Scapholunate (SL) dissociation is part of a spectrum of traumatic carpal bone instabilities and is defined as disruption of the ligamentous complex holding the scaphoid and lunate together.1 The SL ligament complex consists of the volar, dorsal, and intermediate components, with the dorsal component being the strongest and primary stabilizer of the SL joint.2 SL dissociation often results from rupture of the SL interosseous ligament following forceful wrist extension, allowing for widening of the SL joint.3 These injuries typically occur in the setting of a hyperextended wrist that is in ulnar deviation after a fall on an outstretched hand, but they have also been noted to occur in the setting of spastic paresis, rheumatoid arthritis, and congenital ligament laxity.1,4 Approximately 5% of all wrist sprains have an associated SL tear, and SL ligament injuries are often associated with distal radius fracture (40% of the cases on average), particularly fractures of the radial styloid.2 The latter stage of SL ligament instability, with complete diastasis of the SL ligament complex, includes dorsal intercalated segmental instability and perilunate dislocation, which requires emergent reduction. Physical examination of patients with SL dissociation reveals wrist swelling, point tenderness at the dorsal SL interval, and pain with wrist extension and radial deviation.4 In acute injuries the wrist is often positioned in extension, and there is ulnar deviation and carpal supination. A palpable “clunk” can be felt during the Watson shift test (when volar counter pressure over the scaphoid tubercle is removed with movement of the wrist from ulnar to radial deviation).4,5 Imaging on standard posteroanterior radiographs may reveal an increased SL interosseus gap of 5 mm or greater (Figure 1). The normal gap is 2 mm or less.6,7 The SL gap can be accentuated by ulnar deviation of the wrist by 20 degrees on the posteroanterior view (Figure 2) or by a clenched-fist anteroposterior position view (SL gap < 3 mm), and has been dubbed the “Terry Thomas sign,” in reference to the gap between the front teeth of the British comedian.5,8 The signet ring sign (results from the scaphoid’s rotary motion and repositioning of its distal pole in a palmar position) may also be seen on the posteroanterior radiograph (Figure 1) in cases of SL dissociation, but may also be present normally and should be evaluated in light of clinical findings.9 Magnetic resonance imaging can be useful for definitive diagnosis of a ligamentous tear (Figure 3), with magnetic resonance arthrography demonstrating a higher sensitivity for diagnosis of complete and incomplete SL tears, although neither magnetic resonance imaging nor magnetic resonance arthrography need to be obtained during the initial Emergency Department visit.10 Treatment in the Emergency Department for SL dissociations includes splinting of the affected wrist in a thumb spica splint, analgesia, and urgent referral to a hand specialist.1 SL dissociation may require urgent surgical intervention (within 6 weeks) to decrease the risk of severe and debilitating wrist dysfunction.11 Prompt recognition of traumatic carpal instabilities is crucial, as delayed diagnosis and treatment are associated with chronic pain, joint instability, inflammatory arthritis, and long-term degenerative changes including SL advanced collapse, or SLAC wrist.1,2,4 v

INTRODUCTION Brugada syndrome (BrS) is an inherited sodium, calcium, or potassium channelopathy associated with an increased risk of ventricular fibrillation (VF) and sudden cardiac death.1-3 This syndrome is most prevalent in men and individuals of southeast Asian descent, with a mean age of onset of symptoms at 41 ± 15 years.2 The diagnosis is challenging because of the often asymptomatic presentation of affected individuals and the dynamic electrocardiogram (ECG) manifestations that are frequently concealed.2 This case highlights the presentation, ECG findings, and management of a patient with BrS.

