AFP Journal Review January 15, 2010 Issue Katina Robertson, MD

AFP Journal Review January 15, 2010 Issue Katina Robertson, MD
Emory Family Medicine AFP Journal Review January 15, 2010 Issue

Articles Reviewed Peripheral Nerve Entrapment and Injury in the Upper Extremity Vocal Cord Dysfunction Noninfectious Penile Lesions Outdoor Air Pollutants and Patient Health

Peripheral Nerve Entrapment and Injury in the Upper Extremity

Peripheral Nerve injury
Peripheral Nerve Injury (PNI) in UE is common Risk Factors Superficial position Long course through area at high risk of trauma Narrow path through bony canal

Anatomy and Risk Factors
ANATOMY AND RELATED RISK FACTORS OF UPPER EXTREMITY NERVE INJURY Nerve Anatomy Function Risk factors for injury Axillary From brachial plexus, around humeral head, through the quadrilateral space to deltoid/teres minor. Quadrilateral space boundaries: humeral neck, teres major and minor, long head of triceps Motor: deltoid, teres minor. Sensory: skin over lower half of the deltoid Humeral head compresses nerve during extreme abduction. Upward pressure through the axilla. Shoulder dislocation. Compression in quadrilateral space Long thoracic C5 to C7 merge, travel between clavicle and first rib through axilla to serratus anterior muscleLong nerve: 20 to 22 cm Motor: serratus anterior. Sensory: none Sudden upper extremity traction. Shoulder depression with contralateral neck flexion. Prolonged compression (backpacker's palsy) Median Brachial plexus down anterior arm, at antecubital fossa passes through radial tunnel, dives between two heads of pronator muscle, under flexor digitorum superficialis, through carpal tunnel Motor: Injury at elbow or forearm: Weak wrist flexion, no interphalangeal flexion of thumb, index, and long digitInjury at wrist: none or weak thumb abduction. Sensory: Injury at elbow: proximal forearm painInjury at wrist: sensory loss in the thumb, radial 2.5 digits, and thenar eminence Injury at elbow /forearm: radial tunnel, within pronator teres muscle, under flexor digitorum superficialis. Injury at wrist: carpal tunnel syndrome

ANATOMY AND RELATED RISK FACTORS OF UPPER EXTREMITY NERVE INJURY Nerve Anatomy Function Risk factors for injury Musculocutaneous C5 to C7 merge into lateral cord brachial plexus, goes through axilla, under coracobrachialis, through biceps and under deep fascia at the elbow Motor: Injury at shoulder: loss in biceps, coracobrachialis, and brachialis. Injury at elbow: none. Sensory: radial side of forearm (dorsal and volar), but not hand Shoulder dislocation. Hypertrophy of the coracobrachialis. Deep brachial fascia of elbow as nerve exits biceps (sensory symptoms only) Radial From brachial plexus, through axilla, down posterior arm until it circles toward anterior arm at spiral groove of the humerus; down anterior arm and enters radial tunnel just above the lateral epicondyleDivides into superficial and deep (posterior interosseus nerve) branches Motor: Injury in axilla: loss of elbow flexion; weak wrist and digit extension; weak forearm supination Injury at elbow: superficial branch (radial tunnel): forearm pain, normal motor; posterior interosseus nerve: weak or no wrist extension. Injury at wrist: no motor loss. Sensory: variable sensory loss in distal forearm or hand. Injury at elbow: no sensory loss; possible pain with repetitive forearm supination Injury in axilla or proximal humerus (fracture). Injury at elbow: radial tunnel or area of proximal radius (fracture or dislocation); two nerve branches from elbow have injury potential, posterior interosseus nerve has mostly motor loss and the superficial branch has only sensory change (pain) Spinal accessory Emerges through sternocleidomastoid muscle, across posterior neck, dives under trapezius Motor: trapezius. Sensory: none Very superficial course in posterior neck and directly under the trapezius muscle

ANATOMY AND RELATED RISK FACTORS OF UPPER EXTREMITY NERVE INJURY Nerve Anatomy Function Risk factors for injury Suprascapular From upper trunk brachial plexus, through posterior triangle, across top of scapula and through scapular notch, down posterior aspect scapula and across scapular spine to supraspinatus, infraspinatus Motor: supraspinatus, infraspinatus. Sensory: acromioclavicular and glenohumeral joints Entrapment under transverse scapular ligament that covers the suprascapular notchInjury as it crosses scapular spine or under spinoglenoid ligament Ulnar From brachial plexus down anterior arm; just above medial epicondyle it passes to the posterior compartment and into the cubital tunnel; down ulnar side of forearm into Guyon canal (boundaries are hamate and pisiform bones); splits into deep (motor) and superficial (sensory) branches in canal Motor: no loss or weak thumb adduction, weak digit abduction, and adduction toward center of long digit. Sensory: Injury at elbow: pain ulnar side of forearm with or without paresthesias in ulnar digits. Injury at wrist: paresthesias in ulnar digits Injury at elbow or forearm: cubital tunnel, ulnar nerve irritation with medial collateral ligament deficiency. Injury at wrist: Guyon canal Upper trunk cervical plexus Nerve roots C5 and C6 as they exit vertebral foramina and form upper trunk brachial plexus Motor: infraspinatus, supraspinatus, biceps, and deltoid. Sensory: C5 and C6 dermatomes No protective coverings (epineurium and perineurium) on the nerves after they exit the foramina. Increased risk of stretch injury at neck and shoulder regionsContusion or compression of upper trunk at Erb point

Pathophysiology Three categories of nerve injury
Neurapraxia– least severe, focal damage of myelin fibers around axon. Limited course (days-wks) Axonotmesis– more severe, axonal injury. Nerve regeneration possible but prolonged (months) and incomplete recovery Neurotmesis– complete disruption of axon. Little chance of regeneration or clinical recovery Mechanisms of nerve injury Direct pressure Repetitive microtrauma Stretch- or compression- induced ischemia The three categories of nerve injuries are neurapraxia, axonotmesis, and neurotmesis. Neurapraxia is least severe and involves focal damage of the myelin fibers around the axon, with the axon and the connective tissue sheath remaining intact. Neurapraxia typically has a limited course (i.e., days to weeks). Axonotmesis is more severe, and involves injury to the axon itself. Regeneration of the nerve is possible, but typically prolonged (i.e., months), and patients often do not have complete recovery. Neurotmesis involves complete disruption of the axon, with little likelihood of normal regrowth or clinical recovery.2,3 Most nerve injuries result in neurapraxia or axonotmesis. Mechanisms of nerve injury include direct pressure, repetitive microtrauma, and stretch- or compression-induced ischemia. The degree of injury is related to the severity and extent (time) of compression.4

Differential Diagnosis
SYMPTOMS OF UPPER EXTREMITY NERVE INJURIES Differential Diagnosis Consider PNI in pts with pain, weakness, parasthesias not related to known bone/soft tissue/vascular injury Anatomic area Symptom Nerve injuries to consider Shoulder Pain or numbness Axillary Brachial plexus Weakness Long thoracic Spinal accessory Suprascapular Forearm Pronator Radial tunnel Posterior interosseous Hand Radial at wrist Ulnar at wrist or elbow Median at wrist Ulnar at elbow

Cutaneous innervation & Dermatomes
It is helpful to understand the nerves commonly involved, their function, and the corresponding areas of the body at risk of compression or entrapment. Figures 1 and 2 show typical distributions of nerves in the upper extremity

Shoulder & Arm Axillary Brachial Plexus Long Thoracic Spinal Accessory
Suprascapular

Axillary Nerve: Quadrilateral Space Syndrome
Mechanism Shoulder dislocation Upward pressure (e.g., from improper crutch use) Repetitive overload activities (e.g., pitching a ball, swimming) Arthroscopy or Rotator cuff repair Symptoms Arm fatigue w/ overhead activity or throwing +/- associated paresthesias of lateral &posterior upper arm Signs Weak abduction Weak external rotation The axillary nerve is vulnerable to trauma as it passes through the quadrilateral space. Injury can occur from shoulder dislocation; upward pressure (e.g., from improper crutch use); repetitive overload activities (e.g., pitching a ball, swimming); and arthroscopy or rotator cuff repair. The typical symptom is arm fatigue with overhead activity or throwing. There may be associated paresthesias of the lateral and posterior upper arm. Examination reveals weak lateral abduction and external rotation of the arm.

