Presentation on theme: "AFP Journal Review January 15, 2010 Issue Katina Robertson, MD"— Presentation transcript:
1 AFP Journal Review January 15, 2010 Issue Katina Robertson, MD Emory Family MedicineAFP Journal ReviewJanuary 15, 2010 Issue
2 Articles ReviewedPeripheral Nerve Entrapment and Injury in the Upper ExtremityVocal Cord DysfunctionNoninfectious Penile LesionsOutdoor Air Pollutants and Patient Health
3 Peripheral Nerve Entrapment and Injury in the Upper Extremity
4 Peripheral Nerve injury Peripheral Nerve Injury (PNI) in UE is commonRisk FactorsSuperficial positionLong course through area at high risk of traumaNarrow path through bony canal
5 Anatomy and Risk Factors ANATOMY AND RELATED RISK FACTORS OF UPPER EXTREMITY NERVE INJURYNerveAnatomyFunctionRisk factors for injuryAxillaryFrom 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 tricepsMotor: deltoid, teres minor. Sensory: skin over lower half of the deltoidHumeral head compresses nerve during extreme abduction. Upward pressure through the axilla. Shoulder dislocation. Compression in quadrilateral spaceLong thoracicC5 to C7 merge, travel between clavicle and first rib through axilla to serratus anterior muscleLong nerve: 20 to 22 cmMotor: serratus anterior. Sensory: noneSudden upper extremity traction. Shoulder depression with contralateral neck flexion. Prolonged compression (backpacker's palsy)MedianBrachial plexus down anterior arm, at antecubital fossa passes through radial tunnel, dives between two heads of pronator muscle, under flexor digitorum superficialis, through carpal tunnelMotor: 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 eminenceInjury at elbow /forearm: radial tunnel, within pronator teres muscle, under flexor digitorum superficialis.Injury at wrist: carpal tunnel syndrome
6 Anatomy and Risk Factors ANATOMY AND RELATED RISK FACTORS OF UPPER EXTREMITY NERVE INJURYNerveAnatomyFunctionRisk factors for injuryMusculocutaneousC5 to C7 merge into lateral cord brachial plexus, goes through axilla, under coracobrachialis, through biceps and under deep fascia at the elbowMotor: Injury at shoulder: loss in biceps, coracobrachialis, and brachialis. Injury at elbow: none. Sensory: radial side of forearm (dorsal and volar), but not handShoulder dislocation. Hypertrophy of the coracobrachialis. Deep brachial fascia of elbow as nerve exits biceps (sensory symptoms only)RadialFrom 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) branchesMotor: 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 supinationInjury 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 accessoryEmerges through sternocleidomastoid muscle, across posterior neck, dives under trapeziusMotor: trapezius.Sensory: noneVery superficial course in posterior neck and directly under the trapezius muscle
7 Anatomy and Risk Factors ANATOMY AND RELATED RISK FACTORS OF UPPER EXTREMITY NERVE INJURYNerveAnatomyFunctionRisk factors for injurySuprascapularFrom 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, infraspinatusMotor: supraspinatus, infraspinatus. Sensory: acromioclavicular and glenohumeral jointsEntrapment under transverse scapular ligament that covers the suprascapular notchInjury as it crosses scapular spine or under spinoglenoid ligamentUlnarFrom 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 canalMotor: 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 digitsInjury at elbow or forearm: cubital tunnel, ulnar nerve irritation with medial collateral ligament deficiency. Injury at wrist: Guyon canalUpper trunk cervical plexusNerve roots C5 and C6 as they exit vertebral foramina and form upper trunk brachial plexusMotor: infraspinatus, supraspinatus, biceps, and deltoid. Sensory: C5 and C6 dermatomesNo 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
8 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 recoveryNeurotmesis– complete disruption of axon. Little chance of regeneration or clinical recoveryMechanisms of nerve injuryDirect pressureRepetitive microtraumaStretch- or compression- induced ischemiaThe 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.2,3Most 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
9 Differential Diagnosis SYMPTOMS OF UPPER EXTREMITY NERVE INJURIESDifferential DiagnosisConsider PNI in pts with pain, weakness, parasthesias not related to known bone/soft tissue/vascular injuryAnatomic areaSymptomNerve injuries to considerShoulderPain or numbnessAxillaryBrachial plexusWeaknessLong thoracicSpinal accessorySuprascapularForearmPronatorRadial tunnelPosterior interosseousHandRadial at wristUlnar at wrist or elbowMedian at wristUlnar at elbow
10 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
11 Shoulder & Arm Axillary Brachial Plexus Long Thoracic Spinal Accessory Suprascapular
12 Axillary Nerve: Quadrilateral Space Syndrome MechanismShoulder dislocationUpward pressure (e.g., from improper crutch use)Repetitive overload activities (e.g., pitching a ball, swimming)Arthroscopy or Rotator cuff repairSymptomsArm fatigue w/ overhead activity or throwing+/- associated paresthesias of lateral &posterior upper armSignsWeak abductionWeak external rotationThe 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.
