Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Choledocholithiasis is one of the main causes for Obstructive Jaundice.In this ppt presentation, I have discussed the etiology, clinical features, complications, investigations and management of Choledocholithiasis. I have also included a mindmap and 2 algorithms for Choledocholithiasis. I hope you will find it very useful and interesting.
this presentation includes anatomy physiology function of peritoneum ,also includes cause of peritonitis its severity ,various scoring system investigation and treatment.It includes the recent advancement and latest articles from latest books of surgery.
Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Choledocholithiasis is one of the main causes for Obstructive Jaundice.In this ppt presentation, I have discussed the etiology, clinical features, complications, investigations and management of Choledocholithiasis. I have also included a mindmap and 2 algorithms for Choledocholithiasis. I hope you will find it very useful and interesting.
this presentation includes anatomy physiology function of peritoneum ,also includes cause of peritonitis its severity ,various scoring system investigation and treatment.It includes the recent advancement and latest articles from latest books of surgery.
Chest drains also known as under water sealed drains (UWSD) are inserted to allow draining of the pleural spaces of air, blood or fluid, allowing expansion of the lungs.
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool.
Nursing assessment and Management clients with Pancreatic disordersANILKUMAR BR
The pancreas, located in the upper abdomen, has endocrine as well as exocrine functions .
The secretion of pancreatic enzymes into the gastrointestinal tract through the pancreatic duct represents its exocrine function.
The secretion of insulin, glucagon, and somatostatin directly into the bloodstream represents its endocrine function.
Pancreatitis (inflammation of the pancreas) is a serious disorder. The most basic classification system used to describe or categorize the various stages and forms of pancreatitis divides the disorder into acute or chronic forms.
Acute pancreatitis can be a medical emergency associated with a high risk for life-threatening complications and mortality, whereas chronic pancreatitis often goes undetected until 80% to 90% of the exocrine and endocrine tissue is destroyed.
Acute pancreatitis does not usually lead to chronic pancreatitis unless complications develop.
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
ACUTE CHOLECYSTITIS- RUQ ABDOMINAL PAIN
#surgicaleducator #ruqabdominalpain #acutecholecystitis #usmle #babysurgeon #surgicaltutor
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Acute Cholecystitis
• It is one of the common surgical problems you see in surgical wards.
• I have discussed the various causes for RUQ pain, etiology, pathology, clinical features, investigations, complications and treatment of Acute Cholecystitis.
• I have also included a mind map, a diagnostic and a treatment algorithm for Acute Appendicitis.
• I hope the video will be very useful and you will enjoy it.
• You can watch all my surgical teaching videos in the following links:
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
Chest drains also known as under water sealed drains (UWSD) are inserted to allow draining of the pleural spaces of air, blood or fluid, allowing expansion of the lungs.
Gastrointestinal bleeding (GI bleed), also known as gastrointestinal hemorrhage, is all forms of bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time, symptoms may include vomiting red blood, vomiting black blood, bloody stool, or black stool.
Nursing assessment and Management clients with Pancreatic disordersANILKUMAR BR
The pancreas, located in the upper abdomen, has endocrine as well as exocrine functions .
The secretion of pancreatic enzymes into the gastrointestinal tract through the pancreatic duct represents its exocrine function.
The secretion of insulin, glucagon, and somatostatin directly into the bloodstream represents its endocrine function.
Pancreatitis (inflammation of the pancreas) is a serious disorder. The most basic classification system used to describe or categorize the various stages and forms of pancreatitis divides the disorder into acute or chronic forms.
Acute pancreatitis can be a medical emergency associated with a high risk for life-threatening complications and mortality, whereas chronic pancreatitis often goes undetected until 80% to 90% of the exocrine and endocrine tissue is destroyed.
Acute pancreatitis does not usually lead to chronic pancreatitis unless complications develop.
Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.
ACUTE CHOLECYSTITIS- RUQ ABDOMINAL PAIN
#surgicaleducator #ruqabdominalpain #acutecholecystitis #usmle #babysurgeon #surgicaltutor
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Acute Cholecystitis
• It is one of the common surgical problems you see in surgical wards.
• I have discussed the various causes for RUQ pain, etiology, pathology, clinical features, investigations, complications and treatment of Acute Cholecystitis.
• I have also included a mind map, a diagnostic and a treatment algorithm for Acute Appendicitis.
• I hope the video will be very useful and you will enjoy it.
