UPPER G-I

HAEMORRHAGE
 DEFINITION

The upper g-i haemorrhage represents

that digestive haemorrhage, located
between the pharingo-oesophageal
junction and Treitz’s angle
 ETIOLOGY

1. Diseases of the digestive tract;

2. Diseases of the digestive glands;

3. Extra-digestive diseases
 ETIOLOGY
1.Diseases of the digestive tract
A. Oesophagus:
 Varices;
 Acute oesophagitis;
 Benign/malignant tumours;
 Ulcer;
 Trauma;
 Mallory-Weiss syndrome;
 Iatrogenic
 ETIOLOGY
1.Diseases of the digestive tract
B. Stomach:
Acute/chronic ulcer;
Gastritis;
Benign/malignant tumours;
Hiatus hernia;
Specific chronic inflammation (tuberculosis,
syphilis, Crohn’s);
Foreign bodies
 ETIOLOGY
1.Diseases of the digestive tract
C. Duodenum:
Ulcer;
Haemorrhagic duodenitis;
Vater’s ampuloma;
Crohn’s disease
 ETIOLOGY
2. Diseases of the digestive glands
A. Liver cirrhosis;
B. Portal vein thrombosis;
C. Portal vein compressions;
D. Budd-Chiari’s syndrome;
E. Posttraumatic haemobilia;
F. Biliary tract diseases;
G. Acute/chronic pancreatitis;
H. Pancreatic cancer
 ETIOLOGY
3. Extra-digestive diseases
A. Haemophilia, Hodgkin’s lymphoma,
leukemia, Henoch-Schönlein’s
syndrome;
B. Arteriosclerosis, high blood pressure,
haemangiomas, sarcoidosis;
C. Stress – Cushing’s ulcer, Curling’s ulcer;
D. Drugs: NSAIDs, chemotherapy,
anticoagulants
 CLASSIFICATION
(Bockum)
I. Gastro-duodenal ulcer – 61.9%
II. Portal high pressure – 11.9%
III. Gastro-duodenal tumours – 6.4%
IV. Rare causes – 10.8%
V. Undetermined causes – 7.7%
 UPPER G-I
HAEMORRHAGE
-ULCER-
 The most frequent complication of the ulcers;
 It appears during the evolution of the disease
or as its first and only clinical sign;
 Triggers: chronic alcoholism, liver failure,
NSAIDs, high blood pressure;
 Origin: gastric lesser curvature, posterior face
of the duodenum;
 Mechanism: erosion of important blood
vessels, diffuse lesions of the mucosa
 UPPER G-I
HAEMORRHAGE
-HIGH PORTAL PRESSURE-
Generally caused by the rupture of the
oesophageal varices;
Pathophysiological classification:
Pre-sinusoidal (portal vein thrombosis);
Sinusoidal (liver cirrhosis);
Post-sinusoidal (Budd-Chiari’s syndrome)

Cirrhosis – 90%
 UPPER G-I
HAEMORRHAGE
-HIGH PORTAL PRESSURE-
 portal blood quantity and pressure 
dilation of the spleno-portal axis and
opening of the natural derivation paths
(haemorrhoidal veins, superficial veins
of the anterior abdominal wall and the
veins of the eso-gastric junction);
Oesophageal varices – especially in the
lower 1/3 of the oesophagus
 PATHOPHYSIOLOGY
• Blood loss  collapse  ventricular
fibrillation caused by myocardial hypoxia
(cataclysmic haemorrhage);
• When >1,000 mL are lost  initial collapse
 reaction of response, generated by the
sympathetic mechanisms; possible
spontaneous remission; if >1,500 mL are
lost  hypovolemic shock;
 PATHOPHYSIOLOGY
• Compensatory mechanisms:
1.Circulation centralization;
2.Vessel constriction;
3.High heart rate;
4.High respiration rate

Prolonged shock  breakdown of

compensatory mechanisms!
 CLINICAL SIGNS
Hematemesis;

Melena;

Acute anemia
 INVESTIGATIONS
 Laboratory: Ht, Hb, WBC, RBC, liver and
kidney functional tests, coagulation tests,
serum electrolytes;
 ENDOSCOPY: the most important
investigation; sensitivity of 95%; it allows the
treatment in certain cases; Forrest
classification;
 Barium X-ray: important, yet insufficient for
superficial lesions;
 Selective arteriography;
 Ultrasound, CT, MRI;
 Exploratory laparoscopy
 TREATMENT
!EMERGENCY!
1. Absolute rest in bed;
2. Absolute digestive rest;
3. 1-2 venous catheters;
4. Blood group, Rh;
5. Naso-gastric aspiration tube;
6. Central venous catheter;
7. Urinary catheter;
8. Oxygen mask;
9. Haemostatic agents;
10. Volume repletion
 TREATMENT
-haemostatic-
A. Conservatory methods
 Gastric irrigation;
 Local haemostatics;
 Haemostatics;
 Somatostatine: 250 μg/h;
 Antiacid drugs;
 Anti-H2 drugs;
 Proton pump inhibitors;
 Compressive probes (Sengstaken-Blakemore,
Linton, Guevara);
 Endoscopy;
 TREATMENT
-haemostatic-
B. Surgery -indications.
 Severe bleeding (rapid loss of >30% of the
total blood amount);
 Continuous bleeding despite a correct medical
treatment;
 Repetitive bleeding within a short period of
time;
 Haemorrhages associated with haemodynamic
instability;
 Patient over 60 yrs old.
 TREATMENT
-volume repletion-

Hydro-electrolytic correction;

Acid-base correction;

Combating high ammonium levels

 TREATMENT
-surgery-
A. Gastro-duodenal ulcer
 Technique adapted to the pathology of
the lesion;
 Gastric resection, in situ haemostasis,
total gastrectomy;
 Ligation of the vascular pedicles of the
stomach
 TREATMENT
-surgery-
B. High portal vein pressure
 Surgery=palliative treatment;
 Methods:
1. Direct ligation of the varices (Boerema, Juvara)
2. Eso-gastric disconnection (Walker, Tanner,
Sugiura)
3. Porto-systemic shunts (proximal/distal)