Upper GI bleeding is a common medical emergency that requires rapid assessment and management. The main causes are peptic ulcer disease, portal hypertension, and vascular malformations. Treatment involves fluid resuscitation, blood transfusion if needed, acid suppression with PPIs, and somatostatin analogues like octreotide for variceal bleeding. PPIs reduce rates of rebleeding but do not impact mortality. Antibiotics are recommended for cirrhotic patients with GI bleeding to prevent infection.
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.
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool.
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.
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool.
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
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
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
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
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
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
Haemorrhoids is one of the commonest cause of lower GI bleed. Understanding the pathophysiology is important for planning a successful treatment. A thorough check up is essential before offering surgical treatment as this condition could herald the presense of a malignant lesion higher up.
Piles - Also called Haemorrhoids and homeopathy treatmentPranav Pandya
haemorrhoids are vascular structures in the anal canal. Normally they are cushions that help with stool control. They become piles when swollen or inflamed.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
2. Learning Objectives
Background: acute upper GI bleeding (UGIB)
Review MAJOR CAUSES in adults
(Briefly) review general management
Look at the EVIDENCE for specific
MEDICALTHERAPIES used in management
3. Background UGIB
Common medical emergency with associated high morbidity,
mortality(6-11%)* and medical expenditure
Most commonly presents with haematemesis and/or melena (much
less commonly with haematochezia – 3x higher risk of death*)
Requires rapid assessment (particularly evaluation of
haemodynamic stability) and then prompt multi-team
management
* Source: Cameron P, Jelinek G, Kelly AM, Murray L, Brown A.Textbook of Adult Emergency
Medicine. 3rd Edition.Churchill Livingston Elsevier 2009
4. Bleeding
Manifestations
Haematemesis = bleeding proximal
to Ligament ofTreitz
Frank bloody emesis vs coffee ground
Melena = majority due to bleeding
proximal to Ligament ofTreitz,
remainder from small bowel or right
side of LI
Haematochezia = usually in lower
GIT bleed, only if massive UGIB
5. Factors Predictive of Upper GI bleed*
Melena on PR examination (LR 25)
Blood or coffee ground vomit on NG lavage (LR 9.6)
Ratio of blood urea nitrogen to creatinine >30 (LR 7.5)
Self reported history of melena (LR 5.1-5.9)
Blood clots seen in stool (LR 0.05)
* Source: Srygley FD, Gerardo CJ,TranT, Fisher DA. Does this patient have a severe upper
gastrointestinal bleed? JAMA 2012; 307:1072
7. Factors Predictive of a Severe Bleed
History
orthostatic dizziness, confusion, angina, severe palpitations
Examination
tachycardia, orthostatic hypotension or supine hypotension
(even worse), cold/clammy peripheries
Bedside and Laboratory Investigations
Hb <80 g/L, high Ur:Cr ratio, high red blood found on NG lavage
8. Mortality/Morbidity Factors*
Advanced age
Cause of the bleed (particularly varices)
Presence of shock
Fresh bright red blood
Low Hb
Re-bleed presentation
Comorbid disease
Endoscopic findings
*Source: http://lifeinthefastlane.com/ebm-upper-gi-haemorrhage/
9.