In the Emergency Department, the diagnosis of acute myocardial infarction (AMI) relies initially on a patient’s history and the 12-lead electrocardiogram (ECG). Establishing the diagnosis of AMI in the setting of a ventricular-paced rhythm (VPR) is difficult and can result in delay of definitive treatment. In 1996, Sgarbossa et al1 published a retrospective study comparing 17 ventricular-paced ECG controls with 17 ventricular-paced ECGs with AMI, confirmed by cardiac biomarkers. The authors found 3 ECG criteria to evaluate for AMI in patients with VPR: 1) ST-segment elevation (STE) greater than or equal to 1 mm for leads with a positive (concordant) QRS complex; 2) ST-segment depression (STD) greater than or equal to 1 mm in leads V1, V2, or V3; and 3) STE greater than or equal to 5 mm in leads with negative (discordant) QRS complexes. These criteria were identical to the criteria Sgarbossa developed to identify AMI in patients with left bundle branch block (LBBB), except the point scoring system was not used when the criteria were applied to patients with VPRs (Figure 1). Only 1 criterion had both relatively high specificity and statistical significance for the diagnosis of AMI at admission in patients with VPRs: STE greater than or equal to 5 mm in leads with a negative QRS complex. We report a case of an 81-year-old woman with a VPR who presented with chest pain, STE greater than or equal to 5 mm in leads with discordant QRS complexes, STE greater than or equal to 1 mm in a lead with concordant QRS complex, and was diagnosed with an AMI on cardiac catheterization. This case demonstrates the utility of Sgarbossa criteria for detecting AMI in patients with a VPR. Open in a separate window Figure 1 Sgarbossa criteria for acute myocardial infarction in the left bundle branch block. Arrows depict elevation or depression of the ST segment. Reprinted with permission from Cai Q, Mehta N, Sgarossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J 2013 Sep;166(3):409–13.

Ibutilide is recommended by professional society guidelines for the cardioversion of atrial fibrillation and flutter.1,2 Its rapid effect and minimal impact on hemodynamics make it well suited for use in the Emergency Department (ED).3 Ibutilide, however, prolongs the corrected QT (QTc) interval and increases risk for ventricular tachycardia (VT).4–6 The risk of VT can be greatly mitigated by careful selection of low-risk patients, the optimal dose of prophylactic magnesium sulfate, and at least 4 hours of postibutilide electrocardiographic monitoring.3 This case illustrates the dangers of overlooking ibutilide contraindications and provides practical lessons in ibutilide use and management of ibutilide-induced VT.

Dextrocardia with situs inversus (also referred to as situs inversus totalis) is a rare congenital anomaly whereby the position of the abdominal and thoracic viscera are reversed.1 The occurrence of this congenital anomaly has been reported to range between 1/6000 to 1/35000 live births and affects males and females equally.2 The affected population with dextrocardia with situs inversus usually does not need any specific treatment except when they are symptomatic or whenever any treatable congenital heart anomaly is present. However, the recognition of this congenital condition is essential when any interventional procedure or emergency surgery is going to be performed in order to avoid any mishaps.3 In our case, a 43-year-old woman presented to the Emergency Department (ED) with chest pain and was found to have dextrocardia with situs inversus by physical examination, electrocardiogram (ECG), and chest radiography.

Accelerated idioventricular rhythm (AIVR) is a ventricular rhythm consisting of three or more consecutive monomorphic beats, with gradual onset and gradual termination.1,2 AIVR is usually seen during acute myocardial infarction reperfusion (following thrombolytic therapy or percutaneous coronary intervention), and rarely manifests in patients with completely normal hearts or with structural heart disease.2 As percutaneous coronary intervention has become a more common treatment for patients presenting with acute myocardial infarction (versus thrombolytic therapy), the observation of AIVR by Emergency Department physicians has become less common than it was during the thrombolytic era.2 AIVR has also been associated with several drugs (eg, halothane, aconitine, desflurane, cocaine, and digitalis), electrolyte imbalances (eg, hypoand hyperkalemia), cardiomyopathies, and during the postresuscitation period following cardiac arrest.2-5 Electrocardiogram characteristics of AIVR include a regular rhythm, 3 or more ventricular complexes with QRS complex > 120 milliseconds, a ventricular rate between 50 beats/min and 110 beats/min, and occasional fusion or capture beats. This rhythm has two postulated, possibly coexisting causes.6 First, the sinoatrial or atrioventricular node may suffer structural damage with depression of nodal automaticity potentiated by enhanced vagal tone. Second, an abnormal ectopic focus within the ventricle may assume the role of dominant pacemaker.6 The ventricular ectopic focus manifests when the sinus rate slows down (below the ectopic focus) or when the ectopic focus accelerates above the intrinsic rate by 30 beats/min to 40 beats/min.2 When both discharge rates (sinus and ectopic focus) are similar, isorhythmic dissociation, fusion beats, and capture beats can be seen. AIVR is usually a benign and well-tolerated arrhythmia.2 Most cases of AIVR will require no immediate treatment for this dysrhythmia, because AIVR is usually self-limiting and resolves when the sinus rate exceeds that of the ventricular

