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After the structures of the medial joint space and proximal tibia are identified cheap 8mg zofran otc, the ultrasound transducer is slowly moved inferiorly while slowly rotating the superior border of the transducer clockwise when 946 imaging the right medial knee and counterclockwise when imaging the medial left knee until the pes anserine tendon is visualized as it is passing over the medial collateral ligament purchase 8 mg zofran. The pes anserine tendon passes over the medial collateral ligament to attach to the medial tibia generic zofran 4mg overnight delivery. Ultrasound image of the knee joint demonstrating the pes anserine bursa lying beneath the pes anserine tendon order 4mg zofran mastercard. Longitudinal image of the pes anserinus in the presence of a large pes anserinus bursitis (arrows). It should be noted that in addition to the pes anserine bursa, that bursa underlying the medial (tibial) collateral ligament may become inflamed mimicking the pain of pes anserine bursitis (Fig. Sagittal T2-weighted image demonstrating multiple small areas of bursal distention (arrows). The lower collection is a distended semimembranosus–tibial collateral ligament bursa. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers for tendon expanding around the patella and forming the medial and lateral patella retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain; the tendon proper is subject to the development of tendinitis (Fig. These fibers pass over the top of and on each side of the patella to ultimately insert on the tibial tuberosity (Fig. It is at the attachment of the patellar tendon at the tibial tuberosity that is the site of pathogenesis of Osgood–Schlatter disease. The patellar tendon originates at the superior pole of the patella and is composed of fibers from quadriceps tendon, which pass over the top of and on each side of the patella and each side for patella to ultimately insert on the tibial tuberosity. The pathogenesis of Osgood–Schlatter disease is thought to be due to excessive repetitive force on the tibial tuberosity by traction of the patellar tendon from quadriceps muscle contraction. This chronic traction creates inflammation of the ossification center of the proximal tibia with resultant avulsion of the secondary ossification center. If the traction injury continues, a nonunion of the avulsed bony fragments results (Fig. The pain of Osgood–Schlatter disease is bilateral approximately 50% of the time, although one side may be worse than the other. On physical examination, the finding of point tenderness over the tibial tubercle is pathognomonic for Osgood–Schlatter disease. Enlargement of the tibial tubercle is invariably present with consistently reproducible pain with direct palpation, resisted knee extension, and jumping which causes the quadriceps muscle to contract and place traction via the quadriceps tendon, expansions, and patellar tendon on the tibial tuberosity (Figs. Moderate rubor may be present around the tibial tuberosity, but there will be no obvious joint effusion as is seen with bursitis of the knee. The range of motion of the knee is within normal limits as is the neurovascular examination. It is important to rule out other diseases that may cause permanent damage to the knee if left untreated (Fig. Lateral view demonstrating prominence of the tibial tuberosity in Osgood–Schlatter disease. Pain with palpation over the tibial tuberosity is suggestive of Osgood–Schlatter disease. Based on the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Plain radiograph showing prominent tibial tubercle and ossicle consistent with Osgood–Schlatter disease. Surgical treatment of unresolved Osgood-Schlatter disease: ossicle resection with tibial tubercleplasty. Lateral film, obtained with a low-kilovoltage/soft-tissue technique, reveals fragmentation of the tibial tuberosity (black arrows) in association with soft-tissue swelling (white arrow)—characteristic findings in Osgood– Schlatter disease. A: Sagittal proton density-weighted image demonstrates thickening and increased signal intensity in the patellar tendon at the tibial tuberosity (arrow). B: Axial T2-weighted image demonstrates tendon thickening with central increased signal intensity (arrow) and marrow edema (arrowheads). T1-weighted (A) and T2*-weighted (B) sagittal magnetic resonance images of Osgood–Schlatter disease demonstrate focus of decreased signal within normal sharp V-shaped area formed by the patellar ligament and anterior tibia (arrow). A: Lateral radiograph shows soft-tissue swelling and small calcifications at the site of ossification center of tibial tuberosity (arrows). Longitudinal (B) and transverse (C) ultrasound images show a fracture and delamination of the cartilaginous portion of ossification center of tibial tuberosity, characteristic of Osgood–Schlatter disease. Arrows point to the margins of the patellar ligament; double solid arrow indicates the thickness of cartilage between the ossification center and patellar ligament insertion; double dashed arrow indicates delamination