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Post-anaesthetic complications

JEAN MARIE DESMONTS

Studies into the overall risk of anaesthetic care have focused mainly on death
rates after operative procedures; few have examined the incidence of non-
fatal complications or the relationship between the nature of recovery room
complications and eventual outcome.
The incidence of complications occurring during the recovery period
varies between 20 and 40% of the total number of complications related to
anaesthesia (Cohen et al, 1986; Tiret et al, 1986). In the French survey (Tiret
et al, 1986), half of the deaths and cases of cerebral damage totally
attributable to anaesthesia were due to post-anaesthetic respiratory
depression. This finding can possibly be explained by the inadequate
number of recovery rooms in France at that time since about 50% of patients
were returned directly to the ward after anaesthesia.
The high incidence of hypoxic episodes (Marshall and Wyche, 1972) in the
post-anaesthesia care unit (PACU) has been reported in many studies using
pulse oximetry for post-anaesthetic management (Tyler et al, 1985; Cooper
et al, 1987; Moller et al, 1990, 1993). The awareness of certain PACU
problems, such as hypoxaemia and the high incidence of cardiovascular
complications induced by recovery led most scientific societies of developed
countries to establish standards for post-anaesthesia care (Eichhorn, 1992;
Cooper et al, 1993).

INCIDENCE OF POST-ANAESTHETIC COMPLICATIONS

Several large series have attempted to document the actual rate of occur-
rence of adverse events. The French survey, performed between 1978 and
1982, has shown that 42% of major complications associated with anaes-
thesia occurred during the recovery period (Tiret et al, 1986). The delay
between the end of the procedure and the occurrence of post-anaesthetic
complications was short in most cases: half of the overall complications
occurred during the first post-anaesthetic hours and 75% within the first 5
hours. The delay was shorter for complications totally related to anaesthesia
than for those which were partially related (Figure 1). The prognosis was
worst when the complications occurred during the recovery period (37% of
lethal complications) than during anaesthesia (16 % of lethal complications).
Baillibre' s Clinical Anaesthesiology-- 797
Vol. 8, No. 4, December1994 Copyright9 1994,byBailli6reTindall
ISBN0-7020-1947-X All rightsofreproductionin anyformreserved
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798 J. M. DESMONTS

100J.
Or)
e-
s 60

ID
40

O 20

1 2 a 4 5 e 1'2 2:4
Time of occurence (h)

Figure 1. Cumulative percentage of post-anaesthetic complications according to the delay

between the end of procedure and the time of occurrence. *, Totally related to anaesthesia;
e, overall; Q, partially related to anaesthesia. From Tiret et al (1986), with permission.

In the United States, Salem et al (1975) reported that 25% of deaths

related to anaesthesia in children were observed during the recovery. The
same percentage was found in the United Kingdom (Lunn and Mushin,
1982). In Australia, Holland (1987), reported that 18% of the total n u m b e r
of anaesthetic deaths were observed during the recovery period.
The overall incidence of post-anaesthetic complications is substantial as
Zelcer and Wells (1987) reported a 30% incidence in a teaching hospital in
Australia. All patients admitted to the recovery room during a one-month
period were included in the study and each incident was recorded (Table 1).
Ten per cent of patients were unarousable and did not show any response to
verbal stimulation for 15-90 minutes. Twenty per cent of patients had
haemodynamic instability (hypotension, hypertension, arrhythmnias, myo-
cardial ischaemia). Two per cent of patients had a respiratory problem
(hypoventilation, hypoxaemia, laryngospasm).
Cohen and co-workers (1986) found 31.6% of in-patients to have suffered
complications related to anaesthesia. Follow up of 112 961 cases was carried
out over 9-years, made up of two time periods (1975-1978 and 1979-1983).
The major post-operative complication rate per 10000 anaesthetics
increased from 41 in the first period to 45 in the second. The rate of
post-operative myocardial infarction was 3.8 per 10000 in the first period
and 13.7 per 10 000 in the second.
A randomized evaluation of pulse oximetry in 20802 patients was
performed in Denmark (Moller et al, 1993). There was a significant increase
in the detection of respiratory events in the oximetry group in the P A C U ,
with a similar 19-fold increase in the rate of detected hypoxaemia (14.3% in
the oximeter group versus 1.7% in the control group). Similarly, more
cardiovascular events were detected in the oximeter group than in the
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POST-ANAESTHETICCOMPLICATIONS 799

Table 1. Distribution of complicationsin 133 patients during the recoveryperiod.

