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Nicotine poisoning (e-cigarettes, tobacco products, plants, and pesticides)

Nicotine poisoning (e-cigarettes, tobacco products, plants, and pesticides)
Literature review current through: Jan 2024.
This topic last updated: Jun 20, 2022.

INTRODUCTION — This topic will discuss nicotine poisoning after exposure to nicotine-containing plants, tobacco products, and concentrated nicotine solutions such as those used in electronic cigarettes (e-cigarettes) and pesticides.

The clinical diagnosis, manifestations, and management of poisoning by organophosphate or carbamate pesticides and other plants are discussed separately. (See "Organophosphate and carbamate poisoning" and "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation" and "Toxic plant ingestions in children: Management".)

NICOTINE-CONTAINING PLANTS AND PRODUCTS — Nicotine occurs naturally in tobacco and several other plants and is used commercially in many tobacco and nicotine products:

The tobacco plant, Nicotiana tabacum, is the source of tobacco for cigarettes, cigars, and chewing tobacco.

Other plants containing nicotine-like alkaloids are much less commonly involved in nicotine poisoning. Examples include:

Conium maculatum (poison hemlock)

Lobelia inflata (Indian tobacco)

Baptisia australis (blue wild or blue false indigo)

Laburnum anagyroides (golden chain)

Cytisus laburnum (golden chain tree)

Caulophyllum thalictroides (blue cohosh)

Nicotine is also present in patches, gums, lozenges, and liquids for vaporization in e-cigarettes.

Nicotine and chemically similar neonicotinoids can be used as potent insecticides.

EPIDEMIOLOGY — Almost 16,000 cases of nicotine exposure are reported to United States regional poison control centers annually [1]. Cigarettes (approximately 5400 annual cases) and e-cigarettes (approximately 4400 annual cases) account for most United States nicotine exposures [1,2]. The majority of nicotine exposures are exploratory ingestions in young children. However, a significant number arise from attempts at self-harm in adolescents and adults [1,3,4]. Concentrated nicotine solutions, such as those found in e-cigarette refills and pesticides, are the most dangerous [1-3,5,6]. Ingestion of even a small amount of these concentrated liquids can cause serious toxicity. Deaths are rare but have occurred in infants and toddlers [1,2,5].

By contrast, exposure to nicotine-containing plants (most commonly, the tobacco plant [Nicotiana tabacum]) is infrequent, with approximately 100 annual exposures reported to United States regional poison control centers [1]. Most nicotine-plant exposures result in mild or moderate symptoms. However, selected plants (eg, poison hemlock, Conium maculatum) have rarely been associated with serious toxicity and death [7-10]. (See 'Tobacco and other nicotinic plants' below.)

TOXICITY AND TOXICOKINETICS

Mechanism of toxicity — Nicotine binds to nicotinic acetylcholine receptors (nAChRs), which are present in the brain, the spinal cord (postganglionic sympathetic and parasympathetic neurons), and at the neuromuscular junction [11]. Under normal conditions, acetylcholine is the neurotransmitter at these receptors. The nAChR is a cation ionic channel, which causes cell depolarization when activated. Repeated agonism, however, can lead to functional paralysis of the receptor. As a result, nicotine toxicity classically manifests in a biphasic pattern [11]:

Initial activation with neuronal excitation that produces:

Diaphoresis (sympathetic stimulation of the sweat glands)

Tachycardia, hypertension, and pallor (sympathetic stimulation)

Bronchorrhea, bronchospasm, salivation, vomiting, diarrhea, and miosis (parasympathetic stimulation)

Skeletal muscle fasciculations (neuromuscular excitation)

Hyperactivity, agitation, tremor, and/or seizures (brain excitation)

Marked inhibition causing:

Bradycardia, arrhythmias, and hypotension, which can progress to asystole

Skeletal muscle paralysis

Apnea

Coma

Nicotine and neonicotinoids (found in pesticides) differ in their behavior at the nAChr. Nicotine can behave as a full or partial agonist [11]; neonicotinoids can act as agonists, partial agonists, or antagonists [12]. In general, neonicotinoid exposures are less likely to cause major toxicity except after large intentional ingestions. (See 'Neonicotinoids' below.)

Although also causing neuromuscular dysfunction, organophosphates inhibit acetylcholinesterase, causing a buildup of excess acetylcholine, leading to repeated depolarization at the neuromuscular junction (figure 1) rather than direct binding of nicotinic anticholinergic receptors. (See "Organophosphate and carbamate poisoning", section on 'Mechanism of action'.)

Toxic dose — Toxicity depends upon the route of exposure:

Ingestion – The estimated toxic and lethal ingested nicotine doses for children and adults are as follows:

Child [13]:

-Toxic dose: 0.1 mg/kg

-Minimum lethal dose: 1 mg/kg

A total dose of 1 to 2 mg of nicotine is potentially toxic in children. In children, doses as small as 2 mg (approximately 0.1 mg/kg) have produced symptoms such as lethargy or weakness [14]. The table provides an estimated toxic ingested dose for common tobacco and nicotine products (table 1).

An estimated nicotine dose of <0.01 mg/kg typically results in minimal or no symptoms [15].

Adult [5]:

-Toxic dose in adults naïve to nicotine: 4 to 7 mg

-Minimum lethal dose: 60 mg

In adults, 60 mg is an oft-cited lethal dose. However, this threshold is debated based upon survival of adult patients who have measured plasma concentrations after e-cigarette liquid ingestion that are up to 10 times higher than the expected concentration after ingestion of 60 mg of nicotine [5,16].

Dermal (liquid nicotine) – Dermal exposure to concentrated nicotine liquid (eg, e-cigarette solutions, nicotine-containing pesticides, nicotine dermal patches, or exposure to wet tobacco plants [green tobacco sickness]) has the potential to cause poisoning, especially if exposure is prolonged [4,15,17-21]. Severe poisoning and death have occurred with prolonged exposure to multiple transdermal nicotine patches in adults [15,18].

Ocular (liquid nicotine) – Based upon isolated reports of inadvertent ocular administration of e-cigarette solutions, ocular nicotine liquid exposure causes eye redness, pain, and local irritation; systemic effects have not been described [21,22].

