Surgery B Flashcards
What is the Evan’s classification?
Evans classification: Extra-capsular fractures
Type 1:
Stable: Undisplaced or displaced but reduced
Unstable: Displaced not reduced or comminuted
Type 2: Unstable: reversed obliquity
Which arteries supply the femoral head?
The blood supply to the femoral head is variable. Three main arteries supply the femoral head. The lateral epiphyseal branch of the medial femoral circumflex and the ascending branch of the lateral femoral circumflex both ascend from the deep femoral artery. Some blood is supplied through the ligamentum teres which may not be present in older people.
Describe femoral neck fractures
A femoral neck fracture occurs one to two inches from the hip joint. These fractures are common among older adults and can be related to osteoporosis. This type of fracture may cause a complication because the break usually cuts off the blood supply to the head of the femur which forms the hip joint.
Intertrochanteric hip fracture:An intertrochanteric hip fracture occurs three to four inches from the hip joint. This type of fracture does not interrupt the blood supply to the bone and may be easier to repair.
Both should be treated with a dynamic hip screw.
Describe the features of hip fractures
Causes : Osteoporosis or osteopenia , Trauma (often in the elderly)
Pathological fractures - primary bone tumours or metastatic deposits leading to fracture
Common Findings on the History :
Fall - may be atraumatic
Pain - may be felt in the hip, groin or knee, or may be an exacerbation of pre-existing pain from another cause (eg. OA)
Examination Findings :
Classically, the leg is shortened, abducted and externally rotated
Exacerbation of pain on palpation of the greater trochanter
Pain is exacerbated by rotation of the hip
NB - if suspicious of hip fracture, avoid rigorous examination
What is a sub-trochanteric hip fracture?
Typically defined as area from lesser trochanter to 5cm distal
Usually in younger patients with a high-energy mechanism but may occur in elderly patients from a low-energy mechanism
Important to rule out pathologic or atypical femur fracture and denosumab or bisphosphonate use, particularly alendronate, can be risk factor.
What are the investigations for hip fractures?
Investigations
X-ray - AP pelvis and lateral hip
When there is a high clinical suspicion - MRI (gold-standard) for occult fracture or CT
Bone scan - helpful to rule out occult fracture but not helpful in assessing viability of femoral head after fracture
Duplex scanning - rule out DVT if delayed presentation to hospital post-hip fracture .
What is the management of hip fractures?
Pre-Operative Management
Adequate analgesia (if possible regional anaesthesia eg nerve block)
FI blocks
IV access
Bloods - group and save, FBC, U&E, LFTs, bone profile, coagulation
Correct any blood abnormalities - anaemia, dehydration, coagulopathy
Diagnose and treat co-morbidities
Document pre-morbid state - mobility status pre-injury
Screen for cognitive impairment - prognostically significant
Post-Operative Management
If no contra-indications then day 1 mobilisation will be attempted
Thromboprophylaxis (usually low molecular weight heparin)
Daily physiotherapy
Ongoing MDT approach with ortho-geriatric input
Medications review - review bone protection (vitamin D, calcium supplements, bisphosphonates) and look for iatrogenic fall causes
Complications : Infection , Bleeding , Increased risk of thromboembolic events (DVT/PE) and Avascular necrosis of the femoral head .
What is gas gangrene?
Rapidly progressive infection with clostridium which follows a penetrating injury or crush injury.
The most dangerous form of gas gangrene is an infection with clostridium perfringens. The gangrene will spread rapidly and cause evolution of foul smelling gas.
Which bacteria cause necrotising fasciitis?
Gram positive cocci: Staph aureus and Strep progenies
Gram negative rods: E.coli and pseudomonas aeruginosa
Gas gangrene can be caused by any type of clostridium.
How should necrotising fasciitis be investigated?