System Complication Frequency
Central nervous system (86 patients) Unrousable 41
Pain 39
Agitation/dysphoria 13
Cardiovascular (68 patients) Hypotension 33
Hypertension 13
Arrhythmia 32
Ischaemia 3
Respiratory (10 patients) Cyanosis 4
Laryngeal spasm 3
Hypoventilation 4
Stridor 1
Gastrointestinal (24 patients) Nausea 11
Vomiting 13
Other Oliguria 5
Hypothermia 1
Hyperglycaemia/acidosis 1
From Zelcer and Wells (1987), with permission.

control group (2.2 % versus 1.8 %). However, the total number of patients in
w h o m a post-operative complication was identified was the same in both
groups (10% with pulse oximetry and 9.4% without).

TYPES OF COMPLICATION

Few epidemiological studies of anaesthetic morbidity have been focused on

the complications occurring during the recovery period. The volunteer case
review survey conducted in France (Tiret et al, 1986) provide some data
regarding the types of complication associated with post-anaesthetic recovery
(Table 2). Few complications due to failure of equipment or related to
intubation were observed. The most common cause was respiratory depres-
sion (27 cases leading to death in seven cases and to brain damage in five
cases). Almost all the patients had received narcotic analgesics (26 of 27
patients) and muscle relaxants (21 of 27 patients) during anaesthesia.
Seventy per cent of cases of respiratory depression occurred during the
first post-anaesthetic hour. Inhalation of gastric contents was also frequently
reported (13 cases leading to the death of four patients). Circulatory failure
was lethal in half of these cases but most of the patients concerned were in
poor condition, making the assessment of the contribution of anaesthesia
difficult. One-half of the cardiac arrests occurred suddenly while the others
following a long period of refractory hypotension. Thirteen neurological
complications related to cerebrovascular accidents or to head injury were
followed by death in four cases and by irreversible brain damage in three
cases.
In the study from Lunn et al (1983), 16 of the 32 deaths totally attributable
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800 J. M. DESMONTS

Table 2. Causes of complications during the post-anaesthetic period.

Complications Death Brain damage
Respiratory failure
Failure of equipment 1 1 --
Complication of intubation 2 1 --
Inhalation of gastric contents 13 4 --
Pneumothorax 2 1 --
Respiratory depression 27 7 5
Atelectasis 1 -- --
Bronchospasm 2 -- --
Circulatoryfailure
Acute pulmonary oedema 12 2 --
Cardiac arrest 19 16 --
Collapse 4 -- --
Myocardial infarction 7 3 --
Severe arrhythmias 9 3 --
Neurological complications 13 4 3
Total 112 42 8
From Tiret et al (1986), with permission.

to anaesthesia o c c u r r e d during the post-anaesthetic period: 11 were related

to respiratory failure and five to circulatory failure.

RESPIRATORY COMPLICATIONS

Post-operative p u l m o n a r y dysfunction can be caused by mechanical,

h a e m o d y n a m i c and pharmacological influences related to surgery and
anaesthesia (Beard et al, 1986).

Inadequate post-operative ventilation

Several factors m a y contribute to post-anaesthetic hypoventilation and
include i n a d e q u a t e respiratory drive, related to residual effects of i.v. or
inhalational anaesthetics, increased airway resistance, residual curarization,
increased c a r b o n dioxide p r o d u c t i o n due mainly to post-anaesthetic
shivering.

