Box 4.6. Causes of hypocalcaemia (modified from Schenck and Chew, 2008).

      • Puerperal tetany (eclampsia);

      • Renal failure (acute and chronic);

      • Protein-losing enteropathies (hypoalbuminaemia);

      • Acute pancreatitis;

      • Ethylene glycol toxicity;

      • Phosphate enema;

      • Hypoparathyroidism:

      • Primary;

      • Idiopathic or spontaneous;

      • Post-operative bilateral thyroidectomy;

      • After sudden reversal of chronic hypercalcaemia;

      • Secondary to magnesium depletion or excess;

      • Nutritional secondary hyperparathyroidism;

      • Citrate anticoagulant overdose with blood transfusion;

      • Hypovitaminosis D.

       Management

      Diazepam (0.5 to 1.0 mg/kg intravenously, up to a maximum total dose of 20 mg, in dogs and cats, repeated to effect or twice within 2 h; see Chapters 21 and 24) can be used to control the tetany and seizures initially while the diagnosis of hypocalcaemia is confirmed. Hypocalcaemia is treated with 10% calcium gluconate at a dose of 0.5–1.5 ml/kg (providing 5–15 mg/kg of calcium) administered slowly IV (over 10 to 30 min) to effect as individual requirements vary. Clinical improvement is generally obvious within minutes of initiating the infusion. Electrocardiographic monitoring is advisable because of the risk of cardiotoxicity. If bradycardia, premature ventricular complexes, increased P-R interval, prolonged QRS complex or shortening of the Q-T interval is observed, the IV infusion should be briefly discontinued. Maintenance therapy of hypocalcaemia involves calcium gluco-nate (at a dosage equal to the one used IV for the control of tetany), diluted in an equal volume of saline, administered SC every 6 to 8 h. Serum calcium concentration should be monitored every 1–3 days to adjust the calcium gluconate dose. Generally, after serum calcium concentrations have been maintained within reference range for 48 h, the administration of calcium gluconate can be gradually tapered off to every 8–12 h. Long-term maintenance treatment with oral calcium (25 mg/kg every 8–12 h) and vitamin D supplementation may be required. Specific treatment for the underlying aetiology of hypocalcaemia should be instituted as promptly as possible.

       Nutritional Disorders Causing Seizures

       Thiamine (vitamin B1) deficiency

       Overview

      Thiamine (vitamin B1) deficiency has been reported in dogs and cats fed thiamine-deficient diets including commercial canned pet food (Marks et al., 2011; Markovich et al., 2014). Thiamine can be destroyed by heat during cooking or processing, preservatives such as sulfur dioxide, sulfate trace minerals, ultraviolet and gamma irradiation, and thiaminase enzyme activity, which is found predominantly in shellfish, fish viscera and some bacteria. In addition, thiamine deficiency can result from decreased intake due to anorexia or vomiting, decreased intestinal absorption (e.g. diarrhoea), abnormal utilization (e.g. liver dysfunction) or increased requirements (e.g. fever, infection). The metabolically active form of thiamine, thiamine pyrophosphate, plays an essential role in three enzyme systems (pyruvate dehydrogenase, alpha ketoglutarate dehydrogenase, and transketolase), which are essential for complete oxidation of glucose through the Krebs cycle. Tissues dependent on glucose or lactatepyruvate for energy, such as the brain and heart, are particularly compromised in thia-mine deficiency.