Page 1139 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1114 CHAPTER 10

VetBooks.ir Prognosis oedema, intracardiac or extracardiac shunts, pneu-
monia, airway obstruction, pneumothorax, botulism
The prognosis depends on the severity of, and abil-
ity to address, the underlying problem. If untreated,
hypoglycaemia may result in irreversible brain and severe hypotension. Hypoxic or ischaemic brain
damage is thought to be one of the principal factors
damage. in the development of neonatal maladjustment syn-
drome (see p. 1344).
NERVOUS TISSUE HYPOXIA/ISCHAEMIA Effective management depends on treatment of
the underlying disorder, with most cases benefiting
Nervous tissue has a high and continuous demand from insufflation of nasal oxygen. Specific therapies
for oxygen and is therefore vulnerable to impaired for the CNS hypoxia and ischaemia associated with
oxygen delivery resulting from hypoxia or ischaemia. neonatal maladjustment syndrome can be found in
The major effect is altered carbohydrate and energy Chapter 14.
metabolism, with a switch from aerobic to anaerobic
glycolysis. This leads to depletion of brain glucose, HYPONATRAEMIA
decreased energy production and localised lactic aci-
dosis. The resulting neuronal swelling may exacer- Hyponatraemia is most commonly associated with
bate ischaemia, with progression leading to further conditions such as enterocolitis, excessive sweat loss,
oedema, neuronal necrosis and cavitation. The clini- renal failure, uroperitoneum and adrenal insuffi-
cal manifestations depend on the extent of the area ciency, which cause sodium depletion or water reten-
affected. Localised interruption of blood supply can tion. The neurological signs that are seen are a result
occur with fibrocartilaginous emboli, intracarotid of the rapidly developing hypotonic hyponatraemia
injections, verminous thromboembolism and aortic and include depression, seizures (generalised or
thrombosis. When there is acute deprivation of oxy- focal), ataxia and coma. Progressively severe dis-
gen to the entire CNS, the first signs that are seen turbances can be seen as the serum sodium con-
are referable to impaired cerebral function, with centration falls below 115 mmol/l (115 mEq/l). The
depression leading to coma and seizures (Fig. 10.64). severity of signs depends not only on the degree of
Most cases result from respiratory insufficiency, hyponatraemia, but also on how quickly it develops.
which may arise from a variety of causes such as
neonatal respiratory distress syndrome, pulmonary HYPERNATRAEMIA (SALT POISONING)

Clinically significant hypernatraemia is uncom-
mon in horses but may occur in the initial stages
10.64
of diarrhoea, vomiting or renal disease if water loss
exceeds electrolyte loss. Food and water depriva-
tion are associated with decreased urine and fae-
cal output but continued cutaneous and respiratory
insensible water losses may result in hypernatraemia.
Inappropriate oral electrolyte supplementation, par-
ticularly in foals, may also cause hypernatraemia.
Hypernatraemia is associated with severe GI and
neurological signs including head and neck exten-
sion, blindness, aggressiveness, hyperexcitability,
ataxia, proprioceptive deficits and head-pressing.
The pathophysiology involves deposition of sodium
ions in the CNS, which when followed by access to
Fig. 10.64 Foal with chewing seizures secondary to ion-free water results in cerebral oedema, with death
hypoxic–ischaemic encephalopathy. occurring by respiratory failure. Treatment involves