Substance Use & Overdose
SUD High-yield Verified · Sep 2026A substance use disorder is repeated use causing clinically significant distress or impairment, diagnosed by two or more of eleven criteria within twelve months — and overdose is the acute toxicity of that use, most lethally as opioid-induced respiratory depression.
The disorder behind pinpoint pupils and a respiratory rate of four, the titrate-to-breathing naloxone rule, the re-sedation window, the COWS score that gates the first buprenorphine dose, and the two stimulant rules that are the opposite of instinct — no restraints, no antipyretics.
What’s going wrong in the body
The normal physiology, where it fails, and why the body’s compensation backfires.
01 Dependence, tolerance and addiction are three different things
Start with the vocabulary, because the page is unusable without it. Dependence is physiological: "when a person suddenly stops using a drug, their body goes through withdrawal, a group of physical and mental symptoms that can range from mild to life-threatening." Addiction is behavioural: "the continued use of these drugs despite adverse consequences or events." And opioid use disorder is the diagnosis that spans them — chronic opioid use that causes real distress or impairs daily life, with "an overpowering desire to use opioids, increased opioid tolerance, and withdrawal syndrome when opioids are discontinued. Thus, OUD can range from dependence on opioids to addiction."
The diagnostic criteria are one set applied to every substance. For opioids: repeated use within 12 months with two or more of continued use despite worsening physical or psychological health; continued use despite social and interpersonal consequences; decreased social or recreational activities; difficulty fulfilling duties at work or school; excessive time spent obtaining or recovering from use; more taken than intended; cravings; inability to cut down; tolerance; use despite danger; and withdrawal, or continued use to avoid it. Six or more indicates severe opioid use disorder — and the alcohol page uses the identical structure with the same severity cut-offs, which is the point: this is one criteria set wearing different substance names.
The mechanism that makes dependence so hard to escape is that it works in both directions. "Physical dependence on opioids may develop rapidly and is likely the result of many changes in mu-opioid receptors, including receptor desensitization, internalization, and signaling abnormalities… Thus, physical dependence on opioids creates both positive and negative reinforcement for continued opioid use." The drug is taken to feel good and to stop feeling terrible — and once the second reason takes over, "many opioid-dependent patients will seek continued access to opioids, by legal or illegal means, to prevent withdrawal." The receptor doing this is specific: opioids act at mu, delta and kappa G protein-coupled receptors that inhibit adenyl cyclase, and "the mu receptor is crucial for reinforcing the actions of opioids."
02 The opioid chain — from the receptor to the respiratory rate
Opioid overdose kills through one mechanism, and naloxone reverses that one mechanism. Naloxone "is indicated for the treatment of opioid toxicity, specifically to reverse respiratory depression from opioid use." The visible picture is the triad plus a late sign: unconsciousness or inability to awaken; pinpoint pupils; slow, shallow breathing with "choking sounds or a gurgling/snoring noise from a person who cannot be awakened," or respiratory arrest; and fingernails or lips turning blue or purple. The pupil is diagnostically load-bearing: "the presence of miosis in a prehospital patient with altered mental status is highly indicative of responsiveness to naloxone."
Withdrawal comes from one anatomical place, and knowing it explains an entire drug class. "The principal site in the brain that triggers the onset of opioid withdrawal syndrome is the locus coeruleus at the base of the brain. Neurons present in locus coeruleus are noradrenergic and have an increased number of opioid receptors… The noradrenergic activity in locus coeruleus neurons is a prime causative site of opioid withdrawal symptoms." At the cellular level the symptoms are "closely related to pathways of adenylyl cyclase superactivation-based central excitation." That is why an alpha-2 agonist works — lofexidine "binds to receptors on adrenergic neurons, which reduces sympathetic tone and decreases norepinephrine release."
