This document provides an overview of various soft tissue infections, including their presentation, diagnosis, and treatment. It discusses impetigo, folliculitis, furuncles, carbuncles, cellulitis, erysipelas, necrotizing fasciitis, pyomyositis, and clostridial myonecrosis. The key points are: impetigo typically presents as blisters that rupture and form honey-colored crusts in children; cellulitis presents as warm, swollen, tender skin but lacks pus; necrotizing fasciitis is a severe infection requiring urgent debridement and antibiotics to treat widespread fascial necrosis; and clostridial myonecrosis following trauma can
Skin, Soft Tissue, & Bone Infections Symposia - The CRUDEM FoundationThe CRUDEM Foundation
This is the Skin, Soft Tissue, & Bone Infections Symposia presented in Milot, Haiti at Hôpital Sacré Coeur in 2011. CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Skin, Soft Tissue, & Bone Infections Symposia - The CRUDEM FoundationThe CRUDEM Foundation
This is the Skin, Soft Tissue, & Bone Infections Symposia presented in Milot, Haiti at Hôpital Sacré Coeur in 2011. CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Cellulitis is a bacterial infection of the deep dermis and subcutaneous tissue. It is most commonly caused by S. pyogenes and S. aureus.5 Bacteria may gain access to the dermis via a break in the skin barrier in healthy adults, whereas the hematogenous route is more common in immunocompromised patients.
The affected skin is usually erythematous, swollen, painful, and warm to the touch. Severe cellulitis can be complicated by bullae, pustules, or necrotic tissue. Damage to lymphatic vessels can lead to recurrent episodes of cellulitis.6 In areas of the world endemic for lymphatic filariasis, it is important to rule out this disease in cases of recurrent bouts of lower-extremity cellulitis and lymphangitis.
Cellulitis is a bacterial infection of the deep dermis and subcutaneous tissue. It is most commonly caused by S. pyogenes and S. aureus.5 Bacteria may gain access to the dermis via a break in the skin barrier in healthy adults, whereas the hematogenous route is more common in immunocompromised patients.
The affected skin is usually erythematous, swollen, painful, and warm to the touch. Severe cellulitis can be complicated by bullae, pustules, or necrotic tissue. Damage to lymphatic vessels can lead to recurrent episodes of cellulitis.6 In areas of the world endemic for lymphatic filariasis, it is important to rule out this disease in cases of recurrent bouts of lower-extremity cellulitis and lymphangitis.
DETAILED DISCUSSION OF NECROTIZING FASCIITIS.
A SOFT TISSUE INFECTION. USUALLY CALLED AS FLESH EATING BACTERIAL INFECTION. CAUSED BY BACTERIA. AFFECTS THE SOFT SKIN TISSUES
Necrotizing fasciitis has also been referred to as haemolytic streptococcal gangrene, Meleney ulcer, acute dermal gangrene, hospital gangrene, suppurative fasciitis, and synergistic necrotizing cellulitis.
Fournier gangrene is a form of necrotizing fasciitis that is localized to the scrotum and perineal area.
Hidradenitis suppurativa (HS) is an inflammatory disorder that is characterized by chronic deep-seated nodules, abscesses, fistulae, sinus tracts, and scars in the axilla, inguinal area, submammary folds, and perianal area. This disfiguring condition is accompanied by pain, embarrassment, and a significantly decreased quality of life. Although the mechanism of HS has not been entirely elucidated, lesion formation is believed to center around follicular hyperkeratosis within the pilosebaceous-apocrine unit. Recent research has provided new insight into the role of cytokines in the pathogenesis of HS, helping close some existing knowledge gaps in the development of this condition.
Gestational trophoblastic disease is a spectrum of interrelated disease processes originating from the placenta.
GTD is a spectrum of tumours with a wide range of biologic behaviour and potential for metastases
They are characterised by an abnormally high amount of HcG levels in the blood
Is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.
Myobacterium tuberculosis important cause of human TB.
Other closely related species in M. tuberculosis complex
M. bovis
M. africunum
M.microti
M. cannette
Vitamin A defficiency-Hamisi Mkindi.pptMkindi Mkindi
Vitamins
-Water soluble
-Fat soluble
Vitamin A
-fat-soluble vitamin ingested in the diet in
two forms.
-as retinol itself from animal sources or
-as provitamin carotene from plant sources
Previously termed acute renal failure
Reversible deterioration of renal function over hours to days manifested by:
Increase in BUN
Increase in creatinine
Reduced urine output
Oliguria : <400><100 ml urine output in 24 hours
Genital warts are an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV).
