PC 617 Modules 7,8,9 - Sheet1 Flashcards
Percentage of adults that report recurrent headaches
80-90%
Headaches and primary care
Rank as one of the 10 most common presenting problems
Classifications of headaches
Tension, vascular, analgesic rebound, traction/inflammation (secondary)
Tension headaches
More prevalent than migraines; produce little disability and are generally effectively managed with OTC medications; rarely seen in primary care
Length of tension headaches
Episodic and can last 30 minutes to hours
Description essentials of tension headaches
At least 2 of 4 - bilateral; steady and nonpulsatile; mild to moderate intensity (may prohibit but not inhibit activity); not aggravated by routine activity
Tension headaches and nausea
Should not be present
Tension headache and aura symptoms
There can be photophobia or phonophobia but not both
Tension headaches and underly disease
Should be no evidence that accounts for the headache
Migraine without aura
Common migraine
Length of migraine without aura
Lasts 4-12 hours
Characteristics of migraine without aura
Must have 2 of the following - unilateral head pain; throbbing; moderate to severe intensity; pain aggravated by routine activity; N and/or V; photophobia and phonophobia
Migraine with aura
Classic migraine
Prevalence of migraine with aura
Occurs in approximately 15% of migraine attaches
Occurrance of aura with migraine
Generally precede headache by less than 1 hours but may occur durring headache
Characteristics of most auras
Most are visual, ie flashes of light, alternating geometric patterns, alterations in perception - the “Alice in Wonderland” syndrome
Somatosensory auras
Consist primarily of numbness and tingling in the lips and fingers although they can occur anywhere
Phases of migraines
Preheadache or premonitory; headache phase; and postheadache or prostdrome
Preheadache or premonitory
Prodrome is far more common than aura; involves changes in mood or energy level (depression, euphoria, fatigue), alteration in sensory processing, changes in muscle tone, food cravings, fluid retention, yawning and a variety of other nondescript symptoms; probably reflect the chemical milieu of the CNS
Chocolates as a trigger
Traditionally considered a potent migraine trigger, but research has shown it is reflected carbohydrate cravings and was a prodrome and not a trigger
Importance of prodromes
Become important markers for the timing of treatment
Headache phase
Begins mild and progresses from mild to severe over 30 minutes to several hours; can be unilateral or bilateral
Duration of migraine with auras in children and adolescents
Usually less than 4 hours
Duration of migraine with auras in children and adolescents
Usually last 4-72 hours, but menstrual migraines may last longer
Postheadache or prodrome
After headache is resolved, other symptoms may linger for 1-2 days - fatigue, irritability, inability to concentrate, muscle pain, and/or food intolerance are common
4 diagnostic questions of headaches
1) How do your headaches interfere with your life? 2) Has there been any change in your headache pattern? 3) How do you experience headaches of any type? 4) How often do you use medication to treat headaches?
Use of a headache diary
Helps to identify triggers to avoid
Diagnostics of headaches
Testing should not be done unless it will change management. If diagnosis is undertain based on H&P, may need testing to differentiate primary and secondary headaches
Cluster headache
Classification of vascular headaches - extremely severe, most often seen in men - suicide risk
Anangesic rebound headache
Suspect with complain of daily headache - Inquire about frequency of analgesia use
Traction/inflammation (Secondary) headache
Diseases of the bones of the cranium. Referred pain from eyes, sinuses, teeth, TMJ, ears, and back, menigeal irrittion, temporal arteritis
Non-pharmacological migraine management
AVOID triggers, relaxation techniques, accupressure, regular exercise, adequate sleep, good nutrition
Classifications of pharmacological management of migraine
Abortive therapy and preventative therapy
Abortive therapy of migraine treatment
Important to use at first indication of headache
Use of triptans of abortive therapy of migraine treatment
Separate all doses by at least 2 hours; may augment with reglan if N&V severe; pregnancy category C - contraindicated
Classifications of drugs used in abortive migraine treatment
Triptans, NSAIDS, narcotics, combination analgesics, ergots, corticosteroids
Combination abortive drugs used in treatment of migraines
Excedrine migraine and fiorinal
Ergots and use as abortive therapy for migraine
Pregnancy category X
Abortive therapy of migraine and pregnant patients
Generally should be counseled to avoid triggers, use non-pharmacological measures except accupressure and may take tylenol or midrin
Preventative therapy for migraine headaches
