Br. J. Anaesth. (1982), 54, 29
SUPPRESSION OF ANTIDIURETIC HORMONE HYPERSECRETION
DURING SURGERY BY EXTRADURAL ANAESTHESIA
F. BONNET, A. HARARI, M. THIBONNIER AND P. VIARS
SUMMARY
The concentrations of antidiuretic hormone in plasma and urine were determined in three groups of
patients submitted to the same operative procedure. Seven (group I) underwent general anaesthesia with
thiopentone, fcntanyl and nitrous oxide and received an infusion of isotomc saline solution at
5mlmin~ l . Seven patients (group II) anaesthetized similarly, received isotonic saline solution
15 ml mm "'. In group III (five patients) anaesthesia was produced by extradural blockade. Surgery under
general anaesthesia induced a significant increase in plasma and urine ADH concentrations which were
not modified by the fluid load. Extradural anaesthesia suppressed almost completely the release of ADH
during surgery. This effect of ertradural anaesthesia could be related to the interruption of conduction
along nocicepave neural pathways.
An increase in the secretion of antidiuretic
hormone (ADH) in relation to surgery was
suggested by Le Quesne and Lewis (1953) and
Dudley, Boling and Le Quesne (1954), and subsequently confirmed by bioassay (Moran et al.,
1964). More recent studies using a specific radioimmunoassay confirmed these findings (Philbin et
al., 1976; Haas and Glick, 1978). The marked
increase in plasma ADH concentration occurs
primarily during surgery and in the period following operation (Moran et al., 1964; Moran and
Zimmermann, 1967). Anaesthesia per se does not
increase the concentration significantly (Moran et
al., 1964). Although several mechanisms could
induce the release of ADH during surgery two
appear most likely: hypovolaemia from blood loss
(Ishihara, Ishida and Oyama, 1978) and painful
stimuli from the operative field (Ukal, Moran and
Zimmermann, 1968).
In an attempt to delineate the mechanisms, a
randomized study was undertaken to compare the
plasma and urine ADH concentrations in patients
undergoing the same surgical procedure under
either general anaesthesia with or without fluid
loading, or extradural anaesthesia.
mented history of renal, hepatic or cardiac failure
were excluded from the study. During the 10 days
preceding the operation, each patient received a
diet comprising water ad libitum, sodium
lOOmmole and potassium 60mmole daily.
Patients were allocated randomly to three
groups. In group I (control group), surgery was
performed under general anaesthesia. In group
II, general anaesthesia was administered as in
group I with, in addition, an isotonicfluidload. In
group III, extradural blockade was performed.
Each study comprised four periods: first, a 2-h
control period before induction of anaesthesia;
second, 1 h following the induction of general or
extradural anaesthesia; the operative period and a
4-h stay in the recovery room were the third and
fourth periods respectively.
Premedication (atropine 0.5 mg and diazepam
10 mg) was administered i.m. l h before the
arrival in the operating theatre.
Group I comprised four women and three men
whose mean age was 60±5.5yr. General anaesthesia was induced with thiopentone 4mgkg~ 1
and maintained with 70% nitrous oxide in
oxygen. Fentanyl 4ngkg - 1 was administered
before the skin incision. The trachea was intuPATIENTS AND METHODS
bated with the aid of suxamethonium lmgkg" 1
Nineteen patients undergoing total hip replace- and the lungs were ventilated artificially throughment were studied. Informed consent was out the operative procedure with a tidal volume of
obtained from each patient. Patients with a docu- 12 ml kg" 1 and a frequency of 15b.p.m. Nondepolarizing neuromuscular blocking drugs were
F. BONNET, M. D.; A. HARARI, M. D.; M. THIBONNIER, M. D.;
not
administered. The trachea was extubated at
P. VIARS, M. D.; Departement d' Anesthesie, Hopital de la Pitie,
the end of the operation. A solution of isotonic
83 boulevard de PHdpital, 75013 Pans, France.
