Lecture notes on surgery – Part I

– Dr. Yogiram Bolisetty

 2

HEAD INJURIES ..........................................................................................................3

PERIPHERAL NERVE INJURIES.............................................................................21
CHEST INJURIES.......................................................................................................34
DISEASES OF OESOPHAGUS..................................................................................39
2

Yogiram’s Lectures on Surgery

 3
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.

Yogiram’s Lectures on Surgery

 4
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 à Haematoma
- Connective tissue
- Sub aponeurotic
- Sub-periosteal
· Open
- Lacerated
- Incised
- Avulsed
Haematoma of scalp
Haematoma of sub cutaneous tissue

Yogiram’s Lectures on Surgery

 5
· 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

Yogiram’s Lectures on Surgery

 6
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

Yogiram’s Lectures on Surgery

 7
· 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.

Yogiram’s Lectures on Surgery

 8
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 à 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 à
primary neuronal damage
Injury to intracranial structures can produce oedema of brain or haemorrhage in the
cranial cavity producing pressure effects on brain à 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.

Yogiram’s Lectures on Surgery

 9
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-Stoke’s respiration due to
brain stem lesion usually leading to death
· Focal deficits are always present on recovery

Yogiram’s Lectures on Surgery

 10
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

Yogiram’s Lectures on Surgery

 11
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.
Incidence
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 (Hutchinson’s 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

Yogiram’s Lectures on Surgery

 12
- 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 (Hutchinson’s pupil)
§ Initially, ipsilateral pupil constriction
§ Immediately followed by ipsilateral dilatation
§ Later, bilateral fixed and dilated pupils
- C) Ipsilateral hemiplegia
- D) Decerebrate rigidity
Investigations
· 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

Yogiram’s Lectures on Surgery

 13
- 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

Yogiram’s Lectures on Surgery

 14

Plan of management

StepI:ABCD

Step II:
Evaluation of injuries

Admission to ward for Outpatient management

severely injured for less severely injured

Monitor for Management of Surgical

secondary injury unconscious management
and manage, if
present

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”

Yogiram’s Lectures on Surgery

 15
§ 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
- Hutchinson’s 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

Yogiram’s Lectures on Surgery

 16
- 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 >1010 F: pontine injury
4) Other signs
· Papilloedema
· Battle’s 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

Yogiram’s Lectures on Surgery

 17
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
- Coleman’s 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

Yogiram’s Lectures on Surgery

 18
- 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) Indications for surgery
· Compound # skull
· Extra dural haemorrhage
· Subdural haemorrhage
· Intra cerebral haemorrhage
· Depressed # with acute angulation of inner table
· Intracranial abscess

Prognosis

Yogiram’s Lectures on Surgery

 19
“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

Yogiram’s Lectures on Surgery

 20
· 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

Yogiram’s Lectures on Surgery

 21

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.

Yogiram’s Lectures on Surgery

 22
· 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

Yogiram’s Lectures on Surgery

 23
Degenerative injuries (Injuries 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 Tinel’s sign migrates distally 1 mm/ day
· Unfavourable lesions
- Static Tinel’s 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 ½ 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

Yogiram’s Lectures on Surgery

 24
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

Yogiram’s Lectures on Surgery

 25
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

Yogiram’s Lectures on Surgery

 26
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

Yogiram’s Lectures on Surgery

 27
· Operative injury
· Malignant infiltration – e.g., Pancoast’s tumour
Pattern of brachial plexus injuries
· 1) Erb – Duchenne palsy
- Lesions of C5&6 nerve roots or upper trunk
· 2) Klumpke’s 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 5th is involved
· Outer side of arm if 6th 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

Yogiram’s Lectures on Surgery

 28
Sensory loss
· Inner side of forearm, inner 3 ½ fingers
Autonomic
· Horner’s 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,

Yogiram’s Lectures on Surgery

 29
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 ½ 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
- Froment’s 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 ½ fingers –both palmar and dorsal sides

Rapid method of eliminating major nerve injury of upper limbs

· Test for wrist drop – radial nerve
· Ochsner’s clasping test – median nerve
· Froment’s sign – ulnar nerve
· Examine for sensory deficit

Claw hand – DD
· Both median and ulnar nerve paralysis
· Inner cord of brachial plexus injury

Yogiram’s Lectures on Surgery

 30
· Klumpke’s paralysis
· Late and severe Volkmann’s 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
Injury 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 à foot drop and inversion of foot
Sensory loss

Yogiram’s Lectures on Surgery

 31
· 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 àdiplopia
· 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)
· Bell’s palsy
· Parotid tumours or surgery

