Ibuprofen fatal dose

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NCBI Bookshelf. Ibuprofen, 2- 4-isobutylphenyl propionic acid, belongs to the class of drugs called nonsteroidal anti-inflammatory drugs NSAIDs and was discovered by Dr. Stewart Adams in It was first marketed in in the United Kingdom and in the United States.

Ibuprofen is prescribed commonly as an analgesic, antipyretic and anti-inflammatory agent in conditions like osteoarthritis, rheumatoid arthritis, juvenile idiopathic arthritis, and acutely painful musculoskeletal conditions. Off-label uses include for conditions like cystic fibrosis to slow progression. This activity serves to review the basic pharmacological characteristics of ibuprofen, clinical presentations during an overdose, and management of ibuprofen toxicity.

Objectives: Describe the epidemiology of ibuprofen toxicity. Identify common history and physical exam findings in patients with ibuprofen. Summarize the treatment options for ibuprofen toxicity. Explain modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by ibuprofen toxicity. Access free multiple choice questions on this topic.

Ibuprofen, 2- 4-isobutylphenyl propionic acid, belongs to the class of nonsteroidal anti-inflammatory drugs NSAIDs and was discovered by Dr. An overdose of ibuprofen may be self-injurious, suicidal, or accidental. Young children may develop ibuprofen toxicity following exploratory ingestions. Ibuprofen is one of the most commonly used and prescribed medications in the world. The therapeutic effects of ibuprofen are mediated by reversible binding to COX receptors both COX-1 and COX-2 on prostaglandin synthase also called cyclooxygenase, COX , thereby preventing arachidonic acid from binding to these sites.

This prevents the conversion of arachidonic acid to the various prostaglandins that are instrumental in causing the 4 defining features of inflammation, namely redness rubor , heat calor , swelling tumor , and pain dolor. Prostaglandins also play a role in sensitizing pain-sensing nerve fibers, which explains the analgesic effect of ibuprofen and other NSAIDs. Ibuprofen also works on the thermoregulatory center of the hypothalamus to control fever. Adverse effects associated with chronic ibuprofen use stem from prostaglandins' important roles, and thromboxanes play in various organ systems, including maintaining gastric mucosal integrity and renal blood flow.

Ibuprofen can, therefore, cause dyspeptic symptoms and gastrointestinal GI ulcers even at therapeutic doses. In the kidneys, this can lead to decreased renal perfusion in the afferent renal vessels, especially in individuals with preexisting dehydration or renal impairment, thereby leading to reduced glomerular filtration rate GFR. Thromboxane A2, another substance produced by the COX enzyme, is vital for platelet aggregation and hence, coagulation.

The depletion of thromboxane A2 could, therefore, in theory, inhibit platelet aggregation and cause bleeding, especially in patients on anticoagulants or antiplatelets. There have been reports of metabolic acidosis after an acute overdose of ibuprofen and other NSAIDs, which may be explained by the accumulation of acidic metabolites in the blood. Ibuprofen is available as tablets with strengths ranging from to mg.

It is well absorbed orally, with peak plasma concentrations reached in 1 to 2 hours. The onset of action after oral ingestion is 30 to 60 minutes for analgesia. Ibuprofen is completely metabolized and eliminated in 24 hours. Important points to be noted in history include the amount of ibuprofen ingested, the time of ingestion, and any co-ingestants. In children, caregivers should be asked explicitly about acetaminophen ingestion, as it is commonly mistaken for ibuprofen. Most patients report no or mild symptoms following ibuprofen overdose. The COX-1 enzyme is found in the gastric mucosa and is instrumental in producing prostaglandins that regulate blood flow and bicarbonate production in the stomach.

Ibuprofen, being a nonselective inhibitor of COX, can disrupt the mucosal integrity of the gastric mucosa. Intramucosal hemorrhages occur within a few hours of ingestion in all NSAIDs [13] , especially with acidic ones like ibuprofen. These may progress to erosions with continued use but are typically reversible. In susceptible individuals, they may progress to peptic ulcer.

The severity of GI adverse effects can range from dyspepsia to life-threatening upper GI hemorrhage or viscus organ rupture. Symptoms include nausea, vomiting, dyspeptic symptoms, and abdominal pain. GI hemorrhage has been described in multiple case reports, particularly after large ingestions. Renal impairment has been described in individuals who had consumed therapeutic as well as supratherapeutic doses of ibuprofen. Normalization of creatinine occurred after 72 hours. One case report describes a year-old woman who presented comatose after ingesting 40 to 60 ibuprofen mg tablets.

The patient was unresponsive to verbal stimuli but responded to noxious stimuli. She was endotracheally intubated for airway protection. She developed renal failure and GI hemorrhage in the form of a guaiac positive stool test. After a day in the intensive care unit ICU , she clinically improved and was extubated with no further complications. His level of consciousness and other parameters improved with supportive management. Generalized seizures, depressed level of consciousness, and apnea have been reported in children by various authors after large ingestions.

High anion gap metabolic acidosis is the most common abnormality reported, which usually occurs after massive ingestions. Apnea from respiratory depression can result in a concomitant respiratory acidosis. Life-threatening hypokalemia has been reported secondary to renal tubular acidosis after ibuprofen overdose. Thrombocytopenia is common following ibuprofen overdose.

