makubi phinias

1. UGIB
Presenter: Margaret Kisunje
Phinus Makubi
Facilitator: Dr.David Majinge
Date: July 2023

2. Definition and Classification

3. Epidemiology
• UGIB vs LGIB = 5:1
• Incidence: 170 patients/ 100,000 population /year.
• 40% due to peptic ulcer disease (Most common).
• Oesophageal varices (42.3%), followed by
duodenal ulcers (15.4%), hemorrhagic/erosive
gastritis (7.7%), gastric ulcer (4.6%), Mallory Weiss
tear (1.5%) and no cause (27%) at KCMC (Suba et al,
2007-8)

4. Epidemiology – 2
• Pts on anti platelet therapy have two fold increase
in bleed VS normal ones.
• 20% of pts of moderate to high risk, who have
recurrent bleeding (within 48-72 hrs) have poor
prognosis.
• The mortality rate is 5% to 10% for severe UGI
bleed.

5. Clinical features

6. Stool color and origin/pace of bleeding
• Guaiac positive stool
– Occult blood in stool
– Does not provide any localizing information
– Indicates slow pace, usually low volume bleeding
• Melena
– Very dark, tarry, pungent stool
– Usually suggestive of UGI origin (but can be small
intestinal, proximal colon origin if slow pace)
• Hematochezia
– Spectrum: bright red blood, dark red, maroon
– Usually suggestive of colonic origin (but can be UGI origin
if brisk pace/large volume)

7. Laboratory work up
• CBC – assess for blood loss, anemia typing,
platelet count.
• Blood grouping and X - match
• PT/INR, aPTT – assessment of coagulation profile.
• RFT – useful to assess renal co-morbidity
• LFT – assess for liver function
• Stool for H.pylor antigen test
• Stool analysis

8. Diagnostic studies
1. Endoscopy
 Safe & effective investigation of choice {D&T}.
 Can locate the source and site of UGIB
 Should be done within 24hrs of presentation/
immediate after stabilizing the patient.
2. Capsule endoscope
 may identify low risk lesions in UGIB

9. Imaging studies
• Ultrasound elastography
liver and periportal fibrosis.
• Plain abdominal X – ray supine and erect
For suspected GI perforation
• Abdominal USS
may be indicated for evaluation of liver disease
• CT scan
aotoenteric fistula {thickened bowel,
inflammatory changes, fluid collection

10. Classification of Causes

11. Causes of UGIB

12. Varices
• Consequence of Portal HTN.
• The initial factor in portal HTN is the increase in
vascular resistance to portal blood flow.
• This will lead to structural distortion (underlying
disease) and active contraction of portal/septal
cells (hepatic cells, myofibroblasts) in portal
venules. (the dynamic component).
• This will lead to development of porto-systemic
collaterals (possibly from influence of angiogenic
factors, VEGF) will cause shunting of blood
around liver.

13. Varices – 2
• Hepatic venous pressure gradient > 12 mmHg.
• In esophageal varices , prefer variceal ligation
(with multiband ligator) over endoscopic
sclerotherapy.
• In gastric varices, injection with a glue will be
more beneficial.

14. Peptic Ulcer

15. Forrest & Finlayson’s Classification

16. Mallory Weiss Tear
• Mucosal or sub-mucosal
lacerations at the gastro-
esophageal junction and usually
extend distally into a hiatal
hernia .
• History of recent non-bloody
vomiting with excessive retching
followed by hematemesis.
• Endoscopy reveals a single tear
that begins at the gastro-
esophageal junction, extending
several millimetres distally into
a hiatal hernia sac/within
cardiac portion of stomach.

17. Hemorrhagic / Erosive Gastritis
• Stress related mucosal injury
– Occur mostly in extremly sick patients
– Major Trauma or post major surgery
– 3rd Degree burns
– Major intracranial disease
– Severe medical illness (Ventilator dependence, coagulopathy)
– Significant bleeding probably does not develop unless
ulceration occurs.
• IV H2-receptor antagonist is the treatment of choice. Sucralfate
also effective
• Aspirin and NSAIDS
– Half of the patient who chronically ingest NSAIDS have
Erosions. (15 – 30% have Ulcers). Gastric antrum.

