Learn — Musculoskeletal & orthopaedics

13 notes · 28 questions on the topic

Osteomyelitis

Osteomyelitis is infection of bone and its marrow cavity, reaching it through the blood stream, by spread from adjacent infected tissue, or by direct inoculation through an open fracture, a penetrating wound or an operation. It matters because pus under pressure inside a rigid bone strips the periosteum and thromboses the nutrient vessels, so treatment that starts late or stops early leaves dead bone that antibiotics cannot reach and the disease becomes chronic and relapsing.

Staphylococcus aureus, including MRSA, is the commonest organism at every age; sickle-cell disease adds Salmonella, the neonate adds group B streptococcus and Gram-negative bacilli, a nail through a shoe adds Pseudomonas, and a chronic spinal or metaphyseal lesion in India raises the question of tuberculosis.
Acute haematogenous osteomyelitis is a disease of children and lodges in the metaphysis of a long bone — lower femur and upper tibia most often — where the blood flow is sluggish; in adults the vertebral body is the usual site, and diabetes or peripheral vascular disease gives the foot.
Presentation is fever, malaise, severe localised bone pain and exquisite tenderness, refusal to use the limb (pseudoparalysis in an infant) and a limp; the plain X-ray is normal for the first 10 to 14 days, so a normal film never excludes the diagnosis and MRI is the sensitive early test.
Investigations: two sets of blood cultures before the first antibiotic dose, C-reactive protein (the best marker of response, falling within a week of effective treatment), ESR, full blood count, and aspiration or bone biopsy for culture and sensitivity where the diagnosis or the organism is uncertain.
The pathology follows a sequence that explains the treatment: inflammation, suppuration, sequestrum (a piece of dead bone), involucrum (new bone laid down around it), then cloaca and a discharging sinus — once a sequestrum exists, surgery is required because antibiotics do not penetrate dead bone.
Treatment is high-dose intravenous anti-staphylococcal antibiotics started immediately after cultures — cloxacillin or flucloxacillin, with vancomycin or clindamycin where MRSA is likely — then narrowed on sensitivities, for a total course of about 4 to 6 weeks with a switch to oral once the fever has settled and the C-reactive protein is falling; surgical drainage is indicated for an abscess, for failure to improve within 24 to 48 hours, and for a sequestrum.
Nursing: splint and elevate the limb both for pain relief and to prevent pathological fracture, handle it gently supporting the joints above and below, chart temperature and pain, protect the long line on which a six-week course depends, and give analgesia before dressings and physiotherapy.
Complications: septic arthritis (especially of the hip in infants, where the metaphysis is inside the joint capsule), growth-plate damage with limb shortening or deformity, pathological fracture, chronic osteomyelitis with sinuses, and rarely amyloidosis or squamous carcinoma in a long-standing sinus.

Rickets

Rickets is defective mineralisation of the growth plate and of newly formed osteoid in a growing child, almost always from deficiency of vitamin D, calcium or phosphate, so the softened bone bends and deforms under load. It matters to the surgical team because the deformities it leaves — bow legs, knock knees, coxa vara and a contracted pelvis — are what reach the orthopaedic clinic, and because the same child can arrive acutely with hypocalcaemic convulsions or a fracture after trivial injury.

