Suspected Bentonite Toxicosis in a Cat
from Ingestion of Clay Cat Litter
by
Carl S Hornfeldt MS, ABAT
Hennepin Regional Poison Center
701 Park Avenue
Minneapolis, MN 55415
and
Michael L Westfall DVM
Hudson Road Animal Hospital PA
8154 Afton Road
Woodbury, MN 55125
ABSTRACT. A 2 l/2—y-old spayed female cat was presented for lethargy and weakness. The cat was hypokalemic (3.1 m Eq K/L) and severely anemic (60% PVC, 1.3 g hemoglobin/dL). The cat was known to ingest bentonite-containing cat litter. It recovered with treatment of iv fluids, electrolytes and whole blood transfusion and was discharged. Two months later the cat was presented again with signs similar to those seen previously. This occurred 1 mo after the owner resumed the use of bentonite—containing cat litter. The signs were remarkably similar to those reported in humans from the chronic ingestion of bentonite clays. Bentonite toxicosis is suggested by the coexistence of hypokalemia hypochromic anemia in cats presented with lethargy and muscle weakness.
Toxicosis from exposure to products such as pesticides are relatively common in small animals. The highly toxic nature of these substances is quickly clinically apparent. Occasionally, products traditionally thought to be nontoxic produce toxicosis. We report a cat with hypokalemia and macrocytic hypochromic anemia consistent with iron—deficiency anemia that appears to have become ill from the chronic ingestion of a bentonite—containing cat litter.
CASE REPORT
A 2 1/2-y-old spayed female domestic short-hair cat was presented for lethargy. The owners reported the cat had been hiding the previous 2 d during which time it had not eaten. On the evening prior to hospitalization the cat appeared depressed and ataxic. It weighed 3.5 kg, and physical examination revealed a systolic grade II/IV murmur, pale mucous membranes, decreased capillary refill time and approximately 5% dehydration.
The cat was known to chronically ingest cat litter containing 99% bentonite (TIDY CAT, Lowe’s Incorporated, South Bend, IN), and radiography revealed small masses of radiopaque material throughout the colon. Based on history and clinical appearance, an iv infusion of 5% dextrose containing an additional 100 ml of 50% dextrose, 5 mg dexamethasone and 1 ml vitamin B solution/l000 mL was begun at a rate of 7.14 mL/kg/h. The cat also received 50 mL of whole blood. By that afternoon the cat was eating solid food and urinating normally.
The following day the cat was active, alert and eating. Its hydration status had improved, but no stool had been passed so an oral laxative (LAXATONE, Evsco Pharmaceuticals, Vineland, NJ) was administered. A serum chemistry profile from the previous day revealed 3.1 m Eq K/L (normal 4.0-6.0 Eq/L), 145 m Eq Na/L (147-156 mEq/L), 3.3 m Eq P/L (4.5-8.1), 46 mg BUN/dL (14-32 mg/dL), 9.7 g total protein/dL (4.3-7.5 g/dL) and 6.7 g total globulin/dL (2.1-4.3 g/dL). A complete cell count revealed 6.0% PVC (30-45%), 1.3 g hemoglobin/dL (10-15 g/dL), 680,000 RBC (5-10 x 106), 81 MVC (39-55), 25.4 MCHC (30-36) and a 4% reticulocyte count (0-1%). Feline immunodeficiency virus and feline leukemia virus antigen serologies were negative. The iv fluid regimen was changed to Lactated Ringers’ with 100 m L 50% dextrose and 5 mg prednisolone/1000 mL, and the cat was prophylactically given 50 mg oral amoxicillin q 12 h. Because the cat’s condition was markedly improved, additional potassium was not administered.
On the third hospital day, the cat’s appetite remained excellent and a large amount of stool containing cat litter was passed. Fluids, iv and oral medications were continued with the addition of oral multiple vitamins. The cat was discharged on day 3 on 50 mg oral amoxicillin q 12 h and 5 mg prednisolone + multiple vitamins q 24 h. It was recommended that the owners use non—bentonite—containing litter for the cat.
Three days following discharge the cat’s mucous membrane color was improved and no heart murmur was heard. Interestingly, the owner reported that the cat attempted to eat the non-bentonite-containing cat litter (EVERCLEAN ES CAT LITTER, First Brands Company, Danbury, CT).
Two months later, the cat was again presented exhibiting clinical signs similar to those seen previously. The owner indicated they had returned to using the bentonite-containing cat litter approximately 1 mo earlier. On abdominal palpation, the cat’s colon was full and hard. Cat litter ingestion was suspected. The owner declined treatment and the cat was euthanized. Post mortem examination was denied.
DISCUSSION
The chronic ingestion of bentonite-containing cat litter by this cat appeared associated with hypokalemia, lethargy and muscle weakness, dehydration and heart murmur in addition to macrocytic hypochromic anemia. Clinical signs quickly resolved with administration of fluids and whole blood and removal from the cat litter.
