Advances in medical knowledge and our capabilities as physicians, coupled with the transformation of healthcare delivery, call for a reassessment of how we educate,train, and equip physicians to provide safe, high-quality, patient-centered care. A number of national health organizations have begun this process, and many of you maybe familiar with the American Medical Association's (AMA) Initiative to Transform Medical Education (ITME) and the Association of American Medical Colleges' Institute to Improve Medical Education. As every aspect of the medical education continuum is being comprehensively evaluated and critiqued, you have the opportunity to take an active role in this process and influence the future of medical education.

The Initiative to Transform Medical Education

In 2002, the AMA House of Delegates adopted a report of the AMA Council on Medical Education, "Comprehensive Reform at the Interface of Medical Education and Health Care." This report concluded that an evaluation and reform of medical education was needed to ensure that physicians were prepared to practice in a continuously evolving healthcare system. In addition, systematic changes to medical education were recommended to better equip physicians with the knowledge, skills, ethics, and approach necessary to provide quality medical care in this changing environment. Thus the AMA's ITME Task Force was formed, to address goals that were broken down into 3 phases:

Identify current strengths and gaps/opportunities for improvement in the preparation of physicians

Develop plans and strategies for change in medical education across the continuum from premedical preparation and admission to medical school through continuing physician professional development

Form partnerships with appropriate stakeholders within and outside the medical education community to bring about the needed changes.

Phase 1 and phase 2 are now complete, and the full summary/report can be found at 

www.amaassn.org/ama1/pub/upload/mm/16/itme_final_rpt.pdf

. Recommendations from phase 2 that pertain to graduate medical education include:

1. Apportion more weight in admissions decisions to characteristics of applicants that predict success in the interpersonal domains of medicine. Use valid and reliable measures to assess these traits.

To promote the altruistic and compassionate characteristics of physicians, medical schools may consider requiring undergraduate courses in the humanities or social sciences, in addition to the biological and physical science requirements. ITME also suggests the development, validation, and utilization of new tools in the admissions process to assess relevant personalqualities of applicants, such as analytical thinking, service and team orientation, commitment to lifelong learning, and likelihood of maintaining altruism. By identifying personality characteristics that foster the development of these traits and creating methods to assess them using evaluation tools and specialized interviews, these attributes can be accorded more weight during the admissions process. This would have a significant impact on students applying to medical school, as well as on the admissions process itself.

2. Consider creating alternatives to the current sequence of the medical education continuum, including introducing options so that physicians can re-enter or modify their practice.

With so many physicians taking extended leaves from practice for personal reasons or to facilitate a change in their practice, it is important to develop flexible and efficient mechanisms that provide sound training and competency assessment to ease these transitions. This particularly affects residents and young physicians who take time away from medical practice for reasons such as having children, or those who choose to change their training track or specialty.

3. Introduce core competencies across the medical education continuum in new and expanded content areas that are necessary for practice in the evolving healthcare system.

4. Introduce new methods of evaluation that are appropriate to assess the core competencies.

Undergraduate and graduate medical education provides little instruction on skills such as selfassessment, professionalism, and specialized communication skills. The development and implementation of a longitudinal education in these areas would improve physicians' ability to critically evaluate their practice and to develop andcarry out a lifelong learning curriculum. These new methods of evaluation, however, must not only be valid and reliable but also provide an opportunity for formativeas well as critical evaluation. ITME is also searching for ways to incorporate the Accreditation Council Graduate Medical Education core competencies and move them fromthe status of "add-ons" to fundamental elements of graduate medical education training. This new framework, combined with new assessment and evaluation methods, will change not only what we teach but how we teach it.

5. Ensure that the organizational environment in medical schools and teaching institutions values and rewards participation in education.

6. Ensure that the learning environment throughout the medical education continuum is conducive to the development of appropriate attitudes, behaviors, and values, as well as knowledge and skills.

Recommendations 5 and 6 directly address the "hidden curriculum" that underlies the teaching environment, and emphasize the importance that this environment plays in the development of personal qualities in future physicians. Intimidation is a significant issue for residents and fellows today, and these recommendations seek to foster a training environment that is best suited to the development of the positive attitudes, healthy behaviors, and honorable values necessary to provide safe, high-quality, patient-centered care.

Phase 3 of this process is now under way, and will begin by focusing on the "hidden curriculum" and improving the educational environment to facilitate learning and the development of the positive professional attributes of physicians-in-training.

In summary, a substantive remodeling of the "house of medicine" is under way, and your participation is essential to ensure that physicians are thoroughly engaged in this process. You know firsthand what training and skills you need, and what type of learning environment best enables you, as a physician, to learn how to best care for your patients. Armed with that knowledge and with a vision for the future, you, along with your resident and fellow colleagues, can help chart the path this process will take. The opportunity to leave your mark on medical education reform and affect the foundation of our prefession is here. I charge you to work with your colleagues and representatives on ITME and other organizations and councils during this monumental process.

A list of your AMA Resident and Fellow Section representatives on these groups can be found at 

www.ama-assn.org/ama/pub/category/5647.html

; in addition, a list of key stakeholders and participants can be found in the Appendix of the "Recommendations for Change in the System of Medical Education" (ITME, June 2007), available at 

Articles

Resident and Staff

Remodeling the House of Medicine: Update on the Medical Continuum

According to the American Heart Association, as many as 72 million American adults have elevated blood pressure (BP), and many of them do not know they have it. Despite the abundance of antihypertensive medications monotherapies as well as combination agents the rates of BP control among hypertensive patients in the United States are not encouraging. Even among those who are being treated, achieving a BP goal of <140/90 mm Hg has proved elusive, with only about one third of patients reaching their therapeutic goals. Many patients will eventually take more than 1 antihypertensive, which may in part explain the increasing emphasis on combination tablets for hypertension.

Last fall, the US Food and Drug Administration approved a new antihypertensive agent called Exforge, which combines the angiotensin receptor blocker valsartan and the calcium channel blocker amlodipine.