And one sentence explains every precipitated withdrawal on this page. Withdrawal "can also be caused when a patient has an opioid in his/her system and is given an opioid partial agonist like buprenorphine or antagonists like naloxone or naltrexone." That single mechanism produces three different clinical traps: naloxone given in a full-reversal dose to a dependent patient, buprenorphine started before the patient is already in withdrawal, and naltrexone started before seven opioid-free days. Each one is iatrogenic, each one is avoidable, and each one is on the exam.
03 The stimulant chain — and the two rules that are the opposite of instinct
Stimulants work by flooding the monoamine systems, and the damage follows the flood. Amphetamines are "structural analogs of the neurotransmitter phenethylamine," regulating monoamine neurotransmission through trace amine-associated receptor 1 and inhibition of vesicular monoamine transporter 2. That receptor sits in the caudate, putamen, substantia nigra, nucleus accumbens, ventral tegmental area, locus ceruleus, amygdala and raphe nucleus — and "many of these areas play important roles in the development of addiction. Thus, the use of amphetamines begets the desire to continue using amphetamines." Route decides how fast the hit arrives and therefore how reinforcing it is: methamphetamine peaks 3 to 6 hours after oral ingestion, 5 to 10 minutes after nasal insufflation, and within 5 minutes when smoked, with bioavailability of "70% or greater" by those routes.
The vascular damage is a separate mechanism from the sympathetic surge. Downstream effects "may lead to increased reactive oxygen species, mitochondrial dysfunction, and alterations in intracellular calcium… implicated in the accelerated development of cardiovascular disease. Amphetamines also cause necrotizing vasculitis of small- and medium-sized blood vessels, which can yield a myriad of end-organ complications — strokes and neurodegenerative diseases, coronary artery disease, ischemic bowel disease." That is why new abdominal pain in a stimulant user should raise ischaemic bowel, and why a young patient with chest pain and a stimulant history gets a real cardiac work-up.
Two management rules follow from the mechanism and both contradict what an untrained hand would do. First: the hyperthermia is muscular, not hypothalamic. "Antipyretics are not used because the increased body temperature is caused by muscular activity, not an alteration in the hypothalamic temperature set point" — cooling is achieved through "sedation, fluid resuscitation, external cooling blankets, or evaporative cooling techniques." Second: do not use physical restraints. "Physical restraints should be avoided because clients who physically struggle against restraints undergo isometric muscle contractions that are associated with lactic acidosis, hyperthermia, sudden cardiac collapse, and death." Both rules point the same way — sedate the patient, because sedation lowers the temperature, the blood pressure and the heart rate at the same time.
04 The four touchpoints — and the tolerance rule that outranks them
Most overdose deaths had a moment when someone could have intervened. Surveillance data relayed by the nursing text puts it plainly: "nearly 85% of overdose deaths involve illicitly manufactured fentanyl, heroin, cocaine, or methamphetamine," and opportunities to link people to care "have been identified for more than three in five people who died from drug overdose." The four touchpoints: a bystander was present in nearly 40% of opioid and stimulant overdose deaths; about 10% had been recently released from an institution such as jail, prison, inpatient rehabilitation or a psychiatric hospital; about 10% had a previous overdose; 25% had a documented mental health diagnosis; and nearly 20% had previously been treated for substance use.
The institutional-release figure comes with the reason attached, and it is the most important sentence on this page. Risk increased in that group "because they were unaware of decreased tolerance to the drug due to abstinence from it while in the institution." The same rule is stated from the treatment side: "because withdrawal management reduces acquired tolerance, those who attempt to reuse their former substance in the same amount or frequency may overdose, especially those with opioid use disorders," and "patients are at the highest risk for opioid-related death in the first 4 weeks of OUD treatment and for 4 weeks after treatment ends," with the peak "the period between detoxification and the start of maintenance therapy."