• You can watch all my surgical teaching videos in the following links:
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
Acute cholecystitis:Severity assessment and managementKETAN VAGHOLKAR
Acute cholecystitis is one of the commonest biliary tract emergency. Early diagnosis and prompt treatment is essential to reduce the morbidity and mortality associated with the disease. Assessment of the severity of the disease is essential to develop a safe therapeutic plan for the patient. The Tokyo guidelines (TG 18/TG 13) provides a lucid system for grading the severity of acute cholecystitis. Supportive care, antibiotic therapy followed by early laparoscopic cholecystectomy is the mainstay of treatment. Fitness to undergo surgery is determined by the Charlson Comorbidity Index and the American College of Anaesthesiologist’s physical status examination. Those unfit for surgery are best treated by early biliary drainage followed by delayed cholecystectomy. The incidence of iatrogenic bile duct injury is high in severe cases. A low threshold for conversion to open cholecystectomy is essential in such cases to prevent iatrogenic biliovascular injuries. A holistic clinical approach comprising of establishing the diagnosis, grading the severity of acute cholecystitis, assessment of fitness to undergo surgery, administration of supportive care and antibiotics followed by early cholecystectomy constitutes a safe surgical approach to acute cholecystitis.
LOWER GI HEMORRHAGE- PLAYLIST OF 6 VIDEOS
Dear Viewers,
Greetings from “Surgical Educator”.
I have made a playlist for Lower GI Hemorrhage which consists of six videos on various causes of Lower GI Hemorrhage. They are Introduction, diverticular disease, haemorrhoids, fissure-in-ano, colorectal carcinoma and inflammatory bowel disease. If you watch all these videos together you will become confident to tackle the clinical problem of Lower GI Hemorrhage. You can watch these videos in the following link: https://www.youtube.com/playlist…
Thank you for watching the videos.
A quick review of the various benign pathologic conditions of Gallbladder,intended primarily for the Undergraduate students; Based on Bailey & Love's Short Practise of Surgery latest edition.
OSCE ( Organization for security and co-operation in Europe )Vihari Rajaguru
Short presentation about the Organization for security and cooperation in Europe. Including : structure, leaders,history, introduction, activities etc.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
Essay describing cholecystitis
1. 1 | P a g e
Essay describing cholecystitis
Definition
Acute cholecystitis is acute gallbladder inflammation and one of the major
complications of cholelithiasis or gallstones. It develops in up to 10% of
patients with symptomatic gallstones. In most cases (90%), it is caused by
complete cystic duct obstruction usually due to an impacted gallstone in the
gallbladder neck or cystic duct, which leads to inflammation within the
gallbladder wall. n 5% of cases, bile inspissation (due to dehydration) or bile
stasis (due to trauma or severe systemic illness) can block the cystic duct,
causing an acalculous cholecystitis.
Classification
Typesof acute cholecystitis
1. Calculous - 90% to 95%.
2. Acalculous - 3.7% to 14%.
Pathologic classification
1. Edematous
2 to 4 days
Gallbladder tissueis intact histological, with edema in the subserosallayer.
2. Necrotizing
3 to 5 days
Edema with areas of hemorrhageand necrosis
Necrosis does not involve the full thickness of the wall.
3. Suppurative
7 to 10 days
WBCs present within the gallbladder wall, with areas of necrosis and
suppuration
Intrawallabscesses involving theentire thickness of the wall
Pericholecystic abscesses present.
4. Chronic
2. 2 | P a g e
Occurs after repeated episodes of mild attacks
Mucosalatrophy and fibrosis of the gallbladder wall.
5. Emphysematous
Air appears in the gallbladder wall due to infection with gas-forming anaerobes
Often found in diabetic patients.
Epidemiology
More than 20 million Americans are estimated to have gallstones, with
500,000 cholecystectomies performed annually. Most patients with gallstones
do not develop symptoms. About 1% to 2% of asymptomatic gallstones
become symptomatic each year. Acute cholecystitis is the most frequent
complication of gallstones and occurs in 10% of symptomatic patients.
Acute acalculous cholecystitis accounts for 5% to 14% of cases of acute
cholecystitis. The incidence is higher in the intensive care population,
particularly patients in burn and trauma units. The incidence of acute
cholecystitis is approximately the same in western Europe as in the US, but
worldwide the exact incidence is not known. The distribution and incidence
follow that of cholelithiasis because of the close relationship between
gallstones and acute cholecystitis.
Etiology
At least 90% of patients with the condition have gallstones. Helminthic
infection is one of the major causes of biliary disease in Asia, southern Africa,
and Latin America, but not the US. Infection with Salmonella organisms has
been described as a primary event in cholecystitis secondary to typhoid fever.
