Poisoning: quick reference for antidotes and initial management

Basic principle

Manage the patient, not the list of poisons. Stabilisation according to ABCDE, the plasma glucose, a blood gas and an ECG all come before complete identification of the substance. Treatment of acute poisoning consists of four parallel components: supportive treatment, a targeted antidote, reduced absorption and, in selected cases, enhanced elimination. For many poisonings, well-delivered supportive treatment matters more than the antidote [1,2].

Telephone your national or regional poison control centre, which in most countries is staffed around the clock for health care professionals. Contact the centre early in serious, unusual or unclear poisoning, with modified-release preparations, mixed poisoning, pregnancy, children, a need for an antidote or dialysis, and whenever the clinical course deviates from what was expected. The poison control centre is the authoritative local source for the current indication, dosing, sampling and duration of treatment. International guidelines must be adapted to the antidotes, analytical methods and treatment protocols that are available where you practise.

Initial management of all poisonings

ABCDE

A low Glasgow Coma Scale is not on its own an absolute indication for intubation. Assess ventilation, airway protection, the expected course and the possibility of rapid reversal with an antidote. Intubation is recommended for neurological, respiratory or haemodynamic failure that cannot be corrected quickly. Rapid sequence induction is used when intubation is required [1].

In salicylate poisoning, intubation with an inadequate minute ventilation can rapidly worsen the acidaemia and increase the entry of salicylate into the central nervous system. Discuss the case early with the poison control centre and with anaesthesia or intensive care. If intubation is necessary, a high minute ventilation and careful control of the pH must be maintained.

History and gathering information

Ask about:

• the substance, the strength, the formulation and the estimated quantity
• the time, and whether the intake was single or repeated
• a modified-release preparation or a combination product
• concurrent drugs, alcohol and illicit substances
• weight, age, pregnancy and comorbidity
• renal and hepatic function
• regular medication and drug dependence
• epilepsy or previous seizures
• suicidal intent
• packaging, blister packs, photographs, the prescription list and the findings of the ambulance crew

The stated dose is often unreliable and must never be used on its own to declare the patient well. Clinical findings, the ECG and targeted concentration measurements carry more weight. Where serious poisoning is suspected, blood and urine can be saved early for later targeted analysis.

Initial monitoring and investigations

Routine non-specific toxicological urine screens are of limited value in the acute setting. They can be falsely positive or falsely negative and often show previous exposure rather than the cause of the current state. Management should primarily be based on the toxidrome, the ECG and targeted quantitative analyses [1].

Take a paracetamol concentration in unclear intentional drug ingestion, or when the history is unreliable. Paracetamol poisoning often causes few symptoms during the first 24 hours. In a recent observational study, 0.9 per cent of patients with an intentional overdose or suspected poisoning-related impairment of consciousness had detectable paracetamol despite a negative history, and 0.2 per cent had a concentration above 100 micrograms/mL [3]. The low yield must be weighed against the risk of untreated hepatotoxicity.

The ECG as a toxicological vital sign

An ECG must be recorded early and repeated if there are symptoms or if a cardiotoxic substance has been taken. Assess in particular:

• the QRS width
• the QTc
• a terminal R wave in aVR
• AV block
• bradycardia
• ventricular ectopics or ventricular tachycardia
• a Brugada-like pattern
• new ST or T wave changes

A wide QRS suggests sodium channel blockade, for example by tricyclic antidepressants, certain antipsychotics, propranolol, cocaine, flecainide or local anaesthetics. A long QTc increases the risk of torsade de pointes, particularly together with bradycardia, hypokalaemia or hypomagnesaemia.

Toxidromes

Toxidromes help when the substance is unknown, but mixed poisonings often produce incomplete or contradictory findings. Pupil size alone is never diagnostic.

Serotonergic toxicity

Clonus and hyperreflexia, often most marked in the legs, are more specific findings than tachycardia, fever or agitation alone. The Hunter criteria are chiefly validated in overdose or clear serotonergic drug interaction and should be used cautiously in complex patients with alternative causes of fever and delirium [4].