Which is why the last section of this page is about what detoxification is not. "Medically supervised opioid withdrawal, also known as detoxification, involves administering medication to reduce the severity of withdrawal symptoms… However, supervised withdrawal alone does NOT generally result in sustained abstinence from opioids, nor does it address reasons the client became dependent on opioids." It is "considered stabilization — a first step toward recovery, similar to the acute management of a diabetic coma as a first step toward managing the underlying illness of diabetes." And the drop-off is measured: "half to three quarters of individuals with substance use disorders who receive withdrawal management services do not enter treatment. One of the most serious consequences when individuals do not begin continuing care after withdrawal management is overdose."
Causes & risk factors
Modifiable factors are teaching targets — the patient can act on them.
Signs & symptoms
Each finding tied to the mechanism that produces it — and the triage it calls for.
Diagnostics
Complications
Medications for this condition
Why each class is prescribed here — every card links to its full pharmacology page.
This class is on the page as the mechanism of harm, and as the thing being reversed. The disorder-side teaching is the chain: mu-receptor agonism produces analgesia and euphoria, but also tolerance, physical dependence, withdrawal on cessation, and the dose-dependent respiratory depression that is the actual mechanism of death. The numbers that make it a prescribing problem rather than only a street problem: up to 50% of patients on chronic opioid therapy meet the criteria for opioid use disorder, and in the United States, opioids have killed more people than any other drug in history. The prescribing lever, per CDC 2022 guidance as reported by StatPearls: exercise caution before escalating beyond 50 morphine milligram equivalents per day, because higher doses "typically fail to significantly enhance pain relief for most patients while simultaneously increasing the risk of overdose" — and at that threshold, provide naloxone and overdose prevention education to the patient and their household members, with more frequent follow-up. The modern context is contamination: there are "two types of fentanyl — pharmaceutical fentanyl prescribed for severe pain, and illicitly manufactured fentanyl," and "most recent cases of fentanyl-related overdose are associated with illicitly manufactured fentanyl that is added to other street drugs that make them more powerful, more addictive, and more dangerous." Carfentanil is the one potency figure this page can source: "approximately 10,000 times more potent than morphine and 100 times more potent than fentanyl… a miniscule amount of powder containing two milligrams can be lethal," and it "can be accidentally absorbed through the skin or inhaled by unsuspecting parties," so first responders must follow safety protocols. The class page owns equianalgesic dosing, individual agents and adverse-effect profiles. What this page adds is why the legitimate analgesic becomes the disorder, and the one non-opioid alternative the source names — "nonopioid drugs and physical therapy can provide a long-term solution to pain management instead of relying on the use of opioids."
The disorder-side role here is toxicity and its management, and the management is counter-intuitive twice over. Sedation is first-line, and four separate sources say so: "intravenous benzodiazepines are administered immediately for chemical sedation of severely agitated individuals" and "remain the first-line treatment to manage agitation and prevent seizures"; cardiovascular toxicity and agitation are "best treated first-line with benzodiazepines to decrease CNS sympathetic outflow"; "diazepam is an ideal choice if intravenous access is available; otherwise, intramuscular lorazepam or midazolam is appropriate"; and hyperadrenergic symptoms should be managed with benzodiazepines "titrated to effect and repeated as necessary." Titrating to effect means watching the airway while you do it, because the doses that settle a hyperadrenergic patient are not small. Sedation is efficient because it treats several problems at once — "hypertension related to amphetamine toxicity may abate with agitation treatment." On beta-blockers, teach the disagreement rather than the mnemonic. The amphetamine chapter says they "should not be used as SOLE antihypertensive therapies as their use may lead to unopposed alpha-adrenergic tone," preferring nitroglycerin and nicardipine. The methamphetamine chapter names labetalol or carvedilol — combined alpha-1 and beta antagonists — as adjuncts when agitation persists despite adequate benzodiazepines, with alpha-2 agonists dexmedetomidine or clonidine as alternatives. The defensible teaching: sedate first; never a beta-blocker as sole therapy; if one is used, a combined alpha-1/beta agent is the sourced choice. Two other agent notes: non-dihydropyridine calcium channel blockers (diltiazem, verapamil) reliably reduce hypertension but not tachycardia, and dihydropyridines such as nifedipine should be AVOIDED because reflex tachycardia may occur; and haloperidol for stimulant delirium "may cause harm" — it can lower the seizure threshold, cause extrapyramidal effects, increase heat production by altering thermoregulatory function, and prolong the QTc.