thickness within the ossification center; double black arrow indicates fibrosis within deep infrapatellar bursa; asterisk, effusion within deep infrapatellar bursa; dot, ossification center; E, epiphysis; M, metaphysis. A high-frequency linear ultrasound transducer is placed over the center for patella in the transverse plane (Fig. A survey scan is taken which demonstrates the characteristic appearance for fibers for quadriceps tendon passing over and inserting into the hyperechoic anterior margin for dome-shaped patella (Fig. The ultrasound transducer is then moved inferiorly to identify the inferior border for patella and the fibers of the patellar tendon lying inferior to the patella (Fig. After the proximal patellar tendon is identified, the tendon is evaluated for tendinosis, tears, rupture, abnormal mass, crystal tendinopathy, and tendinitis (Figs. The ultrasound transducer is then moved inferiorly to identify and assess the patellar tendons insertion on the tibial tuberosity (Figs. The tibial tuberosity is then assessed for irregularity that is pathognomonic for Osgood–Schlatter disease (Fig. Color Doppler may help identify acute inflammation of the healing tibial tuberosity (Figs. Correct transverse position for ultrasound transducer for ultrasound evaluation of the patellar tendon and its insertion on the tibial tuberosity. Ultrasound image for knee joint demonstrating the medial border for proximal femur (arrow). Transverse ultrasound image demonstrating the inferior pole patella and the patellar tendon. A: Normal tendon with regular and smooth fiber structure, no hypoechoic areas or vascular flow. B: Abnormal tendon with localized widening, including irregular structure and hypoechoic areas. C: Abnormal tendon with localized widening, including irregular structure, hypoechoic areas, and vascular flow (several vessels inside the area with structural changes). Longitudinal ultrasound image of the suprapatellar quadrant demonstrating crystal deposition disease affecting the patellar tendon. Ultrasound of the distal insertion of the patellar tendon shows thickening, apophyseal irregularity, and neovascularization in the adjacent tissues, typical of Osgood–Schlatter disease. Longitudinal ultrasound image of the patella demonstrating the pathognomonic finding of irregularity of the tibial tuberosity that is characteristic of Osgood–Schlatter disease. Osgood–Schlatter disease with abundant irregular bone formation at the tibial insertion.

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He notes that he recently cleaned his laughs 8 mg zofran free shipping, intermittently when talking on the phone buy zofran 4 mg free shipping, and garage and then began having increased wheezing at nighttime when she lays down to sleep 4mg zofran fast delivery. A 44-year-old woman with a history of asthma returns He feels that these symptoms are due to the pollen to follow up with her primary care physician purchase 4mg zofran fast delivery. He recently moved to the area noticed increased effort breathing and dyspnea on and denies known aeroallergen sensitivity but states exertion 4 months ago, and was limiting her physical there were no oak trees where he lived previously. This shortness of breath was asso- His current medications include as-needed albuterol ciated with frequent coughing. She was already using a along with two puffs twice daily of 180 mcg/actuation combination futicasone/salmeterol inhaler at low dose inhaled budesonide (low dose). He has been using his (45 mcg/actuation of futicasone) with two puffs twice albuterol multiple times every day. Lungs have wheeze bilat- noticed improvement of her limitations and dyspnea with erally with diminished air movement. Cardiac exam is exertion gradually over the last 4 months and now feels normal with mild tachycardia. She denies any thrush, hoarseness, dry mouth, or cough The tree pollen seems to have triggered aller- with use of her inhaler. She can’t remember when the last gic disease burden in this patient and subsequently time she needed her rescue inhaler. On exam, her lungs are clear with mildly prolonged expi- What is the next best step in management of the ratory phase on forced exhalation. Control of allergic symptoms should also be What is the next best step in management? She now has lower respiratory symptoms and improved lung func- improved symptoms, and her exam is at baseline. It is critical that a close follow-up appointment be What is a key component of her new management made to reassess the patient’s clinical symptoms and plan? The patient needs to understand her updated The patient returns in 2 weeks and is feeling much asthma action plan and have close follow up to ensure improved. Reassess the patient again in another 3 months to determine if he remains well controlled. He frst in the form of combination futicasone/salmeterol at believed that he had a “chest cold,” but the failure the 250/50 mcg dosing twice a day. Unfortunately, of the cough to improve and chronic mucus produc- she still experiences a chronic productive cough, tion has caused him to seek his physician’s guidance. He