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Lecture notes on surgery Part I

Dr. Yogiram Bolisetty



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HEAD INJURIES ..........................................................................................................3
PERIPHERAL NERVE INJURIES.............................................................................21
CHEST INJURIES.......................................................................................................34
DISEASES OF OESOPHAGUS..................................................................................39
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HEAD INJURIES
Anatomy
Head contains
Scalp
Skull
Brain and its membranes along with vessels and CSF
Scalp
It has five layers
Skin
Connective tissue dense
Aponeurosis of occipito-frontalis
Loose areolar tissue
Pericranium or periosteum
Skin
It is denser than any where in the body. It contains great number of hairs and
sebaceous glands.
Dense connective tissue
It firmly binds skin to aponeurosis. It contains blood vessels and nerves of scalp. The
walls of the blood vessels are adherent to the connective tissue. Hence, the vessels do
not retract and continue to bleed when cut. The haematoma produced due to closed
injury is well limited and does not expand.
Aponeurosis of fronto occipitalis (galea aponeurotica)
It is the aponeurosis of fronto-occipitalis. Frontalis arises from the skin of eyebrows
and occipitalis arises from superior nuchal line.
Lateral extension of the aponeurosis is as temporal fascia covering the temporalis
muscle and is attached to zygomatic arch. Frontalis lifts the eye-brows upwards.
Loose connective tissue
It extends underneath the galea aponeurotica. It extends
Anteriorly into the root of the nose and eye lids
Posteriorly up to the attachment of occipitalis to superior nuchal line
Laterally to zygomatic arch
Hence, any collection of blood or pus in this space extends up to these limits.

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It contains emissary veins connecting the venous sinuses of brain to the veins of
scalp. Haematoma in this compartment manifests as bilateral black eye, which
presents first in the upper lids and usually takes 24 hours to develop.
Pericranium
It is attached to the bone at suture lines. Collection of fluid under this layer causes a
swelling which has the shape of the underlying bone.
Head injuries
Classification of head injuries
Wounds of the scalp
Fractures of skull
Intracerebral injuries
Causes of cranio-cerebral injuries
Trauma
- Dynamic injuries
Acceleration/deceleration injuries
Rotational injuries
- Direct trauma
Penetrating
Blunt trauma
Injuries of scalp
Types
Closed Haematoma
- Connective tissue
- Sub aponeurotic
- Sub-periosteal
Open
- Lacerated
- Incised
- Avulsed
Haematoma of scalp
Haematoma of sub cutaneous tissue

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It is localised, small and painful
Haematoma of loose areolar tissue
It occupies the whole of the scalp. It causes bilateral black eyes starting from upper
lids.
Haematoma of sub-pericranial area
It has the shape of the corresponding bone
Black eye
Causes
Subaponeurotic haematoma
# Anterior cranial fossa
Direct injury to orbit
Subaponeurotic haematoma
It develops 1-2 days after injury
It develops first in the upper lid
Associated bogginess of scalp is present
Fracture of anterior cranial fossa
The black eye develops on either side after 24 hours
First it appears in the lower eye lid
It is limited by attachments of orbital fascia to the margins of orbit
It is associated with flame shaped subconjunctival haemorrhage
In extreme cases, eye ball is fixed and protrudes outwards
Skin around the orbit is not discloured
Direct violence on the orbit
The haematoma develops soon after injury
Colour is reddish purple
Signs of local injury to orbit are present
Bruise of cheek, forehead or nose may be associated
May be associated with conjunctival haemorrhage
- The conjunctival haemorrhage has posterior limit
- It is well localized and it moves with conjunctiva

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Open wounds of scalp
Peculiarities
Severe bleeding occurs usually, which is arrested by eversion of wound margins or
by presuure on the wound margins against the skull
Infection of these wounds is a potential risk for intracerebral abscess due to spread
via emissary veins
Injuries of skull
Types
Simple linear fracture
Depressed fracture
Base of skull fracture
Ping-pong fracture
Blow-out fracture
Simple linear fracture
It indicates the force of injury. It needs no treatment.
Depressed fracture
It usually follows blunt trauma
Types
Compound: if pericranium is opened to exterior
Simple: if pericranium is not opened to exterior
Indications for surgery
Compound fracture
Pressure effect on the brain
Cosmetic
Base of skull fracture
Diagnosed on clinical grounds
Anterior fossa fractures
The features are
Subconjunctival haematoma
CSF rhinorrhoea
Epistaxis

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Anosmia
Middle fossa fractures
The featurea are
CSF otorrhoea/rhinorrhoea
VII and VIII cranial nerve injury
Battle sign: bruise behind the ear 36 hours after injury
Ping-pong or pond fracture
Seen in children
It is a smooth depression of the cranial vault
Blow out fracture
Fracture of orbital walls with herniation of orbital contents resulting in diplopia and
pain
Brain injuries
Mechanism of injury
Dynamic
Direct (Static)
Penetrating
Dynamic injuries
These occur when head is not fixed in the space
These occur because of the jelly nature of brain which moves in relation to skull in
a dynamic injury
The velocity of force at the impact is important
- If the force of impact is dampened by cushioning, e.g., helmet, the severity of
the effects is greatly reduced
Acceleration injury:
It is produced due to abrupt acceleration of the head when a moving object strikes the
head, (e.g., when a stationary vehicle is struck in the rear so that the victim sitting in
the vehicle is suddenly thrown forwards or speeding vehicle hits a person on the road)
Deceleration injury:
It is produced due to abrupt stopping of moving head by striking against a stationary
object. A well fixed head, when sustains a dynamic injury, the force of impact is taken
by the skull bones resulting in fracture and with little or no brain damage.

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Acceleration injuries
Extensive coup injury:
Usually cause extensive brain injury
Deceleration injury
Relatively minor injury at the site of injury coup injury
Extensive injury at the counter point counter coup injury
May be associated with injuries at multiple places
Direct injuries (static injuries)
Most of the force is absorbed by a well supported skull fracture of skull
Usually brain injury is minimal
Penetrating injuries
Due to missiles or sticks
Damage to brain is often localised
Pathogenesis of brain injuries
Injury to brain can cause stretch, disruption or laceration of nerves or its fibers
primary neuronal damage
Injury to intracranial structures can produce oedema of brain or haemorrhage in the
cranial cavity producing pressure effects on brain secondary brain damage
Classification of brain injuries
Primary brain injury
Features of brain trauma manifest immediately following trauma and these changes
are irreversible
Secondary brain injury
The changes are seen subsequent to the impact.
The management of head injuries is principally to detect and treat these secondary
injuries.
Primary brain injury
This is due to stretch of neurons and their fibers produced by displacement and
distortion of cerebral tissues due to movement of impact. The antero-posterior
movement is more and lateral displacements are restricted by septum of falx cerebri.
Hence, the blows on front and back of the head cause maximum displacement of brain
and more severe brain injury. The lateral blows cause little displacement and hence,
little injury.

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As a result of these injuries, there may be
Diffuse neuronal damage, which may be widely distributed
Focal lesions at the points of impact on the skull or falx causing contusions or
lacerations
Depending upon the severity of the cerebral distortion and focal damage, the injuries
are classified as
Cerebral concussion
Cerebral contusion
Cerebral laceration
Cerebral concussion
The stretch is mild and causes temporary physiological dysfunction of brain causing
Instantaneous and transient loss of consciousness
Autonomic abnormalities bradycardia, hypotension, sweating
Amnesia for the event
Varying degrees of temporary lethargy and irritability
Post concussional syndromes
Headache, lassitude, irritability, depression and vertigo
Cerebral contusion
Small areas of haemorrhage occur in the cerebral parenchyma
Neurological effects are seen for more than 24 hours
- Features of cerebral shock as in concussion
- Recovery associated with irritability, delirium, confusion, headache,
photophobia and post traumatic amnesia
There may be deficits
Cerebral oedema is usually associated
Cerebral laceration
The stretch is severe with laceration of brain and intracerebral haemorrhage
Prolonged unconsciousness associated with neurological deficits is present
Features of cerebral irritation curled up posture with universal flexion
In severe cases, deep coma with dilated pupils, Chyne-Stokes respiration due to
brain stem lesion usually leading to death
Focal deficits are always present on recovery

