3. Lower GIB: Overview
F •Introduction
A •Aetiologies
S •Management algorythms
T •Endoscopic hemostasis
4. Introduction:
• LGIB is diagnosed in 20-30% of all patients presenting with
major GI bleeding.
• The annual incidence is 0.03%.
• increases * 200 from 2nd- 8th decades of life.
• The mean age at presentation is 63 - 77 years.
• A full-time gastroenterologist manages >10 cases/ year.
• Blood loss can be trivial or massive & life-threatening, but the
majority have self-limited& uncomplicated hospitalization.
• LGIB tend to present with a higher Hb &less likely to develop
hypotensive shock or require blood transfusions.
• Mortality is 2- 4%, usually from comorbidities& noscom infs.
• Reported decreased incidence of LGIB & lower age/gender-
adjusted fatality rate over the past decade.
5. Definitions:
• Before deep enteroscopy: Bleeding from a source distal to the
ligament of Treitz
• Now: bleeding from a source distal to ICV.
• Now small-bowel sources called midgut bleeding.
• Acute LGIB: of recent duration (<3 days) that may result in
hemodynamic instability, anemia&/or the need for blood
transfusion.
• Chronic LGIB: passage of blood per rectum over a period of
several days or longer& usually implies intermittent or slow
loss of blood& present with occult fecal blood, intermittent
melena or maroon stools, or scant amounts of bright red
blood per rectum.
6.
7. Diverticular bleeding:
• Present in up to 30% >50 ys, to 60% >80 ys.
• Accounts for 20- 65% of acute LGIB episodes.
• Clinically significant bleeding occurs in 3-15% with colon diverticula,
usually as a result of trauma to the vasa recta at the neck or dome
of the diverticulum.
• NSAIDs increase the risk for diverticular bleeding.
• Hypertension&anticoagulation also may contribute to severe
bleeding.
8. Diverticular bleeding:
• The clinical presentation:
• Painless hematochezia, resolves spontaneously in 75-80% but recurs
in 25-40% within 4 years.
• Early rebleeding is uncommon after endoscopic treatment.
• Using epinephrine/or thermal coagulation early (<30 days)
rebleeding 0-38%.
• Using endoscopic clips: no early rebleed & late rebleeding in 18-
22%.
• Late rebleeding may occur from diverticula at a location different
from that of the index bleed.
9. Diverticular bleeding:
• The diagnosis is presumptive in most patients, based on the
presence of colon diverticula& the absence of another obvious
source.
• A definitive diagnosis is made in 22% who have active bleeding or
high-risk stigmata of a visible vessel or clot on colonoscopy.
• Diverticular bleeding is detected by colonoscopy more commonly in
the left side of the colon (50-60%)& by angiography more
commonly in the right side of the colon (50-90%).
10. Ischemic colitis:
• 1- 19% Of LGIB most commonly elderly results from a sudden, often
temporary, reduction in mesenteric blood flow secondary to
hypoperfusion, vasospasm, or occlusion of the mesenteric
vasculature.
• The typical locations affected by non-occlusive colon ischemia are
the “ watershed” areas of the colon: the splenic flexure&
rectosigmoid junction;sigmoid colon in 20.8%, descending colon to
sigmoid colon in 9.9%, transverse colon to sigmoid colon in 4.2%, &
pancolonic involvement in 7.3%.
• Patients often have underlying CVD &present with hypotension or
hypovolemia, which results in mesenteric hypoperfusion&
vasoconstriction&bleeding results from reperfusion injury after the
hypoperfusion has resolved.
11. Ischemic colitis:
• Mesenteric occlusion related to cardiac thromboembolism in 1/3
• Hypercoagulable states,vasculitis&medications are less common.
• The clinical presentation: sudden onset of cramping abdominal
pain, followed by hematochezia or bloody diarrhea within 24 hours.
• Typical endoscopic findings: submucosal hemorrhage& ulcerations
with segmental distribution with an abrupt transition between
abnormal& normal mucosa.
• The rectum usually is spared, because of its dual blood supply.
• A single linear ulcer along the longitudinal axis of the colon on the
antimesenteric border (“ single-strip” sign) also may occur.
• None of these endoscopic findings are pathognomonic of ischemic
colitis&infectious / inflammatory colitides should remain in the DD.