Yogiram’s Lectures on Surgery

 32
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 àdifficulty 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 àdrooping of
shoulder
Hypoglossal nerve

Yogiram’s Lectures on Surgery

 33
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
Horner’s syndrome
Causes
· Injury to cervical sympathetics
- Klumpke’s paralysis and complete brachial plexus injuries
- Neck wounds
- Cervical or thoracic neoplasm
- Cervical sympathectomy
Lesions
· Pseudo-ptosis
· Miosis
· Anhydrosis
· Enopthalmos
· Absence of spinociliary reflex

Yogiram’s Lectures on Surgery

 34

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

Yogiram’s Lectures on Surgery

 35
· 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
¯

Yogiram’s Lectures on Surgery

 36
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

Yogiram’s Lectures on Surgery

 37
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

Yogiram’s Lectures on Surgery

 38
· 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

Yogiram’s Lectures on Surgery

 39

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)

Yogiram’s Lectures on Surgery

 40
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

Yogiram’s Lectures on Surgery

 41
- 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 Trendlenberg’s 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

Yogiram’s Lectures on Surgery

 42
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

Yogiram’s Lectures on Surgery

 43
· 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
à shortening.

Foreign bodies in oesophagus

Causes
· Coins
· Pins

Yogiram’s Lectures on Surgery

 44
· 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 Barret’s ulcer
Full thickness rupture (Boerhaave’s 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

Yogiram’s Lectures on Surgery

 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 Boerhaave’s 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

Yogiram’s Lectures on Surgery

 46
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 Barret’s 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

Yogiram’s Lectures on Surgery

 47
· It is useful in cancer perforation cases
Corrosive injury
· Corrosives: NaOH (lye), H2 SO4 , bleach
· Viscera injured: Oral cavity, pharynx, oesophagus and stomach
· Oesophagus is worst affected with NaOH
Complications
· Perforation
· Stricture (usually multiple and densely fibrotic) à 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

Yogiram’s Lectures on Surgery

 48
· 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

Yogiram’s Lectures on Surgery

 49
· 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

Yogiram’s Lectures on Surgery

 50
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 Trendlenberg’s 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

Yogiram’s Lectures on Surgery

 51
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 Barret’s 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 –

Yogiram’s Lectures on Surgery

 52
· 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, Barret’s 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 Trendlenberg’s 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

Yogiram’s Lectures on Surgery

 53
- 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
- Barret’s oesophagus
Procedures
· Repair of oesophageal hiatus is ineffective and hence, not done (Allison’s repair)
· Total fundoplication – Nissen’s fundoplication
· Partial fundoplication – Toupet’s and Belsey operation
· The Hill procedure
Nissen’s 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 (Toupet’s)

Yogiram’s Lectures on Surgery

 54
· 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
· Barret’s 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

Yogiram’s Lectures on Surgery

 55
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
Barret’s 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, Barret’s 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 Barret’s mucosa (experimental) with laser, photodynamic therapy
or argon beam coagulation
Barret’s ulcer
· Ulcer in the columnar lined portion of Barret’s 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

Yogiram’s Lectures on Surgery

 56
- 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
· Raynaud’s
· 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 Auerbach’s plexus due to –
· Unknown cause
· ? neurotropic virus infection, eg., Varicella zoster
Chagas’ disease in south America has similarities. It differs from Hirschsprung’s
disease in the follwing respects –
· Dilated proximal colon contains normal ganglion cells while dilated oesophagus
contains few ganglion cells

Yogiram’s Lectures on Surgery

 57
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 (bird’s 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

Yogiram’s Lectures on Surgery

 58
Surgery
· Heller’s 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

Yogiram’s Lectures on Surgery

 59
- 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
· Barrett’s 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 Barret’s
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
Barrett’s oesophagus

Yogiram’s Lectures on Surgery

 60
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)

Yogiram’s Lectures on Surgery

 61
- 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-Vinson’s syndrome,
scleroderma

Yogiram’s Lectures on Surgery

 62
§ Diverticulum
§ Neoplasm
§ Spasm: Plummer-Vinson’s 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

Yogiram’s Lectures on Surgery

 63
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

Yogiram’s Lectures on Surgery

 64
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

Yogiram’s Lectures on Surgery

 65
- 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

Yogiram’s Lectures on Surgery

 66
- 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
Zenker’s 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 à fistula into trachea
Schatzki’s 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
Investigations
· 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

Yogiram’s Lectures on Surgery

 67
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

Yogiram’s Lectures on Surgery