Principles of Management of Poisoning in Children

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Prevent Absorption:

Take immediate action to remove the toxin and minimize contact with absorptive surfaces:

Dermal and Ocular Decontamination: Flush the affected area with tepid water. For ocular exposure, at least 10 minutes of flushing is recommended. Use soap and water for skin exposure.
Inhaled Toxins: Move the patient to fresh air or provide oxygen if necessary.
Ingested Toxins: The timing of decontamination depends on whether absorption has occurred from the stomach. Decontamination after absorption poses risks without benefits.
Time of Absorption: Most liquid drugs are absorbed within 30 minutes, and most solid dosage forms within 1-2 hours. Gastrointestinal decontamination beyond this time is unlikely to be effective.

Emesis:

Ipecac syrup can induce vomiting:

The onset of emesis usually occurs 20-30 minutes after dosing, with vomiting occurring in 90-95% of patients. Multiple vomiting episodes may occur over 1-2 hours.
Recommended doses based on age:

Infants (6-12 months): 10 mL
Children (1-12 years): 15 mL
Older children and adults: 30 mL

Ipecac should not be used in infants younger than 6 months. Its use has generally declined.

Gastric Lavage

Gastric lavage involves the insertion of a tube into the stomach to aspirate its contents, followed by flushing with aliquots of fluid, usually normal saline. However, its use in children has limitations:

Disadvantage: Small bore tubes used in children make the process time-consuming.
It removes only a fraction of the gastric contents.

Use of Activated Charcoal

Activated charcoal is effective due to its large adsorptive surface area:

Many toxins are adsorbed onto its surface, preventing their absorption from the gastrointestinal tract.
Not all toxins are significantly bound to charcoal, including heavy metals, iron, lithium, hydrocarbons, cyanide, and low molecular weight alcohols.
Usual doses:

Children: 10-30 g
Adolescents or adults: 30-100 g

Activated charcoal is available commercially, often mixed as a slurry in water or a sorbitol solution (a cathartic).

Use of Cathartics

Cathartics are used alongside activated charcoal to expedite the clearance of the charcoal-toxin complex. However, evidence supporting their value is lacking:

Commonly used cathartics include sorbitol (maximum dose, 1 g/kg), magnesium sulfate (maximum dose, 250 mg/kg), and magnesium citrate (maximum dose, 250 mL/kg).
Caution should be exercised when using cathartics in young children due to the risk of dehydration and electrolyte imbalance.

Whole Bowel Irrigation

Whole bowel irrigation (WBI) involves the introduction of a large volume of a polyethylene glycol electrolyte solution (such as Colyte or GoLYTELY) into the stomach to thoroughly cleanse the entire gastrointestinal tract. This method is utilized to eliminate substances that are slowly absorbed, such as iron or sustained-release preparations.

Enhancing Elimination

Enhancing elimination can be achieved through:

Increasing urine pH with intravenously administered bicarbonate, which enhances the elimination of weak acids like salicylates and phenobarbital.
Haemodialysis

Laboratory Evaluation

Laboratory tests play a crucial role in assessing poisoning cases:

Measurement of serum levels of the toxin
Drug screens to identify the presence of multiple substances
Electrolytes (E), blood urea nitrogen (U), and creatinine (Cr) levels to assess kidney function
Liver function tests (LFT) to evaluate hepatic status
Packed cell volume (PCV) to assess for anemia
Full blood count (FBC) to evaluate for any other blood-related abnormalities

Caustics are substances that include both acids and alkalis, as well as certain oxidizing agents like bleach. They can cause significant harm to the body when ingested or in contact with tissues.

Effects of Acids: Acids coagulate proteins, leading to tissue necrosis. They can cause damage by denaturing proteins and disrupting cellular structures.

Effects of Alkalis: Alkalis have the ability to digest and dissolve proteins, resulting in liquefaction necrosis. When alkalis come into contact with tissues, they can cause tissue destruction and have a risk of perforation, especially if the injury occurs in the intestinal tract.

Factors Influencing Severity: The severity of chemical burns caused by caustics depends on several factors:

The pH of the substance
The concentration of the caustic agent
The duration of contact time

Substances with a pH below 2 or above 12 are more likely to cause significant injury due to their extreme acidity or alkalinity.

