Peritonitis is inflammation of the peritoneum lining the abdominal cavity. It can be caused by infection, injury, or chemical irritation. Acute peritonitis requires prompt treatment to eliminate the infectious source and reduce bacterial load. Treatment involves intravenous antibiotics, surgery to resolve the underlying cause, and intensive care as needed. Prognosis depends on the severity and cause of peritonitis. More severe or generalized cases with organ dysfunction carry a high risk of complications and mortality.
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.
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.
SIGMOID VOLVULUS- GENERALISED ABDOMINAL PAIN
#surgicaleducator #generalisedabdominalpain #sigmoidvolvuus #usmle #babysurgeon #surgicaltutor
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• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Sigmoid Volvulus- a didactic lecture.
• It is one of the life-threatening surgical problems you see in surgical wards.
• I have discussed the various causes for Generalised Abdominal Pain, epidemiology, etiology, pathology, clinical features, investigations, and treatment of Sigmoid volvulus.
• I have also included a mind map, diagnostic algorithm and a treatment algorithm for Sigmoid Volvulus.
• I hope the video will be very useful and you will enjoy it.
• You can watch all my surgical teaching videos in the following link:
• youtube.com/c/surgicaleducator
• Thank you for watching the video.
SIGMOID VOLVULUS- GENERALISED ABDOMINAL PAIN
#surgicaleducator #generalisedabdominalpain #sigmoidvolvuus #usmle #babysurgeon #surgicaltutor
Subscription Link: http://youtube.com/c/surgicaleducator...
Surgical Educator Android App link: https://play.google.com/store/apps/de...
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Sigmoid Volvulus- a didactic lecture.
• It is one of the life-threatening surgical problems you see in surgical wards.
• I have discussed the various causes for Generalised Abdominal Pain, epidemiology, etiology, pathology, clinical features, investigations, and treatment of Sigmoid volvulus.
• I have also included a mind map, diagnostic algorithm and a treatment algorithm for Sigmoid Volvulus.
• I hope the video will be very useful and you will enjoy it.
• You can watch all my surgical teaching videos in the following link:
• youtube.com/c/surgicaleducator
• Thank you for watching the video.
Typhoid perforation is a serious complication of typhoid fever, a bacterial infection caused by Salmonella typhi. It occurs when the infection causes a hole to form in the wall of the intestine, leading to the leakage of contents from the intestine into the abdominal cavity. This can cause severe infection and inflammation of the abdominal cavity, known as peritonitis.
The symptoms of typhoid perforation may include severe abdominal pain, fever, nausea and vomiting, diarrhea or constipation, and signs of shock such as low blood pressure and rapid heart rate. In some cases, there may also be visible signs of a perforation, such as a palpable abdominal mass or signs of fluid accumulation in the abdomen.
The diagnosis of typhoid perforation is typically made through a combination of physical examination, laboratory tests, and imaging studies such as X-rays or CT scans. Treatment typically involves surgical repair of the perforation and aggressive management of the infection and inflammation. This may include antibiotics, intravenous fluids, and other supportive care measures such as pain management and nutritional support.
It is important to seek prompt medical attention if you suspect you or someone you know may have typhoid fever or typhoid perforation. Early diagnosis and treatment are essential for a successful outcome and to prevent further complications.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
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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.
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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?
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
2. Peritonitis
Peritonitis is defined as inflammation of the serosal
membrane that lines the abdominal cavity and the
organs contained there in.
The peritoneum, which is an otherwise sterile
environment, reacts to various pathologic stimuli with
a fairly uniform inflammatory response.
3.
4. Anatomy
The peritoneum is the largest and most complex serous
membrane in the body.
It forms a closed sac by lining the interior surfaces of the
abdominal wall, retroperitoneum, the pelvis and the
diaphragm.
This parietal layer of the peritoneum reflects onto the
abdominal visceral organs to form the visceral peritoneum.