LRINEC score
Investigations
Bloods - FBC, U&Es, CRP, ESR, blood cultures, random blood sugar, CK (myositis)
Imaging - not routinely required or advocated - if gas gangrene débridement immediately // plain films or CT may show gas in subcutaneous tissues
Exploratory Incisions and Biopsy
Incisions made over the affected area show “dishwater” pus and easy separation of the deep fascia from the overlying subcutaneous tissue on blunt / finger dissection
Biopsy specimen should contain skin, subcutaneous tissue, deep fascia and some of the underlying muscle
Histological features: necrosis, angio thrombosis, acute inflammatory cell infiltration and organisms and gas formation
Organisms are detected in 15% of cases - surgical exploration is the only way to definitively establish the diagnosis
Surgical findings show that the muscle does not contract with stimulus nor does it bleed, and oedema and variable colour observed.
What is the management of necrotising fasciitis?
Antibiotics of meropenem, clindamycin and vancomycin
IV access and IV fluids
How should gas gangrene be managed?
IV immunoglobulins for clostridial toxins, hyperbaric oxygen and surgical debridement
Mortality is between 70-100%
What is the initial management of open fractures?
Appropriate IV antibiotics, debridement and fracture stabilisation
Usually cephalosporin is used or gentamycin.
What is an open fracture?
This is where there is a direct communication between the fracture site and the external environment.
What classification system is used for open fractures?
Gustillo-Anderson classification:
Type 1: Wound less than 1cm and minimal contamination or muscle damage
Type 2: Wound 1-10cm with moderate soft tissue injury
Type 3a: Wound greater than 10cm, high energy, extensive soft tissue damage, contamination but there is adequate tissue for flap coverage.
Type 3b: Extensive periosteal stripping and wound requires soft tissue coverage
Type 3c: Vascular injury requiring vascular repair regardless of the amount of soft tissue injury.
What are the causes of compartment syndrome?
High energy limb injuries and crushing injuries. Often seen in tibial fractures.
What is the pathophysiology of compartment syndrome?
Compartment syndrome occurs when the pressure within a closed osteo-fascial muscle compartment rises above a critical level
This critical level is the tissue pressure which collapses the capillary bed and prevents low-pressure blood flow through the capillaries and into the venous drainage
If diastolic arterial pressure is not more than 30 mmHg above tissue pressure, compartmental capillary blood flow is significantly obstructed and severe hypoxia occurs in muscle and nerve tissue
The critical measurement is muscle perfusion pressure (MPP), the difference between diastolic blood pressure (dBP) and measured intramuscular tissue pressure
Muscle tolerates short periods of hypoxia, but after a few hours, progressive necrosis begins
It is generally accepted that after 6-8 hours of inadequate muscle perfusion pressure (MPP), extensive muscle necrosis is likely and effective release of the muscle compartments involved is unlikely to avoid severe muscle contracture.
How are odontoid fractures classified?
Anderson and D’Alonso Classification:
Type 1 fracture - through the upper portion of the odontoid process - thought to be due to apical/alar ligaments
Type 2 fractures - occur at the base of the odontoid - between the level of the transverse ligament and the C2 vertebral body
Type 3 fractures - extend into the vertebral body
What is the initial management of a patient who has suffered a fall?
Initial management based on ATLS principles
Within ‘A’ - triple immobilisation of C-spine
A thorough upper and lower limb neurological examination should be done including a PR when log rolled documented on an ASIA chart
Triple Immobilisation of C-Spine:
Collar - rigid and measured to fit
Blocks - sandbags can be used as a substitute
Tape - wide elastoplast tape at patients ear levels
ASIA Chart
An assessment for minimal elements of neurologic assessment for all patients with a spinal injury
What views of the spine should be asked for when imaging?
AP and lateral
When should a CT C-Spine be offered to under 16s?
- GCS less than 13 on initial assessment
- The patient has been intubated
- Focal peripheral neurological signs
- Paraesthesia in the upper or lower limbs
- A definitive diagnosis of cervical spine injury is needed urgently (for example, before surgery)
- The patient is having other body areas scanned for head injury or multi-region trauma
- There is strong clinical suspicion of injury despite normal X-rays
- Plain X-rays are technically difficult or inadequate
- Plain X-rays identify a significant bony injury
NB - the scan should be performed within 1 hour of the risk factor being identified
When should a C-spine X-ray be offered to under 16s?
- Fall from a height of greater than 1 metre or 5 stairs
- Axial load to the head, for example, diving
- High-speed motor vehicle collision
- Rollover motor accident
- Ejection from a motor vehicle
- Accident involving motorised recreational vehicles
- Bicycle collision
- Safe assessment of range of movement in the neck is not possible
When should a CT C-spine be offered to over 16s?
