surgical anatomy of nose is a humble attempt to make the anatomy of nose simpler and easy for medical students and fellow physicians. at the end of the presentation the students will be able to identify all the structures.
The Nose and nasal cavity, anatomy, and clinical diseases of nasal cavity and...HamzehKYacoub
Nasal cavity is the most superior part of the respiratory system.
Blood supply of nose and Cavernous Sinus.
Epistaxis causes and locations.
Allergic Rhinitis and Non-allergic rhinitis with eosinophilia (NARES).
Ostiomeatal complex (OMC)
Sinusitis.
Nasal polyps.
Headaches types.
Neuralgia.
USMLE RESP 02 nose and paranasal sinuses anatomy medical .pdfAHMED ASHOUR
The nose and paranasal sinuses are interconnected structures in the upper respiratory system that play essential roles in the respiratory and olfactory processes.
Disorders of the nose and paranasal sinuses can include sinusitis (inflammation of the sinuses), nasal polyps, deviated septum, and various infections.
Proper care and treatment are essential to maintain respiratory function and overall health.
The nasal septum is the cartilage and bone in your nose. The septum divides the nasal cavity (inside your nose) into a right and left side. When the septum is off-center or leans to one side of the nasal cavity, it has “deviated.” Healthcare providers call this a deviated nasal septum.
Spaces of middle ear and their surgical importanceDr Soumya Singh
one of the imp topics in ENT that should be understood very thoroughly if u want to pursue as an otologist.I tried to simplify the topic with simple diagrams and models for better understanding .
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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
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
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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ASA GUIDELINE
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2 Case Reports of Gastric Ultrasound
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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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
9. Embyology of nasal septum
5 facial prominences form the nose
• 1-frontal prominence
• Paired medial prominence
• Paired lateral prominence
Septum begins as a downward growth of frontal
prominence,as primary n secondary shelves
join in ,descending septum fuses with the
palate to separate the nasal cavity into 2
distinct nasal passages
10. Nasal septum
Anatomy of nasal septum:
Nasal septum consists of three parts:
1. Columellar septum
2. Membranous septum
3. Septum proper: principle constituents of septum proper
are
a)perpendicular plate of ethmoid
b)vomer
c)septal(quadrilateral cartilage)
minor contributions from crest of nasal bone,nasal spine
of frontal bone,rostrum of sphenoid,crest of palatine and
maxilla and anterior nasal spine of maxilla.
11. Nasal septum
o Mucosa :pseudostratified columnar epithelium
o along inferior two-thirds
o olfactory epithelium along superior one third
o forms a partition between right and left nasal cavities and
provides support to tip and dorsum of cartilagenous part of
nose.
o Septal cartilage lies in a groove in the anterior edge of vomer
and rests anteriorly on anterior nasal spine. during trauma, it
may get dislocated from nasal spine or vomer causing caudal
septal deviation and spur respectively.
15. • FROM ICA >ophthalmic artery >ant. and post.
Ethmoidal arteies
• FROM ECA- sphenopalantine artery br of int.
maxillary artery
Superior labial br of facial artery
19. LITTLE’S AREA (KIESSEL BACH’S PLEXUS)
Anterior ethmoidal
Septal branch of supeior labial
Septal branch of sphenopalotine
Septal branch of greater palatine
20.
21. Vomeronasal organ
Vomeronasal organ for
olfaction (primordial)
Aka Jacoben’s organ
Located on anterior septum
Found with endoscopy 76%
of the time
Don’t biopsy but recognize
as normal anatomic
structure
22. Factors affecting shape and position of
nasal tip
• Lateral crural complex
• Thickness of the overlying skin
• Ligaments and fibrous attachments of nasal
tip structures
23.
24. DOME
Anatmic dome :
Junction of middle and lateral crura
clinical dome:
The most anterior projecting portion of lower
lateral cartilage
Tip defining point:
The external projection of dome
25.
26.
27.
28. Nasal valve
• Narrowest point of upper airway
• Small changes in nasal septal structure can have
significant effects of airflow resistance n
sensation of obstruction
• Boumdaries – 2dimensional plane slicing through
caudal end of upper lateral cartilage superiorly
Alae – laterally
Bony nasal floor inferiorly
Septum medially
29.