The 12-lead electrocardiogram (ECG) in patients with acute intracranial hemorrhage (ICH) can demonstrate several findings associated with ICH and increased intracranial pressure, including deep, inverted “cerebral” T waves, prolonged QT interval, Osborn (J) waves, and U waves.1-3 In addition to the ECG changes described above, cardiac dysrhythmias have been reported in patients with ICH (particularly with subarachnoid hemorrhage), including: sinus bradycardia; sinus tachycardia; atrial pacemaker and atrial fibrillation; premature atrial, junctional, and ventricular complexes; ventricular tachycardia; and atrioventricular blocks.4 ST-T wave changes associated with myocardial ischemia (ST-depression) and infarction (ST-elevation) can also be found on the ECG in association with ICH. The mechanism(s) responsible for ECG changes associated with ICH are not well understood, although hypothalamic stimulation and autonomic dysregulation have been implicated as causative for these ECG findings.4 The differential diagnosis of inverted T waves on the 12-lead ECG includes myocardial ischemia and infarction, bundle branch block, ventricular hypertrophy, pulmonary embolism, hypertrophic cardiomyopathy, and increased intracranial pressure.5 It is important to note that the findings of deep, inverted T waves on the 12-lead ECG are not diagnostic of ICH but can occur in the appropriate clinical setting, and that further diagnostic imaging (ie, noncontrast computed tomography scan of the brain) is required for the diagnosis of ICH. v Disclosure Statement The author(s) have no conflicts of interest to disclose.

Acute posterior wall myocardial infarction (PMI) occurs in up to 20% of cases of acute myocardial infarction (MI), with the vast majority occurring along with inferior or lateral acute MI. 1 A true PMI is considered more rare, with an incidence of approximately 3.3%. 2 The term PMI is used for necro sis of the part of the left ventricle located beneath the atrioventricular sulcus. 3 The majority of patients with the typical electrocardiogram (ECG) abnormalities of PMI have a stenosis or occlusion

After QT prolongation, hyperacute T waves are the earliest-described electrocardiographic sign of acute ischemia, preceding ST-segment elevation. The principle entity to exclude is hyperkalemia-this T-wave morphology may be confused with the hyperacute T wave of early transmural myocardial infarction.

Leukocytoclastic vasculitis (LCV), also termed hypersensitivity vasculitis, is a small-vessel vasculitis. The skin is the organ most commonly involved in LCV. Typical presentation is a painful, burning rash predominantly in the lower extremities. The most common skin manifestation is palpable purpura. Other skin manifestations include maculopapular rash, bullae, papules, plaques, nodules, ulcers, and livedo reticularis.

ST-elevation myocardial infarction (STEMI) is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic ST elevation (STE) and subsequent release of biomarkers of myocardial necrosis. 1 STE is the single best immediately available surrogate marker for detecting acute complete coronary artery occlusion without collateral circulation, signifying a significant region of injured myocardium at imminent risk of irreversible infarction, requiring immediate reperfusion therapy. 2 Diagnostic STE is defined as new STE at the J point in at least 2 contiguous leads > 2 mm (0.2 mV) in men or > 1.5 mm (0.15 mV) in women in leads V2-V3 and/or of > 1 mm (0.1 mV) in other contiguous chest or limb leads. 3 The presence of reciprocal changes (manifested as ST depression in a region that approximates the vector 180 degrees opposite the major vessel of injury) increases the specificity of STE caused by STEMI. 4 New or presumably new left bundle branch block has been considered a STEMI equivalent. Reperfusion therapy should be administered to all eligible patients with STEMI who have experienced symptom onset within the previous 12 hours. 1 Primary percutaneous coronary intervention is the recommended method of reperfusion when it can be performed in a timely fashion by experienced operators, with a goal of first medical contact-toballoon time of 90 minutes or less. 5,6 v