- GCS less than 13 on initial assessment
- The patient has been intubated
- Plain X-rays are technically inadequate (for example, the desired view is unavailable)
- Plain X-rays are suspicious or definitely abnormal
- A definitive diagnosis of cervical spine injury is needed urgently (for example, before surgery)
- The patient is having other body areas scanned for head injury or multi-region trauma
- The patient is alert and stable, there is clinical suspicion of cervical spine injury and any of the following apply:
- 65+
- Dangerous mechanism of injury
- Focal peripheral neurological deficit
- Paraesthesia in the upper or lower limbs
When should a C-spine X-ray be offered to over 16s?
- No indications for a CT C-spine
- It is not considered safe to assess the range of movement in the neck
- Safe assessment of range of neck movement shows that the patient cannot actively rotate their neck to 45 degrees to the left and right
When should range of neck movement be assessed?
- Was involved in a simple rear-end motor vehicle collision
- Comfortable in a sitting position in the emergency department
- Has been ambulatory at any time since injury
- Has no cervical spine tenderness
- Presents with delayed onset of neck pain
What are the management options for an odontoid fracture?
Management options should be described as operative vs non operative.
Operative management can be divided into anterior fixation or posterior fusion and halo immobilisation.
These are all unsuitable for this patient especially the halo, which has a high mortality/morbidity rate.
This patient is therefore not a candidate for surgery and should be treated with a hard cervical collar
These injuries should all be discussed with the local spinal/neurosurgical department
What imaging should be done to investigate discitis?
MRI spine
How should discitis be managed?
Discussion with spinal unit - mention any changes in neurology
Eradication of infection with 6-12 weeks of antibiotics sensitive to a positive culture
Preservation or restoration of spinal structure, stability and neurological deficits
Analgesia
Which bacteria commonly cause discitis?
Staphylococcus aureus – Gram +ve cocci most likely
Pseudomonas in IV drug abuse and Streptococcus in chest infection.
What are the risk factors for discitis?
Over 50s with a 2:1 male to female ratio
Increasing age
More common with increased use of interventional techniques (angiography, surgical etc)
IVDU (hospital and illicit)
T2DM
Smoking
What are the red flags of chronic back pain?
Bilateral sciatica
Severe or progressive bilateral neurological deficit of the legs, such as major motor weakness with knee extension, ankle eversion, or foot dorsiflexion
Difficulty initiating micturition or impaired sensation of urinary flow, if untreated this may lead to irreversible urinary retention with overflow urinary incontinence
Loss of sensation of rectal fullness, if untreated this may lead to irreversible faecal incontinence
Perianal, perineal or genital sensory loss (saddle anaesthesia or paraesthesia)
Laxity of the anal sphincter
What is the pathophysiology of disc degeneration?
Loss of proteoglycan and collagen, and degradation
Fall in osmotic pressure of disc matrix
No longer behaves hydrostatically under pressure
Loose height and weight rapidly
Stress concentration along end plates and annulus
How is cauda equina managed surgically?
Decompressive Laminectomy
20% of all CES patients will have a poor outcome usually with the need for ongoing treatment e.g. management of sexual dysfunction, self-catheterisation, colostomy, urological and gynaecological surgery, spinal injuries rehabilitation and psycho-social support
What is the mechanism of injury for supracondylar fractures of the elbow?
At age of 6-7 yrs, supracondylar area is remodelling, and is thinner than at other ages and the elbow can hyperextend in this age group
Extension type injury in 98% of cases
Extension Type Injury:
Fall onto outstretched hand and the elbow becomes locked in hyperextension
Tension forces anteriorly and the olecranon is forced into the olecranon fossa
The triceps cause posterior and proximal migration of the distal fracture fragment
What other injuries are associated with supracondylar fractures of the elbow?
Neuropraxia (nearly all resolve)
Anterior interosseous nerve (AIN) neuropraxia (branch of median) is the most common
Can also see radial nerve palsy (close second) and ulnar nerve palsy in a flexion type injury
Vascular compromise (~10%) - although rich collateral circulation can maintain supply
How are supracondylar fractures of the elbow classified?