Clinical Presentation of Caustics Poisoning

When individuals ingest caustic substances, it can lead to various clinical manifestations:

Oral burns may be observed as reddened areas or whitish plaques in the mouth.
Common symptoms include pain, drooling, vomiting, and difficulty or refusal to swallow.
Circumferential burns in the esophagus can lead to strictures during the healing process. These strictures might require repeated dilation or surgical correction.
Strong acids might result in scarring around the pylorus, leading to delayed gastric obstruction.
Caustic substances coming into contact with the skin or eyes can cause significant tissue damage.

Treatment of Caustics Poisoning

Initial management of caustic exposure involves:

Thoroughly washing the skin or eye with water to remove the caustic product. Contaminated clothing should be removed as well.
In cases of ingested agents, rinsing the oral cavity. Emesis and lavage are not recommended, and activated charcoal does not effectively bind these agents.
Patients with symptoms should refrain from consuming oral fluids or solids, even if no visible oral injury is present, as significant esophageal lesions can occur.
Endoscopy should be considered in symptomatic patients or those with a history suggesting possible injury.
The use of corticosteroids and esophageal stents remains a topic of debate and controversy.

Introduction

While the incidence of salicylate poisoning has decreased, especially in young children due to the use of alternative antipyretics, it's important to remain vigilant about the potential for salicylate toxicity in both therapeutic scenarios and acute overdose cases.

Pathophysiology of Salicylate Poisoning

Salicylate poisoning affects multiple organ systems, including the central nervous system (CNS), cardiovascular system, pulmonary system, hepatic system, renal system, and metabolic system.

Salicylates exert their effects by directly or indirectly impacting various organ systems. They uncouple oxidative phosphorylation, inhibit enzymes in the Krebs cycle, and hinder amino acid synthesis.

Acid-Base Status in Salicylate Poisoning

Salicylates have notable effects on the body's acid-base balance:

They stimulate the respiratory center, leading to hyperventilation and respiratory alkalosis.
Interference with the Krebs cycle reduces ATP production and increases lactate, resulting in ketosis and a wide anion-gap metabolic acidosis.

Respiratory System Effects of Salicylate Poisoning

Salicylate poisoning has various effects on the respiratory system:

It increases both respiratory rate (tachypnea) and depth (hyperpnea).
In some cases, it may lead to noncardiogenic pulmonary edema (NCPE).

Glucose Metabolism in Salicylate Poisoning

The increased cellular metabolic activity caused by the uncoupling of oxidative phosphorylation in salicylate poisoning can lead to clinical hypoglycemia.

Fluid and Electrolyte Effects of Salicylate Poisoning

Salicylate poisoning can result in fluid and electrolyte imbalances:

Dehydration may occur due to increased gastrointestinal losses (vomiting) and insensible fluid losses (hyperpnea and hyperthermia).
Hypokalemia and hypocalcemia can result from primary respiratory alkalosis.

Central Nervous System Effects of Salicylate Poisoning

The central nervous system (CNS) is affected in various ways:

Neurotoxic effects may include tinnitus and hearing loss. The extent of CNS toxicity correlates with the amount of salicylate bound to CNS tissue.
Initial symptoms such as nausea, vomiting, hyperpnea, and lethargy can progress to disorientation, seizures, cerebral edema, hyperthermia, coma, and ultimately, death.

Gastrointestinal Tract Effects of Salicylate Poisoning

Salicylate poisoning has gastrointestinal effects:

Nausea and vomiting are the most common symptoms.
Large doses can lead to pylorospasm and decreased gastrointestinal motility.

Hepatic Effects of Salicylate Poisoning

Hepatitis can occur in children ingesting doses at or above 30.9 mg/dL, potentially leading to Reye syndrome.

Hematologic Effects of Salicylate Poisoning

The hematologic effects of salicylate poisoning include:

Hypoprothrombinemia and platelet dysfunction.
Bleeding may be promoted by inhibition of vitamin K–dependent enzymes or by the formation of thromboxane A2.