30. Fractures of nasal septum
• Aetiopathogenisis:
-Trauma inflicted from front, side or below.the septum may
buckle on itself, fracture vertically, horizontally or get crushed.
-fracture of septal cartilage or its dislocation can occur without
nasal bones fracture.
septal injuries with mucosal tears cause profuse epistaxis
while with intact mucosa result in septal hematoma.
31. Fractures of nasal septum
Types :
1} Jarjaway fracture: result from blow from front.
fracture line starts just above the anterior nasal spine and
runs horizontally backwards just above the junction of septal
cartilage with the vomer.
2} Chevallet fracture: results from blow from below.
runs vertically from anterior nasal spine upwards to the
junction of bony and cartilaginous dorsum of nose.
33. Fractures of nasal septum
Treatment: -early recognition and treatment of septal injuries is
essential.
-dislocated or fractured fragments should be repositioned and
supported between mucoperichondrial flaps.
-haematomas should be drained.
Complications: a) deviation of cartilagenous nose.
b) asymmetry of nasal tip,columella,or
nostril.
34. DEVIATED NASAL SEPTUM
AETIOLOGY:
1) Trauma:
lateral blow-displacement of septal cartilage from vomer.
blow from front-buckling, fracture, duplication of septum with
telescoping of fragments.
2) Developmental: the septum should grow at the same rate as that of
face. if septum grows at faster rate it becomes buckled. unequal
growth between palate and base of skull may also cause buckling
(high arched palate)
3) Congenital: abnormal intrauterine posture cause compressing
forces acting on nose and upper jaw.
4) Hereditary
5) Racial: Caucasians are more affected
6) Secondary: to a tumour, mass or polyp.
35. DEVIATED NASAL SEPTUM
Types:
1) Deviations: upper or lower, anterior or posterior, C
shaped, S shaped. nasal cavity on the concave side of
the septum will be wider and may show compensatory
hypertrophy of turbinates.
2) Anterior Dislocation: seen on tilting the patients head
backwards.
3) Spurs: shelf like projection at the junction of bone and
cartilage. may predispose for epistaxis and headache.
4) Thickening: it may be due to organized haematoma or
over-riding of dislocated septal fragments
5) impacted septum-despite decongestants
37. Mladina classification for nasal septal
deviation
• Type 1- U/L vertical ridge in the valve region
• Type 2- same as type 1 but more severe obstrution n disturbance of
nasal valve
• Type3- U/L vertical ridge at d level of head of middle turbinate
• Type 4- combination of type3 wid either type ½
• Type 5- HZ septal crest in contrast wid lateral nasal wall
• Type 6- prominent maxillary crest C/L to deviation wid a septal crest
on d deviated side
• Type 7- combination of previously described septal deformity types
38. Clinical features
• Nasal obstruction: the most common symptom mainly on side
of DNS,C/L paradoxical nasal obstruction due to turbinate
hypertrophy may be seen
• Headache-contact with lateral wall sluders neuralgia,sinusitis
• Recurrent attacks of cold due to sinusitis
• Epistaxis-stretched mucosa on DNS-dry crusting n bleeding on
removal-stretched blood vessels over spur
• Anosmia/hyposmia-in high DNS
• External deformity
• Middle ear infection
39. Clinical features
• Cottle’s test: used in nasal obstruction due to
abnormality of nasal valve. In this test cheek is
