Upper GI bleeding

UGI bleding

ONE syndrome: a group of diseases

Definitions

Intraluminal, exteriorised bleeding Hematemesis – above the angle of

Treitz Melena – above the ileo-cecal valve Hematochezia – bellow the spelnic

flexure

A major health problem 100-150/100.000 admission/year in US Mortality is high ~10% even if:

fiberoptic endoscopy - general better understanding of pathology high performance medication

POPULATION IS GROWING OLDER Great variety of pathologies risk of

rebleeding very difficult to evaluate

Major cause

Duodenal ulcer 24% Gastritis 23% Gastric ulcer 21% Esophageal varices 10% Esofagitis 8% Sdr. M-W 7% Duodenitis 6% Tumors 3%

Large variations according to region

DIAGNOSTIC VS TRATAMENT Major emergency Urgent treatment before ethiological

diagnostic Sequence:

» Diagnostic of UGI bleeding» Resuscitation » Empiric treatment» Ethiologic treatment» Specific treatment

Emergency

URGENT EVALUATION

URGENT TREATMENT OF HYPOVOLEMIA

INSSURING A SECURE TRANSPORTATION TO A HOSPITAL

Anamnesis

Describe bleeding» Quantification of blood loss is ridiculous

Other symptoms on onset: ex cough Past medical history – associated with

bleeding: hepatitis, chirrhosis… Family problems Alchool intake Previous bleedings Medication intake in the last week

FIRST AID

Decubitus One or two large vein access Insure vital function Safe transportation A sample for blood typing No macromolecules before sample Nill per mouth +/- nasogastric tube + drainage

Haemodynamic evaluation

Hypovolemic shock if: Systolic blood pressure <90 mmHg = 50% circulating volume

NO shock – check for changes in blood pressure and puls in orthostatism» BP<90 - 25-50% loss» BP-10 or puls rate >120/min - 20-25%

EVALUATION BEFORE ETHIOLOGY IS ESTABLISHED

1. Hemoglobine 2. Platelets 3. Hematocrit 4. Screening test for coagulation 5. BUN 6. Screening for live function tests 7. Abdominal and/or thorax X-Ray for

associated pathology that could change protocol

EVALUATION BEFORE ETHIOLOGY IS ESTABLISHED

Patient in ICU under gastroenterology care Supress HCl secretion (i.v. H2 bloxkers,

PPI) Treat coagulation disfunctions Blood products

» Balance for risks – viral infections» Risks vs benefits in continuous bleeding

SURVEILANCE -MODELES FOR REBLEEDING -

CONTINUOUS BLEEDING– No response– 42% do not present a major episode of rebleeding– Aggressive monitoring = ESSENTIAL

MAJOR EPISODE OF REBLEEDING– 15,2% rebleeding in ICU

» 61% sudden onset– ONLY shock is very unusual but possible

REBLEEDINGMAJOR RISK FACTOR

Definition: new bleeding episode after an initial stop and haemodynamic stability

High mortality: 20% (3x more then average for UGU bleeding)

3 major risk factors for in hospital morbidity and mortality: Major rebleeding during hospital stayOld ageTotal quantity of transfused blood

ETHIOLOGICAL EVALUATION

Clinical Rx + US

endoscopy

“GOLD DIAGNOSTIC”

ANAMNESIS PATIENT + FAMILY

Clinical Evaluation

Haemodyanmic evaluation and stabilisation Confirm the dg of UGI bleeding

– HEMATEMESIS, MELENA + rectal exam– Ex oral cavity + ENT for swallowed blood– Medicaton

Clinical signs suggestive for liver chirrhosis Palpable tumors Other medical problems that can cause UGI

bleeding

IMAGISTICS Can point to a possibel diagnostic Rx thorax

– Pleural efusions– TBC– Primary or secondarty tumors

Abdominal US– Liver chirrhosis + portal hypertension– Abdominal tumors

Rx g-d – Unusual alternative to explore UGI after the remission of

signs or when endoscopic examination is incomplete.