Can use if no more than 4 per month, used for severe headaches, use if patient does not respond well to medication
Comorbid conditions and migraines
Consider conditions such as hypertension and epilepsy
Classes of preventive drugs and treatment of migraines
Beta blockers; calcium channel blockers; anticonvulsants; TCAs; SSRIs
Follow up care and migraine
Return to clinic every 2-4 weeks X 3 months until responding well to medication
Dizziness
A symptom
Vertigo
A condition that causes dizziness
Differentiation of dizziness
The sensation of the person spinning or the environment spinning around the person
Disequalibrium
A loss of balance and lack of coordination
Lightheadedness
The feeling that one is about to faint
Classifications of vestibular problems
Peripheral and central
Vestibular problems
Imbalance in vestibular system
Peripheral vestibular problems
Problems of inner ear or cranial nerve VIII - most common type of vertigo
Central vestibular problems
Includes brainstem ischemia and infarction and demylenating disease such as MS - uncommon
Presentation of central vestibular problems
Typically present with vertigo in association with other brainstem deficits. May be associated with other signs and symtpoms including diplopia and focal, sensory or motor deficits
Nonvestibular causes of vertigo
Systemic viral or bacterial infection causing postural hypotension
Classifications of nonvestibular causes of vertigo
Systemic, metabolic, and drug causes
Metabolic causes of vertigo
Hypo or hyperglycemia; electrolyte disturbances; anemia
Drug causes of vertigo
Hypnotics, antihypertensives, alcohol, analgesics, tranquilizers
Types of peripheral vestibular
Benign positional paroxysmal vertigo (BPPV); Menier’s disease; vestibular neuronitis
Benign positional paroxysmal vertigo (BPPV)
Mot common type of vertigo - caused by free floating particular matter which moves within the semicircular canal with certain head movements; position changes cause an abrupt onset; NO tinnitus or hearing loss but may have associated N&V; a common problem in the elderly
Diagnostic criteria of Meniere’s disease
2 episodes, last at least 20 minutes each; accompanied by hearing loss, tinnitus or aural fullness
Characteristics of meniere’s disease
Vertigo unrelated to position changes, hearing loss is initially reversible but may become permanent in 75% of cases; symptoms are usually unilateral
Vestibular neuronitis (acute labyrinthitis
Involves the cochlea and may cause hearing loss - caused by viral infection of the labyrinth. Frequently occurs after URI followed by vertigo. Symptoms resolve in 3-6 weeks with no sequelae
History of dizziness and vertigo
Describe dizziness. Medical problems? Do episodes occur with any specific activity or movement? Associated symptoms? Describe episodes especially onset, duration, and any hearing involvement. Medications? Recent infections? Any recent head trauma? Ear surgeries?
Physical exam of dizziness and vertigo
General appearance. Vision exam. Ear exam including Weber and Rinne tests. Hallpike maneuver. Perform neuro and cardiovascular exams.
Weber hearing test
Lateralization to unaffected side with sensorineural hearing loss - Meniere’s and labyrinthitis
Rinne hearing test
AC:BC with sensorineural loss. BC and AC are both reduced but ration remains the same.
When will you see conductive bone loss with hearing test
Seen with serous otitis and otitis media
Hallpike maneuver
Produces intense vertigo in patients with vestibular problems. May cause mild vertigo in patients with central problems. Nystagmus with peripheral causes produces a 3-10 second delay in onset, lessens with repetition, and is in a fixed direction. Nystagmus with central causes begins immediately, does not fatigue with repetition and may be in any change of positions
Diagnostics of dizziness and vertigo
Lab tests identify the cause in less than 1% of patients. Audiometry - quantify hearing loss. Electronystagmography (ENG). MRI. CBC/ELECTROLYTES
Electronystagmography (ENG)
can be useful in diagnosing chronic peripheral disorders such as Meniere’s and persistant BPPV
MRI and diagnosis of dizziness and vertigo
Use if vertigo is of sudden onset and accompanied by severe headache, direction changing nystagmus or if risk factors for stroke
CBC/electrolytes and diagnosis of dizziness and vertigo
Use if suspect anemia, diabetes, or electrolytes inbalances
Length of BPPV
May resolve in a few days or weeks without any treatment
Action tht may shorten BPPV recovery time
Referral for vestibular physical therapy
Epley’s maneuver
Patient can be taught to do this at home, especially if recurrent (50% of patients)
Medical treatment for BPPV
Meclizine (antivert) can be used but is not as effective as exercises and do not suppress acute attacks. Pregnancy category B
Meniere’s disease
Refer to otolaryngologist for testing and management. Bed rest during an attack. Recommend decreasing sodium, caffeine, alcohol, and tobacco, but unclear benefit.
