This document provides information about acute cholecystitis, cholangitis, and their management. It begins with the anatomy of the gallbladder and discusses the pathogenesis of acute cholecystitis, typically caused by gallstones obstructing the cystic duct. Signs and symptoms include right upper quadrant pain and fever. Ultrasound is often used for diagnosis. Treatment involves antibiotics, analgesia, and early cholecystectomy to remove the gallbladder. Complications of acute cholangitis from bacterial infection of the bile ducts are also reviewed.
- Viral hepatitis can present asymptomatically, symptomatically before jaundice, or progress to fulminant hepatitis or chronic hepatitis. Diagnosis involves blood tests to check liver enzymes and serology or molecular testing to determine the virus.
- Liver abscesses can be pyogenic (most common), amebic, or fungal. Amebic abscesses are caused by Entamoeba histolytica and present with fever, abdominal pain, and hepatomegaly. Pyogenic abscesses require drainage if large or not improving with antibiotics.
- Hydatid cysts are caused by the tapeworm Echinococcus granulosus. Surgical removal is usually required for large or infected cysts while
This document summarizes key information about liver abscesses, including pyogenic, amebic, and fungal types. Pyogenic liver abscess is most common, with risk factors like cirrhosis, diabetes, and biliary diseases. Organisms usually enter via the biliary tract or bloodstream. Ultrasound and CT are useful for diagnosis, showing hypoechoic or hypodense lesions. Treatment involves antibiotics, with drainage for larger abscesses. Amebic liver abscess is caused by Entamoeba histolytica and presents similarly, treated with metronidazole or other amebicides. Complications of both include rupture and spread of infection.
Aetiopathologenesis and management of acute cholecystitisCHIZOWA EZEAKU
This document summarizes the aetiopathogenesis and management of acute cholecystitis. It begins with an introduction to acute cholecystitis and its classification. It then covers the anatomy and physiology of the gallbladder. Risk factors for acute calculous and acalculous cholecystitis are discussed. The pathogenesis involves obstruction of the cystic duct by a stone leading to inflammation. Conservative management or early cholecystectomy are the main treatment options.
1. Chronic cholestasis can be caused by intrahepatic or extrahepatic conditions. Common intrahepatic causes include primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and drug-induced liver injury (DILI).
2. PBC is an autoimmune disease characterized by progressive destruction of intrahepatic bile ducts, presence of antimitochondrial antibodies (AMA), and histologic findings of florid duct lesions on liver biopsy. PBC diagnosis requires two of three criteria: cholestatic liver enzymes, AMA positivity, or liver biopsy consistent with PBC.
3. PSC is a chronic inflammatory condition of
This document defines various gallstone diseases and provides information on their risk factors, presentations, diagnoses, and treatments. It discusses the definitions of cholelithiasis, cholecystitis, choledocholithiasis, and other conditions. The risk factors include factors like female gender, obesity, and hemolytic states. Imaging studies like ultrasound and CT are used for diagnosis, and treatments involve analgesics, antibiotics, ERCP, and cholecystectomy.
The document provides tips for using a PowerPoint presentation on acute cholecystitis. It recommends:
1) Freely editing, modifying, and adding your name to slides.
2) Not worrying about number of slides, as half are blank except for titles.
3) Showing blank slides first to elicit student responses before presenting information.
4) Repeating this process of blank slide then information slide at the end for active learning.
5) Using this approach for self-study as well.
6) Checking notes for bibliography citations.
This document discusses lower gastrointestinal bleeding (LGIB), which occurs in the small and large intestines, presenting as hematochezia or melaena. Common causes of LGIB include diverticular disease, inflammatory bowel diseases like Crohn's disease and ulcerative colitis, ischemic colitis, vascular malformations, polyps, tumors, and anal issues. LGIB is typically chronic and self-limiting, though some cases are acute and require blood transfusion. The diagnostic workup depends on the patient's age and symptoms, and may involve endoscopy, imaging, or angiography to identify the source of bleeding.
pancreatitis Gi disorder diagnosis managementTHaripriya1
This document discusses acute pancreatitis, defining it as a reversible inflammation of the pancreas that ranges from mild to severe. It presents the epidemiology, signs and symptoms, investigations, management, and complications of acute pancreatitis. The most common causes are gallstones and alcohol, accounting for 80% of cases. Treatment involves supportive care, pain management, IV fluids, and identifying and treating any complications like infections. The mortality rate depends on the severity of the attack, ranging from 1% for mild cases up to 75-90% for severe pancreatitis.
- Viral hepatitis can present asymptomatically, symptomatically before jaundice, or progress to fulminant hepatitis or chronic hepatitis. Diagnosis involves blood tests to check liver enzymes and serology or molecular testing to determine the virus.
- Liver abscesses can be pyogenic (most common), amebic, or fungal. Amebic abscesses are caused by Entamoeba histolytica and present with fever, abdominal pain, and hepatomegaly. Pyogenic abscesses require drainage if large or not improving with antibiotics.
- Hydatid cysts are caused by the tapeworm Echinococcus granulosus. Surgical removal is usually required for large or infected cysts while
This document summarizes key information about liver abscesses, including pyogenic, amebic, and fungal types. Pyogenic liver abscess is most common, with risk factors like cirrhosis, diabetes, and biliary diseases. Organisms usually enter via the biliary tract or bloodstream. Ultrasound and CT are useful for diagnosis, showing hypoechoic or hypodense lesions. Treatment involves antibiotics, with drainage for larger abscesses. Amebic liver abscess is caused by Entamoeba histolytica and presents similarly, treated with metronidazole or other amebicides. Complications of both include rupture and spread of infection.
Aetiopathologenesis and management of acute cholecystitisCHIZOWA EZEAKU
This document summarizes the aetiopathogenesis and management of acute cholecystitis. It begins with an introduction to acute cholecystitis and its classification. It then covers the anatomy and physiology of the gallbladder. Risk factors for acute calculous and acalculous cholecystitis are discussed. The pathogenesis involves obstruction of the cystic duct by a stone leading to inflammation. Conservative management or early cholecystectomy are the main treatment options.
1. Chronic cholestasis can be caused by intrahepatic or extrahepatic conditions. Common intrahepatic causes include primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and drug-induced liver injury (DILI).
2. PBC is an autoimmune disease characterized by progressive destruction of intrahepatic bile ducts, presence of antimitochondrial antibodies (AMA), and histologic findings of florid duct lesions on liver biopsy. PBC diagnosis requires two of three criteria: cholestatic liver enzymes, AMA positivity, or liver biopsy consistent with PBC.