Inhalation – Cigarette and e-cigarette inhalation exposures account for a small minority of nicotine exposures. Cigarette smoking in patients with no prior nicotine exposure can cause self- limited cough, nausea, and vomiting [23]. Because of the higher concentration of nicotine during e-cigarette inhalation, more serious poisoning is possible. For example, in a study of 10 e-cigarette inhalational exposures in children reported to a regional poison control center, excessive vaping from an e-cigarette was associated with vomiting, marked tachycardia, lethargy, seizures, and hallucinations in two adolescents [21]. No symptoms occurred in a three-year-old child who took one or two "drags" from the parent's e-cigarette.

The clinical features of poisoning are described below. (See 'Toxicity by nicotine source' below and 'Clinical features of poisoning' below.)

Toxicokinetics — Toxicokinetics for nicotine are as follows:

Absorption – Nicotine absorption is rapid by all routes. Peak concentration is reached within minutes by inhalation or mucosal exposure.

Because nicotine is a weak base (pKa = 8.0), it is more readily absorbed from basic or neutral environments than acidic ones. Gastric absorption may be delayed or incomplete. While precise pharmacokinetics following oral overdose are not well described, peak plasma concentrations were reached one to two hours following oral administration of a nicotine-replacement product [24].

Dermal absorption can be rapid and varies by nicotine concentration and age [25]. Transdermal nicotine patches are designed to deliver between 0.3 and 0.9 mg per hour, though pharmacokinetic studies have not been evaluated in children. The skin may also serve as a reservoir following patch placement, with 10 percent of total dose being absorbed after removal of a patch in one pharmacokinetic study [26]. Wet tobacco plants or nicotinic pesticides are other potential sources of dermally absorbed nicotine.

Volume of distribution and protein binding – The volume of distribution of nicotine is 2.6 L/kg. It is minimally protein bound (approximately 5 percent).

Metabolism and half-life – Metabolism is predominantly hepatic (80 to 90 percent), largely via cytochrome oxidases 2A6 and 2D6 [27]. The remainder of nicotine is metabolized by the lung or kidney.

The observed half-life is one to four hours but can be lower in chronic users.

Onset of toxicity — Onset of symptoms after nicotine exposure is frequently rapid but also depends upon the type of exposure:

Inhalation or mucosal administration – Inhalation or mucosal administration (such as buccal or rectal) typically has an onset of symptoms within minutes [28].

Ingestion – Initial symptoms of nausea and/or vomiting often appear within 15 to 30 minutes after ingestion. However, because nicotine is a weak base and has poor absorption in the acidic environment of the stomach, peak blood concentrations may not be reached until 60 to 90 minutes after ingestion [24].

A notable exception is ingestion of nicotine patches, in which nicotine release from the patch matrix can be delayed. Biting, piercing, or chewing a nicotine patch may disrupt the matrix and permit large doses of nicotine to be absorbed if swallowed [15].

Dermal – Green tobacco sickness from occupational or farming exposure may have onset of symptoms as early as 15 minutes after contact with dew-laden tobacco leaves [29], but typically, symptoms begin after several hours (mean 10 hours; range 3 to 17 hours in one report).

Dermal absorption from nicotine patches has been demonstrated in vitro [17,30], and cases of toxicity from dermal exposure are reported [15,18]. In children, onset of symptoms after dermal exposure has varied from as short as 15 minutes (nicotine patch mistaken for a bandage and applied to an open wound) to several hours [15]. Severe symptoms including seizures, cardiovascular effects, and respiratory failure have occurred after 1.5 to 24 hours in adults who intentionally serially applied multiple nicotine patches [18].

Toxicity by nicotine source

E-cigarette (nicotine) solution — Although most exposures result in minimal or no toxicity, concentrated nicotine solution used in e-cigarettes can cause major and life-threatening poisoning after ingestion, especially in young children [1,2,5]. E-cigarettes are electronic nicotine delivery systems that vaporize a liquid nicotine solution (also called vape juice, e-liquid, or e-juice) to be inhaled by the user (figure 2). Some e-cigarettes use pre-filled cartridges or pods, while others have a refillable reservoir (figure 3). These vaping liquids contain varying nicotine concentrations, which typically range from 0.5 to 36 mg/mL, though some pod-based nicotine solutions are much more concentrated. (See "Vaping and e-cigarettes", section on 'E-cigarette liquid components'.)

Nicotine- and tobacco-containing products — The potential for toxicity from tobacco and nicotine cessation products correlates with the amount or concentration of nicotine; ingestion of >0.1 mg/kg is associated with toxicity [10] (see 'Toxic dose' above). Ingestion in children is also encouraged by products with fruit or candy flavoring (snus and orbs) and, for orbs, a candy-like appearance. The table provides nicotine concentration and estimated amount of tobacco or nicotine product that may produce nicotine toxicity (table 1).

Tobacco products (cigarettes, cigars, chewing tobacco, snuff, and pipe tobacco) – A typical cigarette contains 7 to 15 mg of nicotine [31]. Cigars vary greatly in size and total tobacco content but generally have more nicotine than cigarettes. Chewing tobacco and dipping tobacco (moist snuff) are shredded or pulverized plant material, which may be flavored or sweetened, and are typically buffered to a neutral or slightly alkaline pH to enhance absorption (table 2). (See "Patterns of tobacco use".)

Smoking cessation products (nicotine gum, snus, and transdermal nicotine patches) – Nicotine gum, often used as an aid to smoking cessation, contains 2 or 4 mg of nicotine [32].

Transdermal nicotine patches are formulated to deliver between 5 and 22 mg of nicotine over a 16- to 24-hour period (0.3 to 0.9 mg/hour) [15,33]. The total content within the transdermal nicotine patches varies by manufacturer but can be as high as 118 mg. Up to 74 percent of the total nicotine content may remain in the patch after use . Children who have applied nicotine patches to their skin can develop symptoms, typically if exposed for 20 minutes or longer [15]. Patches have also been misused by adults in self-harm attempts [18], including one reported fatality [34].

Ingestion of whole patches has the potential to cause delayed and prolonged toxicity [15]. Patches that are torn or bitten and then ingested can result in more rapid toxicity.

Tobacco and other nicotinic plants — Nicotiana is a genus of plants in the Solanaceae family (the nightshades, many of which produce toxic alkaloids). Nicotiana tabacum is the cultivated tobacco plant used for making cigars, cigarettes, pipe tobacco, and chewing tobacco; but many other species within the genus are popular garden plants. The plants can be recognized by their tubular flowers with five petals. Their leaves tend to be large and dark green, and they may be hairy or sticky to the touch.