007-0912/82/010029-08 801.00
© Macmillan Publishers Ltd 1982
30
saline was infused at 5 ml min 1 15 min before the
induction of anaesthesia until the end of the
operation. The rate of infusion was 3 ml min"' for
the 24 h following surgery.
Group II comprised five women and two men;
mean age 56 ± 3 yr. They received the same anaesthetic as the patients in group I with in addition, a
fluid load. An isotonic saline solution was infused
continuously at 15 ml min" 1 from 15 min before
the induction of anaesthesia until the end of the
operation. After operation the rate of infusion was
3 ml min" 1 .
In group III (four women and one man, mean
age 60 + 8 yr) extradural anaesthesia was produced
with 0.5% bupivacaine; after 15 min anaesthesia
extended from S5 to T4 in all patients. A further
injection of bupivacaine was given 2h later
through the extradural catheter. In this group, the
rate of infusion of isotonic saline was as in group
I.
In all the three groups, blood loss was measured
carefully (swabs weighed, suction volume
measured) and replaced promptly during surgery.
In all patients plasma and urine osmolalities
were measured by freezing point depression
(Fiske-Osmometer) and sodium and creatinine
concentrations determined using a Technicon
Autoanalyser. Systemic arterial pressure was
recorded using an electromanometer.
The concentration of ADH was measured in
urine samples collected during a control period of
2h during anaesthesia, during surgery (mean
duration: group I 187 ±34 min, group II
125 + 17 min, group III 172+ 44 min) and for the
first 4h after operation. These urine samples gave
a profile of ADH secretion during the whole
anaesthetic period, the entire surgical procedure
and the period immediately after operation.
Plasma ADH concentration was measured in
blood samples collected on dry heparin in glass
tubes previously chilled in ice. The first blood
sample was collected on arrival in the operating
theatre. Three subsequent collections were made
5, 10 and 15 min after the induction of general
anaesthesia or the onset of extradural anaesthesia,
and were pooled. Three other samples were
obtained 5,10 and 15 min after the skin incision in
each of the three groups of patients and were
pooled also. A final sample was collected in the
4th hour following operation. Thus, plasma ADH
concentrations were known after the induction of
anaesthesia and within the first minutes of surgery
BRITISH JOURNAL OF ANAESTHESIA
and at the end of the study. Since the increase in
ADH secretion could be intermittent (Weitzman
et al., 1977a) the effect of anaesthesia and surgical
stimulation were studied more effectively by pooling the plasma samples. Samples were
immediately
centrifuged
at
4°C,
at
4000 rev min" 1 for 10 min, and the plasma stored
frozen at — 20 °C in 2-ml aliquots acidified to pH
4.5 with hydrogen chloride lmollitre" 1 . ADH
concentration was determined using a previously
described
radioimmunoassay
in
urine
(Fressinaud, Corvol and Menard, 1974) and
plasma (Thibonnier et al., 1981).
Statistical calculations used non-parametric
methods: the Kruskall-Wallis test and the
Spearman rank correlation.
RESULTS
Plasma and urine ADH concentrations
Control period. Plasma ADH concentrations
were within the normal range in all patients and
were similar to those measured in eight healthy
men after overnight fasting (1.57 + 0.17pgml" 1 )
(Thibonnier et al., 1981). There were no significant differences between the three groups (table
I). In all groups the ADH concentrations in urine
were also in the normal range when compared
with the values in 15 healthy subjects after overnight fasting (urine creatinine 53±22pgmg" 1 )
(Alhenc-Gelas et al., 1974).