Nutritional vitamin D deficiency is the usual cause in India — prolonged exclusive breastfeeding without supplementation, dark skin, covered clothing or little sun exposure, and a mother who was deficient in pregnancy; other causes are dietary calcium deficiency, vitamin D-dependent rickets from enzyme or receptor defects, and X-linked hypophosphataemic rickets, which wastes phosphate and does not respond to vitamin D alone.
The signs follow whichever bone is growing fastest at the time of onset: craniotabes and a late-closing anterior fontanelle (normally closed by 18 months) in infancy, frontal bossing, a rachitic rosary at the costochondral junctions, Harrison's sulcus, widened wrists and ankles, and bow legs (genu varum) or knock knees once the child begins to walk.
Non-skeletal features are delayed motor milestones and delayed dentition, hypotonia with a protuberant abdomen, growth failure, and hypocalcaemic tetany, carpopedal spasm, stridor or convulsions in the infant.
Biochemistry: calcium normal or low, phosphate low, alkaline phosphatase high (the most consistent abnormality and the best marker of healing), 25-hydroxyvitamin D low and parathyroid hormone raised in the nutritional form; the wrist X-ray shows cupping, splaying and fraying of the metaphysis with a widened growth plate.
Treatment is vitamin D3 with calcium: the Global Consensus and Indian Academy of Pediatrics regimens give daily oral vitamin D (2000 IU under 12 months, 3000 to 6000 IU in older children) for at least 12 weeks, or the widely used Indian schedule of 60,000 IU orally once a week for about 6 weeks, always with elemental calcium of at least 500 mg a day, followed by a maintenance dose of 400 IU daily in infancy and 600 IU thereafter.
Healing is confirmed by a dense mineralisation line at the metaphysis on X-ray and a falling alkaline phosphatase; deformity that persists 2 years after biochemical cure, or that is severe, is the deformity that needs osteotomy or guided growth surgery rather than more vitamin D.
Prevention is 400 IU of vitamin D daily for every infant, safe sun exposure, and supplementation of pregnant and lactating women — the single change that removes the disease from a family.
Never give calcium as a rapid intravenous push for tetany: 10% calcium gluconate is diluted and given slowly with cardiac monitoring, watching the pulse for bradycardia and the cannula site for extravasation, which causes tissue necrosis.

Osteomalacia

Osteomalacia is the adult counterpart of rickets: a normal amount of osteoid is laid down but fails to mineralise once the growth plates have fused, so the bone is soft rather than merely thin. It matters because it presents as vague bone pain with proximal weakness that is easily dismissed as arthritis or ageing, and because soft bone fractures after trivial injury and holds internal fixation poorly.

Causes are vitamin D deficiency from lack of sunlight, dark or covered skin and poor intake; malabsorption after gastrectomy or bariatric surgery, in coeliac disease and chronic pancreatitis; chronic kidney disease, where 1-alpha-hydroxylation fails; enzyme-inducing anticonvulsants such as phenytoin and phenobarbitone; and phosphate-wasting states including tumour-induced osteomalacia.
Symptoms are diffuse aching bone pain and tenderness over the pelvis, ribs and spine, and a proximal myopathy with a waddling gait and difficulty rising from a chair or climbing stairs — the weakness is what separates it clinically from osteoporosis.
Biochemistry: calcium and phosphate low or low-normal, alkaline phosphatase raised, 25-hydroxyvitamin D low, and parathyroid hormone raised as secondary hyperparathyroidism.
Radiology: generalised loss of density with indistinct trabeculae, and Looser's zones (pseudofractures) — transverse translucent bands on the concave side of the femoral neck, pubic rami, ribs and lateral border of the scapula; severe long-standing disease gives protrusio acetabuli and a triradiate pelvis.
Treatment is vitamin D3 with calcium — in deficiency, 60,000 IU orally once a week for 6 to 8 weeks and then a maintenance dose, with about 1000 mg of elemental calcium daily; malabsorption needs larger or parenteral doses and renal disease needs an activated analogue such as calcitriol or alfacalcidol, because the failing kidney cannot hydroxylate ordinary vitamin D.
Distinguish it from osteoporosis: in osteomalacia the bone is soft with abnormal biochemistry and it hurts; in osteoporosis the bone mass is low, calcium, phosphate and alkaline phosphatase are normal, and there is no pain until something breaks.
Nursing: fall prevention from the day of diagnosis (lighting, footwear, removing loose mats, hip protectors, a walking aid), graded exercise for the proximal myopathy, and teaching that calcium is taken apart from iron and levothyroxine because it blocks their absorption.

Fractures and healing

A fracture is a break in the structural continuity of bone, complete or incomplete, and it always injures the surrounding soft tissue — periosteum, muscle, vessels and nerves — as well as the bone itself. It matters perioperatively because the first assessment is of the limb's circulation, sensation and skin cover rather than the X-ray, and because the complications that kill or cripple — haemorrhage, compartment syndrome, fat embolism and infection of an open fracture — all declare themselves in the first hours and days.