Medication to use to treat Meniere’s disease
Antivert and antiemetics with severe symptoms. Diuretics may reduce severity of attacks
Vestibular neuronitis
Lie down in darkened room. Antibiotics if associated with bacterial infection. Symptoms resolve spontaneously in 3-6 weeks with no sequelea
Medication used to treat vestibular neuronitis
Methylprednisone. Antivert and antiemetics can be helpful during an attack but should be stopped after 3 days since continuing may slow recovery.
Bell’s palsy
Presents with unilateral paralysis of face. Often preceded by viral infection. CN VII affected. Acute onset with maximum paralysis in 48-72 hours. May have altered taste and increased sensitivity to sound
History to obtain regarding Bell’s palsy
Onset and progression. History of recent infections, especially viral. Any chronic diseases. Insect bites - Bell’s palsy is a common neuropathy with Lyme’s disease. Facial trauma? Pregnancy? Occurs more frequently with pregnancy
Physical exam of Bell’s palsy
Head and neck. Cranial nerve assessment. Corneal light reflex may be decreased. Eyeball may roll upward when close eyelid.
Diagnostics of Bell’s palsy
Usually not indicated. May be useful to exclude other conditions such as Lyme disease (titre) or other infection (CBC with diff)
Management of Bell’s palsp
Prevention of eye injury is the most important goal. Prevent exposure keratitis by protecting cornea with eye drops (methylcellulose bid and lubricant at HS). Protective eyewear. Patching at bedtime. Massage of facial muscles.
Pharmacological therapy within first week of onset of Bell’s palsy
Prednisone recommended in all patients. Antiviral (Valacyclovir). Pregnancy category B - recommended for patients with severe facial paralysis. NSAIDS can be used.
Recovery of Bell’s palsy
Majority of patients recover full function in 4-6 months - 12 months at the most
Trigeminal neuralgia
Affects 5th (trigeminal) cranial nerve. Most are idiopathic. Presents with recurrent episodes of intense sharp, penetrating electric like pain on one side of the fact. Frequency and duration varies.
Trigger of pain of trigeminal neuralgia
May be triggered by cold, chewing, touch, talking or facial movements with trigger zone. Info should be elicited in history
Exam of trigeminal neuralgia
Physical should include exam of all cranial nerves. Neuro exam should be normal
Management of trigeminal neuralgia
Tegretal 100 mg bid, may increase to max 1200/day. Need serial blood counts and LFTs. Abrupt withdrawal should be avoided. SSRIs if person is depressed.
Referral of treatment of trigeminal neuralgia
Should be referred to a neurologist for more comprehensive evaluation and initiation of treatment. Care can be managed by the PCP. Refer to neurosurgeon is limited pain relief.
Meningitis
Infection that results in inflammation of the brain’s meningeal membranes. Most often caused by bacterial agent.