Most plants in the genus contain nicotine or similar alkaloids (such as anabasine, another nicotinic receptor agonist), with nicotiana tabacum containing the greatest content by dry weight. This content can vary from 0.1 to 4.9 percent of dry weight [35]. Most cultivated tobacco plant exposures produce mild or moderate symptoms [1]. However, brewed tobacco plant material produces a concentrated nicotine solution that has been used for self-harm resulting in serious toxicity and death [7,8]. Nicotine toxicity from dermal occupational exposure during farming of tobacco is also described. (See 'Green tobacco sickness' below.)

Exposures to other nicotinic plants are rare, but serious toxicity including death has occurred after exploratory ingestions of Conium maculatum (poison hemlock) by young children or from foragers who mistake poison hemlock for wild carrots or parsnips [9,10]. Baptisia australis has been mistaken for wild asparagus and caused nausea, vomiting, diarrhea, generalized weakness, and ataxia [36].

Nicotine-containing pesticides — Although banned in many countries, including the United States, highly concentrated nicotine pesticides may be available in other parts of the world. These agents are rapidly absorbed, and life-threatening nicotinic poisoning or death after ingestion or dermal exposure has been described [2].

Neonicotinoids — Neonicotinoids are widely used as insecticides and include compounds such as imidacloprid, thiamethoxam, clothianidin, acetamiprid, and thiacloprid. Despite having structural similarities to nicotine, neonicotinoids produce varying patterns of activity at nAChR subtypes [12]. (See 'Mechanism of toxicity' above.)

Compared with concentrated liquid nicotine insecticides, neonicotinoid exposures are less dangerous in overdose. For example, even with large, intentional ingestions of neonicotinoids, most patients develop only mild to moderate symptoms of nausea, vomiting, diarrhea, abdominal pain, and headache that resolve with supportive care. However, life-threatening coma, respiratory failure, and/or hepatotoxicity and death have been described [37,38]. The liver injury reported in individuals who ingested imidacloprid-based insecticides includes cholestatic, hepatocellular, and mixed patterns of injury. It is unclear whether imidacloprid, or one of the other chemical components (eg solvents or surfactants) in these insecticide solutions, is responsible for hepatotoxicity [39].

CLINICAL FEATURES OF POISONING

Approximately 20 to 33 percent of patients with a nicotine exposure will become symptomatic [1,40]. The classic biphasic appearance, initial stimulation followed by later depression (see 'Mechanism of toxicity' above), is not frequently observed in clinical practice.

Nicotine poisoning can be classified by the severity of signs and symptoms (table 3) [5,40,41]:

Mild – Clinical findings of mild nicotine poisoning include:

Nausea and vomiting

Salivation

Drowsiness

Hyperactivity (for infants, fussy but consolable)

Tachycardia

Pallor

Diaphoresis

Dizziness

Patients with mild poisoning may develop one or more of the signs or symptoms above within 30 minutes of ingestion or dermal exposure; findings typically resolve over the subsequent four to six hours. Other than patients who have ingested a transdermal nicotine patch, individuals who will progress to moderate or severe nicotine poisoning will usually do so within one hour of exposure.

Moderate – The following clinical findings indicate moderate nicotine poisoning:

Hypertension

Bronchorrhea, wheezing, and tachypnea secondary to bronchorrhea

Repeated vomiting and/or diarrhea

Tremors

Muscle fasciculations

Ataxia

Confusion, agitation, lethargy, and/or irritability (for infants, inconsolable crying)

Individuals with moderate signs or symptoms of poisoning warrant emergency supportive care and close monitoring because they can rapidly progress to severe manifestations of nicotine toxicity.

Severe – Severe findings of nicotine poisoning include:

Bradyarrhythmias and cardiac arrest

Hypotension

Respiratory failure (secondary to muscle paralysis)

Seizures

Coma

TELEPHONE TRIAGE — Patients with the following features of nicotine exposure warrant referral for emergency evaluation and treatment:

Symptomatic individuals with more than minimal symptoms of nausea or self-limited vomiting (see 'Clinical features of poisoning' above)

High-risk exposures, even if initially asymptomatic, including:

Ingestion or dermal exposure to a concentrated nicotine solution (eg, e-cigarette cartridge or refill)

Ingestion of a transdermal nicotine patch [15]

Ingestion of tobacco or tobacco products with estimated dose >0.1 mg/kg (table 1)

Asymptomatic after intentional ingestion

The following nicotine exposures may be observed at home with scheduled telephone or video conference follow-up when available:

Children who ingest:

<1 cigarette or <3 cigarette butts [42,43]

A single piece of 2 mg gum [14]

<1 mouthful of snuff

The clinician should counsel the caregiver that their child may experience mild symptoms, such as nausea, salivation, or self-limited vomiting.

Asymptomatic children who briefly chew or suck on a transdermal nicotine patch or apply it to intact skin for <20 minutes [15]. The clinician should counsel the parent to remove the patch (if not already performed) and wash the skin with soap and water.

EMERGENCY DEPARTMENT EVALUATION

Initial stabilization — Most nicotine exposures result in no or minimal symptoms. However, nicotine poisoning may present with one or more of the following life-threatening conditions:

Cholinergic effects (ie, miosis, bronchorrhea, wheezing, salivation, vomiting, diarrhea)

Tachy- or bradydysrhythmias

Shock due to fluid losses and/or cardiotoxicity

Respiratory depression and apnea

Skeletal muscle fasciculations followed by weakness/paralysis

Seizures

Rhabdomyolysis

Initial stabilization of nicotine poisoning is provided in the rapid overview (table 3).

