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1. MSK Ortho 1 Flashcards

1
Q

Stages of fracture healing:

A

Haematoma formation.

Granulation tissue (7-14 days); causes vascularisation of the haematoma.

Bony callus formation (4-16 weeks) - progenitor cells differentiate into fibroblasts and chondroblasts. Eventually woven bone is replaced by lamellar bone.

Bone remodelling eventually restores cortical structure

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2
Q

3 types of nerve injuries:

A

Neuropraxia
Axonotmesis
Neurotmesis

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3
Q

Outline neuropraxia:

A

Mildest form of traumatic peripheral nerve injury.

Focal segmental demyelination without axon interruption - no anatomical interruption.

Blocks nerve conduction results in transient weakness or parasthesia.

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4
Q

Axonotmesis:

A

Anatomical interruption of nerve conduction with no or partial connective tissue network interruption.

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5
Q

Neurotmesis:

A

Complete anatomical disruption of the nerve and connective tissue network - nerve rupture.
No chance of spontaneous recovery.

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6
Q

Open fractures carry a higher risk of infection, non-union and malunion. What scoring system is used to grade them, and describe it?

A

Gustilo-Anderson:
I - <1cm wound, minimal contamination

II - 1-10cm wound, mod contamination

IIIa - minimal periosteal stripping
IIIb - significant periosteal stripping
IIIc - associated vascular injury

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7
Q

Principles of treating an open fracture:

A

Antibiotics, removal of gross debris, image/XR, sterile covering and splint in A+E first.

Then urgent debridement, reduction and immobilisation.

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8
Q

List 6 orthopaedic emergencies:

A

Dislocations
Open fractures
Septic arthritis
Compartment syndrome
Nec fasc
Cauda equina

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9
Q

Define / pathophys of acute compartment syndrome:

A

Intra-compartmental pressure in a fascial compartment increases to above the capillary perfusion pressure.
Compromised tissue perfusion results in necrosis.

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10
Q

Most important clinical feature of compartment syndrome?

A

Pain out of proportion to what is expected based on physical exam findings.

Other Ps of acute limb ischaemia may be present too (not pulselessness though)

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11
Q

2 main fracture carrying compartment syndrome as a high risk complication:

A

Supra-condylar
Tibial shaft
+ crush injuries

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12
Q

How do you diagnose compartment syndrome?

A

Clinical suspicion + measuring compartment pressures.

Diastolic BP - compartment BP <30mmHg = +ve
OR
Compartment pressure >30-40mmHg = +ve

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13
Q

Treatment of compartment syndrome:

A

Urgent and deep fasciotomy.

Aggressive IV fluids due to excess myoglobinuria which can cause acute renal failure.

Elevate leg to heart level and maintain good BP.

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14
Q

Complications of compartment syndrome:

A

Myoglobinuria leading to renal failure
Contractures
Pain
Rhabdo
Nerve damage
Infection
Death

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15
Q

Most common organisms in septic arthritis:

A

Gram positive anaerobes e.g. S.aureus, beta-haemolytic strep and strep pneumoniae

Neisseria gonorrhoae is a potential cause in young sexually active individuals

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15
Q

6 ways septic arthritis can occur:

A

Haematogenous spread
Direct inoculation
Trauma
Iatrogenic
Adjacent osteomyelitis
Soft tissue infection

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16
Q

Clinical features of septic arthritis:

A

Joint pain, swelling, erythema, warmth.
Rapid onset
Fever
Reduced ROM
Pain on active and passive movement

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17
Q

Management of septic arthritis:

A

Aspirate joint

IV flucloxacillin native joint (after joint aspirate) 4-6 weeks.

Prosthetic joint IV vanc.
Note, abx may be required for several months

Washout of joint - arthroscopic or open

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18
Q

Complications of septic arthritis (7):

A

Rapid destruction of joint if delayed for >24hrs
Degenerative joint disease
Soft tissue injury
Osteomyelitis
Joint fibrosis
Sepsis
Death

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19
Q

Which is the most commonly fractured carpal bone, and what is the characteristic clinical feature?

A

Scaphoid

Pain and tenderness in the anatomical snuffbox

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20
Q

What is a particular risk of a scaphoid fracture and why?

A

Avascular necrosis

Retrograde blood supply - enters at the distal end.

If there is a fracture to the middle / waist of the scaphoid it can interrupt this and render the proximal part avascular

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21
Q

What causes carpal tunnel syndrome?

A

Compression of the median nerve within the carpal tunnel.

