03 May 2013

No.15

POST ANAESTHESIA SHIVERING

NSY Padayachee

Commentator: NH Gokul

Moderator: J Reddy

Department of Anaesthetics

CONTENTS
DEFINITION AND AETIOLOGY.............................................................................3
RISK FACTORS......................................................................................................3
GRADING OF SHIVERING.....................................................................................4
SHIVERING PATTERNS.........................................................................................4
PHYSIOLOGY OF SHIVERING..............................................................................5
MECHANISM OF SHIVERING...............................................................................8
ADVERSE EFFECTS OF SHIVERING INCLUDING HYPOTHERMIA..................9
MECHANISM OF HYPOTHERMIA UNDER ANAESTHESIA................................9
TEMPERATURE MONITORING...........................................................................12
GENERAL VS NEURAXIAL ANAESTHESIA......................................................12
SPINAL VS EPIDURAL ANAESTHESIA.............................................................13
PREGNANCY.......................................................................................................13
TEMPERATURE OF NEURAXIAL INJECTATE/ INTRAVENOUS FLUID...........13
PREVENTION AND TREATMENT MODALITIES................................................14
Non-pharmalogical............................................................................................14
Pharmacological................................................................................................15
CONCLUSION......................................................................................................16
COMMENTARY....................................................................................................17
REFERENCES......................................................................................................18

INTRODUCTION
Page 2 of 19

Shivering is a frequent complication following anaesthesia, with an incidence of

between 40 60% and 56,7% following general and neuraxial anaesthesia
respectively. Post anaesthesia shivering (PAS) is associated with significant
patient discomfort including increase in postoperative pain, sympathetic
stimulation, metabolic oxygen demand, lactic acidosis and carbon dioxide
production. As a result it imposes increased stress on the cardiopulmonary
system, via increases in cardiac output and minute ventilation, which can be
detrimental in patients with limited reserves.[1-4]
Many studies have investigated the mechanism behind PAS, its consequences,
various preventative and treatment modalities including the science behind each
of these entites yet although numerous theories and evidence based literature
exist in animal and human studies there is no clear consensus with regard to the
aetiology of PAS, its prevention and the mechanism and efficacy around its
pharmacological treatment.
Although PAS may prove a conundrum, the value in its understanding and further
investigation is pivotal to anaesthesiologists to reduce patient morbidity and
mortality especially for those at higher risk of cardiac events.
DEFINITION AND AETIOLOGY
Shivering is defined as an involuntary, spontaneous, oscillatory mechanical activity
of skeletal muscle associated with increased oxygen consumption, this can be as
much as 600% [5]
Amoungst the various causes shivering can be divided into thermoregulatory and
nonthermoregulatory in nature[6]. Thermoregulatory shivering occurs as a
consequence of hypothermia, and inorder to maintain normothermia,
vasoconstriction and shivering occurs.
Non thermoregulatory shivering is less well understood and may be associated
with postop-pain, release of endogenous pyrogens, uninhibited spinal reflexes and
adrenal suppression.[7]
Shivering is also seen in normothermic individuals following surgery and in
pregnant patients undergoing labour and delievery.
RISK FACTORS
Some studies have suggested that younger age, male sex, longer duration of
surgery and anaesthesia and type of anaesthesia are associated with increased
risk of PAS.
GRADING OF SHIVERING
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Crossley and Mahajan have graded the intensity of PAS using the following scale:
.
0 = no shivering;
1 = no visible muscle activity but piloerection, peripheral vasoconstriction, or
both are present (other causes excluded);
2 = muscular activity in only one muscle group;
3 = moderate muscular activity in more than one muscle group but no
generalized shaking;
4 = violent muscular activity that involves the whole body. [8]
A scale more specific to neuraxial anaesthesia would incorporate
0 = no shivering
1 = shivering not interfering with monitoring or causing patient distress
2 = shivering interfering with monitoring or causing patient distress [9]
SHIVERING PATTERNS
2 types of shivering patterns have been observed following general anaesthesia
and also confirmed of EMG assessment :
The first is a synchronous waxing and waning at a frequency of 4 -8 cycles.min -1
and is of a tonic nature associated with true thermoregulation shivering as seen in
unanaesthetised volunteers exposed to cold enviroments

