This study included 166 cats with confirmed or presumed poisoning that was presented over 5 years. To the best of our knowledge, this reports the largest cohort of feline poisoning cases within a short period [35].

Reasons for hospital admission based on patient history and clinical presentations at hospital admission were largely consistent and comprised mostly neurologic signs or an altered general condition. Neurologic signs are common with poisonings [5, 7, 12, 36]. Moreover, witnessing seizures alarms many owners to seek immediate veterinary care. Exhibiting reduced general condition is less specific and can occur with any disease. Cats were also often presented for gastrointestinal signs; however, evidence of altered thermoregulation, cardiovascular, and hydration status predominated on physical examination. A previous review of 138 feline poisoning cases reported similar presentations of neurologic, gastrointestinal and respiratory clinical signs, reduced general condition, and bleeding; however, clinical signs based on medical history were not differentiated from those at admission [35]. A possible explanation for more cats showing neurologic clinical signs in this study could be a higher rate of neurotoxic substance intake. However, interpreting clinical signs by medical laypersons versus the veterinary care team and collecting short patient histories during emergency consultations could introduce bias. Furthermore, temporal aspects must be considered as clinical signs may worsen or improve from their onset to hospital admission.

Approximately one-quarter of the cats showed bradycardia or tachycardia, likely due to increased vagal or sympathetic tone associated with the toxicant or specific drug [11, 13, 35]. Tachypnea can also be stress-related or linked to dyspnea. Many hypothermic patients presented intra- or postictally (57.0%) or in advanced shock (28%), and mild hypoglycemia (4.3–4.9 mmol/L) were observed, particularly with rodenticide poisoning (2%). Hypothermia was also detected in cats with comatose states (13%). Only one-third of the hyperthermic cats experienced seizures. More than half of the euthanized cats (56%) and two-thirds of the cats that died were hypothermic. Only one deceased patient was hypothermic. Finally, hypothermia rates were not different between survivors and non-survivors, contrasting with the results of a study that examined one specific toxicant group (organophosphates) [36]. Similar to that study, rectal body temperature was lower in non-survivors than in survivors in this study.

Our data indicate that poisonings primarily impact juvenile and young adult cats, possibly attributed to heightened curiosity behavior and associated elevated risk of ingesting foreign substances. However, the causative toxicant could not be determined in almost half of the patients, possibly due to a lower likelihood of witnessing toxicant ingestion in outdoor cats (with a prevalence of 50% in this study) and limited toxicological screenings. Another investigation reported the detection of the toxicant in a larger proportion of patients (80.4%) that comprised only one-third of outdoor cats, and poisonings were significantly more often classified as “certain” than the more conservative classification in our study (72% vs. 23%) [35]. Moreover, other studies included cats witnessed to have ingested the toxicant; however, without specifying the level of certainty or subcategories [13, 37]. Poisonings with ectoparasite prophylactics have been shown to cluster in cats [6, 7, 18, 32, 33, 38–40]. This involves primarily the accidental administration of spot-on formulations that are labeled only for dogs and are highly toxic to cats, where accidental oral administration by the owner or ingestion by the cat during grooming can cause neurotoxicity [38]. Two-thirds of the permethrin-poisoned cats in the present study survived (4/6; 67%), and survival rates for other toxicants ranged from 63% to 98% [7, 39, 40].

Almost a third of all anemic cats (hematocrit [HCT] <30.3%; median age 5.1 years) in our study were affected by poisoning with coumarin derivates, suggesting (mostly occult) bleeding. Furthermore, chronic kidney disease (CKD, n = 2) was considered to be an important contributor to anemia in these cats, and a small deviation (<1%) from the lower reference limit for HCT was interpreted as an age-related physiological finding in juvenile cats (n = 3). Increased serum creatinine concentrations (>167 μmol/L) in about 10% of the cats suggested direct kidney injury (two-thirds of the cats with Lilium species poisoning were azotemic), shock after dehydration, or CKD. Serial creatinine measurements performed in some cats revealed progressive azotemia (8%) or relevant increases in serum creatinine levels within the high-normal range (21%). Survival of Lilium species-poisoned cats with AKI was 50%. The previous study has shown a remarkably good prognosis with up to 100% survival following decontamination and IV infusion within 48 h without AKI development [37]. As seen in many cats, hyperglycemia can be explained by the physiological stress response. Hypoglycemia suggests severe cardiovascular compromise (e.g., sepsis) and/or consumption of glycogen stores (e.g., post-seizures); however, preanalytic effects cannot be definitively excluded. Prolongation of PT and aPTT was exclusively detected in coumarin derivative poisoning, whereas an isolated aPTT prolongation was also observed. Possible explanations for the increased aPTT are hepatopathy, inflammatory reaction, or disseminated intravascular coagulation. Significant alterations in laboratory parameters are rarely associated with poisoning.

