D’Souza, R

Mekonnen, E

Tacci, S

Varcada, M

Virdis, F

English

PubMed

F. Virdis

E. Mekonnen

R. D’Souza

S. Tacci

M. Varcada

Springer - Publisher Connector

LETTER TO THE EDITOR
Could surgery be the gold standard in moderate and severe
ischaemic colitis? Atypical case description and review
of literature
F. Virdis & E. Mekonnen & R. D’Souza & S. Tacci &
M. Varcada
Accepted: 14 April 2014 /Published online: 14 May 2014
# The Author(s) 2014. This article is published with open access at Springerlink.com
Dear Editor,
Ischaemic colitis (IC) is a rare condition caused by an inade-
quate perfusion leading to colonic inflammation. This condi-
tion has an incidence of 4.5–9.9 per 100,000 population/year
[1]. The exact pathophysiology is still debated; the main
mechanism implicated is an ischaemia-reperfusion phenome-
non with rapid return of normal mesenteric blood flow [2].
Despite suggestive evidence for a vascular or autonomic cause
for IC, most cases have no identifiable cause. These sponta-
neous episodes are thought to be the result of impairment of
the micro-vascularization of the colonic wall. Several risk
factors have been described, which include comorbidities
and medications. Two types of IC are described, defined by
their severity: sever IC with transmural colonic ischaemia and/
or multi-organ failure (MOF) and mild-moderate IC without
MOF [2]. The clinical presentation is variable, and clinical
signs are nonspecific [2]. Lower gastrointestinal bleeding is
often accompanied by urgent diarrhoea. However, blood loss
is usually minimal without haemodynamic compromise or the
need for transfusions and profuse bleeding should suggest
another diagnosis [3].
Surgical treatment is necessary in about 20–28 % of pa-
tients with IC [3]. There is no overall consensus regarding
treatment of IC [2]. Diaz-Nieto et al. reported that surgery is
only generally agreed upon in peritonitis and conservative
treatment is used for remaining cases, with an undefined role
for surgery in the latter [1].
A 70-year-old male was admitted to our institution with
sudden sided left abdominal pain associatedwith two episodes
of bloody diarrhoea, nausea, belching, vomiting, dysuria and
pyrexia. The patient was on Simvastatin on a regular basis
only. On admission, all the patient’s observations were stable,
with blood pressure 153/64 mmHg, heart rate 70 beats/min,
body temperature 36.5 °C and oxygen saturation 100 % in
room air. On clinical examination, the abdomen was soft and
quite tender in the left lower quadrant. There were no palpable
masses or signs of peritoneal irritation. Normal bowel sounds.
On rectal (PR) examination, there was minimal bright red
blood on the glove, with an empty rectum. Blood chemistry
revealed a high white blood cell count (16.47×109/L) with
neutrophils 14.07×109/L, haemoglobin 156 g/L, C-reactive
protein level 2 mg/L, lactate 2.47, BE 1.6, normal PH and
normal clotting. Initially, management was based on bowel
rest, intra venous (IV) fluids, IVantibiotics (ciprofloxacin and
metronidazole) and analgesia (paracetamol, tramadol). An
abdominal computer tomography (CT) scan with contrast,
performed the day after admission, showed a significant ab-
normality of the colon from the ascending colon in a contin-
uous fashion to the descending/sigmoid junction. The caecum,
sigmoid and rectum appeared unremarkable. The colon was
thick walled and oedematous with some fluid in the left
paracolic gutter and within the pelvis. No collections. No
pneumatosis. The colon affected appeared underperfused,
and the final radiologist’s report concluded acute colitis.
Therefore, Clostridium difficile infection was excluded with
blood investigations. A sigmoidoscopy performed 4 days after
the admission showed severely inflamed proximal sigmoid
and distal descending colon with significantly hyperaemic
mucosa, and the histological report of biopsies taken during
the procedure indicated that the distal colon and rectum were
within normal limits; the sigmoid colon was affected by
ulceration and features in keeping with the clinical suspicion
of IC. During the first week of treatment, our patient improved
in terms of abdominal pain, associated with no further PR
bleeding, bowels regularly opened and observations stable.
His blood investigations improved asWCC declined (down to
9.3×109/L), but CRP increased to 247 mg/L. During the
F. Virdis (*) : E. Mekonnen :R. D’Souza : S. Tacci :M. Varcada
Department of Emergency General Surgery, Royal Free Hospital,
Pond Street, London, Greater London NW3 2QG, UK
e-mail: francesco.virdis@hotmail.it
Int J Colorectal Dis (2014) 29:1015–1016
DOI 10.1007/s00384-014-1877-z
second week following the admission, therapeutic tinzaparin
was started. However, despite medical treatment and apparent
improvements, on the 12th hospitalization day, the patient
presented a few episodes of PR bleeding. An abdominal CT
angiogram was performed, and it showed active bleeding
from the anterior wall of the transverse colon, arising from a