Brachial Plexus: Stinger
Mechanism Collision sports (e.g. football) Symptoms Classic: acute onset paresthesias in upper arm Paresthesias in circumferential pattern (not dermatomal) Short duration: last seconds-minutes Motor symptoms can develop at any point Signs Differentiate from C-spine injury (point tenderness, pain w/ neck motion, bilateral symptoms)immobilize Motor weakness, can occur hrs-days after injury re-evaluate @ 24hrs, then every few days x 2wks if recurrent stingers w/up the neck for underlying pathology predisposing to injury sporting event: All sxs resolve in 15 min + no C-spine injury may return to play, but repeat exam during event A brachial plexus injury (i.e., stinger) is common in persons who play football, but it also occurs with other collision sports. The classic presentation is acute onset of paresthesias in the upper arm. A key characteristic is a circumferential rather than dermatomal pattern of paresthesias. Symptoms typically last seconds to minutes. Motor symptoms may be present initially or develop later. A brachial plexus injury must be differentiated from a cervical spine injury. The initial examination should focus on the neck, with palpation of the cervical vertebrae to detect point tenderness and evaluation of neck range of motion. Any indication of a cervical spine injury mandates further emergent neurologic and radiologic evaluation. Point tenderness of the cervical vertebrae or pain with neck movement is a red flag for a cervical spine injury, in which case the patient should be immobilized. Bilateral symptoms or those involving upper and lower extremities are less likely to be from a brachial plexus injury. If motor symptoms occur, the upper extremity muscle group exhibiting weakness correlates with the part of the brachial plexus that has been injured. Because motor symptoms may occur hours to days after the injury, repeated neurologic examinations are necessary—the patient should be reevaluated after 24 hours and then at least every few days for two weeks. If new symptoms or significant worsening of existing symptoms occurs, neuroimaging, electrodiagnostics, or surgical referral should be considered.8 Patients who have multiple occurrences of stingers should also have a more thorough workup, because they may have an underlying neck pathology that predisposes them to this injury.9,10 Occurrence during participation in a sporting event raises the issue of return to play. If all symptoms resolve within 15 minutes and there is no concern for cervical spine injury, the player may return to the same event with at least one repeat examination during that event.11

Long Thoracic Nerve Mechanism Blow to the shoulder
Chronic repetitive traction on nerve (e.g., tennis, swimming, baseball) Symptoms Diffuse shoulder or neck pain, worse with overhead motions Signs Winged scapula and weakness with forward elevation of arm Injury to the long thoracic nerve occurs acutely from a blow to the shoulder, or with activities that involve chronic repetitive traction on the nerve (e.g., tennis, swimming, baseball). Presenting symptoms include diffuse shoulder or neck pain that worsens with overhead activities. Examination reveals scapular winging and weakness with forward elevation of the arm.

Spinal Accessory Nerve
Mechanism Trapezius trauma Shoulder dislocation Iatrogenic (Radical neck dissection, carotid endarterectomy, and cervical node biopsy) Symptoms Generalized shoulder pain and weakness Signs Shoulder asymmetry Shoulder sag, inability to shrug shoulder to ear Weakness of forward arm elevation above horizontal plane Chronic injury trapezius atrophy Injury to the spinal accessory nerve can occur with trapezius trauma or shoulder dislocation. Radical neck dissection, carotid endarterectomy, and cervical node biopsy are iatrogenic sources of injury. Patients usually present with generalized shoulder pain and weakness. Examination of the shoulders reveals asymmetry. The affected side appears to sag and the patient is unable to shrug the shoulder toward the ear. Associated weakness of forward arm elevation above the horizontal plane is common. With chronic injury, the trapezius may atrophy.

Suprascapular Nerve Mechanism Symptoms Signs
repetitive overhead loading Glenoid labrum tear +/- cyst formation at suprascapular notch Symptoms Motor weakness Signs Infraspinatus- weak external rotation of the arm Supraspinatus- weak arm elevation, 90 to 180 degrees Differentiate from rotator cuff tear MRI Injury to the suprascapular nerve is associated with repetitive overhead loading. The suprascapular nerve serves the supraspinatus and infraspinatus muscles. The infraspinatus may be the only muscle affected, depending on the site of injury. Loss of infraspinatus function presents as weak external rotation of the arm. Supraspinatus involvement additionally presents with weak arm elevation, which is most pronounced in the range of 90 to 180 degrees. Suprascapular nerve injury can result from other shoulder pathologies, specifically a glenoid labrum tear. Cyst formation at the suprascapular notch from a labral tear is not uncommon. The cyst compresses the suprascapular nerve, affecting the supraspinatus and infraspinatus muscles.12 Suprascapular nerve injury and rotator cuff tear both lead to supraspinatus and infraspinatus weakness. Differentiating the two injuries may require magnetic resonance imaging (MRI).

Forearm & Elbow Median Radial Ulnar

Median Nerve at the elbow: Pronator Syndrome
Mechanism pronator teres m. -- compress the median nerve Symptoms Forearm discomfort and aching w/activities requiring repetitive pronation (especially w/elbow extended) +/- Paresthesias in the thumb and first two digits Signs Sensory loss over thenar eminence (not seen in carpal tunnel) Negative Tinel Negative Phalen The pronator teres muscle in the forearm can compress the median nerve, which may cause symptoms that mimic carpal tunnel syndrome. Symptoms are discomfort and aching in the forearm with activities requiring repetitive pronation of the forearm, especially with the elbow extended. Paresthesias in the thumb and first two digits may be present. Forearm sensation is normal, and sensation of the digits may also be normal. In pronator syndrome, there is sensory loss over the thenar eminence, which is not a finding of carpal tunnel syndrome. Results of the Tinel sign and Phalen maneuver at the wrist should be negative in patients with pronator syndrome.13

Radial Nerve at the elbow: Radial Tunnel & Posterior Interosseous Nerve Syndromes
Mechanism divides into a superficial branch (sensory only) and a deep branch (posterior interosseous nerve) at the lateral elbow– compression at any point Symptoms Pain that radiates from lateral elbow to forearm and wrist Pain with wrist extension or grip (shaking hands, turning doorknob) Generalized hand and forearm weakness Signs Differentiate from lateral epicondylitis (tennis elbow) Both– pain with supination against resistance w/ elbow and wrist extended Both– pain resisted extension of middle finger **Maximal tenderness over anterior radial neck If motor symptoms (weakness of digit & wrist extension)– likely post. interosseous The radial nerve divides into a superficial branch (sensory only) and a deep branch (posterior interosseous nerve) at the lateral elbow. Forearm pain that is exacerbated by repetitive forearm pronation is the presenting symptom of radial tunnel syndrome, which involves injury to the superficial branch of the radial nerve. Symptoms of radial tunnel syndrome are almost identical to those of tennis elbow (i.e., lateral epicondylitis), and distinguishing the two can be difficult because physical examination maneuvers that aggravate radial tunnel syndrome may also be positive in patients with tennis elbow (e.g., supination against resistance with the elbow and wrist extended, and resisted extension of the middle finger).14 A differentiating factor is the point of maximal tenderness. In radial tunnel syndrome, this point is over the anterior radial neck; in tennis elbow, it is at the origin of the extensor carpi radialis brevis muscle. The presence of any motor symptoms is more likely related to injury of the posterior interosseus nerve, which supplies the extensor muscles of the hand. Generalized hand weakness is the presenting symptom of posterior interosseus nerve syndrome. Examination reveals weakness of digit and wrist extension, although this is usually more prominent in the digits than in the wrist.

