A pneumothorax in any patient who has sustained thoracic trauma should arouse suspicion. The patient may complain of an acute onset of sharp pleuritic chest pain, with radiation to the ipsilateral shoulder and associated dyspnea and anxiety. Typical physical findings in pneumothorax include unilaterally decreased breath sounds, hyperresonance to percussion over the affected lung, and asymmetric chest rise. In tension pneumothorax, the patient displays respiratory distress, tachypnea, and tachycardia, and the patient may also experience cyanosis, jugular venous distention, tracheal deviation away from the affected lung, and a pulsus paradoxus.

The epidemiology of traumatic pneumothoraces has not been well characterized. In the united States, trauma is the leading cause of death in persons younger than 45 years, and it accounts for approximately 150,000 deaths annually.1 The overall mortality for thoracic trauma is 10%, and chest injuries cause approximately 1 in 4 trauma deaths in North America.2 Pneumothorax is a serious complication of thoracic trauma, and it has been described in 1 in 5 patients that survive major trauma.3 Interestingly, in one study, 12% of patients with asymptomatic chest stab wounds had a delayed pneumothorax or hemothorax.8

While pneumothoraces in stable patients can be confirmed radiographically, a tension pneumothorax causing hemodynamic compromise should be diagnosed clinically, and treatment should never be delayed in favor of diagnostic imaging. A chest x-ray may show a linear shadow of visceral pleura, without lateral lung markings. An upright chest x-ray is more sensitive than a supine radiograph, as air tends to accumulate at the lung apex. In recumbent patients, air often accumulates in the anterior portion of the inferior chest and manifests radiographically as a “deep sulcus.” If a pneumothorax without tension physiology is suspected but not seen on the initial upright chest x-ray, a repeat film during exhalation may reveal it. Increasingly, ultrasound is being used as a rapid bedside modality for diagnosing pneumothoraces; some studies have shown that it is more sensitive than radiography for detecting traumatic pneumothoraces.4,5 Computed tomography (CT) is more sensitive and specific than chest x-rays or ultrasonography for the evaluation of small pneumothoraces and hemothoraces. Occult pneumothoraces may be present in 2-55% of trauma patients, although the clinical significance of occult pneumothoraces in patients who are not mechanically ventilated under positive pressure is unclear.6 Making the diagnosis of hemothorax may be more challenging. A minimum of 200-300 mL of blood is needed in the pleural space for blunting of the costophrenic angle to be visible on an upright chest x-ray. Blood is more difficult to appreciate on a supine x-ray because it will typically layer posteriorly, and ever larger volumes (up to 1000 mL) of blood may produce only a mild diffuse radiodensity. Lateral chest films may help differentiate hemothoraces from pulmonary contusions, and ultrasonography may also be useful for detecting fluid above the diaphragm. As with pneumothoraces, CT scanning is the most sensitive modality for diagnosing hemothoraces, although patients with massive hemothoraces may be too unstable for the scan.

The treatment of traumatic pneumothoraces and hemothoraces depends upon the volume of blood or air that has accumulated and on the condition of the patient. Hemodynamically stable patients who are not intubated and have a relatively small pneumothorax (ie, less than 1 cm wide) can be placed under observation. A repeat film should be obtained after 4-6 hours; if the pneumothorax is unchanged in size, the patient can continue to be observed without the need for decompression or tube thoracostomy. These patients should always be placed on 100% oxygen to increase the rate of reabsorption of the air in the pleural space. In unstable patients who, on clinical grounds, are suspected of having a pneumothorax, a needle thoracostomy may be performed to quickly decompress the pleural space. A 14-gauge Angiocath (18-gauge or 20-gauge in an infant) should be placed immediately superior to the rib in the second intercostal space, midclavicular line on the affected side. Once in place, the needle is removed and the Angiocath is secured. A rush of air may be appreciated as the Angiocath enters the pleural space. Pneumothoraces should preferentially be decompressed either by needle decompression or placement of a tube thoracostomy before the patient is intubated, as positive pressure ventilation will exacerbate a pneumothorax; however, definitive management of the airway should never be delayed when indicated. Needle thoracostomy generally necessitates the subsequent placement of a chest tube; however, stable patients who do not require a chest tube may be observed. In simple spontaneous pneumothoraces, a 20F or 22F chest tube may be used; however, larger-caliber chest tubes (28F to 40F) should be used in most traumatic pneumothoraces and hemothoraces to ensure adequate drainage of any fluid. Chest tubes are placed in the fourth or fifth intercostal space in the anterior axillary or midaxillary line, and they should be directed posteriorly and toward the apex of the lung. After the tube is secured, it should be connected to a water seal and vacuum device, and placement should be confirmed by chest x-rays. In the case of a hemothorax, immediate drainage of more than 1500-2000 mL (or 20 mL/kg) of blood, or ongoing hemorrhage exceeding
600-1200 mL/6 hours (or >3 mL/kg/hr) after the initial drainage, constitute the definition of a massive hemothorax and generally are indications for a thoracotomy. Occasionally, placement of an additional chest tube may be necessary to assist in draining of the hemothorax. Additionally, the possibility of a bronchial injury should be considered if a continuing air leak is observed after several chest tubes and an unexpanded lung. In hemothorax, chest tubes should be directed posteriorly and inferiorly to arrive posterior to the diaphragm (as opposed to the placement for a simple pneumothorax).

