Xylazine
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Xylazine — tranq — is a synthetic sedative of the thiazine class. Structurally unrelated to opioids, it converges with them through shared receptor targets. Xylazine is an α2-adrenergic and kappa opioid receptor agonist, producing its effects by suppressing noradrenergic tone and activating opioid pain-modulation pathways.[1][2]
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No dose data on record for this route. The timings below are not a dose guide.
Synthesized by Bayer AG in 1962 as an antihypertensive candidate, xylazine was abandoned for human use after producing excessive sedation and redirected to veterinary medicine.[1] It appeared as a fentanyl adulterant in Puerto Rico's drug supply in the early 2000s,[3] then spread to Philadelphia and across all four US Census regions.[4] It is now detected in a substantial proportion of fentanyl overdose deaths nationwide[5] and is a defining element of the North American overdose crisis.
Subjective effects include profound sedation, muscle relaxation, analgesia, and loss of consciousness. The experience resembles pharmacological unconsciousness — a deep, involuntary shutdown that outlasts the fentanyl it accompanies, leaving users immobile and unresponsive for extended periods.[6] Bradycardia, dangerous drops in blood pressure, and characteristic necrotic skin wounds are unsought effects.[7]
Xylazine produces rapid physical dependence with a withdrawal unresponsive to standard opioid medications,[8] and the gap between non-fatal and fatal doses is dangerously narrow.[9] No antidote exists for xylazine itself — naloxone reverses only the opioid component of fentanyl/xylazine overdose, meaning apparent recovery may mask ongoing xylazine toxicity. No controlled human studies have been published; all understanding rests on case reports, forensic analyses, and animal models.
History[edit]
Discovery
Xylazine was synthesized in 1962 at Bayer AG in Leverkusen, West Germany, during a screening program for thiazine-based antihypertensives.[1] Human trials revealed excessive sedation and profound blood pressure drops at therapeutic doses, and the compound was abandoned for clinical development. Bayer redirected it to veterinary medicine, where it entered the market in the late 1960s under the trade name Rompun and became a foundational sedative-analgesic across large and small animal practice.
Emergence in the Illicit Drug Supply
The first documented large-scale human exposure occurred in Puerto Rico in the early 2000s, where xylazine appeared as a heroin adulterant causing "unprecedented scale and depth" of physical harm.[3] It entered the Philadelphia drug supply in the mid-2010s, rising from fewer than 2% of heroin/fentanyl overdose deaths to 31% of 858 fatal cases by 2019.[5] By 2021, xylazine was present in 91% of Philadelphia's heroin/fentanyl samples, making it the single most prevalent adulterant in that city's supply.[1]
National Spread and Regulation
Xylazine expanded from its Puerto Rican and Philadelphia epicenters to all four US Census regions, rising from 0.36% to 6.7% of overdose deaths between 2015 and 2020.[4] CDC surveillance confirmed a 276% monthly increase in fentanyl-involved deaths with xylazine detected between January 2019 and June 2022.[10] Detection has since spread internationally — Toronto's drug checking service identified xylazine in 7.2% of fentanyl samples in September 2020,[11] and West Coast emergence was documented in San Francisco.[12] Florida became the first US state to schedule xylazine (Schedule I, 2018), and the UK classified it as Class C effective January 2025,[13] but it remains unscheduled at the federal level in the United States.
The street name "tranq" — short for tranquilizer — reflects the compound's veterinary origins and became the dominant identifier in Philadelphia's drug community. "Tranq dope" refers specifically to fentanyl adulterated with xylazine. The term gained national media currency during 2022–2023 as images of xylazine-associated skin wounds drew widespread attention. Unlike most drug slang, which tends toward euphemism, "tranq" carries an openly animal-drug connotation that many users cite as evidence the supply has become indifferent to their survival.[6]
Chemistry[edit]
Structural Class
Xylazine is built on a 5,6-dihydro-4H-1,3-thiazine core — a six-membered ring containing sulfur and nitrogen atoms. The ring is substituted at the 2-position with a 2,6-dimethylphenylamino group, the structural feature responsible for its α2-adrenergic receptor binding. This thiazine scaffold makes xylazine structurally distinct from the imidazoline-class alpha-2 agonists (clonidine, dexmedetomidine) and the guanidine-class agonists (guanfacine) — a unique chemical approach to the same pharmacological target.