Congenital narrow carpal tunnel
Wrist fracture / dislocation
Repetitive movements / forceful gripping / vibration

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22
Q

Contents of the carpal tunnel:

A

Flexor pollicis longus tendon (has its own synovial sheath)

Flexor digitorum profundus x4

Flexor digitorum superficialis x4

+ median nerve

(9 tendons and the median nerve)

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23
Q

Ulnar nerve (C8-T1) motor function (hand):

A

Intrinsic hand muscles - LOAF muscles.

(Deep branch of ulnar nerve)

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23
Ulnar sensory function (hand):
Medial one and a half fingers + associated palm area. 3 branches - dorsal, palmar and superficial.
23
Describe the anatomical course of the ulnar nerve: from spine to elbow:
Arises at the brachial plexus, with C8-T1 nerve roots. Passes posteriorly to the elbow through the ulnar tunnel (between the medial epicondyle and olecranon)
24
What branch of which nerve supplies the elbow joint?
Articular branch of the ulnar nerve
25
Describe the path of the ulnar nerve at the wrist:
At the wrist the ulnar nerve travels superficially to the flexor retinaculum, and is medial to the ulnar artery. It enters the hand via the ulnar canal, and terminates giving rise to superficial and deep branches.
26
What causes cubital tunnel syndrome?
Compression of the ulnar nerve at the elbow as it passes through the cubital tunnel
27
What are the clinical features of cubital tunnel syndrome?
Intermittent then constant numbness and tingling in 4th and 5th fingers. Potential weakness and muscle wasting (hypothenar). Pain leaning on affected elbow. Hx of OA or trauma to area.
28
What is Froment's sign?
Test for ulnar nerve palsy, specifically paralysis of adductor pollicis. Get patient to hold paper between thumb and index finger and pull away.
29
Potential causes of cubital tunnel syndrome:
Repeated use of the elbow joint Prev trauma e.g. fractures, dislocations Arthritis Bone spurs
30
What other elbow condition can present similar to cubital tunnel syndrome?
Medial epicondylitis (Golfer's elbow)
31
Management options for cubital tunnel syndrome:
Avoid exacerbating activity Physiotherapy Steroid injections Surgery
32
Tennis vs Golfer's elbow?
Tennis = Lateral epicondylitis Golfer's = Medial epicondylitis
33
What is lateral epicondylitis and what causes it?
Tennis elbow! Inflammation of the periosteum of the lateral epicondyle. Caused by repeated movement of the superficial extensor muscles, which strains their tendinous attachment to the condyle.
34
Clinical signs of lateral vs medial epicondylitis:
Lateral: Pain worse on wrist extension, or supination of forearm. Medial: Pain worse on wrist flexion, or forearm pronation.
35
Treatment options for lat and med epicondylitis:
Avoidance of triggering movements. Physical therapy NSAIDs Splints / bracing Steroid injections (if refractory)
36
5 stages of medial epicondylitis pathophysiology:
1. Microtrauma, degeneration and tears 2. Tendinosis - collagen degeneration 3. Inflammatory process 4. Angiofibroblastic hyperplasia 5. Ulnar nerve involvement
37
List the stabilising structure of the glenohumeral joint:
Rotator cuff muscles Ligaments Glenoid labrum Biceps tendon
38
4 ligaments of the glenohumeral joint:
Glenohumeral Coracohumeral Coracoacromial Transverse humeral
39
What makes up the shoulder joint?
Glenoid fossa and the humeral head
40
The shoulder joint is the most likely joint to dislocate. Which type of dislocation is most common?
Anterior dislocation
41
Which nerve is at risk in shoulder dislocation, and what symptoms would impingement cause?
Axillary nerve Paralysis of deltoid muscle, and sensory 'badge' sign
42
Management options for carpal tunnel syndrome:
Splinting wrist in dorsiflexion for symptomatic relief NSAIDs and oral steroids for pain relief and inflammation reduction Corticosteroid injections Surgical decompression - open or endoscopic transverse carpal ligament release.
43
Conditions associated with carpal tunnel syndrome (5):
Rheumatoid arthritis Hypothyroidism Diabetes Pregnancy Gout
44
Signs and symptoms of CTS
Intermittent pain, numbness and tingling, worse on wrist flexion / extension Symptoms worse at night Weakness and wasting of the thenar muscles, leading to reduced grip strength and fine motor skills Positive Tinel's / Phalen's tests
45
Predisposing factors for trigger finger / flexor tenosynovitis:
Female Rheumatoid arthritis Diabetes
46
Non-surgical management options for flexor tenosynovitis / trigger finger:
