This document discusses examination and treatment of brachial plexus injuries. It provides an overview of brachial plexus anatomy and classifications of injuries. Common clinical presentations are described including patterns associated with different levels and types of injuries. Timing of surgery is based on the severity and chronicity of the injury. Intraoperative assessment helps determine graftability and motor function to guide repair.
Pain from acute vertebral fracture appears to be due in part to instability (non-union or slow union at the fracture site), while more than 1/3 of patients become chronically painful.
Traditional treatment for patients with painful VCFs includes bed rest, narcotic analgesics and bracing, resulting in increased pain because of acceleration bone loss and muscle weakness.
paediatric injuries around the elbow
supracondylar elbow injuries
pulled elbow in paediatric age r
radiological signs around elbow in supracondylar fracture humerus
Pain from acute vertebral fracture appears to be due in part to instability (non-union or slow union at the fracture site), while more than 1/3 of patients become chronically painful.
Traditional treatment for patients with painful VCFs includes bed rest, narcotic analgesics and bracing, resulting in increased pain because of acceleration bone loss and muscle weakness.
paediatric injuries around the elbow
supracondylar elbow injuries
pulled elbow in paediatric age r
radiological signs around elbow in supracondylar fracture humerus
Spine and extremity injuries are common among people of all ages and can have a significant impact on mobility and quality of life. This PowerPoint presentation provides a comprehensive overview of spine and extremity injuries, including the causes, symptoms, and treatment options.
Through powerful images and personal stories, we showcase the impact of spine and extremity injuries on individuals, families, and communities. We highlight the challenges of accessing healthcare and rehabilitation services, particularly in low-resource settings, and the importance of early intervention and treatment.
The presentation provides detailed information about the various types of spine and extremity injuries, including fractures, dislocations, and soft tissue injuries. We also discuss the diagnostic procedures, including imaging tests and physical exams, and the treatment options, such as surgery, physical therapy, and pain management.
In addition, we explore the efforts being made to prevent and manage spine and extremity injuries. We highlight the importance of safety precautions, such as proper equipment use and ergonomic work practices, and the role of rehabilitation services in promoting recovery and restoring function.
Through this PowerPoint presentation, we aim to raise awareness about spine and extremity injuries and the importance of early diagnosis and treatment. We showcase the latest research and innovations in injury prevention and treatment, and the importance of collaboration and partnership to address the disease.
We urge the audience to take action in the fight against spine and extremity injuries, whether it be through spreading awareness, supporting organizations working on the ground, or advocating for policy change. Let us come together to create a world where everyone has access to the care and support they need to recover from spine and extremity injuries and live healthy, fulfilling lives.
Brachial plexus surgery restores the normal functioning of the shoulder, hands and arms. Ensure that a reputable surgeon providing services at an AAAASF accredited plastic surgery center is chosen.
La hernie du sportif : diagnostic et traitement, technique mini-ainvasive -Dr...VitamineB
La hernie du sportif : diagnostic et traitement, technique mini-invasive
Par le Docteur Ulrike MUSCHAWECK
Lors de la 1ère Journée Européenne de la pubalgie
Clinique du Sport Bordeaux Mérignac
The Important Nerves During Venous AblationVein Global
By: John Mauriello, M.D.