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Secondary brain damage
Causes
Intra cranial haematoma
Cerebral oedema
- Due to vascular engorgement and rise in intra vascular fluid
- Cerebral ischaemia
Due to hypoxia and decreased perfusion (due to failure of regulation of
blood pressure by injured brain)
Infection
- Due to compound # and base of skull #
Epilepsy
- Aggravate the cerebral hypoxia and hence, prophylactic usage of antiepileptics
is beneficial
Clinical features of secondary changes
These changes occur at an interval after the injury. These changes are
Progressive deterioration of level of consciousness
Slowing of pulse
Slowing of respiration
Appearance of new localising signs
These changes are most often produced by intracranial haematoma and occasionally
by oedema.
Intracranial haematoma
Types depending upon the site
Extra dural
Sub dural
Intracerebral
Extra dural haematoma
Sources of haemorrhage
Middle meningeal artery (branch of maxillary) the commonest source
Rarely from accessory meningeal and anterior meningeal artery (branch of
opthalmic artery)
Dural venous sinus haematoma

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Anatomy of middle meningeal artery
It arises from maxillary artery in the infratemporal fossa and enters the middle cranial
fossa through the foramen spinosum. It courses laterally on the floor of the middle
cranial fossa and turns upwards on the greater wing of sphenoid and divides into
anterior and posterior branches.
The anterior branch passes from the bony tunnel near the pterion to the surface of the
dura and courses over the dura covering the motar cortex. The posterior branch
courses over the dura covering the superior temporal gyrus. The arteries are
accompanied by two vena comitantes, which groove the skull.
Surface anatomy
Anterior branch: A point 2.5 cms behind the orbital margin and above the zygomatic
process.
I ncidence
2% of head injuries
Sex: males are commonly affected
Age: middle age, because of loose attachment of dural site at temporal region
Pathogenesis
It usually follows trivial injury such as a blow from a golf or cricket ball striking the
thin bone of temporal fracture of temporal bone the fracture snaps the middle
meningeal artery at the point where it leaves the bony canal near the pterion to gain
attachment to dura.
From the torn blood vessel, the blood flows in three directions
Outwards through the fracture line forming a boggy swelling under the temporalis
muscle
Downwards into middle cranial fossa
Upwards over the motor cortex: the clot over the motor cortex produces certain
pathological changes
- 1) The spreading clot over the motor cortex produces pressure over motor
cortex leading to twitchings followed by progressive paralysis from
contralateral face, arm to leg.
- 2) Clot over the motor cortex Inward and downward displacement of
temporal lobe Inner portion of the temporal lobe presses against the third
nerve above the edge of tentorium ipsilateral pupilary constriction,
immediately followed by dilatation (Hutchinsons pupil)
- 3) If the clot progresses, there will be displacement of brain stem to opposite
side pressure of opposite crus against the edge of tentorium Ipsilateral
hemiplegia

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- 4) If pressure not relieved Coning of midbrain Decerebrate rigidity
with bilateral fixed dilated pupils
Clinical features
1) Bruise with haematoma in the temporal region
2) Features of intra cranial haematoma
- A) Altered level of consciousness
Initial loss of consciousness due to concussion
Recovery from concussion (lucid interval)
Progressive loss of consciousness after a delay of few hours
When the injury is trivial, the initial loss of consciousness is absent
And if the injury is severe, the lucid interval is absent
- B) Bradycardia
- C) Slow respiration
3) Localising signs progressing as
- A) Contralateral hemiplegia first starts in the face
Contralateral plantar extensor
- B) Pupillary changes (Hutchinsons pupil)
Initially, ipsilateral pupil constriction
Immediately followed by ipsilateral dilatation
Later, bilateral fixed and dilated pupils
- C) Ipsilateral hemiplegia
- D) Decerebrate rigidity
I nvestigations
X ray skull
CT scan
Treatment
Emergency surgery is done to relieve the compression.
Side of operation: it is judged by
- Side of bruising
- Side of skull fracture
- Side of initial dilatation of pupil

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- Opposite side of hemiparesis
- CT scan decides
Operation
- Burr hole is made 5cms behind the orbital margin and 5cms above the
zygomatic bone and its margins are nibbled
- The bleeder is identified, ligated or coagulated or if the bleeding is from
foramen spinosum, the foramen is plugged with bone-wax.
Subdural haemorrhage
Types of presentation
Acute
Chronic
Acute subdural haematoma
It is the commonest intracranial mass lesion following head injury. It follows dynamic
injuries due to tearing of bridging veins connecting the dura with the cortical veins.
Usually, it is associated with cerebral laceration. Prognosis is poor in these cases.
Chronic subdural haematoma
It occurs in old people with shrunken brains and wide subdural space and large
ventricles.
Clinical presentation
Insidious symptoms of drowsiness, headache, which mimics intra cranial tumours.
Treatment
Evacuation of clot by four burr holes made on the vault of the skull.
Prognosis
Early detection and treatment gives good prognosis.
Intra cerebral haemorrhage
It is usually associated with laceration of brain. It presents with focal epilepsy,
monoplegia etc.
Management of head injuries





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Management in casualty
First-aid
Resuscitation of the injured by ABCD
Assessment of head injury:
- History from a witness about
Time and nature of injury
Presence and duration of unconsciousness immediately after injury
Presence of fits after the injury
Right or left handed
- Examination
Level of consciousness graded by Glasgow coma scale
StepI :ABCD
Step II:
Evaluation of injuries
Admission to ward for
severely injured
Monitor for
secondary injury
and manage, if
present
Surgical
management
Management of
unconscious
Outpatient management
for less severely injured
Plan of management

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Vital data recording
Neurological examination
Neck stiffness
Wounds of the scalp
v Nature of wounds
v Associated bleeding from nose, ears or mouth
Other injuries
Three base lines should be recorded in every case
1) Level of consciousness
2) Neurological examination (pupils and paresis)
3) TPR & BP
1) Level of consciousness
It is assessed by simple AVPU method (Alert, Verbal response, Pain response,
Unresponsive) or by Glasgow coma scale (Eye opening, verbal response and
motor response)
2) Neurological examination
Examination is done to evaluate the pupils and motor system.
Pupils
- Unequal pupils: extra dural clot or injury to optic nerve, differentiated by
consensual light reflex
- Hutchinsons pupils: extra dural clot
- Bilateral fixed dilated pupils: injury to brain stem or midbrain
- Pinpoint pupils: pontine injury (usually associated with pyrexia and paresis)
Hemiparesis, hemianopia, aphasia: middle meningeal clot
Decrebration: brain stem injury or coning
Flaccid paralysis: cervical spine injury
3) Vital functions
Pulse
- Slow: raised intracranial pressure
- Rapid: decompensated stage of raised ICT
Respirations
- Slow and shallow: concussion

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- Slow and deep: raised tension
- Chyne Stokes respiration: late stages of raised tension
- Very slow or very rapid respiration soon after accident: severe brain injury
Temperature
- Subnormal: concussion
- Pyrexia of >101
0
F: pontine injury
4) Other signs
Papilloedema
Battles sign: post auricular ecchymosis in # base of the skull
Blood and CSF leak from nose: #anterior cranial fossa / injury nose
Blood from ear: # petrous temporal
CSF leak from nose: #anterior cranial fossa
CSF leak from ear: # middle cranial fossa
Neck stiffness: subarachnoid leak / # cervical spine
Injuries of other organs
Evaluated and managed appropriately
Out patient management of less severely injured
Headache
- Paracetamol
- Aspirin
Restlessness
- Phenobarbitone
- Chlorpromazine
Management in the ward
Indications for admission
H/O unconsciousness or amnesia
# skull
Children
Intoxicated persons
H/O vomiting or headache

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The injured are admitted for managing three types of patients
1) unconscious
2) for evaluation and management of secondary damage
3) for surgical management
1) Management of unconscious patient
Observation and progress: these are observed for
Level of consciousness
Pupils
TPR and BP
General care of unconscious patient
Posture
- Colemans posture prone with head end lowered
- Not to restrain the restless patient
Avoid sedatives
Nutritional support by nasogastric feeding / TPN
Bladder
- Retention: continuous drainage (distended bladder causes restlessness)
- Incontinence: condom drainage / indwelling catheterisation
Prevention of bed sores
- 2 hourly change of posture
- Clean and dry back
- Wrinkle - free bed sheets
- Ripple bed
- Avoid urinary soakage of bed clothes
Special care of unconscious patient
Respiratory assistance and care
- Chest physiotherapy
- Suction of pharynx and trachea
- Tracheostomy and oxygen administration
Hyperpyrexia
- Tepid sponging

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- Paracetamol
- Chlorpromazine
Antibiotics
Induced hypothermia in brain stem injuries
Management of complications
Epilepsy
- Phenobarbitone, phenytoin
Status epilepticus
- Diazepam, phenytoin, mechanical ventilation after muscle relaxants
CSF rhinorrhoea (DD: rhinitis; glucose + in CSF rhinorrhoea)
- Do not plug the nose and protect it by sterile gauze
Meningitis
- Antibiotics
Diabetes insipidus
- Fluid balance
- Pitressin
Cerebral oedema
- Dehydration therapy - mannitol, frusemide, 50% dextrose
- ? Dexamethasone
2) For observation and progress to detect and manage secondary
neuronal damage
(The causes, clinical features and management of secondary neuronal damage was
discussed already)
3) I ndications for surgery
Compound # skull
Extra dural haemorrhage
Subdural haemorrhage
Intra cerebral haemorrhage
Depressed # with acute angulation of inner table
Intracranial abscess
Prognosis

