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widely adopted, as physicians were understandably wary of overlooking a preventable etiology of calamitous postoperative demise. Based on these anecdotal reports,
stress-dose or high-dose perioperative steroids became standard practice in any
steroid-dependent patient undergoing surgery.
Stress-dose steroids typically consists of hydrocortisone 100 mg intravenous
(IV) preoperatively then every 8hours postoperatively for the rst 24hours, followed by a taper down to the basal preoperative dose over the subsequent 2–3days
[3]. Current guidelines are variable, but generally recommend an individualized
decision to utilize stress-dosing depending on the home dose, duration of steroid
use, time since last use, and anticipated physiologic burden of the operation.
However, they note the decision to stress-dose must be weighed against the negative
aspects of supra-physiologic steroid administration [4–6].
While suppression of the HPA axis is known to occur with chronic steroid supplementation [7], the dosage and duration of steroid exposure required to induce
suppression is unknown. Further, the duration of time to recover from HPA axis
dysfunction is not known [8]. Historically, HPA axis dysfunction was speculated to
persist for up to 1year [9], thus stress-dose steroids have been recommended in
patients treated with corticosteroids within the past year. However, perioperative
high-dose steroids are not without consequence and have been associated with
hyperglycemia, impaired wound healing, anastomotic leak, hypertension, electrolyte imbalance, immunosuppression and psychological impairments [7]. These
risks are further potentiated and associated with increased perioperative morbidity
if accompanied with malnutrition, advanced age, or concomitant use of immunosuppressive medications [10].
Despite the potential for AI and perioperative cardiac decompensation, a standardized preoperative evaluation algorithm for adrenal insufciency is not established. Furthermore, the clinical signicance of diagnostic tests for adrenal
insufciency is currently debated [11]. Over the past 6 decades, several large case
series have been conducted in both IBD and non-IBD patients challenging the practice of stress-dose steroid administration. Recent recommendations lean towards
avoiding perioperative stress-dose steroids [5, 12]. Still, there remains great variability in perioperative steroid dosing for IBD patients undergoing colorectal surgery [13]. In this chapter, we review the literature and evidence surrounding
perioperative steroid dosing followed by our recommendations for steroid management in patients with IBD undergoing colorectal surgery.
E. D. Adams and K. Zaghiyan
Search Strategy
Relevant PICO (Population, Intervention, Comparator, Outcome) questions were
generated (Table9.1). A Medline and PubMed search was conducted for publications in the English language between January 1952 and July 2022 using the following search terms: (‘inammatory bowel disease’ or ‘IBD’ or ‘ulcerative colitis’ or
‘Crohn’s’ or ‘organ transplant’ or ‘transplant’ or ‘steroid-treated’) and (‘corticosteroid’ or ‘steroid’) and (‘colorectal’ or ‘colorectal surgery’ or ‘surgery’ or ‘surgical’
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Table 9.1 PICO questions
P (Patients)
Steroid-treated patients
with or without IBD
undergoing colorectal or
non-colorectal surgery
Patients with or without
IBD, previously treated
with steroids within
1year undergoing
colorectal or noncolorectal surgery
I (Intervention) C (Comparator)
Low-dose
perioperative
steroids
No
corticosteroids
High-dose or
stress-dose
perioperative
steroids
High-dose or
stress-dose
perioperative
steroids
O (Outcomes)
Perioperative
hemodynamic instability,
adrenal insufciency,
morbidity, mortality,
infectious complications
Perioperative
hemodynamic instability,
adrenal insufciency,
morbidity, mortality,
infectious complications
101
or ‘operation’ or ‘operative’ or ‘perioperative’) and (‘stress-dose’ or ‘high-dose’ or
‘low-dose’ or ‘dosing’ or ‘previous steroid’) and (‘adrenal insufciency’ or ‘hemodynamic’ or ‘outcome’ or ‘complication’ or ‘morbidity’ or ‘mortality’). We additionally searched the reference section of each relevant article to identify additional
articles pertaining to this topic. Retrospective and prospective, observational and
randomized studies were included. Given the paucity of studies investigating IBD
patients undergoing colorectal surgery, the search was expanded to include organ
transplant recipients and other non-IBD steroid treated patients undergoing noncolorectal surgery.