Key interventions include:

For patients with dermal exposure, donning of protective personal equipment by all providers and rapid skin decontamination (see 'Decontamination' below)

For patients with signs of excess cholinergic stimulation (miosis, bronchorrhea, wheezing, salivation, vomiting, and/or diarrhea), administration of atropine targeted to drying of bronchial secretions and clearing of wheezing

Support airway, breathing, and circulation (see 'Moderate to severe poisoning' below):

Administer oxygen

Anticipate need for early endotracheal intubation due to bronchorrhea, coma, seizures, and/or skeletal muscle weakness or paralysis; avoid succinylcholine during rapid sequence intubation (may precipitate or produce prolonged paralysis in nicotine-poisoned patients)

Obtain intravenous (IV) access and, for patients who develop cardiotoxicity or shock caused by significant fluid losses due to vomiting, diarrhea, and/or diaphoresis, provide bolus infusions of normal saline or balanced crystalloid solution (eg, lactated Ringer) and vasoactive infusions as needed for shock (see "Shock in children in resource-abundant settings: Initial management" and "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock")

Treat arrhythmias according to Advanced Cardiac Life Support (ACLS) (algorithm 1 and algorithm 2) and Pediatric Advanced Life Support (PALS) (algorithm 3 and algorithm 4)

Treat seizures initially with benzodiazepines; for patients with persistent seizures, use levetiracetam, valproic acid, or phenobarbital; avoid phenytoin or fosphenytoin (see "Convulsive status epilepticus in adults: Management" and "Management of convulsive status epilepticus in children")

For patients who develop rhabdomyolysis, IV infusion of normal saline to maintain urine output of 200 to 300 mL per hour in adults and 4 mL/kg per hour in children (see "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Volume administration')

History — The following historical information is essential for determining the significance of nicotine or tobacco product exposure and directing further management:

What was the exposure? – Determine the type of nicotine or tobacco product exposure and potential for toxicity. Exposures with the highest potential for serious toxicity include:

Ingestion of or dermal exposure to concentrated liquid nicotine found in e-cigarette products or insecticides [2,3,5]. (See 'E-cigarette (nicotine) solution' above and 'Nicotine-containing pesticides' above.)

Ingested nicotine doses >0.1 mg/kg are potentially toxic; doses >1 mg/kg (60 mg in adults) are potentially lethal (table 1). (See 'Toxic dose' above.)

Ingestion of a transdermal nicotine patch may result in delayed toxicity and has the potential to deliver a high nicotine dose (up to 70 percent of the total dose in the patch is present after being discarded) [15]. (See 'Nicotine- and tobacco-containing products' above.)

Most cultivated tobacco plant exposures produce, at most, mild or moderate symptoms, often after occupational dermal exposure (green tobacco illness). Exploratory ingestions of other nicotine-containing plants by children are rare and typically innocuous. However, deaths of amateur foragers have occurred after consuming poison hemlock (Conium maculatum) roots that were mistaken for wild carrots or parsnips. (See 'Nicotine- and tobacco-containing products' above.)

When did it happen? – Signs and symptoms of nicotine poisoning usually develop soon after exposure (typically within one hour). Important exceptions that may be associated with delayed toxicity include transdermal nicotine patch ingestion and some patients with dermal exposure to wet tobacco (green tobacco sickness). (See 'Onset of toxicity' above.)

How did it happen? – With the exception of exposure to concentrated nicotine solutions, most exploratory exposures in children or unintentional exposures in adults result in minimal or no toxicity [1,13]. By contrast, intentional ingestions (attempts at self-harm) are more likely to involve high doses of nicotine and other toxic substances [7,8,18].

Are there symptoms of nicotine toxicity? – Salivation, nausea, vomiting, weakness, confusion, and dizziness are nonspecific symptoms associated with mild nicotine poisoning. Seizures, lethargy, or coma indicate more serious poisoning. (See 'Clinical features of poisoning' above.)

Physical examination — Most patients will have minimal or no findings after nicotine exposure. In patients with nicotine poisoning, physical examination findings may reflect a spectrum of activation and/or inhibition of nicotinic acetylcholine receptors (nAChRs) (see 'Mechanism of toxicity' above):

General – Altered mental status may arise from central nervous system stimulation (agitation, confusion, or, in infants, irritability) or depression (lethargy or coma).

Vital signs – Sympathetic stimulation produces tachycardia (typically sinus, but tachyarrhythmias are described) and hypertension; parasympathetic stimulation and fluid loses from cholinergic toxicity can cause bradycardia with hypotension.

Bronchorrhea and wheezing from cholinergic activation produces tachypnea. Muscle weakness and central nervous system depression can cause respiratory depression and apnea.

Cholinergic findings – Prominent cholinergic features after nicotine poisoning consist of bronchorrhea, wheezing, salivation, miosis, vomiting, and diarrhea; salivation alone commonly occurs after small oral ingestions.

Musculoskeletal system – Nicotinic stimulation at the neuromuscular junction results in muscle fasciculations initially and can rapidly progress to depolarizing blockade with muscle weakness and then paralysis.

Central nervous system – Central nervous system toxicity may manifest as seizures, lethargy, or coma.

Skin – Diaphoresis and pallor can be prominent findings.

Ancillary studies

Asymptomatic or minimal toxicity — In an unintentional nicotine exposure with minimal toxicity or no symptoms, screening labs are generally not indicated.

In cases of intentional nicotine exposure (ie, attempt at self-harm), the clinician should obtain plasma levels of acetaminophen and salicylate because these patients can have a life-threatening and treatable ingestion. (See "Acetaminophen (paracetamol) poisoning in adults: Pathophysiology, presentation, and evaluation", section on 'General approach and laboratory evaluation' and "Salicylate (aspirin) poisoning: Clinical manifestations and evaluation", section on 'Diagnosis'.)

Symptomatic — Patients with signs or symptoms of serious nicotine toxicity should undergo the following studies:

Rapid bedside test for plasma glucose

Arterial or venous blood gas

Serum electrolytes

Blood urea nitrogen and creatinine

In patients with seizures and all pediatric patients, urine screening for drugs of abuse (see "Testing for drugs of abuse (DOAs)", section on 'Utility of DOA screening')

In postmenarcheal females, urine pregnancy test

Other toxicologic testing as indicated for potential co-ingestants:

Serum acetaminophen and aspirin levels in patients with intentional ingestions

Rapidly available quantitative levels of potentially ingested drugs or toxins (table 4)

Electrocardiogram (ECG)

Serial measures of serum creatine kinase and urinalysis (for patients with muscle fasciculations, seizures, and/or paralysis to identify the presence of rhabdomyolysis)

Plasma and red blood cell cholinesterase (for patients with muscle fasciculations, weakness, and/or paralysis and when history of nicotine exposure is not readily apparent to differentiate nicotine poisoning from organophosphate or carbamate poisoning; results are not immediately available) (see 'Differential diagnosis' below)

Neuroimaging may be indicated for patients with altered mental status if the diagnosis of poisoning is in doubt or there are clinical findings of head trauma or focal neurologic deficit.