3. PSC is a chronic inflammatory condition of
This document defines various gallstone diseases and provides information on their risk factors, presentations, diagnoses, and treatments. It discusses the definitions of cholelithiasis, cholecystitis, choledocholithiasis, and other conditions. The risk factors include factors like female gender, obesity, and hemolytic states. Imaging studies like ultrasound and CT are used for diagnosis, and treatments involve analgesics, antibiotics, ERCP, and cholecystectomy.
The document provides tips for using a PowerPoint presentation on acute cholecystitis. It recommends:
1) Freely editing, modifying, and adding your name to slides.
2) Not worrying about number of slides, as half are blank except for titles.
3) Showing blank slides first to elicit student responses before presenting information.
4) Repeating this process of blank slide then information slide at the end for active learning.
5) Using this approach for self-study as well.
6) Checking notes for bibliography citations.
This document discusses lower gastrointestinal bleeding (LGIB), which occurs in the small and large intestines, presenting as hematochezia or melaena. Common causes of LGIB include diverticular disease, inflammatory bowel diseases like Crohn's disease and ulcerative colitis, ischemic colitis, vascular malformations, polyps, tumors, and anal issues. LGIB is typically chronic and self-limiting, though some cases are acute and require blood transfusion. The diagnostic workup depends on the patient's age and symptoms, and may involve endoscopy, imaging, or angiography to identify the source of bleeding.
pancreatitis Gi disorder diagnosis managementTHaripriya1
This document discusses acute pancreatitis, defining it as a reversible inflammation of the pancreas that ranges from mild to severe. It presents the epidemiology, signs and symptoms, investigations, management, and complications of acute pancreatitis. The most common causes are gallstones and alcohol, accounting for 80% of cases. Treatment involves supportive care, pain management, IV fluids, and identifying and treating any complications like infections. The mortality rate depends on the severity of the attack, ranging from 1% for mild cases up to 75-90% for severe pancreatitis.
This document discusses acute pancreatitis, defining it as a reversible inflammation of the pancreas that ranges from mild to severe. It can be caused by gallstones, alcohol use, metabolic issues, infections, drugs, trauma, and other factors. Symptoms include severe abdominal pain that may radiate to the back. Investigations include blood tests of amylase, lipase, and other enzymes. Treatment focuses on supportive care, pain management, and identifying/treating any complications like infections. The mortality rate ranges from 1% for mild cases to 15-20% overall.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
The document describes the pancreas, pancreatitis, and pancreatic tumors. It discusses the anatomy and function of the pancreas, including that it produces digestive enzymes and hormones. Pancreatitis can be acute or chronic and is defined as inflammation of the pancreas. Acute pancreatitis causes severe abdominal pain and its severity ranges from mild to severe based on organ dysfunction. Chronic pancreatitis is progressive destruction of the pancreas due to recurrent inflammation, causing severe pain and pancreatic insufficiency over time. The document also outlines evaluation and management of pancreatic disorders.
Disorders of the gallbladder and biliary tract include gallstones, cholecystitis, cholangitis, and cancer. Gallstones are usually cholesterol stones in Western countries and pigment stones in Asia. Risk factors for cholesterol stones include age, female sex, obesity, and genetics. Cholecystitis occurs due to gallstone obstruction and inflammation. Obstructive lesions can cause cholangitis and secondary biliary cirrhosis. Biliary atresia is a neonatal condition requiring transplantation. Gallbladder and cholangiocarcinomas are associated with gallstones and inflammation.
Ultrasound is useful for evaluating the pancreas and detecting complications of acute and chronic pancreatitis. In acute pancreatitis, ultrasound can identify changes in the pancreas such as areas of hypoechogenicity and peripancreatic inflammation. Complications like pseudocysts and vascular thromboses are also detectable. Chronic pancreatitis is characterized on ultrasound by ductal dilatation, calcifications, and changes in pancreatic echotexture. Differentiating chronic pancreatitis from pancreatic cancer can be challenging. CT or MRI may be needed when ultrasound findings are inconclusive or to further evaluate necrosis in acute pancreatitis.
This document discusses the anatomy, physiology, diagnostic studies, diseases, and surgical procedures related to the gallbladder and extrahepatic biliary system. Key points include:
- The gallbladder is a pear-shaped sac located in the liver that stores and concentrates bile. Bile is produced by the liver and aids in fat digestion.
- Gallstones are a common problem, forming when bile becomes supersaturated, and can cause conditions like cholecystitis. Surgical interventions include cholecystectomy.
- Other issues discussed include bile duct injuries, tumors, and abnormalities like sclerosing cholangitis. A variety of imaging studies and endoscopic procedures are used for diagnosis and treatment.
The document discusses disorders of the gallbladder and extrahepatic bile ducts. It covers topics like cholelithiasis (gallstones), cholecystitis (gallbladder inflammation), choledocholithiasis (bile duct stones), cholangitis (bile duct inflammation), biliary cirrhosis, biliary atresia, gallbladder and bile duct cancers. The major points are that gallstones are a common cause of gallbladder disease in Western countries. Inflammation of the gallbladder or bile ducts can occur due to stone obstruction or infection and may lead to complications like sepsis. Biliary cirrhosis can develop from longstanding bile duct obstruction. Biliary atresia is a
The document discusses various disorders of the gallbladder and bile ducts. It describes that over 95% of biliary tract diseases are due to cholelithiasis (gallstones), which can be either cholesterol stones or pigment stones. Cholecystitis, an inflammation of the gallbladder, can be acute or chronic and is usually caused by gallstones blocking the cystic duct. Other complications of gallbladder disorders include cholangitis, an inflammation of the bile ducts, and secondary biliary cirrhosis from long-term bile duct obstruction.
The document discusses disorders of the gallbladder and extrahepatic bile ducts. It covers topics like cholelithiasis (gallstones), cholecystitis (gallbladder inflammation), choledocholithiasis (bile duct stones), cholangitis (bile duct inflammation), biliary cirrhosis, biliary atresia, gallbladder and bile duct cancers. Risk factors, pathogenesis, clinical features, and pathology of these conditions are described in detail. Surgical treatment options are also mentioned.
