Bilateral leg edema Drew C. Baird, MD and diffi culty swallowing - MDedge

PHOTO ROUNDS

Bilateral leg edema and difficulty swallowing

This patient's leg pain was the tip of the iceberg. He also had diminished breath sounds and a cachectic appearance.

edia 70-year-old man came to our M medical center for treatment of

A Health painful bilateral leg swelling that

Dowden only had gotten progressively worse over the CopyrigFhotr personal use past week. He had no significant pa?st

medical or surgical history, took an aspirin daily, did not smoke tobacco or drink alcohol, and had not taken any

and lower lung fields, and pitting edema up to the knees bilaterally.

Lab studies showed a normal brain natriuretic peptide of 16 pg/mL, normocytic anemia (hemoglobin, 9.5 g/dL; hematocrit, 29.6%; and a mean corpuscular volume of 82.6 fL), potassium of 2.4 mEq/L, calcium of 5.4 mg/dL, and al-

trips recently. He denied any chest pain, bumin of 1.4 g/dL. An electrocardiogram

dyspnea, or orthopnea, but indicated (EKG) revealed a bifascicular heart block,

that he'd been having difficulty swal- which was not new based on older EKGs.

lowing food for the past month.

A plain chest radiograph was performed

The patient had a cachectic appear- (FIGURES 1A AND 1B).

ance, diminished breath sounds and dull-

ness to percussion over the right middle What is your diagnosis?

FIGURE 1 A

Chest x-rays reveal large mass

B

Drew C. Baird, MD Department of Family and Community Medicine, D.D. Eisenhower Army Medical Center, Fort Gordon, Ga drew.baird@us.army.mil

EDITOR

Richard P. Usatine, MD University of Texas Health Science Center at San Antonio

FAST TRACK

In addition to having difficulty swallowing, the patient had diminished breath sounds and dullness to percussion over the right middle and lower lung fields.

A posterior-anterior chest radiograph (A) revealed a large mass in the right hemithorax with an air-fluid level. A lateral chest radiograph (B) showed the same large mass with an air-fluid level that displaced the trachea anteriorly.



VOL 58, NO 2 / FEBRUARY 2009

89

For mass reproduction, content licensing and permissions contact Dowden Health Media.

PHOTOS COURTESY OF DREW C. BAIRD, MD

PHOTO ROUNDS

FAST TRACK

To aid in the transit of food boluses, patients will eat slowly, stretch, move side-to-side, and walk after meals.

Diagnosis: Achalasia

Achalasia is characterized by an incomplete relaxation of the lower esophageal sphincter (LES) accompanied by aperistalsis of the esophageal body. The etiology of primary achalasia is unknown, but involves the degeneration of inhibitory neurons within the myenteric plexus responsible for LES relaxation and esophageal peristalsis.

Many potential causes. Infectious, inflammatory, autoimmune, and genetic causes have all been proposed. Achalasia has a prevalence of less than 1 in 10,000; its incidence is 0.3 to 1 per 100,000 per year, with peaks in the third and seventh decades of life. Men and women are affected equally.1

Conversely, pseudoachalasia--or secondary achalasia--has a known cause that either destroys the neurons of LES relaxation or has a mass effect that limits LES relaxation. Its most common cause is malignancy involving the gastroesophageal junction. Other causes include Chagas disease, an infection by the parasite Trypanosoma cruzi that affects the myenteric plexus, and amyloidosis.2

A disorder that goes undiagnosed for years In primary achalasia symptom onset is insidious, with the disorder typically going undiagnosed for several years. Patients experience a gradual dysphagia for solids, progressing to liquids. Over time, patients adopt particular behaviors to aid the transit of food boluses down the esophagus and through the contracted LES, including eating slowly, stretching, moving side-to-side, or walking after meals.1 Regurgitation of food, chest pain, weight loss, heartburn, and difficulty belching are also common complaints.3 A more rapid onset and progression of symptoms (less than 6 months) is suggestive of pseudoachalasia and cancer.

Left untreated, primary achalasia leads to a progressively dilating esophagus with increased risk of aspiration, perforation, malnutrition, weight loss,

and esophageal cancer.3 This case is remarkable for how far the patient's disease progressed before he presented with signs and symptoms more indicative of secondary malnutrition than the primary disease.

