This document discusses fat embolism syndrome (FES), including its history, causes, mechanisms, clinical presentation, diagnosis, and treatment. Some key points:
- FES was first identified in 1862 and occurs when fat enters the bloodstream after long bone fractures or other trauma, causing respiratory, neurological and dermal symptoms.
- The exact mechanism is unknown but theories include fat globules entering blood mechanically from bone marrow or biochemically through free fatty acid release.
- Clinical diagnosis is based on respiratory issues, neurological abnormalities like confusion, and a petechial rash occurring 1-3 days post-injury. Treatment focuses on respiratory support.
Seminar presentation by 4th year medical student of Lincoln University College, supervised by HRPZ Orthopedic's specialist.
Reference were from reliable medical websites and also from texttbook; Apley and Solomon's Concise System of Orthopaedics and Trauma, 4th Ed.
This is a lecture presentation on applying external fixator on open fracture specially on tibia. This method is a classical method. Various new and dynamic fixators are there but the basics are the same.
Seminar presentation by 4th year medical student of Lincoln University College, supervised by HRPZ Orthopedic's specialist.
Reference were from reliable medical websites and also from texttbook; Apley and Solomon's Concise System of Orthopaedics and Trauma, 4th Ed.
This is a lecture presentation on applying external fixator on open fracture specially on tibia. This method is a classical method. Various new and dynamic fixators are there but the basics are the same.
Fat Embolism Syndrome (FES) is a Syndrome characterized by: Hypoxia, Confusion and Petechiae. Presenting soon after long bone fracture and soft tissue injury. Diagnosed by exclusion of other causes 0f (Hypoxia & Confusion). It occurs in 0.9 – 8.5% of all fracture patients. Up to 35% of the multiply injured. Mortality 2.5 – 15 - 20%. Rare in upper limb injury and children.
Treatment includes prompt stabilization of long bone fractures and supportive measures which includes: 1- Oxygen Therapy to maintain PaO2. 2- Mechanical Ventilation. 3- Adequate Hydration.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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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
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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
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 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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This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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2. Zenker, a pathologist,1st identified fat embolism
syndrome at autopsy 1862.
First diagnosed in 1873 by Dr Von Bergmann
1879 Fenger and Salisbury published description of
FES
3. Fat Emboli: Fat particles or droplets
that travel through the circulation
Fat Embolism: A process by which fat
emboli passes into the bloodstream
and lodges within a blood vessel.
Fat Embolism Syndrome (FES):
serious manifestation of fat
embolism occasionally causes multi
system dysfunction, the lungs are
always involved and next is brain
4. FAT EMBOLISM SYNDROME:
Clinical diagnosis, No specific laboratory test is
diagnostic
Mostly associated with long bone and pelvic #, and
more frequent in closed # then open #
Single long bone fracture 1-5% chance of
developing FES, and increases with number of #
Onset is 24-72 hours from initial insult
Mortality: 5-15%
8. CAUSES CONTD..
Non Trauma: agglutination of chylomicrons and VLDL
by high levels of plasma CRP.
– disease-related
• Diabetes, acute pancreatitis, burns, SLE, sickle cell crisis
– drug-related
• parenteral lipid infusion
– procedure-related
• Orthopedic surgery, liposuction
9. Exact mechanism unknown, but two main hypothesis
• Mechanical vs. Biochemical
• MECHANICAL – Fat globules from disrupted bone
marrow or adipose tissue are forced into torn venules
in areas of trauma.
• BIOCHEMICAL – Hormonal changes caused by trauma
and/or sepsis induce systemic release of free fatty
acids (FFA) as chylomicrons which cause the systemic
FES.
10. MECHANICAL HYPOTHESIS-
– Fractures of marrow-containing bone (Femur,
Pelvis) have the highest incidence of FES and
cause the largest volume of fat emboli, because the
disrupted venules in the marrow remain tethered open
by their osseous attachments.
– The marrow contents enter the venous circulation
with little difficulty.
11. CONT..
This theory is supported by research on Orthopaedic
long bone (IM reaming) and spinal surgeries which
cause fat globules to enter the blood circulation
when vigorous reaming/fixation is done.
