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ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
+ acetabulum are composed of unossified cartilage) and also useful for monitoring disease +/– arthrography. Majority (
Treatment options include: abduction splint (e.g. Pavlik harness, hip spica)
90%) stabilise by two weeks after birth without intervention.
– used up to age 6–8 months; traction; open surgical reduction or closed manipulation. Family counselling – 10 fold risk of second child being affected.
16.6. Child with a limp
Most common cause of a painful limp in a child is trauma but other causes need to be excluded.
Differential diagnosis of an irritable hip
Trauma
Osteomyelitis of femur
Perthes’ Disease
Tumours of bone/soft tissue
Secondary to abdominal pathology, i.e. psoas abscess, appendicitis
Septic arthritis
Transient synovitis
Slipped upper femoral epiphysis (SUFE)
Inflammatory arthritis
Transient synovitis
Most common non-traumatic cause of an irritable hip. Defined as a transient, non­specific synovitis of the hip, with effusion. Peak age: 3–8 years; male to female ratio is 2:1; can affect both hips.
CLINICAL FEATURES Pain in the hip or thigh (referred pain), with stiffness often
there is a history of preceding recent ear, upper respiratory or gastrointestinal tract infection. Child is reluctant to weight-bear with the hip held in fl exion, abducted and externally rotated. Diagnosis is one of exclusion.
MANAGEMENT Bed rest, analgesia (NSAIDs); occasionally traction. Condition is
self-limiting.
Perthes’ disease
Aseptic necrosis of all or part of the femoral head due to impairment of the blood supply by recurrent infarction; aetiology unknown. Can progress to avascular necrosis. Associated with long-term risk of developing early OA (in 30s) of the hip joint. Peak age: 3–9 years; 3–5 times more common in males; both hips affected in <10%.
CLINICAL FEATURES
Examination can be normal.
Positive fi ndings include:
abnormal gait, positive Trendelenberg test leg length discrepancy restricted hip movement; as well as fi xed flexion, external rotation and
adduction deformities.
MANAGEMENT
Investigations: x-ray (‘frog-lateral’ view).
Treatment
conservative: analgesia; bimonthly follow-up; advise avoidance of contact
sports and physiotherapy surgical: 40% will require surgery, i.e. osteotomy.
184
ORTHOPAEDICS
Slipped upper femoral epiphysis (SUFE)
‘Slippage’ of the epiphysis posteriorly and inferiorly. Can be bilateral. Peak incidence: 14–16 years in boys, 11–13 years in girls (i.e. pre-menarche). 3:1 male to female ratio.
CLINICAL FEATURES
Antalgic limp + hip or knee pain, typically, in a pre-adolescent, obese male.
On examination: inability to weight bear; antalgic or ‘waddling’ gait; limb
shortening; restricted range of hip movements.
MANAGEMENT
Investigations: x-ray (AP + lateral views) confi rms diagnosis.
Treatment includes reduction of the ‘slip’ with surgical fixation, i.e. in situ screw
or osteotomy and rehabilitation. Consider prophylactic pinning of contralateral hip.
16.7. Osteomyelitis
This is an inflammatory reaction of bone in response to a pyogenic organism which, left untreated, will lead to irreversible destruction of the joint/limb. Can be classifi ed according to: route of entry of the infecting pathogen (exogenous, i.e. following surgery or an open fracture, or haematogenous following bacteraemia); or time­course of the clinical presentation, i.e. acute, subacute or chronic. Complications of osteomyelitis: avascular necrosis, pathological fractures, chronic infection, growth disturb ance (arrest, with shortening or angular deformity of the limb), septic arthritis.
AGE PATHOGEN
Neonate Staph. aureus; Group B Streptococcus; E. Coli Infants or pre-school Staph. Aureus; Haemophilus influenzae >5 years – adult Staph. aureus; Salmonella (assoc. with sickle cell),
Pseudomonas, Fungi (chronically ill on long-term antibiotics)
CLINICAL FEATURES
Risk factors: diabetes, immunocompromise (e.g. HIV, IgA defi ciency), chronic
illness, malnutrition, exposure to haematogenous source (dental procedure, abrasion, urethral catheterisation). Systemic symptoms: malaise and pyrexia.
Local symptoms: point bony tenderness, limp (reluctance to weight-bear) or
pseudoparalysis, muscle spasm +/– limited range of movements.