Ulnar Nerve at the elbow: Cubital Tunnel Syndrome
Mechanism Very superficial– injury from acute contusion or chronic compression Symptoms Paresthesias of the fourth and fifth digits elbow pain radiating to the hand (sxs may be worse w/ prolonged or repetitive elbow flexion) Signs Sensory loss Motor: Weak digit abduction, weak thumb abduction, and weak thumb-index finger pinch Late finding– decreased power grip The ulnar nerve at the elbow is very superficial and at risk of injury from acute contusion or chronic compression. Compression can be from an external or internal source. As the elbow flexes, the cubital tunnel volume decreases, causing internal compression. Cubital tunnel syndrome may cause paresthesias of the fourth and fifth digits. There may be elbow pain radiating to the hand, and symptoms may be worse with prolonged or repetitive elbow flexion. Paresthesias precede clinical examination findings of sensory loss. Weakness may occur, but is a late symptom. When present, motor findings are weak digit abduction, weak thumb abduction, and weak thumb-index finger pinch. Power grip is ultimately affected.

Hand & Wrist Median Radial Ulnar

Median Nerve at the wrist: Carpal Tunnel Syndrome
Mechanism Repetitive fine movements– chronic compression Symptoms Paresthesias of thumb, 2nd & 3rd digits +/- forearm pain Signs Hypalgesia (positive LR of 3.1) Abnormality in a Katz hand diagram Positive Tinel & Phalen signs Late findings: weak thumb abduction, thenar atrophy Carpal tunnel syndrome is the most common nerve entrapment injury.15 Early symptoms are paresthesias of the thumb, index digit, and long digit. Some patients also have forearm pain. The most helpful physical examination findings are hypalgesia (decreased pain sensitivity, positive likelihood ratio of 3.1) and abnormality in a Katz hand diagram.16 Although commonly used in patients with carpal tunnel syndrome, Tinel sign and Phalen maneuver are less accurate.16 The sensory examination is normal initially, although late findings include sensory loss in the median nerve distribution, weak thumb abduction, and thenar atrophy. Electrodiagnostic testing can be useful and quantitates severity of entrapment, although false negatives and false positives may occur

Katz Hand Diagram classic carpal tunnel syndrome (CTS) for both hands; B. probable CTS, because of symptoms in palm; C. unlikely CTS

Radial Nerve at the wrist: Handcuff Neuropathy
Mechanism Superficial branch of the radial nerve crosses the volar wrist-- vulnerable to compression by anything wound tightly around the wrist (e.g. handcuffs) Symptoms Numbness on dorsal hand (usually on radial side) Signs Decreased sensation to soft touch and pinprick over the dorsoradial hand, dorsal thumb, and index digit Motor intact The superficial branch of the radial nerve crosses the volar wrist on top of the flexor retinaculum of the carpal tunnel. It is vulnerable to compression by anything wound tightly around the wrist. Historically, this is an area easily injured by tight handcuffs, thus the name “handcuff neuropathy.” The injury leads to numbness on the back of the hand, mostly on the radial side. Examination may reveal decreased sensation to soft touch and pinprick over the dorsoradial hand, dorsal thumb, and index digit. Motor function is typically intact.

Ulnar Nerve at the wrist: Cyclist’s Palsy
Mechanism Common in cyclists -- ulnar nerve compressed against handlebar during cycling Activities involving prolonged pressure on the volar wrist (e.g., jackhammer use) Symptoms Paresthesias in the 4th and 5th digits Weakness uncommon -- motor portion of nerve less superficial at wrist Signs Unless activity is prolonged or chronic-- results of the sensory examination are normal Numbness resolves within hours after stopping the activity Injury of the ulnar nerve at the wrist is common in cyclists because the ulnar nerve gets compressed against the handlebar during cycling, resulting in “cyclist's palsy.” This type of nerve injury occurs with other activities involving prolonged pressure on the volar wrist (e.g., jackhammer use). Symptoms are paresthesias in the fourth and fifth digits. Digit weakness is uncommon because the motor portion of the nerve at the wrist is less superficial. Unless the activity is prolonged or chronic, results of the sensory examination are normal and numbness will resolve within a few hours after stopping the activity.

Shoulder & Arm

Forearm & Elbow

Hand & Wrist

Diagnostic Testing Plain XR: fracture or cervical spondyloarthropathy
Plain radiography is primarily useful for identifying other diagnoses, such as fracture or cervical spondyloarthropathy. MRI is rarely needed for initial evaluation of a typical nerve injury, although it may be helpful for specific nerves (Table 5).18 Chronic nerve injury can lead to denervation changes in muscle. These changes may be visible on MRI as abnormal signal patterns. A normal MRI finding does not rule out nerve injury. Newer techniques, such as gadofluorine M–enhanced MRI, may ultimately be able to assess nerve regeneration.19 Ultrasonography is a less expensive modality to define anatomic entrapment, but its use is limited by lack of standardization of technique and interpretation.20

Electrodiagnostic Testing
Nerve Conduction Studies– Evaluate motor and sensory nerves; Demyelination = slowing of conduction velocity Helpful in confirming diagnosis in pts with atypical presentations In pts with “classic” presentation, NCS do not change diagnosis or management, i.e. don’t bother EMG– useful in conjunction with NCS to distinguish central vs peripheral neuropathies Electrodiagnostic testing consists of nerve conduction studies and electromyography (EMG). Nerve conduction studies assess the integrity of sensory and motor nerves. Areas of nerve injury or demyelination appear as slowing of conduction velocity along the nerve segment in question. EMG records the electrical activity of a muscle from a needle placed into the muscle, looking for signs of denervation.21,22 The combination of nerve conduction studies and EMG can help distinguish peripheral from central nerve injuries. Electrodiagnostic testing is commonly used to evaluate for carpal tunnel syndrome and cubital tunnel syndrome. Nerve conduction studies have been shown to confirm carpal tunnel syndrome with a sensitivity of 85 percent and a specificity of 95 percent.23 Nerve conduction studies also may help confirm the diagnosis in patients who have a history or physical examination findings that are atypical of carpal tunnel syndrome. For most patients who have a typical presentation, nerve conduction studies do not change the diagnosis or management.

