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Fatal pneumomediastinum associated with use of noninvasive mechanical ventilation.

Ruggeri P, Girbino G - Respirol Case Rep (2014)

Bottom Line: Use of NIMV in end stage ILD is not standardized and efficacy is to be proven.No data are reported to manage patient with concomitant COPD and ILD.Pathophysiological mechanisms underlying this fatal complication are explained and suggestions to treat this subgroup of patients discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Experimental Medicine and Surgery with Odontostomatology, Respiratory Unit, Policlinico Universitario "G.Martino" di Messina Messina, Italy.

ABSTRACT
We present a case of fatal pneumomediastinum in a patient with acute respiratory failure caused by acute exacerbated chronic obstructive pulmonary disease (AECOPD) and interstitial lung disease (ILD) precipitated by noninvasive mechanical ventilation (NIMV). To our knowledge, this is the first case reported in the literature. NIMV is very useful to treat acute respiratory failure due to AECOPD improving survival and avoiding endotracheal intubation. Use of NIMV in end stage ILD is not standardized and efficacy is to be proven. No data are reported to manage patient with concomitant COPD and ILD. Pathophysiological mechanisms underlying this fatal complication are explained and suggestions to treat this subgroup of patients discussed.

No MeSH data available.


Related in: MedlinePlus

Chest computed tomography performed after acute event showing clear radiological findings of pneumomediastinum, subcutaneous emphysema, small bilateral pneumothorax, and interstitial lung disease.
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fig02: Chest computed tomography performed after acute event showing clear radiological findings of pneumomediastinum, subcutaneous emphysema, small bilateral pneumothorax, and interstitial lung disease.

Mentions: The patient was a 78-year-old Caucasian man weighing 80 kg who was formerly a heavy smoker. He was admitted to the respiratory unit from the emergency department for the evaluation and treatment of AECOPD. CPFE was diagnosed following high-resolution computed tomography imaging (Fig. 1) three months before exacerbation. At admission, only a chest X-ray was carried out in supine position. At admission, the patient was dyspneic with a respiratory frequency (RF) of 33 breaths per minute. Cyanosis was observed at extremities and the saturation at pulse oxymeter was 88% while the patient was breathing oxygen via nasal cannula at 2 l/min. The patient stated that coughing had increased a few days prior to recovery and that he had coughed up sputum and had a moderate fever (38°C). A physical examination revealed wheezing in the mid-thoracic area and fixed crackles in the lower pulmonary lobes. Arterial blood gas analysis demonstrated an acute decompensated respiratory acidosis with severe hypoxemia (pH 7,28; PaCO2 70 mmHg; PaO2 55 mmHg; Sat 88%; 28 mEq/L). The patient was administered 80 mg of prednisone intravenous and salbutamol aerosol therapy was promptly started with poor patient response. The patient rapidly manifested impaired sensorium. Considering the fast decline of clinical and functional parameters, we promptly started a NIMV trial session. A Viasys Healthcare Vela Ventilator (Carefusion, Savi Ranch Parkway Yorba Linda, CA, USA) was used with a Fisher & Paykel 431 NIV nasobuccal mask (medium) (Fisher & Paykel Healthcare, Panmure, Auckland, New Zeland). Ventilator setting was pressure support (PS) 15 cmH2O; positive end-expiratory pressure (PEEP) 5 cmH2O; mean RF 10; inspiratory trigger 1 l/min; inspiratory time (Tinsp) 0.8 sec; inspiratory oxygen fraction (FiO2) 30%. In the beginning, the patient appeared to be intolerant to the assisted ventilation procedure as it caused more coughing and agitation. After a more detailed explanation of NIMV goals, patient-ventilatory synchronization greatly improved and oxygen saturation stabilized at 92%. Pharmacological sedation was not used in this case. In the first hour of ventilation, PS was progressively increased from 15 cmH2O to 20 cmH2O in order to achieve a target expiratory volume of 10 mL/kg. PEEP remained unchanged. A microbiological culture of the sputum revealed colonies of Pseudomonas aeruginosa. In the first hour from the start of NIMV, the patient coughed continually with peak inspiratory pressure over 30 cmH2O. After about 4 h of ventilation, the patient rapidly became more dyspneic during a coughing attack with deterioration of cyanosis. Hamman's sign with subcutaneous emphysema became rapidly evident, supporting the diagnosis of pneumomediastinum. A chest computed tomography (Fig. 2) confirmed pneumomediastinum in addition to subcutaneous emphysema, small bilateral pneumothorax, and interstitial lung disease. The patient underwent endotracheal intubation and invasive mechanical ventilation. This therapeutic approach was not able to stabilize the patient's clinical conditions and he died after one day in intensive care unit because of the worsening of bilateral pneumothorax and development of cardiac tamponade caused by pneumopericardium.