Differential Dx includes hiatal hernia

The differential diagnosis for achalasia includes hiatal hernia, right middle lobe pneumonia, empyema, and lung abscess. Most patients with hiatal hernias are asymptomatic, and the diagnosis is made incidentally on chest x-ray as a retrocardiac air-fluid level or on upper gastrointestinal studies. Right middle lobe pneumonia would appear on chest x-ray as a well-demarcated opacity within the confines of that lobe, but would not have an air-fluid level. Empyema and lung abscess are complications of pneumonia, and patients present with persistent fever, cough, dyspnea, and malaise. With an empyema, chest x-ray reveals a pleural effusion. A lung abscess is an intrapulmonary cavitary lesion with an air-fluid level, most commonly due to aspiration pneumonia.

This patient's chest x-ray showed a mass outside the lung tissue and pleural space that had an air-fluid level, was within the mediastinum, and displaced the trachea anteriorly, all suggestive of a dilated esophagus filled with undigested food unable to pass the LES.

Esophageal manometry clinches the diagnosis

Esophageal manometry is the gold standard for diagnosis. In achalasia, manometry shows poor peristalsis of the esophageal body and a constricted LES that does not relax sufficiently with swallowing.3 Manometry cannot, however, reliably distinguish primary achalasia from pseudoachalasia.

Barium swallow studies and endos-

copy can assist in the diagnosis and help rule out pseudoachalasia. Timed

90

VOL 58, NO 2 / FEBRUARY 2009 THE JOURNAL OF FAMILY PRACTICE

Bilateral leg edema and difficulty swallowing

barium studies can show a lack of peristalsis, an air-fluid level at the top of a barium column retained within the dilated esophagus, and the narrowing of the distal esophagus into the pathognomonic "bird's beak" of primary achalasia.4 Endoscopy can visualize a mass beyond the LES, but cannot adequately assess esophageal peristalsis or LES relaxation.1

In our patient's initial workup, a CT (FIGURE 2), barium study (FIGURE 3), and endoscopy were all used to rule out an obstructive lesion.

Treatment targets the constricted LES

The goal of treatment in achalasia is to help food move through the constricted LES. Pharmacologic therapy, used to decrease LES resting tone, has limited benefit and becomes less effective as the disease progresses. Calcium channel blockers, particularly nifedipine, and nitrates are the most commonly used agents.5

Pneumatic dilation is the most effective nonsurgical treatment of achalasia. It involves the controlled rupture of LES muscle fibers to dilate the sphincter and allow gravity to move food from the esophagus into the stomach.6 Symptom improvement lasts for 60% of patients at 1 year, 50% at 5 years, and 36% at 10 years. Repeated dilations are possible and sometimes necessary, but have diminishing success rates. The most worrisome complication of pneumatic dilation is esophageal rupture, which occurs 2% of the time.5

Botulinum toxin injection is another accepted nonsurgical therapy and is recommended for patients who would like to avoid more invasive treatment. When injected into the LES, the toxin causes temporary atrophy of the neurons responsible for LES contraction. After the procedure, 70% of patients report improvement in symptoms, with half in remission at 6 months and one-

FIGURE 2

Massively distended esophagus

A chest CT revealed a distended esophagus--at times 8 cm in diameter--from the thoracic inlet to the gastric inlet, strongly suggestive of achalasia. The patient's trachea was displaced anteriorly, his posterior right lung was compressed, he had bilateral pleural effusions, and had generalized edema that was suggestive of anasarca.

FIGURE 3

The "bird's beak" of achalasia

A barium swallow study showed diffuse enlargement of the esophagus with a narrowing "bird's beak" near the esophagogastric junction, consistent with achalasia.

third at 1 year. Patients may require repeat injections every 3 to 4 months, but the toxin's effectiveness diminishes with each injection.6

The laparoscopic Heller myotomy involves cutting the LES muscle, making it incompetent and allowing food boluses to pass through the LES. Ninety percent of patients experience symptom relief after surgery,5 with 10-year remission rates of 67% to 85%.1 Comparisons to

FAST TRACK

It was remarkable how far the patient's disease had progressed before he sought treatment.



VOL 58, NO 2 / FEBRUARY 2009

91

PHOTO ROUNDS

FACULTY

pneumatic dilation do not show significant differences in outcomes over time, although most studies favor myotomy over dilation.

Surgical treatment is indicated for patients who are younger than 40 years of age, those who have failed repeated nonsurgical therapies, and those at high risk of esophageal perforation.5

Correspondence Drew C. Baird, MD, Department of Family and Community Medicine, D.D. Eisenhower Army Medical Center, 300 Hospital Road, Fort Gordon, GA 30905; drew. baird@us.army.mil

Disclosure The author reported no potential conflict of interest relevant to this article. The opinions or assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the Department of Defense.