Double-edged, and both edges are sourced. The positive role is first-line sedation in stimulant toxicity — for agitation, for seizure prevention, and as the intervention that lowers temperature, blood pressure and heart rate together. The second positive role is substitution in sedative withdrawal: "substituting the short-acting benzodiazepine the individual has been using with a long-acting one, such as diazepam or clonazepam, which provides more stable blood levels and reduces the intensity of withdrawal symptoms. The medication is then gradually tapered… The tapering process can last several weeks to several months." The negative role is a co-prescribing rule that exists because of a boxed warning: "use of benzodiazepines and zolpidem is NOT recommended for clients receiving methadone or buprenorphine therapy unless they are under close medical supervision due to the risk of oversedation." The same principle governs methadone generally — it "is medically safe, provided there is no concomitant use of other prescription or illicit drugs." And the withdrawal these drugs produce is the dangerous kind: tremor and rebound anxiety escalating through hallucinations and agitation to seizures within one to five days of abrupt cessation or rapid tapering, with autonomic instability. That is the sourced basis for the contrast this page teaches — GABAergic withdrawal, whether from alcohol or benzodiazepines, has documented seizure and delirium risk, and the Alcohol Withdrawal page carries the parallel picture in full.
Not comfort care — volume protection. The sourced symptomatic regimen for opioid withdrawal is specific by symptom: "nausea/vomiting: ondansetron, prochlorperazine, and promethazine," alongside "loperamide for diarrhea… and ibuprofen for myalgia." The disorder-side rationale is what makes this a nursing priority rather than a convenience: "clients who have associated diarrhea, vomiting, or sweating should be monitored for dehydration and have fluid levels maintained with oral and/or intravenous fluids." Controlling the vomiting is how the nurse prevents the volume loss, and volume loss is one of the two sourced hazards of opioid withdrawal — the other being the collapse of tolerance that follows it. The environment does some of this work too: "a calm, quiet environment with supportive and reassuring staff is instrumental for helping clients overcome most symptoms of acute opioid withdrawal and can decrease the need for pharmacologic interventions," with warm baths, rehydration and gentle stretching named for muscle aches and cramps. The class page owns the antiemetic pharmacology; this page teaches which symptom gets which agent and why the vomiting matters.
Beyond medications
- NALOXONE — what it is, every route, and the dosing rule that depends on dependence. It is "usually administered intravenously. However, if IV access can’t be achieved, it can also be administered via an intraosseous, subcutaneous, intramuscular, or intranasal route," and intravenously it "completely reverses the effects of opioids within a few minutes." Formulations include injectable 0.4 mg/mL and 1 mg/mL solutions and a 5 mg/0.5 mL high-dose prefilled syringe, with intranasal actuations of 3 mg, 4 mg and 8 mg. The critical rule: "the dose is titrated to increase the patient’s respiratory drive and allow for adequate spontaneous respiration and oxygenation, BUT NOT FULL REVERSAL. This can result in withdrawal and include combative or aggressive behavior." A small initial IV dose of 0.04 to 0.1 mg is recommended in a known opioid-dependent patient; 0.4 mg in someone without known dependency. Repeat every 2 to 3 minutes in alternating nostrils for intranasal use, or every 2 to 5 minutes for longer-acting agents, with an IV drip in some cases. The goal is adequate breathing, not complete arousal.
