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Competitive Swimmer With Hip Pain
ANSWER
The radiograph demonstrates no evidence of an acute fracture or dislocation. Normal gas/stool pattern is present. Essentially, this radiograph is normal.
The patient most likely has an acute strain of her hip quadriceps or flexor. On occasion, severe enough strain injuries can cause a slight avulsion fracture within the hip at the muscle origination point. These can sometimes be evident on plain films.
ANSWER
The radiograph demonstrates no evidence of an acute fracture or dislocation. Normal gas/stool pattern is present. Essentially, this radiograph is normal.
The patient most likely has an acute strain of her hip quadriceps or flexor. On occasion, severe enough strain injuries can cause a slight avulsion fracture within the hip at the muscle origination point. These can sometimes be evident on plain films.
ANSWER
The radiograph demonstrates no evidence of an acute fracture or dislocation. Normal gas/stool pattern is present. Essentially, this radiograph is normal.
The patient most likely has an acute strain of her hip quadriceps or flexor. On occasion, severe enough strain injuries can cause a slight avulsion fracture within the hip at the muscle origination point. These can sometimes be evident on plain films.
A 17-year-old girl presents for evaluation of severe pain in her left hip. She is a competitive swimmer; earlier in the day, she was at practice doing dry land (out of the water) activities/exercises. Having completed a series of stretches and warm-up exercises, she and her teammates proceeded to do sprints. During one of these sprints, she immediately felt a “pop” in her left hip followed by severe, debilitating pain in that hip and thigh. Medical history is otherwise unremarkable. Physical exam reveals that it is extremely painful for the patient to bear weight on the affected leg. There is moderate-to-severe tenderness over the lateral hip. Some swelling is noted; no bruising is present. Distal pulses are good, and motor and sensation are intact. Radiograph of the pelvis is obtained (shown). What is your impression?
Obese, Short of Breath, and Rationing Meds
ANSWER
The correct interpretation is sinus rhythm with a first-degree atrioventricular (AV) block, right superior axis deviation, and low voltage QRS complexes. The measured PR interval of 360 ms is correct!
The P waves are best seen in precordial leads V1 to V3. Notice that the P waves fall between the QRS complex and the T wave. The P wave is upright and not inverted, so it is not occurring retrograde from the preceding QRS complex. The sinus node depolarizes, and a long delay occurs within the atria and AV node before conducting down the normal conduction system in the ventricles. This conduction delay is so long that the preceding beat (QRS complex) is still repolarizing (T wave) by the time the sinus node depolarizes again. Thus, the P wave is responsible for the next QRS complex after duration of 360 ms.
A right superior axis deviation, also known as an extreme right axis deviation, is evidenced by an R-wave axis of 192°. Low-voltage QRS complexes are due to the patient’s body habitus. Morbid obesity significantly diminishes the electrical vectors measured by the surface ECG electrodes.
Finally, extra credit is due if you recognize the long QTc interval as well. The maximum normal QTc adjusted for a heart rate of 100 beats/min in men is 310 ms. This ECG barely meets that criteria; in this case, the prolonged QTc interval is of no significance.
ANSWER
The correct interpretation is sinus rhythm with a first-degree atrioventricular (AV) block, right superior axis deviation, and low voltage QRS complexes. The measured PR interval of 360 ms is correct!
The P waves are best seen in precordial leads V1 to V3. Notice that the P waves fall between the QRS complex and the T wave. The P wave is upright and not inverted, so it is not occurring retrograde from the preceding QRS complex. The sinus node depolarizes, and a long delay occurs within the atria and AV node before conducting down the normal conduction system in the ventricles. This conduction delay is so long that the preceding beat (QRS complex) is still repolarizing (T wave) by the time the sinus node depolarizes again. Thus, the P wave is responsible for the next QRS complex after duration of 360 ms.
A right superior axis deviation, also known as an extreme right axis deviation, is evidenced by an R-wave axis of 192°. Low-voltage QRS complexes are due to the patient’s body habitus. Morbid obesity significantly diminishes the electrical vectors measured by the surface ECG electrodes.
Finally, extra credit is due if you recognize the long QTc interval as well. The maximum normal QTc adjusted for a heart rate of 100 beats/min in men is 310 ms. This ECG barely meets that criteria; in this case, the prolonged QTc interval is of no significance.
ANSWER
The correct interpretation is sinus rhythm with a first-degree atrioventricular (AV) block, right superior axis deviation, and low voltage QRS complexes. The measured PR interval of 360 ms is correct!
The P waves are best seen in precordial leads V1 to V3. Notice that the P waves fall between the QRS complex and the T wave. The P wave is upright and not inverted, so it is not occurring retrograde from the preceding QRS complex. The sinus node depolarizes, and a long delay occurs within the atria and AV node before conducting down the normal conduction system in the ventricles. This conduction delay is so long that the preceding beat (QRS complex) is still repolarizing (T wave) by the time the sinus node depolarizes again. Thus, the P wave is responsible for the next QRS complex after duration of 360 ms.
A right superior axis deviation, also known as an extreme right axis deviation, is evidenced by an R-wave axis of 192°. Low-voltage QRS complexes are due to the patient’s body habitus. Morbid obesity significantly diminishes the electrical vectors measured by the surface ECG electrodes.
Finally, extra credit is due if you recognize the long QTc interval as well. The maximum normal QTc adjusted for a heart rate of 100 beats/min in men is 310 ms. This ECG barely meets that criteria; in this case, the prolonged QTc interval is of no significance.