Musculoskeletal Effects of Salicylate Poisoning

Rhabdomyolysis can occur due to the dissipation of heat and energy resulting from uncoupling of oxidative phosphorylation.

Clinical and Laboratory Manifestations of Salicylate Poisoning

Salicylate toxicity is divided into phases:

Phase 1: Hyperventilation, respiratory alkalosis, compensatory alkaluria, potassium, and sodium bicarbonate excretion in urine. This phase can last up to 12 hours.
Phase 2: Paradoxic aciduria with continued respiratory alkalosis, occurring when enough kidney potassium has been lost. This phase may begin within hours and last 12-24 hours.
Phase 3: Dehydration, hypokalemia, and progressive metabolic acidosis. This phase can start 4-6 hours after ingestion in infants or 24 hours or more after ingestion in adolescents.

Early signs and symptoms of salicylate toxicity include nausea, vomiting, diaphoresis, and tinnitus. Other early effects encompass vertigo, hyperventilation, hyperactivity, agitation, delirium, hallucination, convulsion, lethargy, and stupor. Severe toxicity is indicated by hyperthermia.

History of Salicylate Poisoning

When possible, gather the following information:

Type of salicylate
Amount ingested
Approximate time of ingestion
Possibility of long-term ingestion
Co-ingestants that may be present
Presence of other medical conditions (e.g., cardiac, renal diseases)

Treatment should not be delayed in symptomatic patients awaiting serum level tests. Tinnitus can be indicative of salicylate ingestion. Monitoring vital signs can reveal tachypnea, tachycardia, and elevated temperature.

Bedside ferric chloride testing involves adding a few drops of 10% FeCl3 to 1 mL of urine. Presence of salicylates causes the solution to change to a brown-purple color.

Arterial Blood Gas (ABG) should be obtained to evaluate mixed acid-base disturbances.

Initial and serial salicylate levels should be measured. The therapeutic range of salicylate is 15-30 mg/dL. Levels above 40-50 mg/dL are symptomatic, and levels equal to or greater than 100 mg/dL usually indicate serious or life-threatening toxicity.

Salicylate Serum Monitoring

In cases of overdose, the peak serum concentration may not occur for 4-6 hours. Concentrations obtained before that time may not accurately reflect peak levels.
Signs and symptoms of toxicity typically appear at levels >30 mg/dL.
A 6-hour salicylate level exceeding 100 mg/dL is considered potentially lethal and warrants hemodialysis.

Frequency of Serum Salicylate Level Monitoring

Serum salicylate levels should be monitored at least every 2 hours until the peak concentration is reached, and then every 4-6 hours until the peak falls into the nontoxic range.

Other Laboratory Studies

Electrolytes (E/U/Cr)
Serum Calcium
Serum glucose levels
Serum acetaminophen levels
Liver function tests
Prothrombin Time (PT) and Partial Thromboplastin Time (PTTK)
Urinalysis – including urine pH and specific gravity

Principles of Treatment

Principles of treatment for salicylate poisoning include:

Limiting absorption
Enhancing elimination
Correcting metabolic abnormalities
Providing supportive care

No specific antidote is available for salicylates. Assessment of serum salicylate levels is not a reliable substitute for clinical evaluation.

When determining treatment options, the decision should be individualized based on the patient's clinical condition and not solely on a specific salicylate level.

Gastrointestinal Tract Decontamination

Initial treatment strategies include:

Use of oral activated charcoal, particularly within 1 hour of ingestion. Gastric lavage may be recommended in symptomatic patients, regardless of ingestion time.
Activated charcoal binds to salicylates, limiting further gut absorption. The initial dose is 1-2 g/kg of body weight, which can be repeated to enhance elimination.
Discontinuation of multiple doses of activated charcoal may be determined based on the passage of stool with charcoal and resolution of symptoms.
Whole bowel irrigation (WBI) using polyethylene glycol has been compared to single-dose activated charcoal for salicylate absorption in volunteer subjects who ingested enteric-coated aspirin.

