Head Injury, Chest Injury, Oesophagus

Lecture notes on surgery – Part I

– Dr. Yogiram Bolisetty

Yogiram’s Lectures on Surgery

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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 à 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 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.


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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-Stoke’s 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.

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


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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 (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


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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

- 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


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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 >1010F: 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


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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

- 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


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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) Indications 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 (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


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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., 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


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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,


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


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· 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


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


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


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


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


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

¯


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


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


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


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)


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


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


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


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


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


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


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


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


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


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


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


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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 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 –


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


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)


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


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


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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

· 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


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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 (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


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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


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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

· 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


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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-Vinson’s syndrome, scleroderma


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§ 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


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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

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


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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

Documents

Head Injury, Chest Injury, Oesophagus