Congenital talipes equinovarus, or clubfoot, is a deformity where the foot is rotated inward and downward. It involves four components - cavus, adduction, varus, and equinus. Treatment involves serial casting or manipulation to gradually correct the deformity through stretching of contracted soft tissues and remodeling of bones. The Ponseti technique is currently the gold standard non-surgical treatment, involving weekly cast changes over 5-10 weeks to gradually position the foot in a corrected alignment. Surgical release of soft tissues may be required for resistant cases.
Please find the power point on Fracture of Talus with well diagrammatic explanation from very reliable sources. If you need such a power point on different topics related with MBBS then please write it on comment section. Thank you
Please find the power point on Fracture of Talus with well diagrammatic explanation from very reliable sources. If you need such a power point on different topics related with MBBS then please write it on comment section. Thank you
The medicos PDF app was used to collect this information. I stumbled discovered this amazing app when searching for various slides and books and decided to share it with you all. The Google Play Store has a free version of the app.
Importance for learners:
MBBS/Dental
Nursing
Pharmacy
Microbiology
BPH
MPH
MDS
MD
Ophthalmology
Paramedics
It is a form of arthritis that is long-lasting (chronic) and most often affects the spine. It affects joints in the spine and the sacroilium ...
Ankylosing spondylitis,Causes,symptoms, ...
Ankylosing Spondylitis Ankylosing spondylitis is a form of arthritis that mainly affects the spine. Pain In The Lower Back, Hips, And Buttocks ...This pdf consist of introduction, pathophysiology, clinical features, diagnosis,and management of ankylosing spondylitis including physiotherapy management
Anorectal Malformation for BSc Nursing/PB BSc Nursinggautamicharingia
Anorectal Malformation, in which you will learn about its types, incidence, causes, risk factors, signs and symptoms, associated abnormalities, diagnostic evaluation, surgical and nursing management. It also includes anal dilation, colostomy care and family education.
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.
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.
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
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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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
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
2. WHATISCTEV?
• ROTATORY SUBLUXATION OF TALOCALNOENAVICULAR JOINT
(SUBTALAR) COMPLEX WITH TALUS IN PLANTAR FLEXION
AND SUBTALAR COMPLEX IN MEDIAL ROTATION AND
INVERSION.
• ALSO REFFERED AS CLUBFOOT.
• TALIPES DERIVED FROM TERM: TALUS- ANKLE &
PES - FOOT
• EQUINOVARUS DERIVED FROM WORD EQUINO - LIKE A
HORSE &
3. DEFORMITIES:
• 4 CLINICAL COMPONENTS: CAVE
• C- CAVUS- EXAGGERATED MEDIAL LONGITUDINAL ARCH
AT MIDFOOT
• A- ADDUCTION- FOREFOOT IN ADDUCTION
AT TARSOMETATARSAL JUNCTION
• V- VARUS- HINDFOOT ROTATED INWARD AT
TALONAVICULAR JOINT
• E- EQUINUS- FOOT FIXED IN PLANTAR FLEXION ATANKLE
4.
5. EPIDEMIOLOGY:
• INCIDENCE- 1-2 PER 1000 LIVE BIRTH
• INCIDENCE IN MALE:FEMALE- 2.5:1
• LATERALITY- >50% CASES ARE
BILATERAL
• IN UNILATERAL AFFLICTION- RIGHT>
LEFT
6. ETIOLOGY:
• MOST COMMON CAUSE OF
CTEV IS
IDIOPATHIC.
• OTHER THAN IDIOPATHIC
IS
IS
CTEV
WHIC
H WITH
UNDERLYI
NG
SECONDA
RY
ASSOCIAT
ED
7. IDIOPATHICCTEV:
• ARRESTED FETAL DEVELOPMENT: BOHM PROPOSED ARREST OF FETAL
DEVELOPMENT OF THE LOWER LIMB IN 6-8 WKS SO CALLED CLUB FOOT
EMBRYONIC STAGE. HOWEVER DYSMORPHIC TALAR HEAD AND MEDIAL
DISPLACEMENT OF NAVICULAR IS NOT SEEN IN ANY STAGE OF NORMAL FETAL
DEVELOPMENT.
