Acute (UGIB) is a GIT emergency with a mortality of 4%-14% despite advances in critical care monitoring and support. Spontaneous cessation of bleeding occurs in 85% of cases. Main cause is PUD. But in Egypt variceal bleeding is the commonest.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
Upper Gastrointestinal Bleeding (UGIB) - General ApproachMohamed Badheeb
What does the science & evidence say about UGIB ?
Introduction & Background on Upper GI Bleeding.
- Incidence and Epidemiology
- Etiologies
2. Guidelines on UGIB
- Resuscitation, Risk assessment
- Diagnostic Modalities
- Treatment Options
Approach to Hematuria including:
Definition of Hematuria.
Pathophysiology of Hematuria.
Differential Diagnosis of Red Urine.
Causes of Hematuria.
Approach to a patient with Hematuria.
Diagnostic Algorithms.
Management and Disposition.
Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
Diffuse nodular lymphoid hyperplasia (DNLH) is a benign rare condition of unknown etiology characterized microscopically by diffuse hyperplasia of the lymphoid follicles of the gastrointestinal tract (GIT). It is grossly seen during endoscopy as numerous visible mucosal nodules measuring <0.5 cm in diameter. It can involve any part of the GIT, mainly the small intestine, but it may also involve the colon and rarely the stomach. It may have diffuse pattern which is the most common former focal pattern which is much less common. The disease is usually associated with immunodeficiency syndromes such as common variable immunodeficiency or selective IgA deficiency syndrome. Its prognosis is usually benign but it carries the risk of malignant transformation characteristically to lymphoma.
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
Upper Gastrointestinal Bleeding (UGIB) - General ApproachMohamed Badheeb
What does the science & evidence say about UGIB ?
Introduction & Background on Upper GI Bleeding.
- Incidence and Epidemiology
- Etiologies
2. Guidelines on UGIB
- Resuscitation, Risk assessment
- Diagnostic Modalities
- Treatment Options
Approach to Hematuria including:
Definition of Hematuria.
Pathophysiology of Hematuria.
Differential Diagnosis of Red Urine.
Causes of Hematuria.
Approach to a patient with Hematuria.
Diagnostic Algorithms.
Management and Disposition.
Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
Diffuse nodular lymphoid hyperplasia (DNLH) is a benign rare condition of unknown etiology characterized microscopically by diffuse hyperplasia of the lymphoid follicles of the gastrointestinal tract (GIT). It is grossly seen during endoscopy as numerous visible mucosal nodules measuring <0.5 cm in diameter. It can involve any part of the GIT, mainly the small intestine, but it may also involve the colon and rarely the stomach. It may have diffuse pattern which is the most common former focal pattern which is much less common. The disease is usually associated with immunodeficiency syndromes such as common variable immunodeficiency or selective IgA deficiency syndrome. Its prognosis is usually benign but it carries the risk of malignant transformation characteristically to lymphoma.
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
POEM (Per Oral Endoscopic Myotomy) is a rising well known treatment for Achalasia ....... in this ppt we discuss the feasibility of POEM versus dilation and Heller's myotomy
Choledochoduodenal fistula is considered an uncommon complication to peptic ulcer, in this presentation we present a case with a short talk about choledochoduodenal fistulas and also a very interesting video is attached showing it clearly.
Cutaneous involvement is very common in the different types of vasculitis. Skin lesions may be the only manifestation or may occur in the context of systemic disease
Nutritional assessment in chronic liver diseaseShaimaa Elkholy
Protein Energy Malnutrition (PEM) is highly prevalent among patients with chronic liver disease. One of the problems is how to assess these patients nutritionally. yet no standard golden rule for their nutritional assessment.
Primary GIT lymphoma typically refers to a lymphoma that predominantly involves any section of the GIT from the oropharynx to the rectum. The GIT is the predominant site of extra nodal lymphoma involvement, mostly are non-Hodgkin lymphomas (NHLs).
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
5. Definitions:
• Hematemsis: vomiting of blood or coffee-
ground like material suggests bleeding
proximal to the ligament of Treitz.
• Melena: black, tarry stools originates proximal
to the ligament of Treitz (90 %), or from the
small bowel or right colon.
• Hematochezia: red or maroon blood in the
stool is usually due to lower GI bleeding. It can
occur with massive upper GI bleeding.
Shaimaa Elkholy, M.D. Cairo University
6. Epidemiology :
• Acute (UGIB) is a GIT emergency with a
mortality of 4%-14% despite advances in
critical care monitoring and support.