Inadequate respiratory drive. T h e residual effects of intravenous or

inhalational anaesthetics blunt the ventilatory responses to b o t h hypox-
aemia and hypercarbia. T h a n k s to pulse oximetry, it is n o w possible to
routinely m o n i t o r oxygen saturation during the post-anaesthetic period.
Several reports (Moiler et al, 1990; Tyler et al, 1985) have d o c u m e n t e d a
55% incidence of h y p o x a e m i a (SpO2 less than 90%) in healthy patients
breathing r o o m air after general anaesthesia, with up to 12% having severe
h y p o x a e m i a (SpO2 less than 80%).
L o w residual concentrations of volatile agents virtually abolish the
ventilatory response to h y p o x a e m i a and that condition m a y persist for some
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POST-ANAESTHETICCOMPLICATIONS 801

time after the end of anaesthesia (Knill and Gelb, 1978). Certain opiate
anaesthetic techniques might produce biphasic, delayed respiratory
depression and hypoventilation (Becker et al, 1976). An additional increase
in plasma fentanyl concentration during the elimination phase was observed
in some patients during the recovery and might cause delayed respiratory
depression (Stoeckel et al, 1979). Sedatives can augment depression from
opiates and anaesthetics, or ablate the conscious will to ventilate (Bailey et
al, 1990). As shown by Forrest and Belleville (1963), the respiratory effects
of morphine are enhanced while the subjects are asleep. This relationship
between sleep stage and episodes of hypoxaemia and apnoea has been
confirmed by Catley et al (1985). The decrease in ventilatory response to
both hypercarbia and hypoxaemia is related to the level of sleep in adults
(Douglas et al, 1982). In elderly subjects, this response is 50% less than in
control younger subjects (Kronenberg and Drage, 1973).

Increased airway resistance. In the PACU, increased airway resistance is

commonly observed by upper airway obstruction in the pharynx (posterior
tongue displacement, soft-tissue collapse) and in the larynx (laryngospasm,
laryngeal oedema). The high incidence of obstructive apnoeas (Figure 2) in
the post-operative period has been emphasized by Catley et al (1985). Sleep
is known to depress the tonic and phasic activity of the musculature of the
upper airway and rib cage (Tusiewicz et al, 1977; Longobardo et al, 1982). It
is likely that some agents used for anaesthesia affect the muscle airway in a
fashion that is similar to the effects of sleep and then the drug may act with
sleep to cause narrowing of the upper airway and an increase in its airflow
resistance. In volunteers, the administration of 0.1 mg kg -1 of midazolam
produces a marked increase in upper airway resistance (Montravers et al,
1992). The midazolam-induced apnoeas are initially central and later

Central apnoea Obstructive apnoea Paradoxical breathing

lOO , Flll ,
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Figure 2. Histogramsshowingthe total number of episodedisturbances against time after the

end of anaesthesia in patients receivingmorphineinfusions(11)and patients receivingregional
anaesthesia (D). From Catley et al (1985),with permission.
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802 J . M . DESMONTS

obstructive. It has also been shown that midazolam increases the work of
breathing (Molliex et al, 1993). This increased work in breathing may be
poorly tolerated in elderly patients and in those with chronic respiratory
failure.

Residual curarization. If the inspiratory muscles cannot generate sufficient

pressure gradients along airways to overcome resistance, effective venti-
lation can be so reduced that respiratory failure occurs. This post-operative
hypoventilation is sometimes caused by incomplete reversal of intra-
operative neuromuscular relaxation. On arrival in the recovery room, 42%
of patients in a Danish study (Viby-Mogensen et al, 1979) and 21% in a
Australian study (Bemmer and Rozental, 1986) had train-of-four ratios of
less than 0.7. More recently, Bevan et al (1988), in Canada, reported that
the incidence of impaired recovery of neuromuscular activity following the
use of pancuronium and its reversal was 36% of patients and was similar to
previous reports from Denmark and Australia. However, the incidence was
decreased considerably in patients who had received atracurium and
vecuronium (Figure 3).
Lunn et al (1983) have incriminated persistent post-operative paralysis as
an important cause of anaesthesia related mortality since six out of 32 cases
4O Pancuronium Atracurium Vecuronium
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Figure 3. Relationship between TOF and muscle weakness in 150 patients on arrival in recovery
room. From Bevan et al (1988), with permission.
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POST-ANAESTHETIC COMPLICATIONS 803

of death totally due to anaesthesia were caused by residual neuromuscular

blockade. In the French survey (Tiret et al, 1986), 21 of 27 patients having
post-anaesthetic respiratory depression had received muscle relaxants
during anaesthesia for which antagonists had not been used.

