eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Hydrocarbon Inhalation Injury: Treatment & Medication

Author: Jason M Kane, MD, FAAP, Assistant Professor of Pediatrics, Northwestern University Feinberg School of Medicine; Attending Physician, Department of Pediatrics, Section of Pediatric Critical Care and Cardiac Intensive Care, Children's Memorial Hospital
Coauthor(s): Emily B Nazarian, MD, Fellow, Department of Pediatrics, Division of Critical Care, University of Rochester Medical Center; Heidi Connolly, MD, Associate Professor of Pediatrics and Psychiatry, University of Rochester; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Contributor Information and Disclosures

Updated: Jun 25, 2008

Treatment

Medical Care

The care of patients with inhalation abuse is mainly supportive. Because many potential complications involving the pulmonary, cardiovascular, and neurologic systems may be present, careful assessment and stabilization of the ABCs should be paramount in the initial management. In addition to acute medical treatment, patients suspected of chronic solvent-inhalant use should be carefully evaluated by a team trained in the treatment of childhood substance abuse.

  • Acute inhalant abuse
    • Medical care of patients following acute decompensation from hydrocarbon inhalation is primarily supportive. Those with significant neurologic impairment who are unable to protect their airway should undergo endotracheal intubation and mechanical ventilation to prevent aspiration and respiratory deterioration. Hypoxic injury to other organ systems, particularly the heart, should be sought and treated.
    • Because of the sensitization of the myocardium to catecholamines, inotropic agents and bronchodilators should be avoided. Some authors suggest the use of amiodarone to treat ventricular arrhythmias if used early in treatment. Epinephrine administration during resuscitation may be harmful and can lead to recurrence of ventricular fibrillation.
    • Electrolyte abnormalities should be corrected.
  • Chronic inhalant abuse
    • Management of chronic solvent-inhalant abuse should be directed at preventing further abuse.
    • Therapy for commonly involved organs, including the central and peripheral nervous systems, kidneys, liver, lungs, heart, and bone marrow, is primarily supportive.
    • In patients with significant electrolyte abnormalities, typically due to distal renal tubular acidosis, parenteral fluid and electrolyte repletion may be necessary. Correction of potassium and phosphorus deficiency may result in rapid improvement in muscle strength. Hypocalcemia is frequently encountered during fluid and electrolyte repletion.

Consultations

Patients who are suspected of solvent-inhalant abuse should be carefully evaluated by experts who are trained in the treatment of childhood substance abuse. Consultation with specialists, including cardiologists and neurologists, may also be warranted, depending on the individual needs of the patient. Any patient who has unstable hemodynamics or cardiac arrhythmias or who has significantly altered mental status should be admitted to and observed in the pediatric intensive care unit.

Diet

Patients should remain on a diet of nothing by mouth (NPO) until muscle weakness clearly will not necessitate institution of mechanical ventilation. Also, because of the risk of hypocalcemic seizures, patients should remain NPO during initial fluid and electrolyte repletion.

Medication

Electrolyte replacement agents

These agents are used to correct hypokalemia and hypophosphatemia in inhalation cases. Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish osmotic equilibrium of specific ions.


Potassium phosphate (Neutra-Phos-K, K-Phos)

Preferable to potassium chloride because it allows for correction of both hypokalemia and hypophosphatemia. Contains 4.4 mEq of potassium per 3 mmol of phosphate. Elemental phosphorus equals 31.25 mg/mmol. Should be ordered in millimols of phosphorus, not milliequivalents of potassium, to avoid confusion as to the phosphorus content.

Adult

3-4.5 g (95-142.4 mmol) per d PO divided tid/qid
Alternatively, 1.5-2 g (47.5-63.3 mmol) IV over 24 h

Pediatric

0.08-0.24 mmol/kg IV infused over 4-6 h; reassess phosphorus level before additional doses

Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin

Hyperkalemia; renal failure; conditions in which potassium retention is present; oliguria or azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Do not rapidly infuse because rapid or central IV infusion may cause cardiac arrhythmias; high plasma concentrations of potassium may cause death because of cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; patients receiving infusions >0.5 mEq (potassium) per kg/h (>20 mEq/h) should be on an ECG monitor; when a concentration >40 mEq (potassium) per L is infused, local pain and phlebitis may also follow; do not co-infuse with calcium-containing products


Calcium gluconate

Patients with hypocalcemia may need replacement, particularly in the presence of carpopedal spasm or hypocalcemic seizures. One gram of calcium gluconate equals 90 mg of elemental calcium.