A 64-year-old man who is morbidly obese is admitted to the medical service with a two-week history of increasing shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea. He states that he has depleted his finances for the month and has resorted to taking his medications every other day in order to make them last until next payday. He denies chest pain but notes that he has had a lot of “heaviness” in his anterior chest for the past week and now has a persistent, nonproductive cough. His medical history is remarkable for a cardiomyopathy due to alcohol abuse, frequent pneumonias, and renal insufficiency. He has a history of sleep apnea and uses continuous positive airway pressure (CPAP) at night in order to sleep. The patient is divorced, unemployed, lives alone in a subsidized apartment, and collects disability. Prior to filing for disability, he worked as a longshoreman. He is a former smoker who quit two years ago after several pulmonary infections. He attributes quitting smoking to his current weight problem. He states he has been an alcoholic for many years, and at one point consumed one bottle of whiskey per day along with one or two six-packs of beer. He has been to two alcohol rehab programs in the past five years and says he recently started drinking again when he learned his disability checks were not going to be increased. Family history is positive for coronary artery disease (mother) and diabetes (father). His parents and both of his siblings are being treated for hypertension. He has no known drug allergies. Current medications include aspirin, extended-release metoprolol, hydralazine, isosorbide mononitrate, torsemide, docusate, and senna. The review of systems is remarkable for chronic low back pain, corrective lenses, and multiple small venous ulcers on both legs that he states will “just not go away.” The physical exam reveals a morbidly obese male in mild distress. His weight is 494 lb and his height, is 70 in. His blood pressure is 120/82 mm Hg; pulse, 90 beats/min and regular; respiratory rate, 18 breaths/min; temperature, 96.8°F; and O2 saturation, 92% on room air. Pertinent physical findings include jugular venous distension to 12 cm, coarse rales in both lower lung fields, distant heart sounds without evidence of a murmur or rub, an obese abdomen without palpable organomegaly or ascites, and 3+ pitting edema in both lower extremities to the level of the knees. There are multiple old and new small, superficial venous ulcers on both lower legs. The skin is warm and pink; however, pulses are not palpable. Upon his admission, a cardiac catheterization is performed, which shows a right dominant system with angiographically normal coronary arteries, a left ventricular ejection fraction of 44%, and no evidence of valvular disease. Right heart pressures include a pulmonary artery pressure of 70/62 mm Hg with a mean of 51 mm Hg. The wedge pressure is 35 mm Hg, the transpulmonary gradient is 10, and the cardiac output is 12.5 L/min with a cardiac index of 4.4 L/min. These data are consistent with moderate-to-severe pulmonary hypertension with severely elevated left-sided filling pressures. A transthoracic echocardiogram is remarkable for elevated left ventricular end diastolic volumes with diffuse hypokinesis and an ejection fraction of 40%. The patient is also found to have a small pericardial effusion and bilateral pleural effusions. An ECG reveals the following: a ventricular rate of 98 beats/min; PR interval, 360 ms; QRS duration, 116 ms; QT/QTc interval, 24/314 ms; P axis, 54°; R axis, 192°; and T axis, 24°. As you review these measurements, you are skeptical of a PR interval of 360 ms and refer to the tracing. What is your interpretation of this ECG, and is the PR interval of 360 ms correct?
Is Man Balding “Just Like Dad”?
ANSWER
The correct answer is alopecia areata (choice “d”), the causes of which are discussed below. It typically manifests with sudden-onset complete hair loss in a well-defined area or areas.
Androgenetic alopecia (choice “a”) is incorrect, since its onset is remarkably gradual and the areas it affects are patterned differently from those seen with alopecia areata.
Kerion (choice “b”) is the name of an edematous, inflamed mass in the scalp triggered by fungal infection (tinea capitis) and is almost always accompanied by broken skin and palpable lymph nodes in the area.
Lichen planopilaris (choice “c”) is lichen planus of the scalp and hair follicles, an inflammatory condition that can involve hair loss of variable size and shape, but not in the same well-defined pattern seen here.
DISCUSSION
There are dermatologists who specialize in diseases of the scalp, especially those resulting in hair loss. In addition to the differential diagnoses mentioned, they see conditions such as lupus, trichotillomania, and reactions to hair care products.
Alopecia areata (AA) seldom needs the attention of these specialists, except in atypical cases. The total hair loss in these well-defined, oval-to-round areas presents fairly acutely, with obviously excessive hair loss noted not only in the scalp but also in the comb, brush, or sink. Although AA is quite common (and thus well known to barbers and hairdressers), it is still often a total and very distressing mystery to the patient. Stress is one of the factors theorized to trigger it—but unfortunately, the more stressed the patient is about the hair loss, the worse it gets.
In the vast majority of cases, the condition resolves, the hair returns, and the grateful patient breathes a sigh of relief. Recurrences, however, are not at all uncommon. A tiny percentage of AA patients go on to lose all the hair in their scalp (alopecia totalis), and an even smaller percentage of those patients go on to lose every hair on their body, permanently (alopecia universalis).
Much has been reported about the cause, which appears to be autoimmune in nature, with an apparent hereditary predisposition. About 10% to 20% of affected patients have a positive family history of AA, and those with severe AA have a positive family history about 16% to 18% of the time.
The theory of an autoimmune basis is also strongly supported by the significantly increased incidence of other autoimmune diseases (especially thyroid disease and vitiligo) in AA patients and their families. But T-cells almost certainly play a role too: Reductions in their number are usually followed by resolution of AA, while increases have the opposite effect. Increased antibodies to various portions of the hair shaft and related structures have now been tied to AA episodes, but these may be epiphenomenal and not causative.
One constant is the perifollicular lymphocytic infiltrate surrounding anagen phase follicles of AA patients. When corticosteroids are administered (eg, by intralesional injection, orally, or systemically), it is this infiltrate that is thereby dissipated, promoting at least temporary hair regrowth. Topically applied steroid preparations are not as helpful, and no known treatment has a positive effect on the ultimate outcome.
Fortunately, most cases of AA resolve satisfactorily with minimal or no treatment. Numerous treatments have been tried for AA, including minoxidil, topical sensitizers (eg, squaric acid, dintrochlorobenzene), and several types of phototherapy. Studies of the efficacy of the various treatments is complicated by the self-limiting nature of the problem.
Predictors of potentially poor outcomes include youth, atopy, extent of involvement, and the presence of ophiasis, a term used to describe extensive involvement of the periphery of the scalp.
ANSWER
The correct answer is alopecia areata (choice “d”), the causes of which are discussed below. It typically manifests with sudden-onset complete hair loss in a well-defined area or areas.
Androgenetic alopecia (choice “a”) is incorrect, since its onset is remarkably gradual and the areas it affects are patterned differently from those seen with alopecia areata.
Kerion (choice “b”) is the name of an edematous, inflamed mass in the scalp triggered by fungal infection (tinea capitis) and is almost always accompanied by broken skin and palpable lymph nodes in the area.
Lichen planopilaris (choice “c”) is lichen planus of the scalp and hair follicles, an inflammatory condition that can involve hair loss of variable size and shape, but not in the same well-defined pattern seen here.
DISCUSSION
There are dermatologists who specialize in diseases of the scalp, especially those resulting in hair loss. In addition to the differential diagnoses mentioned, they see conditions such as lupus, trichotillomania, and reactions to hair care products.