Treatment is guided by severity:

• stop the serotonergic drugs
• give a benzodiazepine for agitation and muscle activity
• give intravenous fluid according to clinical need
• cool actively in hyperthermia
• intubate, anaesthetise and paralyse early if the temperature is rising rapidly, or with marked rigidity or ventilatory failure

Antipyretics do not help in toxic hyperthermia, since the heat production is caused by muscle activity, not by a change in the temperature set point. Cyproheptadine is sometimes used, but controlled data are lacking and its value in life-threatening serotonergic toxicity is uncertain. Aggressive sedation, cooling and organ support must not be delayed while awaiting a serotonin antagonist [4].

Decontamination

Activated charcoal

Activated charcoal must not be given routinely to every patient. Consider a single dose when essentially all of the following apply:

• the ingestion is potentially serious
• the substance is bound by charcoal
• a clinically relevant amount is judged to remain in the gastrointestinal tract
• the airway is intact or secured
• the gastrointestinal tract is functioning
• giving it does not delay more important treatment or transfer

The greatest effect is seen when charcoal is given within about an hour. There may be an effect later with modified-release preparations, a massive ingestion, an anticholinergic agent, an opioid, salicylate or any other situation with delayed gastric emptying. Volunteer studies show reduced absorption even after later administration, but clinical studies have not clearly shown improved mortality or a shorter length of stay [5,6].

The usual dose is:

• adults: 50 g
• children: 1 g/kg, usually not exceeding the adult dose

Do not give activated charcoal to a patient with a reduced level of consciousness or an expected rapid deterioration without a secured airway. Aspiration of charcoal can cause severe lung injury. Charcoal can also cause vomiting, constipation and, rarely, bowel obstruction.

Activated charcoal does not bind, to any clinically relevant extent:

• iron
• lithium
• potassium
• alcohols, including methanol and ethylene glycol
• strong acids and alkalis
• many solvents

Charcoal is unsuitable in corrosive ingestion, since it does not neutralise the injury and can make endoscopy more difficult. It must not be given in ileus, bowel obstruction or suspected perforation.

Repeated doses of activated charcoal can enhance the elimination of certain substances by reducing enterohepatic circulation and through so-called gut dialysis. This may be considered after a life-threatening ingestion of, among others, carbamazepine, dapsone, phenobarbital, quinine or theophylline, but it must be decided together with the poison control centre [5]. The evidence for first-aid use of activated charcoal is generally of low or very low certainty [7].

Gastric lavage

Gastric lavage has a very limited place and does not reliably improve the outcome compared with supportive treatment or activated charcoal. The complications include aspiration, hypoxia, laryngospasm, arrhythmia and perforation. Consider it only after a very recent, potentially lethal ingestion in which the expected benefit clearly outweighs the risk. Always discuss it with the poison control centre and secure the airway where necessary [5].

Vomiting must not be induced.

Whole bowel irrigation

Whole bowel irrigation with a polyethylene glycol solution may be considered in:

• large ingestions of modified-release preparations
• iron, lithium, potassium or other substances not bound by charcoal
• ingested drug packages
• an accumulation of tablets or a suspected bezoar

The method lacks strong clinical outcome data and must not be used routinely. The contraindications include an unprotected airway, haemodynamic instability, uncontrolled seizures, ileus, bowel obstruction and perforation [5].

Antidotes and targeted treatment

Doses are deliberately not given in the main table. Telephone the poison control centre or follow the current local protocol. The wrong antidote, the wrong route or the wrong monitoring can harm the patient. In time-critical situations, however — for example opioid-induced respiratory arrest, a wide QRS from a tricyclic antidepressant, or severe cholinergic bronchorrhoea — treatment must not be delayed while a complete history is obtained.

Paracetamol

Acetylcysteine is highly effective when given early. Document precisely:

• the time at which the ingestion began
• whether it was a single or a repeated ingestion
• the formulation
• any concurrent opioid or anticholinergic substance
• the patient's weight
• the paracetamol concentration
• the ALT, INR, creatinine, pH and lactate in a late or serious presentation

The nomogram may be used only for an acute, single ingestion with a known time and a concentration taken no earlier than four hours after the ingestion. It must not be used when the time is unknown, after repeated supratherapeutic ingestions, with ongoing ingestion over a longer period, or when the patient already has liver injury. Modified-release preparations and a concurrent opioid or anticholinergic substance can delay absorption and require a repeat concentration [8].