denies any chest pain, palpita- she has been able to cut back to half a pack daily with tions, weight gain, orthopnea, fevers, chills, or recent the use of nicotine replacement. He takes a baby aspirin daily any alternative smoking cessation pharmacothera- for heart protection but is otherwise on no medica- pies and is not sure she can fully quit smoking. He quit smoking 7 years ago when his grandson exam, she has a normal oropharyngeal exam, cardiac was born. On exam, he has normal nasal and ocular exam is normal, lungs have poor air movement bilat- mucosa, there is no cervical lymphadenopathy, there erally with bronchial breath sounds and faint wheeze is no jugular venous distention, cardiac exam is regu- appreciated on force exhalation, abdominal exam is lar and without displacement of point of maximal normal, and there is no pedal edema. The best choice would radiograph demonstrates hyperinfation but no bul- be to add long-acting anticholinergic to her regimen. What other measures would be important for her The patient is presenting with symptoms sugges- physician to consider? He has endured paramount that she receive a pneumococcal vaccine signifcant exposure to tobacco smoke. Lung function (unless she has received this already) and a yearly testing demonstrates an obstructive lung disease infuenza vaccination. The recommended medication would be long- physician to discuss her diffculty breathing. She has acting bronchodilator, either in the form of β2-agonist been having progressive diffculty with exercise toler- or anticholinergic. If either does not control his symp- ance for the last year but has been largely ignoring it. She still had an albuterol inhaler from a pre- vious visit to a walk-in clinic and has been using this 16. R-albuterol is responsible for pack-year history but quit when she was 40 years of the majority of the bronchodilator e ect, which led to the age. On exam, there is a clear oropharynx, there is development of levalbuterol, a single enantiomer formu- no jugular venous distention or cervical lymphade- lation of R-albuterol. Despite its theoretical superiority, nopathy, the cardiac exam is normal and without S3 there does not appear to be a clinical bene t over albuterol, or displaced point of maximal impulse, the lungs have although some patients report fewer adrenergic side e ects diminished breath sounds bilaterally with wheeze 2 with levalbuterol. Onset of action of both medications is noted in the end of the expiratory phase, there is no within minutes of administration and lasts for 4–6 hours. Chest radiograph demonstrates hyperin- dia and other more serious cardiac arrhythmias can be seen fation and bullous changes consistent with emphy- in susceptible patients by activation of β receptors on car- 1 sema. She should be carefully approved for use in asthma and are highly e ective for the monitored for symptom improvement and therapy quick relief of asthma symptoms. No maintenance onset of action within ve minutes whereas salmeterol 6 medications have been shown to improve mortality or rate takes 20–30 minutes to take e ect. Glucocorticoids have a potent anti-in ammatory e ect by increasing transcription of 16. It is important to determine whether the cataracts are posterior versus anterior 16. Leukotrienes are byproducts of the 5-lipoxygenase pathway in arachidonic acid metabolism. Omalizumab also works by reducing FcεR1 expression on the mast cell, basophil cell, and the antigen presenting dendritic cell surface. It is administered as a subcutaneous head-to-head trials comparing these agents, the favorable injection every 2–4 weeks. Clinical trials to date indicate that it too may be an e ective option for the treatment of severe eosinophilic asthma. Patients Anaphylactic reactions have been reported in association must be monitored for anaphylaxis for at least 30 minutes with both medications. Risk of anaphylaxis is higher in patients observed within 20 minutes of administration, whereas with moderate to severe asthma, and in those with poorly mepolizumab has the potential to cause delayed anaphy- controlled asthma. Short-term use of oral corticosteroids can result in hyper- glycemia, increased appetite, uid retention, weight gain, mood alteration, insomnia, peptic ulcer disease, and rarely, 16. Oral corticosteroids can be used as either short-term “burst” therapy to gain control of an exacerbation or as long-term 16. Its use in acute exacerbations reduces the need for referral to the eophylline has a narrow therapeutic index and wide emergency room, reduces hospital admissions, and prevents interpatient variation in metabolism. Oral corticosteroids can be stopped once and medications that may alter theophylline metabolism. In hospitalized patients, oral glucocorticoids tion with very few noticeable side e ects. Chronic toxicity may have a more insidious onset and may e bene ts of long-term oral corticosteroid therapy must not correlate to serum levels. Patients treated with prolonged corticosteroids should e risk of side e ects and the emergence of novel thera- undergo a slow taper before discontinuing.

