A 70-year-old female with a history of diabetes, coronary artery disease, and hypothyroidism was admitted to the intensive care unit (ICU) for pneumonia complicated by acute respiratory distress syndrome (ARDS). She was intubated on the day of admission. Her ICU course was complicated by shock, delirium, and recurrent aspiration. She was successfully extubated on ICU day 14. Following extubation, she was noted to have significant coughing that seemed worse with the consumption of liquids. A barium swallow demonstrated a spillage of contrast from the esophagus into the trachea.
Which of the following is a risk factor for this complication?
Correct Answer: D
This patient has developed an acquired tracheoesophageal fistula (TEF). TEF is a rare but serious complication of prolonged mechanical ventilation. The most common etiology for acquired TEFs is malignancy, with esophageal malignancy as the most frequent cancer leading to TEF. Following malignancy, the most common cause of TEFs is endotracheal intubation. Endotracheal tube–related TEFs can occur in up to 3% of ventilated patients. Risk factors include prolonged intubation, diabetes, overinflation of the endotracheal cuff, hypotension leading to necrosis of the tracheal wall, and recurrent airway infections. In ventilated patients, TEFs can present with weight loss, recurrent infections or inability to liberate from the ventilator. In nonventilated patients, coughing is a common sign with a classic sign of coughing after consuming liquids (Ono’s sign), particularly carbonated liquids. TEFs can be diagnosed via barium swallow, endoscopy, or bronchoscopy. Treatment is typically surgical; however, for nonoperable, malignant cases, stenting is an option. Extubation following correction of the TEF is key as positive pressure ventilation has been associated with poor anastomotic breakdown and stenosis.
Reference:
A 30-year-old female with a past medical history of moderate persistent asthma, substance abuse disorder, and allergic rhinitis was brought to the emergency department (ED) by paramedics after being found down in a subway station surrounded by empty medication bottles and was noted to have needle tracks on her arms. In the ED, she was intubated for airway protection with a 7.0 endotracheal tube. She was then admitted to the ICU where her toxicology panel was positive for cocaine, oxycodone, and methadone. Her mental status improved over the next 72 hours, and she was converted from volume control ventilation to pressure support. She was able to tolerate pressure support 5/5 with an FiO2 of 0.30, a respiratory rate of 18, and tidal volume of 600 mL. Given her clinical improvement, the team contemplated extubation. Prior to extubation, her endotracheal cuff is deflated. The discrepancy between her inspiratory and expiratory volumes is less than 110 mL, but no audible cuff leak is appreciated.
What is the next most appropriate step?
The decision to test for an endotracheal cuff leak is controversial. Endotracheal intubation can lead to laryngeal edema and has been associated with an incidence of postextubation stridor that is 6% to 37%. The American Thoracic Society Guidelines indicate that a “cuff-leak” test to evaluate for laryngeal edema should only be performed in high-risk patients. High-risk patients are defined as those with traumatic intubation, intubation >6 days, large endotracheal tube, those who have been repeatedly reintubated and extubated, and women. This patient’s largest risk factor is her gender. The guidelines then go on to recommend repeating a cuff-leak test if the initial testing demonstrated an absent leak. If no leak is present on the repeat testing, steroids are recommended. Lee et al. performed a randomized control trial of patients with less than 110 mL difference between inspiratory and expiratory volumes. Patients in the treatment arm received dexamethasone 5 mg q6h for 24 hours Cuffleak volumes were checked every 6 hours, and the change in volumes in the steroid group demonstrated significant improvement within the first 6 hours with little additional benefit after.
References:
A 60-year-old male with a history of type 2 diabetes and prior alcohol use presents to the emergency room with complaints of shortness of breath and mouth pain. His initial temperature is 102°F; he has a heart rate of 110, a blood pressure of 120/60, and a respiratory rate of 30. He states he recently had dental work performed. On examination, he appears uncomfortable with increased work of breathing. He is noted to have a swollen submandibular gland with surrounding erythema at the base of his face extending onto the proximal portion of his neck. His oropharyngeal examination is notable for poor dentition and one tooth with increased erythema along the gum line. There is a high-pitch wheeze with inspiration. The rest of his pulmonary examination is clear. His cardiac examination is notable for sinus tachycardia without murmurs. His labs were notable for an elevated white cell count of 16 000 and an elevated ESR and CRP.
What is the next best step in management?
