The Upper GI Bleeder
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This document discusses the management of upper gastrointestinal bleeding. It begins by outlining the goals of resuscitation, which are to provide intravascular volume resuscitation, optimize oxygen-carrying capacity, and reverse coagulopathy. It then discusses various pharmacological and procedural interventions that may be used, including proton pump inhibitors, somatostatin, vasopressin, endoscopy, and balloon tamponade. The key takeaway message is that early recognition and a multidisciplinary team approach are needed to resuscitate the patient and identify the source of bleeding in order to optimize outcomes for those experiencing an upper GI bleed.
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Upper GIT Bleeding
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1. A 32 month old male presented with a 2 day history of abdominal pain, black stools, and fresh blood in stool. Physical exam showed pallor and splenomegaly.
2. Initial workup revealed anemia and thrombocytopenia. Further imaging found portal cavernoma and esophageal varices, indicating extrahepatic portal vein obstruction.
3. The patient was stabilized and treated for upper gastrointestinal bleeding from esophageal varices caused by extrahepatic portal vein obstruction, the most common cause of variceal bleeding in older children in India. Endoscopy is the gold standard for diagnosis and management of upper GI bleeding.
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1. Upper GI bleeding is a medical emergency that requires prompt resuscitation and endoscopy within 24 hours.
2. The leading causes of upper GI bleeding vary between Sri Lanka and Western countries, with varices being much more common in Sri Lanka due to higher rates of cirrhosis.
3. Endoscopic banding is superior to sclerotherapy for treating esophageal varices, while combination medical therapy with Terlipressin and endoscopic treatment works best.
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This document discusses gastrointestinal bleeding, including defining acute upper and lower GI bleeding, assessing the severity of bleeding, determining the location of bleeding, differential diagnoses, and management approaches. It provides details on the signs and symptoms of upper and lower GI bleeding, common causes, and first aid measures. The management of GI bleeding involves assessing the patient's hemodynamic status, localizing the bleeding source, checking blood work, addressing risk factors, and stopping active bleeding while preventing recurrence.
Portal hypertension:A disease better controlled than cured.
Portal hypertension is one of the common causes of upper gastrointestinal bleeding. It is a very lethal condition. Prompt diagnosis and commencement of early medical treatment can help keeping the disease under control. Surgery is a very useful adjunct in uncontrollable bleeding and in long term prevention in certain selected cases.
Portal hypertension (1)
1) A 35-year old female presented with hematemesis and was found to have signs of portal hypertension including splenomegaly and visible veins on her abdominal wall.
2) Portal hypertension is increased blood pressure in the portal vein, usually caused by cirrhosis of the liver. It can lead to dangerous variceal bleeding from enlarged veins in the esophagus or stomach.
3) Diagnosis involves ultrasound, endoscopy, and liver tests. Treatment focuses on stabilizing any bleeding, identifying its cause via endoscopy, and managing the underlying cause of portal hypertension like cirrhosis.
Gastrointestinal bleeding
- Gastrointestinal bleeding (GIB) accounts for around 150 hospitalizations per 100,000 people annually in the United States, with upper GIB being more common than lower GIB. The incidence and mortality of GIB have decreased in recent decades primarily due to a reduction in upper GIB.
- GIB can present as overt or occult bleeding. Overt GIB involves visible bleeding while occult GIB is identified through symptoms of blood loss or anemia. GIB is also categorized by the site of bleeding as upper, lower, or obscure GIB.
- Common causes of upper GIB include peptic ulcers, Mallory-Weiss tears, esophageal varices, and hemorrhagic
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Upper GIT Bleeding
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1. A 32 month old male presented with a 2 day history of abdominal pain, black stools, and fresh blood in stool. Physical exam showed pallor and splenomegaly.
2. Initial workup revealed anemia and thrombocytopenia. Further imaging found portal cavernoma and esophageal varices, indicating extrahepatic portal vein obstruction.
3. The patient was stabilized and treated for upper gastrointestinal bleeding from esophageal varices caused by extrahepatic portal vein obstruction, the most common cause of variceal bleeding in older children in India. Endoscopy is the gold standard for diagnosis and management of upper GI bleeding.