Alopecia areata (AA) seldom needs the attention of these specialists, except in atypical cases. The total hair loss in these well-defined, oval-to-round areas presents fairly acutely, with obviously excessive hair loss noted not only in the scalp but also in the comb, brush, or sink. Although AA is quite common (and thus well known to barbers and hairdressers), it is still often a total and very distressing mystery to the patient. Stress is one of the factors theorized to trigger it—but unfortunately, the more stressed the patient is about the hair loss, the worse it gets.
In the vast majority of cases, the condition resolves, the hair returns, and the grateful patient breathes a sigh of relief. Recurrences, however, are not at all uncommon. A tiny percentage of AA patients go on to lose all the hair in their scalp (alopecia totalis), and an even smaller percentage of those patients go on to lose every hair on their body, permanently (alopecia universalis).
Much has been reported about the cause, which appears to be autoimmune in nature, with an apparent hereditary predisposition. About 10% to 20% of affected patients have a positive family history of AA, and those with severe AA have a positive family history about 16% to 18% of the time.
The theory of an autoimmune basis is also strongly supported by the significantly increased incidence of other autoimmune diseases (especially thyroid disease and vitiligo) in AA patients and their families. But T-cells almost certainly play a role too: Reductions in their number are usually followed by resolution of AA, while increases have the opposite effect. Increased antibodies to various portions of the hair shaft and related structures have now been tied to AA episodes, but these may be epiphenomenal and not causative.
One constant is the perifollicular lymphocytic infiltrate surrounding anagen phase follicles of AA patients. When corticosteroids are administered (eg, by intralesional injection, orally, or systemically), it is this infiltrate that is thereby dissipated, promoting at least temporary hair regrowth. Topically applied steroid preparations are not as helpful, and no known treatment has a positive effect on the ultimate outcome.
Fortunately, most cases of AA resolve satisfactorily with minimal or no treatment. Numerous treatments have been tried for AA, including minoxidil, topical sensitizers (eg, squaric acid, dintrochlorobenzene), and several types of phototherapy. Studies of the efficacy of the various treatments is complicated by the self-limiting nature of the problem.
Predictors of potentially poor outcomes include youth, atopy, extent of involvement, and the presence of ophiasis, a term used to describe extensive involvement of the periphery of the scalp.
ANSWER
The correct answer is alopecia areata (choice “d”), the causes of which are discussed below. It typically manifests with sudden-onset complete hair loss in a well-defined area or areas.
Androgenetic alopecia (choice “a”) is incorrect, since its onset is remarkably gradual and the areas it affects are patterned differently from those seen with alopecia areata.
Kerion (choice “b”) is the name of an edematous, inflamed mass in the scalp triggered by fungal infection (tinea capitis) and is almost always accompanied by broken skin and palpable lymph nodes in the area.
Lichen planopilaris (choice “c”) is lichen planus of the scalp and hair follicles, an inflammatory condition that can involve hair loss of variable size and shape, but not in the same well-defined pattern seen here.
DISCUSSION
There are dermatologists who specialize in diseases of the scalp, especially those resulting in hair loss. In addition to the differential diagnoses mentioned, they see conditions such as lupus, trichotillomania, and reactions to hair care products.
Alopecia areata (AA) seldom needs the attention of these specialists, except in atypical cases. The total hair loss in these well-defined, oval-to-round areas presents fairly acutely, with obviously excessive hair loss noted not only in the scalp but also in the comb, brush, or sink. Although AA is quite common (and thus well known to barbers and hairdressers), it is still often a total and very distressing mystery to the patient. Stress is one of the factors theorized to trigger it—but unfortunately, the more stressed the patient is about the hair loss, the worse it gets.
In the vast majority of cases, the condition resolves, the hair returns, and the grateful patient breathes a sigh of relief. Recurrences, however, are not at all uncommon. A tiny percentage of AA patients go on to lose all the hair in their scalp (alopecia totalis), and an even smaller percentage of those patients go on to lose every hair on their body, permanently (alopecia universalis).
Much has been reported about the cause, which appears to be autoimmune in nature, with an apparent hereditary predisposition. About 10% to 20% of affected patients have a positive family history of AA, and those with severe AA have a positive family history about 16% to 18% of the time.
The theory of an autoimmune basis is also strongly supported by the significantly increased incidence of other autoimmune diseases (especially thyroid disease and vitiligo) in AA patients and their families. But T-cells almost certainly play a role too: Reductions in their number are usually followed by resolution of AA, while increases have the opposite effect. Increased antibodies to various portions of the hair shaft and related structures have now been tied to AA episodes, but these may be epiphenomenal and not causative.
One constant is the perifollicular lymphocytic infiltrate surrounding anagen phase follicles of AA patients. When corticosteroids are administered (eg, by intralesional injection, orally, or systemically), it is this infiltrate that is thereby dissipated, promoting at least temporary hair regrowth. Topically applied steroid preparations are not as helpful, and no known treatment has a positive effect on the ultimate outcome.
Fortunately, most cases of AA resolve satisfactorily with minimal or no treatment. Numerous treatments have been tried for AA, including minoxidil, topical sensitizers (eg, squaric acid, dintrochlorobenzene), and several types of phototherapy. Studies of the efficacy of the various treatments is complicated by the self-limiting nature of the problem.
Predictors of potentially poor outcomes include youth, atopy, extent of involvement, and the presence of ophiasis, a term used to describe extensive involvement of the periphery of the scalp.
A 39-year-old man presents with a two-month history of focal hair loss that has not responded to treatment. His primary care provider prescribed first an antifungal topical cream (clotrimazole/betamethasone bid for two weeks), then an oral antibiotic (cephalexin 500 mg qid for 10 days). Neither helped. His scalp is asymptomatic in the affected area (as well as elsewhere), but the hair loss is extremely upsetting to the patient. He is convinced (and has been told by family members) that he is merely going bald “just like his father.” The onset of his hair loss was rather sudden. It began with increased hair found in his sink and shower, followed by comments from family and coworkers. One friend loaned the patient his minoxidil solution, but twice-daily application for a week failed to slow the rate of hair loss. In general, the patient’s health is excellent; he does not require any maintenance medications. Neither he nor any family members have had any serious illnesses (eg, thyroid disease, lupus, vitiligo) that he could recall. The patient’s hair loss, affecting an approximately 10 x 8–cm area, is confined to the right parietal scalp and has a sharply defined border and strikingly oval shape. The hair loss within this area is complete, with no epidermal disturbance of the involved scalp skin noted on inspection or palpation. No nodes are palpable in the surrounding head or neck. No other areas of hair loss can be seen in hair-bearing areas.