As with most combination agents, the 2 components are complementary: valsartan blocks the renin-angiotensin system (RAS), and amlodipine blocks the calcium channel and affects vasomotor tone more strongly. The combination of another RAS blocker, which combines the angiotensin-converting-enzyme (ACE) inhibitor benazepril HCl and amlodipine, has been shown to be an effective antihypertensive therapy in real-world settings.

Several other combination antihypertensives include a diuretic, because diuretics are considered to be the base of therapy, according to current guidelines. And since patients respond to different drugs in a variety of ways, physicians often prescribe one medication and then switch to another that is better tolerated by the individual patient.

The approval of this new combination agent was based on placebo-controlled and active-controlled trials. In one study that randomized patients with stage 2 hypertension to amlodipine (5-10 mg/d) plus valsartan (160 mg/d) or the ACE inhibitor lisinopril (10-20 mg/d) plus the diuretic hydrochlorothiazide for a period of 6 weeks, similar results were seen with both combinations:

Reduction in mean sitting systolic BP (SBP) of 35.8 mm Hg with amlodipine/valsartan and 31.8 mm Hg with lisinopril/hydrochlorothiazide

Response rates of mean sitting diastolic BP (DBP) <90 mm Hg, or a ≥10-mm Hg reduction from baseline of 100% and 95.5%, respectively

DBP control rates of 79.7% and 77.3%, respectively 

Both combination agents were well-tolerated.

Another report assessed the results of 2 multicenter, 8-week, placebo-controlled trials that evaluated amlodipine and valsartan, alone or in combination. Study 1 randomized 1911 patients to amlodipine (2.5 or 5.0 mg/d), valsartan (40-320 mg/d), the combination of both agents across the same dose ranges, or placebo.

Study 2 randomized 1250 patients to amlodipine (10 mg/d), valsartan (160 or 320 mg/d), the combination of both agents across the same dose ranges, or placebo. All participants in both studies had mild-to-moderate essential hypertension at baseline, and all underwent an initial 2-week washout period, during which any current antihypertensive medications were discontinued.

In both trials, the combination regimens&#8212;except for a few that included the lowest amlodipine dose of 2.5 mg&#8212;resulted in greater reductions in mean sitting DBP and SBP compared with the individual components.

Subgroup analyses of these 2 trials showed similar results in patients with stage 1 hypertension (140-159/90-99 mm Hg) or stage 2 hypertension (≥160/100 mm Hg), the elderly, and African Americans.

The combination regimen was well-tolerated. Combining valsartan with amlodipine significantly decreased the dose-limiting side effect of peripheral edema seen with amlodipine monotherapy.

The daily doses of the new combination tablet are 5 to 10 mg amlodipine and 160 to 320 mg valsartan. The drug is currently not indicated for initial therapy of hypertension. It also should not be prescribed for patients with severe renal disease or for pregnant women. It can be used in those with mild renal disease and in patients with diabetes.

In placebo-controlled trials, 1.8% of patients treated with Exforge discontinued therapy because of side effects, compared with 2.1% of placebo-treated patients.

The most frequently reported side effects with the new combination were peripheral edema (5.4%), nasopharyngitis (4.3%), upper respiratory tract infection (2.9%), and dizziness (2.1%).

New Combination Antihypertensive Therapy with 2 Proven Mechanisms of Action

Prepared by Julie Marie Borba, MPH, medical student, Elena Kret-Sudjian, MD, Assistant Professor, Department of Internal Medicine, University of California Davis School of Medicine, Sacramento

A 72-year-old woman presented with a nonpainful, 10 x 7 cm, fungating mass on her right thumb (Figure). Thirty years earlier, when the mass was significantly smaller, it was biopsied and diagnosed as benign. Current radiographs and magnetic resonance imaging showed the mass to involve most of the hand. Biopsy revealed epithelioid sarcoma, and the hand was amputated.

 Epithelioid sarcoma of the hand is often misdiagnosed because of its benign appearance initially, and because it is often mistaken clinically and pathologically for a granulomatous lesion. Prognosis depends on the location, size, and duration of the tumor. In most cases, however, lymph node and lung metastases are present by the time the diagnosis is established. Treatment consists of radical surgical excision of the tumor and, if indicated, lymph node dissection.

Hand Tumor in a 72-Year-Old Woman

Wamiq Y. Banday, MD, Resident, Internal Medicine Residency Program, Sisters of Charity Hospital, University of Buffalo, Buffalo, and Jawaid Shaw, MD, Resident, Department of Internal Medicine, Rochester General Hospital, Rochester, NY

A 51-year-old African-American man presents to the emergency department with a 1-week history of sudden onset of exertion-induced breathlessness associated with light-headedness. He has no fever, cough, chest pain, orthopnea, or paroxysmal nocturnal dyspnea. His history includes type 2 diabetes and hypertension. His vital signs are: blood pressure, 157/100 mm Hg; heart rate, 93 beats/min; respiratory rate, 15 breaths/min; temperature, 98.7&#176; F. The physical examination is remarkable for pallor and bilateral pedal edema, with no evidence of jugular venous distention or tenderness in the lower limbs. Lungs are clear to auscultation. Arterial blood gases on room air are: pH, 7.48 (normal range, 7.35-7.45); PCO

, 53.0 mm Hg (normal, 80-100); bicarbonate, normal (at 21.4 mmol/L); troponin, normal (at 0.15 &#181;g/L); B-type natriuretic peptide, 217 pg/mL (normal, <100). A 12-lead electrocardiogram (ECG) is obtained (Figure).

Diagnosis: Acute cor pulmonale caused by pulmonary embolism (S

Pulmonary embolism ranges from incidental, clinically unimportant thromboembolism to massive embolism with sudden death. Acute pulmonary embolism causes elevated pulmonary artery and right heart pressures and decreased cardiac output, which will be reflected in the ECG by the S

 pattern. However, when the ECG changes persist even after the pulmonary artery pressure and the right heart size have returned to normal, additional mechanisms are involved,

 including the release of catecholamine or histamine at the cellular level.