Management of acute upper GI hemorrhage
1. Upper GI bleeding is a medical emergency that requires prompt resuscitation and endoscopy within 24 hours.
2. The leading causes of upper GI bleeding vary between Sri Lanka and Western countries, with varices being much more common in Sri Lanka due to higher rates of cirrhosis.
3. Endoscopic banding is superior to sclerotherapy for treating esophageal varices, while combination medical therapy with Terlipressin and endoscopic treatment works best.
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Author: Ms Christa Maria Joel
Supervisor: Dr Roy (Gastroenterologist)
Department of General Surgery
Father Muller Medical College
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This document discusses gastrointestinal bleeding, including defining acute upper and lower GI bleeding, assessing the severity of bleeding, determining the location of bleeding, differential diagnoses, and management approaches. It provides details on the signs and symptoms of upper and lower GI bleeding, common causes, and first aid measures. The management of GI bleeding involves assessing the patient's hemodynamic status, localizing the bleeding source, checking blood work, addressing risk factors, and stopping active bleeding while preventing recurrence.
Portal hypertension:A disease better controlled than cured.
Portal hypertension is one of the common causes of upper gastrointestinal bleeding. It is a very lethal condition. Prompt diagnosis and commencement of early medical treatment can help keeping the disease under control. Surgery is a very useful adjunct in uncontrollable bleeding and in long term prevention in certain selected cases.
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1) A 35-year old female presented with hematemesis and was found to have signs of portal hypertension including splenomegaly and visible veins on her abdominal wall.
2) Portal hypertension is increased blood pressure in the portal vein, usually caused by cirrhosis of the liver. It can lead to dangerous variceal bleeding from enlarged veins in the esophagus or stomach.
3) Diagnosis involves ultrasound, endoscopy, and liver tests. Treatment focuses on stabilizing any bleeding, identifying its cause via endoscopy, and managing the underlying cause of portal hypertension like cirrhosis.
Gastrointestinal bleeding
- Gastrointestinal bleeding (GIB) accounts for around 150 hospitalizations per 100,000 people annually in the United States, with upper GIB being more common than lower GIB. The incidence and mortality of GIB have decreased in recent decades primarily due to a reduction in upper GIB.
- GIB can present as overt or occult bleeding. Overt GIB involves visible bleeding while occult GIB is identified through symptoms of blood loss or anemia. GIB is also categorized by the site of bleeding as upper, lower, or obscure GIB.
- Common causes of upper GIB include peptic ulcers, Mallory-Weiss tears, esophageal varices, and hemorrhagic
hematemesis melena GIT bleeding egypt Draz MY
1. The document discusses gastrointestinal bleeding, describing different types including hematemesis, melena, hematochezia, occult blood, and chronic blood loss.
2. It examines causes of upper and lower GI bleeding such as peptic ulcers, varices, hemorrhoids, and tumors.
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Portal hypertension
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Management of upper gi bleed
This document summarizes the management of upper gastrointestinal bleed. It begins with two clinical scenarios of patients presenting with GI bleed and then covers the epidemiology, causes, signs and symptoms, risk scores for prognosis, and approaches to treatment. It emphasizes the importance of early endoscopy and acid suppression treatment. Medications discussed include PPIs, somatostatin analogs like octreotide, terlipressin, antibiotics and tranexamic acid which is being studied in the HALT-IT trial to reduce mortality from GI bleed. Discharge instructions include avoiding NSAIDs and treating H. pylori infection.
Portal hypertension
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Portal hypertension occurs when scar tissue from liver injuries disrupts blood flow, increasing pressure in the main and portal veins and diverting blood away from the liver. The most common cause is cirrhosis, but it can also be caused by blood clots, fatty liver disease, hepatitis, or schistosomiasis. Symptoms include gastrointestinal bleeding, abdominal fluid buildup, and varicose veins. Diagnosis involves medical history, lab tests, and imaging exams. Treatment focuses on medications and procedures to reduce blood pressure such as sclerotherapy and TIPS or DSRS shunt surgery in severe cases. Lifestyle changes like quitting drinking and smoking can help prevent portal hypertension.
