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CHAPTER 21 Basic Microbiology
381
procedures’ (EPPs). As eective treatment is available for
HBV, all individuals with acute or chronic infection should
be referred to local hepatitis services for further management following diagnosis.
Hepatitis C
• Single-stranded RNA virus.
• Incubation period 2 weeks to 6 months.
• UK prevalence of chronic HCV infection is 0.4%.
• Transmission by blood-borne route from viraemic carriers of infection.
• Routes of transmission:
• IVDUs sharing needles, syringes and other para-
phernalia; 20% seroconversion/year
• recipients of blood transfusions before September
1991
• recipients of pooled plasma products (including
Factor VIII and immunoglobulin) manufactured
prior to 1986
• transplant recipients and haemodialysis patients,
particularly if performed overseas
• healthcare workers from occupational sharps
injuries
• vaccination, cultural rituals, tattooing and acupunc-
ture with unsterile equipment
• mother-to-child transmission (3–10% transmission
at birth without intervention)
• transmission by sexual contact may occur but is
rare.
Clinical presentation
• Oen asymptomatic.
• Only about 25% become symptomatic and jaundiced.
• Severity of symptoms does not necessarily equate to
extent of liver disease.
Serology
• Antibody test used for screening.
• 15–40% of people infected with HCV will clear the virus
in the acute stage but will remain antibody-positive.
• PCR to detect HCV RNA will identify if infection is still
active.
Outcome
Of the 60–85% of patients who do not clear the virus in the
acute stage (within 6 months from infection):
• some will never develop liver damage
• many will develop only moderate liver damage with or
without symptoms
• 20% will progress to cirrhosis within 20 years
• of these, 25% will progress to end-stage liver disease
(oesophageal varices, ascites and/or hepatic encephalopathy) or develop hepatocellular carcinoma.
Eective treatment is available for HCV infection using
combination treatment with interferon-α and ribavirin.
Patients newly diagnosed with HCV infection should be
referred to a specialist hepatitis service for further assessment and management.
HIV
• Single-stranded RNA retrovirus.
• Produces DNA via the enzyme reverse transcriptase.
• DNA integrated into host cell genome (integrase).
• During replication, this proviral DNA is transcribed
into mRNA and translated into viral proteins. ese are
cleaved into constituent parts by protease enzyme.
• ese enzymes act as potential targets for antiretroviral
therapy (ART).
• HIV infection results in widespread immunological
dysfunction by replicating in and eventually exhausting CD4+ T-helper cells, macrophages and antigen presenting cells.
• Loss of immune function causes:
• increased risk of infection (see below) and opportu-
nistic infections
• increased risk of cancer – all types (both HIV- and
non-HIV associated)
• patients infected with HIV also have higher rates
of cardiovascular disease, endocrine abnormalities,
renal dysfunction and osteoporosis.
• HIV may be transmitted by:
• sexual intercourse (MSM and heterosexual – fastest
rate of increase is among heterosexual white couples
in UK)
• blood transfusion
• intravenous drug abuse and needlestick injuries
• mother-to-child transmission (MTCT).
• e following are therefore at risk of becoming HIV
positive:
• anyone of any age who is sexually active
• commercial sex workers (CSWs), both male and
female
• intravenous drug users (IVDUs)
• haemophiliacs or recipients of blood products before
routine testing of donated blood became available,
i.e. October 1995
• sexual partners of the above
• children of infected mothers, particularly in high-
endemicity areas.
Natural history
• During acute infection, rapid viral replication occurs.
• e patient may be asymptomatic for 4–8 weeks prior
to the development of a ‘seroconversion illness’.
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SECTION III Pathology
• is is a u-like or glandular fever-like illness with
symptoms including fever, lymphadenopathy, pharyngitis and rash.
• Patients are highly infectious during this period and
their CD4 cell count may fall suciently to allow the
development of opportunistic infections.
• Subsequently an asymptomatic (‘plateau’) phase occurs;
HIV antibodies are present, controlling viral replication;
CD4 count low normal; may continue for many years.