This patient's ECG shows: sinus tachycardia (with a rate of 100/min), S wave in lead I,Q wave in lead III, and T-wave inversion in lead III (S

 pattern); Q waves are also seen in leads II and aVF; T-wave inversion is seen in leads V

 (anterior leads); complete right bundle-branch block (RBBB); and ST-segment depression in leads V

. These findings make this ECG very suspicious for pulmonary embolism. A computed tomography scan of the chest with contrast showed large bilateral pulmonary embolisms.

 and transient RBBB was first described in 1939.

 pattern varies in about 12% to 50% of cases and is therefore not pathogonomic.

 This pattern will resolve within 14 days of onset of disease. Up to 25% of patients with pulmonary embolism have normal ECG at admission.

 Transient RBBB is seen in 6% to 67% of patients with pulmonary embolism.

 ST elevation or depression is seen in up to 50% of this type of patients.

 T-wave inversion, diffuse or in the inferior leads, is a frequent finding in pulmonary embolism and is a sign of massive disease; however, good prognostic value has been reported when the T-wave inversion is reversed before the sixth day.

Our patient's ECG had all these findings, making this ECG a prototype for pulmonary embolism as described in the literature. However, the sensitivity and specificity of ECG changes in pulmonary embolism are 26.7% and 57.1%, respectively, and are therefore not sufficient for the diagnosis.

Other ECG abnormalities described in the literature include rhythm disturbances, such as sinus tachycardia (8%-69%), first-degree AV block (1%-12%), premature atrial or premature ventricular beats (4%-23%), atrial fibrillation (18%) and atrial flutter (35%), and P-pulmonale (2%-31%)

; as well as PR depression and low-voltage complexes

Chan TC, Vilke GM, Pollack M, et al. Electrocardiographic manifestations: pulmonary embolism. 

Yoshinaga T, Ikeda S, Nishimura E, et al. Serial changes in negative T waves on electrocardiogram in acute pulmonary thromboembolism. 

Ferrari E, Imbert A, Chevalier T, et al. The ECG in pulmonary 80 case reports. 

Palla A, Petruzzelli S, Donnamaria V, et al. The role of suspicion in the diagnosis of pulmonary embolism. 

Durant TM, Ginsberg IW, Roesler H. Transient bundle branch block and other electrocardiographic changes in pulmonary embolism. 

Sreeram N, Cheriex EC, Smeets JL, et al. Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. 

Petruzzelli S, Palla A, Pieraccini F, et al. Routine electrocardiography in screening for pulmonary embolism. 

ECG Rounds

Bhanu Wunnava, MD, Resident, Family Medicine Program, Louisiana State University Health Sciences Center, Monroe, La

Life is full of surprises sometimes good and sometimes bad. Good encounters are enjoyable; however, it is the bad experiences or circumstances that usually help a person to grow and better understand the complexities of life. Such experiences, if properly analyzed, can give new wisdom, understanding, faith, and appreciation of  one's surrounding support system. It is for this reason that I would like to share my recent experience as a patient.

I was recently hospitalized because of excruciating abdominal pain, which turned out to be a hernia that needed to be surgically repaired. Before this episode, I had never been hospitalized. Being a patient was a different experience altogether for me. To play the role of a patient is strange and humbling for a doctor.

I have seen thousands of patients moaning and groaning in pain in my clinical experience, but I could only sympathize with their pain and suffering. I could never empathize or identify completely with their anguish and distress. Many of them would request more and more pain medication, and even increased frequency of doses, as they were unable to tolerate the pain. Before my hospitalization I had always thought that such patients were abusing the pain medications unreasonably and unnecessarily.

However, when the tables were turned on me during my hospital stay, I found myself behaving in the same way. I was constantly pressing the button to call the nurse so that I could get additional pain medication more frequently, because I couldn't bear the pain after my surgery. While doing so, it never crossed my mind that the nurse would think that I, too, was trying to abuse the pain medications.

My hospitalization also taught me the importance of family support and friends. During my practice, I have time and again seen family and friends visiting my patients, and many times I felt it cumbersome to repeat the prognosis of the patient to each visitor. In the past, I never realized the mental and even physical support it provided to the patient. But when I was the patient, my wife, my family, colleagues, and friends were similarly eager for news of my condition. It was comforting and healing beyond words to be taken care of, cared for, and cared about by my loved ones. It was such a wonderful feeling to know how much they were all concerned about me. Moreover, this made me remember my patients who walked through the hospital doors in pain by themselves or who lay in bed for days with no visitors. From now on, I will be sure to give a few extra words of consolation and support, and a few extra minutes of my time to such patients during my practice.

After 36 hours of postsurgery hospital stay I was back on my regular diet, and the doctor on call was supposed to make rounds that evening. I was overjoyed at the prospect that I might be discharged that evening. I was so impatient to go home, even though I was still in pain.

I recall that while working as a resident, I had often been tied up in my clinic and thus had been late to get to my patients' rooms to discharge them. I never realized how fervently patients wait to hear from their doctor that everything looks good and they can be discharged. The waiting is never ending for a patient. Now, playing the role of the patient, I had to go through the same experience.

As it turned out, my doctor was called to perform emergency surgery on another patient that evening, thus delaying my discharge by a couple of hours. I never realized that every minute of the wait feels like an hour. Those 2 hours seemed like 20 hours for me. And as I lay there waiting for my discharge, I vowed to myself that in the future, I would try my best to minimize the waiting time for my patients.

The entire experience of being a patient in the hospital taught me a lot as a doctor, as well as a human being. It taught me to be a more caring, understanding, and compassionate person not just to my patients but also to others in my day-to-day activities. It gave me the strength to face the unexpected, and often agonizing, battles life brings. This incident helped me to learn humility, empathy, and faith.

