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11
J.E. Ilkiw
Anaesthesia and
Disease
Introduction
Hyperthyroidism
225
systems may all be seriously affected (Peterson, renal function (and delaying the clinical and
1981). In one study of 131 hyperthyroid cats, biochemical consequences of severe renal failweight loss, polyphagia, hyperactivity and ure) in some cats with chronic renal failure
tachycardia were the most common clinical (Peterson & Ferguson, 1989). Deterioration of
signs and were found in 98, 81, 76 and 66% of renal function with clinical signs of renal failure
affected cats, respectively. Polydypsia/polyuria, has been reported after correction of the hypervomiting, cardiac murmur, muscle weakness, thyroid state in some cats with normal or
congestive heart failure and dyspnoea were slightly increased values for blood urea nitrofound in 60, 55, 53, 25, 12 and 11% of affected gen (BUN) and creatinine prior to treatment
(Peterson & Randolph, 1989). Maintenance of
cats, respectively (Peterson et al., 1983).
Weight loss may affect the pharmacokinetics renal blood flow during anaesthetic manageof some anaesthetic agents by changing the ment of hyperthyroid cats is therefore very
volume of distribution, and together with important in order to avoid postanaesthetic
excessive shedding of hair, will make these renal dysfunction or failure. Hyperthyroid cats
cats more susceptible to hypothermia under may be unable to concentrate urine even in the
face of clinical dehydration. This may be
anaesthesia.
The restless, apprehensive state induced by important in the hyperthyroid cat presented
hyperthyroidism can cause cats to be difficult to for emergency anaesthesia.
Dyspnoea, panting and hyperventilation have
handle and to become aggressive if restrained.
Some cats with hyperthyroidism tend to become been reported in some cats with hyperthyroidunable to cope with stressful conditions. ism, often associated with some form of stress
Respiratory distress, weakness and develop- (Peterson & Randolph, 1989). Alterations in
ment of cardiac arrhythmias may follow stress respiratory function reported in people with
such as forced restraint (Peterson & Randolph, hyperthyroidism include decreased vital capa1989). Muscle weakness, if present, may predis- city, decreased pulmonary compliance and
pose to hypoventilation under anaesthesia and increased minute respiratory volume (Ingbar &
the increased arterial carbon dioxide tension Woeber, 1981). These abnormalities in respirathat results from this may predispose to tory function probably result from a combination of respiratory muscle weakness and
arrhythmias.
Renal blood flow, glomerular filtration rate increased carbon dioxide production. Ventilaand tubular reabsorptive and secretory capa- tory responses to hypoxaemia or hypercapnia
cities are increased in people with hyperthyr- are increased in hyperthyroidism (Massey et al.,
oidism and in animals given large doses of 1967). Respiratory depression induced by anaesthyroid hormone (Vaamonde & Michael, 1981). thetic drugs is common under general anaesDespite these alterations, electrolyte balance and thesia and control of ventilation in hyperthyroid
serum electrolyte concentrations are usually cats is advisable. Dyspnoea in cats with
normal. Polyuria and polydipsia may be promi- congestive heart failure may be caused by
nent signs and studies in thyrotoxic people pulmonary oedema and/ or pleural effusion. If
usually reveal impaired concentrating ability pleural effusion is extensive, thoracocentesis is
probably due to increased renal blood flow and advisable prior to induction of anaesthesia.
Cardiovascular signs, including tachycardia,
the resultant decline in intramedullary solute
concentration. In cats with hyperthyroidism, systolic murmurs, gallop rhythm, dyspnoea,
renal dysfunction is relatively common, with cardiomegaly and congestive heart failure, are
42% of affected cats being azotaemic (Feldman common in cats with hyperthyroidism. A recent
& Nelson, 1987). Following successful manage- study has reported that 80% of hyperthyroid
ment of hyperthyroidism, 18% of these cats still cats are hypertensive (Kobayashi et al., 1990).
appeared to have renal insufficiency (Feldman & Electrocardiographic changes include tachycarNelson, 1987). In fact, the increased renal blood dia, increased R-wave amplitude in lead II,
flow associated with untreated hyperthyroidism atrial and ventricular arrhythmias and intramay tle beneficial in maintaining sustainable ventricular conduction disturbances (Fig. 11.1).
226
].E. Ilkiw
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Fig. 11.1 Electrocardiogram from a cat with hyperthyroidism showing increased QRS voltage indicative of left
ventricular. enlargement.
227
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J.E. Ilkiw
229
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230
J.E. Ilkiw
placed over the thorax and abdomen. Intravenous fluids and the inspired gases can also be
warmed by placing fluid and gas lines under hot
water containers. Oesophageal or rectal temperature should be continuously monitored
during anaesthesia (Chapter 10).
