✅ Toxidromes Flashcards
Gastric Decontamination
Decontamination Methods:
Activated Charcoal is given orally to absorb toxins that are present in the GI tract. It is most efficacious if given within the first hour post ingestion but still works beyond that point. Toxins bind to the charcoal and are excreted without being digested. Charcoal does not bind metals (such as iron), alcohols or hydrocarbons. It should be avoided in patients with somnolence as they run the risk of aspiration. [pneumonitis]
Whole bowel irrigation involves the administration of an osmotically balanced polyethylene glycol electrolyte solution (like Go Lytely) to flush the bowel to prevent the absorption of ingested toxins. It is used in cases where charcoal is not effective, with certain sustained release products, and in cases of illicit drug packet ingestions (body packers).
Gastric Lavage is rarely used and carries significant risks with questionable benefit. In some cases, however, such as recently ingest lethal substances or an intubated overdose following recent ingestion, the benefits may outway the risks and warrant use. Lavage involves the application of a very large bore (36 – 40 French) orogastric tube and then flushing the stomach with aliquots of water ideally to obtain pill fragments. [e wall tube]
Many patients with potential ingestions may be observed for six hours and then dispositioned (home or psychiatric treatment facility) if clinically asymptomatic (provided the ingestion is not an extended release agent).
DRUGS
PCP (phencyclidine) [Hallucinogen]
- Violent behavior
- Dissociation
- Hallucinations
- Amnesia
- Nystagmus (horizontal or vertical)
- Ataxia
LSD [Hallucinogen]
- Visual hallucinations
- Euphoria
- Dysphoria/panic
- Tachycardia/hypertension
⚪ Cocaine [Stimulant]
- Euphoria
- Agitation /😵 Psychosis
- Chest pain
- Seizures
- Tachycardia/hypertension
- Mydriasis
Methamphetamine [Stimulant]
- Violent behavior
- 😵 Psychosis, diaphoresis
- Tachycardia/hypertension
- Choreiform movements
- Tooth decay
Marijuana (THC, cannabis) [Cannabinoid]
- Increased appetite
- Euphoria
- Dysphoria/panic
- Slow reflexes, impaired time perception
- Dry mouth
- Conjunctival injection
Heroin [Opioid]
- Euphoria
- Depressed mental status
- Miosis
- Respiratory depression
- Constipation
Acetaminophen Overdose
Acetaminophen (APAP) overdose is one of the most common but also one of the most dangerous poisonings in the US. Acetaminophen is available in many formulations and is though an acute overdose usually causes symptoms, patients may present asymptomatic even after a lethal ingestion. Therefore, it is imperative that an acetaminophen level is checked on all overdose patients.
There are four main stages of an acute APAP overdose. Typical symptoms usually involve nausea, vomiting in the first two stages. The lethal dose of APAP is 150mg/kg. In an acute overdose, APAP is metabolized to NAPQI which combines with glutathione and is excreted. When the majority of the glutathione is used, NAPQI causes hepatic toxicity. The toxic level of acetaminophen can be measured on the Rumak nomogram and the toxic plasma level at four hours is 150. In addition to decontamination with repeated doses of activated charcoal, the antidote N-acetylcysteine (Mucomyst) should be administered if indicated by the nomogram.
Acetaminophen is extensively metabolized in the liver to form nontoxic sulfate and glucuronide conjugates. A small proportion of the drug can be metabolized, however, by the cytochrome P450 mixed oxidase enzyme system to form a potentially toxic, intermediate metabolite (NAPQI), which, under normal circumstances, is conjugated with glutathione (a sulfydryl donor) to form nontoxic cysteine and mercapturic acid derivatives. In an overdose setting, the glucuronide and sulfate conjugation pathways often become saturated. A large proportion of the drug is then shunted into the P450 pathway, which results in the depletion of hepatic stores of glutathione and the subsequent binding of NAPQI to hepatic proteins, leading to centrilobular necrosis. Chronic use of ethanol can enhance liver toxicity via induction of P450.