• Spontaneous cessation of bleeding occurs in
85% of cases.
• UGIB in the UK ranges between 84-172 per
100,000 per year, causing 50-70,000 hospital
admissions per year.
• Major cases due to PUD.
Shaimaa Elkholy, M.D. Cairo University
7. • UGIB in the United States is 160 hospital admissions
per 100,000 population, which translates into more
than 400,000 per year.
• 80 to 90% have NVGIB mainly PUD.
• An increasing proportion related to the use of aspirin
/NSAIDs.
• PUD bleed is seen predominantly among the elderly,
68% > 60 years/ 27% > 80 years.
• Mortality remains high at 5-10%&medical costs for
the in-hospital care>$ 2 billion annually in US.
Epidemiology :
Shaimaa Elkholy, M.D. Cairo University
10. Other rare cases:
• Idiopathic angiomas
• Osler-Weber-Rendu syndrome
• Radiation-induced telangiectasia
• Traumatic or post-surgical
• Foreign body ingestion
• Post-surgical anastamosis
• Aortoenteric fistula
• Post gastric/duodenal polypectomy
• Hemobilia
• Hemosuccus pancreaticus
Shaimaa Elkholy, M.D. Cairo University
11. EGYPTIAN scenario:
• Variceal causes of bleeding were the most
common, representing 70.1% followed by
non-variceal causes (26.1%) and obscure
causes (3.8%).
• Gastric lesions were the most common causes
of non variceal bleeding.
Shaimaa Elkholy, M.D. Cairo University
12. VGIB:
• Variceal hemorrhage is the most common
fatal complication of cirrhosis.
• At the time of diagnosis:
30% of cirrhotic patients O.V.
90% after approximately 10 years.
• Bleeding ceases spontaneously in up to 40%
Shaimaa Elkholy, M.D. Cairo University
13. • Correlation to the severity of liver disease:
Child–Pugh A patients: 40% have varices
Child–Pugh C patients: 85% have varices
• Some patients may develop varices and hemorrhage
early in the course of the disease, even in the absence
of cirrhosis
• Patients with hepatitis C and bridging fibrosis: 16%
have esophageal varices
VGIB:
Shaimaa Elkholy, M.D. Cairo University
14. Prognosis:
• Bleeding O.V. occurs 30 % in
the 1st year after diagnosis.
• The mortality during the
attack:
< 10% Child–Pugh grade A
> 70% in advanced Child–
Pugh C cirrhotic stage.
• Bleeding O.V. mortality rate
20% at 6 weeks.
• The risk of re-bleeding is
high, reaching 80% within 1
year.
• High Portal venous pressure
> 20 mmHg :
REBLEEDING : 1st week of
admission
Failure to control bleeding
(83% vs. 29%)
Higher 1-year mortality rate
(64% vs. 20%).
Shaimaa Elkholy, M.D. Cairo University
16. Small varices Large varicesNo varices
7-8%/year 7-8%/year
Varices Increase in Diameter Progressively
Merli et al. J Hepatol 2003;38:266
VARICES INCREASE IN DIAMETER PROGRESSIVELY
Shaimaa Elkholy, M.D. Cairo University
17. I. Dilated venes (< 5mm) still at the level of the surrounding
tissue
II. Dilated, straight venes (> 5 mm) protruding into the
esophageal lumen but not obstructing it
Grades of O.V.:
Shaimaa Elkholy, M.D. Cairo University
18. III. Large, tense and winding venes already obstructing the
esophageal lumen considerably
IV. Near complete obstruction of the esophageal lumen with
impending danger of hemorrhage (cherry red spots)
Shaimaa Elkholy, M.D. Cairo University
19. NVGIB :
Peptic ulcer disease:
• The mortality associated with acute bleeding
from a peptic ulcer remains high (5 to 10%).