Results
Several studies have been performed over the past 60years to assess the clinical
utility and optimal dosage of perioperative steroids in steroid-treated or steroiddependent patients undergoing surgery (Table 9.2). The concept of reducing or
omitting high-dose or stress-dose steroids in steroid-treated patients is not novel,
particularly given serious concerns about surgical wound healing. In the early trials,
steroid-treated patients underwent surgery without perioperative steroids and clinical parameters and HPA function were tested. In 1962, Solem and Lund reported 30
patients whose steroids were stopped more than 4weeks before a variety of surgical
procedures (IBD undergoing major colorectal surgery, n=4) without perioperative
steroid dosing and showed no severe hemodynamic collapse to suggest clinically
relevant AI in any of these patients [14]. Two studies from the 1970s further investigated the consequence of perioperative steroid omission in steroid-treated patients
undergoing surgery. They similarly implemented HPA axis testing and correlated
them with clinical parameters and found that hypotension attributed to AI in only 4
out of 125 patients combined [15, 16]. In a series of 104 patients, Kehlet and Binder
followed steroid-treated patients undergoing major and minor operations. Homedose steroids were stopped 48h before surgery and restarted 24h after minor cases
and 48h after major cases. In these patients, who did not receive high-dose, stressdose, nor any perioperative steroids, clinical adrenal insufciency was minimal with
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Table 9.2 Studies evaluating perioperative steroid dosing
First author
(year)
Solem
(1962)
[14]
Jasani
(1968)
[15]
Kehlet
(1973)
[16]
Knudsen
(1981)
[18]
Lloyd
(1981)
[19]
Symreng
(1981)
[20]
Patients
studied Intervention
Patients
previously
treated with
steroids/
various
surgeries
(n=4 IBD/
CRS).
RA/anterior
synovectomy
Steroidtreated
patients
undergoing
various
major/minor
operations
IBD/CRS 200 with no
RA/
Orthopedic
surgery
Various
patients
(n=7 IBD,
n=16,CRS)
No periop
steroids
No periop
steroids
No periop
steroids
periop
steroids, 50
received
steroids
Stress-dose
vs. usual
daily dose
If impaired
ACTH stim
test>HC
25mg IV
preop then
100mg
IV/24hrs. If
normal
ACTH stim
test: No
periop
steroids.
Return to
usual daily
dose postop
Study
design N Outcome
R 30 No unexplained
PO 21
steroidtreated
vs. 20
controls
PO 104 3 patients with
R 250 11 cases of
PO 61 No difference in
PO 14
steroidtreated
patients
and 8
steroidnaïve
controls
E. D. Adams and K. Zaghiyan
Quality
of
evidence
Very low
death attributed
to AI
1 patient with
abnormal preop
ACTH had
hypotension
responsive to
steroids.
hypotension and
low cortisol
thought to be AI
hypotension
treated with
steroids/possible
AI
periop steroid
supplementation
between the 2
groups
No
hemodynamic
instability
Very low
Low
Very low
Very low
Very low
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Table 9.2 (continued)
Quality
of
evidence
Very low
Very low
Very low
Very low
Very low
Very low
Low
Very low
Moderate
(continued)
First author
(year)
Bromberg
(1991)
[22]
Bromberg
(1995)
[23]
Friedman
(1995)
[24]
Glowniak
(1997)
[26]
Thomason
(1999)
[27]
Mathis
(2004)
[25]
Zaghiyan
(2012)
[31]
Zaghiyan
(2012)
[32]
Zaghiyan
(2011)
[33]
Patients
studied Intervention
Renal
transplant
patients
admitted w/
signicant
physiologic
stress
Renal
transplant
patients/
various
surgeries
Renaltransplant or
RA/major
orthopedic
surgery
Various
(colorectal
n=2) with
positive
ACTH stim
test
Organ
transplant/
gingival
surgery
Organ
transplant/
lymphocele
drainage
IBD/CRS
previously on
steroids
within 1year
IBD/CRS HDS vs.
