03 May 2013
No.15
POST ANAESTHESIA SHIVERING
NSY
Padayachee
Commentator: NH Gokul Moderator:
J Reddy
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Department of
Anaesthetics
CONTENTS
INTRODUCTION
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
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
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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]
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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 TRPV1-4
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 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 (0.5-10
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]
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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 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[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]
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]
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 1-20
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 –
0.40 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 don’t 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.
Figure 6 hypothermia following
general anaesthesia [20]
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TEMPERATURE
MONITORING
Body temperature is heterogeneous, with deeper
structures being 2-40 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]
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]
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]
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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
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 it’s 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. It’s 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.
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.
COMMENTARY
Review of the weight of evidence in articles used
for the production of the booklet
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level
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No.
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References
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1 a
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Systematic reviews & meta- analysis
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12
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6,7,9,11,15,16,17,18,19,20,27,30
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1 b
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Randomised controlled double blinded trials
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4
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3,5,23,29
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2
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Cohort studies
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5
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1,8,10,26,28
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3
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Case control studies
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4
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2,4,24,25
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Case series
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4
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13,14,21,22
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Case report
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0
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4
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Editorials
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0
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