DIAGNOSIS — Nicotine poisoning is a clinical diagnosis based upon a history of nicotine or tobacco exposure and clinical features including one or more of the following (see 'Clinical features of poisoning' above):

Cholinergic findings (typically nausea, vomiting, miosis, salivation, bronchorrhea, and/or wheezing)

Central nervous system stimulation (confusion, agitation, or, in infants, irritability) or depression (lethargy or coma)

Tachy- or bradydysrhythmias

Shock

Seizures

Muscle fasciculations

Muscle weakness or paralysis

Urine cotinine and whole blood or plasma nicotine concentrations can be obtained to confirm exposure [44,45] but are not readily available at most health care centers to provide rapid diagnosis during acute treatment. Cotinine is one of the primary metabolites of nicotine and has a much longer half-life (T 13 to 19 hours) than its parent compound, making it the typical biomarker of exposure [46]. However, low levels of urine cotinine may be detectable as a result of passive inhalation (secondhand smoke) [6,47], and, in cases of nicotine poisoning, plasma nicotine or cotinine levels may not correlate with degree of toxicity [5,18]. Considering these factors, qualitative cotinine assays may not be useful in diagnosing nicotine toxicity, though markedly elevated concentrations of cotinine may be indicative of an acute exposure in a child.

DIFFERENTIAL DIAGNOSIS — In the absence of a clear nicotine exposure history, many of the symptoms of nicotine poisoning are nonspecific and could be confused for other conditions. Additionally, because nicotine poisoning can occur from small quantities, an exposure history may not be immediately apparent.

The differential diagnosis for patients with suspected nicotine poisoning includes toxic causes of cholinergic effects, vomiting, and altered mental status:

Cholinergic effects – The differential diagnosis of toxins causing signs of cholinergic excess (eg, miosis, vomiting, diarrhea, salivation, tachycardia, and/or seizures) is limited:

Organophosphates or carbamates – Organophosphate or carbamate poisoning is the major toxic exposure, other than nicotine, that presents with cholinergic effects. Organophosphate poisoning may be difficult to differentiate from nicotine poisoning because either toxin can cause cholinergic effects and/or muscle fasciculations followed by paralysis [48]. Low cholinesterase activity level as measured by decreased plasma and/or red blood cell cholinesterase levels indicates organophosphate poisoning (see "Organophosphate and carbamate poisoning", section on 'Laboratory abnormalities'). However, results of these studies are typically not rapidly available, and interpretation of cholinesterase levels can be difficult due to variation in enzyme activity among patients and day-to-day variations within the same patient. Unlike organophosphates, nicotine does not bind to cholinesterase and should not impact enzyme activity.

Because cholinesterase levels are not rapidly available, a trial dose of pralidoxime for patients who develop cholinergic findings or neuromuscular dysfunction may be appropriate. If given, atropine should also be administered concurrently. While pralidoxime may reverse neuromuscular signs of organophosphate poisoning, it does not treat nicotine poisoning. Additional details regarding indications and proper administration of pralidoxime are provided separately. (See "Organophosphate and carbamate poisoning", section on 'Pralidoxime'.)

Muscarinic mushrooms – Although rare, ingestion of muscarinic mushrooms (eg, Clitocybe dealbata, Clitocybe illudens, Inocybe fastigiata, or Boletus calopus) can also cause cholinergic effects, but unlike nicotine exposures, seizures or neuromuscular dysfunction do not occur. Cholinergic mushroom ingestion is typically short lived and not life threatening. A recent history of wild mushroom ingestion can help distinguish this poisoning from mild nicotine poisoning. (See "Clinical manifestations and evaluation of mushroom poisoning", section on 'Cholinergic poisoning'.)

Vomiting – Vomiting is one of the earliest signs of nicotine toxicity. Other agents that can cause vomiting after toxic exposure include iron, salicylates, theophylline, caustic agents, toxic alcohols, arsenic and mercurial salts, nonsteroidal antiinflammatory drugs (NSAIDs), plants, mushrooms, and colchicine [49]. In many instances, the history helps to distinguish nicotine from these toxins. Clinical and/or laboratory findings help to distinguish the following selected poisons from nicotine:

Arsenic – Elevated spot urine arsenic level (acute poisoning) in patients with garlic odor on the breath, vomiting, diarrhea, and prolonged QTc and/or torsade de pointes on ECG after acute arsenic poisoning. (See "Arsenic exposure and chronic poisoning".)

Colchicine – History of colchicine ingestion (medication or plant) associated with onset of multisystem organ failure. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Gastroenteritis with systemic toxicity'.)

Iron – Elevated serum iron level in patients with vomiting (may be hemorrhagic), abdominal pain, and an elevated anion gap metabolic acidosis. (See "Acute iron poisoning".)

Mercury salts – Elevated whole blood mercury in patients with hemorrhagic gastroenteritis, shock, and acute kidney injury due to acute tubular necrosis. (See "Mercury toxicity", section on 'Inorganic mercury salts toxicity'.)

Methylxanthines (caffeine or theophylline) – Elevated caffeine or theophylline level, especially when associated with seizures and tachyarrhythmias. (See "Theophylline poisoning".)

Mushrooms – History of mushroom ingestion with vomiting followed by characteristic mushroom syndrome (table 5). (See "Clinical manifestations and evaluation of mushroom poisoning".)

NSAIDS – Serious toxicity occurring only after very large ingestions and consisting of anion gap metabolic acidosis, depressed mental status, and cardiac arrhythmia. (See "Nonsteroidal antiinflammatory drug (NSAID) poisoning".)

Plants – Plants that contain nicotine or nicotine-like substances that can cause nicotine poisoning are described above (see 'Tobacco and other nicotinic plants' above). Many other plants can cause self-limited nausea, vomiting, and diarrhea after ingestion, which either require no therapy or respond to supportive measures (table 6). More severe gastroenteritis and major toxicity can occur after ingestion of pokeweed (Phytolacca americana), castor bean (Ricinus communis), jequirity bean (Abrus precatorius), and May apple (Podophyllum peltatum) (table 7). In addition to history, lack of development of other signs of potential cholinergic effects and absence of neuromuscular dysfunction helps to differentiate plant ingestions from nicotine poisoning. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Gastrointestinal toxicity'.)

Salicylates – Elevated anion gap and serum salicylate concentration, especially when associated with hyperthermia and hyperventilation. (See "Salicylate (aspirin) poisoning: Clinical manifestations and evaluation".)