IBD/CRS HDS vs.
Usual daily
dose
Usual daily
dose
Usual daily
dose
Stress-dose
vs. placebo.
Return to
usual daily
dose postop
Stress-dose
vs. placebo.
Return to
usual daily
dose postop
Stress-dose
vs. no
steroid.
Return to
usual daily
dose postop
No periop
steroids
LDS
LDS
Study
design N Outcome
PO 40 No unexplained
hemodynamic
instability
PO 52 No clinical or
laboratory
evidence of
adrenocortical
insufciency
PO 28 All patients with
endogenous
adrenal function.
No unexplained
hemodynamic
instability.
RCT 18 No episodes of
AI.One in each
group with
hypotension.
RCT 20 No
hemodynamic
instability
R 58 No hypotension,
arthralgia, ileus,
mental status
changes. Blood
glucose higher
with stress-dose
R 49 No difference in
hemodynamic
instability
RO 32 No unexplained
hemodynamic
instability
R 97 No difference in
hemodynamic
instability
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Table 9.2 (continued)
First author
(year)
Aytac
(2013)
[34]
Zaghiyan
(2014)
[36]
Ritter
(2019)
[35]
IBD Inammatory bowel disease, CRS Colorectal Surgery, RA Rheumatoid arthritis, ACTH
Adrenocorticotropic hormone, HDS High-dose steroids, LDS Low-dose steroids, R Retrospective,
PO Prospective observational, RO Retrospective observational, RCT Randomized controlled trial
Patients
studied Intervention
IBD/CRS Stress-dose
vs. usual
daily dose
IBD/CRS HDS vs.
LDS
IBD/CRS Stress dose
with rapid IV
taper vs. PO
taper
Study
design N Outcome
R 235 More tachycardia
RCT 92 Non-inferiority
R 686 Postoperative
E. D. Adams and K. Zaghiyan
Quality
of
evidence
Moderate
with stress-dose
otherwise no
difference in
hemodynamic
instability
High
of LDS vs. HDS
with respect to
postural
hypotension; no
difference in
hemodynamic
instability. More
infections with
HDS.
Low
oral steroid taper
associated with
pelvic sepsis
only 3 patients (2.8%) exhibiting unexplained hypotension and abnormal adrenocorticotropin hormone (ACTH) testing. However, each of these patients recovered
spontaneously without the administration of steroids [16].
The utility and clinical relevance of preoperative ACTH testing has been an area
of interest. In theory, preoperative testing could be utilized to identify potential
steroid-treated patients with HPA suppression who may require perioperative steroids to prevent AI. It may also be used to identify patients whose HPA axis has
recovered, thereby sparing these patients from the side effects of unnecessary steroids. In practice, the link between biochemical HPA axis suppression and clinical
practice has been opaque. In a prospective study of perioperative HPA axis function,
ACTH testing correlated with preoperative HPA function in 48 steroid-treated
patients undergoing elective surgery (colorectal, n=7) without perioperative steroids. While 17 of the 48 steroid-treated patients exhibited a normal response to
both ACTH stimulation and postoperative HPA axis testing, none exhibited any
symptoms consistent with AI or hemodynamic instability and none required steroid
administration including the 31 patients with abnormal ACTH responses [17]. Thus,
while normal HPA testing indicates the safety of foregoing steroids, this may still be
possible in those with abnormal HPA testing.