18. Hemorrhagic / Erosive Gastritis – 2

19. Portal Hypertensive Gastropathy (PHG)
• Mucosa is engorged and friable.
• Caused by increased portal venous pressure and
severe mucosal hyperemia that results in ectatic
blood vessels in the proximal gastric body and
cardia and oozing of blood.
• Less severe grades of PHG appear as a mosaic or
snake skin appearance and are not associated
with bleeding.
• Usually, patients with severe PHG present with
chronic blood loss, but they occasionally can
present with acute bleeding.

20. Gastric Antral Vascular Ectasia (GAVE)
• Described as watermelon stomach. Unknown etiology.
• Characterized by rows or stripes of ectatic mucosal
blood vessels that emanate from the pylorus and
extend proximally into the antrum.
• GAVE is most commonly reported in older women and
also seems to be more common in patients with ESRD
• GAVE has been associated with cirrhosis and
scleroderma.
• Patients with GAVE who do not have portal
hypertension demonstrate linear arrays of angiomas
(classic GAVE).
• Pts with portal hypertension have more diffuse antral
angiomas.

21. GAVE – 2

22. Aortoenteric Fistula
• Bleeding is usually acute and massive, with a high
mortality rate (30 – 100%).
• The A-E fistula is a communication between the
native abdominal aorta (usually an
atherosclerotic abdominal aortic aneurysm) and,
most commonly, the third portion of the
duodenum.
• Often, a self-limited herald bleed occurs hours to
months before a more severe, exsanguinating
bleed.
• Secondary aortoenteric fistula between the third
portion of the duodenum and the proximal end of
the graft but may occur elsewhere in the GI tract.

23. Dieulafoy’s Lesion
• It is a large (1- to 3-mm) submucosal artery
that protrudes through the mucosa.
• It is not associated with a peptic ulcer, and
can cause massive bleeding.
• Located in the gastric fundus, within 6 cm of
the gastroesophageal junction.
• Endoscopic hemostasis of a Dieulafoy's
lesion can be performed with injection
therapy, a thermal probe, or clip device or
by band ligation.

24. Clues to Source of Acute UGIB

25. Approach to Patient with UGIB

26. Initial Assessment
• Always remember to assess A,B,C’s
• Assess degree of hypovolemic shock
Class I Class II Class III Class IV
Blood loss (mL) 750 750-1500 1500-2000 >2000
Blood volume
loss (%)
< 15% 15-30% 30-40% >40%
Blood Pressure normal normal decreased decreased
Heart rate <100 >100 >120 >140
SBP No change Orthostatic Reduced Very low, supine
Urine output/hr >30 20-30 10-20 <10
Mental status Alert Anxious Aggressive/drowsy Confused/LOC
Fluid (3:1rule) crystalloid crystalloid Crystalloid & blood Crystalloid & blood

27. Initial Assessment and Triage
• Identify patients with nonvariceal UGIB at
greatest risk for mortality and rebleeding.
• Pts may be categorised as low, intermediate and
high risk.

30. Management as per Risk
• Low risk(0-2)
–Usually 80 % of the pts recovers spontaneously
with medical Tt ( PPI) +
–Hospitalisation for 24 hrs and may be
discharged if uneventful.
• Intermediate risk(3-5)
–Same Tt + Hospitilisation for at least 72 hrs.
• High risk(>5%)
–Same Tt + Hospitilisation in I.C.U.

31. Initial UGIB management
• Assess hemodynamic status immediately
• Insert 2 large bore IVs and begin resuscitation
• Blood transfusions
– Target hemoglobin ≥ 7g/dl
– In massive bleeding or active cardiac disease ≥ 8-9g/dl
– Platelet transfusion to pts with platelet count <50X109
– PCC/FFP if active bleeding and PT/INR or aPTT > 1.5 UNL
• Risk stratifying patient (low-risk vs. high risk)

32. AIMS 65
• Simple risk score that predicts in-hospital
mortality, LOS, cost in patients with acute UGIB.
lbumin <3.0
NR > 1.5
ental status altered
ystolic BP <90
+ years old
Gastrointest Endosc 2011;74:1215

