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Infectious disease and microbiology – Parvovirus infection
Parvovirus B19 infection is a common viral illness with a wide spectrum of clinical manifestations, ranging from mild childhood disease to severe complications in high-risk groups. It is best known for causing erythema infectiosum (fifth disease), but it can also lead to transient aplastic crisis in patients with chronic hemolytic anemia, chronic anemia in immunocompromised individuals, and serious fetal complications such as hydrops fetalis and fetal death. Notably, it is responsible for the majority of aplastic crises in conditions like sickle cell disease.
The virus has a global distribution, with humans as the only reservoir. Seroprevalence increases with age, reaching 30–60% in adults, and infection commonly occurs in childhood outbreaks, particularly in late winter and early spring. Transmission occurs mainly via respiratory secretions, but can also occur through blood products, vertical (mother-to-fetus) transmission, and rarely nosocomial exposure.
After an incubation period of about one week, viremia develops and is followed by infection of erythroid precursor cells in the bone marrow, leading to temporary suppression of red blood cell production (pure red-cell aplasia). The characteristic rash and joint symptoms appear later and are immune-mediated. In immunocompromised patients, failure to mount an antibody response may result in persistent infection and chronic anemia.
Clinically, infection often begins with mild flu-like symptoms such as fever, malaise, headache, and myalgias. This is followed by the classic “slapped cheek” facial rash, which may spread as a lacy, reticular rash over the extremities. Joint symptoms, particularly symmetric polyarthropathy affecting the hands, wrists, and knees, are more common in adults, especially women. In patients with hemolytic disorders, the presentation may be dominated by severe anemia, often without rash.
Diagnosis in typical childhood cases is clinical, but laboratory confirmation can be achieved through detection of parvovirus-specific IgM antibodies or a rise in IgG titers. In immunocompromised patients, PCR detection of viral DNA is more reliable, as antibody responses may be absent. In aplastic crises, laboratory findings include severe anemia with low reticulocyte count and characteristic bone marrow findings (giant pronormoblasts).
Management is largely supportive, as infection in immunocompetent individuals is usually self-limited. Nonsteroidal anti-inflammatory drugs may help relieve joint symptoms. In severe cases, such as aplastic crisis or chronic anemia, treatment includes blood transfusions and intravenous immunoglobulin (IVIG). In immunocompromised patients, reducing immunosuppression when possible may aid recovery.
Special consideration is required during pregnancy, as fetal infection can result in severe anemia, hydrops fetalis, and fetal death, particularly in the first half of pregnancy. Monitoring with ultrasound and laboratory testing is essential, and intrauterine transfusion may be needed in severe cases.
The prognosis is excellent in healthy individuals, with most cases resolving without complications. However, complications can occur in vulnerable populations and include severe anemia, chronic infection, fetal loss, hepatitis, myocarditis, meningoencephalitis, and hemophagocytic syndrome. Overall, parvovirus B19 infection highlights the contrast between a typically mild childhood illness and its potentially serious impact in high-risk groups.
Parvovirus B19 infection is a common viral illness with a wide spectrum of clinical manifestations, ranging from mild childhood disease to severe complications in high-risk groups. It is best known for causing erythema infectiosum (fifth disease), but it can also lead to transient aplastic crisis in patients with chronic hemolytic anemia, chronic anemia in immunocompromised individuals, and serious fetal complications such as hydrops fetalis and fetal death. Notably, it is responsible for the majority of aplastic crises in conditions like sickle cell disease.
The virus has a global distribution, with humans as the only reservoir. Seroprevalence increases with age, reaching 30–60% in adults, and infection commonly occurs in childhood outbreaks, particularly in late winter and early spring. Transmission occurs mainly via respiratory secretions, but can also occur through blood products, vertical (mother-to-fetus) transmission, and rarely nosocomial exposure.
After an incubation period of about one week, viremia develops and is followed by infection of erythroid precursor cells in the bone marrow, leading to temporary suppression of red blood cell production (pure red-cell aplasia). The characteristic rash and joint symptoms appear later and are immune-mediated. In immunocompromised patients, failure to mount an antibody response may result in persistent infection and chronic anemia.
Clinically, infection often begins with mild flu-like symptoms such as fever, malaise, headache, and myalgias. This is followed by the classic “slapped cheek” facial rash, which may spread as a lacy, reticular rash over the extremities. Joint symptoms, particularly symmetric polyarthropathy affecting the hands, wrists, and knees, are more common in adults, especially women. In patients with hemolytic disorders, the presentation may be dominated by severe anemia, often without rash.
Diagnosis in typical childhood cases is clinical, but laboratory confirmation can be achieved through detection of parvovirus-specific IgM antibodies or a rise in IgG titers. In immunocompromised patients, PCR detection of viral DNA is more reliable, as antibody responses may be absent. In aplastic crises, laboratory findings include severe anemia with low reticulocyte count and characteristic bone marrow findings (giant pronormoblasts).
Management is largely supportive, as infection in immunocompetent individuals is usually self-limited. Nonsteroidal anti-inflammatory drugs may help relieve joint symptoms. In severe cases, such as aplastic crisis or chronic anemia, treatment includes blood transfusions and intravenous immunoglobulin (IVIG). In immunocompromised patients, reducing immunosuppression when possible may aid recovery.
