This document discusses septic arthritis, including its definition, risk factors, common causative organisms, modes of infection, pathogenesis, clinical features, investigations, treatment, and approaches to joint aspiration and drainage. The key points are:
- Septic arthritis is a joint infection caused by bacterial invasion of the synovial membrane. It commonly affects the knee, hip, shoulder and ankle.
- Risk factors include rheumatoid arthritis, prosthetic joints, IV drug use, and diabetes. Common organisms include Staphylococcus aureus and gram-negative bacilli.
- Treatment involves joint drainage, IV antibiotics based on culture and sensitivity results, and splinting the joint. Surgical drainage is often needed if
Acute and Chronic Osteomyelitis - Infection of BoneRahul Singh
Acute and Chronic Osteomyelitis - Infection of Bone
http://essentialinspiration4u.blogspot.com
Osteomyelitis is defined as an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.
Duration , Mechanism & Host response.
Duration - Acute / Subacute / Chronic
Mechanism - Heamatogenous (tonsil , lungs , ear/ GIT) - Exogenous (injection , open fractures)
Host response - Pyogenic / Granulomatous
Introduction of bacteria from :
Outside through a wound or continuity from a neighboring soft tissue infection
Hematogenous spread from a pre existing focus (most common route of infection)
Avascular necrosis (AVN) of the femoral head is a pathologic process that results from interruption of blood supply to the bone. AVN of the hip is poorly understood, but this process is the final common pathway of traumatic or nontraumatic factors that compromise the already precarious circulation of the femoral head. Femoral head ischemia results in the death of marrow and osteocytes and usually results in the collapse of the necrotic segment
SEPTIC ARTHRITIS AS AN INFECTIOUS PROCESS, DESCRIBING THE APPLIED ANATOMY, THE ORGANISMS INVOLVED, STAGES , PRESENTATION ALL THE WAY DOEN TO THE MANAGEMENT PROTOCALS
Acute and Chronic Osteomyelitis - Infection of BoneRahul Singh
Acute and Chronic Osteomyelitis - Infection of Bone
http://essentialinspiration4u.blogspot.com
Osteomyelitis is defined as an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.
Duration , Mechanism & Host response.
Duration - Acute / Subacute / Chronic
Mechanism - Heamatogenous (tonsil , lungs , ear/ GIT) - Exogenous (injection , open fractures)
Host response - Pyogenic / Granulomatous
Introduction of bacteria from :
Outside through a wound or continuity from a neighboring soft tissue infection
Hematogenous spread from a pre existing focus (most common route of infection)
Avascular necrosis (AVN) of the femoral head is a pathologic process that results from interruption of blood supply to the bone. AVN of the hip is poorly understood, but this process is the final common pathway of traumatic or nontraumatic factors that compromise the already precarious circulation of the femoral head. Femoral head ischemia results in the death of marrow and osteocytes and usually results in the collapse of the necrotic segment
SEPTIC ARTHRITIS AS AN INFECTIOUS PROCESS, DESCRIBING THE APPLIED ANATOMY, THE ORGANISMS INVOLVED, STAGES , PRESENTATION ALL THE WAY DOEN TO THE MANAGEMENT PROTOCALS
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 gives a brief idea of Acute osteomyelitis, its cause, predisposing factors, pathogenesis, signs and symptoms, investigation and its management. It also explain Nades principle.
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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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Septic arthritis
1. SEPTIC ARTHRITIS
DR. DEBESH SHRESTHA
1ST YEAR PG RESIDENT
DEPARTMENT OF ORTHOPEDICS
GANDAKI MEDICAL COLLEGE
POKHARA, NEPAL
2.
3. Definition
• Septic arthritis is an inflammation of synovial
membrane with purulent effusion into the
joint capsule due to infection.
• Also referred to as Infectious Arthritis
• Considered as an orthopedic emergency
4. • Acute septic arthritis can occur at any age but
young children and elderly adults are most
susceptible
• Male = female
• The lower extremity weight bearing joints are
predominantly affected (61-79%)
• However any joint can be involved
• Multiple joint infections do occur
6. Organisms found in common clinical
settings of infectious arthritis
Patient age
o Neonate : Staph. aureus
o <2 yr : H.influenzae, S.aureus
o >2 yr : S.aureus
o Young adults : Neisseria gonorrhoea
(sexually active)
o Elderly adults : S.aureus(50%), Streptococci,
gram negative bacilli
9. Medical conditions
o Injecting drug use : atypical gram negative bacilli
(eg. Pseudomonas species)
o Rheumatoid arthritis : S.aureus
o SLE, sickle cell anemia : Salmonella species
o Hemophilia : S.aureus(50%), streptococci, gram
negative bacilli
o Immunosuppression : S.aureus, Mycobacterium
species, fungi
10. Modes of infection
1. Hematogenous spread from a distant site- most
common
2. Direct invasion through a penetrating wound, intra-
articular injection or arthroscopy
3. Direct spread from adjacent bone
o Can develop from osteomyelitis especially in infants in
whom transphyseal vessels allow proximal spread into
the joint in joints with an intra-articular metaphysis
(hip, elbow, shoulder, ankle)
11.