My Experience as a Patient

Fresh Frozen Plasma Beneficial for ACE Inhibitor?Induced Angioedema

 The article "Atypical Presentation of ACE Inhibitor?Induced Angioedema" (October 2007) was interesting. At the Mercy Hospital of Pittsburgh, we admitted a similar case to the intensive care unit through the emergency department.

 Our patient was initially treated with antihistamines and steroids. After receiving 2 units of fresh frozen plasma, her symptoms improved significantly, and she was able to go home the very next day. It is now believed that the kininase activity in the fresh frozen plasma is responsible for breaking down the accumulated bradykinin in patients suffering from angiotensin-converting?enzyme inhibitor?induced angioedema, and that helps resolve the symptoms.

1. Warrier MR, Copilevitz CA, Dykewicz MS, et al. Fresh frozen plasma in the treatment of resistant angiotensin-converting enzyme inhibitorangioedema. 

Rethinking Ethnicity in Thyrotoxic Periodic Paralysis

 We would like to comment on the case report "Hypokalemic Thyrotoxic Periodic Paralysis" (July/August 2007). Although until now it has been accepted that thyrotoxic periodic paralysis is more common in Asians, this condition has also been described sporadically in white, Hispanic, and African-American patients, as is described in this case presented by Drs Dahal and Roy. Thyrotoxic periodic paralysis can indeed be a presenting symptom of thyrotoxicosis. We recently reported on 3 cases involving African Americans who presented with acute weakness and hypokalemia: 2 of them were diagnosed with Grave?s disease and thyrotoxic periodic paralysis (using biochemical laboratory testing and thyroid radioactive iodine uptake scan). The third patient was diagnosed with thyroiditis (using biochemical hyperthyroid). With the current state of international travel and the resulting increase in population migration, what was previously thought of as an  uncommon disease entity in this country must now be considered in tients of any ethnic origin presenting with hypokalemia (ie, <3 mEq/dL) and muscle weakness. Thyroid function tests should be considered in all such patients, regardless of their ethnic background.

Wright State University Boonshoft School of Medicine

 Thank you for the wonderful entry presented in the Picture Perfect entry in the November/December 2007 issue. I am reminded of a patient, now long deceased, who presented with a  mammoth abdominal girth associated with his belly scar and weight loss. When asked ?What have you been told was the diagnosis,? he took out a piece of paper from his wallet, on which was penciled in, "Pseudomyxoma Peritonei," which was referred to as "Jelly Belly" by our professor of pathology, exactly as described in the present case.

? Fresh Frozen Plasma for ACE Inhibitor?Induced Angioedema? Rethinking Ethnicity in Thyrotoxic Periodic Paralysis? Jelly Belly Diagnosis

Letters to the Editor

 Prepared by Paul B. DiDomenico, MD, Resident, Radiology Department, and Peter S. Palka, DO, Neuroradiologist, Department of Diagnostic Imaging, David Grant US Air Force Medical Center, Travis AFB, Calif

A 21-year-old woman was brought to the emergency department after having 2 episodes of generalized tonic-clonic seizures. The patient had a complex medical history that included systemic lupus erythematosus (SLE), hemodialysis-dependent status after bilateral nephrectomy, thrombotic thrombocytopenic purpura (TTP), and poorly controlled hypertension. A computed tomography (CT) scan of the brain (performed at an outside hospital) was reportedly normal. Magnetic resonance imaging (MRI) of the brain suggested the diagnosis (Figure 1).

Posterior reversible encephalopathy syndrome

&#8212;MRI findings included regions of high signal on T2 and fluid attenuation inversion recovery (FLAIR) sequences within the posterior parietal and occipital lobes. These sequences indicated edema in the posterior subcortical white matter, as well as cortical involvement. The patient was admitted to the hospital for blood pressure (BP) control. Repeat MRI 10 days later demonstrated a normal brain, with complete resolution of the previous T2/FLAIR signal abnormalities (Figure 2). This reversibility of the lesion confirmed the diagnosis. The patient improved clinically and did not experienceanother seizure.

Posterior reversible encephalopathy syndrome was first described in 1996 as a syndrome of neurologic findings including headache, altered mental status, visual changes, and seizures in 15 patients who demonstrated evidence of posterior leukoencephalopathy on imaging studies.

 The findings included vasogenic edema predominantly in the posterior cerebral hemispheres, but also in the brain stem and cerebellum. Risk factors included abrupt increases in BP, impaired renal function (secondary to lupus nephritis or acute glomerulonephritis), immunosuppressive therapy, and eclampsia. The neurologic symptoms and imaging abnormalities resolved in all patients after adequate BP control or reduction in immunosuppressive therapy. Although posterior reversible encephalopathy syndrome has been often referred to as hypertensive encephalopathy, several of the patients described in the 1996 study were normotensive.

 Other associations reported in the literature include TTP, SLE, and  several immunosuppressive and cytotoxic drugs.

 The precise pathogenesis is still unknown; however, imaging studies have consistently demonstrated vasogenic edema. This is likely related to a breakdown in cerebral vascular autoregulation, with fluid leakage into the cerebral interstitium.

 but the imaging study of choice is MRI, which has greater sensitivity and can exclude infarction of the occipital lobes from the differential diagnosis (by using diffusion-weighted imaging).

The patient described in this case had at least 4 of the known risk factors for posterior reversible encephalopathy syndrome hypertension, SLE, TTP, andimmunosuppressive therapy. SLE usually involves the central nervous system, resulting in vasculopathy in the cerebral arterioles and capillaries and producing perivascular inflammation.

Lupus cerebritis would be expected to demonstrate a more diffuse pattern of atrophy and T2/FLAIR signal abnormalities that would not be expected to reverse in a short interval, if at all.

Acute infarction would demonstrate high signal on diffusion-weighted imaging, which was not present in this case.