Avoidance of triggering movements e.g. repetitive gripping Splinting for 4-6 weeks to allow to heal Corticosteroid injections into the tendon sheath at the level of the A1 pulley
47
2 types of surgical intervention for flexor tenosynovitis:
Percutaneous release - no visualisation. Better morbidity rates, but higher risk of incomplete release and neurovascular injury. Open release - direct visualisation of the A1 pulley - complete decompression of the flexor tendon.
48
Aetiological / risk factors for Dupuytren's contracture:
Genetics!! (Viking/Northern European gene) Diabetes Alcohol Male Older age
49
Physical signs of Dupuytren's contracture:
Nodules Cords / thickening of palmar fascia Finger contraction - impaired function and grip strength
50
2 conditions related to Dupuytren's contracture:
Plantar fibromatosis (Ledderhose) Penile fibromatosis (Peyronie's)
51
Management options for Dupuytren's contracture:
Conservative Splinting / physio Operative: ~30 degrees of contracture, fasciotomy.
52
Which 4 muscles make up the rotator cuff?
Supraspinatus Infraspinatus Teres Minor Subscapularis
53
What is the most common cause of Cauda Equina Syndrome?
Lumbar disc herniation L5/S1 most common but can occur anywhere 2% of all herniations results in CES
54
Causes of CES, apart from lumbar disc herniation:
Tumours - primary or mets Infection e.g. discitis, abscess Haematoma Trauma
55
Possible clinical features of CES:
Low back pain Bilateral sciatica Reduced anal tone Bladder (incontinence/retention) / bowel / sexual dysfunction Reduced sensation / pins and needles in the perianal area
56
Investigations in suspected CES:
Urgent MRI
57
Management of CES:
Urgent, to minimise permanent neurological damage - surgical spinal decompression.
58
Role of dexamethasone in CES:
If the CES has been caused by primary or metastatic malignancy, IV dexamethasone can be given to try and reduce the oedema, which can worsen the compression.
59
Long term complications of CES:
Paralysis of the lower limbs Bladder / bowel / sexual dysfunction
60
CES can present as acute or chronic. The symptoms can be divided into diagnostic and accompanying:
Diagnostic: Urinary, bowel, sexual dysfunction Saddle anaesthesia Accompanying: Lower back pain +/- sciatica Lower limb sensory loss Lower limb LMN signs Most patients will notice a progression in their symptoms over time, even with acute onset
61
2 categories of CES, and discuss their prognosis:
CESR = CES with retention - established urinary retention +/or overflow incontinence CESI = incomplete. No urinary retention. May have loss of urge / reduced sensation / poor stream. Better prognosis, and more likely to make a full recovery than CESR.
62
What is the standard treatment for lower leg compartment syndrome?
2-incision, 4-compartment decompression. For all, necrotic muscle should be excised and patients should go re-exploration at 48 hours.
63
How quickly should a fasciotomy be done after a decision to operate on compartment syndrome?
<1 hour
64
Debridement timings for open fractures:
Immediately if significant contamination e.g. agricultural, aquatic, sewage, or associated vascular compromise e.g. compartment syndrome / ischaemia. <12 hours if solitary high energy open fracture. <24 hours if low energy open fracture.
65
Differential diagnoses for an acute hot swollen joint:
Septic arthritis Rheumatoid flare Reactive arthritis Gout Trauma / dislocation Soft tissue injury Osteomyelitis
66
Which 4 places does NF occur?
Perineum (most common!), limbs, genitals, abdo wall.
66
NF can be categorised types 1- 4 based on the organism. What does each type represent?
Type I = POLYMICROBIAL. Most common. Occurs in patients with lots of comorbidities. Trunk or perineum. 70-90% of cases. Type 2 = STREP. PYOGENES. Younger patients, limbs over trunk. Type 3 = CLOSTRIDIUM / vibrio. IVDU. Type 4 = Fungal, mainly candida. Immunocompromised patients.
67
Risk factors for NF:
Skin factors: recent TRAUMA!, burns, soft tissue infections DM - most common! Especially if treated with SGLT2i. Other significant comorbidities should increase clinical index of suspicion e.g. peripheral vascular disease / CLD. IVDU Immunosuppression
68
Systemic features that can be present in NF (often later on):
Tachycardia Sepsis / organ dysfunction inc altered mental status Diarrhoea and vomiting Tachycardia Fever Failure to respond to broad spec Abx
69
Local features of NF:
Rapidly progressive 'cellulitis' Pain not in proportion to clinical findings Blistering / bullae Grey dusky skin = necrosis Skin crepitus / gas gangrene Acute onset
70
Which scoring system aims to increase early recognition of NF, and what are it's components?