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No head injury is so slight that it should be neglected or so severe that life
should be dispaired of Hippocrates
Good in concussion, extra dural clot
Guarded in contusion, laceration and intracerebral haemorrhage
SPINA BIFIDA AND MENINGOCELE
Development of spinal cord and vertebral column
Neural groove occurs on the dorsum of embryo, which closes forming the neural
canal. From the walls of the neural canal, nervous system is developed and the central
canal forms spinal canal. The vertebral bodies develop from notochord situated
anterior to the neural tube. Mesodermal ingrowth occurs between the neural tube and
ectoderm forming the vertebral arches of the spinal column, which fuse with the
vertebral bodies. Failure of fusion of the arches causes spina bifida.
Types of spina bifida
Meningocele
- Through the gap in the failed fusion of vertebral arch, meninges herniate
containing CSF
- Swelling occurs usually in the sacral region and is covered with normal skin
and is transilluminant
Meningo- myelocele
- The herniated membranes contains the normally developed spinal cord or
cauda equina (transillumination negative)
- The swelling is covered by unepithelialised membranes rather than skin
- Associated neurological defects may be present
Syringomyelocele
- The herniated membranes contain spinal cord with dilated neural canal
forming a cavity filled with fluid
- Associated neurological lesions present
Rachischisis
- The neural and vertebral arches fail to fuse in the midline and the neural canal
opens on to the surface
- It may be complete involving the whole length of spinal cord or may be partial
(myelocele)
- The infant is stillborn or dies immediately after birth

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Spina bifida occulta
- The gap in the vertebral arches is filled with fibrous tissue and hence, there is
no herniation of the meninges
- A band of fibrous tissue is attached between the gap and the spinal cord called
membrana reuniens
- It may pull the cord, when the vertebral column grows disproportionately to
the spinal cord (around 8-14 yrs) causing neurological lesions
- The defect in the vertebral arches occur usually in the sacral or lumbar regions
and is indicated by a tuft of hair, lipoma or pigmented patch
Associated diseases
Hydrocephalus in 80% of cases
Arnold-Chiari malformation
Investigations
Xray spine
MRI spine and brain
Treatment
The defect in the arch is repaired
Hydrocephalus is corrected by shunting
Encephalocele
Similar to meningocele, if skull bones are not developed, it results in meningocele
(Protrusion of arachnoid through the defect)
Encephalocele
The meningeal herniation contains brain
Hydrencephalocele
The brain in the herniation contains ventricle

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PERIPHERAL NERVE INJURIES
Anatomy
Structure of a nerve trunk
It is made up of a large number of nerve fibres arranged in bundles like a system of
cables. Each fibre consists of an axon and its cell. The cell, neuron is situated in the
CNS or in the ganglion of the autonomic nervous system.
The neuron: it contains
- Cell body
- Dendrites
- Axon
Axon: it is of two types
- Myelinated
- Unmyelinated
Myelinated nerve
Each axon is surrounded by Schwann cells (neurilemma)
Integrity of myelin sheath is necessary for nerve conduction
Unmyelinated nerve
Several axons are wrapped by a single Schwann cell
Nerve sheath
The nerve fibres are enclosed in a connective tissue sheath called nerve sheath.
Endoneural tube
The endoneurium together with the Schwann cell basement membrane forms the
endoneural tube.
Physiology
Changes after nerve injury Wallarian degeneration
After injury to a nerve
Distal to the injury, the nerve undergoes degeneration: there will be lysis of the
axoplasm, fragmentation of myelin sheath producing empty endoneural tube
containing Schwann cells.
Proximal to the injury, degeneration occurs upto the node of Ranvir and later,the
remaining nerve regenerates into the endoneural tube.

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The regeneration process depends upon the presence of endoneural tube.
If endoneural tube is not intact, the proximal and distal stumps proliferate due to
proliferation of neurilemmal cells and form a proximal neuroma and distal glioma
.
Classification of nerve injuries
Neuropraxia
Axontmesis
Neurotmesis
Neuropraxia
It is physiological cessation of nerve function without anatomical disruption. Recovery
is complete, if the cause is removed.
Causes:
Compression caused by tourniquet, streching of nerve or near- miss injury by a
missile
Axontmesis
The nerve fibre has anatomical disruption of axons and myelin sheaths with intact
endoneurium, epineurium and perineurium. Wallerian degeneration occurs because of
intact endoneural tube followed by regeneration.
Nerve conduction is absent and the regeneration occurs at the rate of 1-2 mm/ day.
Recovery is complete
Causes:
Severe stretch injury, bone-fragment pressure
Neurotmesis
There will be anatomical disruption of whole nerve including the sheath. Wallerian
degeneration occurs distally, but regeneration can not occur because of lack of
continuity of endoneural tube. If surgical repair is done, recovery occurs, but is not
perfect.
Causes:
Cut injury, avascular injury, severe stretch, injection of toxic drugs
Clinical manifestations
They depend upon the nature of injury. The types of clinical manifestations are
Degenerative (axontmesis and neurotmesis) injuries
Non-degenerative (neuropraxia) injuries

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Degenerative injuries (I njuries which cause degeneration of the
distal segment)
Signs of degeneration
- Loss of sensory and motor functions
- Loss of sudomotor and vasomotor function: dry and red skin, evident 7-10
days after injury
- Nails become curved non-glossy with ridges in long standing cases
Favourable lesions (axontmesis)
- Spontaneous recovery present
- Positive Tinels sign migrates distally 1 mm/ day
Unfavourable lesions
- Static Tinels sign
Non-degenerative lesions
Signs
- Sudomotor and vasomotor functions are preserved
- Complete paralysis of muscles supplied by that nerve with preservation of
sensory and autonomic function partly
The neurological effects are reversed with in 1 1 hours after release of nerve
compression
MRC classification of motor nerve dysfunction
M0: complete paralysis
M1: flicker of muscle activity
M2: power insufficient to overcome gravity
M3: movement against gravity
M4: movement against resistance
M5: normal full power
MRC classification of sensory nerve dysfunction
S0: no sensation
S1: deep pain sensation
S2: skin touch, pain, thermal sensation
S3: S2 + accurate localisation, but deficient stereognosis
S4: normal sensation

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Investigations
Nerve conduction studies
Electromyography (EMG)
MRI scan
Treatment
Conservative
Indications: neuropraxia, axontmesis
Procedure
- Splintage of limb in the position which prevents contraction of opponent
muscle groups, e.g., cock- up splint for wrist drop
- Passive movements to prevent joint stiffness
- Active movements of recovering muscles
Surgery
Nerve repair
Nerve grafting
Nerve transfer
Tendon or muscle transfer
Arthrodesis
Treatment nerve repair
Open injuries
- Exploration and primary repair of the nerve
Closed injuries (stretch or compression)
- Repair of the nerve may be combined with fixation of skeletal fragments
- Axontmesis and neuropraxia recover completely and hence, conservative
approach is advised
If no recovery is noted after 2-3 months, exploration and repair is done
Surgical repair
Accurate coaptation of nerve ends with out tension in a healthy bed of tissue with fine
sutures (6/0 10/0) to the epineurium is done. In injuries with ragged or contused
ends, trimming of the nerve ends is done till healthy ends are seen. If ends can not be
brought together, nerve grafting is done.
In secondary repair, the scarred nerve ends are cut till healthy nerve fibrils are seen

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and repaired by suturing or nerve grafting.
Timing of repair
Primary repair is ideal. If conditions are not favourable for primary repair, the nerve
ends are fixed to the surrounding tissues with the help of a non-absorbable suture to
identify the nerve at a later date during secondary repair and to prevent its retraction.
PO management
Immobilisation of the limb in POP casing to reduce tension on the suture line for 3
weeks
Passive movements of the affected joints
Factors affecting prognosis
Better prognosis in
- Children, clean cut injuries and early repair
Bad prognosis in
- Traction injuries and high velocity missile injuries and proximal lesions
- Associated injury to vessels and soft tissues
- Mixed nerve injury
Special types of nerve injury
Compression neuropathy
Irradiation neuropathy
Compression neuropathy
E.g., carpal tunnel syndrome, cubital tunnel compression syndrome
Pathology
Chronic compression myelin sheath degeneration and chronic ischaemia of nerve
fibrosis
Clinical features
Initially pain and later sensory and motor disturbances
Treatment
Release of compression
Prognosis
Usually responds to decompression
Radiation neuritis

