Ibuprofen and Diclofenac
Ibuprofen and Diclofenac belong to the group of non-steroidal anti-inflammatory drugs (NSAIDs), which are commonly used as pain relievers in human medicine. These substances have anti-inflammatory (antiphlogistic), pain-relieving (analgesic), and fever-reducing (antipyretic) effects. While they are relatively safe for humans at correct dosages, they can cause severe poisoning symptoms in dogs and cats even in small doses.
The most important facts at a glance
Ibuprofen and Diclofenac poisoning poses a serious threat to dogs and cats. These human pain relievers can cause severe poisoning symptoms even in small doses. The toxic effect is primarily based on the inhibition of prostaglandin synthesis, which can lead to damage to the gastrointestinal mucosa, kidneys, and in severe cases, metabolic derangements and neurological symptoms.
Symptoms typically develop within a few hours and range from vomiting and diarrhea to kidney dysfunction, seizures, and coma. Diagnosis is based on history, clinical examination, and laboratory diagnostic parameters.
Therapy includes decontamination, gastric protection, fluid therapy, and symptomatic measures. With early treatment, the prognosis is good; with existing organ damage, it ranges from cautious to unfavorable.
For prevention, safe storage of medications and educating pet owners about the dangers of human pain relievers are crucial. Pet owners should never administer human NSAIDs to their pets on their own and should immediately seek veterinary help if poisoning is suspected.
Causes, development and progression
Ibuprofen and diclofenac belong to the non-steroidal (not based on glucocorticoid action) anti-inflammatory drugs.
Non-steroidal anti-inflammatory drugs are abbreviated as NSAIDs (Non-Steroidal Anti-Inflammatory Drug).
NSAIDs inhibit the synthesis of prostaglandins, which are essential for inflammatory processes in the body.
Prostaglandins also influence pain transmission and perception.
In this way, they have anti-inflammatory (antiphlogistic), pain-relieving (analgesic), and fever-reducing (antipyretic) effects.
The most common cause of ibuprofen or diclofenac poisoning in pets is improper administration by the pet owner. Often, human pain medications are given under the assumption that they are as safe for animals as they are for humans. This self-medication can have fatal consequences.
Further causes include:
- Accidental ingestion of unsupervised medications left lying around
- Access to unsecured medicine cabinets
- Lack of awareness about the risks of human pain medications in animals
- Confusion with veterinary-approved NSAIDs
The toxic dose for dogs is already 8 mg/kg body weight per day for ibuprofen, which for a 10 kg dog corresponds to only a quarter of a typical 400 mg human tablet. In cats, a single dose of 50 mg/kg body weight can lead to poisoning symptoms. In the presence of pre-existing conditions, especially kidney insufficiency, the toxic threshold can be even lower.
Diclofenac has a similar toxicity profile and can cause severe damage even at low doses. Young animals, older animals, and animals with pre-existing kidney or liver diseases are particularly at risk.
Mechanism of action
The main mechanism of action of these substances is based on the inhibition of cyclooxygenase (COX), an enzyme responsible for the formation of prostaglandins. Prostaglandins play an important role in inflammatory processes, but also in protecting the gastric mucosa and maintaining kidney function. The inhibition of prostaglandin synthesis explains both the therapeutic and toxic effects of these medications.
In dogs and cats, the metabolism of these substances is significantly slower than in humans, leading to a longer retention time in the body and thus increased toxicity. Additionally, the organ systems of dogs and especially cats are more sensitive to the effects of these medications.
The mechanism of action in detail is primarily based locally and systemically (affecting the entire body) on the decrease in prostaglandin synthesis.
It is characterized by:
- Irritation of the mucous membranes in the gastrointestinal tract
- Loss of protective effect on the gastrointestinal tract (increased acid production and reduced mucus formation with prostaglandin decrease)
- Gastrointestinal bleeding due to direct damage and inhibition of blood clotting
- Development of metabolic acidosis
- Kidney damage due to decreased blood flow
Pharmacological Background – COX Inhibition
COX-1 and COX-2
Cyclooxygenase (COX) exists in two main forms:
- COX-1: constitutively expressed, responsible for “housekeeping” prostaglandins, e.g., mucosal protection, renal perfusion, platelet aggregation
- COX-2: inducible in inflammation → mediates pain, fever, inflammatory reactions
NSAIDs like ibuprofen and diclofenac inhibit both isoforms, especially in overdose. The undesirable effects in animals primarily result from the inhibition of COX-1 and thus the absence of protective prostaglandins in the stomach, kidneys, and CNS.
