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CHAPTER 22 System-Specific Pathology
391
Complete Transection of Spinal Cord
• Total loss of voluntary movement distal to the level of
transection; this loss is irreversible.
• Loss of all sensation from those areas which depend on
ascending pathways crossing the site of injury.
Incomplete Spinal Cord Injury (see Fig. 6.10)
• Anterior cord syndrome:
• associated with exion/rotation injuries producing
anterior dislocation; or compression fracture of vertebral body with bone encroaching on the vertebral
canal
• loss of power below level of lesion
• loss of pain and temperature below the lesion
• in addition to direct damage, the anterior spinal
artery may be compressed
• the dorsal columns remain intact and propriocep-
tion is not aected.
• Central cord syndrome:
• occurs in syringomyelia and centrally placed
tumours
• initially involves decussating spinothalamic bres so
that pain and temperature are lost below the lesion
• later the lateral corticospinal tract is involved, with
the more centrally placed cervical tract supplying
the arm being involved more than the peripheral
tracts supplying the legs. Classically there is accid
weakness of the arms, but because the distal leg and
sacral motor and sensory bres are spared, perianal
sensation and some leg movement and sensation are
preserved
• proprioception and ne touch are preserved in the
dorsal columns until late.
• Posterior cord syndrome:
• seen in hyperextension injuries with fractures of the
posterior elements of the vertebrae
• loss of proprioception with profound ataxia and
unsteady faltering gait
• usually good power and pain and temperature sensa-
tion below the lesion.
• Brown-Séquard syndrome:
• hemisection of the cord
• stab injury; or damage to lateral mass of vertebra
• paralysis on aected side below lesion (pyramidal
tract)
• loss of proprioception and ne discrimination (dor-
sal columns on aected side below lesion)
• loss of pain and temperature on opposite side below
lesion (normal on aected side because of decussation below level of hemisection)
• therefore the uninjured side has good power but
absent sensation to pin-prick and temperature.
• Cauda equina syndrome:
• compression of lumbosacral nerve roots below the
conus medullaris
• caused by bony compression or disc protrusion in
lumbosacral area
• lower motor neuron lesion
• bowel and bladder dysfunction, together with leg
numbness and weakness.
PERIPHERAL NERVE INJURIES
Peripheral nerve injuries may be classied as follows:
• Neuropraxia:
• a condition of transient physiological block without
degeneration
• continuity of axons and the myelin sheaths remain
intact
• function returns spontaneously in about 6 weeks.
• Axonotmesis:
• usually the result of compression or traction injuries
causing disruption of the axons with intact myelin
sheaths
• distal axons show degeneration, but since the
myelin sheaths are intact return of function can be
anticipated
• axons regenerate at the rate of about 1 mm a day
• return of function can be anticipated but may take
many months.
• Neurotmesis:
• division of nerve in whole or in part which occurs
aer incised or lacerated wounds, or may be the
complication of a fracture
• complete disruption of both axon and myelin sheath
• surgical repair is required
• residual neurological defect likely and neuroma may
occur.
Wallerian Degeneration
• Damage to neuronal body, e.g. anterior horn cell, spinal
nerve roots or nerve trunks, results in degeneration of
the axon distal to the site of the injury.
• In myelinated bres, this is accompanied by secondary
breakdown of myelin around the degenerating axons.
• Regeneration commences 3–4 days following injury.
• Regenerating axonal sprouts grow at 1–2 mm/day.
• is is accompanied by central chromatolysis in the
neuronal perikaryon.
• Remyelination occurs by Schwann cells.
• If regeneration and remyelination are successful, reinnervation of the target organ occurs.
• Reinnervation may be prevented by the following
factors:
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SECTION III Pathology
• ischaemia
• cytotoxic drugs
• disruption of perineurium
• haematoma
• scar tissue.
MUSCULOSKELETAL SYSTEM
Osteomyelitis
Acute Osteomyelitis
• Inammatory lesion due to bacterial infection of bone.
• Disease of growing bones in children but may occur in
immunosuppressed or diabetic adults.
• Is being seen increasingly in elderly patients.
• Usually due to Staphylococcus aureus and rarely due to
streptococci, pneumococci, Haemophilus or Salmonella.