• MECHANICAL FACTOR IN UTERO: OLDEST THEORY PROPOSED BY HIPPOCRATES
SUGGESTING FOOT WAS HELD IN EQUINO VARUS BY EXTERNAL UTERINE
COMPRESSION. SOME INVESTIGATOR OPINE DIMINUTION OF AMNIOTIC FLUID
AS CAUSE OF CLUB FOOT.
• VASCULAR HYPOTHESIS: KEITH SUGGESTED TEMPORARY CESSATION OF
8. IDIOPATHICCTEV:
• MUSCULOLIGAMENTOUS FIBROSIS: IPPOLITO AND PONSETI FOUND
CONSIDERABLE INCREASE IN COLLEGEN FIBRES AND FIBROBLASTIC CELLS IN
LIGAMENTS AND TENDONS OF CLUBFOOT. THEY CONSIDERED TO BE PRIMARY
DEFECT, CARTILAGINOUS AND BONY CHANGES BEING SECONDARY.
• PRIMARY GERM PLASMA DEFECT: WAISBROD SUGGESTED DEFECT IN
PRIMARY GERM PLASMA OF CARTILAGINOUS TALAR ANALGE RESULTING IN
DYSMORPHIC TALAR NECK AND NAVICULAR SUBLUXATION.
• HEREDITARY: WYNNE- DAVIES SUGGESTED CLUB FOOT ARE PART OF
NUMEROUS SYNDROMES FOLLOWING MANDELIAN PATTERN OF EITHER
AUTOSOMAL DOMINANT OR AUTOSOMAL RECESSIVE INHERITANCE.
10. SECONDARYCTEV:
• GENETIC CAUSES-
N- ACETYLATION GENES NAT1 AND NAT2
XENOBIOTIC METABOLISM GENES CYP1A1
LIMB AND MUSCLE MORPHOGENESIS GENE HOXA, HOXD
AND IGF BP3
GENE FOR LOWER EXTREMITY DEVELOPMENT- CAN D2
AND WNT 7A
GENE FOR CONTACTILE PROTEIN OF SKELETAL
MYOFIBRES- TBX4
11. PATHOLOGICALANATOMY:
1. BONES-
• TALUS-
HEAD AND NECK DEVIATED MEDIALLY AND DOWNWARD.
MEDIAL AND PLANTAR DEVIATION OF NAVICULAR
ARTICULATION.
BODY ROTATED EXTERNALLY AND IS IN EQUINUS OF
NECK IN ANKLE
MORTISE.
BODY EXTRUDED ANTERIORLY
SMALLER THAN NORMAL
NECK- BODY ANGLE IS 90-110* (NORMAL- 150*)
DISLOCATION OF HEAD OF TALUS OUT OF ITS SOCKET.
13. PATHOLOGICALANATOMY:
• CALCANEUM-
OFTEN SMALL IN SIZE
MEDIALLY ROTATED
ANTERIOR PORTION LIES BENEATH
THE HEAD OF TALUS CAUSING VARUS
AND EQUINUS OF HEEL.
SUSTENTACULUM TALI IS
UNDERDEVELOPED.
• CUBOID-
MEDIAL
LY
HEAD
SUBLUXAT
ED
OVE
R
CALCANE
UM
14. PATHOLOGICALANATOMY:
• MUSCLES AND TENDONS-
ATROPHY OF PERONEAL GROUP OF
MUSCLES
CONTRACTURE OF TRICEP
SURAE,TIBIALIS
POSTERIOR,FLEXOR DIGITORUM
LONGUS AND FLEXOR HALLUCIS
LONGUS.
NUMBER OF FIBRES IN MUSCLE IS
NORMAL BUT ARE SMALLER IN SIZE.