Figure 1 emg - tonic - pattern of shivering

[6]

The second is a clonic pattern of shivering occurring 5-7hz associated with

uninhibited spinal reflexes as seen in spinal cord transection, as seen in a study
with 0.2-0.4 end-tidal isoflurane concentration [10]

Page 4 of 19

Figure 2 emg - clonic - pattern of shivering

[6]

PHYSIOLOGY OF SHIVERING
There are 3 components that govern the physiology of shivering :
- Afferent neural pathway
- Central regulation
- Efferent response pathway[11]
The integration of information and modulation of thermal information amongst
these components lend to an efficient system that maintains a narrow therapeutic
range of core body temperature, being 36,5 37,5 0C, by utilising behavioural and
autonomic responses to defend against fluctuations in core temperature hence
ensuring optimal body function.
Afferent Neural Pathway
Thermoreceptors, which comprise of cold and warm sensory receptors are noted
to be central as well as peripheral. Cold signals travel via delta fibres and warm
signals travel via unmyelinated C fibres. These thermal signals get integrated at
the level of the spinal cord which, being itself thermosensitive, senses and
modulates the received input which eventually reaches the hypothalamus via the
lateral spinothalamic tracts. Of importance is the nucleus raphe magnus (inhibits
shivering) and the locus subcoerulus (excites shivering), located in the medulla
and pons respectively, which relays thermal information from the skin to the
hypothalamus. Spinal cord temperature is also known to influence effector
responses. Of note, the hypothalamus itself, other parts of the brain, spinal cord,
deep thoracic and abdominal tissues and skin, each constitute 20% of thermal
afferent input to the central regulatory system. According to recent studies, the
skin and dorsal root ganglia have been found to have special thermoreceptors viz.
Transient Receptor Potential (TRP) vanilloid (V) and menthol (M) receptors. They
are highly thermosensitive receptors with TRPV 1-4 being actiavted by heat whilst
cold activates TRPM8 and TRPA1 .[12-15]
Central Regulation
The preoptic region of the anterior hypothalamus is the most important central
regulator of temperature although the spinal cord and brainstem also subserve
this function.
Warm neurons in this region of the hypothalamus compare thresholds (triggering
core temperatures) with local thermal and non thermal information arriving via the
afferent pathway. They sense and integrate information. Autonomic responses
which are controlled by the anterior hypothalamus are primarily determined by
information received from central structures, whist behavioural responses and the
Page 5 of 19

effector mechanism which are controlled by the posterior hypothalamus are mostly
determined by information from the skin surface .[16]
The current consensus is that thermal inputs are received from a variety of
structures, the effector responses are not concurrent and occurs at different
temperatures, and there exists an interthreshold temperature (range of core
temperature at which no response is elicited )[16] Inhibitory potentials are thought to
govern the thresholds in the hypothalamus which are modulated by noradrenalin,
dopamine, serotonin, acetylcholine, prostaglandin E1 and neuropeptides.
Threshold temperatures are altered with circadian rythm and mentruation (0.5-1 0
C; 0.50 C respectively) together with nutritional status, exercise, infection and
drugs (sedatives, alcohol and nicotine ) The interthreshold range which is
bounded by sweating in the upper end and vasoconstriction in its lower end, is
between 0.2 0.40C. Sweating and vasoconstriction thresholds are higher in
women than men by 0.3 0.50C.
The shivering threshold is poorly regulated in the elderly .[16]

Figure 3 neural pathways involved in shivering

[6]

