Letters to the Editor

Vocal Cord Dysfunction

to the editor: I was pleased that the article "The 'Crashing Asthmatic'"1 included a differential diagnosis of vocal cord dysfunction (VCD). I would like to further discuss this puzzling condition.

VCD is a paradoxic adduction (closure) of the vocal cords during inspiration or expiration, when they should normally remain open. Unfortunately, misdiagnosis of VCD as asthma has led to several unnecessary intubations and iatrogenic side effects from unnecessary medications. The incidence of VCD is unknown and probably underreported, but an estimated 2 to 3 percent of the general population is affected. The majority of cases reported are in adolescent females. One study2 found that almost 10 percent of elite winter athletes had VCD.

The etiology of VCD is unknown, but there are several triggers, including exercise, gastroesophageal reflux disease (GERD), post-nasal drip, allergic rhinitis, and inhaled irritants.3 VCD is most commonly misdiagnosed as exercise-induced bronchospasm. There also seems to be a large psychologic component. A recent case report4 proposed focal dystonia as an etiology, suggesting that neurologic causes may at times need to be considered.4

The typical clinical presentation is acute onset of an inability to catch one's breath, inspiratory stridor, and choking or full sensation in the throat. The "so-called" classic history is an adolescent female who appears with inspiratory stridor just before a major sporting competition. The attack usually abates as quickly as it began. Most patients will appear very anxious, but are almost never hypoxemic, which differentiates VCD from an acute asthma attack. Patients also will have poor to no response from bronchodilators, except for the 30 percent of patients who have VCD and coexistent asthma and may be suffering from a simultaneous attack.

Diagnosis rests with a high clinical suspicion and direct observation of paradoxic vocal cord function. The diagnosis can be strongly suggested by abnormal flow volume loops during an acute or provoked attack showing truncation or irregularity of the inspiratory or expiratory limbs of the flow volume loop (see the accompanying figure on page 1045).5 VCD may be either an inspiratory (most common), expiratory, or combined phenomenon. During pulmonary function testing (PFT), methacholine can be used to induce reactive airway disease, and negative results almost certainly rule out any asthmatic component. Unfortunately, methacholine can act as an irritant and provoke VCD, but the flow volume loops will not reveal the characteristic obstructive pattern. If VCD is considered during PFT, direct laryngoscopy should be available to visually confirm the paradoxic vocal cord motion if induced. The real role of PFT is determining if there is a reversible bronchoconstrictive process. Fluoroscopy has been demonstrated as a reliable and noninvasive technique to confirm the diagnosis of VCD.6

Microscopic Hematuria The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication. FIGURE.

Initial management depends on the severity of the attack. For mild episodes, coughing or panting may break the cycle. Acute, severe episodes of VCD can be managed with oxygen, Heliox (80 percent helium/20 percent oxygen), or sedation. Intermittent, positive pressure also can resolve an attack. Topical lidocaine applied to the larynx and discontinuing unnecessary asthma medication may be useful. Treatment of patients with GERD, allergic rhinitis, or postnasal drip are contributory; treatment of these conditions can greatly decrease the number of attacks. Behavior modification and speech therapy also are necessary. Anxiolytics have a role in the chronic management, because there is a large psychologic component to VCD.

JRFF LEGGIT, M.D.
2203 Delaware Dr.
Harker Heights, TX 76548

REFERENCES

1. Higgins JC. The 'crashing asthmatic'. Am Fam Physician 2003;67:997-1004.

2. Rundell KW, Spiering BA. Inspiratory stridor in elite athletes. Chest 2003;123:468-74.

3. Balkissoon R. Occupational upper airway disease. Clin Chest Med 2002;23:717-25.

4. Vlahakis NE, Patel AM, Maragos NE, Beck KC. Diagnosis of vocal cord dysfunction: the utility of spirometry and plethysmography. Chest 2002;122: 2246-9.

5. Brugman SM, Simons SM. Vocal cord dysfunction: don't mistake it for asthma. Phys Sportsmed 1998; 26:63-74.

6. Mistry DJ, Kramer CM. Imaging of cardiopulmonary diseases. Clin Sports Med 2003;22:197-212.

Management of Swimming-Induced Pulmonary Edema

to the editor: A healthy 20-year-old United States Navy search and rescue swimmer trainee, who was equipped with only a mask and fins, developed hemoptysis, sharp substernal chest pain, and shortness of breath after performing a dive to a depth of 12 feet. He immediately surfaced and began to cough up pink, frothy sputum and have persistent shortness of breath. His initial oxygen saturation was 70 percent on room air and improved to 86 percent on three liters of oxygen via nasal cannula during ambulance transfer. On arrival at the emergency department, the patient had an oxygen saturation of 100 percent on three liters of oxygen with improved shortness of breath and resolved hemoptysis.