Increased carbon dioxide production. Total body carbon dioxide production

varies directly with metabolic rate, substrate availability and body tempera-
ture. Recovery from general anaesthesia is known to be associated with
haemodynamic and ventilatory changes related to post-operative rewarm-
ing and shivering (Bay et al, 1968). Shivering has been observed frequently
after inhalation anaesthesia, and reports of its incidence varied from
21-66% (Vaughan et al, 1981). Ciofolo et al (1989) have shown that the
carbon dioxide output during recovery from isoflurane anaesthesia
increased from 150mlmin -1 at the end of anaesthesia t~) 570 mlmin -1 20
minutes after isoflurane discontinuation (Figure 4). However, PaCO2
remained unchanged, suggesting that ventilation in the ASA class 1
patients, included in this study, was perfectly accommodated to the
increased CO2 production resulting from post-operative shivering. The
ability to change ventilation in response to increased carbon dioxide
production remains to be investigated in the patients with limited cardio-
pulmonary reserve.

Inadequate post-operative oxygenation

The occurrence of post-operative hypoxaemia has been documented in
several studies (Marshall and Wyche, 1972; Moller et al, 1990). The
introduction of pulse oximetry has made it possible to investigate pbst-
operative hypoxaemia with a continuous measuring technique. As shown by
Moller et al (1990), the hypoxaemic episodes were unrecognized by the staff
in 95% of the cases. Significant risk factors associated with a higher
incidence of hypoxaemia were duration of anaesthesia, age and a history of
smoking. Cooper et al (1987) evaluated the effect of pulse oximetry on the
rate and severity of anaesthesia-related problems encountered in the
PACU. Significantly fewer events were recorded when pulse oximetry was
used but the study did not examine outcome beyond the PACU.
The most common causes of hypoxaemia in the PACU are: inadequate
alveolar Po2, hypoventilation and ventilation/perfusion mismatch.

Inadequate alveolar P02 and hypoventilation. Occasionally, post-

anaesthetic hypoxaemia is caused by a global reduction in the alveolar PO2
due to a ventilatory problem that impairs the delivery of fresh gas to alveoli.
Severe hypoventilation caused by respiratory centre depression from
residual effects of opiates may lead to major hypoxaemia with its disastrous
consequences as shown in the French survey (Tiret et al, 1986). Hypoxaemia
may also occur during periodic apnoea or obstruction (Catley et al, 1985).
Complete airway obstruction caused by laryngeal oedema or laryngo-
spasm rapidly depletes alveolar oxygen and a severe hypoxaemia may result
if this situation is not adequately managed.
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804 J. M. DESMONTS

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POST-ANAESTHETIC COMPLICATIONS 805

Occasionally, excessive concentrations of nitrous oxide (diffusion hypox-

aemia) in the alveoli can transiently reduce PAO2 and a significant hypox-
aemia may occur at the end of anaesthesia using this gas (Fink et al, 1954).