When the time is unknown, when a concentration is measurable or when there is liver involvement, acetylcysteine should often be started before the whole course is clear. Treatment must not be stopped automatically merely because a standard infusion schedule has finished. The current stopping criteria comprise the clinical course, the paracetamol concentration and the liver tests. International recommendations set out particular strategies for high-risk ingestions, but the dosing schedule and nomogram in local use must be followed after contact with the poison control centre [9].

Opioids

Bag-mask ventilation with oxygen is the immediate treatment. Naloxone does not replace airway management. The aim is regular, adequate spontaneous breathing and adequate oxygenation, not full wakefulness. Rapid complete reversal can precipitate acute withdrawal with agitation, vomiting, aspiration and sometimes marked sympathetic activation.

The half-life of naloxone is around 60 to 120 minutes and is often shorter than the effect of methadone, modified-release opioids or a large ingestion. Recurrent respiratory depression can therefore appear after an initial improvement. Repeated doses or an infusion may be required. Fentanyl and certain other potent synthetic opioids may require more naloxone than heroin [10].

Observe the patient with continuous respiratory monitoring after a response. A need for repeated doses of naloxone, a long-acting opioid, mixed poisoning, aspiration, pulmonary oedema or persistent hypoxia all argue for admission.

Benzodiazepines and flumazenil

Pure benzodiazepine poisoning often has a favourable course with supportive treatment. Flumazenil must not be used routinely. It can precipitate seizures, withdrawal and arrhythmia, particularly in:

• mixed poisoning with tricyclic antidepressants or another proconvulsant substance
• known epilepsy
• long-term benzodiazepine use
• unclear poisoning
• a wide QRS or other signs of sodium channel blockade

A meta-analysis of 13 randomised trials with 994 participants showed more adverse events with flumazenil than with placebo, risk ratio 2.85, and more serious adverse events, risk ratio 3.81. The serious events included seizures and supraventricular arrhythmias [11]. Flumazenil may be considered in carefully selected cases, for example iatrogenic sedation or a confirmed isolated ingestion in a benzodiazepine-naive patient.

Tricyclic antidepressants and sodium channel blockade

Tricyclic antidepressants can cause rapid-onset seizures, coma, hypotension, a wide QRS and ventricular arrhythmias. A QRS above 100 ms is an important risk marker and warrants immediate consideration of sodium bicarbonate [12].

Sodium bicarbonate is the first-line treatment for:

• a QRS above about 100 ms
• ventricular arrhythmia
• hypotension not responding to initial fluid
• seizures with signs of tricyclic toxicity
• a clear terminal R wave in aVR

Monitor the pH, sodium, potassium and QRS during treatment. Marked alkalaemia, hypokalaemia, hypocalcaemia and volume overload must be avoided. Seizures are treated with a benzodiazepine. Refractory hypotension is treated with a direct-acting vasopressor, usually noradrenaline. Tricyclic antidepressants have a large volume of distribution and high protein binding and cannot be meaningfully eliminated by dialysis [13].

Beta blockers and calcium channel blockers

These poisonings can cause bradycardia, AV block, hypotension, cardiogenic shock and sometimes vasodilatory shock. Modified-release preparations can cause a delayed deterioration. Calcium channel blockers often cause hyperglycaemia, while certain beta blockers can cause hypoglycaemia. Propranolol can in addition cause seizures and sodium channel blockade with a wide QRS.