Acute pancreatitis has an annual incidence of 9.8 per 100,000 people and is most commonly caused by gallstones or alcohol abuse. It involves premature activation of pancreatic enzymes within the pancreas leading to autodigestion. A history, physical exam, serum amylase and lipase levels, and imaging can establish the diagnosis. Severity is assessed using Ranson's criteria, CT severity index, or APACHE II score. Mild cases are treated with bowel rest and IV fluids while severe cases require intensive care monitoring and organ support. Complications include pancreatic necrosis, pseudocysts, abscesses, and systemic complications like respiratory failure and shock.
This document discusses portal hypertension and variceal bleeding. It begins by describing portal hemodynamics and defining clinically significant portal hypertension as a hepatic venous pressure gradient (HVPG) greater than 10-12 mm Hg.
The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
Complications of portal hypertension include variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. Investigations for diagnosis include ultrasound Doppler,
This document provides an overview of acute pancreatitis, including its definition, epidemiology, etiology, pathophysiology, clinical features, investigations, and assessment of disease severity. Acute pancreatitis is defined as acute inflammation and autodigestion of the pancreas presenting with abdominal pain and elevated pancreatic enzymes. Gallstones and alcohol abuse are the most common causes. Clinical features include epigastric pain radiating to the back. Investigations include serum amylase, lipase, imaging like CT scan. Disease severity is assessed using criteria like Ranson score, APACHE II score, CT severity index, and Atlanta criteria.
The document discusses diseases of the gallbladder and biliary tree. It describes the anatomy and physiology of the gallbladder and discusses conditions like gallstones, acute cholecystitis, and obstructive jaundice. Gallstones are the most common pathology of the biliary tract and can cause complications within the gallbladder or bile ducts. Acute cholecystitis is an inflammation of the gallbladder usually due to a gallstone obstructing the cystic duct. Obstructive jaundice is caused by an obstruction of the biliary tree above the entry of the pancreatic duct and results in a yellowish discoloration of skin and eyes.
etiology ,classifications of gall stones & causes,risk factors,presentations, clinical examinations ,investigations including radiological (role of ERCP and MRCP ) and serological ,treatment including surgical and non surgical ,post cholecystectomy syndrome and its management ,Iindicatrions for cholecystectomy and cholecystotomy & when to perform ,complications of gall stones ,preventions of gall stone disease
gall stone disease, etiology , pathogenesis , risk factors ,types of gall stones,clinical feature, diagnosis , medical and surgical treatment of gall stones , prevention of gall stones
Cholecystitis & carcinoma of gallbladder Baiti Basheer
This document discusses cholecystitis and carcinoma of the gallbladder. It defines cholecystitis as inflammation of the gallbladder and classifies it as acute or chronic. Acute cholecystitis is further divided into calculous (caused by gallstones) and acalculous (not caused by stones). Carcinoma of the gallbladder is associated with chronic inflammation from gallstones and has a poor prognosis, as it is often diagnosed at late stages when treatment is unlikely to cure it.
Biliary system disease2023kgadeejanofal.pptxkhadeejanofal
Acute cholecystitis refers to inflammation of the gallbladder, usually caused by gallstones blocking the cystic duct. Key symptoms include right upper quadrant pain that may radiate to the shoulder, fever, nausea, and Murphy's sign on examination. Ultrasound is usually the first imaging test, showing thickened gallbladder walls and stones. Treatment involves antibiotics, nil by mouth, and urgent cholecystectomy to remove the gallbladder within 72 hours of symptoms onset. Complications can include sepsis, empyema, or gallbladder perforation if not treated promptly.
This document discusses gallstone disease and provides definitions and details regarding epidemiology, risk factors, symptoms, diagnosis, and treatment options. It covers conditions such as cholelithiasis, cholecystitis, cholangitis, choledocholithiasis, and gallstone pancreatitis. Complications are outlined including acute cholecystitis, acute cholangitis, and gallstone pancreatitis. Diagnostic tools such as ultrasound and MRCP are mentioned. Management depends on the condition but may involve antibiotics, drainage procedures, ERCP, or cholecystectomy.
This document discusses neurologic diseases in HIV-infected individuals, focusing on Toxoplasmosis and Cryptococcosis. It covers the epidemiology, clinical presentation, diagnosis, treatment and prevention of these two opportunistic infections. Toxoplasmosis commonly causes focal brain lesions that enhance with contrast. Cryptococcosis typically presents as subacute meningitis with fever and headache. Both require prolonged antifungal therapy and secondary prophylaxis to prevent recurrence in those with advanced HIV infection.
This document provides an overview of spinal cord diseases. It begins with an introduction noting that spinal cord diseases can cause paralysis and sensory deficits due to the concentration of motor and sensory pathways in the spinal cord. Many diseases are reversible if recognized early, making them neurologic emergencies. The document then covers the approach to localizing spinal cord lesions based on anatomy and symptoms, different patterns of lesions, distinguishing features of various lesions and diseases, and key details about specific compressive and non-compressive myelopathies.
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This document discusses acute pancreatitis, defining it as a reversible inflammation of the pancreas that ranges from mild to severe. It can be caused by gallstones, alcohol use, metabolic issues, infections, drugs, trauma, and other factors. Symptoms include severe abdominal pain that may radiate to the back. Investigations include blood tests of amylase, lipase, and other enzymes. Treatment focuses on supportive care, pain management, and identifying/treating any complications like infections. The mortality rate ranges from 1% for mild cases to 15-20% overall.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
The document describes the pancreas, pancreatitis, and pancreatic tumors. It discusses the anatomy and function of the pancreas, including that it produces digestive enzymes and hormones. Pancreatitis can be acute or chronic and is defined as inflammation of the pancreas. Acute pancreatitis causes severe abdominal pain and its severity ranges from mild to severe based on organ dysfunction. Chronic pancreatitis is progressive destruction of the pancreas due to recurrent inflammation, causing severe pain and pancreatic insufficiency over time. The document also outlines evaluation and management of pancreatic disorders.
Disorders of the gallbladder and biliary tract include gallstones, cholecystitis, cholangitis, and cancer. Gallstones are usually cholesterol stones in Western countries and pigment stones in Asia. Risk factors for cholesterol stones include age, female sex, obesity, and genetics. Cholecystitis occurs due to gallstone obstruction and inflammation. Obstructive lesions can cause cholangitis and secondary biliary cirrhosis. Biliary atresia is a neonatal condition requiring transplantation. Gallbladder and cholangiocarcinomas are associated with gallstones and inflammation.