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Other action mechanisms may contribute to antiepileptic efcacy Oral bioavailability >95% Time to peak levels 1–3 h Elimination Primarily by conjugation with glucuronic acid Volume of 1 order zofran 8mg without a prescription. Children may have shorter half-lives Serum clearance Patients on monotherapy purchase 4 mg zofran otc, patients on polytherapy receiving neither valproic acid nor enzyme-inducers order 8 mg zofran amex, and patients receiving a combination of valproic acid and enzyme inducers: 0 cheap zofran 8mg otc. Children have higher clearance values Protein binding 55% Active metabolites None Comment A very useful antiepileptic drug which can used as frst- or second-line monotherapy, or as adjunctive therapy, in the treatment of focal seizures and in some of the generalized epilepsy syndromes Introduction poorly soluble in water (0. Its extensive use has also highlighted broadly similar to that of phenytoin and carbamazepine [5,6]. Te manufacturer’s product information is regu- trigine was more potent than phenytoin and carbamazepine in these larly updated, and the clinician should refer to the latest version [2,3]. A recent study using Lamotrigine produces a dose-dependent suppression of second- microdialysis in freely moving animals demonstrated that lamo- ary generalized seizures and aferdischarge duration in amygdaloid trigine blocked release of glutamate and aspartate in hippocampus and hippocampal-kindled seizures in rats (a model of complex par- of pentylenetetrazole-kindled rats [33]. It is not readily understood tial seizures), with the efect lasting as long as 24 h in some cases why lamotrigine has a broader spectrum of clinical activity than the [8,10]. Tis efect was also observed in kindled rats that had previ- other sodium channel blockers, phenytoin or carbamazepine [34]. Lamotrigine is thought to A potential explanation could be its preferential afnity for diferent produce this efect by increasing aferdischarge threshold, that is by sodium channel α subunits which have diferential regional distri- suppression of seizure initiation, not propagation. Te inhibits voltage-sensitive sodium currents through a preferential pharmacokinetics of lamotrigine in adults has previously been ex- interaction with the slow inactivated sodium channel [17], suggest- tensively reviewed [45,46,47,48,49].. Lamotrigine does not afect normal synaptic transmis- children and adults with epilepsy [47,50]. Lamotrigine potently inhibits glu- tamate and aspartate release induced by the sodium channel opener Absorption veratrine in rat cerebral cortical slices, and displaces batrachotoxin Lamotrigine is well absorbed following oral administration and dis- from its sodium channel-binding site [19,25]. Administration of a plays an absolute bioavailability of 98% in healthy adult volunteers. A mean peak concentra- ductance involved in the release of excitatory amino acids in the tion of 1. At clinically relevant concen- adults, while afer a single oral dose of 2 mg/kg a mean peak con- trations, lamotrigine inhibits voltage-activated calcium currents in centration of 1. As the role of limbic structures in the pathophysiology of epi- Distribution leptic seizures is well established, actions of lamotrigine on these Lamotrigine is approximately 55% bound to plasma proteins in vit- structure are especially relevant. Protein binding is unafected by therapeutic concentrations of excitatory transmission in the rat amygdala by its efect on N-type phenytoin, phenobarbital and valproic acid [47]. Renal insufciency Studies in animals show that lamotrigine is widely distributed in Twelve volunteers with chronic renal failure (mean creatinine clear- all tissues and organs, but little is known of its diferential tissue dis- ance 13 mL/min; range 6–23 mL/min) and another six individuals tribution in humans. Measurement of lamotrigine concentrations undergoing haemodialysis were each given a single 100-mg dose of in brain tissue obtained from resected brain tumours [53], and dur- lamotrigine [49]. Te mean lamotrigine half-lives determined were ing autopsies [54], showed good penetration into the brain. Elimination Lamotrigine is metabolized by the liver, predominantly via N-glu- Hepatic dysfunction curonidation, which is the rate-limiting step in lamotrigine elimi- Te clearance of lamotrigine is reduced by about 25% in patients nation [45]. Approximately 