Postanaesthetic shivering.

Epidemiology,
pathophysiology and approaches
to prevention and management
P. ALFONSI
Dpartement of Anesthesia and Resuscitation,
Hpital A. Par, Boulogne, France
Postanaesthetic shivering is one of the lea-
ding causes of discomfort for patients recove-
ring from general anesthesia. During EMG
records, the distinguishing factor from shive-
ring in fully awake patients is the existence of
clonus similar to that recorded in patients
with spinal cord transection. They coexist
with the classic waxing and waning signals
associated with cutaneous vasoconstriction
(thermoregulatory shivering). The causes
responsible for their appearance primarily
include hypothermia, which sets in due to
thermoregulation inhibition by anesthetics.
However, we also note the existence of shive-
ring associated with cutaneous vasodilatation
(non-thermoregulatory shivering) one of the
origins of which is postoperative pain. Apart
from the discomfort and aggravated pain,
postanaesthetic shivering raises metabolic
demand proportionally to the solicited
muscle mass and the patients cardiac capaci-
ties. No link has been demonstrated between
their occurrence and an increase in cardiac
morbidity but it is preferable to avoid posta-
naesthetic shivering since it is oxygen drai-
ning. Prevention mainly entails preventing
hypothermia by actively rewarming the
patient. Postoperative skin surface rewar-
ming is a way of obtaining the threshold shi-
vering temperature while raising the skin
temperature and improving the patients
comfort. However, it is less efficient than cer-
tain drugs such as meperidine, nefopam or
tramadol, which act by reducing the shive-
ring threshold temperature.
Key words: Shivering, physiopathology - Shi-
vering, prevention and control - Anesthesia,
adverse effects.
Epidemiology
Postanesthetic shivering is an involuntary
movement that may affect one or several
muscle groups and which generally occurs
in the early recovery phase after general
anesthesia. According to studies, the inci-
dence ranges between 6.3% and 66%
1-5
.
Male gender
2
, young adult
2,3
and the length
of the anesthesia or surgery
2
seem to be
determinant factors for postanaesthetic shi-
vering. Mild perioperative hypothermia
does not necessarily occur before the
appearance of postanaesthetic shivering but
it encourages it and the more serious the
hypothermia is, the higher the probability
of postanaesthetic shivering incidence
1
.
Lastly, the incidence differs depending on
the perioperative anesthetic used. The use
of a halogenated agent
2,3,6
or penthotal
5
or
administering only peroperatively small
Address reprint requests to: P. Alfonsi, Dpartement dA-
nesthsie, Ranimation, Hpital A Par, 9 Av Ch de Gaulle,
92104 Boulogne Cedex, France - e-mail: pascal.alfonsi@
apr.ap-hop-paris.fr.
438 MINERVA ANESTESIOLOGICA Maggio 2003
MINERVA ANESTESIOL 2003;69:438-41
POSTANAESTHETIC SHIVERING. EPIDEMIOLOGY, PATHOPHYSIOLOGY AND APPROACHES TO PREVENTION ALFONSI
Vol. 69, N. 5 MINERVA ANESTESIOLOGICA 439
quantities of opiates
2
encourage their
appearance. On the contrary, the incidence
is less significant with propofol
7
.
Pathophysiology
Origins of postanaesthetic shivering
Recording of postanaesthetic shivering
electromyographic patterns enables the
identification of 3 types of EMG signals
8
:
tonic EMG activity, spontaneous EMG clo-
nus similar to pathologic clonus observed
in patients with spinal cord transection and
waxing and waning signals identical to tho-
se obtained during cold-induced shivering
in non-anesthetized patients. There are 2
types of postanaesthetic shivering. Among
them, the majority are associated with cuta-
neous vasoconstriction and corresponds to
thermoregulatory shivering
9
. There are the
physiological response to the hypothermia
developed at the perioperative period. The
second ( 15% of postanaesthetic shivering)
corresponds to non-thermoregulatory shi-
vering (shivering associated with cutaneous
vasodilatation). The mechanisms responsi-
ble for non-thermoregulatory shivering are
not fully known. However, it exists a link
between postoperative pain and postanae-
sthetic shivering incidence
10
.
Difference of postanaesthetic shivering
frequency between propofol and other ane-
sthetics such as pentothal or halogenated
agents cannot be explained by the differen-
ces of effect on thermoregulation. It is plau-
sible that the effect of low concentrations of
propofol is less significant on certain central
structures such as the reticulated substance
comparatively to these other drugs thus
enabling a faster recovery of the descen-
ding inhibiting control.
Consequences of postanaesthetic shivering
The first clinical consequence of the
postanaesthetic shivering is the discomfort
for the patient. Moreover, the patient has a
stressful sensation of coldness that is syste-
matically associated with
5,6,8
. Another con-
sequence of postanaesthetic shivering on
the patients comfort is the increased pain
caused by muscular contractions on the
operated site.