- THE FIVE OVERDOSE RESPONSE STEPS, in order. (1) Evaluate and get help — "try to stimulate the person by calling their name or vigorously grinding one’s knuckles into their sternum. If the person does not respond, call 911." (2) Rescue breathing, compressions and oxygen — "be sure the person’s airway is clear. Place one hand on the person’s chin, tilt the head back, and pinch the nose closed… give two slow breaths. Watch for the person’s chest (but not the stomach) to rise. Follow up with one breath every five seconds. If the individual becomes pulseless, provide cardiopulmonary resuscitation." (3) Give the first naloxone dose. (4) Give a second dose if there is no response in 2 to 3 minutes. (5) Monitor the response, including for re-sedation. The American Heart Association position relayed alongside it: "laypersons and others who cannot reliably confirm the presence of a pulse should initiate cardiopulmonary resuscitation in any individual who is unconscious and not breathing normally, with the additional recommendation to administer naloxone if opioid overdose is suspected."
- Who gets naloxone, and who gets missed. "Clinicians should offer naloxone to ALL patients with OUD," and it "is reasonable to prescribe naloxone to any patient with OUD," with prescriptions "also considered for a more general population of patients taking chronic opioids." More than a dozen states have passed good samaritan laws permitting prescription to family members or caregivers. The nasal spray exists specifically "to permit medically untrained individuals to safely administer naloxone," with no concern about venous access, needlestick or sharps disposal — though "the price of this formula is still a major issue." And the equity point is explicitly sourced: "women, older adults, and those without obvious signs of opioid use disorder are undertreated with naloxone and, as a result, have a higher death rate. Therefore, naloxone should be considered for women and the elderly who are found unresponsive." Storage, per SAMHSA as relayed: room temperature in a protective outer case, replaced on expiry and if exposed below 3.8 °C or above 40 °C.
- MEDICATIONS FOR OPIOID USE DISORDER — plain-text notes, and the timing rules are the exam. Buprenorphine is a partial mu agonist, and "it is crucial to ensure that the patient is in opioid withdrawal BEFORE initiation… to avoid precipitated withdrawal." The operational gate: "the client must be in a state of mild to moderate withdrawal before receiving their first dose — that is, have a COWS score greater than 10. The first dose is typically 2 to 4 mg sublingually." The time-based version: 12 to 18 hours after a short-acting agonist, 24 to 48 hours after a long-acting one. Naloxone is added to the combination product because it "is not absorbed orally and only exerts its action when injected," deterring misuse. Methadone is a full mu agonist, dispensed in the US "only for specially monitored clinics," offering "reduced euphoric effects, decreased narcotic cravings, and reduced transmission of infectious diseases" — and, crucially, it "does not induce withdrawal symptoms when administered to a client with opioid in their system because it has an additive effect on opioids that are already present." Watch its long half-life. Naltrexone is an antagonist that "may only be initiated when the patient is free of physiological opioid dependence, and at least seven days without acute withdrawal symptoms are required"; the intramuscular form may be more effective and is FDA-approved for opioid dependence, with monthly dosing aiding compliance.
- What the medications achieve, and how long they run. "Almost half of the patients can maintain abstinence from additional opioids while receiving replacement therapy," and "methadone treatment is associated with a 50% reduction in all-cause mortality, as well as a 50% reduction in the incidence of hepatitis C," plus decreased drug-related crime and improved retention. There is no winner between methadone and buprenorphine — "no consensus among experts… the agent use should be based on patient-specific factors," though methadone "may increase patient retention" and "may treat withdrawal symptoms and cravings better than buprenorphine for patients who use fentanyl." Duration is genuinely contested: some clinicians stop after a year, others "suggest that treatment should be lifelong due to the risk of relapse and overdose death after patients stop." Access changed in December 2022: the MAT Act eliminated the DATA-Waiver (X-Waiver) program, so "all DEA-registered practitioners with Schedule III prescribing authority may now prescribe buprenorphine for OUD," with no patient limits and no tracking, subject to state law. Adjuncts: clonidine may abate withdrawal while the methadone or buprenorphine dose is adjusted, tizanidine helps anxiety and muscle pain, bupropion targets anxiety symptoms, and lofexidine — FDA-approved in May 2018 as "the first non-opioid for managing opioid withdrawal syndrome" — is an alpha-2 agonist usable up to 14 days that works by reducing sympathetic tone and norepinephrine release.