THICKENING AND CONTRACTURE OF
TENDON SHEATHS ESPECIALLY OF
15. PATHOLOGICALANATOMY:
• LIGAMENTS-
THICKENING AND CONTRACTURES
ARE SEEN IN
CALCANEOFIBULAR LIGAMENT
TALOFIBULAR LIGAMENT
DELTOID LIGAMENT
LONG AND SHORT PLANTAR LIGAMENT
SPRING LIGAMENT
BIFURCATE LIGAMENT
INTEROSSEOUS TALO CALCANEUM
LIGAMENT
MASTER KNOT OF HENRY
16. PATHOLOGICALANATOMY:
• JOINTS CAPSULE AND FASCIA-
CONTRACTURES ARE SEEN IN
POSTERIOR ANKLE CAPSULE
SUBTALAR CAPSULE
TALONAVICULAR JOINT CAPSULE
CALCANEOCUBOID JOINT CAPSULE
PLANTAR FASCIA CONTRACTURE ARE SEEN WHICH IS
RESPONSIBLE CAVUS DEFORMITY
17. PATHOLOGICALANATOMY:
• SKIN CHANGES-
DEEP CREASE ON MEDIAL SIDE
DIMPLES IN LATERAL ASPECT OF ANKLE AND
MID FOOT.
SHORTENING ON MEDIAL SIDE OF SOLE
CALLOSITIES AND BURSA ON LATERAL SIDE
OF FOOT
• VASCULAR CHANGES-
HYPOPLASIA OR ABSENCE OF DORSALIS
PAEDIS AND ANTERIOR TIBIAL ARTERY
18. CLINICALFEATURES:
• HEEL IS SMALL AND IN EQUINUS
• FOOT INVERTED ON END OF TIBIA
• DEEP CREASES ON MEDIAL AND POSTERIOR
ASPECT
• ABNORMAL THIN CALF
• VARYING DEGREE OF RESISTANCE/ FIXED
DEFORMITY WHEN TRY TO DORSIFLEX AND EVERT
THE FOOT.
• LACK OF CORRECTABILITY
• OTHER JOINT ABNORMALITY
• ASSOCIATED ANOMALIES
AND CONDITION.
NEUROMUSCU
LAR
19. CLASSIFICATION:
1. IDIOPATHIC AND NON-IDIOPATHIC
2. CUMMIN CLASSIFICATION
3. PONSETI AND SMOLEY CLASSIFICATION- BASED ON EXTENT OF
DEFORMITY
4. HARROLD AND WALKER CLASSIFICATION- BASED ON
ABILITY TO CORRECT THE DEFORMITY.
5. BROWNE’S CLASSIFICATION- BASED ON TYPE OF DEFORMITY
6. DIMEGLIO ET AL SCORING SYSTEM BASED ON SEVERITY OF THE
DEFORMITY
20. CUMMINCLASSIFICATION
• SUPPLE: FOOT CAN BE BROUGHT TO NORMAL POSITION AND
ALL JOINTS ARE MOBILE.
• NEGLECTED: NO TREATMENT FOR 1 YR.
• RELAPSED: CORRECTED DEFORMITIES APPEARS AGAIN.
• RECCURENT: TYPE OF RELAPSE DUE TO MUSCLE IMBALANCE
• RESISTANT: NO CORRECTION AFTER CONSERVATIVE
MANAGEMENT.
• RIGID: AFTER CONSERVATIVE TREATMENT
FOREFOOT DEFORMITY CORRECTED AND
HINDFOOT DEFORMITY REMAIN UNCORRECTED.
21. PIRANISCORINGSYSTEM:
• SIMPLE AND RELIABLE SYSTEM TO DETERMINE SEVERITY AND MONITOR PROGRESS IN THE
ASSESSMENT AND
TREATMENT OF CLUBFOOT.