In this case, the junior emergency medicine resident placed a 14-gauge Angiocath in the second intercostal space, midclavicular line of the left chest. A rush of air was appreciated, and the patient’s blood pressure (as previously noted in the case presentation) improved to 95/60 mm Hg. The resident then prepared the left chest and placed a 38F chest tube in the fifth intercostal space, midaxillary line. There was immediate drainage of 1600 mL of bloody fluid through the chest tube. Uncrossmatched blood was administered, and the surgical team was consulted for the massive hemothorax. The patient was intubated and transported to the operating room (OR). In the OR, the surgery team performed a thoracotomy, repaired the injured lung parenchyma, and ligated several small arteries that were actively bleeding. The patient was transported to the surgical intensive care unit (ICU) and extubated the following day. The chest tube was removed 48 hours later, and the patient was discharged on hospital day 4 in stable condition.

The pathophysiology of atrial flutter includes multiple reentrant or ectopic atrial waveforms reaching the AV node. There are 2 forms of atrial flutter, referred to as type I and type II. Type I, also called typical, common, or isthmus-dependent atrial flutter, involves a reentrant circuit that encircles the tricuspid annulus of the right atrium, with rates that average 240-340 bpm. The depolarizing impulse can travel in a “counterclockwise” fashion around the tricuspid annulus, resulting in negative flutter waves in the inferior leads, or it can travel in a “clockwise” fashion, resulting in positive flutter waves in the inferior leads. Type II atrial flutter, also known as atypical aflutter, is less common and remains uncharacterized except for unusually high rates of
340-440 beats/min.[1,2] The exact etiology of atrial flutter is unknown, but it has been found to occur in patients with a variety of conditions, such as heart failure, pericarditis, valvular disease, pulmonary embolism, chronic obstructive pulmonary disease, and hyperthyroidism, as well as following most types of cardiac surgery. It is estimated that 200,000 new cases of atrial flutter are diagnosed each year in the United States. The condition tends to be more common in elderly men and in patients with the above mentioned comorbidities; however, it can also occur in patients without identifiable risk factors.[1]

After addressing the need for immediate cardioversion in patients with atrial flutter who may be hemodynamically unstable,[1] the general goals for pharmacotherapy include ventricular rate control, conversion to a normal sinus rhythm (NSR), prevention of recurrent episodes, minimization of the risk of thromboembolic complications, and minimization of any adverse effects from pharmacologic therapy.[2] Ventricular rate control can alleviate the symptoms associated with a rapid ventricular response. Two classes of medications are routinely used: calcium channel blockers (eg. diltiazem) and beta-blockers (eg. metoprolol). Both classes of medications work by blocking conduction of the atrial tachydysrhythmia through the AV node. The potential for hypotension associated with the negative inotropic effects of these drugs should be considered when they are used to treat atrial flutter.