ENDOSCOPY

Establishes SOURCE OR SOURCES of bleeding

Evaluation of risk of rebleeding THERAPEUTIC acces directly to the

lesion

ENDOSCOPY - in emergency - not after 24 hourseSHORT LIVED LESIONS

PREPARE FOR ENDOSCOPY

Patient should be stable / in OR Empty stomach if possible +/- sedation – risk of aspiration Patient in left lateral position – prevent

aspiration

ENDOSCOPIC DIAGNOSTIC

Portal hypertension: varices YES/NO– Significant in massive bleeding

Diagnostic for all lesions with potential of bleeding

Evaluation of RISK of rebleeding Type of ACTIVE bleeding Complete vs incomplete examination: which

areas not evaluated

MIRAGE – the first lesion

? the most significant lesion?

TREATMENT

Stabilise and monitor patient STOP THE BLEEDING Prevent recurrent bleeding Treat the disease CAUSE Treat complications and associated

diseases

TRATAMENTaccording to cause

ENDOSCOPY: Oclude the vessel

the least aggressive for patient

immediate after diagnosis

very efficient

required in all cases with major risk of rebleeding

Medication Surgical Interventional radiology

ESOPHAGIAN CAUSES - 4%

a. Congenital Weber-Rendu-Osler Blue rubber bleb

nevus Bullous epidermolisis Esophageal

duplication

b. Inflamatory GERD Barrett disease Infectious esophagitis Caustic lesions RT induced lesions CHT induced lesions Crohn disease Behcet disease pemfigoid

b. Traumatic or mechanic

Hiatus hernia Mallory-Weiss

syndrome Boerhaave syndrome Foreign body Iatrogenic

c. Neoplasia malignant benignd. Vascular Varices Aortic aneurism After cardiac surgerye. Hematological anticoagulants coagulation disorders

ESOPHAGIAN CAUSES

Esophagus varices Mallory-Weiss

sundrome Hiatus hernia and

GERD Tumors

Varices10% of casesAssociated with alcohol abuse and

hepatitis: clinical signs of chirrhosisESSENTIAL to exclude variceal

haemorrhageEndoscopy may be difficult but very

important

VARICELE ESOFAGIENE

Endoscopic difficulties– Important bleeding– Stomach full of cloths– Gastric varices– Encephalopathy

BUT ONLY 60% of patients with chirrhosis bleed from varices

DIAGNOSTIC

TRATAMENT

MEDICATION - OCTREOCTIDE: decreases portal flux and pressure in varices

TAMPONDE – Segstaken Blackmore tube – Not a first choice

SURGICAL SHUNT – ~70% mortality in emergency cases

TIPS – ~50% mortality on emergency

M-W SYNDROM

Diagnostic only with endoscopy in emergency

– Short lived lesions

» Usually with small quantity of blood but may produce shock

» Short monitoring» ~0% risk of rebleeding» Conservative treatment ~ 100%

Mallory Weiss

HIATUS HERNIA AND GERD

dg+ EDS – stigmata of recent bleeding

HH very frequent encounter

Treatment: H2 blockers, PPI

TUMORS of ESOPHAGUS

Very unusual cause of clinical manifest bleeding: occult

Endoscopic hemostasis» Laser YAG» Argon plasma

GASTRIC ORIGINE

Hemorrhagic gastritis Gastric ulcer Benign tumors Malignant tumors

HEMORRHAGIC GASTRITIS

Morfologic criteria EDS aspect may vary Radiology useless and

pointless EDS: if late may not show

anything

HEMORRHAGIC GASTRITIS

H2 blockers and PPI – routine but doubtful benefit

Rebleeding extremely rare Endoscopic treatment: not recommended

(numerous lesions with small risk of rebleeding) SURGICAL(unusual: doubtfull diagnostic +

hemodynamic instability) » In situ hemostasissutura in situ» Vagotomy + gastrectomy

GASTRIC ULCER

Some localisations are difficult to see

EDS needs to evaluate» Stigmata of bleeding» Risk of rebleeding

Treatment

H2, IPP +/- i.v route Endoscopic direct

treatment

•Sclerosis•Thermocoagulation•Clips

Surgical treatment

If so, resection of lesion is better Frozen section pathology: malignnancy

always in doubt Limited resections for bening disease

Benign gastric tumors

Bleding is RARE Polipoid lesions can be

resected endoscopically Surgical excision

Malignant gastric tumors

6% Special

characteristicsHigh mortality 9% Frequently non-

resectableLarge costs little

benefit in survival

ENDOSCOPY

Examination: advanced lesionHemostasis (laser or

argon plasma) Ex. Echografic

Ultrasound: MTS and large LN: inoperable

Surgical treatment

Laparotomy or laparoscopy: confirm advanced disease vs operability

Massive bleeding: most often advanced lesions

Paliation ~25%bypassgastrostomy jejunostomy

Vascular malformations Dielafoy (exulceratio simplex)

