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DMcG: 68 year old man
B/G: bilateral hip replacement, psoriasis
23/08/07: Transferred from Letterkenny
General Hospitaltriple vessel disease
with complete LAD occlusion
24/08/07: CABG x 3uncomplicated
extubated day 1 post op
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Day 3nausea and vomiting, pyrexial
Day 4loose stools
lower sternal wound infection
noted
> flucloxacillin IV commenced
Day 5ongoing vomiting and diarrhoea,
pyrexia 38.9
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Day 6abdominal distension, bowel
sounds present, tachycardic 110
> NPO
> IV fluids and wide bore NG
> CXR and PFA
> general surgical consult
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General surgeryinitial assessment:
> central abdominal pain, diarrhoea
> pyrexial, tachycardic
> abdomen mildly distended, mildly
tender lower abdomen, no guardingor rigidity, bowel sounds.
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PFAdilated large bowel
WCC18
Na133
CRP180
Imp: ?systemic sepsis syndrome
?infective diarrhoea
Advised: antibiotics, micro consult, urgent CT
abdomen/pelvis, stool for CMS
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Day 6norovirus positive
Day 7 morningClostridium difficile positive> flucloxacillin stopped
CT abdomenthick-walled caecum,
ascending colon and descending colon, dilatedtransverse colonconsistent with
pseudomembranous colitis
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Day 7 : deteriorationtachypnoeic,
desaturating, hypotensive, oliguric
S/B anaesthetist immediately
Brought to theatre at 18.30 for total
colectomy and end ileostomy formation
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> grossly dilated, distended colon resected> rectal stump protected with 2-layer
closure> abdominal cavity washed out with saline
> terminal ileostomy fashioned in RIF
> Robinson drain inserted> Transferred to ICU
Commenced on IV tazocin & metronidazole asper microbiology
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ICU day 1 post op:
- anuric requiring CVVHD
- daily proctoscopy to decompress
rectal stump
- requiring inotropic support,intubated and ventilated
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Day 3 post op:
- making urine
- NG feeding commenced 10ml/hr
- stoma functioning
- stopped inotropes- WCC raised - 20
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Day 9extubated, off dialysis
Day 13transferred to cardiothoracic
HDU
Uneventful course
Day 26transferred back toLetterkenny
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Discussion
Clostridium difficile
Diagnosis and management of toxic
megacolon
Medical and surgical treatment
options and outcomes
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Discussion
C difficile is a spore-forming, gram-positive
bacillus first described in 1935 as part of the
normal colonic flora of healthy infants. Asymptomatic carriage in 3-5% of healthy
adults
Leading cause of nosocomial entericinfection
Affects up to 20% of hospitalised patients-
1/3 will become symptomatic
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Pathogenesis
Antibiotic therapy
Disruption of colonic mucosa
C Diff exposure and colonization
Release of toxin A (enterotoxin) and toxin B(cytotoxin)
Mucosal injury and inflammation
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Risk Factors
Advanced age
Antibiotic therapy
Immunosuppressive therapy
Multiple and severe underlying diseases Placement of a nasogastric tube
Recent surgical procedure
Admission to intensive care unit
Prolonged hospital stay
Residing in a nursing home
Sharing a hospital room with a C. diff-infected patient
Use of antacids
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Clinical variants of C. diff
infection Asymptomatic carriage
Antibiotic associated diarrhoea
without colitis
Antibiotic associated colitis withoutpseudomembrane formation
Pseudomembranous colitis
Fulminant colitis
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Causes of Toxic Megacolon
Inflammatory bowel disease
-Ulcerative colitis 46%
-Crohns disease 2%
Infectious colitisBacterial
-Pseudomembranous colitis (Clostridium difficile) 31%
Parasitic
-Amoebiasis 3%
Colitis due to special medical therapy
-Cytotoxic chemotherapy 3%
-Beta mimetics 4%
Ischaemia 11%
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Distribution of aetiology
Time period
Aetiology 1984-94 n (%) 1995-2004 n (%)
IBD 21 (30) 12(17)
Other 10 (14) 27(39)
C. Ausch*, R. D. Madoff, M. Gnant, H. R. Rosen*, J. Garcia-Aguilar, N. Holbling*, F. Herbst, V.Buxhofer*, B. Holzer*, D. A. Rothenberger and R.Schiessel* Aetiology and surgical management of toxicmegacolon. Colorecatal disease (8) 195-201. June 2005
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Diagnosis of Toxic Megacolon
1.Evidence of dilatation:
Clinical: Visible abdominal distension, abdominal tenderness, diarrhoea,bloody diarrhoea, constipation, obstipation, bowel sounds.