> than 100 types of double-stranded HPV papovaviruses have been isolated thus far, and, of these, about 35 types have affinity to genital sites
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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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
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
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
2. Skin and soft tissue infections
(SSTIs)
• Include infections of skin, subcutaneous
tissue, fascia, and muscle, encompass a wide
spectrum of clinical presentations, ranging
from simple cellulitis to rapidly progressive
necrotizing fasciitis.
• Diagnosing the exact extent of the disease is
critical for successful management of a
patient of soft tissue infection.
3. TYPES
The various types of SSTIs, listed according to clinical
presentation and anatomic location, include the
following:
•Impetigo
•Folliculitis
•Furuncles
•Carbuncles
•Erysipelas
•Cellulitis
•Necrotizing fasciitis
•Pyomyositis
4.
5. Impetigo
• Impetigo is an acute, highly contagious gram-
positive bacterial infection of the superficial
layers of the epidermis.
• Skin lesions such as cuts, abrasions, and
chickenpox can also become secondarily infected
(impetiginized) with the same pathogens that
produce classic impetigo.
• Impetigo occurs most commonly in children,
especially those who live in hot, humid climates
8. Impetigo-Treatment
• Treatment is directed at washing the affected
areas and applying topical antistaphylococcal
treatments, and broad-spectrum oral
antibiotics if streptococcal infection is
implicated.
• Mupirocin ointment (Bactroban).
• Oral Cephalexin
9. Folliculitis
• Folliculitis is a primary inflammation of the
hair follicle that occurs as a result of various
infections, or it can be secondary to follicular
trauma or occlusion.
12. Furuncles and Carbunlces
• Furuncles and carbuncles are subcutaneous
abscesses caused by S. aureus.
• The lesions are red, tender nodules that may
have a surrounding cellulitis. They often drain
spontaneously.
• If fluctuant, these lesions should be incised
and drained in conjunction with antibiotics,
especially if systemic symptoms or cellulitis is
present.
14. Cellulitis
• Is an inflammation of the dermal and
subcutaneous tissues due to non suppurative
bacterial invasion.
• Misnomer as lesion is one of the connective
tissues and interstitial tissue and not of the
cells.
• The common causative organisms are GAS
and staphylococcus.
15. Cellulitis-Pathophysiology
• Cellulitis usually follows a breach in the skin.
• In some cases, there is no obvious portal of
entry and the breach may be due to
microscopic changes in the skin or invasive
qualities of certain bacteria.
• There is a widespread swelling and redness at
the area of inflammation but without definite
localization.
18. Cellulitis-O/E
• The affected part is warm,swollen and tender.
• There is pitting oedema and brawny
induration.
• Regional lymph nodes will be enlarged and
tender with acute lymphadenitis.
• Calf tendersness test R/O dvt
21. Cellulitis-Treatment
Consist of:
•Rest and elevation of the part to reduce
oedema.
•Appropriate antibiotic preferably broad
spectrum should be administered.
•Pain relief
•Failure of inflammatory swelling to subside
after 48-72 hours suggest that an abscess has
developed hence I & D UGA.
22. Erysipela
• Is an acute infection of the upper dermis and
superficial lymphatics, usually caused by
streptococcus bacteria.
• Erysipelas is more superficial than cellulitis,
and is typically more raised and demarcated.
23. Erysipela-Pathophysiology
• Bacterial inoculation into an area of skin
trauma is the initial event in developing
erysipelas.
• The infection rapidly invades and spreads
through the lymphatic vessels. This can
produce overlying skin "streaking" and
regional lymph node swelling and tenderness.
26. Erysipelas or Cellulitis???
• Erysipela:
Typical rosy rash dissapears on pressure and
feels stiff.
Raised rash of erysipelas has a sharply defined
margin which is better felt than inspected.
28. Necrotizing fascitis
• A severe and extensive necrosis of the
superficial fascia and subcutaneous fat
with destruction of those tissues.
• Gram + and – bacteria involved
29. Pathophysiology
• Organisms spread from sub Q tissues along
superficial and deep planes, facilitated by
bacterial enzymes and toxins.
• Infection causes vascular occlusion, ischemia,
necrosis.
• Superficial nerves damaged, producing
anesthesia.
• Septicemia ensues
30.
31.
32.
33. Pathophysiology
• M1 and M3 surface proteins increase
adherence of the bacteria to the tissues,
protect from phagocytosis.
• Streptococcal pyrogenic exotoxins release
cytokines and produce hypotension.
34. Nec.Fasc-Symptoms
• pain or soreness of a muscle.