• e classical sequence of changes in osteomyelitis is as
follows:
• transient bacteraemia, e.g. S. aureus
• focus of acute inammation in the metaphysis of
long bone
• necrosis of bone fragments forming the sequestrum
• new subperiosteal bone forms around the dead bone
forming a shell (involucrum)
• in untreated cases, sinuses form draining pus to the
skin surface
• rarely, pus may decompress into the joint, causing
septic arthritis.
Chronic Osteomyelitis
• May follow acute osteomyelitis but is more common following surgery for a common fracture, especially when
foreign material is implanted.
• It may be chronic from the outset, e.g. tuberculosis.
• Chronic osteomyelitis may occur as a result of tuberculosis, tertiary syphilis or mycotic infections; tuberculosis is the most common cause.
• Children with haemoglobinopathies, e.g. sickle cell disease, have an increased risk of osteomyelitis; unusual
organisms such as Salmonella are sometimes responsible.
Septic Arthritis
Most cases of septic arthritis are a result of bacterial infection. Arthralgia may be associated with viral diseases.
• Septic arthritis is the result of blood-borne spread from
a focus of infection elsewhere.
• e epiphyseal plate forms an eective barrier and it is
unusual for an area of osteomyelitis in the metaphysis to
spread and involve adjacent joints; this may occasionally occur in the hip joint where the metaphysis may lie
within the joint capsule.
• Children are more commonly aected than adults.
• Organisms responsible include:
• S. aureus
• Staphylococcus epidermidis (prosthetic joints)
• Streptococcus pyogenes
• Streptococcus pneumoniae
• Neisseria gonorrhoeae
• Haemophilus influenzae (children)
• Gram-negative organisms (drug addicts)
• Mycobacterium tuberculosis
• Brucella abortus (intervertebral discitis).
• Risk factors for septic arthritis include:
• diabetes mellitus
• rheumatoid arthritis
• immunosuppression
• intra-articular injections, e.g. corticosteroids.
Fractures
e healing of fractures has been considered in Chapter 14.
Complications of Fractures
ese may be:
• immediate (at the time of fracture)
• early (during the period of initial treatment)
• late (aer the period of initial treatment).
Immediate
• Haemorrhage: this may be internal or external. Internal
haemorrhage can be considerable at the fracture site, i.e.
up to 1.5 L with a fractured femoral sha.
• Injury to nerves and vessels.
• Injury to underlying structures, e.g. brain damage with
skull fractures, splenic rupture with le lower rib fractures, urethral trauma with pelvic fractures.
Early
ese may be divided into:
• local
• general.
Local
• Gangrene due to vessel damage or tight plasters.
• Nerve palsies from tight plasters or involved in callus.
• Wound infection or wound dehiscence.
• Loss of position.
• Tetanus.
• Gas gangrene.
General
• DVT.
• Acute urinary retention.
• Fat embolism.
• Compartment syndrome.
• Crush syndrome.
CHAPTER 22 System-Specific Pathology
393
Late
• Delayed union.
• Non-union.
• Mal-union.
• Reex sympathetic osteodystrophy (Sudek’s atrophy).
• Avascular necrosis of bone.
• Myositis ossicans.
• Osteoarthritis.
Delayed union
• Fracture does not heal in expected time.
• Absence of callus and mobility at the fracture are
features.
Non-union
• Attempt at repair by normal body mechanisms have
ceased and the fracture remains un-united.
• Persistent mobility of fracture site.
• Radiographs show no trabeculae across the fracture
line.
• A pseudoarthrosis (false joint) may result.
• Causes of non-union include:
• inadequate blood supply
• infection
• poor immobilization
• excessive movement at fracture site
• interposition of so tissue between bone ends
• pathological fracture.
Mal-union
• Healing has resulted in a deformed position.
• is may be shortening, overlap or angulation.
• Deformity may put strain on adjacent joints, resulting in
osteoarthritis.
Complex regional pain syndrome (CRPS)
• Can be related, or unrelated, to a nerve injury.
• Can follow relatively mild hand trauma.
• Limb becomes painful, swollen and sti with a reddened, smooth, shiny appearance to skin.
• e cause is unknown.
Avascular necrosis of bone
• Part of bone necroses when its blood supply is interrupted by the fracture.
• Common sites are:
• the head of the femur in intracapsular fractures
where the retinacular vessels supplying the femoral
head are disrupted
• the proximal part of the scaphoid bone in fractures
across the body; the blood supply enters from the
distal end.