13 Brachial Plexus: Stinger MechanismCollision sports (e.g. football)SymptomsClassic: acute onset paresthesias in upper armParesthesias in circumferential pattern (not dermatomal)Short duration: last seconds-minutesMotor symptoms can develop at any pointSignsDifferentiate from C-spine injury (point tenderness, pain w/ neck motion, bilateral symptoms)immobilizeMotor weakness, can occur hrs-days after injury re-evaluate @ 24hrs, then every few days x 2wksif recurrent stingers w/up the neck for underlying pathology predisposing to injurysporting event: All sxs resolve in 15 min + no C-spine injury may return to play, but repeat exam during eventA 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.9,10Occurrence 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
14 Long Thoracic Nerve Mechanism Blow to the shoulder Chronic repetitive traction on nerve (e.g., tennis, swimming, baseball)SymptomsDiffuse shoulder or neck pain, worse with overhead motionsSignsWinged scapula and weakness with forward elevation of armInjury 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.
15 Spinal Accessory Nerve MechanismTrapezius traumaShoulder dislocationIatrogenic (Radical neck dissection, carotid endarterectomy, and cervical node biopsy)SymptomsGeneralized shoulder pain and weaknessSignsShoulder asymmetryShoulder sag, inability to shrug shoulder to earWeakness of forward arm elevation above horizontal planeChronic injury trapezius atrophyInjury 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.
16 Suprascapular Nerve Mechanism Symptoms Signs repetitive overhead loadingGlenoid labrum tear +/- cyst formation at suprascapular notchSymptomsMotor weaknessSignsInfraspinatus- weak external rotation of the armSupraspinatus- weak arm elevation, 90 to 180 degreesDifferentiate from rotator cuff tear MRIInjury 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).
18 Median Nerve at the elbow: Pronator Syndrome Mechanismpronator teres m. -- compress the median nerveSymptomsForearm discomfort and aching w/activities requiring repetitive pronation (especially w/elbow extended)+/- Paresthesias in the thumb and first two digitsSignsSensory loss over thenar eminence (not seen in carpal tunnel)Negative TinelNegative PhalenThe 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
19 Radial Nerve at the elbow: Radial Tunnel & Posterior Interosseous Nerve Syndromes Mechanismdivides into a superficial branch (sensory only) and a deep branch (posterior interosseous nerve) at the lateral elbow– compression at any pointSymptomsPain that radiates from lateral elbow to forearm and wristPain with wrist extension or grip (shaking hands, turning doorknob)Generalized hand and forearm weaknessSignsDifferentiate from lateral epicondylitis (tennis elbow)Both– pain with supination against resistance w/ elbow and wrist extendedBoth– pain resisted extension of middle finger**Maximal tenderness over anterior radial neckIf motor symptoms (weakness of digit & wrist extension)– likely post. interosseousThe 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.