Special consideration is required during pregnancy, as fetal infection can result in severe anemia, hydrops fetalis, and fetal death, particularly in the first half of pregnancy. Monitoring with ultrasound and laboratory testing is essential, and intrauterine transfusion may be needed in severe cases.
The prognosis is excellent in healthy individuals, with most cases resolving without complications. However, complications can occur in vulnerable populations and include severe anemia, chronic infection, fetal loss, hepatitis, myocarditis, meningoencephalitis, and hemophagocytic syndrome. Overall, parvovirus B19 infection highlights the contrast between a typically mild childhood illness and its potentially serious impact in high-risk groups.
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Infectious disease and microbiology – Pericarditis
Pericarditis is an inflammatory condition of the pericardium, the sac surrounding the heart, and can result from a wide range of infectious (viral, bacterial, fungal, protozoal) and noninfectious causes. In many cases, especially when no specific pathogen is identified, it is presumed to be viral or idiopathic, often involving an immune-mediated mechanism.
The condition is relatively common in clinical practice, accounting for about 5% of emergency visits for chest pain, though it occurs in only about 0.1% of hospitalized patients. Bacterial pericarditis is much rarer but more severe. There is no specific prevention for idiopathic cases, but early diagnosis and treatment can reduce complications and the need for surgical intervention.
Pathophysiologically, pericarditis may result from direct infection of the pericardium, as seen in bacterial cases, or from an autoimmune response, particularly in idiopathic or viral forms. Tuberculous pericarditis involves immune activation with CD4 lymphocytes and interferon-gamma, while viral infections lead to lymphocytic inflammation of the pericardium.
A wide variety of pathogens can cause pericarditis. Viruses are the most common, especially Coxsackie A and B, along with herpes viruses, influenza, adenovirus, HIV, and others. Bacterial causes often arise from nearby infections like pneumonia or from postoperative or hospital-acquired infections, with organisms such as Staphylococcus aureus, Streptococcus pneumoniae, and gram-negative bacteria. Less commonly, fungi (e.g., Candida, Histoplasma) and protozoa (e.g., Toxoplasma, Entamoeba histolytica) are involved, typically in disseminated disease.
Clinically, patients usually present with sharp, retrosternal chest pain and fever, with pain often relieved by sitting forward, which is a classic feature. Viral prodromal symptoms may be present. In bacterial cases, chest pain may be less prominent. Other findings include tachypnea and tachycardia, and in severe cases, progression to cardiac tamponade. On examination, a pericardial friction rub is characteristic, and signs such as pulsus paradoxus and decreased heart sounds may indicate significant effusion.
Diagnosis relies heavily on electrocardiography (ECG), which typically shows diffuse ST-segment elevation and PR depression, making it one of the most important diagnostic tools. Laboratory findings may include elevated white blood cells and inflammatory markers, and sometimes elevated cardiac troponins. Imaging such as chest X-ray, CT, MRI, or echocardiography helps assess pericardial effusion and structural involvement. Pericardiocentesis or biopsy may be necessary for diagnosis and to relieve tamponade, with fluid analysis aiding in identifying the cause.
Management depends on the underlying etiology. Most cases are treated with nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or indomethacin, along with colchicine, which reduces symptoms and recurrence. Steroids are generally avoided except in specific situations like tuberculous pericarditis. If a specific pathogen is identified, targeted therapy is required—for example, antivirals (e.g., acyclovir, ganciclovir), antibiotics for bacterial causes, or antituberculous therapy. Supportive measures include bed rest and gastric protection when using NSAIDs.
Severe complications such as cardiac tamponade require urgent intervention with pericardiocentesis, while purulent or constrictive pericarditis may necessitate surgical procedures like pericardiotomy or pericardiectomy. Hospitalization is indicated in high-risk patients, including those with fever, large effusions, immunosuppression, or failure of initial therapy.
The prognosis is generally excellent in idiopathic or viral pericarditis, with recovery in most patients. However, outcomes are worse in tuberculous or untreated bacterial pericarditis, which can be fatal. Important complications include recurrence, constrictive pericarditis, and cardiac tamponade, all of which require careful monitoring and follow-up, often with repeat echocardiography.
Pericarditis is an inflammatory condition of the pericardium, the sac surrounding the heart, and can result from a wide range of infectious (viral, bacterial, fungal, protozoal) and noninfectious causes. In many cases, especially when no specific pathogen is identified, it is presumed to be viral or idiopathic, often involving an immune-mediated mechanism.
The condition is relatively common in clinical practice, accounting for about 5% of emergency visits for chest pain, though it occurs in only about 0.1% of hospitalized patients. Bacterial pericarditis is much rarer but more severe. There is no specific prevention for idiopathic cases, but early diagnosis and treatment can reduce complications and the need for surgical intervention.
Pathophysiologically, pericarditis may result from direct infection of the pericardium, as seen in bacterial cases, or from an autoimmune response, particularly in idiopathic or viral forms. Tuberculous pericarditis involves immune activation with CD4 lymphocytes and interferon-gamma, while viral infections lead to lymphocytic inflammation of the pericardium.