Pulmonary infiltrates with eosinophilia syndrome has been reported following ibuprofen overdose. Routine laboratory testing is unnecessary following an accidental overdose in asymptomatic patients, provided that a history of acetaminophen overdose be excluded by history. When acetaminophen overdose cannot be excluded, a serum acetaminophen level should be obtained. Assessment for co-ingestants like ethanol, toxic alcohols, and aspirin may be appropriate depending on patent presentation. Serum ibuprofen concentrations are typically not readily available in the acute care setting but may be obtained from reference laboratories if confirmation of ibuprofen exposure is necessary.

Management of an ibuprofen toxicity patient is primarily supportive. Most patients have no symptoms or mild GI symptoms that respond to symptomatic management. Asymptomatic patients with normal vital s and no acetaminophen poisoning may be observed for 4 to 6 hours to develop symptoms. Therapeutic interventions may include airway stabilization, mechanical ventilation, benzodiazepines for seizure control, intravenous fluids, and vasopressors to correct hypotension—monitor life-threatening arrhythmias, which can occur secondary to electrolyte imbalances like hypokalemia, with serial ECGs.

As ibuprofen is heavily protein-bound, hemodialysis cannot remove the drug, although the latter can be used for associated conditions like hyperkalemia or refractory metabolic acidosis. Ibuprofen overdose is rarely fatal although there have been cases of death from ibuprofen toxicity. Gastrointestinal blood loss following ibuprofen intake is dose-related. The more serious gastrointestinal effects are not common and include occult blood loss, GI hemorrhage, ulcer, and pancreatitis.

While some patients experience increases in liver enzymes, hepatic side effects, including cholestasis, jaundice, hepatitis, and hepatic failure, are rare. These are more likely in patients with impaired renal function. Other very rare complications include cardiovascular effects e. Managing ibuprofen overdose requires teamwork from healthcare professionals, including the emergency physician, intensivist, medical toxicologist or poison control center, pharmacist, and nursing staff. The emergency physician is responsible for the following:. The management of ibuprofen toxicity should continue after the patient is admitted to an appropriate level of care.

Patients should be admitted to an ICU level of care for respiratory depression, hypotension or shock, depressed mental status, severe metabolic acidosis, severe GI hemorrhage, life-threatening electrolyte imbalances or arrhythmias, or if the pd clinical course of the patient is predicted to worsen based on the dose of ibuprofen consumed. Symptomatic but otherwise stable patients may be admitted to a general medical floor. Asymptomatic patients may be observed for 4 to 6 hours in the emergency department. Consult with a mental health counselor or psychiatrist to assess self-harm risk and the potential need for psychiatric admission in intentional or self-injurious exposures.

These interprofessional interventions can drive better outcomes irrespective of the underlying cause of toxicity. This book is distributed under the terms of the Creative Commons Attribution 4. Turn recording back on. National Center for Biotechnology Information , U. StatPearls [Internet]. Search term. Affiliations 1 University of Nebraska Medical Center. Continuing Education Activity Ibuprofen, 2- 4-isobutylphenyl propionic acid, belongs to the class of drugs called nonsteroidal anti-inflammatory drugs NSAIDs and was discovered by Dr.

Introduction Ibuprofen, 2- 4-isobutylphenyl propionic acid, belongs to the class of nonsteroidal anti-inflammatory drugs NSAIDs and was discovered by Dr. Etiology An overdose of ibuprofen may be self-injurious, suicidal, or accidental.

Epidemiology Ibuprofen is one of the most commonly used and prescribed medications in the world. Pathophysiology The therapeutic effects of ibuprofen are mediated by reversible binding to COX receptors both COX-1 and COX-2 on prostaglandin synthase also called cyclooxygenase, COX , thereby preventing arachidonic acid from binding to these sites. Toxicokinetics Ibuprofen is available as tablets with strengths ranging from to mg. History and Physical Important points to be noted in history include the amount of ibuprofen ingested, the time of ingestion, and any co-ingestants.

Evaluation Routine laboratory testing is unnecessary following an accidental overdose in asymptomatic patients, provided that a history of acetaminophen overdose be excluded by history. Differential Diagnosis Abdominal pain in elderly persons. Prognosis Ibuprofen overdose is rarely fatal although there have been cases of death from ibuprofen toxicity.

Complications Complications can include both gastrointestinal problems as well as hepatic and renal damage. Enhancing Healthcare Team Outcomes Managing ibuprofen overdose requires teamwork from healthcare professionals, including the emergency physician, intensivist, medical toxicologist or poison control center, pharmacist, and nursing staff. The emergency physician is responsible for the following: A complete history of the substance ingested, any co-ingestion, time of ingestion, any suicidal intent behind the ingestion, and any similar history in the past.

Ordering initial labs, including acetaminophen levels, aspirin levels, blood gas, complete blood count CBC , renal and liver function tests, electrolytes, and blood sugar. If the patient is stable enough, obtaining a psychiatric history to assess the risk of self-harm. Consulting with nephrology if there is resistant metabolic acidosis, hyperkalemia, or renal failure to consider hemodialysis. Review Questions Access free multiple choice questions on this topic.

Comment on this article. References 1. Ann Am Thorac Soc. J Adolesc Health. Ibuprofen overdose: the first two years of over-the-counter sales. Hum Toxicol. Clin Toxicol Phila. Davies NM. Clinical pharmacokinetics of ibuprofen. The first 30 years. Clin Pharmacokinet.

Ibuprofen fatal dose

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Ibuprofen overdose