Poisoning from the chronic ingestion of bentonite clay has been reported in humans (1-3). Signs of toxicosis included myalgias (not appreciated in this cat), muscle weakness and lethargy. Serum chemistries of affected humans consistently revealed hypokalemia, ECG changes consistent with hypokalemia, and hemograms that showed iron deficiency resulting in macrocytic hypochromic anemia (1-2). The neurologic signs in humans quickly resolved when serum potassium was increased to normal levels (1-2) and the anemia resolved with oral iron supplementation (1,4). In vitro experiments have confirmed that bentonite clays adsorb potassium (1-3), and it has been speculated that the presence of bentonite in the gut may inhibit the absorption of dietary iron (5).
While it is not known with certainty that ingestion of bentonite clay was responsible for the hypokalemia and anemia seen in this cat, the clinical similarities between humans poisoned by ingesting clay bentonite and this cat are striking. In addition, the cat became ill a second time with similar clinical signs after the ingestion of bentonite—containing cat litter resumed. This suggests that ingestion of bentonite clay—based cat litter may have been responsible for both illness episodes in this cat. Given the common use of bentonite clay litters for cats, veterinarians should consider bentonite toxicity when a cat is presented for lethargy, weakness and coexisting hypokalemia and anemia.
REFERENCES
- Mengel CE, Carter WA, Horton ES: Geophagia with iron deficiency and hypokalemia. Arch Intern Med 114: 470-474, 1964.
- Gonzales JJ, Owens W, Ungaro PC et al: Clay ingestion: A rare cause of hypokalemia. Ann Intern Med 97: 65-66. 1982.
- Severance HW, Holt I, Patrone NA et al.: Profound muscle weakness and hypokalemia due to clay ingestion. South Med J 81: 273-274, 1988.
- Rosella MA: Association of laundry starch and clay ingestion with anemia in New York City. Arch Int Med 125: 57—61, 1970.
- Okcuoglu A, Aracasoy A, Minnich V et al: Pica in Turkey I. The incidence and association with anemia. American J Clin Nutr 19: l25-131, 1996.
Bentonite Toxicosis in a Cat from Cat Litter?
These letters were published in the Journal of Veterinary and Human Toxicology, Vol. 39, No. 3, June 1997.
Dear Editor,
This letter is written in response to a case report published in your journal: "Suspected Bentonite Toxicosis in a Cat from Ingestion of Clay Cat Litter" (October 1996). It was sent to me by Sorptive Minerals Institute, a trade association based in Washington, DC which represents the marketers and manufacturers of clay-based litters.
In my opinion, there was no evidence presented which supports the authors' conclusions that the ingestion of bentonite was causative of the cat’s problems and there was extensive evidence that it was not. Below are specific inconsistencies in the report that call the author's conclusions into question.
—99% bentonite litter is not TIDY CAT~ Lowe's Incorporated South Bend, IN. The case report is mistitled at best.
—"By that afternoon the cat was eating solid food and urinating normally. The following day the cat was active, alert and eating." The cited case reports of hypokalemia and anemia associated with clay ingestion in humans (see references 1-3) took 3 days to resolve, and required iv supplementation with potassium.
—K+ = 3.1 m Eq/L (normal 4.0-6.0). This is compatible with mild hypokalemia. The authors do not report any clinical cardiac abnormalities referable to potassium deficiency: no tachycardia, no irregular pulse. The human cases cited had much lower serum K+ levels when they were presented with clinical signs (1.5-1.9 m Eq/L).
—4% reticulocyte count. The implication is that the anemia is regenerative. However, this value was not corrected for the degree of anemia. When corrected, the reticulocyte count becomes <1, evidence that this cat had a non-regenerative anemia. Iron deficiency anemia is a regenerative anemia. The formula for figuring this is: Observed pcv over normal pcv (which is 30—45% in the cat) times observed reticulocyte count over X.
—The mean corpuscular volume and the mean corpuscular hemoglobin concentration reported are descriptive of a hypochromic, macrocytic anemia. This does not describe an iron deficiency anemia, which is hypochromic, microotic.
—The iv fluid therapy, even though changed to Lactated Ringers', did not have very much potassium. The food that the cat consumed after receiving a blood transfusion would probably have provided some potassium. No post treatment laboratory values were evaluated (see above).
—Non-bentonite containing cat litter is not EVERCLEAN ES CAT LITTER, First Brands Company, Danbury, CT.
—The cited literature does not indicate the type of clay that the hypokalemic, anemic humans ingested. "Poisoning from the chronic ingestion of bentonite clay has been reported in humans (1-3)." This fact plus the discrepancy in just what the cat ate—bentonite or TIDY cat—may or may not be of any importance.
Anemia causes pica in cats. This well-known fact is not acknowledged or discussed in the report.
There were no postmortem, no bone marrow biopsy, no confirmation of the FeLV negative status found on the ELISA testing, no investigation of the elevated BUN (renal failure causes non-regenerative anemia) or other laboratory abnormalities, no follow up lab work, and no cardiac work up for the cause of the heart murmur.