The initial management of most nerve injuries is nonsurgical
The initial management of most nerve injuries is nonsurgical. The main components of treatment are relative rest and protection of the injured area. Anti-inflammatory medications are often added, although it is unknown if they aid healing. Mobility of associated joints should be maintained at full range of motion, and effort should be made to increase the strength of any supporting or accessory muscles. Specifics of conservative therapy and indications for surgical referral are shown in Table 6.13,15,25–46 Systematic reviews of carpal tunnel syndrome have found short-term benefit from local corticosteroid injection, splinting, oral corticosteroids, ultrasound, yoga, and carpal bone mobilization.29 Symptom relief from local injection has not been shown to last longer than one month, and there is no demonstrated benefit from a second injection.30 Clinical outcome from local corticosteroid injection is similar to that from splinting combined with anti-inflammatory medication.29 Vitamin B6, ergonomic keyboards, diuretics, and nonsteroidal anti-inflammatory drugs have not been shown to be beneficial.29,30 Patient characteristics that predict a poor response to nonsurgical therapy include age older than 50 years, symptom duration longer than 10 months, history of trigger digit, constant paresthesias, and Phalen maneuver that is positive in less than 30 seconds.47 Surgical treatment likely has better outcomes than splinting, but it is unclear if surgical treatment is better than corticosteroid injection.48 Treatment Options

Recommendations

Peripheral Nerve Injury
A football player presents with upper arm paresthesias following a tackle. Which one of the following statements about a brachial plexus nerve injury (i.e., stinger) is correct? (check one) A. Paresthesias typically have a dermatomal pattern. B. The athlete should not return to competition or activity for two weeks. C. Bilateral symptoms make the diagnosis more likely. D. Paresthesias typically have a circumferential pattern.

A patient works on an assembly line doing repetitive overhead work. He has weakness with external rotation of the right arm and when he raises his right arm above his shoulder. Which one of the following nerves is likely involved? (check one) A. Suprascapular nerve. B. Posterior interosseus nerve. C. Radial nerve. D. Ulnar nerve.

Which of the following has/have been shown to provide short-term benefit for patients with carpal tunnel syndrome? (check all that apply) A. Nonsteroidal anti-inflammatory drugs. B. Corticosteroid injection. C. Vitamin B6. D. Splinting.

Vocal Cord Dysfunction

Definition: inappropriate vocal cord motion produces partial airway obstructionsubjective respiratory distress Normal-- person breathes  cords move away from midline during inspiration & slightly toward the midline during expiration Dysfunction-- person breathes  cords move toward the midline during inspiration or expiration = obstruction Other terms: paradoxical vocal cord dysfunction, paradoxical vocal fold motion, factitious asthma Vocal cord dysfunction is a syndrome in which inappropriate vocal cord motion produces partial airway obstruction, leading to subjective respiratory distress. When a person breathes normally, the vocal cords move away from the midline during inspiration and only slightly toward the midline during expiration.1 However, in patients with vocal cord dysfunction, the vocal cords move toward the midline during inspiration or expiration, which creates varying degrees of obstruction.2 Vocal cord dysfunction has numerous labels in the literature, including paradoxical vocal cord dysfunction,3 paradoxical vocal fold motion,4 and factitious asthma.

Clinical Presentation
Women >men; Ages 20-40 Symptoms -- recurrent , subj. resp distress Inspiratory stridor Cough Choking sensation Throat tightness 59% with VCD, previously Dx of asthma Sxs usually mild, intermittent Laryngospasm (subtype of VCD) brief involuntary spasm of vocal cords producing aphonia and acute resp distress common complication of anesthesia Spasmodic Dysphonia hoarseness and voice strain when the abnormal vocal cord motion occurs during speech Vocal Cord Dysfunction Vocal cord dysfunction occurs more often in women than in men, and is common in persons 20 to 40 years of age.2,6,7 However, studies have identified vocal cord dysfunction in adolescents and in children as young as eight years.8 Patients with vocal cord dysfunction typically present with recurrent episodes of subjective respiratory distress that are associated with inspiratory stridor, cough, choking sensations, and throat tightness.3 The presence of wheezing can indicate an asthma exacerbation, but is commonly a mistaken description of the stridor characteristic of vocal cord dysfunction.9,10 In one study, 59 percent of patients with vocal cord dysfunction had been previously diagnosed with asthma.8 Most patients with vocal cord dysfunction have intermittent and relatively mild symptoms, although some patients may have prolonged and severe symptoms. Laryngospasm, a subtype of vocal cord dysfunction, is a brief involuntary spasm of the vocal cords that often produces aphonia and acute respiratory distress. Laryngospasm is a common complication of anesthesia.11 Another variation of vocal cord dysfunction is spasmodic dysphonia, which causes hoarseness and strained vocalization when the abnormal vocal cord motion occurs during speech.12

Differential Diagnosis
Vocal Cord Dysfunction The primary diagnosis to consider in patients with respiratory distress or wheezing is asthma. Vocal cord dysfunction is often misdiagnosed as asthma, and a considerable subset of patients with vocal cord dysfunction also have asthma, making the diagnosis more difficult.2,8 A careful patient history may help to differentiate between the two conditions. Unlike asthma, vocal cord dysfunction causes more difficulty with inspiration than expiration, and is commonly associated with a sensation of throat tightness or choking. However, further testing, including pulmonary function testing and laryngoscopy, is usually required to make the diagnosis.13 Additional conditions in the differential diagnosis of vocal cord dysfunction are listed in

Precipitating Factors
Exercise: consider in pts with exercise-induced asthma not improved with bronchodilators Psychosocial Conditions: stress disorder, anxiety, depression, and panic attack Irritants: environmental/occupational ammonia, dust, smoke, soldering fumes, and cleaning chemicals Rhinosinusitis GERD Medications: neuroleptics can cause transient VCD (considered focal dystonic reaction) Vocal Cord Dysfunction EXERCISE Exercise is a common cause of vocal cord dysfunction. Exercise-induced vocal cord dysfunction is often misdiagnosed as exercise-induced asthma.8 It should be strongly considered in patients with dyspnea on exertion who have been diagnosed with exercise-induced asthma, particularly if they respond poorly to usual treatment with bronchodilators.7 PSYCHOLOGICAL CONDITIONS Studies have reported associations between vocal cord dysfunction and multiple psychological conditions, including posttraumatic stress disorder, anxiety, depression, and panic attack.14 Anxiety disorders appear to be particularly common in adolescent patients with vocal cord dysfunction.15 However, associated depression and anxiety may also be consequences of persistent respiratory symptoms, rather than causes.16 IRRITANTS Exposure to environmental and occupational irritants has been found to precipitate respiratory symptoms consistent with vocal cord dysfunction. Common airborne irritants associated with vocal cord dysfunction include ammonia, dust, smoke, soldering fumes, and cleaning chemicals. Studies have shown a clear temporal relationship between exposure and onset of symptoms.17 RHINOSINUSITIS Postnasal drip associated with rhinosinusitis has been linked to airway hyperresponsiveness.18 A high prevalence of rhinosinusitis in patients with vocal cord dysfunction and case reports of resolution of vocal cord dysfunction symptoms with treatment suggest that rhinosinusitis may play a role in some patients.17 GASTROESOPHOGEAL REFLUX DISEASE Gastroesophageal reflux disease (GERD) has been implicated in triggering vocal cord dysfunction.19 In some studies, a high prevalence of GERD was identified in patients with vocal cord dysfunction20; however, treatment of GERD was only effective in decreasing vocal cord dysfunction in some patients. MEDICATION USE Neuroleptic drugs, specifically phenothiazines, may cause transient vocal cord dysfunction. This appears to be a focal dystonic reaction and is associated with extra-pyramidal signs, such as torticollis.21

