Colonic bleeding (Shackelford)

1. COLONIC BLEEDING AND ISCHEMIA
ALVIN T. LORENZANA, MD
GENERAL SURGERY RESIDENT
REGION II TRAUMA AND MEDICAL CENTER

2. COLONIC BLEEDING
•LOWER GI BLEEDING – DISTAL TO THE LIGAMENT OF
TREITZ
• SMALL BOWEL BLEEDING
• COLONIC BLEEDING– ASSOCIATED WITH INCREASED HEALTH CARE USE – COST TO
SOCIETY
IN-HOSPITAL MORTALITY RATE – 2-4%
• ADVANCED AGE (>70 YEARS)
• INTESTINAL ISCHEMIA
• COMNRBID ILLNESS

3. COLONIC BLEEDING
•PREDICTORS OF SEVERE BLEEDING
• TACHYCARDIA (>100 BPM)
• HYPOTENSION (SBP < 115 MMHG)
• SYNCOPE
• NONTENDER ABDOMINAL EXAMINATION
• RECTAL BLEEDING IN THE FIRST 4 HOURS OF EVALUATION
• ASPIRIN USE
• MORE THAN 2 COMORBID CONDITIONS

4. COLONIC BLEEDING
• ETIOLOGIES
• DIVERTICULOSIS
• NEOPLASIA
• VASCULAR ECTASIA
• OTHERS
• INFLAMMATORY BOWEL DISEASE
• INFECTIOUS COLITIS
• POSTPOLYPECTOMY
• ISCHEMIC COLITIS

5. COLONIC BLEEDING
• ANORECTAL
• Hemorrhoids
• Neoplasm
• Pressure necrosis (indwelling rectal tubes)
• Radiation proctitis

6. PROFILE
• MORE LIKELY TO BE MALE
• ALCOHOL USE
• TOBACCO
• ASPIRIN USE
• NONSTEROIDAL ANTINFLAMMATORY AGENTS

7. • CARCINOMA – MOST COMMON CAUSE OF LOWER INTESTINAL
BLEEDING
• DIVERTICULOSIS – MOST COMMON CAUSE OF ACUTE SYMPTOMATIC
LOWER GI BLEEDING

8. DIVERTICULOSIS
• 30% IN OLDER THAN 50 YEARS
• 60% IN OLDE THAN 80 YEARS
• PAINLESS HEMATOCHEZIA
• 70-80% WILL HAVE SPONTANEOUS RESOLUTION
• 20% OBTAIN A DEFINITIVE DIAGNOSIS OF A DIVERTICULAR BLEED
BASED ON COLONOSCOPIC FINDINGS AOF ACTIVE BLEEDING OR A
VISIBLE VESSEL OR CLOT.
• MOSTLY ARE DIAGNOSED PRESUMPTIVELY – DUE TO PRESENCE OF
DIVERTICULA DURING COLONOSCOPY

9. NEOPLASIA
MAJORITY OF PATIENTS WITH COLORECTAL NEOPLASIA –
OCCULT BLOOD LOSS AND ARE MORE LIKELY TO PRESENT
WITH IRON DEFICIENCY ANEMIA
• LOWER GI BLEEDING + WEIGHT LOSS + CHANGE IN
BOWEL HABITS = SUSPICION FOR NEOPLASIA
• DRE is imperative
• Most common cause of bleeding: Ulceration of the tumor
surface

10. VASCULAR ECTASIA
• AKA angiodysplasia, arteriovenous malformation, angioectasia
• Frequent cause of recurrent Lower GI bleeding
• Age related degeneration of previously normal colonic blood
vessels
• CECUM AND ascending colon
• Typically are less than 5mm in diameter and are multiple
• Characteristic findings: small red flat lesion with ectatic vessels
radiating from the central lesion
Factors for bleeding:
a. number of lesions
b. presence of coagulopathy or bleeding disorder

12. DIAGNOSIS OF LOWER GI BLEEDING
• Varies with:
• Age
• Presence or absence of active bleeding
• Severity of hemodynamic compromise
• All patients patients with lower GI bleeding require a physical examination,
including DRE

13. LABORATORY
• Performed to:
• Evaluate level of anemia
• Rule out coagulopathy

14. DEFINITION OF TERMS
• OCCULT BLEED: Absence of gross bleeding
Heme positive stools
• MELENA: Passage of dark, black, or tarry stools
• SCANT INTERMITTENT HEMATOCHEZIA: Intermittent passage of
usually bright red blood per rectum
• SEVERE HEMATOCHEZIA: Large-volume bright red blood per rectum
•

15. BLEEDING SEVERITY AND MANAGEMENT
American Society of Gastrointestinal Endoscopy (ASGE)

17. ENDOSCOPIC TREATMENT of ACUTE HEMORRHAGE
• Depends on:
• THE ENDOSCOPIST
• THE LOCATION OF THE LESION
• THE SIZE OF THE LESION
• MOST COMMONLY USED METHOD
• Epinephrine injection
• Heater probe coagulation
• Endoscopic clip placement