Efferent Response Pathway

Efferent responses are based on thermal disturbances that trigger responses that
either increase heat loss or promote heat gain. Each response is governed by a
specific threshold. Heat balance is maintained by behavioural modification, which
in a conscious individual is more important than autonomic control. Vasomotor
control constitutes vasoconstriction and piloerection in response to cold in an
Page 6 of 19

attempt to increase heat gain whilst vasodilatation and sweating increase heat
loss in response to increased warmth.[17]
Non shivering thermogenesis is essentially a form of increasing metabolic heat
production without an increase in mechanical work. It occurs in brown fat and
primarily a means of heat gain in infants.[16]
Shivering is regarded as a final means to increase metabolic heat production
when behavioral modification and vasoconstriction together with peripheral
arterio-venous shunting of blood in an attempt to increase core body temperature
is inadequate.[17] The shivering threshold is an entire 10 C less than the
vasoconstriction threshold. Shivering is not well developed in newborn infants .[16]

Figure 4 hypothalamic thermoregulation

Page 7 of 19

[18]

Figure 5 hypothalamic responses to temperature inputs

[18]

MECHANISM OF SHIVERING
When the preoptic region of the anterior hypothalamus is cooled this stimulates
the motor centre of shivering which is located in the posterior hypothalamus.
As a result the descending shivering pathway is activated and through
temperature induced neuronal activation of the mesenchephalic, dorsolateral
pontine and medullary recticular formation there is an increase of spinal muscle
tone manifested as shivering. Stimulation of the alpha motor neurons is the final
common pathway and synchronous discharge is brought about by inhibition of
renshaw cells (inhibitory interneurons) [11]

Page 8 of 19

ADVERSE EFFECTS OF SHIVERING INCLUDING HYPOTHERMIA

Post anaesthesia shivering, apart from patient discomfort also has several
deletrious effects including difficulty with monitoring techniques (ecg, bp, sp02),
increased oxygen consumption and metabolic demand, increased introcular and
intracranial pressure, metabolic acidosis and increased carbon dioxide production,
increased post-operative pain from surgical incision stretching, increase in cardiac
output, minute ventilation and systemic vascular resistence as well as raised
plasma catecholemine levels which may be linked to morbid cardiac events in
high risk patients.[6]
Post anaesthesia shivering is predominantly thermoregulatory in nature as a result
of the anaesthetic induced inhibition of thermal defense mechanisms and
subsequent hypothermia.
Hypothermia, according to the strict physiological definition, is a core temperature
greater than one standard deviation below mean core temperature for that
mammal under resting conditions in a thermoneutral environment, for practical
purposes however mild hypothermia is defined as a core body temperature of
between 33.0 36.40C, at which cellular and tissue dysfucntion may develop.
There is no consensus at which level mild hypothermia progresses to moderate
hypothermia.[17]
During periods of cerebral or cardiac ischaemia, it is thought that hypothermia
maybe protective on the basis on decreased metabolic demand, however
hypothermia, just like many other entites in anaesthesia, has a risk benefit ratio to
consider.
Mild hypothermia itself, is associated with numerous adverse side effects which
the shivering patient maybe at risk of, including, impaired immunity and surgical
site infection, delayed wound healing, coagulopathy, increase in allogenic blood
transfusions, delayed post anaesthetic recovery, prolonged hospitalistion, patient
discomfort, and morbid myocardial outcomes secondary to sympathetic nervous
system stimulation and increased plasma catecholemines [16]
It is thus imperative that temperature monitoring be done in patients undergoing
general anaesthesia longer than 30min and major operations under neuraxial
anaesthesia.[16]
MECHANISM OF HYPOTHERMIA UNDER ANAESTHESIA
Ineffective thermoregulation during anaesthesia, more so than environmental cold
exposure (lower ambient temperatures, cold intravenous fluids, evaporation from
surgical sites) is responsible for temperature changes in surgical patients. [16]

