Should we be using 3% hydrogen peroxide as an emetic agent in dogs | VETgirl Veterinary Continuing Education Podcasts
In this VETgirl online veterinary continuing education podcast, we discuss whether or not we should be using 3% hydrogen peroxide (H202) as an emetic agent in dogs. With most of our pets’ toxin ingestions occurring outside the veterinary hospital, we, as veterinary professionals, must use our best judgment when making recommendations to pet owners regarding how best to help their pet. If the pet has ingested a toxic substance or an overdose of medication, and you know the best course of action is to prevent further absorption by way of emesis, what do you recommend to the client? Does your hospital induce emesis with apomorphine or with hydrogen peroxide? Do you sometimes recommend to clients to induce emesis at home? Or do you just direct them to the ASPCA Animal Poison Control Center instead?
If pet owners can’t transport their dog safely to a veterinary hospital in time for emesis induction, we often advise the client to attempt this on their pet at home. (Remember, there are NO safe emetic agents that pet owners can use at home for cats, so get those feline patients seen at your veterinary clinic immediately!). Hydrogen peroxide is a common household disinfectant used as one of our agents for gastric decontamination in dogs. Concentrations of hydrogen peroxide solutions range from 3% in our disinfectants to >10% in cleaning solutions (with higher concentrations being corrosive). The veterinary recommendations for inducing emesis are to administer 1-2ml/kg of the 3% hydrogen peroxide solution with 1 additional dose if emesis is not achieved.1
While we often assume that a small volume of 3% hydrogen peroxide is benign when ingested, we don’t presently have veterinary studies to support this assumption. Reports from the human side of medicine document some significant – albeit rare – complications from ingesting hydrogen peroxide such as gastric ulcers, hemorrhagic gastritis, gas emboli, and even death.2,3 That said, these humans had ingested much higher concentrations (e.g., 35% hydrogen peroxide)!
So, Niedzwecki et al wanted to investigate this in the study Effect of oral 3% hydrogen peroxide used as an emetic on the gastroduodenal mucosa of healthy dogs. They performed a prospective study aimed to investigate the effects of 3% hydrogen peroxide on the gastrointestinal mucosa in healthy dogs when ingested in amounts we routinely use for emesis induction. The investigators hypothesized that these ingested doses of hydrogen peroxide would in fact cause significant mucosal injuries in the stomach and the small intestines of otherwise healthy dogs. In this study, a total of 6 staff-owned dogs (Best work colleagues ever!) were selected to represent the study group after first ruling out pre-existing gastroduodenal lesions by way of bloodwork screening and gastroduodenoscopy with gastric and duodenal biopsies. All dogs in this study group were administered 2 ml/kg of 3% hydrogen peroxide orally to induce emesis. One dog did not vomit after this initial dose and needed another dose 10 minutes later (also 2 ml/kg). One dog was used as the control group after going through the same baseline screening for preexisting gastrointestinal disease and received subconjunctival apomorphine instead of hydrogen peroxide. This dog only required a single dose of 0.25 mg/kg apomorphine to achieve successful emesis. Actually, this one dog was documented to have vomited about 4 times more than the mean number of times of vomit found in the hydrogen peroxide group.
Next, all dogs underwent gastroduodenoscopy for visual screening of the esophagus, stomach, and duodenal mucosa with gastric and duodenal biopsy sampling at 4 hours, 24 hours, 1 week, and 2 weeks. When examining the esophagus alone for injury, most dogs in the hydrogen peroxide group experienced mild esophageal lesions noticeable at the first 4-hour examination. These minor gross lesions lasted anywhere from 24 hours to 2 weeks. There were 2 cases in the study group that developed esophagitis at the 1-week mark, but there is the possibility that the gastroduodenoscopy procedure alone is a precipitating factor for the development of reflux. The one dog that received apomorphine did not exhibit any grossly visible esophageal lesions at any time point.
So what’d they find? All dogs in both groups had visible evidence of gastric lesions at the very first 4-hour examination. All dogs in the hydrogen peroxide group experienced worsening of gastric lesions within the first 24 hours, with improvement seen in all dogs in both groups over the 2-week period. The biopsy samples taken from the stomach showed that in all dogs administered hydrogen peroxide there were significant histopathologic injury to the gastric mucosa including gastric ulcers, degeneration, and necrosis. The apomorphine dog did not exhibit any histopathologic lesions in the gastric samples provided. Lastly, 83% of the dogs in the study group suffered visible duodenal mucosal lesions, but these all improved over the 2-week period. Interestingly, although most of the visible duodenal lesions were mild in nature, the dog that suffered the most severe duodenal lesions of the study group exhibited a decreased appetite for 1 month and the gastrointestinal lesions were still visualized at 2 weeks out in both the stomach and the duodenum. The biopsies from this dog’s stomach at the 2-week examination revealed a moderate multifocal lymphoplasmacytic gastritis. There were no gross abnormalities seen on the duodenal mucosa at any time point in the control dog that received apomorphine. Despite the grossly visible duodenal lesions observed in the study group, there were no histopathologic lesions identified on duodenal biopsies in any of the dogs in either group.