A wide variety of pathogens can cause pericarditis. Viruses are the most common, especially Coxsackie A and B, along with herpes viruses, influenza, adenovirus, HIV, and others. Bacterial causes often arise from nearby infections like pneumonia or from postoperative or hospital-acquired infections, with organisms such as Staphylococcus aureus, Streptococcus pneumoniae, and gram-negative bacteria. Less commonly, fungi (e.g., Candida, Histoplasma) and protozoa (e.g., Toxoplasma, Entamoeba histolytica) are involved, typically in disseminated disease.
Clinically, patients usually present with sharp, retrosternal chest pain and fever, with pain often relieved by sitting forward, which is a classic feature. Viral prodromal symptoms may be present. In bacterial cases, chest pain may be less prominent. Other findings include tachypnea and tachycardia, and in severe cases, progression to cardiac tamponade. On examination, a pericardial friction rub is characteristic, and signs such as pulsus paradoxus and decreased heart sounds may indicate significant effusion.
Diagnosis relies heavily on electrocardiography (ECG), which typically shows diffuse ST-segment elevation and PR depression, making it one of the most important diagnostic tools. Laboratory findings may include elevated white blood cells and inflammatory markers, and sometimes elevated cardiac troponins. Imaging such as chest X-ray, CT, MRI, or echocardiography helps assess pericardial effusion and structural involvement. Pericardiocentesis or biopsy may be necessary for diagnosis and to relieve tamponade, with fluid analysis aiding in identifying the cause.
Management depends on the underlying etiology. Most cases are treated with nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or indomethacin, along with colchicine, which reduces symptoms and recurrence. Steroids are generally avoided except in specific situations like tuberculous pericarditis. If a specific pathogen is identified, targeted therapy is required—for example, antivirals (e.g., acyclovir, ganciclovir), antibiotics for bacterial causes, or antituberculous therapy. Supportive measures include bed rest and gastric protection when using NSAIDs.
Severe complications such as cardiac tamponade require urgent intervention with pericardiocentesis, while purulent or constrictive pericarditis may necessitate surgical procedures like pericardiotomy or pericardiectomy. Hospitalization is indicated in high-risk patients, including those with fever, large effusions, immunosuppression, or failure of initial therapy.
The prognosis is generally excellent in idiopathic or viral pericarditis, with recovery in most patients. However, outcomes are worse in tuberculous or untreated bacterial pericarditis, which can be fatal. Important complications include recurrence, constrictive pericarditis, and cardiac tamponade, all of which require careful monitoring and follow-up, often with repeat echocardiography.
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Toxicology – Drugs Causing Hypoventilation
Opiates
Opiates are the most significant contributors to respiratory depression among toxicologic agents. They suppress the brainstem respiratory center, leading to decreased respiratory rate and depth. Reversal with naloxone is effective but should be carefully titrated to avoid precipitating acute withdrawal.
Sedative–Hypnotics
This class of central nervous system depressants reduces respiratory drive in overdose situations, potentially leading to hypoventilation and respiratory failure.
Liquor (Ethanol)
At very high concentrations, ethanol can cause marked central nervous system depression, resulting in clinically significant respiratory suppression.
Weed (Cannabinoids)
Cannabinoid receptor agonists such as marijuana generally have mild respiratory effects. However, slight reductions in respiratory rate may occur as part of overall central nervous system depression.
Treatment
In patients with decreased consciousness, central nervous system depression, or inadequate ventilation, airway protection with endotracheal intubation is essential. Opiate toxicity can be reversed with naloxone, and continuous infusion may be required due to its shorter duration of action compared to many opioids. Flumazenil may reverse certain sedative–hypnotics like benzodiazepines, but it must be used cautiously as it can trigger withdrawal seizures or status epilepticus in dependent individuals.
Opiates
Opiates are the most significant contributors to respiratory depression among toxicologic agents. They suppress the brainstem respiratory center, leading to decreased respiratory rate and depth. Reversal with naloxone is effective but should be carefully titrated to avoid precipitating acute withdrawal.
Sedative–Hypnotics
This class of central nervous system depressants reduces respiratory drive in overdose situations, potentially leading to hypoventilation and respiratory failure.
Liquor (Ethanol)
At very high concentrations, ethanol can cause marked central nervous system depression, resulting in clinically significant respiratory suppression.
Weed (Cannabinoids)
Cannabinoid receptor agonists such as marijuana generally have mild respiratory effects. However, slight reductions in respiratory rate may occur as part of overall central nervous system depression.
Treatment
In patients with decreased consciousness, central nervous system depression, or inadequate ventilation, airway protection with endotracheal intubation is essential. Opiate toxicity can be reversed with naloxone, and continuous infusion may be required due to its shorter duration of action compared to many opioids. Flumazenil may reverse certain sedative–hypnotics like benzodiazepines, but it must be used cautiously as it can trigger withdrawal seizures or status epilepticus in dependent individuals.
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Toxicology – Drugs Causing Bradycardia
Beta-Blockers (e.g., Propranolol)
Beta-blockers reduce sinoatrial (SA) and atrioventricular (AV) nodal conduction, leading to decreased heart rate and, in severe cases, heart block.
Opiates (Poppies)
Opiates increase vagal tone and exert a depressant effect on SA and AV nodal conduction, contributing to bradycardia.
Anticholinesterase Inhibitors
By inhibiting acetylcholinesterase, these agents increase acetylcholine levels, producing a cholinergic toxidrome in which bradycardia is a prominent feature.