Diagnosis PFT w/ a flow-volume loop = most common diagnostic test
expiratory loop = normal inspiratory loop = flattened (c/w extrathoracic upper airway obstruction) Flexible Laryngoscopy = diagnostic standard, direct visualization Vocal Cord Dysfunction Pulmonary function testing with a flow-volume loop is the most commonly used diagnostic test to confirm vocal cord dysfunction. In the flow-volume loop, it is typical for the expiratory loop to be normal and the inspiratory loop to be flattened, which is consistent with an extrathoracic upper airway obstruction (Figure 1). This pattern is characteristic of patients when they are symptomatic.22 Even when asymptomatic, some patients with vocal cord dysfunction will demonstrate inspiratory loop flattening.2 Exercise flow-volume loops, performed in conjunction with exercise testing, may be useful in identifying patients with exercise-induced vocal cord dysfunction Pulmonary function testing is particularly useful in differentiating vocal cord dysfunction from asthma because bronchospasm produces an impaired expiratory loop that is different from that seen in vocal cord dysfunction.24 In cases with an unclear etiology, or if concurrent asthma and vocal cord dysfunction are suspected, methacholine challenge testing may help to clarify the diagnosis.25 FLEXIBLE LARYNGOSCOPY Flexible laryngoscopy is considered the diagnostic standard for vocal cord dysfunction. Direct observation of abnormal vocal cord movement toward the midline during inspiration or expiration confirms the diagnosis. Most patients with symptomatic vocal cord dysfunction will demonstrate the abnormal movement, and more than one half of patients who are asymptomatic will be diagnosed.2,26 Stimulating asymptomatic patients with panting, deep breathing, phonating, or exercising may increase the sensitivity of the test.

Treatment Vocal Cord Dysfunction SHORT-TERM
Patients with vocal cord dysfunction may present with acute respiratory distress in the emergency department or outpatient setting.10 After other causes have been ruled out, vocal cord dysfunction can be treated with a variety of interventions (Table 2). Reassurance and breathing instruction may resolve an acute episode of vocal cord dysfunction. Published case reports suggest that having the patient breathe rapidly and shallowly (i.e., pant) can result in immediate resolution of symptoms.27 Additional breathing maneuvers include diaphragmatic breathing, breathing through the nose, breathing through a straw, pursed-lip breathing, and exhaling with a hissing sound. Administering a helium and oxygen mixture (heliox) reduces airway resistance and may result in rapid improvement in patients with acute vocal cord dysfunction. A trial of heliox may be appropriate because of its relatively low cost and minimal adverse effects, although this has been reported in only one case series

Which of the following is/are common triggers of vocal cord dysfunction? (check all that apply) A. Gastroesophageal reflux disease. B. Airborne irritants. C. Anticholinergics. D. Exercise.

Which of the following is/are the most valuable diagnostic tests for confirming vocal cord dysfunction? (check all that apply) A. Methacholine challenge test. B. Flexible laryngoscopy. C. Pulmonary function testing with a flow-volume loop. D. Arterial blood gases.

Which of the following symptoms is/are often present in patients with vocal cord dysfunction? (check all that apply) A. Cough. B. Inspiratory stridor. C. Choking sensation. D. Throat tightness.

Noninfectious Penile Lesions
Inflammatory Papulosquamous Neoplastics

Anatomy Noninfectious Penile Lesions

Psoriasis Epidemiology Symptoms bimodal peaks at 16-22 yo & 57-60 yo
Prevalence 1-2%, up to 40% have GU involvement Symptoms red or salmon-colored, papulosquamous, circinate plaques, w/ white or silvery scales Pruritis Exacerbated by-- stress, excess etoh &tobacco use, acute infections (strep), medications(e.g., beta blockers, lithium) Noninfectious Penile Lesions Psoriasis may occur at any age, with bimodal peaks at 16 to 22 years of age and at 57 to 60 years of age.2,3 The prevalence of psoriasis in the United States is 1 to 2 percent,4 with genital involvement occurring in up to 40 percent of patients.3,5–7 Psoriasis presents as red or salmon-colored, papulosquamous, circinate plaques (Figure 1), often associated with white or silvery scales.2,5 Pruritus and psychosocial distress are common. Exacerbating factors include stress, excessive alcohol and tobacco use, acute infections (particularly streptococcal), and some medication use (e.g., beta blockers, lithium).8 Extragenital psoriasis occurs on the extensor surfaces of elbows and knees, scalp, lumbosacral region, umbilicus, and nails. Psoriatic arthritis occurs in up to 25 percent of patients. Psoriasis is usually clinically apparent in the presence of nail pitting or confirmatory lesions elsewhere on the body.3 Punch or shave biopsy is indicated if lesions are atypical. Treatment depends on whether the disease is localized or disseminated.3,5,7,9 First-line localized treatment includes mild to midstrength topical corticosteroids.3,6,8,9 Once-daily application of corticosteroids is sufficient because genital skin is permeable, and corticosteroid receptors remain saturated for almost 24 hours. As a general rule, no more than 50 g of ultrapotent or 100 mg of potent topical corticosteroids should be applied over a long-term period9 because continuous use may cause skin atrophy. Lesions may reappear when corticosteroid use is discontinued.10 To avoid overdose, daily ultrapotent topical corticosteroid use should be limited to two weeks, followed by weekend dosing.10 If long-term therapy is required, tacrolimus (Protopic) or pimecrolimus (Elidel) may be appropriate, without the risk of atrophy.11 Vitamin D3 analogues are a first-line option for localized disease, and are usually applied once or twice daily. Patients with refractory disease should be referred to a dermatologist.

Psoriasis Noninfectious Penile Lesions Diagnosis
Clinical systemic signs (nail pitting, arthritis, other skin) If atypical– punch or shave biopsy Treatment 1st line options for localized disease mild to mod strength topical corticosteroids (CS)—qDay Vitamin D3 analogues– qDay or BID Prevent skin atrophy– use <50 mg ultrapotent or <100 mg potent topical CS over long-term dose ultrapotent daily x 2wks then q weekend Lesions may recur when CS discontinued If long-term therapy required, tacrolimus (Protopic) or pimecrolimus (Elidel) may decrease risk of atrophy Refractory cases– dermatology referral Noninfectious Penile Lesions Psoriasis may occur at any age, with bimodal peaks at 16 to 22 years of age and at 57 to 60 years of age.2,3 The prevalence of psoriasis in the United States is 1 to 2 percent,4 with genital involvement occurring in up to 40 percent of patients.3,5–7 Psoriasis presents as red or salmon-colored, papulosquamous, circinate plaques (Figure 1), often associated with white or silvery scales.2,5 Pruritus and psychosocial distress are common. Exacerbating factors include stress, excessive alcohol and tobacco use, acute infections (particularly streptococcal), and some medication use (e.g., beta blockers, lithium).8 Extragenital psoriasis occurs on the extensor surfaces of elbows and knees, scalp, lumbosacral region, umbilicus, and nails. Psoriatic arthritis occurs in up to 25 percent of patients. Psoriasis is usually clinically apparent in the presence of nail pitting or confirmatory lesions elsewhere on the body.3 Punch or shave biopsy is indicated if lesions are atypical. Treatment depends on whether the disease is localized or disseminated.3,5,7,9 First-line localized treatment includes mild to midstrength topical corticosteroids.3,6,8,9 Once-daily application of corticosteroids is sufficient because genital skin is permeable, and corticosteroid receptors remain saturated for almost 24 hours. As a general rule, no more than 50 g of ultrapotent or 100 mg of potent topical corticosteroids should be applied over a long-term period9 because continuous use may cause skin atrophy. Lesions may reappear when corticosteroid use is discontinued.10 To avoid overdose, daily ultrapotent topical corticosteroid use should be limited to two weeks, followed by weekend dosing.10 If long-term therapy is required, tacrolimus (Protopic) or pimecrolimus (Elidel) may be appropriate, without the risk of atrophy.11 Vitamin D3 analogues are a first-line option for localized disease, and are usually applied once or twice daily. Patients with refractory disease should be referred to a dermatologist.