Patient's course highlights Tx risks

Due to the severity of the patient's achalasia, a Heller myotomy was performed. During the postoperative period he had several complications. He ultimately died from an uncontrollable hemorrhage after an esophageal perforation, highlighting the seriousness of this disease and the risks inherent to its treatment.

References

1. Pohl D, Tutuian R. Achalasia: an overview of diagnosis and treatment. J Gastrointestin Liver Dis. 2007;16:297-303.

2. Spechler SJ, Castell DO. Classification of oesophageal motility abnormalities. Gut. 2001;49:145-151.

3. Farrokhi F, Vaezi MF. Idiopathic (primary) achalasia. Orphanet J Rare Dis. 2007;2:38.

4. Levine MS, Rubesin SE. Diseases of the esophagus: diagnosis with esophagography. Radiology. 2005;237:414-427.

5. Roberts KE, Duffy AJ, Bell RL. Controversies in the treatment of gastroesophageal reflux and achalasia. World J Gastroenterol. 2006;12:3155-3161.

6. Annese V, Bassotti G. Non-surgical treatment of esophageal achalasia. World J Gastroenterol. 2006;12:5763-5766.

READ ABOUT BIPOLAR SPECTRUM DISORDERS AND EARN 2.5 FREE CME CREDITS

HENRY A. NASRALLAH, MD, PROGRAM CHAIR Professor of Psychiatry, Neurology, and Neuroscience University of Cincinnati College of Medicine Cincinnati, Ohio

DONALD W. BLACK, MD Professor of Psychiatry University of Iowa Carver College of Medicine Iowa City, Iowa

JOSEPH F. GOLDBERG, MD Associate Clinical Professor of Psychiatry Mt Sinai School of Medicine, New York, New York Silver Hill Hospital, New Canaan, Connecticut

DAVID J. MUZINA, MD Vice Chair for Research & Education Associate Professor of Medicine Cleveland Clinic Department of Psychiatry & Psychology Cleveland, Ohio

STEPHEN F. PARISER, MD Professor of Psychiatry, Obstetrics and Gynecology Medical Director, Psychiatry Clinics Medical Director, Neuropsychiatry Ohio State University College of Medicine Columbus, Ohio

RELEASE DATE: DECEMBER 1, 2008 EXPIRATION DATE: DECEMBER 1, 2009

LEARNING OBJECTIVES After reviewing this material, clinicians should be better able to: ? Achieve early and accurate diagnosis of patients with mood disorders ? Utilize available screening tools effectively ? Understand the mechanisms of action, hepatic effects, and other

metabolic effects of available agents and their potential impact on treatment ? Develop an effective treatment plan that includes monotherapy or combination therapy ? Select the most appropriate agent(s) for short- and long-term treatment to meet individual patient needs

TARGET AUDIENCE Psychiatrists, primary care physicians, and other health care professionals who treat patients with psychotic and mood disorders

CME ACCREDITATION STATEMENT The University of Cincinnati designates this educational activity for a maximum of 2.5 AMA PRA Category 1 creditsTM. Physicians should only claim credit commensurate with the extent of their participation in the activity. This CME activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the sponsorship of the University of Cincinnati College of Medicine. The University of Cincinnati College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

FINANCIAL DISCLOSURES AND CONFLICTS OF INTEREST According to the disclosure policy of the University of Cincinnati, faculty, editors, managers, and other individuals who are in a position to control content are required to disclose any relevant financial relationships with the commercial companies related to this activity. All relevant relationships that are identified are reviewed for potential conflicts of interest. If a conflict of interest is identified, it is the responsibility of the University of Cincinnati to initiate a mechanism to resolve the conflict(s). The existence of these interests or relationships is not viewed as implying bias or decreasing the value of the presentation. All educational materials are reviewed for fair balance, scientific objectivity of studies reported, and levels of evidence.