After controlling the ventricular rate, the safety of attempting restoration of an NSR must be established; addressing the need for anticoagulation therapy for the prevention of thromboembolic phenomenon should be the first consideration. The success rate of direct current (DC) synchronized cardioversion is >95% for returning the heart to an NSR; however, as with atrial fibrillation, the success rate of sinus rhythm maintenance after 1 year of DC cardioversion without the aid of antiarrhythmic pharmacotherapy varies from 20 to 50%. Atrial flutter generally requires less energy for conversion than atrial fibrillation; in many cases, conversion is achieved with as little as 50 joules. Pharmacologic cardioversion is an alternative to electrical cardioversion, and it offers several choices with regard to specific medications. Procainamide is effective in 0-13% of patients; flecainide, in approximately 10% of patients; and dofetilide, in approximately 70-80% of patients. Ibutilide can convert recent-onset atrial flutter to an NSR in 63% of patients with a single infusion. Large, single oral doses of type IC antiarrhythmic agents, such as propafenone
(450-600 mg) or flecainide (200-300 mg), have been shown to be effective in converting recent-onset atrial fibrillation to an NSR as well.[2] Oral amiodarone during the loading period (>1 mo) has been shown to convert 18% of cases of atrial fibrillation or flutter to an NSR. Intravenous amiodarone is also effective in converting an atrial flutter to an NSR, and it slows the ventricular rate in patients with a rapid ventricular response. A final option is atrial overdrive pacing, which can be performed invasively or through the use of a transesophageal electrode to pace the left atrium; this therapy has a success rate of approximately 50%.[2] A combination of DC cardioversion and antiarrhythmic therapy is most commonly used to effectively restore an NSR and maintain sinus rhythm.[1,2]

After the initial episode of atrial flutter has terminated and any underlying precipitating factors have been treated, some patients may not need any further intervention, except for avoidance of the precipitating factor (eg, alcohol, caffeine); however, as mentioned above, approximately 30% of patients remain in sinus rhythm at 1 year without antiarrhythmic therapy, requiring some sort of maintenance therapy. The guidelines regarding the use of antiarrhythmic agents in atrial flutter are similar to those for using antiarrhythmic agents in atrial fibrillation. In addition, radiofrequency ablation has a high success rate and low complication rate for treating atrial flutter, and in some cases, it may be a more favorable option when compared with lifelong antiarrhythmic drug therapy because of adverse reactions that can include fatal proarrhythmic events and organ toxicity. Antiarrhythmics used to treat atrial fibrillation have been shown to be effective in treating fibrillation or flutter during a 6- to 12-month follow-up; the specific characteristics and the adverse effects of each antiarrhythmic agent should be considered when selecting which pharmacologic agent to use. Generally speaking, class IC agents may be used in patients without structural
heart disease[3]; however, for patients with left ventricular hypertrophy with or without ischemia or conduction delay, class III agents (specifically, sotalol or amiodarone) are the drugs of choice. For patients with significant systolic dysfunction, dofetilide can be an effective option provided that there is no evidence of renal dysfunction.[1,2]

There is an increased risk of thromboembolic complications for patients who have been in atrial flutter for more than 48 hours, which may result from episodic atrial fibrillation leading to impaired left atrial appendage function and subsequent thrombus formation. The same anticoagulation strategy used in patients with atrial fibrillation may be applied to patients with atrial flutter.[2] Some reports have demonstrated thrombus in the left atrium appendage in as many as 43% of patients with atrial flutter, with postcardioversion thromboembolic events occurring in up to 7% of patients who were not anticoagulated. These events, if not occurring immediately after cardioversion, typically occur at about 3 days following cardioversion, with almost all cases occurring within 10 days after restoration of an NSR. Stunning of the left atrial appendage is thought to contribute to thrombogenicity and may play a role for as long as 4 weeks following cardioversion. This is believed to be the source of emboli in patients who have had a thromboembolic event after cardioversion despite no evidence of thrombus found on transesophageal electrocardiography (TEE). Anticoagulation is also recommended for at least 1 week after any ablation of an atrial flutter that persists for more than 48 hours. Adequate anticoagulation, as recommended by the American College of Chest Physicians, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.[2]

