Synthetic cannabinoid induced acute respiratory depression: Case series and literature review b Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, New Medical marijuana can potentially alleviate the symptoms associated with COPD (Chronic Obstructive Pulmonary Disease) and improve long term outcomes. Learn more here.
Synthetic cannabinoid induced acute respiratory depression: Case series and literature review
b Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, New York City Health+Hospitals Harlem, Columbia University College of Physicians and Surgeons, New York, NY, USA
a Department of Internal Medicine, New York City Health+Hospitals Harlem, Columbia University College of Physicians and Surgeons, New York, NY, USA
b Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, New York City Health+Hospitals Harlem, Columbia University College of Physicians and Surgeons, New York, NY, USA
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Synthetic Cannabinoids are a street drug that is widely attainable and cheap compared to natural cannabis, and has variable potency and unpredictable effects with no commercially available diagnostic test to confirm its presence. Similar to natural cannabis, Synthetic Cannabinoid intoxication can present in several ways with the most common emergency room presentations to be of neurologic and psychiatric manifestation. The respiratory depressive effect of Synthetic Cannabinoids has not been well documented in medical literature.
We report four patients admitted in the Intensive Care Unit with acute respiratory failure necessitating endotracheal intubation after use of Synthetic Cannabinoid. All patients had a reversal of respiratory failure in less than 24 h, three patients had a complicated course due to aspiration pneumonia. All four patients exhibited aggressive behavior, with two of them diagnosed with Bipolar Disorder and Cocaine Use Disorder.
The effect of Synthetic Cannabinoids in peripheral receptors such as chemoreceptors and baroreceptors can increase bronchial airway resistance. It is postulated that CB1 receptor stimulation could be one of the possible mechanisms of synthetic cannabinoid-induced respiratory depression. Chemical gases released after its inhalation may also cause damage to the bronchiolar epithelium and has the potential to disrupt the protective surfactant layer in the alveoli, which then could interfere with effective gas exchange leading to hypoxia and acidosis. The stimulation of CB1 receptors have a series of downstream signaling effects in the G protein-coupled pathway and mitogen-activated protein kinase (MAPK) pathway, causing suppression of both excitatory and inhibitory neuronal activity. The aforementioned molecular changes in the central nervous system after CB1 receptor stimulation could impact respiration.
The use of Synthetic Cannabinoids can cause respiratory depression in individuals without an underlying pulmonary disease and adds to the growing number of literature about the presentation and debilitating adverse events from its consumption. Although there is no specific toxidrome associated with it, clinicians should have a high index of suspicion with its use especially in patients presenting with a history of drug overdose.
Synthetic cannabinoid-related emergency department visits in the northeast region of the United States have been steadily increasing, with more than 1200 emergency room encounters occurring every month since July 2016 , , . Males account for 90% of these visits with a median age of 37. Most of the patients are residents of shelters and individuals with psychiatric illnesses . It is reasonable to project that this current epidemic will slowly affect every state as its use becomes more rampant.
In the advent of marijuana legalization in some states such as Colorado, California, Maine, and Nevada, consumption of synthetic cannabinoids has been very appealing due to its availability and cheaper price compared to its natural counterpart. It is usually purchased as pulverized herbs to be ingested, used as incense or rolled with natural marijuana to be smoked. They are cleverly packaged as well to entice consumers who would not otherwise consume cannabis , .
There are more than 50 types of synthetic cannabinoids known and they are often mixed in every packet, making each packet unique with variable potency and unpredictable effects . Currently, a synthetic cannabinoid Enzyme Linked ImmunoSorbent Assay (ELISA) test was developed as a presumptive initial test, which for forensic purposes has to be confirmed through chromatography and mass spectrometry technique. These tests can only screen a handful of the metabolites and are not commercially available .
The use of synthetic cannabinoid is associated with variable but surely debilitating adverse events . Similar to natural cannabis, being intoxicated with synthetic cannabinoid can present in a number of ways, with the most common symptomatic presentations as nausea, vomiting, anxiety, agitation, paranoid ideations and psychosis , . Case reports have been published with outcomes of seizures, encephalopathy, acute stroke, hypertension, cardiotoxicity, pneumonia, diffuse alveolar hemorrhage, severe lung injury and consequences such as death from coronary ischemic event and arrhythmias , . The depressive effects of the synthetic cannabinoid in the respiratory system have not been thoroughly described, with just one published case report in 2012, long before it has been identified as an impending epidemic . We present four cases of synthetic cannabinoid-induced respiratory depression necessitating endotracheal intubation for airway support. All of the cases were encountered during a span of one week in the intensive care unit of a city hospital. This is during a week when multiple hospitals are receiving drug intoxications from a new street drug that cannot be detected by a standard toxicology test .