• HIV oen progresses within 5–10 years from infection.
• When CD4 count falls <350 cells/mm3, treatment
should be initiated (current recommendations).
• When CD4 count falls <200 cells/mm3, risk of developing opportunistic infection and HIV-associated malignancy increases.
• ese used to be termed AIDS-dening conditions, and
are important indicators of underlying potential HIV
infection (see below).
• Without treatment, net median survival time in developed countries is 9–11 years.
HIV tests
• HIV antibody tests will be negative until seroconversion occurs (the window period).
• Modern 4th-generation tests look for both antibody
and antigen (the p24 antigen) to shorten this to about
4 weeks. If the patient is at ‘on-going’ risk then repeat
testing should be performed.
• Only verbal consent is required to perform a routine
HIV test, and can be obtained by any medical/surgical
practitioner. Higher-risk patients should be counselled
by those with training to do so (health advisors, ID/GU
department).
• Measurement of CD4 count in those presenting with
surgical complaints may be useful to determine risk of
opportunistic infection/malignancy and (if relevant)
treatment compliance.
HIV indicator diseases
HIV testing is strongly recommended when the following
conditions are suspected (RCP Guidelines):
• Any unusual manifestation of bacterial, fungal or viral
disease, i.e.
• tuberculosis infection (any site including
pulmonary)
• suspected Pneumocystis jirovecii (formerly carinii)
pneumonia
• suspected cerebral toxoplasmosis
• oral/oesophageal candidiasis
• oral hairy leucoplakia
• persistent genital ulceration
• presence of blood-borne or sexually transmitted
infection, e.g. syphilis, HBV
• suspected primary seroconversion illness
• also anyone with recurrent bacterial infections (see
list below).
• Unusual tumours, i.e. cerebral lymphoma, non-Hodgkin's lymphoma or Kaposi's sarcoma.
• Unexplained thrombocytopenia or lymphopenia.
• Unusual skin problems, including severe seborrhoeic
dermatitis, atypical psoriasis or extensive molluscum,
and recurring shingles or shingles in a young person.
• Persistent lymphadenopathy or unexplained lympho edema.
• Neurological problems including peripheral neuropathy or focal signs due to a space-occupying intracerebral lesion.
• Unexplained weight loss or diarrhoea, night sweats, or
pyrexia of unknown origin.
• Any other unexplained ill health or diagnostic problem.
Sites of bacterial infection in those with underlying HIV
infection may include:
• recurrent pneumonia
• boils, carbuncles, cellulitis
• anorectal abscesses
• empyema thoracis
• necrotizing fasciitis
• osteomyelitis
• septic arthritis
• epididymo-orchitis
• pelvic inammatory disease.
Precautions in Hepatitis B, Hepatitis C and
HIV Patients
Sources of infection are:
• contact: blood, urine, faeces, saliva, tears, CSF, etc.
• aerosol: use of power tools
• inoculation: sharps injuries – needlestick, scalpels.
Universal Precautions
is refers to those precautions taken to protect theatre
sta from infection from every patient. ey include:
• washing hands before and aer contact with every patient
and before putting on and aer removing surgical gloves
• cover existing wounds and skin lesions
• avoid sharps use where possible
• avoid wearing open footwear
• clearing blood spillages promptly.
Special Precautions
ese are used for all high-risk patients, e.g. hepatitis, HIV,
or patients suspected of having these conditions:
• All personnel involved in patient care should be aware
of the risk.
• Any patient considered a risk should be indicated as
belonging to a high-risk category on the operating list
(under no circumstances should the disease causing
CHAPTER 21 Basic Microbiology
383
the risk be placed on the operating list, for reasons of
patient condentiality).
• Arrangements should be made for contaminated uid,
dressings, etc., to be handled and disposed of correctly.