Group I (figs 1, 2, table I). General anaesthesia
produced insignificant increases in plasma and
urine ADH concentrations. The immediate response to surgery was a dramatic and significant
TABLE I. ADH concentrations in plasma and urine. *P<0 05,
**P<0.0I
Group
Control
Anaesthesia
Surgery
After
operation
I
II
III
I
II
III
I
II
III
I
II
III
Plasma
(pgmr 1 )
1.29±0.43
0.98±0.29
1.21 ±0.28
4 10±2.84
0.83±0.14
0.95±0.29
8 82±3 03*
12 2117 08*
3.1012.72
14.1216.81**
22.3617.90**
19.5618 36**
Urine
creatinine
(pgmg"1)
65115
48112
32115
239125
144197
39110
12861513**
14081671**
5541288**
8351390**
16741801**
3401288**
EXTRADURAL ANAESTHESIA AND ADH
31
increase in plasma ADH values substantiated by
an increase in the amount of ADH excreted
during the whole operation. A further increase in
plasma and urine ADH concentrations occurred
after operation.
Group II (figs 1, 3, table I). There were no
changes in plasma and urine ADH concentrations
with the induction of anaesthesia but a marked
increase occurred, as in group I, following the
skin incision. After operation ADH concentrations increased and were identical to those of
group I in both plasma and urine.
Group III (figs 1, 4, table I). ExtradunJ anaesthesia by itself did not modify plasma and urine
ADH secretion. Surgery under extradural anaesthesia was not followed by any significant change
in plasma ADH. A slight increase in the urinary
concentration of ADH was noticed during surgery
but remained well below the values observed in
the first two groups (P<0.01). Following surgery
(effective extradural anaesthesia lasted for 1 h) the
increase in ADH concentration in the urine was
much less marked than in the first two groups
(P<0.01). By the 4th hour, plasma values were
identical with those in groups I and II.
Circulatory changes.
After the induction of general anaesthesia
systolic arterial pressure decreased by 8% and 4%
in groups I and II respectively. There were
insignificant fluctuations during the rest of the
study. Following the production of extradural
anaesthesia, a decrease of 15% was observed in
arterial pressure, which gradually returned to its
initial value.
When the third sample for plasma ADH was
taken at the 15thmin after the skin incision blood
losses were 160 ±30 ml in group I, 140 ±20 ml in
group II and 145 ± 25 ml in group III. During the
whole procedure blood loss was comparable in the
three groups: group I 1850 ±600 ml, group II
1700±450ml, group III 1600±450ml. Fluid
retention throughout the study, estimated by the
difference between the volume of saline infused
25
2000
20
S
*
15
1000
*
o
<
10
1
2
3
4
FIG. 1. Changes in ADH concentrations in urine. Values are
expressed in pgmg" 1 of creatinine because of changes in
glomerular
filtration
during
surgery.
1 = Control,
2 = anaesthesia; 3 = surgery; 4 = postoperative period.
**P<0.01
0
J±l
1
FIG. 2. Group I: changes in ADH concentrations in plasma
under general anaesthesia. 1 = Control; 2 = induction of
anaesthesia; 3 = skin incision; 4 = 4th hour after operation.
32
BRITISH JOURNAL OF ANAESTHESIA
301-
30-
25
25• •
~
20
20
1
2
Q
<
as
0.
E
S
x
15
15
Q
10
10
0
1
2
3
4
FIG 3 Group II: effect of fluid load on plasma ADH
concentrations during general anaesthesia. Periods as in
figure 2.
FIG 4. Group III: changes in plasma ADH concentrations
under extradural anaesthesia. Periods of study as in figure 2.