18. ANGIOGRAPHIC TREATMENT of ACUTE HEMORRHAGE
• Follows unsuccessful endoscopy or if there is rapid ongoing bleeding
• IN ORDER:
• Selective SMA
• Selective IMA
• Celiac axis studies
• Intraarterial injection of Vasopressin – used most of the time for active bleeding
• Others: selective embolization with coils, gels, or cellulose materials
• Success rate: 40-78%
• COMPLICATIONS: renal toxicity, arterial injury, ischemia (higher than in endoscopy)
– explains why it is done after a colonoscopy

19. SURGICAL TREATMENT
• Reserved for bleeding that cannot be controlled with endoscopy or angiography.
Indications:
• Hemodynamic instability
• ongoing transfusion requirements
• Persistent hemorrhage not responsive to other methods
• Preop preparation: Endoscopic tattooing or angiographic identification of the
bleeding source
• Intraoperative endoscopy – needed if bleeding is not perioperatively localized – if
still not localized, subtotal colectomy is recommended.

20. COLONIC ISCHEMIA
• Before: synonymous with colonic infarction or gangrene
• DEFINITION:
• Colonic ischemia – hypoperfusion of the colon
• Mesenteric ischemia – hypoperfusion of the small intestine
• ETIOLOGIES:
A. Occlusive or non-occlusive arterial obstruction
• B. Obstruction of venous outflow

22. COLONIC CIRCULATION
• protected from ischemia by its abundant collateral circulation (between the celiac artery, SMA,
IMA, and iliac artery)
• Arch of Riolan
• Marginal artery of Drummond
• Network of communicating submucosal vessels exists within the bowel wall

24. PATHOPHYSIOLOGY OF COLONIC ISCHEMIA
• Whether it is increased demand by colonic tissue
superimposed on already marginal blood flow or
whether the flow itself is acutely diminished – not yet
determined

25. COLONIC ISCHEMIA
• Tends to be a disease of older adults and may therefore result from:
• age-related alteration in the mesenteric vasculature
• age-related tortuosity of the longer colonic arteries (increased
resistance)
• MOST CASES HAVE NO IDENTIFIABLE CAUSE (thought to be
the result of local nonocclusive ischemia - low-flow state in
association with small vessel disease
• Thromboembolic disease – less often cause of ischemia

26. MEDICAL COMORBIDITIES
• cardiovascular disease
• diabetes mellitus
• chronic kidney disease
• chronic obstructive pulmonary disease
• Irritable bowel syndrome and constipation may also increase the risk of developing colonic
ischemi
• postoperative complication of procedures requiring ligation or exclusion of the IMA
A. Aortic surgery for the treatment of aneurysmal disease
B. Colonic resection for carcinoma.

28. SYMPTOMS
• sudden onset of mild, crampy abdominal pain, usually localized to
the lower left quadrant
• Less commonly the pain is severe, or conversely, in other patients
the description of pain can be elicited only retrospectively
• An urgent desire to defecate frequently accompanies the pain and
is followed, within 24 hours, by the passage of either bright red or
maroon blood in the stool.
• Physical examination may reveal mild to severe abdominal
tenderness elicited in the location of the involved segment of bowel

29. Distribution of Colonic Ischemia
•MOST COMMON
• Splenic flexure
• Descending colon
• Sigmoid colon
• Segmental involvement is the most common distribution (Involvement
of the whole colon is rare)

30. • The rectum is very rarely involved because of its abundant dual
blood supply from both the splanchnic and systemic arcades.
Patients noted to have right-sided–only ischemia more commonly
have atrial fibrillation, coronary artery disease, and chronic kidney
disease
• Depending on the severity and duration of the ischemic insult, fever
or leukocytosis may develop. Patients with severe ischemia leading
to transmural necrosis, gangrene, or perforation may develop
peritonitis.

31. Natural History of Colonic Ischemia
• ultimate course of an ischemic insult depends on many
factors:
• the cause (i.e., occlusive or nonocclusive)
• the caliber of an occluded vessel
• the duration and degree of ischemia
• the rapidity of onset of the ischemia
• the condition of the collateral circulation
• the metabolic requirements of the affected bowel
• the presence and virulence of the bowel flora, and
• the presence of associated conditions (colonic distention)

33. COLONIC ISCHEMIA
• Symptoms subside within 24 to 48 hours
• Clinical, radiographic, and endoscopic evidence of healing is
seen within 2 weeks
• More severe, but still reversible, ischemic damage may take 1
to 6 months to resolve.
• The majority of patients with reversible disease develop
colopathy, whereas transient colitis develops in approximately
one-third.
• Severe reversible ischemia may result in diffuse mucosal
sloughing.