Describe every fracture the same way: which bone, which part (proximal, shaft or distal), the pattern (transverse, oblique, spiral, comminuted, segmental, impacted, avulsion, and greenstick or buckle in children), the displacement, angulation and rotation, and whether it is closed or open.
Open (compound) fractures are graded by the Gustilo–Anderson classification from type I to type III: photograph the wound once, cover it with a saline-soaked sterile dressing, splint the limb, give intravenous antibiotics as early as possible and ideally within an hour of injury, check tetanus immunisation status, and arrange formal debridement and irrigation in theatre — early antibiotics and a proper debridement matter more than the old arbitrary six-hour rule.
Secondary (callus) healing runs in four overlapping stages: haematoma and inflammation over the first days, soft fibrocartilaginous callus at about 2 to 3 weeks, hard bony callus at roughly 6 to 12 weeks, and remodelling over months to years; rigid compression fixation with a plate heals by primary (direct) union with no visible callus on the X-ray.
Rough union times: upper limb about 6 to 8 weeks, lower limb about 12 to 16 weeks, and children roughly half the adult time. Delayed union, non-union with a false joint and abnormal movement, and malunion follow infection, inadequate immobilisation, distraction of the fragments, poor blood supply and smoking.
Treatment is the four Rs — resuscitate, reduce (closed or open), retain (cast, traction, external fixator, plate and screws, or intramedullary nail) and rehabilitate; a cast is never applied circumferentially over an acutely swelling limb, and every plastered limb is checked for the five Ps: pain, pallor, paraesthesia, paralysis and pulselessness.
Compartment syndrome is the ward emergency: pain out of proportion to the injury and pain on passive stretch of the muscles are the early signs, while pulselessness and paralysis are late and mean the muscle is already dying. Split the cast and all dressings down to skin, keep the limb at heart level rather than elevated, and call the surgeon for fasciotomy.
Fat embolism syndrome appears 24 to 72 hours after a long-bone or pelvic fracture with hypoxia and breathlessness, confusion or restlessness, fever, tachycardia and a petechial rash over the chest, axillae and conjunctivae; treatment is supportive with oxygen and ventilation, and prevention is early fixation and good resuscitation.
Blood loss to expect at the trauma call: about 750 mL into a closed humerus or tibia, 1000 to 1500 mL into a femur, and 2000 mL or more into a pelvic fracture — which is why a hypotensive patient with a femoral fracture is resuscitated before being sent for imaging.
Nursing after fixation: neurovascular observations of the limb hourly at first, elevation to control swelling, analgesia given before physiotherapy, pin-site care for an external fixator, thromboprophylaxis, early mobilisation, and cast advice on discharge — keep it dry, never push anything inside to scratch, and return for increasing pain, numbness, discolouration, a bad smell or a loose cast.

Rheumatic fever

Acute rheumatic fever is a delayed, immune-mediated inflammatory illness that follows a group A streptococcal throat infection after a latent period of about 2 to 4 weeks, affecting the joints, heart, skin, subcutaneous tissue and brain. It matters in India because it is still the commonest cause of acquired heart disease in children and young adults, and because carditis is the only feature that leaves permanent damage, in the form of rheumatic valve disease years later.

It follows streptococcal pharyngitis, never streptococcal skin infection, and peaks between 5 and 15 years of age; treating a sore throat with penicillin within about 9 days of onset prevents the first attack, which is the whole basis of primary prevention.
A first episode is diagnosed by the revised Jones criteria as two major criteria, or one major plus two minor criteria, together with evidence of a preceding streptococcal infection such as a rising or raised ASO titre or a positive throat culture or rapid antigen test; a recurrence may also be diagnosed on three minor criteria with that evidence.
Major criteria are carditis (clinical or subclinical on echocardiography), arthritis, chorea, erythema marginatum and subcutaneous nodules; minor criteria are fever, arthralgia, a raised ESR or CRP and a prolonged PR interval on the ECG.
The revised criteria are stratified by population risk, and India is treated as a moderate-to-high-risk population, so monoarthritis and polyarthralgia count as the major arthritis criterion and monoarthralgia counts as a minor criterion, thresholds that would not apply in a low-risk population.
The arthritis is migratory, involves large joints such as knees, ankles, elbows and wrists, is exquisitely painful, leaves no deformity and responds dramatically to salicylates; the mnemonic is that rheumatic fever licks the joints but bites the heart.
Sydenham chorea appears late, up to 6 months after the infection, may be the only feature, and can therefore make the diagnosis on its own even when the inflammatory markers have normalised.
Treatment of the acute attack is benzathine penicillin G as a single intramuscular dose of 1.2 million units for a patient of 27 kg or more and 600 000 units below that weight (or oral penicillin V for 10 days), with aspirin for arthritis and corticosteroids added for severe carditis with heart failure.
Secondary prophylaxis is intramuscular benzathine penicillin every 3 to 4 weeks, and Indian practice uses the 3-weekly interval in high-incidence settings; it continues for 5 years or until age 21 (whichever is longer) after an attack without carditis, 10 years or until age 21 after carditis without residual valve disease, and 10 years or until age 40 and often lifelong when there is residual valve disease.
The mitral valve is affected most often, giving mitral regurgitation during the acute attack and mitral stenosis years later, and the ECG finding to look for in the acute phase is first-degree AV block.