12. Ischemic colitis:
• Angiography should be considered in severe ischemic colitis or
right-sided involvement, when there is suspicion for an underlying
thromboembolism or concomitant mesenteric ischemia involving
the small bowel.
• The majority improve with conservative management including:
• IV hydration.
• Correction of the underlying etiology.
• Involvement of the right side of the colon& total colon ischemia
(usually after a major abd surgery) may have unfavorable outcome
because of concomitant small-bowel ischemia or transmural
infarction & may require surgical management.
13.
14. Angioectasias(angiodysplasias):
• The prevalence varies with clinical presentation (1-2% in
asymptomatic patients undergoing screening colonoscopy; 40- 50%
in those presenting with hematochezia).
• Account for 3-15% of patients with LGIB.
• The incidence increases with age& >2/3 of these lesions are seen in
> 70 years.
• Angioectasias are caused by degenerative changes& chronic
intermittent low-grade obstruction in the submucosal vessels.
• They are located predominantly in the cecum & the ascending
colon.
• Multiple angioectasias may be seen on colonoscopy appear as red,
flat lesions, 2 mm- several cms, with ectatic blood vessels radiating
from a central feeding vessel
15. Angioectasias(angiodysplasias):
• Risk factors include:
• Advanced age, comorbidities, the presence of multiple
angioectasias & the use of anticoagulants or antiplatelet agents.
• Patients can present with occult bleeding, melena, or painless
intermittent hematochezia.
• Colonoscopy has a sensitivity of 80% for detection of angioectasias.
• Narcotics for sedation may reduce mucosal blood flow and impair
the detection of these lesions at colonoscopy.
• Bleeding from angioectasias in AS( Heyde syndrome) explained that
severe AS may result in type 2 VWD, which precipitates bleeding in
patients with underlying angioectasias.
• There is a high rebleeding rate despite endoscopic treatment& defi
nitive management may involve AV replacement.
16.
17. Hemorrhoids:
• Aplexus of dilated AV vessels that arise from the superior & inferior
hemorrhoidal veins,located in the submucosa of the distal rectum
classified as internal or external, based on their location relative to
the dentate line.
• Although may be present in up to 75% with LGIB, the majority are
considered incidental findings.
• Hemorrhoidal bleeding accounts for only 2- 10- 24- 64.4% of acute
LGIB or hematochezia.
• Patients typically present with painless, intermittent, scant
hematochezia characterized by bright red blood on the toilet paper,
coating the stool, or dripping into the toilet bowl.
18.
19. CR neoplasias:
• Bowel habit changes&weight loss should raise suspicion for a
colorectal neoplasia&prompt colonoscopy in patients with LGIB.
• Accounts for up to 17% of GIB & presents more commonly with
occult bleeding.
• Acute LGIB associated with colorectal neoplasia usually results from
surface ulcerations of an advanced tumor.
• Patients with tumors in the right side of the colon are more likely to
present with occult blood loss &IDA whereas those with left-sided
tumors more commonly present with hematochezia.
• Endoscopic hemostasis is rarely required because bleeding is slow
in the majority.
21. NSAID use :
• Associated with increased risk of LGIB, including DD.
• NSAID users had a significantly higher incidence of lower GI
adverse events, including bleeding
• The prevalence of NSAID use is up to 86% LGIB.
• Mechanisms not well understood: local mucosal trauma
&platelet inhibition in susceptible individuals & concomitant
use of warfarin&other antiplatelets.
• Use of NSAIDs is associated with exacerbations of IBD.
• NSAIDs can induce NSAID colopathy, which may be
misdiagnosed as IBD, characterized by colon ulcerations and
diaphragm-like strictures, predominantly located in the
terminal ileum& right side of the colon.
• NSAID colopathy may be associated with LGIB &perforation.
22. Rectal ulcers :
• 8% of severe hematochezia&32% LGIB after ICU admissions for
other critical illnesses.
• Patients often have major medical comorbidities:
• ESRD on HD
• Respiratory failure requiring mechanical ventilation,
• Decompensated cirrhosis
• Malignancy.
• Endoscopic findings:clean-based ulcers (82%),adherent clots
(17%),nonbleeding visible vessels (33%),active bleeding (50%).
• Early rebleeding after endoscopic treatment is 44% -48%
&mortality rate of 33-48% in high-risk stigmata who have
multiple comorbidities.