It thereby creates a potential space between the 2 layers (ie,
the peritoneal cavity).
The compartmentalization of the peritoneal cavity, in
conjunction with the greater omentum, influences the
localization and spread of peritoneal inflammation and
infections.
5. Anatomy
Normally, the amount of peritoneal fluid present is
less than 50 mL, and only small volumes are
transferred across the considerable surface area in a
steady state each day.
The peritoneal fluid represents a plasma ultrafiltrate.
In addition, peritoneal fluid contains small numbers
of desquamated mesothelial cells and various numbers
and morphologies of migrating immune cells.
6. Practical significance and clinical actuality
of the pathology
Acute peritonitis reveals in 16% of hospitalized
patients with surgical abdomenal pathology
The cause of death in 50% of moribund after
abdomenal operations is peritonitis.
Severe forms (stages) of this surgical state have
a 25-30% lethality rate.
In cases of multi-organs insufficiency it raises
till 85-90%
Lethality rate was in : 1936 – 1941гг = 23,8%,
1980- 1986г. = 21,9%.
8. Primary (spontaneous) peritonitis
Idiopathic peritonitis is uncommon, constituting
about 1% of all cases of peritonitis and occurs when no
obvious source for the peritoneal infection can be
demonstrated.
It was classically described in young girls where the
port of entry was presumed to be through the fallopian
tubes.
Adult primary peritonitis arises via haematogenous
spread or translocation of bacteria through the bowel
wall, especially in the presence of exogenous or
endogenous immunosuppresssion.
9. Secondary:
Acute suppurative
This is the most common form of peritonitis
encountered by the surgeon and results from
the perforation of a viscus (e.g. appendix, peptic
ulcer, colonic diverticulum, or gallbladder),
ischaemia of an intra-abdominal organ (e.g.
strangulated hernia, volvulus, mesenteric artery
occlusion),
or extension of an existing infection of an
abdominal organ (e.g. appendix abscess, liver
abscess, pyosalpinx).
10. Secondary:
Chemical (aseptic) peritonitis
Aseptic peritonitis refers to the peritoneal inflammation from
substances other than bacteria.
A perforated peptic ulcer provides the chemical peritonitis with
gastric juice and bile contaminating the peritoneal cavity.
Biliary peritonitis alone may follow gangrene and perforation of
the gallbladder, or, after open or laparoscopic cholecystectomy.
Blood in the peritoneum is also a cause of peritoneal irritation
after slow bleeding.
Meconium and urine may also precipitate chemical peritonitis.
Acute pancreatitis causes the release and activation of potent
lipolytic and proteolytic enzymes, which produce a severe
peritonitis and fat necrosis.
11. Secondary:
Interventional peritonitis
Endoscopy of the gastrointestinal tract may precipitate acute
peritonitis through perforation of the hollow organs (stomach,
bowel, oesophageal dilatation, diverticulum, urinary bladder).
The expansion of interventional radiological procedures has
precipitated a multitude of assaults on the abdominal cavity,
such as CT-guided biopsy and drainage of abscesses, mesenteric
angiography and therapeutic embolization, and percutaneous
transhepatic cholangiography and stenting, all providing further
potential for peritonitis.
Peritonitis may follow abdominal surgery where bowel and
gastric contents, blood, and urine escape into the abdominal
cavity following anastomotic dehiscence.
In patients with renal failure treated by continuous ambulatory
peritoneal dialysis, a permanent indwelling catheter in the
abdominal cavity provides a portal of entry for exogenous
bacteria.
12. Secondary:
Traumatic peritonitis
Abdominal trauma may produce acute peritonitis in
several ways. Penetrating wounds of the abdomen
without visceral injury may provide a route for
exogenous bacterial contamination.
Several blunt trauma may disrupt intra-abdominal
organs directly or indirectly through disruption of
their vascular supply.