VentiIation/perfusion mismatch. Ventilation/perfusion mismatch can be

caused by any process that leads to decreased ventilation in some alveoli while
perfusion to these alveoli is maintained. Atelectasis is the commonest cause of
the intrapulmonary shunt and bronchial obstruction from secretion is a
frequent cause of it. Decreased ventilation to dependent lungs during
anaesthesia in patients lying supine has also been well documented (Tokics et
al, 1987). Pneumothorax as a result of surgical lung trauma or attempts at
percutaneous vascular cannulation is a cause of hypoxaemia due to atelectasis
and intrapulmonary shunts. Pulmonary oedema is another process that can
result in hypoxaemia during the post-operative period. Though rare, this
complication does occur in the PACU even in patients without predisposing
disease states (Warner et al, 1990). Most described cases have an onset within
60 min after anaesthesia (Cooperman and Price, 1970) and were preceded by
hypertension in more than one half of these cases.
However, the ordinary cause of intrapulmonary shunt is the decrease of
lung volume. A reduction in functional residual capacity (FRC) is
commonly observed in patients during and after surgery (Craig, 1981). The
risk for reduction of FRC is increased in certain patients such as elderly
patients, obese patients and those with chronic obstructive pulmonary
disease.
Because of the high risk of hypoxaemia during the recovery, all patients
should receive supplemental oxygen during transfer and initial recovery in
the PACU. The routine use of pulse oximetry was found to change PACU
care including higher flow rate of supplemental oxygen and increased use of
supplemental oxygen at discharge in monitored patients when compared
with those not monitored with pulse oximetry (Moller et al, 1993).

Aspiration
Aspiration of gastric contents is a recognized hazard for post-operative
patients whose laryngeal reflexes are inhibited by sedatives or residual
effects of general anaesthesia (Laxmaiah et al, 1985). Recovery of sufficient
neuromuscular function does not necessarily indicate that airway protection
is restored (Pavlin et al, 1989). Siedlecki et al (1974) found aspiration of
radio-opaque dye in 21% of responsive patients immediately upon tracheal
extubation at the end of anaesthesia. Burgess et al (1979) demonstrated that
some patients had laryngeal incompetence persisting several hours after
tracheal extubation following elective coronary artery bypass surgery. A
recent study has confirmed that prolonged endotracheal intubation impairs
the swallowing reflex for up to 48 hours (de Larminat et al, 1992). This could
contribute in part to the development of aspiration pneumonitis. Depres-
sion of the swallowing reflex was also observed during sedation produced by
inhalation of 50% nitrous oxide in oxygen (Nishino et al, 1987).
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806 J. M. DESMONTS

In the French survey (Tiret et al, 1986), 13 of 48 respiratory post-

anaesthetic complications were related to the inhalation of gastric contents
and led to death in four cases.

CARDIOVASCULAR COMPLICATIONS

Post-operative hypotension
Hypotension is the most frequent of the cardiovascular complications in all
series. Complications of hypotension include myocardial ischaemia or
infarction and brain infarction specially in patients with cardiac disease. Of
the various causes of hypotension, decreased cardiac output due to a
reduction in circulatory intravascular volume is surely the most common.
Blood loss frequently causes post-operative hypovolaemia. Blood loss is
sometimes occult and related to either a surgical problem or acute
coagulopathy. Rewarming following intra-operative hypothermia may
produce a decrease in systemic vascular resistances (SVR) and enhance
hypovolaemia related hypotension. Other causes for decreased SVR
include vasodilation from anaphylactoid reactions to medications or endo-
toxic shock. Post-operative hypotension caused by ventricular dysfunction
usually occurs in patients with pre-operative impaired ventricular con-
tractility. Left ventricular dysfunction related to post-operative myocardial
ischaemia is often initiated by intra-operative hypotension (Mangano, 1990)
in patients with coronary artery disease.

Post-operative hypertension
Most hypertension seen in the PACU develops during the emergence from
anaesthesia. Sympathetic stimulation due to pain, hypothermia, inadequate
ventilation or bladder distension is the most common cause. In patients with
pre-existing hypertension, post-operative hypertension may be severe
enough to require an antihypertensive treatment (Kataria et al, 1990; IV
Nicardipine Study Group, 1991). Thus, cardiovascular complications
including serious dysrhythmias, myocardial infarction or heart failure may
occur when untreated post-operative hypertension lasts over 3 hours (Gal
and Cooperman, 1975). Cerebral vascular accidents due to hypertension are
uncommon in normal patients but they can be observed more frequently
after carotid endarterectomy. Assidao et al (1982) have shown that there is a
correlation between the incidence of post-operative hypertensive episodes
and the occurrence of cerebrovascular accidents after carotid endarter-
ectomy.