23. Radiation proctopathy:
• LGIB occurs in 4-13% with rad colitis.
• This disorder is caused by radiation-induced endarteritis
obliterans, which results in neovascularization&
telangioectasias in the rectum.
24. IBD:
• Commonly present with LGIB.
• Acute LGIB requiring hospitalization is uncommon & reported
to account for only 1.2-6% of all admissions in patients with
Crohn’ s disease &0.1- 4.2% in patients with ulcerative colitis.
• Clinically significant bleeding in Crohn’ s disease is more
common in patients with colon involvement than in those
with isolated small-bowel disease.
• Bleeding resolves spontaneously in up to 50% of patients, but
there is a recurrence rate of up to 35%.
• Medical management with biologics can be effective in the
management.
25. HIV:
• LGIB occurs in 2.6% of patients with HIV, usually in the setting
of AIDS-related thrombocytopenia&associated with an
inpatient mortality rate of 28%.
• The most common etiologies of LGIB in these patients are
opportunistic infections, including cytomegalovirus, herpes
simplex virus, Kaposi’ s sarcoma& idiopathic proctocolitis.
26. U& SI source of LGIB :
• UGI source may be present in 11- 15% of patients with
suspected LGIB
• Small-bowel sources constitute 2-15% of cases.
27. Management: Resuscitation/ evaluation
• Initial assessment: whether or not an urgent intervention is
necessary.
• The majority, manifesting as occult fecal blood or scant
hematochezia, can be managed electively in OP.
• Patients presenting with acute LGIB with melena or
hematochezia usually require inpatient management, because
the majority are elderly with significant comorbidities.
• Should undergo stabilization&resuscitation with crystalloids or
blood products.
• Coagulation factors &platelets may be necessary in patients
who are on antithrombotics or with underlying bleeding
disorders.
28. Management: Resuscitation/ evaluation
• ICU admission:
• Clinical evidence of ongoing or severe bleeding.
• Transfusion > 2 units of packed RBCs
• Significant comorbidities.
• NGT lavage to exclude an upper GI bleeding source should be
considered in patients presenting with hematochezia &
hemodynamic instability.
• An actively bleeding upper GI source is unlikely if bile is seen
in NG Lavage, but it cannot be ruled out with clear aspirate.
• A targeted history: NSAID use, prior bleeding episodes, recent
polypectomy, radiation therapy for prostate or pelvic
malignancies, IBD, CRC risk.
29. Management: Resuscitation/ evaluation
• Risk stratification:
• High risk of severe bleeding 80%: > 3 the following RFs.
• Moderate risk (45%) with 1-3 RFs.
• Low risk No Rfs (< 10%):.
• HR 100/minute, systolic blood pressure % 115 mm Hg,
syncope, nontender abdominal exam, rectal bleeding during
the first 4 hours of evaluation, aspirin use, multiple comorbid
illnesses.
30. Management: Resuscitation/ evaluation
• Another model: independent predictors of severe LGIB.
• Initial hematocrit! 35%, presence of abnormal vital signs
(SBP<100 mm Hg or HR> 100/minute) 1 hour after initial
medical evaluation& gross blood on initial rectal exam. Kollef
et al100 developed and validated another
• BLEED model; Outcome prediction tool for UGIB&LGIB: predict
resource utilization& inpatient adverse events, including
mortality.
• Ongoing bleeding, low SBP, elevated PT, erratic mental status,
&unstable comorbid illness.
31. Occult GI bleeding
• Colonoscopy for evaluation of underlying CR neoplasia.
• CT colonography may be an alternative if high risk for
colonoscopy-related adverse events& for the detection of
proximal lesions in those who have had an incomplete
colonoscopy.
• An EGD should be considered if a bleeding source is not
identifi ed in the colon, especially in those patients with upper
GI symptoms, IDA, or NSAID use( overall yield 13- 41%, with
PUD &esophagitis)
• Small-bowel evaluation if fecal occult blood&persistent
anemia, after negative EGD &colonoscopy.
32. Melena:
• EGD is the initial test in the evaluation of melena
• Melena also may result from slow bleeding emanating from
the colon or small-bowel.
• Colonoscopy should, be pursued after negative EGD.
• Persistent melena after negative results with bidirectional
endoscopy warrant small-bowel endoscopy.
33. Intermitent scant hematochesia:
• Is the most common pattern of LGIB.