• Appropriate theatre techniques should be adopted:
• minimize theatre sta: only essential personnel; no
spectators
• remove all but essential equipment
• disposable drapes and gowns
• double-gloving and use of ‘indicator’ glove systems
• visors to prevent splashing in eyes
• blunt suture needles
• stapling devices rather than needles where possible
• pass instruments in kidney dish
• ‘no-touch’ technique
• all disposable equipment should be removed in spe-
cically marked containers
• theatre should be thoroughly cleansed with dilute
bleach solution at the end of the procedure.
• Recovery sta must also be aware of the risk.
ese special precautions should also be used for other
cases where spread of infection is possible, e.g. patients
with MRSA.
Immunization
Immunization is available against hepatitis B but not hepatitis C or HIV.
Hepatitis B
Hepatitis B vaccine is oered to all high-risk sta, i.e. those
performing exposure-prone procedures (EPPs). ese
include:
• surgeons
• theatre nurses and other operating department personnel
• pathology department sta
• A&E sta
• liver transplant unit sta
• GI unit sta
• workers in residential units for those with learning
disabilities
• sta of infectious diseases units.
Dialysis units are oen quoted as being ‘high-risk’ areas;
however, following outbreaks of hepatitis B several years ago,
all sta and patients of dialysis units are tested for HBsAg.
Management of Sharp Injuries
Immediately aer the injury:
• let the site of injury bleed
• wash area with soap and water
• report the incident to supervisor/senior ocer/occupational health immediately
• contact the occupational health department or nearest
emergency department as soon as possible, according
to local protocols.
Procedure at occupational health (OH) or emergency
department:
• Take detailed information:
• source patient risk factors for having a blood-borne
virus (including IVDU, born in sub-Saharan Africa,
etc.)
• nature of the incident – type of injury and sharp
involved (open-bore needle, probe, etc.)
• HBV vaccination status of the exposed person
• when the incident occurred.
• Explain transmission risks; risk is small.
• Depending on local protocol (your hospital will have its
own), take serum/blood to store in case future testing
required.
• If the source patient is known (i.e. the original use of
the needle in needlestick injury), they should be asked
to consent for testing for HIV, HBV and HCV. ey
should be counselled before the tests are done, by someone other than the person exposed.
• e person sustaining the ‘sharps’ injury should be
advised about the risks of transmission until the test
results are received. ey should practise safe sex and
not donate blood. ey may continue operating and
performing EPP. Follow-up testing must be performed
as directed by the OH department, the timing of which
will depend on the source patient's status. Generally,
antibody tests to HBV, HCV and HIV are performed at 3
and 6 months, but additional testing for HCV RNA and/
or HIV RNA may be required if the patient is known to
be infectious.
Post-Exposure Prophylaxis
Hepatitis B
• OH or exposed person should be aware of their
own HBV vaccine status, particularly if they have
not responded to the initial immunization course
(‘non-responder’).
• If the exposed person has responded to HB vaccine (documented anti-HBsAg >10 mIU/mL) then a booster dose
may be given regardless of the source patient's status.
• If the exposed person has received two or more doses of
HB vaccine, then the course is completed regardless of
the source patient’s status.
• If the exposed person has received one or no doses of
HB vaccine or is a known ‘non-responder’ and a signicant exposure from an HBsAg-positive source has
occurred, then HB immunoglobulin will be required
and an accelerated HB vaccine course may be initiated.
• Similar procedures should be followed when the source
patient cannot be identied or refuses to be tested.
Liaison with OH and a microbiology/virology consultant is mandatory.
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SECTION III Pathology
Hepatitis C
• No vaccine or post-exposure prophylaxis is currently
available.
• Risk of infection only if source patient is viraemic.
HIV
• Carry out tests aer counselling at 3 months and 6
months.
• No vaccine available.
• Post-exposure prophylaxis (PEP) may be recommended depending on the nature of the injury and the
risk of transmission (which is always low). Which drugs
are used varies although commonly a combination of
two NRTIs (nucleoside reverse transcriptase inhibitors,
e.g. zidovudine, lamivudine) and a PI (protease inhibitor, e.g. lopinavir, ritonavir) are used.