• SIX “SIGNS” ARE ASSESSED
• 3 SIGNS IN MIDFOOT
• 3 SIGNS IN HINDFOOT
• BASED ON 6 WELL-DESCRIBED CLINICAL SIGNS OF CONTRACTURE CHARACTERIZING A SEVERE
CLUBFOOT:
• IF THE SIGN IS SEVERELY ABNORMAL IT SCORES 1
• IF IT IS PARTIALLY ABNORMAL IT SCORES 0.5
• IF IT IS NORMAL IT SCORES 0
• TOTAL SCORE (TS) VARIES FROM 0 TO 6 AND IS THE SUM OF MIDFOOT AND HINDFOOT
CONTRACTURE SCORES
23. RADIOGRAPHICEVALUATION:
• FOR NON AMBULATORY CHILD-
ANTEROPOSTERIOR
STRESS DORSIFLEXION LATERAL
VIEW
• FOR OLDER CHILD-
STANDING ANTEROPOSTERIOR
STANDING LATERAL
• IMPORTANT ANGLE WE MEASURE-
TALOCALCANEAL ANGLE ON AP AND
LAT VIEW
TIBIOCALCANEAL ANGLE ON LAT VIEW
TALUS- FIRST METATARSAL ANGLE
24. RADIOGRAPHIC
EVALUATION:
TALOCALCANEAL ANGLE-
• ON AP VIEW-
1ST LINE THROUGH THE CENTRE OF
LONG AXIS OF TALUS (PARALLEL TO
MEDIAL BORDER)
2ND LINE THROUGH LONG AXIS
OFCALCANEUM (PARALLEL TO
LATERAL BORDER)
NORMAL 25-40*
• ON LATERAL VIEW-
1ST LINE MIDPOINT OF HEAD AND
BODY OF TALUS
2ND LINE ALONG BOTTOM OF
CALCANEUM
NORMAL 35-50*
25. RADIOGRAPHICEVALUATION
• RADIOLOGICAL FINDING SEEN-
• ON LATERAL VIEW-
DECREASED TALOCALCANEAL ANGLE (TALOCALCANEAL PARALLELISM)
DISRUPTED TALAR FIRST METATARSALANGLE
LONG AXIS OF TALUS AND CALCANEUM PASSES INFERIOR TO CUBOID (NORMALLY
CROSSES CUBOID)
• ON ANTEROPOSTERIOR VIEW-
INCREASED TALOCALCANEAL ANGLE
INCREASED TALAR FIRST METATARSALANGLE
LONG AXIS OF TALUS DEVIATE LATERALLY AND PASSES ALONG 3RD OR 4TH
METATARSALBONE
28. TREATMENT:
• GOAL: TO ACHIEVE
PLANTIGRADE FOOT
FLEXIBILTY
COSMETICALLY ACCEPTABLE FUNCTIONAL AND PAIN FREE FOOT IN SHORTEST
TREATMENT TIME
• PRINCIPLES:
SOFT TISSUE CONTRACTURE RELEASE OR STRETCHING TO
RESTORE NORMAL TARSAL RELATIONSHIP.
ONCE NORMAL TARSAL RELATIONSHIP ATTAINED, CORRECTION SHOULD BE
MAINTAINED TILL TARSAL BONES REMOULDS STABLE ARTICULAR SURFACE.
29. NONOPERATIVETREATMENT:
• SEVERAL REGIME HAVE BEEN PROPOSED INCLUDING SPLINTING
TAPING AND CASTING.
• KITE’S METHOD:
CORRECTION OF EACH COMPONENT SEPARATELY
CORRECTION WAS DONE IN FOLLOWING ORDER
PRONATION/ EVERSION OF 1ST METATARSAL.
PREMATURE DORSIFLEXION OF HEEL.
USED CALCANEOCUBOID JOINT AS FULCRUM THAT BLOCKS ABDUCTION OF CALCANEUS ,
THERBY PREVENTS EVERSION OF CALCANEUS.
FOREFO
OT
ADDUCTI
ON
KITE’S
ERRORS:
HEEL VARUS
EQUINU
S
30.
31.