So how does hydrogen peroxide cause the mucosal damage seen in this study? There are 3 known mechanisms behind hydrogen peroxide’s damaging affects:
1) It causes direct caustic injury to the mucosal tissues
2) In the presence of catalase, which is found in mucus membranes, the liver, kidney, RBCs, and bone marrow,4 hydrogen peroxide will dissociate into water and oxygen which can lead to gas-induced perforation or gas embolism
3) It can cause lipid peroxidation in all cell membranes it comes in contact with by creating those not-so-fun free radical chain reactions that ultimately destroys the cell membrane.
Overall, what can we learn from this VETgirl podcast?
This study suggests that hydrogen peroxide’s direct affect on the gastric mucosa is the causative agent for the histopathologic lesions seen on gastric biopsies in the study group. The authors came to this conclusion based on the lack of any gastric histopathologic lesions in the control dog (despite the fact that this canine vomited many more times than the study dogs). An interesting discovery in this study was the degree of gastric mucosa friability seen in all dogs that received hydrogen peroxide. This is also a common finding in humans ingesting hydrogen peroxide. There are some important clinical implications with this finding. In our canine patients with a known disease that is affecting the integrity of gastrointestinal mucosa, we should seriously consider how the hydrogen peroxide will affect the already friable mucosal tissues. Disease conditions of importance would include things such as gastroenteritis, IBD, hypovolemic shock (that results in poor gut perfusion), or if the substance we are trying to evacuate was a caustic or corrosive substance that has already started to affect the gastric mucosa.
The pro of this study? First, it’s a prospective study, so huge kudos to the authors. Second, this study is the first to document that mucosal lesions can develop from administration of hydrogen peroxide when used at “common” doses used in dogs as an emetic agent. The cons? The major limitation to this study was the number of dogs used in both the study group and in the control group. Also, not all of the dogs were initially fasted (withheld from food) and we toxicologists often feel that hydrogen peroxide is more effective as an emetic agent when food is present in the stomach. This may have affected the severity of the direct gastritis in some of the dogs.
In conclusion, the findings from this study support that hydrogen peroxide is not as benign as perhaps we once thought. While the authors’ take away from this study was that the use of hydrogen peroxide shouldn’t be recommended for at-home use in pet owners unless the benefits outweigh the risks, the toxicologist in me is going to take a little bit of a different take on it. VETgirl will likely still use it as an emetic agent (again, only in dogs), but now I’m going to add on gastric protectants and antacids for 1-2 weeks post-administration of hydrogen peroxide. Also, in human medicine, they recommend administering large quantities of water following hydrogen peroxide ingestion in order to prevent esophageal injury. Are any of us making this recommendation to our canine patients? Just like when giving doxycycline, this might be something we should be considering (once an anti-emetic agent is on board)?
Keep in mind that if a poisoned dog cannot be presented in a timely fashion to a veterinary clinic that can administer apomorphine, and if the substance ingested is too dangerous to treat supportively, then the recommendation for hydrogen peroxide administration can be made, but the pet owner should be warned of the gastrointestinal consequences that can arise. Special consideration should be made for patients with known preexisting gastrointestinal disease before recommending emesis induction with hydrogen peroxide. When in doubt, contact the ASPCA Animal Poison Control Center for life-saving advice!
1. Schildt JC, Jutkowitz LA. Approach to poisoning and drug overdose. In: Silverstein DC, Hopper K. eds. Small Animal Critical Care Medicine. 1st ed. St. Louis: Saunders Elsevier; 2009, pp.326-329.
2. Caraccio TR, Comer GM, Hnery MC, et al. Hydrogen peroxide 3% exposures. J Toxicol Clin Toxicol 1996; 34(3):323-327.
3. Moon JM, Chun BJ, Min YI. Hemorrhagic gastroenteritis and gas emboli after ingesting 3% hydrogen peroxide. J Emerg Med 2006; 30(4):403-406.
4. Pritchett A, Green D, Rossos P. Accidental ingestion of 35% hydrogen peroxide. Can J Gastroenterol 2007;21(7):665-667.
5. Schindler AE, Schneider JA, Obstein KL. Foaming at the mouth: ingestion of 35% hydrogen peroxide solution (with video). Clin Gastroenterol Hepatol 2012;10:e13-e14.
6. Niedzwecki AH, Book BP, Lewis KM, et al. Effect of oral 3% hydrogen peroxide used as an emetic on the gastroduodenal mucosa of healthy dogs. JVECC 27(2):178-184.