A Different Source of Elbow Pain
ANSWER
The radiograph shows no obvious fracture or dislocation. However, there are two small, radiopaque densities noted within the soft tissue. These are most likely consistent with broken glass pieces.
When the laceration was irrigated and the wound probed, the glass bits were found and removed prior to wound closure.
ANSWER
The radiograph shows no obvious fracture or dislocation. However, there are two small, radiopaque densities noted within the soft tissue. These are most likely consistent with broken glass pieces.
When the laceration was irrigated and the wound probed, the glass bits were found and removed prior to wound closure.
ANSWER
The radiograph shows no obvious fracture or dislocation. However, there are two small, radiopaque densities noted within the soft tissue. These are most likely consistent with broken glass pieces.
When the laceration was irrigated and the wound probed, the glass bits were found and removed prior to wound closure.
A 30-year-old man is brought to your facility after being in a motor vehicle collision. He was an unrestrained driver who lost control of his vehicle, went off the road, and hit a tree. Emergency personnel on the scene indicated there was moderate damage to his vehicle, including a broken windshield, and no air bag deployment. The patient is complaining of right shoulder, chest, hip, and left elbow pain. His medical history is unremarkable. His vital signs are normal. On physical examination, he has superficial lacerations on his forehead, face, and both forearms. Bleeding from all wounds is controlled. Palpation reveals some bruising of the right shoulder, chest, right hip, and left elbow; no obvious deformity or neurovascular compromise is noted. Multiple radiographs are ordered; the left elbow is shown. What is your impression?
Young Man Thinks He is Having a Heart Attack
ANSWER
The correct interpretation of this patient’s ECG is atrial flutter with variable atrioventricular block. Atrial flutter is a macro re-entrant supraventricular arrhythmia arising in the right atrium and usually (but not always!) identified by saw-tooth–appearing flutter waves.
The atrial rate in atrial flutter typically ranges from 200 to 350 beats/min. The QRS appearance will be narrow and similar to that of sinus rhythm, because conduction occurs normally down the atrioventricular node unless there is aberrant conduction.
The ventricular rate is dependent on the ability of the node to control rapid conduction. In this case, there appear to be three flutter waves for each QRS complex (3:1 flutter). If the ventricular rate is 80 beats/min, the rate in the atrium is approximately 240 beats/min. A regular ventricular rate of 150 beats/min should make you suspicious for atrial flutter (2:1 flutter).
The variable atrioventricular block on this ECG is evidenced by the presence of two, rather than three, flutter waves per QRS complex (seen after the fourth, fifth, and 10th QRS complexes on the rhythm strip). This case illustrates that flutter may be present with a ventricular rate of less than 100 beats/min.
ANSWER
The correct interpretation of this patient’s ECG is atrial flutter with variable atrioventricular block. Atrial flutter is a macro re-entrant supraventricular arrhythmia arising in the right atrium and usually (but not always!) identified by saw-tooth–appearing flutter waves.
The atrial rate in atrial flutter typically ranges from 200 to 350 beats/min. The QRS appearance will be narrow and similar to that of sinus rhythm, because conduction occurs normally down the atrioventricular node unless there is aberrant conduction.
The ventricular rate is dependent on the ability of the node to control rapid conduction. In this case, there appear to be three flutter waves for each QRS complex (3:1 flutter). If the ventricular rate is 80 beats/min, the rate in the atrium is approximately 240 beats/min. A regular ventricular rate of 150 beats/min should make you suspicious for atrial flutter (2:1 flutter).
The variable atrioventricular block on this ECG is evidenced by the presence of two, rather than three, flutter waves per QRS complex (seen after the fourth, fifth, and 10th QRS complexes on the rhythm strip). This case illustrates that flutter may be present with a ventricular rate of less than 100 beats/min.
ANSWER
The correct interpretation of this patient’s ECG is atrial flutter with variable atrioventricular block. Atrial flutter is a macro re-entrant supraventricular arrhythmia arising in the right atrium and usually (but not always!) identified by saw-tooth–appearing flutter waves.
The atrial rate in atrial flutter typically ranges from 200 to 350 beats/min. The QRS appearance will be narrow and similar to that of sinus rhythm, because conduction occurs normally down the atrioventricular node unless there is aberrant conduction.
The ventricular rate is dependent on the ability of the node to control rapid conduction. In this case, there appear to be three flutter waves for each QRS complex (3:1 flutter). If the ventricular rate is 80 beats/min, the rate in the atrium is approximately 240 beats/min. A regular ventricular rate of 150 beats/min should make you suspicious for atrial flutter (2:1 flutter).
The variable atrioventricular block on this ECG is evidenced by the presence of two, rather than three, flutter waves per QRS complex (seen after the fourth, fifth, and 10th QRS complexes on the rhythm strip). This case illustrates that flutter may be present with a ventricular rate of less than 100 beats/min.
The 24-year-old male graduate student whom you saw one month ago for palpitations (see July 2013 ECG Challenge) returns without an appointment, stating that his heart is “flip-flopping” just as it has in the past. The problem started abruptly about 45 minutes ago, and he is afraid he might be having a heart attack. A quick check of his pulse reveals a rate of 80 beats/min. At his previous visit, an ECG showed sinus rhythm with sinus arrhythmia and a blocked premature atrial contraction (PAC). A rhythm strip documented that his palpitations coincided with blocked PACs. You recall that he reported having two episodes of tachycardia in the past, while “pulling all-nighters” for finals as an undergraduate. Today, he denies shortness of breath, nausea, vomiting, chest pain, and symptoms of near-syncope or syncope, but says his heart is “flopping around” in his chest and he can feel his heart beat in his throat. He has no prior cardiac or pulmonary history and has not recently been ill. Medical history, medication list, allergies, family history, and review of systems are unchanged since his last visit: Medical history is remarkable only for fractures of the right ankle and the left clavicle. He takes no medications and has no drug allergies. Family history is significant for stroke (paternal grandfather), diabetes (maternal grandmother), and hypertension (father). The patient consumes alcohol socially, primarily on weekends, and does not binge drink. He smokes marijuana during snowboard season, but denies use at other times of the year. A 12-point review of systems is positive only for athlete’s foot and psoriasis on both upper extremities. The physical exam reveals an anxious but otherwise healthy, athletic-appearing male. Vital signs include a blood pressure of 140/88 mm Hg; pulse, 80 beats/min; respiratory rate, 20 breaths/min-1; and O2 saturation, 99% on room air. His height is 70” and his weight, 161 lb. His lungs are clear, there is no jugular venous distention, and cardiac auscultation reveals no murmurs, gallops, or rubs. The abdominal exam is normal without organomegaly, and peripheral pulses are regular and strong bilaterally. His neurologic exam yields normal results. As you examine the ECG, you note the following: a ventricular rate of 80 beats/min; PR interval, unmeasurable; QRS duration, 92 ms; QT/QTc interval, 388/444 ms; P axis, 265°; R axis, 72°; and T axis, 66°. What is your interpretation of this ECG?