TABLE II. Changes in plasma and urmary indices. *P<0 05, **P<0 01
Group
Plasma osmolality
(mosmolkg"1)
Urine osmolality
(mosmolkg"1)
Urine output
(mlmin"1)
Creatuune clearance
(mlmin"1)
Osmolar clearance
(mlmin"1)
Free water clearance
(mlmin"1)
I
II
III
I
II
III
I
II
III
I
II
III
I
II
III
I
II
III
Control
Anaesthesia
Surgery
After
operation
288 ±4
282 ±2
288 ±2
699 ±72
547 ±77
544±75
1.0±0.1
2.2±04
2.0±0 5
121 ±27
122± 16
117±7
2.3 ±0.4
3.9±1.6
3.1 ±0.8
- 1 3 ±0.2
-1.8±0.4
-1.3±04
289±3
280±2
289±2
683±69
498 ±85
549 ±70
0.9±0 1
2.6±0 6
1.6±0.4
125±21
125±31
84±15**
2.9±0.7
4 1±1 3
22±06
- 1 5±0.2
-1.6±0.8
—1.1 ±0.5
289±5
283±2
291 ±3
637 ±79
437 ±89*
520 ±49
1.3±0.5
2 4±0.8
1.3±0.5
74±11**
76±13**
68±17**
1.9±0.6
29±1.1
1 l±0.2*
- 0 6±0.2
-0.4±0.7
-0.5±0.1
293 ±4
284±2
288±3
681 ±58
580 ±67
609 ±103
0.6±0.1*
1.0±0.3*
1.1 ±0.3*
68±13**
67 ±17**
5O±9**
1.3±0 3*
1.6±0.3**
1.5±0.3*
-1.0±0.3
-0.9 ±0.4
-0.7 ±0.2
EXTRADURAL ANAESTHESIA AND ADH
33
and the urinary volume, was more marked in observed in normal subjects (Robertson, 1977)
group II (1740±340ml; P<0.01) than in groups reinforces this assertion.
I (831 ± 179ml) or III (994±299ml).
In thefirsttwo groups variations in arterial pressure were less than 10% from control. Since a relationship is documented between the changes in arterial pressure and the release of ADH (Robertson,
Plasma osmolahty and renal function (table II)
Plasma osmolality remained constant through- 1977), this small decrease in systolic arterial presout the study in all the three groups. Urine sure could account for the slight increase in ADH
osmolality decreased significantly in group II values observed after the induction of anaesthesia.
during the operative period coinciding with the However, in the group submitted to extradural
saline load. A significant decrease in urinary anaesthesia, despite a larger decrease in arterial
output and osmolar clearance was noted in all pressure the concentrations of ADH remained
three groups after operation. Creatinine clearance constant in plasma and urine. Only a decrease in
was decreased in groups I and II during surgery blood volume greater than 10% can stimulate
and in the period after operation. As expected, in ADH release (Robertson, 1977). In our study, any
group III creatinine clearance decreased influence of such volume regulation can be
immediately following induction of extradural excluded because of careful replacement of blood
anaesthesia without fluid loading, whereas the loss and the infusion of saline making a significant
free water clearance was negative during all decrease in blood volume improbable. Moreover,
the increase in plasma ADH concentration was
periods in the three groups.
observed within a few minutes of the start of
surgery before any significant blood loss had
occurred. In group III when blood loss and fluid
Statistics
retention were identical to those observed in the
Plasma and urine ADH concentrations were control group, secretion of ADH was less.
closely related in the three groups of patients Furthermore, the fluid load in group II was
(r = 0.61, P < 0.001), but these indices were not unable to prevent the ADH hypersecretion
related to plasma osmolality, plasma sodium con- induced by surgery but led to fluid retention as
centration, urine osmolality or free water clear- previously observed (Sinnatamby et al., 1974).
ance, when considering the whole study.
Such an infusion has been demonstrated to be
sufficient to decrease the release of ADH in
normal subjects and in subjects in whom fluids
have been restricted (Moore, 1971). In a recent
DISCUSSION
Simultaneous measurements of the concentration study Ishihara, Ishida and Oyama (1978) also
after operaof ADH in plasma and urine demonstrated release failed to block ADH hypersecretion
1
tion
using
a
15-mlmin"
infusion
in
dogs. Only
of this hormone during surgery conducted under
1
general anaesthesia. A fluid load did not prevent an infusion of fluid of about SOmlmin" —10
this hypersecretion, whereas extradural anaes- times greater than in our control group, was able
to prevent the release of ADH (Ishihara, Ishida
thesia suppressed it almost completely.