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E.g., infraclavicular brachial plexus after radiation to carcinoma breast
Clinical features
Severe pain with some sensory and motor disturbances
Treatment
It is very difficult
Casualgia (casua=heat, lgia=pain)
It is paroxysmal attack of pain produced due to partial nerve injury, especially of
brachial plexus or sciatic nerves.
Pathology:
Incomplete lesion of the nerve

Artificial synapses of autonomic with sensory nerves

Sends antidromic* impulses to the sensory nerves

H-like substance produced at the sensory nerve endings

Vasodilatation

Severe burning pain and hyperaesthesia associated with sweating
The affected skin is atrophic due to trophic changes
(*Dromic= impulses in the normal direction)
Treatment
Sympathectomy

Specific nerve injuries
Brachial plexus injuries
Aetiology
Traumatic following traction of hand, shoulder dislocation and cervical injuries
including penetrating injuries

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Operative injury
Malignant infiltration e.g., Pancoasts tumour
Pattern of brachial plexus injuries
1) Erb Duchenne palsy
- Lesions of C5&6 nerve roots or upper trunk
2) Klumpkes paralysis
- Lesions of T1 root or lower trunk
Erb Duchenne palsy
Causes
Difficult confinement (obstetric brachial plexus palsy)
Fall on shoulder
Motor palsy
Biceps, brachialis, brachioradialis, supinator, spinati and deltoid
Position of limb
Receiving a tip position
Sensory changes
Absent if only 5
th
is involved
Outer side of arm if 6
th
is involved
Treatment
Muscle transfer from pectoral group to humerus
Klumpke paralysis
Causes
Inclusion while ligating subclavian aretry
Dislocation of shoulder
Stretching of arm, e.g., failing to obtain a foot hold on a running bus
Motor palsy
Small muscles of hand
Position
Claw hand

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Sensory loss
Inner side of forearm, inner 3 fingers
Autonomic
Horners syndrome
Prognosis
Usually poor
Radial nerve injury
Causes
Fracture of shaft of humerus
Saturday night palsy
Injection into triceps
Site of injury
Radial groove commonly
Motor palsy
Brachioradialis, extensors of wrist and extensor digitorum longus
In higher lesions triceps also
Position of limb
Wrist drop
Sensory loss
Dorsum of thumb and I web space
In higher lesions over back of forearm
Treatment
Conservative: cock-up splint
Tendon transfer, if no response
Median nerve injury
Sites of injury
Elbow (#lower end of humerus, dislocation of elbow)
Wrist (# lunate, lower radius and carpal tunnel syndrome)
Motor paralysis
At elbow: Flexors of wrist and fingers, except medial half of flexor profoundus,

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and flexor carpi ulnaris, pronators of forearm
- Sign = Pointing index finger
At wrist: Thenar muscles
- Loss of abduction and opposition of thumb
- Wasting of thenar eminence
Sensory loss
Palmar aspect of lateral 3 fingers
Dorsum of radial aspect of ring finger
Ulnar nerve injury
Causes
Entrapment behind epicondyle of humerus
Lacerated wound of fore arm
Motor paralysis
Small muscles of hand except thenar muscles and lateral two lumbricals
Signs:
- Claw type deformity
- Loss of abduction and adduction of fingers
- Froments sign: flexion of thumb when a paper is held between the thumb and
index finger
In lesions above elbow, medial half of flexor profundus and flexor carpi ulnaris
Sensory loss
Medial 1 fingers both palmar and dorsal sides
Rapid method of eliminating major nerve injury of upper limbs
Test for wrist drop radial nerve
Ochsners clasping test median nerve
Froments sign ulnar nerve
Examine for sensory deficit
Claw hand DD
Both median and ulnar nerve paralysis
Inner cord of brachial plexus injury

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Klumpkes paralysis
Late and severe Volkmanns ischaemic contracture
Anterior poliomyelitis
End result of neglected suppurative tenosynovitis of ulnar bursa
Advanced rheumatoid arthritis
Dupuytren's contracture
Post burn contracture
Neurological conditions
- Syringomyelia
- Progressive muscular atrophy
- Polyneuritis
- Amyotrophic lateral sclerosis
Sciatic nerve injury
Causes
Wounds, # pelvis, post dislocation of hip, operations on hip
Motor paralysis
I njury above hamstrings
Flexors of knee and all the muscles below knee foot drop
Sensory loss
Complete loss below knee except the medial border of foot, supplied by long
saphenous nerve
Casualgia in partial injuries
Common peroneal (lateral popliteal) nerve injury
Causes
# and dislocations around the knee
Pressure from POP casing
Operations around knee
Motor paralysis
Extensor and peroneal muscles of ankle and toes foot drop and inversion of foot
Sensory loss

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Dorsum of foot and toes
Rapid method of eliminating nerve injury of lower limb
Ask to flex big toe
- +: intact medial popliteal and posterior tibial nerves
Ask to extend the big toe
- +: intact lateral popliteal and anterior tibial
Knee extension
- +: intact femoral nerve
Olfactory nerve injury
Causes
Head injuries
Meningioma from floor of the anterior cranial fossa
Lesions
Anosmia
Occulomotor nerve injury
Ptosis
Eye is deviated downwards and outwards diplopia
Mydriasis
Trochlear nerve injury
Mild diplopia
Trigeminal nerve
Commonest lesion is trigeminal neuralgia
Abducent nerve
Diplopia
Facial nerve
Causes
Cerebello-pontine angle lesions (acoustic neuroma)
Bells palsy
Parotid tumours or surgery

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Motor
All facial muscles and platysma
Sensory
Loss of taste for anterior 2/3 of tongue
Auditory nerve
Causes
Acoustic neuroma
# middle cranial fossa
Glossopharyngeal nerve
Causes
# base of skull
Lesions
Paralysis of stylopharyngeus, which could not be tested
Absence of gag reflex and sensation of palate and posterior third of tongue
Vagus nerve
Clinical presentation
Affect muscles of palate and larynx difficulty in swallowing and vocal cord
paralysis
Recurrent laryngeal nerve lesion
Partial paramedian position
Complete cadaveric position
Accessory nerve
Causes
# base of skull
Operations on posterior triangle of neck
Lesions
In anterior triangle of neck, it causes paralysis of sternomastoid and trapezius
In posterior triangle of neck, it causes paralysis of trapezius drooping of
shoulder
Hypoglossal nerve

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Causes
Intracranial lesions
Operations on sub mandibular salivary gland
Lesions
Wasting, weakness and fasciculations of the ipsilateral half of the tongue
Tongue deviates to the side of lesion
Horners syndrome
Causes
Injury to cervical sympathetics
- Klumpkes paralysis and complete brachial plexus injuries
- Neck wounds
- Cervical or thoracic neoplasm
- Cervical sympathectomy
Lesions
Pseudo-ptosis
Miosis
Anhydrosis
Enopthalmos
Absence of spinociliary reflex

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CHEST INJURIES
Classification
According to nature of injury
Blunt injuries
Open injuries
- Crush injuries
Road traffic injuries
Blast injuries
Under water explosions
- Penetrating wounds stabs, gunshot wounds
According to the organs injured
Chest wall injuries
- Contusion chest wall
- Rib fracture
Isolated
Multiple
Haemo thorax, pneumo thorax or both
Lung injuries
- Contusion or laceration
Aorta and great vessels injury
Diaphragmatic injuries
Abdomino-thoracic injuries
Incidence
Thoracic trauma is responsible for 70% of deaths following road traffic accidents
Fracture ribs
Types of presentation
Fracture of isolated rib

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Fracture of multiple ribs
- Stove in chest
- Flial chest
Isolated rib fracture
Commonest complication of chest trauma
It produces severe pain and localised tenderness over the site of fracture, elicited
by direct pressure and by chest compression test
Crepitus may be present
May lead to pulmonary complications in elderly or in those with lung disease
Treatment:
Analgesics, intercostal nerve block, physio to lungs
Strapping of chest is contraindicated
Isolated first rib fracture
It is always associated with major vessel injury, injury to abdomen, head and neck
Isolated fracture of lower ribs
They may be associated with injuries of spleen or liver
Multiple rib fractures
Cause:
Crushing of chest wall
Site of fractures
At the maximum curvature of ribs anterior and posterior angles
Types of injuries
Stove in chest
Flial chest
Stove in chest
Pathology
Extensive and localised crushing force

Localised indentation of chest wall


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Reduced lung volume and expansion on the affected side

Collection of broncho-pulmonary secretions

Pulmonary infections
Treatment
Same as for isolated rib fracture
Severe forms require surgical correction
Flial chest
It is caused by automobile accidents of serious nature. It is usually associated with
other major injuries. Several adjacent ribs are fractured in two places either on one
side or on either side of the sternum
Pathology
1) The fractured segment (flial segment) of chest wall moves inwards during
inspiration and outwards during expiration (paradoxical respiration)