Gartland Classification (all based on lateral elbow radiograph)
Type 1 - non displaced - treated with cast immobilisation for 3-4 weeks with radiographs at 1 week
Type 2 - displaced (posterior cortex and posterior periosteal hinge are intact) - deformity only in the sagittal plane and typically treated with CRPP or open reduction
2a is not rotated and 2b is rotated
Type 3 - displaced, often in 2/3 planes - treated with CRPP or open reduction
Type 4 - complete periosteal disruption with instability in flexion and extension - diagnosed during surgery and treated with CRPP or open reduction
Medial communition - collapse of the medial column, loss of Baumann angle - leads to a virus malunion (gunstock deformity) - treated with CRPP and often requires significant values force to reduce
Flexion type injury - generally due to fall on the olecranon, treated with CRPP, more likely to require open reduction
How do supracondylar fractures of the elbow present?
Presentation
Symptoms - pain and refusal to move the elbow
Physical exam
Inspection - gross deformity, swelling, ecchymosis in antecubital fossa
Motion - limited
Neuro - may show AIN neuropraxia (ok sign), median nerve injury or radial nerve injury
Also vascular exam to assess perfusion
S-Shape Deformity and Puckering of the Skin
How should supracondylar fractures of the elbow be investigated?
AP and lateral x-rays of the elbow
Posterior fat pad sign - lucent on a lateral view along poster distal humerus and olecranon fossa suggestive if occult fracture around the elbow
Displacement of the anterior humeral line and alteration of Baumann’s angle
Angiography indicated if vascular compromise
What are the treatment options for supracondylar fractures of the elbow?
Non-Operative Treatment :
Long arm casting with less than 30% of elbow flexion
Indications - warm perfused hand with no neuro deficit in type 1 fractures and type 2 fractures where the anterior humeral line intersects the capitellum, minimal swelling and no medial communities
3 weeks and repeat radiographs at 1 week to assess for interval displacement
Operative Treatment :
Closed reduction and percutaneous pinning (CRPP)
Indications - type 2 and 3 supracondylar fractures, flexion type and medial column collapse
Non urgent (can wait overnight) - warm perfused hand with no neuro deficits - splint overnight 30-40° elbow flexion and elevate in preparation for surgery
Urgent (same day) - pulseless, well perfused hand, sensory nerve deficit, XS swelling, brachialis sign and floating elbow - check vascular status after reduction
Emergent (within hours) - pulseless, poorly perfused hand - check vascular after reduction
Open Reduction, Percutaneous Pinning +/- Vascular Exploration
Indications - open fracture, failed closed reduction (more frequently flexion fracture), pulseless white that is unable to be reduced and remains a gap (gap may represent entrapped vasculature)
What are the mechanisms of injury for knee dislocation?
High energy is usually from MVC, crush injury, fall from a height, or dashboard injury resulting in axial load to a flexed knee
Low energy may be from an athletic injury or routine walking
Hyperextension injury leads to anterior dislocations
Posteriorly directed force across the proximal tibia (dashboard injuries) leads to posterior dislocations
What other injuries are associated with knee dislocation?
Vascular injury
Nervous injury - usually common peroneal (25% incidence) and tibial is much less common
Fractures - present in 60% dislocations
Soft tissue injury - patellar tendon rupture, periarticular avulsion and displaced menisci
How are knee dislocations classified?
Kennedy Classification (based on direction of tibial displacement(
Anterior (most common) - due to hyperextension, usually involves PCL tear, highest rate of peroneal injury
Posterior - due to axial load of flexed knee (dashboard injury) - highest rate of vascular injury - highest incidence of popliteal artery tear
Lateral - due to varus or valgus forces, usually involves ACL and PCL
Medial - due to varus or values forces - usually disrupted PLC and PCL
Rotational - posterolateral is most common rotational dislocation, usually irreducible and may present with buttoning of femoral condyle through the capsule
How do knee dislocations present?