Molecular Properties
| Molecular formula | C₁₂H₁₆N₂S |
| Molecular weight | 220.34 g/mol |
The 2,6-dimethyl substitution pattern on the phenyl ring is pharmacologically significant and is shared with the local anesthetic lidocaine. The molecule contains no chirality centers and exists as a single achiral species — no stereoisomeric considerations apply to its activity.
Physical Properties
Xylazine is highly lipophilic, enabling rapid penetration of the blood-brain barrier and preferential concentration in the central nervous system and kidneys.[1] It is commercially available as the hydrochloride salt in veterinary injectable formulations at concentrations of 20, 100, and 300 mg/mL.[1]
Pharmacology[edit]
Mechanism of Action
Alpha-2 Adrenergic Agonism
Xylazine's primary mechanism is agonism at α2-adrenergic receptors, which suppresses norepinephrine release throughout the central nervous system.[1] The resulting drop in sympathetic nervous system activity produces dose-dependent sedation, pain suppression, slowed heart rate, and low blood pressure. At higher concentrations, brief activation of other adrenergic receptor subtypes can cause a transient blood pressure spike before the dominant hypotensive phase.[14][1]
The alpha-2 antagonists yohimbine and idazoxan completely block xylazine's pain-relieving effects in animal models.[15] The veterinary reversal agent atipamezole reverses xylazine sedation in animals but is not approved for human use.[16][17]
Kappa Opioid Receptor Agonism
A 2024 study established that xylazine is also a full agonist at kappa opioid receptors — an activity unique among all approved alpha-2 adrenergic drugs.[2][18] This dual mechanism helps explain several distinctive clinical features: withdrawal that can be precipitated by naloxone in some models,[2] characteristic skin wounds driven by kappa receptor activation on skin cells,[7] and sex-specific differences in withdrawal severity.
An earlier study reported involvement of endogenous opioids and mu-opioid receptors in xylazine's pain relief.[19] This finding is not necessarily contradictory — it may reflect downstream endogenous opioid signaling rather than direct mu receptor agonism. The kappa opioid data from 2024–2026 represent more direct mechanistic evidence and constitute the current consensus.
Additional Mechanisms
Xylazine inhibits the NET independently of its receptor activity[20] and produces peripheral pain relief through the nitric oxide/cGMP pathway.[21] It also suppresses insulin release from pancreatic cells, producing elevated blood sugar in animal models.[22][23] The clinical significance of these additional mechanisms at illicit human doses has not been established.
Pharmacokinetics
No controlled human pharmacokinetic studies have been published. Xylazine has a plasma half-life of 23–50 minutes,[1][24] though clinical effects persist well beyond this window. High lipophilicity drives rapid blood-brain barrier penetration and preferential distribution to the central nervous system and kidneys.[1]
The liver produces two primary metabolites: 2,6-dimethylaniline and 4-hydroxyxylazine, with the latter detected in 78% of xylazine-positive forensic cases.[25] Illicit use occurs via intravenous injection (predominant), intramuscular and subcutaneous injection, oral ingestion, and inhalation.[9] Intravenous effects appear within minutes; systemic toxicity has been documented within 2 hours of accidental eye exposure.[26] Oral bioavailability in humans has not been established.
Urinary detection is possible using mass spectrometry methods[27] and point-of-care immunoassay strips, though strip performance varies by type.[28]
Neuroscience[edit]
Where It Acts
Xylazine's sedative effects originate in the locus coeruleus, the brain's principal norepinephrine-producing center. Alpha-2 receptor activation there suppresses arousal-promoting norepinephrine release — the same mechanism exploited by dexmedetomidine in intensive care sedation, but at illicit doses producing far deeper loss of consciousness. The kappa opioid component adds a second layer: kappa receptor activation in the brain's mesolimbic pathway reduces dopamine release, producing aversion and low mood that oppose the euphoria of co-administered fentanyl.
Why It Matters
Xylazine's dual alpha-2/kappa opioid mechanism creates a pharmacological paradox. Users consistently report it as an unwanted adulterant,[6] yet continued exposure drives physical dependence — a dissociation between stated preference and compulsive behavior consistent with incentive salience theory.