Clonidine
Clonidine is a central α₂ receptor agonist that can cause bradycardia along with hypotension and respiratory depression.
Calcium Channel Blockers
These medications impair SA and AV nodal conduction, resulting in decreased heart rate and potential heart block.
Digoxin
Digoxin increases vagal tone while slowing conduction through the SA and AV nodes, leading to bradycardia despite its positive inotropic effects.
Ethanol
At high doses, ethanol can depress cardiac function and contribute to bradycardia.
Treatment
Atropine may be administered to counteract increased vagal tone and raise heart rate. If ineffective, external pacing should be considered. Definitive management involves identifying the causative toxin and administering the appropriate antidote or targeted therapy.
Beta-Blockers (e.g., Propranolol)
Beta-blockers reduce sinoatrial (SA) and atrioventricular (AV) nodal conduction, leading to decreased heart rate and, in severe cases, heart block.
Opiates (Poppies)
Opiates increase vagal tone and exert a depressant effect on SA and AV nodal conduction, contributing to bradycardia.
Anticholinesterase Inhibitors
By inhibiting acetylcholinesterase, these agents increase acetylcholine levels, producing a cholinergic toxidrome in which bradycardia is a prominent feature.
Clonidine
Clonidine is a central α₂ receptor agonist that can cause bradycardia along with hypotension and respiratory depression.
Calcium Channel Blockers
These medications impair SA and AV nodal conduction, resulting in decreased heart rate and potential heart block.
Digoxin
Digoxin increases vagal tone while slowing conduction through the SA and AV nodes, leading to bradycardia despite its positive inotropic effects.
Ethanol
At high doses, ethanol can depress cardiac function and contribute to bradycardia.
Treatment
Atropine may be administered to counteract increased vagal tone and raise heart rate. If ineffective, external pacing should be considered. Definitive management involves identifying the causative toxin and administering the appropriate antidote or targeted therapy.
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Toxicology – Nystagmus-Inducing Toxins
Sedative–Hypnotics
Medications in this class commonly produce nystagmus as part of central nervous system depression.
Alcohols (Ethanol, Methanol, Ethylene Glycol, Isopropanol)
All alcohols can induce nystagmus. Ethanol is particularly associated with horizontal and downbeat nystagmus and is often assessed clinically using the horizontal gaze nystagmus test.
Phencyclidine and Dissociatives
Dissociative agents such as PCP, ketamine, and dextromethorphan can produce a characteristic rotatory nystagmus.
Phenytoin
Phenytoin toxicity is associated with horizontal and sometimes upbeat nystagmus.
Carbamazepine (Tegretol)
Carbamazepine can cause both horizontal and downbeat nystagmus.
Lithium
Lithium toxicity may lead to downbeat nystagmus.
Solvents (Inhalants)
Exposure to inhaled solvents has been associated with positional nystagmus, with severity correlating to the degree of exposure.
Thiamine Deficiency (Wernicke Encephalopathy)
Thiamine deficiency can result in Wernicke encephalopathy, characterized by ataxia, confusion, ophthalmoplegia, and nystagmus.
Overview
Nystagmus is an involuntary, rhythmic oscillation of the eyes that may occur in toxicologic conditions. It can present as horizontal (side-to-side), vertical (upbeat or downbeat), or rotatory movement. Horizontal nystagmus is the most common and is best observed during lateral gaze. Alcohol intoxication frequently produces nystagmus, which is often assessed in clinical and roadside settings. Certain agents such as anticonvulsants and lithium may produce vertical nystagmus, while phenytoin has been associated with upbeat nystagmus and PCP with rotatory nystagmus.
Sedative–Hypnotics
Medications in this class commonly produce nystagmus as part of central nervous system depression.
Alcohols (Ethanol, Methanol, Ethylene Glycol, Isopropanol)
All alcohols can induce nystagmus. Ethanol is particularly associated with horizontal and downbeat nystagmus and is often assessed clinically using the horizontal gaze nystagmus test.
Phencyclidine and Dissociatives
Dissociative agents such as PCP, ketamine, and dextromethorphan can produce a characteristic rotatory nystagmus.
Phenytoin
Phenytoin toxicity is associated with horizontal and sometimes upbeat nystagmus.
Carbamazepine (Tegretol)
Carbamazepine can cause both horizontal and downbeat nystagmus.
Lithium
Lithium toxicity may lead to downbeat nystagmus.
Solvents (Inhalants)
Exposure to inhaled solvents has been associated with positional nystagmus, with severity correlating to the degree of exposure.
Thiamine Deficiency (Wernicke Encephalopathy)
Thiamine deficiency can result in Wernicke encephalopathy, characterized by ataxia, confusion, ophthalmoplegia, and nystagmus.
Overview
Nystagmus is an involuntary, rhythmic oscillation of the eyes that may occur in toxicologic conditions. It can present as horizontal (side-to-side), vertical (upbeat or downbeat), or rotatory movement. Horizontal nystagmus is the most common and is best observed during lateral gaze. Alcohol intoxication frequently produces nystagmus, which is often assessed in clinical and roadside settings. Certain agents such as anticonvulsants and lithium may produce vertical nystagmus, while phenytoin has been associated with upbeat nystagmus and PCP with rotatory nystagmus.