Myositis ossificans
• Calcication with subsequent ossication occurs in a
haematoma associated with stripping of the periosteum
and release of osteoblasts into the surrounding muscle
and tissue.
• Most common in injuries around the elbow and those
involving quadriceps femoris.
Osteoarthritis
• Results from misaligned fractures putting strain on
joints.
• Aer intra-articular fractures.
PATHOLOGICAL FRACTURES
A pathological fracture is one that occurs through a bone
already weakened by an underlying disease. Causes of
pathological fractures may be:
• general
• local.
General
• Osteoporosis.
• Metabolic conditions, e.g. rickets, osteomalacia.
• Adrenal overactivity or excessive steroid therapy.
• Hyperparathyroidism.
• Paget’s disease of bone.
• Neuropathic conditions, e.g. syphilis, syringomyelia.
• Osteogenesis imperfecta.
Local
• Bony metastases from:
• breast
• prostate
• thyroid
• kidney
• bronchus.
• Benign and malignant primary bone tumours.
• Simple bone cysts.
• Irradiation of bone.
• Bone atrophy, e.g. polio.
Compartment Syndrome
• Compartment syndrome is caused by increased tissue
pressure in a closed fascial compartment, compromising circulation to the nerves and muscles within the
involved compartment.
• e fascial compartments to the leg and forearm are
most commonly involved.
• Causes include:
• fracture with subsequent haemorrhage and oedema
in the compartment
• limb compression or crush
• vigorous exercise.
• Ischaemia results from pressure on surrounding small
arteries.
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SECTION III Pathology
• Distal pulses may still be palpable and the diagnosis
therefore missed.
• In the lower limb, the posterior compartment (exors of
the ankle), anterior compartment (extensors) or peroneal compartment (evertors) may be involved.
• Treatment is by prompt fasciotomy, which allows
the muscle to expand and relieves pressure on the
vessels.
ARTHRITIS
Osteoarthritis
• Common, painful, disabling, degenerative joint disease.
• Primarily aects cartilage of weight-bearing joints, e.g.
hips, knees.
• Occurs spontaneously in older age groups and is
increasingly common above the age of 60 years.
• Occurs in joints of younger persons following any form
of previous mechanical damage, e.g. trauma, developmental dysplasia of hip, osteochondritis.
• Macroscopic features include:
• erosive changes in cartilage (brillation)
• exposed bone develops an ivory-like surface
(eburnation)
• thickening of the subchondral bone plate
• subchondral bone pseudocyst may form, due to
entry of synovium under pressure into the subchondral plate
• at margins of the articular cartilage, bony outgrowths
develop (osteophytes).
• Pain results from stimulation of nerve endings in joint
capsule and synovium by inammation or abnormal
load-bearing/joint movement.
• Deformity results due to:
• synovial inammation
• eusion into joint
• erosion of articular surfaces
• abnormal remodelling of subchondral bone
• loss of alignment of joint surfaces by cartilage
destruction and bone deformity.
• Restricted movement occurs because of:
• synovial swelling
• brosis
• limitation by pain.
Rheumatoid Arthritis
• Common systemic chronic inammatory disorder
involving joints.
• Associated with rheumatoid factor – an autoantibody
reactive with altered autologous immunoglobulin.
• Females aected more than males.
• Occurs in all age groups, e.g. Still’s disease in children.
• Up to 75% of patients are HLA-DR4 positive.
• Multisystem disease characterized by chronic inammatory granulomatous lesions (rheumatoid nodules).
• Aects many small joints, particularly those of the ngers, hands and wrists, but larger joints such as ankle,
hip and knee are also aected.
• Joints are painful, swollen and tender.
• e synovial membrane is thickened with villus overgrowth, increased vascularity, and pannus, which grows
over and replaces the articular cartilage.
• Extra-articular features of rheumatoid disease are:
• subcutaneous rheumatoid nodules
• anaemia
• lymphadenopathy
• splenomegaly
• pericarditis
• dry eyes and mouth (Sjögren’s syndrome)
• uveitis and scleritis
• vasculitis, especially ngers and nail beds
• pulmonary changes (nodules, interstitial brosis,
obstructive airways disease)
• amyloidosis.