drawn laterally while the patient breathes
quietly. If the nasal airway improves on test
side the test is positive and indicates
abnormality of nasal valve
43. History of septoplasty
• Edwin smith papyrus
treating broken nose by placing 2 plugs of linen coated wid grease& ext packing
wid stiff rolls of linen
• Bosworth opeartion (late 19th)
deviated part of septum amputed wid mucosa on convex side
• Asch (1899)- full thickness cruciate incision on septal cartilage
• Freer (1902) -SMR of total septal cartilage
• Killian (1904) -SMR wid preservation of dorsal&caudal portion of cartilage
• Metzenbaum (1929)-swinging door technique for caudal dislocation
• Peer (1937)-removal of caudal septum n replacement after its alterartion
• Cottle (1948)-maxilla –premaxilla septoplasty
44. Preoperative assessment
History
1. Allergies
2. Nasal obstruction (unilateral/bilateral, constant/intermittent, seasonal)
3. Bilateral symptoms that change in severity (mucosal disease)
4. Constant obstruction (fixed structural abnormality)
5. Presence of epistaxis or rhinorrhea
6. Prior nasal surgery
7. Medication history (especially vasoconstrictive sprays, OC’s)
8. Trauma
9. Symptoms (crusting, dry mouth, frequent sore throats, sinus problems)
45. Anosmia/hyposmia
University of Pennsylvania Smell Identification
Test (UPSIT)
Help identify malingering and gross degree of
impairment
34% of patients scored lower postoperatively after
septal surgery
66% improved or were unchanged
46. Rhinomanometry
Anterior rhinomanometry
Posterior rhinomanometry
Pernasal rhinomanometry
Objective information regarding respiratory
function
Quantifies nasal air flow and pressure
Nasal resistance (pressure/flow)
47. Acoustic rhinomanometry
Measures the cross-
sectional area of the
nasal cavity as a
function of distance
from the nostril
Sound generator, wave
tube, microphone, and
a computer
48. Optimizing acoustic rhinomanometry
Must form an acoustic seal with wave tube
without distorting the nasal tip
Results represent cross sectional area as a
function of distance (cm) from end of
nosepiece
Does not detail shape of the airway, cannot
provide information on nasal airway resistance
49. Physical exam
• External appearance of nose
• Mouth breather
• Adenoid facies (maxillary hypoplasia)
• Location of deviation
• Tip support
• Nasal valve
• Remove all crusts (? Underlying perforation,
exophytic lesion, etc)
• Any abnormal crusts, ulcerations, or polypoid
changes should delay elective surgery for
possible underlying systemic condition
• Examine with vasoconstrictor, endoscope
50. Goals of surgery
Exposure of the pathologic portion of septum
Removal or reconstruction of the defective
portions
Preserve nasal mucosa and lining
Prevent external deformity of patient
51. Anaesthesia
• Lignocaine 2% wid epinephrine 1/100,000
• Solution injected subperichondrially (not used only as a hemostatic
agent but for hydrodissection-with pressure lifting the mucosa and
perichondrium from cartilage
• Performed in anterior to posterior direction and d mucosa should
blanch as injection proceeds
• Injected bilaterally
• more the time taken for infillteration less is the time rqrd for Sx
52. You inject lidocaine with epinephrine and the patient becomes
tachycardic, hypotensive, and syncope…
Vasovagal?, Allergic Reaction to PABA?, Intravascular Injection of
Epinephrine?