INVESTIGATIONS
Blood tests: CRP, ESR and WCC elevated.
X-ray: osseous changes are not evident in the first 7–10 days; in chronic
osteomyelitis characteristic periosteal elevation and a sequestrum of dead bone surrounded by a sleeve of involucrum (new bone) may be seen +/– Brodie’s abscess (seen as a cavity with sclerotic margins). MRI: 100% sensitive; detects early changes.
Ultrasound: may show early subperiosteal oedema; useful for excluding an
effusion. Bone scan: useful for differentiating multi- from unifocal infections.
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ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
MANAGEMENT
Fluid resuscitation.
Blood cultures followed by commencement of antibiotics, i.e. fl ucloxacillin +
fucidin in adults and third generation cephalo sporins in children <5 years old. Aspiration of joint if appropriate – send aspirate for urgent Gram stain and
MC&S. Analgesia +/– splinting of the affected limb.
Surgical options: soft tissue/abscess drainage +/– biopsy (for histology and
microbiology) +/– seques trectomy and bone grafting in chronic osteomyelitis.
16.8. Bone tumours
Can be primary or secondary, i.e. metastatic.
Metastatic bone tumours
Commonly arise from prostate, breast, kidney, lung and thyroid primaries. Rarely, skin (e.g. melanoma). Spread is haematogenous. The spine, long bones, pelvis and ribs are the most frequently affected sites. Lesions are typically lytic with the exception of prostatic metastases, which are sclerotic.
CLINICAL FEATURES
Can be asymptomatic (in early stages) and may be discovered following
diagnosis of the primary tumour. 50% develop symptoms: constant bone pain; antalgic/altered gait;
pathological fractures (commonly of the femur, humerus and spine). Spinal deposits +/– spinal instability or cord compression.
Hypercalcaemia.
MANAGEMENT
Involves treatment of:
primary malignancy symptoms: e.g. analgesia for bony pain +/– radiotherapy complications: e.g. hypercalcaemia and fractures (with bisphosphonates +/–
prophylactic fixation of bones at risk).
Malignant primary bone tumours
Rare. Accounts for 0.5% of all tumours. Often misdiagnosed. Evaluation requires careful history, examination (including the breasts in women and prostate in men), investigation and staging.
CLINICAL FEATURES Include bony pain (typically worse with activity and at
night), restricted movement of adjacent joints and pathological fractures. Can be asymptomatic. Examination may reveal a limp (if lower limb affected) and the presence of a painless soft tissue mass.
INVESTIGATIONS
Imaging may include:
plain x-ray of affected bone MRI/CT of the bone involved whole body MRI, technetium bone scanning ultrasound and mammography (in females) chest x-ray (for metastases; only useful if mass >2 cm) or chest CT scan.
186
ORTHOPAEDICS
Blood tests: FBC, CRP, ESR, calcium, phosphate, ALP, serum PSA in males,
serum and urine protein electrophoresis (for myeloma).
MANAGEMENT
Medical: primarily chemotherapy.
Surgical options include curretage/wide excision of primary tumour +/– limb
reconstruction; excision of pulmonary metastases; amputation.
Differential diagnosis for bone tumours
AGE 0–5 YEARS AGE 5–20 YEARS AGE 20–40 YEARS >40 YEARS
Osteomyelitis Bone cyst Ewing’s sarcoma Metastases Metastastatic Osteosarcoma Giant cell tumour Myeloma/lymphoma
neuroblastoma Leukaemia Ewing’s sarcoma Osteosarcoma Chondrosarcoma
Spindle cell tumours
Osteomyelitis Chondrosarcoma Osteosarcoma due to
Paget’s/irradiation
Osteosarcoma
Rapidly-growing tumour; metastasises early; 5-year survival 60–65%. Majority
occur between the ages of 10–25 years; 1.5:1 male to female ratio. Characteristically found in metaphysis of long bones (especially around knee).
ALP typically elevated (prognostic indicator).
Management: wide excision +/– limb reconstruction + chemotherapy.
Chondrosarcoma
Second most common primary bone tumour; onset between 30–70 years.
Can arise in long or flat bones, i.e. pelvis, scapula.
Treatment: wide local resection; local recurrence common.