32. NONOPERATIVETREATMENT:
• PONSETI TECHNIQUE:
2 PHASE- TREATMENT AND MAINTENANCE PHASE
TREATMENT PHASE-
BEGINS AS EARLY AS POSSIBLE. DURING FIRST WEEK OF LIFE ONLY
MANIPULATION IS CARRIED OUT BUT CAST IS NOT APPLIED.
ORDER OF CORRECTION-
TALUS HEAD IS USED AS FULCRUM.
5-6 SERIAL CASTING WITH MANIPULATION IS GENERALLY ENOUGH TO CORRECT
THE DEFORMITY. MAXIMUM UPTO 1O CASTING CAN BE DONE.
CAVU
S
ADDUCTION
WITH
VARUS
EQUINU
S
33. PONSETITECHNIQUE:
• CORRECTION OF CAVUS
DEFORMITY:
CORRECTED BY FOREFOOT
SUPINATION RELATIVE TO
HINDFOOT ALONG WITH
ADDUCTION OF FOREFOOT.
TENDS TO EXAGGERATE FOOT
INVERSION.
PRONATION OF FOREFOOT
SHOULD NOT BE DONE AS
IT INCREASES CAVUS
DEFORMITY BECAUSE 1ST
METATARSAL IS FURTHER
PLANTAR FLEXED.
E- RIGHT MANEUVER TO CORRECT CAVUS
DEFORMITY
F- WRONG MANEUVER TO CORRECT CAVUS
34. PONSETITECHNIQUE
A: THUMB IS POSITIONED OVER LATERAL ASPECT OF HEAD OF TALUS AND FINGER
CORRECT THE FOREFOOT.
B: CAVUS AND ADDUCTION ARE CORRECTED BY SLIGHT SUPINATION OF FOREFOOT IN
35. PONSETITECHNIQUE
• CORRECTION OF VARUS AND ADDUCTION:
CORRECTION OF CAVUS BRINGS METATARSAL, CUNIEFORM,
NAVICULAR, AND CUBOID IN SAME PLANE OF SUPINATION.
NOW FOOT IS ABDUCTED AND HELD IN FLEXION AND
SUPINATION TO ACCOMMODATE THE INVERSION OF TARSAL
BONES WHILE COUNTER PRESSURE IS APPLIED WITH THUMB
ON LATERAL ASPECT OF HEAD OF TALUS.
THIS MANEUVER NECESSITATES PROLONG STRETCHING OF
MEDIAL TARSAL LIGAMENTS AND TENDONS.
36. PRESSURE EXERTED ON METATARSALAND COUNTERPRESSURE ON LATERALASPECT
OF HEAD OF TALUS. FURTHER ABDUCTION OF FOOT HELD IN FLEXION AND
SUPINATION.
38. PONSETITECHNIQUE
• CORRECTION OF EQUINUS:
• SHOULD BE ATTEMPTED WHEN HINDFOOT
IS IN NEUTRAL POSITION TO SLIGHT
VALGUS AND FOOT IS ABDUCTED 70* RELATIVE TO LEG.
• EQUINUS IS COORECTED BY PROGRESSIVE DORSIFLEXING
THE FOOT.
• TO FACILITATE RAPID CORRECTION SUBCUTANEOUS
TENOTOMY IS DONE.
• CARESHOULDBE TAKEN WHILE DORSIFLEXING FOOTBY
39. FOOT IS FURTHER ABDUCTED UPTO 70*
TO
STRETCH TO STRETCH MEDIAL TARSAL
LIGAMENT.
NOTE: HEEL IS NOT GRASPED BY HAND
THUS ALLOWING CALCANEUS TO
ABDUCT WITH FOOT AND HEEL VARUS
TO CORRECT
41. PERCUTANEOUSTENOTOMY
FOOT HELD IN DORSIFLEXION AND
TENDON IS FELT
BLADE OF 11 SIZE ENTERS PARALLEL TO MEDIAL
BORDER OF
TENDOACHILLES 1CM ABOVE INSERTION AT
CALCANEUM.