Increased Pressure + Volume Extravasation
Measuring fat globules pre and post reaming
shows significant difference in concentration
12. CONT..
Fat droplets are deposited in the pulmonary capillary
beds and travel through arteriovenous shunts to the
brain. Systems affected include LUNG, BRAIN and
CIRCULATION.
Microvascular lodging of droplets produces local
ischemia and inflammation, with concomitant release
of inflammatory mediators, platelet aggregation, and
vasoactive amines
13. BIOCHEMICAL :
FES is dependent upon degradation of the embolized fat
into free fatty acids.
Neutral fat does not cause an acute lung injury, it is
hydrolyzed over the course of hours to several products,
including FFA, which cause ARDS in animal models.
CRP (acute phase reactant), which is elevated in trauma
patients, appears to be responsible in lipid agglutination
(FES) for both traumatic and non- traumatic FES.
14. CONT..
The process of Neutral fat cells -> FFA ->
Agglutination with CRP may explain the time
sequence of clinical findings in FES.
Onset of symptoms may coincide with
Agglutination.
This theory is animal model based and
circumstantial at best.
15. Diagnosis is made CLINICALLY NOT
CHEMICALLY. It does not matter how much
fat globules are in your circulation, it just matters if
you have their side effects.
FES typically manifests 24 to 72 hours after the
initial insult. Rarely <12 hrs or >72 hrs.
18. PULMONARY:
Hypoxia, rales, pleural friction rub
Breath sounds: Loud harsh, Crepts & wheeze
ARDS may develop(fat emboli obstructs lung vessel
(20microns) platelets and fibrin adhere.)
½ of pts with FES require mechanical ventilation (Bulger,
Archives of Surgery 1997; 132: 435-9)
CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
CT chest: ground glass opacification with interlobular
septal thickening
19.
20. NEUROLOGICAL FINDINGS:
Usually occur after respiratory symptoms.
Incidence 80% patients with FES
Minor global dysfunction most common, but ranges from
mild delirium to coma.
Seizures/focal deficits not common but can occur
Transient and reversible in most cases
CT Head: general edema, usually nonspecific
MRI brain: Low density on T1, and high intensity T2
signal, correlates to degree of impairment
21. RASH:
Petechial
Usually on conjuntiva , neck, axillae
Results from occlusion of dermal capillaries by fat
globules and then extravasations of RBC
Fleeting & last short.Resolves in 5-7 days
PATHOGNOMONIC, but only present in 20-50% of
patients
25. DIAGNOSIS
FES is CLINICAL diagnosis, not biochemical.
A high degree of suspicion is needed to make diagnosis
.
-Common misconception that the presence of fat
globules, either in sputum, urine, or a wedged PA
catheter, is necessary to confirm the diagnosis of FES
In 50% of fracture patients, fat globules was
demonstrated in the serum, without symptoms of FES.
HOWEVER
Growing literature on the use of bronchoscopy with
bronchoalveolar lavage to detect fat droplets in alveolar
macrophages as a means to diagnose fat embolism.
Sensitivity and specificity are unknown, being studied in
Trauma patients
26. FES = 1 major + 4 minor + fat microglobulinemia
Still widely used today
27. FES = femur fracture ± tibia fracture + 1 feature
Based on respiratory parameters
28. 3 TYPES- In 1962
SUBCLINICAL FES
NON FULMINANT FES
FULMINANT FES
29. SUBCLINICAL FES:
Around 3 days post trauma
Probably occurs in almost all long bone
fractures of the lower extremity and fractures of
the pelvis
Characterised by decreased PaO2, decreased
Hb% and decreased platelets. No clinical signs
and symptoms of respiratory insufficiency.
30. NONFULMINANT FES:
- Any time ,upto 6 days post trauma
-Clinical signs and symptoms are clearly evident.
Petechiae, tachycardia, respiratory failure, and signs of CNS
embolism.