13. Secondary:
Drug-induced peritonitis
Warfarin anticoagulation can cause peritoneal
irritation and peritonitis through leakage from a
spontaneous retroperitoneal haematoma.
The symptoms of acute peritonitis have also been
described during treatment with the antituberculous
agent, isoniazid.
14. Classification and forms of peritonitis
(continuation)
Simonyan K.S.
reactive phase – 24 hours.,
toxic – 24-72 hours,
terminal – 72 hours.
15. Classification and forms of
peritonitis (continuation)
Кusin M.I.:
I st. – without functional insufficiency of
abdominal organs (compensation)
II st. – with functional deficiency of
abdominal organs (subcompensation)
III st. – with multiple organ failure
(decompensation)
16. Classification and forms of
peritonitis (continuation)
serous peritonitis
fibrinous peritonitis
fibrinopurulent peritonitis
purulent (suppurative) peritonitis
hemorrhagic peritonitis
putrid peritonitis
17. Classification and forms of
peritonitis (continuation)
Fedorov V.D.
localized peritonitis
circumscribed (encloused) peritonitis
(infiltration, abscess)
unlimited (not encloused) peritonitis (no more
than 2 of 9 anatomical region)
generalized peritonitis
diffuse peritonitis (3-5 anatomical region)
general peritonitis
18. Classification and forms of
peritonitis (continuation)
Кusin M.I. (1994)
circumscribed peritonitis (infiltration,
abscess)
diffuse peritonitis
local peritonitis (1 anatomical region)
generalized peritonitis (several anatomical
regions)
general peritonitis (all peritoneum
19. Pathogenesis
Initially, peritoneal inflammation is often localized
and the affected area contained by a wrapping of
greater omentum, adjacent bowel, and fibrinous
adhesions.
If the inflammatory focus is part of an ongoing
process, or if host defences are lowered, localized
peritonitis may progress to life-threatening
generalized peritonitis.
There is massive exudation of inflammatory fluid into
the peritoneal cavity causing hypovolaemia, often
compounded by toxaemia from absorbed products and
septicaemia if infection is present.
Diffuse peritoneal irritation causes peristaltic paralysis
with the cessation of bowel motility.
20. Signs and symptoms
The clinical features of peritonitis are dependent on both
the aetiology and the progression of the inflammation.
The early manifestations of peritonitis following disease of
an abdominal viscus are characterized by the primary
disease process itself.
Irritation of the nearby parietal peritoneum results in
localization of the pain.
Associated symptoms include malaise, nausea and
vomiting, and a low-grade fever.
When the peritonitis is generalized the patient is clearly
unwell, with marked fever, dehydration, and absent bowel
sounds. Pain is diffuse throughout the abdomen and is
exacerbated by even the slightest movement. Shoulder-tip
pain is diagnostic of diaphragmatic inflammation.
21. Signs and symptoms
Physical findings can be divided into abdominal
signs and manifestations of systemic infection.
Local findings include
abdominal pain,
tenderness,
guarding or rigidity,
distention,
free peritoneal air,
and diminished bowel.
22. Signs and symptoms
Systemic findings include
fever,
chills or rigors,
tachycardia,
sweating,
tachypnea,
restlessness,
dehydration,
oliguria,
Disorientation
Shock is due to the combined effects of hypovolemia and
septicemia with multiple organ dysfunction. Recurrent
unexplained shock is highly predictive of serious
intraperitoneal sepsis.
Vital functions depend on the stage of the process: reactive
(or initial), toxic (or late) and terminal.
23. Laboratory findings
blood cell count,
arterial blood gases,
electrolytes,
liver and renal function tests.
A white blood cell count of greater than 200 cells/uL is
indicative of peritonitis, with virtually no false-positive and
minimal false-negative errors.
24. Instrumental investigations
Radiography (X-ray plan of abdomen)
Diagnostic puncture, abdominocentesis
Diagnostic peritoneal lavage
Ultrasonography
Magnetic resonanse tomography
Laparoscopy
25. Treatment
Surgery remains a cornerstone of peritonitis treatment.
