Neurological signs of uraemic encephalopathy include obtunded mental status that can progress to stupor, muscle fasciculations (especially in facial muscles), head bobbing, generalized seizures and generalized weakness. In one retrospective study including 29 dogs, altered mental status was more common in dogs with chronic renal disease, whereas seizures were more common in dogs with acute renal failure (Fenner, 1995). Other clinical signs such as polyuria, polydipsia, vomiting and dehydration are reflective of renal failure.
Diagnosis
Diagnosis of renal-associated encephalopathy is based on signs of cerebral (mainly forebrain) dysfunction in an animal with renal failure or soon after haemodialysis or renal transplantation and no other cause of brain disease. Serum biochemistry shows very severe azotaemia, hyperkalaemia, and hyperphosphataemia with or without hypocalcaemia. Urinalysis performed before fluid therapy shows isosthenuria.
Management
Treatment should be aimed at the causes of the renal failure, if possible, as well as symptomatic and supportive. Fluid, electrolyte and acid-base imbalances should be corrected. Hypertension, if present, should be treated. Seizures can be treated as described in Chapters 12 and 24, however dosages of AEMs may need to be decreased in case of impaired renal excretion.
Hyponatraemia
Overview
Hyponatraemia occurs when plasma sodium concentration is below reference levels (usually 140 mEq/l or mmol/l in dogs, and 149 mEq/l or mmol/l in cats) (Benitah, 2010). Occurrence of clinical signs depends more on rapidity of onset of hyponatraemia than to magnitude of change. Neurologic signs may occur with sodium concentrations less than 120 mEq/l or mmol/l in dogs and less than 130 mEq/l or mmol/l in cats (de Morais and DiBartola, 2008a). Serum sodium concentration reflects the amount of sodium relative to the volume of water in the body and not total body sodium content. Hyponatraemic animals may have decreased, increased or normal total body sodium content and therefore volemic status also needs to be considered when investigating serum hyponatraemia (de Morais and DiBartola, 2008a). Hyponatraemia may result primarily from increased water gain, administration of fluids low in sodium (e.g. 5% dextrose in water, 0.45% sodium chloride), hypertonic solution without sodium (e.g. mannitol, glucose) and an excessive sodium loss (e.g. loop diuretics, thiazides). Causes of hyponatraemia classified based on plasma osmolality and hydration status are listed in Box 4.4.
Clinical presentation
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).
Diagnostic investigation
In hypovolemic and hyponatraemic animals calculation of the fractional excretion of sodium (FENa) can be used to determine if the kidneys are the source of excessive sodium loss (see equation below). The FENa should be less than 1% for nonrenal sources of sodium loss and 1% or greater if sodium is being lost by the kidneys (de Morais and DiBartola, 2008a).
Calculation of the fractional excretion of sodium is:
where FENa = fractional excretion of sodium, UNa = urine concentration of sodium (mEq/l), SNa = serum concentration of sodium (mEq/l), UCr = urine concentration of creatinine (mg/dl) and SCr = serum concentration of creatinine (mg/dl).
Additional diagnostic investigations including laboratory analysis and imaging will vary depending on the suspected underlying aetiologies of hyponatraemia (see Box 4.4). The reader is referred to internal medicine textbooks for further details on diagnosis and treatment of each condition.
Management
Treatment is aimed at increasing serum sodium levels and treating the underlying cause of the hyponatraemia. Isotonic (0.9%) saline or balanced electrolytes solutions can be administered to hypovolemic animals, while water restriction (i.e. limiting water intake to less than urine output) can be performed for animals with normovolaemia or hypervolaemia associated with excessive water intake or renal retention.