Thrombocytopaenia, anaemia, and coagulation
abnormalities can be found, as can pulmonary alveolar and
interstitial opacities on chest x ray
31. There is no definitive test for this version of the
syndrome, as most of the changes described can
occur as a result of trauma as well as a result of fat
embolism, the diagnosis remains a clinical one,
and the significance is uncertain
32. FULMINANT FES:
Occurs very suddenly and rapidly after injury, and
progresses very quickly, often resulting in death within a
few hours of the initial trauma.
Clinical features are acute respiratory failure, acute
cor pulmonale and embolic neurological changes.
These occur shortly after injury and often result in the
death of the patient.
33. Pats. with multiple fractures are particularly
susceptible to this form of the syndrome, which,
although it is relatively rare, is of immense clinical
significance because of its high mortality.
34.
35. TREATMENT IS LARGELY SUPPORTIVE
Constant Positive Airway pressure(CPAP)
Mechanical Ventilation
Antibiotics
Nutritional support
Corticosteroids
Heparins
Have all been used
36. INITIAL TREATMENT
Adequate airway
Start IV line – correct fluid deficit
Basic investigation – including baseline chest X-ray
and ABG assay (v. imp).
Nasogastric tube – should be inserted in patient
with severe trauma and gastric contents suctioned
to prevent aspiration and ARDS
37. MONITORING
TPR, BP
I/O chart – maintain output 50-100cc/hr
CVP – to correct fluid deficit
If overload pulmn. Edema (4-8cm H2O)
Pulmonary haemodynamics– PCWP for accurate mean
of deficit correction (5-12mm of Hg)
Arterial blood gas monitoring
38. SPECIFIC DRUG THERAPY:
Many drugs have tried, most without demonstrable
benefit in established ARDS except Corticosteroids
but with some prophylactic benefit.
39. Drugs which may be tried in Fat embolism associated
ARDS are:
1.Ethanol : Lipase inhibitor, low incidence when level
>20mg.
2.Heparin : PL aggregation useful in DIC assoc
ARDS also.Controversial in trials.10000-15000 iu stat &
10000 iu 4-6hly with PTT at 1.5-2.5 INR.
3.Hypertonic glucose: block post traumatic
mobilization of FFA – may improve oxygenation.
40. 4.Corticosteroids – stabilize cell member, PMN
adhesion, prevent surfactant reduction, protect
capillary endothelium, compliment activation and
minimize transudation.
41. CORTICOSTEROIDS –
Value in ARDS of Fat embolism, aspiration,
sepsis, shock and cerebral edema.
Helpful in late stage in recovering patients in
reducing fibrotic change.
Improve and preserve arterial oxygenation and
stimulate proliferation and maturation of Type II
pneumocyte.
43. ATLS Protocol :
1. Early immobilization of fracture and early definitive
reduction (open or closed).
2. Maintain intravascular volume to maintain
cardiovascular stability (hypovolemic shock
resuscitation), may use colloids (albumin) as it can
expand fluid and bind FFA.
3. Mechanical ventilation with PEEP
44. 4. IV Ethanol has been used in Russia, Europe and
some American centres to decrease rate of FES.
J Bone Joint Surg Am. 1977 Oct;59(7):878-80
“A raised level of alcohol in the blood was
associated with a lower incidence of fat embolism” all
other variables controlled.
- Other studies
- Can J Surg. 1970 Jan;13(1):41-9
- Br Med J. 1978 May 13;1(6122):1232-4
45. ROLE OF FRACTURE STABILIZATION
Highly debated issue
- Accumulated evidence over past decade support
early fixation within 24 hours of injury.
46. Early IF – decompress # hematoma as ongoing
source of fat emboli and retained necrotic debris,
eliminate pain and physiologic stress with continued
# motion, optimize pulmn function, contributes to
reduced ventilatory dependence and improve
survival.
47. But transient increasing pulmn Ar pressure and
worsening pulmn gas exchange observed during
reaming of medullary canal. So undreamed nailing
is suggested for femoral fixation in multiple #
patients.
48. PROGNOSIS
Mild -undetected
Mod -low mortality
Severe -fatal unless if treatement
instituted early. Survivors have pulmonary sequele.