Week 36: Upper Airway, Lung US, and More EKGs

Tracheomalacia results from abnormally soft, undeveloped supporting cartilage of the tracheal rings. The stridor worsens with agitation, supine position, and infection. It is the most common cause of chronic stridor in infants. It is rarely associated with respiratory distress, feeding difficulties, or failure to thrive. Most patients experience complete resolution of symptoms by age 2.

Asphyxia from foreign body aspiration (A) most commonly occurs in children younger than 3 years. Clinical signs of complete obstruction include cough, severe distress, and cyanosis. Tracheal stenosis (B) is a congenital anomaly that results from complete tracheal rings. Infants have persistent stridor that worsens over age. Viral croup (D) is a common pediatric infection associated with a barky cough, hoarse voice, and high-pitched, inspiratory stridor.

This child is presumed to have epiglottitis, given his acutely high fever, dysphagia, drooling, and discomfort. While a conservative approach to airway management in children with epiglottitis exists, this child is leaning forward, will not lie back, and is not able to swallow his secretions. This suggests that he has impending airway compromise. A definitive airway should be sought while disrupting the patient as little as possible. There are several options for artificial airway establishment, which may involve consulting anesthesiology or otolaryngology for more controlled intubating conditions in the operating room.

Airway management takes precedence; antibiotics (B) can be administered afterward. Steroids (C) are controversial and are unlikely to change this patient’s need for a definitive airway. Further diagnostic tests such as lateral neck X-rays (D) may be considered after intubation. The patient should not be repositioned until his airway is secured.

This patient has an unstable ventricular tachycardia. Her ECG demonstrates a monomorphic wide-complex tachycardia. Regardless of the etiology (underlying bundle branch block, supraventricular tachycardia with aberrancy), the patient is unstable (hypotensive). Unstable patients demonstrate signs related to organ hypoperfusion including hypotension, altered sensorium, syncope, shortness of breath or chest pain consistent with myocardial ischemia. When the dysrhythmia is unstable, the patient requires synchronized cardioversion. The etiologies of ventricular tachycardia include ischemic and non-ischemic cardiomyopathy, coronary artery disease (acute MI or scar tissue from previous infarction), electrolyte abnormalities or medications.

For stable patients with ventricular tachycardia, medical therapy with amiodarone 150 mg IV (A) or procainamide 17 mg/kg IV at a rate of 30-50 mg/min (C) are both potential options. Both of these agents may medically cardiovert the patient into a stable rhythm. Amiodarone does not typically cause hemodynamic instability when administered. Procainamide may cause hypotension and widening of the QRS complex over the course of its infusion. If either of these occurs, the infusion should be held. Defibrillation (B) is indicated for the treatment of a wide complex tachycardia without a pulse.

Commotio cordis occurs when an object such as a baseball strikes the chest and produces sudden death. It most commonly occurs in children between 5 and 15 years of age with no known predisposing cardiac conditions. Of the few cases where a documented cardiac rhythm post-blunt trauma to the chest has been captured, the most common identified rhythm is ventricular fibrillation. The majority of patients do not survive.

Asystole (A) is the end result of commotio cordis if ventricular fibrillation is not addressed, but it is not the most common immediate dysrhythmia. Supraventricular tachycardia (B) and ventricular tachycardia (D) are less commonly associated with commotio cordis.

This patient has bacterial tracheitis. Patients who have bacterial tracheitis usually present with a history of a recent upper respiratory tract infection or croup that improves initially and then worsens. Definitive diagnosis of bacterial tracheitis requires direct visualization with bronchoscopy or laryngoscopy showing laryngotracheal erythema, edema, and thick purulent secretions. Antibiotic therapy should be directed at Staphylococcus aureus, Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, and beta-hemolytic Streptococcus. A third-generation cephalosporin agent combined with a penicillinase-resistant penicillin such as nafcillin is appropriate for first-line therapy. Vancomycin should be substituted if methicillin-resistant S. aureus is locally prevalent.

Croup, not bacterial tracheitis, is a clinical diagnosis (B). An anteroposterior neck radiograph (C) can show a steeple sign consistent with croup; a lateral radiograph can show the thumbprint sign consistent with epiglottitis. Given that this child’s clinical status is worsening after the treatment for croup (steroids and racemic epinephrine), this is unlikely a recurrence of croup. A lateral neck X-ray would be needed (not AP) and presents as subglottic narrowing that may be irregular as opposed to the symmetric tapering typical of croup. A neck CT scan with IV contrast (D) is helpful for deep neck infections such as retropharyngeal abscesses. A retropharyngeal abscess usually presents with a sore throat and decreased range of motion of neck rather than stridor, making it a less likely diagnosis.

