Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 97

Clinical signs of hypernatraemia are mainly neurological and include anorexia, lethargy, vomiting, behavioural changes, head pressing, ataxia, generalized muscular weakness, muscle fasciculations, seizures, blindness, obtunded mental status progressing to stupor and coma, and death in severe cases. The severity of the neurological signs depends more on the rate of increase in sodium concentration than on the degree of hypernatraemia. With acute hypernatraemia water moves out of cells into the hyperosmolar extracellular space producing neuronal dehydration. The resulting decrease in cerebral volume may cause stretching and tearing of small cerebral vessels, leading to intracranial haemorrhage (subarachnoid, subdural, and/or intraparenchymal). Both cellular dehydration and intracranial haemorrhage may contribute to cerebral dysfunction in the acutely hypernatraemic animal (Benitah, 2010). When hypernatraemia develops slowly and gradually (e.g. <1 mEq/l/h or <1 mmol/l/h), the cerebral neurons compensate by increasing intracellular osmolality by movement of sodium, potassium, chloride and glucose intracellularly and by producing osmotically active solutes, called idiogenic osmoles (such as taurine, sorbitol and inositol) to adapt to the hypertonicity and minimize cerebral cellular dehydration. Clinical signs may be minimal or absent with slowly developing hypernatraemia. In addition to the clinical signs caused by the hypernatraemia and associated hyperosmolality, clinical signs of hypovolaemia (decreased skin turgor, dry mucous membranes, delayed capillary refill time, tachycardia, hypotension, increased PCV and total protein concentration, and high urine specific gravity) or hypervolaemia (ascites, peripheral or pulmonary oedema and jugular distension) may be present.