• The skin may be warm with red or purplish
areas of swelling that spread rapidly.
• There may be ulcers, blisters or black spots on
the skin.
• Fever, chills, fatigue (tiredness) or vomiting
may follow the initial wound or soreness
35. Diagnosis of Nec. Fas.
• History and Physical examination of the
patient !!!!! This is a simple diagnostic test that
works every time.
• Microbiology: group A Streptococcus
pyogenes , Coliforms, Staphylococcus Aureus,
Bacteroides species, and rarely Clostridium
septicum
36. Six Clinical Criteria of Nec. Fas.
1) Necrosis of the superficial fascia with undermining
of the surrounding tissues
2) Systemic toxic reaction with altered mental status
3) Absence of muscle involvement
4) No Clostridia species isolated
5) No arterial inflow occlusion
6) Pathological exam of debrided tissue shows
intense leukocytic infiltration, focal fascial and
surrounding tissue necrosis and thrombosis of
microvasculature
ref: Fisher’s criteria
38. Diagnosis-LRINEC
• The Laboratory Risk Indicator for Necrotizing
Fasciitis (LRINEC) score.
• It uses six serologic measures: C-reactive
protein, total white blood cell count,
hemoglobin, sodium, creatinine and glucose.
• A score greater than or eqaul to 6 indicates
that necrotizing fasciitis should be seriously
considered.
39. LRINEC-Criteria
The scoring criteria are as follows:
CRP (mg/L) ≥150: 4 points
WBC count (×103/mm3)
• <15: 0 points
• 15–25: 1 point
• >25: 2 points
41. Radiology
• Standard x-rays of little use.
• CT more sensitive.
• MRI and CT can delineate and determine
extent of surgical resection.
42. Imaging of Nec. Fas.
•Radiology
–Plain x-ray
shows gas in
tissues only
30% of cases
–Ultrasound:
not useful
43. Nec.Fasc-Treatment
• Regardless of the etiology, the primary
therapy is emergent surgical debridement and
treatment with antibiotics that are active
against streptococci, clostridium species, and
mixed aerobes and anaerobes.
• Clindamycin and pen G IV or Ceftriaxone 2gm
q12h IV .
44. Pyomyositis
• Pyomyositis, also known as tropical
pyomyositis or myositis tropicans, is a
bacterial infection of the skeletal muscles which
results in a pus-filled abscess
• Deep infection of muscle usually caused by S. aureus
and occasionally by group A streptococci or enteric
bacilli.
• Patients present with fever and tender swelling of
the muscle;Following exercise or muscle injury, the
skin is usually minimally involved.
45. Pyomyostis-Diagnosis
• Most often infects the large muscle groups.
• The diagnosis can be readily made, if
suspected, by needle aspiration and x-rays.
• Within 1-2 days of injury, the involved
extremity becomes painful and swollen. Gas
present in tissue may be obvious by physical
exam, x-ray or CT.
47. Clostridial Myonecrosis
• Principally C. perfringens but C. novyi and C.
septicum also seen.
• Predisposing event
–Deep trauma with gross contamination
–Surgical wound
–Hematogenous spread from colonic lesion
• Incubation Period 2-3 days; then explosive
spread.
48. Clostridial Myonecrosis
•Presentation
– Severe pain out of
proportion to
clinical findings
– Erythema and
cutaneous blisters
– Gangrene
– Crepitus
– Brown foul smelling
discharge
– Loss of motor
function
49. Pathophysiology
• Clostridia spores Tissues
Contamination, severe and open wounds
Germinate and grow rapidly
If normal tissue ox-red potential lowered eg.cell injury
• Lesion involve co-infection
• Alpha toxin and other exotoxins secreted.
• Enzymes break down ground substance
facilitating spread.
51. Treatment
• Debridement and excision, with amputation
necessary in many cases.
• Antibiotics alone are not effective because
they do not penetrate ischaemic muscles
sufficiently to be effective.
52. Treatment-cont
• Penicillin is given as an adjuvant treatment to
surgery.
• In addition to surgery and
antibiotics, hypercarbic oxygen
therapy (HBOT) is used and acts to inhibit the
growth of and kill the anaerobic C.
perfringens.
53. References
• WWW.emedecine.medscape/Skin soft tissue
infections.
• Bailey & Love’s short practice of surgery
• Ovadia D, Ezra E, Ben-Sira L et al. (2007).
"Primary pyomyositis in children: a
retrospective analysis of 11 cases".
• Lippincot illustrated review of microbiology
• Consise textbook of surgery by S DAS