Tracheitis

S. aureus
3-5 years old
URI prodrome → suddenly worsens with airway obstruction, toxic appearance
CXR: subglottic narrowing
Gold standard dx: bronchoscopy
ABX, intubation

Atropine 0.5 mg administered intravenously is indicated for symptomatic sinus bradycardia, defined as a heart rate < 60 beats/minute with intact P waves followed by a QRS complex at constant intervals. Symptoms are variable and may include lightheadedness, chest pain, dyspnea, syncope, nausea, or diaphoresis. Patients may also present with hypotension due to poor cardiac output. Atropine inhibits parasympathetic activity in cardiac myocytes and and thus increases cardiac output. It has a rapid onset of action and should be administered at a rate of 0.5 mg every 3 to 5 minutes up to a maximum dose of 3 mg. Care should be taken when giving atropine to certain patient populations, particularly those with known coronary artery disease, congestive heart failure, hypertension or acute myocardial ischemia. Side effects of atropine include tachydysrhythmias, blurred vision, photophobia, constipation and xerostomia.

Adenosine 6 mg (A) is indicated for narrow-complex supraventricular tachycardia that has failed vagal maneuvers. It may also be used as a diagnostic agent in stable, monomorphic wide-complex tachycardia. Amiodarone 300 mg (B) is indicated for cardiac arrest from ventricular fibrillation or ventricular tachycardia without a pulse. Transvenous pacing (D) is reserved for patients with symptomatic or unstable bradycardia who are unresponsive to atropine or have contraindications for its use. This patient may require a pacemaker, but there should be no delay in administering atropine.

This patient has atrial fibrillation with a rapid ventricular rate and is hemodynamically unstable (BP 80/50 mm Hg and pulse ox 88%). This dysrhythmia needs to be emergently corrected in order to stabilize the patient; failure to do so could result in sudden cardiac death. In such circumstances, emergent synchronized cardioversion is required.

If the patient is hemodynamically stable, the approach to management (rate vs. rhythm control) depends on the time of dysrhythmia onset. If the onset is unknown or greater than 48 hours, then cardioversion should be delayed until the patient can be adequately anticoagulated with enoxaparin (A) followed by warfarin. In the interim, rate control would be accomplished with either esmolol (D), a short acting ß-blocker, or diltiazem (C), a calcium channel blocker. For patients with stable paroxysmal atrial fibrillation and duration of onset < 48 hours, chemical cardioversion using procainamide (B) can be attempted. In unstable patients, regardless of the rhythm duration, synchronized electrical cardioversion is recommended. Alternatives to procainamide include amiodarone, ibutilide, and, to a lesser degree, flecainide.

When a patient’s body is rotated, the retropharyngeal soft tissue space may appear falsely enlarged because part of the soft tissue in the lateral neck is brought into view. This commonly occurs in young children and is well documented in the literature.

Other causes include exhalation and neck flexion, the opposites of (B) and (C). Shoulder lowering (D) has not been associated with radiographic changes in the retropharyngeal space.

Case link.

This is not pericarditis, nor is it STEMI. Get to know this pattern just like you would get to know a friend. I called him “Jack,” and told the residents to get to know Jack.

Jack often has high voltage QRS, has marked J-waves (they look almost like Osborn waves). There is a relatively short QT interval. The ST Elevation is towards leads II and V5. Thus, there is no reciprocal ST depression in aVL. [In fact, these could be Osborn waves, but they were not: the patient was not hypothermic.]

Although the T-wave is negative in aVL, it is NOT T-wave inversion, as the QRS-T angle is narrow (QRS axis is 85 degrees, almost directly inferior; T-wave axis is 68 degrees — angle is only 17 degrees. Both these measurements are accurately made by the computer algorithm.)

How do I know it is not pericarditis? First, the patient denied any chest pain! Second, normal variant STE is far more common that pericarditis. There are J-waves, no PR depression, and no Spodick’s sign (downsloping T-P segment — of questionable reliability).

It is very common for Normal Variant STE to be misdiagnosed as pericarditis. Does this have adverse consequences?? It may. Take a look at this case that was written by Pendell Meyers when he was a medical student: due to misdiagnosis of the ECG as “pericarditis”, a patient’s chest pain was misattributed to pericarditis and the correct diagnosis of pulmonary embolism was ignored:

B lines are created by increased density in the lungs, not necessarily by fluid collection. If the increased density in the lung is focal (meaning focal, not diffuse, B lines will be present), this could represent a pneumonia, atelectasis, or contusion. If the B lines are more diffuse, this is likely secondary to pulmonary edema, acute respiratory distress syndrome, or interstitial lung disease.