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Indian J. Anaesth. 2003; 47 (2) : 88-93

INDIAN JOURNAL OF ANAESTHESIA, APRIL 2003

88

REVIEW ARTICLE

POST ANAESTHESIA SHIVERING (PAS): A REVIEW

Dr. Pradip K. Bhattacharya1 Dr. Lata Bhattacharya2
Dr. Rajnish K. Jain3 Dr. Ramesh C. Agarwal 4
SUMMARY
Post Anaesthesia Shivering (PAS) occurs in 40% of patients recovering from general anaesthesia and most of the times is preceded
by central hypothermia and peripheral vasoconstriction indicating that it almost is always thermoregulatory mechanism, which even
today is ill understood. Some shivering may not be thermoregulatory, thus making the management of PAS complex.
The physiology of PAS, organisation of the thermoregulatory mechanism, various measures for prevention and the methods both
pharmacological and non pharmacological, of effective managements are reviewed in this article.

Introduction
In homeothermic species, a thermoregulatory
system coordinates defenses against environmental
temperature to maintain internal body temperature within
a narrow range, thus optimizing normal body function.
The combination of anaesthetic induced thermoregulatory
impairment and exposure to a cool environment makes
most unwarmed surgical patients hypothermic, as Pickering
wrote in 1956: The most effective system for cooling a
man is to subject him to anaesthesia. Santorio discovered
the clinical value of temperature in 1646 but it took two
centuries more, before body temperature was recognized
by Wunderlich as a key parameter. In anaesthesia its
importance was not understood till mid of 1960s when
first case of malignant hyperthermia was observed.
Unfortunately, except in some isolated cases temperature
monitoring has not yet become a standard practice, nor
is the measures instituted to lessen changes in core
temperature during the perioperative period.
Inadvertent hypothermia is associated with numerous
adverse outcomes in the postoperative period. Shivering
is an important complication of hypothermia, it is a
complicated response of the body that includes at least
three different patterns of muscular activity1 It occurs
frequently i.e. 40 to 60 % after volatile anaesthetic, but
still it remains poorly understood. Obvious etiology
although is said to be cold induced, but some shivering
1.
2.
3.
4.

MD., Assistant Prof., Anaesthesia, BMHRC, Bhopal

MD., Reader, Anaesthesia , JLN Cancer Hospital, Bhopal
MD., Associate Prof. Anaesthesia, BMHRC, Bhopal
DA., MD., Professor, Anaesthesia, BMHRC, Bhopal
Correspond to :
Dr. Rajnish K. Jain
Associate Prof. Anaesthesiology & Critical Care,
Bhopal Memorial Hospital & Research Centre,
Bhopal- 462 038
Tele-Fax: +91-755-742692
E-mail : rajnishkjain@hotmail.com

like tremors are not thermoregulatory.2,3 Despite the

availability of various drugs and technologies to prevent
hypothermia it continues to remain an ongoing problem
in the perioperative period. First of all our goal will be
to review the organization of the thermoregulatory
system, and particularly the physiology of postanaesthetic
shivering, followed by discussion considering
consequences, preventive and curative measures.
Thermoregulation
The processing of thermoregulatory response has
three components: Afferent thermal sensing, Central
regulation and Efferent responses. Together they work to
maintain normal core body temperature (Fig-1).

Afferent thermal sensing

Signals from cold receptors travel along a delta
fibres and Signals from warmth receptors are conveyed
by C fibres. Thermal inputs get integrated at the level of
spinal cord, its ability to sense and modulate thermal
signals was pivotal for development of currently accepted
multiple multilevel concept of thermoregulation.4 In
fact all thermoregulatory effector mechanisms are
modulated by spinal cord, eventually it arrives at the
hypothalamus, the primary thermoregulatory control center
in mammals.