branch of the middle colic artery. Embolisation using micro
coils was then successfully performed. Moreover, on the 14th
day of hospitalization, the general condition of the patient
started to deteriorate, with increasing abdominal pain associ-
ated with diffuse tenderness, pyrexia and tachycardia.
Therefore, after 14 days of conservativemanagement, surgical
intervention with laparotomy, total colectomy and end
ileostomy was performed. On-table colonoscopy was per-
formed and showed pancolitis.
There is no overall consensus regarding treatment of IC; no
studies with a sufficient level of evidence are available in the
literature to establish clinical practice guidelines [1]. Any part
of the bowel may be affected, but the splenic flexure and
descending and sigmoid colon are the most common sites.
In our case, the initial CT scan showed that the disease
diffusion was quite uncommon, with sparing of the sigmoid
colon. However, the biopsy performed during the sigmoidos-
copy, which was done 2 days after the CT scan, reported an
involvement of the proximal sigmoid.
Following an initial improvement with conservative man-
agement (intravenous fluids, bowel rest, parenteral nutrition,
heparin prophylaxis and antibiotics), after 14 days, the condi-
tion of the patient deteriorated and surgery was necessary.
Another atypical disease complication was the profuse epi-
sode of bleeding after 2 weeks of medical management.
Treatment guidelines can be standardized depending on the
depth of colonic mural ischaemia and its impact on vital
function: surgical treatment is advocated for deep ischaemia
with colonic necrosis and/or MOF, whereas observation and
medical management are recommended for patients with su-
perficial ischaemia without organ dysfunction [2]. Favier et al.
described an endoscopic classification of IC, which included
ischaemia limited to the mucosa with petechiae and small
ulcerations with intervening healthy mucosa as stage I, ischae-
mia extending to the muscularis mucosa with large ulcerations
as stage II and transmural ischaemia with necrosis of the
muscularis and possible perforation as stage III [4].
Basically, in agreement with literature, patients with a con-
firmed IC diagnosis, without surgical abdomen and/or evi-
dence of pneumoperitoneum, need surgery only if they have
Favier stage 2 with MOF or Favier stage 3. A question could
be why, in patients with ischaemia extending to the muscularis
mucosa with large ulceration (Favier stage 2), we should wait
for the appearance of sepsis, or MOF, before deciding on
surgical treatment? We found, in the literature, how most
patients with IC will clinically improve within 24 or 48 h.
However, an indication for surgery is persistent symptoms
beyond 2–3 weeks. Obviously, a septic patient, with MOF,
or with perforation and/or peritonitis, has more risk of devel-
oping post-surgical complications than a patient who has
surgery before the appearance of these conditions. A possible
suggestion could be to decide on surgical management in all
patients with Favier stage 2 in which there is no evidence of
clinical improvement after 48–72 h. In our patient, we had a
clinical improvement 6 days following admission but another
worsening during the second week; this can suggest that the
role of endoscopy and the grade of disease based on Favier
classification could be a better prognostic index than a slow
improvement in the clinical condition. Moreover, colonosco-
py performed on table showed the extent of disease and
allowed the right edges of resection to be identified. This is
our conclusion after a comparison of our experience and a
review of literature. However, we cannot reach a definitive
conclusion without a sufficient sample of patients, but we
would like to suggest a new possible strategy in the manage-
ment of mild and severe IC, with the hope that it could be
helpful for other studies in the future.
Open Access This article is distributed under the terms of the Creative
Commons Attribution License which permits any use, distribution, and
reproduction in any medium, provided the original author(s) and the
source are credited.
References
1. Diaz Nieto R, VarcadaM,Ogunbiyi OA et al (2011) Systematic review
on the treatment of ischaemic colitis. The Association of
Coloproctology of Great Britain and Ireland. Color Dis 13:744–47.
doi:10.1111/j.1463-1318.2010.02272.x
2. Moszkowicz D, Mariani A, Trèsallet C et al (2013) Ischaemic colitis:
the ABCs of diagnosis and surgical management. J Visceral Surg 150:
19–28
3. Baixauli J, Kiran RP, Delaney CP (2003) Investigation and manage-
ment of ischemic colitis. Cleve Clin J Med 70(11):920–34
4. Favier C, Bonneau HP, TranMinh Vet al (1976) Endoscopic diagnosis
of regressive ischemic colitis. Endoscopic, histologic and arteriograph-
ic correlations. Nouv Presse Med 5:77–9
1016 Int J Colorectal Dis (2014) 29:1015–1016


Could surgery be the gold standard in moderate and severe ischaemic colitis? Atypical case description and review of literature