Acute disseminated encephalomyelitis is a monophasic demyelinating disease that is usually preceded by viral infection. In cases of posterior reversible encephalopathy syndrome, documentation and reversibility of imaging findings is an important part of the diagnosis and management. Early recognition allows for corrective action with BP control and withdrawal of cytotoxic medications, thus avoiding potentially permanent brain damage. 

Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. 

Bartynski WS, Boardman JF, Zeigler ZR, et al. Posterior reversible encephalopathy syndrome in infection, sepsis, and shock. 

Bartynski WS, Boardman JF. Distinct imaging patterns and lesion distribution in posterior reversible encephalopathy syndrome. 

Brubaker LM, Smith JK, Lee YZ, et al. Hemodynamic and permeability changes in posterior reversible encephalopathy syndrome measured by dynamic susceptibility perfusion-weighted MR imaging. 

Radiology

 Prepared by Richmond McCarty, DO, USAF Flight Surgeon, and Terri Nutt, MD, Chief of Dermatology, David Grant Medical Center, Travis AFB, Calif

A 37-year-old woman presented with a 1-week history of multiple erythematous, scaly papules on her scalp, trunk (Figure), upper extremities, and pelvic area. She stated that the lesions did not itch and were not painful. On further questioning, the patient admitted to taking some leftover penicillin 2 weeks earlier for a self-diagnosed "strep throat." The patient denied any recent travel outside the United States and reported minimal improvement with the use of over-the-counter hydrocortisone cream. She also denied any sexual contact outside her marriage for herself and her husband.

&#8212;This condition is classically preceded by streptococcal pharyngitis or by an upper respiratory viral infection a week or two earlier. It is characterized by the sudden appearance of plaques and round, scaling papules on the trunk and extremities, sparing the soles of the feet and palms of the hands. These dropletlike lesions serve as a hallmark for the disease and usually exhibit some degree of central clearing. Guttate psoriasis usually occurs in children and young adults and resolves spontaneously within weeks to months after the initial eruption. It is estimated that 33% to 66% of patients with a history of guttate psoriasis will develop chronic plaque psoriasis.

 Our patient had an elevated antistreptolysin-O titer, and her tissue biopsy confirmed the diagnosis of guttate psoriasis.

 She was subsequently referred to a local dermatologist for ultraviolet B light therapy.

Secondary syphilis is characterized by mucocutaneous lesions, flulike symptoms, and adenopathy (which is usually painless). It manifests approximately 6 weeks after the primary chancre and can last between 2 and 10 weeks. It is generally associated with low or no fever during the initial onset, and the lesions tend to develop slowly, with little or no inflammation. Pain and itching are usually minimal, and various types of lesions often present simultaneously rather than as a single uniform eruption. In the majority of patients, lesions are typically found on the hands and feet and are distributed throughout the trunk. Our patient had no other systemic symptoms or associated lesions on the palms of her hands or the soles of her feet, and denied any unfaithfulness on her or her husband?s part. A Venereal Disease Research Laboratory test for syphilis was ordered, but the laboratory was unable to process the sample for an unknown reason.

Drug reactions can occur within hours after ingestion, or up to several weeks after the initial exposure. The reactions tend to be pruritic and present with a diffuse and symmetrical maculopapular rash and with generalized urticaria. These eruptions are very similar to that of a viral exanthema; it can be hard to differentiate between the two. Our patient did not exhibit fever or urticaria, and her lesions presented gradually, whereas drug reactions tend to present with a moresudden onset.

Pityriasis rosea is a benign, asymptomatic, self-limited skin eruption of unknown etiology. It is often preceded by a history of acute infection and presents with multiple oval lesions that have a thin collarette scale and can be mildly pruritic. The long axis of the lesions tends to be oriented with the skin lines, which can give a characteristic "Christmas tree" distribution. Only a small percentage of patients present with a herald patch, which our patient did not have. This condition was high on the differential diagnosis list for our patient; the tissue biopsy helped rule it out.

Scatena L. What triggered this sudden eruption? 

Gudjonsson JE, Thorarinsson AM, Sigurgeirsson B, et al. Streptococcal throat infections and exacerbation of chronic plaque psoriasis: a prospective study. 

Dermatology

Avneet Singh, MD, Resident, Colleen McEvoy, BS, Medical Student, Nadish Garg, MD, Resident, Department of Internal Medicine, University of Missouri, Columbia.

An 80-year-old man with diabetes, hypertension, chronic kidney disease, and coronary artery disease was admitted to the hospital for chest pain. segment elevation myocardial infarction. Other medications initiated in the hospital included metoprolol, simvastatin, insulin, and calcitriol for secondary hyperparathyroidism (parathyroid hormone level >150 pg/mL). At 12 hours after admission, a skin lesion was noted at the site of the insulin administration on the abdominal wall (Figure). A biopsy of the lesion revealed the diagnosis.

&#8212;The skin biopsy confirmed the diagnosis. The likely precipitating event was subcutaneous insulin injection at that site, in addition to an elevated activated partial thromboplastin time (aPTT) from heparin infusion. Heparin is a known cause of subcutaneous and deep-tissue hematomas in patients with a prolonged aPTT. Unless the patient is hemodynamically unstable, the treatment is usually conservative. In this case, the heparin therapy was stopped, which contained the hemorrhage. The skin biopsy was negative for thrombi or necrosis (heparin-induced skin necrosis), medial calcification (calciphylaxis), and cholesterol clefts (cholesterol emboli).

Calciphylaxis is mostly seen in patients with end-stage renal disease who are on hemodialysis or who have recently received a renal transplant. Calciphylaxis is related to vascular and soft-tissue calcification and can be precipitated acutely by the initiation of calcitriol therapy for secondary hyperthyroidism. The diagnosis is confirmed by skin biopsy, which shows arterial occlusion and calcification in the absence of vasculitic change.

Heparin-induced skin necrosis is a rare entity that has been described only in patients receiving subcutaneous heparin.