70% of a single oral dose is recovered with mild hepatic dysfunction. A more prominent reduction in in the urine during the frst 6 days and about 2% of an oral dose is lamotrigine clearance is observed in patients with moderate and excreted in the faeces. Clearance is increased by 20– syndrome, the clearance of lamotrigine clearance is moderately 170% in children, but not for the frst week of life. In comparative reduced and the lamotrigine half-life is prolonged by about 35% studies of lamotrigine monotherapy, apparent oral clearance and compared with values found in healthy subjects [58]. In the study in children, weight-normalized clearance a clear understanding of possible interactions between lamotrigine appeared to be higher in children younger than 6 years (0. Te pharmacokinetics of lamotrigine afer multiple dose admin- istration conforms to that predicted from single-dose studies [45], Effects of co-administered drugs on lamotrigine indicating that clinically signifcant autoinduction does not occur pharmacokinetics [57]. Diminished glucuronidation of lamotrigine accounts for an Other antiepileptic drugs age-related decline in the clearance of the drug in the elderly [55]. Co-administration of valproic acid, an inhibitor of lamotrigine A comparison of the pharmacokinetics of lamotrigine (150 mg oral glucuronidation, has been shown to markedly reduce lamotrig- dose) in healthy young (26–38 years) and elderly (65–76 years) vol- ine clearance and to prolong markedly lamotrigine half-life [25]. Tese changes reverse rapidly within the frst pronounced peak–trough fuctuations in serum lamotrigine con- few days post partum. Te changes in lamotrigine pharmacokinet- centrations at steady state, particularly in children under 6 years of ics during pregnancy seem to be much less signifcant in women age [47]. Synergistic therapeutic efects, as well as some adverse efects (par- Dosing guidelines have been developed to optimize dose titra- ticularly development of tremor), have been observed when com- tion and target dosages in relation to age and type of co-medication. Diplopia, dizziness, nausea, ataxia and nystagmus – classic signs While some reports have suggested that lamotrigine clearance may of carbamazepine toxicity – were reported in some adult and pae- be accelerated by oxcarbazepine, a carefully conducted study in diatric patients when lamotrigine was added to carbamazepine healthy volunteers found no evidence of a pharmacokinetic inter- therapy [83,84,85]. However, the efects of lamotrigine Oral contraceptives and hormone replacement therapy on the serum concentration of carbamazepine-10,11-epoxide are Addition of combined oral contraceptive decreases lamotrigine lev- ambiguous. In adults, the addition of lamotrigine to existing car- els by around 50% on average [77]. Te interaction, which is caused bamazepine therapy has variously been reported to increase serum by stimulation of lamotrigine metabolism by the oestrogen com- carbamazepine-10,11-epoxide concentrations by 10–45% [84] or ponent of the contraceptive, may result in loss of seizure control if to leave them unaltered [85,86]. In children, the mean serum con- lamotrigine dosage is not appropriately adjusted. Tis interaction centration of carbamazepine-10,11-epoxide decreased signifcant- shows a biphasic time course, with a prominent decrease in serum ly when lamotrigine was added to carbamazepine therapy in one lamotrigine concentration during the period of pill intake, and study [87]. A pharmacodynamic interaction resulting in reciprocal gradual return toward baseline levels during the 7-day pill-free in- facilitation of adverse efects has also been reported between lamo- terval. A decrease in serum lamotrigine concentration is also seen A clear relationship between serum lamotrigine concentrations with hormone replacement therapy in postmenopausal women and clinical response has not been established in clinical trials [86]. Cessation of intake of oestrogen-containing medications can A target range of between 1 and 4 µg/mL was initially suggested result in a marked rise in serum lamotrigine levels, with the atten- [80,88,89] but children and adults with refractory epilepsy fre- dant risk of manifestations of toxicity. Interestingly, concomitant quently require higher serum concentrations to gain optimum sei- intake of valproic acid seems to antagonize the stimulating efects zure control [80]. Although