Other Measures

Additional measures in the treatment of salicylate poisoning include:

Rehydration and correction of electrolyte abnormalities

Urinary Alkalization

Urinary alkalization involves:

Increasing urine pH to 7.5 to prevent salicylic acid reabsorption from urine.
Concomitant alkalinization of blood and urine to prevent salicylates from entering brain tissue and enhance urinary excretion.
Raising urine pH from 5 to 8 can increase renal clearance of salicylate by 10-20 times.
Adequate serum potassium levels are crucial for successful urinary alkalinization.

Hemodialysis

Hemodialysis is indicated when rapid salicylate elimination is necessary:

In severely ill patients with salicylate poisoning
If salicylate levels are very high (>90-100 mg/dL after acute overdose or >40-50 mg/dL in long-term toxicity)
In cases of severe fluid or electrolyte disturbances
If the patient is unable to eliminate the salicylate

Iron poisoning is a significant concern, especially in children. Iron-containing products are commonly found in households and can be mistaken for candy.

The severity of exposure to iron is determined by the amount of elemental iron ingested. Many vitamin products that contain iron specify the amount of elemental iron on the label.

Different formulations of iron contain varying percentages of elemental iron:

Ferrous sulfate: 20%
Ferrous gluconate: 12%
Ferrous fumarate: 33%
Ferrous lactate: 19%
Ferrous chloride: 28%

Pathophysiology

Iron poisoning can occur with toxic doses ranging from 20 mg/kg to over 60 mg/kg.

Iron has both local and systemic effects, as it is corrosive to the gastrointestinal (GI) mucosa and affects the lungs and liver.

Excessive free iron acts as a mitochondrial toxin, disrupting energy metabolism.

The pathophysiology of iron poisoning involves metabolic acidosis and its impact on multiple organ systems:

Phase 1: Within the first 6 hours after ingestion, characterized by hemorrhagic vomiting, diarrhea, and abdominal pain. This phase is due to the corrosive effects of iron on the GI mucosa.
Phase 2: Occurs 6-12 hours after ingestion, often showing symptom improvement with supportive care provided during phase 1.
Phase 3: Starting after 12-24 hours, involves multisystem damage. It includes metabolic acidosis, coagulopathy, shock, seizures, and altered mental status due to mitochondrial damage and hepatocellular injury.
Phase 4: Takes place 2-6 weeks after ingestion. It is characterized by late scarring of the GI tract causing issues like pyloric obstruction or hepatic cirrhosis.

Investigations

Clinical Diagnosis: Diagnosis is primarily based on clinical presentation.
Iron Levels: Obtain serum iron levels approximately 4 hours after ingestion.
Serum Iron Levels: These levels often correlate with clinical severity:

Mild: <300 mg/dL
Moderate: 300-500 mg/dL
Severe: >500 mg/dL

Toxic Effects: Toxic effects may occur at doses of 10-20 mg/kg elemental iron.
Calculation of Ingested Iron: For example, to calculate iron ingestion for a 10-kg child who took ten 320-mg tablets of ferrous gluconate:

10 tablets X 320 mg (12% elemental iron per tablet) = 10 X 38.4 mg elemental iron per tablet = 384 mg/10 kg = 38.4 mg/kg

PCV: Packed cell volume (hematocrit) should be measured.
Electrolytes and Creatinine (EU/CR): These tests provide information about kidney function and electrolyte imbalances.
Arterial Blood Gas (ABG): ABG analysis evaluates acid-base disturbances.
Serum Glucose: Glucose levels should be monitored.
Liver Function Tests (LFT): Assess liver function to monitor any potential hepatic involvement.
Prothrombin Time/Partial Thromboplastin Time (PT/PTTK): Coagulation parameters are important to evaluate.

Diagnostic Imaging

Plain Abdominal X-ray: This radiographic examination can confirm iron ingestion as iron is radiopaque. A negative result doesn't rule out iron ingestion since only undissolved tablets may be visible.

