. The reliance on comprehensive toxicology screenings means that many cases may go undiagnosed in the initial stages, leading to delayed treatment and increased risk of severe outcomes. Developing rapid testing methods is crucial for improving response times and patient outcomes.

The treatment of Medetomidine overdose focuses primarily on supportive care. This includes maintaining airway patency, providing respiratory support, and monitoring vital signs. In severe cases, mechanical ventilation may be required. The absence of a specific antidote further complicates treatment, emphasizing the need for medical personnel to be well-versed in managing the symptoms associated with alpha-2 adrenergic agonist toxicity.

 

Public Health Implications, Policy, and Regulatory Considerations

The rise of Medetomidine as a drug of abuse underscores the need for increased vigilance and proactive measures within the public health and law enforcement sectors. Hospitals and emergency responders must be aware of the signs and symptoms of Medetomidine overdose to provide appropriate care. Moreover, the development and deployment of specific drug tests for Medetomidine and similar substances are crucial for early detection and intervention.

Raising public awareness about the dangers of Medetomidine is essential in curbing its spread. Educational campaigns targeting both the general public and healthcare professionals can help disseminate vital information about the risks and signs of Medetomidine misuse. Community outreach programs, informative workshops, and the distribution of educational materials can play significant roles in these efforts.

Addressing the issue of Medetomidine abuse also requires robust policy and regulatory measures. This includes tighter control over the distribution and sale of veterinary tranquilizers and increased surveillance of the illicit drug market. Law enforcement agencies must collaborate with public health officials to monitor and respond to trends in Medetomidine usage and distribution effectively.

 

Conclusion

Medetomidine represents a growing threat within the landscape of illicit drug use. Its potent effects, combined with its presence as an additive in street opioids and counterfeit pills, make it a significant public health concern. The current lack of effective detection methods and antidotes exacerbates the risk it poses to communities. Addressing this issue requires a coordinated effort between public health officials, law enforcement, and healthcare providers to mitigate the impact of Medetomidine and prevent further harm.

As this situation evolves, staying informed and vigilant is essential. Public awareness and education about the dangers of Medetomidine can play a pivotal role in curbing its spread and ensuring that appropriate measures are taken to protect public health. The development of rapid testing methods and effective treatment protocols is also critical in enhancing the response to Medetomidine-related incidents. By addressing these challenges head-on, we can work towards reducing the incidence of Medetomidine abuse and its associated harms.

 

Additional Considerations:

 

Research and Development

Investing in research to better understand Medetomidine’s effects on humans and to develop targeted interventions is crucial. This includes studying its pharmacokinetics and pharmacodynamics in human subjects, as well as exploring potential reversal agents that could mitigate its toxic effects. Collaborative efforts between academic institutions, government agencies, and the pharmaceutical industry can drive advancements in this area.

International Perspectives

While Medetomidine misuse is currently a pressing issue in North America, it is essential to consider its potential impact on a global scale. International cooperation and information sharing can help prevent the spread of Medetomidine abuse to other regions. Learning from the experiences of countries that have successfully managed similar drug crises can provide valuable insights and strategies.

Long-term Public Health Strategies

To combat the rising threat of Medetomidine, long-term public health strategies must be implemented. This includes enhancing substance abuse prevention programs, improving access to addiction treatment services, and addressing the underlying social determinants of drug abuse. A comprehensive approach that combines immediate response efforts with long-term preventive measures can create a more resilient public health system.

Final Thoughts

The emergence of Medetomidine as a drug of abuse highlights the ever-evolving nature of the illicit drug landscape. As new substances enter the market, staying ahead of these trends is essential for protecting public health and safety. By fostering collaboration, investing in research, and prioritizing education and awareness, we can better equip ourselves to handle current and future challenges posed by drugs like Medetomidine. In summary, Medetomidine is a powerful veterinary tranquilizer whose misuse in humans has led to significant public health concerns. Its detection and treatment present unique challenges, necessitating a multi-faceted approach to mitigate its impact. Through concerted efforts across various sectors, we can work towards reducing the harm caused by Medetomidine and safeguarding the health of our communities.

A metabolite is defined as “a substance produced during metabolism, which is the process of digestion and other bodily chemical processes”. Essentially anything you put into your body is metabolized in one way or another. Food, for example, metabolizes into vitamins, proteins, fats, sugars, etc. Some food metabolites are useful chemicals your body needs, and some are discarded and excreted as waste byproducts.