• e decision on whether PEP is appropriate should be
taken by someone experienced in HIV medicine as the
drugs are always poorly tolerated, and specic counselling is needed. If the source patient has a drug-resistant
virus (which is known about), then alternative agents
may be used.
CJD and vCJD
• Two types of human prion protein (PrP) disease causing spongiform degeneration of the brain (transmissible spongiform encephalopathy).
• Creutzfeld–Jakob disease (CJD) is a progressive sporadic disease occurring over the age of 50.
• Variant CJD (vCJD) has been directly linked to BSE
(bovine spongiform encephalopathy) in cattle and
arises following the consumption of infected meat. It
has a longer clinical course (years rather than months)
and aects a younger age group (mean age is 25 years).
• No eective management exists and the conditions are
usually fatal.
• Although no evidence exists for person-to-person
spread by close contact, transmission may occur with
specic surgical or medical treatment (iatrogenic).
• Hospitals have strict guidelines in place to prevent
spread from those suspected or known to have the condition or from those with a greater than average risk,
due either to their medical or family history, or from
patients undergoing brain biopsy.
• Examples of precautions taken include:
• including screening questions in preoperative
checklists to determine risk
• provision of single-use equipment for neurosurgical
and endoscopic procedures
• use of leucocyte-depleted blood in transfusions
• appropriate disposal of waste and post-mortem
material.
OSCE SCENARIOS
OSCE Scenario 21.1
A 37-year-old male attends A&E, complaining bitterly of pain
in his le groin. On examination the skin appears red and cellulitic. He is in severe pain when it is touched, and he has a
tachycardia of 133 beats/min and a temperature of 38.8°C.
1. Given the above information, what broad dierential
diagnoses are you considering?
2. What questions would you like to ask this patient to get
a rapid idea of the diagnosis?
3. What investigations and management plan would you
initiate?
e patient rapidly becomes haemodynamically unstable
and a diagnosis of septic shock due to severe so tissue
infection is assumed. He is taken to theatre where extensive debridement of infected and necrotic tissue is performed along the fascial planes of his leg.
4. What are the diagnosis and prognosis, and which organ-
isms are commonly associated with this condition?
OSCE Scenario 21.2
A 68-year-old male patient develops acute retention of
urine aer repair of a right inguinal hernia. An indwelling
urethral catheter was inserted and he has now developed
a urinary tract infection. He was started on appropriate
broad-spectrum antibiotics and is now systemically much
better. He has asked to speak to one of the surgical team as
he is upset about developing a hospital-acquired infection
(HAI).
1. Answer the patient’s questions about HAI.
He is satised with your explanation and feels much happier now; however, he is worried about the possibility of
getting an MRSA infection whilst he is in hospital, as he
has read so much about it in the newspapers.
2. Explain what MRSA is, the dierent sources of infec-
tion and methods of spread.
3. Explain the methods employed in hospitals for preven-
tion and control of HAI.
OSCE Scenario 21.3
A 31-year-old male patient who admits to regular intravenous drug use is admitted with cellulitis of his right
groin, which began 48 h aer repeated attempts to inject
his femoral vessels. He saw his GP and was started on oral
antibiotics but tells you the redness is increasing, although
he is systemically well. On examination, the area is warm,
pink and swollen but there is no evidence of abscess.
CHAPTER 21 Basic Microbiology
385
1. Which two bacterial species are the most likely to be the
cause of this patient’s infection?
Microbiology culture results of a wound swab taken by
the patient’s GP report that a resistant organism has been
isolated.
2. Explain how organisms develop resistance to
antimicrobials.
e antibiotics are changed, but as the erythema settles
the patient develops a uctuant area in the skin, consistent
with an abscess. e patient is prepped for theatre.
3. What special considerations and precautions should be
taken when operating on this patient?
OSCE Scenario 21.4
A 67-year-old male patient was admitted with perforated
duodenal ulcer that necessitated laparotomy and repair.
