Aluminium intoxication in a dog

Toor, Arifa; Voet, Gijsbert B. van der; Ellen, G.; Voorst, J van

doi:10.1080/01652176.1990.9694271

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…Aluminium intoxication has been reported in a dog presenting with muscle twitching, convulsions, tetraparesis and coma which resolved following removal of a gastric foreign body containing aluminium (van Toor et al 1990) (Table 2). Diet has been associated with some types of canine urolithiasis (Osborne et al 1981) and avoidance of dietary silica (a type of silicate) has been recommended to minimise recurrence of silica uroliths (Minnesota Urolith Centre 2020).…”

Section: Adsorbent Claysmentioning

confidence: 99%

Additives in pet food: are they safe?

Craig¹

2021

J of Small Animal Practice

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A good, nutritious diet is essential for the health and well‐being of our domestic pets. Today, most pet dogs and cats are fed highly processed food bearing little resemblance to canine and feline ancestral diets. Additives are included in processed pet food to provide nutritional benefits, ensure food safety, and maintain the desirable features of colour, flavour, texture, stability and resistance to spoilage. This paper reviews the safety of various additives in processed pet food. Labelling, safety assessment, and ethical concerns regarding existing toxicity testing procedures are also considered. The adequacy of testing for many additives and the scientific basis for determining safety are questioned. Additives can be synthetic or ‘natural’ although the distinction can be blurred when naturally derived substances are synthesised in the laboratory, or extracted using a high level of physical and chemical processing. Although additives play important roles in processed food production, updated strategies and technologies may be required to establish their safety in the pet food industry.

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Section: Adsorbent Claysmentioning

confidence: 99%

Additives in pet food: are they safe?

Craig¹

2021

J of Small Animal Practice

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“…To date, there is no documentation of aluminum toxicity associated with administration of phosphate‐binding agents in dogs with naturally occurring kidney disease. van Toor et al 13 reported a case of aluminum toxicity in a dog after ingestion of an aluminum foreign object. Clinical signs included convulsions and muscle twitching, which resolved gradually after removal of the foreign object.…”

Section: Casementioning

confidence: 99%

Aluminum Toxicity Following Administration of Aluminum‐Based Phosphate Binders in 2 Dogs with Renal Failure

Segev

Bandt

Francey

et al. 2008

Veterinary Internal Medicne

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A n 11-year-old, female spayed, Brittany Spaniel, weighing 22 kg, was referred to the Emergency Service of the Veterinary Medical Teaching Hospital (VMTH) at the University of California, Davis, and hospitalized for evaluation and treatment of acute kidney injury, following ingestion of an unknown amount of ethylene glycol, 3 days earlier. At presentation at the VMTH (day 1), the dog was ambulatory, but lethargic, and overhydrated. The remainder of the physical examination was unremarkable. A CBC revealed normocytic normochromic, nonregenerative anemia (Hct, 29%; reference range [RR], 40-55%). Serum chemistry abnormalities included azotemia (serum creatinine concentration, 8.1 mg/dL; RR, 0.5-1.6 mg/dL; blood urea nitrogen [BUN], 67 mg/dL; RR, 8-21 mg/dL), hyperphosphatemia (13.8 mg/dL; RR, 3.0-6.2 mg/dL), hypocalcemia (8.3 mg/dL; RR, 9.7-11.5 mg/dL), normokalemia (4.97 mmol/L; RR, 3.6-5.3 mmol/L), and metabolic acidosis (serum bicarbonate, 10 mmol/L; RR, 16-26 mmol/L). On urinalysis, specific gravity was 1.009, pH was 5, and occasional calcium oxalate crystals were observed. Urine culture for aerobic and anaerobic bacteria was negative. Abdominal ultrasound examination disclosed normal-sized kidneys with hyperechoic cortices bilaterally, consistent with ethylene glycol intoxication and focal hyperechoic appearance to the mesentery in the right cranial abdominal quadrant suggestive of pancreatitis.Owing to azotemia, clinical signs, and presumed ethylene glycol exposure, hemodialysis was initiated, using standard procedures as established for dogs.1,2 By day 11, clinical signs had resolved with the combination of hemodialysis and symptomatic treatment, and all caloric requirements and medications were provided via a gastrostomy tube placed during initial hospitalization. Renal function, however, did not improve, necessitating continued thrice weekly hemodialysis treatments on an outpatient basis. On the day of discharge (day 11), aluminum hydroxide a was added to the blended diet to provide 84 mg/kg/d in order to control the hyperphosphatemia. This dosage was increased to 126 mg/kg/d on day 22, because the serum phosphorus concentration exceeded the target range (o6 mg/dL). On day 36, erythropoietin b therapy was initiated at 100 U/kg thrice weekly, SC in combination with iron dextran c supplementation at 10 mg/kg IM every 3 weeks.The dog remained stable for the next 26 days on hemodialysis but no improvement in the kidney function was noticed. Mean serum creatinine and BUN concentrations before each dialysis treatment were 6.8 and 75 mg/dL, respectively. On day 62, lethargy and a decreased activity were noted by the owners. Both conditions worsened progressively to obtundation and complete recumbency by day 70. Neurologic examination revealed an inconsistent menace response, normal cranial reflexes, tetraparesis, reduced patellar reflexes in the hind limbs, and markedly reduced withdrawal reflexes in all 4 limbs. On the basis of these findings, the neurologic deficits were localized as diffuse cerebral and periph...