12.
13. Pathogenesis
• The usual trigger is a hematogenous infection
which settles in the synovial membrane
• There is an acute inflammatory reaction with a
serous or seropurulent exudate and an
increase in synovial fluid
14. • As pus appears, articular cartilage is eroded
and destroyed, partly by bacterial enzymes
and partly by proteolytic enzymes released
from synovial cells, inflammatory cells and pus
• Spread to the underlying bone or burst out of
the joint to form abscesses and sinuses
15. With healing there may be
1. Complete resolution and a return to normal
2. Partial loss of articular cartilage and fibrosis
of the joint
3. Loss of articular cartilage and bony ankylosis
4. Bone destruction and permanent deformity
of the joint
16.
17. Clinical features
In neonates
o Emphasis on septicemia rather than joint pain
o Irritable
o Refusal to feed
o Fever
o Rapid pulse
o Joint warm, tender and resistant to movement
o a/w umbilical cord inflammation, IV site
inflammation
18. • Baby’s chest, spine and abdomen should be
examined for any infection
• Look for concomitant osteomyelitis in an
adjacent bone end
19. In children
• Acute pain in a single large joint (commonly
the hip or the knee)
• Reluctance to move the limb
(pseudoparesis)
• Fever
• Rapid pulse
• Joint swelling and redness
• Joint tenderness
• All movements are restricted and often
completely abolished by pain and spasm
• Look for source of infection
20. In adults
• Often involve a superficial joint (knee,
wrist, finger, ankle or toe)
• Joint painful, swollen and inflamed
• Unable to bear weight
• Warm and tender
• Evidence of gonococcal infection or drug
abuse
• Patients with RA and on corticosteroids
may develop silent joint infection
23. Aspiration of joint fluid and analysis
• May be frankly purulent or in early cases clear
• White cell count and Gram stain
• Fluid culture and sensitivity
24.
25. Imaging –
May help confirm the suspicion but not diagnostic
Radiographs
• Usually normal- in first few days of infection
• Soft tissue swelling, displacement of fat pad
or joint space widening from localized edema
• As infection progresses, joint space narrowing
from destruction of cartilage
26. Ultrasonography
• Used to detect even small collections of fluid
deep in the large joints such as hip
• Widening of space between capsule and bone
of more than 2 mm is indicative of an effusion
• Echogenic fluid- likely septic
• Echo-free fluid- likely synovitis
• Used to guide joint aspiration and drainage
27. MRI and Radionuclide bone scans
o Helpful in diagnosing infections that are
difficult to assess
o In obscure sites such as sacro-iliac and
sternoclavicular joints
30. Treatment
• Principles
1. Adequate drainage of the joint and resection
of infected tissue
2. Antibiotics to diminish the systemic effects of
sepsis
3. Resting of the joint in a stable position
31. • Suspected arthritis suspected
• Blood and synovial fluid sample
• Empiric parenteral antibiotics based on Gram stain
• Joint drainage
• Adjust antibiotics based on culture and sensitivity result
32. • Empirical antibiotic treatment is based on the
patient’s age and risk factors
• Empirical antibiotic therapy should be given until
culture and sensitivity results are available, at
which time definitive treatment is initiated
• If no organism is isolated, empirical therapy
should be continued
33. Empirical Antimicrobial Therapy
Pathogen Empirical antimicrobial
Gram positive cocci in clusters with MRSA
risk factor or Beta lactam allergy
Vancomycin 15 mg/kg IV q12h
Gram positive cocci in clusters, no MRSA risk
factors
Nafcillin or oxacillin 2 g IV q4h
Gram positive cocci, no MRSA risk factors Cefazolin 2 g IV q8h
Gram positive cocci in chains (Streptococci
presumed)
Penicillin G 12-18 MU/d or ampicillin 2 g IV
q4h
Gram negative cocci ( Neisseria presumed) Ceftriaxone 1-2 g IV/ IM q12-24h or
cefotaxime 2 g IV q8h
Gram negative rods Ceftazidime 2 g IV q8h or cefepime 2 g IV q8h
34. Negative Gram stain, previously healthy,