Postoperatively, he recovered on the high-dependency unit
and was stepped down to the ward and deemed medically
t for discharge. He was commenced on H. pylori eradication therapy and was awaiting a social package. However,
he developed severe diarrhoea a few days later along with
abdominal pain and distension. He had T of 39.5°C, PR of
140/min, RR of 25/min and his blood tests showed WBC
count of 35,000 106/dL. Abdominal X-ray showed very
dilated colon.
1. What is the most likely diagnosis and responsible
microorganism?
2. What are the predisposing risk factors for acquiring
this infection in this context?
3. How do you conrm the diagnosis?
4. How do you manage this condition?
5. What are the precautions required to prevent this infec-
tion from occurring and spreading in hospitals?
OSCE Scenario 21.5
You attend the minor operation room to perform excision
of skin lesions under local anaesthesia. Your consultant
reminds you of using the pink disinfectant for skin preparation and performing the procedures under strict sterile
measures using sterile instruments, gloves and gowns.
1. What disinfection agents are used on skin?
2. What is the dierence between cleaning, disinfection,
and sterilization?
3. What are the four main methods of sterilization?
Answers in Appendix pages 481–484
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
22
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System-Specific Pathology
NERVOUS SYSTEM
Head Injury
In the UK, head injuries account for annual attendance
rates at A&E of almost 1 million patients. Head injuries
account for 9 deaths per 100 000 population and in young
males, account for 15–20% of all deaths. Head injuries may
be classied as follows:
• missile injury to the brain
• non-missile injury to the brain.
Missile Injury to the Brain
Typically caused by bullets. May result in:
• depressed injuries: missile causes depressed skull fracture with contusion, but does not enter brain
• penetrating injuries: where missile enters cranial cavity
but does not exit, resulting in focal damage
• perforating injury: where missile enters and exits from
cranial cavity, usually resulting in severe extensive
haemorrhage around the track of the bullet.
Non-Missile Injury to Brain
• More common than missile injury.
• Range from relatively minor injuries to severe injuries,
which may be fatal.
• Main damage to brain occurs as a result of acceleration/deceleration forces causing rotational and shearing forces acting on the mobile brain anchored within a
rigid skull.
e types of brain damage occurring in non-missile injuries may be classied as:
• Primary brain injury:
• immediate result of trauma
• results in contusions, lacerations and diuse brain
damage
• treatment cannot reverse primary brain injury.
• Secondary brain injury:
• result of complications
• prevention, recognition, and treatment is mainstay
of management of patients with head injuries.
Primary Brain Damage
ere are two main forms:
• Focal damage:
• commonest type of focal damage is contusion
• oen occurs at site of impact, particularly if skull
fracture
• may be more severe on the side opposite the impact,
i.e. contrecoup
• large contusions may be associated with intracerebral haemorrhage
• may be associated with tears of cranial nerves.
• Diuse axonal injury:
• results where there is shearing of axons as a result of
acceleration/deceleration/torsional forces
• changes are usually only detectable histologically
• useful pointers to an occurrence are petechial haemorrhages in the corpus callosum and the cerebellar
peduncles
• patients who have sustained diuse axonal injury
and survive are generally severely disabled.
Secondary Brain Damage
• Results from complications developing aer the moment
of injury.
• Complications include:
• intracranial haemorrhage
• cerebral hypoxia
• cerebral oedema
• intracranial herniation
• cerebral infection, e.g. meningitis.
Outcome of Non-Missile Head Injury
Complications include:
• Post-concussion syndrome resulting in:
• headache
• dizziness
• fatigue
• poor memory
• labile emotional state.
386
CHAPTER 22 System-Specific Pathology
387
• Post-traumatic epilepsy.
• Persistent vegetative state.
• Post-traumatic dementia.
• Brainstem death.
INTRACRANIAL HAEMORRHAGE
is may be:
• extracerebral: occurring in relation to the coverings of
the brain
• intracerebral: occurring within the brain.
Extracerebral
Extracerebral intracranial haemorrhage may be divided
into dierent types according to the anatomical space in
which it occurs in relation to the meninges:
• extradural
• subdural
• subarachnoid.