The compound also potentiates fentanyl-induced brain oxygen deprivation and eliminates the rebound effect oxygen recovery that normally follows opioid respiratory depression.[17] This suggests the fentanyl/xylazine combination produces qualitatively different brain oxygen dynamics than either drug alone. Xylazine's pain-relieving effects operate through at least three distinct pathways — alpha-2 spinal/supraspinal, kappa opioid descending inhibition, and peripheral nitric oxide/cGMP[21] — an unusual convergence for a single compound.
No neuroimaging or receptor occupancy studies have been performed in humans, leaving the relative contributions of alpha-2 versus kappa opioid agonism to subjective experience unknown. The disconnect between xylazine's short plasma half-life (23–50 minutes) and its prolonged clinical effects is unexplained — tissue redistribution, receptor binding kinetics, and active metabolites are all plausible but uncharacterized.
Subjective Effects[edit]
Xylazine produces pharmacological loss of consciousness qualitatively distinct from opioid sedation or benzodiazepine drowsiness. Because virtually all human exposure occurs through fentanyl-adulterated supply, the xylazine component is rarely experienced in isolation. Users describe an extended shutdown that outlasts fentanyl's short euphoric window — deep, involuntary sedation accompanied by cardiovascular depression and complete loss of motor control.[6] There is no capacity for dose titration, and the experience more closely resembles general anesthesia than typical sedative intoxication.
Relative to other alpha-2 agonists encountered in clinical settings, xylazine produces more profound loss of consciousness and carries the unique burden of necrotic skin wound formation absent from clonidine or dexmedetomidine exposure. Unlike opioid nodding, which retains intermittent awareness, xylazine sedation is a near-total absence of consciousness with minimal recall.
Effect Grid
The typical adulterant exposure produces extended sedation well beyond fentanyl's duration — the defining characteristic reported by users. Deep drowsiness progresses toward involuntary sleep or unconsciousness. Cognitive impairment is substantial, with confusion, amnesia, and marked information processing suppression.
Bradycardia (heart rate 50–60 bpm), hypotension, and significant muscle relaxation are expected. Motor control impairment prevents coordinated movement. Pain suppression is substantial. Temperature dysregulation may produce hypothermia in uncontrolled environments.
Sedation typically outlasts the opioid component by hours, leaving users unconscious and vulnerable after fentanyl's effects have waned. Tissue necrosis risk increases with repeated exposure at this level.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual acuity suppression · Internal hallucinations
Pain suppression · Pupil constriction · Vasoconstriction · Abnormal heartbeat · Bodily heaviness · Dizziness · Temperature dysregulation · Dry mouth · Nystagmus (eye wobbles) · Constipation · Heart rate perception changes · Nausea · Body schema distortion · Involuntary body movements · Vomiting · Bodily dissociation
Abnormal heartbeat · Dizziness · Temperature dysregulation · Dry mouth · Nystagmus (eye wobbles) · Constipation · Heart rate perception changes · Nausea · Body schema distortion · Involuntary body movements · Vomiting · Bodily dissociation
Information processing suppression · Confusion · Motivation suppression · Thought deceleration · Language suppression · Memory suppression · Memory fragmentation · Thought disorganization · Cognitive dysphoria · Amnesia · Delirium
Thought deceleration · Language suppression · Memory suppression · Memory fragmentation · Thought disorganization · Cognitive dysphoria · Delirium
Anhedonia · Anxiety
Derealization · Cognitive disconnection
Timeline
Rapid onset of sedation within seconds to minutes. An initial brief hypertensive phase may precede the predominant hypotension. First signs include drowsiness and decreasing heart rate.
Deep sedation or unconsciousness with bradycardia (40–50 bpm), hypotension, miosis, muscle relaxation, and substantial pain suppression. Cognitive function is effectively absent. Duration outlasts plasma half-life due to receptor binding kinetics and lipophilic tissue accumulation.
Gradual return of consciousness with persistent confusion, motor control impairment, and cardiovascular depression. May be prolonged hours when concurrent opioids are present. Recovery is unpredictable and does not correlate reliably with dose.