33. Initial UGIB management
• Assess hemodynamic status immediately
– 1L if tachycardic – reassess in 2hrs
– 2L if orthostatic – reassess in 2hrs
– 2L if in shock – reassess in 30minutes
• Urinary catheterization to ensure UOP >/=
0.5ml/kg/hr

34. Initial UGIB management
• Assess the severity of blood loss.
– Tachycardia – 10% of volume loss
– Orthostatic hypotension – 20% of volume loss
– Shock – 30% of volume loss.
Laine L, Jensen D. ACG Practice Guidelines.
Am J Gastroentol 2012; 107:345-360

35. Management of UGIB

36. Nasogastric lavage
• Randomized trial with 280 patients with UGIB,
showed no differences in rebleeding rates or
mortality between patients who underwent
NGT lavage and those who did not.
• Patients should only undergo NGT lavage if
particulate matter, fresh blood, or clots need
to be removed from the stomach to facilitate
endoscopy.

37. General Management
• Supplemental oxygen by nasal cannula and NPO
• Two large caliber (18 gauge or larger) peripheral
IV catheters or a central venous line should be
inserted.
• Elective Endotracheal Intubation in pts with
ongoing hematemesis, or AMS or altered
respiratory may:
–Facilitate endoscopy
–Decrease risk of aspiration

38. General Management
Fluid Resuscitation
• Patients with active bleeding should receive IVF
(eg, 500 mL of N/S or R/L solution over 30
minutes) while being typed and cross-matched
for blood transfusion.
• If BP fails to respond to initial resuscitation
efforts, the rate of fluid administration should be
increased.
• In some patients, temporary support with
vasopressor drugs may be required.

39. Role of Blood Transfusion
Anemia
• Initiate BT if Hb is <8 g/dL for most patients with a
goal of maintaining the Hb ≥8 g/dL
• Goal is Hb ≥9 g/dL for patients
–With unstable coronary artery disease,
–with evidence of ongoing active bleeding.
• Patients with signs of active ischemia, maintaining
the Hb ≥10 g/dL is appropriate.

40. Role of Blood Transfusion
• Initiate BT if Hb <7 g/dL, if variceal bleeding is
suspected.
• Avoid overtransfusion as it can precipitate
worsening of the bleeding.
• Liberal (Hb < 9 – 10 g/dL) VS restrictive (Hb < 7
g/dL) transfusion strategies.

41. Role of Blood Transfusion
Coagulopathy
• FFP transfusion in pts with non-cirrhotic
coagulopathy with a prolonged PT and INR > 2.0
• Endoscopy to be performed when INR < 2.5
• A unit of FFP should also be given after every four
units of packed red blood cells because packed
red blood cells do not contain coagulation factors.

42. Role of Blood Transfusion

43. ESGE guideline on endoscopic timing
• Following hemodynamic resuscitation, ESGE
recommends early (≤ 24 hours) upper GI endoscopy
• Very early/emergent endoscopy (< 12 hours) upper
endoscopy ma be considered in patients with high risk
clinical features
– Hemodynamic instability
– In-hospital bloody emesis/nasogastric aspirate
– Contraindication to the interruption of anticoagulant
Gralnek IM. Endoscopy 2015;47;a1-a46

44. Medical Management
Acid Suppression:
• Options include giving an IV PPI every 12 hours or
starting a continuous infusion.
• High-dose bolus (eg, esomeprazole 80 mg) to pts
with signs of active bleeding (eg, hematemesis,
hemodynamic instability).
• Endoscopy on these patients within 12 hours.
• If endoscopy is delayed, 2nd dose of IV PPI should
be given 12 hours later (eg, esomeprazole 40 mg).

45. Medical management
• For patients with bleeidng ulcers with high-risk
stigmata who have undergone successful endoscopic
therapy, we recommend using PPI therapy via IV
leading dose followed by continuous-infusion IV
• Following 3 days of IV PPI’s, we suggest using twice
daily oral PPI (vs. once daily) through 14 days followed
by once daily
Barkun AN international Consensus Guidelines Ann Intern Med 2019

46. Medical Management
Prokinetics:
• Use of prokinetic agent is to improve gastric
visualization at the time of endoscopy by clearing
the stomach of blood, clots, and food residue
• Erythromycin promotes gastric emptying based
upon its ability to be an agonist of motilin
receptors.
• Using erythromycin to improve gastric
visualization has been studied in at least four
randomized controlled trials.