10. Ulcerative or Erosive
Disease
Peptic Ulcer Disease
*MOST COMMON CAUSE UGIB*
Idiopathic
Drug induced
Aspirin
NSAID (approx doubles risk)
Infectious
H.pylori,CMV, HSV
Stress induced ulcer (burns, major
trauma, sepsis, hypotension, HI)
Zollinger-Ellison Syndrome
14. Traumatic or Post Surgical
Mallory-WeissTear (classic N+V then bleeding in 1/3) Post surgical anastomosis
FB ingestion Post gastric/duodenal
polypectomy
Aortoenteric fistula (Hx aortic surgery + bright red haematemesis + haematochezia)
16. General Management
General Management Principles
1. supplemental oxygen
2. crystalloid/colloid fluid resuscitation
3. +/- blood transfusion
4. consider correcting coagulopathy (?benefit vs risk)
5. medical management
6. endoscopic (pretreat with erythromycin) / embolisation /
surgical management
17. General Management
BloodTransfusion
consider on individual basis (particularly comorbidities)
indication: Hb <70 g/L
(except unstable CHD aim Hb > 90 g/L)1-3
avoid transfusing patients with suspected variceal
bleeding to Hb >100 g/L
(portal P may worsen bleeding)4, 5-8
give one unit FFP for each four units of packed RBC
transfused9
18. General Management
Consider reversal of coagulopathy (in those actively bleeding)
FFP if INR >1.5 or platelets if count <50 x 109/L
simultaneous replacement + scope if INR <3
delay scope until INR <3 if it is initially higher10
Consider platelet transfusion if life threatening bleeding and
taking antiplatelet agents eg aspirin or clopidogrel
If stent or ACS – recommend discuss with cardiologist
prior to stopping antiplatelet agent or transfusing platelets11
19. Medical Management
Acid Suppression
Proton pump inhibitor
H2 R antagonists
Somatostatin Analogue
Octreotide
Other
Terlipressin
Antibiotics
Tranexamic acid
20. Acid Suppression
Proton Pump Inhibitor (PPI) / H2 Receptor Antagonist
Recommended Practice (Up to Date 2014):12
Give PPI (empirically) to all patients with acute UGIB:
esomeprazole or pantoprazole: 80mg IV bolus, followed by
8mg/hour IVI (continued for 72 hours)
Start PPI at presentation (often don’t know source of
bleeding)
Once source known (and treated), decision can be made
before discharge home if PPI needs to be continued
21. Acid Suppression
Evidence?
Meta analysis (2002): Pharmacotherapies for NonVariceal UGIB13,14 :
PPI (IVI) significantly reduces rate of rebleeding
compared to H2 R antagonists or placebo
H2 R antagonists had only modest effects in bleeding
gastric ulcers and no longer recommended15:
- reduced rebleeding by 7.2%
- reduced surgery by 6.7%
- reduced mortality by 3.2%
22. Acid Suppression
Evidence cont?
Peptic Ulcers:
PPIs (oral and IV) have additional benefits16,17:
decrease LOHS
decreased need for blood transfusion (in those with high
risk ulcers treated with endoscopic therapy)
MAY promote haemostasis in other, non ulcer, lesions
23. Acid Suppression
However, NO demonstrable effect on all cause mortality
What we know (oops!) think18:
Asians patients likely benefit best from PPI
(related to drug metabolism and ability to raise intragastric
pH)
PPI may decrease rate rebleeding, LOHS, need for blood
transfusion but likely doesn’t effect mortality
Unfortunately no good data to guide us on best route of
administration or dose
Oral dose needs to be at least double std clinical dose
24. Acid Suppression
What do we know about the timing of administration*??
If given PPI pre – endoscopy: reduces high risk stigmata and the need for
endoscopic therapy (OR 0.67)
If given PPI post – endoscopy: reduces risk of requiring surgery, risk of
rebleeding and death in high risk patients (RR 0.43, 0.4, 0.41 respectively)
---------------------------------------------------------------------------------------------
*Source: http://lifeinthefastlane.com/ebm-upper-gi-haemorrhage/
References:
1. Lau J, Leung W, Wu J et al. Omeprazole before endoscopy in patients with gastrointestinal
bleeding. NEJM 2007; 356:1631- 40.
2. Leontiadis GI, SharmaVK, Howden CW. Proton pump inhibitor treatment for acute peptic
ulcer bleeding. Cochrane Database Syst Rev 2006;1:CD002094. [2006 Reference] [2010 Reference]
25. Somatostatin Analogue
Octreotide
Recommended Practice (UpTo Date 2014)12:
In suspected or known cases of variceal bleeding,
give octreotide 20-50 mcg bolus followed by 25-50 mcg/hr IVI
may also reduce risk of bleeding due to nonvariceal causes19
(however NOT recommended for routine use in these
circumstances – but can be used as an adjunct in some cases)
MOA in this setting: reduces splanchnic arterial blood flow (via vasoconstriction) and portal venous
pressure (while still maintaining systemic BP and cardiac output)
26. Somatostatin Analogue
Octreotide Indications
Suspected or known variceal bleeding
controls bleeding in 74-92% cases18
comparable to injection sclerotherapy and vasopressin for
bleeding control and survival, however, with less SE18
reduces rebleeding, blood transfusion requirement and
surgery
does NOT reduce mortality significantly
(RR 0.80, 95% CI 0.63-1.01)20
27. Somatostatin Analogue
Octreotide Indications continued….