~5% Congenital anomaly Abnormal artery

protruding in submucoasa

Echoendoscopy

Treatment

Mechanic destruction of the vascular anomaly» Surgery: in situ hemostasis» Endoscopy – GOLD STANDARD

– Correct diagnostic– Banding – Hemoclips– Laser thermocoagulation

Bading

DUODENAL ORIGIN

Very frequent Justifies the empiric

treatment with PPI

EROSIVE DUODENITIS

BIG BAG with different pathologies: erosions

Confusion in term with ulcer/superficial ulcer

Frequent association with Helicobacter Pylori

Treatment conservative: H2 blockers, PPI and antiobiotics

DUODENAL ULCER

Incidence is constant 53% known ulcer in PMH HDS iterative: 17%

High gravity and high risk25% in difficult localizationsRequires a new approach

ASSOCIATED LESIONS

Multiple ulcers Association with varices!!!!! Duodenal stenosis: may be associated

with postbulbar ulcer Association of bleeding and perforation

RISK QUANTIFICATION

ENDOSCOPIC TREATAMENT

Standard Very good results Little requirement of surgical procedures

Heater probe

Very good on visible vessels

Clips

Visible vessels Difficult and

expensive

SURGICAL

Emergency operation Major indication:

Massive bleeding More then 6 units of blood/24 hours =

continuous bleeding

SURGICAL PROCEDURES

In situ hemostasis: the most used technique

Resections (limited in number and extent)

CONCLUSIONS

UGI bleeding is still a significant problem Endoscopy is mandatory for diagnostic

and treatment Surgery is limited in emergency

situations

LOWER GI BLEEDNG

ETIOLOGY

Differential Diagnosis of Lower Gastrointestinal Hemorrhage

COLONIC BLEEDING (95%) % SMALL BOWEL BLEEDING (5%)

Diverticular disease 30-40 Angiodysplasias

Ischemia 5-10 Erosions or ulcers (potassium, NSAIDs)

Anorectal disease 5-15 Crohn's disease

Neoplasia 5-10 Radiation

Infectious colitis 3-8 Meckel's diverticulum

Postpolypectomy 3-7 Neoplasia

Inflammatory bowel disease 3-4 Aortoenteric fistula

Angiodysplasia 3

Radiation colitis/proctitis 1-3

Other 1-5

Unknown 10-25

CLINICAL PRESENTATION

History taking-type of bleeding» Careful interpretation of data» Blood on paper» Red blood vs feaces mixed with blood» Quantity» etc

Paraclinical

Wbc Hct Plt Coagulation profile LFT + numerous other

according to associated pathology

Risk stratificationInitial Emergency Department Risk Stratification for Patients with Gastrointestinal Bleeding

Low Risk Moderate Risk High Risk

Age <60 Age >60

Initial SBP ≥100 mm Hg

Initial SBP <100 mm Hg

Persistent SBP <100 mm Hg

Normal vitals for 1 hr Mild ongoing tachycardia for 1 hr

Persistent moderate/severe tachycardia

No transfusion requirement

Transfusions required ≤4 U

Transfusion required >4 U

No active major comorbid diseases

Stable major comorbid diseases

Unstable major comorbid diseases

No liver disease Mild liver disease—PT normal or near-normal

Decompensated liver disease—i.e., coagulopathy, ascites, encephalopathy

No moderate-risk or high-risk clinical features

No high-risk clinical features

Risk stratification

Seven independent predictors of severity in acute LGIB» hypotension» tachycardia, » syncope, » nontender abdominal exam, » bleeding within 4 hours of presentation, » aspirin use, and » more than two comorbid diseases

LOCALIZATION

The duration, frequency, and color of blood passed per rectum.