BLADE IS PUSHED MEDIAL TO TENDON AND
ROTATED 90* UNDERNEATH IT. TENDON IS CUT
FROM MEDIAL TO LATERAL DIRECTION.
"POP" IS FELT AND CAST IS APPLIED IN
MAXIMAL
45. PONSETITECHNIQUE
• MAINTENANCE PHASE:
• AFTER REMOVAL OF CAST INFANT IS PLACED IN FOOT ABDUCTION
ORTHOSIS.
• BRACE IS WORN FOR 23HRS PER DAY FOR FIRST 3 MONTH THEN
ONLY WHILE SLEEPING FOR 3-4 YEARS.
• FREQUENT FOLLOW UP IS IMPORTANT TO DETECT EARLY
RECCURENCE.
• IT PREVENT RECURRENCE OF DEFORMITY
• IT FAVORS REMODELLING OF JOINTS WITH THE BONES IN PROPER
ALINGMENT AND TO INCREASE LEG AND FOOT MUSCLE STRENGTH.
46. FOOTABDUCTION
ORTHOSIS
• ALSO KNOWN AS DENIS BROWN
SPLINT.
• CONSIST OF SHOES MOUNTED TO
CROSSBAR IN POSITION OF 70*
EXTERNAL ROTATION AND 15*
DORSIFLEXION.
• DISTANCE BETWEEN SHOES IS SET
AT ABOUT 1INCH WIDER THAN THE
WIDTH OF INFANT’S SHOULDER.
• IN UNILATERAL CASES NORMAL
FOOT SHOULD IN 40* OUTWARD
47. CTEVSHOES
• MODIFIED SHOES
FOR CHILD WHO
START WALKING.
• THESE SHOES ARE
USE UNTILL 5
YEARS OF AGE.
• SPECIAL FEATURES:
STRAIGHT INNER
BORDER
OUTER SHOE RISE
48. NONOPERATIVETREATMENT
• STRETCHING AND ADHESIVE STRAPPING(ROBERT JONES):
PRINCIPLE- APPLY EVERSION CORRECTION FORCE ON FOOT
WITH HELP OF ADHESIVE STRAPPING.
• FRENCH TECHNIQUE:
GOAL IS TO REDUCE TALONAVICULAR JOINT, STRETCH OUT
MEDIAL TISSUES AND THEN SEQUENTIALLY CORRECT FOREFOOT
ADDUCTION, HINDFOOT VARUS AND EQUINUS OF CALCANEUM.
50. SURGICALTREATMENT
• INDICATION:
IN CASE OF NEGLECTED CTEV, RELAPSED CTEV, RECCURENT CTEV,
RESISTANT CTEV, RIGID CTEV.
• CHOICE OF SURGERY:
1-4 YEARS-
SOFT TISSUE RELEASE
4-11 YEARS-
SOFT TISSUE RELEASE WITH
OSTEOTOMY PERFORMED ACCORDING TO THE DEFORMITIES
>11YRS- SALVAGE PROCEDURES
TRIPLE ARTHRODESIS
TALECTOMY
51. SOFT TISSUE RELEASEOPERATION
TURCO’S OPERATION- IT IS ONE STAGE POSTEROMEDIAL RELEASE. HE
EMPHASIZED ON SUBTALAR
RELEASE ALONG WITH CALCANEOFIBULAR LIGAMENT.
CAROLL’S INCISION- CAROLL EMPHASIZED ON PLANTAR FASCIA RELEASE AND
CAPSULOTOMY OF
CALCANEOCUBOID JOINT. IT INCLUDE 2 INCISIONS, MEDIAL AND POSTERO-
LATERAL INCISION.
CINCINATTI INCISION- IT IS DONE FOR POSTEROMEDIAL AND POSTEROLATERAL
SOFT TISSUE RELEASE. PREFFERED TECHNIQUE FOR INITIAL SURGICAL
MANAGEMENT OF CLUB FOOT.