Postoperative Management
Many potential complications are associated
with thyroidectomy (Peterson, 1984) including
hypoparathyroidism, Horner's syndrome, vocal
cord paralysis, haematoma formation and airway obstruction.
The most serious complication is hypocalcaemia, which develops after the parathyroid
glands are injured, devascularized or inadvertently removed in the course of bilateral
thyroidectomy. After bilateral thyroidectomy,
serum calcium concentration should be monitored on a daily basis for 4-7 days or until it has
stabilized within the normal range (Feldman &
Nelson, 1987). Thyrotoxicosis depletes bone
calcium concentrations and following successful surgery, the serum calcium concentration
may decline below normal for several days as
skeletal reserves are restored (McDougall, 1981).
This mild hypocalcaemia (serum calcium concentration 1.75-2.25 mmol/1) must be differentiated from severe, acute hypocalcaemia (serum
calcium concentration < 1.75 mmol/1) associated with iatrogenic hypoparathyroidism. In
the latter case, clinical signs associated with
hypocalcaemia will develop within 1-3 days of
surgery. If clinical signs of restlessness, abnormal behaviour, muscle cramping or muscle pain,
muscle tremors, tetany or convulsions develop,
in association with a serum calcium concentration of < 1.75 mmol/1, the cat should be treated
(Feldman & Nelson, 1987). Severe tetany should
be treated by administration of calcium gluconate intravenously to effect, with ECG monitoring for bradycardia. Tetany can then be
controlled by the same dose of calcium gluconate diluted with an equal amount of normal
saline and administered subcutaneously, three
to four times daily (Feldman & Nelson, 1987).
Cats with less severe signs should be treated
with oral vitamin D and calcium supplementation (Feldman & Nelson, 1987). Plasma thyroid
hormone concentrations decline, often to subnormal levels, within 24-72h of a total thyroidectomy. This is not, however, an absolute
indication to initiate thyroid hormone supplementation (Feldman & Nelson, 1987). Thyroid
hormone levels should be checked 1 week after
total thyroidectomy and if T4 is < 12.87nmol/l,
supplementation with L-thyroxine should be
started. If T4 is > 12.87 nmol/1 then the level
should be checked again in 2 weeks (Nelson,
1993 pers. commum.).
Bilateral recurrent laryngeal nerve injury
causes stridor and laryngeal obstruction due to
unopposed adduction of the vocal cords and
closure of the glottic aperture. Immediate
endotracheal intubation is necessary to establish an airway, usually followed by tracheostomy (Roizen, 1990). Unilateral recurrent nerve
injury usually goes unnoticed. If laryngeal nerve
damage is suspected, function can be assessed at
the end of surgery by placing the patient in
sternal recumbency and viewing arytenoid
cartilage movement during a light plane of
anaesthesia.
Postoperative bleeding can lead to haematoma formation which can compromise the
airway. If this occurs, the cat should be reanaesthetized, the surgical area explored and all
bleeding vessels ligated.
Urethral Obstruction
Disease of the lower urinary tract is a common
health problem in cats. The reported incidence
varies from 52 to 85 new cases per 10 000 cats
each year (Fennell, 1975; Lawler et al., 1985). The
reported proportional morbidity rate in both
male and female cats varies from 1 to 6% (Lees et
al., 1989). Males and females have similar risks
of occurrence of non-obstructive forms of feline
urologic syndrome (FUS), but urethral obstruction is almost exclusively an affliction of male
cats. Occurrence is highly age-related; lower
urinary tract disorders are diagnosed predominantly in cats aged 2-6 years. Urinary tract
diseases can be categorized into one of several
clinical syndromes based on how they are
encolfntered in small animal practice (Lees et
231
al., 1989). Acute urethral obstruction can be lifethreatening and can induce acute renal failure,
while chronic partial obstruction can reduce
renal function. Male cats presenting with acute
urethral obstruction require some form of
restraint, usually chemical in nature, to enable
urine flow to be restored.
232
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Fig. 11.2 Electrocardiogram from a cat with hyperkalaemia (plasma potassium concentration 9.1 mmol/1)
showing absence of P waves, increased duration of QRS and increased voltage of T wave.
transport; tissue catabolism and parasympathetic activity (Schaer, 1975). Because of its farreaching effects, acidaemia should be corrected
prior to inducing anaesthesia (Schaer, 1975).