• Usually is caused by an anorectal or distal colon source
• A digital rectal exam&flexible sigmoidoscopy ( yield of 9-58%),
with or without anoscopy, may be sufficient for the evaluation
of healthy patients aged< 40 years.
• A colonoscopy should be pursued in the absence of a defi
nitive source of bleeding on flexible sigmoidoscopy, patients
aged> 50 years, IDA, CRC risk, or alarm symptoms of weight
loss or bowel habit changes.
34. Severe hematochesia:
• An emergent EGD is the test of choice for patients presenting
with severe hematochezia & hemodynamic instability,
followed by a colonoscopy after if the later is normal.
• In hemodynamically stable patients with severe
hematochezia, colonoscopy should be performed first,
followed by an EGD, if the colonoscopy is negative.
• The main advantage of colonoscopy lies in the ability to
perform a therapeutic intervention in conjunction with
diagnosis of the underlying lesion.
• The diagnostic yield of colonoscopy is 45-100% in LGIB &
significantly higher than radiologic evaluation with RBC scan &
angiography.
35. Severe hematochesia:
• Urgent colonoscopy should be performed within 8-24 hours of
admission.
• Early colonoscopy increases its diagnostic yield &likelihood of
a therapeutic intervention.
• Endoscopic therapy is performed in 10-40%, with immediate
hemostasis achieved in 50-100%.
• Earlier colonoscopy is associated with higher higher successful
hemostasis,reduced duration of hospitalization&cost of care
but no improvement rebleeding or surgery.
36. Severe hematochesia:
• Colon preparation is important to improve visualization,
increase the diagnostic yield&reduce the risk of perforation.
• Polyethylene glycol– based solutions can be administered
orally (or via NGT in patients at increased risk of aspiration or
who are unable to complete oral consumption) at 1 L/30-45
minutes until the effluent is free of fecal material.
• Colonoscopy is performed within 1- 2 hours of preparation.
• The reaccumulation of blood in the colon after preparation
may be helpful in localizing the bleeding source.
• Endoscopic hemostatic interventions include epinephrine
solution injection, thermal contact coagulation, argon plasma
coagulation, hemostatic clips&band ligation.
37. Endoscopic hemostasis : Bleeding DD
• Thermal contact modalities:heater probe&bipolar coagulation
alone or in combination with epinephrine injection.
• Epinephrine solution in a dilution of 1:10,000 or 1:20,000 is
injected in aliquots of 1 mL-2 mL at the site of active bleeding
or around a non-bleeding visible vessel.
• An adherent clot, may be guillotined by using a polypectomy
snare.
• The visible vessel can be treated effectively by using a heater
probe (10 J-15 J) or bipolar coagulation (10 W-16 W) with 2 to
3– second pulse&application of mild contact pressure.
• Perforation reported with contact thermal coag in thin-walled
right side colon in up to 2.5%, so higher settings or repeated
applications avoided to prevent transmural injury.
38. Endoscopic hemostasis: Bleeding DD
• Endoscopic clips is an alternative to thermal coagulation&has
the advantage of quick&easy application.
• Clips can be deployed over a bleeding vessel at the neck of the
diverticulum or to oppose the walls& close the diverticular
orifice, thereby tamponading a vessel within the dome.
• The use of an endocap has been described to evert the
diverticulum and facilitate clipping of bleeding vessels within
the dome of a diverticulum.
• There are no reports of early rebleeding after endoscopic
treatment with clips.
39. Endoscopic hemostasis : Bleeding DD
• Endoscopic band ligation described in some small series ,but
limited by inadequate suction of diverticula with small orifi
ces or large domes&high early rebleeding.
• A tattoo should be placed adjacent to the bleeding
diverticulum, if identified at colonoscopy, for future identifi
cation in recurrent bleeding &necessity for repeat endoscopic
or surgical intervention.
• Placement of an endoscopic clip also may be useful to allow
localization of the bleeding source at angiography.
40. Endoscopic hemostasis : Bleeding AD
• Both contact& noncontact thermal coagulation
• APC is useful in the endoscopic treatment of angioectasias.
• APC is the preferred technique because of its ease use, ability
to treat large surface areas& predictable depth of penetration.
• Lower APC power settings of 30- 45 W & 1 L/minute, 1-3 mm
away from the mucosal surface &at 1- 2– second pulses used
to decrease the risk for perforation in the thin-walled right
side of the colon.