Page 9 of 19

Anaesthesia results in impairment in thermoregulatory defence mechanisms

resulting in core to periphery heat redistribution which is the primary cause of
hypothermia with a decrease of 1-2 0 C of core body temperature during the first
hour of general anaesthesia [19] (Phase 1)
Heat loss to the environment is responsible for the more gradual decline in body
temperature over the next 3-4hrs (phase 2) [19]
Eventually an equilibrium is reached such that heat loss equals heat production
(phase 3) [18]
General anaesthesia inhibits central thermoregulation by interfering with
hypothalamic function as well as causing dose dependent reduction in
thermoregulatory thresholds as seen with volatiles. [19] The interthreshold range is
increased by a tenfold factor from 0.2 0.4 0 C, in unanaesthetised individuals to,
2-40 C, under anaesthesia, thus limiting thermal defence responsiveness. [6,16,17]
Similar mechanisms surround neuraxial anaesthesia with the initial decrease in
core body temperature being due internal heat redistribution due to vasodilatation
(Phase 1). Failure of vasoconstriction below the level of the blockade promotes
ongoing heat loss (phase 2) and the decrease in the shivering threshold is
attributed to the altered perception of temperature in the blocked dermatomes by
the hypothalamus, which senses the elevation in skin temperature .[19]
This also results in a lack of perception of cold in patients who routinely dont have
intraoperative temperature monitoring when under neuraxial blockade. This further
increases the risk of hypothermia which generally goes undetected in this
subgroup of patients until shivering eventually manifests.

Page 10 of 19

Figure 6 hypothermia following general anaesthesia

[20]

Figure 7thermoregulation thresholds in unanaesthetised and

anaesthetised humans

[11]

Page 11 of 19

TEMPERATURE MONITORING
Body temperature is heterogeneous, with deeper structures being 2-4 0 C warmer
than peripheral structures. Skin temperature varies according to environmental
exposure, temperature of peripheral tissues (arms and legs), exposure history and
core temperature. Core temperature is the best measure of the thermal status in
humans which can be monitored via the tympanic membrane, pulmonary artery,
nasopharynx, distal oesophagus. Core temperature monitoring is used to assess
and monitor for intraoperative hypothermia, hyperthermia and the
pharmocogenetic entity of malignant hyperthermia .[16]
Inconvenience or unavailability of core temperature sites allow near core sites to
be used (mouth, axillae, bladder, rectum, skin surface). Each site and modality of
monitoring has its own limitations, the combination of which should not exceed
0.50C level of inaccuracy as this could be associated with hypothermia induced
complications[16]
Infrared sensors have emerged as the most popular form of thermometers as they
are accurate and inexpensive.[16] Tympanic probes being soft and pliable, pose
little risk of tympanic membrane perforation but cerumen insulation and incorrect
positioning are disadvantages of using such a modality.[16,19]
Oesophageal probes incorporated into oesophageal stethoscopes are safe
economical and accurate when positioned into the distal oesophagus .[19]
Nasopharyngeal probes are best placed a few centimetres distal to the nares
adjacent to the nasopharyngeal mucosa but they carry the obvious risk of
epistaxis with traumatic insertion.[16,19] Oral, axillary, bladder and rectal temperature
can measure core temperature with fair accuracy in the absence of extreme
temperature disturbances.[16]
GENERAL VS NEURAXIAL ANAESTHESIA
The mechanisms behind impairment of thermoregulation following general and
neuraxial anaesthesia is noted to be similar, however general anaesthesia is
associated with central inhibition of thermal defences and a greater degree of
suppression of threshold responses as manifested by shivering in the
postoperative period when general anaesthesia dissipates and threshold
responses return to baseline. This commonly results in thermoregulatory shivering
in response to hypothermia.
In contrast to this, neuraxial anaesthesia does not cause central inhibition and
results in a lesser suppression of threshold responses hence vasoconstriction and
shivering can still occur above the level of the neuraxial block, though such
thermal defences are inadequate in generating metabolic heat as the muscle
mass cephalad to the block is small.[9]