Not Just Another Groin Rash
ANSWER
The correct answer is fungal infection (choice “a”). If this condition had been fungal, it would have responded to one or more of the medications used to treat it. In this case, treatment failure demanded consideration of alternate diagnostic possibilities.
Lichen simplex chronicus (choice “b”), also known as neurodermatitis, was a good possibility, since it is the consequence of chronic rubbing or scratching in response to the itching caused by, for example, eczema.
Psoriasis (choice “c”) usually has adherent white scale on its surface, unless it’s in an intertriginous (skin on skin) area where scale gets rubbed off by friction.
The patient’s actual diagnosis, however, turned out to be Paget’s disease (choice “d”). See the Discussion for relevant details.
DISCUSSION
Biopsy showed changes consistent with a type of skin cancer called extramammary Paget’s disease (EMPD), an intradermal adenocarcinoma that tends to develop in areas where apocrine glands are found (eg, the anogenital and axillary areas).
The majority of EMPD cases represent adenocarcinoma in situ with extension from adnexal structures. Intraepidermal metastasis from noncutaneous adenocarcinomas (via local or lymphatic routes) accounts for a significant minority of cases (< 25%). Urogenital and colorectal carcinomas are the most common.
EMPD is more common in women and is rare before age 40. In addition to the usual intertriginous areas, other sites in which it may be found include eyelids and ears. The lesions typically itch but rarely hurt; they do, however, inevitably grow larger and more extensive.
The histologic changes of EMPD are identical to those seen in mammary Paget’s disease, though the latter virtually always involves the areola and nipple. It also signals the presence of an underlying intraductal breast cancer.
The main teaching point to be gleaned from this case is the concept of “cancer presenting as a rash,” of which there are several examples: cutaneous T-cell lymphoma, B-cell lymphoma, metastatic breast cancer, superficial basal cell carcinoma, and intraepidermal squamous cell carcinoma (Bowen’s disease).
EMPD is especially prone to being overlooked, not only because groin rashes are so common but also because most skin cancers are “lesional” (ie, they take the form of a papule or nodule). Any rash that proves to be unresponsive to ordinary treatment should be either referred to dermatology or biopsied.
TREATMENT
This patient was prescribed imiquimod 5% cream, to be applied three times a week, which has a good chance of clearing the condition (but only after three to four months of application). If this fails, the patient will be referred for Mohs surgery.
Even so, recurrences are common. About 25% of EMPD patients with underlying malignancies eventually die of their disease. For these reasons, the patient was referred back to his primary care provider for workup for a possible underlying malignancy.
ANSWER
The correct answer is fungal infection (choice “a”). If this condition had been fungal, it would have responded to one or more of the medications used to treat it. In this case, treatment failure demanded consideration of alternate diagnostic possibilities.
Lichen simplex chronicus (choice “b”), also known as neurodermatitis, was a good possibility, since it is the consequence of chronic rubbing or scratching in response to the itching caused by, for example, eczema.
Psoriasis (choice “c”) usually has adherent white scale on its surface, unless it’s in an intertriginous (skin on skin) area where scale gets rubbed off by friction.
The patient’s actual diagnosis, however, turned out to be Paget’s disease (choice “d”). See the Discussion for relevant details.
DISCUSSION
Biopsy showed changes consistent with a type of skin cancer called extramammary Paget’s disease (EMPD), an intradermal adenocarcinoma that tends to develop in areas where apocrine glands are found (eg, the anogenital and axillary areas).
The majority of EMPD cases represent adenocarcinoma in situ with extension from adnexal structures. Intraepidermal metastasis from noncutaneous adenocarcinomas (via local or lymphatic routes) accounts for a significant minority of cases (< 25%). Urogenital and colorectal carcinomas are the most common.
EMPD is more common in women and is rare before age 40. In addition to the usual intertriginous areas, other sites in which it may be found include eyelids and ears. The lesions typically itch but rarely hurt; they do, however, inevitably grow larger and more extensive.
The histologic changes of EMPD are identical to those seen in mammary Paget’s disease, though the latter virtually always involves the areola and nipple. It also signals the presence of an underlying intraductal breast cancer.
The main teaching point to be gleaned from this case is the concept of “cancer presenting as a rash,” of which there are several examples: cutaneous T-cell lymphoma, B-cell lymphoma, metastatic breast cancer, superficial basal cell carcinoma, and intraepidermal squamous cell carcinoma (Bowen’s disease).
EMPD is especially prone to being overlooked, not only because groin rashes are so common but also because most skin cancers are “lesional” (ie, they take the form of a papule or nodule). Any rash that proves to be unresponsive to ordinary treatment should be either referred to dermatology or biopsied.
TREATMENT
This patient was prescribed imiquimod 5% cream, to be applied three times a week, which has a good chance of clearing the condition (but only after three to four months of application). If this fails, the patient will be referred for Mohs surgery.
Even so, recurrences are common. About 25% of EMPD patients with underlying malignancies eventually die of their disease. For these reasons, the patient was referred back to his primary care provider for workup for a possible underlying malignancy.
ANSWER
The correct answer is fungal infection (choice “a”). If this condition had been fungal, it would have responded to one or more of the medications used to treat it. In this case, treatment failure demanded consideration of alternate diagnostic possibilities.
Lichen simplex chronicus (choice “b”), also known as neurodermatitis, was a good possibility, since it is the consequence of chronic rubbing or scratching in response to the itching caused by, for example, eczema.
Psoriasis (choice “c”) usually has adherent white scale on its surface, unless it’s in an intertriginous (skin on skin) area where scale gets rubbed off by friction.
The patient’s actual diagnosis, however, turned out to be Paget’s disease (choice “d”). See the Discussion for relevant details.
DISCUSSION
Biopsy showed changes consistent with a type of skin cancer called extramammary Paget’s disease (EMPD), an intradermal adenocarcinoma that tends to develop in areas where apocrine glands are found (eg, the anogenital and axillary areas).
