Page 423 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

398 CHAPTER 1

VetBooks.ir depression, petechiation on the mucous membranes supporting table padding and poor positioning.
There may be a predisposition of certain individuals
and limb oedema may also be observed. Infarction of
the gastrointestinal tract can occur simultaneously,
sensitivity to anaesthetic agents.
leading to signs of colic. to generalised myopathy, probably through hyper-
This condition is thought to be similar to com-
Diagnosis partment syndrome in humans. Prolonged pressure
Blood work usually reveals a leucocytosis with a applied to muscle masses causes a decreased perfu-
left shift and toxic changes. Globulins are usually sion and blood stasis in the muscles. Hypotension
increased while albumin may be low. Muscle enzyme worsens the situation, leading to hypoxia and
activity is increased with CK frequently >47,000 ischaemia. This induces an anaerobic metabo-
IU/L and AST >1000 IU/L. High serum antibody lism, with accumulation of lactate, decreased pH
titres to SeM protein (>1:1600) and characteristic and oedema. The inelastic fascia surrounding the
histopathology can confirm the diagnosis. muscle masses causes the compartment pressure
to increase. Electrolyte imbalances are associ-
Management ated with muscle hyperexcitability and sustained
Corticosteroids are the mainstay of treatment with myotonic contractions. These phenomena lead to
dexamethasone administered at 0.04–0.2 mg/kg. fibre necrosis. During recovery, reperfusion brings
oxygen to the damaged cells, causing free radi-
Prognosis cal accumulation. Halothane may also lead to the
The prognosis for horses with infarctive purpura formation of toxic radicals. These induce further
haemorrhagica is poor and the condition is often muscle degeneration.
fatal.
Clinical presentation
POST-ANAESTHETIC MYOPATHY The signs become apparent during the recovery
from anaesthesia or soon afterwards. Recovery is
Definition/overview prolonged, with difficulty or an inability to stand
This is a myopathy that is identified during the up, depending on the affected muscles. Muscles are
anaesthetic recovery period and causes rapid, pro- swollen, hard to touch and feel abnormally warm
gressive degeneration of the muscle fibres. Two syn- (Fig. 1.766). There is localised to generalised sweat-
dromes are recognised: localised myoneuropathy ing and pain when pressure is applied to the affected
affecting one muscle or muscle group, and gener- muscle masses. Two forms are encountered:
alised myopathy causing diffuse myodegeneration.
It is generally accepted that there may be a periph- • Localised form. A distinct muscle mass is
eral neurological component, but post-anaesthetic affected, particularly the triceps, biceps and
neuropathy primarily involves the muscles, hence quadriceps femoris, masseter, longissimus dorsi,
the use of the term ‘myoneuropathy’ gluteal and hindlimb adductor muscles. The
affected muscle mass is hard, hot and painful
Aetiology/pathophysiology with localised sweating (Fig. 1.767). There
Post-anaesthetic myoneuropathy occurs after may be mild to severe lameness in the affected
general anaesthesia. Intrinsic predisposing fac- limb(s) (Fig. 1.768) or complete paresis. If the
tors include the weight of the animal, its muscular horse is recumbent, the condition may worsen
development, intensive training and nervous tem- significantly. In more severe cases the urine may
perament. Extrinsic factors relate to the anaesthe- appear orange to dark chocolate brown due to
sia, with the risk of problems increasing with the myoglobinuria. The signs usually resolve after
duration of anaesthesia, arterial blood pressure ≤70 a few hours to several days, but muscle atrophy
mmHg, inadequate perfusion of dependent muscles, and/or fibrosis may appear in 2–3 weeks and
use of positive pressure ventilation, hard or poorly remain.