The patient in this case was placed on noninvasive positive pressure ventilation for her pulmonary edema and treated with intravenous diltiazem for the rapid ventricular response to the underlying 2:1 atrial flutter rhythm. Administration of diltiazem resulted in conversion to a variable block that was mainly 4:1, resulting in a heart rate of around 80 bpm. Additional intravenous pharmacologic therapy with furosemide, nitroglycerin, and morphine sulfate was administered for her congestive heart failure. Heparin was administered as an anticoagulant for the atrial flutter. After several hours, the patient improved notably and was in no evident respiratory distress. The initial examination of cardiac enzymes was unremarkable, and she was admitted to a cardiac unit on a monitored floor for further management of her congestive heart failure, evaluation for possible myocardial ischemia, and workup for her atrial flutter. She continued to improve with intravenous diuretic therapy; on hospital day 2, she underwent a TEE that did not reveal structural heart disease or thrombus in the left atrium. She was DC cardioverted successfully (see ECG in Figure 2) and discharged on warfarin therapy with follow-up.

Dyshidrotic eczema is estimated to be present in 0.5-1% of the population, with an equal distribution between men and women. The majority of cases present before the patients reach 40 years of age, and there is no racial predominance. It is more commonly found in warmer, more humid climates, especially during the spring and summer. Recurrences may occur throughout a patient’s lifetime, with or without treatment. The pathophysiology of dyshidrotic eczema has not been definitively established,[5] but several hypotheses have been proposed. The term “dyshidrosis” is a misnomer that refers to the original hypothesis of sweat gland dysfunction, which has fallen out of favor. In addition, patients are not typically noted to experience hyperhidrosis. There is interest in the association of the condition with atopy,[4] as approximately 20% of patients experience concomitant hand eczema and approximately 50% of patients have a general disposition to an atopic diathesis (eg, asthma, hay fever, and sinusitis).[2] Other exogenous factors that have been implicated and may trigger episodes include contact dermatitis to heavy metals (such as with exposure to costume jewelry, nickel,[2,5] cobalt,[5] or chromates); sensitivity to ingested metals[5]; exposure to other contact allergens such as balsam,[5] paraphenylenediamine, and sesquiterpene lactones; and infection by dermatophytes or bacteria. Emotional stress (many patients report recurrences during stressful periods of their life) and environmental factors (eg, seasonal changes, hot or cold temperatures, and humidity) are also reported to exacerbate dyshidrosis.[2,5] There have also been case reports of dyshidrotic eczema occurring in patients recently treated with intravenous immunoglobulin therapy; in HIV-positive patients with an immune reconstitution inflammatory syndrome shortly after starting active antiretroviral therapy[5]; with the use of aspirin or oral contraceptives; and with cigarette smoking. In most cases, the condition remains idiopathic.

Dyshidrotic eczema is a recurrent or chronic, relapsing form of vesicular dermatitis. The classic presentation is of crops of vesicles or bullae that erupt bilaterally on the palms and the lateral aspects of the fingers. The vesicles may coalesce over time to form multiloculated bullae. The majority of cases involve the hands alone (cheiropompholyx), but roughly 10% of patients have lesions on both the hands and feet, and another 10% have lesions on just the feet (podopompholyx). The lesions may be intensely pruritic, leading to secondary desquamation and erosions and ulcerations from scratching. Dyshidrotic eczema developing near the tips of the fingers or toes may lead to dystrophic changes of the nails. Cellulitis, lymphangitis, or infection of the lesions themselves may all develop with the long-standing presence of lesions and/or poor hygiene. The vesicular crops usually resolve spontaneously after 3-4 weeks, leaving behind collarettes of scale. Although self-limited, outbreaks will frequently alternate with disease-free intervals of weeks to months and, if severe, may be extremely disabling.[5]

The differential diagnosis includes immunobullous disorders, such as bullous pemphigoid and pemphigus vulgaris, or other dermatoses, such as contact dermatitis, herpes simplex virus infection, bullous tinea pedis, and pustular psoriasis. The diagnosis is usually made on the basis of the clinical history, the physical examination, and the exclusion of alternative diagnoses. Bacterial culture and sensitivities may be evaluated for secondary infections. Additionally, potassium hydroxide wet mount preparations may be useful for excluding dermatophyte infections. A skin biopsy may also be useful for confirming the clinical impression in unresponsive cases and for excluding alternative diagnoses. It can be difficult to differentiate dyshidrotic eczema from an id reaction (autoeczematization), which is a cutaneous eruption that develops in response to a variety of infectious and inflammatory stimuli at a distant site from the primary dermatosis.[5]