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Toxicology – Drugs Causing Tachycardia
Cocaine (Freebase)
Cocaine produces strong sympathomimetic effects by blocking the reuptake of serotonin, dopamine, and norepinephrine, leading to increased heart rate and blood pressure.
Amphetamines
Amphetamines stimulate the release of catecholamines from presynaptic nerve terminals, resulting in marked tachycardia and hypertension.
Sympathomimetics
This group of drugs elevates heart rate and blood pressure by increasing catecholamine release, decreasing reuptake, or inhibiting metabolism.
Anticholinergics
Anticholinergic agents inhibit parasympathetic activity, causing an increase in heart rate and often accompanying hypertension.
Antihistamines
Many antihistamines possess anticholinergic properties, which can lead to tachycardia as part of their toxic effects.
Theophylline (Methylxanthines)
Theophylline acts as an adenosine receptor antagonist, β-agonist, and phosphodiesterase inhibitor, all of which contribute to increased heart rate and potential arrhythmias.
Thyroid Hormone
Excess thyroid hormone elevates metabolic rate and enhances sensitivity to catecholamines, leading to tachycardia.
Solvents (Inhalants)
Inhaled solvents may displace oxygen in the lungs, causing hypoxemia and reflex tachycardia. They can also sensitize the myocardium to catecholamines, increasing the risk of fatal arrhythmias.
Fever
An increase in body temperature raises basal metabolic rate, which in turn increases heart rate.
Treatment
Benzodiazepines are the first-line treatment for undifferentiated tachycardia in toxicologic settings. Intravenous fluids should be administered in cases of hypovolemia, and active cooling measures should be initiated for patients with hyperthermia.
Cocaine (Freebase)
Cocaine produces strong sympathomimetic effects by blocking the reuptake of serotonin, dopamine, and norepinephrine, leading to increased heart rate and blood pressure.
Amphetamines
Amphetamines stimulate the release of catecholamines from presynaptic nerve terminals, resulting in marked tachycardia and hypertension.
Sympathomimetics
This group of drugs elevates heart rate and blood pressure by increasing catecholamine release, decreasing reuptake, or inhibiting metabolism.
Anticholinergics
Anticholinergic agents inhibit parasympathetic activity, causing an increase in heart rate and often accompanying hypertension.
Antihistamines
Many antihistamines possess anticholinergic properties, which can lead to tachycardia as part of their toxic effects.
Theophylline (Methylxanthines)
Theophylline acts as an adenosine receptor antagonist, β-agonist, and phosphodiesterase inhibitor, all of which contribute to increased heart rate and potential arrhythmias.
Thyroid Hormone
Excess thyroid hormone elevates metabolic rate and enhances sensitivity to catecholamines, leading to tachycardia.
Solvents (Inhalants)
Inhaled solvents may displace oxygen in the lungs, causing hypoxemia and reflex tachycardia. They can also sensitize the myocardium to catecholamines, increasing the risk of fatal arrhythmias.
Fever
An increase in body temperature raises basal metabolic rate, which in turn increases heart rate.
Treatment
Benzodiazepines are the first-line treatment for undifferentiated tachycardia in toxicologic settings. Intravenous fluids should be administered in cases of hypovolemia, and active cooling measures should be initiated for patients with hyperthermia.
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Toxicology – Odor-Associated Toxins
Bitter Almond Odor
This characteristic smell is classically associated with cyanide exposure, although a significant portion of the population cannot detect it due to genetic variation.
Garlic-Like Odor
Substances such as phosphorus, arsenic compounds (arsine), organophosphates, selenium, thallium, and dimethyl sulfoxide (DMSO) may produce a garlic-like smell.
Rotten Egg Odor
Hydrogen sulfide, carbon disulfide, mercaptans, disulfiram, and N-acetylcysteine are known to emit a sulfurous “rotten egg” odor.
Fruity Odor
A sweet or fruity smell may be present in exposures involving nitriles, ketoacidosis, ethanol, isopropanol, chloroform, trichloroethane, paraldehyde, chloral hydrate, methyl bromide, and certain nitrites.
Fishy or Musty Odor
Compounds such as zinc phosphide, aluminum phosphide, and nickel carbonyl may produce a fishy or musty scent.
Ammonia-Like Odor
Ammonia exposure is associated with a sharp, pungent odor that is easily recognizable.
Mothball Odor
Naphthalene, camphor, and p-dichlorobenzene commonly produce the classic mothball smell.
Minty Odor
Methylsalicylate (oil of wintergreen) and menthol can give off a distinct mint-like aroma.
Disinfectant Odor
Phenol and creosote are associated with a strong antiseptic or disinfectant-like smell.
Burnt Rope Odor
This smell may be linked to marijuana or opium exposure.
Carrot-Like Odor
Cicutoxin, found in water hemlock, can produce an odor reminiscent of carrots.
Hay-Like Odor
Phosgene exposure may be associated with a freshly cut hay smell.
Pear-Like Odor
Chloral hydrate may produce a scent resembling pears.
Pepper Odor
Exposure to riot control agents such as CS (tear gas) can result in a pepper-like smell.
Pine Odor
Pine oil is associated with a characteristic pine-like scent.
Peanut Butter Odor
Vacor, a rodenticide, has been described as having a peanut butter-like odor.
Shoe Polish Odor
Nitrobenzene exposure may produce a smell similar to shoe polish.