Lichen Sclerosus (balanitis xerotica obliterans)
Epidemiology All ages; ave age 42yo Prevalence..? 1 in 300 4-6% assoc w/ squamous cell carcinoma (SCC) Signs/Symptoms hypopigmented lesion texture like crinkled paper/cellophane. glans penis and prepuce involv Bullae, erosions, or atrophy phimosis, painful erections, obstructive voiding, itching, pain, and bleeding DDX: carcinoma in situ, leukoplakia, and scleroderma Noninfectious Penile Lesions Penile lichen sclerosus, also known as balanitis xerotica obliterans, occurs in males of all ages.12 The average age at diagnosis is 42 years The estimated prevalence may be as high as one in 300 males.16,17 Lichen sclerosus is associated with squamous cell carcinoma in 4 to 6 percent of patients.6,14,18 Many physicians consider genital lichen sclerosus in males to be a precancerous condition that is similar to its counterpart in females.12,16 Lichen sclerosus appears as a hypopigmented lesion with a skin texture similar to crinkled paper or cellophane. It primarily affects the glans penis and prepuce (Figure 2). Bullae, erosions, or atrophy may be prominent. Patients typically present with phimosis, painful erections, obstructive voiding, itching, pain, and bleeding.16,19 Because the progression of the lesions may lead to obstruction, urinary retention may be the initial complaint.16,18,20 Almost all parts of the body can be affected, although they may be asymptomatic.12,16,20 Lichen sclerosus should be differentiated from carcinoma in situ (Figure 3), leukoplakia, and scleroderma.16,20

Lichen Sclerosus (balanitis xerotica obliterans)
Treatment Goal: decr symptoms & prevent malignant transformation mod to ultrapotent fluorinated topical CS Surgery if persistent dz or h/o SCC Circumcision if limited to glans and prepuce Severe cases– reconstructive surgery Systemic agents (e.g. retinoids) for severe refractory cases Long term f/u to monitor for malignant transformation Noninfectious Penile Lesions The goal of treatment is to reduce symptoms and prevent malignant transformation.13 Lichen sclerosus can be treated with moderate to ultrapotent fluorinated topical corticosteroids. Biopsy is indicated if squamous cell carcinoma is suspected.20 Surgery is needed in patients with persistent disease or a history of squamous cell carcinoma.18 Circumcision may be indicated in patients with lichen sclerosus limited to the glans penis and prepuce. Severe cases may require reconstructive surgery,16,19 although conservative management may be appropriate if the risks of surgery outweigh the potential benefits.16 Systemic agents, such as retinoids, are reserved for severe cases of lichen sclerosus and when local therapy fails.19 Long-term follow-up is appropriate to monitor for malignant transformation.18

Angiokeratomas Epidemiology Signs/Symptoms Age >40yo; white males
Prevalence <1% Signs/Symptoms well-circumscribed, red or blue papules, 1 to 6 mm Clinical diagnosis Usu glans penis; also involv scrotum, groin, thighs, abdominal wall Involv of penile shaft, suprapubic area, and sacrum a/w Fabry disease– referral needed rare intermittent bleeding, pain, or pruritus Tx options: (if symptomatic) surgery, cryoablation, electrocautery, and laser ablation Noninfectious Penile Lesions The prevalence of angiokeratomas is unknown, but is believed to be less than 1 percent.21 These lesions occur more often in men than women, and are more common in white persons. Angiokeratomas are benign, well-circumscribed, red or blue papules measuring 1 to 6 mm that typically occur in patients older than 40 years The diagnosis is usually made by characteristic appearance, although it may be misdiagnosed as penile cancer or pearly papules. Angiokeratomas may affect only the glans penis, or they may also affect the scrotum, groin, thighs, and abdominal wall26 (Figure 4). Patients with angiokeratomas may experience rare intermittent bleeding, pain, or pruritus.27 Angiokeratomas affecting the penile shaft, suprapubic region, and sacrum are associated with Fabry disease and should prompt referral.28 Treatment is indicated if the patient is symptomatic or if the lesions bleed. Options include surgery, cryoablation, electrocautery, and laser ablation.22,29,30 Treatment may be difficult in patients with extensive lesions.

Lichen Nitidus Epidemiology: uncommon Signs/Symptoms
Discrete, slightly elevated, hypopigmented papules, approx 1 mm Can involve upper limbs &abdomen Diff from pearly papulesring-like distribution on coronal sulcus Tx options: for cosmesis-- corticosteroids, vitamin A analogues, cyclosporine (Sandimmune), itraconazole (Sporanox), and phototherapy Noninfectious Penile Lesions Lichen nitidus is uncommon. The diagnosis is made on examination. Patients with lichen nitidus present with discrete, slightly elevated, hypopigmented papules measuring approximately 1 mm31,32 (Figure 5). These lesions should be distinguished from pearly papules, which have a ring-like distribution on the coronal sulcus (Figure 6). Lichen nitidus papules may occur on the penis, as well as the upper limbs and abdomen.31,33 Patients are typically asymptomatic and do not require treatment.31,33 Patients rarely experience pruritus.32,33 The course of lichen nitidus is variable and can resolve spontaneously.31 When treatment is indicated for cosmesis, options include corticosteroids, vitamin A analogues, cyclosporine (Sandimmune), itraconazole (Sporanox), and phototherapy.33 Laser ablation should be avoided because of the potential for scarring.

Lichen Planus Epidemiology: uncommon but ¼ affected have GU lesions
Signs/Symptoms raised, violaceous, flat-topped, polygonal papules Fine white streaks (Wickham striae), on surface Pts c/o pruritus and soreness Biopsy ulcerated/indurated lesions to r/o SCC Tx options: variable response Potent CS daily vs Ultrapotent CS qWknd If refractory and isolated to prepuce-- circumcision Noninfectious Penile Lesions Lichen planus is also uncommon. It is typically systemic, affecting mucous membranes, nails, acral sites, and the scalp.34 One fourth of patients with lichen planus have lesions on the genitalia, and most patients also have extra-genital involvement.35 Lichen planus lesions are raised, violaceous, flat-topped, polygonal papules36 (Figure 7). Fine white streaks (Wickham striae) may appear on the surface of the lesions. In uncircumcised patients, the lesions assume a lacy, white, reticulated pattern. Patients with lichen planus often complain of pruritus and soreness. Lesions may be associated with ulceration.34 Ulcerated or indurated lesions may suggest squamous cell carcinoma and require a biopsy.37 The response to treatment of lichen planus is variable.37,38 Daily potent topical corticosteroids are usually effective but carry a risk of atrophy; however, weekend dosing of ultrapotent topical corticosteroids may be effective. For isolated lichen planus of the prepuce, circumcision is indicated when medical management fails.