Treatment for dyshidrotic eczema begins with topical corticosteroid therapy; topical class I steroids are the first-line treatment regimen, with oral steroids reserved for more severe cases. Large lesions should be drained, but not unroofed, in order to prevent rupture and subsequent infection. Wet compresses will help shrink bullae, and the physician could consider a course of oral antibiotics if infection is suspected. In many patients, antihistamines or other antipruritic agents may be extremely helpful for symptomatic relief. The patient should make appropriate modifications to daily activities and should avoid scratching in order to limit unwarranted skin irritation, exacerbation, and subsequent infection. In addition, there are a number of other adjuvant therapies, such as ultraviolet light, botulinum toxin, irradiation, occlusive dressings, and immunosuppressive agents, which may be helpful on a case-by-base basis for refractory patients. Unfortunately, there is no established preventive therapy except for avoidance in patients with well-established triggers. Untreated dyshidrotic eczema can lead to concomitant infections; therefore, prompt detection and treatment is essential.

One of the bullae, measuring approximately 3 cm by 1.5 cm, was percutaneously drained with a 10 cc syringe. Approximately 3 mL of a yellow, cloudy fluid was aspirated. The roof of the vesicle was left intact. In order to confirm the diagnosis and exclude alternative diagnoses, a punch biopsy of the skin was performed from the foot (see Figures 1-3). Histologically, spongiotic dermatitis and an intraepidermal vesicle were present, which were consistent with the diagnosis of dyshidrotic eczema. A periodic acid-Schiff (PAS) stain performed on this specimen did not reveal any fungal elements; scrapings of skin from the feet were negative for fungal infection as well. The patient was instructed to begin a regimen of topical steroids and moisturizing emollient, as well as wet compresses. An over-the-counter moisturizer was recommended, and prescriptions for Burrow’s solution (10% aluminum acetate) and clobetasol propionate were written. Additionally, prophylactic antibiotics were prescribed to prevent superinfection by typical organisms. The patient was instructed to limit his ambulation to avoid further blister rupturing. At a follow-up visit, the patient underwent patch testing, but a causative contact allergen was not identified.

Although dyshidrotic eczema is frequently idiopathic, which one of the following has not been described as being associated with an outbreak of dyshidrotic eczema?
Answer: Person-to-person contact
The exact etiology of dyshidrotic eczema is not completely understood; however, studies have elucidated associations with contact allergens (notably nickel), IVIg therapy, emotional stress, and concomitant tinea pedis infection. Unfortunately, in many cases, the causative agent is not discovered. There is no evidence to support person-to-person transmission.
What is the most common anatomic location for the presentation of dyshidrotic eczema?
Answer: Hands
Approximately 80% of cases of dyshidrotic eczema are localized to the hands only; 10% of cases are limited to the feet only; and 10% include both the hands and the feet, as in the patient in this case. Vesicles are rarely found elsewhere on the body.

WPW syndrome can be identified by a classic fusion QRS complex ECG pattern that is a combination of simultaneous normal conduction through the AV node and aberrant conduction through the accessory tract. This fusion QRS complex leads to particular ECG features that include a shortened PR interval (<120 msec) and a widened QRS complex with a delta wave representing preexcitation of the ventricle through the accessory pathway. The distinctive ECG pattern of the accessory pathway was initially described by Wolff, Parkinson, and White in 1930 as a bundle branch block with a short PR interval. Additionally, as mentioned, WPW syndrome is recognized as the most common form of ventricular preexcitation, although it likely represents a collection of pathologic conditions rather than a single structural abnormality.

Normal cardiac conduction of action potentials from the atria to the ventricles occurs exclusively through the AV node; the atrial impulses are subsequently propagated through a specialized conduction system (the AV-His-Purkinje system) and finally terminate in the ventricular myocardium. Action potential conduction through the AV node depends on slow inward calcium currents. In addition, the AV nodal system exhibits decremental conduction, which provides a protective effect; as the cardiac cycle is shortened (eg, the heart rate increases), there is decreased conduction through the AV node. This phenomenon limits the ventricular response to rapid atrial rates, such as those observed in atrial fibrillation or atrial flutter.