LRINEC (Lab Risk Indicator for NEC fasc.) Hb, wcc, Na, creat, glucose, CRP. Score 5 or less = low risk 6-7 = mod >7 = high risk
71
Investigations that aid in the diagnosis of NF (4):
Wound culture, for Abx sensitivity Plain x-ray, for subcut gas CT + MRI, for asymmetrical fascial thickening, and fluid collection and gas tracking across fascial planes. Incisional biopsy
72
3 differentials for NF:
Cellulitis Erysipelas Pyoderma gangrenosum
73
Management of NF:
Surgical debridement inc fasciotomies Recovery in ICU Antibiotics good in combination with debridement.
74
Which IV Abx are used in NF (GGC guidelines):
Flucloxacillin Benzylpenicillin Metronidazole Clindamycin Gentamicin
75
4 common post-op orthopaedic complaints:
delirium pain nausea pyrexia
76
Orthopaedic patients more at risk of post-operative delirium:
Elderly Hip # Poor pain management Alcohol withdrawal
77
Patient risk factors for PONV:
Female Younger age Non-smoker Opioid analgesia use Prev. PONV or motion sickness
78
Anaesthetic risk factors for PONV:
Prolonged anaesthetic Opiates or spinal Inhaled agents Intraoperative dehydration or bleeding Overuse of BVM (gastric dilatation)
79
Surgical risk factors for PONV:
Laparoscopic, cranial, middle ear or gynae surgery. Poor post-op pain control
79
Clinical features associated with haemorrhage:
Hypotension Tachycardia Altered consciousness Low urine output
80
Post-op pyrexia can be normal, or can be a specific complication. What are the potential causes?
Infection Iatrogenic e.g. drug or transfusion reaction Secondary to prosthesis - low grade fever not uncommon VTE (rare) PUO
81
How do you investigate post-op pyrexia?
A to E screen for any obvious sources of infection Septic screen inc bloods, urine dipstick, cultures, imaging
82
Causes of post-op dehydration:
Lack of fluids Blood loss PONV Frailty? Losses via drains
83
Risk factors for developing FES:
Poly trauma Long bone fractures Hip and knee arthroplasty patients Increased exposure to bone marrow e.g. intramedullary nailing
84
Outline the major criteria in the diagnosis of FES:
Respiratory distress / radiographic changes Cerebral symptoms in non-head trauma Petechial rash (2 major, or 1 major + 4 minor)
85
Outline the minor criteria in the diagnosis of FES (8):
Jaundice Sudden onset thrombocytopenia Raised ESR Retinal changes Renal changes e.g. an/oliguria Fever >38.5 Tachycardia >110 Hb drop Fat macroglobulinaemia (2 major, or 1 major + 4 minor)
86
FES is the term for when fat emboli enter the systemic circulation and cause symptoms. Symptoms would usually present 24-72 hours post trauma. What are the 2 theories about how the fat enters the circulation?
Mechanical - fatty tissue release into the circulation during the operation as a result of trauma. Biochemical - inflammation caused by the trauma of the surgery causes release of free fatty acids into venous system from bone marrow.
87
What is the pathophysiology of the effects of fatty emboli on the body?
Fatty emboli cause a severe inflammatory response, increasing permeability of the vasculature, leading to cerebral oedema and ARDS. There is also a theory that the emboli cause occlusion of the vessels, causing symptoms this way.
88
DDx of FES:
PE Meningococcal septicaemia - neuro sx + petechial rash
89
Investigating FES:
Standard bloods including FBC, U+Es, CRP, LFTs, clotting CXR; diffuse bilateral pulmonary infiltrates ABG; T1RF Blood film; fat globules? CTPA; global ground glass Monitor pulse oximetry closely
90
Principles of management in FES:
Supportive, with a focus on respiratory management; mechanical ventilation may be required. Monitor pulse ox regularly in high risk patients. DVT prophylaxis. Prompt fixation of any long bone fractures.
91
Red flags for lower back pain:
Age <20 or >50 Hx of previous malignancy Night pain Hx of trauma Systemically unwell e.g. fever, weight loss Cauda equina symptoms
92
Discuss the types of osteoporosis (Primary/Secondary etc):
Primary Type 1 = post menopause, loss of protective oestrogen, >resorption Type 2 = 'senile' - older age, men Secondary Iatrogenic - steroids, PPIs, antiepileptics, aromatase inhibitors Endocrine - hypogonadism, renal failure, hyperparathyroidism, cortisol increased, overcorrection of hypothyroidism Alcohol Immobilization
93
Respiratory symptoms in FES:
Tachypnoea, dyspnoea and hypoxia, usually 72 hours post trauma Early, persistent tachycardia Pyrexia
94
Dermatological symptoms in FES:
25-50% have a petechial rash Subconjunctival and oral haemorrhage / petechiae
95
CNS symptoms of FES:
Confusion and agitation Retinal haemorrhage and intra-arterial fat globules on fundoscopy

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