Myocardial ischaemia
Recovery from anaesthesia and surgery constitutes a major risk period for
patients with coronary artery disease (CAD). Post-anaesthetic haemo-
dynamic disturbances such as hypotension, hypertension, tachycardia have
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POST-ANAESTHETIC COMPLICATIONS 807

been considered responsible for myocardial injury and left ventricular

dysfunction. Fegert et al (1988) studied 50 patients with CAD investigated
before, during and up to 32 hours after non-cardiac surgery with automated
ECG recordings and demonstrated that 30% of the patients had evidence of
myocardial ischaemia in the post-operative period (Figure 5). All post-
operative ischaemic events were reported to be silent and only 24% of them
were accompanied by increases in heart rate (Figure 6). Cardiac outcomes
(death, myocardial infarction and left ventricular failures) occurred in seven
of 50 patients (14%). Reiz and Hohner (1989) studied 95 patients with CAD
undergoing abdominal aortic reconstructive surgery and reported that 31%
of these patients demonstrated ischaemia in at least one of their four

6~F i n=20 n=16

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Figure 5. Incidence of post-operative ischaemia among patients with peri-operative ischaemia.

From Mangano et al (1989).

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Mangano et al (1989).
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808 J.M. DESMONTS

post-operative ECG recordings. In contrast to the study of Fegert et al

(1988), they found that all ischaemic changes in the first 24 post-operative
hours were accompanied by marked haemodynamic changes, most
commonly tachycardia.
Wong et al (1988) studied the post-operative ischaemic pattern in 102
patients with CAD over the first week following surgery. ST segment
changes were detected in 27% of the patients. Most of ischaemic patients
had early ischaemia (post-operative day 0-3) and 64% of all ST segment
depression episodes were associated with tachycardia. Cardiac outcomes
(death myocardial infarction, heart failure) occurred in eight patients (8%)
and six of eight had ischaemic ST depression.

Myocardial infarction
Myocardial infarction remains the main post-surgical cardiac complication
and is responsible for approximately one half of the 4-8% mortality
following abdominal aortic surgery (Crawford et al, 1981; Jamieson et al,
1982; Diehl et al, 1983). The incidence of non-lethal myocardial infarction
following major vascular surgery ranges from 4-7% (Jamieson et al, 1982;
Diehl et al, 1983). The risk is increased in patients who have suffered a
previous myocardial infarction (Tarhan et al, 1972). However, recent data
seem to indicate that aggressive monitoring and circulatory management in
an intensive care unit might reduce the reinfarction rate to the range of
5-12% (Rao et al, 1983). The relationship between post-operative myo-
cardial infarction and peri-operative myocardial ischaemia is not clearly
established (Slogoff and Keats, 1985). In the study by Fegert et al (1988),
adverse cardiac outcome occurred in seven of their 50 patients with only two
out of seven having peri-operative ischaemia. Intra-operative hypotension is
probably the commonest cause--by reducing or abolishing the blood flood
through a critical coronary artery stenosis (Mangano, 1990).

Left ventricular failure

The incidence of acute post-operative left ventricular failure is poorly
documented in the literature. Goldman (1983) reported a 5% incidence of
post-operative pulmonary oedema in 437 patients undergoing thoracic,
abdominal or aortic procedures. Diehl et al (1983) reported that 3%
subjected to abdominal aortic surgery had evidence of post-operative con-
gestive failure. Nine per cent of patients with previous myocardial infarction
studied by Eerola et al (1980) had post-operative dyspnoea, suggesting left
ventricular failure.
However, Reiz and Hohner (1989) reported that in their series of 95
patients, five with global post-operative left ventricular dysfunction had
pre-operative echocardiographic and scintigrpahic evidence of segmental
left ventricular dysfunction. These data suggest that left ventricular dys-
function during the first 24 hours after non-cardiac surgery is related to the
presence of previous myocardial injury rather than to peri-operative myo-
cardial ischaemia detected by electrocardiographic ST segment changes.
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POST-ANAESTHETIC COMPLICATIONS 809

However, brief episodes of myocardial ischaemia may alter contractile

function over several hours. This dysfunction would be related to the
stunning phenomenon as suggested by Coriat et al (1985). These authors
using nuclear ventriculography and long-term ECG recording showed a
close concordance between prolonged peri-operative myocardial ischaemia
and new global dysfunction at 24 hours after surgery. The existence of a
stunned myocardium following surgery documented by two-dimension
transoesophageal echocardiography was confirmed by Smith and colleagues
(1985).