Ewing’s sarcoma
Small round cell tumour of bone; majority occur <20 years old; more common
in males; 5-year survival about 50%. Typically, affects diaphysis of long and fl at bones.
Characteristic ‘onion-skin’ (periosteal elevation) appearance + soft tissue mass
on imaging. Management: chemotherapy, tumour resection +/– post-operative
radiotherapy.
Spindle cell sarcomas
Includes: fibrosarcomas, malignant fibrous histiocytomas and leiomyosarcomas.
Treatment and prognosis similar to osteosarcomas.
16.9. Short cases in orthopaedics
Dupuytren’s disease
Benign condition, where nodular fibromatosis of the palmar or plantar fascia leads to permanent and often progressive contracture of the associated digit. Aetiology is unknown but can be familial or associated with previous hand trauma, phenytoin, alcohol, diabetes mellitus.
187
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
CLINICAL FEATURES Presents with deformity and loss of hand/foot function; the
ring finger, little finger and middle finger are most commonly affected. Bilateral in 65% of cases.
MANAGEMENT Consider steroid injections, splints and surgical excision of the
affected fascia. Recurrence rates are high.
Ganglion
A benign cystic swelling arising from a joint or tendon sheath; contents resemble synovial fluid. 3:1 male to female ratio. Causes: trauma, joint overuse, or idiopathic.
MANAGEMENT If symptomatic, aspiration ( 50% recur) or surgical excision
followed by immobilisation of the joint for 1–2 weeks.
Trigger finger/thumb (aka tenosynovitis)
Painful locking of the thumb or fi nger which is functionally limiting. Thought to be due to focal degeneration within the fl exor tendon sheath, leading to localised inflammation and limiting movement of the tendon within its sheath. 1:4 male to female ratio.
CLINICAL FEATURES Palpable nodule in the distal palm which moves with fl exion
and extension; triggering or locking at the MCP/DIP joint which in later stages requires release by passive manipulation using the other hand +/– clicking or crepitus.
MANAGEMENT Splinting, corticosteroid injection or surgical release.
Tennis elbow (aka lateral epicondylitis)
The most common cause of elbow pain.
CLINICAL FEATURES Pain and tenderness over the lateral epicondyle radiating
down forearm, typically exacerbated by wrist extension.
MANAGEMENT NSAIDs and physiotherapy, or surgical release of the extensor
origin at the elbow, if conservative treatment fails.
Golfer’s elbow (aka medial epicondylitis)
Pain over the medial epicondyle exacerbated by resisted pronation of the forearm and wrist fl exion.
MANAGEMENT NSAIDs and physiotherapy, or surgical release of the fl exor origin
at the elbow in a few cases.
Charcot’s joint (aka neuropathic joint)
Chronic, progressive, destructive arthropathy. Causes: chronic neuropathies, e.g. diabetes, syringomyelia (and traditionally infection such as syphilis and leprosy).
CLINICAL FEATURES Loss of pain and proprioceptive sensation. The foot, ankle and
knee are commonly affected.
MANAGEMENT Treat the underlying cause; advise and educate regarding protection
of the joint; surgery – rarely, usually reserved for severe disease.
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17

Ophthalmology

17.1. Painful red eye
17.2. Unilateral sudden loss of vision
17.3. Uveitis
17.4. Cataracts
17.5. Glaucoma
17.6. Retinal disease
17.1. Painful red eye
Beware that eyesight may be threatened and action may be required immediately. Causes:
Conjunctivitis (bacterial, viral or allergic):
(severe pain should alert you to other possible causes) with discharge (purulent suggests a bacterial cause, whereas viral is associated with a watery discharge). Eyes are itchy in allergic conjunctivitis.
Keratitis (bacterial, viral, fungal or protozoal):
cornea. May cause severe pain, reduced vision and discharge (which may be watery, mucoid or purulent). There may be ulceration: this threatens eyesight and is an emergency – refer to ophthalmologists immediately. Causes: Staphylococcus or Pseudomonas (bacterial), HSV (viral – causes ‘dendritic’ ulcers), acanthamoeba (protozoal – more common in contact lens wearers).
Episcleritis: produces
Scleritis: more severe pain than episcleritis and commonly associated with
systemic disease, e.g. rheumatoid arthritis. Patient may also complain of reduced vision.
Anterior uveitis:
Trauma to the cornea/foreign body.
Acute glaucoma – see below.