Toxic alcohols (isopropyl alcohol, methanol, or ethylene glycol) – Elevated serum osmolal gap (soon after ingestion), anion gap acidosis (several hours after ingestion) associated with vomiting (which may be hemorrhagic), inebriation, and/or coma. (See "Isopropyl alcohol poisoning" and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

The general approach to vomiting in children and adults is discussed in detail separately. (See "Approach to the infant or child with nausea and vomiting" and "Approach to the adult with nausea and vomiting".)

Depressed mental status – The differential diagnosis and evaluation of lethargy and coma is broad (table 8). Hypoglycemia is a life-threatening condition that should be assessed with a rapid blood glucose in all patients with depressed mental status. Most organic causes, such as infection or metabolic derangement, would be expected to develop over hours or days, while toxic ingestions typically manifest rapidly. The evaluation of stupor and coma, including initial emergency stabilization and treatment, is discussed in detail separately. (See "Evaluation of stupor and coma in children" and "Stupor and coma in adults".)

Seizures – Except for organophosphate or carbamate poisoning, nicotine poisoning differs from most toxic and other conditions that cause seizures because of the presence of cholinergic effects and/or skeletal muscle fasciculations and paralysis. Acute onset of seizures and seizure-like movements are a common, important feature of many other poisonings and medical conditions including:

Hypoglycemia (see "Hypoglycemia in adults without diabetes mellitus: Determining the etiology" and "Approach to hypoglycemia in infants and children")

Sympathomimetic overdose (see "Cocaine: Acute intoxication" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication")

Anticholinergic poisoning (see "Anticholinergic poisoning")

Serotonin syndrome (see "Serotonin syndrome (serotonin toxicity)")

Phencyclidine intoxication (see "Phencyclidine (PCP) intoxication in adults" and "Phencyclidine (PCP) intoxication in children and adolescents")

Isoniazid poisoning (see "Isoniazid (INH) poisoning")

Lidocaine toxicity (see "Local anesthetic systemic toxicity")

Strychnine poisoning (see "Strychnine poisoning")

Meningitis (see "Viral meningitis in children: Clinical features and diagnosis" and "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Bacterial meningitis in children older than one month: Clinical features and diagnosis" and "Aseptic meningitis in adults")

Encephalitis (see "Viral encephalitis in adults" and "Acute viral encephalitis in children: Clinical manifestations and diagnosis")

Tetanus (see "Tetanus")

Intracranial hemorrhage (see "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis")

Stroke (see "Initial assessment and management of acute stroke" and "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis")

The evaluation of new-onset seizures is discussed in detail separately. (See "Evaluation and management of the first seizure in adults" and "Seizures and epilepsy in children: Clinical and laboratory diagnosis".)

MANAGEMENT

Decontamination — The approach to decontamination of patients with nicotine exposure is as follows:

Personal protective equipment – For patients who ingest nicotine, no special personal protective equipment is required.

For dermal exposures with concentrated nicotine products or industrial, agricultural, or insecticide exposures, providers should wear a waterproof gown, gloves, and eye protection.

External decontamination of dermal exposure – All patients with possible dermal exposure to nicotine should undergo careful skin inspection and removal of any transdermal nicotine patches. In addition, check the vagina, rectum, and roof of the mouth.

Patients with dermal exposure to concentrated liquid nicotine (eg, spilled e-cigarette liquid, nicotinic pesticides) or damp plant material (as in green tobacco sickness) should undergo external decontamination by health care providers in personal protective equipment as follows [41]:

Remove all clothing (at least down to their undergarments) and place in a labeled, waterproof, and durable 6-mil polyethylene or similar bag

Avoid breaking the patient's skin during the decontamination process; cover all open wounds

Starting at the head and working down to the feet, thoroughly wash and rinse the contaminated skin of the patient using soap and, preferably, warm water at low pressure

Gently pat the patient dry and cover with clean, dry linen or other appropriate barrier to prevent hypothermia

Gastrointestinal decontamination — Although evidence of clinical benefit in patients who ingest nicotine or tobacco products is lacking, activated charcoal can effectively bind to and reduce absorption of nicotine. For patients who present within one hour of a potentially toxic ingestion of nicotine or a tobacco product or within three hours of ingestion of a transdermal nicotine patch, we suggest administration of activated charcoal (dose: 1 g/kg up to 50 g; activated charcoal without sorbitol preferred in pediatric patients) (see "Gastrointestinal decontamination of the poisoned patient", section on 'Activated charcoal'). Vomiting may prevent administration of activated charcoal.

Activated charcoal should not be given to patients with depressed mental status unless the airway is first secured. It is also contraindicated if there has been co-ingestion of a caustic substance or a hydrocarbon.

For patients who present within one hour after a large ingestion of a concentrated liquid nicotine product, nasogastric aspiration and lavage with normal saline may be attempted, but benefit of this approach is not established. Whenever possible, this decision should be made in consultation with a medical toxicologist. For patients who cannot protect their airway, endotracheal intubation should be performed before nasogastric aspiration. Otherwise, gastric lavage is generally not recommended for patients with nicotine, tobacco, or tobacco product ingestion because the potential risks of the procedure likely outweigh the benefit, considering that most nicotine exposures can be managed supportively.

Moderate to severe poisoning — There is no specific antidote for nicotine poisoning. Excellent supportive care, directed at clinical findings, is the mainstay of treatment as provided in the rapid overview (table 3).

Cholinergic signs and symptoms — Cholinergic signs and symptoms (eg, bronchorrhea, wheezing, bradycardia, salivation, miosis, vomiting, and/or diarrhea) are treated as follows:

Atropine – Intramuscular (IM) or intravenous (IV) atropine (0.01 to 0.02 mg/kg, maximum single dose 1 to 2 mg); atropine dosing should be repeated every three to five minutes as needed until drying of respiratory secretions has occurred. Tachycardia is not a contraindication to atropine because respiratory secretions may contribute to respiratory failure; tachycardia is typically well-tolerated.

Ipratropium bromide – For patients with wheezing, inhaled ipratropium bromide (500 mcg) may be administered with atropine and may be repeated every 15 minutes for a total of three doses in patients with persistent wheezing.

Antiemetics – Relative to other antiemetics, ondansetron has a low risk for dystonia or other neurologic side effects and may be used to treat either isolated vomiting or vomiting in association with other cholinergic findings.

Seizures — Initial treatment of generalized seizures caused by nicotine poisoning consists of:

Benzodiazepines – Benzodiazepines such as IV lorazepam or diazepam are the first-line therapy for all patients.