Residual sedation, cognitive fog, and subclinical cardiovascular depression may persist for hours after apparent recovery. One case report documented symptoms persisting approximately 25 hours after exposure.
⚠ Do not drive or operate machinery — residual sedation, impaired motor control, and cardiovascular depression may persist for hours after apparent recovery.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- High
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- —
- Physical
- High
- Psychological
- Moderate
- Compulsive redosing
- Low
- Dose escalation
- Moderate
- Cross-tol.
- mu opioid agonists (supraspinal) · delta opioid agonists (supraspinal) · fentanyl
Toxicity
Acute Toxicity
Xylazine poisoning produces a recognizable pattern: coma, constricted pupils, slowed breathing, slow heart rate, low blood pressure, and low body temperature.[30][26] This presentation overlaps substantially with opioid overdose, but naloxone does not reverse xylazine's effects — it addresses only the opioid component of fentanyl/xylazine overdose.[8][10]
A review of 59 published cases found dose ranges of 40–4,300 mg across all routes, with an average fatal dose of approximately 1,200 mg and an average non-fatal dose of approximately 525 mg.[9] These ranges overlap substantially — individual lethality is unpredictable and confounded by polydrug use. The fatal outcome rate in this series was 35.6%, with most deaths involving co-administration with opioids.[9]
Heart and Circulation
Slow heart rate (40–50 bpm) and sustained low blood pressure are the primary cardiovascular effects.[26][14] Heart rhythm disturbances including premature ventricular contractions are documented. The fentanyl/xylazine combination produces additive cardiovascular and respiratory depression.[16]
Skin Wounds
Chronic xylazine use produces characteristic deep necrotic skin ulcers that occur at and beyond injection sites, confirming a systemic mechanism rather than local injection trauma alone.[31][32] Two pathways drive the damage: vasoconstriction reduces skin blood flow and impairs healing,[32][33] while kappa opioid receptor activation directly disrupts skin cell integrity.[7]
Severe cases progress to deep bone infection, bloodstream infection with drug-resistant bacteria (MRSA, Streptococcus, E. coli, Enterococcus),[33] and limb amputation.[34]
Blood Sugar
Xylazine inhibits insulin release, causing elevated blood sugar in animal models.[22][23] The clinical significance in chronic human use is not well-characterized.[35]
Pregnancy
Xylazine crosses the placenta, confirmed by umbilical cord detection in a human case.[36] Animal models demonstrate reduced blood flow to the uterus, restricted fetal growth, and pregnancy loss. No controlled human pregnancy safety data exist.
Psychological Risks
No controlled studies have characterized xylazine's psychological effects in humans. The compound produces profound sedation rather than psychotic or anxiety-producing effects at typical exposure levels.
Psychological risks are primarily indirect: prolonged unconsciousness in uncontrolled settings increases vulnerability to assault, hypothermia, positional suffocation, and choking on vomit. Withdrawal-associated distress is reported by users[6] and may drive compulsive continued use despite perceived harm from the adulterant itself. Kappa opioid receptor agonism is associated with low mood and aversive states, though whether these effects are distinguishable from the opioid co-exposure context is unknown.
Tolerance and Dependence
Xylazine produces physical dependence with a withdrawal syndrome distinct from opioid withdrawal. In a user survey, 53% of respondents reported xylazine-specific withdrawal symptoms.[6] Higher xylazine exposure levels are associated with more severe early withdrawal symptoms in patients with opioid use disorder.[37]
Animal studies show sex-specific withdrawal patterns, with females showing delayed onset and enhanced sensitivity to motor-suppressing effects.[29] Naloxone precipitates withdrawal from xylazine in mice, consistent with kappa opioid receptor activity, with enhanced sensitivity in females.[2]
Cross-tolerance between xylazine and opioid receptor agonists has been demonstrated in animal models.[38] Alpha-2 agonist co-administration may prevent the development of fentanyl tolerance,[39] suggesting chronic xylazine exposure could modify opioid tolerance trajectories. Human tolerance data for xylazine itself have not been published.