20 Ulnar Nerve at the elbow: Cubital Tunnel Syndrome MechanismVery superficial– injury from acute contusion or chronic compressionSymptomsParesthesias of the fourth and fifth digitselbow pain radiating to the hand (sxs may be worse w/ prolonged or repetitive elbow flexion)SignsSensory lossMotor: Weak digit abduction, weak thumb abduction, and weak thumb-index finger pinchLate finding– decreased power gripThe 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.
22 Median Nerve at the wrist: Carpal Tunnel Syndrome MechanismRepetitive fine movements– chronic compressionSymptomsParesthesias of thumb, 2nd & 3rd digits+/- forearm painSignsHypalgesia (positive LR of 3.1)Abnormality in a Katz hand diagramPositive Tinel & Phalen signsLate findings: weak thumb abduction, thenar atrophyCarpal 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
23 Katz Hand Diagramclassic carpal tunnel syndrome (CTS) for both hands; B. probable CTS, because of symptoms in palm; C. unlikely CTS
24 Radial Nerve at the wrist: Handcuff Neuropathy MechanismSuperficial branch of the radial nerve crosses the volar wrist-- vulnerable to compression by anything wound tightly around the wrist (e.g. handcuffs)SymptomsNumbness on dorsal hand (usually on radial side)SignsDecreased sensation to soft touch and pinprick over the dorsoradial hand, dorsal thumb, and index digitMotor intactThe 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.
25 Ulnar Nerve at the wrist: Cyclist’s Palsy MechanismCommon in cyclists -- ulnar nerve compressed against handlebar during cyclingActivities involving prolonged pressure on the volar wrist (e.g., jackhammer use)SymptomsParesthesias in the 4th and 5th digitsWeakness uncommon -- motor portion of nerve less superficial at wristSignsUnless activity is prolonged or chronic-- results of the sensory examination are normalNumbness resolves within hours after stopping the activityInjury 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.
29 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).18Chronic 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
30 Electrodiagnostic Testing Nerve Conduction Studies– Evaluate motor and sensory nerves; Demyelination = slowing of conduction velocityHelpful in confirming diagnosis in pts with atypical presentationsIn pts with “classic” presentation, NCS do not change diagnosis or management, i.e. don’t botherEMG– useful in conjunction with NCS to distinguish central vs peripheral neuropathiesElectrodiagnostic 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.
31 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 6.13,15,25–46Systematic 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.48Treatment Options
33 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.
34 Peripheral Nerve Injury 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.
35 Peripheral Nerve Injury 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.
37 Vocal Cord Dysfunction Definition: inappropriate vocal cord motion produces partial airway obstructionsubjective respiratory distressNormal-- person breathes cords move away from midline during inspiration & slightly toward the midline during expirationDysfunction-- person breathes cords move toward the midline during inspiration or expiration = obstructionOther terms: paradoxical vocal cord dysfunction, paradoxical vocal fold motion, factitious asthmaVocal 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.
38 Clinical Presentation Women >men; Ages 20-40Symptoms -- recurrent , subj. resp distressInspiratory stridorCoughChoking sensationThroat tightness59% with VCD, previously Dx of asthmaSxs usually mild, intermittentLaryngospasm (subtype of VCD)brief involuntary spasm of vocal cords producing aphonia and acute resp distresscommon complication of anesthesiaSpasmodic Dysphoniahoarseness and voice strain when the abnormal vocal cord motion occurs during speechVocal Cord DysfunctionVocal 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.8Patients 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
39 Differential Diagnosis Vocal Cord DysfunctionThe 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
40 Precipitating Factors Exercise: consider in pts with exercise-induced asthma not improved with bronchodilatorsPsychosocial Conditions: stress disorder, anxiety, depression, and panic attackIrritants: environmental/occupational ammonia, dust, smoke, soldering fumes, and cleaning chemicalsRhinosinusitisGERDMedications: neuroleptics can cause transient VCD (considered focal dystonic reaction)Vocal Cord DysfunctionEXERCISEExercise 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.7PSYCHOLOGICAL CONDITIONSStudies 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.16IRRITANTSExposure 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.17RHINOSINUSITISPostnasal 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.17GASTROESOPHOGEAL REFLUX DISEASEGastroesophageal 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 USENeuroleptic 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
41 Diagnosis PFT w/ a flow-volume loop = most common diagnostic test expiratory loop = normalinspiratory loop = flattened (c/w extrathoracic upper airway obstruction)Flexible Laryngoscopy = diagnostic standard, direct visualizationVocal Cord DysfunctionPulmonary 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 dysfunctionPulmonary 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.25FLEXIBLE LARYNGOSCOPYFlexible 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.