(Some) bleeding peptic ulcers18:
may be reduction in rebleeding
may be reduction in need for subsequent surgery
NO effect on mortality
NOT routinely given, consider if high risk
(to avoid the above complications)
OR delay until emergency endoscopy
28. Vasopressin Analogue
Terlipressin
Recommended Practice21:
in suspected or known cases of variceal bleeding
give 2mg bolus IV injection (2mg 6 hourly for 24 hours, then 1mg
6 hourly for 24 hours if bleeding stabilised, then stop)
34% relative risk reduction in mortality
Systematic review has shown NO difference between21:
- terlipressin and somatostatin treatment
- terlipressin and endoscopy therapy
MOA: synthetic analogue of vasopressin with fewer SE, vasoactive, specificity for splanchnic vessels causing
vasoconstriction and reduction in portal pressure
29. ‘Other’ MedicalTreatments
Antibiotics
Recommended Practice (Up to Date 2014)12:
patients with cirrhosis andUGIB (what ever the cause) –
20% will have a bacterial infection, further 50% will develop one
while in hospital (assoc HIGH mortality)
give ceftriaxone, quinolone or amoxyicillin-clavulanate
30. ‘Other’ MedicalTreatments
Evidence?
Prophylactic antibiotics in patients with cirrhosis + UGIB have
been shown to 12 :
reduce infectious complications
decreased mortality
may decrease risk of rebleeding from oesoph varices
Timing? benefits shown when given both before and after
endoscopy (before preferred)
31. ‘Other’ MedicalTreatments
Tranexamic Acid
Recommended practice (UpTo Date 2014)12 :
NO role in medical management of UGIB
Evidence?
A meta analysis of 7 RCTs found in those patients
treated with antiulcer and /or endoscopy for UGIB (the mainstay
treatment), tranexamic acid did not provide any
additional beneficial effect22
MOA: Anti fibrinolytic agent which competitively inhibits activation of plasminogen to plasmin
(plasmin degrades fibrin clots)
32. Summary
Careful history and examination important – consider source,
assess severity, identify comorbid condition, look for signs
that indicate complications
Blood transfusion for12:
• Haemodynamic instability despite crystalloid
resusc (at least 2L)
• Hb < 70 g/L in low risk patients
• Hb <90 g/L in high risk (elderly, CAD, COPD)
• Give FFP for coagulopathy (IRN>1.5, PTT 3 sec
greater then control)
• Give platelets if < 50 x109 /L or platelet
dysfunction (chronic aspirin therapy)
33. Summary
ALL patients with acute upper GI bleeding should be treated
at presentation with PPI until source of bleeding is known
Majority of existing studies use omeprazole, we SUSPECT that
other PPIs offer the same benefit (?dose ?route)
Evidence PPI in peptic ulcers (major cause of UGIB) reduces
most things (!) EXCEPT mortality
(however high risk patients may have improved mortality rates if
PPI given post endoscopy)
H2 R antagonists are no longer recommended
34. Summary
Patients who present with UGIB and have known cirrhosis
should have antibiotics before endoscopy
35. Summary
Patients with known or suspected gastro - oesophageal
variceal bleed should have:
octreotide (bolus and then IVI) PLUS antibiotics
Avoid blood transfusing to Hb>100 g/L
OR
terlipressin boluses six hourly PLUS antibiotics
*note: octreotide remains the therapy of choice18
37. References
1. Laine L, Jensen DM. Management of patients with ulcer bleeding.
Am J Gastroenterol 2012; 107:345
2. Duggan JM.Gastrointestinal hemorrhage: should we transfuse less?
Dig Dis Sci 2009; 54:1662
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