Symptoms - trauma history, knee pain, instability
Inspection
No obvious deformity - 50% reduced before ED arrival and may present with subtle signs of the trauma (swelling, effusions, abrasions, ecchymosis)
Obvious deformity - reduce immediately (especially if absent pulses), dimple sign (buttonholing of medial femoral condyles through the medial capsules - indicative of an irreducible posterolateral dislocation - contraindication to closed reduction due to risks of skin necrosis
Vascular exam - rule out injury before and after reduction
If pulses present and normal - measure ABPI - if abnormal - arterial duplex USS or CT angiography
If pulses are absent and diminished - immediate surgical exploration - ischaemia time >8 hours is 86% amputation rate - imaging contraindicated if surgery delayed
Neurological exam - assess sensory and motor function of peroneal and tibial nerves
Stability - diagnosis based on instability on physical exam, may see recurvatum when in extension, assess ACL, PCL, MCL, LCL and PLC
How should knee dislocations be investigated?
Imaging
Radiographs
Pre-reduction AP and lateral of the knee - look for asymmetric or irregular joint space, avulsion fractures, osteochondral defects
Post reduction AP and lateral of the knee
Optional - 45 degree oblique if fracture suspected
CT - indicated if fracture identified on post reduction plain films, obtain post reduction CT for characterisation of fractures
MRI - obtain MRI after acute reduction but prior to hardware placement - required to evaluated soft tissue injury and for surgical planning
How are knee dislocations treated?
Nonoperative Treatment
Emergent closed reduction followed by vascular assessment - considered in an orthopaedic emergency and consider vascular input if pulses diminished post reduction
Immobilisation as definitive
Operative Treatment
Open reduction - indications include irreducible knee, posterolateral dislocation, open fracture dislocation, obesity, vascular injury
External fixation - indications include vascular repair (takes precedence), open fracture dislocation, compartment syndrome, obese (if difficult to maintain reduction) or poly trauma patient
Delayed ligamentous reconstruction - indications include instability - patients can be placed in a knee immobiliser for 3 weeks until treated operatively
Define acute limb ischaemia
Acute limb ischaemia is defined as the sudden decrease in limb perfusion that threatens the viability of the limb
What are the three main causes of acute limb ischaemia?
Thrombus in situ - (60%) whereby an atheroma plaque in the artery ruptures and a thrombus forms on the plaque’s cap; can present acutely or acute-on-chronic
Embolisation - (30%) whereby a thrombus from a proximal source travels distally to occlude the artery; original thrombus may be due to AF, post MI mural thrombus, AAA or prosthetic heart valves
Trauma - long bone fractures and dislocations
How does acute limb ischaemia present?
Pain, pallor, pulselessness, paraesthesia, perishingly cold, paralysis
Sudden onset, Hx of cause of potential embolisation
What are the signs of chronic limb ischaemia?
Rest pain, gangrene, ulcers and erythema
How should critical limb ischaemia be investigated?
Serum lactate (asses level of ischaemia), a thrombophilia screen and group and save
ECG
CT angiography
Duplex ultrasound (if available)
How should acute critical limb ischaemia be managed?
Initial Management
Complete arterial occlusion will lead to irreversible tissue damage within 6 hours
Start the patient on high flow oxygen and ensure adequate IV access
A heparin bolus doe then heparin infusion should be initiated
Conservative Management
Considered in Rutherford 1 and 2a - consider a prolonged course of heparin may be effective - but will require regular assessment
Surgical Intervention
Mandatory for Rutherford 2b
If embolic cause - embolectomy via a Fogerty catheter, local intra-arterial thrombolysis or bypass surgery
If thrombotic cause - local intra-arterial thrombolysis in combination with angioplasty or bypass surgery
Angioplasty
What is the definition of an abdominal aortic aneurysm?
Dilatation of the aorta greater than 3cm.
What are the risk factors for AAA?
Main cause is atherosclerosis
Other causes include trauma, infections connective tissue disease (Marfan’s, Ehler’s Danlos, Loey Gietz) or inflammatory disease (Takayasu’s disease)
Risk factors for AAA include smoking, hypertension, hyperlipidaemia, family history, male gender, and increasing age
Diabetes mellitus is considered a negative risk factor - mechanism unknown
What are the clinical features of AAA?