Page 12 of 19

This is supported by emg studies of volunteers undergoing general anaesthesia

without surgery revealing the 2 patterns of shivering as mentioned earlier
indicating both shivering related to hypothermia(tonic) and shivering related to
uninhibited spinal reflexes (clonic), whilst non-pregnant volunteers undergoing
epidural blocks revealed only the tonic pattern of shivering. [6]
SPINAL VS EPIDURAL ANAESTHESIA
There is evidence revealing a greater intensity of shivering following epidural vs
spinal anaesthesia. Spinal anaesthesia results in a greater widespread
vasodilatation and increased core to peripheral heat redistribution with greater
depression of shivering threshold compared to epidural anaesthesia.
Shivering threshold in spinal anaesthesia is directly related to the number of
dermatomes blocked. Spinal anaesthesia is associated with complete motor
blockade whilst epidural anaesthesia spares the sacral nerve roots, so for the
same block height there is reduced thermal afferent input in patients undergoing
epidural vs spinal anaesthesia so the shivering threshold is reduced to a lesser
extent. This is supported by Saito et al [21] who revealed higher shivering
thresholds in epidural versus spinal anaesthesia in pregnant parturients
undergoing caesarean sections whilst Ozaki et al [22] failed to show a difference in
shivering thresholds amongst male volunteers undergoing epidural vs spinal
anaesthesia.
It is postulated that the epidural and intrathecal space differ in terms of
thermoreceptors and their respective sensitivity. [9]
PREGNANCY
Despite the lack of extensive control studies on this subset of population, it is
found that there is an increase in temperature in patients undergoing labour and
those that have epidural anaesthesia. Several reasons for the hyperthermia have
been postulated including infection, placental inflammation, increase in metabolic
heat production secondary to muscular effort and the presence of the fetus.
Shivering during labour occurs with or without neuraxial anaesthesia. Patients with
epidural anaesthesia are more likely to shiver if they shivered prior to epidural
anaesthesia and also received N20. Immunological reasons have been postulated
for peripartum shivering. The shivering threshold however is noted to be higher in
females than males. [9,16]
TEMPERATURE OF NEURAXIAL INJECTATE/ INTRAVENOUS FLUID
Numerous studies have shown a correlation between the temperatures of the
local anaesthetic injected into the epidural space and the outcome on shivering .[9]
Epidural injections with cold local anaesthetic are associated with significantly
greater incidence and intensity of shivering whilst other studies remain
controversial and postulate other reasons.[9]
Page 13 of 19

A study by Mirzaei et al 2012 revealed a decreased incidence and intensity of

shivering in patients who received warm bupivacaine for spinal anaesthesia
undergoing caesarean section, 8.3% shivered in the warm group whilst 39.1%
shivered in the cold group.[23]
Chung et al 2012, revealed a decrease in shivering in patients that received warm
intravenous fluids compared to controls.[24]

Figure 8 frequency of shivering intensity in warm and cold bupivacaine groups [23]

PREVENTION AND TREATMENT MODALITIES

Non-pharmalogical
Most authors impress upon the importance of prevention as opposed to treatment
of post anaesthesia shivering as the majority of cases are associated with
hypothermia. Simple physical measures have been described including increasing
the ambient temperature of the operative room, preventing convective heat loss
by insulation with surgical drapes, space blankets, warm cotton blankets, ensuring
warm skin disinfectant is used prior to draping, and the use of warm intravenous
fluids and warm local anaesthetics for neuriaxial blockade .[9,11,17]
Forced air-warming devices have been associated with a significant decrease in
post anaesthesia shivering if applied for 15minutes prior to induction of
anaesthesia.[24]
The efficacy is based on increasing the skin temperature without appreciably
increasing core body temperature; this decreases the temperature gradient
between the central and peripheral compartments and subsequently decreases
internal heat redistribution on induction. Such patients exhibit higher skin
temperatures, lower decreases in core temperatures and a lower incidence of
shivering compared to unwarmed controls.[9]