Ultrasound is useful for evaluating the pancreas and detecting complications of acute and chronic pancreatitis. In acute pancreatitis, ultrasound can identify changes in the pancreas such as areas of hypoechogenicity and peripancreatic inflammation. Complications like pseudocysts and vascular thromboses are also detectable. Chronic pancreatitis is characterized on ultrasound by ductal dilatation, calcifications, and changes in pancreatic echotexture. Differentiating chronic pancreatitis from pancreatic cancer can be challenging. CT or MRI may be needed when ultrasound findings are inconclusive or to further evaluate necrosis in acute pancreatitis.
This document discusses the anatomy, physiology, diagnostic studies, diseases, and surgical procedures related to the gallbladder and extrahepatic biliary system. Key points include:
- The gallbladder is a pear-shaped sac located in the liver that stores and concentrates bile. Bile is produced by the liver and aids in fat digestion.
- Gallstones are a common problem, forming when bile becomes supersaturated, and can cause conditions like cholecystitis. Surgical interventions include cholecystectomy.
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The document discusses disorders of the gallbladder and extrahepatic bile ducts. It covers topics like cholelithiasis (gallstones), cholecystitis (gallbladder inflammation), choledocholithiasis (bile duct stones), cholangitis (bile duct inflammation), biliary cirrhosis, biliary atresia, gallbladder and bile duct cancers. The major points are that gallstones are a common cause of gallbladder disease in Western countries. Inflammation of the gallbladder or bile ducts can occur due to stone obstruction or infection and may lead to complications like sepsis. Biliary cirrhosis can develop from longstanding bile duct obstruction. Biliary atresia is a
The document discusses various disorders of the gallbladder and bile ducts. It describes that over 95% of biliary tract diseases are due to cholelithiasis (gallstones), which can be either cholesterol stones or pigment stones. Cholecystitis, an inflammation of the gallbladder, can be acute or chronic and is usually caused by gallstones blocking the cystic duct. Other complications of gallbladder disorders include cholangitis, an inflammation of the bile ducts, and secondary biliary cirrhosis from long-term bile duct obstruction.
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Acute pancreatitis has an annual incidence of 9.8 per 100,000 people and is most commonly caused by gallstones or alcohol abuse. It involves premature activation of pancreatic enzymes within the pancreas leading to autodigestion. A history, physical exam, serum amylase and lipase levels, and imaging can establish the diagnosis. Severity is assessed using Ranson's criteria, CT severity index, or APACHE II score. Mild cases are treated with bowel rest and IV fluids while severe cases require intensive care monitoring and organ support. Complications include pancreatic necrosis, pseudocysts, abscesses, and systemic complications like respiratory failure and shock.
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The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
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This document discusses cholecystitis and carcinoma of the gallbladder. It defines cholecystitis as inflammation of the gallbladder and classifies it as acute or chronic. Acute cholecystitis is further divided into calculous (caused by gallstones) and acalculous (not caused by stones). Carcinoma of the gallbladder is associated with chronic inflammation from gallstones and has a poor prognosis, as it is often diagnosed at late stages when treatment is unlikely to cure it.
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Acute cholecystitis refers to inflammation of the gallbladder, usually caused by gallstones blocking the cystic duct. Key symptoms include right upper quadrant pain that may radiate to the shoulder, fever, nausea, and Murphy's sign on examination. Ultrasound is usually the first imaging test, showing thickened gallbladder walls and stones. Treatment involves antibiotics, nil by mouth, and urgent cholecystectomy to remove the gallbladder within 72 hours of symptoms onset. Complications can include sepsis, empyema, or gallbladder perforation if not treated promptly.
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Recurrent ARF: 2 major or 1 major plus 2 minor or 3
minor manifestations PLUS evidence of recent strep
No ARF: No criteria met
Management of ARF
Management of ARF
1. Treatment of acute attack:
- Bed rest
- Salicylates (Aspirin)
- Antibiotics (Penicillin) if carditis
- Corticosteroids for severe carditis
2. Secondary prophylaxis:
- Benzathine penicillin G every 4 weeks lifelong
- Or
The document provides information on chronic obstructive pulmonary disease (COPD), including its definition, epidemiology, risk factors, pathogenesis, clinical manifestations, diagnosis, screening tools, management, and preventive strategies. It describes COPD as a common lung disease characterized by persistent respiratory symptoms and airway limitation usually caused by significant exposure to noxious particles or gases like smoke. The summary discusses COPD's prevalence, risk factors like smoking and indoor air pollution, methods of diagnosis including spirometry, and approaches to management such as reducing exacerbations and risk factors.
This document provides definitions and information about diabetes mellitus. It begins by defining diabetes as a metabolic disorder characterized by chronic hyperglycemia according to the WHO. Diagnosis is made through laboratory tests measuring blood glucose or glycosylated hemoglobin levels. The diagnostic criteria for diabetes and prediabetes are outlined. The document then discusses the global, regional, and national epidemiology of diabetes, noting its increasing prevalence worldwide and the large number of people affected. It identifies factors contributing to the rise in diabetes cases and explains strategies for screening and preventing the disease.
Unit 7_Hypertension in Special Groups.pptxImanuIliyas
This document discusses hypertension in special groups. It begins by outlining objectives to identify special groups with hypertension and appropriate management strategies. It then discusses hypertension among groups such as those with diabetes, chronic kidney disease, pregnant women, HIV/AIDS patients, the elderly, and children. For each group, it provides considerations for evaluating and managing their hypertension. It also includes case studies and classifications to illustrate approaches to hypertension in pregnancy.
This document discusses complications of hypertension, including their mechanisms and management. It describes how high blood pressure can lead to left ventricular hypertrophy and atherosclerosis over time. Major complications discussed include heart failure, stroke, kidney failure, coronary artery disease/heart attack, and peripheral vascular disease. For each complication, key signs and symptoms are outlined as well as recommended actions like referral protocols. The document emphasizes preventing complications through proper treatment and control of hypertension and associated risk factors like diabetes and dyslipidemia.
Unit 2_Classif and Pathoge. of DM2.pptxImanuIliyas
This document provides an overview of the classification and pathogenesis of diabetes mellitus. It begins by outlining the learning objectives, which are to classify diabetes based on pathogenesis, describe the role of the endocrine pancreas in glucose homeostasis, and understand the pathogenesis of types 1 and 2 diabetes. It then discusses glucose regulation by hormones like insulin and the role of the pancreatic islets and beta cells in secreting insulin. The document classifies diabetes into four main types - type 1, type 2, gestational diabetes, and specific types - based on etiology. It provides details on the autoimmune pathogenesis of type 1 diabetes and the roles of genetic and environmental factors. For type 2 diabetes, it describes the pathogenesis as involving insulin resistance,
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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.