Complications of cirrhosis review
This document discusses complications that can arise in patients with cirrhosis, including portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. It provides details on the pathophysiology, clinical presentation, diagnosis, and treatment of these complications. Specifically, it focuses on portal hypertension and the development of varices, describing the risks of variceal bleeding and approaches to prevention and management. It also covers ascites extensively, explaining how and why it develops in cirrhosis and its treatment with diuretics and sodium restriction.
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This document discusses the pathophysiology of upper GI bleeding. It describes how portal hypertension can lead to esophageal varices and the development of portosystemic collaterals. It also discusses how peptic ulcer disease associated with H. pylori infection can cause ulcers that weaken blood vessels and rupture. Acute stress gastritis is described as resulting from conditions that alter mucosal barriers like decreased blood flow or ischemia from shock/trauma. Mallory-Weiss tears occur when forceful vomiting causes tears in the gastric mucosa at the gastroesophageal junction.
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Portal hypertension occurs when blood pressure within the portal venous system increases. It is commonly caused by liver cirrhosis and affects 5-10% of patients in developed countries. Cirrhosis results from chronic liver damage and scarring of the liver tissue. It can be caused by alcoholism, viral hepatitis, NASH, or genetic diseases. Common signs include fatigue, abdominal pain, and jaundice. Treatment focuses on managing complications through medications, procedures like TIPS or banding of varices, and potentially liver transplantation.
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This document provides information on gastrointestinal bleeding, including:
- Causes of upper and lower GI bleeding such as peptic ulcers, varices, angiodysplasia
- Clinical presentations including hematemesis, melena, hematochezia
- Evaluations including endoscopy, angiography, CT angiography
- Anatomy of arteries supplying the GI tract including celiac, SMA, IMA
- Imaging findings of active bleeding and various pathologies
- Management of different causes such as endoscopic therapy for ulcers or TIPS procedure for variceal bleeding
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1. Ascites is an accumulation of fluid in the peritoneal cavity, most commonly caused by cirrhosis of the liver.
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3. Initial treatment involves sodium restriction, diuretics like spironolactone and furosemide, and therapeutic paracentesis if needed. Refractory ascites may require transjugular intrahepatic portosystemic shunt or liver transplantation.
Portal hypertension
This document discusses portal hypertension and its causes and complications. It defines portal hypertension as a pathological increase in portal venous pressure. Cirrhosis is a major cause of portal hypertension and can lead to complications like ascites, hepatic encephalopathy, and variceal hemorrhage. Variceal bleeding from esophageal varices is a severe complication and a common cause of death in cirrhotic patients. The document also discusses classifications of portal hypertension and different pathways for the development of portal systemic collaterals.
1. portal hypertension converted
Here are the revisions to the document:
1. Normal portal venous pressure is less than 5 mm Hg.
2. Oesophageal balloon used to achieve temporary haemostasis is Sengstaken-Blakemore tube.
3. TIPSS stands for transjugular intrahepatic portosystemic shunt.
4. Median GCS score in hepatic coma is below 8.
5. Diet recommended for hepatic coma is low in protein and sodium.
TAEM10:Upper Gi Hemorrhage Ems
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This document discusses signs and symptoms of gastrointestinal bleeding, including melena, haematemesis, and haematochezia. It covers evaluation, treatment, and management of variceal bleeding including pharmacologic therapies, endoscopic procedures like band ligation and sclerotherapy, and surgical options like shunts and transplantation.
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This document discusses oesophageal varices, which are dilated and tortuous veins in the oesophageal wall caused by increased venous pressure. Varices are prone to rupture and bleeding. The document defines portal hypertension and discusses the epidemiology, etiology, risk factors, pathophysiology, clinical manifestations, diagnostic evaluations, medical and surgical management, nursing care, and conclusions regarding oesophageal varices. It also summarizes two research articles on using capsule endoscopy to diagnose varices and using blood ammonia levels to predict variceal presence and bleeding risk.
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1. The document discusses gastrointestinal bleeding, describing different types including hematemesis, melena, hematochezia, occult blood, and chronic blood loss.