Treatment is multimodal:

• cautious fluid therapy
• calcium in calcium channel blocker poisoning
• high-dose insulin with concurrent glucose and close monitoring of the glucose and potassium
• glucagon, chiefly in beta blockade
• adrenaline or another inotrope for myocardial depression
• noradrenaline for marked vasodilatation
• early intensive care
• consider ECMO in refractory cardiogenic shock or cardiac arrest

High-dose insulin improves myocardial energy utilisation and contractility and should be considered early when there is myocardial depression [14,15]. Hypoglycaemia and hypokalaemia are expected complications requiring structured monitoring. Controlled studies are few, and a systematic review of calcium channel blocker poisoning was based mainly on case reports, one case series and one cohort. It supports a multimodal approach but cannot reliably rank the treatments [16].

Toxic alcohols

Suspect methanol or ethylene glycol in:

• a metabolic acidosis with a high anion gap
• a raised osmolal gap, particularly early in the course
• visual disturbance after suspected methanol
• acute kidney injury or hypocalcaemia after suspected ethylene glycol
• unexplained impairment of consciousness
• a relevant history of exposure

A normal osmolal gap does not exclude late poisoning. As the alcohol is metabolised, the osmolal gap can fall while the anion gap and the acidosis increase. Start fomepizole, or alternatively ethanol, on a strong clinical suspicion, without awaiting the definitive analysis.

Ethylene glycol is dialysable. EXTRIP recommends dialysis for severe clinical findings such as coma, seizures or acute kidney injury, and for a marked metabolite burden, for example a high anion gap. Intermittent haemodialysis is preferred where it is available [17]. The antidote dose must be adjusted during dialysis. The exact dialysis thresholds and local practice must be discussed with the poison control centre, intensive care and nephrology.

Lithium

Acute, acute-on-chronic and chronic lithium poisoning differ clinically. The neurological findings can be marked despite a moderate serum concentration in chronic poisoning. Monitor:

• repeated lithium concentrations
• creatinine and urine output
• sodium
• the level of consciousness
• tremor, ataxia, myoclonus and seizures
• the ECG

Give isotonic fluid in volume depletion. Activated charcoal has no effect. EXTRIP recommends dialysis in severe lithium poisoning, in renal failure with a lithium above 4 mmol/L, and in a reduced level of consciousness, seizures or life-threatening arrhythmia irrespective of the concentration. Dialysis is suggested for, among other situations, a lithium above 5 mmol/L, significant confusion, or when the time to a concentration below 1 mmol/L is judged to exceed 36 hours [18]. The evidence is, however, mainly observational, and randomised trials are lacking [19]. The decision must be taken together with the poison control centre and nephrology.

Salicylate

The clinical findings are tinnitus, nausea, tachypnoea, fever, sweating, agitation, pulmonary oedema, hypoglycaemia in the central nervous system, and a mixed respiratory alkalosis with metabolic acidosis. A single early salicylate concentration can be misleading, particularly with enteric-coated preparations or an accumulation of tablets. Take repeated concentrations until there is a clearly falling trend together with clinical improvement.

Treatment comprises:

• activated charcoal in selected cases, including later than one hour
• correction of hypovolaemia
• glucose when the glucose is low or low-normal in a neurologically compromised patient
• sodium bicarbonate for serum and urinary alkalinisation
• correction of the potassium
• early discussion of dialysis in a serious clinical picture, renal failure, pulmonary oedema, marked acidaemia or a rising concentration despite treatment

Digoxin

Suspect serious digoxin toxicity in bradyarrhythmia, AV block, ventricular arrhythmia, gastrointestinal symptoms, visual phenomena or hyperkalaemia. Take a digoxin concentration, potassium, creatinine and an ECG. A concentration taken too soon after an acute ingestion can be hard to interpret, since distribution is not complete.

Digoxin-specific antibody fragments are used for life-threatening arrhythmia, circulatory failure or marked hyperkalaemia. After administration, ordinary digoxin assays can show misleadingly high total levels and must not be used uncritically to guide further dosing. Discuss the case with the poison control centre.

Sulfonylureas and insulin

Both insulin and sulfonylureas can cause prolonged or delayed hypoglycaemia. Give glucose for symptomatic hypoglycaemia and monitor the plasma glucose closely.