Acetaminophen overdose typically presents with initial nonspecific symptoms such as nausea, vomiting, and lethargy, followed by hepatotoxicity and occasional nephrotoxicity. N-acetylcysteine (Mucormyst) reduces acetaminophen-induced liver injury by restoring hepatic glutathione stores. Serious hepatotoxicity is uncommon if NAC is administered within 8 hours of overdose.
🍗 Rhabdomyolysis
Etiology
- Skeletal muscle lysis/necrosis due to:
- Crush injury or prolonged immobilization
- Intense muscle activity (eg, seizure, exertion)
- Drug/medication toxicity (eg, statins)
Clinical features
- Muscle pain and weakness
- Dark urine (myoglobinuria/pigmenturia)
- blood on urinalysis & no RBCs on microscopy
- ↑ serum K and PO4, ↓ serum Ca, ↑ AST > ALT
- Acute kidney injury
Diagnosis
- Serum creatine kinase >1,000 U/L
- Consistent clinical features
Management
- Aggressive intravenous fluid resuscitation
- Sodium bicarbonate in some cases
Alcohol binges can cause acute alcohol myopathy that predominantly affects the lower extremities, causing pain, weakness, and swelling. It likely occurs via direct toxicity of ethanol and its metabolites, leading to disruption of myocyte membranes. Cocaine abuse further contributes to muscle damage via both vasoconstrictive skeletal muscle ischemia and direct myocyte toxicity.
Up to 50% of patients with rhabdomyolysis will develop acute kidney injury (AKI). During muscle cell lysis, intravascular fluid is shifted into the damaged muscle tissue, and heme-containing myoglobin is released into the bloodstream. The intravascular volume depletion causes an initial prerenal insult, which is followed by a subsequent insult from direct tubular toxicity of heme (pigment nephropathy).
Alcohol(s)
These “toxic” alcohols include isopropanol, methanol, and ethylene glycol. Isopropyl alcohol is found in many solvents, mouthwashes, and rubbing alcohols.
- Methanol is found in windshield wiper fluid.
- Ethylene Glycol is typically found in antifreeze.
Patients who have ingested any of these agents may appear to be intoxicated or even comatose.
Alcohol ketoacidosis
- Slurred speech
- Unsteady gait
- Altered mentation
- High osmolar gap
- Increased anion gap metabolic acidosis (ketosis)
Methanol ingestion
- Visual blurring, central scotomata
- Afferent pupillary defect
- Altered mentation
- High osmolar gap
- Increased anion gap metabolic acidosis
Ethylene glycol ingestion
- Flank pain
- Hematuria, oliguria
- Cranial nerve palsies, tetany
- High osmolar gap
- Increased anion gap metabolic acidosis
- Calcium oxalate crystals in urine
Isopropyl alcohol ingestion
- CNS depression
- Disconjugate gaze
- Absent ciliary reflex
- High osmolar gap
- No increased anion gap or metabolic acidosis
Additional diagnostic measures include the application of a wood’s lamp to the urine of a patient with an ethylene glycol ingestions. Since the source is antifreeze, sometimes the urine in the setting will fluoresce. The urine can also be examined for the presence of calcium oxalate crystals.
Isopropanol is usually not life threatening and can be managed by supportive care. In rare instances hemodialysis may be required.
Tx: Methanol and ethylene glycol, on the other hand, are more lethal and should be aggressively treated as soon as suspected. Methanol is metabolized to formaldehyde, and ethylene glycol is broken down into oxalate. All alcohols are metabolized by alcohol dehydrogenase (ADH). Therefore, the initial treatment for methanol and ethylene glycol involves the blockade of ADH. This can be accomplished by either simple ethanol or fomepizole. In addition, removal of the toxin may be necessary by hemodialysis. Sodium bicarbonate and glucose may also be necessary.
🍻 Alcohol
Alcohol intoxication can cause impaired judgement.