2. Gall bladder Anatomy
• Pear-shaped sac, 7 to 10 cm
long, 30 to 50 mL
• Differs histologically from
the rest of the GIT
( Lacks a muscularis mucosa
and submucosa.)
• Along with bile ducts, and
the sphincter of Oddi, Store
and regulate bile flow.
• Concentrate and store
hepatic bile and deliver bile
into the duodenum in
response to a meal.
2
3. • Could be:
Acute or chronic inflammation
Calculus or acalculous
• Risk factors: obstruction and bile stasis
• Bacterial growth common but secondary
3
Cholecystitis
4. Acute Cholecystitis
Pathogenesis
• Gallstones in 90% to 95% of cases.
• Obstruction of the cystic duct by a gallstone
( Only occasionally )
↓↓↓
Gallbladder distention, inflammation, and wall edema
↓↓↓
Hyperemia and patchy necrosis the mucosa
( - Ischemia and necrosis of the GB wall – 5 – 10%)
( - Gallstone is dislodged and inflammation resolves)
4
5. Pathogenesis…
When the GB remains obstructed and secondary bacterial
infection supervenes
↓↓↓
Acute gangrenous cholecystitis develops
Abscess or empyema forms within the gallbladder.
Perforation of ischemic areas (Rare)
↓↓↓
- Usually contained in the subhepatic
- Free perforation with peritonitis,
- Intrahepatic perforation with intrahepatic abscesses
- Perforation into adjacent organs (duodenum or colon)
( Cholecystoenteric Fistula)
5
6. Acute Cholecystitis: Diagnosis
History
• Compatible with chronic cholecystitis – 80%.
• Begins as an attack of biliary colic, but, more severe,
unremitting and may persist for several days.
• The pain is typically in the right upper quadrant or
epigastrium and may radiate to the right upper part of
the back or the interscapular area.
• Fever, anorexia, nausea, and vomiting
Physical Examination
• Jaundice – CBD Stones or Mirizzi’s syndrome
• Focal tenderness and guarding in the RUQ
• A mass (gallbladder and adherent Omentum), is
occasionally palpable.
• Murphy’s sign
6
7. Acute Cholecystitis: Diagnosis …
• Leukocytosis (12,000 –15,000
cells/mm3, >20,000
cells/mm3)
• Some may have a normal
WBC.
• Serum liver chemistries -
Usually normal
• Abdominal U/S
- Sensitivity and specificity of
95%.
- Presence or absence of stones,
- Thickening of the gallbladder
wall and pericholecystic fluid
- Sonographic Murphy’s sign 7
8. Acute Cholecystitis: Diagnosis …
• Elderly and diabetic patients may have a
subtle presentation
↓↓
Delay in diagnosis.
↓↓
• Increased incidence of complications
• 10-fold the mortality rate compared to that of
younger and healthier patients.
8
10. Acute Cholecystitis: Management
• IV fluids
• Antibiotics
- Cover gram-negative aerobes and anaerobes
- 3rd generation cephalosporin with good
anaerobic coverage or
- Second-generation cephalosporin combined
with metronidazole or
- Aminoglycoside with metronidazole or
- Ciprofloxacin with metronidazole
• Analgesia.
10
11. Acute Cholecystitis: Management …
• Definitive treatment – Cholecystectomy
• Timing of cholecystectomy
- Early cholecystectomy - within 2 to 3 days of
the illness Vs Interval/delayed
cholecystectomy ( 6 to 10 weeks after initial
medical treatment)
• When patients present late, or unfit for surgery,
treat with antibiotics, then cholecystectomy
scheduled for 2 months later.
11
12. Acute Cholecystitis: Management …
Fail to respond to initial medical therapy
↓↓ ↓↓
Those fit for Surgery Not fit for surgery
↓↓ ↓↓
Cholecystectomy Percut. cholecystostomy or
Open cholecystostomy (LA)
12
13. Acute Cholecystitis: Management …
After percutaneous or open cholecystostomy
↓ ↓
Failure to improve Respond after cholecystostomy
↓ ↓
Gangrene of the GB or Remove the tube after cholangiography
Perforation ↓
↓ Schedule for Cholecystectomy
Surgery is unavoidable.
• For the rare patients who can’t tolerate surgery,
the stones can be extracted via the
cholecystostomy tube before its removal
13
15. ACALCULAS CHOLECYSTITIS
pts with major abdominal & thoracic surgery & TPN
recovering from major trauma
severe burns
Acute emphysematous cholecystitis
serious form of Ac.
Characterized by gas in the lumen or wall of the GB
In the elderly pts
25% have DM
CF as AC but pts are more toxic
DX ….air in the gallbladder or wall on plain abdominal
Film
15
16. INVESTIGATION AND DIAGNOSIS
1. History & P/E
2. Standard base line investigation
- CBC
- LFT
-Serum Amylase ….. Acute pancreatitis
- Blood culture
3. Plain radiography
- 10% of GS are radio opaque
-not routinely indicated
-in acutely ill pts to R/O perforated viscus
- Gas in the GB or BD
16
17. 4. ULTRASOUND
primary screening
procedure
can show us….
Calculi with acoustic
shadow
thickened wall ,
distension of GB
localized pericholecystic
collection
dilated CBD
17
18. 5. Oral cholecystography (OCG)
- replaced by U/S
- used to assess GB function
6. IV cholangiography
-to see extrahepatic biliary tree
-effective in jaundiced pts.
7. CT & MRI
- to R/O pancreatic head tumour
8. Scintography … to Dx acute cholecystitis
18
19. 9. PTC & ERCP
- in pts with comp. acute biliary dd. & jaundice
- clotting studies before PTC
- prophylactic antibiotics
indicated in pts.
- Known GBS with increased bilirubin >10 mg/dl
- Symptomatic pts with previous cholecystectomy
- Pts with biliary Sx & inconclusive evidence
19
20. Acute Cholangitis
• Bacterial infection superimposed on an obstruction
of the biliary tree
• Most commonly from a gallstone, but it may be
associated with neoplasm or stricture.
• Biliary tract obstruction Elevated intraluminal
pressure Infection of bile
• Bacteria gain access to the biliary tree by retrograde
ascent from the duodenum or from portal venous
blood.
• Primary sclerosing cholangitis
- inflammation and fibrosis of the intrahepatic and
extrahepatic bile ducts (Autoimmune mechanism).