Many abdominal aortic aneurysms are asymptomatic and are simply detected on incidental finding or screening
Symptomatic patients present with abdominal pain, back/loin pain, distal embolisation producing limb ischaemia and/or aortoenteric fistula (rare cause of GI bleed)
On examination, pulsatile mass in the abdomen (above umbilical level) and rarely, signs of retroperitoneal haemorrhage may be evident
A ruptured AAA presents with pain (abdominal/back/loin), a degree of shock or syncope and pulsatile mass
Who is offered AAA screening?
Men aged 65 receive a one-off USS
How are AAAs managed?
Medical Management
Any AAA < 5.5cm can be monitored via Duplex USS, as surgery prior to this diameter provides no survival benefit
- 0-4.4 cm = yearly USS
- 5-4.9 cm = 6 monthly USS
- 0-5.4 cm = 3 monthly USS
Any small (3.0-5.5 cm) have a 3% / year mortality, and should reduced CVS risk factors: smoking cessation, improve BP control, commence statin and aspirin therapy and weight loss
What are the surgical interventions for AAAs?
Surgery should be considered for an AAA >5.5 cm in diameter, AAA expanding at >1 cm per year or a symptomatic AAA in a patient who is otherwise fit
If patient less fit for surgery - then can be left to until 6 cm
Open repair - involves a midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally, before the segment is then removed and replaced with a prosthetic graft
Endovascular repair (EVAR) - involves introducing a graft via the femoral arteries and fixing the stent across the aneurysm
Both have the same outcomes at 2 years +, but EVAR has an improved short term outcome but higher rate of reintervention
What are endoleaks?
Important complication of EVAR, whereby an incomplete seal forms around the aneurysm resulting in the blood leaking around the graft
Usually asymptomatic hence regular surveillance (usually ultrasound unless a complication is noted) is needed
How does a ruptured AAA present?
AAA rupture increases exponentially with aneurysmal diameter - and risk increased by smoking, hypertension and female gender
An AAA rupture can present with abdominal/groin pain, back pain or syncope
On examination they will typically be haemodynamically compromised, with a pulsatile abdominal mass and tenderness
Classic triad (50% of rAAA cases) - flank/back pain, hypotension, pulsatile abdominal mass
How are ruptured AAAs managed?
Immediate high flow oxygen, IV access (2x large bore cannula) and urgent bloods (FBC, U&Es, clotting) with crossmatch for minimum 6U units
Treat shock with care - fluids may dislodge clots precipitating further bleeding so aim for BP<100mmHg (permissive hyptension)
Unstable patient - immediate transfer to local vascular unit
Stable patient - CT angiogram to determine whether the aneurysm is suitable for EVAR
What is shoulder impingement?
This generally occurs in younger patients (30-60) and the differential diagnosis is frozen shoulder and AC joint arthritis. Shoulder impingement occurs when the supraspinatus tendon catches on the acromion as the shoulder elevates.
Primary impingement is caused by collagen degeneration, vascular damage or subacromial spurs.
Secondary shoulder instability is the cause of secondary impingement syndrome.
What are the symptoms of shoulder impingement?
The symptoms are pain in the shoulder when lifting the arms above the head, they will have the palm sign where they localise pain to the deltoid because they cannot localise the pain. They may also have a mid range painful arc between 60-120 degrees. The Hawkins test is where the arm is taken to 90 degrees and internally rotated to see if it causes pain. Steroids can be used to confirm diagnosis as this will remove the pain.
Which muscles make up the rotator cuff?
The rotator cuff includes the subscapulairis (internal rotation), supraspinatus, infraspinatus and teres minor.
The rotator cuff’s function is to balance the deltoid action to permit shoulder movement that is stable and concentric.
What are the symptoms of rotator cuff tears and how are they treated?
Rotator cuff tears: Present in the over 60s, history of impingement pain, affects dominant arm more commonly, pain with overhead activities and pain at night and weakness. Acute large tears following dislocation in patients over 40s need urgent care because they will have a complete tear.
Strength testing all 4 muscles is vital. The empty can test is used for supraspinatus which will be painful and weak if positive.The lift off test is used for subscapularis tears.
Most tears are chronic and can be managed non-operatively with physiotherapy, NSAIDs, rest and possibly steroid injections.