2. It examines causes of upper and lower GI bleeding such as peptic ulcers, varices, hemorrhoids, and tumors.
3. Evaluation and management are outlined, including resuscitation of hypovolemic shock, determining bleeding location, and considering high risk patients.
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Portal hypertension occurs when blood pressure increases in the portal venous system, which normally carries blood from the gastrointestinal tract to the liver. It is defined as a hepatic venous pressure gradient over 10mm Hg. There are three types - pre-hepatic, intra-hepatic, and post-hepatic - depending on the site of vascular obstruction. Common causes include cirrhosis, schistosomiasis, and portal vein thrombosis. Clinical manifestations involve complications from increased portosystemic shunting and include ascites, esophageal varices, hemorrhoids, and hepatic encephalopathy. Diagnostic evaluations involve blood tests, imaging, and endoscopy. Treatment options include medications, endoscopic therapy, TIPS procedure,
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This document summarizes the management of upper gastrointestinal bleed. It begins with two clinical scenarios of patients presenting with GI bleed and then covers the epidemiology, causes, signs and symptoms, risk scores for prognosis, and approaches to treatment. It emphasizes the importance of early endoscopy and acid suppression treatment. Medications discussed include PPIs, somatostatin analogs like octreotide, terlipressin, antibiotics and tranexamic acid which is being studied in the HALT-IT trial to reduce mortality from GI bleed. Discharge instructions include avoiding NSAIDs and treating H. pylori infection.
Portal hypertension
Portal hypertension is caused by increased vascular resistance and blood flow and can result from cirrhosis, vascular diseases, or other conditions. It leads to complications like ascites, variceal bleeding, and hepatic encephalopathy. Treatment involves general measures, variceal treatment including banding, TIPS procedure, and in some cases transplantation. Ascites is treated with paracentesis and diuretics along with albumin to prevent renal failure.
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Portal Hypertension
Portal hypertension occurs when scar tissue from liver injuries disrupts blood flow, increasing pressure in the main and portal veins and diverting blood away from the liver. The most common cause is cirrhosis, but it can also be caused by blood clots, fatty liver disease, hepatitis, or schistosomiasis. Symptoms include gastrointestinal bleeding, abdominal fluid buildup, and varicose veins. Diagnosis involves medical history, lab tests, and imaging exams. Treatment focuses on medications and procedures to reduce blood pressure such as sclerotherapy and TIPS or DSRS shunt surgery in severe cases. Lifestyle changes like quitting drinking and smoking can help prevent portal hypertension.
Complications of cirrhosis review
This document discusses complications that can arise in patients with cirrhosis, including portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. It provides details on the pathophysiology, clinical presentation, diagnosis, and treatment of these complications. Specifically, it focuses on portal hypertension and the development of varices, describing the risks of variceal bleeding and approaches to prevention and management. It also covers ascites extensively, explaining how and why it develops in cirrhosis and its treatment with diuretics and sodium restriction.
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Portal hypertension syndrome is characterized by increased pressure in the portal vein system due to obstructed blood flow out of the liver. The causes of obstructed blood flow can be divided into intrahepatic, subhepatic, and prehepatic blocks. Clinical features include collateral vein circulation around the liver, ascites, and splenomegaly. Ascites and hepatic encephalopathy are also signs of hepatocellular failure, where all liver functions are disrupted. Cholestasis syndrome results from obstructed bile flow and causes jaundice, itching, and fat malabsorption.
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This document discusses the pathophysiology of upper GI bleeding. It describes how portal hypertension can lead to esophageal varices and the development of portosystemic collaterals. It also discusses how peptic ulcer disease associated with H. pylori infection can cause ulcers that weaken blood vessels and rupture. Acute stress gastritis is described as resulting from conditions that alter mucosal barriers like decreased blood flow or ischemia from shock/trauma. Mallory-Weiss tears occur when forceful vomiting causes tears in the gastric mucosa at the gastroesophageal junction.