Mechanism of Action of Ibuprofen in Dogs and Cats
Gastrointestinal Tract
- Prostaglandins protect the gastric mucosa by stimulating mucus and bicarbonate secretion and regulating blood flow.
- COX inhibition creates an imbalance: increased stomach acid, reduced mucus protection → gastritis, ulcers, bleeding.
- Cats are particularly sensitive because they lack important glucuronidation mechanisms → delayed metabolism.
Kidneys
- Prostaglandins regulate renal blood flow, primarily under stress (e.g., dehydration).
- COX inhibition leads to renal vasoconstriction, which reduces renal blood flow and glomerular filtration rate (GFR) → acute kidney failure, especially in predisposed animals (older, dehydrated animals, heart patients).
Central Nervous System
- At high doses, ibuprofen can directly affect the CNS: seizures, ataxia, lethargy.
- Possible Cause: Imbalance of neurotransmitters or secondary effects due to metabolic acidosis.
Mechanism of Action of Diclofenac in Dogs and Cats
Diclofenac is similarly toxic but even more potent in its COX inhibition, leading to severe symptoms even at low doses.
Gastrointestinal Damage
- Very aggressive ulceration due to strong inhibition of protective prostaglandins.
- Hemorrhagic gastroenteritis is typical: bloody vomiting, tarry stools, abdominal pain.
Nephrotoxicity
- Pronounced renal dysfunction due to decreased GFR → increase in urea, creatinine, electrolyte disturbances (especially hyperkalemia), acidosis.
- Even single doses can trigger acute kidney failure in animals with impaired renal reserve (older animals, pre-existing conditions).
CNS Effects
- High diclofenac levels can lead to disturbances of consciousness, seizures, and loss of coordination.
- In combination with metabolic imbalances (acidosis, electrolyte disturbances), this can quickly become life-threatening.
Species-Specific Characteristics
Dog:
- Toxic dose for Ibuprofen: from approx. 25 mg/kg → first symptoms, from 100 mg/kg → potentially fatal.
- Diclofenac is already critical at 5–10 mg/kg.
- Common symptoms: vomiting, loss of appetite, lethargy, diarrhea, possibly CNS disturbances and circulatory problems.
Cat:
- Very low tolerance, as cats can hardly detoxify NSAIDs (missing UDP-glucuronosyltransferase).
- Toxic dose for Ibuprofen: already possible from 5–10 mg/kg!
- Diclofenac in any amount is potentially fatal.
- Symptoms often appear delayed but then severely: hypersalivation, inappetence, vomiting, hematemesis, apathy, kidney failure.
Summary of Mechanisms of Action
| Organ System | Mechanism of Action by Ibuprofen/Diclofenac | Consequences |
| Gastrointestinal Tract | COX-1 inhibition → ↓ mucus, ↑ acid secretion → mucosal damage | Ulcers, Hemorrhage, Perforation, Pain |
| Kidney | COX inhibition → ↓ prostaglandins → vasoconstriction of renal vessels | Acute Kidney Failure, Oliguria, Azotemia |
| Central Nervous System | indirect metabolic effects, also direct influence in case of overdose | Seizures, Ataxia, Coma |
| Blood Count | In very high doses: potentially hemolytic anemia or thrombocytopenia | Pale Mucous Membranes, Petechiae, Weakness |
Ibuprofen and Diclofenac are among the most common household poisons for dogs and cats. They lead to the suppression of vital prostaglandins through non-selective inhibition of cyclooxygenase. The result is multi-system poisoning focusing on the gastrointestinal tract, kidneys, and CNS. Cats, in particular, are extremely sensitive, as they can hardly metabolize these substances. Any ingestion is considered potentially toxic and requires immediate veterinary treatment.
Symptoms of intoxication
For dogs and cats, Ibuprofen and Diclofenac are toxic even at low doses.
They must not be used in dogs and cats!
In dogs, even 8 mg/kg/day, and in cats, a single dose of 50 mg/kg body weight, lead to poisoning symptoms.
The symptoms of poisoning with Ibuprofen or Diclofenac typically develop within 2–6 hours after ingestion and can be divided into different phases.