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“…4,5 Epidemiological investigations in people have identified important therapeutic considerations and prognostic information based upon signalment and presenting clinicopathologic signs. 4,[6][7][8] Literature pertaining to the underlying etiology and outcome of dogs and cats with coma and stupor is scarce, and largely limited to individual case reports [9][10][11][12][13][14][15][16][17][18][19][20][21] and cases indirectly reported as part of larger populations suffering other systemic illness. [22][23][24][25][26][27][28][29] The objective of this study was to summarize the signalment, clinical findings, underlying etiology, and short-term outcome in a large population of dogs and cats presenting with coma and stupor to a multicenter out-of-hours emergency care provider in the United Kingdom.…”

Section: Introductionmentioning

confidence: 99%

“…Literature pertaining to the underlying etiology and outcome of dogs and cats with coma and stupor is scarce, and largely limited to individual case reports and cases indirectly reported as part of larger populations suffering other systemic illness …”

Section: Introductionmentioning

confidence: 99%

Retrospective characterization of coma and stupor in dogs and cats presenting to a multicenter out‐of‐hours service (2012–2015): 386 animals

Parratt¹,

Firth²,

Boag

et al. 2018

J Vet Emergen Crit Care

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Objective -To describe the signalment, etiology, and short-term outcome of dogs and cats presenting in a coma or stupor. Design -Retrospective study conducted between May 2012 and February 2015.Setting -Multicenter out-of-hours emergency service provider. Animals -Three hundred eighty-six patients presenting in a coma or stupor to a multicenter out-of-hours emergency care provider. Interventions -None.Measurements and Main Results -Records were reviewed to determine the most likely etiology of coma or stupor. Short-term outcomes were defined as deceased (died or euthanized) or transferred (case handed over to a daytime clinic or discharged). There were 168 dogs (coma n = 112, stupor n = 56) and 218 cats (coma n = 148, stupor n = 70) identified. Coma and stupor were more prevalent in cats compared to dogs, and Chihuahuas were over represented. Blood glucose concentrations were frequently outside established reference intervals. Excluding undetermined causes, the most common causes in dogs included traumatic brain injury (TBI) 16.0% (n = 27, deceased n = 22), hypoglycemia 10.7% (n = 18, deceased n = 8), shock 10.1% (n = 17, deceased n = 16), seizure 9.5% (n = 16, deceased n = 13), and renal or hepatic dysfunction 5.3% (n = 9, deceased n = 7). For cats, the most common causes included TBI 21.6% (n = 47, deceased n = 38), renal or hepatic dysfunction 13.3% (n = 29, deceased n = 25), intoxication 10.1% (n = 22, deceased n = 18), hypoglycemia 6.0% (n = 13, deceased n = 4), and shock 5.0% (n = 11, deceased n = 8). When treatment was attempted, 46.0% of dogs (n = 44/96) and 41.2% of cats (n = 35/85) survived to be transferred. Compared to all other etiologies, death was less likely when coma or stupor was attributed to hypoglycemia. Conclusion -In cases where a cause was determined, TBI was the predominant etiology of coma and stupor for both species. With the exception of coma and stupor attributed to hypoglycemia, the overall short-term prognosis was poor. (J Vet Emerg Crit Care 2018; 28(6): 559-565)

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Aluminium intoxication in a dog

Cited by 4 publications

References 22 publications

Additives in pet food: are they safe?

Additives in pet food: are they safe?

Aluminum Toxicity Following Administration of Aluminum‐Based Phosphate Binders in 2 Dogs with Renal Failure

Retrospective characterization of coma and stupor in dogs and cats presenting to a multicenter out‐of‐hours service (2012–2015): 386 animals

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