In sulfonylurea poisoning, repeated large doses of glucose can stimulate further insulin release. After the initial correction of the glucose, octreotide is the central treatment to counteract recurrent hypoglycaemia. In insulin overdose, continuous glucose administration is the main treatment. Observation is needed after glucose and octreotide have been stopped, since the hypoglycaemia can recur [20].

Organophosphates and carbamates

Protect staff from secondary contamination. Remove contaminated clothing and wash the skin. Bronchorrhoea, bronchospasm and respiratory failure are more immediately life-threatening than the pupillary findings.

Atropine is titrated against:

• reduced bronchial secretions
• improved ventilation
• improved oxygenation and circulation

Tachycardia or persistent miosis are not in themselves reasons to stop atropine if bronchorrhoea persists. An oxime, for example obidoxime or pralidoxime, may be considered in organophosphate poisoning. The evidence is uncertain. A Cochrane review found insufficient evidence to establish benefit or harm, partly because of methodological problems and low dosing in the studies [21]. Follow the current protocol of your poison control centre.

Methaemoglobinaemia

Suspect methaemoglobinaemia in central cyanosis that does not improve as expected with oxygen, a saturation of around 85 per cent despite a normal or high PaO2, and chocolate-brown blood. The diagnosis is confirmed with co-oximetry [22].

Methylthioninium chloride (methylene blue) is the first-line treatment for symptomatic acquired methaemoglobinaemia. Treat the patient, not merely the percentage figure. A lower threshold is used in anaemia, cardiac or pulmonary disease and other states of impaired oxygen transport.

Methylthioninium chloride can be ineffective and can cause haemolysis in G6PD deficiency. It inhibits monoamine oxidase and can precipitate serotonergic toxicity in patients taking serotonergic drugs. If there is no response, the diagnosis, any continuing exposure, G6PD deficiency and alternative treatment must be discussed immediately with the poison control centre and intensive care [23].

Cyanide

Cyanide poisoning is a clinical diagnosis. The smell of bitter almonds and cherry-red skin are uncommon and must not be required for the diagnosis. In a systematic review of isolated cyanide cases, unconsciousness, respiratory failure, hypotension and marked lactic acidosis were considerably more common [24].

Consider hydroxocobalamin in a relevant exposure together with:

• a marked lactic acidosis
• impaired consciousness
• seizures
• hypotension or cardiac arrest
• a fire in an enclosed space with soot in the airways and a serious clinical picture

Hydroxocobalamin can colour the skin, urine and plasma red and can interfere with several laboratory analyses and with the optical blood leak alarm of dialysis equipment.

Systemic local anaesthetic toxicity

Systemic local anaesthetic toxicity, LAST, can begin with perioral numbness, tinnitus, a metallic taste, agitation or seizures and progress to hypotension, a wide QRS, ventricular arrhythmia and cardiac arrest. Stop the injection, secure the airway and ventilation, treat the seizures and give lipid emulsion according to the local LAST protocol. Use small doses of adrenaline according to the specific protocol and avoid further local anaesthetic.

Anticoagulants

In serious bleeding, anticoagulant treatment must be stopped and reversal carried out in parallel with surgical, endoscopic or interventional control of the bleeding.

• Warfarin is reversed with vitamin K and prothrombin complex concentrate in serious bleeding.
• Unfractionated heparin is reversed with protamine.
• Low-molecular-weight heparin is only partly reversed with protamine.
• Dabigatran can be reversed with idarucizumab.
• Factor Xa inhibitors can in some situations be reversed with andexanet alfa or prothrombin complex concentrate.

International guidelines give separate recommendations for the different antithrombotic drugs [25]. Swedish restrictions on availability and local bleeding protocols may differ and must be followed.

Enhanced elimination and intensive care

Discuss dialysis early in suspected serious poisoning with:

• lithium
• methanol
• ethylene glycol
• salicylate
• valproate
• metformin with severe lactic acidosis
• theophylline
• certain other small, water-soluble substances with low protein binding and a small volume of distribution

The decision about dialysis is not governed by the concentration alone. The clinical findings, the pH, renal function, the trend, the type of exposure and the expected natural elimination are all decisive.