Second-line antiseizure medications – If seizures persist despite repeated doses of benzodiazepines, phenobarbital is typically recommended as a second-line agent in patients with toxin-induced seizures; phenytoin or fosphenytoin should be avoided because they are typically less effective or (for certain agents such as cocaine, lindane, or theophylline) may intensify seizures (see "Convulsive status epilepticus in adults: Management", section on 'Fosphenytoin and phenytoin'). Evidence for the use of levetiracetam or valproic acid for toxin-induced seizures is lacking.

Refractory convulsive status epilepticus – For refractory convulsive status epilepticus, treatment consists of a continuous infusion of:

Midazolam (preferred for adults and children)

Propofol (older adolescents and adults only, avoid in children)

Pentobarbital (adults and children)

Patients with refractory convulsive status epilepticus warrant continuous electroencephalogram (EEG) to monitor for continued seizure activity. Drug dosing is provided in the algorithms for adults (algorithm 5) and children (algorithm 6) and provided separately. (See "Management of convulsive status epilepticus in children", section on 'Emergency antiseizure treatment' and "Convulsive status epilepticus in adults: Management", section on 'Emergency antiseizure treatment'.)

Lethargy or coma — Lethargy or coma may be seen as a primary sign of nicotine poisoning or become established after an initial presentation marked by agitation or seizures. Patients with lethargy or coma should have close monitoring of oxygenation and ventilation. Endotracheal intubation by rapid sequence intubation and mechanical ventilation are indicated for patients who appear unable to protect their airway or develop hypercarbia or hypoxia. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Approach" and "Rapid sequence intubation in adults for emergency medicine and critical care".)

During rapid sequence intubation, non-depolarizing agents such as rocuronium should be used, and succinylcholine, which also has direct effect on the neuromuscular junction and may precipitate or prolong toxin-induced paralysis, should be avoided. Mechanical ventilation may be complicated by bronchorrhea and bronchospasm; initial ventilation settings similar to those used for patients with status asthmaticus are advised. (See "Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation", section on 'Endotracheal intubation and mechanical ventilation' and "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

Muscle fasciculations and paralysis — Muscle fasciculations indicate activation of the nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction and signal a high risk for progression to generalized skeletal muscle weakness and paralysis.

Endotracheal intubation and mechanical ventilation – The clinician should anticipate the need for endotracheal intubation and mechanical ventilation as indicated by rising end-tidal carbon dioxide (EtCO2), hypercarbia on blood gases, or significant hypoxia.

For patients with nicotine-induced paralysis, lower-than-normal doses (ie, half-dose) of muscle relaxants may permit safe intubating conditions.

Presumptive administration of pralidoxime – For patients with neuromuscular effects following an exposure poisoning but uncertainty as to the specific toxic agent, presumptive administration of pralidoxime for possible organophosphate poisoning is a reasonable approach, especially in regions where organophosphates are widely used [38]. Pralidoxime may benefit patients with organophosphate poisoning but is ineffective for nicotine poisoning. If pralidoxime is given, atropine should also be administered concurrently.

Pralidoxime dosing and administration is discussed in greater detail separately. (See "Organophosphate and carbamate poisoning", section on 'Pralidoxime'.)

Shock — Shock with or without hypotension after nicotine poisoning may arise from fluid losses, bradyarrhythmias, and/or myocardial depression. Treatment includes:

Treatment of bradycardia (see discussion of cardiac arrhythmias below)

Rapid infusion of IV isotonic crystalloid (eg, normal saline or balanced crystalloid solutions [eg, lactated Ringer]). The volume and rate depend upon the degree of shock and whether pre-existing conditions (eg, heart failure) are present. (See "Shock in children in resource-abundant settings: Initial management", section on 'Fluid resuscitation' and "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Intravenous fluids'.)

If hypotensive shock persists despite fluid administration, give vasoactive agents such as norepinephrine (patients with high heart rate) or epinephrine (patients with relative bradycardia).

Cardiac arrhythmias — Sinus tachycardia is the most common arrhythmia after nicotine poisoning. It does not typically require specific treatment although it may indicate hypovolemia caused by vomiting and diarrhea.

Atropine as described above is the primary treatment for bradycardia with poor perfusion after nicotine poisoning. If persistent, the clinician should provide further treatment according to Advanced Cardiac Life Support (ACLS) (algorithm 1) or Pediatric Advanced Life Support (PALS) (algorithm 3) guidelines.

Tachyarrhythmias (eg, supraventricular tachycardia or ventricular tachycardia) may occur due to sympathetic stimulation during nicotine poisoning and should be managed according to ACLS (algorithm 2) or PALS guidelines (algorithm 4).

Rhabdomyolysis — Patients with rhabdomyolysis should receive IV isotonic saline titrated to produce a urine output of 200 to 300 mL/hour in adults (4 mL/kg per hour in children). The suggested initial fluid volume and rate in adults is 1 to 2 L/hour (20 to 40 mL/kg per hour in children). (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

Mild poisoning or asymptomatic — Asymptomatic patients and those with signs of mild poisoning should undergo decontamination (see 'Decontamination' above) as needed and undergo careful monitoring for progression of toxicity for four to six hours following exposure to liquids, plant material, or cigarettes/cigars. patients who are asymptomatic after six hours of observation may be discharged home or, for patients who intended self-harm, cleared for mental health evaluation.

If a nicotine patch is ingested, observation for 24 hours is warranted because toxicity may be delayed.

PREVENTION — As with prevention of other poisonings, public awareness campaigns and child-resistant packaging may reduce exposures to nicotine-containing products and substances. For example, in an observational study of e-cigarette and liquid nicotine exposures in the United States, institution of child-resistant packaging laws was associated with a significant decrease in reported exposures [3].

GREEN TOBACCO SICKNESS — Green tobacco sickness refers to nicotine toxicity caused by dermal absorption from tobacco leaves in field workers during harvest [50]. Factors associated with green tobacco sickness include:

Working in tobacco fields when the crop is wet (eg, early morning dew, during or shortly after a rainstorm, or days with high ambient humidity) [50,51]

Nonsmoking workers (due to lower tolerance to nicotine when compared with smokers) [50]

Younger age, with children and adolescents at highest risk [51]

Clinical manifestations and diagnosis — Green tobacco sickness may have rapid onset while the worker is in the field or can be delayed for several hours [50]. Typical clinical findings consist of pallor, nausea, vomiting, lightheadedness, and headache [19,20,52]. Less commonly, diaphoresis, salivation, copious bronchial secretions, diarrhea, muscle weakness, and fluctuations in heart rate and blood pressure may occur [50,51]. Rarely, seizures have been described [51,53]. Green tobacco sickness typically resolves within three days.