Gi bleeding presentation
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This document provides information on gastrointestinal bleeding, including:
- Causes of upper and lower GI bleeding such as peptic ulcers, varices, angiodysplasia
- Clinical presentations including hematemesis, melena, hematochezia
- Evaluations including endoscopy, angiography, CT angiography
- Anatomy of arteries supplying the GI tract including celiac, SMA, IMA
- Imaging findings of active bleeding and various pathologies
- Management of different causes such as endoscopic therapy for ulcers or TIPS procedure for variceal bleeding
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Portal hypertension is elevation of portal venous pressure
above 10-12 mm Hg (normal 5-10 mm Hg). Portal
hypertension results from (a) increased resistance to portal
blood flow and (b) high portal blood flow.
Ascites by_ Dr Mohammed Hussien
1. Ascites is an accumulation of fluid in the peritoneal cavity, most commonly caused by cirrhosis of the liver.
2. Diagnosis involves physical exam findings, ultrasound imaging, and analysis of ascitic fluid. A serum ascites albumin gradient (SAAG) can help determine if ascites is caused by portal hypertension.
3. Initial treatment involves sodium restriction, diuretics like spironolactone and furosemide, and therapeutic paracentesis if needed. Refractory ascites may require transjugular intrahepatic portosystemic shunt or liver transplantation.
Portal hypertension
This document discusses portal hypertension and its causes and complications. It defines portal hypertension as a pathological increase in portal venous pressure. Cirrhosis is a major cause of portal hypertension and can lead to complications like ascites, hepatic encephalopathy, and variceal hemorrhage. Variceal bleeding from esophageal varices is a severe complication and a common cause of death in cirrhotic patients. The document also discusses classifications of portal hypertension and different pathways for the development of portal systemic collaterals.
1. portal hypertension converted
Here are the revisions to the document:
1. Normal portal venous pressure is less than 5 mm Hg.
2. Oesophageal balloon used to achieve temporary haemostasis is Sengstaken-Blakemore tube.
3. TIPSS stands for transjugular intrahepatic portosystemic shunt.
4. Median GCS score in hepatic coma is below 8.
5. Diet recommended for hepatic coma is low in protein and sodium.
TAEM10:Upper Gi Hemorrhage Ems
This document summarizes the management of upper gastrointestinal hemorrhage. It discusses risk stratification tools like the Rockall score to determine a patient's risk level. For low risk patients, outpatient care may be appropriate. It also reviews the causes, evaluation, and endoscopic and pharmacologic treatment approaches for acute non-variceal and variceal bleeding.
Upper GI bleeding & portal hypertension in Children
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This document discusses oesophageal varices, which are dilated and tortuous veins in the oesophageal wall caused by increased venous pressure. Varices are prone to rupture and bleeding. The document defines portal hypertension and discusses the epidemiology, etiology, risk factors, pathophysiology, clinical manifestations, diagnostic evaluations, medical and surgical management, nursing care, and conclusions regarding oesophageal varices. It also summarizes two research articles on using capsule endoscopy to diagnose varices and using blood ammonia levels to predict variceal presence and bleeding risk.
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- Abdominal xray (pneumatosis intestinalis - malrotation)
- Rectal exam, CBC, imaging (intussusception)
- Scrotal exam (testicular torsion)
- Urinalysis (renal calculi)
- Blood
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This document discusses how to assess and describe rashes, including key factors in the patient history and physical exam. It provides case studies on common rashes such as measles, chickenpox, meningococcal disease, and anaphylaxis. The document emphasizes that most rashes are not serious but can be anxiety-provoking. It provides tips on characterizing rashes and determining when isolation may be necessary. Treatment is often supportive with focus on identifying any infectious causes or allergic reactions.
Mental health in the Emergency Department
This document provides information on managing mental health patients in the emergency department. It outlines the psychiatric resources available, the ED's role in stabilization and assessment, how to conduct a brief mental status exam, evaluate for medical causes, manage common disorders like depression and psychosis, and handle suicidal patients. Key aspects of care include ensuring safety, conducting a thorough assessment, ruling out medical causes, providing support and determining an appropriate disposition.