AIDS-related cholecystitis and cholangiopathy may be secondary to CMV
and Cryptosporidium organisms. Various microorganisms can be identified
early in the onset of disease.
These include Escherichia coli, Klebsiella, enterococci, Pseudomonas,
and Bacteroides fragilis. It has been suggested that this bacterial invasion is
not a primary perpetrator of injury, because in >40% of patients no bacterial
growth is obtained from surgical specimens. Generally, bacterial infection is a
secondary feature and not an initiating event. Occasionally, acute cholecystitis
occurs in the absence of gallstones. Starvation, total parenteral nutrition,
3. 3 | P a g e
narcotic analgesics, and immobility are predisposing factors for acalculous
acute cholecystitis. Secondary infection with gram-negative flora occurs in
most cases.
Pathophysiology
Fixed obstruction or passage of gallstones into the gallbladder neck or cystic
duct causes acute inflammation of the gallbladder wall. The impacted gallstone
causes bile to become trapped in the gallbladder, which causes irritation and
increases pressure in the gallbladder. Trauma caused by the gallstone
stimulates prostaglandin synthesis (PGI2, PGE2), which mediates the
inflammatory response. This can result in secondary bacterial infection leading
to necrosis and gallbladder perforation.
The pathophysiology of acalculous cholecystitis is poorly understood, but it is
most likely multifactorial. Functional cystic duct obstruction is often present
and related to biliary sludge or bile inspissation caused by dehydration or bile
stasis (due to trauma or systemic illness). Occasionally, extrinsic compression
may play a role in the development of bile stasis. Some patients with sepsis
may have direct gallbladder wall inflammation and localized or generalized
tissue ischemia without obstruction.
Jaundice occurs in up to 10% of patients and is caused by inflammation of
contiguous biliary ducts (Mirizzi syndrome).
Acute cholecystitis may resolve spontaneously 5 to 7 days after symptom
onset. The impacted stone becomes dislodged, with re-establishment of cystic
duct patency. If cystic duct patency is not re-established, inflammation and
pressure necrosis may develop, leading to mural and mucosal hemorrhagic
necrosis. Untreated acute cholecystitis can lead to suppurative, gangrenous,
and emphysematous cholecystitis.
Diagnostic Approach
Early diagnosis is essential for prompt therapeutic decisions and prevention of
complications. Diagnosis is based on the signs and symptoms of inflammation
in the presence of peritonitis localized to the RUQ of the abdomen. However,
no clinical or laboratory finding has a high or low enough likelihood ratio to
predict the presence or absence of the condition.
4. 4 | P a g e
History
Patients typically complain of nausea and pain that lasts >3 to 6 hours, which is
unremitting and may be associated with fever. The pain is severe and steady.
The duration of pain can be shorter if the gallstone returns into the gallbladder
lumen or passes into the duodenum.
Physical exam
Physical exam may reveal RUQ tenderness or a palpable mass. A positive
Murphy sign (the examiner's hand rests along the costal margin and deep
inspiration causes pain) has a specificity of 79% to 96% for acute cholecystitis.
Persistent pain, fever, chills, and more severe localized or generalized
tenderness may indicate complicated disease (e.g., abscess formation or
gallbladder perforation).
Acalculous cholecystitis is more difficult to diagnoseclinically, as it often occurs
in critically ill patients who may not be able to express pain. Patients receiving
total parental nutrition are at increased risk. Fever, jaundice, vomiting,
abdominal tenderness, leukocytosis, and hyperbilirubinemia should lead to a
high index of clinical suspicion. Typically acalculous cholecystitis is a diagnosis
of exclusion.
Blood tests
CBC and C-reactive protein (CRP) should be assessed to look for evidence of an
inflammatory process. LFTs may show elevated bilirubin, alkaline phosphatase,
and gamma-GT.
Imaging
RUQ ultrasound should be the first test ordered and can be performed at the
patient's bedside. Detection of gallstones alone does not definitively diagnose
the condition. To make an accurate diagnosis the findings of stones and an
ultrasonographic Murphy sign are required. About 92% of patients with a
positive Murphy sign in the presence of gallstones have the condition. [29]
Ultrasound allows for evaluation of all the abdominal structures. It provides
anatomic information about gallbladder size, stone size, gallbladder wall, and
bile duct size.
Scintigraphy with hepatobiliary iminodiacetic acid (HIDA) scan should be
obtained if ultrasound results are equivocal.
5. 5 | P a g e
Abdominal CT scan is inferior to ultrasound in assessing acute biliary disease,
but it is useful when obesity or gaseous distension limits ultrasound
interpretation. It is also indicated for evaluation of suspected complications
(such as abscess) and concurrentintra-abdominalconditions. Abdominal MRI is
appropriate for pregnant patients with abdominal pain.