In the early phase, general symptoms first appear:
- Apathy and lethargy
- Impaired consciousness
- Restlessness or stupor
- Loss of appetite
As poisoning progresses, symptoms of the gastrointestinal tract dominate:
- Excessive salivation
- Abdominal pain (recognizable by a tense abdominal wall or expressions of pain upon touch)
- Vomiting, which can become bloody as poisoning progresses
- Diarrhea, which can also become bloody
- Dark, tarry stools (melena) as a sign of bleeding in the upper gastrointestinal tract
In severe cases or with advanced poisoning, the following symptoms may occur:
- Shallow, rapid breathing
- Increasing apathy up to lateral recumbency
- Increased body temperature (hyperthermia)
- Metabolic acidosis
- Seizures
- Coma
Additionally, signs of kidney damage may occur:
- Increased or decreased urination
- Dark or bloody urine
- Dehydration
In cats, symptoms can be particularly dramatic, as they metabolize NSAIDs even worse than dogs.
Diagnosis
The diagnosis of Ibuprofen or Diclofenac poisoning rests on several pillars:
History: A thorough history is crucial. Pet owners should be asked whether:
- there was access to pain relievers
- self-medication occurred
- empty medication packaging was found
- the time of possible ingestion is known
- the approximate amount of the ingested substance can be estimated
Clinical Examination: During the clinical examination, the above-mentioned symptoms are recorded and evaluated. Special attention is paid to:
- Vital parameters (heart rate, respiratory rate, body temperature)
- Mucous membrane color and capillary refill time
- Hydration status
- Neurological status
- Abdominal palpation
Laboratory Diagnostics: To confirm the diagnosis and assess the severity, the following laboratory tests are performed:
- Complete blood count (CBC) to detect anemia due to blood loss
- Blood chemistry with renal and hepatic parameters
- Electrolytes and acid-base status
- Coagulation parameters
- Urinalysis to detect blood or protein in the urine
Imaging Procedures: Ultrasound examinations can help detect changes in the stomach, intestines, kidneys, and liver. X-rays can provide indications of stomach contents or free fluid in the abdominal cavity.
Toxicological Detection: In specialized laboratories, direct detection of Ibuprofen or Diclofenac in blood or stomach contents is possible, but is rarely performed due to time constraints.
If NSAID poisoning is suspected, treatment should be started immediately, even if not all diagnostic results are available yet.
Therapeutic principles
Therapy should be initiated in dogs at a single intake of 10 mg/kg body weight.
If pre-existing renal insufficiency is known, therapy should be initiated at a single intake of 5 mg/kg body weight.
Prostaglandins promote kidney blood flow. A decrease in prostaglandin synthesis and the associated reduction in kidney blood flow can exacerbate an existing renal insufficiency.
Decontamination. In the case of sustained-release preparations, decontamination by vomiting, gastric lavage, and bowel lavage can still be helpful more than 5 hours after ingestion. Activated charcoal should be administered multiple times.
Misoprostol, a synthetically produced prostaglandin, is used as an antidote in dogs. Misoprostol reduces the stomach’s acid production.
There is little experience with the use of misoprostol in cats, so its use cannot be recommended.
Symptomatic therapy serves to stabilize vital functions and treat the animals’ complaints such as pain, vomiting, and seizures.
A continuous drip infusion, in addition to compensating for fluid loss, optimizes electrolyte concentrations and the acid-base balance in the blood. The acid-base balance is sustainably disturbed. In the advanced stage of intoxication, acidosis (metabolic acidosis) dominates.
Fluid replacement simultaneously supports cardiovascular and kidney function.
Therapy for ibuprofen or diclofenac poisoning should begin as early as possible and includes several approaches:
Decontamination: If ingestion occurred less than 2–3 hours ago, decontamination may be useful:
- Inducing vomiting (only in conscious animals and early presentation)
- Gastric lavage under anesthesia for larger quantities
- Administration of activated charcoal to bind unabsorbed substances (initially 1–4 g/kg body weight)
- Repeated administration of activated charcoal every 4–6 hours, as NSAIDs undergo enterohepatic circulation
- For sustained-release preparations, decontamination may still be useful even after more than 5 hours
Antidote: In dogs, misoprostol, a synthetic prostaglandin E1 analog, can be used as a partial antidote. It protects the gastric mucosa and can prevent ulcerations. The usual dosage is 2–5 μg/kg every 6–8 hours. There is little experience in cats, so its use cannot be generally recommended.