• APC showed a significant improvement in Hb& reduction in
transfusion requirements with no adverse events.
• The use of endoscopic clips with APC reported.
41. Non- endoscopic treatments:
• Mesenteric angiography with or without a preceding RBC scan
is reserved for patients with:
• Severe bleeding who cannot be stabilized or prepped for a
colonoscopy
• Failed endoscopic management.
• The multidetector row CT scan may be superior to the nuclear
RBC scan for evaluation of LGIB& replaced RBC scan at several
centers.
• It decreases scan time, allows accurate acquisition of arterial
images&demonstrates contrast material extravasation into
any portion of the GI tract.
• A mesenteric angiogram can detect bleeding at 0.5 mL/min.
42. Non - endoscopic treatments:
• Superselective embolization with microcoils, polyvinyl alcohol
particles, or water-insoluble gelatin (gel foam) improved the
success rate of this technique&decreased the occurrence of
the adverse event of bowel infarction.
• Angiography & embolization as first-line therapy for LGIB
found embolization to be an effective treatment for
diverticular bleeding, with successful hemostasis in 85%
compared with 50% of those with bleeding from other sources
at 30-day follow-up with early re-bleeding after embolization
in 22%.
• The technique is less successful in angiodysplasia & with more
re-bleeding 40%.
• Major adverse events, including bowel infarction,
nephrotoxicity,hematomas.
43. Non endoscopic treatments: Surgery
• Surgery is rarely required &reserved for minority of patients
who have persistent or refractory diverticular bleeding.
• Indications for surgery:
• Hypotension&shock despite resuscitation.
• Persistent bleeding with transfusion of >units of Packed RBCs.
• Lack of a diagnosis despite a pan-intestinal evaluation for
persistent bleeding in a surgical candidate.
• It is important to attempt localization of the bleeding site for a
segmental colectomy opposed to a subtotal colectomy with
significantly higher mortality rate.
• Surgery should be performed elective, because there is a high
mortality with emergent one.
44. Recommendations:
• 1. We recommend colonoscopy in patients with occult GIB.
• 2. We recommend EGD in patients with occult GIB if a bleeding
source is not identified in the colon, especially in those
patients with UGI symptoms, IDA or NSAIDs use.
• 3. We suggest small-bowel evaluation after negative EGD&
colonoscopy results in patients with occult GIB who have
persistent anemia.
• 4. We recommend colonoscopy for the evaluation of chronic
intermittent scant hematochezia in patients > 50 years& for
patients who have IDA, risk factors for CR neoplasia, or the
alarm symptoms of weight loss or bowel habit changes.
• 5. We suggest that in younger patients presenting with chronic
intermittent scant hematochezia without alarm symptoms, a
DRE &flexible sigmoidoscopy may be sufficient evaluation.
45. Recommendations:
• 6. We recommend EGD in the initial evaluation of patients
with melena followed by colonoscopy if the EGD is negative.
• 7. We recommend an initial EGD in patients with severe
hematochezia&hemodynamic instability to evaluate for a
high-risk UGI lesion, followed by colonoscopy if EGD is –VE.
• 8. We suggest colonoscopy within 24 hours of admission after
a rapid bowel preparation in the evaluation of patients with
severe hematochezia.
• 9. We recommend endoscopic treatment with epinephrine
solution injection combined with thermal coagulation or
endoscopic clip placement as the preferred management in
patients presenting with diverticular bleeding.
46. Recommendations:
• 10. We recommend endoscopic clip or tattoo placement
adjacent to a bleeding diverticulum if identifi ed at
colonoscopy for future localization in the event of recurrent
bleeding.
• 11. We recommend endoscopic treatment with APC as the
preferred management in patients with bleeding
angioectasias.
• 12. We recommend surgical &radiologic consultation in
patients presenting with severe hematochezia who cannot be
stabilized for endoscopy or in whom endoscopic evaluation
has failed to reveal a bleeding source.
Notes de l'éditeur
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Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.
Make a natural segue to the next slide so that your presentation flows naturally.
The gradual reveal of your points serves to keep anticipation up and enables you to flow naturally to the next point.
Note: Level one text on the Title and Content layout used by this slide contains no bullet. To demote your text to level two, which is the bulleted text level shown on this slide, on the Home tab, under Paragraph, click Increase Indent.