Lordosis, scoliosis, kyphosis

The normal spine is straight when seen from behind and carries gentle front-to-back curves when seen from the side — cervical and lumbar lordosis, thoracic and sacral kyphosis. Deformity is either an exaggeration of a normal curve (hyperlordosis, hyperkyphosis) or a curve that should not exist at all (scoliosis, a lateral curvature with vertebral rotation), and it matters because a large curve restricts the lungs and deforms the chest, and because a curve with pain or neurological signs points to a tumour, infection or syrinx rather than idiopathic disease.

Scoliosis is a lateral curvature of more than 10 degrees measured as the Cobb angle on a standing full-spine radiograph, together with rotation of the vertebrae; anything under 10 degrees is called spinal asymmetry and not scoliosis.
Adolescent idiopathic scoliosis is the commonest form, appears around the growth spurt, is far more likely to progress in girls, and classically produces a RIGHT thoracic curve.
The Adams forward-bend test is the screening examination: with the patient bent forward the vertebral rotation shows as a rib hump on one side, and a scoliometer reading of about 5 to 7 degrees or more is the usual threshold for referral for radiography.
Skeletal maturity decides the risk of progression: the Risser sign grades ossification of the iliac apophysis from 0 to 5, and a curve in a Risser 0 to 2 child has far more remaining growth in which to worsen than the same curve at Risser 4 or 5.
Management by Cobb angle: curves under 25 degrees are observed with review every 4 to 6 months during growth, curves of about 25 to 40 degrees in a growing child are braced, and curves beyond about 45 to 50 degrees are considered for posterior spinal fusion with instrumentation.
Bracing works only if it is worn — the effect is dose-dependent, and a Boston thoracolumbosacral brace or a Milwaukee brace is prescribed for most of the day and night, typically 18 to 23 hours, until skeletal maturity; the brace stops the curve getting worse and does not straighten the spine.
Kyphosis: the normal thoracic curve is about 20 to 45 degrees. Scheuermann disease gives a rigid adolescent hyperkyphosis with anterior wedging of at least 5 degrees in three consecutive vertebrae, while postural kyphosis is a smooth flexible curve that corrects when the patient lies down or is asked to stand straight.
Hyperlordosis is an exaggerated lumbar curve seen in pregnancy, obesity, a fixed hip flexion contracture and muscular dystrophy; the pot-bellied lordotic stance of a boy with Duchenne muscular dystrophy is the classic example.
Curves that are painful, rapidly progressive, present before the age of 10, LEFT-sided in the thorax, or associated with abnormal neurology or absent abdominal reflexes are not idiopathic and need MRI to look for a syrinx, tethered cord or tumour.
After spinal fusion the nursing priorities are log-rolling with the spine kept in alignment, hourly neurovascular checks of the limbs, chest physiotherapy because the thoracic cage has been operated on, and close watch on the drain output and the urine output.

Paget disease

Paget disease of bone is a localised disorder of bone remodelling in which osteoclasts become large, overactive and disorganised, and the osteoblasts that follow them lay down structurally weak, mosaic-patterned woven bone. The affected bones become larger and look denser on radiographs but are mechanically weaker, so the patient presents with bone pain, deformity, fracture or deafness rather than with a fall in bone mass.