42 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
43 Vocal Cord Dysfunction 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.
44 Vocal Cord Dysfunction 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.
45 Vocal Cord Dysfunction 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.
48 Psoriasis Epidemiology Symptoms bimodal peaks at 16-22 yo & 57-60 yo Prevalence 1-2%, up to 40% have GU involvementSymptomsred or salmon-colored, papulosquamous, circinate plaques, w/ white or silvery scalesPruritisExacerbated by-- stress, excess etoh &tobacco use, acute infections (strep), medications(e.g., beta blockers, lithium)Noninfectious Penile LesionsPsoriasis 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.
49 Psoriasis Noninfectious Penile Lesions Diagnosis Clinical systemic signs (nail pitting, arthritis, other skin)If atypical– punch or shave biopsyTreatment1st line options for localized diseasemild to mod strength topical corticosteroids (CS)—qDayVitamin D3 analogues– qDay or BIDPrevent skin atrophy–use <50 mg ultrapotent or <100 mg potent topical CS over long-termdose ultrapotent daily x 2wks then q weekendLesions may recur when CS discontinuedIf long-term therapy required, tacrolimus (Protopic) or pimecrolimus (Elidel) may decrease risk of atrophyRefractory cases– dermatology referralNoninfectious Penile LesionsPsoriasis 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.
50 Lichen Sclerosus (balanitis xerotica obliterans) EpidemiologyAll ages; ave age 42yoPrevalence..? 1 in 3004-6% assoc w/ squamous cell carcinoma (SCC)Signs/Symptomshypopigmented lesiontexture like crinkled paper/cellophane.glans penis and prepuce involvBullae, erosions, or atrophyphimosis, painful erections, obstructive voiding, itching, pain, and bleedingDDX: carcinoma in situ, leukoplakia, and sclerodermaNoninfectious Penile LesionsPenile 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.12,16Lichen 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
51 Lichen Sclerosus (balanitis xerotica obliterans) TreatmentGoal: decr symptoms & prevent malignant transformationmod to ultrapotent fluorinated topical CSSurgery if persistent dz or h/o SCCCircumcision if limited to glans and prepuceSevere cases– reconstructive surgerySystemic agents (e.g. retinoids) for severe refractory casesLong term f/u to monitor for malignant transformationNoninfectious Penile LesionsThe 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
52 Angiokeratomas Epidemiology Signs/Symptoms Age >40yo; white males Prevalence <1%Signs/Symptomswell-circumscribed, red or blue papules, 1 to 6 mmClinical diagnosisUsu glans penis; also involv scrotum, groin, thighs, abdominal wallInvolv of penile shaft, suprapubic area, and sacrum a/w Fabry disease– referral neededrare intermittent bleeding, pain, or pruritusTx options: (if symptomatic) surgery, cryoablation, electrocautery, and laser ablationNoninfectious Penile LesionsThe 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.
53 Lichen Nitidus Epidemiology: uncommon Signs/Symptoms Discrete, slightly elevated, hypopigmented papules, approx 1 mmCan involve upper limbs &abdomenDiff from pearly papulesring-like distribution on coronal sulcusTx options: for cosmesis-- corticosteroids, vitamin A analogues, cyclosporine (Sandimmune), itraconazole (Sporanox), and phototherapyNoninfectious Penile LesionsLichen 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.
