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Clinical signs of hyponatraemia include lethargy, anorexia, vomiting, generalized weakness, ataxia, obtunded mental status progressing to stupor and coma, and seizures. The severity of neurologic signs is greater when hyponatraemia develops rapidly. In acute hyponatraemia, water flows down its concentration gradient and enters brain cells producing cerebral oedema and increased intracranial pressure. In addition, hypervolemic animals may be presented with ascites, peripheral or pulmonary oedema, and jugular distension; whereas hypovolemic animals may present with signs of dehydration including decreased skin turgor, dry mucous membranes, delayed capillary refill time, tachycardia, hypotension, increased packed cell volume (PCV) and total protein concentration, and high urine specific gravity. Determination of the animal’s volume status helps to identify the underlying cause of the hyponatraemia and initiate correct treatment.

Box 4.4. Causes of hyponatraemia classified based on plasma osmolality and hydration status (modified from de Morais and DiBartola, 2008a).

With plasma hyperosmolality (>310 mOsm/kg):

• Hyperglycaemia;

• Mannitol infusion.

With normal plasma osmolality (290–310 mOsm/kg):

• Hyperglycaemia;

• Severe hyperproteinaemia.

With plasma hypo-osmolality (<290 mOsm/kg):

• Hypervolaemia:

• Severe liver disease causing ascites;

• Congestive heart failure;

• Advanced renal failure;

• Nephrotic syndrome;

• Normovolaemia:

• Psychogenic polydipsia;

• Hypotonic fluid infusion;

• Syndrome of inappropriate antidiuretic hormone secretion;

• Antidiuretic medications (e.g. narcotics, nonsteroidal anti-inflammatory drugs, vincristine);

• Myxedaema coma due to severe hypothyroidism;

• Hypovolaemia:

• Gastrointestinal loss (diarrhoea with or without vomiting);

• Third-space loss (pancreatitis, peritonitis, uroabdomen, cavitary effusion);

• Cutaneous burns;

• Renal loss (hypoadrenocorticism, diuretic administration).