Cardiac dysrhythmias
In patients without previous cardiac problems, sinus tachycardia is
undoubtedly the most common rhythm change enconntered during the
post-operative period (Goldman and Braunwald, 1992). Multiple non-
cardiac aetiological factors have been identified including pain, hypo-
volaemia, hypervolaemia, hypoxaemia, pulmonary embolism, anxiety,
infection and hypotension. Post-operative sinus tachycardia is best treated
by controlling its underlying cause.
In one study reported by Goldman and Braunwald (1992), 916 patients
with sinus rhythm throughout the course of major non-cardiac surgery, 35
(4%) developed new supraventricular tachyarrhythmias. Of these patients,
46% had acute cardiac conditions, 31% had major infection, 29% had
pre-existing hypotension and 20% were hypoxic. More commonly, post-
operative cardiac dysrhythmias are observed in patients with pre-existing
cardiac diseases. Atrial fibrillation may be precipitated by hypovolaemia as
well as hypervolaemia. The incidence of acute post-operative atrial fibril-
lation reported in the study from Reiz and Hohner (1989) was 30%.
Six per cent of patients over the age of 40 subjected to thoracic, abdominal
or aortic procedures exhibited new supraventricular tachycardia but its
relationship to adverse cardiac outcome was not reported (Goldman, 1983).
Premature ventricular contractions are commonly observed in post-
operative patients with CAD. Myocardial ischaemia may induce ventricular
tachyarrhythmias and precipitate ventricular fibrillation. Reiz and Hohner
reported post-operative multiple premature ventricular contractions in
three of 95 abdominal aortic surgical patients. However, no relation
between post-operative premature ventricular contractions and adverse
cardiac outcome could be demonstrated.

TEMPERATURE DISORDERS

Many patients undergoing surgery exhibit post-operative hypothermia. One

study observed that the average body temperature in recovering adults was
35.6~ and that 13% had a temperature less than 35~ (Vaughan et al,
1981). Elderly patients and infants are at increased risk of intra-operative
hypothermia. Hypothermia can increase the risk of post-operative mor-
bidity (Slotman et al, 1985) by increasing sympathetic nervous system
activity and oxygen demand during rewarming. Severe shivering can
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810 J . M . DESMONTS

increase peripheral oxygen consumption by 200-300% requiring augmented

cardiac output and minute ventilation (Ciofolo et al, 1989). This situation
may be poorly tolerated in patients with limited cardiac and poor ventilatory
reserve.
In contrast, hyperthermia is uncommon in the PACU. Acute post-
operative fever is often caused by exacerbation of an existing infection by the
surgical procedure. Other causes have been identified such as atelectasis,
unrecognized intra-operative aspiration, drug or transfusion reaction and
thyroid storm. The onset of malignant hyperthermia may be delayed until in
the PACU period (Rosenberg, 1988). Concomitant manifestations include
unexplained tachycardia, muscle rigidity and acidaemia and will establish the
diagnosis before marked temperature elevation occurs.