Adult

5-15 g/d PO/IV divided q6h

Pediatric

Infants: 400-800 mg/kg/d PO divided q6h; alternatively, 200-500 mg/kg/24 h IV divided q6h
Children: 200-500 mg/kg/d PO/IV divided q6h

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity; IV push

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not exceed 100 mg/min IV if undiluted; for diluted IV infusion, do not exceed 120-240 mg/kg/h, with a maximum concentration of 50 mg/mL; do not administer IM or SC; avoid scalp veins; watch peripheral infusion because extravasation may cause tissue necrosis; IV infusion may be associated with hypotension and bradycardia; in digitalized patients, may be associated with arrhythmias

Anticonvulsants and sedatives

These agents are used for withdrawal symptoms or seizure activity in inhalation cases.


Phenobarbital (Luminal, Solfoton)

Most helpful if withdrawal symptoms are evident. Can be continued for sedation for 5-10 d. Therapeutic level is 15-40 mg/L.

Adult

Seizures:
Loading dose: 15-20 mg/kg IV, start with 10 mg/kg and follow with the subsequent 10 mg/kg if needed; not to exceed 20 mg/kg
Maintenance dose: 60-200 mg/d PO/IV divided bid/tid
Sedation: 30-120 mg/d PO/IV divided bid/tid

Pediatric

Seizures:
Loading dose for neonates, infants, or children: 5-20 mg/kg/dose IV in a single or divided dose; may administer an additional 5 mg/kg/dose q15-30 min; not to exceed a cumulative dose of 30 mg/kg for seizure activity
Maintenance dose (monitor levels):
Neonates: 3-5 mg/kg/d PO/IV qd or divided bid
Infants: 5-6 mg/kg/d PO/IV qd or divided bid
Children 1-5 years: 6-8 mg/kg/d PO/IV qd or divided bid
Children 6-12 years: 4-6 mg/kg/d PO/IV qd or divided bid
>12 years: 1-3 mg/kg/d PO/IV qd or divided bid
Sedation of children: 6 mg/kg/d PO divided tid

CYP450 inducer; may decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of PO contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis; porphyria

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

IV push not to exceed 1 mg/kg/min or 100 mg/min; IV administration may cause respiratory arrest and hypotension or paradoxical reactions in children (eg, hyperactivity, irritability, insomnia); caution in hepatic or renal disease; adverse effects include drowsiness, cognitive impairment, ataxia, hypotension, hepatitis, rash, respiratory depression, apnea, megaloblastic anemia, and anticonvulsant hypersensitivity syndrome


Diazepam (Valium)

Used for sedation if withdrawal symptoms present. Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.

Adult

2-10 mg/dose PO q6-12h prn
2-10 mg/dose IV/IM prn; not to exceed 30 mg/8 h

Pediatric

0.12-0.8 mg/kg/d PO divided q6-8h
0.04-0.2 mg/kg/dose IV/IM q2-4h prn; not to exceed 0.6 mg/kg within an 8-h period

CNS toxicity increased with coadministration of other CNS depressants (eg, phenothiazines, barbiturates, alcohol, MAOIs)

Documented hypersensitivity; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Hypotension and respiratory depression may occur; use with caution in glaucoma, shock, and depression; administer the conventional IV product undiluted no faster than 2 mg/min; do not mix with IV fluids


Phenytoin (Dilantin)

May act in motor cortex where may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited. Dose should be individualized. Administer larger dose before retiring if dose cannot be divided equally. Therapeutic level is 10-20 mg/L.

Adult

100 mg/dose PO/IV q8h initially and carefully titrate to 300-600 mg/d (or 6-7 mg/kg/d) divided q8-24h

Pediatric

Loading dose: 15-20 mg/kg IV; not to exceed 1500 mg/d
Maintenance dose: 5 mg/kg/d PO/IV divided q8-12h initially
Divide daily doses bid/tid unless extended cap
Typical dosage ranges:
Neonates: 5-8 mg/kg/d
6 months to 3 years: 8-10 mg/kg/d
4-6 years: 7.5-9 mg/kg/d
7-9 years: 7-8 mg/kg/d
10-16 years: 6-7 mg/kg/d

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; CYP450 inducer; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, PO contraceptives, and valproic acid

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform CBC counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction occurs


Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Important to monitor patient's blood pressure after administering dose. Adjust as necessary.

Adult

4 mg/dose IV slowly over 2-5 min and repeat in 10-15 min prn; cumulative dose of 8 mg/d typically considered maximum
1-10 mg/d PO/IV/IM divided bid/tid

Pediatric

Infants and children: 0.1 mg/kg IV slowly over 2-5 min; may repeat with dose of 0.05 mg/kg in 10-15 min if needed; not to exceed 4 mg/dose
Adolescents: 0.07 mg/kg IV slowly over 2-5 min and repeat in 10-15 min prn; not to exceed 4 mg/dose

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma; reversal agents (eg, flumazenil) contraindicated when lorazepam used for life-threatening conditions (eg, control of intracranial pressure or status epilepticus)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Antiarrhythmic agents

These agents may be required to treat tachycardias.