Presentation of meningitis
Typically with high fever, headache, photophobia and neck pain and stiffness (nuchal rigidty)
History regarding meningitis
Should include exposures, recent travels, food consumptions, sexual practices, drug use, history of infectious diseases, immunocompromised, systemic disorders
Physical exam regarding meningitis
Temp, pulse, respiratory rate; signs of meningeal irritation - Brudinski’s and Kernig’s sign; LOC - confusion, lethargy, stupor, coma; cranial nerves - diplopia, deafness, facial weakness, pupillary abnormalities
Brudinski’s sign
Hip and knee flexion with the neck flexed
Kernig’s sign
Inability to fully extend the legs
Initial diagnostics of meningitis
CBC - marked elevation of WBC’s; blood cultures; serum glucose; LP is indicated but will be done after referral
Management of meningitis
If sign and symptoms indicate possibility of meningitis, immediate referral to a neurologist or ED is warranted
Prevention of meningitis of unexposed individual
Pneumococcal and H Influenza vaccines - all ages; meningococcal vaccine - young adolescents, college freshmen and military, also high risk patients and travelers to endemic areas
Prevention of meningitis of exposed individual
Meningococcal of H influenza - Rifampin or cipro; pneumococcal - none recommended
Most challenging decision regarding PCP care of chest pain
The determination if the presenting symptoms are life threatening, requiring immediate referral
Common causes of non-cardiac chest pain
Peptic ulcer disease (PUD), GERD, costochondritis, acute anxiety
Consideration of life-threatening conditions regarding chest pain
Determine there is no immediate risk of severe O2 deprivation to vital organs such as - MI, aortic dissection, PE. Most life-threatening conditions present as acute rather than chronic pain
Symptoms of MI
Sudden onset not relieved by rest or nitro. associated symptoms
Aortic dissection
Sudden tearing pain located in the anterior or posterior chest. May radiate to arms, legs, abdomen, or back
Pulmonary embolism
Able to point to area of pain over lung; dyspnea; apprehension; hemoptysis; gripping or stabbing pain of moderate to severe intensity that may increase with deep breathing; may radiate to neck or shoulder; bed rest or other surgery are risk factors
Known risk factors for CAD
Male >45; female > 55; family history of premature CAD; cigarette smoking; HTN; low HDL 130
Patients who present with CP that should be sent to ED
Non-localized pain lasting > 20 minutes. Associated with diaphoresis, dyspnea, N&V, dizziness, radiation to neck, jaw, shoulder, arm.
CP patients who present with atypical symptoms
Women, older adults, and diabetic patients
Physical of patients who present with CP
General appearance. Vital signs. Inspect skin. Palpate chest wall. Auscultate breath sounds. Auscultate heart sounds. Examine abdomen. Examine extremities.
Costochondritis
Pain with palpation over the cartilage between the sternum and ribs
Musculoskeletal pain assessment in patient with CP
Can it be reproduced with movement or palpation?
Breath sounds with patient with PE
Crackles may be heard over the site of PE
Auscultation of heart sounds in patient with CP
A new, transient, paradoxical S2 during pain can indicate coronary ischemia. S4 indicates stressed heart which can result from MI, HTN, or CAD. Irregular rhythms are often heard during MI. Aortic diastolic murmur can occur with a dissecting aorta.
Physical appearance with patient with CP
Grimacing, diaphroesis, cyanosis, pallor, tachypnea
Vital signs in patient with CP
BP may be elevated with MI. Aortic dissection can have hypotension. Hyperventiltion can cause chest pain.
Skin inspection with patient with CP
May have cool, pale, moist skin with acute MI, PE, or aortic dissection. Palpate entire chest wall.
Abdominal exam of patient with CP
PUD, cholecystitis, pancreatitis may cause referred pain
Extremity exam in patient with CP
Observe for peripheral cyanosis which can indicate hypoxia. Lower extremity edema can indicate heart failure. Absent peripheral pulses can occur with PE
Diagnostic tests of costochondritis
None needed if physical exam is normal
Treatment of costochondritis
Application of heat and NSAIDs
Education regarding costochondritis
Condition is self-limiting. Avoid overuse and trauam. Take NSAIDs with food
Follow up care regarding costochondritis
Return to clinic if symptoms worsens or no improvement
GERD
If suspect give trial dose of PPI and check for improvement. If risk factors for CAD, may also do EKG and check lipids.
