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Anaesthesiology Intensive Therapy
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vol. 54
Letter to the Editor

Extracorporeal life support as rescue therapy in severe bronchiectasis with Kartagener’s syndrome

Riddhi Kundu
Ajeet Singh
Priyankar Kumar Datta
Ashish Shrivastava
Shrikanth Srinivasan
1, 2

Department of Critical Care Medicine, Manipal Hospitals, New Delhi, India
Manipal Hospitals, New Delhi, India
Anaesthesiol Intensive Ther 2022; 54, 4: 334–338
Online publish date: 2022/11/17
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Dear Editor,
Recent years have seen increasing interest in the use of extracorporeal life support (ECLS) in the context of acute hypercapnic respiratory failure due to near-fatal asthma and chronic obstructive pulmonary disease [1, 2]. We describe a case of ECLS use as a rescue measure in a patient with infective exacerbation of chronic bronchiectasis (Kartagener’s syndrome). A 43-year-old man was admitted with complaints of fever associated with chills and rigor for 10 days, cough with purulent expectoration for one week, with worsening shortness of breath for 2 days preceding admission. His medical history was significant for bronchiectasis, sinusitis, and complete situs inversus as part of Kartagener’s syndrome. He had recovered from COVID-19-related pneumonia one year before the current admission.
He was conscious and oriented at the time of admission but severely tachypneic, using accessory muscles of respiration, and he had a silent chest on auscultation. Hypercarbia and hypoxia were worsening despite continuous nebulization with bronchodilators, O2 support, steroids, and other supportive therapy. After a brief trial of non-invasive ventilation (NIV), the patient was intubated on arrival to the intensive care unit due to further CO2 cumulation, progressive drow­siness, and impending respiratory arrest. Severe bronchospasm, refractory to nebulization, steroids, magnesium, and aminophylline infusion persisted. Copious amounts of purulent secretions were present, requiring frequent suctioning. Chest radiograph showed patchy non-homogeneous opacities (Figure 1). Post intubation his airway pressures remained extremely high (ACMV mode, TV 400 mL, PEEP 5, RR 18 min–1, FiO2 0.6, Ppeak around 60–70 cm H2O, compliance 24– 28 mL cm–1 H2O–1, resistance 22– 24 cm H2O L–1 s–1). He started developing haemodynamic instability requiring dual vasopressor support (norepinephrine 0.35 μg kg–1 min–1 and vasopressin 2.4 IU h–1) despite optimizing ventilatory settings for severe expiratory flow limitation. He was started on an intravenous keta­mine infusion, to no avail, after which he was given inhaled sevoflurane therapy because of persistent refractory spasms. Despite all the supportive therapy for relieving spasm, reducing secretions, and causing bronchodilation, the patient’s condition continued to deteriorate, and his haemodynamic condition remained unstable (probably secondary to the severe air trapping). His blood gases showed severe respiratory...

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