Note: some of the causes above more commonly cause minor irritation or mild discomfort, e.g. conjunctivitis, episcleritis. Other causes of a red eye (usually painless) include subconjunctival haemorrhage and blepharitis.
normally only mild discomfort and self-limiting.
see below.
mild discomfort and irritation
i.e. inflammation of the
17.2. Unilateral sudden loss of vision
It is important to distinguish between painless versus painful (identified in brackets) causes.
Acute glaucoma (painful).
Vitreous haemorrhage.
Central retinal artery occlusion (pale retina with ‘cherry red’ spot).
Central retinal vein occlusion.
Retinal detachment.
189
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
Age-related macular degeneration (usually gradual but can be sudden).
Anterior ischaemic optic neuropathy.
Temporal arteritis.
Non-arteritic.
Optic neuritis (painful).
17.3. Uveitis
Anterior uveitis (iritis)
Associated with systemic disease in 50% cases, e.g. sarcoidosis, seronegative arthritis, Behcet’s disease.
CLINICAL FEATURES Can present acutely as a painful red eye with blurred vision
and photophobia or more chronically with milder symptoms. A hypopyon may be present and there may be keratic precipitates (clumps of inflammatory cells) and synechiae (adhesions of the iris to the lens).
TREATMENT With topical steroids, and drops to dilate the pupil (e.g. cyclopentolate)
to prevent synechiae (adhesions of iris to lens).
Posterior uveitis
Normally presents with blurred vision without pain or red eye.
May be associated with systemic disease, e.g. toxoplasmosis or Behcet’s disease.
17.4. Cataracts
Opacity of the lens. Incidence increases with age.
CLINICAL FEATURES Gradual painless loss of vision with glare; with loss of the red
reflex on fundoscopy. Associated with:
Increasing age.
Ocular disease, e.g. high myopia.
Systemic disease, e.g. diabetes, myotonic dystrophy.
Drugs, e.g. steroids.
MANAGEMENT Surgery if symptoms affect quality of life.
17.5. Glaucoma
Damage to the optic nerve secondary to raised intraocular pressure. Classifi ed as primary or secondary (associated with ocular disease); acute or chronic; and closed-angle (iris in contact with the trabecular meshwork) or open-angle (iris not in contact with the trabecular meshwork):
Chronic (open angle) – asymptomatic until well-advanced but causes
progressive visual field defect with cupped optic disc; routine screening necessary for early diagnosis; familial – check relatives. Treatment: with topical eye drops, e.g. latanoprost, β-blockers (e.g. timolol), pilocarpine. Rarely surgery is necessary – trabeculectomy. Acute closed angle – presents with painful, red eye with loss of vision. Pupil
may be fixed and dilated. Urgent treatment is required with IV acetazolamide, topical pilocarpine and then laser iridotomy or iridectomy.
190
OPHTHALMOLOGY
17.6. Retinal disease
Diabetic retinopathy
Occurs in virtually all type I diabetics after 15–20 years and 80% of type II diabetics ( 10% at diagnosis and 50% at 10 years). Commonest cause of blindness in developed world in 30–60 year olds. Normally classifi ed as:
Background: microaneurysms; dot, blot and flame haemorrhages; hard
exudates. Pre-proliferative: as for background + cotton wool spots; dilation and beading of veins; and intraretinal microvascular abnormalities (IRMAs). Proliferative: neovascularisation, vitreous haemorrhage, retinal detachment,
glaucoma (rubeosis iridis).
Maculopathy = retinopathy involving the macula, therefore likely to cause visual loss even with less severe disease: typically causes poor central vision with relatively intact peripheral vision.
Patients need good glycaemic control but other management depends on the
type:
Background: monitor for progression.
Pre-proliferative: monitor closely +/– panretinal laser photocoagulation in
some circumstances. Proliferative: panretinal laser photocoagulation.
Maculopathy: focal laser photocoagulation.
Note: that patients with diabetes are also more likely to develop glaucoma and cataracts.
Hypertensive retinopathy
Associated with compensated hypertension (often called grades 1 and 2):
1: ‘copper’ or ‘silver’ wiring (attenuation of the arterioles).
2: AV nipping.
Associated with accelerated hypertension (often called grades 3 and 4):
3: flame haemorrhages, cotton wool spots, hard exudates.