Cardiac work up - Suspected post-MI in no acute distress
Cardiac troponins (I&T), serum cardiac enzymes (CPK), SGOT adn LDH, elevated leukocytes & ESR - non-specific indicators, EKG, and refer
Cardiac tropinins
Rise within 2-4 hours post MI and remain elevated 7-10 days
Serum cardiac enzymes (CPK)
Rise 4-8 hours after MI and return to normal 48-72 hours
SGOT and LDH
Elevated later and not indicators of acute MI
Neck pain and paresthesias - cervical radiculopathy
Caused by compression of the cervical nerve roots - radiculopathy. Most comonly affected are C6 and C7
Radiculopathy
A pathologic process affecting the nerve root
Causes of radiculopathy
Compressive - most common - and noncompressive etiologies
Predominant mechanisms of compressive cervical radiculopathy
Cervical spondylosis and disc herniation
Causes of noncompressive radiculopathy
Infectious processes (especially herpes zoster and Lyme disease), nerve root infarction, root avulsion, infiltration by tumor, infiltration by granulomatous tissue, and demyelination
Clinical symptoms of cevical radiculopathy
Neck pain and radicular pain associated with numbness and paresthesias in the upper extremities; muscle spasms or fasciculations in involved myotomes; weakness, lack of coordination, changes in handwriting or strength, radiation of pain into paraspinal and scapular regions. Pain may be relieved by placing hands on top of head to relieve tension of involved nerve root.
Reflexes in patients affected with cervical radiculopathy
Reflexes are typically reduced with involvement of C5, C6, or C7, but there are no standard reflexes that reflect the distribution of C8 and T1
Major aim of neurologic exam in patient with neck pain and paresthesias
To look for evidence of weakness and sensory disturbance in myotomal and dermatomal patterns
Clinical exam of patient with neck pain and paresthesias
Evaluate ROM of neck and extremities, Spurling’s maneuver, abduction relief test, palpate for tendeness, muscle spasm, or lymphadenopathy, assess sensory and motor functions, DTRs
Spurlings maneuver
Highly specificity for the prsence of cervical radiculopathy, but its sensitivity is low to moderate. Positive test - if limb pain or paresthesias are produced test should be stopped. Production of neck pain alone is nonspecific and constitutes a negative test.
Caution with Spurling’s maneuver
Never perform in patients who may have instability o the C-spine (RA, cervical malformations, or metastatic disease, since it may cause further injury to the spine). Should not be performed when associated cervical myelopathy is suspected.
Abduction relief test
Patient is asked to lift the symptmatic arm above the head, resing hand on top of head. If test is positive, the patient has a decrease or disappearance of radicular symptoms.
Diagnostics of neck pain and paresthesias
Based on history and clinical findings. neuroimaging and electrodiagnostic testing, MRI, EMG, plain radiographs
When neuroimaging and electrodiagnostic testing is indicated
Persistent symptoms that do not resolve with 4-6 weeks of conservative therapy. Significant neurologic findings or localizing symptoms are present, including myotomal weakness or myelopathy
MRI and diagnosis of neck pain and paresthesias
Most currently the study of choice in most patients for the initial neuroimaging eval of the C-spine
EMG and diagnosis of neck pain and paresthesias
Usually confirms radiculopathy and frequently reveals a myotomal pattern of denervation. Nerve conduction studies alone are not sensitive for radiculopathy. Symptoms should be present for more than 3 weeks when use this test
Plain radiographs in use of neck pain and paresthesias diagnosis
They are rarely diagnostic in setting on non-traumatic cervical radiculopathy
Differential diagnoses of neck pain and paresthesias
Adhesive capsulitis, demylenating conditions, myocardial ischemia, peripheral nerve entrapment, rotator cuff disease, thoracid outlet syndrome
Conservative treatment of neck pain and paresthesias
NSAIDs, avoidance of provocative activities, add a short course of oral prednisone if pain severe. Once pain is tolerable, initiate physical therapy with exercise and gradual mobilization.
Treatment for patients with severe or disabling pain related to neck pain and paresthesias
If conservative treatment has failed and if no progressive worsening of neurologic deficits, recommend use of epidural steroid injections rather than surgery
Surgical candidates of neck pain and paresthesias
Symptoms and signs of cervical radiculopathy. Cervical nerve root compression by MRI or CT myelography. Persistence of radicular pain despite non-surgical therapy for at least 6-12 weeks, or progressive motor weakness that imapirs function
Cervical strain
A common condition that is usually self-limited. It is a muscle injury.
Sprain
Ligamentous stretching-type injury
Whiplash
Ligament is torn, usually C7
Clinical symptoms of cervical strain or sprain
May occur after trauma or may be spontaneous. Report of non-radicular, non-focal pain, noted anywhere from the base of the skill to cervicothoracid junction. Pain worse with motion and may accompanied by paraspinal spasm. Occipital headaches may occur early and may persist longer than pain. May report increased irritability, fatigue, sleep disturbances, and difficulty concentrating.