Vasovagal-Bradycardic, Cool skin, Hypotensive, Impending sense of doom
Allergic Reaction-Tachycardic, Hypotensive, Flushed and warm skin
Intravascular Epinephrine-Tachycardic (from epinephrine), Hypotensive
from impaired ventricular filling of heart, Peripheral Vasodilation
(depending on the dose) can occur
53. Incisions
Kilian incision
Preserves projection the best
Should not be too far posterior (difficult to close)
Hemitransfixion incision
Full transfixion incision
High and Low transfixion incision
Open rhinoplasty incision
56. Treatment- surgery
• Submucous resection of nasal septum (SMR)
It is generally done in adults
It consists of elevating mucoperichondrial and
mucoperiosteal flap on either side of the
septum, removing the deflected parts of bony
and cartilagenous septum and then
repositioning the flaps
57. SMR
• Indications
Deviated nasal septum causing nasal obstruction and
recurrent headaches
Deviated nasal septum causing obstruction to ventilation of
paranasal sinuses and middle ear resulting in recurrent
infections
Recurrent epistaxis from septal spur
As a part of septorhinoplasty
Harvesting cartilage graft for tympanoplasty and
rhinoplasty
As an approach to surgeries of sphenoidal sinus, vidian
nerve and pituitary gland
59. SMR
• Anesthesia - Local anesthesia/ general
anesthesia
• Positioning: reclining position with head end of
the table raised
60. SMR - STEPS
• Infiltration: subperichondrial infiltration with 2% xylocaine with
adrenaline
• Incision: killian’s incision- curvilinear incision 2-3mm behind the
anterior end of septal cartilage
• Elevation of flaps: the mucoperichondrial and mucoperiosteal flap
is elevated
• Incision of the cartilage- cartilage is incised just posterior to the
first incision
• Elevation of opposite mucoperichondrial and mucoperiosteal flap
61. SMR – STEPS (cont…)
• Removal of cartilage and bone - cartilage can be
removed with Ballinger swivel knife or luc’s
forceps. Bony spur is removed using gouge and
hammer
• Preserve a strip of 1cm wide cartilage along the
dorsal and caudal borders ( L-struts)
• Nasal packing
63. Keystone areas
Preserve along bony
cartilaginous junction
Preserve along nasal floor
Diagram showing area of L
SHAPED STRUT cartilage
preserved
64. Submucous resection limitations
and comlications
Caudal end deformities are not addressed
Poor access to nasal spine
Dorsal deformities not addressed
Saddle back defomity
Septal hematoma
Collopse of nasal tip n columella
Nasal obstruction
Mucosal tear
TSS
Septal perforation
Cartilage n bone may have memory to return to original
deformed position
65. Reconstitution
Morselized cartilage replaced between flaps
Less risk of septal perforation
Future source of cartilage for rhinoplasty and
easier dissection
80. complications
• Bleeding
• Septal haematoma
• Damage to surrounding structures
• Septal abscess
• Septal Perforation
• Depression of bridge
• Retraction of columella
• Synichae
• Flapping septum
• Infection- sinus and middle ear
• CSF rhinorrhoea
81. Cottle’s line
• A vertical line between the
nasal process of frontal
bone and nasal spine of
maxillary crest. it divides
septum into anterior and
posterior segments
82. Septoplasty
• It is a conservative approach to septal surgery as much of the septal
framework is retained
• Indications:
Deviated nasal septum causing nasal obstruction and recurrent
headaches
Deviated nasal septum causing obstruction to ventilation of
paranasal sinuses and middle ear resulting in recurrent infections
Recurrent epistaxis from septal spur
As a part of septorhinoplasty
As an approach to surgeries of sphenoidal sinus, vidian nerve and
pituitary gland
84. Septoplasty (cont…)
• Anesthesia: local or general anesthesia
• Position: same as SMR
• Steps :
Infiltration
Incision: Freer’s incision– a unilateral hemitransfixation
incision at the caudal border of the septum
Exposure: the mucoperichondrial and mucoperiosteal
flap is elevated on only one side
85. Septoplasty (cont…)
Separate septal cartilage from vomer and ethmoid
plate
Inferior strip of cartilage is removed
Correct the bony septum by removing deformed parts
Minor deviations of cartilage are corrected by criss
cross incision which breaks spring action of cartilage
Nasal packing
86. Post-operative complications
• Bleeding
• Septal haematoma
• Saddle nose
• Damage to surrounding structures
• Septal abscess
• Septal Perforation
• Depression of bridge
• Retraction of columella
• Synechiae
• Persistent deviation
• Infection- sinus and middle ear
• CSF rhinorrhoea
• Toxic shock syndrome
87. Differences between SMR and septoplasty
SMR
1. Radical surgery
2. Not done in children
3. Killian’s incision
4. Flaps elevated on both sides
5. Most of cartilage removed
6. Caudal dislocation not corrected
7. Perforation chance higher
8. Post operative saddling may be
present
9. Revision surgery difficult
10. Rhinoplasty incision cant combine
11. Cartilage graft can be harvested
Septoplasty
1. Conservative surgery
2. Can be done in children
3. Freer’s incision
4. Flap elevated on concave side only
5. Most of cartilage preserved
6. Caudal dislocation corrected
7. Perforation rare
8. Post operative deformity absent
9. Revision surgery easier
10. Can combine
11. Cannot be harvested
88. ENDOSCOPIC SEPTOPLASTY
• Described by LANZA and STAMMBERGER
ADVANTAGES :
• Minimally invasive
• Better for treatment of isolated spurs
• Improved access to deviation posterior to septal perforation
• Better assessment of relationship b/w septum n middle turbinate
• Possible to see d separation of collagenous fibres connecting the
perichondrium and periosteum to underlying bone and cartilage
• Can be used as a teaching tool for residents
• mucosal disruptions are recognized immediately
89. Procedure
• Infilteration is given
• The nasal cavity is examined with a 0 degree
endoscope to see location of deviation and spur
• Rest of the steps are same as conventional
septoplasty
90. Directed septoplasty
• This approach is useful for managing isolated spurs in
absence of larger septal deviations
• HZ incision is made over the apex of spur,mucosal
flaps elevated in superior and inferior direction
• Spur incised using microdebrider or by traditional
septal transfixion with resection of spurring
cartilage/bone.