and Oyama, 1978). Such a fluid load overcomes
The physiological control of ADH secretion the compensation of hypovolaemia. The need to
involves alteration in plasma osmolality, arterial infuse such large amounts to counteract ADH
pressure and blood volume. In our study plasma hypersecretion induced by surgery, suggests that
osmolality remained constant throughout the other factors are more important.
operative and the postoperative periods. The
ADH concentrations achieved during these
The release of ADH may be influenced by
periods were markedly greater than those factors other than the physiological, such as
observed after a strong stimulation of hypo- factors related directly to anaesthesia and the
thalamic osmoreceptors (Moran and Zimmer- surgical procedure. In this study it appeared that
mann, 1967). Thus, alterations in plasma osmo- thiopentone and suxamethonium did not have a
lality are not likely to be the factor promoting major influence on ADH release and therefore,
ADH hypersecretion. The lack of correlation are similar to previous reports about thiopentone
between ADH and plasma osmolality, usually (Ishihara, Ishida and Oyama, 1978; Leedy,
34
BRITISH JOURNAL OF ANAESTHESIA
Forsling and Forsling, 1979), ether (Ishihara, affecting innervation above the level of extradural
Ishida and Oyama, 1978; Leedy, Fossling and anaesthesia, the suppression by extradural anaesFossling, 1979) and halothane (Oyama, Sato and thesia disappeared (Moran et al., 1964). The
Kimura, 1971; Forsling and Ullmann, 1975; importance of nociceptive stimuli is supported by
Simpson and Forsling, 1976; Ishihara, Ishida and the depressant effect of very high doses of morOyama, 1978; Leedy, Forsling and Forsling, phine or fentanyl on surgically-induced release of
1979). It has been suggested that morphine and ADH (Philbin and Coggins, 1978; Stanley,
beta-endorphin could stimulate the secretion of Philbin and Coggins, 1979). Furthermore, plasma
ADH (De Bodo, 1944; Schnieden and Blackmore, and urine concentrations reached their greatest
1955; Weitzman et al., 1977b). However, the values when opiate or extradural analgesia had
influence of morphine on the release of ADH decreased during the early postoperative period, at
during balanced anaesthesia is similar to that of which point pain was the main factor stimulating
other anaesthetic drugs (Philbin et al., 1976; further ADH hypersecretion.
Ishihara, Ishida and Oyama, 1978).
Hypersecretion of other hormones, induced by
Mechanical ventilation could influence the surgery, can be blocked by extradural anaesthesia
secretion of ADH (Hemmer et al., 1980), but it (Kehlet, 1979): growth hormone (Brandt et al.,
has been demonstrated that intermittent positive 1976), cortisol (Engquist et al., 1975) renin, aldopressure ventilation has no significant effect on sterone (Brandt, 01gaard, and Kehlet, 1979) and
the release of ADH (Philbin, Baratz and catecholamines (Roizen and Horrigan, 1979).
Patterson, 1970; Hemmer et al., 1980). We could Since surgically-induced release of hormones may
observe no significant difference in ADH con- be implicated in immune depression and metacentrations in plasma and urine during the anaes- bolic disturbances after operation (Kehlet et al.,
thetic period before surgery when comparing the 1979; Rem, Brandt and Kefilet, 1980) this
first two groups submitted to arterial ventilation inhibition of the endocrine response to surgery
and extradural group of patients breathing could be beneficial, but that fact is yet to be
spontaneously.
proven for ADH.