BHATTACHARYA P., BHATTACHARYA L., JAIN R., AGARWAL R. : POST ANAESTHESIA SHIVERING

Two anatomically separate groups of neurons are

involved in thermal responsiveness and control the
thermoregulatory muscle tone and shivering in the reticular
formation of rat.5 A comparative study in vertebrates also
concludes that peripheral thermal input to the hypothalamic
areas is via the polysynaptic nonspecific reticular areas in
the brain stem. The nucleus raphe magnus and the
subcoeruleus area of the brainstem are important relay
stations in the transmission of thermal information from
skin to hypothalamus.
Central regulation
Preoptic region of the anterior hypothalamus is the
dominant autonomic thermoregulatory controller in
mammals. Much of the excitatory input to warm sensitive
neurons comes from hippocampus, which links the limbic
system (emotion, memory, and behavior) to
thermoregulatory responses. Warm sensitive neurons in
the preoptic anterior hypothalamus along with sensing of
core temperature also compare local information with
thermal and nonthermal synaptic afferents arriving from
ascending pathways.
Electrophysiological studies suggest that some
anterior hypothalamic neurons act as Sensors as well as
integrators. These interactions are inevitable because
the thermoregulatory system has few specific effector
organs, and must be understood as a part of adaptive
response of the organism as a whole6 (Fig.2 and 3).

89

Efferent responses
Multiple inputs are integrated into a common
efferent signal to the effector systems. In both animals
and humans,7 effector mechanisms are called upon in an
orderly fashion, ensuring optimal regulation.
The principle defense against hypothermia in
humans includes skin vasomotor activity, nonshivering
thermogenesis, shivering and sweating.
Heat loss is normally regulated by cutaneous
vasodilatation or vasoconstriction, sweating and shivering
are major response of the body to heat regulation.7
Thermoregulatory shivering is thus a last resort defense
that is activated only when behavioral compensations and
maximal arterio-venous shunt vasoconstriction are
insufficient to maintain core temperature. Nonshivering
thermogenesis is the result of cellular metabolic process
that does not produce mechanical work; it has been
demonstrated in human neonate8 and in rodents.
Shivering
It is an involuntary, oscillatory muscular activity
that augments metabolic heat production upto 600%
above basal level.9 Shivering is elicited when the preoptic
region of the hypothalamus is cooled. Efferent shivering
pathway arises and descends from the posterior
hypothalamus. Increase in muscle tone during shivering
is due to temperature-induced changes in neuronal
activity in mesencephalic reticular formation and
dorsolateral pontine and medullary reticular formation.5
Synchronization of motor neurons during shivering
may be mediated by recurrent inhibition through
renshaw cells, a group of inhibitory interneurons identified
in cats.10
Heat balance and shivering
The processes that lead to core hypothermia in
regional and general anaesthesia are similar.11 As in
general anaesthesia, the initial hypothermia in regional
anaesthesia results from redistribution of body heat from
the core to the periphery.12 Patients given spinal or epidural
anaesthetics cannot reestablish core temperature
equilibrium, because peripheral vasoconstriction remains
impaired. Shivering in these patients produces relatively
little amount of heat, because it is restricted to the small
muscle mass cephalad to the block.
Shivering occurs in approximately 40% of
unwarmed patients who are recovering from general
anaesthesia and in about 50% of patients with a core
temperature of 35.5 degree centigrade and in 90% of
patients with a core temperature of 34.5 degree centigrade.

90

It is associated with substantial adrenergic activation13 and

discomfort.14 Some patients find accompanying cold
sensation worse than surgical pain.
Consequences of shivering
Shivering can double or even triple oxygen
consumption and carbon dioxide production. Prospective
randomized data suggest that high risk patients assigned
to only 1.3 degree Celsius core hypothermia were three
times more likely to experience adverse myocardial
outcomes.15 Marked increase in plasma catecholamine
level is perhaps associated with high-risk cardiac
complications.13
Shivering increases intraocular16 and intracranial17
pressures. It is especially disturbing to mothers during
labour and delivery. Since shivering intensity is markedly
reduced in elderly and frail patients, it is unlikely that
shivering itself provokes serious adverse outcomes in these
patients. Similarly shivering is rarely associated with
clinically important hypoxemia, because hypoxemia itself
inhibits this response.18
Tremor patterns
Three patterns of muscular activity were observed
in hypothermic volunteers during emergence from
isoflurane anaesthesia.1 The first was a tonic stiffening
and appeared to be largely a direct non-temperature
dependant effect of isoflurane anaesthesia. A second pattern
was overt synchronous tonic waxing and waning at near
0.3% end tidal isoflurane concentration. This was the
commonest pattern and resembled that produced by cold
induced shivering true thermoregulatory shivering.19 The
third pattern was spontaneous electromyographic clonus
that required both hypothermia and residual isoflurane
end tidal concentration between 0.4 and 0.2%. During
epidural anaesthesia, synchronous waxing and waning
patterns were present, however no abnormal EMG patterns
were detected.20
Dissipation of anaesthetic induced thermoregulatory
inhibition, with the increase in shivering threshold towards
normal is the conventional explanation for the post
anaesthetic tremor. Tremor frequency is not observed in
markedly hypothermic patients, it occurs commonly in
normothermic patients.2 Contradictory to this, one study1
suggested that special factors related to surgery such as
stress or pain might contribute to the genesis of
postoperative tremor, since it failed to identify any
shivering- like activity in normothermic volunteers. Pain
might facilitate shivering like tremor in both postoperative
patients7 and in women having spontaneous term labour.3
25% of postoperative patients reach a core temperature of