The majority of EMPD cases represent adenocarcinoma in situ with extension from adnexal structures. Intraepidermal metastasis from noncutaneous adenocarcinomas (via local or lymphatic routes) accounts for a significant minority of cases (< 25%). Urogenital and colorectal carcinomas are the most common.
EMPD is more common in women and is rare before age 40. In addition to the usual intertriginous areas, other sites in which it may be found include eyelids and ears. The lesions typically itch but rarely hurt; they do, however, inevitably grow larger and more extensive.
The histologic changes of EMPD are identical to those seen in mammary Paget’s disease, though the latter virtually always involves the areola and nipple. It also signals the presence of an underlying intraductal breast cancer.
The main teaching point to be gleaned from this case is the concept of “cancer presenting as a rash,” of which there are several examples: cutaneous T-cell lymphoma, B-cell lymphoma, metastatic breast cancer, superficial basal cell carcinoma, and intraepidermal squamous cell carcinoma (Bowen’s disease).
EMPD is especially prone to being overlooked, not only because groin rashes are so common but also because most skin cancers are “lesional” (ie, they take the form of a papule or nodule). Any rash that proves to be unresponsive to ordinary treatment should be either referred to dermatology or biopsied.
TREATMENT
This patient was prescribed imiquimod 5% cream, to be applied three times a week, which has a good chance of clearing the condition (but only after three to four months of application). If this fails, the patient will be referred for Mohs surgery.
Even so, recurrences are common. About 25% of EMPD patients with underlying malignancies eventually die of their disease. For these reasons, the patient was referred back to his primary care provider for workup for a possible underlying malignancy.
A 60-year-old man is referred to dermatology for evaluation of a somewhat itchy, unilateral groin rash. For several years, it has waxed and waned, never completely resolving. Recently, the rash has grown in size, and the itching has intensified, causing the patient to lose sleep. The patient has tried several OTC and prescription topical medications for this problem: creams containing clotrimazole, tolnaftate, 1% hydrocortisone, and betamethasone/clotrimazole, as well as triple-antibiotic ointment and several different moisturizing creams and lotions. He also tried a two-week course of oral terbinafine (250 mg/d). Additional questioning reveals a history of atopy, eczema, and asthma as a child. There is a strong family history of similar problems. This strikingly red, blistery-appearing rash is palm-sized and confined to the right groin. It has a fairly well–defined, scaly border that is KOH-negative on microscopic examination. Within the borders of this lesion are several focal, shiny, somewhat atrophic areas in which no epidermal adnexae (pores, follicles, hair, skin lines) can be seen.
Woman With Hip Pain After Car Accident
ANSWER
The radiograph demonstrates evidence of contrast material within the bladder. There is evidence of fixation of an old subcapital femoral neck fracture on the left.
There is an acute, mildly displaced right intertrochanteric fracture of the right hip. The orthopedic service was consulted, and plans were established to subsequently fix this fracture surgically.
ANSWER
The radiograph demonstrates evidence of contrast material within the bladder. There is evidence of fixation of an old subcapital femoral neck fracture on the left.
There is an acute, mildly displaced right intertrochanteric fracture of the right hip. The orthopedic service was consulted, and plans were established to subsequently fix this fracture surgically.
ANSWER
The radiograph demonstrates evidence of contrast material within the bladder. There is evidence of fixation of an old subcapital femoral neck fracture on the left.
There is an acute, mildly displaced right intertrochanteric fracture of the right hip. The orthopedic service was consulted, and plans were established to subsequently fix this fracture surgically.
A 55-year-old woman is transferred to your facility with injuries sustained in a motor vehicle collision. She was an unrestrained front-seat passenger in a vehicle that rear-ended another vehicle. There was no airbag deployment, and the patient believes she struck her face on the windshield. At the outside facility, it was determined that she had a cervical fracture and facial fractures. Upon arrival at your facility, she is complaining of bilateral hip pain as well. Her medical history is significant for coronary artery disease, several myocardial infarctions, hypertension, and stroke. She has a pacemaker. Six months ago, she had an open reduction internal fixation of her left hip for a fracture she sustained in a fall. Primary survey reveals a female who is uncomfortable but alert and oriented. Vital signs are normal. She has some facial swelling and bruising. Her heart and lungs are clear; abdomen is benign. She is able to move her upper extremities with-out any problems. She has limited movement of her lower extremities due to pain in her pelvis. She is able to move both feet and toes, and distal pulses and sensation are intact. No obvious leg shortening is noted. A portable radiograph of the pelvis is obtained. What is your impression?
Child hit by car
ANSWER
The chest radiograph demonstrates no acute abnormalities within the lungs, ribs, or chest. Of note, there are two radiodensities consistent with teeth, which are presumed to be in the patient’s stomach (most likely secondary to being swallowed following trauma to his face). Upon reexamination, it is noted that the child’s two front incisors are missing, with minimally bleeding sockets. Other than reassurance, no specific intervention was required.
ANSWER
The chest radiograph demonstrates no acute abnormalities within the lungs, ribs, or chest. Of note, there are two radiodensities consistent with teeth, which are presumed to be in the patient’s stomach (most likely secondary to being swallowed following trauma to his face). Upon reexamination, it is noted that the child’s two front incisors are missing, with minimally bleeding sockets. Other than reassurance, no specific intervention was required.
ANSWER
The chest radiograph demonstrates no acute abnormalities within the lungs, ribs, or chest. Of note, there are two radiodensities consistent with teeth, which are presumed to be in the patient’s stomach (most likely secondary to being swallowed following trauma to his face). Upon reexamination, it is noted that the child’s two front incisors are missing, with minimally bleeding sockets. Other than reassurance, no specific intervention was required.
A 6-year-old boy is brought to your facility by ambulance after being hit by a car. The child was apparently riding his bike when a slow-moving vehicle turned onto the street and accidentally bumped him, knocking him to the ground. He was not wearing a helmet. The child is crying but somewhat consolable. His medical history is unremarkable. On initial assessment, he is awake, crying, and moving all of his extremities spontaneously. His vital signs include a temperature of 36.3°C; blood pressure, 149/72 mm Hg; pulse, 110 beats/min; and respiratory rate, 22 breaths/min. Physical examination reveals several abrasions to his face, nose, and lips. Otherwise, he is normocephalic. His pupils are equal and react appropriately. Heart and lung sounds are clear, and the abdomen appears benign. You order some preliminary labwork and CT of the head. In addition, a portable chest radiograph is obtained (shown). What is your impression?
Is Active Patient a “Picture of Health”?
ANSWER
The correct interpretation includes marked sinus bradycardia, a right bundle branch block, and T-wave abnormalities in the lateral leads.