47. Medical Management
• There were no differences in units of blood
transfused, endoscopy duration, or need for
emergent surgery between those who received
erythromycin and those who did not.
• ESGE recommends a 250 mg erythromycin
infusion 30–120 min pre-endoscopy in patients
with clinically severe/ongoing AUGIB [1].
1. Gralnek I, Dumonceau J, Kuipers E et al. Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European
Society of Gastrointestinal Endoscopy (ESGE) Guideline. Endoscopy 2015; 47: 1–46

48. Medical Management – 2

49. Medical Management
Variceal Measures:
• Terlipressin (or alternative) and antibiotics in
suspected variceal haemorrhage
– increases systemic vascular resistance,
– reduces cardiac output, and
– reduces portal pressures by approximately 20%.
• 2 mg four times a day.

50. Medical Management
• Contraindications to terlipressin:
–arterial disease,
–hyponatraemia,
–myocardial ischaemia,
–severe cardiac failure and
–prolonged QTc interval.
• Somatostatin or octreotide may be considered for
patients with contraindications.
–IV bolus of 50 mcg, followed by a continuous
infusion at a rate of 50 mcg per hour.

51. Medical Management
Antibiotics in Patients with Cirrhosis:
• Bacterial infections are common in cirrhotic
patients with AUGIB.
• 20% of patients have infections within 48 h,
increasing to 36% after 7 days.
• Infection is associated with significantly increased
rebleeding risk (43.5% vs 9.8%) and mortality
(47.8% vs 14.6%) [4].
4. Bernard B, Cadranel J, Valla DO. Prognostic significance of bacterial infection in bleeding cirrhotic patients: a prospective study.
Gastroenterology 1995; 108: 1828–34.

52. Endoscopic Management

53. • Determine the cause of the bleeding, prognosis
and therapeutic interventions.
• Endoscopic haemostasis in PUD reduces:
–mortality,
–rebleeding risk and
–the need for surgery.
• Endoscopic therapies for NVUGIB comprise
–injection therapy,
–thermal treatments,
–mechanical adjuncts and
–spray therapy.

54. Thermal treatment:
• Two Types: contact and non-contact.
• Contact treatments: involve applying pressure and
heat via a heater probe using monopolar
diathermy; to compress and seal a bleeding lesion.
• The probe is applied until the treated areas are
black and depressed.
• Non-contact thermal haemostasis includes: argon
plasma coagulation, which is sufficient for the
treatment for superficial angiodysplastic lesions.

55. Mechanical Treatment:
• Most common: the endoclip or haemoclip.
• Stainless steel clips which are passed through the
endoscope and deployed to the bleeding lesion.
• Clips provide mechanical compression to the
bleeding vessel, resulting in haemostasis.
• In a meta-analysis, clip application VS injection
therapy in achieving definitive haemostasis (86.5%
vs 75.4%, RR 1.14) [6].
6. Sung J, Tsoi K, Lai L et al. Endoscopic clipping versus injection and thermo-coagulation in the treatment of non-variceal upper gastrointestinal
bleeding: a meta-analysis. Gut 2007; 56: 1364–73.

56. Haemostatic Agents:
• Topical – Hemospray
• Mechanically adhering to a bleeding site, resulting
in mechanical tamponade, and by activating
coagulation factors to promote thrombus
formation.
• Safe, not absorbed systemically.

57. Haemostatic Agents:
• Hemospray is sprayed via an endoscopically-
directed catheter, covers large areas with multiple
bleeding points, without the need for precise lesion
targeting.
• It is a suitable choice for bleeding lesions such as:
–haemorrhagic gastritis,
–portal hypertensive gastropathy,
–gastric antral vascular ectasia,
–radiation-induced mucosal injury and
–malignancy-related bleeding.

58. • Endoscopic therapies for
VUGIB comprise
–Variceal Band
Ligation,
–Cyanoacrylate and
Thrombin,
–Balloon
Tamponade and
–Oesophageal
Stenting.

