Ortho/rheum Flashcards
general ortho considerations (2 reasons for fixation, what are intramedullary nails esp good for, when would you do external fixation, 3 reasons for osteotomy, reason for bone graft, how bone lengthening works, 2 reasons for arthrodesis inc 3 best joints to do it for)
fixation - internal (using screws, plates, wires, nails etc for fractures to stop displacement or malunion, intramedullary nails often useful, v good for stabilising shaft in long bone fracture), and external which is often if severe soft tissue injury as nails driven into bone, fragments aligned, then nails attached to external device so soft tissues still exposed for procedures after eg severe open fracture
osteotomy - correct deformity, relieve pain in arthritis by redirecting load trajectory; can inc or dec length of bone with open and close wedge osteotomy respectively
bone grafts - to fill cavity etc
bone lengthening - using external fixator to gradually distract bone 1mm a day with callus and cortex forming, can also be used to plug gaps in shaft if bone removed; thus can lengthen one leg to match the other
arthrodesis - joint fusion for painful or unstable joint, esp if stiffness wont affect function too much eg spine, wrist, IP joints; even large joints can be done
vte prophylaxis in ortho patients
THR/hemi - 28 days LMWH or DOAC (some elective protocols prefer 35 days)
TKR - 14 days LMWH or DOAC
some surgeons use aspirin for 28/14 days respectively
ankle can also require 14 days LMWH/DOAC if not mobilising the calf; nothing needed after removal of ilizarov frame
fracture mx - hold (meaning, when is traction needed (inc 4 egs), x2 common ways to hold, 3 important principles of plasters inc how many joints to cross, when is VTE proph given for casts, what to advise pt about), rehab (why important after fracture, what to advise pt at start, what other important thing can OT offer)
‘Hold’ is the generic term used to describe immobilising a fracture.
Initially, it is important to consider whether traction is needed, such as for subtrochanteric neck of femur fractures, femoral shaft fractures, displaced acetabular fractures, or certain pelvic fractures. Most commonly this is where the muscular pull across the fracture site is strong and the fracture is inherently unstable.
There most common ways to immobilise a fracture are via simple splints or plaster casts. When applying a plaster cast, the most important principles to remember are:
For the first 2-weeks, plasters are not circumferential (not always the case in children)
They must have an area which is only covered by the overlying dressing, to allow the fracture to swell; if this principle is not adhered to, the cast will become tight (and subsequently painful) overnight, and if left the patient is at risk of compartment syndrome
If there is axial instability (whereby the fracture is able to rotate along its long axis), such as combined tibia-fibula metaphyseal fractures or combined radius-ulna metaphyseal fractures, the plaster should cross both the joint above and below
These are usually termed ‘above knee’ or ‘above elbow’ plasters, respectively, preventing the limb to rotate on its long axis; for most other fractures, the plaster need only cross the joint immediately distal to it
Do they need thromboprophylaxis?
If the patient is immobilised in a cast and is non-weight bearing, it is common to provide thromboprophylaxis
Have you provided advice about the symptoms of compartment syndrome?
Patients should be advised that if they develop any features of compartment syndrome to return to A&E for further assessment
rehab: need for most patients to undergo an intensive period of physiotherapy following fracture management.
Invariably, patients are stiff following immobilisation and therapists are therefore essential to successful recovery. It is therefore also important to ensure that patients are advised to move non-immobilised unaffected joints from the outset.
It is also important to remember that many fractures occur in frailty and render the patient with an inability to weight bear or use an arm, having profound effects on their ability to cope at home. Therapists are therefore essential in making sure that this group have suitable adaptations implemented for them during their recovery
entonox and penthrox
Penthrox is an inhaler that contains a drug called methoxyflurane, which is poured into the device. A piece of gauze inside soaks up the liquid and you inhale the vapours
Entonox consists of two gases, 50% nitrous oxide (N2O) and 50% oxygen and is more commonly known as gas and air
both suitable options for pain mx in ED/trauma settings for things like fracture reduction, nail removal, burns, dressing changes etc - some studies show penthrox is superior and others find no difference; note penthrox not licensed for kids in the UK, so may have to stick to entonox
entonox has multiple mechanisms of action:
The anesthetic effect of nitrous oxide is through non-competitive NMDA inhibition in the central nervous system. The analgesic effects occur by releasing endogenous opioids that act on opioid receptors; its analgesic actions are like morphine. The anxiolytic effects are through GABA-A activation
Entonox is given using a mouthpiece which is held firmly between the teeth/lips to form a good seal. Pt should breathe deeply for 1 – 2 minutes before the procedure begins
intranasal fentanyl is a good adjunct/first line for prehospital analgesia and covering painful procedures
fracture healing - 2 types, what factor determines which type happens (and what governs that); what is the first type and what kind of fracture do you usually see this in; second type is what and occurs in what kind of fractures; 4 stages of second type; 9 things that affect healing; non-union and delayed healing definitions (inc how long healing should take to begin); what does non-union normally need
2 types - primary and secondary
mechanical stability governs the mechanical strain
when the strain is below 2%, primary bone healing will occur
when the strain is between 2% and 10%, secondary bone healing will occur
if strain over 10% (too much movement) then no healing will occur
primary is intramembranous via haversian remodelling and occurs with compression plates and other absolute stability constructs due to low strain
secondary is endochondral and occurs with non-rigid fixation, inc casts, braces, IM nails, external fixation, bridge plating etc
stages of secondary: haematoma forms (step 1) and macros, neuts, plats release PGDF and other cytokines - haematoma important, provides structure and materials for callus and so prefer external fixation or casts etc to preserve this; BMPs, fibroblasts etc migrate to site and granulation tissue forms (stage 2) and runx2 causes osteoblast differentiation; stage 3 is repair with prim callus within 2 weeks with soft callus bridging between bone where not touching, then this soft callus becoming hard callus via endochondral ossification, with COX2 and prostanoids playing role in guiding this; 4th stage remodelling via osteoblasts and osteoclasts responding to mechanical stress, VEGF guides new blood vessel formation
good blood supply important for healing; DM impairs healing (takes 1.6 times longer), vit D and Ca deficiency delays, nicotine inhibits new vessel formation and gives worse blood flow so 70% longer to heal and inc’d non-union risk; NSAIDs inhibit COX and runx2/ALP, quinolones toxic to chondrocytes, steroids and bisphos may also affect healing; infection also reduces healing and inc’s risk of non-union
non-union - no signs of healing after 3 months; delayed healing, some healing by 3 months but taking longer than expected (most 6-8 weeks, wrist quick 4-6 and tibia may be 20 or more + rehab time; hips may take 3mo); pain often persists; if non-union often needs internal fixation to ensure proper alignment and healing
complications of ortho ops (4 ways to reduce swelling + complication, 4 other things you might see)
swelling common, esp if tourniquet used to stop bone bleeding too much; split cast, early movement of neighbour joints, elevate limb, dressing not too tight, watch for comp syndrome
haematoma - ensure bleeding vessels dealt with before closing up
DVT, PE, chronic venous insufficiency - common after lower limb op, rare but poss after other joint/limb op
infection and poor wound healing can occur
thromboembolism (what day are platelets etc highest post op, 4 other things that inc thrombosis risk, 2 areas where surgery esp high risk and why; 5 other things that inc risk of clotting; 3 aspects of reducing risk; how might PE present in elderly pt; what day post-op is highest risk and when might it acutely be triggered, why is lung infarction uncommon but when is it more likely)
platelets and fibrinogen may rise post-op after initially falling, levels peak ~10 days after, inc tendency to thrombose; stasis due to dec mobility during and post op; pressure from mattress; inflam/sepsis; damage to vessels during op all lead to damaged venous endothelium so inc thrombosis risk
pelvic and hip surgery esp risk as veins often damaged
OCP/HRT, obesity, malignancy, elderly, hypercoaguable state all inc risk
early mobilisation, minimise/treat risk factors, subcut LMWH; beware inc bleeding risk post-op
note in the elderly confusion due to hypoxia may be how PE presents; 10th post-op day is day of highest suspicion but can be before or after too, often occurred when eg straining at stool as raised abdo pressure dislodges pelvic thrombus
lung infarction from PE uncommon as bronchial a’s perfuse the lungs themselves, but can occur esp if preexisting pulm hypertension
Heparin - UF vs LMWH (admin route, duration/mech of action (inc 5 factors for UH vs 1 for LMWH), s/e (3), monitoring for each inc why that is used, 2 times when UH better)
Administration
Intravenous vs subcutaneous
Duration of action
Short vs long
Mechanism of action
Activates antithrombin III. Forms a complex that inhibits thrombin + factors Xa most and IIa, IXa, XIa and XIIa decently
Activates antithrombin III. Forms a complex that inhibits factor Xa, the others to some extent but much less so
Side-effects
Bleeding
Heparin-induced thrombocytopaenia (HIT)
Osteoporosis
Lower risk of all with LMWH
Monitoring
Activated partial thromboplastin time (APTT) for UH - may titrate to target APTT
Anti-Factor Xa for LMWH (although routine monitoring is not required)
Administration of UH results in approximately equal inhibition of Xa and IIa but LMWH, because of their shorter chain length preferentially inhibit Xa. As a result, doses of LMWH required to achieve an antithrombotic effect possess only weak inhibitory activity against thrombin and thus have less effect on APTT and a decreased risk of bleeding compared with UFH therapy
Notes
UH useful in situations where there is a high risk of bleeding as anticoagulation can be terminated rapidly. Also useful in renal failure
arterial trauma - 6 consequences, recognition and 7 mx of acute limb ischaemia
open or closed and may result in H+, thrombosis, AVF formation, dissection, downstream compartment syndrome from ischaemic muscle swelling
downstream acute limb ischaemia (6 Ps)
management: discuss with seniors and keep NBM. give O2 and insert large bore iv cannula, iv opioids, fluids to keep abp >100mmHg, manage any hyperkal; iv bolus unfractionated heparin then infusion
compartment syndrome (3 common causes, 4 other causes, why does it happen, why does it have a positive feedback loop, what is the next structure to be compressed and what do you see, then next (at what level of pressure), how long does it take to dev, most reliable sx (and how to exacerbate it), how to differentiate the neuropraxia of this from initial nerve damage, how will the compartment appear on exam, then what features will dev; how to diagnose (inc if uncertainty - normal comp pressure), how will CK level be, how is it mx’d, prior to definitive mx 5 mx steps, after def mx what procedure is done, what needs to be monitored closely in blood)
typically occurs following high-energy trauma, crush injuries, or fractures that cause vascular injury. Other causes include iatrogenic vascular injury, tight casts or splints, deep vein thrombosis, and post-reperfusion swelling.