Gout
• Painful, acute, inammatory response to tissue deposition of urate crystals, e.g. subcutaneous tophi or in periarticular tissues.
• Usually occurs in middle-aged or elderly males,
although females may be aected, especially when there
is a family history of gout.
• e rst metatarsophalangeal joint is the predominant
site but many other joints including those of hands may
be aected.
• Joint is swollen, red and shows white ‘chalky’ patches in
the skin through which crystals can oen be expressed.
• Serum uric levels are raised.
• May be associated with chronic renal failure.
Neuropathic Arthritis (Charcot’s Joint)
• A degenerative joint disease which occurs due to loss of
sensory nerve supply.
• Most frequently seen in knee or hip joints in tabes dorsalis, and shoulder or elbow joint in syringomyelia.
• Clinical features include:
• recurrent swelling
• degenerative changes in ligaments and tendons,
resulting in subluxation of the joint.
BONE TUMOURS
ese may be benign or malignant. Secondary tumours
are much more common than primary. Primary malignant tumours are rare, but they have a bad prognosis and
aect patients in a younger age group. Benign tumours
include:
CHAPTER 22 System-Specific Pathology
395
• osteoma (‘ivory’ osteoma)
• osteoid osteoma
• chondroma
• broma and brous dysplasia
• bone cysts.
Primary Malignant Tumours
ese include:
• osteosarcoma (osteogenic sarcoma)
• osteoclastoma (giant cell tumour)
• Ewing’s tumour
• chondrosarcoma
• brosarcoma
• myeloma.
Secondary Malignant Tumours
ese occur from:
• lung
• thyroid
• breast
• prostate
• kidney.
Benign Tumours
Osteoma (‘Ivory’ Osteoma)
• Growth from surface of bone
• Common on the surface of the vault of the skull.
• A smooth, non-tender mound, rarely causing symptoms.
• If symptomatic, can be cured by excision.
• Occasionally multiple enchondromatosis occurs in long
bones (Ollier’s disease).
Fibroma and Fibrous Dysplasia
• A spectrum of conditions with failure or partial failure
of ossication replaced by brous tissue.
• Usually asymptomatic and oen regress at puberty or
aer a fracture.
Bone Cysts
• Fluid- or blood-lled cavities.
• Vary from multiloculated cysts containing clear uid in
children and adolescence to large aneurysmal bone cysts
which may cause ‘bulging out’ of one side of a bone.
• Pathological fractures common.
• Treatment is by excision and bone graing.
Primary Malignant Tumours
Osteosarcoma (Osteogenic Sarcoma)
• Most common primary tumour of bone.
• More common in males.
• Occurs under the age of 30 years.
• Occurs in long bones.
• In the young it commonly aects the lower end of
the femur or upper end of tibia, usually aecting the
metaphysis.
• In older patients, may be associated with Paget’s disease.
• Spread is via the bloodstream to the lungs.
Osteoid Osteoma
• Usually occurs in long bones in young males.
• Continuous, severe, boring pain, usually worse at night
and relieved by aspirin.
• Probably not a true neoplasm.
• Radiographs show dense sclerosis surrounded by a central small lucent zone (osteoid).
• Treatment is by excision, which gives dramatic relief of
pain.
Chondroma
• A cartilaginous tumour common in the phalanges and
metacarpals.
• Enchondroma: a chondroma growing in the centre of a
bone.
• Ecchondroma: a chondroma growing on the surface of a
bone.
• Osteochondroma: a cartilage-capped bony outgrowth
(commonest bone tumour; malignant potential; especially if >2 cm or multiple).
• Treatment consists of observation for malignant transformation or bony destruction, and removal only if the
Chondroma is causing pain or fracture.
Osteoclastoma (Giant Cell Tumour)
• Occurs in young adults.
• Occurs at end of long bones.
• Has low malignant potential but is locally recurrent.
• Metastases uncommon, occur late and are to the lungs.
• Pathological fractures may occur.
Ewing’s Tumour
• Highly malignant.
• Arises from marrow.
• It is not conned to the ends of long bones and may
occur in any bone.
• Aects children and young adults.
• Spreads rapidly via the bloodstream to lungs, liver and
other bones.
Chondrosarcoma
• Slow-growing tumour arising from chondroblasts.
• Occurs between 30 and 50 years.
• May arise de novo or in a pre-existing osteochondroma.