Plain radiographs may detect a radiopaque gallstone in 15% of cases and
provide information about bowel gas pattern or free air, but offer no
incremental information if ultrasound or CT is performed.
Treatment Approach
When a diagnosis of acute cholecystitis is suspected, medical treatment,
including NPO, intravenous fluids, antibiotics, and analgesia, together with
close monitoring of blood pressure, pulse, and urinary output, should be
initiated. Simultaneously, the grade of severity needs to be established.
Appropriate treatment should be performed in accordance with the severity
grade. Operative risk should also be evaluated based on the severity grade.
Cholecystectomy
Cholecystectomy is the definitive treatment, as gallbladder inflammation often
persists despite medical therapy. This can be performed by laparoscopy or
laparotomy (i.e., open approach). It is carried out as soon as possible after the
onset of cholecystitis unless the patient is critically ill with severe cholecystitis
and is thoughtto havea high operativerisk, or inflammation is thought to have
been present for more than 7 days. This is because of the high risk of liver
failure and heavy hemorrhage.
Laparoscopic
Now the preferred treatment. Early laparoscopic cholecystectomy (ELC)
showed a significant reduction in hospital stay evidence but did not
significantly affect conversion rate to open cholecystectomy. Evidence Optimal
timing (≤7 days after symptomonset) is critical for the best results. Conversion
to the open procedure may be required if there is significant inflammation,
difficulty delineating the anatomy, or significant bleeding.
Conversion rates vary depending on the patient population but not the
surgeon's experience. Patients with Child-Turcotte-Pugh grade A or B liver
6. 6 | P a g e
cirrhosis have fewer overall postoperative complications than those who
undergo the open procedure.
Open
May be appropriate for patients with gallbladder mass, extensive upper
abdominal surgery, suspicion of malignancy, or late third trimester of
pregnancy. It is also indicated if there is significant gallbladder inflammation,
difficulty delineating the anatomy, significant bleeding, presence of adhesions,
or laparoscopic cholecystectomy complications.
Percutaneous cholecystostomy tube
If medical management fails, and patients are poor surgical candidates (e.g.,
medically not suitable for surgery), a percutaneous cholecystostomy tube
should be considered. This has been shown to give clinical improvement in
80% of patients within 5 days after placement.
Age over 70 years, diabetes, a distended gallbladder, and persistently elevated
WBC (>15,000 cells/microliter) are prognostic factors for the development of
complications such as gangrenous cholecystitis and predictors for failure of
conservative treatment. These patients should be considered for early
percutaneous cholecystostomy tube.
It is a minimally invasive procedure most often performed in patients who
have a high surgical risk and occasionally in critically ill patients. Initially it was
used as a bridging procedure to help patients recover from a serious
underlying illness and before definitive surgery.
Based on available evidence from RCTs, the management of people at high risk
of perioperative death due to their general condition (i.e., high-risk surgical
patients) with percutaneous cholecystostomy is unclear. Further data are
needed.
The inflamed gallbladder is localized with sonography or fluoroscopy after the
oral administration of contrast medium. CT-guided access may help if no
sonographic window is found. A tube is then placed through the skin to drain
or decompress the gallbladder.
An incomplete or poor response within the first 48 hours may indicate
complications (e.g., tube dislodgment, gallbladder wall necrosis) or the wrong
diagnosis. Extrahepatic and transhepatic approaches have been advocated. A
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transhepatic route minimizes the risk of intraperitoneal bile leakage and
inadvertent injury to the hepatic flexure of the colon. A subhepatic or
transperitoneal approach is more favorable if stone extraction is planned due
to the need for tract dilation.
Contraindications include coagulopathy that cannot be corrected, massive
ascites that cannot be drained, and suspicion for gangrenous or perforated
cholecystitis. Technical success of percutaneous cholecystostomy is high in
experienced hands (95% to 100%), and complication rates are low.
Complications include catheter dislodgment, vagal reaction, bile leakage and
peritonitis, and hemorrhage.
Patients treated with cholecystostomy tube can be discharged with their tube
in place after the inflammatory process has resolved clinically. These patients
should subsequently undergo a cholangiogram through the cholecystostomy
tube (6-8 weeks) to see whether the cystic duct is open. If the duct is open and
the patient is a good surgical candidate, he or she should be referred for
cholecystectomy.
Management based on severity grade
Mild (grade I)
Defined as acute cholecystitis in a healthy patient with no organ dysfunction
and mild inflammatory changes in the gallbladder; responds to initial medical
treatment.