Fascial compartments are closed and cannot be distended; consequently, any fluid that is deposited therein will cause an increase in the intra-compartmental pressure
the veins will be compressed. This increases the hydrostatic pressure within them, causing fluid to move out of the veins in to the compartment. This increases the intra-compartmental pressure further.
Next, the traversing nerves are compressed. This causes a sensory +/- motor deficit in the distal distribution. Paraesthesia is therefore a common symptom.
As the intra-compartmental pressure reaches the diastolic blood pressure, the arterial inflow will be compromised, and the leg will become ischaemic
Symptoms tend to present within hours, although it can develop up to 48 hours post-insult.
The most reliable symptom of compartment syndrome is severe pain, disproportionate to the injury, which is not readily improved with initial measures (such as analgesia, elevation to the level of the heart, and splitting a tight cast). The pain is made worse by passively stretching the muscle bellies traversing the affected fascial compartment.
Parasthesia can occur, however whilst the patient may have had a neuropraxia at the time of the injury, it is the presence of evolving neurology that is most important.
The affected compartment may feel tense (compared to the contralateral side), but will not generally be swollen (as the fascial compartment is only minimally distensible).
If the disease progresses, the features are acute limb ischaemia will subsequently develop (often referred to as the ‘5 P’s’)
clinical diagnosis usually, but most reliable diagnostic test is siting an intra-compartmental pressure monitor, which may be utilised where there is clinical uncertainty, such as in atypical presentations or if the patient is unconscious / intubated (normal compartmental pressures are 0-8mm Hg)
A creatine kinase (CK) level may aid diagnosis, if elevated (or trending upwards).
most important part of the management is early recognition and immediate surgical treatment via urgent fasciotomies.
Prior to definitive intervention, additional management steps should include:
Keep the limb at a neutral level with the patient (do not elevate or lower)
Improve oxygen delivery with high flow oxygen
Augment blood pressure with bolus of intravenous crystalloid fluids - this transiently improves perfusion of the affected limb
Remove all dressings / splints / casts, down to the skin (no layers of any dressing must be left circumferentially)
Treat symptomatically with opioid analgesia (usually intravenous)
Once fasciotomies have been performed, the skin incisions are left open and a re-look is planned for 24-48 hours. This is to assess for any dead tissue that needs to be debrided. If the remaining tissues are healthy, the wounds can then be closed (the subtending fascia is often left open).
Monitor renal function closely, due to the potential effects of rhabdomyolysis or reperfusion injury, and danger of hyperkal
oestoarth (3 broad reasons to dev OA, common ways it presents, 8 mx, surgery x2 reasons, neuropathic OA definition and 5 causes, likely cause of OA if <20yo)
joint incongruity, excess loading (eg someone who bends knee a lot at work), or weakening of cart due to certain genes or inflam conditions
classic form is pain and dysfunction in one or two large joints, multi joints inc DIPs esp in older women; stiffness worse after rest
NSAIDs, keep active, reduce overstressing, physio to keep range of motion; soft shoes, lose weight, maybe walking stick all for load reduction; can step up the pain ladder, can do intra-articular steroid injections
if symptoms severe and marked loss of function, joint replacement is treatment of choice
neuropathic arth is rapid progressing OA in joint that has lost position sense and protective pain sense; often due to periph neuropathy (eg DM), tabes dorsalis, cauda equina damage, congen pain insensitvity, syringomelia
repeat bleeding into joint can give OA in ppl <20yo
arthroplasty (shoulder (3 reasons, 5 complications, effect on rom and pain, which part of joint does ball component go in), knee (3 reasons, what else is removed often, 4 complications, rom in artificial vs healthy knee, how long does it last), hip (6 reasons, risks inc most common and when it tends to occur, why metal on metal implants not used; when is hemiarth done vs total arth (why latter is better), how long it lasts, when back to light activity)
shoulder: bad OA and RA if medical treatment fails, prox humeral fractures may sometimes need it; complications include infection, instability of joint, rotator cuff failure, periprosthetic fracture, implant loosening; rom often disappointing but pain relief good; remove head of humerus, put in cup with polyphene liner, put the ball component into the glenoid fossa
knee: most often for OA but also eg RA, PA; ACL and often PCL removed; DVT, periprosthetic fracture, infection, loosening; often get 110deg rom back (130 is normal healthy knee); intense rehab after but can last 15-20 years
hip: for OA, RA, AVN, certain hip fractures, problems with paget’s disease or tumour; risks similar to other types, with dislocation most common problem usually in first 3mo as soft tissues not yet healed; DVT and PE common problems after too; metal-on-metal not used due to risk of toxicity (esp cobalt/chromium), also fail more often; so stainless steel femoral head, polythene acetabulum; fixed using PMMA bone cement; hemiarth done after fracture of neck of femur in elderly or frail patients, if adult is healthy and independently mobile then total replacement better (as hemiarth fem replacement often wears acetabulum down over time); lasts 10-15 years, back to light activity within 6 weeks
trauma surg (3 inds for c spine immobilisation, triad of death, what causes trauma induced coagulopathy x3)
should have low threshold for c-spine immobilisation inc blunt/penetrating trauma above clavicle, head injury, polytrauma
beware triad of death in trauma: (met) acidosis, hypothermia, coagulopathy (leading to massive bleeding)
believed trauma induced coagulopathy comes from acidosis, hypothermia, haemodilution by inflam etc all acting together and may well be a form of DIC
secondary survey (when it happens, 5 things in quick history, what else to ask, what to check next (inc spotting hypovol shock early), 8 things to assess with head, how to clear the c-spine, 4 things in chest, 4 things in abdo, perineum inc when to do DRE x2 (+3 things you’re looking for), what to do if blood at meatus, how to assess extremities (+what to do if injured joint found), how to assess pelvis, how to assess neuro x2, last thing to not forget)
After A-E
AMPLE History:
Allergy
Medications
Previous medical history or illness/pregnancy
Last Meal
Events/environment related to injury
Ask if pain anywhere
Assess vital signs; A narrow pulse pressure and tachycardia indicate hypovolemic shock in a trauma setting until proven otherwise. Vital signs should be closely monitored
Examine the head for scalp hematoma, skull depression, or laceration. The scalp should be palpated, since scalp lacerations or bony step-offs may be identified only by careful palpation. Palpate the entire facial bony margins including orbit, the maxilla, the nose and jaw
Ears should be evaluated for hemotympanum or retro-auricular ecchymosis (Battle’s sign) and look for nasal septal haematoma
The pupillary size and response, as well as eye movements should be assessed. The ocular examination should also include ocular mobility/entrapment, or periorbital ecchymosis (Raccoon eyes)
The neck should be carefully inspected and palpated while it is carefully immobilized; C-spine can be cleared either clinically by applying decision rules, or by obtaining imaging studies
Palpate the entire chest wall for crepitus (subcutaneous emphysema) and tenderness; Assess any respiratory effort and work of breathing. Evaluate whether breath sounds are symmetrical and heart sounds are normal and not muffled
Abdomen should be examined for distension, bowel sounds, bruising, skin marks or tenderness; also do a FAST scan
Perineum should be inspected for any evidence of injury. Historically, a digital rectal examination has been included. However, its necessity as been questioned. A digital rectal examination should be performed when there is a suspicion of urethral injury or penetrating rectal injury.
Look for the following:
Gross blood in the rectal vault, which may indicate bowel injury
Displaced or high-riding prostate, which may suggest urethral injury
Abnormal sphincter tone and sensation, which may be due to a spinal cord injury.
If blood is present at the meatus, urethral injury should be suspected. In this situation, retrograde urethrography should be performed before a Foley catheter is inserted
extremities should be assessed for fractures by carefully palpating each extremity over its entire length for tenderness and decreased the range of motion. Assess the integrity of uninjured joints by both active and passive movements. Injured joints should also be immobilized, and radiographs should be obtained; neurovasc status of each limb should be assessed and documented
pubis and anterior iliac spines should be evaluated for any signs of pelvic instability
GCS and motor/sensory function
log-roll to check the skin of the back
assessing head injury (definition of head injury, definition of TBI; classifying head injury using GCS, what is a concussion; how to assess (x3) and monitor (x3) a head injury pt, when examining x3 things to look for and 5 signs of basal skull fracture, 6 red flags in head injury, what ix to consider)
Head Injury = a patient who has sustained any form of trauma to the head, regardless of whether they have any symptoms of neurological damage
Traumatic Brain Injury = evidence of damage to the brain as a result from trauma to the head, represented with a reduced Glasgow Coma Scale or presence of a focal neurological deficit
Head injury is classified as minimal, mild, moderate, or severe based on the patient’s Glasgow Coma Scale (GCS); mild head injury/TBI is also known as concussion.
mild: GCS 13-15, mod 9-13, sev 8 or less
A-E assessment initially inc GCS, full periph and cranial exam if pt awake; check blood glucose as brain glucose need may be up after injury; GCS every 30-60mins, also assess for size and reactivity of pupils at same time + limb movements
Examine carefully for lacerations, evidence of facial fractures, or depressed skull fractures. Ensure to check for signs of basal skull fractures, such as bruising around eyes (‘racoon eyes’), bruising behind the ears (Battle’s sign), clear discharge from nose or ear (CSF rhinorrhoea or CSF otorrhoea), blood bulging from middle ear (haemotympanum), or any obvious penetrating injury
Key red flag signs in head injury include
Impaired consciousness level
Dilated pupils which do not respond to light (“fixed and dilated”)
Signs of basal skull fracture
Focal neurological deficit or visual disturbances
Seizures or amnesia
Significant headache or nausea and vomiting
Consider need for CT head
EDH (how common, commonest group affected, commonest mechanism of injury inc commonest source of bleeding and site fractured; classic history and 3 other sx; 3 things you might find on exam; initial assessment and 5 bloods, what imaging to get; once stabilised what’s the next step (who is candidate for surgery and who isn’t), what to do for conservative mx, 2 aspects of surgery, post-op assessment/mx, mortality including 4 poor prognostic indicators)
Around 2% of all head injuries presenting to the emergency department are extradural haematomas (EDHs), with associated significant morbidity and mortality, especially with advancing age.
The incidence of EDHs is higher in men, with the most common age group affected being the 2nd to 3rd decades
Extradural haematomas typically occur following blunt force head trauma resulting in a linear skull fracture, with no or minimal displacement. Parieto-temporal fractures are most commonly implicated (73.5%), typically secondary to events such as road traffic collisions (in 57%), assault (in 22%) and falls (in 9%).
The middle meningeal artery is the most common source of bleeding (around 85%), occurring due to a fracture at the pterion, lacerating the anterior branch of this vessel as it runs beneath
classic picture is of an initial loss of consciousness at the time of injury, followed by a lucid period, before further deterioration (albeit this is present in only around 30% cases). Other symptoms may include headache, nausea or vomiting, or progressive drowsiness.