Emergency Nursing of the Obese Patient
The document discusses emergency nursing considerations for obese patients. It covers key topics such as:
- The pathophysiological effects of obesity including impacts to the cardiovascular, respiratory, gastrointestinal and other body systems.
- Critical care management challenges such as difficult intubation, ventilation needs, positioning patients, and vascular access.
- Trauma management implications like atypical injury patterns, assessment difficulties, and hemorrhage risk.
- Pharmacological considerations as obese patients often require different drug dosing than non-obese patients.
The document emphasizes preparing for the unique needs of obese emergency patients, such as having proper equipment available and prioritizing staff safety during patient handling and transport.
Street Drug Update 2013
This document discusses various street drugs presenting to emergency departments, including synthetic cannabinoids, designer amphetamines, and prescription drug abuse. It provides three case studies of patients presenting after using synthetic cannabinoids, mephedrone, and excessive nurofen plus abuse. For each drug, it covers symptoms, management in the emergency department, and complications. The key messages are that street drugs are continually evolving but present similar management challenges, and to consider medical causes for any unexpected presentations.
Time Critical Procedures Part 2
This document discusses several time-critical procedures for trauma patients including emergency resuscitative thoracotomy, pericardial tamponade, tension pneumothorax, and peri-mortem c-section. It provides indications, contraindications, techniques, and outcomes for each procedure. Case studies are presented and steps for performing the procedures like opening the chest and internal cardiac compressions are outlined. Key signs and treatments for conditions like tension pneumothorax are also reviewed. The importance of having the right equipment and team support for complex, life-saving procedures is emphasized.
Time Critical Procedures Part 1
This document discusses various time-critical procedures that may need to be performed in emergency situations. It provides guidance on being cognitively and materially prepared to perform these procedures. Specific procedures covered include intraosseous access, fasciotomy for compartment syndrome, lateral canthotomy for orbital compartment syndrome, and escharotomy for severe circumferential burns. Case examples are also provided to demonstrate how to apply these procedures.
Can Social Media/FOAM Influence Nursing Education?
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Resuscitating the Hypotensive Patient
This document discusses the resuscitation of hypotensive patients through fluid resuscitation and vasoactive medications. It defines shock, outlines the epidemiology and diagnosis of shock, and explains how to assess shocked patients both physically and through laboratory tests like lactate levels. Fluid resuscitation is presented as the initial treatment, followed by vasoactive agents if fluids fail to improve the patient's condition. Examples of inotropes, vasopressors, and push dose pressors are provided, along with their indications and mechanisms of action. Finally, case studies demonstrate the application of specific vasoactive medications in anaphylaxis, sepsis, post-intubation hypotension, and cardiogenic shock.
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This document provides checklists for responding to common ventilator alarms and troubleshooting a crashing ventilated patient. For high airway pressures, possible causes include a tube in the right main bronchus, bronchospasm, mucous plugs, and pneumothorax. For low minute volumes, possible causes are an endotracheal tube cuff deflation allowing an air leak or chest wounds allowing air to escape. The checklist for a crashing ventilated patient follows the acronym D.O.P.E.S. to identify potential problems, then D.O.T.T.S. to address them, such as checking tube position or ventilator settings.
Triage basics
Presentation on the basics of Triage for the Emergency Nurse working in Australian Emergency Department.
Medico-Legal Issues at Triage
This document discusses several important medico-legal issues that triage nurses need to be aware of, including: obtaining informed consent, duty of care, negligence, documentation, confidentiality, and preserving forensic evidence. The triage nurse must be knowledgeable, skilled, educated, professional and accountable. They use tools like the Australasian Triage Scale, physiological discriminators, and local policies/protocols. Triage involves assessing patients in a chaotic environment with many factors that can increase risk. Proper documentation, obtaining consent, maintaining confidentiality and adhering to the standard of care are important to avoid legal issues like charges of negligence or battery.
Managing Spider Bites in the ED
Redback spiders are the most common cause of spider envenomation in Australia, resulting in 5-10,000 bites per year. While the symptoms can be distressing, including inconsolable crying in children and priapism, redback bites are rarely life-threatening. Funnel-web spiders are the most dangerous spiders in Australia; their bites can cause symptoms ranging from local pain and swelling to autonomic effects like sweating and vomiting as well as cardiac or neurological issues. While white-tailed spider bites are often blamed, the venom has not been proven to cause tissue necrosis. Most spider bites result in only localized symptoms, but funnel-web bites require antivenom treatment in the emergency department.