Our patient did have atherosclerotic vascular disease that predisposed him to cholesterol embolization, characterized by skin lesions such as livedo reticularis, subcutaneous nodule, and ischemic ulceration. However, cholesterol embolization typically occurs after angiography, cardiac catheterization, vascular surgery, or abdominal trauma. Biopsy in cholesterol embolism shows cholesterol clefts within the vessel.

Internal Medicine

University of Texas Health Science Center

Posterior ischemic optic neuropathy (PION) is an uncommon condition that occurs after acute hypoperfusion of the intraorbital optic nerve and is manifested as substantial vision loss.

 The optic nerve head typically appears normal at the initial examination, despite a profound loss of vision. Pallor of the optic nerve head develops in 6 to 8 weeks. PION has been divided into 3 subtypes, according to the etiology:

Perioperative PION occurs as a consequence of profound hypotension and anemia during surgical procedures

Arteritic PION is associated with systemic vasculitis, most often with giant-cell arteritis

Nonarteritic PION has been associated with a variety of conditions, including internal carotid dissection, intranasal corticosteroids, methanol intoxication, migraine, sickle-cell disease, lung carcinoma, 

A 55-year-old woman with a history of hypertension, depression, and several suicide attempts was transported to the emergency department by emergency medical services after her husband found her unconscious next to an empty bottle of nifedipine. The precise amount ingested could not be determined accurately. Physical examination showed a lethargic and confused patient, with a heart rate of 20 to 30 beats/min and a systolic blood pressure of 60 to 74 mm Hg (diastolic blood pressures were not recorded by the emergency department). Initial management included normal saline, calcium chloride, dopamine, glucagon, and norepinephrine to treat her bradycardia and hypotension. A transcutaneous pacemaker was also used to treat her bradycardia. Because the transcutaneous pacemaker did not capture her ventricular sinus rhythm, she was transferred to the intensive care unit (ICU), where a transvenous pacemaker was placed, capturing her ventricular sinus rhythm at 80 beats/min.She was in the emergency department for a total of 55 minutes before being transferred to the ICU.

The patient regained full consciousness 6 days later. She was noted to use tactile sensation to locate objects at her bedside as opposed to vision. She reported that she could not see anything. The ophthalmology inpatient consultation service was called.

The initial ophthalmic examination revealed visual acuity of light perception (without projection) in the right eye and no light perception in the left eye. Her pupils were 7 mm (reacting to light sluggishly to 6.5 mm) in the right eye, and 7 mm (nonreactive to light) in the left eye. She had a relative afferent pupillary defect in the left eye. The optic discs appeared normal and did not show evidence of pallor or disc swelling (Figure 1). Visual field analysis and color vision examination could not be conducted because of the profound vision loss. A computed tomography (CT) scan of the head was unremarkable.

 The right (A) and left (B) optic discs appear normal during the initial ocular examination of a patient with PION.

A presumptive diagnosis of PION was made based on the history and the ocular examination. The patient was scheduled for a follow-up visit in the neuro-ophthalmology clinic 8 weeks later. When she returned, her vision was unchanged in both eyes from the initial examination, but repeated funduscopic examination revealed diffusely pale optic discs, with sharp margins, and no swelling or atrophy (Figure 2). The retina, vessels, and choroid remained unchanged&#8212;a finding that lends support to the clinical diagnosis of PION secondary to an acute episode of hypotension and bradycardia after a calcium channel blocker overdose.

 The right (A) and left (B) optic discs develop diffuse pallor 8 weeks after the initial diagnosis of PION.

PION is caused by a compromised vascular supply to the intraorbital optic nerve through the posterior ciliary arteries. To our knowledge, this is the first report of PION as a consequence of calcium channel blocker overdose. Based on the patient's history, CT scan, and physical/ocular examination, PION was the most likely cause of her vision loss; however, other potential etiologies were entertained, including cortical blindness and toxic optic neuropathy. If the visual loss was secondary to cortical ischemia, pupillary responses would have been present, and the CT scan would have shown characteristic changes. According to available information about nifedipine, this medication has never been implicated as a cause of toxic optic neuropathy, although we cannot completely rule out toxicity as a potential contributorto this patient's visual loss.

One study suggests that normal doses of antihypertensive medications can lead to nocturnal arterial hypotension, which can reduce optic nerve head blood flow.

 The authors suggest that this mechanism may play a role in the pathogenesis of anterior ischemic optic neuropathy and glaucomatous optic neuropathy, but no mention of PION is included in the study.

In contrast, another case report suggests use of calcium channel blockers at normal dosages for the treatment of ocular ischemic syndrome caused by vasospasm.

 Therefore, it appears that calcium channel blockers can be used to improve blood flow to the optic nerve in some conditions, but as our case suggests, a quantity large enough to cause bradycardia and hypotension can be detrimental to the optic nerve blood flow and lead to permanent visual loss.

PION, leading to visual loss, is a potential complication of bradycardia and hypotension secondary to a calcium channel blocker overdose. Because these medications are often prescribed for hypertension, all physicians should be aware of the possibility of PION occurring in patients who present with vision loss after ingesting quantities larger than the recommended dose.

This manuscript was supported by a grant from Research to Prevent Blindness, New York, NY.

Hayreh SS. Posterior ischemic optic neuropathy. 

Sadda SR, Nee M, Miller NR, et al. Clinical spectrum of posterior ischemic optic neuropathy. 

Hayreh SS, Podhajsky PA, Zimmerman B. Ocular manifestations of giant cell arteritis. 

Buono LM, Foroozan R, Savino PJ, et al. Posterior ischemic optic neuropathy after hemodialysis. 

Hayreh SS, Podhajsky P, Zimmerman MB. Role of nocturnal arterial hypotension in optic nerve head ischemic disorders. 

Winterkorn JM, Beckman RL. Recovery from ocular ischemic syndrome after treatment with verapamil. 

The first report of a calcium channel blocker overdose as a cause of this condition.