TENDOACHILLES TENDON RELEASE WITH POSTERIOR CAPSULOTOMY- TO
CORRECT RESIDUAL
52. TURCOOPERATION
• MEDIAL INCISION GIVEN
• EXPOSE TIBIALIS POSTERIOR, FDL,FHL, TENDOACHILLES AND POSTERIOR NEUROVASCULAR BUNDLE.
• DIVIDE MASTER KNOT OF HENRY.
• DIVIDE CALCANEONAVICULAR LIGAMENT AND ABDUCTOR HALLUCIS FROM TIBIALIS POSTERIOR
TENDON,NAVICULAR TUBEROSITY AND 1ST METATARSAL.
• POSTERIOR RELEASE- BY DOING Z-PLASTY OF TENDO ACHILLES, INCISING POSTERIOR CAPSULE OF ANKLE
JOIN, SUBTALAR JOINT AND DIVIDING TALOFIBULAR LIGAMENT AND CALCANEOFIBULAR LIGAMENT.
• MEDIAL PLANTAR RELEASE- DIVIDE TIBIALIS POSTERIOR, SUPERFICIAL DELTOID LIGAMENT, TALONAVICULAR
CAPSULE AND SPRING LIGAMENT.
• SUTALAR RELEASE- DIVIDE MEDIAL PART OF TALOCALCANEAL INTERROSEOUS LIGAMENT AND BIFURCATION OF Y
LIGAMENT.
• AFTER REDUCING NAVICULAR BONE TRANSFIX TALONAVICULAR JOINT BY K-WIRE AND SUBTALAR JOINT BY 2ND K-
WIRE.
55. ACHILLESTENDON
LENTHENINGAND
POSTERIORCAPSULOTOMY
• TO CORRECT RESIDUAL HINDFOOT
EQUINUS
• Z-PLASTY IS DONE TO LENGTHEN
THE ACHILLES TENDON.
• RELEASING MEDIAL HALF DISTALLY
AND LATERAL HALF PROXIMALLY.
• POSTERIOR CAPSULOTOMY OF
ANKLE AND SUBTALAR JOINT TO
RELEASE CAPSULE CONTRACTURE.
56. TENDONTRANSFER
• INDICATION- PASSIVELY
CORRECTABLE DEFORMITY
RESULTING FROM MUSCLE
IMBALANCE.
• ANTERIOR TIBIALIS TENDON
TRANSFER- TENDON IS
TRANSFERRED EITHER TO
MIDDLE CUNIEFORM OR TO BASE
OF 5TH METATARSAL.
• SPLATT (SPLit ANTERIOR TIBIALIS
TENDON TRANSFER)- LATERAL
57. DWYER
OSTEOTOMY
• INDICATION- PERSISTENT
VARUS DEFORMITY OF
HEEL WHEN SOFT TISSUE
SURGERIES ARE
CONTRAINDICATED.
• AGE- 3-4YRS
• DONE BY MEDIAL OPEN
WEDGE OSTEOTOMY OR
BY LATERAL CLOSED
WEDGE OSTEOTOMY
58. LATERALCOLUMNSHORTENINGPROCEDURE
• INDICATION- RECURRENCE OF CLUBFOOT
DEFORMITY
AFTER SURGICAL RELEASE IS MOSTLY DUE
TO DISPARITY BETWEEN MEDIAL AND
LATERAL BORDER OF FOOT. ANY ATTEMPT
TO CORRECT DEFORMITY IS RESISTED BY
MEDIAL CONTRACTURE AND EXCESSIVE
LENGTH OF LATERAL COLUMN.
• DIFFERENT PROCEDURE TO DO SHORTEN
LATERAL COLUMN ARE-
DILLWYNN EVANS PROCEDURE
LICHTBLAU PROCEDURE
59. LATERALCOLUMNSHORTENINGPROCEDURE
DILLWYN EVANS PROCEDURE LICHTBLAU
PROCEDURE
AGE- 4-8 YRS
INDICATION- MIDFOOT IN VARUS
DUE TO TALONAVICULAR AND
CALCANEOCUBOID SUBLUXATION
AGE- 3-4 YRS
INDICATION- HEEL VARUS & RESIDUAL
INTERNAL DEFORMITY OF CALCANEUS
WITH LONG LATERAL COLUMN
60. FOWLER
PROCEDURE
• INDICATION- SUFFICIENT
SCARRING THAT MEDIAL SOFT
TISSUE AND SUBTALAR RELEASE
WOULD BE IN EFFECTIVE.
