A 2-year-old 14.9-kg (32.8-lb) neutered female Shetland Sheepdog was admitted to the University of Liverpool Small Animal Teaching Hospital for evaluation of acute collapse. The dog had collapsed 2 hours prior to admission after a short period of exercise in the proximity of derelict buildings in rural Wales. The dog had vomited once during transport to the hospital. The owners reported that the vomitus appeared to consist only of water and food. Prior to collapse, the dog had no history of relevant medical problems and was not receiving any medications.
Physical examination revealed that the dog was nonambulatory but was responsive and able to maintain sternal recumbency. Ventroflexion of the neck was evident. The dog was in good body condition (body condition score of 5; scale of 1 to 9). Respiratory rate was 80 breaths/min, and heart rate was 100 beats/min. No adventitious lung sounds or murmurs were evident during auscultation of the thorax. Peripheral pulse quality was good, and no pulse deficits were detected. Abdominal palpation did not reveal any abnormalities.
Neurologic examination did not reveal abnormalities of the cranial nerves, panniculus reflex, or withdrawal reflexes. Forelimb and hind limb reflexes were reduced, and muscle tone was diminished. Findings of the neurologic examination were consistent with diffuse lower motor neuron dysfunction.
Blood samples were obtained for hematologic and biochemical analyses and blood gas analysis. Hematologic evaluationa revealed neutrophilia (neutrophil count, 20.5 × 109 cells/L; reference range, 3.5 × 109 cells/L to 12.5 × 109 cells/L) and monocytosis (monocyte count, 3.51 × 109 cells/L; reference range, 0.3 × 109 cells/L to 2 × 109 cells/L), which were considered consistent with a stress leukogram. Changes consistent with hemoconcentration (hemoglobin concentration, 20.1 g/L; reference range, 12 to 18 g/L; Hct, 57.6%; reference range, 37% to 55%) were also evident. The only abnormality detected during biochemical analysisb,c was severe hypokalemia (1.7 mEq/L; reference range, 3.5 to 5.8 mEq/L). Blood gas analysisd of a sample of venous blood collected at the time of admission revealed no acid-base abnormalities.
Urinalysis of a sample obtained via cystocentesis revealed an increase in specific gravity (1.055), which was compatible with the suspected hemoconcentration. Other results of the urinalysis were unremarkable. Examination of an ECG revealed a prolonged QT interval (0.35 seconds; reference range, 0.15 to 0.25 seconds). Abdominal ultrasonography did not reveal any abnormalities.
Intravenous administration of lactated Ringer's solution was initiated; the solution was supplemented with potassium chloridee (0.5 mEq/kg/h [0.23 mEq/lb/h]). Despite this treatment, the clinical status of the dog continued to deteriorate. One hour after admission, muscle twitching was evident. The dog remained tachypneic (80 breaths/min). Muscle weakness progressed, and 3 hours after admission, the dog was unable to maintain sternal recumbency. Respiratory rate slowed to 28 to 36 breaths/min. The gag reflex was no longer detected; thus, the dog was moved into a head-down position to prevent aspiration of saliva.
Clinical deterioration was accompanied by marked irregularities on the ECG. Large numbers of ventricular premature complexes were seen, followed by the appearance of ventricular couplets and triplets and then runs of ventricular tachycardia. Antiarrhythmic medications were not administered because the pulse quality and capillary refill time of the dog remained adequate.
Blood gas analysis of a venous sample obtained at that time revealed the development of acidemia (pH, 7.18; reference range, 7.35 to 7.45) and consequent ionized hypercalcemia (0.39 mg/dL; reference range, 0.28 to 0.35 mg/dL). The hypokalemia worsened (1.4 mEq/L). The Pco2, which was not abnormal at the time of admission (reference range, 35 to 38 mm Hg), increased to 50 mm Hg. The increase in Pco2 was associated with a reduction in respiratory rate and depth of respiration. Muscle paralysis was generalized, and the onset of ventilatory failure as a result of respiratory muscle weakness was suspected.
At 3.5 hours after admission, the dog had signs of clinical improvement (muscle strength, mentation, and a more physiologically appropriate tachypnea). By 4.5 hours after admission, the dog was able to attain a sitting position and appeared bright and alert. The potassium concentration and acid-base status had correspondingly returned to within the respective reference ranges.
The dog remained hospitalized for 52 additional hours. During that time, blood gas analysis and hematologic and biochemical analyses were repeated 3 times. The results were within the respective reference ranges for all analyses at these 3 times.