THE FACULTY HAS REPORTED THE FOLLOWING: DR NASRALLAH reports that he is on the advisory board of Abbott, AstraZeneca, Cephalon, Janssen, Pfizer, and Vanda Pharmaceuticals; is a consultant for AstraZeneca, Janssen, Pfizer, and Vanda Pharmaceuticals; receives grants from AstraZeneca, Forest Laboratories, Janssen, Otsuka America Pharmaceutical Inc., Pfizer, Roche, and sanofi-aventis; and is on the speakers bureau of AstraZeneca, Janssen, and Pfizer. DR BLACK reports that he is a consultant for Forest Laboratories and Jazz Pharmaceuticals and receives grant(s) from Forest Laboratories. DR GOLDBERG reports that he is on the advisory board, speakers bureau, and serves as a consultant for AstraZeneca, Eli Lilly & Co, and Glaxo SmithKline. DR PARISER reports that he receives grants from Pfizer and is on the speakers bureau for AstraZeneca, GlaxoSmithKline, and Pfizer. DR MUZINA reports that he is on the advisory board of AstraZeneca and Bristol-Myers Squibb; and is on the speakers bureau of AstraZeneca, Bristol-Myers Squibb, Pfizer, Sepracor, and Wyeth. PLANNING COMMITTEE: Kay Weigand, University of Cincinnati; and Kristen Georgi, Charles Williams, and Katherine Wandersee for Dowden Health Media have disclosed no relevant financial relationship(s) with any commercial interests. No off-label use of drugs or devices are discussed in this supplement.

SUPPORT Supported by an educational grant from AstraZeneca.

ACKNOWLEDGEMENT This CME activity was developed through the joint sponsorship of the University of Cincinnati and Dowden Health Media. It was edited and peer reviewed by The Journal of Family Practice.

? 2008 AMERICAN ACADEMY OF CLINICAL PSYCHIATRISTS AND DOWDEN HEALTH MEDIA

and

2FC.RR5ECEDMEITES

Recognizing and managing psychotic and mood disorders in primary care

INTRODUCTION > HENRY A. NASRALLAH, MD

T he diagnosis and management of psychotic and mood disorders is an evolving process and an important clinical topic for primary care clinicians (PCPs). Although many reports exist on the prevalence and treatment of depression in primary care, far less information is available about patients in this setting with depression accompanied by symptoms of mania or hypomania.1

To facilitate a dialogue on the identification and treatment of psychotic and mood disorders, we invited 4 expert faculty members to present actual patient cases followed by a panel discussion in which the collective experience of all the faculty lends further practical insights into the nuances of management of such patients in both inpatient and outpatient settings. In particular, these cases underscore the importance of being alert to critical clues in a patient's history or the family's history. A larger version of this panel discussion appears in a supplement to the December 2008 issue of CURRENT PSYCHIATRY. We've extracted the portion that we felt would be of most interest to primary care providers.

The case selected for presentation here is by David Muzina, MD, and concerns a 20-year-old man who was referred for psychiatric evaluation by his PCP and psychologist for treatment of mood swings, anxiety, and confusion. He had been given sertraline and then venlafaxine, but discontinued both medications on his own. His symptoms began rather abruptly 14 months earlier, coinciding with an intense program of weight lifting and supplement use to change his self-described smallness. Profound, persistent sadness and feeling "dead inside" were his chief complaints, and they had led to a break-up with his girlfriend, which distressed him greatly and preoccupied his thinking. He also believed his parents were hiding from him the truth of a significant birth defect.

Following the case presentation is a faculty discussion of several pivotal issues in the management of mood disorders:

? Pitfalls to avoid during the diagnostic evaluation ? Pros and cons of monotherapy and combination therapy ? Mechanisms of action of available medications and implications for an effective treatment plan ? Suggestions for enabling patient compliance with prescribed regimens We hope the insights you glean from this exchange of practical clinical issues will enhance and confirm your own approach to diagnosing and treating patients with psychotic and mood disorders.

REFERENCE 1. Das AK, Olfson M, Gameroff MJ, et al. Screening for bipolar disorder in a primary care practice. JAMA.

2005;293:956-963.

Supplement to The Journal of Family Practice Vol 57, No 12s December 2008 S5

DON'T MISS THIS 12-PAGE CME SUPPLEMENT

AVAILABLE ONLINE AT

Recognizing and managing psychotic and mood disorders in primary care

Read a case referred to psychiatry by primary care and find out how experts manage the care of patients with psychotic and mood disorders.

FAC U LT Y

} HENRY A. NASRALLAH, MD, PROGRAM CHAIR } DONALD W. BLACK, MD } JOSEPH F. GOLDBERG, MD } DAVID J. MUZINA, MD } STEPHEN F. PARISER, MD

THIS CME AC TIVIT Y IS SUPPORTED BY AN EDUCATIONAL GRANT FROM ASTRAZENECA AND DEVELOPED

THROUGH THE JOINT SPONSORSHIP OF THE UNIVERSIT Y OF CINCINNATI AND DOWDEN HEALTH MEDIA.

92

VOL 58, NO 2 / FEBRUARY 2009 THE JOURNAL OF FAMILY PRACTICE

 ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download