• 4 risk factors:
H. pylori infection
NSAIDs
Stress
Gastric acid
Alcoholism
Shaimaa Elkholy, M.D. Cairo University
20. FORREST - classification of upper gastrointestinal hemorrhage
Acute hemorrhage
Forrest IA Active spurting hemorrhage
Forrest IB Oozing hemorrhage
Signs of recent hemorrhage
Forrest IIA Non-bleeding visible vessel
Forrest IIB Adherent clot
Forrest IIC Hematin on ulcer base
Lesions without active bleeding
Forrest III Clean-base ulcers
Bleeding PUD
Shaimaa Elkholy, M.D. Cairo University
21. Endoscopic Stigmata of Bleeding Peptic Ulcer, Classified as High Risk or Low Risk
Spurt blood (grade IA) Ooze blood (grade IB) Nonbleeding visible
vessel (grade IIA)
Adherent clot (grade IIB) Flat, pigmented spot
(grade IIC)
Clean base (grade III)
Shaimaa Elkholy, M.D. Cairo University
22. DIEULAFOY'S LESION:
• Dilated aberrant submucosal vessel
which erodes the overlying
epithelium in the absence of a
primary ulcer.
• It’s caliber 1 to 3 mm, 10-times
the normal caliber of mucosal
capillaries.
• Usually on lesser curve below the
cardia, may be found any where.
Shaimaa Elkholy, M.D. Cairo University
23. DIEULAFOY'S LESION:
• unknown, but may be congenital.
• Events triggering bleeding are also not well-
understood(?? NSAIDs).
• Male patients with comorbidities including
cardiovascular disease, hypertension, CKD ,
diabetes, or alcohol abuse.
• Bleeding is usually self limited but it may be
severe.
Shaimaa Elkholy, M.D. Cairo University
25. Mallory-Weiss syndrome:
• longitudinal mucosal lacerations
s in the distal esophagus and
proximal stomach, which are
usually associated with forceful
retching.
• secondary to a sudden increase
in intraabdominal pressure e.g.
vomiting, straining or lifting,
coughing, epileptic convulsions,
hiccups under anesthesia,
closed-chest massage, blunt
abdominal injury.
Shaimaa Elkholy, M.D. Cairo University
30. Resuscitation and initial management:
Initial evaluation: “QUICK”
Triage.
General support.
Fluid resuscitation.
Blood transfusions.
Nasogastric lavage.
Shaimaa Elkholy, M.D. Cairo University
31. General management:
• Triage: “QUICK”
ICU admission
Hemodynamic instability (shock, orthostatic
hypotension).
Active bleeding (manifested by hematemesis,
bright red blood per nasogastric tube, or
hematochezia).
Shaimaa Elkholy, M.D. Cairo University
32. General management:
• Support :
oxygen by nasal cannula.
NPO.
Two large caliber (16-18 gauge) peripheral I.V.
Catheters.
Central venous line if possible.
Pulmonary artery catheter should be considered in
patients with hemodynamic instability or who need
close monitoring during resuscitation.
Elective endotracheal intubation in patients with
ongoing hematemesis with altered respiratory or
mental status.
Shaimaa Elkholy, M.D. Cairo University
33. General management:
• Fluid resuscitation:
resuscitation and stabilization is essential prior to
endoscopy
Patients with active bleeding should receive
intravenous fluids (crystalloids or colloids)
while being typed and cross-matched for blood
transfusion.
Patients at risk of fluid overload may require
intensive monitoring with a pulmonary artery
catheter.
Shaimaa Elkholy, M.D. Cairo University
34. General management:
• Indications of blood transfusion:
• Hb below 7mg/dl (low risk).
• High risk patients (old or comorbid) 10mg/dl.
• Active (fresh) bleeding & Hypovolemea even with normal HB.
• Indications of platelet & FFP transfusion:
• low platelet count (<50,000/microL) OR INR > 1.5.
• life-threatening bleeding receiving antiplatelet or anti coagulation.
• Patients receiving massive blood transfusion due to dilutional
coagulopathy.
• Over-transfuse patients with suspected variceal bleeding can precipitate
worsening of bleeding (10 mg/dl).
Shaimaa Elkholy, M.D. Cairo University
35. General management:
• Nasogastric lavage:
• Its use before endoscopy in the ER remains
controversial.
• Benefits:
To confirm an UGI source of bleeding(can still miss up
to 15%)
Prognostic index for identifying high-risk lesions as
presence fresh red blood in the NGT aspirate.
May exclude false hematemsis.
To facilitate lavage of the upper GI tract to improve
mucosal views at subsequent endoscopy.
Shaimaa Elkholy, M.D. Cairo University
36. Risk assessment:
• Blatchford score at first assessment.
• Rockall score after endoscopy.
Shaimaa Elkholy, M.D. Cairo University
38. ScoreLow risk
defined as score
of <=2
4.3% rebleeding
0.1% mortality
Shaimaa Elkholy, M.D. Cairo University
39. Medications (pre- endoscopy):
• Acid suppression.