The main effect of postanaesthetic shive-
ring is the oxygen consumption (VO
2
)
increase. By affecting several muscular
groups for periods that sometimes last lon-
ger than 45 minutes, postanaesthetic shive-
ring triggers an increase in metabolic
demand, which generally translates into
higher VO
2
combined with increased minu-
te ventilation. Regarding VO
2
increase, the
figures reported in the literature are very
variable, presenting percentages ranging
from 7% to more than 700%
11
. The hetero-
geneous samples, measuring methods and
the differences between clinical situations
can explain such significant differences.
Also, postanaesthetic shivering probably
increases VO
2
by roughly 40 to 120%.
Mild perioperative hypothermia multi-
plies by 2 the incidence of morbid cardiac
events among patients who either have
coronary artery disease or are at high risk
for coronary disease
12
. On the contrary,
Frank et al.
12
do not found relationship
between incidence of myocardial ischemia
and postanaesthetic shivering, which is a
specific consequence of hypothermia.
However, many authors observe in shive-
ring patients significant decreases in vein
oxygen saturation (SvO
2
)
4,13
or higher con-
sumption of inotropic drugs
13
. That shows,
in certain situations, the inability of the ven-
tricular function to cope with the increase
in metabolic demand.
Prevention and management
Peroperative hypothermia prevention
Hypothermia is responsible for most
cases of postanaesthetic shivering. Therefo-
re, peroperative hypothermia prevention
will not only have a beneficial effect on the
patient
12,14
, but will also automatically redu-
ce the postanaesthetic shivering incidence.
Hypothermia prevention during general
anesthesia entails first, limiting the effects of
internal redistribution and second, reducing
and making up for the heat losses. Preope-
rative skin surface rewarming is efficient for
limiting the effects of internal redistri-
bution
15
. Another method entails increasing
the organisms heat content by causing
endogenous production. Raise of the ope-
rating room temperature (>23C) and the
fact of covering the patient as much as pos-
sible are sufficient to reduce significantly
the skin losses. When a perfusion of a large
volume of crystalloid or colloid or of cold
blood products are needed, intravenous
solution rewarming prevents the patient
from cooling down. The use of passive
means will not prevent the heat balance
from being negative during surgery and an
active heat transfer is necessary. The cuta-
neous path is the most efficient.
Physical treatment of postanaesthetic
shivering
A linear relationship between core tem-
perature and the average skin temperature
exists at the shivering appearance thre-
shold. In the awake patient
16
, cutaneous
contribution factor for shivering is equal to
18-20%. In practice, this means that, to inhi-
bit postanaesthetic shivering, the average
skin temperature must be raised by at least
4C to be as efficient as a 1C increase in
core temperature. Furthermore, heat tran-
sfer from the periphery and the deep tis-
sues is hindered by cutaneous vasoconstric-
tion. In all cases and regardless of the
means used, increasing the skin temperatu-
re significantly improves thermal comfort
17
.
Medical treatment of postanaesthetic
shivering
Thermoregulatory shivering is principally
modulated via bioamines (mainly serotonin
and noradrenalin), peptides and cholinergic
receptors
18
. There are numerous efficient
drugs for preventing or stopping postanae-
sthetic shivering acting by one or different
ways on thermoregulatory shivering. This is
the case of 2-agonists, opiates, tramadol,
ketanserin, physostigmine, nefopam, and 5-
HT3 antagonists.
OPIATES
Mu-receptor agonists inhibit postanae-
sthetic shivering. Alfentanil acts centrally by
increasing the interthreshold range in
volunteers
19
. And, in the postoperative
period, there is a linear relationship
between the threshold temperature of
postanaesthetic shivering and the plasmatic
concentration of sufentanil
20
. However,
results of clinical studies are contradictory
and, at plasmatic concentration allowing
spontaneous breathing, m-receptor agonists
do not seem as potent as others antishive-
ring drugs. In fact, only meperidine (or
pethidine) presents a constantly remarkable
effect on postanaesthetic shivering
20,21
.
Moreover, meperidine possesses a specific
anti-shivering effect
22
. Meperidine has
various different pharmacological proper-
ties
18
: mu and kappa-receptor agonists,
alpha2 adrenoceptor agonists and an anti-
cholinergic effect. To date, it seems that the
combination of all the pharmacological
properties of meperidine contributes to its
specific anti-shivering effect.
2-ADRENERGIC AGONIST
In volunteers, clonidine and dexmedeto-
midine lower cutaneous vasoconstriction
threshold and shivering
23,24
. Clonidine
25
administration in premedication and during
the surgery reduces the incidence of posta-
naesthetic shivering. When recovering from
general anesthesia, 75 g of clonidine injec-
ted in bolus stops postanaesthetic shivering
in 5 minutes in all patients
26
.
