Case Report

The Use Of High Frequency Oscillatory Ventilation In Hydrocarbon Pneumonitis

Lois K. Lee, MD, MPH
Michael Shannon, MD, MPH
John Arnold, MD

The Division of Emergency Medicine and the Division of Anaesthesia and Critical Care, Children’s Hospital; Harvard Medical School, Boston

Int J Med Toxicol 2003; 6(2):10


Correspondence

Lois Lee, MD, MPH
Children’s Hospital Boston
300 Longwood Ave.
Boston, MA 02115
Phone: 617-355-6624
Fax: 617-731-3279
Email: lois.lee@tch.harvard.edu

Abstract

Two patients are described who presented with severe pneumonitis from hydrocarbon ingestion and aspiration. Conventional ventilation did not adequately oxygenate and ventilate the patients despite the use of very high airway pressures. One of the patients improved with high frequency oscillatory ventilation (HFOV); the other patient required HFOV and extracorporeal membrane oxygenation. This provided adequate respiratory support while minimizing barotrauma as the pneumonitis resolved. HFOV can be an alternative to conventional ventilation for respiratory failure secondary to hydrocarbon aspiration.

Key Words

High frequency oscillatory ventilation (HFOV)
Hydrocarbon aspiration
Acute respiratory distress syndrome (ARDS)

Abbreviations

ABG: Arterial blood gas
ARDS: Acute respiratory distress syndrome
CV: Conventional ventilation
ECMO: Extracorporeal membrane oxygenation
FiO2: Fraction of inspiratory oxygen
HFJV: High frequency jet ventilation
HFOV: High frequency oscillatory ventilation
ICU: Intensive care unit
MAP: Mean airway pressure
PEEP: Positive end-expiratory pressure
PIP: Positive inspiratory pressure
SSU: Saybolt seconds universal

Introduction

High frequency jet ventilation (HFJV) has been described in the successful treatment of hydrocarbon pneumonitis.1  HFJV is a mode of mechanical ventilation, which uses a jet injector to actively deliver inspiratory gas at low tidal volumes into the trachea at supraphysiological ventilatory frequencies of 100-600 cycles/min.2 The expiration phase is passive, relying on lung and chest wall passive recoil for expiratory flow. 3 Conventional ventilation (CV) can be combined with HFJV in some situations to provide “sigh breaths” to prevent atelectasis and maintain lung volumes during HFJV. 2 High frequency oscillatory ventilation (HFOV) is an alternate mode of mechanical ventilation where gas is actively driven into and withdrawn from the lung. 3 It uses a steady inflating pressure to maintain lung recruitment while high-frequency pressure oscillations (4-15 Hz) generate alveolar ventilation. In HFOV, low tidal volumes and high ventilatory frequencies of 900-3600 cycles/min result in gas exchange with lower airway pressures. 2,4 Most of the clinical experience with HFOV has been in premature infants; there has been less published information about the use of HFOV in older children and adults. We report the successful use of HFOV in two cases of hydrocarbon pneumonitis.

Case Reports

Case 1: A previously well fifteen-month-old, 10-kilogram, female ingested an unknown amount of lamp oil. She coughed immediately and was given back blows, after which she developed noisy breathing. She was taken to a nearby hospital, lethargic and grunting. Her initial oxygen saturation was 90-91% on room air; initial arterial blood gas (ABG) values revealed a pH of 7.21 with a PaCO2of 65 mm Hg. Bibasilar infiltrates were seen on her chest x-ray. She was intubated and transferred to the pediatric Intensive Care Unit (ICU) for further management.