Gastric protection: For the prevention and treatment of gastrointestinal ulcerations, the following are used:
- Proton pump inhibitors such as omeprazole (0.5-1.0 mg/kg once daily)
- H2 receptor antagonists such as famotidine (0.5-1.0 mg/kg 1-2 times daily)
- Sucralfate as mucosal protection (0.5-1.0 g per animal 3-4 times daily)
Fluid therapy: Aggressive fluid therapy is crucial for:
- Maintaining kidney function by promoting diuresis
- Compensating for fluid loss due to vomiting and diarrhea
- Correcting electrolyte imbalances
- Correcting metabolic acidosis
Symptomatic therapy:
- Antiemetics for persistent vomiting (e.g., maropitant)
- Anticonvulsant medications for seizures
- Oxygen administration for respiratory distress
- Pain management with opioids (no NSAIDs!)
- In case of severe blood loss, a blood transfusion may be necessary
Treatment of complications:
- In case of kidney failure, dialysis may be considered
- For cerebral edema: elevate the head, osmotherapy, glucocorticoids
- For liver failure: liver protective therapy
Close monitoring of vital parameters, kidney function, and acid-base balance should be performed. Therapy often needs to be continued for several days, even if clinical symptoms are already subsiding.
In case of severe blood loss, a blood transfusion can be life-saving.
The development of cerebral edema is a severe complication and potentially life-threatening. Treatment options are limited and include elevating the body, osmotherapy, maximal stimulation of urine excretion, administration of special glucocorticoids, and sedatives.
Prognosis & follow-up care
The prognosis is very good with timely therapy. In advanced intoxications with existing kidney damage, the prognosis is rather cautious.
The prognosis of ibuprofen or diclofenac poisoning depends on several factors:
- Time of therapy initiation after ingestion
- Amount ingested
- General condition and pre-existing illnesses of the animal
- Severity of existing organ damage
With early therapy within the first 2–4 hours after ingestion and at low doses, the prognosis is generally good. In cases of existing kidney damage, severe gastrointestinal bleeding, or neurological symptoms, the prognosis is cautious to unfavorable.
Aftercare following acute poisoning includes:
Short-term aftercare:
- Regular monitoring of kidney and liver values (initially after 24–48 hours, then after 5–7 days)
- Continuation of gastric protection for 1–2 weeks
- Easily digestible, gentle diet
Long-term aftercare:
- In case of kidney damage: regular monitoring of kidney values over several months
- Diet adjustment for chronic kidney insufficiency
- Avoidance of nephrotoxic medications in the future
Preventive measures:
- Educating pet owners about the dangers of human NSAIDs
- Secure storage of medications out of reach of pets
- Use of child-resistant medicine cabinets
- Information on veterinary-approved alternatives for pain therapy
Full recovery can take weeks to months depending on the severity of the poisoning. Some animals may retain permanent damage, especially to the kidneys.
Research outlook
Research in the field of NSAID poisoning in small animals currently focuses on several promising approaches:
Improved Antidotes: Researchers are working on the development of more specific antidotes for NSAID poisoning. Substances are being investigated that can selectively neutralize the toxic effects without affecting the underlying disease.
Biomarkers for Early Diagnosis: New biomarkers in blood and urine could enable earlier detection of organ damage. Particularly promising are markers for acute kidney injury such as NGAL (Neutrophil Gelatinase-Associated Lipocalin) and KIM-1 (Kidney Injury Molecule-1), which allow kidney damage to be detected even before conventional parameters like creatinine rise.
Innovative Dialysis Procedures: For severe poisoning cases, improved extracorporeal elimination procedures are being developed that can filter toxic substances from the blood more effectively than conventional dialysis methods.
Regenerative Therapies: Stem cell therapies and other regenerative approaches are being researched to regenerate damaged organs after NSAID poisoning. Initial studies show promising results in the regeneration of kidney and liver tissue.
Improved Risk Assessment: Genetic factors influencing susceptibility to NSAID toxicity are being investigated. In the future, genetic tests could help identify particularly at-risk animals.
Development of Safer Alternatives: Research into veterinary pain relievers with an improved safety profile is progressing. New drug classes with more selective mechanisms of action could reduce the risk of adverse effects.