It is a disease of people over 55 and affects the pelvis, femur, skull, tibia and lumbar spine most often; many patients are asymptomatic and are found through an isolated raised alkaline phosphatase or an incidental radiograph.
The biochemical hallmark is a markedly raised serum alkaline phosphatase with a NORMAL serum calcium and phosphate, and that combination is what separates it from hyperparathyroidism and from metastatic bone disease.
Radiographs show cortical thickening, coarse trabeculae, expansion of the bone, osteoporosis circumscripta and a cotton-wool appearance in the skull, and a flame-shaped or blade-of-grass lytic front advancing along a long bone; a radionuclide bone scan shows how many sites are involved.
Complications are pathological fracture across the convexity of a bowed bone, osteoarthritis of the adjacent joint, deafness and other cranial nerve palsies from skull involvement, spinal stenosis, high-output cardiac failure from the increased vascularity of extensive disease, and hypercalcaemia if the patient is immobilised.
A sudden increase in pain, a new soft-tissue mass or a rapid rise in alkaline phosphatase suggests malignant transformation to osteosarcoma; it occurs in under 1% of patients but carries a very poor prognosis.
Treatment is a potent bisphosphonate, usually a single intravenous zoledronic acid infusion, with calcium and vitamin D repletion started BEFORE the infusion, because a bisphosphonate given to a vitamin D deficient patient can precipitate symptomatic hypocalcaemia.
Treatment is indicated for pain, for disease at a site where complications would be serious such as the skull, a weight-bearing long bone, the spine or the area next to a major joint, and before elective surgery on pagetic bone to reduce bleeding; the response is followed by the fall in alkaline phosphatase.
Nursing care centres on pain control, fall prevention because the bones fracture easily, hearing assessment with referral for hearing aids, and the practical adjustments needed by a patient whose hat size has changed or whose leg has bowed.

Colles fracture

A Colles fracture is a fracture of the distal radius within about 2.5 cm of the wrist joint in which the distal fragment is displaced and angulated DORSALLY, with radial shortening and radial deviation, and it usually follows a fall on the outstretched hand. It is the commonest fracture in women over 50 and is a fragility fracture, which means that the wrist is only the presenting problem and osteoporosis is the disease.

The mechanism is a fall on an outstretched dorsiflexed hand, and the resulting deformity — dorsal displacement making the wrist look like an upturned dinner fork from the side — is the dinner-fork or bayonet deformity.
Radiographs show dorsal displacement and dorsal angulation of the distal fragment with radial shortening and loss of radial height, and often an avulsed ulnar styloid; posteroanterior and lateral views of the wrist are the minimum.
Smith fracture is the reverse injury, with the distal fragment displaced VOLARLY after a fall on the flexed wrist, giving a garden-spade deformity; Barton fracture is an intra-articular fracture-dislocation of the distal radius and a chauffeur fracture is an isolated fracture of the radial styloid.
Undisplaced or minimally displaced fractures are treated in a below-elbow cast for about 6 weeks; displaced fractures are reduced closed under haematoma block, Bier block or sedation and held in a cast, while comminuted, unstable or intra-articular fractures need percutaneous wires or open reduction with a volar plate.
Median nerve compression is the commonest early nerve complication, giving numbness and tingling in the thumb, index and middle fingers and the radial half of the ring finger; the answer is to split the cast and check the wrist position, not to increase the analgesia.
Neurovascular observation of the fingers after casting is the core nursing duty — colour, warmth, capillary refill under 3 seconds, sensation, active movement and pain on passive stretch, recorded and compared with the other hand.
The cast rules taught to the patient are to elevate the hand above the level of the heart for the first 48 to 72 hours, to move the fingers, elbow and shoulder every hour to prevent stiffness, to keep the cast dry, never to push anything down inside it, and to return at once if the fingers become numb, blue or cold or if the pain increases despite elevation and analgesia.
Late complications are malunion with a residual dinner-fork deformity and weak grip, joint stiffness, rupture of the extensor pollicis longus tendon typically 6 to 12 weeks later (the thumb can no longer be lifted off a flat table), carpal tunnel syndrome, and complex regional pain syndrome or Sudeck atrophy with a swollen, shiny, painful, stiff hand.
Every Colles fracture in a person over 50 is a signal to assess bone health — arrange DEXA and fracture-risk assessment, ensure adequate calcium and vitamin D and address the falls risk, because the next fracture is likely to be the hip.