Tobacco Odor
Nicotine-containing substances often have a distinct tobacco-like smell.
Vinegar Odor
Acetic acid and hydrofluoric acid may emit a sharp, vinegar-like odor.
Violet Odor
Turpentine metabolites excreted in urine may produce a violet-like scent.
New Car Smell
Chemicals such as benzene, cyclohexanone, and styrene, often found in new materials, can produce this recognizable odor.
PEARLS
Bitter Almond Odor
This characteristic smell is classically associated with cyanide exposure, although a significant portion of the population cannot detect it due to genetic variation.
Garlic-Like Odor
Substances such as phosphorus, arsenic compounds (arsine), organophosphates, selenium, thallium, and dimethyl sulfoxide (DMSO) may produce a garlic-like smell.
Rotten Egg Odor
Hydrogen sulfide, carbon disulfide, mercaptans, disulfiram, and N-acetylcysteine are known to emit a sulfurous “rotten egg” odor.
Fruity Odor
A sweet or fruity smell may be present in exposures involving nitriles, ketoacidosis, ethanol, isopropanol, chloroform, trichloroethane, paraldehyde, chloral hydrate, methyl bromide, and certain nitrites.
Fishy or Musty Odor
Compounds such as zinc phosphide, aluminum phosphide, and nickel carbonyl may produce a fishy or musty scent.
Ammonia-Like Odor
Ammonia exposure is associated with a sharp, pungent odor that is easily recognizable.
Mothball Odor
Naphthalene, camphor, and p-dichlorobenzene commonly produce the classic mothball smell.
Minty Odor
Methylsalicylate (oil of wintergreen) and menthol can give off a distinct mint-like aroma.
Disinfectant Odor
Phenol and creosote are associated with a strong antiseptic or disinfectant-like smell.
Burnt Rope Odor
This smell may be linked to marijuana or opium exposure.
Carrot-Like Odor
Cicutoxin, found in water hemlock, can produce an odor reminiscent of carrots.
Hay-Like Odor
Phosgene exposure may be associated with a freshly cut hay smell.
Pear-Like Odor
Chloral hydrate may produce a scent resembling pears.
Pepper Odor
Exposure to riot control agents such as CS (tear gas) can result in a pepper-like smell.
Pine Odor
Pine oil is associated with a characteristic pine-like scent.
Peanut Butter Odor
Vacor, a rodenticide, has been described as having a peanut butter-like odor.
Shoe Polish Odor
Nitrobenzene exposure may produce a smell similar to shoe polish.
Tobacco Odor
Nicotine-containing substances often have a distinct tobacco-like smell.
Vinegar Odor
Acetic acid and hydrofluoric acid may emit a sharp, vinegar-like odor.
Violet Odor
Turpentine metabolites excreted in urine may produce a violet-like scent.
New Car Smell
Chemicals such as benzene, cyclohexanone, and styrene, often found in new materials, can produce this recognizable odor.
PEARLS
- Approximately 40% of individuals are unable to detect the bitter almond odor of cyanide.
- Hydrogen sulfide exposure can quickly lead to olfactory fatigue, reducing the ability to perceive its smell.
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Toxicology – Seizure-Inducing Toxins
Cocaine
Cocaine lowers the seizure threshold through potent stimulation of the central nervous system, similar to other sympathomimetic agents.
Isoniazid
Isoniazid toxicity can cause severe, refractory seizures that are characteristically resistant to standard therapy and require treatment with pyridoxine.
Anticholinergics
Seizures may occur as a late and severe manifestation of anticholinergic toxicity.
Amphetamines
Amphetamines increase catecholamine release and significantly lower the seizure threshold, increasing the risk of seizures.
Organophosphates
These insecticides produce a cholinergic toxidrome and can lead to seizures due to excessive acetylcholine accumulation.
Ethanol Withdrawal
Seizures may develop within 6 to 48 hours after abrupt cessation of alcohol in dependent individuals.
Tricyclic Antidepressants (TCAs)
At high doses, TCAs can induce seizures, often occurring before serious cardiac complications such as arrhythmias or arrest.
Methylanthines
Agents such as theophylline can cause seizures in overdose due to central nervous system stimulation.
Phencyclidine (PCP)
Large doses of PCP may result in severe toxicity, including seizures, hyperthermia, coma, and death.
Lidocaine
Intravenous toxicity from local anesthetics like lidocaine can initially cause seizures, followed by cardiovascular collapse.
Camphor
Camphor exposure, especially in children, can lead to seizures due to increased absorption through ingestion or skin contact.
Sympathomimetics
This class of drugs broadly lowers the seizure threshold through increased adrenergic activity.
Benzodiazepine Withdrawal
Abrupt discontinuation of benzodiazepines can lead to withdrawal symptoms, including seizures. Use of flumazenil may precipitate acute withdrawal in dependent individuals.
Lithium
Severe lithium toxicity may present with neurological complications, including seizures.
Lindane
Lindane, used topically for lice and scabies, can cause seizures when absorbed in excessive amounts, particularly in infants and children.
Lead (Severe Toxicity)
Extremely elevated lead levels can result in neurological toxicity, including seizures.