FIGURE. Chest radiograph showing fluffy perihilar infiltrates bilaterally in patient with swimming-induced pulmonary edema.

Auscultation of the lungs revealed bilateral rhonchi. The remainder of the physical examination was unremarkable with all vital signs being normal. Electrocardiogram, complete blood count, electrolytes, creatine kinase, troponin, and coagulation studies were all within normal limits. A chest radiograph showed fluffy perihilar infiltrates bilaterally (see the accompanying figure on page 1048). A chest radiograph taken several hours later showed resolving infiltrates. The patient was diagnosed with swimming-induced pulmonary edema (SIPE) and discharged.

While the exact pathophysiology of SIPE remains uncertain, it is believed to be related to exertion, immersion in cold water, and overhydration. The body's normal response to exercise is to increase cardiac output to meet the increased oxygen demand. Although an increased cardiac output is known to cause pulmonary edema in racehorses, this increase is rarely enough to produce such an effect in humans.1 Cold-water immersion is instrumental in this process because the peripheral vasculature constricts to divert blood away from the extremities in an effort to maintain the core body temperature. This results in a central pooling of blood, leading to an increased preload, increased pulmonary artery pressure, and an increased cardiac output. The vasoconstriction also causes an increase in afterload, which leads to an increase in pulmonary vasculature resistance. The increased cardiac output from exertional activities coupled with an increased preload and afterload from immersion appear to be sufficient to rupture the pulmonary capillary membranes, thus resulting in pulmonary edema. In several documented cases of SIPE, it has been noted that the patients consumed anywhere from two to four liters of water in the hours leading up to their swim in an effort to remain well hydrated.2 It is believed that this degree of hydration led to a fluid overload that contributed to the onset of pulmonary edema by increasing the pulmonary capillary pressure.2 Patients may present with symptoms, such as cough, dyspnea, hemoptysis, tachypnea, and confusion with hypoxia, after exertional cold water activity such as swimming and scuba diving.3

Treatment for patients with SIPE consists primarily of supportive measures such as removing the patient from the wet and/or cold environment and providing supplemental oxygen. Although useful in treating pulmonary edema in racehorses, diuretics are typically not necessary because patients tend to show relief of symptoms soon after being placed on supplemental oxygen.4 Full resolution of radiographic findings typically occurs within 24 to 48 hours.

JASON A. YODER, MS3, ENS, MC, USNR
Uniformed Services University of the Health Sciences
4301 Jones Bridge Rd.
Bethesda, MD 20814

ANTHONY J. VIERA, LCDR, MC, USNR
Naval Hospital Jacksonville
2080 Child St.
Jacksonville, FL 32214

REFERENCES

1. Hopkins SR, Schoene RB, Henderson WR, Spragg RG, Martin TR, West JB. Intense exercise impairs the integrity of the pulmonary blood-gas barrier in elite athletes. Am J Respir Crit Care Med 1997; 155:1090-4.

2. Weiler-Ravell D, Shupak A, Goldenberg I, Halpern P, Shoshani O, Hirschhorn G, et al. Pulmonary oedema and haemoptysis induced by strenuous swimming. BMJ 1995;311:361-2.

3. Pons M, Blickenstorfer D, Oechslin E, Hold G, Greminger P, Franzeck UK, et al. Pulmonary oedema in healthy persons during scuba-diving and swimming. Eur Respir J 1995;8:762-7.

4. Lund KL, Mahon RT, Tanen DA, Bakhda S. Swimming-induced pulmonary edema. Ann Emerg Med 2003; 41:251-6.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U.S. Navy Medical Department or the U.S. Navy Service at large.

FIGURE 1. Trendelenburg's Sign. The pelvis tilts toward the normal hip when weight is borne on the affected side.

Corrections

The article "Antidepressants: Update on New Agents and Indications" (February 1, 2003, page 547) contained an error in the augmentation dosage of lithium and triiodothyronine (T3). On page 553, the last sentence of the fourth paragraph should have given the augmentation dosage of T3 as 25 mcg per day, not 25 mg per day. The online version of the article has been corrected.

The article "A Practical Guide to Anaphylaxis" (October 1, 2003, page 1325) contained an error in the concentration of epinephrine for intravenous infusion. On page 1328, in the second paragraph under the heading "Emergency Management," the fifth sentence should have given the concentration as 1:10,000 (100 mcg per mL) epinephrine at 1 mcg per minute, not 10 mcg per mL. The online version of this article has been corrected.

The article "Lower Extremity Abnormalities in Children" (August 1, 2003, page 461) contained an error in Figure 1 on page 462. The arrows identifying the normal and weak hip abductors were inadvertently transposed during production. The arrows should be pointing to the left side of the hip, rather than to the right. The corrected figure is reprinted below. The online version of the article has been corrected.