We prospectively gathered data on patients who were admitted to the intensive care unit during a one-week span of time. A diagnosis of synthetic cannabinoid-induced acute respiratory failure was made in patients presenting with signs and symptoms requiring an advanced airway, specifically an endotracheal tube. We noted that while there is no diagnostic test that will confirm the use of synthetic cannabinoid, a history of its use a few hours prior to presentation as stated by the patient or emergency medical personnel is sufficient.
The patients in the present case series all have in common (see Table 1 , Table 2 ):
Arterial blood gas results on admission and after 24-h with the reference ranges.
|ARTERIAL BLOOD GAS|
|Test||Patient 1||Patient 2||Patient 3||Patient 4||Reference Range|
|On Admission||After 24 hours||On Admission||After 24 hours||On Admission||After 24 hours||On Admission||After 24 hours|
|pCO2||88.2 mmHg||38.1 mmHg||57.9 mmHg||36.3 mmHg||70.3 mmHg||46.7 mmHg||84.0 mmHg||44.7 mmHg||35-45 mmHg|
|pO2||78.0 mmHg||132.0 mmHg||58.9 mmHg||92.0 mmHg||107.0 mmHg||71.0 mmHg||83.1 mmHg||59.0 mmHg||80-105 mmHg|
Summary of serum and urine test results on admission with the reference ranges.
|Test||Patient 1||Patient 2||Patient 3||Patient 4||Reference range|
|Complete Blood Count (CBC)|
|Hemoglobin||13.7 g/dL||14.1 g/dL||13 g/dL||14.8 g/dL||14-18 g/dL|
|White cell count||10.1 K/uL||25.1 K/uL||11 K/uL||6.2 K/uL||4.5–11.5 K/uL|
|Platelet||228 K/uL||434 K/uL||287 K/uL||429 K/uL||150-450 K/uL|
|Neutrophil||4.3 K/uL||14.9 K/uL||5.3 K/uL||2.5 K/uL||1.9–7.7 K/uL|
|Lymphocyte||4.1 K/uL||7.7 K/uL||6.9 K/uL||2.3 K/uL||0.7–5.0 K/uL|
|Monocyte||0.8 K/uL||2.2 K/uL||0.7 K/uL||0.9 K/uL||0.16–1.25 K/uL|
|Eosinophil||0.8 K/uL||0.2 K/uL||0.0 K/uL||0.5 K/uL||0.0–0.8 K/uL|
|Basophil||0.1 K/uL||0.1 K/uL||0.0 K/uL||0.1 K/uL||0.0–1.0 K/uL|
|Sodium||139 mmol/L||135 mmol/L||146 mmol/L||135 mmol/L||136-145 mmol/L|
|Potassium||3.51 mmol/L||4.45 mmol/L||4.06 mmol/L||3.72 mmol/L||3.5–5.1 mmol/L|
|Chloride||104 mmol/L||99 mmol/L||107 mmol/L||103 mmol/L||98-107 mmol/L|
|Bicarbonate||28 mmol/L||14 mmol/L||31 mmol/L||22 mmol/L||21-32 mmol/L|
|BUN||18 mg/dL||13 mg/dL||11 mg/dL||14 mg/dL||7-18 mg/dL|
|Creatinine||1.1 mg/dL||1.8 mg/dL||0.7 mg/dL||0.8 mg/dL||0.44–1.10 mg/dL|
|Glucose||103 mg/dL||233 mg/dL||127 mg/dL||111 mg/dL||70-99 mg/dL|
|Magnesium||1.8 mg/dL||2.4 mg/dL||2.2 mg/dL||2.0 mg/dL||1.8–2.4 mg/dL|
|Phosphorus||4.1 mg/dL||2.6 mg/dL||5.5 mg/dL||5.0 mg/dL||2.5–4.9 mg/dL|
|Serum Alcohol||2 mg/dL|
|Creatine Kinase||135 Units/L||1163 Units/L||233 Units/L||364 Units/L||39-308 Units/L|
The use of synthetic cannabinoid remains a clinical diagnosis. However, work up for the following cases relied on widely available tests to rule out other causes of acute respiratory failure. In each situation, each patient received a chest radiograph, urine toxicology, arterial blood gas, trending of serum chemistries, bicarbonate, electrolytes and a complete blood count. The diagnosis of synthetic cannabinoid-induced acute respiratory failure is confirmed either through reports by emergency medical services that patient was found with packets of the synthetic cannabinoid in their pockets, saw their consumption of the substance or when patients report their use upon return to baseline mental status.