Reduced gasseous exchange

Hypoxia

2) Pressure of flial segment over the lung parenchyma

Lung injury

Hypoxia
Treatment
Minor flial segment without respiratory embarassment
- Analgesics, regular blood gas analysis, physio to lungs
Severe cases
- Endotracheal intubation and positive pressure ventilation for 3 weeks
- If lung injury is present repair of lung parenchyma and fixation of flial
segment

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Traumatic pneumothorax
Sources
Air leak from a damaged lung common cause
Sometimes, it may be a valvular opening in the lung tension pneumothorax
Air sucked through a wound in the thorax
Pneumothorax is usually associated with haemothorax in most of the cases
Treatment
Sucking wounds of the chest
- First aid: cover the wound with an occlusive pad
- Later, repair of the wound and provision of under-water seal drainage
Tension pneumo-thorax
- First aid: insertion of aspiration needle through an intercostal space
- Later, underwater seal drainage
Traumatic haemothorax
Sources
Chest wall, lung, heart and great vessels
Complications
Pleural thickening
Empyema
Treatment
Mild: aspiration every 24 hours
Rapidly accumulating or associated with pneumothorax: under water seal drainage
Progressive (>200ml/hr): thoracotomy and arrest of bleeding
Pulmonary contusion and laceration
Lung is injured in majority of moderate and severe chest trauma
Types of injury
Minor consolidation, which resolves spontaneously
Severe collapse of lung and pneumo/haemothorax
Treatment

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Conservative for mild: antibiotics, physio and bronchial aspirations
Thoracotomy for severe cases
Diaphragm injuries
It presents as diaphragmatic hernia, which can be
Acute or
Chronic
Management of chest injuries
Resuscitation: ABCD
Most are managed by under -water seal drainage
Indications for thoracotomy
More than one litre of blood aspirated at the initial aspiration
Progressive bleeding
Rupture of bronchus, aorta, oesophagus, diaphragm
Cardiac tamponade
Swellings of chest wall
Solid
- Skin and soft tissue lesions
- Rib tumours
Benign chondroma, osteochondroma
Malignant secondaries (more common), chondrosarcoma
Cystic
- Cold abscess from intercostal lymphnodes, spine, ribs or sternum
- Lipoma (soft mass with out fluctuation)
- Empyema necessitates



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DISEASES OF OESOPHAGUS
Anatomy
It measures 25 cms in length extending from cricopharyngeal junction (15 cms from
incisor teeth) to cardiac orifice (40 cms from incisor teeth). It has 3 physiological
constrictions
From incisor teeth at 15cms (cricopharyngeal jn) narrowest part of alimentary
tract
From incisor teeth at 25cms (crossing of aorta)
From incisor teeth at 40cms (OG jn)
Its muscle coat has striated muscle in its upper part and much of lower part has smooth
muscle.
Nerve supply: vagus by its oesophageal plexus
Mucosa is lined by stratified squamous epithelium except its lower 2 3 cms , which
is lined by columnar epithelium .
Physiology
Functions
Propagation of food into stomach
Clearance from refluxed food or fluid
Prevention of reflux of acid gastric juice
Prevention of reflux of food into trachea
These functions are due to its peristalsis, lower oesophageal sphincter and upper
oesophageal sphincter (cricopharyngeus)
Peristalsis
Primary peristalsis
It occurs in response to a food bolus and it is for clearance and neutralisation of
acid
Secondary peristalsis
It occurs in response to a stubborn food bolus or to the presence of fluid in the
lower oesophagus (refluxed material from stomach)

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Tertiary peristalsis
It occurs occasionally and are mainly contractions and are not peristaltic waves
Lower oesophageal sphincter
It is a physiological sphincter
It prevents reflux of gastric and duodenal contents
Its tone varies with
- Gastric distension
- Smoking
- G.I hormones
- Nature of food
Cricopharyngeal sphincter
It prevents regurgitation of food into trachea and air into oesophagus
Normally, it is closed at rest and relaxes on swallowing
Failure to relax on swallowing predisposes to pharyngeal diverticulum
Symptoms of oesophageal disease
Dysphagia:
- Difficulty in swallowing with or without pain
- It may be for solids or liquids
- It may be Intermittent or progressive
- Localisation of the holdup is possible in many, but, in some it is imprecise
Odynophagia:
- Painful swallowing
Globus:
- Feeling of lump in the throat, unaffected by swallowing
Reflux:
- Return of gastric and biliary contents
Regurgitation:
- Return of oesophageal contents above an obstruction
Chest pain:
- Resembles cardiac pain

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- Mucosal lesions and reflux produce chest pain
Heartburn:
- Cardinal symptom of reflux
- It presents as presternal pain radiating to neck
Investigations
1) Radiography
Plain X-ray: Not useful
Barium swallow: it is indicated in motility disorders, identification of hiatus hernia
(done in Trendlenbergs posture), and in space occupying lesions.
2) Upper GI endoscopy
- To evaluate mucosal lesions
- It is the most commonly performed investigation
Diagnostic endoscopy
- Biopsy or cytology from suspected lesions
Therapeutic endoscopy: it is done for
- Removal of foreign bodies,
- Dilatation of strictures,
- Injection of varices,
- Insertion of stents,
- Luminisation of tumours
Types of endoscopy
Rigid endoscopy
- Negus oesophagoscope or Earlam oesophagoscope is used. It is useful in
examination of cricopharyngeal area and the lower pharynx. The risk of
perforation is high. It needs high skill.
Flexible fibre-optic endoscopy
- It has supplanted rigid scope. It is safer to use.
3) Manometry
It is a gold standard in the assessment of motor disorders. A polyvinyl tube of about 4
mm in dia is passed into the oesophagus. This tube consists of multiple microcapillary
tubes connected to external presuure transducers, which pass signals to a computer for
real time displayIt is useful in evaluating motility disorders like achalasia, diffuse

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spasm, nut cracker oesophagus, and systemic sclerosis
4) pH monitoring
It is the most accurate method of diagnosing reflux disease
5) Radionucleide scan
It is experimental and is used to evaluate oesophageal clearance

Congenital diseases
Atresia with or without tracheo-oesophageal fistula
Stenosis (rare)
Short oesophagus with hiatus hernia (rare)
Dysphagia lusoria
Atresia and tracheo-oesophageal fistula
Pathology
Types:
The oesophagus is atretic and the upper or lower segments of the oesophagus open
into the trachea in one of the four ways
A) Lower segment opens into trachea (85%),
B) Upper segment opens into trachea (2%),
C) Both segments open into trachea (1%),
D) Both segments end blindly and the mid oesophagus is absent (12%)
Clinical features
Regurgitation of first and subsequent feeds by new born baby with pouring out of
saliva from the mouth the sign
Coughing and cyanosis on feeding
Associated with hydramniosis in the mother
It may be part of VACTER anomalies
VACTOR anomalies
V vertebral body defects
A anal atresia
C cardiovascular disease:- VSD/PDA

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TO Tracheo-oesophageal fistula
R renal agenesis / radial ray hypoplasia
Diagnosis
Naso gastric tube insertion gets hindrance at less than 10cms.
X-ray chest:
- Anteriorly displaced trachea on lateral view
- If fundic gas is present, it suggests fistula between the trachea and lower
segment
- Dionosil (via naso- gastric catheter) X-ray demonstrates the fistula
Treatment
Surgery:
Resection of fistula and anastomosis of both the ends
- Complications: Pneumonia and anastomotic leak
Prognosis
Good
2) Oesophageal stenosis
It is rare. It can occur anywhere in the oesophagus and it presents as dysphagia.
3) Dysphagia lusoria
(Lusoria = sport of nature)
Vascular anamolies like aberrant subclavian artery and double aortic arch cause
compression of oesophagus Dysphagia. It manifests in early childhood or late teens
Treatment
Division of nondominant component of the arch of aorta.
4) Short oesophagus
It is a misnomer. It is not a congenital anomaly.It is secondary to severe oesophagitis
shortening.
Foreign bodies in oesophagus
Causes
Coins
Pins

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Dentures
Button batteries
Food bolus (due to underlying distal obstruction)
Diagnosis
Plain X-ray chest
Endoscopy
Treatment
Endoscopic retrieval
- Accessories needed: Grasping forceps, basket, snare and overtube
Injuries of oesophagus
Causes
Spontaneous injury
- Full thickness rupture
- Partial thickness rupture
Iatrogenic injury
Penetrating injury
Foreign body
Corrosive injury
Drug- induced injury
Due to Barrets ulcer
Full thickness rupture (Boerhaaves syndrome)
Causes
Rupture of oesophagus due to severe barotrauma when a person vomits against
closed glottis
Site
At the weakest point of oesophagus, i.e., lower 1/3 of oesophagus
Pathology
Rupture