Amiodarone (Cordarone)

Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.
Has low risk of proarrhythmia effects, and any proarrhythmic reactions are generally delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Before administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
PO efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta blockade and initial therapy with other agents.

Adult

Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk, and decrease to 600-800 mg/d in 1-2 doses for 1 mo Maintenance dose: 400 mg/d PO Alternatively, 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h and, then, 540 mg over next 18 h

Pediatric

10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until arrhythmia controlled

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by macrolide antibiotics, ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers, may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism resulting in increased serum levels and may prolong QT interval; coadministration may increase myopathy/rhabdomyolysis risk; associated with HMG-CoA reductase inhibitors (eg, simvastatin); other drugs that prolong the QT interval (eg, fluoroquinolones, erythromycin, dofetilide, tricyclic antidepressants, thioridazine) may increase life-threatening arrhythmia risk

Documented hypersensitivity, complete AV block, and intraventricular conduction defects

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Known to cause serious (and at times fatal) toxicities, including pulmonary and liver toxicities; may cause prolonged proarrhythmic effects; may cause optic neuritis/neuropathy or hypothyroidism or hyperthyroidism; CNS and GI toxicity may occur and typically dissipates with dose reduction

More on Hydrocarbon Inhalation Injury

Overview: Hydrocarbon Inhalation Injury
Differential Diagnoses & Workup: Hydrocarbon Inhalation Injury
Treatment & Medication: Hydrocarbon Inhalation Injury
Follow-up: Hydrocarbon Inhalation Injury
References
Further Reading

References

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  3. Jones HE, Balster RL. Inhalant abuse in pregnancy. Obstet Gynecol Clin North Am. Mar 1998;25(1):153-67. [Medline].

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  5. LoVecchio F, Fulton SE. Ventricular fibrillation following inhalation of Glade Air Freshener. Eur J Emerg Med. Jun 2001;8(2):153-4. [Medline].

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  7. El-Menyar AA, El-Tawil M, Al Suwaidi J. A teenager with angiographically normal epicardial coronary arteries and acute myocardial infarction after butane inhalation. Eur J Emerg Med. Jun 2005;12(3):137-41. [Medline].

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Further Reading

National Institute on Drug Abuse. NIDA Research Report - Inhalant Abuse. National Institutes of Health. Available at http://www.nida.nih.gov/researchreports/inhalants/Inhalants.html

Keywords

hydrocarbon inhalation injury, volatile substance abuse, inhalant abuse, solvent abuse, sniffing, huffing, bagging, solvent, butane, toluene, sudden cardiac events, sudden sniffing death syndrome, ventricular dysrhythmias, sudden death, myocardial infarction, renal tubular acidosis, hypokalemia, hyperchloremia, frostbite, bone marrow damage, aplastic anemia, leukemia, toxic hepatitis, pulmonary injury, microcephaly, narrow bifrontal diameter, short palpebral fissures, hypoplastic mid face, wide nasal bridge, abnormal palmar creases, blunt fingertips, pulmonary hypertension, hydrocarbon aspiration, Parkinson disease, attention deficit, rhabdomyolysis, rhinitis, nasal mucosal erosions, epistaxis, hoarse voice, conjunctivitis, hypophosphatemia, hypercalcemia

Contributor Information and Disclosures

Author

Jason M Kane, MD, FAAP, Assistant Professor of Pediatrics, Northwestern University Feinberg School of Medicine; Attending Physician, Department of Pediatrics, Section of Pediatric Critical Care and Cardiac Intensive Care, Children's Memorial Hospital
Jason M Kane, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Emily B Nazarian, MD, Fellow, Department of Pediatrics, Division of Critical Care, University of Rochester Medical Center
Emily B Nazarian, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Heidi Connolly, MD, Associate Professor of Pediatrics and Psychiatry, University of Rochester; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Girish D Sharma, MD, Associate Professor, Department of Pediatrics, Rush University Medical Center, Rush Children's Hospital; Director of Pediatric Pulmonary Section and Rush Cystic Fibrosis Center
Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Charles Callahan, DO, Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center
Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Associate Professor, Department of Clinical Pediatrics, State University of New York at Stony Brook
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD, Attending Physician, Pediatric Pulmonary Medicine, Columbia University Medical Center; Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Merck Honoraria Speaking and teaching

 
 
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