54 Lichen Planus Epidemiology: uncommon but ¼ affected have GU lesions Signs/Symptomsraised, violaceous, flat-topped, polygonal papulesFine white streaks (Wickham striae), on surfacePts c/o pruritus and sorenessBiopsy ulcerated/indurated lesions to r/o SCCTx options: variable responsePotent CS daily vs Ultrapotent CS qWkndIf refractory and isolated to prepuce-- circumcisionNoninfectious Penile LesionsLichen 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.37The 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.
55 Zoon Balanitis Epidemiology: Signs/Symptoms Men ; usu Ages 50-62 yo Patchesbright red or brown,shiny with red specks /spotssharply demarcatedoccur on glans penis, inner prepuce, or coronal sulcusLesions – tend to bleed +/- erodeMimic carcinoma in situ-- biopsyNoninfectious Penile LesionsPenile 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.
56 Carcinoma in Situ Pre-malignant, restricted to skin Epidemiology: uncircumcised men >60 yoProgress to SCC in 5-30% ptsEtiology:Primarily HPVOther factors: smegma, traumaSigns/Symptoms2-35 mm; involv glans penis, urethral meatus, frenulum, coronal sulcus, and prepuceLesions= raised, beefy red, velvety, irreg shaped plaques, may ulcerateVelvety plaques of glans = erythroplasia of QueyratKeratotic plaques on shaft, scrotum, or perineum = Bowen diseaseapprox 50% have pruritus and painNoninfectious Penile LesionsCARCINOMA IN SITUPenile 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.41,42Pruritus 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
57 Carcinoma in Situ Dx: shave biopsy adequate Treatment Prepuce only-- circumcisionOther-- Mohs micrographic surgery? Radiation for non-surgical candidates? Imiquimod (Aldara)fluorouracil, curettage, local excision, laser ablation a/w significant recurrenceNoninfectious Penile LesionsCARCINOMA IN SITUPenile 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.41,42Pruritus 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
58 Invasive Squamous Cell Carcinoma Epidemiology:Rare; 2-3 cases/100,000 menPeak Incidence men >70 yoSCC 95% of penile cancersRisk FactorsHPVLichen sclerosusSmegmaSmokingOlder agePoor hygeineForeskinphimosisSigns/symptomsEarly stage: painless lump/ ulcerProgress to thickened skin & wart-like growthsometimes a/w foul dischargeNoninfectious Penile LesionsPenile 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 retractedThe 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.
59 Invasive Squamous Cell Carcinoma Signs/symptoms (Cont’d)Exophytic or fungating SCC--large, irreg shapeExophytic lesions -- can cause phimosis (mass not visible until prepuce retracted)Endophytic SCC -- ulcerative and infiltrating lesionsNoninfectious Penile LesionsPenile 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
60 Invasive Squamous Cell Carcinoma Diagnosis: confirmed w/ biopsy (excision vs incision based on size)Treatmentlow-grade/low-stage tumors: organ-sparing techniques, (e.g. Mohs micrographic surgery)Prepuce only: circumcisionHigher-stage tumors (i.e., T2 to T4): Penile amputation is standard treatmentPartial penectomy, laser therapy, radiation, and brachytherapy have been attempted as alternatives to radical penectomyNoninfectious Penile LesionsThe 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.
64 Noninfectious Penile Lesions 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.
65 Noninfectious Penile Lesions 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.
66 Noninfectious Penile Lesions 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.
67 Outdoor Air Pollutants & Patient Health OzonePM
68 Air pollutantsFederal Clean Air Act– requires EPA to set National Ambient Air Quality Standards (NAAQS) for certain pollutantsSix Major Pollutantsozone, particulate matter (PM), carbon monoxide, nitrogen oxides, sulfur dioxide, and leadOutdoor Air PollutantsThe 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
69 Air pollutantsDoes your local area meet EPA standards? Go toOutdoor Air PollutantsFigure 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
70 Air pollutantsAQI = information about local air quality, potential health effects, and actions to take to protect when air pollutants reach unhealthy levelsOutdoor Air PollutantsAir 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
72 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
73 Air Pollutants & Patient Health 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.
74 Air Pollutants & Patient Health 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.