Behavioral changes, slowing of motor performance, and decrease in the ability to think clearly may appear with a blood alcohol level as low as 20 to 30 mg/dL. Most people show significant impairment of motor and mental performance when their alcohol levels reach 100 mg/dL. With blood alcohol concentration between 200 and 300 mg/dL, slurred speech is more intense and memory impairment, such as blackout and anterograde amnesia, becomes common. In a nontolerant person, a blood alcohol level over 400 mg/dL can produce respiratory failure, coma, and death. Because of tolerance, chronic heavy drinkers can present with fewer symptoms, even with blood alcohol levels greater than 500 mg/dL.
Alcohol withdrawal syndrome
Mild withdrawal
- Autonomic hyperarousal (anxiety, insomnia, tremors, diaphoresis, palpitations), gastrointestinal upset, intact orientation
- 6-24 hr
Seizures
- Single or multiple generalized tonic-clonic
- 12-48 hr
Alcoholic hallucinosis 😵
- Alert sensorium, visual, auditory, or 🕷 tactile hallucinations; intact orientation; stable vital signs
- 12 - 48 hr (lasts)
Delirium tremens (alcohol withdral delerium) (DT)
- Confusion, agitation, fever, tachycardia, ♨ hypertension, diaphoresis, hallucinations
- 48-96 hr
Tx: Chlordiazepoxide (Librium) should be given orally, or if this is not possible, lorazepam should be given IV or IM.
🕰 Alcohol Dependence
Tx:
Naltrexone: Competitive antagonist at the mu and kappa opioid receptors. Decreases cravings and blocks dopamine reward pathways, thereby decreasing reinforcing effects of use (i.e. use is less enjoyable)
Acamprosate: Blocks glutamate NMDA receptors and activates GABA-A receptors. EtOH is inhibitory and chronic use leads to upregulation of NMDA receptors. Withdrawal of EtOH leads to glutamate excitation (i.e. seizures, tachycardia, etc). By blocking NMDA receptors, acamprosate decreases the sign/symptoms of withdrawal as well as decreasing glutamate-driven cravings.
🥞 Benzodiazepines
Sedative-hypnotic
Overdose
- Altered level of consciousness, ataxia, and slurred speech.
- Most patients with isolated benzodiazepine overdose are arousable and have normal vital signs.
Co-ingestion of other sedative-hypnotics (🍻 alcohol)
- Bradycardia, hypotension, respiratory depression, and hyporeflexia.
👴🏾As people age, they metabolize benzodiazepines more slowly and are more likely to experience confusion and increased risk of falls. Another adverse effect of benzodiazepines is paradoxical agitation is characterized by increased agitation, confusion, aggression, and disinhibition, typically within an hour of administration.
Tx: 🐩 Flumazenil can precipitate seizures in those with preexisting seizure disorders.
Cx: Because flumazenil can induce acute withdrawal symptoms in long-term benzodiazepine abusers, it is contraindicated in patients with a history of long-term benzodiazepine use, seizure disorder, and concomitant TCA ingestion. Flumazenil should not be used routinely to arouse an unconscious patient with overdose because it is often unknown whether a patient is a chronic benzodiazepine user.
Withdrawal:
Worsening anxiety, insomnia, tremor, psychomotor agitation, and dysphoria. Following abrupt discontinuation of benzodiazepines, early rebound effects of insomnia and increased anxiety are common, sometimes making it difficult to distinguish benzodiazepine withdrawal from a return of the underlying psychiatric disorder. Benzodiazepine withdrawal may also present with psychosis and seizures and may be life-threatening in severe cases.
Onset and severity of benzodiazepine withdrawal depend on the half-life of the drug, with shorter-acting drugs (5 hours)
- Alprazolam (Xanax)
- Lorazepam (Ativan)
producing earlier and more severe symptoms.
Intermediate acting
- clorazepate (Tranxene) (5-24 hours)
Strategies for managing withdrawal include using a longer half-life benzodiazepine (24+ hours)
Diazepam (Valium)
Chlordiazepoxide (Librium)
and gradually tapering it over several months.
