(F) 42 yr.
old Bah K/C/O HTN diagnosed in 2015
Presented to A/E H/O black stool, vomiting, abdominal
pain for 2 days.
- Stool: notice black stool but no streaks of blood.
- Vomit: twice food content and fresh blood.
- Abdominal pain: epigastric, localized, colic in nature,
aggravated by eating food and retrieved by laying flat.
Pt. recently had ERCP for stone reveled in CBD and
discharged on 26-4-15
H/O cholecystectomy
Pt. on Norvasc OD for HTN
He is teacher and ex-smoker.
Examinations
Vitally stable, afebrile.
On visual examination: pale, conscious, alert, not in RD.
Chest: N .CVS: N.Abdomen: N.PR: not examined
ECG done was normal.
X-ray done was normal.
Previous was 14.3
DDx
Peptic ulcer disease
Most
Gastroesophageal varices
common
Erosive esophagitis/gastritis/duodenitis
Mallory Weiss tear
Vascular ectasia
Neoplasm
Dieulafoys lesion
Rare, but cannot afford to miss
Aortoenteric fistula
Hemobilia, hemosuccus pancreaticus
Pt. had diagnostic gastroscopy:
* Mild gastritis
* No bleeding
Pt. given Omeprazole 40mg BD for tow days
and
DISCHARGED ON IT
UPPER GI BLEEDING
ESOPHAGEAL VARICES
DR. ALI M.J
2015
WHAT IS IT ?
UGIB is a common medical emergency
Defined as bleeding arising from the
esophagus, stomach, or duodenum.
HOW IT PRESENT ?
UGIB may present in five ways:
1. Hematemesis is vomitus of red blood or coffeegrounds material.
2. Melena is black, tarry, foul smelling stool.
3. Hematochezia is the passage of bright red or maroon
blood from the rectum.
4. Maybe identified in the absence of overt bleeding by a
fecal occult blood test or the presence of iron deficiency.
5. Patients may present only with symptoms of blood loss
or anemia such as lightheadedness, syncope, angina, or
dyspnea.
TYPES OF UGIB :
Two types:
VARICEAL:
1. Chronic liver disease usually cirrhosis
2. Prolonged INR
3. Low platelets
NON-VARICEAL:
1. Peptic Ulcer
2. Erosions
3. Esophagitis
4. Malignancy
5. Miscellaneous*
MISCELLANEOUS
Oesophagus
Mallory-Weiss tear, Reflux oesophagitis, Oesophageal ulcer, Barrets
ulcer, Cameron ulcer within hiatus hernia*, Oesophageal neoplasm
Stomach
Gastric ulcer, Gastric erosions, Haemorrhagic gastritis,Gastric
carcinoma, Gastric lymphoma, Leiomyoma, Gastric polyp, Hereditary
haemorrhagic telangiectasia, Dieulafoy lesion*,Gastric Antral
Vascular Ectasia (GAVE)*,Angiodysplasia*
Duodenum
Duodenal ulcer, Duodenal erosions, Vascular malformation, Aortaduodenal fistula,Polyps (including Peutz-Jeghers syndrome and
other polyposis syndromes), Carcinoma of ampulla, Carcinoma of
pancrease, Haemobilia*
Small bowel
Stomal ulcer, Diverticulum, Vascular malformation, Tumor
Initial Assessment
Always remember to assess A,B,Cs
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%
Heart rate
<100
>100
>120
>140
SBP
No change
Orthostatic
change
Reduced
Very low,
supine
Urine output
(mL/hr)
>30
20-30
10-20
<10
Mental status
Alert
Anxious
Aggressive/dro Confused/unco
wsy
nscious
PEPTIC ULCERS
Focal defects in the mucosal that penetrate the muscularis
mucosal layer results in scarring
(defects superficial to the muscularis mucosa have erosions
and no scarring)
Peptic ulcers are the most common cause of UGIB,
accounting for up to ~50% of cases; an increasing
proportion is due to NSAIDs,
with the prevalence of H.pylori decreasing.
ETIOLOGY OF PEPTIC ULCER
DISEASE
H. pylori infection
NSAIDs, ASA
Physiologic stress-induced
Zollinger-Ellison (ZE) syndrome
Idiopathic
Duodenal
Gastric
80%
7%
<3%
<1%
15%
50%
35%
<5%
<1%
10%
NSAID negative, H. pylori negative ulcers becoming
more commonly recognized
others: CMV, ischemic, idiopathic
alcohol: damages gastric mucosa but rarely causes ulcers
peptic ulcer associated with tobacco, cirrhosis of liver,
COPD and chronic renal failure
HEMORRHAGIC AND
EROSIVE GASTROPATHY
Hemorrhagic and erosive gastropathy, often labeled
gastritis, refers to endoscopically visualized subepithelial hemorrhages and erosions.
These are mucosal lesions and thus do not cause major
bleeding. They develop in various clinical settings, the
most important of which are NSAID use, alcohol intake,
and stress.
VARICES
Varices are abnormal distended veins usually in the
esophagus (esophageal varices) and less frequently in the
stomach (gastric varices) or other sites (ectopic varices)
usually occurring as a consequence of liver disease.
Esophageal varices
Are extremely dilated submucosal veins in the lower
third of the esophagus.
HOW IT
HAPPENED ?