Contact intensive care early in:

• airway or ventilatory failure
• a need for an antidote infusion
• seizures
• hyperthermia
• a wide QRS or a serious arrhythmia
• a rising lactate or metabolic acidosis
• shock
• a need for dialysis
• expected delayed toxicity after a modified-release preparation
• a need for ECMO or other advanced circulatory support

Body packers and body stuffers

Distinguish between:

• the body packer, who deliberately swallows many well-wrapped drug packages
• the body stuffer, who hastily swallows fewer and more poorly wrapped packages to avoid detection

Body stuffers are at higher risk of leakage, since the packages are often poorly sealed. Symptoms of opioid or sympathomimetic toxicity may signal leakage or rupture of a package.

Non-contrast computed tomography of the abdomen is the most reliable imaging method when body packing is suspected. A negative plain abdominal radiograph does not exclude packages [26]. Contrast media can make visualisation more difficult.

Asymptomatic body packers can often be managed with observation and whole bowel irrigation after specialist assessment. Emergency surgery is required for:

• toxic effects suggesting leakage or rupture
• bowel obstruction
• perforation
• packages that do not progress despite adequate conservative treatment

Endoscopic manipulation carries a risk of rupture and must not be undertaken without a multidisciplinary plan.

Red flags

• A wide QRS complex, particularly after a tricyclic antidepressant, propranolol, flecainide, cocaine or a local anaesthetic.
• A long QTc together with bradycardia or an electrolyte disturbance.
• A rising lactate or a worsening metabolic acidosis.
• A high anion gap with or without a high osmolal gap.
• Hyperthermia, particularly together with agitation, clonus or rigidity.
• Recurrent hypoglycaemia.
• Seizures, even if they stop after a benzodiazepine.
• A modified-release preparation or a large tablet ingestion, where symptoms can be delayed.
• Paracetamol with an unknown time, repeated ingestions or liver involvement.
• Salicylate with neurological symptoms, pulmonary oedema or acidaemia.
• Lithium with neurological symptoms or renal failure.
• Smoke inhalation with impaired consciousness and marked lactic acidosis.
• Suspected body packing with abdominal pain or a toxidrome.
• A rising vasopressor requirement in cardiotoxic poisoning.
• Pregnancy, a small child or a frail older patient, in whom smaller doses can have greater consequences.
• Suicidal intent, a persisting suicide risk, or inadequate social protection.

Observation, discharge and psychiatric assessment

Discharge presupposes that:

• the substance ingested and its formulation are reasonably established
• the relevant period of observation has elapsed
• the patient is awake and orientated with no residual psychoactive effect
• the vital signs are normal
• the relevant laboratory tests are normal or following a reassuring trend
• the ECG is normal when a cardiotoxic substance may have been taken
• recurrent toxicity is not expected
• there is a plan for continued physical and psychiatric care

A generic observation period does not suit every poisoning. Six symptom-free hours may be sufficient after certain rapid-acting preparations, but it is inadequate with a modified-release preparation, methadone, a sulfonylurea, lithium, a calcium channel blocker, certain beta blockers or delayed paracetamol absorption.

After deliberate self-poisoning, the suicide risk must be assessed before discharge. The assessment must be made when the patient is sufficiently sober and cognitively recovered to take part. A persisting serious suicide risk may warrant psychiatric inpatient care and consideration of compulsory admission.

A short checklist

1. ABCDE and the plasma glucose.
2. Oxygen and ventilation as needed.
3. An ECG now; repeat it with a cardiotoxic substance or symptoms.
4. A blood gas with lactate, and targeted laboratory tests.
5. Paracetamol in intentional or unclear poisoning.
6. Identify the toxidrome, but assume mixed poisoning until that is no longer plausible.
7. Consider activated charcoal only after assessing the substance, the timing and the airway.
8. Give a time-critical antidote without unnecessary delay.
9. Telephone the poison control centre early in serious, unclear or unusual poisoning.
10. Plan observation, intensive care, dialysis and psychiatric assessment during the initial management.