What are the symptoms of acromioclavicular joint OA, investigations and how is this managed?
Symptoms are well localised AC joint region pain. They will have a high painful arc to elevation with pain at the top of the arc. Pain can be elicited by stressing the AC joint with the cross shoulder adduction test.
Investigation are with X-Ray, MRI and steroid injections. Steroid injections will almost certainly abolish OA pain so can be a positive diagnostic test.
Non-operative treatment is with rest, NSAIDs and up to 3 injections. Operative is with resection of the lateral end clavicle arthroscopically and should be done if non-operative treatment only provides transient relief.
What are the symptoms of biceps tendinopathy?
Symptoms include pain with lifting or tendon rupture. They will be tender of the bicep groove, speeds test and yergason test. Long head biceps rupture can be assessed with Popeye’s sign where the tone is lost so the muscle belly bunches up. A distal rupture can be assessed with hook test where the muscle belly moves proximally and there is a distal defect associated with bruising, the hook test is where the tendon cannot be felt at the distal end.
How is biceps tendinopathy investigated and treated?
Investigations are with USS, MRI or diagnostic USS guided injection for localising pain.
Management depends on the pathology as secondary tendonitis needs to treat the rotator cuff pathology, beginning conservatively. Proximal ruptures do not need surgery but distal biceps rupture will need acute surgical repair within 3 weeks.
What is the pathophysiology of carpal tunnel syndrome?
Definition is symptoms of median nerve compression within the carpal tunnel. The carpal tunnel is enclosed radially by the scaphoid, trapezium and fascial septum overlying the flexor carpi radialis. The ulnar border consists of the hook of the hamate, triquetrum and pisiform.
The median nerve is the most superficial part of the carpal tunnel and so is susceptible to damage. The recurrent branch of the median nerve supplies the abductor pollices brevis, opponens pollices and superficial part of the flexor pollices brevis.
Pathology is caused by inability of the carpal tunnel to expand which causes increased pressure. This leads to the cessation of blood flow and oedematous changes.
How is carpal tunnel syndrome categorised?
Acute carpal tunnel may require immediate surgical intervention of decompression. This is seen in wrist trauma and infection.
Chronic carpal tunnel can be subdivided into:
Idiopathic (most common) with women more affected than men
Anatomic - persistent medial artery, infection, ganglion cyst or tumours
Systemic - obesity, drug toxicity, alcoholism, diabetes, hypothyroidism, rheumatoid arthritis, primary amyloidosis and renal failure
Exertional - repeated impact on the palm or vibratory tools
How is carpal tunnel syndrome diagnosed and treated?
Diagnosis is based on the history of nocturnal pain, tingling in the thumb and on or more radial fingers. Shaking and wringing of hands may improve symptoms and in chronic median nerve compression there may be motor symptoms.
On examination there may be thenar atrophy, sensory testing and physical examination of the cervical spine and entire upper extremities. Phalen’s test is where the patient places their hands back to back pointing downwards for 60 seconds.
This is positive if the patient experiences paraesthesia. Durken’s test involves direct compression of the median nerve at the carpal tunnel for 30 seconds.
Electrodiagnostic nerve studies can be done to exclude other pathologies. Management is with splinting and immobilisation of the wrist at night and intermittently during the day. Steroids injections can be beneficial conservatively and surgically.
Surgical interventions include open release, endoscopic carpal tunnel release and limited open carpal tunnel release.
What is the pathology of achilles tendon rupture?
The pathophysiology is first there is a reactive phase (mins-days) where there is an increased tenocyte response, large proteoglycans, no vessels but this is reversible. The second phase is disrepair where there is collagen disorganisation with type 3 collagen present (repair collagen), increased chondrocyte activity and some vessels possible. This stage is also reversible. The third stage is degeneration with areas of cell death, minimal fibrillar collagen, Neo-vessels present and this stage is irreversible.
How does achilles tendon rupture present?
This presents with sudden pain, audible noise, unable to walk afterwards and there was be a genetic association with the O blood group. It is more common in people who have rheumatoid arthritis, gout, ankylosing spondylitis, chronic uraemia, hyperparathyroidism or on medications such as fluroquinolones and phenytoin.