Snake Bite Management for the ED Nurse
This document provides guidance for emergency department nurses on snake bite management in Australia. It discusses the most common poisonous snakes found in Australia and their characteristic clinical envenoming syndromes. It emphasizes the importance of a thorough risk assessment, physical exam, and investigations to determine if envenoming has occurred. The document also reviews pressure immobilization bandaging techniques, indications for antivenom administration, and supportive care for the different clinical envenoming syndromes caused by Australia's major snake groups: brown snakes, tiger snakes, mulga/black snakes, taipans, and death adders.
The Four-Hour Rule- Lesson's Learnt from the WA Experience
The document discusses the four-hour rule implemented in Western Australian tertiary public hospitals in 2009. It aimed to improve patient flow and quality of care by requiring all patients be admitted, discharged or transferred within four hours of presenting to the emergency department. Initial targets were set at 85% by 2010 and 95% by 2011. While the rule has helped reduce overcrowding and access block, ongoing challenges include increasing patient presentations and acuity without a rise in hospital beds. Lessons learned indicate factors like patient navigators and assessment units help flow, while issues like isolation rooms, paperwork and ramping impede it. Sustainability remains a challenge moving forward.
Best Practice in Sepsis
Sepsis is a life-threatening condition that occurs when a localized infection spreads through the bloodstream, producing an uncontrolled immune response. It is a major public health problem associated with high mortality. Early recognition, screening, and time-critical treatment are important to combat sepsis but are often lacking. The document outlines interventions for septic patients including administering oxygen, collecting blood cultures, giving IV antibiotics and fluids, monitoring lactate levels and urine output. It discusses approaches to respiratory support, fluid resuscitation, vasopressors and inotropes, appropriate antibiotic selection, source control and supportive care.
Foam in review
FOAMed in 2012 focused on airway management, checklists, and optimizing resuscitation room performance. Key topics included new airway devices, using checklists to guide procedures like intubation, and approaches like the "Vortex" to manage difficult airways. FOAMed resources highlighted evidence-based practices and innovative techniques to improve patient care and guide the future of emergency medicine.
Excited delirium syndrome
This document describes a case of excited delirium syndrome (EDS) and provides information about the condition. A man experiencing EDS required 6 people to restrain him and was unresponsive to sedation. He later went into asystole and died despite resuscitation efforts. EDS is characterized by acute agitation, exceptional strength, and hyperthermia. It can be triggered by drug use or mental illness and often involves interactions with law enforcement. Rapid sedation is critical to changing the downward trajectory and preventing fatal complications like cardiac arrest.
Resuscitating the injured brain
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Post Cardiac Arrest Syndrome
1) Therapeutic hypothermia, early defibrillation, and high-quality chest compressions are the three evidence-based approaches that help cardiac arrest patients.
2) The case study describes a 68-year-old man who suffered cardiac arrest but achieved return of spontaneous circulation. He was treated with therapeutic hypothermia, circulatory support, and taken for cardiac catheterization, resulting in successful recovery.
3) Therapeutic hypothermia aims to reduce reperfusion injury and improves outcomes after cardiac arrest by slowing the pathological cascade through induced hypothermia between 32-34°C for 12-24 hours.
Post Intubation Care
(1) Post intubation care is crucial for critically ill patients in the ED. (2) Proper ventilator settings including low tidal volumes and PEEP can prevent ventilator induced lung injury. (3) Preventing ventilator associated pneumonia requires keeping the head of the bed elevated, maintaining proper cuff pressure, and using chlorhexidine mouthwash. (4) Adequate sedation and analgesia is important to prevent stress responses and immunosuppression in intubated patients.