Zoon Balanitis Epidemiology: Signs/Symptoms Men ; usu Ages 50-62 yo
Patches bright red or brown, shiny with red specks /spots sharply demarcated occur on glans penis, inner prepuce, or coronal sulcus Lesions – tend to bleed +/- erode Mimic carcinoma in situ-- biopsy Noninfectious Penile Lesions Penile carcinoma in situ can be difficult to distinguish from other lesions, such as psoriasis. The differential diagnosis includes Zoon balanitis, a condition of unknown etiology usually affecting men 50 to 62 years of age. Zoon balanitis lesions generally appear as bright red or brown, shiny patches with red specks or as pinpoint red spots. Characteristic patches are sharply demarcated, glistening red, and occur on the glans penis, inner prepuce, or coronal sulcus. Lesions tend to bleed and may erode. Although Zoon balanitis is benign, the lesions may mimic carcinoma in situ; therefore, biopsy is needed.

Carcinoma in Situ Pre-malignant, restricted to skin Epidemiology:
uncircumcised men >60 yo Progress to SCC in 5-30% pts Etiology: Primarily HPV Other factors: smegma, trauma Signs/Symptoms 2-35 mm; involv glans penis, urethral meatus, frenulum, coronal sulcus, and prepuce Lesions= raised, beefy red, velvety, irreg shaped plaques, may ulcerate Velvety plaques of glans = erythroplasia of Queyrat Keratotic plaques on shaft, scrotum, or perineum = Bowen disease approx 50% have pruritus and pain Noninfectious Penile Lesions CARCINOMA IN SITU Penile carcinoma in situ is a premalignant lesion restricted to the skin. It typically affects uncircumcised men older than 60 years. Velvety plaques of the glans penis are known as erythroplasia of Queyrat. Keratotic plaques are known as Bowen disease (Figure 3A), which occurs on the penile shaft, scrotal skin, or perineum.6,19 Human papilloma virus (HPV) is the primary etiology of penile carcinoma in situ, although other factors may include smegma and trauma from friction, heat, and inflammation.40 Penile carcinoma in situ progresses to squamous cell carcinoma in approximately 5 to 30 percent of patients.41,42 Pruritus and pain occur in approximately 50 percent of patients with penile carcinoma in situ.41 Lesions usually appear as raised, beefy red, velvety, irregularly shaped plaques that may ulcerate (Figure 3B). The lesions are generally 2 to 35 mm in size and occur on the glans penis, urethral meatus, frenulum, coronal sulcus, and prepuce. In uncircumcised men, the lesions may be encrusted without a velvety appearance. Lesions on the shaft may appear erythematous; display fissuring; and have soft, white scales. Biopsy is needed for the diagnosis of penile carcinoma in situ; shave biopsy is generally adequate. Lesions restricted to the prepuce are treated with circumcision. Mohs micrographic surgery is indicated for other penile carcinoma in situ lesions.40 Treatment with fluorouracil, curettage, local excision, or laser ablation is associated with significant recurrence rates. Radiation may be an option for patients who are not surgical candidates or who refuse surgery. Imiquimod (Aldara) is an immune response modifier that has also been studied as a treatment option for penile carcinoma in situ.40

Carcinoma in Situ Dx: shave biopsy adequate Treatment
Prepuce only-- circumcision Other-- Mohs micrographic surgery ? Radiation for non-surgical candidates ? Imiquimod (Aldara) fluorouracil, curettage, local excision, laser ablation a/w significant recurrence Noninfectious Penile Lesions CARCINOMA IN SITU Penile carcinoma in situ is a premalignant lesion restricted to the skin. It typically affects uncircumcised men older than 60 years. Velvety plaques of the glans penis are known as erythroplasia of Queyrat. Keratotic plaques are known as Bowen disease (Figure 3A), which occurs on the penile shaft, scrotal skin, or perineum.6,19 Human papilloma virus (HPV) is the primary etiology of penile carcinoma in situ, although other factors may include smegma and trauma from friction, heat, and inflammation.40 Penile carcinoma in situ progresses to squamous cell carcinoma in approximately 5 to 30 percent of patients.41,42 Pruritus and pain occur in approximately 50 percent of patients with penile carcinoma in situ.41 Lesions usually appear as raised, beefy red, velvety, irregularly shaped plaques that may ulcerate (Figure 3B). The lesions are generally 2 to 35 mm in size and occur on the glans penis, urethral meatus, frenulum, coronal sulcus, and prepuce. In uncircumcised men, the lesions may be encrusted without a velvety appearance. Lesions on the shaft may appear erythematous; display fissuring; and have soft, white scales. Biopsy is needed for the diagnosis of penile carcinoma in situ; shave biopsy is generally adequate. Lesions restricted to the prepuce are treated with circumcision. Mohs micrographic surgery is indicated for other penile carcinoma in situ lesions.40 Treatment with fluorouracil, curettage, local excision, or laser ablation is associated with significant recurrence rates. Radiation may be an option for patients who are not surgical candidates or who refuse surgery. Imiquimod (Aldara) is an immune response modifier that has also been studied as a treatment option for penile carcinoma in situ.40

Invasive Squamous Cell Carcinoma
Epidemiology: Rare; 2-3 cases/100,000 men Peak Incidence men >70 yo SCC 95% of penile cancers Risk Factors HPV Lichen sclerosus Smegma Smoking Older age Poor hygeine Foreskin phimosis Signs/symptoms Early stage: painless lump/ ulcer Progress to thickened skin & wart-like growth sometimes a/w foul discharge Noninfectious Penile Lesions Penile cancer is rare, with a prevalence of two or three cases per 100,000 men. The peak incidence is in men older than 70 years.42 Squamous cell carcinoma accounts for 95 percent of penile cancers.40,42 Risk factors include some types of HPV infection, lichen sclerosus, smegma, smoking, older age, poor hygiene, presence of foreskin, and phimosis.6,19,40 Giant condyloma (Figure 9) may be difficult to distinguish from squamous cell carcinoma, and biopsy is indicated if the diagnosis is in doubt. The presentation of squamous cell carcinoma is variable because patients commonly delay seeking medical care, with average delays of six months or longer.42,46,47 In the early stages, squamous cell carcinoma can present as a painless lump or ulcer that progresses to thickened skin and a wart-like growth, sometimes associated with foul discharge (Figure 10A). Rashes and changes in skin coloration may occur.48 Exophytic or fungating squamous cell carcinoma typically appears as a large, irregularly shaped mass, whereas endophytic squamous cell carcinoma commonly presents as ulcerative and infiltrating lesions.42,49 Exophytic lesions occasionally lead to phimosis with the mass not visible until the prepuce is retracted The diagnosis of squamous cell carcinoma is confirmed with biopsy. The lesion size determines whether incisional or excisional biopsy should be performed.42 Treatment options have not been compared in randomized trials because of the rarity of the disease. In general, low-grade and low-stage tumors can be treated with organ-sparing techniques, such as Mohs micrographic surgery. Lesions restricted to the prepuce are generally best treated by circumcision.42 Partial penectomy, laser therapy, radiation, and brachytherapy have been attempted as alternatives to radical penectomy.6,40,49 However, penile amputation is the standard treatment for higher-stage tumors (i.e., T2 to T4).42,49 Patients should receive lifelong surveillance for recurrence.