On examination there will be a palpable gap where the achilles should be connected. The Simmonds test is where the calf is squeezed which causes the foot to plantar flex, if this does not happen then the test is positive.
How is achilles tendon rupture treated?
Treatment can be conservative as collagen can repair the achilles tendon over a number of months. Immobilisation increases the amount of scar tissue so more movement will improve the quality of the healed tendon.
The chronic achilles tendon rupture is rare and is caused by defects in the tendon. They need surgical intervention to replace the tendon from another site, known as a BOX graft.
What is Morton’s neuroma?
Defined as a nerve thickening due to perineurial fibrosis. The intermetatarsal space is narrower in the 2nd and 3rd interspace and there are strong intermetatarsal ligaments whereas the 4th and 5th move a lot.
The nerve sits underneath these strong metatarsal ligaments so it gets battered. The medial and lateral plantar nerve have a common branch at the third space which is a common area for compression.
What are the causes of Morton’s neuroma?
It may be associated with high heels or running shoes. It is more common in women and in over 50s. 70% are affected in the third space. They present with burning pain on the plantar aspect of the foot, located between the metatarsal heads and radiating to the two corresponding toes. They may have some numbness and is made worse by wearing heels or tight shoes. They can also have some shock sensation. It can cause a separation of the toes known as collateral ligament injury.
Other causes of metatarsalgia include intractable plantar keratoses, RA, DM, OA, neuromuscular, Freiburg’s (avascular necrosis) and plantar plate rupture.
On examination, it is important to palpate under the metatarsal heads as pain is unlikely to cause Morton’s neuroma. Mulder’s click test. Investigate with X ray to rule out other diseases and see size of the space. Ultrasound is the main investigation.
What is Hallux Rigidus?
OA of the big toe
This can be caused by mechanical factors (post trauma, deformity or OA) or chemical (gout, infection to inflammatory such as RA). They may describe pain when barefoot, wearing shoes or at night. They may have stiffness, ulcers and other foot pains.
Classification is with the Hattrup and Johnson system which divides it into three grades. Conservative management is with NSAIDs and shoe modification. Cortisone injections may be beneficial. Grade 3 need arthroplasty.
How is Hallux valgus defined, investigated and treated?
Defined as a progressive foot deformity in which the first metatarsalphalangeal joint is affected and is often accompanied by disability and foot pain. This joint is gradually subluxed (lateral deviation) causing abduction. Soft tissue develops on the bony prominence which is known as a bunion.
Caused by genetics, excessive load, silly shoes, age, forefoot overload and metatarsus Primus varus. The second toe may be deformed with the progressive adduction of the head of the big toe.
Investigate with a weight bearing X ray. The metatarsal angle should be less than 9 degrees and the hallux valgus angle less than 15 degrees. Severe is over 40 degrees. Operative treatments include scarf osteotomy and the lateral release technique.
What is Blumensaat’s line?
Blumensaat’s line is a line which corresponds to the roof of theintercondylar fossa of femuras seen on a lateral radiograph of theknee joint.The angle at which this line appears on the radiograph can be used to determine the position of the patella or diagnose an ACL injury
What is Patella Baja?
Patella baja is an abnormally low lyingpatella, which is associated with restricted range of motion, crepitations, and retropatellar pain. If longstanding, extensor dysfunction may ensue with significant morbidity.
What is the Salter-Harris classification system?
The salter Harris classification system is used to determine whether radius fractures in young people will effect the growth plate or cause growth plate arrest. The higher the number the greater the concern.
type I:
slipped, fracture plane passes all the way through the growth plate, not involving bone
cannot occur if the growth plate is fused. This has a good prognosis
type II:
Fracture passes across most of the growth plate and up through the metaphysis
good prognosis
type III:
Fracture plane passes some distance along with the growth plate and down through the epiphysis
poorer prognosis as the proliferative and reserve zones are interrupted
type IV:
Through or transverse or together
intra-articular
Fracture plane passes directly through the metaphysis, growth plate and down through the epiphysis
poor prognosis as the proliferative and reserve zones are interrupted
type V: Ruined or rammed uncommon <1% crushing type injury does not displace the growth plate but damages it by direct compression worst prognosis