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Physiology of Chemical Sensation of smell.pdf
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
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Physiology of Special Chemical Sensation of Taste
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
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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
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The Electrocardiogram - Physiologic Principles
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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The Upper GI Bleeder
- 1. The Upper GI Bleeder By Kane Guthrie FCENA
- 2. Upper GI Bleeds • • • • Understand the causes Goals of resuscitation Pharmacological resuscitation Procedural resuscitation
- 3. Upper GI Bleeds in ED • • • • • Its challenging Effective Mx = good PT outcomes Underlying comorbidities ∧ complexities Team approach Pharmacology & procedural approach
- 4. Upper Vs Lower • Consider upper first – More life threatening • Haematemisis = Upper GI source • Bright red blood not always = LOWER GI
- 5. Case Study • 52 Male • Chronic ETOH abuse • Known varices C/O – Vomiting blood post binge
- 6. What to Look for!
- 7. His Vitals
- 8. The Upper GI Bleeder Multi Team Approach: • ED, ICU – resuscitate • Gastro – scope • Interventional Radiologist – therapeutic Ix • Surgeons – surgical intervention
- 9. The Source • • • • • Duodenal ulcers- 28% Gastric ulcers- 26% Gastritis- 13% Varices - 12% Esophagitis - 8% • “Massive GI Bleed Mortality rate 20-39%”
- 10. The DDx! • Intranasal • Intrapulmonary
- 11. Remember! Early Intervention can mean difference between Life & Death
- 12. The 3 Goals of Resuscitation 1 Provide Intravascular Volume Resuscitation 2 Optimise Oxygen-Carrying Capacity 3 Reverse Coagulopathy
- 13. Initial Resuscitating • • • • • • Start with ABCDE x2 Large bore IVC – Bloods Full monitoring Get specialties involved Arrange blood products Consider limitations of care!
- 14. Intravascular Volume Resuscitation • Limit crystalloid fluid –to early phase Prepare for transfusion: • HB <80 • Coagulopathy • Persistent hypotension
- 15. Intravascular Volume Resuscitation • • • • PRBC’s not enough Replace clotting factors Consider massive transfusion protocol “PRBC:FFP:platelet ratio 1:1:1” • Tranexamic Acid?
- 16. Optimise Oxygenation Signs of decreased O2 delivery: – Decreased LOC – Evidence of cardiac ischaemia – Increased lactate – Cold peripheries
- 17. Optimise Oxygenation • Give blood so oxygen can get to the tissue Initially: – Provide High Flow 02 Crashing: • Intubate early Stablised: • Titrate oxygen to need • Considered humidified
- 18. Intubating Isn’t Easy! 1. 2. 3. 4. 5. 6. 7. Intubate early Empty stomach (NGT) Intubate with HOB at 45° Preoxygenation Limit BVM Use experience Prepare for vomit
- 20. Reverse Coagulopathy • Tailor to etiology. Causes: • Anticoagulation • Shock – Metabolic acidosis –tissue hypoperfusion • Chronic disorders – ETOH abusers
- 21. Pharmacological Interventions • Proton Pump Inhibitors • Somatostatin • Vasopressin
- 22. Proton Pump Inhibitors • Suppress gastric acid production • Potential reduction haemorrhage during scope The evidence though:
- 23. Somatostatin • (Octreotide) Reduces: • Portal venous blood flow • Splachinic vasoconstriction =decrease GI Bleeding Use • Variceal GI bleeds • Limited evidence – low side effect profile
- 24. Vasopressin (Telipressin) • Reduces portal hypertension • Splachnic vasoconstrictor • Can cause ischaemia • Last ditch effort in bleeding varices
- 25. Antibiotics • Infection on varices – Causes bleeding • Give antibiotics (broad spectrum)
- 26. Procedural Interventions • Endoscopy • Balloon Tamponade
- 27. Endoscopy • Diagnostic & therapeutic tool Interventions: • Clips • Banding • Thermocoagulation • Sclerosant injection % adrenaline
- 30. Balloon Tamponade • Temporising rescue device Indicated: – Endoscopy not available – Endoscopy not successful • Need to secure airway prior
- 31. Questions
- 32. Take Home Points • • • • Early recognition Team approach is needed Resuscitate with blood products Advocate for early intervention