On examination, patients may have a low conscious level, localising neurological signs, or clinical features of brain herniation or raised intracranial pressure
All patients presenting with a suspected traumatic head injury should be investigated and managed as per ATLS guidelines.
For initial investigations, routine urgent bloods, including FBC, U&Es, CRP, clotting profile, and a group and save, should be taken.
CT imaging of the head is required for any suspected of EDH. A EDH classically show as hyperdense biconvex* lesions, potentially with an associated skull fracture
Once the patient has been stabilised and the EDH is confirmed, urgent neurosurgical opinion is required (if deemed suitable for surgical intervention).
Current management guidelines from the Brain Trauma Foundation suggest that not all EDHs require surgery:
> 30cm3 should be managed surgically regardless of other factors
<30cm3 with low thickness, minimal midline shift and GCS >8 without any focal neurological deficits are candidates for conservative management
Conservative management typically involves serial CT imaging and close neurological observation.
Whilst no specific surgical procedure shows definitive benefit, craniotomy may be preferred in certain circumstances versus Burr holes in others.
Any bleeding source identified and localised should be controlled through ligation or cauterisation, if necessary.
Post-operatively, patients should be observed on either a neuro-critical care or high dependency unit with close neuro-observations and routine post-operative CT scans to ensure adequate clot removal. Ongoing neurorehabilitation is often required.
30% mortality, esp if increasing age, temporal location, low GCS at presentation, and evidence of herniation or raised intra-cranial pressure
SDH (acute vs subacute vs chronic, simple vs complicated; bleeding from where (vulnerable to what kind of injury), what does this bleeding lead to, 4 risk factors, 5 sx, what else is important to do with children, 5 bloods needed, ix, medical mx x2, what if they fell, conservative mx when, surgical mx acute and chronic, 6 complications)
can be classified as acute (< 3 days after injury), subacute (3-21 days), or chronic SDH (>21 days), or as simple (no associated parenchymal injury) versus complicated (associated underlying parenchymal injury)
Bleeding in a SDH occurs from tearing of the bridging veins that cross from the cortex to the dural venous sinuses, which are vulnerable to deceleration injury.
This subsequently leads to accumulation of blood between the dura and arachnoid and results in a gradual rise in intracranial pressure (ICP)
Risk factors for SDHs include increasing age*, alcohol excess, epileptics (as prone to falls and head injury), and those with clotting disorders or taking anti-coagulants
Patients can present with clinical features including altered level of consciousness, headaches, focal neurology, features of raised intracranial pressure (such as blurred vision, worsening headache), or even seizure activity.
Clinical features of an acute SDH occur quickly, whilst those of a chronic SDH have a latent period of weeks (or even months) before symptoms appear. Indeed, the initial injury may be relatively trivial or forgotten, especially in the elderly patients or those with recent alcohol excess.
In children, it is important to survey for other injuries with suspected SDH as there might be signs of non-accidental injury
patients should have initial routine bloods, including FBC, CRP, U&Es, LFTs, and a clotting, which will also aid in assessing for differential diagnosis. A group and screen will be requiring for any surgical intervention required.
The gold-standard initial imaging modality* for a suspected SDH is a non-contrast CT scan of the head
All patients on anticoagulation should have this reversed appropriately, which may require discussion with haematology colleagues. Patients may also started on anti-epileptic medications for 1 week after presentation of a SDH but this is controversial
For those that present with a SDH following a fall, they should also be investigated for potential underlying reasons for falls
Conservative management is generally appropriate for small acute SDH that do not cause significant midline shift or cisternal encroachment without any significant neurologic impairment.
For acute SDHs requiring surgical intervention, a trauma craniotomy may be warranted, with a hemicraniectomy if there is significant cerebral swelling or associated contusions.
For chronic SDHs, surgical intervention can be either a burr hole craniotomy with irrigation or a twist-drill craniotomy with drain placement
Complications following a SDH include cerebral oedema and raised ICP, seizures, herniation, persistent vegetative state, and permanent neurological or cognitive deficits. There is also an increased risk of recurrent haematoma formation or bleeding into the injury
diffuse axonal injury (what it is/how it happens, 4 common causes, classification, which part of the axons are most vulnerable, after injury what happens to microtubules and tau/APP, what are 3 delayed axonal problems, affect on consciousness immediately and over time, when is it often suspected, appearance on CT and MRI, general mx strategy inc monitoring, surgery and 2x medications; 3 aspects of rehab)
One of the most common and detrimental forms of traumatic brain injury (TBI).
The resistant inertia that occurs to the brain at the time of injury, preceding and following its sudden acceleration against the solid skull, causes shearing of the axonal tracts of the white matter -normally the tracts are disrupted, but not completely avulsed
Road traffic accidents (RTAs) are the most frequent cause of DAI, with assault or falls also common aetiologies. DAI may also present as a consequence of child abuse, particularly in shaken baby syndrome and abusive head trauma
A classification for grading of DAI characterises into 3 distinct categories, based upon histological findings in the anatomical distribution of injury:
Grade Pathology
Effect on Consciousness
Grade 1 Diffuse axonal damage within the white matter of the cerebral hemispheres (esp frontal) and grey-white matter interfaces Brief loss of consciousness
Grade 2 Tissue tear haemorrhages present; axonal damage of the white matter including grade 1 regions and the territory of the corpus callosum Variable recovery process, coma of unclear duration
Grade 3 Grade 2 findings in addition to tissue tear haemorrhages within the brainstem Instant coma with posturing and incomplete recovery
grey and white matter of the axons are of distinct specific gravities, therefore the axons present at the grey-white matter junction are particularly susceptible to injury.
Axonal disconnection and mechanical disruption to axonal cytoskeletal structure results in immediate severe brain injury. Destroyed axon microtubules will align incorrectly, with Tau and amyloid precursor protein (APP) are aberrantly deposited.
The delayed secondary axonal disconnection develops in a progressive manner, so majority of DAI damage evolves over time. Secondary physiological alterations include disrupted axonal transport, diffuse swelling (axonal varicosities), and axonal degeneration
Patients will have loss of consciousness at the time of injury with a prolonged post-traumatic coma (often attributed to co-existent injury, e.g. acute haemorrhage or cerebral contusions), in some cases persistent vegetative state
The diagnosis is often only suspected when patients do not make a neurological recovery, based on initial imaging
Even severe cases of DAI can have relatively normal CT imaging.
MRI imaging serves as the best imaging modality for DAI detection. Artefact regions are seen at the junctions of the grey-white matter, such as in the corpus callosum or brainstem, and hypertinense FLAIR
Treatment options are all aimed to preventing secondary effects such as cerebral oedema or haemorrhage, however guidelines in treatment for DAI are variable
Patients will warrant close monitoring, including intracranial pressure monitoring, however the role of surgical intervention is also variable.
Management via steroids and short-term anticonvulsant therapy can be considered on a case by case basis.
Physiotherapy, speech therapy, and occupational therapy within brain injury rehabilitation programs should be provided to optimise patient follow-up
salter harris clasffication inc which need closed reduction; 3 things open fractures need, 3 painful limb causes after open fracture
salter-harris: t1 transverse through plate, t2 splits off some metaphysis too, t3 along physis then into epi and joint so physis affected, t4 epi, physis, into metaphy too esp liable to displacement and so asym growth, t5 compression injury of physis, may result in growth arrest; t3/4 need closed reduction under GA then cast for 4-8 weeks or open reduction if not poss plus int fixation
open fractures need tetanus proph and antibiotics, usually co-amox, then to theatre with one dose of gentamicin and surgical debridement with removal of detritus and devitalised tissue, then continue doses of co-amox for 72hrs max, stabilise fracture and wound closure
beware comp syndrome due to bleeding or inflam; gas gangrene within 24 hrs of injury giving pain, swelling, brown discharge, oft little fever but pulse up and smells bad, toxaemia thence death if not treated; also risk of nec fasc
note comp syndrome can come from closed fracture or crush injury too
principles of fracture management - 3 steps, 4th step in high energy injury; 1st step 2 general approaches and what is needed during the process
most important adage to remember for the surgical management in traumatic orthopaedic complaints is ‘Reduce – Hold – Rehabilitate’
In the context of high-energy injuries, this is precluded by resuscitation
Reduction involves restoring the anatomical alignment of a fracture or dislocation of the deformed limb; Fracture reduction is typically performed closed in the Emergency Room. However, some fractures need to be reduced open; Reduction is painful and requires analgesia. Where regional or local blockade is both sufficient and easily provided (e.g. phalangeal/metacarpal/distal radius fractures), this would be the method of choice.