Sprain vs strain

A sprain is an injury to a LIGAMENT, the tissue that joins bone to bone across a joint, and it follows a joint being forced beyond its normal range — the inverted ankle is the classic example. A strain is an injury to a MUSCLE or its TENDON, the tissue that joins muscle to bone, and it follows a sudden overstretch or a violent contraction such as a pulled hamstring while sprinting; patients use the two words interchangeably but an examination answer never does.

Sprain means ligament and joint, strain means muscle or tendon. The commonest sprain is of the anterior talofibular ligament from an inversion injury of the ankle, and the commonest strains involve the hamstrings, the calf and the lower back.
Both are graded in three: grade 1 is a stretch with microscopic tearing, minimal swelling and no instability; grade 2 is a partial tear with moderate swelling, bruising and some loss of function; grade 3 is a complete rupture with marked swelling, inability to bear weight or to contract, and, for a ligament, a demonstrably unstable joint.
The Ottawa ankle rules decide who needs a radiograph: bony tenderness at the posterior edge or tip of either malleolus, tenderness over the navicular or the base of the fifth metatarsal, or an inability to take four steps both immediately after the injury and in the department.
First aid is PRICE or POLICE — protection, optimal loading with brief rest followed by controlled movement, ice, compression and elevation; apply ice wrapped in a cloth for 15 to 20 minutes every 2 to 3 hours for the first 48 hours and never directly on the skin.
Avoid HARM in the first 72 hours: heat, alcohol, running and massage all increase bleeding and swelling into the injured tissue.
Elevate the part above the level of the heart, apply the compression bandage from distal to proximal with even pressure, and then check the toes or fingers for colour, warmth, sensation and capillary refill, because a bandage that is too tight causes more harm than the original injury.
Paracetamol or a short course of an NSAID is used for pain, and early protected weight-bearing with a rehabilitation programme of range-of-motion, strengthening and proprioception work is what prevents the chronic instability that follows a badly managed ankle sprain.
Refer when there is a grade 3 tear, demonstrable joint instability, a positive Ottawa rule, an inability to bear weight after a few days, or a palpable gap in a muscle or tendon; in a child the growth plate is weaker than the ligament, so what looks like a sprain near a physis is often a Salter-Harris fracture.

Amputation

Amputation is the surgical removal of all or part of a limb, done when the tissue is dead, dangerous or useless, and the level chosen is the lowest one that will heal and still allow a functional prosthesis. In India, as elsewhere, the great majority of non-traumatic amputations are done for peripheral vascular disease and the diabetic foot, so most patients arrive with the systemic disease that caused the problem still active in the other leg.

Indications are a dead limb (peripheral arterial disease, gangrene), a dangerous limb (spreading sepsis, gas gangrene, malignancy), a damaged limb (crush, burn, irreparable trauma) and a useless painful limb, with diabetes and peripheral vascular disease the commonest single cause.
Levels from distal to proximal are toe, ray, transmetatarsal, Syme at the ankle, below-knee (transtibial), through-knee, above-knee (transfemoral) and hip disarticulation. Preserving the knee matters enormously because a below-knee amputee uses far less energy to walk than an above-knee amputee, so saving the knee is the operative principle.
The immediate post-operative priority is haemorrhage: a large tourniquet is kept at the bedside for the first 24 hours, the stump dressing and the sheets under it are inspected for bleeding every 15 to 30 minutes at first, and a rising pulse with a falling blood pressure is the early warning of concealed loss.
Positioning prevents the contracture that would make a prosthesis impossible — elevate the stump on a pillow only for the first 24 hours to control oedema and then stop, lie the patient prone for 20 to 30 minutes three or four times a day to extend the hip, keep the residual limb flat with no pillow under the knee, and do not allow long periods sitting in a chair with the knee flexed.
Phantom limb SENSATION, the feeling that the limb is still there, happens to almost everyone and settles; phantom limb PAIN is a burning, cramping or shooting pain in the absent limb and is treated with gabapentin or pregabalin, amitriptyline, mirror therapy and TENS rather than with opioids alone. Stump pain is a different problem and points to infection, a neuroma, ischaemia or a poorly fitting socket.
Stump bandaging is applied in a figure-of-eight with firmer pressure distally than proximally so that the stump is shaped into a smooth cone that will take a socket; circular turns are avoided because they act as a tourniquet, and the bandage is reapplied several times a day.
Stump care is taught before discharge: wash and dry the stump daily, inspect it with a mirror for redness, blisters and breaks, do not apply oils or creams under the socket, wear a clean stump sock every day, and report any wound that does not heal.
Rehabilitation is multidisciplinary from day one — physiotherapy for upper-body and remaining-limb strength, early ambulation with a walker, prosthetic fitting once the wound has healed and the stump has matured, and equal attention to the OTHER foot, because the same vascular disease threatens it.
Body-image disturbance and grief are expected reactions; assess mood, involve the family and connect the patient with peer support, because rejection of a prosthesis is more often psychological than mechanical.