Blood from esophagus is drained via esophagus veins, which
carry deoxygenated blood from esophagus to azygos vein
Drains directly into superior vena cava.
THESE VEINS ARE NOT PART OF ESOPHAGUS
VARICES
Remaining blood from esophagus drained into superficial veins
lining esophageal mucosa.
Then it drains into left gastric vein
Then it will drain into portal vein
THE ISSUE WILL START NOW IF PT. HAS
RELATED PROBLEMS (RISK FACTORS)
Cirrhotic Liver without Esophageal Varices
superficial veins approximately 1 mm in diameter
pressure 2-6 mmHg which is low comparing to portal vein (9 mmHg)
If presenting complications of known liver disease or when clinical
assessment identifies stigmata of CHRONIC LIVER DISEASE or
PORTAL HYPERTENSION
portal vein pressure
>10 .. Superficial veins pressure 7-10
Will distend superficial veins into 1-2 cm in diameter
Which means collateral circulation develops in lower esophagus, abdominal wall,
stomach and rectum
The small blood vessels of these area become distended, more thin-walled
And appear as varicosities
Cirrhotic Liver with Esophageal Varices
1- Evidence of recent variceal hemorrhage
includes necrosis and ulceration of the mucosa.
2- Evidence of past variceal hemorrhage includes
inflammation and venous thrombosis.
SPLENECTOMY
Splenic vein thrombosis is a rare condition
that causes esophageal varices. Splenectomy
can cure the variceal bleeding due to
splenic vein thrombosis
without a raised portal pressure
Risk factors
Development of varices
High portal vein pressure: HVPG >10 mmHg in
patients who have no varices at initial endoscopic screening
Progression from small to large varices
Decompensated cirrhosis
Alcoholic cirrhosis
Presence of red wale marks at baseline endoscopy (=longitudinal
dilated venules resembling whip marks on the variceal surface)
Initial variceal bleeding episode
Large varices (>5 mm) with red color signs
Continuing alcohol consumption
High HVPG >16 mm Hg
Coagulopathy
Patients presenting with variceal haemorrhage should be
assessed and resuscitated as for any other patient with
evidence of UGIB.
Variceal haemorrhage may be suspected when there is
a history of previous variceal bleeding, known liver
disease or when clinical assessment identifies stigmata
of chronic liver disease or portal hypertension. These
include the presence of:
1.
2.
3.
4.
5.
Jaundice
Ascites
Splenomegaly
Encephalopathy
Caput medusae and spider naevi.
DIFFERENTIAL DIAGNOSIS
Schistosomiasis
Severe congestive heart failure
Hemochromatosis
Wilson disease
Autoimmune hepatitis
Portal/splenic vein thrombosis
Sarcoidosis
BuddChiari syndrome
Chronic pancreatitis
Hepatitis B
Hepatitis C
Alcoholic cirrhosis
Primary biliary cirrhosis (PBC)
Primary sclerosing cholangitis (PSC)
DIAGNOSIS GUIDELINE
TREATMENT
Patients with confirmed esophageal variceal hemorrhage
should undergo variceal band ligation.
Splanchnic vasoconstrictors
Vasopressin (analogues)
Somatostatin (analogues)
Non-cardioselective -blockers
Pharmacotherapy with somatostatin (analogues) is effective in stopping hemorrhage, at least
temporarily, in up to 80% of patients. Somatostatin may be superior to its analogue octreotide.
About 30% of patients do not respond to -blockers with a reduction in the hepatic venous
pressure gradient (HVPG), despite adequate dosing. These non-responders can only be detected by
invasive HVPG measurements. Moreover, -blockers may cause side effects such as fatigue and
impotence, which may impair compliance (especially in younger males), or - blockers may be
contraindicated for other reasons.
Venodilators
Nitrates
Nitrates alone are not recommended. Isosorbide 5-mononitrate reduces portal pressure, but its use
in cirrhotic patients is limited by its systemic vasodilatory effects, often leading to a further
decrease in blood pressure and potentially to (prerenal) impairment of kidney function.
Vasoconstrictors and vasodilators
Combination therapy leads to a synergistic effect in reducing portal pressure
Combining isosorbide 5-mononitrate with nonselective -blockers has been shown to have
additive effects in lowering portal pressure and to be particularly effective in patients who do
not respond to initial therapy with -blockers alone. However, these beneficial effects may be
outweighed by detrimental effects on kidney function and long-term mortality, especially in
those aged over 50. Routine use of combination therapy is therefore not recommended.
Ligation technique
Patients with confirmed oesophageal variceal
hemorrhage should undergo variceal band ligation.
Banding may be technically difficult in cases of
continued bleeding, and sclerotherapy may then be
necessary
A meta-analysis of vasoactive drug treatment versus
sclerotherapy indicated similar rates of hemostasis,
rebleeding and mortality for both interventions, with
greater adverse events in the sclerotherapy group
Sclerotherapy technique
Balloon tamponade
Harrison's Gastroenterology and Hepatology
Sources
Toronto notes 2014
Harrison's Gastroenterology and Hepatology
Scottish guideline 2008
Academy of medicine, Malaysia 2003
World Gastroenterology Organization Global Guidelines
2014
Wikipedia
medscape
UpToDate
..
THANK YOU FOR ATTENDING
ALI MJ - 2015
[email protected]