Visit VeinGlobal at http://www.veinglobal.com/ for more presentations and videos on this topic, or for more information on venous disease news, education and research.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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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
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
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
1. Hands II & Brachial Plexus
Chye Yew Ng
MBChB(Hons) FRCS(Tr&Orth) British Diploma in Hand Surgery
European Board of Hand Surgery Diploma
Consultant Hand & Peripheral Nerve Surgeon
Upper Limb Fellowship Director
Wrightington Hospital
2. www.slideshare.net/ChyeYewNg
www.vumedi.com (search for chye yew ng)
Clinical examination of brachial plexus
Examination of a patient with upper roots BPI
Nerve transfers for C5,C6 BPI
Exploration of infraclavicular brachial plexus
www.youtube.com (search for CY Ng or brachial plexus exam)
@CY_Hand @Nerve_Clinic
6. Cross Section of a Peripheral Nerve
Axon
Fascicle
Nerve
Endoneuriu
m
Epineurium
Perineurium
EpiPEn = Epi – Peri – Endo
A&E
Extrinsic & Intrinsic vascular supply
Longitudinal – Segmental - Interconnected
7. Central Neuronal Death &
Neuroprotection
Neuronal death after peripheral nerve injury
Acetyl-L-carnitine
Arrests sensory neuronal death
Speeds up regeneration
N-acetyl-cysteine
Provides sensory and motor neuronal protection
Hart et al. Neurological Research 2008
8. Mechanoreceptors
Slowly Adapting Rapidly Adapting
Cutaneous
Low
frequency
vibration
Merkel
discs
Meissner
corpuscles
Subcutaneous
High
frequency
vibration
Ruffini
terminals
Pacinian
corpuscles
10. Classification of Nerve Injuries
Seddon
BMJ
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in Continuity)
Neurotmesis
(Division of a nerve)
Brain
1943
• Localised
degeneration of
the myelin
sheaths
• Complete
interruption of
axons
• Preservation of
supporting
structures
(Schwann tubes,
endoneurium,
perineurium)
• All essential parts
destroyed
• Interruption can
occur without
apparent loss of
continuity
11. Classification of Nerve Injuries
Neurapraxia Axonotmesis Neurotmesis
Motor
- - -
Sensory
+/- - -
Autonomic
+/- - -
NCS
Conduction block at the site
Distal conduction preserved
Loss of conduction both at
and distal to the lesion
Loss of conduction both at
and distal to the lesion
EMG No fibrillation Fibrillation ++ Fibrillation ++
Recovery
Days to weeks provided the
cause is removed
Months provided the cause
is removed
No recovery unless repaired
13. In clinical practice, how do you distinguish?
Axonotmesis versus Neurotmesis
Nature of injury
Serial observations
Exploration
Seddon BMJ 1942
(Imaging)
14. Classification of Nerve Injuries
Sunderland
1951 I II III IV V
Focal
conduction
block
NO Wallerian
degeneration
Axonal
Disruption
Axon
+
Endoneurium
Disruption
Axon
+
Endoneurium
+
Perineurium
Disruption
Axon
+
Endoneurium
+
Perineurium
+
Epineurium
Disruption
Cross-innervation
16. Physiological Conduction Block
Type A
Intraneural circulatory arrest
Metabolic block with no nerve fibre pathology
Immediately reversible
Type B
Intraneural oedema
Increased endoneurial fluid pressure
Reversible within days or weeks
17. Classification of Nerve Injuries
Lundborg
1988
Physiological
conduction
block
Myelin
damage
Axonal
damage
Axon
+
Endo
damage
Axon
+
Endo
+
Peri
damage
Axon
+
Endoneuriu
m
+
Perineurium
+
Epineurium
damage
Type
A
Type
B
Sunder
land
1951
I II III IV V
Seddon
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in
Continuity)
Neurotmesis
(Division of a nerve)
18. Classification of Nerve Injuries
Lundborg
1988
Physiological
conduction
block
Myelin
damage
Axonal
disruption
Axon
+
Endo
Axon
+
Endo
+
Peri
Axon
+
Endoneuriu
m
+
Perineurium
+
Epineurium
Type
A
Type
B
Sunder
land
1951
I II III IV V
Seddon
1942
Neurapraxia
(Transient Block)
Axonotmesis
(Lesion in
Continuity)
Neurotmesis
(Division of a nerve)
Non-
degenerative
Degenerative
19. Nerve in Danger!
Pain, Pain, Pain
• Burning
• Severe
Autonomic dysfunction
• Absence of sweating
• Smoothness & dryness of skin
Tinel sign
• Distal to Proximal
• Regenerating touch fibres
20. BRITISH ORTHOPAEDIC ASSOCIATION
STANDARDS for TRAUMA (BOAST)
Sept 2012
BOAST 5: PERIPHERAL NERVE INJURY
All surgeons undertaking Musculoskeletal Trauma Surgery will be involved in the management of peripheral
nerve injury, either as a result of injury or a postoperative complication. Nerve repair and complex nerve injuries
(e.g. brachial plexus) is now a specialist field but all surgeons involved in trauma surgery must be able to di-
agnose nerve injuries and identify those that need referral to a specialist. These audit standards have been dis-
tilled from the recent BOA blue book on peripheral nerve injury which provides evidence-based guidelines for
management.