Trochanter rolls

A trochanter roll is a firmly rolled towel, blanket or foam wedge placed along the outer side of the hip and thigh and tucked under the patient so that it braces the greater trochanter and stops the leg from rolling outwards. It is used in any patient who cannot control the position of the leg — after a stroke, in an unconscious or sedated patient, after hip surgery or during prolonged bed rest — because a hip left externally rotated for days shortens the external rotators and leaves a deformity that physiotherapy cannot easily undo.

The roll prevents EXTERNAL ROTATION of the hip. It does not prevent foot drop: foot drop is prevented by a footboard, a foot splint or a boot that holds the ankle at 90 degrees, and confusing the two devices is the classic trap on this topic.
Placement runs from the crest of the ilium down to the middle of the thigh along the lateral aspect, with the rolled edge tucked snugly under the buttock and thigh; a roll placed under the knee or extended beyond mid-thigh compresses the common peroneal nerve at the head of the fibula and can itself cause the foot drop it was meant to avoid.
Each positioning device has exactly one job: a trochanter roll stops external rotation of the hip, a footboard or foot splint stops plantar flexion contracture, a hand roll stops finger flexion contracture, and an abduction pillow keeps the legs apart after total hip replacement.
The hip is held in neutral with the patella pointing at the ceiling, the leg in slight abduction and the knee in about 5 to 10 degrees of flexion; full extension for long periods is uncomfortable and sustained flexion invites a knee contracture.
The device never replaces turning — reposition the patient at least every 2 hours, inspect the skin over the greater trochanter, sacrum, heels and lateral malleolus at every turn, and score pressure risk with a tool such as the Braden or Waterlow scale.
After total hip replacement by the posterior approach the correct device is an ABDUCTION pillow between the legs, with the hip kept from flexing beyond 90 degrees, from adducting past the midline and from rotating internally for about 6 to 12 weeks; a trochanter roll on its own does not maintain abduction.
The roll must be firm but not hard, must not wrinkle underneath the patient, and must be reapplied after every turn, bed bath and linen change, because a roll that has slipped is doing nothing at all.

Arthroplasty, arthrodesis, arthrotomy

These are the three surgical answers to a destroyed or diseased joint, and their suffixes say exactly what was done: -plasty means to reshape or replace, -desis means to fuse and -tomy means to cut open. Arthroplasty replaces or resurfaces the joint and keeps movement, arthrodesis deliberately abolishes movement to give a stable painless joint, and arthrotomy simply opens the joint, usually to drain pus, remove debris or take a biopsy.