Further studies investigated if the timing of steroids impacted the requirement
for perioperative steroids. In 1981, Knudsen and colleagues performed a
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retrospective study evaluating 250 steroid-treated IBD patients undergoing major
colorectal surgery [18]. The study included 3 groups of patients: (1) patients on
steroids at the time of surgery (n= 48); (2) patients whose steroids were stopped
1week to 2months before surgery (n=76); and (3) patients with steroid cessation
greater than 2months before surgery (n=126). Intraoperative hypotension occurred
in 29 patients overall (11.6%) but was less common in those furthest from steroid
use (>2 months, 5.6%). In 9 patients, intraoperative rescue hydrocortisone was
given, however none of these patients had biochemically proven AI.These early
studies elaborated on the inconsistency between positive ACTH testing and clinically signicant AI and reinforced the need for perioperative steroids in some
patients, though the optimal patient cohort and steroid dose remained unclear.
Subsequent studies evaluated various perioperative steroid dosing regimens consisting of low-dose steroids or maintaining patients on their preoperative steroid
dose without the addition of a stress-dose steroid. In 1981, Lloyd completed a prospective observational trial of 61 arthritic patients requiring orthopedic surgery
comparing a single preoperative stress-dose of steroids (hydrocortisone 100mg
intramuscular) against omission of any stress-dose steroids [19]. They found no
signicant difference in the need for perioperative rescue steroids in patients treated
with preoperative stress-dose steroids (24%) compared to those patients without
stress dose steroids (17%). These ndings provide evidence that steroid-treated
patients may not require rescue medication despite receiving no stress-dose steroids. Furthermore, they showed that the physiologic requirement for perioperative
steroid supplementation may be lower than expected. Further justication for lowdose perioperative steroid safety was evidenced by Symreng in a small study of 14
steroid-treated patients (IBD, n=7) compared to 8 steroid-naïve controls undergoing various operations (major colorectal surgery, n = 16) [20]. They report that
steroid- treated patients with abnormal preoperative ACTH-stimulation testing
(n=6) may be managed with low-dose steroids (hydrocortisone 15mg IV upon
induction of anesthesia followed by 100mg IV over the next 24h) followed by
reinstitution of the preoperative dose, whereas patients with normal ACTH- stimulation testing may be managed without steroids on the day of the surgery.
In the 1990s, Shapiro and colleagues prospectively observed 13 pediatric transplant patients whose home-dose steroid regimen were either weaned or abruptly
stopped before an allograft nephrectomy [21]. The range of overall steroid use was
broad (range: 21days to 5years) and although 6 patients, had evidence of HPA-axis
dysfunction on preoperative ACTH testing, no patient in the entire series developed
signs or symptoms of AI.This indicates the potential for adrenal reserve regardless
of immunosuppression duration. Bromberg and colleagues later performed two prospective cohort studies evaluating renal transplant recipients admitted with signicant physiologic stress (n= 40) or for various operations (n=52), both managed
with continuation of their home-dose steroid dosing [22, 23]. Almost all patients
had normal urinary cortisol levels and no clinical expression of hemodynamic compromise yet ACTH-stimulation testing appeared to overestimate adrenal dysfunction in a majority of patients. Friedman and colleagues prospectively evaluated 28
renal-transplant or rheumatoid arthritis patients on an average prednisone dose of
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E. D. Adams and K. Zaghiyan
10mg/day undergoing major orthopedic surgery [24], and similarly found that all
patients had endogenous adrenal function and no episodes of clinically signicant
adrenal insufciency. Further, another retrospective study of 58 pancreas and kidney transplant recipients undergoing lymphocele drainage showed no difference in
hypotension, arthralgia, mental status changes, ileus, or wound healing in patients
treated with stress-dose steroids or not, but patients treated with stress-dose steroids
had more hyperglycemia [25].