• A careful examination of the peripheral nervous and vascular systems must be performed and clearly
recorded for all injuries. This examination must be repeated and recorded after any manipulation or sur-
gery.
• If a laceration is near a nerve or associated with a neurological deficit, the urgent advice of a surgeon
who treats nerve injuries should be obtained.
• If a nerve injury is present with an unstable fracture or dislocation, the urgent priority (after life-saving
interventions) is reduction and stabilisation of the skeleton.
• When internal fixation of a fracture associated with a nerve injury is performed, in general, the nerve must
be explored. Possible exceptions are an axillary nerve palsy associated with low-energy shoulder trauma
and sacro-iliac screw fixation with a lumbosacral plexus injury.
• If a nerve is explored during fracture surgery, this must be clearly recorded in the operation record in-
cluding an indication of the nerve’s relationship to any internal fixation device.
• Nerves will occasionally be damaged during surgery and recognition and urgent treatment is essential.
Basic science evidence strongly supports very urgent repair as this will give the best possible outcome.
• If a divided nerve is found at surgery, and the surgeon does not have the skills to perform a definitive
repair, the nerve ends should be gently opposed with fine, coloured sutures. The patient should then be
discussed with a surgeon experienced in nerve repair.
• When a nerve or vascular deficit is identified following surgery, immediate measures include loosening
bandages, splitting Plaster of Paris splints (to the skin) and gentle repositioning of the limb. If these
measures are ineffective, a senior surgeon should be alerted to decide whether urgent re-exploration is
required.
• Painful, postoperative paralysis must be explored urgently. It may be due to compartment syndrome or
nerve compression from bone fragments, suture, haematoma or hardware.
• Pain and progressing loss of sensation is the hallmark of critical ischaemia. Immediate surgical explo-
ration is required. By the time paralysis occurs it is too late.
• Neurophysiological investigations are rarely needed in the acute injury and requesting neurophysiology
must not delay referral or treatment. MRI is not essential before surgery but can assist in preoperative
planning. Referral or surgery should not be delayed to wait for a scan.
• Brachial plexus injuries should be discussed with a plexus/complex nerve injury specialist within 3 days
of injury, or sooner if possible.
Evidence Base:
Predominantly retrospective case series but with good expert reviews and
an evolved, multi-national, professional consensus over 15 years.
HOT
22. Prerequisites for Nerve Repair
Skeletal stability
Healthy tissue bed
Healthy nerve ends
No undue tension
Adequate soft tissue coverage
23. Epineurial versus Group Fascicular Repairs
Epineurial
Less exact
Simple
Group Fascicular
Better alignment
More dissection (scarring)
The functional results of group fascicular repair
has not been shown to be more superior than that
of epineurial repair.
Lee & Wolfe. Peripheral nerve injury & repair. JAAOS 2000
24. Prognostic Factors of Outcomes
• Age
• DM, alcohol
Patient
factors
• Level of injury (distal vs proximal)
• Type of nerve (pure vs mixed)
• Condition of nerve ends
Injury
factors
• Delay to repair
• Length of gap
Surgical
factors
25. Which of the following is false regarding fibrin glue?
a) Fibrin glue is nontoxic and does not block axon regeneration
b) It may be used in combination with suture repair
c) The outcome of fibrin glue repair is inferior to that of suture
repair
d) The common components of fibrin sealants include
fibrinogen, thrombin and calcium chloride
e) It has low tensile strength
Tse & Ko. Nerve glue for upper extremity reconstruction. Hand Clinics 2012
26. Nerve Grafts/Conduits
Autologous Source
Nerve autograft
Vein (+/- muscle)
Off-the-shelf
Type I collagen
Caprolactone
Polyglycolic acid (PGA)
Submucosal ECM
Processed nerve
allograft
Lin et al. Nerve Allografts & Conduits in Peripheral Nerve Repair. Hand Clinics 2013
Kaushik & Hammert. Options for Digital Nerve Gap. JHSAm 2015
27. A 35 year-old male presented with numbness along the radial border of his
right index finger 9 months after he sustained a cut in his first web. After
surgical exploration and debridement, there is a 3.5cm nerve defect in the
radial digital nerve.