Extradural Haemorrhage
• Bleeding into the extradural space, i.e. between skull
and dura.
• Usually caused by trauma to the skull associated with a
fracture tearing an artery or dural venous sinus.
• Particularly common with fractures of the temporal
bone tearing the middle meningeal artery.
• Haematoma develops outside the dura, causing compression of the underlying brain, resulting in transtentorial herniation.
• Commonly fatal unless diagnosed early and treated by
surgical evacuation.
• Clinical features include:
• temporary concussion
• recovery (‘lucid interval’)
• decreased conscious level
• coma
• falling pulse rate
• rising BP
• dilated ipsilateral pupil
• contralateral hemiparesis
• focal ts
• may be boggy swelling overlying the site of fracture
as extradural blood tracks through the fracture into
the subcutaneous tissues.
Subdural Haemorrhage
• Bleeding into the subdural space between dura and
arachnoid.
• Caused by bleeding from veins which cross the subdural
space.
• Divided into:
• acute subdural haemorrhage: seen following head
injury caused by falls or assaults
• chronic subdural haemorrhage: usually seen in the
elderly, where brain shrinkage makes the bridging
veins between cortex and venous sinuses vulnerable;
may result from trivial and forgotten head injury.
• Haematoma appears as a layer of gelatinous blood
(acute type) or an organized layer of granulation tissue
and clot (chronic type).
• Compression of underlying brain causes decline in conscious level.
Subarachnoid Haemorrhage
• Bleeding into the subarachnoid space, i.e. between
arachnoid and pia.
• Causes include:
• traumatic: in association with head injury
• spontaneous:
• rupture of berry aneurysm
• rupture of vascular malformation
• rupture of intracerebral haematoma into subarachnoid space.
• Pathologically there is a layer of blood over the cerebral
surface in the subarachnoid space.
• Blood present in CSF.
• Presents with headache and signs of meningeal
irritation.
• 60% of cases die immediately.
• One-third of survivors are permanently disabled as a
consequence of hypoxic brain damage.
• Hydrocephalus can occur in survivors where brous
obliteration of the subarachnoid space or arachnoid
granulations may occur.
Intracerebral Haemorrhage
• An expansile haematoma within the brain substance.
• Causes include:
• hypertensive vascular disease (most common cause)
• trauma
• bleeding into a tumour
• vascular malformation
• cerebral vasculitis
• associated with coagulopathies.
• Commonest sites for intracerebral haematoma include
basal ganglia, internal capsule, thalamus, cerebellum
and pons.
Diffuse Petechial Haemorrhages
• Small pin-point haemorrhages scattered throughout
brain.
• Result from disruption of wall of small cerebral blood
vessels.
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SECTION III Pathology
• Causes include:
• vasculitis
• acute hypertensive encephalopathy
• fat embolism
• head injury.
RAISED INTRACRANIAL PRESSURE
• Skull contains brain, CSF and blood.
• At normal intracranial pressures (10–15 mmHg or 12–18
cmH2O), these three components are in volumetric equilibrium. If one component is elevated, intracranial pressure
will increase unless the volume of the other two components decreases proportionately (Monro–Kellie doctrine)
(see Ch. 22, Raised Intracranial Pressure section).
• Compensatory properties among the intracranial contents follow a pressure/volume exponential curve.
• Increased volume of any of three components can be
balanced up to a certain level without any increase in
intracranial pressure.
• Eventually a critical volume is reached where any further
volume increase results in raised intracranial pressure.
• e eects of raised intracranial pressure include:
• hydrocephalus
• cerebral ischaemia
• brain shi and herniation
• systemic eects.
Hydrocephalus
• Common complication of space-occupying lesions of
posterior cranial fossa, which compress cerebral aqueduct and fourth ventricle.
Cerebral Ischaemia
• Eects of raised intracranial pressure are exerted on
vascular component and result in progressive reduction
in cerebral perfusion pressure (cerebral perfusion pressure = blood pressure − intracranial pressure).