Exam of cervical strain or sprain
Tenderness in paraspinous muscles, trapexii, sternocleidomastoid muscles, spinous processes, interspinous ligaments, and/or the medial border of the scapula. Limited ROm common. Pain often noted in extremes of motion. Neuro exam is usually normal.
Diagnostics of cervical strain or sprain
AP and lateral and open mouth (odontoid) radiographs are necessary if patient has history of trauma or if the patient is elderly
Differential diagnoses of cervical strain or sprains
Cervical disk herniation; cervical spine tumor or infection; dislocation of subluxation of spine; inflammatory condition of C-spine (RA); spinal fracture; symptom amplification/secondary gain
Treatment of cervical strain or sprain
Mild to moderate axial pain improves in 2-3 weeks. Posture modification, especially in sleep. Home exercise. Tylenol or NSAIDs and mild opioid analgesics short term. TCAs at bedtime for pts with chronic pain and sleep problems. Muscle relaxant at night for pts with severe muscle spasm. Cervical collars. Physical therapy. No c-spine traction or massage for neck pain. TENS units, medical branch blocks.
Prevelance of low back pain
2nd most common reason for clinician visits. 84% of adults suffer. Most common cause of disability. By age 50, 80-90% of population have evidence of DDD.
Risk factors for the onset of back pain
Smoking, obesity, older age, female gender, physical strenuous work, sedentary work, psychologically strenuous work, low education level, Worker’s comp insurance, job dissatisfaction and psychological factors such as somatization disorder, anxiety, and depression
Subjective data of low back pain
Sudden onset of back pain after an event or injury; information needed - OLDCART, any associated neuro deficits, med/surg history, current meds; allergies
Clinical symptoms of low back pain
Low back pain, pain often radiates to buttocks and posterior thighs, may have difficulty standing erect or may need frequent position changes
Clinical exam of low back pain
Inspection, palpation, straight leg raises, range of motion, sensory and motor function, DTRs, abdominal exam
Inspection of low back pain
Reveal anatomic abnormalities such as scoliosis (lateral spinal curvature) or kyphosis (spinal curvature with posterior convexity)
Palpation of low back pain
Assess vertebral or soft tissue tenderness. Vertebral tenderness is not a specific finding for spinal infection
Straight leg raises
May be useful to help confirm radiculopathy. Done with pt supine. Examiner raises the pt’s extended leg with ankle dirsiflexed, being careful that the pt is not actively helping in lifting. Considered positive when the sciatics is reproduced between 10-60 degrees of elevation
“Red flags” for a potentially serious underlying cause for low back pain
Trauma, unexplained weight loss, age >50, female, unesplained fever, immunosuppression, diabetes, history of cancer, IV drug use, prolonged use of corticosteroids, osterporosis, age >70, focal neurologic deficits with progressive or disabling symptoms, duration longer than 6 weeks, prior surgery
Management of low back pain
Usually self-limiting; 90% resolve in 1-6 weeks. Tylenol, NSAIDS, muscle relaxants. Activity as tolerated. Bed rest no longer than 2 days. Walk. Weight loss. Physical activity. Exercise 30 min per day. No smoking. Return to clinic in 2 weeks if problems persist or sooner if worsen
Assessment of shoulder pain
Inspection, range of motion of elbow, palpation, rotator cuff testing, stability testing
Rotator cuff testing
Positive or negative drop arm test, empty can test, push off test, Hawkin’s test, Neer’s test
Cervical testing regarding shoulder pain
Positive or negative Spurling’s test
General shoulder clinical pearls
Acute shoulder pain often seek treatment following trauma. Diagnosis made by observation, gentle palpation, and x-ray
Shoulder pain unrelated to trauma
Must distinguish between extrinsic and intrinsic causes. Rule out potentially dangerous extrinsic causes, then move on to more common patterns of shoulder pain.