• Occurs in long bones, pelvis and ribs.
• Metastases occur to lungs.
• Treatment is by wide excision or amputation.
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SECTION III Pathology
Fibrosarcoma
• More common in so tissues (malignant brous histio cytoma).
• Much less aggressive in bone.
Myeloma
• Common primary bone malignancy.
• It arises from marrow plasma cells.
• Rare before 50 years.
• Early dissemination with widespread marrow replacement (multiple myelomatosis).
• Clinically presents with:
• anaemia
• malaise
• bone pain (backache)
• pathological fracture.
Secondary Bone Malignancy
• Secondaries may occur from lung, thyroid, breast, prostate and kidney.
• Clinical features include:
• past history of primary tumour
• primary may not be apparent
• bone pain
• pathological fracture.
METABOLIC BONE DISEASE
Rickets and Osteomalacia
• Decient mineralization of organic bone matrix.
• Rickets is the name given to osteomalacia aecting the
growth of the skeleton in children.
• Rickets is characterized by bone deformities.
• Osteomalacia occurs in adults, causing susceptibility to
fractures but few deformities.
• Causes of osteomalacia/rickets include:
• dietary deciency of vitamin D
• deciency of vitamin D metabolites
• intestinal malabsorption
• renal disease
• liver disease.
• In children, classical deformities occur:
• bowing of the femur and tibia
• large head (‘bossing’ of the skull due to persistence of
suture lines and fontanelles)
• pronounced swelling of the costochondral junctions
(‘rickety rosary’)
• enlarged epiphyses
• stunted growth
• delayed dentition.
• Treatment is with vitamin D and calcium.
Osteoporosis
• Reduction in bone mass per unit volume.
• Common in the elderly, particularly females.
• May be complication of steroid therapy and Cushing’s
syndrome.
• Common predisposing cause of fractures, e.g. neck of
femur, Colles’ fracture, wedge fractures of vertebra.
• Occurs with any form of immobility.
• Associated with alcoholism, diabetes, liver disease and
smoking.
• Localized osteoporosis is inevitable aer immobilization of any part of the skeleton.
Hyperparathyroidism
See Chapter 12.
Paget’s Disease of Bone
• Dicult disease to categorize, probably not metabolic.
• Aetiology unknown.
• Localized increase in bone turnover.
• May aect part of one bone, an entire bone or many
bones.
• Disorderly bone resorption and replacement leads to
soening, increased vascularity, painful enlargement
and bowing of bones.
• Occurs in middle to old age and is more common in
males.
• Skull, vertebra, pelvis and long bones are aected.
• Some cases are symptomless, being picked up on routine radiography.
• Complications include:
• compressive symptoms due to skull enlargement, e.g.
blindness, deafness, cranial nerve entrapment
• paraplegia
• pathological fractures
• high-output cardiac failure, due to vascularity of
bone
• osteogenic sarcoma may develop aer many years.
LUNG TUMOURS
Lung tumours may be primary or secondary. Both are
common.
Primary Carcinoma of the Lung
• Most common primary malignant tumour worldwide.
• Largest cancer-causing death in UK: 35 000/year.
• 30% of all male cancer deaths.
• Male/female ratio 2 : 1 (was 7 : 1 but rise in incidence
in women parallels increase in numbers of female
smokers).
CHAPTER 22 System-Specific Pathology
397
• Directly related to cigarette smoking.
• Associated with occupational exposure to carcinogens.
• Overall 5-year survival rate around 5%.
Aetiology
Major risk factors are:
• Cigarette smoking.
• Occupational hazards:
• asbestos
• haematite
• radioactive gases, e.g. radon.
• Other factors:
• nickel
• chromates
• mustard gas
• arsenic
• coal-tar distillates
• brosis: peripheral lung cancers may arise in areas
of previous scarring, e.g. old tuberculous foci or
infarcts.
Classification of Lung Cancer
Four histological types are described:
• adenocarcinoma (30–45%)
• squamous cell carcinoma (35–40%)
• small cell (oat cell) carcinoma (15–25%)
• undierentiated large cell carcinoma (rarest).
Clinical Features
Primary
• May be asymptomatic and seen on routine chest X-ray.
• Cough.
• Haemoptysis.
• Dyspnoea.
• Chest pain.
• Wheeze.
• Hoarseness.