INDIAN JOURNAL OF ANAESTHESIA, APRIL 2003

380 C and 50% of them reach 38.40 C7 and this eventually

leads to an increase in thermoregulatory set point, which
may be associated with normal thermoregulatory shivering.
Normal thermoregulatory shivering remains by far the
most common cause of postoperative shivering.
Temperature monitoring
Temperature monitoring must be accurate and
consistant. Research indicates that during the perioperative
period when core temperature rapidly changes, the
relationship between the temperatures measured at various
body sites may differ considerably.21 Core temperature is
measured in the pulmonary artery, distal esophagus,
nasopharynx and tympanic membrane.22 A recent survey
found that infrared tympanic monitoring to be the preferred
route of temperature measurement pre and post operatively.
Research has indicated that the accuracy of temperature
reading is dependent on the operator, patient anatomy,
and the instrument.23
Prevention of post anaesthesia shivering
If we restrict ourselves to combat shivering solely
with pharmaceuticals, than heat recovery will be still
slower and the patient will be deprived of an important
defense mechanism against reduction of core temperature,
shivering therefore should first of all be prevented, thereby
offsetting hypothermia. If it does occur, it should be
treated, mainly by warming the patient and than
administering medication to inhibit it.
The benefits of cutaneous warming in the
postoperative patients have been controversial, with some
studies identifying benefits 24 and others failing to confirm
faster rewarming.25 Two factors contribute to rapid
intraoperative transfer of heat from peripheral tissues to
the core, the first is vasodilatation induced by central
inhibition of thermoregulatory control26,27 the second is
that general anaesthesia itself induces peripherally mediated
vasodilatation, which facilitates intracompartmental heat
transfer. Taken together, these studies suggest that
intraoperative cutaneous warming is faster than comparable
postoperative warming. It seems clear that patients should
be warmed during surgery rather than allowed to cool
and then rescued postoperatively for prevention of post
anaesthesia shivering.
Cutaneous heat loss can be decreased by covering
the skin (e.g. with surgical drapes, blankets or plastic
bags). A single layer of an insulator reduces the heat loss
by approximately 30%; unfortunately adding additional
layers does not proportionately increase the benefit.28 In
most cases some form of active warming is required to
prevent hypothermia. Forced air warming is generally the

BHATTACHARYA P., BHATTACHARYA L., JAIN R., AGARWAL R. : POST ANAESTHESIA SHIVERING

91

most effective available method,29 but any method or

combination of methods that maintain the core temperature
above 360C is adequate. Forced air warming or a
combination of forced air warming along with fluid
warming is required to maintain normal intraoperative
and postoperative core temperatures.

Physostigmine a nonselective centrally acting

cholinesterase inhibitor is a potent antishivering drug.7 In
a prospective, randomized and double blind study, healthy
adult patients who were premedicated with anticholinergic
drug had a significant greater incidence of postoperative
shivering than those in control group.39

Pharmacotherapy
Potent antishivering properties have been attributed
to numerous drugs.7,18,30 These drugs are substances of
several classes including biogenic monoamines,
cholinomimetics, cations, endogenous peptides and possibly
N-methyl-D- aspartate

Activity of preoptic warm-sensitive neurons

decreases and cold sensitive neurons increases with local
application of thyrotropin releasing hormone thereby
producing cold defense response and hyperthermia.40 In
contrast, activity of preoptic anterior warm sensitive
neurons increases and cold sensitive neurons decreases
with angiotensin II41 and morphine42 thereby producing
hypothermia.