20
21. • The most common pathogens isolated in blood
cultures
• E coli (59%),
• Klebsiella species (16%),
• Pseudomonas aeruginosa (5%),
• Enterococcus species (4%).
21
22. • Ranges from mild symptoms to fulminant
overwhelming sepsis.
• History of abdominal pain or symptoms of
gallbladder colic before
• Charcot's Triad consists of fever, RUQ pain, and
jaundice.
• Reynolds Pentad - Charcot's triad + ( Mental status
changes and sepsis )
• Previous history of diagnosed Gallstones, CBD
stones
• History of Recent cholecystectomy
• Endoscopic manipulation or ERCP, cholangiogram 22
23. • CBC: Leukocytosis, 79% had a WBC greater than
10,000/mL,
• Electrolyte panel with renal function.
• Calcium level is necessary to check if pancreatitis
• LFT- Hyperbilirubinemia and increased ALP
• PT, PTT – Sepsis related DIC
• Pancreatic enzymes - elevations suggest bile duct
stones caused the cholangitis, with or without
gallstone pancreatitis.
• Biliary and blood cultures cultures
• Abdominal U/S, CT scan
23
24. 1. Medical Therapy
• Broad-spectrum IV antibiotics
• Correction of fluid and electrolyte imbalances
• Analgesics
2. Surgical Therapy - Decompression and drainage of
the biliary system.
• Endoscopic biliary drainage and decompression
• Surgical decompression – If endoscopic or
transhepatic drainage is unsuccessful or
unavailable.
24
25. Complications
• Liver failure, hepatic abscesses, and micro
abscesses
• Bacteremia (25-40%); gram-negative sepsis
• Acute renal failure
• Catheter-related problems in patients treated
with percutaneous or endoscopic drainage:
• Bleeding (intra-abdominally or percutaneously)
• Catheter-related sepsis
• Fistulae
• Bile leak (intraperitoneally or percutaneously)
25
26. Management of Urologic Emergencies
• Acute Scrotum
• Bladder and Uretheral Injury
• Acute Urinary Retention
• Phimosis and Paraphimosis
• Priapism and Penile Fracture
26
27. Acute SCROTUM
• Acute onset of scrotal pain and or swelling
• With or without fever
• Anorexia, Nausia and vomitting
27
28. Causes of Acute Scrotum
• Ischemia:
- Torsion of the testis ( Intravaginal Vs Extravaginal ),
(Prenatal or Neonatal)
- Appendiceal torsion ( testis or epididymis )
- Testicular infarction due to other vascular insult
(cord injury, thrombosis)
• Trauma:
- Testicular rupture
- Intratesticular hematoma,
- Testicular contusion
- Hematocele
28
30. Causes ….
• Acute on chronic events:
- Spermatocele ( rupture or hemorrhage)
- Hydrocele (rupture, hemorrhage or infection)
- Testicular tumor ( with rupture, hemorrhage,
infarction or infection)
- Varicocele
30
31. 1. Testicular Torsion
Testicular Anatomy
• The normal testis is oriented
in the vertical axis and the
epididymis is above the
superior pole in the
posterolateral position.
• Tunica Vaginalis
• Cremasteric reflex:
Stroking/pinching the inner
thigh should result in
elevation of > 0.5 cm of the
ipsilateral testicle
31
32. 1. Testicular Torsion …
• Incidence 1:4000
• Only 50% salvageability with testicular loss from
either atrophy or ochidectomy
• Age - 70% occur prenatally and 30% occur
postnatally
• Two peak periods: First year of life and at
puberty
• 10 times more likely in an undescended testis
Left side is more commonly involved
32
33. 1. Testicular Torsion …
• Most torsions due to
bilateral anatomic
abnormality.
• Tunica vaginalis has a
high insertion about the
spermatic cord.
↓
Bell-clapper deformity
↓
Testis dangles in the
scrotum and is mobile
33
34. 1.Testicular Torsion: Pathophysiology
• Initially venous return is obstructed and then
venous thrombosis is followed by arterial
thrombosis
• Degree of obstruction is a function of the degree
of rotation
• 720° twist is required to compromise flow
through the testicular artery and result in
ischemia.
• Necrosis develops in testicle with complete
obstruction and infarction develops after arterial
thrombosis
34
35. 1. Testicular Torsion…
• Rapid swelling and edema of the testis and
scrotum, followed by scrotal erythema
• Damage proportional to duration/extent of
vascular obstruction
• Testis salvage rate
- ~ 100% in patients who undergo detorsion within
6 hours of the start of pain.
- 20% viability rate if detorsion occurs >12 hours
- Virtually no viability if detorsion is delayed >24 hrs
35
36. 1. Testicular Torsion …
• 40% report a history of similar pain that
resolved spontaneously in the past
• The onset of pain may be preceded trauma,
physical activity, or by no activity (e.g. during
sleep).
• Typically no urinary symptoms
• Sudden onset of scrotal pain, but can be
inguinal or lower abdominal.
• May be constant or intermittent.
• Nausea and Vomiting
36
37. 1. Testicular Torsion ….
• Hemiscrotum is swollen, tender,
firm
• High-riding testis with a transverse
lie is classic sign
• Loss of Cremasteric reflex – almost
universal
• May see the bell-clapper deformity,
with horizontal lie of the
contralateral testicle
• Prehn’s sign: Checking for relief of
scrotal pain by elevating testicle.
• Pain NOT relieved – Negative
Prehn’s test
Testicular Torsion
37
38. 1. Testicular Torsion: Diagnosis
• Doppler Ultrasound
- Test of choice for Dx of torsion.
- Sensitivity comparable to radioisotope scans (86%-100%)
and greater specificity (100%).
- More rapid and more available than radioisotope scans.
- testicular perfusion is the key to the ultrasound diagnosis
of torsion.
- Tests such as nuclear testicular scans, CT or MRI, have
essentially no role in the contemporary management of
the acute scrotum.
38
39. 1.Testicular Torsion: Management
• Immediate Urologic consultation
for surgical exploration and
possible bilateral orchidopexy if
diagnosis is obvious
• Manual detorsion - Only a
temporizing measure. Endpoint for
successful detorsion is pain relief.
• Most torsions occur lateral to
medial, therefore detorsion should
be attempted in a medial to lateral
direction - “open the book”
maneuver
• Imaging if diagnosis unclear, should
NOT delay exploration if high
suspicion exists
39
40. 1.Testicular Torsion: Management
• Sharply entering the scrotum,
open the tunica vaginalis
• Detorse the testis and wrapp in a
warm, moist gauze.