• Prokinetics.
• Somatostatin and its analogs in VUGIB.
• Antibiotics for patients with cirrhosis.
Shaimaa Elkholy, M.D. Cairo University
40. • Acid suppression:
• starte empirically on an I.V. PPI &continued
until confirmation of the cause of bleeding.
• I.V. of a PPI significantly reduces the rate of
rebleeding compared& hospital stay in
comparison to H2 blockers.
• 80 mg bolus followed by 8 mg/hr infusion for
72 days then switched to oral.
Medications (pre- endoscopy):
Shaimaa Elkholy, M.D. Cairo University
41. • Prokinetics: erythromycin & metchlopromide.
• Somatostatin, or its analog Octreotide
splanchnic vasoconstriction and decreased
portal inflow
50 mcg bolus followed by a continuous
infusion of 50 mcg per hour and is continued
for 3-5 days.
Medications (pre- endoscopy):
Shaimaa Elkholy, M.D. Cairo University
42. • Antibiotics for patients with cirrhosis:
• The AASLD guidelines : (max.7 days)
Oral norfloxacin (400 mg twice daily) or
intravenous ciprofloxacin
In patients with advanced cirrhosis,
I.V. ceftriaxone (1 g/day) & with a high
prevalence of quinolone-resistant organisms.
Medications (pre- endoscopy):
Shaimaa Elkholy, M.D. Cairo University
43. :Timing of endoscopy
• Patients with UGIB should generally undergo
endoscopy within 24 h of admission, following
resuscitative efforts to optimize hemodynamic
parameters and other medical problems
Shaimaa Elkholy, M.D. Cairo University
44. Timing of endoscopy
• Patients who are hemodynamically stable and
without serious comorbidities:
Endoscopy as soon as possible in a non-emergent
setting to identify the substantial proportion of
patients with low-risk endoscopic findings who can
be safely discharged
Shaimaa Elkholy, M.D. Cairo University
45. Timing of endoscopy
• Patients with higher risk clinical features endoscopy
within 12 h may be considered to potentially improve
clinical outcomes
Shaimaa Elkholy, M.D. Cairo University
46. Endoscopic management VUGIB:
• EIS
( endoscopic injection
sclerotherapy)
Sclerosing materials :
ethanolamin oleate(E/O)
cyanoacrylate (H/A).
• Local complications :
Ulceration
Bleeding
stricture formation
portal hypertensive gastropathy
• Regional complications
esophageal perforation and
mediastinitis.
• Systemic complications
sepsis and aspiration with
ventilation perfusion mismatch and
hypoxemia
Shaimaa Elkholy, M.D. Cairo University
49. • Endoscopic therapy should be provided to patients with
Forrest grade IA, IB, or IIA.
• Endoscopic therapy may be considered for patients with an
adherent clot resistant to vigorous irrigation.
• Endoscopic therapy should not be provided to patients who
have an ulcer with a clean base or a flat pigmented spot
(Forrest grade IIC, or III).
Endoscopic management NVUGIB:
Shaimaa Elkholy, M.D. Cairo University
50. Endoscopic Stigmata of Bleeding Peptic Ulcer, Classified as High Risk or Low Risk
Spurt blood (grade IA) Ooze blood (grade IB) Nonbleeding visible
vessel (grade IIA)
Adherent clot (grade IIB) Flat, pigmented spot
(grade IIC)
Clean base (grade III)
Shaimaa Elkholy, M.D. Cairo University
51. • Mechanical method (for example, clips) with
or without adrenaline
• Thermal coagulation with adrenaline
• Fibrin or thrombin with adrenaline
• No single method of endoscopic thermal
coaptive therapy is superior to another
Endoscopic management NVUGIB:
Shaimaa Elkholy, M.D. Cairo University
52. Take home messeges
• Patient with UGIB is critically ill patient with different
presentations.
• PUD is the commonest cause world wide.
• VUGIB is commonest cause in Egypt.
• Stepped approach to UGIB has to be known.
• Resuscitation is essential prior to endoscopy.
• Indications of blood , platelets & FFP transfusion differs from one
patient to another.
• Target HB differs according to the patient.
• Risk assessment is essential in those patients by different scoring
systems.
• Forrest classification is essential to determine the line of
management.
• EVL is much preferred than injection sclerotherapy.
Shaimaa Elkholy, M.D. Cairo University