UCL Discovery

LETTER TO THE EDITORCould surgery be the gold standard in moderate and severeischaemic colitis? Atypical case description and reviewof literatureF. Virdis & E. Mekonnen & R. D’Souza & S. Tacci &M. VarcadaAccepted: 14 April 2014 /Published online: 14 May 2014# The Author(s) 2014. This article is published with open access at Springerlink.comDear Editor,Ischaemic colitis (IC) is a rare condition caused by an inade-quate perfusion leading to colonic inflammation. This condi-tion has an incidence of 4.5–9.9 per 100,000 population/year[1]. The exact pathophysiology is still debated; the mainmechanism implicated is an ischaemia-reperfusion phenome-non with rapid return of normal mesenteric blood flow [2].Despitesuggestiveevidenceforavascularorautonomiccausefor IC, most cases have no identifiable cause. These sponta-neous episodes are thought to be the result of impairment ofthe micro-vascularization of the colonic wall. Several riskfactors have been described, which include comorbiditiesand medications. Two types of IC are described, defined bytheirseverity:severICwithtransmuralcolonicischaemiaand/or multi-organ failure (MOF) and mild-moderate IC withoutMOF [2]. The clinical presentation is variable, and clinicalsigns are nonspecific [2]. Lower gastrointestinal bleeding isoften accompanied by urgent diarrhoea. However, blood lossisusually minimal without haemodynamiccompromiseor theneed for transfusions and profuse bleeding should suggestanother diagnosis [3].Surgical treatment is necessary in about 20–28 % of pa-tients with IC [3]. There is no overall consensus regardingtreatment of IC [2]. Diaz-Nieto et al. reported that surgery isonly generally agreed upon in peritonitis and conservativetreatment is used for remaining cases, with an undefined rolefor surgery in the latter [1].A 70-year-old male was admitted to our institution withsuddensidedleftabdominalpainassociatedwithtwoepisodesof bloody diarrhoea, nausea, belching, vomiting, dysuria andpyrexia. The patient was on Simvastatin on a regular basisonly. On admission, all the patient’s observations were stable,with blood pressure 153/64 mmHg, heart rate 70 beats/min,body temperature 36.5 °C and oxygen saturation 100 % inroom air. On clinical examination, the abdomen was soft andquitetenderinthe leftlower quadrant.There werenopalpablemasses or signs of peritoneal irritation. Normal bowel sounds.On rectal (PR) examination, there was minimal bright redblood on the glove, with an empty rectum. Blood chemistryrevealed a high white blood cell count (16.47×109/L) withneutrophils 14.07×109/L, haemoglobin 156 g/L, C-reactiveprotein level 2 mg/L, lactate 2.47, BE 1.6, normal PH andnormal clotting. Initially, management was based on bowelrest, intra venous (IV) fluids, IVantibiotics (ciprofloxacin andmetronidazole) and analgesia (paracetamol, tramadol). Anabdominal computer tomography (CT) scan with contrast,performed the day after admission, showed a significant ab-normality of the colon from the ascending colon in a contin-uousfashiontothedescending/sigmoidjunction.Thecaecum,sigmoid and rectum appeared unremarkable. The colon wasthick walled and oedematous with some fluid in the leftparacolic gutter and within the pelvis. No collections. Nopneumatosis. The colon affected appeared underperfused,and the final radiologist’s report concluded acute colitis.Therefore, Clostridium difficile infection was excluded withbloodinvestigations.Asigmoidoscopyperformed4daysafterthe admission showed severely inflamed proximal sigmoidand distal descending colon with significantly hyperaemicmucosa, and the histological report of biopsies taken duringthe procedure indicated that the distal colon and rectum werewithin normal limits; the sigmoid colon was affected byulceration and features in keeping with the clinical suspicionofIC.Duringthefirstweekoftreatment,ourpatientimprovedin terms of abdominal pain, associated with no further PRbleeding, bowels regularly opened and observations stable.HisbloodinvestigationsimprovedasWCCdeclined(downto9.3×109/L), but CRP increased to 247 mg/L. During theF. Virdis (*): E. Mekonnen:R. D’Souza: S. Tacci: M. VarcadaDepartment of Emergency General Surgery, Royal Free Hospital,Pond Street, London, Greater London NW3 2QG, UKe-mail: francesco.virdis@hotmail.itInt J Colorectal Dis (2014) 29:1015–1016DOI 10.1007/s00384-014-1877-zsecond week following the admission, therapeutic tinzaparinwas started. However, despite medical treatment and apparentimprovements, on the 12th hospitalization day, the patientpresented a few episodes of PR bleeding. An abdominal CTangiogram was performed, and it showed active bleedingfrom the anterior wall of the transverse colon, arising from abranch of the middle colic artery. Embolisation using microcoils was then successfully performed. Moreover, on the 14thday of hospitalization, the general condition of the patientstarted to deteriorate, with increasing abdominal pain associ-ated with diffuse tenderness, pyrexia and