Treatment
Benzodiazepines such as diazepam or lorazepam are first-line therapy for toxin-induced seizures. If seizures persist, phenobarbital is considered second-line. In refractory cases, propofol with airway protection may be required. Phenytoin and fosphenytoin are generally not effective for toxin-induced seizures. Pyridoxine should be administered when isoniazid or certain mushroom toxicities are suspected.
Cocaine
Cocaine lowers the seizure threshold through potent stimulation of the central nervous system, similar to other sympathomimetic agents.
Isoniazid
Isoniazid toxicity can cause severe, refractory seizures that are characteristically resistant to standard therapy and require treatment with pyridoxine.
Anticholinergics
Seizures may occur as a late and severe manifestation of anticholinergic toxicity.
Amphetamines
Amphetamines increase catecholamine release and significantly lower the seizure threshold, increasing the risk of seizures.
Organophosphates
These insecticides produce a cholinergic toxidrome and can lead to seizures due to excessive acetylcholine accumulation.
Ethanol Withdrawal
Seizures may develop within 6 to 48 hours after abrupt cessation of alcohol in dependent individuals.
Tricyclic Antidepressants (TCAs)
At high doses, TCAs can induce seizures, often occurring before serious cardiac complications such as arrhythmias or arrest.
Methylanthines
Agents such as theophylline can cause seizures in overdose due to central nervous system stimulation.
Phencyclidine (PCP)
Large doses of PCP may result in severe toxicity, including seizures, hyperthermia, coma, and death.
Lidocaine
Intravenous toxicity from local anesthetics like lidocaine can initially cause seizures, followed by cardiovascular collapse.
Camphor
Camphor exposure, especially in children, can lead to seizures due to increased absorption through ingestion or skin contact.
Sympathomimetics
This class of drugs broadly lowers the seizure threshold through increased adrenergic activity.
Benzodiazepine Withdrawal
Abrupt discontinuation of benzodiazepines can lead to withdrawal symptoms, including seizures. Use of flumazenil may precipitate acute withdrawal in dependent individuals.
Lithium
Severe lithium toxicity may present with neurological complications, including seizures.
Lindane
Lindane, used topically for lice and scabies, can cause seizures when absorbed in excessive amounts, particularly in infants and children.
Lead (Severe Toxicity)
Extremely elevated lead levels can result in neurological toxicity, including seizures.
Treatment
Benzodiazepines such as diazepam or lorazepam are first-line therapy for toxin-induced seizures. If seizures persist, phenobarbital is considered second-line. In refractory cases, propofol with airway protection may be required. Phenytoin and fosphenytoin are generally not effective for toxin-induced seizures. Pyridoxine should be administered when isoniazid or certain mushroom toxicities are suspected.
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Toxicology – Radiopaque Toxins
Iron
Iron preparations, particularly ferrous sulfate tablets, are clearly visible on radiographs. In large ingestions, they may accumulate and form a radiopaque pharmacobezoar.
Lead (Pb)
Lead-containing objects such as paint chips, bullets, toys, and figurines are highly radiopaque and easily identified on imaging.
Calcium
Calcium-containing substances are radiopaque, and significant ingestion can result in formation of a visible mass within the gastrointestinal tract.
Barium
Barium is inherently radiopaque and readily detectable on imaging studies.
Potassium
Potassium tablets may be visualized on radiographs, especially when ingested in large amounts, sometimes forming a pharmacobezoar.
Heavy Metals
Various heavy metals are radiopaque and can be identified on plain radiographs.
Enteric-Coated or Sustained-Release Tablets
Large ingestions of these formulations can lead to the formation of a radiopaque pharmacobezoar visible on imaging.
Arsenic
As a metallic element, arsenic is radiopaque and may be seen on radiographic studies.
Iodine
Iodine-containing compounds are radiopaque and can appear on imaging.
Chloral Hydrate and Halogenated Compounds
Certain halogenated substances, such as chloral hydrate and chloroform, may be detectable on x-ray due to their radiopaque properties.
Condom Packets (Body Packers)
Individuals who ingest drug-filled packets may show multiple uniform radiopaque densities on abdominal imaging.
Tricyclic Antidepressants (TCAs)
These medications may demonstrate variable radiopacity depending on dose and preparation.
Phosphorus
Phosphorus can be visualized on radiographs due to its radiopaque nature.
Iron
Iron preparations, particularly ferrous sulfate tablets, are clearly visible on radiographs. In large ingestions, they may accumulate and form a radiopaque pharmacobezoar.
Lead (Pb)
Lead-containing objects such as paint chips, bullets, toys, and figurines are highly radiopaque and easily identified on imaging.
Calcium
Calcium-containing substances are radiopaque, and significant ingestion can result in formation of a visible mass within the gastrointestinal tract.
Barium
Barium is inherently radiopaque and readily detectable on imaging studies.
Potassium
Potassium tablets may be visualized on radiographs, especially when ingested in large amounts, sometimes forming a pharmacobezoar.
Heavy Metals
Various heavy metals are radiopaque and can be identified on plain radiographs.
Enteric-Coated or Sustained-Release Tablets
Large ingestions of these formulations can lead to the formation of a radiopaque pharmacobezoar visible on imaging.
Arsenic
As a metallic element, arsenic is radiopaque and may be seen on radiographic studies.
Iodine
Iodine-containing compounds are radiopaque and can appear on imaging.