Anticholinergic syndrome:
“Blind as a bat, mad as a hatter (delirium), red as a beet, hot as a hare (hyperthermia), dry as a bone (skin and mucous membranes), the bowel and bladder lose their tone, and the heart runs alone.”
Heart: diminished vagal tone at the SA node causes relative tachycardia.
Blood vessels: vasoconstriction via muscarinic receptor blockade in endothelial cells results in decreased nitric oxide synthesis. In spite of this effect, atropine poisoning is associated with cutaneous flushing; the pathogenesis of this effect is unknown.
GI: delayed gastric emptying, decreased intestinal motility, and secretion.
Respiratory: bronchodilatation.
GU: urinary retention via detrusor relaxation and contraction of the external urethral sphincter.
Secretions: decreased lacrimation (dry eyes), salivation (dry mouth) and sweating (dry and hot skin). Atropine decreases one’s ability to sweat, contributing to hyperthermia.
Eye: mydriasis (dilated pupils - loss of accommodation) and cycloplegia (inability to focus on the near objects, blurry vision).
In the eye, atropine causes mydriasis, resulting in narrowing of the anterior chamber angle and diminished outflow of aqueous humor. This can precipitate angle-closure glaucoma in patients with shallow anterior chambers or higher than normal intraocular pressures. Acute closed-angle glaucoma presents with unilateral severe eye pain and visual disturbances (eg, halos). Individuals of Inuit and Asian descent are at increased risk of angle-closure glaucoma.
CNS: hallucinations, agitation and delirium.
Possible toxins with anticholinergic properties include the following:
TCA’s Tricyclic antidepressants
Antihistamines
Overactive bladder medication
Aspirin
Patients with an acute overdose of aspirin are usually quite ill appearing, breathing fast, vomiting, confused, and sometimes febrile. The toxic effects are complex and involve an uncoupling of oxidative phosphorylation. This causes a profound anoin gap metabolic acidosis. The general approach to aspirin overdose is the management of the airway, gastric decontamination, the administration of sodium bicarbonate, and hemodialysis.
Bath salts
Bath salts are synthetic cathinones, which consist of a large family of amphetamine analogues. As such, they may increase the release, or inhibit the reuptake, of norepinephrine, dopamine, and serotonin. Symptoms of intoxication include severe agitation, combativeness, psychosis, delirium, myoclonus, and, rarely, seizures. Increased sympathetic outflow may lead to significantly increased blood pressure and heart rate. The most distinguishing feature of synthetic cathinone intoxication is the prolonged duration of effect. Delirium and psychosis due to bath salts may last up to a week, whereas the effects of intoxication with other amphetamines or hallucinogens are usually of much shorter duration.
Bath salts are usually sold as a white powder in small packages labeled as “bath salts,” “plant food,” “cleaners,” or other substances. Bath salts may be ingested orally, inhaled, or injected. They are not related to the product Epsom salts or any other substances used in bathing. Routine toxicology screens do not test for bath salts.
Cholinergic poisoning
Sources: organophosphate poisoning (pesticides) and nerve agents
SLUDGE:
Salivation
Lacrimation
Urination
Diaphoresis and defecation
Gastrointestinal upset
Excessive bradycardia or tachycardia (muscarinic or nicotinic)
DUMBBELLS:
Diarrhea.
Urination.
Miosis/muscle weakness.
Bronchorrhea.
Bradycardia.
Emesis.
Lacrimation.
Salivation/sweating.
Treatment: Atropine (2-6 mg IV q 15-30 min), pralidoxime (2-PAM) 1-2 g, decontaminate
☕ Caffeine
Caffeine is a stimulant that, when used excessively, can result in insomnia, jitteriness, anxiety, gastrointestinal symptoms, and headaches, as well as more serious adverse effects including tachycardia, hypertension, cardiac arrhythmias, panic attacks, agitation, psychosis, and seizures. Energy drink consumption is especially popular among adolescents and young men, and it should be considered in anyone with signs or symptoms of stimulant intoxication.