Fatal pneumomediastinum associated with use of noninvasive mechanical ventilation.

Ruggeri P, Girbino G - Respirol Case Rep (2014)

Chest computed tomography performed after acute event showing clear radiological findings of pneumomediastinum, subcutaneous emphysema, small bilateral pneumothorax, and interstitial lung disease.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4263491&req=5

fig02: Chest computed tomography performed after acute event showing clear radiological findings of pneumomediastinum, subcutaneous emphysema, small bilateral pneumothorax, and interstitial lung disease.
Mentions: The patient was a 78-year-old Caucasian man weighing 80 kg who was formerly a heavy smoker. He was admitted to the respiratory unit from the emergency department for the evaluation and treatment of AECOPD. CPFE was diagnosed following high-resolution computed tomography imaging (Fig. 1) three months before exacerbation. At admission, only a chest X-ray was carried out in supine position. At admission, the patient was dyspneic with a respiratory frequency (RF) of 33 breaths per minute. Cyanosis was observed at extremities and the saturation at pulse oxymeter was 88% while the patient was breathing oxygen via nasal cannula at 2 l/min. The patient stated that coughing had increased a few days prior to recovery and that he had coughed up sputum and had a moderate fever (38°C). A physical examination revealed wheezing in the mid-thoracic area and fixed crackles in the lower pulmonary lobes. Arterial blood gas analysis demonstrated an acute decompensated respiratory acidosis with severe hypoxemia (pH 7,28; PaCO2 70 mmHg; PaO2 55 mmHg; Sat 88%; 28 mEq/L). The patient was administered 80 mg of prednisone intravenous and salbutamol aerosol therapy was promptly started with poor patient response. The patient rapidly manifested impaired sensorium. Considering the fast decline of clinical and functional parameters, we promptly started a NIMV trial session. A Viasys Healthcare Vela Ventilator (Carefusion, Savi Ranch Parkway Yorba Linda, CA, USA) was used with a Fisher & Paykel 431 NIV nasobuccal mask (medium) (Fisher & Paykel Healthcare, Panmure, Auckland, New Zeland). Ventilator setting was pressure support (PS) 15 cmH2O; positive end-expiratory pressure (PEEP) 5 cmH2O; mean RF 10; inspiratory trigger 1 l/min; inspiratory time (Tinsp) 0.8 sec; inspiratory oxygen fraction (FiO2) 30%. In the beginning, the patient appeared to be intolerant to the assisted ventilation procedure as it caused more coughing and agitation. After a more detailed explanation of NIMV goals, patient-ventilatory synchronization greatly improved and oxygen saturation stabilized at 92%. Pharmacological sedation was not used in this case. In the first hour of ventilation, PS was progressively increased from 15 cmH2O to 20 cmH2O in order to achieve a target expiratory volume of 10 mL/kg. PEEP remained unchanged. A microbiological culture of the sputum revealed colonies of Pseudomonas aeruginosa. In the first hour from the start of NIMV, the patient coughed continually with peak inspiratory pressure over 30 cmH2O. After about 4 h of ventilation, the patient rapidly became more dyspneic during a coughing attack with deterioration of cyanosis. Hamman's sign with subcutaneous emphysema became rapidly evident, supporting the diagnosis of pneumomediastinum. A chest computed tomography (Fig. 2) confirmed pneumomediastinum in addition to subcutaneous emphysema, small bilateral pneumothorax, and interstitial lung disease. The patient underwent endotracheal intubation and invasive mechanical ventilation. This therapeutic approach was not able to stabilize the patient's clinical conditions and he died after one day in intensive care unit because of the worsening of bilateral pneumothorax and development of cardiac tamponade caused by pneumopericardium.

Bottom Line: Use of NIMV in end stage ILD is not standardized and efficacy is to be proven.No data are reported to manage patient with concomitant COPD and ILD.Pathophysiological mechanisms underlying this fatal complication are explained and suggestions to treat this subgroup of patients discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Experimental Medicine and Surgery with Odontostomatology, Respiratory Unit, Policlinico Universitario "G.Martino" di Messina Messina, Italy.

ABSTRACT
We present a case of fatal pneumomediastinum in a patient with acute respiratory failure caused by acute exacerbated chronic obstructive pulmonary disease (AECOPD) and interstitial lung disease (ILD) precipitated by noninvasive mechanical ventilation (NIMV). To our knowledge, this is the first case reported in the literature. NIMV is very useful to treat acute respiratory failure due to AECOPD improving survival and avoiding endotracheal intubation. Use of NIMV in end stage ILD is not standardized and efficacy is to be proven. No data are reported to manage patient with concomitant COPD and ILD. Pathophysiological mechanisms underlying this fatal complication are explained and suggestions to treat this subgroup of patients discussed.

No MeSH data available.


Related in: MedlinePlus