Introduction: During major disasters, hospitals experience varied levels of absenteeism among healthcare workers (HCWs) in the immediate response period. Loss of critical hospital personnel, including Emergency Department (ED) staff, during this time can negatively impact a facility's ability to effectively treat large numbers of ill and injured patients. Prior studies have examined factors contributing to HCW ability and willingness to report for duty during a disaster. The purpose of this study was to determine if the degree of readiness of ED personnel, as measured by household preparedness, is associated with predicted likelihood of reporting for duty. Additionally, the authors sought to elucidate other factors associated with absenteeism among ED staff during a disaster.Methods: ED staff of five hospitals participated in this survey-based study, answering questions regarding demographic information, past disaster experience, household disaster preparedness (using a novel,15-point scale), and likelihood of reporting to work during various categories of disaster. The primary outcome was personal predicted likelihood of reporting for duty following a disaster.Results: A total of 399 subjects participated in the study. ED staffs were most likely to report for duty in the setting of an earthquake (95 percent) or other natural disaster, followed by an epidemic (90 percent) and were less likely to report for work during a biological, chemical, or a nuclear event (63 percent). Degree of household preparedness was determined to have no association with an ED HCW's predicted likelihood of reporting for duty. Factors associated with predicted absenteeism varied based on type of disaster and included having dependents in the home, female gender, past disaster relief experience, having a spouse or domestic partner, and not owning pets. Having dependents in the home was associated with predicted absenteeism for all disaster types (OR 0.30-0.66). However, when stratified by gender, the presence of dependents at home was only a significantly associated with predicted absenteeism among women as opposed to men (OR 0.07-0.59 versus OR 0.41-1.02).Discussion: Personal household preparedness, while an admirable goal, appears to have no effect on predicted absenteeism among ED staff following a disaster. Having responsibilities for dependents is the most consistent factor associated with predicted absenteeism among female staff. Hospital and ED disaster planners should consider focusing preparedness efforts less toward household preparedness for staff and instead concentrate on addressing dependent care needs in addition to professional preparedness.

Atrial flutter (AFl) is a cardiac dysrhythmia characterized by rapid and regular depolarization of the atria that appears as a sawtooth pattern on the electrocardiogram (ECG) and is categorized into type I (typical) and type II (atypical) AFl.1 The ECG in type I (typical) AFl is characterized by an inverted sawtooth flutter (F) wave pattern in the inferior leads II, III, and aVF, low amplitude biphasic F waves in leads I and aVL, an upright F wave in precordial lead V1, and an inverted F wave in lead V6.2 Type I AFl is most commonly caused by the presence of a macro-reentrant circuit in the right atrium that includes a small strip of tissue between the inferior vena cava and the tricuspid annulus known as the cavotricuspid isthmus.3 The ECG in atypical (type II) AFl is characterized by upright F waves in leads II, III, aVF, and V6 and by biphasic F waves in leads I, aVL, and V1. The underlying mechanism of type II AFl is unclear.1 Risk factors for AFl include presence of heart failure, chronic obstructive pulmonary disease, antiarrhythmic medications, thyrotoxicosis, pulmonary embolism, prior cardiac surgery or prior atrial ablation. Common symptoms of AFl include palpitations, light-headedness, fatigue, presyncope, mild shortness of breath, and possibly chest pain or hypotension. The initial treatment for AFl focuses on rate control of the ventricular response with AV nodal blocking agents such as beta-blockers and calcium channel blockers.4 If rhythm identification is unclear and the patient is stable, adenosine or Valsalva maneuver may be employed to slow conduction through the AV node such that the atrial flutter waves are more readily apparent.1 Hemodynamically unstable patients with AFl should receive synchronized electrical cardioversion.1

Acute pericarditis is an inflammation of the pericardium that can result in chest pain, pericardial friction rub, and serial electrocardiogram (ECG) changes. The most common causes of pericarditis are viral or idiopathic in developed countries, and tuberculosis in developing countries.1 Other causes of pericarditis include bacterial and fungal infections, myocardial infarction, chest trauma, neoplasm, renal failure, radiation therapy, autoimmune disorders, and certain medications (eg, phenytoin, rifampin).2 Patients must have 2 of the following 4 clinical criteria for diagnosis: typical pericardial chest pain, pericardial friction rub, widespread ST-segment elevation or PR depression, and new or worsening pericardial effusion on echocardiography.1,3 In patients with acute pericarditis, chest pain is generally abrupt in onset; pleuritic, and substernal or left precordial in location; may radiate to the neck, arms, or jaw; and is relieved by leaning forward and worsened by lying supine.2 The 4 ECG stages of pericarditis include: 1) diffuse ST elevation and/or PR depression, 2) normalization of ST- and PR-segments, 3) diffuse T-wave inversions with isoelectric ST-segments, and 4) normalization of the ECG.4,5 Plasma troponin concentrations are elevated in 35% to 50% of patients with pericarditis, a finding that is thought to be caused by epicardial inflammation rather than myocardial necrosis.5 Transthoracic echocardiography is often recommended in patients with suspected pericarditis, because the presence of an effusion helps to confirm the diagnosis, and clinical or echocardiographic evidence of tamponade indicates the need for pericardiocente-sis.5 Although the mainstay of treatment includes nonsteroidal anti-inflammatory drugs, colchicine is an efficacious adjunct to nonsteroidal anti-inflammatory drugs therapy, reducing recurrence rates by 50%.1,3,5 Admission is recommended in patients with fever > 38°C (100.4°F), subacute onset (several days or weeks), tamponade or pericardial effusion > 20 mm, or lack of response after one week of treatment, as patients with these findings are at increased risk of complications.1,5