Elevation of blood urea nitrogen concentration occurs in obstructive uropathy. In one
study, the blood urea nitrogen was 57
39 mmol/1 and 71 37 mmol/1 after obstructions of 48 and 72 h, respectively (Finco &
Cornelius, 1977). Uraemic 'toxaemia' causes
central nervous system and myocardial depression. In uraemia, the effects of general anaesthetic agents are potentiated and drug dosages
should be decreased (Haskins, 1992).
233
234
J.E. Ilkiw
thereby lowering the serum potassium concentration. While some advocate administration of
both dextrose and insulin (Schaer, 1975) others
have found administration of dextrose alone to
decrease serum potassium concentration due to
endogenous insulin release (Lees et al., 1989).
With the first regime, a total dose of 0.5 units of
regular insulin/kg is added to lactated Ringer's
solution, together with 2 g of dextrose/unit of
insulin. The fluids are administered so that 40%
of the estimated deficit from dehydration is
administered over the first few hours (Schaer,
1975). In the second regime, the initial fluid
deficit is replaced using a solution which is
made with half 0.45% saline and half dextrose
5% (Lees et al., 1989).
If cats are not depressed, hyperkalaemic or
uraemic, a balanced electrolyte solution, such as
lactated Ringer's solution can be administered
subcutaneously. Approximately 90 ml/kg, divided into three daily doses, has been recommended until the patient is no longer azotaemic
and then tapered off over 1-3 days (Barsanti &
Finco, 1984). In sicker cats, the amount of fluid
to be administered depends on the severity of
the dehydration, uraemic signs and hyperkalaemia. One recommendation is to deliver
over 2-4 h a quantity of fluid equal to 5% of
body weight if signs are mild, 8% if moderate
and 12% if severe (Barsanti & Finco, 1984).
However, these are guidelines only and actual
volumes should be given according to individual requirements based on vital signs, hydration status and urine output.
Anaesthetic Management
Even in healthy animals, general anaesthesia
depresses renal function by decreasing renal
blood flow, glomerular filtration rate and
electrolyte excretion and by increasing renal
vascular resistance (Benson & Thurmon, 1987)
(Chapter 2). This is due to both direct and
indirect effects on renal function, with indirect
effects thought to play a more important role.
Indirect effects include changes in cardiovascular function as well as in sympathetic system
and endocrine activity, while anaesthetic agents
can directly affect tubular transport mechanisms. After short uncomplicated anaesthesia,
235
236
].E. Ilkiw
Postanaesthetic Management
Fluid therapy should be continued until azotaemia is resolved. Some cats will undergo a
marked diuresis (postobstructive diuresis) following relief of the obstruction. This is believed
to be due to both clearance of accumulated
metabolites and transient inability of the
proximal tubules to concentrate urine effectively. Substantial losses of water, sodium and
potassium can occur during this diuresis and,
since it may lead to volume depletion and
reduced renal function, it is important that it
be identified and adequate amounts of fluids
administered. Measurement of urine volume
every 2-4 h will help to identify diuresis and
can be used to calculate fluid requirements.
Haematocrit, total protein, blood urea nitrogen, creatinine and serum electrolyte concentrations should be reassessed as needed to ensure
adequate hydration and recovery of renal
function. The time interval between measurements will depend on the degree of uraemia and
the response to therapy.
237
hepatic insufficiency. In these cases, surface examination. Evaluation of liver function may
haemorrhages, haematuria and gastrointestinal detect severe lipidosis even before hyperbilirubinaemia has developed. Serum bile acid
blood loss may be found.
Cats with severe lipidosis may demonstrate concentrations after a 12-h fast and 2 h after a
obvious hepatic encephalopathy. In one study, meal may be used to detect functional impair25% of cats had some neurological deficit at ment. Bile acid concentrations exceeding
presentation, while signs of central nervous 20 j..lmol/1 indicate impaired hepatic function
system dysfunction developed in the remaining and warrant biopsy for histologic diagnosis of
cats as the disease progressed (Burrows et al., the underlying liver disorder (Center, 1991).