In the ICU her ABG values were pH 7.35, PaCO2 of 41mm Hg, and PaO2 of 84 mm Hg on conventional ventilator settings of rate 22, positive inspiratory pressure (PIP) of 25 cm H2O, positive end-expiratory pressure (PEEP) of 5 cm of H2O, and FiO2 of 0.6. Her hematocrit was 33.8%, with WBC 30,000 /ml, and platelet count 561,000 /ml. The following day she had respiratory deterioration; ventilatory settings were adjusted to rate 20, PIP of 30 cm of H2O, PEEP of 8 cm of H2O, and FiO2 of 0.6 with ABG values of pH 7.28, PaCO2 of 48 mm Hg, and PaO2 of 42 mm Hg. Her chest x-ray had the radiographic appearance of acute respiratory distress syndrome (ARDS). She was placed on HFOV with mean airway pressure (MAP) of 22 and amplitude of 40. Her hospital course was also complicated by cardiovascular instability requiring inotropic support for four days. On hospital day seven, an attempt was made to wean her to CV; however, she required PIPs greater than 30 cm of H2O and FiO2 of 1.0 so was placed back on HFOV. The following day she had respiratory deterioration requiring increased settings with MAP 27, amplitude 38, and FiO2 of 0.8. Over the next six days the FiO2 then other settings were slowly weaned. A chest x-ray on hospital day 12 revealed a left lower lobe pneumatocele. On hospital day 13 she was weaned to CV in pressure control mode with settings of rate 18, PIP of 30 cm of H2O, PEEP of 7 cm of H2O, and FiO2 of 0.6. Her ABG values were pH 7.42, PaCO2 of 58 mm Hg, and PaO2 of 103 mm Hg. She was extubated four days later. On hospital day 23 she was discharged home.

Case 2: A 17-year-old male ingested approximately 17 ounces of lamp oil in a suicide attempt; subsequently he coughed and vomited. Upon EMS arrival his respiratory rate was 30, pulse 108, and his oxygen saturation was 92% on room air. He was given oxygen by nasal cannula and 10 grams of charcoal by mouth. He vomited charcoal and oil in the ambulance; his cough persisted. Upon arrival to the emergency department, he was pale with acrocyanosis and significant respiratory distress. A nasogastric tube was placed; he vomited and aspirated part of the charcoal/oil mixture. His initial ABG values were pH 7.31, PaCO2 of 51 mm Hg, and PaO2 of 92 mm Hg on FiO2 of 1.0 via non-rebreathing oxygen mask. His chest x-ray showed right middle and lower lobe, left lower lobe, and retrocardiac infiltrates. He became somnolent and developed worsening respiratory distress. He was intubated and placed on ventilatory settings of rate 12, PEEP of 7.5 cm of H2O, tidal volume of 700 ml, and FiO2 of 1.0. He was transferred to a tertiary facility for further management.

Initially his respiratory status improved and then stabilized on CV. A Staphylococcus aureus superinfection, cultured from sputum on hospital day 9, and empyema complicated his hospital course. On hospital day 11, a tracheostomy was placed to provide chronic ventilatory support. Over the next few days his respiratory status worsened, and he developed ARDS requiring ventilatory settings of rate 12, PEEP of 12 cm of H2O, tidal volume of 700 ml, FiO2 of 1.0, and pressure control of 20. His ABG values on hospital day 14 were pH 7.16, PaCO2 of 97 mm Hg, and PaO2 of 60 mm Hg with an oxygen saturation of 80-82 % on FiO2 of 1.0. He was subsequently transferred to the pediatric ICU. Upon arrival to the ICU he was placed on HFOV with a MAP of 40, amplitude of 72, and FiO2 of 1.0, eventually requiring maximum amplitude of 74. His initial ABG on HFOV was pH 7.27, PaCO2 of 81 mm Hg, and PaO2 of 112 mm Hg. His chest x-ray on admission showed bilateral fluffy infiltrates, consolidations of bilateral lower lobes, and a cystic area on the right, suggestive of a pneumatocele. A thoracostomy tube was placed on hospital day 16 for the right lung pneumatocele. On hospital day 17 he had worsening respiratory function and oxygenation with increasing respiratory acidosis. He underwent uneventful internal jugular/femoral venous cannulation and was placed on veno-venous extracorporeal membrane oxygenation (ECMO) because of concerns for severe ventilator induced lung injury given the pressures needed to ventilate and oxygenate him. He remained on HFOV with lower settings and FiO2. Inotropic support was required for hemodynamic instability for the first 3 days on ECMO. On hospital day 23, corticosteroid therapy was added to control the inflammatory and fibrotic processes in the lung. He was successfully weaned from ECMO after 15 days and was on HFOV for one day before being weaned to CV. He required CV until hospital day 56 when he was weaned to continuous positive airway pressure. Systemic methicillin resistant S. aureus, Candida, and enterococcus infections and a persistent right bronchopulmonary fistula complicated his hospital course. On hospital day 85 he was discharged to a rehabilitation facility requiring no supplemental respiratory support.