TRAMADOL/KETANSERIN/NEFOPAM/ONDANSETRON
Tramadol, an inhibitor of amine re-up-
take with opiate properties, inhibits posta-
naesthetic shivering
27
. Nefopam (0.15
mg/kg or 20 mg), another inhibitor of ami-
ne re-uptake, inhibits it or prevents it
28
.
Ketanserin (10 mg), a 5-HT2 antagonist,
inhibits postanaesthetic shivering
26
. In the
same way, 8 mg-ondansetron, a 5-HT3
antagonist, are effective to prevent posta-
naesthetic shivering at recovery of a general
anaesthesia
29
.
ALFONSI POSTANAESTHETIC SHIVERING. EPIDEMIOLOGY, PATHOPHYSIOLOGY AND APPROACHES TO PREVENTION
440 MINERVA ANESTESIOLOGICA Maggio 2003
POSTANAESTHETIC SHIVERING. EPIDEMIOLOGY, PATHOPHYSIOLOGY AND APPROACHES TO PREVENTION ALFONSI
Vol. 69, N. 5 MINERVA ANESTESIOLOGICA 441
Postanaesthetic shivering: how to do?
Postanesthetic shivering is a phenome-
non that tends to decline thanks to the
more systematic prevention of hypothermia
in the peroperative stage. Prevention of
hypothermia consists in limiting heat losses
and in actively rewarming the patient.
However, if shivering occurs, it must be
systematically treated in order to improve
patient comfort and analgesia. It is difficult
to list and compare the different treatments
deemed to efficiently prevent or stop posta-
naesthetic shivering due to the scarcity of
comparative elements between the diffe-
rent studies. In order to be able to compare
various drugs used to prevent or stop shive-
ring we can use the number-needed-to-
treat with their 95% confidence intervals
30
.
Only studies where the product tested was
compared with a placebo and of which the
effect was statistically significant were retai-
ned. Utilisation of the number-needed-to-
treat enables to calculate the number of
patients that must be treated to stop or pre-
vent postanaesthetic shivering in a patient.
This method has revealed that with meperi-
dine (0.4 to 0.85 mg.kg
-1
) treatment of less
than 2 patients is necessary for stopping
postanaesthetic shivering. With tramadol (1
or 2 mg/kg) or nefopam (20 mg), the NNT
is also lower than 2 for treating or for pre-
venting postanaesthetic shivering.
Riassunto
Epidemiologia, fisiopatologia e approccio alle misu-
re preventive e terapeutiche dei brividi post-aneste-
sia
I brividi post-anestesia rappresentano una delle
principali cause di disagio per i pazienti che sono
stati sottoposti ad anestesia generale. Nel corso del-
le registrazioni elettromiografiche, il fattore di diffe-
renziazione rispetto ai brividi che si riscontrano nei
pazienti in completo stato di veglia risultato essere
lesistenza di un clono simile a quello registrato nei
pazienti con sezione del midollo spinale. Insieme a
questo tipo di brividi sono presenti i classici segnali
di accensione e spegnimento che si associano alla
vasocostrizione cutanea (brividi termoregolatori).
Tra le cause responsabili della loro comparsa si tro-
va innanzi tutto lipotermia, che si instaura in segui-
to allinibizione della termoregolazione operata
dagli agenti anestetici. Tuttavia, noi abbiamo notato
anche lesistenza di brividi associati alla vasodilata-
zione cutanea (brividi non-termoregolatori), che
riconosce molte cause, fra cui il dolore postoperato-
rio. Indipendentemente dal disagio e dallaggrava-
mento del dolore che provocano, i brividi post-ane-
stesia aumentano le richieste metaboliche in misura
proporzionale alla massa muscolare sollecitata e
alle capacit cardiache del paziente. Non stata
dimostrata alcuna associazione tra il verificarsi di
questi brividi e una aumentata morbilit cardiaca,
ma preferibile evitare i brividi post-anestesia, dal
momento che fanno consumare ossigeno. Le misure
preventive riguardano essenzialmente la prevenzio-
ne dellipotermia per mezzo di un riscaldamento
attivo del paziente. Il riscaldamento post-operatorio
della superficie cutanea un mezzo per determina-
re la temperatura di soglia dei brividi mentre si
aumenta la temperatura della pelle e si limita il disa-
gio del paziente. Tuttavia, questa procedura risulta
meno efficace rispetto allimpiego di farmaci come
la meperidina, il nefopam o il tramadolo, che sono
attivi nel ridurre la temperatura di soglia dei brividi.
Parole chiave: Brividi, fisiopatologia - Brividi, pre-
venzione e controllo - Anestesia, complicanze.
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