• AGE- 6-8 YEARS
• PROCEDURE- LATERAL COLUMN
SHORTENING COMBINING WITH
MEDIAL
COLUMN LENGTHING BY
REMOVING
WEDGE FROM
CUBOI
D
AN
AN
D
OPENIN
G
TRANSFERING IT
TO
WEDGE.
61. SALVAGEPROCEDURE
• INDICATION-
UNCORRECTED CLUBFOOT OR WITH RESIDUAL DEFORMITY AFTER THE
AGE OF 10 YRS.
PAINFUL STIFF FOOT WITH POOR FUNCTION
DIFFICULT TO ACCOMMODATE TO FOOT WEAR
• GOAL-
CORRECT RESIDUAL DEFORMITY WHICH IS RESISTANT TO SOFT
TISSUE RELEASE.
TO ATTAIN FUNCTIONALLY AND COSMETICALLY ACCEPTABLE FOOT.
• PROCEDURE-
TRIPLE ARTHRODESIS
TALECTOMY
62. TRIPLE
ARTHRODESIS
• INDICATION-
PAINFUL STIFF FOOT WITH POOR
FUNCTION
DIFFICULT TO
ACCOMMODATE TO
FOOT WEAR
ALL OTHER CORRECTION FAILED
• AGE – 10 – 12 YEARS
• PROCEDURE-
OSTEOTOMY FOLLOWED BY
FUSION OF TALONAVICULAR,
63. TALECTOMY
• INDICATION-
RESERVEDFOR
SEVERE CLUBFOOT
• AGE - <6 YEARS
• PROCEDURE-
UNTREAT
ED
COMPLETE EXCISION OF TALUS
DEROTATE THE FOOT AND
DISPLACE THE CALCANEUS
POSTERIORLY INTO ANKLE
MORTISE UNTIL NAVICULAR ABUTS
THE ANTERIOR EDGE OF TIBIAL
PLAFOND.
• COMPLICATION-
64. EXTERNALFIXATOR
• INDICATION-
IN CASE OF NEGLECTED AND RECCURENT DEFORMITY WITH
SEVERE SCARRING
• MODALITIES-
ILLIZAROV’S EXTERNAL FIXATOR
JESS (JOSHI EXTERNAL STABILIZING SYSTEM)
• ADVANTAGE-
PREVENT CRUSHING OF THE TISSUES ON CONVEX SIDE
LENGHTENS THE LIMB
EFFECTIVELY CORRECT THE DEFORMITY AT SAME TIME
65. ILLIZAROV’SEXTERNAL
FIXATOR
• PRINCIPLE- FRACTIONAL DISTRACTION
• INDICATION- SEVERE DEFORMITIES
WITH SEVERE SCARING OR TROPHIC
ULCERS WHICH MAKE OPERATIVE
INTERVENTION CONTRAINDICATION
BECAUSE OF RISK OF TISSUE
NECROSIS.
• STEPS OF CORRECTION-
ANGULAR CORRECTION
OF HINDFOOTCORRECTION OF
FOREFOOT
SUPINATION
CORRECTION OF
FOOT
EQUINUS
66. JESS
• PRINCIPLE- DIFFERENTIAL
DISTRACTION
• ADVANTAGE-
LENTHENS ALL CONTRACTED
TISSUES PREVENTING
HISTIOGENESIS AND THUS
AVOID CUTTING OF THESE
IMMINENT SCARRING.
POSSIBLE TO CONTROL
MAGNITUDE
OF CORRECTION.
NO FURTHER SHORTHENING
OF FOOT
RESULTANT FEET IS VERY