Although most healthy adults can safely consume ≤400 mg of caffeine daily, the caffeine content of one energy drink can range from 50 to 500 mg.
Cocaine
Cocaine is a stimulant that produces increased energy, decreased appetite, and reduced need for sleep. Individuals who abuse cocaine often have mood changes (eg, euphoria, irritability) and weight loss secondary to decreased appetite. The diagnostic hallmark in this scenario is erythema of the nasal mucosa, which is a common finding in individuals who snort cocaine. In severe cases, perforation of the nasal septum can occur.
Patients under the influence of cocaine or other stimulants may exhibit elevated or irritable mood, hyperactivity, agitation, and grandiosity that are indistinguishable from an acute manic episode of 💫bipolar disorder.
- Increased arousal
- Agitation
- Dilated pupils
- Hyperthermia
- Tachycardia
- Hypertension
- Tachypnea
- Diaphoresis
- Hyperreflexia.
Psychiatric effects of cocaine use include:
- Anxiety
- Irritability
- Hypervilliagance
- Mood swings
- Panic attacks
- Grandiosity
- Impaired judgement
- Psychotic symptoms (paranoia and visual / tactile hallucinations 🕷[bugs crawling]).
- When intoxicated, patients using cocaine are frequently energetic, restless, and hypervigilant and may exhibit euphoria and grandiosity that resemble an acute manic episode.
The dopaminergic system is thought to be involved in the brain’s “reward system,” and this involvement is thought to explain the very high addiction potential with regard to
cocaine.
Cocaine withdrawal involves predominantly psychological features. Common symptoms include depression, fatigue, 💤 hypersomnia, increased dreaming, 🍗 hyperphagia, impaired concentration, and intense drug craving. Physical symptoms are minor and rarely require treatment.
LSD
Patients ingesting LSD may have a wide variety of sensory disturbances, and because of the sympathomimetic effects of the drug, may experience tremors, hypertension, tachycardia,
mydriasis, hyperthermia, sweating, and blurry vision. Patients may die when they act on their false perceptions (belief that they can fly) or accidentally kill themselves. When the subject is not clear about which drug was taken, the unexpected sensory disturbances can be quite terrifying, and patients can fear losing their minds.
Marijuana
intoxication typically presents with tachycardia, increased respiratory rate, dry mouth, and conjunctival injection.
MDMA (Ecstasy)
After ingestion, there is an initial phase of disorientation, followed by a “rush” that includes increased blood pressure and pulse rate as well as sweating. Users experience euphoria, increased self-confidence, and peaceful feelings of empathy and closeness to other people; effects usually last 4 to 6 hours. MDMA decreases appetite. It has been associated with
bruxism (grinding of the teeth 🦷 ), shortness of breath, cardiac arrhythmia, and death.
Intoxication may manifest as:
- Amphetamine toxicity: hypertension, tachycardia, and hyperthermia
- Serotonin toxicity: serotonin syndrome (characterized by autonomic dysregulation, high fever, altered mental status, neuromuscular irritability, and seizures) and hyponatremia (due to drug-induced inappropriate antidiuretic hormone secretion as well as excessive water intake to reduce hyperthermia)
Methamphetamine
“meth,” “crystal,” “ice,” and “glass” is a highly addictive and very potent central nervous system stimulant. Heavy use frequently causes marked weight loss, psychotic symptoms, and excoriations due to chronic skin picking. Severe dental problems (“meth mouth”) can include brown discoloration, tooth decay, and cracked teeth due to severe bruxism and dry mouth. Other features of intoxication include mood disturbances, anxiety, irritability, confusion, violent behavior, and signs of sympathetic overactivity (eg, elevated pulse and blood pressure, hyperthermia, sweating, pupillary dilation).