More commonly, the patient requires a short period of conscious sedation, often can provided in the Emergency Department where there is access to anaesthetic agents, airway adjuncts, and monitoring
15 common ortho xrays in paeds
supracondylar fracture - fall on extended outstretched arm; beware damage to median and ulnar nerves, and if brachial art then volkmann’s contracture
greenstick (due to thick and elastic periosteum)
perthes - AVN of fem head, almost always unilat and if bilat think of epiphyseal dysplasia; consider sickle cell, trauma, septic arth, TB
SUFE - posteroinf displacement of fem head relative to nexk (looks medial), 25% of cases bilat; frog legged xray best; use line of klein to see: line drawn along the superior edge of the femoral neck on the frontal projection which hould normally intersect the lateral aspect of the superior femoral epiphysis. Failure of intersection can indicate SUFE
osgood-schlatter - soft tissue swelling around tibial tubercle, or distortion/fragmentation of it
toddlers fracture - minimally displaced or undisplaced spiral fractures, usually of the distal tibia, commonly encountered in toddlers; vague symptoms not clearly related to the tibia presenting with non-specific pain, inability to weight-bear, and localised tenderness; from trip or fall while walking, may be subtle
congen hip dislocation - shallow/dysplastic acetabulum, hypoplastic femoral head (cant see in first 3-6mo until femoral epiphysis ossifies)
dysplastic femoral epiphyses - think hypothyroid
radial aplasia - think TAR/VATER or holt-oram syndromes, or fanconi
may see OA - eg haemarth repeated
osteosarcoma - metaphysis vs diaphysis for ewing; cortical bone destruction; soft tissue swelling, maybe elevation of periosteum giving codman triangle, may see sun burst radiating bone spicules
osteopetrosis - inc’d bone density, flask shaped deform of end of long bones; AR/AD; bone marrow involvement gives pancytopenia, extramed haematopoiesis giving organomeg, nerve compression can give blindness/deafness/other CN palsies; steroids and bone marrow transplant can help
horizontal growth arrest lines - malnutrition, severe stress or infection, trauma to bone, ALL, other chronic diseases affecting bone inc eg JIA
multiple skull lesions - leukaemia, neuroblastoma, histiocytosis X
wormian bones - down syndrome, hypothyroid, cleidocranial dysostosis, osteogensis imperfecta and more
osteopetrosis - MIOP is what; pathphys leading to 7 sx, imaging appearance x3; mx
Malignant infantile osteopetrosis (MIOP) is a rare genetic disorder that is characterised by increased bone density due to abnormal osteoclast activity
impaired bone resorption and endochondral formation replaces haematopoietic cells in the medullary cavity, with relative sparing of the cortices, and also increases the incidence of fractures due to bone fragility. The reduction in haematopoietic cells can also cause haematological abnormalities including thrombocytopenia, anaemia, susceptibility to infections and extramedullary haematopoiesis - can result in liver and spleen dysfunction/organomegaly. Neurological manifestations of osteopetrosis can also occur due to narrowing of osseous foramina and inc CN dysfunction and hydrocephalus
characterized by a unique radiographic appearance of generalized hyperostosis; Loss of differentiation between the medullary and cortical portions of bone; pathologic fractures; endobone or “bone-within-bone” appearance in the spine, pelvis, long bones; where areas of osteosclerosis intermingle with areas of relatively hypodense bone; ends of humerus/femur fail to remodel so get flask shaped deformity
mx involves HSC transplantation
craniosynostosis - what it is, 5 causes, 7 consequences, crouzon syndrome, apert syndrome, carpenter syndrome (for all inheritance, which suture, affect on appearance), dolichocephaly/scaphocephaly, brachycephaly, trigonocephaly, plagiocephaly, turricephaly, pansynostosis; mx)
premature fusion of sutures which can be idiopathic, sec to hyperthyroid (or over treatment of hypothyroid), hypophos/rickets, hypercalc, or various syndromes
may get raised icp, CN palsies (esp deafness/strabismus), exophthalmos, OSA, hydrocephalus, chiari malformation, sometimes problems with attention, IQ etc
crouzon syndrome is AD w all 3 sutures fused giving hypertelorism, prominent forehead, beaking of nose, low set ears
apert syndrome is AD w high mut rate, prem fusion of coronal suture giving reduced AP diameter, prom forehead, flat occiput and high vertex (acrocephaly/tower head), syndactyly
carpenter syndrome AR and similar to apert except polydactyly
dolichocephaly prem fusion of sagg suture incs AP diameter of skull
brachycephaly from prem fusion of coronal sutures giving flat occiput
trigonocephaly from the premature closure of the metopic suture giving narrow pushed forwards forehead with hypotelorism
ant/post plagiocephaly from unilat coronal or lambdoid synostosis giving asymmetrical flattening
turricephaly is coronal plus any other suture eg lambdoid, skull is tall and twisted
pansynostosis when 3+ sutures closed; can look like microcephaly, or eg clover leaf deformity
mx by ref to specialist teams to reconstruct skull
sprengel deformity - what it is, associated with what, what happens in severe form
one scapula hypoplastic and higher than the other w reduced movement, and due to failure of scap to descend to correct final position in fetal life
associated w klippel-feil syndrome
in severe forms an omovertebral bone may bridge gap between scap and cervical vertebra
childhood torticollis - congenital x2 causes and what might complicate, 9 acquired causes inc a syndrome
common
congen or acquired
congen may be due to intrauterine positioning, or sternomastoid haematoma after traumatic delivery may fibrose causing contracture of ipsi scm muscle
acquired inc most commonly idiopathic and self resolving but also BG disorders, neuro tumours, cervical spine bony abnorms/tumours/infs, post-traumatic, peritonsillar abscess or phayryngeal infection, strabismus (esp trochlear palsy), rarely associated with severe GORD (sandifer syndrome), drug induced dystonia (antipsychs, DAr antag antiemetics)
scoliosis - who most common in, postural vs structural, what might shoulders/scapulae look like, which direction in different spine regions usually and how to make more pronounced, 5 causes, mx
80% in girls, may be postural (they can correct by standing differently) or structural; may see one shoulder higher than the other or prominent scapula
usually to the right in thoracic region and left in lumbar - more pronounced if child bends forwards
80-85% idiopathic, rest eg hemivertebrae, neuromusc problems like dystrophies, marfan syndrome, mucopolysaccharidoses
refer severe for poss surgical correction
scoliosis
Non-structural lateral curvature can masquerade as scoliosis. Common causes include:
Poor posture
Leg length discrepancy
Trauma
Tumour
Infection
structural/true scoliosis causes include:
cerebral palsy
Friedreich’s ataxia
Polio
Spinomuscular atrophy
Spina bifida
Myopathic
Muscular dystrophy
Neurofibromatosis
Skeletal dysplasia
Metabolic disorders
Collagen disorders
Congenital
Or in 75% of time, idiopathic - adolescent if onset >10yo and early onset otherwise
hallmark of a structural curve is axial rotation, which clinically manifests as a rib prominence; this is generally not seen in the non structural causes
diagnosis of idiopathic scoliosis is
dependent on excluding the other causes
typical adolescent idiopathic scoliosis patient is a female with a convex right thoracic curve or convex left lumbar curve, right shoulder elevated, right rib prominence, left lumbar loin bolster, no abnormal neurology and no significant pain. Deviation from typical features should prompt a search for underlying causes
red flags:
Structural scoliosis in a male patient
Significant pain, particularly night pain
Left-sided thoracic curves
Abnormal neurological signs/symptoms
Rapidly progressive curves
Onset in childhood rather than adolescence
While scoliosis has cosmetic implications, its clinical significance is related to growth potential and respiratory function. Thoracic idiopathic curves may be associated with decreased respiratory function when >50° and increased shortness of breath when >80°. Scoliosis in children under 10 years of age may result in pulmonary hypoplasia and long-term respiratory failure
important to document curve location as well as shoulder and pelvis symmetry. Leg length discrepancy can be assessed by palpating both iliac crests while the patient is standing. Rib prominence, resulting from rotational deformity, is measured by the Adam’s forward bend test. A detailed neurological examination is required to assess tone, power, reflexes and sensation of upper and lower limbs
standing whole-spine plain posteroanterior and lateral radiograph should be obtained for patients with structural scoliosis. The Cobb angle measures the most significant magnitude of the curve from the superior endplate of the upper vertebral body to the inferior endplate of the lower vertebral body involved in the curve; Cobb angle <25° is unlikely to progress, 25–50° will likely progress during skeletal immaturity and >50° will likely progress even after skeletal maturity; Peak growth velocity (growth of 5–6 cm in six months) usually occurs 6–12 months before menses. This growth spurt represents the period of highest risk of curve progression
Early referral to a paediatric spinal specialist is recommended, especially for skeletally immature patients with curves >20°, patients with significant rotation or those with red flags
Observation is appropriate for curves <20° in patients with high growth potential (Risser 0–2) and curves <40° in patients with minimal growth potential (Risser 3–5). If the curve is <20° without rotation, it is appropriate for the general practitioner to repeat plain radiograph imaging in six months’ time to assess progression. At each consultation, the patient should perform an Adam’s forward bend test. Bracing is appropriate for patients with a curve of 20–40° with high growth potential. Brace prevents progression but doesn’t cure
Symptomatic treatment includes an exercise regimen for core strengthening and posture control. Physiotherapy can help obtain and maintain muscle condition
Indications for the surgical management of scoliosis vary considerably depending on patient and curve factors; however, surgery can be indicated when the curve is >40–50°.
scheuermann disease
Postural kyphosis is the most common form of kyphosis and tends to occur in teenagers. As its name implies, this curve is due to bad posture and becomes more apparent during the teenage growth spurt. It is more common in boys than girls. Requires PT.
Scheuermann’s kyphosis usually occurs during a growth spurt. It is when the back of the vertebrae in the upper spine grow faster than the front. On an x-ray, the vertebrae, instead of looking like rectangular building blocks, look wedged at the front so that the spine curves forward.