While every veterinary practitioner regrets the financial and personal realities that limit the thoroughness with which some cases are investigated, in this situation, the lack of documentation renders this case report worse than valueless. The veterinary literature is ill served by publication of misleading speculation; indeed the conclusions drawn are incongruent with the data presented.
Susan McDonough VMD
Cat Hospital of Philadelphia
225 South 20th Street
Philadelphia PA 19103
AUTHOR'S RESPONSE
Dear Editor,
Thank you for the opportunity to respond to Dr McDonough's comments on our case report, "Suspected Bentonite Toxicosis in a Cat from Ingestion of Clay Cat Litter," which recently appeared in this journal. Because confirmation of bentonite toxicosis was not possible, we entitled this case report a suspected case of toxicosis, recognizing that the clinical findings in this case are subject to interpretation. Nevertheless, as Dr McDonough has chosen to comment on our report so vigorously, we shall attempt to address her numerous remarks regarding this case.
The owner of the cat in this case used a product called TIDY CAT. Information on this product was obtained from a computerized database called Poisindex, published quarterly by Micromedex Inc, Denver, CO, commonly used by poison information centers. According to this source, based on information supplied by the manufacturer, Lowe’s Inc, South Bend, IN, 2 formulations are provided for TIDY CAT. One is comprised of 99% de-dusted montmorillonite (bentonite) clay and the other contains Fuller's earth which, according to one source, is synonymous for montmorillonite (1).
The cat in this case showed marked improvement during the first 24 hours of therapy; however, we do not mean to infer that the anemia or hypokalemia had resolved. Regrettably, financial constraints prevented laboratory tests to be repeated on days two and three of treatment. While the similarities between the cat in this case and humans similarly affected by chronic clay ingestion seem obvious, we are reluctant to suggest a cat and a human would necessarily follow an identical response to therapy.
On admission, the cat was hypokalemic, with a serum potassium of 3.1 m Eq/L, and examination of the cat revealed a systolic grade II/IV murmur. As Dr McDonough points out, the hypokalemia was not as severe as that reported in humans, who have had associated cardiac dysrhythmias. As the cat's hypokalemia was not as profound as other cases, it should not be surprising that the cardiac manifestations were not as serious as those reported in humans, although, again, we are reluctant to make direct comparisons between humans and cats.
With respect to the type of anemia displayed in this case, it is unequivocally associate with increased red blood cell production, commonly referred to as a regenerative anemia. Three points support this conclusion. The formula presented by Dr McDonough is most applicable to dogs who may have substantially elevated aggregate reticulocyte counts, so that a reticulocyte count of 4% in a dog might bear correcting. On the other hand, cats do not release reticulocytes into circulation readily and a 4% reticulocyte count in a cat is quite high, perhaps as high as one might expect. Similarly, the MCV in dogs normally ranges in the 60's, so a value of 81 in a dog might need to be interpreted after correction. Cats normally have a MCV in the 40's, so 81 is a doubling of the normal value. Cats do release proportionally larger red cells than dogs when under anemic stress, leading to our interpretation of a macrocytic anemia. The cat returned to the clinic two months later after ingesting of cat litter resumed. Dr McDonough is inferring that the cat having a PVC of 6% and a non-regenerative anemia survived during the interim without rather extensive therapy which the cat did not receive. Collectively, these points support the presence of a regenerative anemia.
As Dr McDonough points out, it is true we cannot ascertain the nature of clays eaten in the various cases of poisoning in humans. Again, this is why we refer to this case as a suspected case of bentonite toxicosis. While anemia allegedly causes pica in cats, a retrospective Commonwealth Agriculture Bureau VETCD literature search to 1973 failed to provide any reference to support this.
The increased BUN was interpreted as dehydration and possible prerenal azotemia. Creatinine was within normal limits and therefore not reported. The cat recovered clinically within 24 hours and returned to eating and drinking normally. It would seem unlikely that a cat with chronic renal failure sufficient to cause a non-regenerative anemia, as suggested, with a PCV of 6.0 and Hb of 1.3 would respond this quickly and without relapse for two months.
While we regret that Dr McDonough found our report to be of no value, it may be of interest that this case inspired an in vitro research project. This experiment, examining the use of oral bentonite for the treatment of acute iron poisoning, was supported by the American Association of Poison Control Centers. In this study, we found bentonite significantly absorbed soluble iron dissolved in distilled water, although not in simulated gastric fluid (2), suggesting bentonite may be impractical for the treatment of acute iron poisoning. Never-the-less, it supports the notion that chronic ingestion of bentonite may cause decreased absorption of dietary iron.
Carl S Hornfeldt MS, RPh, ABAT
Hennepin Regional Poison Center
701 Park Avenue, Minneapolis, MN 55415
Michael L Westfall DVM
Hudson Road Animal Hospital PA
8154 Afton Road, Woodbury, MN 55125