Pharmacological
Page 14 of 19

Many drugs of various classes have been documented in the prevention and
treatment of post anaesthesia shivering, with different mechanisms of action,
varying doses, efficacy and side effect profiles. Hence the choice of
pharmacological agent for the treatment of post anaesthesia shivering should be
based on patient profile, drug characteristics as well as route of administration .[11]
Opiates
Pethidine is the most widely studied drug in the treatment of post anaesthesia
shivering. 25mg of pethidine has been found to be an effective antishivering agent
when administered intravenously. Its noted to cause inhibition of 5HT and
noradrenalin reuptake. This effect is not inhibited by naloxone and thus is not
opioid receptor mediated according to one author [25] whilst another[26] states that
the use of high dose naloxone in the presence of pethidine, fails to reduce
shivering. Pethidine decreases the shivering threshold twice as much as the
vasoconstriction threshold. Its antishivering action however according to studies
suggest that its a combination of stimulating alpha 2 adrenoreceptors, k opioid
receptors, NMDA antagonism and monoamine reuptake inhibition .[6]
Tramadol inhibits the reuptake of 5HT, dopamine and noradrenaline and
stimulates 5HT release. Its an opioid analgesic whose action is mediated through
the mu receptor. One study suggests that a dose of 2mg/kg at the time of surgical
wound closure provides sufficient analgesia and antishivering effects without
increasing adverse side effect potential (Mohta M et al 2009) [27], whilst another
study suggests that 0.25mg/kg in combination with 0.25mg/kg of ketamine is
superior to tramadol 0.5mg/kg alone in the prevention of shivering [28]
Pure mu receptor agonists morphine(2.5mg), fentanyl(25ug) and alfentanil(250ug)
are shown to be significantly superior to placebo in treatment of post anaesthesia
shivering, with alfentanil showing a linear relationship between increasing plasma
levels and a linear reduction in the shivering threshold. A study by Sadegh et al
2012, revealed that 25ug of intrathecal fentanyl with hyperbaric bupivacaine
compared to control in patients undergoing elective caesarean section under
spinal anaesthesia significantly decreases the incidence and severity of post
anaesthesia shivering.[29]
Non-opiates
Nefopam is a centrally acting non-opioid analgesic with powerful antishivering
properties via inhibition of 5HT, noradrenaline and dopamine reuptake. Clonidine
an alpha 2 agonist at a dose of 150ug proved to decrease the incidence of
shivering compared to placebo in at least 3 trials .[30] Doxapram, a respiratory
stimulant, is shown to be effective in the treatment of post anaesthesia shivering
with doses of 100mg noting to be effective in studies.Magnesium and ketamine
through NMDA receptor antagonism have been implicated in stopping shivering.
Studies* in rats have shown that the preoptic anterior hypothalamus is stimulated
via NMDA.
Page 15 of 19

Magnesium is also noted to decrease the shivering threshold via it being a natural
calcium antagonist. Calcium influx into the posterior hypothalamus on cold
exposure stimulating shivering has been implicated in rat studies. Physostigmine,
a cholinesterase inhibitor, also is successful in the prevention of post anaesthesia
shivering indicating that cholinergic pathways are involved in thermoregulation.
Ketanserin and ondansetron, serotonin antagonists, have proved to be effective
against post anaesthesia shivering.[6]
*reference available on request

CONCLUSION
Patients presenting for surgery and anaesthesia are invariably at risk of
inadvertent hypothermia and post anaesthesia shivering due to inhibition of
thermoregulatory defence mechanisms and ongoing heat loss to the environment.
Core temperature monitoring together with passive and active measures to
maintain normothermia are effective combative strategies in minimising the risk of
these undesirable clinical consequences. Though much research has been
dedicated to the pharmacology of post anaesthesia shivering, its complexity,
various mechanisms and lack of extensive conclusive evidence renders it an area
that requires further research and investigation. Prevention through simple
physical or non pharmacological methods should form the mainstay of our
intervention with drug treatment being based on clinical emergence of shivering.
Our choice of antishivering agent must consider our patients clinical status, drug
profile also taking into account dosing with respective side effects and our own
personal experience with each agent.

Page 16 of 19

COMMENTARY
Review of the weight of evidence in articles used for the production of the booklet
level
No.
1a
Systematic reviews & meta- 12
analysis
1b
Randomised controlled double 4
blinded trials
2
Cohort studies
5
3
Case control studies
4
Case series
4
Case report
0
4
Editorials
0

Page 17 of 19

References
6,7,9,11,15,16,17,18,19,20,27,30
3,5,23,29
1,8,10,26,28
2,4,24,25
13,14,21,22

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