Congenital kyphosis is rare but occurs when a baby is born with an abnormal spine. The spine has not developed properly and the curve can get worse as the child grows
a condition of hyperkyphosis that involves the vertebral bodies and discs of the spine identified by anterior wedging of greater than or equal to 5 degrees in 3 or more adjacent vertebral bodies
thoracic spine is most commonly involved, although involvement can include the thoracolumbar/lumbar region as well
Likely, genetic inheritance results in discordant vertebral endplate mineralization and ossification during growth, causing disproportional vertebral body growth with the resultant classic wedge-shaped vertebral bodies that lead to kyphosis
the deformity is typically appreciated in the early-mid teenage years by the child or parents; there may be subacute thoracic pain; the curve is rigid, ie does not resolve with an extension or lying prone/supine
although neurologic deficits are uncommon, a thorough neurologic exam must be completed
obtain AP/lateral radiographs, then diagnostic criteria include the following:
Rigid hyperkyphosis, greater than 40 degrees
Anterior wedging, greater than or equal to 5 degrees in three or more adjacent vertebral bodies
stretches, NSAIDs when needed, PT if kyphosis less than 60 degrees and generally asymptomatic
above + extension bracing if kyphosis 60 to 80 degrees plus/minus symptomatic
surgery if:
Kyphosis greater than 75 degrees causing unacceptable deformity
Kyphosis greater than 75 degrees with associated pain
Neurologic deficit/spinal cord compression
Severe refractory pain
ddx
Postural kyphosis (flexible postural deformity)
Hyperkyphosis attributable to another known disease state
Postsurgical kyphosis
Ankylosing spondylitis
Scoliosis
acute back strain (what it is and common causes, pain is in what 3 places usually,3 factors that support diagnosis, how long does pain last; sacroiliac lig pain distribution, what worsens it, and what to distinguish it from; how long to rest, what exercises to do, position to relieve pain in back strain and sacroiliac strain, 5 ways to mx pain, mx if chronic x3 and 4 other dd to consider)
minor self limiting injury, usually due to lifting heavy load, prolonged uncomfortable posture, a fall, or sudden unexpected motion as in accident
pain usually lower back, either in midline, across waist, or just on one side; localised tenderness and increased pain in postural changes supports diagnosis as does history; pain should resolve in few days to a week
strain of sacroiliac lig will have tenderness over that joint and pain radiating into buttock and post thigh, usually worsened by abduction of thigh against resistance and pain may refer to symphysis pubis or groin; week or two and will heal, be sure to distinguish it from sciatica
bed rest doesnt help, get active slowly with no more than 48hrs off, do trunk strengthening exercises esp abs; while pain initially bad lying on side with knees and hips flexed or supine with pillows under knees will help relieve, or hyperextend legs by lying prone or with pillow under lumbar spine if sacroiliac sprain; ice or heat and massage help, NSAIDs in first few days but not for too long; chiropractic can help some pts return to work sooner; yoga is beneficial in both acute and chronic back pain for many people
aching and stiffness may become chronic and radiate into buttocks and post thigh but no motor, sensory reflex abnorms; same treatments as for acute can help end an attack but often recur; long term chiropractor helps some ppl but not all; changing firmness of mattress often helps; worth considering arthropathy; metastatic disease if percussion tenderness over one vertebra, OA, spinal stenosis
OA of spine (how the pain presents, differentiating from slipped disc; facet syndrome presentation and mx)
stiff pain often worst in the morning with progressive mobilization making better in contrast with some other back pain causes; straight leg raising tests dont give pain unlike radiculopathy
facet syndrome due to degen of a facet joint, will be tender on palpation with no signs of nerve root compression, NSAIDs helpful
obscure (ie not biological) low back pain - 3 causes, features that you might see in malingering
fairly common, may be attributed to posture or injury, or else to mental illness; low back pain may occur in anxiety, depression but always consider bio causes first
sometimes ppl will play up pain as seeking eg compensation: usually describe pain vaguely and prefer to discuss extent of their disability; description may vary from time to time or region and radiation not make sense; pt may wince over slightest pressure, even over sacrum, or may fail to bend forward despite lack of muscle spasm
6 spine pain red flags
Age <20 >65
* Constant progressive pain
* Thoracic pain
* PMH HIV drug abuse
* Widespread neurological signs
* Sphincter disturbance
back pain (transient after muscle activity, sudden acute +/- sciatica (4 causes), intermittent chronic (5 ddx), back pain plus pseudoclaudication, severe localised pain (4 causes), 4 things in chronic backache syndrome and mx x2
5 types of backache: transient after muscular activity, suggests simple strain needing some rest then increasing activity;
sudden acute pain and sciatica may be infection or spondylolisthesis (if under 20 these most likely cause), acute disc prolapse (20-40yo, recent lifting), compression fractures but possibly mets or multiple myeloma if a bit older
intermittent low back pain after exertion poss relieved by rest, may be OA of facet joints, lumbar spondylosis, ankylosing spondylitis, chronic infection, mult myeloma
back pain plus pseudoclaudication may be spinal stenosis
severe constant localised pain may be fracture, paget’s disease, tumour, or infection and remember osteoporosis in man <60 suspicious and needs raft of test for all the poss causes
chronic backache syndrome from self perpetuating illness behaviour may have non physiological signs, variable responses to tests, exaggerated behaviours like falling, hypervent etc; exclude all organic causes, important to address psychosocial need, then consider completementary therapies, pain clinic referral
low back pain (16dd, red flags for cauda equina x3, malignancy x2, infection x2, aaa x2, fracture (inc 2 things making that less likely), when is mechanical cause unlikely
mechanical back pain most common but diagnosis of exclusion
vertebral fracture if onset coincides with injury or if bony tenderness, LXR
prolapsed disc, straight leg test
renal colic from loin to groin, micro haematuria in 95% cases, loin tenderness common but abdo tenderness rare so if thats present consider other options
pyelonephritis
symptomatic aortic aneurysm: shock and sudden pain if noncontained bleed, pain if contained bleed, rapidly growing w/o rupture hurt due to stretching of the a wall; beware esp in those >55, and often they present with what seems to be left sided renal colic due to bleed contained in left retroperitoneal space, but may have abdo tenderness; abdo uss to rule out as exam alone often doesnt pick up
bony mets - constant, chronic, unremitting, worse at night; radionucleotide bone scan if suspect; myeloma can also be a cause, diagnosis from plasma electrophoresis and urinary bence jones protein test
pancreatitis relatively common but usually abdo pain radiating to back, check serum amylase
discitis, osteomyelitis, epidural abscess, cauda equina or spinal cord compression; prostatitis often has severe pain in lower back and perineum, prostate exam v tender, sometimes fevers and rigors, often associated uti
OA, lumbar stenosis
red flags for cauda equina: saddle area paraesthesia, urinary retention or incontinence, faecal incontinence
red flags malignancy - constant pain inc at rest and worst at night
red flags infection - fever, constant pain inc at rest
aaa red flags - abdo pain, sudden cv collapse
fracture red flags - history of trauma w/ pain starting soon after; fractures unlikely if pain free after accident then pain devs, or if no bony tenderness; mechanical cause unlikely if pain not made worse by movement
vertebral fracture (7 causes, pain and affect on lumbar muscles x2, 7 features of rotary tear, body fracture mx)
usually from violent impact eg fall or jump from height or vehicle accident; osteoporosis often the cause, esp in older ppl, inc due to hyperparathroidism, prolonged corticosteroid use; osetomalacia, myeloma, bony met
pain usually immediate but may be delayed up to days after; all lumbar movements limited, spasm of lower lumbar muscles
high impact rotary injury can break transverse process and tear paravert muscle giving limited movements, deep tenderness, local haematoma, and poss bleeding into retroperitoneal space giving groin pain, prox leg weakness and loss of patellar reflex, and grey turner sign
body fractures usually need bed rest and good analgesia; discuss with neurosurg or T&O; get a standing XR once pain allows to rule out secondary kyphosis or collapse; brace generally only for comfort if needed but can get neurosurg or T&O opinion
lumbar stenosis - narrowing where, major cause and 10 other things that can cause; presents how (exacerbates, relieves); sx distribution pattern; how might stairs be affected; 5 red flags for CE/CM syndromes; sign differentiating from disc prolapse, and what else you need to examine
a narrowing in the vertebra, in the areas of the central canal, lateral recess, or the neural foramen
degenerative spondylosis is a significant etiology of lumbar spinal stenosis; degenerative changes can also lead to posterior vertebral osteophyte formation (uncinate spurs), facet hypertrophy, synovial facet cysts, and ligamentum flavum hypertrophy; Degenerative spondylolisthesis is another cause of lumbar spinal stenosis; also more rarely things like SOLs, post-surgical fibrosis, rheumatoid conditions like AS, hyperostosis, achondroplasia
presents as pain exacerbated by prolonged ambulation, standing, and with lumbar extension, and is relieved by forward flexion and rest. Neurogenic claudication is an important feature of lumbar spinal stenosis. Symptoms are typically bilateral, but usually asymmetric. Low back pain, numbness, and tingling are present in a majority of patients. Numbness and tingling in lumbar spinal stenosis typically involve the entire leg and rarely affect only a single nerve root distribution
may also report walking upstairs being easier than walking downstairs, as the back is forward flexed with stairs climbing
if present with new-onset bowel or bladder dysfunction, saddle anesthesia, bilateral lower extremity weakness, and/or increased lower extremity pain, the patient may have developed cauda equina or conus medullaris syndromes
Patients presenting with radicular pain will not have their pain exacerbated by Valsalva as is the case with intervertebral disc prolapse.
check pedal pulses due to dd of vascular claudication
traumatic spinal cord injury - 3 commonest causes,complete vs incomplete, 2 ways trauma can injure the cord, mechanism of oedema and ischaemia, who do c-spine rules apply to, 3 c-spine indications for immediate imaging (inc 5 high risk injurie), 5 low risk factors suggesting imaging not needed and what to do after that.; what imaging to use for c-spine x2, what imaging for any other spine injury x2 + follow up imaging, why restrict the spine initially, 4 steps conservative mx, 2 absolute indications for surgical mx, 3 aims for surgical mx, what other input to get early
majority are due to preventable causes such as falls (40%), road traffic collisions (35%), or sport injuries (12%).
TSCI can be classified* as complete or incomplete:
A complete injury is damage occurring across the whole spinal cord width, leading to complete loss of sensation and paralysis below the level of injury
An incomplete injury is the injury is spread across part of the spinal cord thereby only partially affecting sensation or movement below the level of injury
Trauma causes injury to the spinal cord from (1) the initial acute impact, resulting in a concussion on the spinal cord (2) compression on the spinal cord from increased pressures from nearby rigid structures
In the latter cases, such changes result in increased tissue pressure, which can block venous return and result in oedema around the spinal cord. Arterial blood supply to the spinal cord can also be compromised, and therefore lead to ischaemia
Canadian C-spine rules can help further stratify risk of cervical spine injury and therefore potential imaging modality.
rules apply to patients who are alert (Glasgow Coma Scale score 15/15) and are in a stable condition following trauma where C-spine injury is a possibility.
Patients who have a high-risk factor require immediate radiological imaging, which includes either age ≥ 65yrs, a dangerous mechanism, or paraesthesia in extremities. dangerous mechanism: fall from 3feet+, load to head eg from diving, vehicle rollover/ejection or 100kph speed+, if in any motorized recreational vehicle, bicycle accident
If none of these are present, those who have a low-risk factor present do not require radiological imaging prior to assessment. These factors include those involved in a simple rear-end motor vehicle collision, those who are waiting in a sitting position, those ambulatory at any time, presence of delayed onset neck pain, or the absence of midline C-spine tenderness.