Brain Shift and Herniation
• Occurs following a critical increase in intracranial
pressure.
• Lumbar puncture contraindicated as there is a risk of
precipitating a potentially fatal brainstem herniation.
• Herniation may occur at the following sites:
• transtentorial herniation (clinical manifestation
shown in Box 22.1)
• tonsillar herniation
• herniation of cerebellar tonsils into foramen mag-
num, causing compression of medulla
• medullary compression results in decerebrate pos-
ture, respiratory failure and death.
BOX 22.1 Clinical Manifestations of
Tentorial Herniation
Affected (Compressed)
Structure Clinical Manifestation
Oculomotor nerve
(cranial nerve III)
Ipsilateral cerebral
peduncle
Contralateral cerebral
peduncle
Posterior cerebral artery Cortical blindness
Cerebral aqueduct Headache and vomiting
Reticular formation Coma
Midbrain Decerebrate rigidity,
Ipsilateral pupillary
dilatation
Contralateral
hemiparesis
Ipsilateral hemiparesis
from hydrocephalus
death
Systemic Effects
ese include:
• hypertension
• bradycardia
• slowing of respiration
• pulmonary oedema
• gastrointestinal ulceration (Cushing’s ulcer).
Clinical Manifestations of Raised Intracranial
Pressure
ese include:
• headache, due to distortion and compression of pain
receptors within the dura mater and around the cerebral
vessels
• nausea and vomiting, due to pressure on the vomiting
centre in the pons and medulla
• papilloedema, due to venous obstruction
• decrease in level of consciousness ranging from drowsiness to coma, depending upon the level of the intracranial pressure.
CEREBRAL ABSCESS
Cerebral abscesses usually develop following focal inammation of the brain parenchyma. ey usually occur as a
result of:
• direct spread of infection from sepsis in the middle ear
or paranasal sinuses
• septic cerebral sinus thrombosis, due to spread of infection from the mastoid or middle ear via the sigmoid sinus
CHAPTER 22 System-Specific Pathology
389
• blood-borne infection, e.g. from infective endocarditis or bronchiectasis; in immunocompromised patients
abscesses may be caused by fungal or protozoal organisms
• trauma, e.g. following open skull fractures.
Abscesses may occur at preferential sites according to their
aetiology:
• temporal lobe or cerebellum from otitis media
• frontal lobe from paranasal sinuses
• parietal lobe from haematogenous spread.
Complications
Complications of cerebral abscesses include:
• meningitis
• intracranial herniation
• focal neurological decit
• epilepsy.
TUMOURS OF THE NERVOUS SYSTEM
Classication of cerebral tumours is shown in Box 22.2.
Astrocytoma
• Peak incidence in early middle age.
• Vary in malignancy, some being slow growing and
inltrative.
• Most malignant astrocytomas are radioresistant and
overall survival is usually less than 5 years.
• In children the tumour is oen well dierentiated
and cystic and occurs in the cerebellum. is type is
BOX 22.2 Classification of Cerebral
Tumours
Primary
Glial (gliomas)
Astrocytomas
Glioblastoma multiforme
Medulloblastomas
Ependymomas
Oligodendrogliomas
Non-glial
Meningiomas
Acoustic neuromas
Pituitary tumours
Secondary
Lung
Breast
Kidney
Melanoma
histologically benign and may oen be completely
excised with potential cure.
Glioblastoma Multiforme
• Most malignant brain tumour.
• Grows rapidly.
• Occurs between 40 and 60 years old.
• Rarely removable surgically.
• Radioresistant.
• Most patients die within 1 year.
Medulloblastoma
• Commonest glioma of childhood.
• Occurs in rst decade of life.
• Arises in roof of fourth ventricle and inltrates into
cerebellum.
• May cause obstructive hydrocephalus.
• Spreads by CSF and may seed on spinal cord.
Ependymomas
• ose arising from the choroid plexuses of the ventricles may be totally removable.
• ose arising from the ventricular walls are dicult to
remove.
• Most are well dierentiated.