References

1. Mégarbane B et al. Management of pharmaceutical and recreational drug poisoning. Annals of Intensive Care 2020. PMID: 33226502
2. Smith SW. Drugs and pharmaceuticals: management of intoxication and antidotes. EXS 2010. PMID: 20358691
3. Alyahya B et al. The clinical value of screening for acetaminophen in all patients with intentional overdose or altered mental status suspected to be secondary to overdose. Frontiers in Pharmacology 2025. PMID: 40808679
4. Chiew AL, Isbister GK. Management of serotonin syndrome (toxicity). British Journal of Clinical Pharmacology 2025. PMID: 38926083
5. Albertson TE et al. Gastrointestinal decontamination in the acutely poisoned patient. International Journal of Emergency Medicine 2011. PMID: 21992527
6. Olson KR. Activated charcoal for acute poisoning: one toxicologist's journey. Journal of Medical Toxicology 2010. PMID: 20490748
7. Avau B et al. First aid interventions by laypeople for acute oral poisoning. Cochrane Database of Systematic Reviews 2018. PMID: 30565220
8. Dart RC et al. Acetaminophen poisoning: an evidence-based consensus guideline for out-of-hospital management. Clinical Toxicology 2006. PMID: 16496488
9. Dart RC et al. Management of Acetaminophen Poisoning in the US and Canada: A Consensus Statement. JAMA Network Open 2023. PMID: 37552484
10. Saari TI, Strang J, Dale O. Clinical Pharmacokinetics and Pharmacodynamics of Naloxone. Clinical Pharmacokinetics 2024. PMID: 38485851
11. Penninga EI et al. Adverse Events Associated with Flumazenil Treatment for the Management of Suspected Benzodiazepine Intoxication: A Systematic Review with Meta-Analyses of Randomised Trials. Basic and Clinical Pharmacology and Toxicology 2016. PMID: 26096314
12. Woolf AD et al. Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management. Clinical Toxicology 2007. PMID: 17453872
13. Yates C et al. Extracorporeal treatment for tricyclic antidepressant poisoning: recommendations from the EXTRIP Workgroup. Seminars in Dialysis 2014. PMID: 24712820
14. Graudins A, Lee HM, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. British Journal of Clinical Pharmacology 2016. PMID: 26344579
15. Hamzić J, Raos D, Radulović B. High-dose insulin euglycemic therapy. Acta Clinica Croatica 2022. PMID: 36304811
16. Baid H et al. Treatment Modalities in Calcium Channel Blocker Overdose: A Systematic Review. Cureus 2023. PMID: 37664357
17. Ghannoum M et al. Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations from the EXTRIP workgroup. Critical Care 2023. PMID: 36765419
18. Decker BS et al. Extracorporeal Treatment for Lithium Poisoning: Systematic Review and Recommendations from the EXTRIP Workgroup. Clinical Journal of the American Society of Nephrology 2015. PMID: 25583292
19. Lavonas EJ, Buchanan J. Hemodialysis for lithium poisoning. Cochrane Database of Systematic Reviews 2015. PMID: 26374731
20. Klein-Schwartz W, Stassinos GL, Isbister GK. Treatment of sulfonylurea and insulin overdose. British Journal of Clinical Pharmacology 2016. PMID: 26551662
21. Buckley NA, Eddleston M, Szinicz L. Oximes for acute organophosphate pesticide poisoning. Cochrane Database of Systematic Reviews 2005. PMID: 15654704
22. Ivek I et al. Methemoglobinemia: a case report and literature review. Acta Clinica Croatica 2022. PMID: 36304805
23. Iolascon A et al. Recommendations for diagnosis and treatment of methemoglobinemia. American Journal of Hematology 2021. PMID: 34467556
24. Parker-Cote JL et al. Challenges in the diagnosis of acute cyanide poisoning. Clinical Toxicology 2018. PMID: 29417853
25. Frontera JA et al. Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage. Neurocritical Care 2016. PMID: 26714677
26. Shahnazi M, Sanei Taheri M, Pourghorban R. Body packing and its radiologic manifestations: a review article. Iranian Journal of Radiology 2011. PMID: 23329942