• The contralateral side then
undergoes orchidopexy to
prevent torsion on that side.
• The affected testis is re inspected
for signs of improved perfusion
(“pinking up”).
40
41. 2. Torsion of Appendage
• Torsion of appendages is more
common than testicular torsion
• Testicular and Epididymal
appendages are vestigial
remnants of the wolffian and
mullerian ducts respectively
• Most frequent in preadolescent
males 3-13yrs
• Cause unclear
• Twisting causes obstruction,
edema and then painful
necrosis
41
43. 2. Torsion of Appendage
• Discrete, painful testicular mass
• Symptoms less severe than
torsion.
• No nausea, vomiting, or fevers
• Transillumination of scrotum may
reveal the cyanotic appendage as a
pathognomonic blue dot
• U/S should reveal normal to
increased blood flow
43
44. 2. Torsion of Appendage: Management
• Scrotal Support
• Pelvic rest
• Analgesia
• Expect resolution of symptoms in 7-10 days
with degeneration of appendages
44
45. 3. Epididymitis
• Average age 25 years
• Most common misdiagnosis for testicular torsion
• Rarely affects a prepubertal child without an
underlying urinary tract infection
• Result of retrograde ascent of urethral and
bladder pathogens
• Peritubular fibrosis may develop and occlude the
ductules, if bilateral may lead to sterility
45
46. Epididymitis
• In men > 40 yrs, E. coli is the predominant
pathogen.
• Pseudomonas, and gram positive cocci.
• Associated w/ underlying urologic pathology --
Recent GU tract manipulation or bacterial
prostatitis.
• In men < 40, Chlamydia and N. gonorrhea are
the major pathogens
46
47. Epididymitis
• Gradual Scrotal pain, peaks over days
• Low grade fever, average 38 degrees C
• Cremasteric reflex usually preserved
• Due to inflammatory nature of pain, may have
some transient pain relief from scrotal elevation
(Prehn’s Test Positive)
• Localized epididymal swelling initially, then may
progress to single, large testicular mass
• Urethral discharge and voiding symptoms may
be present
47
48. Epididymitis
• Pyuria and bacteriuria on U/A
• Urethral discharge should be
examined for gram stain and
culture
• Leukocytosis between 10,000 -
30,000 cells/ml
• Torsion should not be excluded
by pyuria, fever, or dysuria.
• An equivocal exam demands
Imaging.
• U/S with increased or normal
testicular blood flow is c/w
epididymitis
48
49. Epididymitis: Management
• Sexually acquired: Ceftriaxone 250 mg IM and
Doxycycline 100 mg PO bid x 10d. Treat sexual
partners.
• Nonsexually acquired: TMP-SMX or
Fluoroquinolone x 14d. Check urine C&S.
• Bed rest, scrotal support, analgesics, sitz
baths, and Urology follow up
49
50. Complications of Epididymitis
• Infertility - Sexually transmitted epididymitis
• Abscess - Gonococcal epididymitis
• Chronic epididymitis
• U/S indicated if no response to medical
therapy
50
51. Orchitis
• Acute infection of the testis
• Rare without initial epididymitis, Consider testicular
tumor.
• Bacterial infection secondary to spread from
epididymitis of E. coli, Klebsiella, Pseudomonas
• Viral orchitis – Mumps.
- 4-6 days after onset of parotitis usually.
- 50% of involved testes atrophy but infertility rare
• Syphilis
• Treatment: Antibiotics for bacterial orchitis and local
scrotal measures for viral orchitis
51
52. Testicular Tumor
• Testicular CA – Most common cause of malignancy
to afflict young men
• Average age of incidence is 32 Years
• DDx: Epididymitis and torsion
• Increased incidence with cryptorchidism in
bilateral testes
• Majority are Seminomas, then embryonal cell CA
and teratomas
52
53. Testicular Tumor
• Classic presentation – Painless, firm testicular
mass
• Acute hemorrhage within the tumor can lead to
acute scrotal pain (10%)
• Ultrasound – Distinct Intratesticular Mass
• CXR if suspect Metastases
• Treatment: Immediate Urology referral.
• Radical orchidectomy.
• Cisplatin chemotherapy and Radiation for
seminomas.
53
54. Trauma to scrotum
• Blunt injury may result in:
Testicular rupture,
Intratesticular hematoma,
Testicular contusion (bruising) or
Hematocele (Blood collection within the TV
space).
• Only testicular rupture requires surgical repair.
• Large or painful hematoceles may benefit from
drainage.
54
57. Bladder Injury
• protected position of the bladder deep in the
bony pelvis
• Bladder injuries after blunt or penetrating
trauma are rare, (< 2% of abdominal injuries
requiring surgery)
• Usually associated with other severe injuries
• 83- 100% have pelvic fracture, and 6-10% of
patients with pelvic fracture have bladder
injuries.
57
58. Bladder Injury…
• Most (95%- 100%) of patients with bladder injury
will have gross hematuria,
• Only 5% have had only microscopic hematuria
• Gross hematuria is felt to be associated with more
significant injuries (rupture), while
• microhematuria has been seen more commonly
with bladder contusion .
58
60. Bladder Injury…
• Major diagnostic goals in patients with Bladder
Injury:
1.Determine if urethral injury is present
2. Determine if bladder rupture is present,
• Classify it as intraperitoneal (which requires
exploration and repair) or
• extraperitoneal (which can usually be managed
by bladder drainage alone).
3. Determine if renal injuries are associated and if
they require surgical exploration
60
61. Bladder Injury…
Evaluation
• Local Signs and Symptoms
- Lower abdominal pain, tenderness, and
bruising
- Urethral catheter does not return urine.
- Fever, absence of voiding, peritoneal irritation,
and elevated BUN
• Blood at the Urethral Meatus
- 10-17% of patients with bladder injuries will
have associated urethral rupture. 61
63. Bladder Injury: MANAGEMENT
1. Intraperitoneal Ruptures
• 25% of all bladder injuries
• Combined with extraperitoneal rupture in
another 12%
• Caused by rapidly rising intraperitoneal pressure
causing the bladder to burst (Dome)
• Operative repair with two-layer closure with
absorbable suture.
• If conservative management is attempted,
persistent urinary leakage can ensue, with
consequent and often fatal peritonitis.
63
64. Bladder Injury…
2. Extraperitoneal Ruptures
• Found alone in 62% of cases
• In combination with intraperitoneal ruptures in
another 12%.
• Result from direct laceration, usually by bone
spicules from the fractured pelvis.
