Symposium: Emergencies in GI and liver disease Upper ...

Symposium:Emergencies in GI and liver disease

Upper gastrointestinalbleeding

Piyapan P. M.D. M.Sc.Division of Gastroenterology, Department of Medicine,

Chulalongkorn University

Thursday 26th April 201834th Annual Meeting of the Royal College of Physicians of Thailand

GI bleeding:a clinical challenge

•To anticipate the anatomy and etiology of bleeding

•To assess the patients’ risk (how urgent?)

Choose the right procedure

At the right time

Prevent re-bleeding and reduce mortality

GI hemorrhageor not?

•Per mouth:

•Vomiting blood (hematemesis), coffee ground emesis

•Definitely an upper GI hemorrhage

•Differential diagnosis:

•Coughing up blood (hemoptysis), oral bleeding, epistaxis

and vomiting swallowed blood

GI hemorrhageor not?

•Rectal bleeding:

•Hematochezia, maroon stool, melena

•The destination of blood from any part of GI tract

•Differential diagnosis:

•Hemorrhoid, anal fissure

•Mucous bloody diarrhea?!

Anatomy of GI hemorrhage

•Upper GIB

•Variceal or Non-variceal

•Obscure GIB

•Overt or Occult

•Active or Inactive

•Lower GIB

Ligament of Treitz

IC valve

How to anticipate the anatomy of bleeding?

Patient’s risk factor(s) andthe presenting symptoms

Vomiting blood = upper GIH (but not vice versa)

Rectal bleeding

Character of the rectal content

Color and consistency- Melena vs maroon color vs hematochezia- Vital signs?

Mixing up with fecal material?

Evaluation

•Lab: Based on History & Physical examination (Optional:

Coagulogram, CXR, EKG, M/G, Chemistry, UPT)

•Risk stratification

•Age > 60 years

•Multiple co-morbidities

• Large amount of blood. Fresh blood. Continuous bleeding.

•Unstable vital signs. Sign and symptom of inadequate tissue

perfusion.

• Severe anemia

How urgent should endoscopy be performed?Condition Urgency

Upper GIH: high risk

Portal hypertensive patients or suspected variceal bleeding

Unstable vital signs despite of an adequate resuscitation

Vomiting fresh blood or fresh blood from NG aspiration

Anticoagulant which can not be discontinued

Multiple co-morbidities

Very early EGD

Within 12 hours

Upper GIH without high risk featuresEarly EGD

Within 24 hours

Lower GIH: high risk and continuous bleedingWithin 24 hours

After a rapid bowel purge

Lower GIH without high risk features

Within 24-48 hours

After adequate bowel

preparation

Gralnek Ian M et al. ESGE guideline Endoscopy 2015

Risk score

•Glasgow-Blatchford score for patients with UGIH

•Score 0-1 “safely D/C without early endoscopy”

•Allow early discharge in 16-25% of patients

•Sn 99-100% for a severe bleed

(<1% chance requiring intervention)

•Sp 4-44%

•Score 2 or above “therapeutic endoscopy needed”. Refer if

necessary.


Alan N. Barkun et al. Ann Intern Med.2010Non-variceal UGIB GIE 2012

Admission risk markers Scores

BUN (mg/dl) 6.5-7.9 2

8.0-9.9 3

10.0-24.9 4

≥ 25.0 6

Hemoglobin (g/L) 12-12.9(M), 10-11.9(F) 1

10-11.9g/L(M) 3

<10 (M and F) 6

Systolic BP (mmHg) 100-109 1

90-99 2

<90 3

Other markers

Pulse ≥ 100/min 1

Presentation with melena 1

Presentation with syncope 2

Hepatic disease 2

Cardiac failure 2

NG tube

•2 purposes

Distinguish between upper and lower GIH?

Determine whether or not a patient has a massive

upper GIH?

•Good for “rule in” Bad for “rule out”

•Not necessary in cases with clinically obvious upper GIH or

massive upper GIH

•No therapeutic role!

•Example: a patient with rectal bleeding

!

Blood transfusion

•Red blood cells transfusion:

•Hemoglobin <7 g/dL, unstable vital signs, continuous or recurrent bleeding

•Patients without significant co-morbidities: 7-9 g/dL•Patients with CAD, COPD: >10 g/dL

•Platelets transfusion:

•In general: 50,000 -75,000 x 106/L

•Patients with platelets dysfunction: 100,000 x 106/L

•INR:•Less than 1.5 or the lowest limit of therapeutic range


!