Posterior Ischemic Optic Neuropathy Associated with Calcium Channel Blocker Overdose

Pneumococcal sepsis can usually be traced back to a primary site that was left untreated, facilitating spread of the infection into the bloodstream. Most patients have predisposing factors, such as splenectomy, recent surgery, or other immunocompromised states. Typically the blood is seeded from pneumonia or meningitis. Cases of primary pneumococcemia resulting in death within 4 hours of presentation in a patient who had not had splenectomy and with no significant medical history are exceedingly uncommon.

A 46-year-old woman was brought to the emergency department by a basic life support ambulance. She was triaged with a chief complaint of "leg burning." Vital signs on arrival were: blood pressure, 119/51 mm Hg; heart rate, 84 beats/min; respiratory rate, 20 breaths/min; temperature, 36.8 F; oxygen saturation, 98% on room air. The  patient was awake, alert, and oriented to person, place, and time. Physical examination showed mottled, nonblanching skin, which was worst on her abdomen and  extremities, and petechiae on the trunk and back. Her hands and feet were pale and cool, although the distal pulses were intact. No cellulitis, skin abscess, or cervical or inguinal lymphadenopathy were evident. Her lips and mucous membranes were cyanotic but moist. The rest of the examination was unremarkable.

Her primary complaint was bilateral burning in her anterior thighs and numbness in her feet, which began 3 hours before presentation. She had traveled to New Jersey from San Francisco for business and was staying at a local hotel. She denied any other recent travel, including outside of the United States. She reported she had a few episodes of vomiting and diarrhea, with chills but without fever, the previous night. She had no other significant medical history.

The initial presumed diagnosis was meningococcemia, and she was immediately given intravenous (IV) vancomycin 1 g and IV ceftriaxone sodium 2 g. After an emergent consult with the infectious diseases attending physician, the patient was given hydrocortisone sodium succinate 100 mg IV. Two large-bore IV lines were also placed in the antecubital region.

An immediate spinal tap was performed, during which the patient remained awake and alert, with stable vital signs, although she did have a transient nosebleed after the procedure. Because of disseminated intravascular coagulation, 4 units of fresh frozen plasma were ordered, along with 2 units of packed red blood cells (RBCs). The  cerebrospinal fluid (CSF) Gram's stain showed no white blood cells or organisms. The underlying cause of illness remained unclear.

A Foley catheter was placed, with no urine output returned. Her heart rate increased to 110 beats/min, and her blood pressure decreased to 100 mm Hg systolic, but she remained neurologically intact. The patient continued to complain of severe, bilateral, burning pain in the thighs and was given morphine sulfate IV in 2-mg  increments. Her hands and feet were becoming paler, and her skin appeared more mottled.

The patient was moved to the intensive care unit (ICU) before the laboratory results arrived. An emergent hematology consult was obtained in the ICU, and a peripheral smear showed no evidence of schistocytes. Bone marrow aspiration was not done because of the patient's acute deterioration. A renal consult was immediately obtained to evaluate the anuria. Laboratory test results were returned at this time (Table 1).

During the next 30 minutes, the patient became increasingly tachycardic and hypotensive and then went into cardiac arrest. Advanced cardiac life support measures were performed, but she was pronounced dead 2 hours after arriving at the hospital. The following day, blood and CSF cultures grew 

. Autopsy did not reveal a focal site of infection or any other pathology.

 is an encapsulated gram-positive coccus. The capsule helps the bacteria escape phagocytosis and leads to a decreased inflammatory response by na?ve hosts. In contrast, some immunity is provided to those who have been previously exposed to 

. As a result, infection rarely causes invasive disease in healthy adults; when it does, immunodeficiency should be suspected.

Many conditions predispose to pneumococcal infection, including asplenia, splenectomy, complement disorders, and defective antibody formation (often the result of HIV infection, lymphoma, leukemia, or hypogammaglobulinemia).

Our case is unique in that an otherwise healthy woman, with no known medical problems, presented with pneumococcal sepsis that proved to be rapidly fatal. Another unusual aspect of this case is the presentation of purpura fulminans.

Purpura fulminans is characterized by widespread ecchymosis and ischemic infarction of the skin. The lesions can progress to hemorrhagic bullae and skin necrosis and are usually seen on the extremities, buttocks, and abdomen; the chest, face, scalp, and mucous membranes are typically spared. Although the lesions of purpura fulminans are normally confined to the skin, any organ system can be affected, including the kidneys, brain, gastrointestinal tract, and lungs. Patients are often acutely ill at presentation, with high fever, tachycardia, and shock. Other clinical manifestations can include hypotension and disseminated intravascular coagulation.

Laboratory findings often indicate a consumptive coagulopathy, with a low platelet count, low concentrations of fibrinogen and clotting factors, and increased fibrin degradation products.

The management of purpura fulminans remains controversial. Treatment modalities range from reversing the precipitating cause and providing supportive care to administering fresh frozen plasma, antibiotics, steroids, hyperbaric oxygen therapy, heparin, and IV low-molecular-weight dextran. Despite this, the mortalityrate is approximately 18%.

Purpura fulminans is often secondary to a bacterial, fungal, or viral illness, most often meningococcemia, varicella, or scarlet fever. Patients with pneumococcemiaare more vulnerable to developing purpura fulminans if they have one of the following conditions

An underlying medical condition, such as HIV infection, sickle-cell anemia, alcoholism, hypogammaglobulinemia, upper respiratory tract infection, or diabetes mellitus

Undergone splenectomy or any recent surgery

Our patient presented with purpura fulminans, secondary to widespread sepsis from 

. The ecchymotic and purpuric rash was observed over her trunk, back, and extremities; her face was spared, but the lips and mucous membranes were cyanotic. Although she appeared to have disseminated intravascular coagulation, laboratory workup for this condition was not processed. Despite treatment with fresh frozen plasma, fluids, packed RBCs, and IV antibiotics, she rapidly decompensated and died. She had no underlying conditions, such as HIV infection or malignancy, which are normally associated with a presentation of overwhelming pneumococcal sepsis.

