A 45-year-old man with a history of idiopathic pulmonary fibrosis is admitted to the ICU intubated and sedated after single lung transplantation. On postoperative day 1, the patient’s oxygen requirement increases. He remains afebrile, and his arterial blood gas shows PaO2 90 mm Hg on FiO2 50%. The respiratory therapist reports increased secretions from his endotracheal tube. The patient is on ceftazidime, vancomycin, voriconazole, inhaled amphotericin B, and valganciclovir.
Which of the following is the BEST next step in management?
Correct Answer: C
Acute graft rejection after lung transplantation is one of the major causes of early graft loss. There are two mechanisms in which acute rejection could present: acute cellular rejection (ACR) and antibodymediated rejection (AMR). ACR is the leading cause of acute graft rejection in lung transplant patients. AMR is uncommon due to the extensive crossmatching between the donor and recipient for patients undergoing lung transplantation.
ACR could present with a wide range of symptoms, from asymptomatic, cough, shortness of breath to acute respiratory failure. Pulse steroids are the treatment of choice of ACR (answer C). AMR, on the other hand, can be resistant to steroids, and plasmapheresis might be an effective option.
Primary graft dysfunction (PGD) is another major cause of early morbidity and mortality after lung transplantation. It can present as mild to severe lung injury, and chest x-ray can reveal diffuse allograft infiltrations. Donor risk factors such as smoking history, alcohol use, African American race, female gender, and age are associated with increased risk of PGD. Prevention and treatment of PGD are unclear due to lack of appropriately powered clinical studies. However, lung protective ventilation therapy is recommended. ECMO could be used as salvage therapy for patients that remains hypoxemic despite maximum ventilation support.
Lung transplant patient should remain intubated (answer A) if there is a suspicion of acute rejection, as this process is progressive and may lead to severe respiratory failure. Since this patient is afebrile and on appropriate antimicrobial prophylaxis, the addition of a carbapenem (answer B) would not add any benefit. Increasing FiO2 does not add any clinical benefits to this patient, and may be harmful.
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A 52-year-old man with severe COPD underwent bilateral lung transplant 10 days ago. His postoperative course was unremarkable. He was extubated and transferred to the floor on postoperative day 5. Today, he starts to complain of shortness of breath. The physical examination is significant for chest wall subcutaneous emphysema. Images from a chest CT scan below:
What is the BEST next step in management?
Correct Answer: B
Bronchial dehiscence is a feared complication after lung transplantation. Its incidence ranges between 1% and 10% of all lung transplantation. Bronchial arterial circulation is usually not reconstructed during transplant which could lead to bronchial ischemia and dehiscence. Bronchial artery circulation typically reestablished within 4 weeks by collateral formation. Bronchial dehiscence is classified as a partial or complete, and it usually occurs within the first 5 weeks postoperatively. Patients typically present with dyspnea, pneumomediastinum, pneumothorax, persistent chest tube air leak, or subcutaneous emphysema.
Chest CT is highly sensitive and specific for diagnosing bronchial dehiscence. Radiological signs such as bronchial wall defects, bronchial wall irregularities, or extraluminal air around anastomosis area are suggestive for bronchial dehiscence. Although CT scan is an excellent diagnostic modality, flexible bronchoscopy remains essential for making the final diagnosis. CT scan is not reliable for detecting mucosal necrosis as bronchoscopy. Moreover, bronchoscopy is superior to CT scan in assessing the severity of dehiscence. Depending on the severity of bronchial dehiscence, management could include conservative treatment, bronchoscopic or open repair. Conservative treatment includes antibiotics and close monitoring. Bronchoscopic interventions include the use of stents, cyanoacrylate glue, growth factors, and autologous platelet-derived wound-healing factor. Open repair includes reanastomosis, flap bronchoplasty, pneumonectomy, or retransplantation.
Acute rejection (answer A) is in the differential diagnosis for any posttransplant lung transplant patients with shortness of breath; however, CT scan results and physical examination in this patient suggest airway complication rather than rejection. Confirmation of diagnosis and severity assessment should be done by flexible bronchoscopy to guide management (answer B). Serial chest x-ray has no role in confirming or evaluation of the severity of bronchial dehiscence (answer D).
A previously healthy 28-year-old man presents to the emergency department with severe respiratory distress, flu-like symptoms, and cough. The emergency physician intubates the patient for hypoxic respiratory failure. His postintubation chest x-ray shows diffuse, bilateral pulmonary infiltrations, and appropriate endotracheal tube position. The initial mechanical ventilation settings are FiO2 50%, PEEP 18 cm H2O, and tidal volume (TV) 6 mL/kg ideal body weight (IBW). The patient is transferred to the ICU, and 6 hours later you are informed that the patient is hypoxic on FiO2 100%, PEEP 24 cm H2O, and tidal volume (TV) 8 mL/kg ideal body weight (IBW). His plateau pressure is 42 cm H2O, and his ABG shows PaO2 of 54. You decided to place the patient on venovenous extracorporeal membrane oxygenation (V-V ECMO).