• Recurrent chest infections.
• Dysphagia.
Complications
• oracic: pleural eusion, recurrent laryngeal nerve
palsy (hoarseness).
• Superior vena cava obstruction, Horner's syndrome
(ptosis, miosis, enophthalmos, anhidrosis), especially
with Pancoast tumour (invasive cancer of apex of lung).
• Metastatic (cachexia, malaise), brain (headaches, ts,
personality change), bone (pathological fractures), liver
(jaundice), adrenal (Addison’s disease).
• Non-metastatic, extrapulmonary, ADH, ACTH secretion, hypercalcaemia, myasthenic neuropathy, hypertrophic pulmonary osteoarthropathy, thrombophlebitis
migrans, gynaecomastia, clubbing.
Prognosis
• Ultimately depends on cell type and stage of disease at
time of diagnosis.
• Small cell carcinoma has the worst prognosis.
Other Primary Lung Tumours
Primary tumours other than carcinomas are rare. ey may
be classied as:
• benign, e.g. bronchial gland adenomas, benign mesenchymal tumours
• malignant, e.g. sarcomas, adenocystic carcinomas, lymphomas, carcinoid tumours.
Pneumothorax
is is air in the pleural cavity. e causes are as follows:
• Spontaneous:
• primary: blebs on the pleural surface leak spontane-
ously or are triggered by a minor event, e.g. exertion;
more common in young males; may be bilateral; may
be familial
• secondary: to lung disease that breaches pleura, e.g.
COPD, bullous emphysema.
• Traumatic, e.g. following trauma to the chest, fractured
ribs.
• Iatrogenic, e.g. following central lines for CVP, intravenous feeding or haemodialysis.
Pneumothorax may be further classied as follows:
• Open, e.g. following stabbing or shooting. Air is sucked
into the pleural cavity during inspiration. is causes a
to-and-fro movement of the mediastinum during respiration, leading to respiratory embarrassment.
• Closed: this is when the chest wall is intact, e.g. with rib
fractures.
• Tension: occurs when there is a valve-like mechanism
at the site of communication between the air and the
pleural cavity, allowing air to enter the cavity in inspiration but not to escape in expiration. As pressure
rises:
• the lung collapses
• mediastinal shi occurs to the opposite side with tra-
cheal deviation to the opposite side
• compression of the contralateral lung
• compromise of venous return.
Tension pneumothorax is a life-threatening condition.
Pleural Effusions
• Haemothorax:
• blood in the pleural cavity
• due to chest injury, ruptured thoracic aortic aneurysm.
• Hydrothorax:
• transudate (low-protein uid) due to liver failure,
cardiac failure, renal failure
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SECTION III Pathology
• exudate (high-protein uid) due to tumours, infection, inammation.
• Chylothorax:
• lymph in the pleural cavity
• due to neoplastic obstruction of the thoracic duct.
• Pyothorax (empyema):
• pus in the pleural cavity
• due to infection.
LUNG INFECTIONS
Respiratory infections are very common. e general factors predisposing to lung infections include:
• loss or suppression of cough reex, e.g. anaesthesia,
aer surgery, coma, neuromuscular disorders
• ciliary defects, e.g. non-motile cilia or loss of ciliated
cells with squamous metaplasia
• mucus disorders, e.g. cystic brosis, chronic bronchitis
• immunological defects, e.g. hypogammaglobulinaemia
• inhibition of macrophage function, e.g. smokers
• pulmonary oedema.
Mode of Infection
Pathogens may reach the lung via:
• inhalation from the environment, e.g. nebulizers
• aspiration of oropharyngeal ora
• colonization of diseased/abnormal lower respiratory
tract, e.g. bronchiectasis
• blood spread: bacteraemia, septicaemia.
Predisposing Conditions
ese include:
• chronic obstructive pulmonary disease
• mucus disorders, e.g. cystic brosis
• immunosuppressive disorders
• immunosuppressive drugs.
Bronchopneumonia
• Chiey in old age and infancy.
• Occurs in patients with debilitating disease, e.g. cancer,
cardiac failure, renal failure.
• Predisposing factors include COPD and cystic brosis.
• Occurs in early post-operative period due to failure to
remove respiratory tract infections.