- WITHDRAWAL MANAGEMENT IS NOT TREATMENT — and the sources say so twice. "Supervised withdrawal alone does NOT generally result in sustained abstinence from opioids, nor does it address reasons the client became dependent on opioids," and "by itself, it is not an effective treatment for any substance use disorder. It is considered stabilization… a first step toward recovery, similar to the acute management of a diabetic coma as a first step toward managing the underlying illness of diabetes." The four sourced reasons patients enter it: getting clean and staying clean; treating withdrawal in a patient hospitalised for something else who now lacks access to the substance; beginning treatment and transitioning to medication-assisted treatment; and establishing abstinence required by a setting such as incarceration, probation or a drug-free residence. The second of those is the one a medical-surgical nurse meets most often.
- Psychosocial treatment and harm reduction. Rehabilitation "begins with a cognitive behavioral approach similar to that used in the treatment of other chronic conditions," aiming "to minimize drug relapses," with patients "encouraged to participate in self-help programs such as Narcotics Anonymous"; group therapy "helps maintain self-control and restraint" and "is also cost-effective compared to individualized therapy." CBT "is most effective if combined with medications." Harm reduction — exactly the four strategies the sources name: "outreach and education programs, needle/syringe exchange programs, overdose prevention education, and improving public access to naloxone," designed for people who are "not yet ready to participate in treatment," to reduce overdose and infection transmission and to encourage individuals to seek treatment.
- Stimulant overdose care beyond sedation. Immediate goals are "sedation, cardiovascular stabilization, airway protection, and cooling," escalating in severe cases to "endotracheal intubation, mechanical ventilation, and advanced cardiac life support," with "continuous cardiac monitoring… critical due to the high risk of arrhythmias and myocardial infarction," and supportive care including IV hydration or renal replacement therapy for rhabdomyolysis and acute kidney injury. Cooling is physical, not pharmacological: "aggressive cooling is achieved through sedation, fluid resuscitation, external cooling blankets, or evaporative cooling techniques," with rapid cooling above a body temperature of 41 °C, or temperatures exceeding 107 °F in the amphetamine source. There is no antidote.
Nursing considerations
The RN-specific layer — each action paired with the reason it matters.
How a real nurse thinks
The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.
- 1 Recognize cues
At the scene the triad is complete. Pinpoint pupils, a respiratory rate of 4, and an unrousable patient — with blue lips and nail beds as the late visible sign. Miosis in a patient with altered mental status "is highly indicative of responsiveness to naloxone," and respiratory depression is the specific finding naloxone is indicated for. The second cue set is the history, and it is the one that explains why tonight. He was released from jail eleven days ago and used the amount he used to use. That is the single most lethal combination on this page: tolerance fell during the enforced abstinence while the remembered dose did not. About 10% of overdose deaths involve someone recently released from an institution, for exactly this reason. The third cue is the sister herself — a bystander was present, as in nearly 40% of overdose deaths, and unlike most of them she had naloxone and knew how to use it.
- 2 Analyze cues
The combativeness is not a behavioural problem, it is a drug effect. "The most common adverse effects associated with naloxone occur after acute withdrawal from opioids," including anxiety and aggression — and full reversal "can result in withdrawal and include combative or aggressive behavior," which is why the dosing goal is adequate breathing rather than complete arousal. The next question is time, not appearance. Naloxone’s half-life is 30 to 80 minutes, shorter than the opioid he took, so re-sedation is expected. He is not ready for discharge because he woke up; discharge requires the full criteria, including a Glasgow coma scale of 15, no further naloxone needed, saturation at least 92% on room air, and someone to monitor him for 12 to 24 hours. Then the day-2 picture is the mirror image of day 0. Lacrimation, rhinorrhea, gooseflesh, myalgia, vomiting, diarrhea, yawning and dilated pupils are opioid withdrawal — and the discriminator from sedative withdrawal is exactly those first three, since "sedative-hypnotic withdrawal symptoms may resemble opioid withdrawal characteristics, but opioid withdrawal is also characterized by lacrimation, rhinorrhea, and pupillary dilation."