The diagnosis of green tobacco sickness is based upon a history of tobacco leaf exposure and clinical findings. If the diagnosis is in doubt, elevated blood, urine, or salivary cotinine levels can confirm the diagnosis in nonsmokers and smokers with mild to moderate use [50,54]. However, toxic cotinine levels have not been well established in heavy tobacco users.

Management — In most patients, treatment requires prevention of further exposure and supportive care as follows [50]:

Remove the worker from the field

Have the worker shower and change clothing

Encourage adequate hydration and rest

Give antiemetics (eg, ondansetron) and intravenous (IV) fluids to patients with persistent vomiting but no other muscarinic signs (eg, bronchorrhea, salivation, or wheezing)

Prevent the worker from returning to the tobacco field until all signs and symptoms have resolved

Management of more serious nicotine poisoning caused by green tobacco sickness is as for moderate to severe nicotine poisoning. (See 'Management' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Poisoning prevention".)

SUMMARY AND RECOMMENDATIONS

Epidemiology and toxicity – Most nicotine exposures arise from exploratory ingestions in children and result in no effect or minimal symptoms. However, severe toxicity can occur. High-risk exposures include (see 'Epidemiology' above and 'Toxicity by nicotine source' above):

Ingestion or dermal exposure to a concentrated nicotine solution (eg, e-cigarette cartridge or refill)

Ingestion of a transdermal nicotine patch

Ingestion of tobacco or tobacco products with estimated dose >0.1 mg/kg (table 1)

Onset of toxicity – Signs and symptoms of nicotine poisoning usually develop soon after exposure (typically within one hour). Important exposures associated with delayed toxicity include transdermal nicotine patch ingestion, cutaneous patch application, or dermal exposure to wet tobacco plants (green tobacco sickness). (See 'Onset of toxicity' above.)

Clinical features and diagnosis – Nicotine poisoning is a clinical diagnosis based upon a history of nicotine or tobacco exposure. Salivation, nausea, vomiting, weakness, confusion, and dizziness are nonspecific symptoms associated with mild nicotine poisoning. Clinical features of severe poisoning include (see 'Clinical features of poisoning' above):

Cholinergic findings (typically nausea, vomiting, miosis, salivation, bronchorrhea, and/or wheezing)

Central nervous system stimulation (confusion, agitation, or, in infants, irritability) or depression (lethargy or coma)

Tachy- or bradydysrhythmias

Shock

Seizures

Muscle fasciculations

Muscle weakness or paralysis

Definitive laboratory testing is not available in a timely fashion but may be indicated to confirm exposure (obtain blood and urine samples for cotinine and other nicotine metabolites).

Rapid overview – A summary table provides guidance for the emergency evaluation and management of patients with nicotine poisoning (table 3). Management is based upon the type of exposure and anticipated toxicity.

Decontamination – Carefully inspect the skin, vagina, rectum, and roof of the mouth and remove any transdermal nicotine patches. Patients with dermal exposure to concentrated liquid nicotine (eg, spilled e-cigarette liquid, nicotinic pesticides) or damp plant material (as in green tobacco sickness) should undergo external decontamination by health care providers in personal protective equipment. (See 'Decontamination' above.)

For patients who present within one hour of a potentially toxic ingestion of nicotine or a tobacco product or within three hours of ingestion of a transdermal nicotine patch, we suggest administration of activated charcoal without sorbitol (Grade 2C).

Moderate to severe poisoning – There is no antidote for nicotine poisoning. For moderate to severe nicotine poisoning, treatment is supportive based upon physical findings (see 'Initial stabilization' above and 'Moderate to severe poisoning' above):

Cholinergic toxicity (miosis, bronchorrhea, wheezing, salivation, vomiting, and/or diarrhea) – Key interventions include administration of atropine targeted to drying of bronchial secretions and clearing of wheezing, inhaled ipratropium bromide for wheezing, and ondansetron for vomiting. (See 'Cholinergic signs and symptoms' above.)

Bronchorrhea unresponsive to atropine therapy, coma, seizures, and/or skeletal muscle weakness or paralysis – Perform timely endotracheal intubation; avoid succinylcholine during rapid sequence intubation (may precipitate or produce prolonged paralysis). For patients with fasciculations, muscle weakness, or paralysis but uncertainty as to the specific toxic agent, presumptive administration of pralidoxime for possible organophosphate poisoning is a reasonable approach, especially in regions where organophosphates are widely used. Pralidoxime is ineffective for paralysis caused by nicotine. (See 'Muscle fasciculations and paralysis' above.)

Shock from vomiting, diarrhea, diaphoresis, and/or myocardial depression – Provide rapid infusion of isotonic saline or balanced crystalloid solutions according to the degree of shock and presence of pre-existing conditions (eg, heart failure). Vasoactive infusions of norepinephrine, epinephrine, or dopamine are warranted for fluid refractory shock. (See "Shock in children in resource-abundant settings: Initial management" and "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock".)

Bradyarrhythmias or tachyarrhythmias – Provide resuscitation according to Advanced Cardiac Life Support (ACLS) (algorithm 1 and algorithm 2) and Pediatric Advanced Life Support (PALS) (algorithm 3 and algorithm 4) guidelines.

Status epilepticus – First-line therapy is a benzodiazepine (eg, lorazepam), if additional antiseizure medication is needed, phenobarbital is preferred. For refractory convulsive status epilepticus, midazolam infusion is preferred. (See 'Seizures' above.)

Rhabdomyolysis – Provide an intravenous (IV) infusion of normal saline to maintain urine output of 200 to 300 mL per hour in adults and 4 mL/kg per hour in children and urinary alkalinization. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Volume administration'.)

Asymptomatic exposure or mild poisoning – Asymptomatic patients and those with mild poisoning after ingestion of nicotine or a tobacco product can rapidly progress to moderate or severe poisoning and require close monitoring. Patients who ingest a transdermal patch require observation for 24 hours because toxicity may be delayed; otherwise, patients who are asymptomatic after six hours of observation may be discharged home or, for patients who intended self-harm, cleared for mental health evaluation.

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Topic 130609 Version 3.0

References

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