(NMDA) receptor antagonists. All these appear to

modulate central thermoregulatory control mechanisms.
The normal functions of these drugs are diverse and the
predominant site of action of most of these drugs is difficult
to establish.
5 HT caused shivering and vasoconstriction and a
concomitant rise in core temperature while, nor epinephrine
and epinephrine lowered the normal resting temperature
in cat and attenuated the 5 HT induced hyperthermia.31
The balance between the modulatory 5 HT and nor
epinephrine inputs may be responsible for short and long
term thermoregulatory adaptive modifications of the
shivering threshold.32 Dopamine has also been found to
induce hypothermia to a lesser extent in unanaesthetised
monkey when injected into hypothalamus.33
Nefopam an analgesic with powerful antishivering
properties18 is a potent inhibitor of synaptosomal uptake
of 5 HT, nor epinephrine and dopamine. Tramadol is an
antishivering drug7 with a similar mechanism of action, it
inhibits reuptake of 5 HT, norepinephrine and dopamine
and, facilitates 5 HT release.34 Cerebral a2- adrenoceptors
are also thought to play a role in the attenuation of
postoperative shivering by tramadol.35
Acetylcholine and nicotine apparently induce
vasoconstriction, shivering, and a hyperthermic reaction
when injected into the hypothalamus of a conscious
monkey,34 in rabbits, intravenous injection of nicotine
stops shivering.36 Release of acetylcholine is markedly
increased by 88% at the active acetylcholine releasing
sites within the preoptic anterior hypothalamic area by
peripheral cooling but suppressed by 80% at the same
perfusion sites by peripheral warming.37 Microinjection
of the cholinoceptor agonists, carbachol and pilocarpine,
into the mesencephalic nucleus raphe magnus caused
significant hyperthermia which was blocked by local
pretreatment with muscarinic receptor antagonist as well
as a nicotinic receptor antagonist.38

Arginine vasopressin, adrenocorticotrophic hormone

and melanocyte stimulating hormone are thought to act as
endogenous antipyretics during fever.
Pure m agonists including morphine, fentanyl and
alfentanyl are better for treatment of postanaesthetic
shivering. Alfentanyl is probably effective because
increasing plasma concentrations linearly reduces the
shivering threshold.43 Epidurally administered sufentanyl
in patients produces a dose dependant decrease in
shivering response and body temperature.44 Epidural
fentanyl also reduces the shivering threshold when added
to lignocaine for epidural anaesthesia.45 Meperidine
decreases the shivering threshold almost twice as much as
vasoconstriction threshold46 and is not only an effective
treatment for shivering,47 but clearly more effective than
equianalgesic concentrations of pure m receptor agonists.48
The antishivering activity of meperidine may be partially
mediated by k- opiod receptors.
The positive ions calcium (Ca2+) and sodium (Na+)
may play a functionally opposing role in mediation of
body temperature. Excess of Ca2+ into the posterior
hypothalamus leads to a decrease in body temperature
while excess of Na+ ions increases body temperature.49
Magnesium may be considered as physiologic calcium
channel blocker. During cold exposure, magnesium
concentration in plasma increases and in heat acclimatized
volunteers plasma magnesium decreases.50 The possible
physiological role in cold adaptation may thus explain the
effectiveness of magnesium in decreasing the threshold of
postanaesthetic shivering.
Magnesium sulfate is a physiologically occurring
competitive antagonist at NMDA-receptors and was
found to stop post-anaesthetic shivering.7 Ketamine,
which is a competitive NMDA-receptor antagonist,
also inhibits postanaesthetic shivering. It is likely that

92

NMDA-receptor antagonist modulate thermoregulation at

multiple levels, these areas are preoptic anterior
hypothalamus and locus coerulus. The NMDA-receptors
at dorsal horn of spinal cord modulate ascending
nociceptive transmission.
Methylphenidate is an analeptic agent that binds
presynaptic sites on dopamine, nor epinephrine and 5-HT
transport complexes, which in turn blocks reuptake of the
respective neurotransmitters7 and thus is effective for
prevention and treatment of postanaesthetic shivering.
Conclusion
Since shivering is an accompanying part of
general and regional anaesthesia and it leads to various
consequences and discomfort to the patient, proper steps
must be taken for its prevention and treatment. The most
effective measures for prevention and treatment are forced
air warming and fluid warming. The pharmacological
agents for combating it are Nefopam, Tramadol,
Physostigmine, Morphine, Fentanyl, and Pethidine etc.
As the dictum says, prevention is better than cure,
it holds true for shivering also and it should be practiced.
The purpose of writing this article is to highlight the fact
that there is still a lot to understand about the pathophysiology
and management of post anaesthesia shivering, and thus
more research is required in this subject.
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