• Malignant forms, however, may seed via the subarachnoid space.
Oligodendrogliomas
• Occur in the cerebral hemispheres.
• Slow growing.
• Usually ill-dened inltrating neoplasms.
• Most patients die within 5 years of diagnosis.
Meningiomas
• Arise from arachnoid cells.
• Usually occur in females in the 40–60 age group.
• Compress cerebral cortex early in their growth and
therefore ts may be an early sign.
• May cause osteoblastic change in overlying bone, giving
rise to exostosis, producing a palpable lump over vault
of skull.
• Most frequent sites are parasagittal region, sphenoidal
wing, olfactory groove and foramen magnum.
• Usually slow growing; do not invade brain tissue but
compress it.
• Small tumours are usually curable by excision.
• Even with subtotal excision for large tumours the prognosis is good.
Acoustic Neuroma
• Arises from Schwann cells of the nerve sheath of cranial
nerve VIII at the internal auditory meatus.
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SECTION III Pathology
• As tumour grows it expands the internal auditory
meatus, extending into the cerebellopontine angle and
compressing the pons, cerebellum and adjacent cranial
nerves.
• May be a feature of von Recklinghausen’s disease.
• Diagnosis should always be considered in patient with
unilateral sensorineural deafness with tinnitus.
• Usually occurs in 30–60 age group.
• Facial weakness with unilateral taste loss is a later
manifestation.
• Corneal reexes are lost relatively early when trigeminal
nerve is stretched by the tumour.
• Dysphagia, hoarseness and dysarthria may arise due to
involvement of cranial nerves IX, X and XI.
• Unilateral cerebellar signs and features of raised intracranial pressure may occur.
Secondary Tumours
• CNS common site for metastases.
• Commonest neoplasms metastasizing to CNS are:
• breast
• bronchus
• kidney
• colon
• malignant melanoma.
Clinical Features of CNS Tumours
CNS tumours may present clinically in two main ways:
• Local eects, including:
• cranial nerve palsy
• epilepsy
• paraplegia with spinal cord tumour.
• Mass eects:
• many tumours may present with non-specic signs
of space-occupying lesions without any localizing
signs; these symptoms include confusion, drowsiness, headache and vomiting
• other features may relate to development of hydro-
cephalus and intracranial herniation.
Pituitary Tumours
ese may cause symptoms because of:
• endocrine capacity
• eects on optic chiasma.
Secretory Tumours (e.g. Prolactinoma)
• Many tumours contain a mixture of secretory cells.
• Presentation is inuenced by the hormonal production
and size of the tumour.
• Secretory tumours are usually small.
• Secretory tumours may result in the following:
• overproduction of growth hormone: before fusion of
the epiphysis, this will result in gigantism; in adult
life, acromegaly results
• hyperprolactinaemia: this is characterized by amenorrhoea, infertility, galactorrhoea and impotence
• Cushing’s disease (see Chapter 12).
Non-Secretory Tumours
• Usually grow to a large size and present through local
eects.
• Symptoms and signs depend upon whether tumour is
due to endocrine capacity or local pressure eects.
• Bitemporal hemianopia results from compression of the
optic chiasma.
• Compression of secretory cells by non-secretory
tumours may result in hypopituitarism.
• Symptoms of hypopituitarism include:
• reduced libido
• infertility
• amenorrhoea
• myxoedema
• depression
• loss of sex characteristics
• hypoadrenalism
• in children, growth arrest may occur.
SPINAL CORD INJURIES
Two main groups of injury are recognized clinically:
• open injuries
• closed injuries.
Open Injuries
• Cause direct trauma to the spinal cord and nerve roots.
• Penetrating injuries may result in incomplete cord transection (see below).
Closed Injuries
• Account for most spinal injuries and are usually associated with fractures/dislocation of the vertebral column.
• Damage to the cord depends upon the extent of bony
injury and may result in:
• primary damage
• contusion
• nerve bre transection
• haemorrhagic necrosis
• secondary damage
• extradural haematoma
• infarction
• infection
• oedema.
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