Differential diagnoses for hypokalemia included reduced dietary intake, increased renal losses (attributable to renal pathological conditions, diuretics, or chronic lithium exposure1), increased gastrointestinal losses (attributable to gastrointestinal pathological conditions or exposure to laxatives2), or intracellular sequestration of potassium. Intracellular sequestration of potassium may result from alkalosis, hypoglycemia-inducing medications (insulin, orally administered hypoglycemics, or xylitol), β-receptor agonists and other sympathomimetics,2 thyroxicosis,3 barium toxicosis, and breed-specific hypokalemic periodic paralysis.
The dog did not have a history of a reduced dietary intake or gastrointestinal or renal abnormalities to support these as the cause of the hypokalemia. Although the dog had no known access to toxicants or pharmaceuticals commonly associated with hypokalemia, toxicant exposure was suspected given the acute onset and subsequent rapid response to treatment. Unfortunately, the vomitus produced by the dog during transportation to the hospital was not available for toxicological analysis. Urine and plasma (lithium heparin) samples acquired during the period of collapse were submitted to the SAS Unit for Trace Elements of Southampton General Hospital for barium analysis because barium toxicosis reportedly causes similar clinical signs in humans.3–6 Barium analysis was performed by use of ICP-MS,f with rhodium as an internal standard. Detection limit was 0.06 μg/dL for plasma and 0.027 μg/dL for urine. Within-batch CV for lithium heparin plasma was 2.4% for a concentration of 2.4 μg/dL and 3.3% for a concentration of 13.7 μg/dL. Within-batch CV for urine was 4.6% for a concentration of 2.7 μg/dL and 8.6% for a concentration of 1.2 μg/dL.
High barium concentrations were detected in plasma samples obtained 1 (47.4 μg/dL), 3 (45.1 μg/dL), and 5.5 (41.9 μg/dL) hours after admission, and a high barium concentration was detected in a urine sample (14.7 μg/dL) collected 1 hour after admission. The urinary barium-tocreatinine ratio was 24.5 for the sample obtained 1 hour after admission. Given the infrequency with which this assay is performed on samples obtained from dogs, no reference range has been established for barium content in plasma or urine obtained from healthy dogs. Reference ranges for barium concentration in the plasma7 and urine8 of humans have been calculated as < 0.1 μg/dL and 0.01 to 0.85 μg/dL, respectively, and the reference range for the urinary barium-to-creatinine ratio in humans is 0.2 to 7.1. The concentrations detected in the dog reported here were comparable with those detected in humans with confirmed barium intoxication.9 No substantial increases in 30 other potentially toxic trace elements (including arsenic, lead, and molybdenum) were detected in the initial urine and plasma samples when screened semiquantitatively via ICP-MS by use of a multiple-element scanning program.
Paired urine and plasma (lithium heparin) samples were obtained from 5 randomly selected control dogs admitted to our small animal teaching hospital for various non–toxin-related reasons. The 5 control dogs were a 12-year-old neutered female Jack Russell Terrier with chronic bronchitis, a 2-year-old sexually intact male German Shepherd Dog with a fractured tibia as a result of being struck by a car, a 10-year-old sexually intact male Rhodesian Ridgeback with a parathyroid gland adenoma, a 10-year-old neutered male German Shepherd Dog with a cutaneous hemangiosarcoma, and a 3-year-old neutered female Saluki with hepatopathy.
Samples were submitted for analysis to assess the range of barium concentrations in plasma and urine samples of the control dogs. Barium concentrations ranged from 0.07 to 0.19 μg/dL for the plasma samples and from 0.21 to 3.15 μg/dL for the urine samples, and the urinary barium-to-creatinine ratio ranged from 1.9 to 14.4. These results further strengthened the diagnosis of barium toxicosis in the dog reported here.
A plasma sample was obtained for electrolyte analysis 10 days after the dog collapsed (7 days after discharge from our facility); the results were unremarkable. Electrolyte concentrations of the dog were analyzed again on day 56 after collapse, and these results also were within the respective reference ranges. On day 56, urine and plasma (lithium heparin) samples were submitted for barium analysis. The results revealed a decrease in the barium concentration in the plasma (0.3 μg/dL) and urine (1.7 μg/dL); however, the urinary barium-to-creatinine ratio was 34.4 and was still elevated. Ninety days after collapse, the dog remained clinically normal.
Coefficient of variation
Inductively coupled plasma mass spectrometry
LaserCyte hematology analyzer, Idexx Laboratories, Chalfont St Peter, Buckinghamshire, England.
VetTest biochemistry analyzer, Idexx Laboratories, Chalfont St Peter, Buckinghamshire, England.
Vetlyte analyzer, Idexx Laboratories, Chalfont St Peter, Buckinghamshire, England.
iSTAT, Abbott, Birmingham, West Midlands, England.
Potassium chloride concentrate BP 20% wt/vol, Martindale Pharmaceuticals, Brentwood, Essex, England.
Elan 6100DRC plus, SCIEX Perkin Elmer, Beaconsfield, Buckinghamshire, England.
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