- 3 Prioritize
Day 0, first: airway and breathing, then continued monitoring for re-sedation — not discharge. Second: screening he will not get if he leaves, since he injects — HIV and hepatitis B and C, plus CBC, basic metabolic panel, ECG, blood alcohol and a urine drug screen, remembering that methadone and buprenorphine will not show on an opiate screen. Day 2, first: volume. He is vomiting, having diarrhea and sweating simultaneously, and that combination is the sourced hazard of opioid withdrawal — monitor for dehydration and replace fluids. Second: symptom control that protects the volume — ondansetron for the nausea, loperamide for the diarrhea, ibuprofen for the myalgia — alongside the calm, quiet environment that "can decrease the need for pharmacologic interventions." Third: COWS, scored serially, because it gates the buprenorphine. Fourth, and the one most often skipped: the discharge plan, because withdrawal management alone is stabilisation, not treatment.
- 4 Generate solutions
Anticipate observation for at least 4 hours from the last naloxone dose per the nursing text, or 6 to 12 hours per StatPearls, with the longer window if a long-acting opioid is suspected. Anticipate that his COWS of 14 is moderate withdrawal and is above the threshold of 10, so buprenorphine 2 to 4 mg sublingually can be started — given yesterday it would have precipitated withdrawal rather than treated it. Know the alternative shapes: methadone could have been given with opioid still on board, because "it has an additive effect on opioids that are already present," but is clinic-dispensed with a long half-life; naltrexone is not an option yet, because it "may only be initiated when the patient is free of physiological opioid dependence, and at least seven days without acute withdrawal symptoms are required." Plan the discharge package: naloxone and overdose-prevention education for him and for his sister; a linked referral for continuing treatment; and the explicit warning that the first 4 weeks of treatment and the 4 weeks after it ends are his highest-risk periods.
- 5 Take action
On day 0, stay with him through the agitation, keep him safe, and explain what is happening — the sourced instruction is safety, reassurance and explanation, because he is experiencing a withdrawal syndrome that the treatment caused. Escalate with an SBAR: "29-year-old man, found unresponsive with pinpoint pupils and a respiratory rate of 4, reversed with two doses of intranasal naloxone given by a family member. He is now breathing at 16 with a saturation of 96%, but agitated with precipitated withdrawal. He injects heroin and was released from jail eleven days ago, using his pre-incarceration amount — this is a tolerance-loss overdose. I am monitoring for re-sedation because naloxone’s half-life is shorter than the opioid. Requesting HIV and hepatitis B and C screening, and I would like him seen by the addiction team before discharge." Three traps to avoid. Discharging him because he woke up. Reading the agitation as non-cooperation. And giving buprenorphine on day 0 to settle him — it would have precipitated the withdrawal it is meant to relieve.
- 6 Evaluate
Day 0 success: he stays awake and breathing without further naloxone, meets every discharge criterion rather than just looking better, and has bloods drawn that would never have been taken if he had walked out. Day 2 success: vomiting and diarrhea controlled, volume maintained, COWS trending down after the first buprenorphine dose, and no precipitated withdrawal because the dose was given at a score above 10. Discharge success is the part that decides whether he is here again: naloxone in the house and his sister taught to use it; a linked referral rather than a leaflet, because half to three quarters of people who complete withdrawal management never enter treatment and "one of the most serious consequences… is overdose"; and the tolerance rule said out loud — the amount that was normal before jail is not normal now, and the same is true after every hospital stay. Re-escalation triggers: any drop in respiratory rate or level of consciousness during observation; persistent hypoxia despite adequate breathing, which suggests noncardiogenic pulmonary edema; and signs of volume depletion during withdrawal.