4: papilloedema.
Age-related macular degeneration
Commonest cause of blindness in over 65s in the developed world: normally gradual loss of central vision with peripheral vision intact. Two types: dry or non-exudative (presence of lipid deposits or drusen) and the more severe wet or exudative (new vessel formation causing a subretinal neovascular membrane).
Retinitis pigmentosa
Hereditary condition with clinical features of night blindness, tunnel vision and classical fundus appearance (bone-spicule pigmentation, pale disc, attenuated blood vessels).
191
18

Ear, nose and throat

18.1. Disorders of the ear
18.2. Disorders of the nose and throat
18.1. Disorders of the ear
Hearing loss
Conductive, i.e. due to pathology in the middle or outer ear.
Sensorineural, i.e. due to pathology in the cochlea or auditory nerve.
Mixed conductive/sensorineural.
Causes of conductive hearing loss
Wax (although wax impaction has to be very severe to cause hearing loss)
Otitis media (acute, chronic or with effusion)
Perforation
Cholesteatoma
Otosclerosis
Causes of sensorineural hearing loss
Presbycusis
Noise-induced
Ménière’s disease (although vertigo is more of a problem in this condition)
Congenital, e.g. maternal rubella infection
Drugs, e.g. aminoglyosides
Infections, e.g. mumps
Acoustic neuroma
Otitis externa
Infection of the external meatus, most commonly bacterial, e.g. Staph. or Pseudomonas. Clinical features: pain and tenderness over the ear, mild discharge,
and sometimes deafness. Treatment: short course of topical antibiotics generally effective.
Otitis media (OM)
Inflammation of the middle ear.
Acute
Normally follows an URTI (either viral or bacterial), frequently bilateral and most common in children. Clinical features: ear pain/tenderness, conductive deafness, fever and an ab normal ear drum on otoscopy (e.g. bulging, redness, perforation with otorrhoea). Management: many will resolve spontaneously but if not, antibiotic therapy should be started.
192
EAR, NOSE AND THROAT
Chronic suppurative (CSOM)
Failure of acute OM to resolve may lead to chronic OM with persistent discharge and worsening deafness. Classified as active (presence of infection) or inactive, and by whether there is a perforation or presence of cholesteatoma (growth of squamous epithelium in the middle ear). Complications are classified as intratemporal (e.g. ossicular erosion, facial nerve palsy) or intracranial (e.g. meningitis, brain abscess).
With effusion (‘glue ear’)
Collection of serous or viscous fluid in the middle ear. Very common in children, causing conductive deafness and mild ear discomfort. Ear drum is usually abnormal on examination (e.g. dull or immobile).
MANAGEMENT If it does not spontaneously resolve, consider adenoidectomy +/–
myringotomy and grommet insertion. Occurs rarely in adults when it may be a sign of a nasopharyngeal cancer – therefore important to examine post-nasal space with nasendoscope (or mirror).
18.2. Disorders of the nose and throat
Sinusitis
Inflammation of the mucous membranes of the paranasal sinuses. More commonly acute but in a small proportion of cases which do not resolve, it becomes chronic. Usually related to an URTI (viral or bacterial) but in some cases will follow dental infection.
CLINICAL FEATURES Include nasal obstruction, post-nasal drip, headache or pain
over the sinuses.
MANAGEMENT Acute treatment with intranasal decongestants to facilitate sinus
drainage and if it does not resolve spontaneously then appropriate antibiotics should be given; in chronic disease, washout or surgery may be necessary.
Epistaxis
Very common but usually self-limiting and does not require medical intervention. The site of bleeding is commonly Little’s area (a plexus of vessels on the anterior part of the nasal septum). Normally no cause is identified but causes include trauma, clotting disorders and anticoagulant therapy.
Severe epistaxis is an emergency!
ABC important, particularly management of the airway. Patients may need IV fluids +/– blood if very severe (also check FBC, clotting and cross-match)
Sit patient up with head leant forward; if simple compression or nasal plugging does not help and bleeding is persistent – options include cautery (with silver nitrate), nasal packing (e.g. anteriorly with nasal tampons or bismuth, iodoform and paraffin paste (BIPP) or if posterior can use Foley catheter), or rarely surgery (e.g. arterial ligation +/– neuroradiological embolisation)
Patient may need admission if elderly and persistent bleeding
193