Decontamination measures were performed less often (35%) than in a recent study [37]. As the initial emergency action, decontamination must be carefully balanced against potential risks and contraindications for each patient [21, 27, 41]. Decontamination is unhelpful or contraindicated for remote toxicant ingestion, absence of toxic effects, and in patients with impaired consciousness, seizures, compromised swallowing, or other aspiration pneumonia risk factors. Unlike non-volatile oily substances, emesis should not be induced for foaming, corrosive, sharp objects, or volatile hydrocarbons (e.g., gasoline) to prevent aspiration and severe esophageal injuries [24]. Induced emesis is reasonable within 1–2 h of toxicant ingestion; however, little evidence exists to support this narrow window of opportunity, and successful decontamination is described up to 4 h after toxicant ingestion if performed promptly [21, 24, 27, 42]. Gastric lavage could be considered if emesis induction has failed or is contraindicated, although the clinical benefit remains controversial [19, 21, 43, 44]. Additional IV fluid therapy should be considered in most cats with suspected poisoning and needs to be tailored to the individual toxicant and patient status [41]. It can support cardiovascular function and needs to be carefully titrated or even avoided with, for example, toxicants that can cause cerebral edema (e.g., bromethalin) or underlying heart disease. A toxicant-specific antidote was applied only for coumarin derivative poisonings (Vitamin K1). Elimination measures were performed almost twice as often as decontamination attempts, which was mainly IV lipid therapy (Lipofundin 20%, B. Braun, Melsungen, Germany) given to 60% of the cats, particularly to those with α-chloralose, permethrin, other biocides, NSAIDs, or THC poisoning.

Approximately 60% of cats were empirically treated with intravenous lipid emulsion (ILE), as no established protocols existed for managing feline poisoning cases involving hydrophobic agents and severe symptoms at that time. Along these lines, the attending clinician decided to treat, for example, α-chloralose poisoning cases with ILE (log P = 0.99). Particularly in light of possible treatment-associated complications (which also occurred), veterinarians should carefully consider routine ILE administration for hydrophobic toxicants for as long as sufficient evidence is lacking (e.g., log P < 1.0) [44, 45].

A survival rate of almost 90% and low mortality rates is consistent with other studies reporting an 86%, 83%, and 85% survival rate, respectively [3, 35, 36]. However, data for comparison are sparse in feline medicine. As most studies distinguish survival versus non-survival, this study differentiated natural death (2%) and euthanasia (10%) as lethal outcomes. Owners’ reasons for choosing euthanasia vary, and it is conceivable that some of these cats might have survived with additional therapy.

Toxicant-associated complications were more frequent (48%) than in a recent study with 39 cats (28%) [36]. Hypothermia was observed predominantly in rodenticides, hyperthermia due to local inflammation in the oral cavity, and pain triggered by didecyldimethylammonium chloride. Respiratory complications were most frequently noted, likely associated with cardiovascular depression and decreased oxygenation with hemorrhage or anemia. Gastrointestinal signs, including vomiting and superficial tongue lesions, can result from absorption and local effects of the toxicant, which may be prolonged. Nephrotoxicity was primarily associated with the ingestion of Lilium species, evident hemorrhage with coumarin derivatives, and a postictal comatose state with poisonings that did not result in hemorrhage. The hepatic metabolization of several toxicants can contribute to the development of liver failure.

We acknowledge the limitation of this study being retrospective in nature, carrying some risk of bias or lack of information. A standard assessment of the neurological status (e.g., Glasgow coma scale) was not utilized, and respiratory rates were mostly reported if abnormal. Laboratory trends were available from only a few patients. Retrospectively evaluating the likelihood of poisoning is challenging, and toxicological screening was rarely performed. Conclusions from suspected or “unknown” poisonings are generally limited and remain speculative for some clinical signs and treatment options.