Arthroplasty is joint replacement or reconstruction; total hip replacement and total knee replacement are the common ones, done for osteoarthritis, rheumatoid arthritis, avascular necrosis and fracture of the neck of femur, and the aim is a pain-free joint that still moves.
Arthrodesis is surgical fusion of the joint surfaces so that bone unites across the joint — used at the ankle, wrist, first metatarsophalangeal joint and spine when a joint is unstable, infected or too damaged to replace — and it trades movement for stability and pain relief.
Arthrotomy is surgical opening of the joint capsule, typically to drain a septic joint, remove a loose body or take a synovial biopsy; septic arthritis needs urgent arthrotomy or arthroscopic washout because pus destroys articular cartilage within days.
The related words in the same family are arthroscopy (inspecting the joint with a camera through small portals), arthrocentesis (aspirating joint fluid with a needle, both to diagnose and to relieve pressure), synovectomy (removing inflamed synovium) and osteotomy (cutting and realigning bone to unload a joint).
After total hip replacement through the posterior approach the three precautions for about 6 to 12 weeks are: do not flex the hip beyond 90 degrees, do not adduct the leg past the midline and do not rotate the hip internally — in practice, no low chairs or low toilet seats, no crossing the legs, no bending to the floor, and an abduction pillow in bed.
The signs of a dislocated prosthetic hip are sudden severe pain, a shortened and internally rotated leg in posterior dislocation, an inability to move the limb and often a palpable lump in the buttock; the nurse stops all movement, keeps the patient flat and calls the surgeon.
Venous thromboembolism is the main systemic risk after lower-limb arthroplasty, so mechanical prophylaxis, prescribed anticoagulation, ambulation on the first post-operative day, ankle pump exercises and adequate hydration are routine, and calf pain with swelling is reported rather than massaged.
Prosthetic joint infection is the feared local complication — report a wound that keeps discharging, spreading redness, fever or increasing pain after the first week, and remember that these patients may need antibiotic cover for invasive dental and surgical procedures as advised by the surgeon.
After total knee replacement the priorities are quadriceps setting exercises, straight-leg raises, keeping the knee in extension with NO pillow under it because a pillow there produces a flexion contracture, and progressive flexion with the wound drain and neurovascular status monitored.

Gout

Gout is an inflammatory arthritis caused by monosodium urate crystals precipitating in and around joints when the serum urate has stayed above its solubility limit for long enough. It announces itself as an exquisitely painful, red, hot, swollen joint that comes on over a few hours, classically in the early hours of the morning at the first metatarsophalangeal joint of the great toe, an attack called podagra.

Diagnosis is confirmed by polarised light microscopy of joint fluid showing needle-shaped, NEGATIVELY birefringent monosodium urate crystals that look yellow when lying parallel to the axis of the compensator; pseudogout from calcium pyrophosphate gives rhomboid, POSITIVELY birefringent crystals that look blue in the same orientation.
The serum urate is often normal or even low during an acute attack because urate has shifted into the joint, so a normal urate never excludes gout — repeat it two weeks after the attack has settled.
Risk factors are male sex, obesity, alcohol and especially beer, red meat, organ meat, shellfish, fructose-sweetened drinks, chronic kidney disease, and drugs that raise urate such as thiazide and loop diuretics, low-dose aspirin, ciclosporin, pyrazinamide and ethambutol.
The must-not-miss differential is SEPTIC ARTHRITIS, which looks identical as a single hot swollen joint with fever; the joint is aspirated and the fluid sent for Gram stain, culture and crystals before steroids are given, because treating sepsis as gout destroys the joint.
The acute attack is treated with a full-dose NSAID, or with colchicine started within 24 hours using a loading dose of 1.2 mg followed by 0.6 mg an hour later and then usual dosing, or with a corticosteroid given orally, intramuscularly or into the joint, which is the choice when the kidneys are poor or NSAIDs are contraindicated.
Colchicine causes diarrhoea, nausea and vomiting at higher doses, needs a reduced dose in renal impairment, and interacts dangerously with clarithromycin and with statins; the old high-dose regimen of giving it until diarrhoea appears is obsolete.
Urate-lowering therapy — allopurinol first line, started low at 100 mg a day and at 50 mg a day in advanced chronic kidney disease and then titrated up, or febuxostat — is indicated for two or more attacks a year, tophi, radiographic joint damage or urate stones, and it is titrated to a serum urate below 6 mg/dL, or below 5 mg/dL when there are tophi.
Two rules govern urate-lowering drugs: do not start one in the middle of an attack in routine practice, and never STOP one the patient is already taking when an attack occurs; whenever one is started, cover the first 3 to 6 months with low-dose colchicine or an NSAID, because a falling urate mobilises crystals and provokes flares.
Chronic tophaceous gout produces chalky white subcutaneous deposits on the helix of the ear, the olecranon bursa, the fingers and the Achilles tendon, with punched-out juxta-articular erosions carrying overhanging edges on radiographs.

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