3. Case presentation
3.1. Patient 1
The patient is a 27-year-old male of Hispanic ethnicity found in the courtyard of a homeless shelter by emergency medical personnel. He was found to be in significant respiratory distress and received endotracheal intubation while in the field. In addition, EMS administered naloxone which did not produce a response. He was transported to our emergency department for further care. The arterial blood gas result in the ED showed acute respiratory acidosis while other serum laboratory tests showed unremarkable results. Urine toxicology was obtained which showed positive for the use of opiates and benzodiazepines. The chest radiograph that was performed on initial presentation did not show any significant results. However, subsequent imaging showed a developing right lower lobe consolidation and atelectasis with an associated small pleural effusion. The patient received sedation and analgesia with concurrent supportive care. He gradually regained full faculties the following morning with difficulty in keeping him calm. The patient exhibited combative and aggressive behavior which resulted into self-extubation. He signed out against medical advice after evaluation by Psychiatry that he has the capacity to decide what he wants with his care. He conveyed that he smoked synthetic cannabinoids before experiencing shortness of breath. The patient was lost to follow up and the long-term outcome is unknown.
3.2. Patient 2
The patient is a 28-year-old African American male with Bipolar Disorder who was brought in by emergency medical personnel due to a seizure episode while in his homeless shelter. He had a witnessed seizure while in the emergency department with development of fever, altered mental status and inability to protect his airway prompting endotracheal intubation. While awaiting transfer to the intensive care unit, he received additional sedation due to restlessness. He was eventually transferred to the adult intensive care unit where he received care. The arterial blood gas showed acute respiratory acidosis together with serum laboratory tests which revealed lactic acidosis, rhabdomyolysis, and acute kidney injury. His Chest radiograph is unremarkable. The patient regained capability to protect his airway and was successfully extubated with the resolution of acute respiratory acidosis the following morning. The patient was irritable and fought with medical staff regarding his care and demanded to be discharged. However, he developed fever and was evaluated by Psychiatry to have no decisional capacity. The patient stayed and received additional treatment for aspiration pneumonia. He was discharged after staying in the hospital for 3 days and confessed that he inhaled synthetic cannabinoids and ingested marijuana seeds before having a seizure. The patient was given a referral to follow up with chemical dependency clinic. Unfortunately, he never followed up and has never been seen in the facility since.
3.3. Patient 3
The patient is a 55-year-old African American female with a history of Cocaine use brought in by emergency medical personnel due to seizures. She was intubated upon arrival to the emergency department due to the development of stupor with concomitant oxygen desaturation with arterial blood gas showing acute respiratory acidosis. Additional information from the emergency medical personnel stated that the patient was picked up from the street while seen smoking the synthetic cannabinoid followed by seizures. All other serum laboratory results were unremarkable during that time with negative urine toxicology for any detectable substances. The chest radiograph did not show any infiltrates, consolidations or any acute diseases either. Prior to the patient’s transfer from the emergency department to the intensive care unit, she regained full faculties, exhibited agitation and extubated herself. Instead, she was placed in bi-level positive airway pressure and was monitored in the intensive care unit for 24 hours. She was subsequently transferred to the medicine floors after significant clinical improvement and resolution of acute respiratory acidosis. The patient had an uneventful medicine floor course and was discharged the same day with recommendations to follow up with medicine and neurology clinic. She was never started on any anti-seizure medication when she was seen in neurology clinic a week after discharge due to the absence of seizure recurrence. The patient never showed up in her scheduled medicine clinic appointment and was lost to follow up.