Confirmation of hepatic lipidosis requires
1981). Encephalopathic signs may include
lethargy, behavioural changes, intermittent histopathologic examination of liver tissue. The
blindness, dementia, ptyalism, seizures, rage coagulation status must be evaluated prior to
and coma. Changes in response to anaesthetic liver biopsy, especially if the patient is jaundiced
drugs can occur through changes in receptors (Center, 1991). This should include prothrombin
such as gamma aminobutyric acid (GABA) and time, partial thromboplastin time, fibrinogen
opioid, as well as changes in neurotransmitters. concentration and a platelet count. Prolonged
Cats with hepatic lipidosis have varying clotting times, a fibrinogen concentration less
degrees of hepatic dysfunction. Virtually all than 0.5 g/1 or a platelet count less than 50 X
cats develop increased activity of serum 109 /l should be corrected prior to liver biopsy
alkaline phosphatase (ALP). Many cats also by administration of a transfusion of fresh
develop increased serum activities of alanine whole blood or platelet-rich plasma depending
aminotransferase (ALT) and aspartate amino- on the haematocrit. A haematocrit of 0.251/l is
transferase (AST). The increase in gamma- generally recommended as the minimum accepglutamyltransferase (GGT) is usually less than table level prior to anaesthesia and surgery
that "of ALP. Cats with moderate to severe (Dodman et al., 1987) although, in this disease, it
disease usually are hyperbilirubinaemic and is generally unnecessary to transfuse prior to
appear jaundiced. These changes induce induction of anaesthesia provided the haematodecreased hepatocyte function and drugs that crit is above 0.20 1/l. A blood cross-match,
are dependent on the liver for metabolism or however, is carried out on these cats prior to
excretion should be avoided. Serum albumin liver biopsy or tube gastrostomy placement.
Cats that are dehydrated should be rehydrated
and globulin concentrations are usually within
the normal range, although hyperglobulinaemia prior to induction of anaesthesia by intravenous
may develop with chronically impaired hepatic administration of a balanced electrolyte solution
with appropriate potassium supplementation.
function.
Hyperglycaemia has been recognized in some Serum electrolyte concentration$ should be
cats with hepatic lipidosis. Overt diabetes monitored to guide fluid supplementation.
mellitus is not commonly associated with Administration of glucose as a calorie supplesevere hepatic lipidosis in cats and glucose ment should be avoided until a well balanced
intolerance may be the result of changed nutritional ration is successfully ingested
concentrations of endogenous catecholamines (Center, 1991).
and glucocorticoids.
In patients with normal liver function, anaesthesia and surgery uniformly and consistently
lower hepatic blood flow. In most instances, the
decrease in hepatic blood flow induced by
anaesthesia parallels and is proportional to the
decrease in systemic arterial pressure or cardiac
output. Maintenance of an adequate circulating
238
J.E. Ilkiw
hepatic disease to a drug is virtually unpredictable. Therefore, each drug must be carefully
selected and, more importantly, carefully
titrated to the desirable effect (Gelman, 1989).
239
Postanaesthetic Management
Maintenance fluids should be administered in
the postanaesthetic period. Cats recovering from
liver biopsy should be watched closely for signs
of haemorrhage. Signs of haemorrhage may
include a delayed awakening from anaesthesia,
pale mucous membranes, slow capillary refill
time, rapid heart rate, decreasing haematocrit
and total protein and abdominal paracentesis
which is positive for blood. Haemorrhage
should be treated initially by transfusion with
fresh whole blood and, if bleeding continues,
exploratory laparotomy.
The only known treatment for cats with
hepatic lipidosis is dietary support, hence tube
gastrostomy placement. Once the cat has
recovered from anaesthesia, supplementation
of food via the tube can be started. Recommendations for nutritional management are available (Biourge et al., 1990; Riggs, 1991).
Hypertrophic Cardiomyopathy
Cardiomyopathies represent the majority of
feline cardiovascular diseases (see Chapter 4).
An incidence of 8.5% was found in cats
autopsied at the Animal Medical Center
between 1962 and 1976, compared with an
incidence of 1.9% for congenital heart disease
(Lui, 1977). In 1987, a direct link between
decreased taurine concentration in the myocardium and dilated cardiomyopathy was proposed (Pion et al., 1987) and the concentration of
taurine in commercial cat food was increased.
The incidence of dilated cardiomyopathy in one
echocardiographic study has fallen from 28%
in 1986 to 6% in 1989 (Skiles et al., 1990).
Hypertrophic cardiomyopathy is now the most
prevalent feline cardiac disorder, its relative
240
J.E. Ilkiw
241
Fig. 11.3 Electrocardiogram from a cat with hypertrophic cardiomyopathy showing premature ventricular
contractions.
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Fig. 11.4 Electrocardiogram from a cat with hypertrophic cardiomyopathy showing left axis deviation
(which is sometimes referred to as left anterior
fascicular block).
242
J.E. Ilkiw
Fig. 11.5 Electrocardiogram from a cat with hypertrophic cardiomyopathy showing atrial fibrillation and
increased QRS voltage and duration. The latter are indicative of left ventricular enlargement.