Just like food, some substance metabolites are used by your body for various functions, and some are discarded and excreted as waste byproducts. In almost all cases, the process does not metabolize 100% of whatever was ingested, and to varying degrees is excreted unchanged from what was ingested (we call this the “parent compound”). A good common example of this is when you take too much Vitamin C, some of it is excreted unchanged; this is why we sometimes see bright orange urine when we take Vitamin C.

So why does this matter to us regarding drug testing? Since both the parent and the metabolite compounds are present in urine, it is important for a drug test to detect both. Moreover, the metabolites are detectable in urine much longer than their parents. Because of the longer window of detection, virtually all screens for drugs of abuse use metabolites as their target substance; this target substance is also known as the calibrator. When we talk about the cut-off level of a test, we are referring to the concentration at which the calibrator substance (again, typically the metabolite) will trigger a positive result.

While extremely oversimplified, the chart below gives us an idea of how parents and metabolites are excreted via urine. We can see at the far-left side of our timeline (we’ll call that the “onset” of the window of detection), the level of parent substance being excreted is much higher than the metabolite. Then about halfway through our timeline, we see equal amounts of parent and metabolite. Lastly, toward the “outset” of our window of detection we can still detect the metabolite, but the parent has fallen below the concentration needed for detection. So, for example, when testing for Fentanyl we will be able to detect Norfentanyl – its metabolite – for a much longer period of time after use than the parent Fentanyl.

While instant urine tests for drugs of abuse have improved tremendously over the years, the simple fact that it is still just a method of screening tells us that there are some limitations in the amount of information that they provide. Here we will discuss some of the obvious (and less obvious) reasons why laboratory confirmations should be considered a crucial part of your testing program.

First and foremost, it is part of the manufacturers’ instructions for use; usually worded to the effect of “This assay provides only a preliminary analytical test result. A more specific alternate methodology must be used in order to obtain a confirmed analytical result. Gas chromatography/mass spectrometry (GC/MS) and liquid chromatography/mass spectrometry (LC/MS) are the preferred confirmatory methods”. If I provided no additional reasons beyond this, that it is listed as a “must” in the instructions is a pretty compelling argument.

Let’s discuss some of the reasons that test manufacturers (and the FDA, whose guidance compels these instructions) find this so important…

Firstly, it is no secret that drugs screens – whether an instant device, or a “desktop analyzer” type device – are not 100% accurate. While most panels on our instant tests are greater than 99% accurate, it is this remaining 1% that needs to be accounted for. A good example of this is known cross-reacting substances; using the Fentanyl panel as our example, we know that the medication Buspirone (Buspar) can cause a false positive on the Fentanyl panel. The only way to be sure that the positive result is due solely to the Buspirone would be to have the specimen confirmed via laboratory. There are no cross-reactions on a laboratory confirmation.

Another reason lab confirmations are crucial is the fact that most of the panels on an instant test react with many substances within that drug class. An example I like to use for this instance would be the Benzodiazepine (BZO) panel. Let’s say you have an individual who is prescribed Alprazolam (Xanax), but maybe you have suspicions of other Benzos being used. You would expect to see a positive BZO due to the Xanax, but only a lab confirmation could determine if the positive was from the prescribed BZO, or a different BZO that may have been taken illicitly.

Levels in urine tests don’t provide much (if any) useful information, with one exception: checking for THC level over time. Of course, all instant screens are qualitative (positive or negative) and cannot provide a quantitative result (level). In this instance, with the lab confirmation providing the quantitative result, you are able to check for THC level over time to monitor continued abstinence.

Lastly, I’m sure you have encountered outright denial of use, at least on a couple of occasions; something to the effect of “that can’t be right”, or “your tests are broken”, where they are hoping by some miracle the lab result will confirm their story. Of course, some will admit use after the results of the instant test, reducing the importance of confirming. The other side of the coin here is someone admitting use where nothing shows on the instant. In these instances, the lab will confirm at a lower cut-off level, and will typically show that the concentration of substance was just not high enough to react on the instant.

In summary, while the use of instant tests is a hugely beneficial tool, it can’t always tell the whole story. They do reduce the lost time and cost of having to send every specimen out, but do not completely preclude the need for laboratory testing.