Which of the following mechanical ventilation settings are BEST after VV ECMO initiation?
Correct Answer: A
Venovenous ECMO can be used as salvage therapy in severe acute respiratory distress syndrome (ARDS). The ECMO circuit membrane lung (often called the oxygenator) can provide full gas exchange without relying on the patient lungs. It improves oxygenation by providing prepulmonary oxygen-rich blood and ventilation by removing CO2 with the sweep gas in the membrane lung. When a patient is on full V-V ECMO support, mechanical ventilation strategy should focus on preventing ventilatorinduced lung injuries. High PEEP during the early course of V-V ECMO (10- 14 cm H2O) is associated with decreased mortality in ARDS patients. The Extracorporeal Life Support Organization (ESLO) recommends placing the patient on pressure controlled ventilation at 25/15, I:E 2:1, rate 5, and FiO2 50% for the first 24 hours (answer A). After 24 to 48 hours, ELSO recommends reducing the pressure to 20/10, but keeping I:E ratio at 2:1, FiO2 20% to 40%, rate at 5 and allow for spontaneous breathing.
References
A 5′7″ middle-aged man, with unknown medical history, has just arrived in the operating room for emergent exploratory laparotomy following intubation in the emergency department with appropriate hypnotic and 100 mg rocuronium. The initial ventilator settings are tidal volume 450 mL, rate 16 breaths/min, PEEP 5 cm H2O and FiO2 40%, and inspiratory:expiratory (I:E) ratio 1:2. The EtCO2 waveform follows.
Based on the EtCO2 waveform, what would be the BEST next course of action?
Correct Answer: D
A biphasic EtCO2 waveform suggests that the patient had undergone single lung transplantation, most likely from severe emphysema. The first peak shows CO2 emptying of an allograft with normal compliance and airway resistance. The second peak reflects the obstruction of the native emphysematous lung. Since the emphysematous lung is more compliant than the donor lung, most of the tidal volume will preferably go to the native lung. As a result, the native lung, which has a severe expiratory obstruction, is prone to hyperinflation and auto-PEEP. Therefore, expiratory time should be allowed as long as possible to allow time to completely empty the native lung (answer D).
Answer A is incorrect because the waveform does not show recovery from muscle relaxation. When the patient recovers from muscle relaxation, a curare cleft will appear in the EtCO2 tracing as shown below:
Answer B is incorrect because the patient predicted body weight given his height and gender is around 66 kg. A tidal volume of 600 mL then would be 9 mL/kg IBW. Since we want to use lung protective ventilation, especially in a patient with a history of lung transplant, this tidal volume would be too high.
A 59-year-old male with history of COPD is admitted to the ICU for pneumonia and hypoxic respiratory failure. Four hours after admission, the patient continues to be in severe respiratory distress with O2 saturation of 85% on BiPAP (10 cm H2O IPAP, 5 cm H2O EPAP, and FiO2 100%). You decided to intubate the patient, and immediately after rapidsequence intubation, the patient oxygen saturation decreases to 78% with blood pressure 110/65 mm Hg and heart rate 95 bpm. Ventilator settings were tidal volume 6 mL/kg, respiratory rate 14 breaths/min, FiO2 100%, and PEEP 5 cm H2O. The ventilator is alarming for peak air pressure of 45 cm H2O with plateau pressure of 40 cm H2O. You next perform a point-of-care ultrasound of the lungs, and it shows an absence of pleural sliding on the left lung with positive A-lines and positive pulse sign on the left lung.
Which of the following is the MOST appropriate next step in management?
Lung sliding sign is a created by the movement of visceral pleura on parietal pleura. The presence of lung sliding suggests that visceral and parietal pleurae are opposing, which excludes pneumothorax. The absence of lung sliding alone, however, does not diagnose pneumothorax. It has to be accompanied by the presence of lung point and absence of B-lines and lung pulse.
B-lines originate from visceral pleura, and their presence indicates that parietal and visceral pleurae are in contact and excludes pneumothorax. Lung pulse was described by Lichtenstein et al. as a sign of mainstem intubation. A completely atelectatic lung transmits the rhythmic movement of the heart to the pleura. An opposed parietal and visceral pleurae are required to transfer the heart pulses; hence, the presence of lung pulse excludes pneumothorax.
Neuromuscular blockade can help patient-ventilator synchrony. However, this is not the reason for this patient’s acute hypoxemia.
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