Correct Answer: A
Ludwig angina is characterized by cellulitis and edema of the floor of the mouth and soft tissues of the neck. Mortality is close to 8%. Risk factors for developing Ludwig angina include recent dental treatment, dental infections, diabetes, alcoholism, and immunosuppression. This patient is demonstrating evidence of airway compromise with increased respiratory rate, submandibular swelling, and stridor. The leading cause of death in Ludwig angina is airway compromise; therefore, the primary concern is securing the airway. Given that this patient appears to already have upper airway swelling, there is a high risk of failing with endotracheal intubation. If nasotracheal intubation is not an option or fails, then cricothyrotomy and tracheostomy should be performed. Once the airway has been secured, the focus should then switch to treating the underlying infection with antibiotics. Streptococcus and Staphylococcus are the most common bacteria that have been associated with Ludwig angina. A CT neck and chest would not be a good option for this patient given his tenuous airway.
A 70-year-old male with a history of chronic obstructive pulmonary disease (COPD), requiring prior intubation, and active tobacco use presents to the emergency department with shortness of breath. He states that over the last 24 hours, he has had increasing difficulty breathing. He denies fevers or chills at home and is not aware of any sick contacts. His initial vitals are:
On examination, he appears to have a mild increase in work of breathing. He is noted to have scattered wheezing throughout both lung fields. He is started on albuterol nebulizers and IV steroids. Three hours into his emergency room stay you are called to the bedside as the patient appears to be in more distress. His vitals demonstrate:
On examination, the patient is using accessory muscles, and his lung examination is notable for poor air movement with no wheezing. An arterial blood gas is performed:
A chest x-ray is performed and demonstrates hyperinflation of both lung fields with no infiltrate. He is intubated for hypoxemic respiratory failure and is subsequently paralyzed with a neuromuscular blocker secondary to ventilator dyssynchrony. He arrives to the ICU ventilated, with an FiO2 of 0.8, PEEP 10, RR 30, and TV 420 mL/kg (the patient weighs 70 kg). His arterial blood gas demonstrates a pH 7.29/PCO2 50/PaO2 200. His blood pressure upon arrival to the ICU is 80/50 mm Hg.
His flow/time wave form is noted in the following figure:
What would be the next step in management?
Correct Answer: C
The figure above demonstrates air trapping or “auto-PEEP” as the exhalation wave form fails to reach zero before the next breath is taken. Auto-PEEP can cause decreased venous return which leads to a decrease in cardiac output and results in hypotension which was seen in this patient. To address air trapping, the key is to increase the expiratory time. Decreasing the respiratory rate is an affective way to achieve a longer exhalation period. Another way to enhance the expiratory time is to change the inspiration:expiratory ratio or the I:E time. This can be accomplished by increasing the inspiratory flow rate thus decreasing the inspiratory time. Increasing the patient’s tidal volume could enhance the minute ventilation; however, it would not address the dynamic hyperinflation. Finally increasing PEEP can have variable effects on the intrathoracic pressure depending on the degree of expiratory flow limitation but is unlikely to decrease the auto-PEEP.
A 65-year-old male with a history of COPD and active tobacco use with no prior intubations presented to the emergency department with increased work of breathing and increased wheezing. In the emergency department, he was given stacked nebulizers and IV steroids and initiated on BIPAP. His initial blood gas demonstrated:
Following intubation, he was placed on volume control ventilation. His initial peak pressure (peak inspiratory pressure [PIP]) was 45 cm H2O, and his plateau pressure (Pplat) was 35 cm H2O. He was placed on a respiratory rate of 30, PEEP 15, FiO2 0.40 and his SpO2 was 90%. Two hours after arrival to the ICU, his ventilator starts to alarm for high pressures. His peak pressures have increased to 65 cm H2O, and his plateau pressure has increased to 55 cm H2O. His heart rate increases from 80 beats per minutes to 110, and his blood pressure drops from 110/70 to 80/50 mm Hg. His SpO2 drops to 75%. His examination is notable for continual wheezing and slight deviation of the trachea toward the left.
What is the most likely cause for this acute change?
Correct Answer: B
The incidence of overt barotrauma in mechanical ventilation ranges from 4% to 15% COPD is commonly associated with pneumothoraxes, as these patients may have underlying bullous disease and can require high airway pressures to overcome bronchial obstruction. In this case, the patient had a baseline elevated plateau pressure which placed him at higher risk for developing overdistention leading to a pneumothorax. Given that both parameters changed, the underlying issue does not deal solely with resistance. If resistance had suddenly increased, for example, with worsening bronchoconstriction, the peak airway pressures would likely have increased without an increase in the plateau pressures. Along with the increases in both pressures, there was also evidence of hemodynamic changes concerning for a tension pneumothorax. As the lung collapses, intrathoracic pressure causes a shift in mediastinal structures toward the noncollapsed lung which can cause tracheal deviation on examination. Biting on the endotracheal tube could result in an increase in airway pressures, but it is unlikely to have severe hemodynamic effects. Abdominal distention can also cause an increase in peak and plateau pressures and, in the setting of abdominal compartment syndrome, could cause hypotension; however, this would be less likely to occur so acutely and less likely to be associated with tracheal deviation.
Click to expand