243
factors that usually impair contractile performance, such as myocardial depression, systemic
vasoconstriction and ventricular over-distension
characteristically improve systolic function
(Jackson & Thomas, 1993). In this situation, the
mitral regurgitation associated with hypertrophic cardiomyopathy with outflow obstruction, responds to pharmacologic intervention in
a manner opposite to classic mitral regurgitation. Vasodilating agents augment the outflow
obstruction with a resultant increase in mitral
regurgitation, while vasoconstricting drugs
attenuate obstruction and decrease mitral regurgitation (Jackson & Thomas, 1993).
Cats are generally premedicated with a J.Lopioid agonist (such as oxymorphone, 0.03-0.05
mg/kg or methadone 0.1 mg/kg subcutaneously) and an anticholinergic such as glycopyrrolate (0.01 mg/kg subcutaneously). Opioid
agonists have minimal effects on myocardial
contractility, preload and afterload (Copland et
al., 1987). Glycopyrrolate is chosen in preference
to atropine because it is less likely to induce
sinus tachycardia or arrhythmias. If the cat will
tolerate a facemask, oxygen is administered
prior to, and during, induction of anaesthesia.
An intravenous rather than mask or chamber
induction is preferred to avoid excitement and
increased circulating catecholamine. At Davis,
the injectable drugs most commonly used to
induce anaesthesia are etomidate and diazepam.
One quarter (0.25 mg/kg) of the calculated dose
of etomidate (1.0 mg/kg), followed by half
(0.25 mg/kg) of the calculated dose (0.5 mg/
kg) of diazepam are administered together with
a replacement solution at a very slow rate.
Depth of anaesthesia is assessed after 30 s and if
the patient cannot be intubated another dose of
etomidate and diazepam is administered. The
dissociatives ketamine and tiletamine should be
avoided, as drugs which stimulate the sympathetic nervous system increase heart rate,
myocardial oxygen demand, shorten diastolic
filling time (Mason & Atkins, 1991) and may
increase outflow tract obstruction. Propofol,
thiopentone and thiamylal should also be
avoided. Propofol has been reported to impair
regional myocardial function in ischaemic
myocardium (Mayer et al., 1993), while the
increase in heart rate following thiobarbiturate
244
J.E. Ilkiw
Postanaesthetic Management
References
Allan, D.G. (1991) Special techniques. In: Small Animal
Medicine (ed. D.G. Allen), p. 1035-1096. J.B.
Lippincott, Philadelphia.
Atkins, C.E. & Snyder, P.S. (1991) Cardiomyopathy.
In: Small Animal Medicine (ed. D.G. Allen) p. 269297. J.B. Lippincott, Philadelphia.
Atkins, C.E., Gallo, A.M., Kurzman, I.D. & Cowen, P.
(1992) Risk factors, clinical signs, and survival in
cats with a clinical diagnosis of idiopathic
hypertrophic cardiomyopathy: 74 cases (19851989).]. Am. Vet. Med. Ass. 20~, 613-618.
Babad, A.A. & Eger, E.I. (1968) The effects of hyperthyroidism and hypothyroidism on halothane and
oxygen requirements in dogs. Anesthesiology 29,
1087-1093.
Baggot, J.D. & Blake, J.W. (1976) Disposition kinetics
of ketamine in the domestic cat. Arch. Int.
Pharmacodyn. Ther. 220, 115-124.
Barsanti, J.A. & Pineo, D.R. (1984) Management of
post-renal uremia. Vet. Clin. N Am.: Small Anim.
Pract. 14, 609-616.
Barsanti, J.A., Jones, B.D., Spano, J.S. & Taylor, H.W.
(1977) Prolonged anorexia associated with hepatic
lipidosis in three cats. Feline Pract. 7, 52-57.
Bedford, P.G.C. (1991) Small Animal Anaesthesia, The
Increased Risk Patient. Bailliere Tindall, London.
Benson, G.J. & Thurmon, J.C. (1987) Anesthesia and
the kidney: Special considerations. In: Principles
and Practice of Veterinary Anesthesia, (ed. C.E.
Short), p. 237-250. Williams & Wilkins, Baltimore.
Berman, M.L. & Holaday, D.A. (1989) Inhalation
anesthetic metabolism and toxicity. In: Clinical
Anesthesia (ed. P.G. Barash, B.F. Cullen & R.K.
Stoelting), p. 323-338. J.B. Lippincott, Philadelphia.
Berman, M.L., Kuhnert, L., Phythyon, J.M. et al. (1983)
Isoflurane and enflurane-induced hepatic necrosis
in triiodothyronine-pretreated rats. Anesthesiology
58, 1.
Bilezikian, J.P., Loeb, J.N. & Gammon, D.E. (1979) The
influelice of hyperthyroidism and hypothyroidism
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T
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J.E. Ilkiw
12
P.M. Taylor
Accidents and
Em.ergencies
Introduction