Characteristically, melena or black, tarry stool, indicates bleeding from an upper gastrointestinal or small bowel source

Maroon color suggests rt. Sided lesion

whereas bright red blood per rectum signifies bleeding from the left colon or rectum. However, patient and physician reports of stool color are often inaccurate and inconsistent

In addition, even with objectively defined bright red bleeding, significant proximal lesions can be found on colonoscopy

LOCALIZATION

past medical history. antecedent constipation or diarrhea (hemorrhoids, colitis), the presence of diverticulosis (diverticular bleeding), receipt of radiation therapy (radiation enteritis), recent polypectomy (postpolypectomy bleeding), and vascular disease/hypotension (ischemic colitis). A family history of colon cancer Nonetheless, even after a detailed history, physicians

cannot reliably predict which patients with hematochezia will have significant pathology and a history of bleeding from one source does not eliminate the possibility of bleeding from a different source.

LOCALIZATION

Multiple factors make the identification of a precise bleeding source in LGIB challenging.

The diversity of potential sources, The length of bowel involved, The need for colon cleansing, and The intermittent nature of bleeding. In up to 40% of patients with LGIB, more than one

potential bleeding source will be noted and Stigmata of recent bleeding in LGIB are

infrequently identified As a result, no definitive source will be found in a

large percentage of patients

Clinical scenarios

Pt. continued to bleed with hypotension and tachycardia. Patient requires 2 units of PRBCs

Pt. stopped bleeding. Vitals normalizes

Options to diagnose and control the

bleeding

RBC scan, requires 0.5-1 ml/min bleeding

Mesenteric angiography, requires 1-1.5 ml/min bleeding

Colonoscopy Surgery Meckels scan

Scenario one- Pt. continues to bleed and is unstable.

Rbc scan vs colonoscopy

COLONOSCOPY

Colonoscopy is undoubtedly the best test for confirming the source of LGIB and for excluding ominous diagnoses, such as malignancy.

The diagnostic yield of colonoscopy ranges from 45% to 95%

Identifies lesion in 75 % or more Can provide endoscopic therapy most patients undergoing radiographic evaluation

for LGIB regardless of findings and interventions will subsequently require a colonoscopy to establish the cause of bleeding.

CLINICAL SCENARIO

Patient continues to bleed RBC scan is positive on the left side?

How much true this information is?? What to do next? surgery, ?angio

with embolization?

RADIONUCLIDE SCAN

radionuclide scanning has variable accuracy, cannot confirm the source of bleeding, Correct localization rate is 41-100%

Accuracy appears to be best when the scan becomes positive within a short period of time

In one study, 42% of patients underwent an incorrect surgical procedure based on scintigraphy results.

CLINICAL SCENARIO

Patient underwent angiogram with embolization

Vitals improved What are the chances that pt. will

rebleed? Colonoscopy?

MESENTERIC ANGIOGRAM

Selective embolization initially controls hemorrhage in up to 100% of patients, but rebleeding rates are 15% to 40%

Advantages:» Precise localization» Can provide therapy with intra-arterial

vasopressin or coil embolization» Procedure of choice in briskly bleeding pts» Minor complication rate of 9% and a 0%

major complication rate

Disadvantages:» Invasive» Less sensitive in detecting venous

bleeding» Can cause ischemia, contrast

reactions, arterial injury

DIAGNOSTIC DIFFICULTIES

the diagnostic modalities for lower GI bleeding are not as sensitive or specific in making an accurate diagnosis (versus UGIB)

Diagnostic evaluation is complicated: more than one potential source of hemorrhage is identified.

If more than one source is identified, it is critical to confirm the responsible lesion before initiating aggressive therapy.

This approach may occasionally require a period of observation with several episodes of bleeding before a definitive diagnosis can be made.

In fact, in up to 25% of patients with lower GI hemorrhage, the bleeding source is never accurately identified.

SURGERY

Surgery usually is employed for hemorrhage in two settings: massive or recurrent bleeding.

It is required in 15% to 25% of patients who have diverticular Recurrent bleeding from diverticula occurs in 20% to 40% of

patients and generally is considered an indication for surgery

In patients with serious comorbid medical conditions and without exsanguinating hemorrhage, this decision should be made carefully.

Great effort should be made to accurately localize the site of bleeding preoperatively so that segmental rather than subtotal colectomy can be performed Operative mortality is 10% even with accurate localization and up to 57% with blind subtotal colectomy.