• Flaps redrapped to minimize exposure of raw mucosa
• Advantage :limited dissection and quicker post op
healing
91. Complications
• Major complications are rare
• Minor complications include epistaxis. Septal
hematoma, injury to nasopalantine nerve wid dental
numbness, scarring,perforation and CSF leak are rare
complications.
93. • A child coming wid nasal obstructions should be properly evaluated
very rarely cause will be septal deviation alone
Factors contributing are:
• Congenital nasal mass(dermoid,encephalocele,glioma)
• Nasal polyp
• Choanal atresia
• Foreign body
• Septal hematoma
• Adenoid hypertrophy
• Reversible obstruction (acut URTI,chronic sinusitis,allergic
inflammation)
• Isolated spur
• Turbinate hypertrophy
• Deviated septum
• Midface hypoplasia
94. Nasal septal perforation
Etiology :
Traumatic - post surgical, habitual nose picking, cauterization of septum with
chemicals or galvano-cautery for epistaxis
Pathological perforation
a) Septal abscess
b) Nasal myasis
c) Rhinolith or neglected foreign body
d) Chronic granulomatous conditions like TB, lupus, leprosy, syphilis, wegener’s
Inhalant irritants- snuff and cocaine irritant, industrial toxins
Malignancy
idiopathic
95. Septal Perforation
History
Crusting, bleeding, whistling
if perforation is small
Rhinorrhea and disruption
of lamellar flow if
perforation is large
Pain signifies chondritis
More anterior the
perforation the more likely
the patient will become
occult
96. Septal Perforation
Must rule out a chronic inflammatory disease
process, cocaine abuse, granulomatous
process in face of granulation tissue on
perforation
97. Physical Exam
Crusting on mucosa due to dry
nonlaminar flow, not
necessarily at site of
perforation
Bleeding at edge of
perforation
Picture with endoscope and
ruler to assess size of
perforation
98. What tests do I order?
Nasal cultures for fungal
and bacterial infections
Skin testing for TB, fungi
and anergy
VDRL, FTA-Abs, C-ANCA
Biopsy to rule out
autoimmune process
99. Principle
Perforation is unlikely to
heal on its own
More likely to contract
and create a larger
opening
100. Medical Therapy
Petroleum based ointments
Antiseptic wash per
Fairbanks (1 teaspoon salt
in warm water delivered by
Water-Pik device +/-
glycerin to moisturize +
boric acid or vinegar)
Medical button
101. Surgical therapy
Endonasal repair
Small perforations
External approach
Most perforations less than 2cm
Tissue expander
Free flap
102.
103. Nasal septal perforation
• Clinical features
• Whistling sound
• Irritation and crusting
• Epistaxis
• Nasal obstruction
104. Nasal septal perforation
Treatment :
Treat the root cause
Inactive small perforation can be surgically closed
by plastic flaps or septal mucosal flaps
Larger perforations are difficult to close: their
treatment is aimed to keep the nose crust free by
alkaline nasal douch and application of lubricants,
silastic obturator may also be used