Joel T Levis, MD, PhD, FACEP, FAAEM Perm J 2013 Spring; 17(2):84 http://dx.doi.org/10.7812/TPP/12-089 Apical hypertrophic cardiomyopathy (HCM) is an atypical phenotype of nonobstructive HCM with an indistinguishable histology.1 In Japan this apical varia

Phlegmasia cerulea dolens (PCD) is a rare form of massive venous thrombosis of the lower extremities associated with a high degree of morbidity including venous gangrene, compartment syndrome, and arterial compromise.1 Risk factors for PCD include malignancy, immobility, heart failure, heparin-induced thrombocytopenia, prothrombin states (eg, antiphospholipid syndrome), pregnancy, surgery and venous instrumentation (eg, placement of central venous catheters and inferior vena cava filters).2 Clinically, PCD is characterized by sudden pain, swelling, purple ecchymosis, and arterial ischemia with loss of distal pulses.3 Edema develops rapidly, and the skin of the affected extremity is usually tense, firm, and tender to palpation. Doppler ultrasound of the affected extremity should be used to confirm the diagnosis of PCD, and initial treatment includes bed rest, elevation of the affected limb, and systemic anticoagulation with heparin.2 Catheter-directed thrombolysis and venous thrombectomy should also be considered as early treatment options for PCD.4

Flecainide acetate is a Vaughn-Williams class IC antiarrhythmic and a sodium channel blocking agent used mainly for the treatment of supraventricular dysrhythmias.1 Adverse cardiac effects include moderate negative inotropic action and depression of all major conduction pathways.2 With increasing concentration, flecainide's action on conduction pathways is manifested on electrocardiogram as an increased PR interval and QRS duration. Toxicity is suggested when a 50% increase in QRS duration (0.18 sec) or 30% prolongation in PR interval (0.26 sec) occurs. The QTc interval can also be prolonged in cases of flecainide overdose.3 Treatment of acute flecainide overdose includes administration of activated charcoal (for patient presenting early in course of ingestion), administration of sodium bicarbonate (reverses action of sodium channel blockade), pressors (eg, dobutamine) for profound hypotension, and transthoracic or transvenous pacing.1,4 Figure 1 12-lead Electrocardiogram from a 46-year-old woman with flecainide toxicity. Figure 2 12-lead Electrocardiogram from same patient obtained 24 hours later.

Joel T Levis, MD, PhD, FACEP, FAAEM Fall 2011 - Volume 15 Number 4 The S1Q3T3 sign (prominent S wave in lead I, Q wave and inverted T wave in lead III) is a sign of acute cor pulmonale (acute pressure and volume overload of the right ventricle becau

Acute occlusive embolism to the coronary arteries resulting in acute myocardial infarction (AMI) is an uncommon occurrence. Although cases of patients with mechanical prosthetic heart valves resulting in this phenomenon have been reported in the setting of inadequate anticoagulation, reported cases resulting years after tissue aortic valve replacement (AVR) are rare. We report the case of a 50-year-old man who underwent a tissue AVR four years earlier and presented to the Emergency Department (ED) with an ST-segment elevation myocardial infarction. ED door-to-balloon time was delayed (at 115 minutes) because of pre-existing left bundle branch block on electrocardiogram. Emergent coronary angiography demonstrated complete occlusion of the left anterior descending coronary artery by a coronary embolus. The patient was successfully treated with percutaneous transluminal coronary angioplasty and aspiration thrombectomy, and subsequently underwent a transesophageal echocardiogram demonstrating thrombus on the tissue aortic valve prosthesis. This case demonstrates that coronary embolism resulting in AMI, while rare, can occur in patients years after tissue AVR surgery.