Several years later, Glowniak and Loriaux conducted a randomized double-blind
study of 18 steroid-treated patients with positive ACTH stimulation tests undergoing various surgical procedures (colorectal, n=2) managed with either stress-dose
steroids or placebo plus the patient’s baseline steroid dose and observed no episodes
of hypotension related to AI [26]. Their conclusion was that patients with secondary
AI do not manifest symptoms consistent with cardiovascular collapse when given,
at minimum, their preoperative steroid dose. Another randomized double-blind
crossover study of 20 organ transplant recipients on prednisone (5–10mg) undergoing gingival surgery, randomized to hydrocortisone 100mg IV or placebo preoperatively during their rst surgery and then then received the opposite for the second
surgery, similarly observed no symptoms consistent with AI in any patients despite
several cases of abnormal ACTH stimulation testing [27]. Despite obvious sample
size limitations, these studies suggest that stress-doses of corticosteroids are not
required even with biochemical evidence of AI, and advanced the concept that
steroid- treated patients may be continued on their preoperative-dose of corticosteroids during the perioperative period despite abnormal ACTH stimulation testing
without risk of clinically signicant adrenal insufciency. Multiple meta-analysis
have reported safety continuing basal glucocorticoids in minor to moderate surgeries, citing a low incidence of adrenal insufciency secondary to exogenous corticosteroid use [28, 29].
Despite increasing evidence against stress-dose steroids during the perioperative
period for steroid-treated patients, colorectal surgeons managing perioperative IBD
patients on high doses of preoperative steroids remained reluctant to change their
practices [3, 13, 30]. Amidst a paucity of colorectal surgery-specic data, our group
performed several studies comparing low-dose steroids (LDS) to high-dose steroids
(HDS) in steroid-treated IBD patients undergoing major colorectal surgery. Our
LDS protocol consisted of one-third of the daily preoperative steroid dose in hydrocortisone intravenous equivalents (IVED) given at the time of surgical incision followed by one-third IVED every 8h postoperatively, followed by a taper. For patients
off steroids at the time of surgery, no perioperative steroids were given. HDS
entailed hydrocortisone 100mg IV administered preoperatively followed by 100mg
IV every 8hours postoperatively for 24hours, then a taper to oral prednisone over
3days. On hospital discharge, steroids were either discontinued or tapered.
In 2012, we performed a retrospective pilot study evaluating 32 steroid-treated
IBD patients (10 patients on steroids up until surgery and 22 patients treated with
steroids within the past year) managed with LDS [31]. Hypotension occurred in
16% of patients, but all cases resolved spontaneously with no patients requiring
uid bolus, blood transfusion, vasopressors, or high-dose corticosteroid rescue for
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AI.We later compared LDS (n=54) versus HDS (n=43) in IBD patients who were
actively receiving steroid treatment (n=48) or who had previously received steroid
treatment (n=49) undergoing major colorectal surgery [32, 33]. For patients previ-
ously treated with steroids, median duration since last steroid dose was 4months
(range: 0.1–12 months) and median maximum steroid dose in the past year was
equivalent to prednisone 25mg/day (range: 5–60 mg/day). Aside from a higher
incidence of tachycardia in patients previously treated with steroids managed with
HDS [33], we found no signicant difference in hemodynamic instability between
the 2 patient groups and no patients required high-dose steroid rescue for AI.
Aytac and colleagues performed a large volume IBD-specic retrospective analysis of IBD patients on steroids (n = 48) compared to IBD patients off steroids
(n= 187) at the time of proctocolectomy [34]. Eighty-nine patients were treated
with stress-dose steroids and 146 without. There was a higher incidence of sinus
tachycardia in patients managed with stress-dose steroids. While no episodes of
adrenal crisis occurred, one patient in the stress-dose group was readmitted with
hypotension, fatigue and bloating and diagnosed with AI.Another patient in the
stress-dose group died on postoperative day 25 due to an anastomotic leak. Further
underscoring the dangers of postoperative steroids, another retrospective series of
IBD patients undergoing IPAA reported that compared to stress dosing with rapid
IV taper, prolonged oral taper associated with an increased rate of pelvic sepsis [35].
In 2014, our group performed a prospective, randomized non-inferiority study
evaluating 92 steroid-treated IBD patients undergoing major colorectal surgery randomized to HDS or LDS [36]. LDS was non-inferior to HDS with respect to our
primary outcome, absence of postural hypotension on postoperative day 1, which
occurred in 95% of patients randomized to HDS versus 96% of patients assigned to
LDS, p= 0.007. This study included 41 patients previously treated with steroids
(median duration since last steroid dose of 4 months; interquartile range:
2–6 months), of which 25 were randomized to LDS (no perioperative steroids
given). There was no difference in hemodynamic instability between the 2 patient
groups and no patients were treated with rescue HDS for AI.There was, however,
an insignicant trend toward more infectious complications in HDS (16%) versus
LDS-treated patients (4%); p=0.11.