3.4. Patient 4
The patient is a 30-year-old African American male brought in after he was found unresponsive while lying in the street. Upon arrival of EMS, they have found that the patient was hypoventilating at 4 to 6 breaths per minute and in a pool of vomitus. A dose of Naloxone was administered which was ineffective prompting subsequent intubation while in the field. A bystander reported to EMS that the patient has seen earlier smoking synthetic cannabinoid. The report mentioned that the intoxicated patient was aggressively picking a fight prior to being found unresponsive in the street. His arterial blood gas upon presentation showed acute respiratory acidosis with unremarkable serum laboratory tests and chest radiograph. The patient was admitted to the intensive care unit and his respiratory status improved upon optimization of mechanical ventilation. On the third day of management, the patient developed a fever of 103° Fahrenheit accompanied by a new right lower lobe consolidation on chest radiograph prompting the start of antibiotic coverage for Aspiration pneumonia. After 5 days, he improved significantly with normalization of arterial blood gases and was extubated. The patient was transferred to the medicine floor with the continuation of the antibiotic course. He was discharged with a scheduled outpatient follow up to chemical dependency clinic. The patient mentioned that he had been smoking synthetic cannabinoids before losing consciousness and being found by EMS. He never showed up in his scheduled clinic appointment and was lost to follow up with unknown long-term outcomes.
In order to recognize the effects of synthetic cannabinoids in respiration, it is vital to understand the role and distribution of the cannabinoid receptors and the different molecules that act as ligands to them. The cannabinoid receptors are mainly found in the central nervous system and immune system with CB1 receptors being predominant in the brain’s hippocampus, basal ganglia, cortex, amygdala, and cerebellum, while CB2 receptors actively interact peripherally in the immune system . CB1 and CB2 receptors may also modulate non-cannabinoid receptors such as muscarinic, nicotinic, opioid and serotogenic receptors leading to a multitude of physiological effects .
After the discovery of the cannabinoid receptors, several studies in the pharmaceutical industry were conducted to develop molecules that could act as ligands for these receptors . They were initially developed to investigate possible therapeutic effects and to further the research on endocannabinoid receptor systems . These cannabinoid ligands are categorized into five distinct types based on their molecular structure and are termed classical, non-classical or cyclohexylphenols, naphthoylindoles, eicosanoids and the unclassified group respectively , , , .
These cannabinoids vary in their potency, efficacy, affinity, selectivity, metabolic and molecular activity. They vary from acting as a full agonist, partial agonist, and inverse agonist compared to the partial agonist activity of natural marijuana which has the tetrahydrocannabinol (THC) structure , , . The majority of their metabolites also have longer half-lives. Notable among them is the JWH-018 which retains its metabolic activity in the CB1 receptor explaining the increased prevalence of adverse events with the JWH-018 compared to natural cannabis. In addition, it also has a four-fold affinity to the CB1 receptor and a ten-fold affinity to the CB2 receptor .
The effect of Synthetic Cannabinoids in respiration has not been extensively detailed in humans and likely involves multiple mechanisms of action. Research involving rats have demonstrated marked respiratory depression, characterized by a decrease in respiratory rate, hypoxia, hypercapnia and arterial blood gas acidosis. Synthetic Cannabinoid effect on peripheral receptors such as chemoreceptors and baroreceptors, can increase bronchial airway resistance postulating that CB1 receptor stimulation could be one of the possible mechanism of synthetic cannabinoid-induced respiratory depression . Chemical gases released after inhalation of Synthetic Cannabinoids may also cause damage to the bronchiolar epithelium . It also has the potential to disrupt the protective surfactant layer in the alveoli and interfere with the effective gas exchange, leading to hypoxia and acidosis manifesting as acute respiratory distress which could progress to respiratory failure.
The stimulation of CB1 receptors has a series of downstream signaling effects, notably the G protein-coupled pathways and mitogen-activated protein kinase (MAPK) pathway. The CB1 receptor is particularly linked to the Gi/o, which upon stimulation inhibits adenylyl cyclase and decreases cellular cyclic adenosine monophosphate (cAMP) levels. As CB1 receptors are found in both glutaminergic and GABAergic terminals, their stimulation, theoretically can suppress excitatory and inhibitory neuronal activity. On the other hand, the MAPK pathway is specifically linked to synthetic cannabinoid agonist activity. This results in the phosphorylation of nuclear transcription factors, which in turn impacts cellular transcription, translation, motility, shape, proliferation, and differentiation. In addition to these pathways, prolonged phosphorylation of CB1 receptor leads to desensitization and internalization. These molecular changes that occur in the central nervous system after CB1 receptor stimulation could impact respiration .