dose-related improvements in seizure of combined steroid contraceptives on lamotrigine metabolism, control have been observed in children over the serum concentra- and in women co-medicated with valproic acid, serum lamotrigine tion range of 4–21 µg/mL [80], most investigators have not found levels appear to be comparable in the presence and in the absence of this [44,75,80]. Likewise, there is a variable relationship between serum con- Other drugs centration and incidence of adverse efects [44,80,93,94], although Olanzapine can cause a modest (about 25%) reduction in serum some studies suggest that a useful correlation does exist. Rifampicin also reduces serum lamotrigine con- atric study of high-dose lamotrigine therapy, increases in lamotrig- centrations. With respect to interactions with antiretroviral drugs, ine serum concentrations above 21 µg/mL were prevented because serum lamotrigine concentrations are reduced by about 50% by of the development of unacceptable levels of nausea that did not lopinavir/ritonavir, and by about 30% by atanazavir/ritonavir [79]. In a ret- Conversely, atanazir alone and raltegravir do not afect lamotrigine rospective study of 811 patients, reviewing 3731 lamotrigine serum exposure. Te correlation between serum lamotrigine levels and tolera- to a clinically important extent (for review see [[39,49,80]. Lamotrigine 503 Effcacy 50% reduction in focal seizures compared with baseline was seen in Te frst randomized trials of the antiepileptic efcacy of lamotrigi- 42% in the lamotrigine group and 16% in the placebo group [80]. A greater than 50% A large number of short-term, randomized, double-blind, seizure reduction was seen in 42% of lamotrigine-treated patients placebo-controlled studies, many with a cross-over design, have compared with 24% for the placebo group. Because of the uncontrolled nature of the study, these re- py, reducing total seizure frequency by 36%, with a responder rate sults should be interpreted with caution. A pooled analysis of pivotal trial data focusing on seizure free- Efcacy has also been demonstrated against focal seizures in dom indicated that lamotrigine was only infrequently associated childhood.

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Flex and internally rotate the knee and then slowly extend the knee to stress the lateral meniscus buy zofran 8mg fast delivery. Palpate for click and assess for focal tenderness during the test as it may suggest a tear order zofran 8mg visa. Patella Lateral apprehension test – With the patient’s knee in extension quality 8 mg zofran, apply pressure against the medial border of the patella buy 8mg zofran amex. Maintain the pressure, whilst flexing the knee to 30°and assess the degree of patella movement. Complete the knee joint examination Assess the neurovascular status of the lower limbs. The examination of the shoulder (ball and socket) joint follows the same logical pattern as examination of any other joint. This includes Look Feel Move Special tests Look General Look around bed for aids (slings). Specific Whilst the patient is standing: Inspect for swelling, muscle wasting, signs of inflammation and sinus formation. Anterior – Arthroscopic scars, sinuses, contour of the shoulder/squaring off, muscle wasting of deltoid and trapezius. Inspect for winging of the scapula (serratus anterior muscle supplied by long thoracic nerve of Bell, C5/6/7). Feel (ask the patient whether they are in pain before you begin) Temperature of the joint (with the back of the hand). Continue posteriorly to assess the greater tuberosity of humerus, spine of scapula, inferior pole of scapula, supraspinatus and infraspinatus. With the patient’s arm by the side, ask the patient to flex the shoulder forward (90°). Flex the patient’s elbows to 90° and then ask the patient to place their hands behind their head. Ask the patient to place their hands behind their back (normally one should be able to reach up as high as the sixth thoracic vertebrae). Special tests Rotator cuff muscles Supraspinatus (thumbs down test/Jobe’s test/Empty can test). To exclude rupture, passively abduct the patient’s arm to 40°, then the patient should be able to continue active abduction. Impingement test – This is impairment of rotator cuff function within the subacromial bursa. Impingement is characterised by pain and weakness on abduction and internal rotation. Neer’s sign and test – With the patient’s thumb down, place