59. Variceal Band Ligation:
• Superseded sclerotherapy in oesophageal varices
• A meta-analysis of seven randomised trials found
VBL to be superior to sclerotherapy in reducing
– rebleeding (OR 0.52, 95% CI 0.37–0.74) and
– mortality (OR 0.67, 95% CI 0.46–0.98). [7]
• VBL should be used in conjunction with
terlipressin, somatostatin or octreotide.
7. Laine L, Cooke D. Endoscopic ligation compared with sclerotherapy for treatment of esophageal variceal bleeding. Ann Intern Med 1995; 123:
280–7.

60. Cyanoacrylate and thrombin:
• Cyanoacrylate, a.k.a ‘glue’, is a strong adhesive
• For type 2 gastro-oesophageal varices (GOV-2) and
isolated gastric varices (IGV), cyanoacrylate has
been shown to be superior to VBL in achieving
haemostasis and reducing rebleeding, and has
been approved by NICE and BSG.
• Recently, thrombin injection has been accepted as
an alternative to cyanoacrylate for gastric varices,
with haemostasis rates of 94% and rebleeding rates
of 18%.

61. Balloon tamponade:
• Balloon tamponade is indicated in failure of
haemostasis with bleeding oesophageal varices.
• The Sengstaken- Blakemore tube (SBT) - the most
common device for balloon tamponade.
• It achieves haemostasis in 91.5% of cases, with
recurrence of bleeding in approximately 50% of
cases after balloon deflation.

62. • Complications of SBT occur in 15–20% of patients,
and include:
–pressure necrosis,
–misplacement,
–aspiration pneumonia and
–oesophageal rupture.
• Due to its poor tolerability, patients often require
heavy sedation and intubation prior to SBT and ICU
management.

64. Oesophageal stenting:
• Self-expanding metal stents have been shown to be
superior to SBT in OV refractory bleeding.
• Recent RCT showing improved treatment success,
as survival at day 15 with control of bleeding and
without serious adverse events (66% vs 20%, p =
0.025) [8].
• Self-expanding metal stents can be deployed
without radiological guidance and can be left in for
14 days (vs 2 days for SBT).
8. Àngels E, Oana P, Andrés C, et al. Esophageal balloon tamponade versus esophageal stent in controlling acute refractory variceal bleeding: A
multicenter randomized, controlled trial. Hepatology 2016; 63: 1957–67.

65. Post–Endoscopic Management

66. Helicobacter Pylori Treatment:
• Detection and eradication are important for
improved outcomes, and obviate the need for long
term PPI.
• In a Cochrane meta-analysis of patients with H.
pylori-related bleeding PUD (without NSAID use),
H. pylori eradication was superior to non-
eradication (OR 0.16) or long-term antisecretory
therapy (OR 0.14) for preventing rebleeding [12].
• During endoscopy with biopsy methods, urea
breath testing or monoclonal SAT.
12. Gisbert J, Khorrami S, Carballo F et al. Helicobacter pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-
term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. Cochrane Database Syst Rev 2004; 2:
CD004062.

67. Medical Management – 3

68. VUGIB
Non-selective Beta Blockers:
• After 1st episode, the risk of rebleeding is 15–30%
within the subsequent 6 weeks.
• Non-selective beta-blockers, such as propranolol
or carvedilol for secondary prophylaxis.
• Propranolol reduces portal pressures through
splanchnic vasoconstriction and reduced cardiac
output.

69. • A meta-analysis of 12 RCTs (11 with propranolol)
for secondary prophylaxis of variceal bleeding
showed that, over 2 years, non-selective beta-
blockers was associated with:
– Freedom from variceal rebleeding (20% mean
difference, p < 0.001), and
– Increased survival (5.4% mean difference, p < 0.05, RR
1.27). [15]
• BSG guidelines recommend use of propranolol or
nadolol for secondary prevention of variceal
bleeding, with carvedilol as an alternative.
15. Bernard B, Lebrec D, Mathurin P et al. Beta-adrenergic antagonists in the prevention of gastrointestinal rebleeding in patients with cirrhosis:
A meta-analysis. Hepatology 1997; 25: 63–70.