Any operation should address the first 2 principles of the
treatment of intraperitoneal infections: early and definitive
source control and elimination of bacteria and toxins from
the abdominal cavity.
The operative approach is directed by the underlying
disease process and the type and severity of the intra-
abdominal infection. The surgeon should always strive to
arrive at a specific diagnosis and delineate the intra-
abdominal anatomy as accurately as possible prior to the
operation.
26. Treatment
In severe abdominal sepsis, however, delays in
operative management may lead to a significantly
higher need for reoperations and to worse outcomes
overall.
To reduce the bacterial load, a lavage of the abdominal
cavity is performed, with particular attention to areas
prone to abscess formation (eg, paracolic gutters,
subphrenic area).
Initial laparoscopic examination of the abdomen can
assist in determination of the etiology of peritonitis.
27. Preoperative preparations
Volume resuscitation and the prevention of secondary organ
system dysfunction are of utmost importance in the treatment of
patients with intra-abdominal infections. Correct existing serum
electrolyte disturbances and coagulation abnormalities as best as
possible before any intervention.
Begin empiric, broad-spectrum, systemic antibiotic therapy as
soon as the diagnosis of intra-abdominal infection is suspected
and tailor therapy according to the underlying disease process
and culture results.
Because patients with peritonitis often have severe abdominal
pain, provide adequate analgesia with parenteral narcotic agents
as soon as possible.
In the setting of significant nausea, vomiting, or abdominal
distension caused by obstruction or ileus, institute nasogastric
decompression as soon as possible.
28. Treatment
The goals of operative treatment of peritonitis are to
eliminate the source of contamination, to reduce the
bacterial inoculum, and to prevent recurrent or
persistent sepsis.
29. Treatment
A vertical midline incision is the incision of choice in
most patients with generalized peritonitis, because it
allows access to the entire peritoneal cavity.
In patients with localized peritonitis (eg, acute
appendicitis, cholecystitis), an incision directly over
the site of pathology (eg, right lower quadrant, right
subcostal) is usually adequate.
In patients with an unclear etiology of the peritonitis,
initial diagnostic laparoscopy may be useful.
Careful dissection and meticulous hemostasis are of
utmost importance.
30. Treatment
When faced with extensive abdominal inflammatory
disease and septic shock, draining the infection
temporarily, controlling the visceral leak quickly, and
deferring any definitive repair until after the patient
has recovered from the initial insult may be better.
31. Intensive care monitoring, often with ventilatory support
Program sanations
Flowing (running) or fractinal peritoneal lavage (Drains should be
removed or advanced once drainage diminishes and becomes more
serous in nature).
Achieving hemodynamic stability to perfuse major organs
(hypogidratation Ht >48%, CVP < 40 mm Hg; hypergidratation Ht <
35% CBP > 100; impaired cardial function Ht = № CVP – enlarged)
and this may entail the use of cardiac inotropic agents besides fluid and
blood product supportive measures.
Antibiotic therapy. Antibiotics are given for 10-14 days, depending on
the severity of peritonitis
Restoration of intestinal motor activity: procaine blocks, enemas,
peridural anesthesia
Enterosorbtion
Postoperative Care
32. Mannheim Peritonitis Index (МРI)
20 points(I degree of peritonitis) lethelity rate-0
20-30 points (II ст) 29%
More than 30 points (III ст) 100%
Risk factor Assessment of
severity (points)
1 Age 50 years 5
2 Sex (female) 5
3 Presence of organ’s failure 7
4 Presence of malignant tumor 4
5 Duration of peritonitis >24ч 4
6 Large bowel is the cause of peritonitis 4
7 Defuse peritonitis 6
8 Exudate (only one answer):
transparent 0
muddy-purulent 6
Fecal and saprogenic 12