Passage of oesophageal contents into mediastinum

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45

Mediastinitis and left pleural effusion
Clinical features
Severe pain in chest or upper abdomen following vomiting immediately after a
meal or bout of alcohol (Suspect Boerhaaves if severe pain in chest follows
vomiting)
Rigidity of upper abdomen
Differential diagnosis
Perforated peptic ulcer
Acute pancreatitis
Myocardial infarction
Partial rupture (Mallory-Weiss syndrome)
Forcible vomiting

Vertical split in the gastric and oesophageal mucosa immediately below the Z- line

Haematemesis
Treatment
Conservative
Endoscopic injection
Rarely, surgery (suturing of the tear)
Iatrogenic perforation
Causes
Rigid endoscopy: it produces perforation on the posterior wall of pharynx above
the cricopharyngeal sphincter
Flexible endoscopy (1 in 4000 cases): it occurs during retrieval of F.B, especially
dentures, fish bone without the use of overtube, or during dilatation of benign
strictures, cancers, achalasia and during insertion of stents for palliation of cancer.
Diagnosis
Severe chest pain after the procedure
Subcutaneous emphysema of neck or upper chest
X-ray chest: it shows gas in the mediastinum

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Traumatic perforation
It is rare because oesophagus is surrounded by other vital organs. It occurs due to
penetrating injuries or missile injuries.
Pathological perforation
It is unusual. It is perforation of Barrets ulcer or cancer ulcer. The ulcer perforates
into mediastinum or aorta or ventricle with immediate fatal results
Treatment of perforation of oesophagus
Conservative
Surgery
Endoscopy
Conservative treatment
Indications
- Small leak
- Minimal cardio vascular upset
- Perforation by flexible scope
- Perforation of cervical oesophagus
Treatment
Analgesia
Nil by mouth and enteral feeding by jejunostomy or by TPN
Antibiotics
Operative management
(usually with in few hours of perforation)
Thorocotomy
Repair of the tear, strengthened with adjacent gastric fundus, diaphragm or
intercostal muscle
Resection of the part, if the perforated part is not healthy
Late diagnosis or failed non-operative and operated cases
Oesophageal exclusion and resection
Oesophagostomy, gastrostomy and delayed reconstruction
Endoscopic management
Insertion of stent

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It is useful in cancer perforation cases
Corrosive injury
Corrosives: NaOH (lye), H
2
SO
4
, bleach
Viscera injured: Oral cavity, pharynx, oesophagus and stomach
Oesophagus is worst affected with NaOH
Complications
Perforation
Stricture (usually multiple and densely fibrotic) malignancy
Treatment

Early endoscopy by an experienced endoscopist to assess the severity of mucosal
injury
Minimal injury
Supportive treatment
Severe injury: Steroids for 3 weeks and later dilatations
Full thickness necrosis: Early resection
Late presentation with strictures: Resection and replacement of oesphagus
Drug induced injury
Mucosal injury tooesophagus occurs when antiboitics and potassium preparations are
taken with inadequate water.
Clinical features
Dysphagia or odynophagia for 2-3 weeks
Stricture may follow rarely
Treatment
Supportive
Diaphragmatic hernia
The diaphragm has certain defects through which herniation of abdominal contents
can occur into the chest. These foramina are
Congenital foramen
- Foramen of Morgagni
- Foramen of Bochdalek

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Oesophageal hiatus
Types of diaphragmatic hernia
1) Congenital (through congenital foramen)
- Hernia through foramen of Bochdalek ( postero lateral hernia)
- Hernia through foramen of Morgagni (Anterior hernia)
2) Traumatic
- Violence or accidents Blunt or penetrating injuries abdomen or chest
- Post operative following thoraco-abdominal operations
3) Eventration of diaphragm (paralysis or atrophy of diaphragm muscles leads to
abnormally elevated diaphragm)
4) Hiatus hernia: herniation of abdominal contents through the oesophageal hiatus
Congenital diaphragmatic hernia
Incidence
Neonates usually and rarely young
1) Morgagni hernia:
It is a herniation through congential opening situated between costal attachment and
sternal attachment of diaphragm. It occurs usually on right side as heart prevents it on
left side. Transverse colon herniates commonly into this hernia.
2) Bochdalek hernia:
It is herniation through postero - lateral or pleuroperitoneal canal. It is the most
common type and it occurs on the left side, because the liver on the right side prevents
the hernia
Clinical features of diaphragmatic hernia:
Severe respiratory distress
Apparent dextrocardia (due to mediastinal shift)
Scaphoid abdomen
Investigations
X ray chest:
- Displaced cardiac shadow (apparent dextrocardia)
- Absence of diaphragm outline
- Presence of gas & fluid filled bowel loops in chest
Treatment

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Resuscitation of child:
- ECMO (extra corporeal membrane oxygenator)
- Nasogastric aspiration
Surgery:
- Reduction of hernial contents
- Repair of the defect
Hiatus Hernia
TYPES
Sliding or oesophago-gastric hiatus hernia 85%
Rolling or paraoesophageal hiatus hernia 5%
Mixed or transitional hiatus hernia 10%

Sliding hiatus hernia
It is due to herniation of cardiac orifice and a portion of adjacent stomach into the
chest along with a small peritoneal sac on the left side through oesophageal hiatus. It
manifests due to the associated reflux oesophagitis.
Anatomy of cardiac sphincter
Anatomically a sphincter cannot be demonstrated at the lower end of the oesophagus.
Physiologically, an intrinsic sphincteric mechanism exists preventing the gastro-
oesophageal reflux.
The factors maintaining this function are
Pinch-cock action of right crus
Rosette like folds of gastric mucosa at the cardia
The presence of a length of intra abdominal oesophagus
The valvular effect of oesophago-gastric angle
A band of muscle on the fundus of the stomach acting as a sling accentuating the
oesophago- gastric angle.
Pathogenesis of mechanism of hernia
The factors responsible for the hernia are weakening of the normal defences. They are

Muscular degeneration of right crus due to advanced age
Increased intra-abdominal pressure due to large ovarian cysts, obesity, pregnancy

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and tight corsets
Increase of fatty tissue around the hiatus in the elderly obese women
Pathology
Herniation of cardio-oesophageal region into the hiatus

Loss of anti-reflux mechanisms

GORD
Aetiology, clinical features, investigations and management are same as GORD (see
topic on reflux oesophagitis)
Rolling or para-oesophageal hernia
Pathology
The greater curvature of the stomach rolls into the chest by the side of oesophagus,
sometimes the whole of the stomach lies with in the mediastinum. This can lead to
Volvulus of stomach (acute or chronic) causing perforation or gangrene of the
stomach.
Sometimes transverse colon occupies the hernial sac.
The cardiac orifice remains in its normal position and hence, reflux oesophagitis does
not occur in these cases.
Clinical features
Dysphagia, chest pain due to twisting and distortion of oesophagus and stomach
The pain is relieved by a loud belch
Symptoms of GORD are usually absent
Pressure symptoms on heart may be associated
Diagnosis
X-ray chest
- A gas shadow with a fluid level is seen behind the cardiac shadow
Barium meal, especially in Trendlenbergs position
Treatment
It always requires surgical repair, because of their potential dangers.
Procedure: Reduction of hernia and gastro-pexy by abdominal, thoracic or
laparoscopic methods

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Mixed hiatus hernia
It is more common than rolling hernia
The presentation is like GORD with dysphagia
Treatment: Reduction of hernia and repair of the defect
Gastro Oesophageal Reflux Disease (GORD / GERD)
Pathophysiology
Causes of reflux
Decreased lower oesophageal sphincter tone
- The competence of LOS is dependent mostly upon the intra-abdominal length
of the oesophagus
Impaired oesophageal clearance
- Due to decreased amplitude of secondary peristaltic waves
Delayed gastric emptying
Sliding hiatus hernia
All GORD patients do not have sliding hernia and ll sliding hernia cases do not suffer
from GORD
Pathology
Reflux of acid

Oesophagitis (grade I)

Linear superficial ulcers (GradeII)

Linear confluent ulcers (Grade III)

Stricture(grade IV)
In long standing cases, metapalstic changes occur leading to Barrets oesophagus,
which is precancerous.
Clinical features
It is the commonest problem affecting many people (about 7% of population suffer
from this problem). The presenting features are