• Causative organisms include:
• S. pneumoniae
• H. influenzae
• rarer causes include S. aureus and coliforms
• S. aureus pneumonia seen in hospital patients,
after influenza as a severe secondary bacterial
pneumonia; intravenous drug abusers; in the
immunocompromised. It may be fulminating and
rapidly fatal
• coliform bronchopneumonia is rare: may be encountered in hospital patients, the immunocompromised
and those on ventilatory support in ITUs.
• Bronchopneumonia is of characteristically patchy distribution and tends to be basal and bilateral.
• Histological examination reveals inammatory cells
in the bronchi and bronchioles with alveoli lled with
inammatory exudate.
Lobar Pneumonia
• Rarely seen in surgical patients.
• May result in referred pain to the abdomen, particularly
right lower lobar pneumonia; enters into the dierential
diagnosis of appendicitis, the intercostal nerves being
irritated and pain being referred to the right iliac fossa.
• Commonly caused by S. pneumoniae.
• Part of post-splenectomy sepsis.
• Relatively uncommon in infancy and old age.
• Clinical features include:
• cough
• fever
• ‘rusty’ sputum
• rigors may occur
• acute pleuritic chest pain
• consolidation of a lobe or part of lobe results.
• Classically, four stages of the disease are recognized
pathologically:
• congestion: lasts about 24 h and is due to pro-
tein-rich exudate filling alveoli, with venous
congestion
• red ‘hepatization’: lasts a few days, with inflam-
matory cells and red cells in the alveolar spaces;
fibrinous exudate on pleura; lung is red, solid, airless and bears a resemblance to the cut surface of
fresh liver
• grey ‘hepatization’: accumulation of brin with the
destruction of white cells and red cells; lung appears
grey and solid
• resolution: occurs in 8–10 days; inammatory cells
and brin are re-absorbed and the underlying lung
architecture is preserved.
e above is a classical pattern of lobar pneumonia. Most
cases resolve as above, although the pattern may be modied by early and appropriate antibiotic therapy.
Aspiration Pneumonia
• Occurs when upper gastrointestinal contents are aspi-
rated in lung.
• Results in consolidation and inammation.
• Clinical situations in which this may occur include:
• induction of anaesthesia
• recovery from anaesthesia
CHAPTER 22 System-Specific Pathology
399
• sedation
• coma
• severe debility.
• Part of lung aected depends on the patient's posture.
• Abscess and empyema may result.
• Causative organisms are usually commensals of the
upper respiratory tract, principally S. pneumoniae,
although anaerobes are also involved in the majority of
cases.
Atypical Pneumonia
• Main causative organisms are:
• Mycoplasma pneumoniae
• Coxiella burnetii
• Chlamydia psittaci
• Chlamydia pneumoniae.
• Mycoplasma pneumoniae is responsible for most cases
of primary atypical pneumonia.
• School-aged children and young adults are the group
most aected.
• Spread by droplet infection.
• Eective drugs include tetracycline and erythromycin.
Legionnaires’ Disease
• Caused by Legionella pneumophila.
• Patients typically middle-aged smokers, oen in poor
general health.
• May also aect patients who are previously healthy.
• Spread by water droplets from contaminated air humidiers or water storage tanks.
• Symptoms initially those of u-like illness, which progresses to severe pneumonia and respiratory failure.
• Other features include:
• headache
• mental confusion
• myalgia
• nausea
• vomiting
• diarrhoea
• acute renal failure.
• 10–20% of cases are fatal.
• Treatment usually with erythromycin, but those failing
to respond may be treated with rifampicin or ciprooxacin, either singly or in combination.
Chest Infections in the Immunocompromised
• ese are opportunistic infections and include:
• f ungi, e.g. Candida, Aspergil lus fumigatus, Pneumocystis
jirovecii (formerly carinii)
• viruses, e.g. cytomegalovirus (CMV).
• Characterized by:
• fever
• cough
• shortness of breath
• pulmonary inltrates on chest X-ray.
Pneumocystis jirovecii (formerly carinii)
• Results from reactivation of latent infection.
• Common in patients with AIDS, and transplant patients.
• Diagnosis depends on identication of characteristic
organisms in bronchial aspirates, bronchial lavage or
lung biopsy.
• Treatment with intravenous co-trimoxazole.
Fungi
• Both Candida and Aspergillus can cause widespread
areas of necrosis.