70. Transjugular intrahepatic portosystemic shunt
(TIPSS):
• Patients who rebleed should be considered for urgent
repeat endoscopy and VBL.
• If rebleeding is difficult to control, SBT or self-expanding
metal stent can be attempted until salvage TIPSS or
surgical shunt surgery is performed.
• The aim of TIPSS is to rapidly reduce portal pressures by
creating a portosystemic shunt across the liver
parenchyma

73. • TIPSS has been shown to be superior to VBL for
preventing rebleeding (19.0% vs 43.8%, p <
0.00001), but with increased rate of post-
procedural encephalopathy (OR 2.21, p < 0.00001).
• There is RCT evidence [16], recently endorsed by
BSG,18 to support the role for early TIPSS in select
patients (Child B and Child C cirrhosis with score <
14) within 72 h of a variceal bleed.
16. Garcia-Pagan J, Caca K, Bureau C et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010; 362:
2370–9.

74. Follow up:
• All patients with cirrhosis should receive
hepatology follow- up after discharge.
• This includes:
–hepatocellular carcinoma surveillance (6-
monthly α-fetoprotein and ultrasound
assessment),
–monitoring and managing liver disease and its
complications,
–consideration of transplant assessment, and
–addressing variceal surveillance.

75. REFERENCES:
• (World J Gastroenterol. 2013 Oct 28; 19(40):
6919–6927. Published online 2013 Oct 28. Juan
Wang, et al)
• Gralnek I, Dumonceau J, Kuipers E et al. Diagnosis
and management of nonvariceal upper
gastrointestinal hemorrhage: European Society of
Gastrointestinal Endoscopy (ESGE) Guideline.
Endoscopy 2015; 47: 1–46
• Loannou G, Doust J, Rockey D. Terlipressin for
acute esophageal variceal hemorrhage. Cochrane
Database Syst Rev 2003; 1: CD002147.

76. • Seo Y, Park, S, Kim M et al. Lack of difference
among terlipressin, somatostatin, and octreotide
in the control of acute gastroesophageal variceal
hemorrhage. Hepatology 2014; 60: 954–63.
• Bernard B, Cadranel J, Valla DO. Prognostic
significance of bacterial infection in bleeding
cirrhotic patients: a prospective study.
Gastroenterology 1995; 108: 1828–34.
• Chavez-Tapia N, Barrientos-Gutierrez T, Tellez-
Avila F et al. Meta- analysis: antibiotic prophylaxis
for cirrhotic patients with upper gastrointestinal
bleeding – an updated Cochrane review. Aliment
Pharmacol Ther 2011; 34: 509–18.

77. • Sung J, Tsoi K, Lai L et al. Endoscopic clipping versus
injection and thermo-coagulation in the treatment of
non-variceal upper gastrointestinal bleeding: a meta-
analysis. Gut 2007; 56: 1364–73.
• Laine L, Cooke D. Endoscopic ligation compared with
sclerotherapy for treatment of esophageal variceal
bleeding. Ann Intern Med 1995; 123: 280–7.
• Àngels E, Oana P, Andrés C, et al. Esophageal balloon
tamponade versus esophageal stent in controlling
acute refractory variceal bleeding: A multicenter
randomized, controlled trial. Hepatology 2016; 63:
1957–67.

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79. • Gisbert J, Khorrami S, Carballo F et al. Helicobacter
pylori eradication therapy vs. antisecretory non-
eradication therapy (with or without long-term
maintenance antisecretory therapy) for the
prevention of recurrent bleeding from peptic ulcer.
Cochrane Database Syst Rev 2004; 2: CD004062.
• National Institute for Health and Care Excellence
(NICE). Acute upper gastrointestinal bleeding in over
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https://www.nice.org.uk/guidance/cg141 (accessed
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and management of nonvariceal upper
gastrointestinal hemorrhage: European Society of
Gastrointestinal Endoscopy (ESGE) Guideline.
Endoscopy 2015; 47: 1–46

80. • Bernard B, Lebrec D, Mathurin P et al. Beta-
adrenergic antagonists in the prevention of
gastrointestinal rebleeding in patients with
cirrhosis: A meta-analysis. Hepatology 1997; 25:
63–70.
• Garcia-Pagan J, Caca K, Bureau C et al. Early use of
TIPS in patients with cirrhosis and variceal
bleeding. N Engl J Med 2010; 362: 2370–9.

81. Thank you for your Attention!