Poorly localized shoulder pain
Often describes extrinsic cause
Trauma of shoulder and pain
Acute symptoms with history of recent trauma are usually due to acromioclavicul separation, glenohumeral dislocation, fracture, or rotator cuff tear
Anteriolateral shoulder pain
Aggravated by reaching overhead is common. Often associated with impingement syndrome and various stages of rotator cuff tendinopathy
Adhesive capsulitis (frozen shoulder)
Most likely diagnosis when pain is accompanied by stiffness and a significant loss of movement in both active and passive motion of shoulder
Cervical nerve root impingement and shoulder pain
Can produce sharp pain radiating from the neck into the posterior shoulder area and arm
Bursitis of the olecranon (swelling)
Most common complaint of elbow swelling. Warmth and redness and rapid swelling indicate trauma, sepsis, or gout. Ability to extend and flex elbow completely excludes an intraarticular process as cause of elbow pain
Medical epicondylitis - golfer’s elbow - pain
2nd most common elbow complaint. Frequently arises from medical epicondyle or ulner nerve as it travels through the cubital tunnel. Pain is well localized and aggravated by actions that contract the wrist flexors, such as lifting or repetitious use of forearm and wrist
Lateral epicondylitis - tennis elbow - pain
Most common elbow complaint. Source may be due to joint injury or referred shoulder or neck pain. Pain typically well localized and aggravated by activity that contracts the wrist extensors, including repetitious use of forearm and wrist and shaking hands
Differential diagnoses of olecranon bursitis
Fracture of olecranon process of ulna and gouty tophus or RA
Treatment of small mass and mild symptoms with olecranon bursitis
Bursitis should be left alone or treated symptomatically with activity modification and possible NSAIDs. Wear elbow pain and avoid hyperflexion against hard surfaces
Treatment of more symptomatic bursitis with olecranon bursitis
Undergo aspiration followed by gram stain and culture of fluid. If no indication of sepsis, compression bandage. Reassess in 2-7 days
Treatment of septic bursitis with olecranon bursitis
Requires organ-specific antibiotics based on C&S of aspirate and decompression either by surgical drainage or daily aspiration
Carpal tunnel syndrome
Entrapment of median nerve at wrist. Most common compression neuropathy in upper extremity. Most common in middle-aged or pregnant women. Can occur in adjacent flexor tendon repetitive overuse, RA, tumors, pregnancy, diabetes, and thyroid dysfunction
Clinical symptoms of carpal tunnel syndrome
Vague aching that radiates into the thenar area. Aching can extend into shoulder. Pain typically accompanied by paresthesias or numbness in thumb through radial half of ring finger. Symptoms worse at night. Dropping objects, can’t open jars or twist lids
Exam of carpal tunnel syndrome
Inspect for sensation in fingers, swelling, redness, nodules, deformity, muscle atrophy, active ROM, tenderness. Phalen’s sign is most useful clinical test. Tinel’s sign.
Diagnostic tests of carpal tunnel syndrome
X-rays of limited ROM. Electrophysiologic testing can be used for confirmation
Treatment of mild to moderate carpal tunnel syndrome
Splinting, glucocorticoid injections, referral to occupational therapy, nocturnal wrist splinting, bone mobilization and yoga
Failure of conservative treatment of carpal tunnel syndrome
Duration of symptoms >10 months, age >50, constant paresthesias, positive Phalen’s sign <30 seconds, prolonged motor and sensory latencies. Surgery most effective - decompression
Osteoarthritis
Results from multiple factors, including joint integrity, genetics, local inflammation, mechanical forces, and cellular and biochemical processes. Most common in pts over 40. Principal symtpom is pain exacerbated by activity and relieved by rest
Additional symptoms of osteoarthritis
Stiffness, which typically resolvesin the morning less than 30 minutes after awakening; recurrenceof stiffness that may occur with inactivity is termed gelling
Exam of osteoarthritis
Tenderness to palpation, absence of inflammation, crepitus; bony enlargement; decreased ROM; malalighment
Places osteoarthritis typically affects
Fingers, knees, hips, and spine. Rarely affects elbows, wrists, and ankle.