In preexcitation syndromes such as WPW, however, the action potential conducts to the ventricles at least partially through an accessory pathway termed the AV bypass tract or the bundle of Kent. Action potential propagation in the accessory pathway in WPW syndrome occurs through a rapid cellular influx of sodium. The consequence of the sodium-dependent action potential propagation mechanism is an accelerated conduction of impulses by the accessory bypass tracts, which leads to early activation of the ventricle as demonstrated by a shortened PR interval and a “slurred” QRS complex (ie, delta wave). Ventricular depolarization slowly spreads out from the bypass tract, while normal conduction that has been somewhat delayed through the AV node begins to conduct through the His-Purkinje system and spreads quickly to the remaining ventricular musculature. Although conduction velocity through the accessory pathway is faster than it is through the AV node, the accessory pathway often has a longer refractory period and, as such, is slower to recover excitability. Interestingly, the conduction of action potentials through the accessory pathway is nondecremental; therefore, the protective effect achieved by the AV node at higher heart rates is lost. These differences have important clinical implications. For example, a premature beat may conduct through the AV node normally while the accessory pathway remains refractory to conduction. The impulse then travels in a retrograde direction through the accessory pathway after ventricular depolarization, when it has recovered excitability. The consequence of this is the propagation of a reentry loop termed an orthodromic AV reciprocating tachycardia. This can then lead to rapid ventricular response rates that can degenerate into ventricular tachyarrhythmias. Rarely, antidromic tachycardias occur; conduction occurs in an anterograde direction through the accessory pathway and in a retrograde direction through the AV node.

Ventricular depolarization occurs through both the AV node-His bundle pathway and the accessory pathway; each pathway affects the ventricles by various degrees, depending on their relative activation times. As AV nodal conduction is delayed by either rapid atrial pacing or premature atrial beats, the accessory pathway contributes to a greater degree, resulting in a wider QRS morphology with an increasingly slurred delta wave. If the relative conduction time through the AV node is sufficiently delayed, total activation of the ventricle may occur through the accessory pathway.

The presence of accessory bypass tracts is not uncommon in the general population; however, less than half of the people with bypass tracts actually sustain a tachyarrhythmia. WPW syndrome affects approximately 0.15-0.2% of the general population, and of these individuals, 60-70% have no other evidence of heart disease. Mortality and morbidity associated with WPW syndrome occur as a result of associated dysrhythmias or from mistreatment of these dysrhythmias with inappropriate medications. Most studies report that the incidence of sudden death is in the 0-4% range. Men are affected more often than women,[5] accounting for 60-70% of all cases. Although this disease affects people of all ages, it is typically first recognized in children and young adults who present to the ED or their primary care physician with symptoms secondary to a dysrhythmia. Genetic mutations have been identified (by mapping genetic defects to specific loci) that account for the increased incidence of WPW syndrome in certain families.[2]

In patients with suspected WPW syndrome, evaluation should initially be directed at confirming the diagnosis and recognizing any potentially life-threatening arrhythmias. In patients with life-threatening arrhythmias, direct-current cardioversion should be immediately administered. In stable patients with tachyarrhythmias, an antiarrhythmic medication may be administered to terminate the arrhythmic episode, rather than immediately performing electrical cardioversion.

Studies have demonstrated that the best and most cost-effective treatment for patients with asymptomatic WPW syndrome is simple observation.[5] Most patients with symptomatic arrhythmias, drug-refractory WPW syndrome, or significant life-threatening arrhythmias are treated with nonpharmacologic therapy. Surgical ablation, previously the standard technique for drug-refractory WPW syndrome, has been replaced by catheter-based procedures. Compared with surgical techniques, catheter ablation has comparable success rates, lower mortality and complication rates, and improved cost-effectiveness. Moreover, newer catheter mapping systems now allow shorter procedure times. Surgical ablation, however, may be necessary in patients in whom catheter ablation has failed. Because this patient had a symptomatic tachyarrhythmia, he underwent electrophysiologic mapping followed by transvenous catheter ablation. He has remained asymptomatic since this procedure.

Patients with infrequent or minimally symptomatic arrhythmias may be treated pharmacologically. The aim of pharmacologic therapy is to alter the electrophysiologic properties, such as the refractoriness or conduction velocity of the AV node or the accessory bypass tracts.