These research approaches promise improved diagnostic and treatment options for NSAID poisoning in the future, which could ultimately lead to a better prognosis for affected animals.
Frequently asked questions (FAQs)
- Can I give my dog or cat Ibuprofen or Diclofenac for pain?
No, absolutely not. These medications are highly toxic to dogs and cats and can cause life-threatening poisoning even in small doses. Always consult a veterinarian who can prescribe appropriate, veterinary-approved pain relievers. - How quickly do poisoning symptoms appear after ingestion of Ibuprofen or Diclofenac?
First symptoms can appear as early as 2–6 hours after ingestion. The severity of symptoms generally increases over the following 12–24 hours. - What should I do if my pet has accidentally ingested Ibuprofen or Diclofenac?
Immediately seek veterinary attention, even if no symptoms are yet visible. Bring the medication packaging with you and inform the veterinarian about the possible amount and time of ingestion. - Can Ibuprofen or Diclofenac poisoning be fatal?
Yes, if left untreated, poisoning by these substances can lead to death, especially due to kidney failure or gastrointestinal bleeding. - Which pain relievers are safe for dogs and cats?
There are specific, veterinary-approved NSAIDs such as Carprofen, Meloxicam, or Robenacoxib, which can be safely used under veterinary supervision. Opioids can also be used for pain management. - How can I protect my pet from accidental poisoning?
Store all medications in locked cabinets that are inaccessible to animals. Do not leave any pills lying around openly and inform all household members about the dangers. - Are there long-term consequences after surviving poisoning?
Yes, primarily, the kidneys can suffer permanent damage, which can lead to chronic kidney failure. Chronic gastrointestinal problems can also occur as a result. - How long does the treatment for poisoning last?
Acute treatment usually lasts 2–5 days, depending on the severity of the poisoning. Follow-up care can extend over weeks to months. - Are certain dog or cat breeds more susceptible to NSAID poisoning?
In principle, all breeds are at risk. However, animals with pre-existing kidney or liver diseases, very young or very old animals, as well as small breeds (due to lower body weight with the same amount of active ingredient) may carry a higher risk. - How can I tell if my pet is in pain and needs veterinary help?
Signs of pain can include: altered posture, lameness, decreased activity, loss of appetite, vocalizations when touched, aggressive behavior, or withdrawal. If you suspect pain, you should always consult a veterinarian.
Literature
- Dunayer, E., 2004. Ibuprofen toxicity in dogs, cats, and ferrets. Veterinary Medicine – Bonner Springs, later Edwardsville, 99, pages 580–586.
- Gwaltney-Brant, S. M. and Meadows, I., 2018. Nonsteroidal anti-inflammatory drug toxicosis. Veterinary Clinics of North America: Small Animal Practice, 48(6), pages 1033–1044. Available at: https://doi.org/10.1016/j.cvsm.2018.06.003.
- Khan, S. A. and McLean, M. K., 2021. Toxicology of frequently encountered nonsteroidal anti-inflammatory drugs in dogs and cats. Veterinary Clinics of North America: Small Animal Practice, 51(6), pages 1133–1147. Available at: https://doi.org/10.1016/j.cvsm.2021.05.004.
- Lomas, A. L. and Grauer, G. F., 2015. The renal effects of NSAIDs in dogs. Journal of the American Animal Hospital Association, 51(3), pages 197–203. Available at: https://doi.org/10.5326/JAAHA-MS-6239.
- Löwe, G. and Löwe, O., 2021. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 208 pages.
- Marks, S. L., Kook, P. H., Papich, M. G., Tolbert, M. K. and Willard, M. D., 2018. ACVIM consensus statement: Support for rational administration of gastrointestinal protectants to dogs and cats. Journal of Veterinary Internal Medicine, 32(6), pages 1823–1840. Available at: https://doi.org/10.1111/jvim.15337.
- Martínez-Subiela, S., Cerón, J. J., Strauss-Ayali, D., Garcia-Martinez, J. D., Tecles, F. and Tvarijonaviciute, A., 2020. Urinary biomarkers for early detection of acute kidney injury in dogs and cats: A review. Journal of Veterinary Internal Medicine, 34(6), pages 2293–2308. Available at: https://doi.org/10.1111/jvim.15891