Treatment

The first step in treating acute iron overdose involves providing appropriate supportive care with a focus on fluid balance and cardiovascular stabilization. Additionally:

Ipecac-Induced Emesis: This is recommended within 2 hours after ingestion if the patient hasn't vomited spontaneously.
Gastric Lavage: Not recommended due to iron tablets' size and stickiness in gastric fluid.
Whole Bowel Irrigation: Used to accelerate passage of undissolved iron tablets through the GI tract. Administer a polyethylene glycol electrolyte solution orally or via NG tube at specified rates.
Deferoxamine: Iron-chelating agent used to bind absorbed iron. Excreted in urine. Administered via continuous infusion at a standard dose of 15 mg/kg/h.

Continuously monitor and manage the patient throughout treatment.

Indications for Chelation Therapy

Shock
Altered Mental Status
Persistent GI Symptoms
Metabolic Acidosis
Pills Visible on Radiographs
Serum Iron Greater than 500 mcg/dL
Estimated Dose Greater than 60 mg Elemental Iron per Kilogram

Complications:

Infectious - Yersinia enterocolitica Septicemia
Pulmonary - Acute Respiratory Distress Syndrome (ARDS)
Gastrointestinal - Fulminant Hepatic Failure, Hepatic Cirrhosis, Pyloric or Duodenal Stenosis

Prognosis:

If a patient does not develop symptoms of iron toxicity within 6 hours of ingestion, iron toxicity is unlikely to develop.
Expect clinical toxicity following an ingestion of 20 mg/kg of elemental iron.
Expect systemic toxicity with an ingestion of 60 mg/kg.
Ingestion of more than 250 mg/kg of elemental iron is potentially lethal.

Preventive Measures:

Keep bottles of iron supplements with childproof tops inaccessible to children.

Acetaminophen is the most widely used analgesic and the most commonly used drug in pediatrics. It is available in various formulations, including liquid, tablet, capsule, and suppository.

Causes: The maximum daily dose of acetaminophen is 4 g in adults and 90 mg/kg in children. A single ingestion of 7.5 g in an adult or more than 150 mg/kg in a child is a potentially toxic dose of acetaminophen (APAP).

Pathophysiology:

Acetaminophen is rapidly absorbed in therapeutic doses, with peak levels in 1-2 hours and 2-4 hours in the overdose setting. Therapeutic levels range from 10-20 mcg/mL. The metabolism is primarily hepatic, with a half-life of 2-4 hours.

Hepatic metabolism of acetaminophen leads to the formation of a toxic metabolite, N-acetyl-benzoquinoneimine (NAPQI). The liver metabolizes more than 90% of acetaminophen to glucuronide and sulfate conjugates, which are eliminated in the urine.

In children, sulfation is the primary pathway until age 10-12 years; glucuronidation predominates in adolescents and adults. Only a small amount of acetaminophen (2%) is excreted unchanged by the kidney.

Hepatotoxicity is the result of the formation of the reactive and toxic metabolite NAPQI by the cytochrome P-450 system. Glutathione can bind NAPQI and lead to the excretion of nontoxic mercapturate conjugates. As glutathione stores are diminished, NAPQI is not detoxified and covalently binds to the lipid bilayer of hepatocytes causing centrilobular necrosis.

History:

The disease presentation is in four phases:

Phase 1: The first phase lasts up to 24 hours.
- Symptoms include anorexia, nausea, and vomiting; some have no initial symptoms.
- Physical findings are nonspecific and include pallor, malaise, vomiting, and diaphoresis. Presence of neurologic, respiratory, and cardiac symptoms is rare in this phase.
Phase 2: Occurs 24-48 hours post-ingestion.
- Patients present with right upper quadrant pain and tenderness that coincides with transaminase elevation.
- Tachycardia and hypotension may occur with volume loss.
Phase 3: Occurs 3-4 days post-ingestion.
- Symptoms of hepatic failure with jaundice, bleeding, or encephalopathy.
- Physical findings include jaundice, gastrointestinal bleeding, abdominal pain, and encephalopathy.
- Only about 3.5% of patients who develop hepatotoxicity eventually develop fulminant hepatic failure. Death may occur due to cerebral edema or toxicity.
Phase 4: Occurs 4-14 days post-ingestion.
- Depending on the extent of damage, patients may have complete recovery of liver function or death.