The drug concentration of synthetic cannabinoids to produce the aforementioned effects were observed in an in vivo study involving mice, which noted that analgesia is observed at a median effective dose (ED50) of 0.09 mg/kg and hypothermia was recorded at doses of 1.47 mg/kg. In a separate study involving rats, a drug concentration of 10 mg/kg decreased the rate of breathing of animal subjects with subsequent demise .
A common misconception regarding the use of synthetic cannabinoids is the absence of a diagnostic test to confirm its use. In a study done in 2011, the researchers determined that the structure of JWH-018 metabolites can be excreted in the urine, which therefore can be used to detect its presence using a urine sample . Another study done in the same year showed that several monohydroxylated metabolites, a carboxy metabolite, a dihydroxy metabolite and a trihydroxy metabolite can be detected in oral fluid and urine samples provided by human subjects after smoking synthetic cannabinoid . These data propose that mass spectroscopy using saliva and urine could be used to confirm the recent use of some synthetic cannabinoids. However, this technology is not commercially available at the moment and several types of synthetic cannabinoids are formulated as of this day with unknown pharmacokinetics and pharmacodynamics .
This case series present that synthetic cannabinoids can cause respiratory depression in patients without an underlying pulmonary disease and adds to the growing number of literature about the presentation and debilitating adverse events from its consumption. Although there is no specific toxidrome associated with its use, clinicians should have a high index of suspicion in patients presenting with a history of a drug overdose. Further studies are needed to investigate the effects of synthetic cannabinoids to behavioral pathways in the brain and to address the molecular interaction of other unknown types and their vehicles with receptors to subsequently predict and learn their pharmacokinetics and pharmacodynamics.
The authors have no financial relationships or competing interests to declare.
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Cannabis for Chronic Obstructive Pulmonary Disease (COPD)
COPD is a class of chronic lung conditions when the lung airways and air sacs do not inflate and deflate appropriately due to inflammation, less elasticity, and mucus that destroys or obstructs the airflow, making it hard to breathe (23).
Emphysema and chronic bronchitis are the two most common forms of COPD, causing weight loss, weakness, and swelling. COPD News Today reports aside from avoiding inhaling medical cannabis, treating the condition with anti-inflammatory and pain-relieving properties of the plant could be positive (9).
Smoking should be avoided because according to research there are associations between heavy cannabis smoking and developing chronic bronchitis and COPD (10). Vaping concentrates may also cause airway irritation and other potential health risks like lipoid pneumonia. However, there is no statistical link between inhalation and lung cancer. When taken by a non-inhalational route, cannabis may reduce inflammation, relieve insomnia , support the immune system, and reduce mucus, according to the news source.
COPD Risks, Complications and Symptoms
The Centers for Disease Control and Prevention (CDC) breaks down COPD statistics, reporting in 2020 that 5% of the adult population have COPD (6). In 2020, there were over 140,000 deaths due to COPD.
The four most significant risks to contracting COPD are smoking, including tobacco and cannabis; asthma; occupational hazards including long-term exposure to dust, toxic chemicals, and fumes; age, and genetics like alpha-1-antitrypsin deficiency that causes frequent, heavy-mucus coughing, wheezing, shortness of breath, and chest tightening.
According to Mayo Clinic COPD can cause many complications, including respiratory infections, heart problems, lung cancer, high blood pressure in lung arteries, and depression (14).
Symptoms of COPD
According to the National Heart, Lung, and Blood Institute, common symptoms of COPD include:
- An ongoing cough or a cough that produces a lot of mucus, sometimes called smoker’s cough. This is often the first symptom of COPD.
- Shortness of breath, especially with physical activity. You may feel like breathing takes more effort or that you are gasping for air.