What is the most appropriate surgical reconstructive option?
a) Flexion of digit to achieve primary repair before gradual distraction
b) Type I collagen nerve conduit
c) Autologous vein graft
d) Posterior interosseous nerve graft
e) Polyglycolic acid (PGA) conduit
28. Principles of Motor Nerve Transfers
Donor nerve near target motor end plates
Expendable donor nerve
Pure motor donor nerve
Donor-recipient size match
Donor function synergy with recipient function
Motor re-education improves function
Mackinnon SE, Novak CB. Hand Clin 1999
30. Brachial Plexus Injuries
• Time• Breadth
• Length• Depth
Severity
(Seddon,
Sunderland)
Level
(Supra vs
Infra
clavicular)
Acute
vs
Chronic
Number
of roots
(C5-T1)
HOT
31. Leffert Classification
I Open
II Closed
IIA Supraclavicular
Pre-ganglionic
Post-ganglionic
IIB Infraclavicular
III Radiation induced
IV Obstetric
IVA Erb’s (upper root)
IVB Klumpke’s (lower root)
IVC Mixed
32. Objectives of Examination
Where is the lesion?
What functions are lost?
What functions are present?
How can you improve functions of the limb?
50. Common Clinical Patterns
Closed traction
BPI
Supraclavicular
Upper roots
Total palsy
Infraclavicular
Cord(s)
Terminal
branch(es)
Motorcycle
accident
Shoulder
trauma
51. Common Clinical Patterns
25yo RTA polytrauma
No shoulder motion
No elbow flexion
GOOD HAND
25yo RTA polytrauma
FLAIL UPPER LIMB
65yo anterior dislocation
of shoulder
NO DELTOID
C5, C6
C5 – T1
Axillary nerve
52. Common Clinical Patterns
25yo RTA polytrauma
No shoulder motion
No elbow flexion
GOOD HAND
C5, C6
XR neck chest shoulder
MRI cervical spine, BP
NCS/EMG at 3 weeks
25yo RTA polytrauma
FLAIL UPPER LIMB
C5 – T1
XR
MRI
NCS/EMG at 3 weeks
65yo anterior dislocation
of shoulder
NO DELTOID
Axillary nerve
NCS/EMG at 6 weeks
if no recovery
54. Intraoperative Assessment
- Is there a graftable nerve stump?
• Direct inspection
• Palpation
Surgical
• Somatosensory Evoked Potentials
(SSEP)
• Motor Evoked Potentials (MEP)
Neurophysiology
• Frozen section (fascicles / scar)
• Choline acetyltransferase (CAT)
activity – identify motor fascicles
Laboratory
55. Timing of Surgery
Emergent
- Open injury
- Arterial injury
- Deteriorating neurology
Early (<3months)
- Closed injury
- Complete/partial palsy
- Neurolysis/grafts/
transfers
Late (>12months)
- Muscle transfers
- Bony procedures
56. Surgical Priorities
1 – Restore elbow flexion
2 – Restore shoulder abduction & ER (stability)
3 – Restore hand function
57. Common Nerve Transfers
Palsy Donor Recipient
C5, 6
Spinal accessory
Radial (long head of triceps)
Ulnar fascicle
Median fascicle
Suprascapular
Axillary (anterior)
Biceps branch
Brachialis branch
C5, C6, C7
Spinal accessory
Intercostals
Ulnar fascicle
Median fascicle
Suprascapular
Axillary (anterior)