The most important finding of the present
study is that extradural anaesthesia almost completely suppressed the increase in ADH concentration induced by surgery. No changes in
plasma and urine concentrations were observed
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SUPPRESSION DE L'HYPERSECRETION
D'HORMONE ANTIDIURETIQUE PENDANT UNE
INTERVENTION CHIRURGICALE GRACE A
L'ANESTHESIE EXTRADURALE
RESUME
Nous avons determine sur trois groupes de patients devant
subir la mane intervenuon chirurgicale, le conccntrauons
d'hormonc antidiureuque dans le plasma et l'urine. Sept
personnes (groupe I) ont etc soumises a une anesthesie
gencrale a l'aide de thiopentone, fentanyl et protoxyde d'azote,
puis ellcs ont recu unc perfusion de soluuon physiologique a
raison de 5mlmn~L. Sept patients (groupe II), anesthesies
d'une mamere similaire ont recu une soluuon physiologique a
raison de 15ml mn~'. En ce qui concerne lc groupe III (cinq
patients), l'anesthesie a ete provoquee par blocage extradural
L'operauon effectuce sous anesthesie generale a provoque une
augmentation sensible des concentrations ADH dans le plasma
et l'urine, concentrauons qui n'ont pas etc modifices par la
charge hquide. L'anesthesie extradurale a presque
enuerement suppnme le degagement d'ADH pendant
1'intervenuon chirurgicale. Cet effet de l'anesthesie
extradurale peut etre relie a 1'interrupuon de la transmission le
long des voies d'acces nociceptives neurales
UNTERDRUCKUNG DER DIURESEHEMMENDEN
HORMONHYPERSEKRETION WAHREND DER
CHIRURGIE MITTELS EXTRADURALER
ANASTHESIE
ZUSAMMENFASSUNG
Die Konzentrauonen des diuresehemmenden Hormons un
Plasma und un Unn wurden bei drei Gruppcn von Paucnten
bestimmt, die sich derselben Operauon unterzogen. Sieben
Patienten (Gruppe I) bekamen eine Allgemeinnarkose nut
Thiopenton, Fentanyl und Stickoxydul in Verbindung mit
einer Infusion von isotonischer Salzlosung 5 ml mm" 1 .
Weitere sieben Pauenten (Gruppe II) bekamen erne ahnhche
Narkosc und eine isotonische Salzlosung 15 ml mm"'. Bei der
Gruppe III (5 Pauenten) wurde die Anasthesie durch extradurale Blockade herbeigefuhrt Die Chirurgie unter Allgemeinnarkose fuhrte eine bedeutende Zunahme der diuresehemmenden Hormonkonzentrationen im Plasma und lm Unn
herbei, die durch die Flussigkeitsbelastung mcht abgeandert
BRITISH JOURNAL OF ANAESTHESIA
36
wurden. Die extradurale Anasthesie unterdruckte fast volstandig die Abgabe des diuresehemmenden Hormons wahrend
der Chirurgie Diese Auswirkung der extraduralen Anasthesie
konnte nut der Unterbrechung der Obertragung uber
schmerzvermittelnde Bahncn in Verbindung stehen
SUPRESION DE LA HIPERTENSION
OCASIONADA POR HORMONAS
ANTIDIURETICAS MEDIANTE ANESTHESIA
EXTRADURAL ADMINISTRADA DURANTE
INTERVENCION QUIRURJICA
SUMARIO
Se determinaron las concentraciones de hormona antidiuretica, en el plasma y en la onna, en tres grupos de pacientes
somendos a los mismos procedimientos operativos. Siete
(grupo I) se sometieron a anestesia general con uopentona,
fentanilo y oxido nitroso y recibieron una infusion de una
solucion isotonica salina a un regimen de 5 ml nun" 1 Otros
siete pacientes (grupo II), anestesiados de forma similar,
recibieron una solucion isotonica salina a un regimen de
15 ml min "'. En el grupo III (consatuido por cinco pacientes)
la anestesia se produjo mediante bloqueo extradural. La
intervention quinirjica bajo condiciones de anestesia general,
indujo un incremento sigmficativo en las concentraciones de
hormona antidiureuca en el plasma y en la unna, que no
vinieron modificades por la carga de fliiido. La anestesia
extradural supnmio, casi completamente, la hberacion de la
hormona antidiurctica durante la intervencion quirurjica. Este
efecto de la anesthesia extradural podria estar relacionado con
la interrupcion de la conduction a lo largo de las rutas neurales
nociceptoras
1
y