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Circulatory Collapse Due to Hyperinflation in a Patient with Tracheobronchomalacia: a Case Report and Brief Review

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Circulatory Collapse Due to Hyperinflation in a Patient with Tracheobronchomalacia: a Case Report and Brief Review Hindawi Case Reports in Critical Care Volume 2019, Article ID 2921819, 5 pages https://doi.org/10.1155/2019/2921819 Case Report Circulatory Collapse due to Hyperinflation in a Patient with Tracheobronchomalacia: A Case Report and Brief Review Niclas Lundström ,1 Gert Henriksson,2 Ola Börjesson,3 Malin Jonsson Fagerlund,1 and Johan Petersson1 Function Perioperative Medicine and Intensive Care (PMI), Karolinska University Hospital, Sweden Department of ENT Surgery, Karolinska University Hospital, Sweden Department of Rheumatology, Karolinska University Hospital, Sweden Correspondence should be addressed to Niclas Lundstr¨om; [email protected] Received 13 December 2018; Accepted 13 January 2019; Published 29 January 2019 Academic Editor: Kenneth S. Waxman Copyright © 2019 Niclas Lundstr¨om et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We present a case of repeated cardiac arrests derived from dynamic hyperinfation in a patient with severe tracheobronchomalacia. Mechanical ventilation led to auto-PEEP with hemodynamic impairment and pulseless electric activity. Adjusted ventilation settings, deep sedation, and muscle paralysis followed by acute stenting of the afected collapsing airways restored ventilation and prevented recurrent circulatory collapse. We briefy review the pathophysiology and treatment options in patients with dynamic hyperinfation. 1. Introduction tracheobronchial infammation had led to stenosis and sec- ondary tracheobronchomalacia, with the distal trachea and Patients with expiratory fow limitation are at risk of devel- main bronchi most afected on previous CT scans. At the oping dynamic hyperinfation and auto-PEEP, which in time of the reported events, he received treatment with extreme cases can cause circulatory collapse [1]. Aggravated azathioprine 100 mg per day and prednisolone 10 mg per day. by overzealous positive pressure ventilation, it is crucial Noninvasive mask ventilation with positive airway pressure that the cause of collapse is immediately recognized in was used at night because of worsened symptoms when order to relieve intrathoracic pressure and adapt ventilator recumbent. Tere was a plan to consult ENT surgeons treatment [2]. Previously described in patients with severe regarding the possibility of placing airway stents to treat the asthma and COPD [3–5], this case also demonstrates the condition. risk of hyperinfation causing cardiac arrest in patients with Pulmonary function test done the month before showed tracheobronchomalacia. In such a case, rapid stenting of marked nonreversible expiratory fow limitation with forced the collapsing airways can be a lifesaving procedure. Patient expiratory volume in 1 second (0.6 L, 18% of expected) and informed consent was obtained. hyperinfation with a reduced forced vital capacity (2.7L, 58% of expected), an increased residual volume (3.0L, 139% of 2. Case expected), and functional residual capacity (4.3L, 131% of expected). Total lung capacity and difusion capacity were A 66-year-old man arrived at the emergency room afer a normal. cardiac arrest with successful prehospital resuscitation. Te patient had undergone bronchoscopy under gen- He had a medical history of hypertension, diabetes, eral anesthesia the previous year which was complicated and obstructive sleep apnea. Recently he had also been by severe bronchospasm, hypoventilation, and subsequent diagnosed with granulomatosis polyangiitis (GPA) with pos- hypercapnia requiring unplanned delayed extubation and itive C-ANCA and respiratory tract involvement. Severe ICU admission. 2 Case Reports in Critical Care (a) (b) Figure 1: CT imaging before (a) and afer (b) stenting. Arrows pointing at main bronchi. Te cardiac arrest took place during a visit at an out- anesthesia. Te diameter of the right main bronchus was of-hospital urology clinic. It was preceded by obstructive approximately 2-3 mm wide and in the lef main bronchus breathing and coughing leading up to respiratory arrest, hardly any lumen was seen. and he became pulseless before the arrival of paramedics. With the stents in place (Figure 1(b)), respiratory com- Cardiopulmonary resuscitation (CPR) was started. When pliance improved immediately, and peak pressure and PEEP paramedics arrived, they found pulseless electrical activity, could be reduced with maintained minute volume. Te CPR was continued including administration of adrenaline, patient was extubated in the operation room. He was neu- and afer 10 minutes there was return of spontaneous circula- rologically intact and the continued