Scenario — you’re the nurse
Work each question before revealing the answer. Rationales explain the wrong options too.
A 29-year-old man is found unresponsive on the bathroom floor by his sister. He was released from jail eleven days ago. She calls 911, and while waiting she gives him naloxone from a kit she was given when he was discharged. He arrives in the emergency department breathing spontaneously but confused and briefly combative, and is admitted for observation.
Q1 Select all that apply Which findings at the scene indicate opioid overdose? Select all that apply. - A. Pinpoint pupils
- B. Respiratory rate of 4 with gurgling breathing
- C. Unrousable to sternal rub
- D. Blue lips and nail beds
- E. Temperature 37.1 °C
Reveal answer & rationale
Q2 Multiple choice The patient wakes after naloxone and is briefly combative. The nurse should recognize that: - A. The naloxone dose was too low and should be repeated immediately
- B. This is precipitated withdrawal, which is an expected effect of reversal — provide safety, reassurance and explanation
- C. The patient is exhibiting drug-seeking behavior and should be discharged once calm
- D. A benzodiazepine should be given routinely to any patient who is agitated after naloxone
Reveal answer & rationale
Q3 Put in order Put the nurse’s actions in order for this patient: - A. Arrange linked referral for continuing treatment and give naloxone plus teaching to the patient and his sister
- B. Monitor for re-sedation, knowing naloxone’s half-life is shorter than the opioid
- C. Score COWS serially and hold buprenorphine until the score exceeds 10
- D. Replace fluids and control the vomiting and diarrhea
Reveal answer & rationale
Q4 Multiple choice A different patient arrives agitated, febrile at 40.5 °C, tachycardic and hypertensive after using methamphetamine. Which action is contraindicated? - A. Administering a parenteral benzodiazepine for sedation
- B. Applying physical restraints to control the agitation
- C. Using external cooling blankets and intravenous fluids
- D. Obtaining a creatine kinase and lactic acid level
Reveal answer & rationale
Q5 Multiple choice Which statement by the patient’s sister indicates that discharge teaching has been effective? - A. "Now that he has finished detox, the hardest part is behind him."
- B. "If he uses again, the amount he used before jail could kill him now, so I am keeping the naloxone where I can reach it."
- C. "If the naloxone wakes him up, we can stay home and watch him."
- D. "He should be able to stop the buprenorphine once he feels better in a few weeks."
Reveal answer & rationale
Common questions
What causes substance use & overdose?
Which findings should a nurse report immediately in substance use & overdose?
Which medications are used to treat substance use & overdose?
Why is the period right after detox the most dangerous time?
How much naloxone, and when do you stop watching?
Why can buprenorphine not be given as soon as the patient asks for it?
Sources
- Opioid Use Disorder: Evaluation and Management — StatPearls — StatPearls (NCBI Bookshelf)
- Naloxone — StatPearls — StatPearls (NCBI Bookshelf)
- Opioid Withdrawal — StatPearls — StatPearls (NCBI Bookshelf)
- Clinical Practice Guideline for Prescribing Opioids for Pain — United States, 2022 (MMWR Recomm Rep 2022;71:RR-3) — Centers for Disease Control and Prevention
- Amphetamine Toxicity — StatPearls — StatPearls (NCBI Bookshelf)
- Substance Use Disorders — Nursing: Mental Health and Community Concepts, 2nd ed., Ch. 14 — Open RN / Chippewa Valley Technical College (NCBI Bookshelf)
- Opioid overdose and naloxone — MedlinePlus — MedlinePlus (NLM)
Reviewed by Hae Suk Lee, RN
Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.