Biceps branch
Brachialis branch
C8, T1
Brachioradialis or brachialis branch
Supinator branch
AIN
PIN
58. Common Clinical Patterns
?Prognosis
25yo RTA polytrauma
No shoulder motion
No elbow flexion
GOOD HAND
C5, C6
Regain good elbow
flexion, moderate
shoulder movement
Return to work
25yo RTA polytrauma
FLAIL UPPER LIMB
C5 – T1
Poor-to-fair function
Long-term disability
65yo anterior dislocation
of shoulder
NO DELTOID
Axillary nerve Fair-to-good recovery
60. What do (I think) you need to learn?
Carpal tunnel syndrome
Cubital tunnel syndrome
Guyon canal syndrome
Radial tunnel syndrome / PIN palsy
Pronator syndrome / AIN palsy
61. Carpal Tunnel Syndrome
A collection of symptoms and signs due to
increased pressure within the carpal tunnel
leading to compression of the median nerve
• Pins & needles or Tingling
• Numbness
• Pain
• Weakness or clumsiness
• Wasting of thenar muscles
62. What are the contents of the carpal tunnel?
Median nerve
FDS x4
FDP x4
FPL
64. Who is affected? Risk Factors
Age: 45- 65
Females > males
Family history
Pregnancy
Medical conditions: Diabetes mellitus, Rheumatoid
arthritis, Hypothyroidism
Obesity
Vibration
Anatomical abnormalities of the wrist
65. What is the Gold Standard?
CTS
Signs Symptoms
Neurophysiology
66. Treatment Options Comments
Nocturnal neutral
wrist splint
• Those with night symptoms
Steroid injection
• Consider in pregnancy-related CTS
• 1 in 4-5 symptom-free at 1 year
Carpal tunnel release
• Complete division of transverse carpal ligament
• Open and endoscopic CTR both equally effective.
Endoscopic CTR may offer earlier return to work
but this may not be justifiable by its increased risks
of nerve injury and costs (in the NHS).
69. Cubital tunnel syndrome
What is your preferred surgical treatment for
primary cubital tunnel syndrome?
I would perform in-situ decompression because meta-
analyses have shown comparable clinical outcomes but
lesser complications/morbidity when compared to
anterior transposition.
71. Cubital tunnel syndrome
What are the indications of anterior
transposition?
• Revision
• Subluxation/Instability of ulnar nerve
• Poor tissue bed for the nerve
• (Elbow trauma surgery)
73. Superficial branch
(sensory only after
Palmaris brevis)
Ulnar artery
aneurysm or
thrombosis
Deep motor
branch
Ganglion or hook
of hamate
fracture (zones 1
& 2)
MixedLEFT HAND
74. Posterior Interosseous Nerve
Radial tunnel syndrome
Pain syndrome
EMG normal
PIN palsy
Motor deficit
EMG abnormal
Common Sites of Compression:
Fibrous band btw brachialis & BR
Recurrent leash of Henry
Extensor carpi radialis brevis edge
Arcade of Fröhse
Supinator muscle edge
75. Proximal Median Nerve
Pronator syndrome
Pain (forearm) syndrome
Paraesthesia
EMG/NCS inconclusive
AIN palsy
Motor deficit only
EMG/NCS abnormal
Sites of Compression:
Supracondylar process
Ligament of Struthers
Lacertus fibrosus
Btw two heads of pronator teres
FDS arch
Sites of Compression:
Tendinous edge of deep head of PT
Lacertus fibrosus
FDS arch
Accessory head of FPL (Gantzer’s muscle)
Accessory muscle from FDS to FDP
Aberrant muscles (FCRB, palmaris profundus)
Thrombosis of ulnar collateral vessels
Aberrant radial artery
Bicipital bursa
78. International Association for Study of Pain
CRPS Type I
Reflex sympathetic
dystrophy (RSD)
No definable nerve injury
CRPS Type II
Causalgia
Definable nerve injury
Symptoms NOT restricted
to dermatome
83. Decision making
What is missing
What needs reconstructing (think of FUNCTION)
What is available
What is appropriate
What?