An assessment of range of motion can then be carried out, if imaging deemed not required
Suspected Cervical Spine Injury
Perform a CT scan in adults, if suggested by Canadian C-spine rules
Perform MRI for children, if suggested by Canadian C-spine rules
Consider a plain film radiograph in those who do not fulfil the criteria for MRI but clinical suspicion remains after repeated clinical assessment
Suspected Thoracic or Lumbosacral Spine Injury
Perform a plain film radiograph as the first‑line investigation for those with suspected spinal column injury without abnormal neurological signs or symptoms
Perform a CT scan if the radiograph is abnormal or there are clinical signs or symptoms suggestive of a spinal column injury
If a new spinal column fracture is confirmed, image the rest of the spinal column
*Whole body imaging should be considered with blunt major trauma and suspected multiple injuries
Restricting movement of the spine is recommended to prevent further damage to the spinal cord, with the patient is initially strapped to a backboard prior to further assessment or imaging
Conservative management includes a combination of bed rest, cervical collars/motion restriction devices, and traction, followed by early mobilisation and rehabilitation
absolute indications for surgical management of a traumatic spinal cord injury are evidence of a progressive neurological deficit or a dislocation-type injury to the spinal column (displaced and unstable)
Cervical spine surgery aims to realign the spine, decompress the neural tissue, and stabilise the spine with internal fixation (screws, plates, cages)
Thoracolumbar spine surgery typically involves spinal decompression, discectomy, spinal fixation, or spinal cord simulation
Physiotherapy and other specialist therapy input (e.g. speech and language or occupation therapy) should be utilised early (as soon as deemed safe), as TSCI patients often require extensive rehabilitation both as inpatient and outpatient
assessing injuries to c-spine - CT within what timeframe if high risk (13 high risk factors); if no high risk factors when to do CT x3, 4 times to do 3 view plain XR first, MRI as well as CT when, CT/MR angiography x3 reasons)
For people 16 and over who have sustained a head injury (including people with delayed presentation), do a CT cervical spine scan within 1 hour of the risk factor being identified if any of these high-risk factors apply:
the GCS score is <15 on initial assessment*
the person has been intubated*
a definitive diagnosis of a cervical spine injury is urgently needed (for example, if cervical spine manipulation is needed during surgery or anaesthesia)*
there has been blunt polytrauma involving the head and chest, abdomen or pelvis in someone who is alert and stable
there is clinical suspicion of a cervical spine injury (pain, tenderness, stiffness) and any of these factors:
age 65 or over
a dangerous mechanism of injury (that is, a fall from a height of more than 1 m or 5 stairs, an axial load to the head such as from diving, a high-speed motor vehicle collision, a rollover motor accident, ejection from a motor vehicle, an accident involving motorised recreational vehicles or a bicycle collision)**
focal peripheral neurological deficit*
paraesthesia in the upper or lower limbs.*
if none of the above, but neck pain/tenderness is present, then do CT c-spine if cannot actively rotate neck 45 deg to left and right, or condition putting them at risk eg axial spondyloarthritis (collagen vascular disease, or osteogenesis imperfecta), safe assessment not possible**
- = within 1hr in <16yos
**= 3 view plain x-rays, follow up with CT if they show an abnormality
Do MRI in addition to CT if there are neurological signs and symptoms suggesting injury to the cervical spine
Do CT or MRI angiography of the neck vessels if there is a suspicion of vascular injury, for example, because of:
vertebral malalignment
a high-risk fracture (that is, a high-grade or complex facial fracture or a base of skull fracture likely to involve the internal carotid artery or vertebral artery)
posterior circulation syndrome
cervical fractures
Among younger patients, cervical fractures are usually the result of high-energy trauma, whilst older patients can develop cervical fractures from low impact injuries
Patients can present with neck pain, but this is not always the case; may be varying degrees of neurological involvement present, depending on the level of spinal cord involvement and besides potential sensory and motor deficits, innervation to the diaphragm and vasomotor tone can also be affected; injury to the vertebral artery from a cervical fracture (especially in high cervical fractures) may present with a posterior circulation stroke
Differentials for patients presenting with cervical neck pain, with or without neurology, following injury include cervical spondylosis, cervical dislocation, or whiplash injury
Jefferson fracture is the eponymous name given to a burst fracture of the atlas; caused by axial loading of the cervical spine resulting in the occipital condyles being driven into the lateral masses of C1; Hangman’s fracture, also termed as traumatic spondylolisthesis of the axis, describes a fracture through the pars interarticularis of C2 bilaterally, sually with subluxation of the C2 vertebra on C3. These are caused by cervical hyperextension and distraction; Odontoid peg fractures are common cervical fractures, most common in older patients
3-point C-spine immobilisation, CT in adults or MRI in children (sometimes XR based on c-spine rules), discuss with spine specialists; Non-operative management can be appropriate for stable injuries - rigid collar during initial assessment, then possibly a halo vest; unstable get surgical fusion
soft and hard collars
Rigid collars do restrict neck motion compared with soft collars but only for flexion, extension, and rotation. Side bending was the same for both types of collars; thought they may restrict motion less than previously believed, hence things like halo used for long-term immobilisation or conservative management of unstable fracture, where collars can be used for stable injuries, esp of lower c-spine
Collars may still be beneficial for patients with neck pain that goes down the arm. The collar will restrict neck motion and take the pressure off the nerve roots that are irritated or compressed causing pain.
Soft collars are more comfortable, allow necessary motion needed for daily function, and may increase patient compliance after cervical spine surgery
cervical orthoses are effective for short term pain relief, they are not an alternative to physiotherapy treatment
collars can be used for people who are in less pain, but who need the collar to immobilise the neck and for a sense of security. In this case, the collars act primarily as proprioceptive guides to regulate the movement of the cervical spine rather than as a restraint to physically impede motion
collar should be worn constantly for one week only then gradually increased, to prevent soft tissue contractures, muscular atrophy and deconditioning, and psychological dependence
There is conflicting research regarding the effectiveness of cervical collars in treating patients, especially following trauma or injury, but they do seem to be effective for pain
asia scoring - what it is and based on, scoring system for sensation, defining sensory level and what is max score, scoring system for motor, defining motor level and max score, 5 grades, 5 subclasses for incomplete
for classifying spinal cord injury, based on examination of sensory and motor performance (dermatomes and myotomes) to identify the sensory and motor level
each sensory level scored with:
0 = Absent
1 = Altered - Impaired or Partial Appreciation, including Hyperesthesia
2 = Normal or Intact - Similar as on the Cheek
sensory level is most caudal, intact dermatome for both light touch and pin prick (sharp/dull discrimination) sensation. The sensory level is determined by performing an examination of the key sensory points within each of the 28 dermatomes on each side of the body, as above, and may be different for the right and left side
max score 56 for each modality or 112 overall, can be used to track recovery
each motor level scored with normal power grading of 10 Paired Myotomes C5 - T1 and L2 - S1
Motor Level is defined by the lowest key muscle function that has a grade of at least 3 (on supine testing), providing the key muscle functions represented by segments above that level are judged to be intact (graded as a 5)
Max of 25 for each extremity so 50 for upper limbs and 50 for lower limbs (should consider separately)
Grade A: No Sensory or Motor Function is preserved in the Sacral Segments S4-S5
Grade B: Sensory but not Motor Function is preserved below the neurological level and includes the Sacral Segments S4-S5
Grade C: Motor Function is preserved below the Neurological Level AND More than half of key muscle functions below the Neurological Level of Injury have a muscle grade less than 3
Grade D: Motor function is preserved below the neurological level AND At least half (half or more) of key muscle functions below the NLI have a muscle grade ≥ 3
Grade E: Normal if had prev deficits (no AIS grade given if no SCI)
Incomplete further subclassified:
Brown-Sequard Syndrome
Anterior Cord Syndrome
Posterior Cord Syndrome
Conus Medullaris Syndrome
Cauda Equina Syndrome
discitis
infection of intervertebral disc space
relatively scarce blood supply to this region compared to the vertebra themselves makes it difficult both for infection to reach the area but also to then treat infection here
frequency of discitis is more common in pediatric patients than in the adult population, which is thought to be due to the vascular supply of the intervertebral discs, which diminish later in life: in kids the blood vessels extend from the cartilaginous endplates into the nucleus pulposus, whereas in adults these vascular supplies degenerate, and only extend into the annulus fibrosis
back pain, refusal to walk, even abdo pain in younger kids; in adults back pain, fever, anorexia, neurological sx rare but poss; pain normally localises to the disc without radiation, and will have point tenderness; commonest in lumbar region
blood cultures, MRI, biopsy for histology and culture; treat with abx for 4-6 weeks (so PICC line needed)
epidural abscess
infection within the epidural space anywhere in the brain or spinal cord; part of collection of disease with vertebral OM and discitis
Acute SEA is usually less than 2 weeks in duration with fever and signs of systemic inflammation from a hematogenous source. This is in contrast with subtle, afebrile, and long-standing chronic SEA that has resulted from a direct extension of vertebral osteomyelitis. Both present with back and radicular pain, but leukocytosis (in serum and CSF) is more likely in the acute form and not so much in the chronic form
intracerebral form 9x rarer than spinal, and 3rd commonest purulent intracerebral disease after brain abscess and subdural empyema; was historically a result of head and neck infections such as sinusitis, mastoiditis, and otitis; but nowadays is mostly a complication of neurosurgical procedures
early symptoms of backache may be indolent and persist for weeks; severe back pain usually progresses to root pain within 3 to 4 days. This pain is followed by advanced signs of spinal cord dysfunction within the next 4 to 5 days. The neurologic deficits at this stage are often still reversible; yet, rapid surgical intervention may be needed; Most patients will also develop fevers above 38 C. Other nonspecific findings may also be present such as generalized malaise, fatigue, headaches, irritability, or vomiting
progression of neurologic deterioration to severe spinal cord dysfunction can occur in a matter of just a few hours, making the diagnosis and treatment imperative; neurological deficit can become permanent
blood cultures, CT or MRI, and all abscess needs neurosurg discussion; may need CT guided aspiration to decompress or else surgery; abx for 4-6 weeks, 6-8 if also osteomyelitis
get imaging within 6 hrs for sure if neuro signs, otherwise just as quickly as possible; MRI with and without contrast of the complete spine is the preferred imaging study; CT myelogram if MRI contra’d, if not possible then CT with contrast
abx for this, vertebral osteomyelitis, or discitis hold off until biopsy if haem stable and no neuro sx otherwise start broad spectrum immediately
caffey disease - what it is, when seen, what looks like on imaging, mx, 2 dd)
aka infantile cortical hyperostosis, usually seen in first year of life
tender swelling of flat bones like mandible and tubular bones like radius/ulna; intense periosteal reaction on x-ray due to inflam
mx may need steroids, and can be mistaken for osteomyelitis or healing fractures after physical abuse
the hip (3 acquired dislocation causes, OA presentation x5, advice to pt x3)
acquired dislocation: usually either pyogenic (septic) arthritis, muscle imbalance (cerebral palsy, polio etc), or trauma
hip OA: pain oft in groin radiating down to knee, starting off after activity but may become constant and disturb sleep; stiffness inc over time, leg held in adduction so appears short, trendelenburg sign pos eventually; lose weight, keep active but try to reduce eg uphill walking, carrying heavy things etc