Sinus bradycardia is evidenced by a sinus rate less than 60 beats/min and may be considered “marked” if the rate is less than 50 beats/min.
A right bundle branch block is indicated by a QRS duration ≥ 120 ms, a terminal broad S wave in lead I, and the presence of an RSR’ pattern in lead V1.
Small or nonexistent T waves in leads V5 and V6 are suggestive of lateral ischemia but are not diagnostic in this individual.
His marked bradycardia was attributed to his exceptional athleticism and the fact that the ECG was taken “at rest.” It was not of concern, nor did it require treatment.
ANSWER
The correct interpretation includes marked sinus bradycardia, a right bundle branch block, and T-wave abnormalities in the lateral leads.
Sinus bradycardia is evidenced by a sinus rate less than 60 beats/min and may be considered “marked” if the rate is less than 50 beats/min.
A right bundle branch block is indicated by a QRS duration ≥ 120 ms, a terminal broad S wave in lead I, and the presence of an RSR’ pattern in lead V1.
Small or nonexistent T waves in leads V5 and V6 are suggestive of lateral ischemia but are not diagnostic in this individual.
His marked bradycardia was attributed to his exceptional athleticism and the fact that the ECG was taken “at rest.” It was not of concern, nor did it require treatment.
ANSWER
The correct interpretation includes marked sinus bradycardia, a right bundle branch block, and T-wave abnormalities in the lateral leads.
Sinus bradycardia is evidenced by a sinus rate less than 60 beats/min and may be considered “marked” if the rate is less than 50 beats/min.
A right bundle branch block is indicated by a QRS duration ≥ 120 ms, a terminal broad S wave in lead I, and the presence of an RSR’ pattern in lead V1.
Small or nonexistent T waves in leads V5 and V6 are suggestive of lateral ischemia but are not diagnostic in this individual.
His marked bradycardia was attributed to his exceptional athleticism and the fact that the ECG was taken “at rest.” It was not of concern, nor did it require treatment.
A 62-year-old man presents for a preoperative history and physical exam prior to surgical repair of an injury to his right anterior cruciate ligament (ACL). He reports that he has been healthy all his life and has never had an injury or illness requiring hospitalization. He is an accountant at a local financial institution and has a very active lifestyle, which includes competitive cycling, running, and skiing. He recently completed his fourth triathlon and was training for his sixth marathon until his injury occurred. One week ago, he was skiing moguls on a black diamond course when he fell and tumbled about 20 feet before stopping. His right ski binding did not release from the boot. He felt his right knee “pop” and knew immediately that he had sustained a serious injury. When he tried to stand, he was unable to bear weight on his right leg. The ski patrol transported him off the slope via basket. He was then taken to a local hospital by a colleague. Physical exam and MRI confirmed an avulsion of the ACL. He has been convalescing at home (having delayed his surgery in order to catch up on paper-work for work) and is scheduled for surgery in two days’ time. Medical history is unremarkable. Aside from the usual childhood illnesses (eg, ear infections, chicken pox, mumps), he has been very healthy and attributes this to a strict diet and rigorous exercise. Social history reveals that he is married to an attorney and has no children. He has never smoked or taken recreational drugs, and he consumes approximately one bottle of wine per week. His current medications include naproxen as needed for pain, a daily aspirin, fish oil, a multivitamin, and omeprazole on rare occasions. The review of systems is remarkable only for occasional gastroesophageal re-flux, which is exacerbated by spicy dishes containing curry. Physical exam reveals a thin, athletic male in no acute distress. His weight is 168 lb, and his height is 74”. Vital signs include a blood pressure of 104/62 mm Hg; pulse, 50 beats/min; respiratory rate, 14 breaths/min-1; and temperature, 98°F. Examination of the head, neck, lungs, heart, abdomen, skin, and nervous system yields normal findings. Lachman, pivot shift, and anterior drawer maneuvers of the right knee are all positive. A routine ECG is performed that reveals the following: a ventricular rate of 49 beats/min; PR interval, 176 ms; QRS dura-tion, 120 ms; QT/QTc interval, 430/388 ms; P axis, 14°; R axis, 38°; and T axis, 103°. What is your interpretation of this ECG?
A Compulsion to Scratch, But Is There an Itch?
ANSWER
The correct answer is neurotic excoriations (choice “d”), a chronic condition thought to be a psychologic process with dermatologic manifestations, consciously created by repetitive scratching and rubbing. Focally, it can manifest with skin alterations very similar to lichen simplex chronicus (choice “a”; also known as neurodermatitis), but the latter refers to very limited, localized processes and does not involve the psychiatric overlay seen with neurotic excoriations.
Patients with dermatitis artefacta (choice “b”; formerly called factitial dermatitis) consciously create their lesions for secondary gain, often using sharp objects such as nail files, kitchen utensils, or even shards of broken glass. Dermatitis artefacta lesions, which are relatively sparse and bizarre in appearance, can also be created by the application of caustic chemicals, or even by injection of foreign substances.
The differential rightly includes any number of skin conditions such as bullous pemphigoid (choice “c”). However, this was effectively ruled out by the biopsy and also by the morphology and extended chronicity of the patient’s complaint.
DISCUSSION
Neurotic excoriations (NE) are usually created by unconscious picking, scratching, or rubbing. There may be a precipitating minor skin pathology (eg, insect bite, folliculitis or acne), but it can develop independent of any such process. Its origins can often be tied to upsetting life events, such as divorce, death, or early dementia.
More history taking from this patient and her family revealed that her skin problems began after her husband died in an accident, after which, according to her children, “she has never been the same.” Her picking accelerated when she moved to an assisted living setting.
Because patients create neurotic excoriations, their lesions have the quality of an “outside job,” with clean linear erosions, crusts, and scars that can be hypopigmented or hyperpigmented, depending on the patient’s skin type. Similar in size and shape, the lesions tend to be bilaterally and symmetrically distributed and confined to areas within easy reach, such as the extensor surfaces of the arms and the upper part of the back.
The vast majority of NE patients are adult women, though it is also seen in children as a manifestation of comorbid psychopathology or other psychosocial stressor.
TREATMENT
As one might expect, treatment of NE is difficult, particularly since many patients find it impossible to accept the role their mental state plays in the creation and perpetuation of their condition. In the best of all possible scenarios, the patient would be seen and followed by a psychiatrist, who would probably prescribe psychoactive medication.