NEUROLOGICAL COMPLICATIONS

Delayed emergence and persistent coma

Residual sedation from anaesthetic medications is the most frequent cause
of somnolence in the PACU (Denlinger, 1983). Emergence from prolonged
anaesthetics with volatile agents may be slow particularly after long surgical
procedures in obese patients, reflecting saturation of tissue compartments.
Once the residual effects of anaesthetic agents have been eliminated,
other causes of post-operative unresponsiveness should be considered.
Untoward intra-operative events such as prolonged hypoxaemia or severe
hypotension must be sought as potential causes of post-anoxic encepha-
lopathy. This complication has also to be considered when an intra-
operative cardiac arrest requiring a prolonged cardiopulmonary resusci-
tation has occurred.
Intra-operative cerebral thromboembolism is another possibility in
patients with a history of atrial fibrillation or hypercoagulable states or in
those who have undergone internal jugular or subclavian cannulation. Post-
operative cerebrovascular accidents are usually observed in elderly patients
when a prolonged hypotension occurs intra-operatively (Larsen et al, 1988).
In the French survey (Tiret et al, 1986), 10% of the total number of
complications related to anaesthesia had a neurological origin. Half of them
were observed in elderly patients who had prolonged hypotension during
surgery. Other causes of unresponsiveness should be borne in mind when
emergence is delayed. Hypoglycaemia and severe hyperglycaemia will
produce unresponsiveness in patients at risk. Hypothermia produces
obtundation when body temperature is below 31~ (Wong, 1983).

Agitation
In the PACU, some patients exhibit altered mental reaction ranging from
confusion and disorientation to extreme agitation (Chaplan and Feeley,
1990). Agitation may be related simply to post-operative pain and admini-
stration of analgesics may easily resolve the problem. Pre-operative anxiety
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POST-ANAESTHETIC COMPLICATIONS 811

or intra-operative medications as phenothiazine or ketamine may give rise

to disorientation. Ketamine is known to cause post-operative dysphoria and
hallucination.
Patients taking psychogenic medication or those who abuse alcohol,
opioids, cocaine or other drugs can exhibit extreme agitation and dis-
orientation in the PACU (Mecca, 1992). Confusion and delirium after
anaesthesia can also indicate severe respiratory dysfunction. Hypoxaemia
may cause disorientation and agitation and should be recognized before the
administration of sedatives.

MISCELLANEOUS COMPLICATIONS

Nausea and vomiting

Nausea and vomiting are common problems during recovery from anaes-
thesia. Besides the discomfort from vomiting, the risk of aspirating gastric
contents should be borne in mind especially if some laryngeal incompetence
persists after extubation (Burgess et al, 1979). The incidence of emesis
during recovery is very high in some patients, especially those with obesity,
hiatal hernia or having surgical procedures such as extraocular muscle or
middle ear manipulation, and peritoneal intestinal traction. The administra-
tion of opioid analgesics and neostigmine increases the incidence of post-
operative nausea (Hunt et al, 1979; King et al, 1988).

Post-operative myalgias
The incidence of post-operative muscle pain is quite high after the admini-
stration of succinyl-choline (Trepanier et al, 1988) but may be reduced by
administration of a subparalysing dose of non-depolarizing relaxant (Pace,
199.0). However, acute myalgia may be also observed after administration of
non-depolarizing relaxants and even in patients receiving no muscle
relaxants.

Incidental trauma
Corneal injury during anaesthesia produces pain and photophobia in the
PACU (Batra and Bali, 1977). Corneal abrasion related to pulse oximetry
sensor has been observed by the author in an unrestrained patient during
recovery.
Compression injuries caused by improper positioning during anaesthesia
can generate serious long-term peripheral neuropathies (Kroll et al, 1990).
Nerve injury is the second largest class of injury in the ASA Closed Claims
database. Three specific nerve distributions comprised nearly three quarters
of all claims for nerve damage. These distributions were ulnar (34 %), brachial
plexus (23%) and lumbosacral nerve root (16%). Symptoms of ulnar nerve
injury were noted by five patients on emergence from anaesthesia and by
three others on the first post-operative day.
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812 J.M. DESMONTS

SUMMARY

Increasing emphasis on the unsafe period of time following emergence from

anaesthesia has been aided by the use of anaesthetic morbidity studies. The
analysis of such studies supports the contention that the prognosis of post-
anaesthetic complications appears to be related to the availability of a
post-anaesthetic recovery room and the observation of formal standards for
post-anaesthesia care. Although it is extremely difficult to prove that patient
safety is enhanced by the adoption of these standards, there is an intuitive
logic to the assumption that the availability of minimal equipment in the
PACU and the training of staff working in these units will help to optimize
safety for patients recovering from anaesthesia.

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