no MRSA risk factors
Cefazolin 2 g IV q8h
Negative Gram stain, health care
associated or other MRSA risk factors
Vancomycin 15 mg/kg IV q12h plus
ceftazidime 2 g IV q8h, cefepime 2 g IV
q8h or piperacillin/tazobactam 4.5 g IV
q6h
Human, dog or cat bite Ampicillin sulbactam 1.5-3 g IV q4h
35. Pathogen directed Anti-microbial
Therapy
Pathogen Anti-microbial therapy
S. aureus( methicillin sensitive) Nafcillin or oxacillin 2 g IV q4h x 3 weeks
Cefazolin 2 g IV q8h x 3 wk
S. aureus (methicillin resistant or type I
penicillin allergy)
Vancomycin 15 mg/kg IV q12h x 3 wks
Streptococci including penicillin-sensitive
S.pneumonia
Penicillin G 12-18 MU IV qd divided dose
or ampicillin 2 g IV q4h
S. Pneumonia(penicillin resistant) Ceftriaxone 1-2 g IV q12h or
Cefotaxime 2 g IV q8h if susceptible or
vancomycin 15 mg/kg IV q12h x 2 wk
Enteric gram negative
bacilli
Ceftriaxone 1-2 g IV q12h or
cefotaxime 2 g IV q8h × 3 wk
Gram-negative bacilli
(P. aeruginosa)
Ceftazidime 2 g IV q8h or cefepime
2 g IV q8h, plus gentamicin or
tobramycin 5 mg/kg IV q24h ×
3 wk
36. Gram-negative bacilli Ciprofloxacin 400 mg IV q8-12h or
750 mg PO q12h or levofloxacin
750 mg IV or 750 mg PO qd × 3 wk
Polymicrobial Ampicillin/sulbactam 1.5-3 g IV q4h
× 3 wk
Clindamycin 600 mg IV q6-8h ×
3 wk plus ciprofloxacin 400 mg IV
or 750 mg PO q12h or levofloxacin
750 mg IV or 750 mg PO qd × 3 wk
Gram-positive
etiology and type I
penicillin allergy
Vancomycin 15 mg/kg IV q12h ×
3 wk
37. • If the diagnosis is made early and the involved
joint is superficial, such as the elbow or ankle,
aspiration should be performed and repeated
if necessary
• Appropriate antibiotics should be
administered, and the joint should be splinted
in a position of function.
38. • If the response is not favorable and repeat
aspiration does not show a decrease in the
synovial leukocyte count within 24 to 48
hours, open surgical drainage is necessary.
• If purulent material is deeply situated in a
joint, such as the shoulder or hip, open
surgical drainage should be done
39. • Arthroscopic drainage is a good alternative to
open drainage in many instances, especially
for infections involving the knee, elbow,
shoulder, or ankle
40. • Except for gonococcal arthritis, which usually
can be treated effectively with antibiotics,
drainage should be performed for all other
infectious arthritis.
44. POSTEROLATERAL DRAINAGE
OF THE ANKLE
• Hold the foot in dorsiflexion
• Begin the incision 5 cm proximal to the tip of the
lateral malleolus and just lateral to the Achilles
tendon. Extend the incision distally to the
calcaneus and curve it along the superior border
of that bone for 2.5 cm.
• Retract the sural nerve and small saphenous vein
laterally.
• Retract the peroneal tendons laterally
• Incise the posterior capsule under direct vision
45. Aspiration of knee
needle is inserted on the lateral side at the
level of the superior pole of the patella. It is
advanced through the lateral retinaculum and
into the joint.
46. Knee - Drainage
1. Anteromedial- most common
2. Anterolateral
3. Posteromedial
4. Posterolateral
47. ANTERIOR DRAINAGE OF THE KNEE
• Make parallel anterior incisions 7.5 to 10 cm long
on each side of the patella and sufficiently medial
or lateral to the sides of the patellar tendon.
• Incise the capsule and synovium, carefully
evacuate the purulent material, and disrupt any
loculations or adhesions. Use copious saline
irrigation.
• Leave the synovium open, but loosely close the
capsule and skin over drains. Use absorbable
monofilament sutures for closing the capsule.
48. • If the posterior compartment of the knee is
distended and a popliteal abscess is well
established, parallel anterior incisions
combined with posterolateral and
posteromedial (Henderson) incisions usually
are best.
49. POSTEROMEDIAL AND
POSTEROLATERAL DRAINAGE
OF THE KNEE• (KELIKIAN)
• Make a posterior longitudinal incision 7.5 to 10 cm long centered over the joint and the
semimembranosus tendon.