• They can most commonly be managed with
catheter drainage alone,
64
65. 2. Extraperitoneal Ruptures …
• Contraindications for conservative Management
- Bone fragment projecting into the rupture,
- open pelvic fracture, and
- Rectal Perforation
- If clots obstruct the urinary catheter within 48
hours of injury
- Undergoing laparotomy for other reasons
65
69. 1. Anterior urethral injuries
Blunt Trauma
• Bulbar urethra - the most common site injured.
Penetrating injuries of the penile or bulbar
urethra - Rare.
Insertion of foreign bodies
Penile fractures – 10 - 20% of anterior injuries.
Urethral Instrumentation - affect all segments
of the anterior urethra
69
70. 2. Posterior urethral injuries
• Most often related to pelvic fractures ~ 72%
• Iatrogenic posterior injuries - Irradiation or
surgery to the prostate - 3-25%
• Crush or deceleration impact injury
Detachments of the perineal membrane
and puboprostatic ligaments
• Bulbomembranous junction, just distal of the
external urethral sphincter.
• Direct transection of the urethra by a bony
fragment - Rare
70
72. 2. Posterior urethral injuries …
• Injuries of the bladder neck and prostate - Rare.
• They mostly occur at the anterior midline of both
the bladder neck and prostatic urethra.
• Complete transection of the bladder neck or an
avulsion of the anterior part of the prostate
• Penetrating injuries of the pelvis, perineum or
buttocks
72
73. Morbidities of Uretheral Injuries
• Strictures
• Incontinence and
• Erectile Dysfunction (ED)
73
74. Urethral injuries in females
• Very rare -
• Pelvic Fracture
• Usually a partial longitudinal tear of
the anterior wall.
• Complete avulsion- Extremely rare.
74
75. Diagnosis
• Clinical signs and symptoms
• Blood at the meatus
• An inability to void
• Haematuria and pain on urination
• Urinary extravasation and bleeding
• A ‘high-riding’ prostate
• Difficulty or an inability to pass a urethral
catheter
75
78. Anterior urethral injuries
Blunt anterior urethral injuries
• Acute or early urethroplasty – not indicated.
• Therapeutic options:
1. ( A trial of ) early endoscopic realignment with
transurethral catheterization
2. Suprapubic diversion
Urinary diversion should be maintained:
For2 weeks for partial rupture
For 3 Weeks for complete rupture
78
79. Anterior urethral injuries …
Penetrating anterior urethral injuries
• Immediate exploration and Debridement.
• Spatulation of the urethral ends and primary
anastomosis - defects 1.5 cm in the penile
urethra and 2-3 cm in the bulbar urethra,
• Larger defects or apparent infection,
a staged repair with urethral marsupialization
and a suprapubic catheter
• Peri- and post-operative antibiotic treatment is
necessary.
79
80. Posterior urethral injuries
Blunt posterior urethral injuries
• Complete Vs Partial
• Timing
• Immediate: < 48 hours after injury
• Delayed primary: 2 days to 2 weeks after injury
• Deferred: > 3 months after injury
80
81. Posterior urethral injuries
Immediate Management
• Urinary diversion
• To monitor urinary output
• To treat symptomatic retention
• To minimize urinary extravasation and its
secondary effects, such as infection and
fibrosis.
• Attempt at urethral catheterization by
experienced hands if SPC not
possible/difficult
81
82. Partial posterior urethral rupture
• Suprapubic or urethral catheter
• Urethrography - at 2-weekly intervals until
healing has occurred.
• A residual or subsequent stricture should be
managed with:
• Internal urethrotomy if it is short and non-
obliterative;
• Anastomotic urethroplasty - long and dense,
complete obliteration or failed internal
urethrotomy
82
83. Complete posterior urethral rupture
• Acute treatment options:
• Immediate realignment:
- Apposition of the urethral ends over a catheter;
- To correct severe distraction injuries rather than to
prevent a stricture
• Immediate urethroplasty:
- Suturing of urethral ends
- Difficult and not recommended
83
84. Delayed primary treatment
• Delayed treatment options:
1. Delayed primary realignment
- Performed within 14 days
(i.e. before fibrosis begins)
2. Delayed primary urethroplasty
- Performed no later than 14 days after the initial
injury
- Only a few reports have been published in the
literature
- Not recommended.
84
85. Deferred treatment
1. Deferred urethroplasty
• Procedure of choice for the treatment of
posterior urethral distraction defects.
• Excellent outcome
2. Deferred endoscopic optical incision
• For short, non-obliterative strictures following
realignment or urethroplasty,
85
86. Penetrating posterior urethral injuries
• Immediate exploration by retropubic route
and primary repair or realignment.
• Life-threatening associated injuries:
Suprapubic diversion with delayed
abdominoperineal urethroplasty
• In the case of rectal injury, a diverting
colostomy.
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87. Female urethral injuries
Immediate exploration and primary repair:
• Proximal Disruptions – Retropubic approach
• Mid-urethral Disruptions - Transvaginal
approach
• Distal urethral injuries - Managed vaginally by
primary suturing and closure of the vaginal
laceration.
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Introduction
• Urinary obstruction is a common cause of acute
and chronic renal failure.
• A wide variety of pathological processes,
intrinsic and extrinsic to the urinary system, can
cause obstruction.
• Symptoms and signs of obstruction are often
mild, occurring over long periods of time and
requiring a high index of suspicion for diagnosis.
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Management
1. Medical Therapy
• Analgesics
• Antibiotics
• Other medications: Prazosin
2. Surgical Therapy
• The goal of surgical intervention is to completely relieve the urinary tract
obstruction.
• Point of obstruction should be identified
A. Urethral catheterization
– A urethral catheter (size 8F-24F)
– May need to perform urethral dilation, cystoscopy, or both to pass the
catheter.
– Indwelling / clean intermittent catheterization.
– If blood is present at the urethral meatus after pelvic trauma and
suspicion of urethral injury exists, retrograde urethrography needs to be
performed to rule out urethral injury.
B. Suprapubic Cystostomy
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Suprapubic Cystostomy:
• Percutaneously (at the bedside)
• Open Cystostomy (in the operating room).
• A suprapubic tube is placed ~2 finger-breadths
above the pubic symphysis.
• Ultrasound guidance should be used for bedside
procedures to ensure proper placement without
injury to adjacent structures.
• In patients with previous abdominal surgery,
adhesions and scar tissue may have changed
the normal bowel location, so an open approach
may be preferred.