can be considered in hypervolaemic animals. To avoid life-threatening neurologic complications such as brain stem myelinolysis, recommended rates of correction for chronic (>2 days) hyponatraemia are 10–12 mEq/l/day or approximately 0.5 mEq/l/h (0.5 mmol/l/h) (Benitah, 2010). When hyponatraemia is corrected too rapidly, the increasing osmolality of the extracellular space results in water movement from the intracellular to the extra-cellular space, and consequent cellular dehydration and shrinkage. This cellular shrinkage can separate the neurons from their myelin sheaths leading to myelinolysis. Mental status, hydration and electrolytes (particularly serum sodium concentration) need to be monitored frequently (e.g. every 4–6 h) during correction of hyponatraemia. Seizure can be treated as described in Chapters 12 and 24, however dosage and choice of AEMs will vary depending on the underlying aetiology of hyponatraemia.
Hypernatraemia
Overview
Hypernatraemia occurs when plasma sodium concentration is above reference levels (usually 155 mEq/l or mmol/l in dogs, and 162 mEq/l or mmol/l in cats) (Benitah, 2010). Occurrence of clinical signs depends more on rapidity of onset of hypernatraemia than to magnitude of change. Neurological signs generally occur when serum sodium levels exceed 170 mEq/l or mmol/l in dogs and 175 mEq/l or mmol/l in cats (>350 mOsm/kg) (de Morais and DiBartola, 2008b). Hyper-natraemia can result from water or hypotonic fluid loss, or excessive sodium gain (Box 4.5).
Sodium and its attendant anions account for approximately 95% of the osmotically active substances in the extracellular water. Therefore hypernatraemia is associated with hyper-osmolality (de Morais and DiBartola, 2008b).
Box 4.5. Causes of hypernatraemia (modified from de Morais and DiBartola, 2008b).
Pure water deficit (normovolaemic hyper-natraemia):
• Inadequate water intake;
• Animal unable to drink or no access to water;
• Primary hypodipsia;
• Diabetes insipidus (central or nephrogenic).
Hypotonic fluid loss (hypovolaemic hypernatraemia):
• Gastrointestinal;
• Vomiting;
• Diarrhoea;
• Small intestinal obstruction;
• Renal:
• Osmotic diuresis (mannitol infusion, hyperglycaemia);
• Non-osmotic diuresis (furosemide administration);
• Chronic renal failure;
• Non-oliguric renal failure;
• Post-obstructive diuresis;
• Third-space loss;
• Pancreatitis;
• Peritonitis;
• Cutaneous;
• Burns.
Excessive sodium gain (hypervolaemic hypernatraemia):
• Hypertonic fluid administration (intravenous hypertonic saline, sodium bicarbonate, sodium phosphate enema);
• Hyperaldosteronism;
• Hyperadrenocorticism;
• Excessive sodium chloride intake (e.g. salt poisoning).
Clinical presentation
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.
Diagnosis
Diagnostic investigations including laboratory analysis and imaging will vary depending on the suspected underlying aetiologies of hypernatraemia (see Box 4.5). The reader is referred to internal medicine textbooks for further details on diagnosis and treatment of each condition.
Management
Treatment is aimed at restoring normal extra-cellular fluid volume, decreasing sodium serum levels and treating the underlying cause of the hypernatraemia. Serum sodium concentration should be corrected at a rate of less than 0.5 mEq/l/h (0.5 mmol/l/h) to minimize the risk of cerebral cellular swelling, cerebral oedema and increased intracranial pressure. Free water deficit can be calculated based on the formula in equation 4.2 at bottom of page.
Oral water administration is the preferred method to correct water deficits in normovolaemic animals. Isotonic intravenous fluids should be used in normovolaemic animals that cannot drink and in hypovolaemic animals. Once the extracellular fluid volume has been restored, hypotonic fluids can be administered as maintenance treatment. Normovolaemic animals with pure water deficits can be administered 5% dextrose in water intravenously. Hypernatraemia secondary to excessive sodium gain can be treated with 5% dextrose in water intravenously and a loop diuretic to promote natriuresis (Benitah, 2010). Mental status, hydration and electrolytes (particularly serum sodium concentration) need to be monitored frequently (e.g. every 4–6 h) during correction of hypernatraemia. Seizures can be treated as described in Chapters 12 and 24; however, dosage and choice of AEMs will vary depending on the underlying aetiology of hypernatraemia.