hip capsule boundaries, blood supply inc perthes diseases and when that blood supply less relevant, #nof categorisation x5 plus garden system and mx types x4
NOFs can be split into intra and extra capsular; intracapsular may be head, subcapital (most common), transcervical, basicervical
hip capsule boundaries: capsule of the hip joint attaches to the edge of the acetabulum proximally. Distally, it attaches to the intertrochanteric line anteriorly and the femoral neck posteriorly (so more proximal on the posterior aspect)
Most of the femoral head blood supply is done by the extracapsular arterial ring, which is formed by the lateral femoral circumflex and the medial femoral circumflex arteries, both of which arise from the profunda femoris artery; thus, intracapsular fractures will disrupt the blood supply causing osteonecrosis of the head, and so the joint is replaced; THR is preferred, unless poor functional status or v old in which case hemiarthroplasty is done
in children the artery running in the ligamentum teres of the hip supplies blood and if disrupted leads to perthes disease of the hip; after 8 years of age the MFCA is most important with negligible flow through ligamentum teres artery and LFCA
subcapital fractured NOFs are further classified using the garden system: stage 1 is undisplaced incomplete, stage 2 is undisplaced complete (both of these stages can have internal fixation), then stage 3 is complete fracture incompletely displaced and stage 4 is complete fracture completely displaced
extracapsular tend to be intertrochanteric or subtrochanteric
displaced subcapital get arthroplasty; non-dsiplaced intracapsular get cannulated hip screws; inter-trochanteric and basicervical get dynamic hip screws or short IM nail; subtrochanteric get IM nail
fascia iliac block (FIB) - commonly used after what, 3 nerves you block, what if catheter puller out
commonly used for #NOF fracture, after regular paracetamol and opioids used (as tolerated/not contraindicated)
idea is to give large volume of LA under fascia iliaca to block femoral nerve, lateral femoral cutaneous nerve, and obturator nerve (last one oft only partially blocked); rather than injecting, you can insert a catheter to the nerve site allowing for infusion of LA (eg bupivicaine) - note if pt pulls this out can try and control pain using conventional analgesia, and only bleep anaesthetics to replace if this is not successful
local anaesthetics - admin routes, pKa and potency including effect of pH of LA solution vs body, bind to what channel and how, use-dep block, differential block, bupivacaine vs lidocaine
numerous possible routes of administration (IV, IM, SC, topical, neb, etc)
pKa determines their lipid solubility, which in turn determines potency; at physiological pH they become more lipid soluble which allows them to penetrate the cell and bind to the intracellular part of the voltage-gated sodium channel, which is their site of action; this is bc the LA solution will be pH 5-6 so more water soluble, then enters body and this solution buffered to physiological pH of 7.35-7.45
preferentially bind to the channel in its open state, stabilising it in the inactive state which gives rise to use-dependent block, where repeated stimulation of the axon makes more open channels available, and increases the blockade effect; preferentially affect pain and temperature fibres (“Differential block”), possible because they are largely unmyelinated (C-fibres) but experiments are inconclusive
bupivacaine is common long acting, with slower time of onset and longer half life, where lidocaine has faster onset and shorter half life being a common short acting LA
local anaesthetic toxicity - toxic dose for lido and bupi, affect if co-admin with adr, 8 neuro sx, 5 cardio sx, mx how inc bolus and infusion dose (and adjustment if BP doesn’t respond)
lidocaine toxic dose is 4.5mg/kg; bupivacaine is 2.5mg/kg; note if given with adrenaline then max dose is higher as the vasoconstriction slows systemic redistribution allowing more to be excreted while more is absorbing
inhibitory neuronal activity is preferentially suppressed first by systemic local anaesthetics; initially see perioral paraesthesia and visual disturbances, light headedness and tinnitus, then shivering, twitching/tremors, slurred speech, and GTC seizures
CNS is more sensitive than CVS, but with large doses may see bradycardia, short QTc, depressed contractility, hypotension and cardiac arrest
give lipid infusion to treat, as this will bind the lipophillic LA and as plasma conc falls this will pull more from the affected organs, then the lipid and LA will be metabolised in the liver
give intralipid bolus 1.5 mL/kg then continuous infusion 0.25ml/kg/min (double if BP remains low)
perthe’s disease of hip (4 sx, ix, 3x normal mx and 2 if older or more severe, what age has better outcomes), DDH (how often girls, what incs risk, 2 tests, 2 things might see in 3-6mo, how older children might present; imaging x2, how to brace inc age cutoff, what if not responding or above this cut off; major risk)
perthe’s disease - limp, often pain in hip and groin, sometimes referred to thigh/knee; affected leg may be shorter; worsen over weeks, hip stiffens and muscles weaken; hip joint regrows and remodels but can take 2 years or so, and incs risk of OA; hip examination and x ray; observation, physio, basic analgesia; crutches may be needed if bad; surgery maybe if badly affected or older children; younger the child, better the outcome
ddh - 80% cases in girls; breech presentation incs risk; ortolani and barlow tests; if 3-6mo then asym abduction and galeazzi sign; older children may have painless limp or walk on toes of affected side; uss in under 4.5mo may help, x rays after that as femoral epiphysis ossified by then (4-6mo); most stabilise by 2-6weeks of age, if dont then bracing if under 6mo; ideally dynamic harness, can start up to 4.5-6mo but best before 6 weeks; if not respond or older than 6mo then surgery; surg comes with risk of avn
DDH - how common, 7 risk factors, which hip more commonly affected, 3 groups who need US screening and screening for everyone else, 2 main screening tests and 3 other factors, which imaging to use (+ what is disrupted), spont stabilisation, pavlik harness vs surgery
affects around 1-3% of newborns.
Risk factors
female sex: 6 times greater risk
breech presentation
positive family history
firstborn children
oligohydramnios
birth weight > 5 kg
congenital calcaneovalgus foot deformity
DDH is slightly more common in the left hip. Around 20% of cases are bilateral.
Screening for DDH
the following infants require a routine ultrasound examination
first-degree family history of hip problems in early life
breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery
multiple pregnancy
all infants are screened at both the newborn check and also the six-week baby check using the Barlow and Ortolani tests
Clinical examination
Barlow test: attempts to dislocate an articulated femoral head
Ortolani test: attempts to relocate a dislocated femoral head
other important factors include:
symmetry of leg length
level of knees when hips and knees are bilaterally flexed - galeazzi sign
restricted abduction of the hip in flexion
Imaging
ultrasound is generally used to confirm the diagnosis if clinically suspected
however, if the infant is > 4.5 months then x-ray is the first line investigation - you can see interruption of shentons line (imaginary line following superior pubic ramus down inferomedial nof - also disrupted in #nof)
All breech babies at or after 36 weeks gestation require USS for DDH screening at 6 weeks regardless of mode of delivery
Management
most unstable hips will spontaneously stabilise by 3-6 weeks of age
Pavlik harness (dynamic flexion-abduction orthosis) in children younger than 4-5 months
older children may require surgery
perthes catterall staging (1-4), mx x3, prognosis
Stage
Features
Stage 1
Clinical and histological features only
Stage 2
Sclerosis with or without cystic changes and preservation of the articular surface
Stage 3
Loss of structural integrity of the femoral head
Stage 4
Loss of acetabular integrity
Management
To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities <6yo eg fracture or joint collapse
Prognosis
Most cases will resolve with conservative management
femoroacetabular impingement what it is x2 forms, pt usual age and sx x2, leads to what, ix to diagnose
femoral head and acetabulum dont fit together properly (socket too deep/retroverted so head rubs on its ant edge, or head/neck junction too thick so neck jams against ant acet)
pt usually in 30s/40s, complains of pain in groin esp after activity, hip movements may be restricted or provoke pain
leads to damage/degen of joint cartilage and is big cause of OA
MRI needed to diagnose
mx of perthes disease (x2, how long healing takes, later complication) and SUFE (mild vs large mx)
perthe - containment of femoral head w abduction bracing, maybe osteotomy; healing can take upto 2 years; may get OA later
SUFE - consider an emergency, epiphysiodesis if mild slip and open reduction + fixation or osteotomy for larger slips; child needs to be kept non weight bearing in mean time, give analgesia, and obtain AP and frog leg XR views
Increased risk in adolescence because:
-the perichondrial ring thins and weakens
-physis is still vertical in this age group (160° at birth to 125° at skeletal maturity), which results in increased shearing forces
-the epiphyseal tubercle can provide a rotational pivot point - this structure shrinks with skeletal maturity
ASIS avulsion
traumatic avulsion of the ASIS due to a sudden and forceful contraction of the sartorius and tensor fascia lata that occurs in young athletes
occurs during hip extension (sprinting or swinging a baseball bat)
athlete will often report a pop or snap at the time of injury
may complain of weakness
may be confused or misdiagnosed as an acute muscle strain
may see weakness to hip flexion and knee extension
severe injuries may result in a limp
XR will generally show unless non-displaced, in which case CT/MRI might be needed after ortho discussion
rest, protected weight bearing with crutches and routine/VFC follow up
if >3cm displacement will need ORIF
AIIS avulsion is also possible, usually as hip extends and knee is flexed eg in kicking sports, also seen in adolescents; conservative mx with hip rest in flexion then protected weight bearing
another ddx is adductor strain:
a result of forceful hip extension & external rotation of an abducted leg, usually in sports and esp football and hockey
pain is immediate and severe in the groin region with tenderness is at the site of injury along the subcutaneous border of the pubic ramus and pain and/or decreased strength with resisted leg adduction compared to the other leg
XR won’t show anything unless avulsion injury also present but useful to rule those out
MRI can confirm
generally rest, ice, protected weight bearing
transient synovitis - usual age range and joint affecting, what often see in history, how pain presents, differentiating from septic arth x5 and ix to tell, natural course of illness (inc 2x common mx) and a possible dd inc how many are that
commonest cause of limp in children, usually between age 2-12yo, often after URTI, affects hip
sudden onset of limp + pain (may refer to knee), child may not be weight bearing; no local inflam signs; septic arth more painful and immobile vs reduced movements in transient synovitis; may be tender to palpation anteriorly, esr and wcc usually normal or only mildly elevated vs septic arth; may be fluid in joint space but less than in SA, but aspirate if you’re not sure - may be cloudy but not pustulent
usually improves in couple of weeks with bed rest, analgesics; 6% of cases turn out to actually be perthes
pelvis fracture (how common in polytrauma, 2 things that may bleed inc how commonly second is found in ppl, 5 other structures in danger, 3 consequences of damage to membranous urethra)
20% of polytrauma cases esp older ppl (may be non-traumatic in them too) and younger ppl (think motorbikes, falls etc); generally high energy with multiple other injuries to thorax, long bones, spine, intracranial etc
presacral venous plexus sits in pelvic fascia ant to sacrum and may bleed heavily in these fractures
corona mortis common variant anastomosis between ext iliac/deep inf epigastric and obturator, post to sup pubic ramus and so also vulnerable to injury and bleeding (is found in 1/3 ppl)
ext/int iliac arteries potentially in danger too, and lumbar/sacral plexi
membranous urethra in men may be torn as prostate forced back but mem urethra fixed so tears - bleeds and haematoma may cause retention, later incontinence and sexual dysfunction
chondromalacia patellae (what it is, common in who, how presents, mx), osgood-schlatter (what it is, common in who, how presents), osteochondritis dissecans (how it presents x2), patellar subluxation (sx x2), patellar tendonitis (common in who, how presents x2)
Chondromalacia patellae
Softening of the cartilage of the patella
Common in teenage girls
Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
Usually responds to physiotherapy
Osgood-Schlatter disease
(tibial apophysitis)
Seen in sporty teenagers
Pain, tenderness and swelling over the tibial tubercle; generally clinically diagnosed if atraumatic, localised to tubercle, knee exam otherwise normal, settles with rest and at night, and systemically well; settles over weeks-months (para/NSAIDs and ice pack in meantime + continue but modify exercise); if not settling refer to PT, if unsure of diagnosis refer to T&O