Radiological: segmental or total colonic distension >6cm, small bowel
and gastric distension.
2.Evidence of toxicity:
3 of -Pyrexia >38.6 1 of -Dehydration
-Tachycardia >120bpm -Cognitive changes
-Leucocytosis >10.5 x109 -
Electrolyte disturbance
-Anaemia -Hypotension
3. Subsequent pathological confirmation of dilatation andtransmural extension of the inflammatory process
Jalan KN, Sircus W, Card WI, Falconer CW, Bruce CB, Crean GP, McManus JP, Small WP, Smith AN. An experience of ulcerative colitis. I. Toxicdilation in 55 cases. Gastroenterology. 1969 Jul;57(1):6882.
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Management
General
IV fluids
Correct e- abnormalities
Complete bowel rest
Discontinue anticholenergics and narcotics Stool CMS
Blood cultures (bacteraemia in up to 25%)
Decompression
Rectal tube
NG tube
Repositioning manoeuvres
Endoscopy: with extreme caution as risk of perforation
Radiology
Frequent assessment with plain films CT
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Treatment: Medical
Conservative: Stop causative antibiotic
Trial of medical therapy
Oral metronidazole +/- oral vancomycin
IV metronidazole
Bacitracin, teicoplanin
Toxin binding agents eg. Cholestyramine Probiotics
IV immunoglobulin
Faecal reconsistution
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Treatment: SurgicalSave the patient, not the colon
Surgery required in up to 80% of cases in some studies
Reserved for the most severe cases
Absolute indications include:
free perforation; massive haemorrhage; increasingtransfusion requirement; worsening signs of toxicity;progression of colonic dilatation.
Most surgical studies recommend colectomy if there ispersistent colonic distension after 48-72hrs.
Early intervention is associated with lower morbidity andmortality
Surgery of choice is subtotal colectomy with end ileostomyand Hartmann closure of the rectum or sigmoid mucousfistula.
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Outcomes: Morbidity
C. Ausch*, R. D. Madoff, M. Gnant, H. R. Rosen*, J. Garcia-Aguilar, N. Holbling*, F. Herbst, V.Buxhofer*, B. Holzer*, D. A. Rothenberger andR. Schiessel* Aetiology and surgical management of toxicmegacolon. Colorecatal disease (8) 195-201. June 2005
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Outcomes: Mortality
C. Ausch*, R. D. Madoff, M. Gnant, H. R. Rosen*, J. Garcia-Aguilar, N. Holbling*, F. Herbst, V.Buxhofer*, B. Holzer*, D. A.Rothenberger and R. Schiessel* Aetiology and surgical management of toxicmegacolon. Colorecatal disease (8) 195 -201. June 2005
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Outcomes
Perforation is a major factor in and mortality:
8.7% if no perforation, 51% with perforation1
Overall mortality has improved some recentstudies showing no mortality compared with
>50% in 19692
Difficult to show objective difference between
outcome of TM due to IBD and other aetiologies
due to significant changes in aetiology and
recent developments in ICU medicine1 Binderow SR, Wexner SD. Current surgical therapy for mucosal ulcerative colitis. Dis Col Rectum 1994; 37: 61024
2. Jalan KN, Sircus W, Card WI, Falconer CW, Bruce CB, Crean GP, McManus JP, Small WP, Smith AN. An experience of ulcerative colitis. I.
Toxic dilation in 55 cases. Gastroenterology. 1969 Jul;57(1):6882.
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Conclusions
Toxic megacolon complicating
pseudomembranous colitis carries a high
morbidity and mortality rate Early surgical intervention when
conservative and medical treatment have
failed is associated with better outcomesand quality of life