Chloral Hydrate and Halogenated Compounds
Certain halogenated substances, such as chloral hydrate and chloroform, may be detectable on x-ray due to their radiopaque properties.
Condom Packets (Body Packers)
Individuals who ingest drug-filled packets may show multiple uniform radiopaque densities on abdominal imaging.
Tricyclic Antidepressants (TCAs)
These medications may demonstrate variable radiopacity depending on dose and preparation.
Phosphorus
Phosphorus can be visualized on radiographs due to its radiopaque nature.
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Toxicology – Causes of Anion Gap Metabolic Acidosis
Alcohol (Ethanol)
Ethanol intoxication may lead to hypoglycemia, lactic acidosis, and alcoholic ketoacidosis, all of which contribute to an increased anion gap.
Aspirin (Salicylates)
Salicylate toxicity should be suspected in patients with anion gap metabolic acidosis and altered mental status. It typically produces a mixed disorder with metabolic acidosis and respiratory alkalosis due to direct stimulation of the respiratory center. It also increases renal loss of bicarbonate and potassium while promoting lactic and pyruvic acid formation.
Methanol
Methanol poisoning results in a high anion gap and hyperosmolar metabolic acidosis due to accumulation of formic acid, a toxic metabolite.
Ethylene Glycol
Commonly found in antifreeze, ethylene glycol is metabolized into glycolic, glyoxylic, and oxalic acids, producing a severe high anion gap metabolic acidosis.
Metformin
Metformin toxicity can lead to lactic acidosis by increasing production of lactate and other metabolic intermediates, particularly in patients with renal impairment or after contrast exposure.
Diabetic Ketoacidosis (DKA)
DKA occurs due to insulin deficiency, resulting in increased fatty acid metabolism and accumulation of ketoacids such as acetoacetate and β-hydroxybutyrate. Starvation and alcoholic ketosis can produce similar effects.
Uremia
Advanced kidney failure leads to accumulation of nitrogenous waste products and acids such as sulfuric and phosphoric acid, causing an anion gap metabolic acidosis.
Lactic Acidosis
Lactic acid accumulation from anaerobic metabolism is a common cause of anion gap acidosis and may result from hypoxia, hypoperfusion, toxins, or metabolic disorders.
Toluene
Toluene exposure, often through inhalation of solvents, increases production of organic acids such as benzoic and hippuric acid and may also cause renal tubular acidosis with chronic use.
Carbamazepine
Overdose of this antiepileptic drug can lead to metabolic acidosis along with hyperglycemia, ketonuria, altered mental status, seizures, and coma.
Isoniazid (INH)
Isoniazid toxicity can result in lactic acidosis, often accompanied by seizures and altered mental status.
Iron
Iron overdose contributes to metabolic acidosis through hypovolemia, hypotension, and the release of hydrogen ions during its metabolic conversion.
Paraldehyde
This older sedative-hypnotic agent, historically used for seizures, can contribute to anion gap metabolic acidosis in toxic exposures.
Alcohol (Ethanol)
Ethanol intoxication may lead to hypoglycemia, lactic acidosis, and alcoholic ketoacidosis, all of which contribute to an increased anion gap.
Aspirin (Salicylates)
Salicylate toxicity should be suspected in patients with anion gap metabolic acidosis and altered mental status. It typically produces a mixed disorder with metabolic acidosis and respiratory alkalosis due to direct stimulation of the respiratory center. It also increases renal loss of bicarbonate and potassium while promoting lactic and pyruvic acid formation.
Methanol
Methanol poisoning results in a high anion gap and hyperosmolar metabolic acidosis due to accumulation of formic acid, a toxic metabolite.
Ethylene Glycol
Commonly found in antifreeze, ethylene glycol is metabolized into glycolic, glyoxylic, and oxalic acids, producing a severe high anion gap metabolic acidosis.
Metformin
Metformin toxicity can lead to lactic acidosis by increasing production of lactate and other metabolic intermediates, particularly in patients with renal impairment or after contrast exposure.
Diabetic Ketoacidosis (DKA)
DKA occurs due to insulin deficiency, resulting in increased fatty acid metabolism and accumulation of ketoacids such as acetoacetate and β-hydroxybutyrate. Starvation and alcoholic ketosis can produce similar effects.
Uremia
Advanced kidney failure leads to accumulation of nitrogenous waste products and acids such as sulfuric and phosphoric acid, causing an anion gap metabolic acidosis.
Lactic Acidosis
Lactic acid accumulation from anaerobic metabolism is a common cause of anion gap acidosis and may result from hypoxia, hypoperfusion, toxins, or metabolic disorders.
Toluene
Toluene exposure, often through inhalation of solvents, increases production of organic acids such as benzoic and hippuric acid and may also cause renal tubular acidosis with chronic use.
Carbamazepine
Overdose of this antiepileptic drug can lead to metabolic acidosis along with hyperglycemia, ketonuria, altered mental status, seizures, and coma.
Isoniazid (INH)
Isoniazid toxicity can result in lactic acidosis, often accompanied by seizures and altered mental status.
Iron
Iron overdose contributes to metabolic acidosis through hypovolemia, hypotension, and the release of hydrogen ions during its metabolic conversion.
Paraldehyde
This older sedative-hypnotic agent, historically used for seizures, can contribute to anion gap metabolic acidosis in toxic exposures.