Management of bleeding patients treated with NOACs

•The time of last intake of NOAC.

•The half-life by measurement of serum creatinine.

•Minor bleeding:

•Temporary drug withdrawal

•Time is the most important antidote

Veitch AM, Vanbiervliet G, Gershlick AH, et al. Gut 2016;65: 374–389.

Ruben D. Acosta et al. ASGE.GIE 2016

•Antidotes for more severe bleeding:

•Dabigatran - adequate diuresis and hemodialysis, Idarucizumab

•Others - Andexanet alfa (Acts as a decoy factor Xa receptor),

Aripazine (A universal reversal agent )

•Prothrombin complex concentrate, Recombinant factor VIIa (NovoSeven)

•Tranexamic acid (anti-fibrinolytics), Desmopressin (DDAVP)

•Activated charcoal for major ingestion (within 1-2 hours)

•No benefit: Protamine sulfate, vitamin K, FFP

Veitch AM, Vanbiervliet G, Gershlick AH, et al. Gut 2016;65: 374–389.

Ruben D. Acosta et al. ASGE.GIE 2016

Management of bleeding patients treated with NOACs

Endotracheal tube

•To prevent aspiration in patients with upper GIH

•Risk factors:

•Massive upper GIH, impaired consciousness, other

risks for aspiration

Proton pump inhibitor

•Pre-endoscopic IV PPI:

•Reducing rate of high risk ulcer (OR, 0.67) and need for

endoscopic intervention (OR, 0.68)

•Does not reduce rebleeding rate, surgery and mortality

•Additional treatment while waiting for endoscopy

Can not take over the role of endoscopy!

•Prokinetic: “not routinely recommended”


When would variceal bleeding be suspected?

•Presentation

•Most common: upper GIH from esophageal and gastric

varices, vomiting large amount of fresh blood

•Caution: ectopic varices can be anywhere

•Evidences suspecting a presence of portal

hypertension

Evidences suspecting a presence

of portal hypertension•History:

•Chronic liver disease, cirrhosis, chronic alcoholism,

splenic vein thrombosis (isolated gastric varices)

•Physical examination:

•Chronic liver stigmata: spider nevi, palmar erythema

•Signs of portal hypertension: ascites, splenomegaly

•Lab:

•Bilirubin, albumin, platelets, INR

Suspected variceal bleeding:5 to survive

1.) Admit at critical care unit if possible

• Not only to survive GI hemorrhage but also liver

deterioration

2.) Overly transfused red blood cells may increase rebleeding

rate

3.) Prophylactic antibiotic reduce bacterial infection rate, LOS,

and mortality rate:

• Ceftriaxone 1 gm IV OD for a max. duration of 7 days

GARCIA-TSAO ET AL. Hepatology 2017

4.) Vasoactive agent reduces the mortality rate

• Start ASAP in combination with prophylactic antibiotic

5.) Endotracheal intubation

• Massive upper GIH in patients with hepatic

encephalopathy. Ascites may be present.

Suspected variceal bleeding:5 to survive


!

Vasoactive agents

•Octreotide (SMT analogue)

• Initial IV bolus of 50 micrograms (can be repeated in first hour if

ongoing bleeding) Continuous IV infusion of 50mg/hr

•Somatostatin

• Initial IV bolus 250mcg (can be repeated in the first hour if ongoing

bleeding) Continuous IV infusion of 250-500mcg/h

•Terlipressin (VP analogue)

• Initial 48 hours: 2 mg IV every 4 hours until control of bleeding

•Maintenance: 1 mg IV every 4 hours to prevent rebleeding


Imaging is required when..

• GI hemorrhage with severe abdominal pain

• Hemobilia, hemosuccus pancreaticus, ischemic bowel

disease

• Patients with a disease of abdominal aorta

• Aorto-enteric fistula

• Mass / Cancer / Gut obstruction

!

Remember to look at a whole clinical picture…

• Patients with

• Septic shock and a small amount of coffee ground per NG

• Acute anemia with stool occult blood positive without

any overt GI bleeding

•Anemia ≠ GI bleeding

• Patients with

• Secondary myocardial ischemia from acute GI

hemorrhage

NG tube lavage Massive bleeding

Negative aspiratePositive aspirate or risk factors for UGI lesion

EGD Colonoscopy

Surgical consult

Angiography

Refractory bleeding

Successful embolization

Surgery Observe

negative

Initial management

CT angiography

Endoscopic treatment

•High risk ulcer:

•Endoscopic treatment: epinephrine injection + thermal

or mechanical

•Low risk ulcer:

•No endoscopic treatment required

•A black box:

•F IIb: peptic ulcer with adherent clot

•Open it!!