34. • Because the clinical course of colonic ischemia is difficult to predict, there is a
need for serial examinations to evaluate for signs of clinical deterioration
suggesting development of gangrene or perforation:
• rising temperature
• elevated white blood cell count
• worsening metabolic acidosis
• hemodynamic instability
• or peritonitis.
• Persistent diarrhea or bleeding beyond the first 10 to 14 days - risk for development of perforation
or, less frequently, a protein-wasting enteropathy.
• Strictures may develop over a period of weeks to months and may be asymptomatic or produce
progressive bowel obstruction

35. DIAGNOSIS
•CT scan combined with early colonoscopy
•Barium enema – “thumbprinting” or ”pseudotumors”
– subepithelial hemorrhagic nodules or bullae
• It is now being used to follow the course of ischemic
stricture

36. DIAGNOSIS
• CT findings consistent with colonic ischemia include:
• segmental bowel wall thickening
• Edema
• Thumbprinting
• Pericolic fat stranding and
• Ascites
• CT findings that suggest transmural colonic infarction:
• Findings of colonic pneumatosis or portal venous gas
• CT angiography should be performed in patients with clinical suspicion for acute
mesenteric ischemia

38. DIAGNOSIS
• EARLY COLONOSCOPY
• confirm the diagnosis of colonic ischemia – by direct visualization
• Establish the severity of the disease
• Has the benefit of obtaining sample via biopsy
• Done within 48 hours of presentation – done when CT findings are
consistent with colonic ischemia
• Findings of dusky, cyanotic mucosa is highly suggestive of gangrene
• Should be done cautiously in the setting of colonic ischemia – perforation
• Should not be performed in the setting of peritonitis or irreversible
ischemia (surgery)
• Mucosal infartction by biopsy – pathognomonic of ischemia

39. MANAGEMENT
• GENERAL PRINCIPLES
• Once diagnosis is established, the patient is treated expectantly with fluid resuscitation and bowel
rest, unless signs and symptoms of gangrene or perforation develop
• Optimization of cardiac function ensures adequate systemic perfusion
• Medications that cause mesenteric vasoconstriction (e.g., digitalis and vasopressors) should be
withdrawn if possible
• Urine output is monitored and maintained with parenteral isotonic fluids
• There is limited evidence to support the utility of administration of antibiotics; however, ACG
guidelines recommend antimicrobial therapy for patients with “moderate” or “severe” disease.
• If the colon appears distended, either clinically or radiographically, it can be decompressed with a
rectal tube, with or without gentle saline irrigation
• Corticosteroids are not recommended for colonic ischemia, except in cases of vasculitis

40. MANAGEMENT
• GENERAL PRINCIPLES
• CBC is repeated frequently in acute episode
• Athough rarely needed, blood products should be administered according to the patient’s
requirements
• Serum potassium and magnesium levels must be monitored (diarrhea and tissue necrosis)
• Elevated systemic levels of lactate dehydrogenase may indicate bowel ischemia but is neither
sensitive nor specific for necrosis or gangrene.
• Patients with significant diarrhea are started on parenteral nutrition early.
• Narcotics should be administered judiciously
• Mechanical bowel preparation is contraindicated because it may cause perforation.

41. • In the mildest cases of colonic ischemia, signs and symptoms of illness disappear (24 to 48 hours)
• Complete clinical resolution (1 to 2 weeks)
• No further therapy is required in these patients
• Treatment includes a high-residue diet, and follow-up
endoscopy is performed to confirm complete healing and
exclude alternative diagnosis
Management of Reversible Ischemia

42. Management of Irreversible Acute and
Subacute Ischemia
• Acute signs of clinical deterioration during the period of observation (rising temperature, elevated white
blood cell count, worsening metabolic acidosis, hemodynamic instability, or peritonitis) suggest colonic
infarction and are an indication for operative intervention
• Patients with persistent symptoms, such as diarrhea, rectal bleeding, or recurrent sepsis, for more than
10 to 14 days may require operative intervention.
• Despite a normal serosal appearance, there may be extensive mucosal injury, and the extent of
resection should be guided by the distribution of disease as seen on preoperative studies rather than
by the appearance of the serosal surface of the colon at the time of surgery
• As in all resections for colonic ischemia, the specimen must be opened at the time of surgery to
ensure normal mucosa at the margins. If at the time of surgery the segmental colitis is found to
involve the rectum, a mucous fistula or Hartmann procedure with an end colostomy should be
performed.
• Simultaneous proctocolectomy is rarely indicated but should be performed for gangrene of the
rectum.

43. MANAGEMENT OF CHRONIC ISCHEMIA
• Colonic ischemia may not be accompanied by clinical
symptoms during the acute insult but may still produce chronic
segmental colitis
• Regardless, de novo occurrence of a segmental area of colitis
with stricture in an older patient is most likely ischemic.
• How to address:
• Elective bowel resection is indicated for patients with
chronic segmental colonic ischemia and recurrent episodes
of sepsis. The underlying etiology of these septic episodes is
likely bacterial translocation from areas of unhealed
segmental colitis

44. Management of Ischemic Strictures
• Stenosis or stricture
• Asymptomatic – observe (some of them will return to normal over a
12- to 24-month period with no further therapy)
• Symptomatic - segmental resection is required
• Endoscopic dilation of chronic colonic strictures as a result of
ischemia is generally not recommended

45. • THANK YOU!