Some chronic methamphetamine users can develop persistent psychosis that may be difficult to distinguish from primary psychiatric disorders. Visual and tactile hallucinations tend to be more common in substance-induced psychotic disorders. Long-term management includes both cognitive-behavioral treatment to prevent relapse and antipsychotic medication.
However, the decongestant pseudoephedrine and the antidepressants bupropion and selegiline can cause false positives for amphetamines on urine toxicology testing.
Opiates
intoxication
Signs & symptoms
- Decreased mental status
- Decreased respiratory rate & shallow breaths
- Miosis (normal/enlarged if coingestions)
- Bradycardia
- Decreased bowel sounds
- Hypothermia (or normothermia)
Workup
- Arterial blood gas (respiratory acidosis)
- Fingerstick blood glucose (hypoglycemia)
- Evaluate for presence of other drugs (eg, acetaminophen)
- ECG for prolonged QTc with methadone overdose
Treatment
- Naloxone, may need repeated doses
- Airway management & ventilation
- Consider continuous cardiac monitoring (if QTc >500 msec)
The most reliable and predictive sign of OI is a decreased respiratory rate. Other evidence includes decreased bowel sounds and hypotension. Hypothermia results from environmental exposure and impaired thermogenesis, and can occur even at room temperature in severely intoxicated patients. In addition, although many patients with OI have miosis, its absence does not exclude the diagnosis. Normal or even enlarged pupils may be seen in patients who have co-exposures to other agents that can counteract miosis (eg, methamphetamine).
Tx: Management of patients with OI should focus on airway protection and improving ventilation. The prompt administration of naloxone can result in rapid improvements in respiration in both apneic and bradypneic patients, thereby reducing the need for more invasive interventions. Naloxone should be titrated to achieve a respiratory rate >12/min but not to achieve normal mental status.
A word on Naloxone. The Naloxone will wear off before the opiate so the patient can NOT be discharged without a period of observation. Administration of Naloxone may cause the patient to go into opiate withdrawal (aspiration, pulmonary edema), so be prepared for a very violent and combative response and use only the dose necessary to return a normal respiratory rate.
Withdrawl:
Withdrawal may begin 6-12 hours after cessation of a short-acting opioid and 24-48 hours after the last dose of methadone and generally reach peak severity 48 hours after the last dose.
Symptoms include: Myalgias, nausea, diarrhea, abdominal cramping, hyperactive bowel sounds, and pupillary dilation. Other typical symptoms include irritability, yawning, piloerection, rhinorrhea, and lacrimation. Patients are usually afebrile and alert and oriented. Although uncomfortable, opioid withdrawal is rarely dangerous.
Tx: Involves supportive care
Rx: 🕯🕯 alpha-2 adrenergic agonists, methadone, or buprenorphine.
Misuse:
Prescription drug misuse: Age <45, psychiatric disorder, personal or family history of substance use disorder, or a legal history. If the benefits of an opioid prescription outweigh the risks, the physician can reduce the risk of long-term opioid misuse by checking the prescription drug-monitoring program data (available in almost all states) for undisclosed coprescriptions, performing random urine drug screening (UDS), and scheduling frequent follow-up visits. Patients prescribed long-term opioids should be seen at least once every 3 months throughout the course of treatment and even more frequently in high-risk situations.
Phencyclidine (PCP)
Intoxication commonly presents with severe agitation, delusions of enhanced strength, psychosis (eg, paranoia, hallucinations), analgesia, and aggression. Physical examination findings include multidirectional 👀nystagmus (horizontal, vertical, and/or rotary), hypertension, tachycardia, and disorientation. Severe cases may present with hyperthermia, ataxia, muscle rigidity, seizures, and coma.
Tx: Supportive management and targeted treatment of agitation and aggression to maintain safety. Benzodiazepines are the most commonly used agents for the treatment of PCP-associated agitation. Benzodiazepine agents that are available in a parenteral formulation (eg, lorazepam, diazepam) are preferred because patients are often so agitated that they are unable to take medications by mouth.