Drug Interactions
Opioids
The fentanyl/xylazine combination produces additive nervous system and respiratory depression.[15][16] Xylazine worsens fentanyl-induced brain oxygen deprivation and eliminates the normal oxygen recovery response.[17] Naloxone reverses the opioid component only — xylazine effects persist after naloxone, causing prolonged unconsciousness even after apparent partial recovery.[8]
In death investigations, 87% of xylazine-associated deaths involved multiple drugs,[40] and 98% of xylazine-positive opioid deaths involved fentanyl.[41]
Reversal Agents
Atipamezole (veterinary alpha-2 blocker) reverses xylazine sedation in animals; combined with naloxone, it is more effective than either agent alone.[17][42] However, the combination produces cardiovascular instability — rebound effect fast heart rate followed by sustained slow heart rate.[16] Atipamezole is not approved for human use.
Other Sedatives
Additive nervous system depression is expected with benzodiazepines, alcohol, barbiturates, and other sedatives, supported by polydrug toxicity patterns in overdose death series.[40]
Metabolic Interactions
Metabolic interactions between oxycodone and xylazine have been documented in laboratory studies.[43] Xylazine's insulin-suppressing effect may interact with diabetes medications.[22][23]
Haloperidol
In rodent studies, haloperidol significantly altered the potency of both fentanyl and xylazine.[15] The clinical significance of this interaction is unknown.
Contraindications
Opioid Co-Administration
Co-administration with opioids dramatically increases overdose risk through additive cardiorespiratory depression — the context in which virtually all human xylazine exposure occurs.
Other Sedatives
Combination with benzodiazepines, alcohol, barbiturates, GHB, or other sedative-hypnotics increases risk of respiratory arrest and death.
Heart Conditions
Pre-existing slow heart rate, heart rhythm abnormalities, or low blood pressure are relative contraindications given xylazine's cardiovascular depressant effects.
Diabetes
Xylazine's inhibition of insulin release may cause clinically significant blood sugar elevation, particularly in individuals with diabetes.[22][23]
Pregnancy
Documented placental transfer with evidence of restricted fetal growth and pregnancy loss in animal models.[36]
Harm Reduction[edit]
Forms & Identification
Xylazine cannot be identified by sight, smell, or taste in the drug supply. It appears as a white or off-white powder indistinguishable from fentanyl or heroin, and may be present in counterfeit pressed pills. The only reliable way to confirm its presence before use is chemical testing — xylazine-specific immunoassay test strips are available and inexpensive, though accuracy varies between brands.[28] Drug checking services using mass spectrometry provide definitive identification.
Because xylazine is present in the majority of the fentanyl supply in some regions, anyone using unregulated opioids should assume xylazine may be present until testing proves otherwise.
Guidelines
- Test every batch with xylazine-specific test strips before use
- Never use alone — prolonged unconsciousness requires someone to monitor breathing and body position
- Keep naloxone available and administer it in any suspected overdose, even though it will not reverse xylazine's effects — most fentanyl/xylazine overdoses involve both drugs
- Avoid injecting into the same site repeatedly — rotate injection sites to reduce wound risk
- Inspect skin daily for any new sores, discoloration, or areas of numbness
- Seek wound care early — xylazine wounds worsen rapidly without treatment and can progress to limb-threatening infections[34]
- Do not assume naloxone failure means the situation is not an opioid overdose — xylazine prolongs unconsciousness after naloxone administration
Set & Setting
Xylazine-contaminated opioids produce prolonged loss of consciousness that far outlasts the fentanyl component. Using alone is the single greatest risk amplifier — extended periods of immobility increase vulnerability to positional suffocation, aspiration, hypothermia, assault, and delayed wound discovery.
If use cannot be avoided, the presence of another person who can monitor breathing and body position is the most consequential harm reduction measure available. Indoor settings with temperature control reduce hypothermia risk during prolonged unconsciousness.
Aftercare & integration. After xylazine exposure, inspect all skin surfaces — particularly injection sites and extremities — for new wounds, discoloration, or areas of reduced sensation. Xylazine wounds can develop at sites distant from injection and may appear minor before progressing rapidly. Low-barrier wound care clinics have been established in some cities[44] and should be accessed at the earliest sign of tissue damage.
Monitor blood sugar if diabetic or experiencing symptoms of elevated blood sugar (excessive thirst, frequent urination, confusion). Hydration and nutritional recovery support the body after prolonged unconsciousness and cardiovascular depression.