Hemostatic powders

•TC-325 (Hemospray, Cook Medical)

•Action: binds to actively bleeding sites, and the granules

absorb all of the water from blood or secretions, and then

swell and adhere to the bleeding sites.

•Advantages: Easy. Non-contact. Spray onto the bleeding

site.

•Disadvantages: Limited data. Safety. Price.

Forrest classification

StigmataPre-

valenceRebleeding Surgery Mortality

IAActive spurting

12% 55% 35% 11%

IB Active oozing

IIA NBVV 8% 43% 34% 11%

IIB Adherent clot 8% 22% 10% 7%

IIC Flat pigmented spot

16% 10% 6% 3%

III Clean based 55% 5% 0.5% 2%

Loren Laine et al. AJG 2012

Endoscopic treatment for a variceal hemorrhage

• Varices with active bleeding or with a sign of

recent bleeding “white nipple sign”

• Varices with absence of those but..

• Blood in stomach without other more possible etiology

• Delayed > 24 hours after bleeding


• Esophageal varices:• Endoscopic variceal band ligation; EVL

• Gastric varices:

• GOV1 – cardia type:

• EVL or cyanoacrylate glue injection

• GOV2 – fundal type or IGV:

• Cyanoacrylate glue injection or transjugular intrahepatic

portosystemic shunt (TIPS)

Endoscopic treatment for a variceal hemorrhage


Post-endoscopic treatment

• High risk ulcer:• Continue IV PPI and NPO for 72 hours (reduce rebleeding 57%,

surgery 40%, mortality 43%), discharge with a single daily oral

PPI

• Recurrent bleeding: 2/3 of patients with rebleeding did so

within the first 72 hours

• Rescue treatments: repeated endoscopy. Intervention “TAE”.

Surgery.

• Routine second look: not recommended



• Low risk ulcer:

• Discharge with oral PPI

• Also consider: serious co-morbidities (CHF, recent CV

event, chronic alcoholism or active cancer), patient

location /transportation, social support



• H. pylori infection:

• Test and treat with confirmation of eradication

• More effective than PPI alone in preventing rebleeding PUD

• Biopsy-based test: false negative 25-55% during acute bleeding. UBT

or repeat at OPD.

• NSAIDs:

• Discontinuation. Choose other options.

• COX-2 plus prophylactic oral PPI

!


• ASA:

• Primary prevention: risks and benefits. Discontinue.

• Secondary prevention: restart within 1-3 days, at most not more than 7

days. Long term prophylactic oral PPI.

• Dual antiplatelets: ASA as above. Risks and benefits reconsideration of

second antiplatelets.

• Anticoagulant:

• Restart within 7 days

• When CV risk outweighs GI bleeding risk


!

•Continue vasoactive agents and NPO for 2-5 days.

•Continue prophylactic antibiotic for a maximum of 7 days.

•Proton pump inhibitor can be discontinued.

• In subgroup patients with high risk of rebleeding: consider early

or preemptive TIPS within 72 hours despite the absence of

rebleeding.

•Re-bleeding: repeat endoscopy. TIPS.


Post-endoscopic treatment:Variceal hemorrhage

Secondary Prevention

Therapy Recommended Dose Therapy Goals Maintenance, F/U

Propranolol

- 20-40 mg po BID- Adjust every 2-3 days until treatment goal is achieved- Maximal daily dose:

- 320 mg/day in patients without ascites

- 160 mg/day in patients with ascites

- Resting HR 55-60 bpm

- SBP should not decrease below 90

mmHg

- At every outpatient visit make sure that heart rate is on target- Continue indefinitely

EVLEvery 1-4 weeks until the

eradication of varices

Variceal eradication (no further ligation

possible)

First EGD performed 3-6 months after

eradication and every 6-12 months

thereafter


AND

• Buying time before a definite treatment

• Indication

• Before endoscopy: unstable vital signs or during transfer

• After endoscopy: failure to stop bleeding or recurrent

bleeding

• Maximum duration of 24 hours

• Complications: aspiration, esophageal rupture

Sengstaken-Blakemore tube

Take home message!!

•Remember to look at a whole clinical picture.

•We need a good doctor and also a good team.

•The best way to stop the variceal bleeding is to

prevent people from a liver disease.

“Do I not destroy my enemies when I make them my friends?”

― Abraham Lincoln

Thank you

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