HOT
84. Principles
Tissue equilibrium is achieved
Bony stability
Good soft tissue envelope/gliding plane
Full passive range of motion
Expendable donor
Minimum 1 wrist extensor, 1 wrist flexor
1 extrinsic flexor & extensor to each digit
When?
85. Force proportional to cross-sectional area of muscle
Average fibre length proportional to potential excursion
Amplitude/Excursion (The 3-5-7 rule)
Wrist flexors/extensors: 33mm
Finger extensors, FPL, EPL: 50mm
Finger flexors: 70mm
Tenodesis effect +20mm
Expect decrease of one MRC grade after transfer
PrinciplesHow?
87. Median Nerve Palsy
Low
Donor Tendon
Camitz Palmaris longus
Burkhalter Extensor indicis
proprius
Bunnell FDS IV
Huber Abductor digiti minimi
High
Lost Function Donor Tendon
Opposition EIP APB
Thumb IPJ
flexion
Brachioradialis
FPL
Index finger
flexion
FDP I Sutured to
neighbour FDPs
88.
89. Radial Nerve Palsy
PIN High
Lost Function Donor Tendon
Wrist extension PT ECRB
Fingers extension FCR EDC
Thumb extension PL EPL
Lost Function Donor Tendon
Fingers extension FCR EDC
Thumb extension PL EPL
90. Ulnar Nerve Palsy
Low
Lost Function Donor Tendon
Clawing (Grasp) FDS III slips
lateral bands
Thumb adduction ECRB + PL graft
Adductor
pollicis
Index finger
abduction
Accessory APL
1st dorsal
interosseous
Little finger
adduction
(Wartenberg sign)
EDM
radial lateral
band
High
Lost Function Donor Tendon
In addition to low
FDP IV/V DIPJ
flexion
Side-to-side
tenorrhaphy
FDP III
94. Dupuytren’s Disease
A benign proliferative disease that occurs in the
fascia of the palm and digits resulting in nodules,
cords and contractures.
Epidemiology
Caucasian of northern European ancestry
5th-7th decades M>F until 70 then M=F
Autosomal dominant pattern with variable penetrance
Ectopic manifestations
Ledderhose disease (plantar fascia)
Peyronie's disease (dartos fascia of penis)
Garrod’s pads (knuckle pads)
95.
96. Components of Spiral Cord?
4 – Grayson ligament
3 – Lateral digital sheet
2 – Spiral band
1 – Pretendinous band
97. Luck Stages of Dupuytren
Proliferative (Myofibroblasts predominate)
Involutional (Type III > I collagen)
Residual (Fibrocytes predominate)
98. Risk factors / associations
Hueston diathesis
Caucasians
Positive family history
Bilateral disease
Ectopic lesion
Male
Age of onset < 50
Other conditions
Diabetes mellitus
Alcoholism
HIV
Anti-epileptics
Trauma
(Vibration)
105. Zones Treatment
I (II)
• Mallet injury
• Open: repair and pin
• Closed: splint 8/52
• If chronic, risk of Swan-neck
III (IV)
• Open: repair and splint
• Closed: immobilise PIPJ for 3/52 &
leave DIPJ free
• If chronic, risk of Boutonniere
V VI
• Watch out for fight bites!
• Rehab: Static vs Dynamic vs EAM
VII
• Repair retinaculum
• Splint wrist in extension for 4/52
VIII • Core suture-type tendon repair
IX
• Muscle belly injury
• Beware of PIN injury
109. Flexor Tendon Repair
Challenges
Rupture, adhesion, joint stiffness, infection
Surgical Aim
To restore continuity to the tendon with a repair that is robust for EAM
Philosophy/Concept
Managing a number of compromises according to a hierarchy of priorities
110. How do you manage a zone II flexor tendon injury?
Anaesthesia GA, regional, Wide-awake technique (LA + adrenaline)
Core suture
At least 4 strands (Kessler, Cruciate, Adelaide)
4-0 monofilament (Prolene)
Epitendinous suture
Continuous configuration
6-0 monofilament (Prolene)
Rehabilitation
Dorsal splint for 6 weeks
Early active mobilisation