Rheumatoid arthritis
Chronic, systemic, inflammatory disorder of unknown etiology that primarily involves joints. Typically symmetrical. Usually progresses from periphery to more proximal joints with significant disability within 10-20 years
Clinical characteristics of rheumatoid arthritis
Morening stiffness for at least 1 hr; swelling of 3 or more joints for 6 weeks; swelling of wrist, metacarpophalangeal, or proximal interphalangeal joints; symmetric joint swelling; elevated sed rate; rheumatoid subcutaneous nodules
Hip pain
A careful history and physical exam can determine etiology of hip pain. Character and location is the key element in establishing the diagnosis.
Increased hip pain with or after use
Increased pain after weight-bearing movement that improves at rest is the hallmark of a structural joint problem, particularly osteoarthritis
Constant hip pain, especially at night
Suggests an infectious, inflammatory, or neoplastic process
Diagnostic tests of hip pain
Plain x-ray should be performed to exclude fracture with moderate to severe hip pain. MRI may be necessary when history, physical, or plain x-rays are inconclusive
Management of hip pain related to DJD
Tylenol, NSAIDS, glucosamine with or without chondroitin, capsaicin
Management of hip pain related to bursitis
Avoid triggers that aggravate, moist heat application, ROM exercises, NSAIDs
Knee pain
Most complaints related to exercise or sports. Most common is a meniscus tear
Physical exam of knee
Most common is tenderness over medial or lateral joint line, limited ROM due to pain or effusion, positive McMurry sign
Diagnosis of meniscus tear
Trauma or effusion - x-ray. Chronic conditions - x-ray and while weight-bearing. Definitive diagnostic test - MRI
Management of meniscus tear
If no mechanical problem - RICE, crutches, improve strength. With trauma - refer
1st degree ankle sprain
Mild stretching of ligament with microscopic tears. Mild swelling and tenderness. No joint instability. Can bear weight and ambulate
2nd degree ankle sprain
More severe injury with incomplete tear. Moderate pain, swelling, tenderness, and ecchymosis. mild to moderate joint instability with restriction of ROM. Weight-bearing and ambulation are painful
3rd degree ankle sprain
Involves a complete tear. Severe pain, swelling, tenderness, and ecchymosis. Significant medical instability and loss of function. No weight-bearing or ambulation
Exam of ankle sprains
How did injury occur? Assess ROM. Diagnostic - x-ray
Management of ankle sprains
Goal - prevent chronic pain and instability. Limit inflammation and swelling and maintain ROM. Early treatment RICE for 2-3 days. NSAIDs
Fibromyalgia
Chronic, generalized musculoskeletal pain. Mostly women. Diagnosis relies on history, reseach-supported tender point criteria. Altered central pain processing.
Pathophysiology of fibromyalgia
Elevated CSF substance P; altered pain inhibitory mediators serotonin, norepi; dysregulated response to HPA axis
Criteria for diagnosis of fibromyalgia
Pain in the axial skeleton and all 4 quadrants for 3 or more months. Excessive tenderness to 4 kg of point pressure in 11 of 18 specific muscle tendon sites
Subjective data of fibromyalgia
Pain from sources that do not usually cause pain. If painful to others, then exaggerated to patient. Pain worsens with repetition of stimulus. Pain and stiffness uniform throughout the day.
Associated symptoms of fibromyalgia
Sleep disturbances, fatigue, diminished cognitive function, lightheadedness, dizziness, palpitations
Co-morbidities of fibromyalgia
Depression, anxiety, chronic fatigue syndrome, migraine, IBS, restless leg, TMJ dysfunction, female urethral syndrome
Physical exam of fibromyalgia
Complete exam. Look for signs of inflammation and palpation of tender points
Diagnostics of fibromyalgia
No specific test. Diagnosis made on history and physical findings
Management of fibromyalgia
Education. Information. Fibromyalgia impace questionnaire at baseline ad with each chane in treatment
Non-pharmacoligic treatment of fibromyalgia
Exercise - aerobic. Cognitive behavioral therapy. Strength training, acupuncture, hypnotherapy, biofeedback, medicinal baths
Pharmacological treatment of fibromyalgia
NSAIDs, TCAs at night to improve sleep. Cyclobenzaprine. FDA approved drugs - alpha-2deltoid ligand pregabalin (Lyrica). SNRI (Cymbalta and milnacipran)
Use of opioids to treat fibromyalgia
Chronic use will cause neuroadaptive changes that maintain or enhance central sensitivity to pain