Osteochondritis dissecans
Pain after exercise
Intermittent swelling and locking
Patellar subluxation
Medial knee pain due to lateral subluxation of the patella
Knee may give way
Patellar tendonitis
More common in athletic teenage boys
Chronic anterior knee pain that worsens after running
Tender below the patella on examination
the knee (timing of haemarthrosis vs reactive synovitis and ix that can help tell difference, 4 other dd for acute painful swelling, chronic swelling x3 dd; 3 common swellings in pop fossa inc causes of bakers cyst and what happens if bursts, RA knee signs x4, OA knee signs x6)
acute swelling: reactive synovitis dev within hours of mod severe injury eg lig/men tear, swelling immediately after means haemarthrosis with painful warm knee (x ray to see if fracture, if not suspect lig damage), also non traum haemarth from clotting disorder, may also be acute septic arthritis (systemic symptoms too, aspirate pus from joint and send for culture before drainage and iv antibiotics); acute swelling without sign of infection nor trauma may be gout or pseudogout, also reactive arthritis is poss after urogen/GI infection
chronic swelling: OA and RA most common reasons, TB is poss, rarer causes too
swellings not involving joint: pre/infapat bursitis, pop/bakers cyst or aneurysm (pop cyst most commonly caused by RA or OA as post capsule bulges and synovium herniates, cyst may rupture causing painful swollen calf (rule out DVT, it is self resolving with time, elevation, analgesia)
RA causes chronic swelling of knee, wasting of quad, restricted movements and valgus deformity
OA causes joint to be stiff after rest and hurt to get going again, giving way and locking may occur, quad wasting and varus deform (usually), no fluid or warmth but crepitus present
knee effusion
septic arth, lyme, syphilis, TB, crystal, reactive arth, IBD, osteoarth flare, autoimmune, injury (fracture, ligament)
get XR: AP, lateral +/- axial views
bloods: looking mainly at inflam markers but also check urate and calcium levels; consider ASOT, lyme serology, RPR for syphilis, and consider autoimmune screen
Arthrocentesis and subsequent synovial fluid analysis should be done in all cases of unexplained knee effusion; may show crystals, raised white cells, culture or gram stain bugs, blood if haemarthrosis, fat drops if fracture
saline load test may be utilized to determine if a wound near a joint communicates with the joint. In the knee, 155 mL of saline is needed
colchicine/NSAID + ice pack; brace and hot knee clinic if ligament injury, rheum referral if suspect autoimmune; abx for septic arthritis + T&O for washout
locked knee and pseudolocking
locked knee: mechanical block preventing knee fully extending
pseudolocking: appears locked but due to pain meaning pt holds knee in place
most common cause of a locked knee is a tear in the cartilage that cushions the knee joint, or loose body from a fracture or arthritis damage, or from remnants of surgery; pseudolocking may be caused by anything that makes the knee painful or due to patella dislocation/maltracking
a true locked knee may require MRI to find the cause and surgery to remove/fix it
patella dislocation (motion that causes, what pt may feel x2, how it might look x2, chance of rec dislocation, 5 things that inc risk and if high risk what sign you might see, what else might be damaged commonly)
sudden quad contraction while knee valgus and extern rotated, commonly when runner dodges to one side;
may feel tearing sensation and like knee has gone out of joint, may collapse; patella may spring back, or remain displaced (it is lateral and hard to see, but med fem condyle is prominent)
can push it back in, 15-20% chance of rec dislocation;
risk higher if patella alta, general lax joint, marked valgus knee, flat lat condyle, small patella - in these risky cases initial dislocate may not have obvious trauma behind it; but pos apprehension test
often medial part of patellofemoral lig may tear too, repair doesnt seem to help reduce odds of it happening again
ACL injury
ACL tear typically occurs in an athlete with a history of twisting the knee whilst weight-bearing.
The majority of ACL injuries occur without contact and result from a sudden change of direction twisting the flexed knee. The patient is usually unable to weight bear.
An ACL tear will typically present with a rapid joint swelling* and significant pain. If the presentation is delayed, instability may also be evident, in which the patient describes the leg ‘giving way’.
A plain film radiograph of the knee (AP and lateral) should be taken to exclude bony injuries, any joint effusion, or a lipohaemarthrosis present. A Segond fracture (bony avulsion of the lateral proximal tibia) is pathognomic of ACL injury.
An MRI scan of the knee is gold-standard to confirm the diagnosis (>90% sensitivity), also picking up any associated meniscal tears*
*50% of ACL tears will also have a meniscal tear, with the medial meniscus the more commonly affected
RICE, then
Conservative treatment involves rehabilitation, which utilises strength training of the quadriceps to stabilise the knee
In the emergency setting, inpatient admission is rarely required; the patient can often partially weight bear and a cricket pad knee splint can be applied for comfort.
Surgical reconstruction of the ACL involves the use of a tendon or an artificial graft
This is not performed acutely but following a period of ‘prehabilitation’, whereby the patient will engage with a physiotherapist for a period of months prior to the surgery
Acute surgical repair of the ACL is possible in some cases dependent on the location of the tear within the ligament
If the imaging on MRI is favourable, the patient can be further assessed under GA knee arthroscopy, proceeding to an acute repair where possible
Post-traumatic osteoarthritis is a well-established complication of both ACL injury and ACL reconstructive surgery.
tibial plateau fracture
most commonly fractures following high-energy trauma, such as a fall from height or a road traffic accident, from the impaction of the femoral condyle onto the tibial plateau. Less commonly they can occur in elderly patients following a fall, especially those with osteoporosis.
It is typically a varus-deforming force, meaning that the lateral tibial plateau is more frequently fractured than the medial side. They are often found alongside other bony and soft tissue injuries, such as meniscal tears or cruciate or collateral ligament injury.
It is important to recognise that this is a significant injury, as there is disruption of the congruence of the articular surface that, if left, will lead to rapid degenerative change within the knee
Patients will present with sudden onset pain in the affected knee, being unable to weight-bear, and swelling of the knee*.
On examination, significant swelling will be evident, alongside tenderness over the medial or lateral aspects of the proximal tibia, with potential ligament instability (albeit not clinically assessed initially, due to the pain it would cause).
Ensure to check peripheral neurovascular status of the patient, as neurovascular injuries (such as popliteal vessel dissection or common fibular nerve damage) are an important association of high grade injuries.
For patients presenting with knee pain following trauma, other differentials to consider are knee dislocation, other knee fractures (including patella or distal femur), meniscal injuries, ligamentous injuries, patella dislocation, or patella/quadriceps tendon rupture
first line investigation for a suspected plateau fracture is plain film radiographs (anteroposterior and lateral), often features on radiograph are subtle. There will also be a lipohaemarthrosis present.
CT scanning is needed in almost all cases, apart from undisplaced fractures
can be classified through the Schatzker Classification
Non-operative management can be trialled in uncomplicated tibial plateau fractures (including no evidence of ligamentous damage, tibial subluxation, or articular step <2mm)
These can typically be treated with a hinged knee brace and non- or partial-weight bearing for around 8-12 weeks, alongside ongoing physiotherapy and suitable analgesia
Operative management is typically warranted in complicated tibial plateau fractures*, or any evidence of open fracture or compartment syndrome. Any form of medial tibial plateau fractures may also require surgical intervention, even if undisplaced, as they have a great potential for displacement.
Open reduction and internal fixation (ORIF) is the mainstay of most tibial plateau fractures, with the aim to restore the joint surface congruence and ensure joint stability
Postoperatively, a hinged knee brace is fitted with early passive range of movement but limited or non-weight bearing for around 8-12 weeks months is typically required.
External fixation with delayed definitive surgery is indicated in cases of significant soft tissue injury, polytrauma and highly comminuted fractures where an immediate ORIF may not be suitable
main long-term complication following a tibial plateau fracture is post-traumatic osteoarthritis to the affected joint
meniscal tears of knee
menisci rest on the tibial plateau and have two main functions (1) shock-absorbers of the knee joint (2) increase articulating surface area.
The medial meniscus is less circular than the lateral and is attached to the medial collateral ligament, whilst the lateral meniscus is not attached to the lateral collateral ligament
most common causes for meniscal tears are trauma-related injury and degenerative disease (the latter more common in older patients).
In traumatic tears, the mechanism typically involves a young patient who has twisted their knee whilst it is flexed and weight-bearing, with the onset of symptoms following soon after
Patients often report a ‘tearing’ sensation in their knee, associated with an intense sudden-onset pain. The knee invariably swells slowly subsequently over a period of 6-12 hours.
In cases where the meniscal tear results in a free body within the knee (typically the bucket-handle type), it may be locked in flexion and unable to extend.
On examination, there is a joint line tenderness, significant joint effusion, and limited knee flexion
x-ray and MRI
immediate management of an acutely swollen knee is for rest and elevation with compression and ice. Most small (<1cm) meniscal tears will initially swell however the pain will subside over the next few days as the tear heals.
For larger tears or those remaining symptomatic, arthroscopic surgery is indicated:
If the tear is in the outer third of the meniscus (where it has a rich vascular supply), then the tear can often be repaired using sutures
If the tear is in the inner third, then the tear is usually trimmed to reduce locking symptoms (and middle third tears may either be repaired or trimmed)
meniscal tear is a risk factor for developing secondary osteoarthritis.
Knee arthroscopy carries a risk of deep vein thrombosis and damage to local structures, such as the saphenous nerve and vein, the peroneal nerve, and the popliteal vessels.
medial collateral lig injury
medial collateral ligament (MCL) is the most commonly injured ligament of the knee*.
The MCL primary function is to act as a valgus stabiliser of the knee and is most often injured when external rotational forces are applied to the lateral knee, such as a impact to the outside of the knee.
MCL injuries can be graded from one to three:
Grade I – mild injury, with minimally torn fibres and no loss of MCL integrity
Grade II – moderate injury, with an incomplete tear and increased laxity of the MCL
Grade III – severe injury, with a complete tear and gross laxity of the MCL
patient may report hearing a ‘pop’ with immediate medial joint line pain. Swelling tends to follow after a few hours (unless there is an associated haemarthrosis, in which case it will occur within minutes).
The main clinical finding on examination will be increased laxity when testing the MCL*, via the valgus stress test. The patient will be extremely tender along the medial joint line, but may be able to weight bear.
*A Grade II and III tear can be distinguished clinically on medial stress testing; Grade II is lax in 30 degrees of knee flexion but solid in full extension, whereas Grade III is lax in both these positions.
Any patient following trauma with significant knee pain and swelling should have a plain film radiograph to exclude any fracture.
The gold-standard investigation to confirm the diagnosis for an MCL tear is via MRI scanning
management of an MCL injury is dependent on the grade of injury:
Grade I Injury: Rest, Ice, Compression, and Elevation (RICE) with analgesia (typically NSAIDs) as the mainstay. Strength training as tolerated should be incorporated, with an aim to return to full exercise within around 6 weeks.
Grade II Injury: Analgesia with a knee brace and weight-bearing/strength training as tolerated. Patients should aim to be able to return to full exercise within around 10 weeks
Grade III Injury: Analgesia with a knee brace and crutches, however any associated distal avulsion then surgery is considered. Patients should aim to be able to return to full exercise within around 12 weeks
main complications following a MCL tear are instability in the joint and damage to the saphenous nerve