Investigations:

APAP serum concentration
Liver function tests
E, U, and Cr (Electrolytes, Urea, and Creatinine)

Medical Treatment:

Gastric Lavage: Administer within 60 minutes post-ingestion
Gastrointestinal Decontamination: Consider activated charcoal decontamination in any patient who presents within 4 hours of ingestion
NAC (N-Acetylcysteine):

The antidote is NAC.

NAC is converted to cysteine, which can replenish glutathione stores. NAC also directly detoxifies NAPQI to nontoxic metabolites. NAC can provide a substrate for sulfation, thereby increasing the capacity for nontoxic metabolism. NAC can directly conjugate NAPQI to reduce toxicity.

Organophosphates and carbamates are the most frequently used insecticides worldwide.

They account for 80% of the reported toxic exposures to insecticides.

Pathogenesis:

Both organophosphates and carbamates bind to cholinesterase enzymes, preventing the degradation of acetylcholine, resulting in its accumulation at nerve synapses.
Enzymes affected include acetylcholinesterase or red blood cell cholinesterase, pseudocholinesterase (found in plasma), and neurotoxic esterase (found in the nervous system).
Cholinesterases rapidly hydrolyze acetylcholine into inactive fragments.
Acetylcholine is found in:
- Sympathetic and parasympathetic ganglia
- In the terminal nerve endings of postganglionic parasympathetic nerves at the motor endplates of nerves in the skeletal muscle.
Failure of inactivation of acetylcholine leads to its accumulation at the synapse, resulting in overstimulation and disruption of nerve impulses.
Skeletal muscle depolarization and fasciculations occur secondary to nicotinic stimulation at the motor endplate.
If left untreated, organophosphates form a permanent bond to these enzymes, inactivating them. This process, called aging, occurs over the 2-3 days after exposure. Weeks to months are required for the body to regenerate inactivated enzymes. In contrast, carbamates form a temporary bond to the enzymes, allowing regeneration of the enzymes over several hours.
Muscarinic effects occur at the postganglionic parasympathetic synapses, causing smooth-muscle contractions in various organs including the GI tract, bladder, and secretory glands.
Conduction can be delayed in the sinus and atrioventricular (AV) nodes.
Acetylcholine receptors are widely dispersed throughout the CNS.
Stimulation of these receptors causes a wide range of effects, including stimulation, seizures, confusion, ataxia, coma, and respiratory or cardiovascular depression.
Organophosphates are highly lipid soluble and are well absorbed from the skin, mucous membranes, conjunctiva, GI system, and respiratory system.

History

Exposure can occur via ingestion, dermal exposure, or inhalation.
Children often ingest home pesticides found in unmarked or poorly stored containers.
Children can also be exposed while playing in areas recently treated with organophosphate compounds.
Most symptoms appear within 12-24 hours of exposure.
A history of possible exposure combined with physical signs and symptoms consistent with exposure often lead to the diagnosis.

Physical Examination:

Findings vary according to:

the route of exposure,
the age of the patient, and
the specific chemical.

Muscarinic Findings:

Salivation, lacrimation, urination, defecation, and/or diarrhea (SLUD)
Wheezing and/or bronchoconstriction
Pulmonary edema
Increased pulmonary and oropharyngeal secretions
Sweating
Bradycardia
Abdominal cramping and intestinal hypermotility
Miosis

Nicotinic Findings:

Muscle fasciculations (twitching)
Fatigue
Paralysis
Respiratory muscle weakness
Diminished respiratory effort
Tachycardia
Hypertension

CNS Findings:

Anxiety
Restlessness
Confusion
Headache
Slurred speech
Ataxia
Seizures
Coma
Central respiratory paralysis
Altered level of consciousness and/or hypotonia

Prehospital Presentation:

Ensure ABC (Airway, Breathing, Circulation) of resuscitation
Decontamination by removing all clothing and washing with water and soap
Bring clothing and insecticide container to hospital

At the Hospital:

Ensure ABC (Airway, Breathing, Circulation) of resuscitation
Remove clothing to discontinue skin exposure
Gastric decontamination with activated charcoal for cases of oral ingestion
Anticholinergic therapy: Atropine antagonizes central and muscarinic effects by blocking these receptors (not nicotinic receptors)
Administer Atropine at a dose of 0.05 mg/kg until atropinization is achieved
Pralidoxime (2-PAM): Cholinesterase reactivator and antidote for organophosphate poisoning
Primarily affects nicotinic receptors and does not reverse CNS effects
Administer 2-PAM at a dose of 50 mg/kg
Use benzodiazepines for seizures
Provide supportive therapy

Hydrocarbons are easily accessible in products such as gasoline, turpentine, furniture polish, household cleansers, propellants, kerosene, and other fuels
The toxic potential of hydrocarbons is directly related to their physical properties.
Viscosity refers to the compound's resistance to flow; as the viscosity increases, the aspiration potential decreases.
Volatility refers to the compound's ability to vaporize. Highly volatile compounds with low viscosity are more likely to be inhaled or aspirated into the respiratory system.
Compounds with low viscosity, such as mineral spirits, naphtha, kerosene, gasoline, and lamp oil, spread rapidly across surfaces and cover large areas of the lungs when aspirated.
A number of volatile hydrocarbons, including toluene, propellants, refrigerants, and volatile nitrites, are commonly abused by inhalation.

Pulmonary Effects

Due to hydrocarbon aspiration: The lower the viscosity and higher the volatility, the greater the risk of pulmonary aspiration.
Mechanism: The hydrophobic nature of hydrocarbons allows them to penetrate deep into the tracheobronchial tree, producing inflammation and bronchospasm.
The volatile chemical may displace alveolar oxygen, leading to hypoxia.
Direct contact with alveolar membranes can lead to hemorrhage, hyperemia, edema, surfactant inactivation, leukocyte infiltration, and vascular thrombosis.
Overall result is poor oxygen exchange, atelectasis, and pneumonitis.
Respiratory findings include coughing, choking, fever, tachypnea, grunting, cyanosis, rales, and wheezing.
Respiratory symptoms generally begin in the first few hours after exposure and usually resolve in 2-8 days.
Complications include hypoxia, and acute respiratory distress syndrome (ARDS). Prolonged hypoxia may result in encephalopathy, seizures, and death.

Gastrointestinal Effects

Local irritation is the usual GI manifestation of hydrocarbon ingestion.
Abdominal pain and nausea are common.
Vomiting increases the likelihood of pulmonary aspiration.

CNS Findings

Headache
Dizziness
Lethargy
Ataxia
Seizures
Coma

Cardiac Findings

Dysrhythmias

Investigations

Respiratory symptoms may remain mild or rapidly progress to respiratory failure.
Fever occurs and may persist for up to 10 days after aspiration.
Accompanying leukocytosis may be misleading because, in most cases of aspiration pneumonitis, no bacteria are present in the lungs.
Chest radiographs may be normal for as long as 8-12 hours after aspiration. Pneumatoceles may appear on the chest radiograph 2-3 weeks after exposure.

Medical Care

Airway, breathing, and circulation: Stabilization of the airway is the top priority of treatment.
Provide supplemental oxygen to all patients and perform bedside pulse oximetry.
Early intubation, mechanical ventilation, and the use of positive end-expiratory pressure may be necessary.
Decontaminate the skin promptly by removing involved clothing and thoroughly washing the skin with soap and water. Vapor inhalation and cutaneous absorption can continue long after exposure.
Avoid the use of corticosteroids, as they are ineffective and may be harmful.
Do not administer prophylactic antibiotics, as bacterial pneumonia occurs in only a very small percentage of cases.
Do not induce emesis after ingestion of a low-viscosity hydrocarbon (e.g., gasoline, kerosene, furniture polish, mineral spirits) due to the high risk of aspiration.
Gastric lavage is also contraindicated in these cases.
Reserve the use of gastric decontamination for cases of large intentional ingestions or those involving an increased risk of systemic toxicity.
Remember the mnemonic "CHAMP" for hydrocarbons that should not induce emesis or undergo gastric lavage: camphor, halogenated hydrocarbons, aromatic hydrocarbons, (heavy) metal-containing hydrocarbons, and pesticide-containing hydrocarbons.

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