🕶 Minimization of environmental stimuli: PCP disrupts sensory input, so those intoxicated with it can be extremely unpredictable
Standard urine drug screen (UDS)
A standard urine drug screen (UDS) tests for amphetamine, cocaine, cannabis, phencyclidine, and opioids. However, it is important to remember that standard tests performed by immunoassay identify opioid use by measuring morphine, a breakdown product of all natural opioids (eg, heroin, codeine). ❗ Semisynthetic (eg, oxycodone, hydrocodone, hydromorphone) and synthetic (eg, fentanyl, meperidine, methadone, tramadol) opioids DO NOT trigger a positive result on a standard UDS.
sympathomimetic syndrome
MATHS:
Mydriasis
Agitation
Tachycardia
Hypertension
Hyperthermia
Diaphoresis
Sources include nonprescription sympathomimetic agents include the over-the-counter cold agents (containing ephedrine), illegal street drugs (eg, cocaine, amphetamines, methamphetamine), dietary supplements (ephedra), and illicit designer drugs (eg, 3,4-methylenedioxy methamphetamine (MDMA, “ecstasy”)
Treatment involves sedation, hydration, and treatment of complications such as rhabdomyalysis and hyperthermia.
TCA
Tricyclic antidepressant (TCA) overdose causes mental status changes, seizures, tachycardia, hypotension, cardiac conduction delay, and anticholinergic effects (eg, dilated pupils, hyperthermia, flushed and dry skin, intestinal ileus).
Cardiotoxicity is due to blockade of cardiac fast sodium channels, leading to QRS prolongation and risk of developing ventricular arrhythmia (similar to class IA antiarrhythmic drugs such as quinidine).
ECG should be obtained immediately and monitored frequently in suspected TCA overdose. QRS duration >100 msec is associated with increased risk for ventricular arrhythmia and seizures and is used as an indication for sodium bicarbonate therapy.
Tx: Sodium Bicarbonate
Acute lead toxicity
Gastrointestinal manifestations: Constipation
- Neuropsychiatric manifestations: Sensorimotor neuropathy (eg, weakness with dorsiflexion), short-term memory loss
- Hematologic manifestations: Microcytic anemia (often with basophilic stippling on peripheral smear), 🧶 hyperuricemia (due to impaired purine metabolism)
- Chronic lead toxicity can cause hypertension, nephropathy, and more pronounced neuropsychiatric symptoms (eg, psychosis).
Lead is absorbed predominantly via the lungs in adults. It is stored predominantly in the skeleton and is released slowly, exerting its pathologic effects over decades. Diagnosis depends on establishing a history of lead exposure accompanied by corroborating physical examination findings (eg, neurologic manifestations) and elevated blood lead levels.
The treatment for symptomatic lead poisoning is chelation therapy with an agent such as calcium disodium EDTA. It is important to separate the patient from further lead exposure as the chelating agent may otherwise increase lead absorption from the source.
Inhalant abuse
Commonly abused inhalants include glue, toluene, nitrous oxide (“whip-its”), amyl nitrite (“poppers”), and spray paints. Inhalants may be abused by sniffing, huffing (inhaled from a saturated cloth), or bagging (bag over mouth or nose) to concentrate the inhaled substance. Inhalants are highly lipid soluble and produce immediate effects that typically last 15-45 minutes. They act as central nervous system depressants and may cause death.
Dermatitis (“glue sniffer’s rash”) due to chemical exposure can be seen around the mouth or nostrils.
Liver function tests may be elevated with repeated use. Chronic abuse of nitrous oxide is associated with vitamin B12 deficiency and resultant polyneuropathy.
Inhalant abuse is associated with very serious medical problems. 👂🏾 Hearing loss, peripheral neuritis, 🧦 paresthesias, cerebellar signs, and motor impairment are common neurological manifestations. Muscle weakness caused by rhabdomyolysis, irreversible hepatic and renal damage, cardiovascular symptoms, and gastrointestinal symptoms such as vomiting and hematemesis are also common with chronic severe abuse.