- Wheezing or a whistling or squeaky sound when you breathe
- Chest tightness or heaviness (22)
Treatments for COPD
When treating COPD your plan may include medication, surgery, or both. Several treatments for COPD range from steroids, inhalers, pulmonary rehabilitation, supplemental oxygen, and surgery depending on the severity and exacerbation status.
Your treatment plan may include:
- Combination inhalers
- Roflumilast (Daliresp)
- Flu and pneumonia vaccines
- Pulmonary rehabilitation
- Oxygen therapy
- Lung volume reduction surgery
- Lung transplant
The ECS and COPD
The endocannabinoid system (ECS) is a complex cell signaling system that can be found throughout the body and the central nervous system (CNS). It is responsible for maintaining homeostasis in the body through regulating several key bodily functions such as memory, sleep, fertility, memory, pain perception, and more.
Cannabinoids such as delta-9 tetrahydrocannabinol (THC) and cannabidiol (CBD) are able to interact with the ECS. Several studies suggest that modulating the ECS may help provide symptomatic relief to patients with COPD. It could potentially provide symptom relief without severe adverse side effects.
The Effects of THC and CBD on COPD
Medical News Today cited a journal, Nature 2016, which summarized the results of 19 studies on COPD and cannabis and forced vital capacity (FVC), which is the force and speed of exhaling after inhaling. With several trial components, including dose-related exposure to medical cannabis, it was demonstrated that when consumed, medical cannabis increases the FVC, whereas COPD decreases FVC (19).
However, it is important to note that these bronchodilation effects are only short-term. The review study also notes that “chronic cannabis users have an increased incidence of respiratory symptoms such as chronic cough, sputum production, dyspnoea, hoarse voice, and chest tightness. As marijuana smoke contains many of the same compounds as—and shares similar properties with—cigarette smoke, respiratory symptoms would be expected.” Other studies generally agree that long-term cannabis smoking is still modestly associated with an increase in developing chronic bronchitis and COPD (10). Inhalational methods should be avoided for optimal lung health especially in people already with COPD, but patients may use medical cannabis in other ways.
Medical News Today reports medical cannabis alleviated COPD symptoms due to its antimicrobial properties and ability to act as an expectorant, reduce mucus, relieve pain and bolster better sleep patterns. This means there could be temporary, symptomatic relief from using THC and CBD. The institute details the alternative methods to smoke medical cannabis, which could put COPD sufferers at risk for further airway and air sac obstruction. Consuming THC and CBD as sublingual oil, tinctures or edibles are some of the most popular, non-inhalational ways to administer medical cannabis (15).
“Though the topic is a controversial one, as time moves forward, the use of medical marijuana has generally become more widely accepted,” reports the Lung Institute.
Medical cannabis has been demonstrated to alleviate inflammation and chronic pain caused by various conditions, as well as relieve pain. COPD is just one of almost 60 listed conditions medical cannabis could continue to help treat, and that list keeps getting longer.
As far back as 1976 THC in particular has been studied and found to be an effective bronchodilator (24). This means that cannabis has been found effective in widening the bronchi—the large air passages that lead from the trachea (windpipe) to the lungs. THC and CBD are both well-known anti-inflammatory agents (16).
One study that explored the trends in outcomes of cannabis use among patients with COPD that were hospitalized found that “Among hospitalized patients with a diagnosis of COPD, cannabis users had statistically significant lower odds of in-hospital mortality and pneumonia compared to non-cannabis users. The association between cannabis use and these favorable outcomes deserves further study to understand the interaction between cannabis use and COPD (8).” It is encouraging that cannabis users with COPD were associated with a lower risk of death and pneumonia. Still, there is still much to be understood about the relationship between cannabis use and COPD.
Another study found that cannabis oil containing diluted CBD, CBDA, and THC extract, “may affect expression of specific airway epithelial cell genes that could modulate pro-inflammatory or Th1 processes in COPD (12).” Further research will have to elucidate which specific doses and ratios might be useful for COPD patients’ symptomatic relief. Additionally, studies need to determine the short-term bronchodilator effects of THC and elucidate the possible detriments of smoking or vaping cannabis and other long-term effects including the development of bronchitis and COPD.
COPD, Medical Cannabis, and Sleep Disorders
The prevalence of sleep disorders among COPD patients has been long recognized. The increased rates of COPD patients that also have conditions such as insomnia , restless leg syndrome , sleep apnea , and hypoxemia, are well documented (5). In order to improve COPD patients’ quality of life it is essential to treat comorbid conditions such as sleep disorders.