Failing that—or even in addition to that treatment—one could, at a minimum, find ways to distract the patient, trim her nails as much as possible, and/or place barriers between the offending nails and the skin in question.
Topical medications, such as steroid creams, are of very limited usefulness, as are oral antibiotics and antihistamines.
ANSWER
The correct answer is neurotic excoriations (choice “d”), a chronic condition thought to be a psychologic process with dermatologic manifestations, consciously created by repetitive scratching and rubbing. Focally, it can manifest with skin alterations very similar to lichen simplex chronicus (choice “a”; also known as neurodermatitis), but the latter refers to very limited, localized processes and does not involve the psychiatric overlay seen with neurotic excoriations.
Patients with dermatitis artefacta (choice “b”; formerly called factitial dermatitis) consciously create their lesions for secondary gain, often using sharp objects such as nail files, kitchen utensils, or even shards of broken glass. Dermatitis artefacta lesions, which are relatively sparse and bizarre in appearance, can also be created by the application of caustic chemicals, or even by injection of foreign substances.
The differential rightly includes any number of skin conditions such as bullous pemphigoid (choice “c”). However, this was effectively ruled out by the biopsy and also by the morphology and extended chronicity of the patient’s complaint.
DISCUSSION
Neurotic excoriations (NE) are usually created by unconscious picking, scratching, or rubbing. There may be a precipitating minor skin pathology (eg, insect bite, folliculitis or acne), but it can develop independent of any such process. Its origins can often be tied to upsetting life events, such as divorce, death, or early dementia.
More history taking from this patient and her family revealed that her skin problems began after her husband died in an accident, after which, according to her children, “she has never been the same.” Her picking accelerated when she moved to an assisted living setting.
Because patients create neurotic excoriations, their lesions have the quality of an “outside job,” with clean linear erosions, crusts, and scars that can be hypopigmented or hyperpigmented, depending on the patient’s skin type. Similar in size and shape, the lesions tend to be bilaterally and symmetrically distributed and confined to areas within easy reach, such as the extensor surfaces of the arms and the upper part of the back.
The vast majority of NE patients are adult women, though it is also seen in children as a manifestation of comorbid psychopathology or other psychosocial stressor.
TREATMENT
As one might expect, treatment of NE is difficult, particularly since many patients find it impossible to accept the role their mental state plays in the creation and perpetuation of their condition. In the best of all possible scenarios, the patient would be seen and followed by a psychiatrist, who would probably prescribe psychoactive medication.
Failing that—or even in addition to that treatment—one could, at a minimum, find ways to distract the patient, trim her nails as much as possible, and/or place barriers between the offending nails and the skin in question.
Topical medications, such as steroid creams, are of very limited usefulness, as are oral antibiotics and antihistamines.
ANSWER
The correct answer is neurotic excoriations (choice “d”), a chronic condition thought to be a psychologic process with dermatologic manifestations, consciously created by repetitive scratching and rubbing. Focally, it can manifest with skin alterations very similar to lichen simplex chronicus (choice “a”; also known as neurodermatitis), but the latter refers to very limited, localized processes and does not involve the psychiatric overlay seen with neurotic excoriations.
Patients with dermatitis artefacta (choice “b”; formerly called factitial dermatitis) consciously create their lesions for secondary gain, often using sharp objects such as nail files, kitchen utensils, or even shards of broken glass. Dermatitis artefacta lesions, which are relatively sparse and bizarre in appearance, can also be created by the application of caustic chemicals, or even by injection of foreign substances.
The differential rightly includes any number of skin conditions such as bullous pemphigoid (choice “c”). However, this was effectively ruled out by the biopsy and also by the morphology and extended chronicity of the patient’s complaint.
DISCUSSION
Neurotic excoriations (NE) are usually created by unconscious picking, scratching, or rubbing. There may be a precipitating minor skin pathology (eg, insect bite, folliculitis or acne), but it can develop independent of any such process. Its origins can often be tied to upsetting life events, such as divorce, death, or early dementia.
More history taking from this patient and her family revealed that her skin problems began after her husband died in an accident, after which, according to her children, “she has never been the same.” Her picking accelerated when she moved to an assisted living setting.
Because patients create neurotic excoriations, their lesions have the quality of an “outside job,” with clean linear erosions, crusts, and scars that can be hypopigmented or hyperpigmented, depending on the patient’s skin type. Similar in size and shape, the lesions tend to be bilaterally and symmetrically distributed and confined to areas within easy reach, such as the extensor surfaces of the arms and the upper part of the back.
The vast majority of NE patients are adult women, though it is also seen in children as a manifestation of comorbid psychopathology or other psychosocial stressor.
TREATMENT
As one might expect, treatment of NE is difficult, particularly since many patients find it impossible to accept the role their mental state plays in the creation and perpetuation of their condition. In the best of all possible scenarios, the patient would be seen and followed by a psychiatrist, who would probably prescribe psychoactive medication.
Failing that—or even in addition to that treatment—one could, at a minimum, find ways to distract the patient, trim her nails as much as possible, and/or place barriers between the offending nails and the skin in question.
Topical medications, such as steroid creams, are of very limited usefulness, as are oral antibiotics and antihistamines.
At her daughters’ insistence, this 69-year-old woman requests referral to dermatology for a skin condition that has been present for at least 20 years. During that time, she has seen many medical providers (including dermatologists) and has tried many different treatments (eg, creams, oral antibiotics, oral steroids, and antihistamines). While some of these helped a bit, most did not help at all—nor did the constant nagging at the patient by family and caregivers. Nonetheless, her daughters feel strongly that their mother is perpetuating the problem with her “scratching and picking.” They have observed that when she is able to leave her arms alone, the improvement in her skin is dramatic. For example, years ago, she broke her wrist and was placed in a cast for six weeks; when it was removed, the affected arm was completely clear (except for multiple old scars). Everyone, including the patient, was ecstatic—but a week later, the lesions returned. The extensor aspects of both arms and hands are covered with linear excoriations, scars, and scabs, with focal hyperpigmentation in many of the excoriated areas. Overall, the skin in these areas is re-markably thickened and focally shiny. Her skin elsewhere—such as her palms and the volar aspects of her arms—is relatively clear. Throughout the examination, the patient’s hands never stop rubbing and scratching her arms, even as she weakly denies doing so. “Whatever happens, I’m not going to see a shrink,” she says. Clearly, a biopsy is in order, with a sample taken from a typical section of her forearm. The results show minimal changes but demonstrate hyperkeratosis. Blood work, including a complete metabolic profile and complete blood count, fail to show any evidence of systemic disease.