• Develop the interval between this tendon and the medial head of the gastrocnemius
muscle.
• Divide the semimembranosus and suture its proximal end to the deep fascia
• Make a generous window in the joint capsule and excise the posterior horn of the
medial meniscus.
• If the posterior compartment is divided by a median septum and complete drainage is
impossible through the posteromedial incision, or if drainage of only the lateral
compartment is desired, make a longitudinal incision 7.5 to 10 cm long over the biceps
femoris tendon.
50. • Incise the deep fascia lateral and anterior to this tendon
and free the tendon from the head of the fibula. Also free
the popliteus tendon from its insertion on the lateral
femoral condyle.
• Suture the free ends of both tendons to the deep fascia
• Window the joint capsule and remove a wedge of the
lateral meniscus.
• Kelikian advises that drains not be used but rather that
skeletal traction be applied to separate the joint surfaces.
51.
52. Aspiration of Hip
• Insert the needle 2.5 cm
lateral and 2.5 cm distal
to the point joining
inguinal ligament and
femoral artery at a 45-
degree angle to the skin
surface.
• Advance the needle 5 to
7.5 cm medially and
proximally into the joint.
53. Insert the needle at a 45-degree angle with the
surface of the thigh just inferior and anterior to
the greater trochanter
55. POSTERIOR DRAINAGE OF THE HIP
• Make an oblique incision in the line of the femoral neck
extending from the greater trochanter toward the
posterior superior iliac spine
• Split the gluteus maximus muscle in line with its fibers,
ligating branches of the inferior gluteal vessels as they
are encountered.
• Identify and protect the sciatic nerve in the medial
angle of the incision.
• Divide the external rotators of the hip at their
insertions on the greater trochanter.
• Incise the capsule
• Irrigate the joint profusely with saline
56. ANTERIOR DRAINAGE OF THE HIP
• Make a vertical incision beginning about 1 cm below the anterior
superior iliac spine inferiorly.
• Expose the sartorius muscle on the medial side and the tensor
fasciae latae and vastus lateralis muscles on the lateral side. Use
blunt dissection to separate these muscles.
• Identify the lateral border of the rectus femoris and retract this
muscle medially ; this exposes the hip joint capsule.
• Incise the capsule, evacuate the pus, and irrigate the joint with
saline.
• Leave the capsule open, but close the skin loosely over drains.
57.
58. Aspiration of Shoulder
The aspiration site is located half the distance
between the coracoid process and the anterolateral
edge of the acromion. The needle is directed
posteriorly through the joint capsule, and the joint
is aspirated.
59. Shoulder- Drainage
• The shoulder may be drained through an
anterior incision or a posterior incision, but
the anterior incision is preferable.
60. ANTERIOR DRAINAGE OF
THE SHOULDER
■• Begin an anterior longitudinal incision at the anterior
border of the acromion and extend it 5 to 7.5 cm over the
center of the humeral head.
• Split the fibers of the deltoid muscle 5 cm from the
acromion, divide the subscapularis tendon, and open the
capsule under direct vision.
• Open the synovial sheath of the long head of the biceps
tendon. Evacuate the pus and irrigate the joint copiously
with saline.
• In children, drill the proximal humeral metaphysis to
decompress any abscess but take care not to injure the
physis.
• Close the wound loosely over drains.
61. Elbow- Aspiration
Flex the elbow and insert the needle on its
posterior aspect just lateral to the
olecranon
63. MEDIAL DRAINAGE OF THE ELBOW
• Make an incision over the medial humeral
epicondyle and extend it 5 cm proximally and 2.5
cm distally.
• Develop the interval between the triceps
posteriorly and the brachialis anteriorly, taking
care not to injure the ulnar nerve.
• Elevate the periosteum laterally and distally until
the capsule is exposed.
• Incise the capsule and evacuate the pus.
• Irrigate the joint with saline and close the skin
loosely over drains.
64. LATERAL DRAINAGE OF THE ELBOW
• Make an incision over the lateral humeral epicondyle and
extend it 5 cm proximally and 2.5 cm distally.
• Separate the triceps muscle posteriorly from the extensor
carpi radialis longus anteriorly and expose the joint capsule.
Dissect close to the bone to avoid injuring the radial nerve.
• Incise the capsule, evacuate the pus, and irrigate the joint
with saline.
• Close the skin loosely over drains.
• The posterior compartment of the joint also may be
drained through this incision by dissecting posteriorly on
the humerus and elevating the attachment of the triceps
from the lateral surface of the bone.