According to a systematic review of cannabinoids and sleep published in 2017, cannabidiol (CBD)—the nonpsychoactive cannabinoid found in the Cannabis sativa L. plant—may have therapeutic potential for insomnia patients. The review also found that delta-9 tetrahydrocannabinol (THC) may increase sleep latency (e.g., how fast an individual falls asleep), but may impair sleep quality long term (2).
Unfortunately, there is still mixed and inconclusive data to support the use of cannabinoids for obstructive sleep apnea (OSA). COPD patients with OSA should adhere to their provider’s recommendations in regards to sleep studies and airway pressure support devices like CPAPs to prevent further cardiopulmonary complications and exacerbations (18).
COPD, Medical Cannabis, Inflammation and Immune Support
COPD is ultimately an inflammatory disease of the airways and is associated with lung-specific and systemic immune dysfunction. Inflammation is a biological response of the immune system that can be triggered by a variety of factors such as pathogens or toxic compounds. There are many similar compounds present both in tobacco smoke and cannabis smoke that may contribute to the development of COPD (10).
According to an Oncotarget article in the National Library of Medicine, “These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system, potentially leading to tissue damage or disease (7).”
When the lungs of COPD patients are chronically inflamed it contributes to further lung damage and disrupts both the innate and adaptive immune responses (3).
Endocannabinoids in the body’s ECS have an important role in the immune response (17). Research has shown that, “ manipulation of endocannabinoids and/or use of exogenous cannabinoids in vivo can constitute a potent treatment modality against inflammatory disorders (16).”
Since COPD is characterized by chronic inflammation and immune dysfunction, medical cannabis may provide symptom relief through its ability to interact with the body’s ECS and regulate the immune system and inflammation. Further randomized, controlled clinical research into the COPD population specifically is needed in order to fully understand medical cannabis’ therapeutic potential as an immunosupportive and anti-inflammatory drug.
COPD, Medical Cannabis, and Depression
Depression is a common comorbid condition seen in patients with COPD. According to one analysis of this phenomenon, “around 40% are affected by severe depressive symptoms or clinical depression (20).” It is important to address co-occurring conditions such as depression when treating patients with COPD.
There is some evidence that shows medical cannabis may be effective in treating depression and other mood disorders. Though research exploring the potential anxiolytic (anxiety-reducing) and antidepressant effects of cannabis is still in its infancy, some preliminary research suggests it could be effective in providing relief to patients with depression. CBD, on the other hand, has stronger evidence to support its claims as an anti-anxiety agent at least in the short term (4).
According to one study that surveyed published in 2021, “Medicinal cannabis use was associated with lower self-reported depression, but not anxiety, at baseline. Medicinal cannabis users also reported superior sleep, quality of life, and less pain on average (13).”
What Preparations of Cannabis are Recommended for COPD?
When it comes to drug administration and medical cannabis it’s important to consider different consumption methods. It is not advisable to smoke or vape medical marijuana or any substance when treating lung diseases such as COPD (21).
A randomized controlled trial conducted in 2018 that explored the effects of vaporizing cannabis and COPD patients found that “ single-dose inhalation of vaporized cannabis had no clinically meaningful positive or negative effect on airway function, exertional breathlessness, and exercise endurance in adults with advanced COPD (1).”
One study that investigated cannabis and lung health concluded that “when used, cannabis should be used safely without causing respiratory harm and should not be used combusted or combined with tobacco in a cigarette (11).” Oral preparations of cannabis are safest for patients with COPD such as edibles, pill or capsule form, or sublingual forms of cannabis. It is critical that COPD patients avoid serious exacerbations therefore avoiding inhalational routes is paramount.
Talk to Your Doctor About Medical Cannabis
Talk to your doctor about medical cannabis and if it could be a useful addition to your treatment plan. A cannabis coach can help you determine the method of consumption that is best for your condition and make appropriate product recommendations that you can find in your local dispensary.
Note: The content on this page is for informational purposes only and is not intended to be professional medical advice. Do not attempt to self-diagnose or prescribe treatment based on the information provided. Always consult a physician before making any decision on the treatment of a medical condition.