• Microabscesses containing characteristic fungal laments may occur in the lungs.
• Treatment requires intravenous amphotericin B alone
or in combination with 5-uorocytosine.
New imidazoles, e.g. uconazole, may be eective.
Viruses
• Cytomegalovirus causes diuse alveolar damage.
• Characteristic intranuclear inclusions are seen with
CMV infections.
• Treatment is with intravenous ganciclovir.
Bronchiectasis
• Abnormal and irreversible dilatation of bronchi.
• Now relatively uncommon in Western countries due to
the decline in predisposing childhood infections, particularly whooping cough and measles.
• Condition may be congenital or acquired.
• Chief congenital cause is cystic brosis; may be seen in
immunodeciency syndromes.
• Chief acquired causes include:
• whooping cough
• measles
• bronchial obstruction (enlarged lymph nodes from
tuberculosis)
• bronchial tumours.
• Recurrent infection and inammation lead to further
airway damage and destruction of lung tissue.
• Destruction of alveolar walls, brosis of lung
parenchyma.
• Clinical features include:
• production of large amounts of foul-smelling sputum
• dyspnoea.
• Complications include:
• pneumonia
• lung abscess
• empyema
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SECTION III Pathology
• septicaemia
• amyloid formation
• pulmonary brosis
• cor pulmonale
• remote abscesses, e.g. cerebral abscesses and
meningitis.
EMPYEMA
is is pus within the pleural cavity. e causes include:
• pulmonary infection: complication of intrapulmonary
infection, e.g. pneumonia, tuberculosis, lung abscess
• other infections: spread from subphrenic abscess, acute
mediastinitis, distant infective foci
• surgery: as a complication of thoracic surgery
• penetrating chest wall injury.
Organisms
ese include:
• Gram-positive organisms, e.g. S. pneumoniae or S.
aureus, especially when empyema complicates pulmonary parenchymal infection
• empyema secondary to surgery, trauma or oesophageal
disease may be due to Gram-negative organisms.
Complications
• Systemic sepsis.
• Lung collapse.
• Bronchopleural stula.
• Pleural scarring.
Lung Abscess
• May be single or multiple.
• Usually occur in patients who are malnourished,
cachectic or immunocompromised.
• Causes include:
• aspiration pneumonia
• bronchiectasis
• carcinoma
• inhaled foreign bodies
• infected pulmonary infarcts
• infection from drug abuse.
• Organisms include:
• S. pneumoniae
• H. influenzae
• S. aureus
• Klebsiella
• Entamoeba histolytica (spreading from the liver via
the diaphragm).
BREAST DISORDERS
Benign Tumours
Benign breast tumours comprise:
• broadenoma
• duct papilloma
• adenoma
• connective tissue tumours.
Fibroadenoma
• Commonest type of benign tumour, mainly in young
women (15–35).
• Arises from connective tissue and epithelium.
• Clinically mobile on palpation (breast mouse).
• Firm rubbery masses that are well circumscribed. Rarely
larger than 3 cm.
• Cut surface has a characteristic appearance which is
greyish-white with a whorled appearance.
• May calcify with age.
• Juvenile broadenomas occurring in the breasts of
young girls may grow quite rapidly and reach up to 10
cm in diameter; more frequent in Africans and West
Indians than Caucasians.
Duct Papilloma
• More frequent in middle-aged females.
• Commonest cause of nipple discharge, oen blood-stained.
• Consist of branching brovascular cores covered by epithelium, which is benign.
• Solitary duct papillomas are not premalignant.
• Multiple duct papillomas arising in smaller ducts at a
younger age may be associated with an increased risk of
malignancy.
Adenoma
• Rare.
• Tubuloadenomas are well-circumscribed tumours occurring mainly in women in their early 20s.
• Lactating adenomas are tubuloadenomas that undergo
secretory changes during pregnancy.
• Nipple adenomas occur as nodules under the nipple;
may occur at any age but most common between 30 and
50 years; overlying skin may ulcerate and there may be
blood-stained discharge; nipple adenomas may be mistaken for Paget’s disease.
Connective Tissue Tumours
• Lipomas and haemangiomas may occur but are rare.
Carcinoma of the Breast
is accounts for 20% of all cancers in women and is the commonest cause of death among women in 35–55 age group.
Risk Factors
ese include:
• Female sex:
• risk increases with age.
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