tachycardia.Therefore,after14daysofconservativemanagement,surgicalintervention with laparotomy, total colectomy and endileostomy was performed. On-table colonoscopy was per-formed and showed pancolitis.There isnooverall consensus regardingtreatment ofIC; nostudies with a sufficient level of evidence are available in theliterature to establish clinical practice guidelines [1]. Any partof the bowel may be affected, but the splenic flexure anddescending and sigmoid colon are the most common sites.In our case, the initial CT scan showed that the diseasediffusion was quite uncommon, with sparing of the sigmoidcolon. However, the biopsy performed during the sigmoidos-copy, which was done 2 days after the CT scan, reported aninvolvement of the proximal sigmoid.Following an initial improvement with conservative man-agement (intravenous fluids, bowel rest, parenteral nutrition,heparin prophylaxis and antibiotics), after 14 days, the condi-tion of the patient deteriorated and surgery was necessary.Another atypical disease complication was the profuse epi-sode of bleeding after 2 weeks of medical management.Treatment guidelines can be standardized depending on thedepth of colonic mural ischaemia and its impact on vitalfunction: surgical treatment is advocated for deep ischaemiawith colonic necrosis and/or MOF, whereas observation andmedical management are recommended for patients with su-perficialischaemiawithoutorgandysfunction[2].Favieretal.described an endoscopic classification of IC, which includedischaemia limited to the mucosa with petechiae and smallulcerationswithinterveninghealthymucosaasstageI,ischae-miaextendingtothemuscularismucosawithlargeulcerationsas stage II and transmural ischaemia with necrosis of themuscularis and possible perforation as stage III [4].Basically, in agreement with literature, patients with a con-firmed IC diagnosis, without surgical abdomen and/or evi-dence of pneumoperitoneum, need surgery only if they haveFavier stage 2 with MOF or Favier stage 3. A question couldbewhy,inpatientswithischaemiaextendingtothemuscularismucosa with large ulceration (Favier stage 2), we should waitfor the appearance of sepsis, or MOF, before deciding onsurgical treatment? We found, in the literature, how mostpatients with IC will clinically improve within 24 or 48 h.However, an indication for surgery is persistent symptomsbeyond 2–3 weeks. Obviously, a septic patient, with MOF,or with perforation and/or peritonitis, has more risk of devel-oping post-surgical complications than a patient who hassurgery before the appearance of these conditions. A possiblesuggestion could be to decide on surgical management in allpatients with Favier stage 2 in which there is no evidence ofclinical improvement after 48–72 h. In our patient, we had aclinical improvement 6 days following admission but anotherworsening during the second week; this can suggest that therole of endoscopy and the grade of disease based on Favierclassification could be a better prognostic index than a slowimprovement in the clinical condition. Moreover, colonosco-py performed on table showed the extent of disease andallowed the right edges of resection to be identified. This isour conclusion after a comparison of our experience and areview of literature. However, we cannot reach a definitiveconclusion without a sufficient sample of patients, but wewould like to suggest a new possible strategy in the manage-ment of mild and severe IC, with the hope that it could behelpful for other studies in the future.Open Access This article is distributed under the terms of the CreativeCommons Attribution License which permits any use, distribution, andreproduction in any medium, provided the original author(s) and thesource are credited.References1. DiazNietoR,VarcadaM,OgunbiyiOAetal(2011)Systematicreviewon the treatment of ischaemic colitis. The Association ofColoproctology of Great Britain and Ireland. Color Dis 13:744–47.doi:10.1111/j.1463-1318.2010.02272.x2. Moszkowicz D, Mariani A, Trèsallet C et al (2013) Ischaemic colitis:the ABCs of diagnosis and surgical management. J Visceral Surg 150:19–283. Baixauli J, Kiran RP, Delaney CP (2003) Investigation and manage-ment of ischemic colitis. Cleve Clin J Med 70(11):920–344. FavierC,BonneauHP,TranMinhVetal(1976)Endoscopicdiagnosisofregressiveischemiccolitis.Endoscopic,histologicandarteriograph-ic correlations. Nouv Presse Med 5:77–91016 Int J Colorectal Dis (2014) 29:1015–1016

DiazNietoR,VarcadaM,OgunbiyiOAetal(2011)Systematicreview on the treatment of ischaemic colitis.

FavierC,BonneauHP,TranMinhVetal(1976)Endoscopicdiagnosis ofregressiveischemiccolitis.Endoscopic,histologicandarteriographic correlations. Nouv Presse Med 5:77–9 1016

Investigation and management of ischemic colitis.

Trèsallet C et al (2013) Ischaemic colitis: the ABCs of diagnosis and surgical management.

Could surgery be the gold standard in moderate and severe ischaemic colitis? Atypical case description and review of literature

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