Patients are observed and treated with oral antibiotic drugs or even observed
without antibiotics. The pathophysiology of acute cholecystitis is cystic duct
obstruction, which causes an acute sterile inflammation. Secondary infection
of the gallbladder space by bacteria may follow. Antibiotics are required if
infection is suspected on the basis of laboratory and clinical findings.
Antibiotic therapy should include coverage against microorganisms in the
Enterobacteriaceae family (e.g., a second-generation cephalosporin or a
combination of a quinolone and metronidazole); activity against enterococci is
not required.
Nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac or
indomethacin are recommended as part of the medical treatment for their
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analgesic effects and their inhibition of prostaglandin release from the
gallbladder wall.
Medical treatment may be sufficient for patients with mild (grade I) disease,
and urgent surgery may not be required. However, for most patients ELC
should be considered the primary approach (within 1 week of onset of
symptoms). For patients who received preoperative and intraoperative
antibiotics, postoperative antibiotic therapy may not be required.
The Tokyo guidelines state that ELC is the preferred treatment. ELC (within 72
hours of onset of symptoms) has a clear benefit compared with delayed
cholecystectomy (>6 weeks after index admission) in terms of complication
rate, cost, quality of life, and hospital stay.
There is no advantage to delaying cholecystectomy for acute cholecystitis on
the basis of outcomes. Also favoring early cholecystectomy is that
approximately 15% to 20% of patients who underwent delayed procedures in
the randomized trials had persistent or recurrent symptoms requiring
intervention before their planned operation.
If medical management fails, and patients are poor surgical candidates, a
percutaneous cholecystostomy tube should be considered, with consideration
of referral for cholecystectomy if clinical situation improves.
Moderate (grade II)
Defined as acute cholecystitis associated with any one of the following:
elevated white blood cell count (>18,000/microliter), palpable tender mass in
the right upper abdominal quadrant, duration of complaints >72 hours, and
marked local inflammation (gangrenous cholecystitis, pericholecystic abscess,
hepatic abscess, biliary peritonitis, emphysematous cholecystitis).
Moderate-grade cholecystitis usually does not respond to the initial medical
treatment. Patients who do not improve under conservative treatment are
referred for either surgery or percutaneous cholecystostomy, usually within 1
week of onset of symptoms.
ELC could be indicated if advanced laparoscopic techniques and skills are
available. Controversy lies within the group with moderately severe
cholecystitis, where there is no organ dysfunction but there is extensive
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disease in the gallbladder, which can confer difficulty in safely carrying out a
cholecystectomy. In this group, ELC or open cholecystectomy is preferred but
should be carried out only by a highly experienced surgeon. If operative
conditions make anatomic identification difficult, ELC should be promptly
terminated by conversion to open cholecystostomy.
Interval cholecystectomy can then be performed in 6 to 8 weeks. Limiting
factors to emergency surgery include availability of surgical staff, theatre
space, and radiologic investigations. Percutaneous cholecystostomy tube
should be considered for poor surgical candidates, with consideration of
referral for cholecystectomy if clinical situation improves.
Severe (grade III)
Defined as organ dysfunction in at least any one of the following
organs/systems of cardiovascular (hypotension requiring treatment with
dopamine ≥5 micrograms/kg per minute, or any dose of norepinephrine), CNS
(decreased level of consciousness), respiratory (PaO2/FiO2 ratio <300), renal
(oliguria, creatinine >2.0 mg/dL), hepatic (INR >1.5), or hematologic (platelet
count <100,000 cells/microliter), and/or severe local inflammation.
Intensive supportive care is required to monitor and treat organ dysfunction.
Requires urgent management of severe local inflammation by percutaneous
gallbladder drainage (i.e., percutaneous cholecystostomy tube) followed where
indicated by delayed elective cholecystectomy 2 to 3 months later, when the
patient's general condition has improved.
Patients treated with cholecystostomy tube can be discharged with their tube
in place after the inflammatory process has resolved clinically. These patients
should subsequently undergo a cholangiogram through the cholecystostomy
tube (6-8 weeks) to see whether the cystic duct is open. If the duct is open and
the patient is a good surgical candidate, he or she should be referred for
cholecystectomy.
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References
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784509/
https://en.wikipedia.org/wiki/Cholecystitis
http://www.uptodate.com/contents/acute-cholecystitis-
pathogenesis-clinical-features-and-diagnosis
https://online.epocrates.com/diseases/7811/Cholecystitis/Key-
Highlights
http://www.mayoclinic.org/diseases-
conditions/cholecystitis/basics/definition/con-20034277