While current anesthesia guidelines reference the growing body of evidence
against perioperative stress-dose steroid administration for patients at low-risk for
HPA axis suppression, they remain conservative and continue to recommend stressdoses of up to 100mg hydrocortisone IV for patients with documented HPA axis
dysfunction by ACTH stimulation test or those at high-risk despite evidence stating
otherwise [6, 37]. These recommendations reect the 2016 Endocrine Society
Clinical Practice Guidelines [38] prioritizing adrenal crisis prevention over the
potential adverse effects of short-term overtreatment with stress-dose steroids.
Although both societies advocate for ACTH testing, a study by Khoo provided evidence that the threshold for diagnosis of HPA axis dysfunction may be too low [39].
They trended total serum cortisol and cortisol binding protein using modern and
specic immunoassays of 93 euadrenal patients undergoing surgeries of varying
severity. They concluded that (1) endogenous stress cortisol responses correlated
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with surgery severity, (2) a downregulation of cortisol binding protein correlated
with surgery, effectively increasing free and active cortisol, and (3) their minimum
peak stress cortisol response was 375nmol/L suggesting that the previous lower
limit of 580 nmol/L for diagnosis hypoadrenalism needed redenition. A recent
review article and practice recommendations summarizing perioperative optimization strategies in IBD surgery, however, recommended a gradual wean off steroids
in patients undergoing IBD surgery with a goal to have patients off steroids for one
week before surgery [12]. If this is not possible, the authors recommended continuing the preoperative daily dose without the need for additional steroids.
E. D. Adams and K. Zaghiyan
Recommendations Based onData
Based on various retrospective and observational studies and few randomized prospective studies, stress-dose steroids appear to be unnecessary and potentially harmful in IBD patients undergoing major colorectal surgery. Several studies in both IBD
and non-IBD patients have suggested that steroid-treated patients can be maintained
on their usual preoperative steroid dose in the perioperative period. For patients
previously treated with steroids within the past year, perioperative steroids may be
avoided altogether. While preoperative ACTH stimulation and perioperative plasma
cortisol levels may be evaluated, these tests tend to overestimate adrenal insufciency with a majority of patients not exhibiting clinically signicant hemodynamic
instability even when perioperative steroids are held altogether. Thus, a low-dose
perioperative steroid protocol consisting of the patient’s preoperative dose appears
to not only be sufcient but may avoid complications associated with high-dose
steroids. Based on the available data, we recommend that steroid-treated IBD
patients undergoing major colorectal surgery be managed with low-dose perioperative steroids equivalent to their preoperative steroid dose in the perioperative period (evidence quality high; strong recommendation).
Personal View oftheData
In our view, high-dose perioperative steroids are unnecessary and likely increase
perioperative risk. In our practice we maintain patients on their preoperative steroid
dose in the perioperative period. Our perioperative protocol entails hydrocortisone
one-third IVED given at the time of surgical incision, followed postoperatively by
oral prednisone equivalent to the patient’s preoperative steroid dose or in patients
unable to tolerate perioperative oral medications, hydrocortisone equivalent to the
preoperative steroid dose is administered followed by a taper. Preoperative HPA
axis testing is likely oversensitive, does not correlate with practical physiology, and
does not need to be pursued. For patients off steroids at the time of surgery, no perioperative steroids are given.
Patients are monitored closely in the perioperative period and any unexplained
hemodynamic instability is followed by ACTH stimulation testing. Patients are
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109
initially managed conservatively, and high-dose steroids are added only if the
patient remains unresponsive to conservative measures and ACTH stimulation testing is positive. However, in our experience no patients have required additional
high-dose steroids for AI with this protocol.
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