Recovery & Support
Xylazine dependence presents unique treatment challenges. Standard opioid use disorder medications (buprenorphine, methadone) do not address xylazine withdrawal,[1][8] meaning individuals may continue to experience withdrawal symptoms even when stabilized on these treatments. No approved medication for xylazine withdrawal currently exists.
Individuals seeking to reduce or stop use should communicate xylazine exposure to treatment providers, as symptom management may require approaches outside standard opioid treatment protocols. Wound management is often a concurrent need — treatment programs that integrate wound care with addiction services offer the most comprehensive support. Peer support from others who have navigated xylazine withdrawal can provide practical guidance that clinical protocols have not yet formalized.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Blue or grey lips, slow or stopped breathing, unresponsive to voice and sternal rub, seizure, or prolonged unconsciousness in an unusual position all require immediate action. Xylazine-involved overdoses may appear partially responsive to naloxone — the person may resume breathing but remain deeply unconscious.
Immediate steps:
- 1. Call emergency services immediately
- 2. Administer naloxone if available — it reverses the fentanyl component even though xylazine effects persist
- 3. If the person is breathing, place them in the recovery position (on their side) to prevent choking
- 4. If breathing has stopped, begin rescue breathing or CPR
- 5. Do not leave the person alone — xylazine sedation can last far longer than naloxone's duration of action
- 6. Keep the person warm — hypothermia risk is elevated during prolonged unconsciousness
What to tell the dispatcher: State that the person is unresponsive, report suspected fentanyl/xylazine exposure, note the time and any naloxone administered, and describe breathing status. Good Samaritan laws in many jurisdictions protect callers from drug-related prosecution.
Reversal agents: Naloxone reverses the opioid component only.[8] No approved human reversal agent exists for xylazine itself. Administer naloxone regardless — fentanyl/xylazine overdoses still benefit from opioid reversal.
Legal Status[edit]
Xylazine occupies an unusual regulatory position: widely used in veterinary medicine and readily available through veterinary supply channels, yet never approved for human use in any jurisdiction. Regulatory responses to its emergence in the illicit drug supply have been uneven — the United States maintains no federal controlled substance scheduling while the United Kingdom has moved to Class C classification.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not a controlled substance | Regulated under FD&C Act only; TRANQ Research Act enacted December 2023 mandates research coordination; Combating Illicit Xylazine Act (proposed) would classify as Schedule III[45] |
| Florida (US state) | Schedule I | First state to schedule xylazine (2018)[45] |
| Ohio (US state) | Schedule III | Governor executive order, March 2023[45] |
| United Kingdom | Class C, Schedule 4 Part 1 | Effective January 15, 2025; Misuse of Drugs Act 1971; preserves legitimate veterinary access[13] |
| European Union | Not scheduled (EU-wide) | Detected in Estonia and Latvia (13% of used syringes in Riga); no EU-wide scheduling action[13] |
| Canada | Not scheduled federally | Veterinary use approved; first detected in illicit supply September 2020 in Toronto[11] |
| Australia | Unknown | No scheduling data identified in reviewed literaturecitation needed |
More than 26 US states have considered xylazine-specific legislation or regulatory action beyond the federal status quo.[45] The absence of federal scheduling means xylazine is not subject to DEA manufacturing quotas or distribution controls, and possession for human use (outside states with specific scheduling) does not carry controlled substance penalties.
references
- [1]
- [2]
- [3] ^abTorruella RA (2011) Xylazine (veterinary sedative) use in Puerto Rico — Substance Abuse Treatment, Prevention, and Policy doi:10.1186/1747-597x-6-7
- [4] ^abFriedman J, Montero F, Bourgois P, et al. (2022) Xylazine spreads across the US: A growing component of the increasingly synthetic and polysubstance overdose crisis — Drug and Alcohol Dependence doi:10.1016/j.drugalcdep.2022.109380
- [5] ^abJohnson J, Pizzicato L, Johnson C, Viner K (2021) Increasing presence of xylazine in heroin and/or fentanyl deaths, Philadelphia, Pennsylvania, 2010-2019 — Injury Prevention doi:10.1136/injuryprev-2020-043968
- [6]