care was uneventful. tion and breathing. Te following years though, he has needed treatment at At the hospital emergency room he was unresponsive hospital several times, due to recurrent respiratory problems but with stable pulse and blood pressure. Afer intubation he with mucus stagnation, infections and granulation tissue in was taken to the ICU. Arterial blood gas showed respiratory proximity to the stents, well-known complications to long acidosis with pH at 6.88, PaCO2 16.6 kPa. Ventilating the term stent treatment. However, he has experienced no further patient sufciently to normalize PaCO2 was difcult. Regard- episode of circulatory collapse. less of ventilation mode, high inspiratory and end-expiratory pressures were needed for acceptable tidal volumes and 3. Discussion gas exchange. PEEP at 14-16 cmH2O was considered opti- mal. Remaining air fow at end-expiration indicated auto- Tis case illustrates the risk of dynamic hyperinfation and PEEP; therefore, the expiratory phase was prolonged with circulatory collapse in patients with severe expiratory fow I:E ratio 1:4. Bronchoscopy showed very narrow bronchi limitation and the potentially lifesaving efects of timely and infammation. CT scan confrmed narrow conditions airway stenting in patients with obstruction of the central in the proximal airways, especially in the main bronchi airways as in tracheobronchomalacia. In the following, we (Figure 1(a)). No signs of pulmonary embolism were seen. briefy discuss lung hyperinfation, auto-PEEP and circula- Te second day at the ICU, the situation quickly dete- tory compromise and lastly tracheobronchomalacia. riorated, with increasing respiratory acidosis. Te patient Lung hyperinfation essentially means that the lung seemed stressed and hypertensive and triggered the ventila- volume at the end of expiration is above normal [6, 7]. tor. Suddenly the blood pressure dropped to immeasurable. Static hyperinfation refers to a consistent increase in the CRP was started, the ventilator was disconnected, and bag functional residual capacity (FRC). Dynamic hyperinfation ventilation was attempted. Adrenaline was administered and refers to a variable increase in end-expiratory lung volume afer about 2-3 minutes of CPR circulation returned. During (EELV), ofen caused by expiratory fow limitation that the CPR, muscle relaxant with rocuronium (Esmeron5)was prevents the lung from emptying to its resting volume before also administered to ease continued ventilation afer return inspiration. Dynamic hyperinfation varies with changes in of circulation. Te assessment at this point was that hyperin- fow limitation, minute ventilation, and breathing pattern. In fation and auto-PEEP due to the expiratory fow obstruction this situation of incomplete expiration, alveolar pressure at likely had caused the circulatory collapse. Increasing sedation end-expiration remains higher than proximal airway pressure and muscle paralysis stabilized the situation and the patient at the start of next inspiration. Tis is called intrinsic PEEP or was therefore kept deeply sedated. auto-PEEP [1]. Physiologically, auto-PEEP difers from exter- Te ENT surgeons were consulted to discuss urgent stent- nally applied PEEP set on a ventilator, as auto-PEEP is present ing of the collapsing airways. Stenting of each main bronchus only distal to airways with fow limitation and not equally using two stents was conducted a few hours later in the distributed in the lungs [2, 8]. During invasive ventilation operating theater. Te procedure was done with aid of rigid auto-PEEP leads to decreased lung compliance, resulting in bronchoscopy with ongoing jet ventilation during general reduced tidal volumes during pressure controlled ventilation Case Reports in Critical Care 3 Airway pressure Occlusion Auto-PEEP External PEEP Insp air flow Time Time Remaining air flow Exp air flow Lung volume EELV Hyperinflation Time Figure 2: Ventilatory curves for three consecutive breaths during pressure controlled ventilation in a patient with dynamic hyperinfation and auto-PEEP, measurement of static auto-PEEP afer occlusion. and increased peak pressures in volume controlled modes [9]. Te second cardiac arrest during invasive ventilation was Auto-PEEP can be measured in most ventilators from the preceded by acceptable oxygenation but ventilation difcul- airway pressure during prolonged expiration with a closed ties with reduced tidal volumes and hypercapnia. Afer a expiration valve (Figure 2). Tis requires a passive patient. brief period of hypertension, blood pressure dropped quickly Auto-PEEP can generate the same hemodynamic efects before onset of the cardiac arrest (Figure 3). Te circulatory as externally added PEEP.Te resulting elevated intrathoracic collapse can in this case be considered caused directly by pressure reduces venous return and
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