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Retrosternal burning pain (heart burn)
Epigastric pain
Flatulent dyspepsia for fatty foods (The commonest cause for fat dyspepsia is
GORD and not cholecystitis)
Reflux of acid and later, food into the mouth
Odynophagia with hot beverages or sour citrus food and alcohol (confirmatory
symptom)
Angina like pain, pulmonary or laryngeal problems
Dysphagia, if stricture develops
Diagnosis
Endoscopy
- Oesophagitis, Barrets oesophagus, stricture if observed makes the diagnosis
definite
- Sliding hiatus hernia with reflux of stomach is noted in cases of hiatus hernia
- No definite features are seen in patients with only reflux and no complications
24 hour oesophageal pH recording (it is a gold standard test)
Oesophageal manometry
Barium swallow and meal: (Especially in Trendlenbergs posture) helps to identify
sliding hiatus hernia.
Management Medical
Change in life-style
Diet: Avoidance of citrus, fatty foods, chocolates, alcohol, coffee, tea, mint etc.
Drugs: To avoid NSAID, slow-release KCl, theophyllin, nitrates, Ca blockers
Avoidance of smoking
Reduction of obesity
Modest degree of head- up tilt of the bed (The effect is equivalent to HRA)
Avoidance of stooping, lying flat or lifting heavy weights for 3 hours after food
Small and frequent feeds (not practicable)
Drugs
- PPI: It is the most effective drug
Omeprazole, lansoprazole, pantoprazole, rabiprazole, esomiprazole etc
Long-term treatment is needed

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- HRA: It is also useful, but not as effective as PPI
- Antacid gel with alginate:
Short acting and with no action on mucosal inflamation
- Prokinetic drugs
Increase the LOS pressure and motility of the oesophagus and stomach
Metaclopramide, domperidone, mosapride, cisapride, itopride
Management Surgical
Indications
Failure of PPI treatment
- Poor compliance due to side effects of the drug
- Change in life style leads to emergence of symptoms
Complications
- Stricture
- Barrets oesophagus
Procedures
Repair of oesophageal hiatus is ineffective and hence, not done (Allisons repair)
Total fundoplication Nissens fundoplication
Partial fundoplication Toupets and Belsey operation
The Hill procedure
Nissens fundoplication
It is the commonly performed procedure.
Approach
Abdominal
Laparoscopic
Thoracic (rarely done)
Procedure
The fundus is mobilised by dividing short gastric vessels and is wrapped around
lower end of oesophagus behind the oesophagus and brought infront of it and
sutured.
Hiatus is narrowed
Partial fundoplication (Toupets)

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The fundus is sutured to either side of oesophagus after wrapping behind the
oesophagus leaving a strip of oesophagus in the front
Belsey mark IV operation
By thoracic approach, the hernia is reduced and the oesophagus is sutured to
diaphragm and fundus to produce anterior fundoplication
Hill procedure
By abdominal approach, the cardia is tightened and fixed to pre aortic fascia
Angle-chick prosthesis
A silastic prosthetic collar is placed around the lower end of oesophagus after reducing
the hernia. The collar acts by preventing the reflux and by maintaining the abdominal
oesophagus.
Surgery for recurrence
Partial gastrectomy with Roux-en-Y procedure
Complications of surgery
Mortality rate: 0.1% 0.5%
Recurrence rate: 5% -- 10%
Side effects: 10%
- Dysphagia
- Gas bloat syndrome

Complications of reflux oesophagitis
Stricture
Barrets oesophagus
Oesophageal shortening
Stricture
It is common in middle aged and elderly, rarely in children.
Treatment:
Dilatation and PPI
Anti-reflux surgery is usually not considered because of technical difficulty due to
oesophageal shortening
Oesophageal shortening

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Pathology
Long standing oesophagitis

Longitudinal contraction

Shortening of oesophagus

Secondary hiatus hernia
Surgery is difficult because of shortening and Collis gastroplasty and Collis
Nissen fundoplication is done
Barrets oesophagus (Columnar-lined lower oesophagus)
Pathology
Chronic gastro-oesophageal reflux Metaplasia of oesophageal epithelium by
Columnar cell lined gastric mucosa or intestinal type mucosa Adenocarcinoma.
Endoscopically, Barrets oesophagus is differentiated from sliding hernia by absence
of gastric folds.
Treatment
Aggressive treatment of GORD
Repeated endoscopy with multiple biopsies to monitor cancer in situ
Ablation of Barrets mucosa (experimental) with laser, photodynamic therapy
or argon beam coagulation
Barrets ulcer
Ulcer in the columnar lined portion of Barrets oesophagus
Prone to bleeding (ulcers of simple reflux oesophagitis do not severely bleed
usually)
Oesophageal motility disorders
General features
Usually the motility disorders affect whole of the gut. In oesophagus, it manifests as
dysphagia.
Classification
Disorders of pharyngo-oesophageal junction
- Stroke

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- Myasthenia
- Cricopharyngeal achalasia
Disorders of motility of body of oesophagus
- Diffuse spasm
- Hypertensive (nutcracker) oesophagus
- Hypo-peristalsis: systemic sclerosis (CREST*), GORD associated, idiopathic
- Allergic: eosinophilic oesophagitis
Disorders of LOS
- Achalasia
- Hypertensive lower sphincter
- Incompetent lower sphincter (GORD)
*CREST
Calcinosis
Raynauds
Esophageal motility disorders
Sclerodactyly &
Telangectasia
Treatment of motility disorders
Treatment of anxiety and depression
Nitrites, calcium channel blockers
Balloon dilatation in certain disorders
No role for anticholenergic and prokinetic drugs
Achalasia
Pathology
Achalasia is due to loss of ganglion cells in Auerbachs plexus due to
Unknown cause
? neurotropic virus infection, eg., Varicella zoster
Chagas disease in south America has similarities. It differs from Hirschsprungs
disease in the follwing respects
Dilated proximal colon contains normal ganglion cells while dilated oesophagus
contains few ganglion cells

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Loss of peristalsis in the body of oesophagus & absent or incomplete relaxation of
LOS occur due to aganglionosis of oesophageal plexus Gross dilatation of
oesophagus (mega oesophagus) Gross food and fluid residue in the dilated mega
oesophagus Retention oesophagitis due to fermentation of food Cancer
Clinical features
It is commonest in middle life
The main presentation is dysphagia
Regurgitation of food and fluid occur frequently and is mistaken for GORD
Regurgitation leads to aspiration pneumonitis
Diagnosis
Endoscopy
- Tight cardiac orifice with food residue in oesophagus
Barium swallow
- Hold-up in the distal oesophagus
- Peristaltic dysfunction
- Tapering stricture in the distal oesophagus (birds beak)
- Absence of fundic gas bubble
Oesophageal manometry
- Gold standard for diagnosis because other tests may be normal in early stage
- Hypertensive LOS which does not relax on swallowing
- Aperistalsis of body of oesophagus
- Raised resting pressure in the oesophagus
Treatment
- Endoscopic dilatation
- Surgery
Dilatation
Forceful dilatation of contracted (achalasia) segment is done with plastic balloons
of 30-40mm diameter by passing the balloon through a fiberoptic endoscope.
Complications
Perforation
Reflux

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Surgery
Hellers myotomy: it is done by either
- Open surgery
- Laparoscopic surgery
Procedure
Division of muscle of lower oesophagus and cardia (not more than 1 cm below the
hiatus)
If myotomy is carried more on to the stomach, anti-reflux operation should be
performed
Other modes of treatment
Botulinum toxin injection
- Given by endoscope into LOS
- Role is not yet fully established
- It acts by interfering with cholinergic neural activity at the LOS
Drugs
- Calcium channel blockers are useful as transient relievers of symptoms till
surgery is done
Treatment of other motility disorders
Cricopharyngeal achalasia
- Cricopharyngeal myotomy
Diffuse spasm
- May respond to forceful dilatation
- In severe cases, extended myotomy upto aortic arch may be required
CREST syndrome
- Prokinetic drugs
Eosinophilic oesophagitis
- Anti- histamines, sodium chromoglycate, steroids
Tumours of Oesophagus
Classification
Benign (very rare)
- Leiomyoma

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- Granular cell tumours
- Fibro vascular polyps
Malignant
- Carcinoma
- Melanoma (rare)
- Sarcoma (rare)
Carcinoma of oesophagus
Aetiology
Smoking
Alcohol
? Fungal contamination of food
Pre cancerous conditions
Barretts oesophagus
Corrosive stricture
Pathology
Types
Squamous cell carcinoma arising from squamous cell layer of upper 2/3 of
oesophagus
Adenocarcinoma arising from lower 1/3 of oesophagus and from Barrets
oesophagus
Incidence
Geographical variation
Highest incidence in the world is in Linxian in Henan provinence of China (100 in
1,00,000popultion)
Common in Transkei region of South Africa and mid-Asia and some areas of
France
Japan does not have a high incidence of oesophageal cancer
Type
Squamous cell carcinoma was the commonest type during earlier days, but now,
adenocarcinoma is commonest (60-70%)
The change in the incidence of type is probably due to increased incidence of
Barretts oesophagus