Several similar reported cases involve women of different ages (Table 2). One case is a 43-year-old woman who had pneumococcal sepsis complicated by purpura fulminans  after she had a cut on her finger that was infected with pneumococcus.

 This patient's course of illness progressed more slowly. Within 24 hours, she developed thrombocytopenia and had an increased blood urea nitrogen/creatinine ratio and elevations in alanine aminotransferase, total bilirubin, prothrombin time, and partial thromboplastin time. She later became disoriented, confused, afebrile, jaundiced, and anuric, and she had respiratory failure. Despite this, the woman survived after treatment with IV antibiotics, dialysis, and plasma exchange. Although no identifiable source of infection was found, she had a more indolent course of illness and survived with supportive therapy.

 With the exception of plasma exchange, our patient received the same initial treatment.

Another case of pneumococcal sepsis complicated by purpura fulminans involved a 50-year-old patient who had a prodrome of upper respiratory tract infection, with fevers, headache, and a nonproductive cough.

 This woman also rapidly decompensated, presented the next morning with nausea, vomiting, bowel and bladder incontinence, confusion, and purple discoloration of her skin. She rapidly went into shock, was intubated, and developed cold, mottled extremities with ecchymosis extending to the extremities, face, and trunk. She died rapidly, despite supportive treatment with fresh frozen plasma, platelet transfusion, dopamine, IV antibiotics, and mechanical ventilation.

Despite some similarities, that patient differed significantly from ours, except for her prodrome. She was elderly, had a history of fevers before admission, and had a more protracted course, dying 36 hours after admission. In addition, postmortem examination revealed diffuse interstitial and alveolar edema with hemorrhagic exudate, hemorrhagic necrosis of the adrenal glands, and hemorrhagic gastritis, consistent with acute respiratory distress syndrome (ARDS) and Waterhouse-Friderichsen syndrome.

 Our patient had only mild ARDS on autopsy; she was younger, afebrile, and had no known medical conditions.

Perhaps most similar in initial presentation to our patient was a case involving a 15-month-old girl.

 Like our patient, the girl had prodromal symptoms of nausea, vomiting, and fatigue. However, 2 days after she began vomiting, she was unresponsive and had an erythematous, nonblanching, perioral rash. At the time of presentation  to the emergency department, the child had a diffuse petechial and purpuric rash over her face and trunk; her legs and arms were cool. This child also had leukocytosis, thrombocytosis, and elevated liver enzymes. However, CSF culture grew 

 within 24 hours. Despite treatment with IV ceftriaxone sodium and vancomycin, mechanical ventilation, fluid resuscitation, peritoneal dialysis, and blood product transfusion, her pupils became fixed and dilated, and she developed hypertension within 9 hours of presentation. Life support was withdrawn the next day. The cause of death was determined to be meningitis, with edema and cerebellum tonsillar herniation, sepsis, and disseminated intravascular coagulation.

 sepsis with purpura fulminans involved a woman who had undergone bariatric surgery 1 year earlier.

 This 63-year-old patient had a more indolent course of illness than our patient. She had lost 57 kg during the year after her surgery. She presented with severe dehydration and diarrhea, and a stool culture was positive for 

. On her third hospital day, the patient became dyspneic, and was diagnosed with deep-vein thrombosis and pulmonary embolism. At that time, her blood cultures grew 

. The following day she became hypotensive, hypoxic, and azotemic; a petechial rash appeared over her feet, and she was diagnosed with disseminated intravascular coagulation. She continued to receive IV antibiotics, and dopamine and drotrecogin alfa were added to her regimen. She was also started on vitamins A, C, and D replacement therapy, because she was believed to be malnourished as a result of the diarrhea. This patient eventually recovered and became fully ambulatory.

It is postulated that she was more susceptible to illness because of her malnutrition; she continued to take the vitamin supplementation. Unlike our patient, this woman was malnourished and had been hospitalized for 4 days before developing purpura fulminans, during which time she also developed a pulmonary embolus, which she survived. In contrast, our patient, who was younger and did not have any premorbid medical conditions, died 2 hours after arriving at the hospital.

Primary pneumococcal sepsis is unusual in adults without predisposing factors, such as HIV infection, splenectomy, lymphoma, and immunocompromised states. Purpura fulminans is a focal ischemic skin manifestation often seen secondary to bacterial, viral, and fungal infections. Our case is unusual in that it involved a young woman who rapidly decompensated, despite supportive treatment. Although she was later found to have overwhelming sepsis from 

, no primary site was ever identified. In addition, no underlying medical conditions were found, which could have made her more susceptible to pneumococcal sepsis and purpura fulminans.

Warner PM, Kagan RJ, Yakuboff KP, et al. Current management of purpura fulminans: a multicenter study. 

Childers BJ, Cobanov B. Acute infectious purpura fulminans: a 15-year retrospective review of 28 consecutive cases. 

An exceptional case of a patient who died within 4 hours of presentation, yet had no history of splenectomy or other predisposing factors.

February 2008 Vol 54 No 2

Remodeling the House of Medicine: Update on the Medical Continuum

New Combination Antihypertensive Therapy with 2 Proven Mechanisms of Action

Hand Tumor in a 72-Year-Old Woman

ECG Rounds

My Experience as a Patient

Letters to the Editor

Radiology

Dermatology

Internal Medicine

Posterior Ischemic Optic Neuropathy Associated with Calcium Channel Blocker Overdose

Rapidly Deteriorating Pneumococcal Sepsis and Systemic Purpura Fulminans in a Young Woman with No Predisposing Factors

Abnormal Nails and Hypohidrosis in a 22-Month-Old Boy

Calciphylaxis: Necrotizing Skin Ulcers in End-Stage Renal Disease

Human Papillomavirus Infection: Current Approach to Prevention

Sinoatrial Nodal Reentry Tachycardia: An Unusual Type of Sinus Tachyarrhythmia