your hand on their shoulder and with your other hand passively lift up their hand in the plane of the scapula (forward flexion) until they express pain (Figure 7. Pain during this manoeuvre is a positive Neer’s sign and pain abolished with local anaesthetic is a positive Neer’s test. Hawkin’s test – Raise the patient’s arm to 90° forward flexion and bend the elbow to 90°. Jobe’s test (empty can) – Ask the patient to abduct the arc to 90° elevation in the scapula plane with full internal rotation (empty can). Ruptured head of biceps Assess for a ‘biceps bulge’ on flexing the patient’s elbow against resistance. Axillary nerve function Assess for deltoid muscle power and sensation (fine touch) in regimental badge area (Figure 7. Complete the shoulder joint examination Offer to perform apprehension test to test for shoulder instability (Figure 7. Impingement pain is reproduced when the shoulder is internally rotated with 90° of forward flexion, thereby locating the greater tuberosity underneath the acromion; (b) Neer’s impingement test. The patient’s upper limbs should be fully exposed and their hands resting on a pillow. The hand examination may represent a rheumatologic, orthopaedic, neurological or vascular case. The examination of the hands follows the same logical pattern as examination of any other joint. This includes Look Feel Move Special tests Look General Look around bed for aids and supports. Ensure you assess for extra-articular manifestations of systemic disease (see below). Assess for a dropped finger/thumb (evidence of extensor tendon rupture) and wrist drop. Palpate each joint to ascertain the levels affected in the hand and whether active inflammation or inactive disease is present. Palpate for tendon ruptures (start your palpation on the ulnar side of the hands). Ask the patient to perform the following movements: Grip and squeeze two of your fingers and perform a fine pinch. Place their hands in a ‘pray position’ to demonstrate wrist dorsiflexion (Figure 7. Place their hands in a ‘reverse pray position’ to demonstrate wrist flexion (Figure 7. Special tests Functional assessment: Power grip Pincer grip (pick up a coin or key) Button and unbutton shirt Hold a pen and write Neurological assessment (Sensation): Radial nerve (dorsum of first interosseous webspace) Median nerve (palmar/volar aspect of index finger) Ulnar nerves (palmar/volar aspect of little finger) Table top test: Ask the patient to place their hands flat on a table. Extra-articular manifestations of rheumatoid disease: Systemic – Weight loss, fever, malaise, vasculitis and amyloidosis Skin – Subcutaneous (rheumatoid) nodules Eyes – Keratoconjunctivitis sicca, scleritis, episcleritis Cardiovascular – Pericardial effusion, pericarditis, myocarditis Respiratory – Pleurisy, pleural effusion, nodules and fibrosing alveolitis Neurological – Entrapment neuropathy (carpal tunnel syndrome), atlantoaxial instability and multifocal neuropathies Abdominal – Splenomegaly, Felty’s syndrome Haematological – Anaemia, leucopenia and lymphadenopathy Muscular-Skeletal – Knees (valgus/varus deformity, popliteal ‘Baker’s’ cysts), scars for shoulder, knee or hip replacements Complete the hand examination Perform a full neurological assessment of the upper limbs. Assess for extra-articular manifestations of rheumatoid disease (eyes, respiratory, cardiovascular, neurological systems). The examination of the spine follows the same logical pattern as examination of any other joint. This includes Look Feel Move Special tests Look General Look around bed for walking aids and supports (Miami J collar, thoracolumbar brace). Specific Whilst the patient is standing, inspect Skin – Scars, sinuses, hairy tufts, café au lait spots Soft tissues – Muscle wasting Bone – Scoliosis, kyphosis, lumbar lordosis, gibbus Feel Ask the patient whether they are in pain before you begin. Palpate and percuss over the entire spine for any bony or muscle tenderness and assess for step deformities. Ask the patient to tilt their head to the right and left towards their ear (lateral flexion 45° each direction). Lateral flexion – Ask the patient to slide their hand down one side of the body (30°). Rotation – Ask the patient to sit down, cross their hands across their body and rotate their body (40°). Special tests Cervical spine Lhermitte’s sign (the barber-chair phenomenon) is demonstrated when you ask the patient to bend their cervical neck forward.