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Site
Lower 1/3: 47%
Middle 1/3: 13%
Upper 1/3: 4%
OG jn: 36%
Spread
Local
- Satellite nodules in submucosa and mucosa upto 10 cms proximal to the
growth
- Later to neighbouring organs trachea, RLN, aorta, pericardium and
mediastinum
Lymphatic spread
- Lesions of cervical oesophagus spreads to
Cervical paraoesophageal, deep cervical, retropharyngeal and
supraclavicular nodes
- Lesions of thoracic oesophagus to
Paraoesophageal, paratracheal, diaphragmatic and posterior mediastinal
nodes
- Lesions of abdominal oesophagus to
Left gastric, coeliac, splenic hilar, splenic nodes

Systemic spread
- To liver, bone, brain, skin etc
Clinical features
Early disease
- Feeling of something sticking in the throat
- Non-specific dyspeptic symptoms
Late disease
Painless, progressive dysphagia
Weight loss
Features due to infiltration
- Hoarseness of voice ( recurrent laryngeal n. involvement)

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- Cough, stridor (tracheo-bronchial involvement)
- Pain radiating to back and to neck, if infiltrates to mediastinum
Features due to secondaries
- Mass in the neck (lymph nodal metastasis)
- Hepatomegaly (liver secondaries)
Investigations
Endoscopy
- Assessment of the site and extent of lesion
- Biopsy of the lesion
Barium swallow
- Cork-screw or irregular narrowing of lumen
US scan of abdomen and CT scan of chest and abdomen
It is mandatory to perform these tests before surgery.
Endoscopic ultrasonography
- For evaluating local infiltration
Bronchoscopy
- For upper 1/3 lesions
Laparoscopy
- For lower 1/3 tumours to assess peritoneal involvement
Differential diagnosis
It has to be differentiated from other causes of chronic dysphagia
Congenital
- Stenosis
- Webs
- Dysphagia lusoria
Acquired
- In the lumen
Foreign body, Schatzki ring
- In the wall
Stricture: GORD, corrosive poisoning, Plummer-Vinsons syndrome,
scleroderma

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Diverticulum
Neoplasm
Spasm: Plummer-Vinsons syndrome, achalasia, motility disorders
- Outside the wall
Goitre, pharyngeal pouch, aortic aneurysm, mediastinal mass, rolling hiatus
hernia
Treatment
Treatment options
Curative treatments (possible only in 25% of cases)
- Surgery
- Radio-therapy
Palliative treatments
- Radio-therapy
- Endoscopy
- Chemotherapy
- Surgery
Curative treatments which is ideal?
Surgery
- Carries high morbidity and mortality
- It is ideal in a fit case
Radiotherapy
- It can cure both types of cancers
- It is technically difficult for lower end tumours
- Tumours involving stomach are less sensitive for radio-therapy (however, they
improve with concurrent usage of chemotherapy chemo-radiotherapy)
Curative surgery
Principles
To remove the tumour and oesophagus 10cms proximal to the palpable margin of
the tumour
To restore continuity by mobilisation of stomach or by interposing colon or
jejunum between oesophageal remnant and stomach
Lymph node dissection is controversial

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Preop treatment
Correction of malnutrition by I.V. hyperalimentation or by naso-gastric tube
feeding with high protein liquid diet
Proper assessment of respiratory and cardiac systems
Types of surgery
Dependent upon the site of the tumour
Lower 1/3 tumours
Oesophago-gastrectomy by thoraco-abdominal approach or by Ivor-Lewis
approach
Reconstruction is done by stomach, colon or jejunal replacement
Approach: Left abdominothoracic approach
Stomach is mobilised by detaching lesser and greater omentum after ligating the
vessels short gastric, left gastroepiploic and left gastric and their branches
Kockerisation and pyloroplasty is done
Upper 1/3 of stomach is resected
Oesophagus is dissected and resected 10 cms above the palpable margin of tumour
Stomach is anastomosed to the oesophageal stump
Middle 1/3 tumours
Ivor-Lewis procedure or McKeown procedure
Anastomosis is done above the level of aortic arch
Ivor-Lewis procedure
Laparotomy is done and stomach is mobilised as in the previous surgery
Abdomen closed and patient is turned to left lateral position and right thoracotomy
is done
Oesophagus is mobilised and stomach is pulled into the chest and resection and
anastomosis is performed in the chest and chest closed
Upper 1/3 tumours
Early diagnosis is rare as the lymphnodal metastasis or tracheo-broncheal
involvement occurs by the time dysphagia is the presenting symptom
Mckeown three-stage procedure for curable tumours in fit patients
- Ivor-Lewis two stages are performed and the patient is turned into supine, neck
opened and oesophagus mobilsed and delivered into neck and resection-
anastomosis performed in the neck

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Anastomosis
It is done by hand sewn in single interrupted nonabsorbable sutures or by stapler
anastomosis.
P.O. nutrition
Feeding jejunostomy
I.V. alimentation
Duration of PO enteral or IV alimentation
- 5-7 days or till no leak is found from the anastomosis on contrast radiography
Other methods of surgery
Transhiatal oesophagectomy (Orringer)
Thoracoscopic oesophagectomy not yet established
Curative radiotherapy
Indications
- Patients unfit for surgery
- Upper 1/3 and cricopharyngeal tumours
5-year survival rate
9-19% (c.f : surgery 20-35%)
Palliative treatment
Features of advanced disease
- Dysphagia, especially for saliva is the most distressing feature associated with
aspiration pneumonitis
- Survival is very short with any form of therapy
Principles
It should be simple and effective
It should relieve dysphagia, especially of saliva
Palliative surgery
Its role is debatable
Resection or by-pass is done in selected cases
Morbidity is very high
Procedures
Kirschner gastric bypass

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- Stomach is brought to the neck via retrosternal or subcutaneous tunnel and
anastomosed to divided cervical oesophagus
- The abdominal oesophagus is anastomosed to loop of small bowel
Colon bypass
Jejunum bypass
Palliative endoscopy treatment
Intubation is done with any of the following tubes
- Souttar tube
- Celestin tube
- Atkinson tube
- Procter-Livingstone tube
- Expanding metal stents
Laser luminisation: the tumour is burnt with laser passed through the laser guide
which is passed through the endoscope to form a lumen inside the tumour. It has to
be repeated every few weeks.
Palliative radiotherapy
Brachitherapy or interstittial irradiation (delivering intraluminal radiation with a
short penetration distance)
Palliative treatment of tracheo-oesophageal fistula
Life expectancy is very short
Stents are best , especially self expanding metallic stents
Surgery carries high mortality
Summary of surgical treatments
Curative resection
Cervical oesophagus
- Pharyngo- laryngo-oesophagectomy
- Free jejunal transfer
Upper and middle 1/3
- Three- phase oesophagectomy
Middle and lower third
- Ivor-Lewis operation
- Left thoraco-abdominal oesophagectomy

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- Transhiatal oesophagectomy
Cardia
- Oesophago-gastrectomy left thoraco-abdominal
- Oesophago-gastrectomy Ivor- lewis
- Abdominal total gastrectomy
Other Oesophageal Conditions
Oesophageal diverticula
Types
- Pulsion diverticula
- Traction diverticula
Zenkers diverticulum (Pharyngeal pouch)
Pouch protruding between oblique and horizontal fibers of inferior pharyngeal
constrictor due to cricopharyngeal achalasia
Commonest diverticulum
Treatment: Excision of diverticulum and cricopharyngeal myotomy
Mid oesophageal diverticula
Small pulsion diverticulum due to underlying motility disorder
Traction diverticula due to TB lymph nodes fistula into trachea
Schatzkis ring
It is a circular ring in the distal oesophagus, usually at Z- line. The ring is formed by
fibrous tissue and cellular infiltrate.
Clinical features
Dysphagia
I nvestigations
Endoscopy, barium swallow
Treatment:
Dilatation
Monilial oesophagitis
Aetiology
Infection by Candida albicans in patients with immuno-suppression, steroid usage
including steroid inhalers, broad spectrum antibiotics

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Clinical features
Dysphagia
Visible thrush in the throat
Investigations
Endoscopy and biopsy of the lesion
Treatment
Nystatin lozenzes
Flucanozole for 15 days
Plummer-Vinson syndrome
Syn:Brown Kelly-Paterson syndrome, Sideropenic dysphagia
Clinical features
Iron-deficiency anaemia
Kaolinychia
Dysphagia
- Due to web or spasm in the post cricoid area
Glossitis
Complications
Ulcer
Stricture
Carcinoma