Signs/symptoms (Cont’d) Exophytic or fungating SCC--large, irreg shape Exophytic lesions -- can cause phimosis (mass not visible until prepuce retracted) Endophytic SCC -- ulcerative and infiltrating lesions Noninfectious Penile Lesions Penile cancer is rare, with a prevalence of two or three cases per 100,000 men. The peak incidence is in men older than 70 years.42 Squamous cell carcinoma accounts for 95 percent of penile cancers.40,42 Risk factors include some types of HPV infection, lichen sclerosus, smegma, smoking, older age, poor hygiene, presence of foreskin, and phimosis.6,19,40 Giant condyloma (Figure 9) may be difficult to distinguish from squamous cell carcinoma, and biopsy is indicated if the diagnosis is in doubt. The presentation of squamous cell carcinoma is variable because patients commonly delay seeking medical care, with average delays of six months or longer.42,46,47 In the early stages, squamous cell carcinoma can present as a painless lump or ulcer that progresses to thickened skin and a wart-like growth, sometimes associated with foul discharge (Figure 10A). Rashes and changes in skin coloration may occur.48 Exophytic or fungating squamous cell carcinoma typically appears as a large, irregularly shaped mass, whereas endophytic squamous cell carcinoma commonly presents as ulcerative and infiltrating lesions.42,49 Exophytic lesions occasionally lead to phimosis with the mass not visible until the prepuce is retracted

Diagnosis: confirmed w/ biopsy (excision vs incision based on size) Treatment low-grade/low-stage tumors: organ-sparing techniques, (e.g. Mohs micrographic surgery) Prepuce only: circumcision Higher-stage tumors (i.e., T2 to T4): Penile amputation is standard treatment Partial penectomy, laser therapy, radiation, and brachytherapy have been attempted as alternatives to radical penectomy Noninfectious Penile Lesions The diagnosis of squamous cell carcinoma is confirmed with biopsy. The lesion size determines whether incisional or excisional biopsy should be performed.42 Treatment options have not been compared in randomized trials because of the rarity of the disease. In general, low-grade and low-stage tumors can be treated with organ-sparing techniques, such as Mohs micrographic surgery. Lesions restricted to the prepuce are generally best treated by circumcision.42 Partial penectomy, laser therapy, radiation, and brachytherapy have been attempted as alternatives to radical penectomy.6,40,49 However, penile amputation is the standard treatment for higher-stage tumors (i.e., T2 to T4).42,49 Patients should receive lifelong surveillance for recurrence.

Recommendations

Summary DDx

Summary Tx Options

A patient presents with red plaques on his penis. He also reports a history of silvery scales on his elbows that were diagnosed as psoriasis. Which one of the following statements about this patient’s treatment is correct? (check one) A. A minimum daily dosage of 50 g of ultrapotent topical corticosteroids is recommended. B. First-line treatment includes oral corticosteroids. C. Tacrolimus (Protopic) is inappropriate for long-term use. D. Vitamin D3 analogues should be reserved for refractory cases. E. Weekend dosing of topical corticosteroids reduces the risk of atrophy.

A 40-year-old man presents with hypopigmented penile lesions, phimosis, painful erections, and erosions that itch and bleed. The lesions are limited to the glans penis and prepuce. Which one of the following statements about this patient’s condition is correct? (check one) A. Topical corticosteroids aggravate the lesions. B. Lichen sclerosus is usually self-limiting. C. Timely treatment may prevent malignant transformation. D. Circumcision is contraindicated.

Which of the following penile lesions has/have potential for malignant transformation? (check all that apply) A. Zoon balanitis. B. Lichen sclerosis. C. Angiokeratomas. D. Erythroplasia of Queyrat.

Outdoor Air Pollutants & Patient Health
Ozone PM

Air pollutants Federal Clean Air Act– requires EPA to set National Ambient Air Quality Standards (NAAQS) for certain pollutants Six Major Pollutants ozone, particulate matter (PM), carbon monoxide, nitrogen oxides, sulfur dioxide, and lead Outdoor Air Pollutants The federal Clean Air Act requires the EPA to set National Ambient Air Quality Standards (NAAQS) for pollutants to protect the health of all persons in the United States, including vulnerable populations. The EPA standards cover six major air pollutants, also known as “criteria” pollutants: ozone, particulate matter (PM), carbon monoxide, nitrogen oxides (NOx), sulfur dioxide, and lead. This article focuses on ozone and PM, the most widespread and serious threats to health. More than 1,000 monitoring stations across the United States measure ambient concentrations of criteria air pollutants. Locations that fail to meet one or more standards are designated “nonattainment” areas. Table 1 summarizes the standards, sources of pollutants, at-risk groups, and numbers of persons in the United States living in nonattainment areas for ozone and PM.1,3,5,6 Figure 1 shows current U.S. nonattainment areas for one or more NAAQS.7 Physicians and patients can determine if their local area meets the standards by going to The EPA also provides an online training course, “Ozone and Your Patients' Health,” at

Air pollutants Does your local area meet EPA standards? Go to Outdoor Air Pollutants Figure 1 shows current U.S. nonattainment areas for one or more NAAQS.7 Physicians and patients can determine if their local area meets the standards by going to The EPA also provides an online training course, “Ozone and Your Patients' Health,” at

Air pollutants AQI = information about local air quality, potential health effects, and actions to take to protect when air pollutants reach unhealthy levels Outdoor Air Pollutants Air concentrations of criteria pollutants at most locations show substantial short-term variation, mainly because of changing weather conditions. The EPA offers daily information about air quality, including forecasts, in the form of the AQI. The AQI provides the public with concise information about local air quality, potential health effects, and actions persons can take to protect their health when air pollutants reach unhealthy levels. Pollutant concentrations are reported on a normalized, color-coded scale of 0 to 500 to convey the levels of air pollutant and related health concerns (Table 2).2 The AQI value of the day is the highest individual pollutant AQI value. An AQI value of 100 generally corresponds to the NAAQS for the pollutant. Values greater than 100 are considered unhealthy, first for vulnerable groups and then, as values get higher, for everyone. Values rarely exceed 300 in the United States. The AQI is widely publicized, usually in weather reports, using radio, newspapers, television, the Internet, and many state and local telephone hotlines. For a given AQI, pollutant-specific cautionary statements identify groups at risk and recommend actions to reduce or avoid exposure to prevent health effects (Table 2).2 The demonstrated health effects of these air pollutants are drawn from a wide range of epidemiologic studies and placebo-controlled exposure studies, and provide a sound basis for recommending risk reduction by avoiding or reducing exposure.5,8–10

Air pollutants Outdoor Air Pollutants

Air Pollutants & Patient Health
Which one of the following major air pollutants, or “criteria” pollutants, is thought to be the most widespread and serious threat to health in the United States? (check one) A. Carbon monoxide. B. Particulate matter. C. Nitrogen oxides. D. Sulfur dioxide

Which one of the following statements most accurately reflects the health advice of the U.S. Environmental Protection Agency to the general population when the Air Quality Index is 130 for ozone? (check one) A. Everyone should reduce prolonged outdoor exertion. B. No specific health advice is given. C. Persons with asthma should avoid all outdoor exertion. D. Persons with chronic obstructive pulmonary disease should reduce prolonged outdoor exertion. E. Older adults should avoid prolonged outdoor exertion.

Which of the following actions is/are recommended to reduce exposure to air pollution? (check all that apply) A. Opening windows on sunny days to reduce indoor ozone levels. B. Increasing physical activity. C. Using air conditioning in recirculation mode. D. Adjusting exercise schedules to avoid times of day when air pollution levels are highest.

Questions

AFP Journal Review January 15, 2010 Issue Katina Robertson, MD

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AFP Journal Review January 15, 2010 Issue Katina Robertson, MD

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