One month later at pulmonary follow up he was neurologically intact with no pulmonary complaints. A chest x-ray revealed bilateral interstitial fibrosis with decreased right pleural effusion and a 9 x 5-cm pneumatocele in the right lower lobe. Pulmonary function tests showed a restrictive lung defect with total lung capacity at 76% of predicted.

Discussion

Hydrocarbons are organic compounds derived primarily from plants and petroleum distillates. They accounted for 2.6% of all human exposures and 1.9% of pediatric (children less than 6 years) exposures reported to the American Association of Poison Control Centers in 2001. Seven deaths were reported as a result of hydrocarbon ingestion. 5

Hydrocarbon ingestion can affect the gastrointestinal and central nervous systems, but the most serious effect is pulmonary toxicity from aspiration and the resulting pneumonitis. The properties of hydrocarbons that determine their aspiration potential are volatility, surface tension and viscosity. Volatility refers to the tendency of a liquid to become a gas. Substances with high volatility are more likely to result in pulmonary absorption. Hydrocarbons with low surface tension have increased aspiration potential since they may spread more easily from the upper GI tract to the trachea. 6

Viscosity is the most important property determining aspiration potential, and it is measured in Saybolt seconds universal (SSU). A SSU of less than 45 correlates with a high potential for aspiration (e.g. gasoline, kerosene), and a SSU greater than 100 indicates a high tendency to resist flow, and therefore, a low potential for aspiration (e.g. mineral oil). Low surface tension facilitates direct spread of hydrocarbons from the upper gastrointestinal tract to the trachea. Aspirated hydrocarbons inhibit surfactant resulting in alveolar collapse. 6 Experimental studies have demonstrated that alveolitis develops and peaks within 3 days; alveolar thickening then develops and peaks at 10 days. After the first week, there is typically a progressive resolution of lung inflammation. 7

Pulmonary symptoms may not be apparent initially, but can develop 6-24 hours after exposure. 8 Most children will remain asymptomatic, but those who become symptomatic can vary widely in illness severity, ranging from minimal symptoms to severe ARDS. In children who develop ARDS from any etiology, HFOV is increasingly becoming an important ventilation technique. In our cases, HFOV was used alone and with ECMO for hydrocarbon pneumonitis. The use of ECMO after the failure of CV in the treatment of hydrocarbon pneumonitis has been previously reported. 9,10

The majority of studies on the use of HFOV in respiratory failure have involved neonates; however, there are several studies on the use of HFOV in pediatric patients and two studies involving adults. 11, 12  A randomized controlled trial in 1994 comparing HFOV and CV in 58 pediatric patients showed that HFOV resulted in significantly improved oxygenation with less barotrauma and fewer patients required supplemental oxygen at 30 days. 13  HFOV is able to maintain a consistent lung volume preventing cyclic derecruitment since the MAP is most commonly set above closing pressure. 4 Bulk axial flow, interregional gas mixing, and molecular diffusion are the important mechanisms for gas exchange. Theoretically, HFOV provides a smaller change in phasic volume and pressure, reversal of atelectasis in the dependent lung, and less depression of surfactant production. 14 Therefore HFOV is advantageous in respiratory failure and ARDS because it can maintain a high lung volume while using small tidal volumes, resulting in decreased ventilator induced lung injury from barotrauma.11 This is important in hydrocarbon aspiration where surfactant is inhibited leading to areas of atelectasis that would normally require high airway pressures to achieve and maintain lung recruitment. Thus HFOV can provide respiratory support while enabling the lungs to heal with the possibility of less ventilator induced lung injury.

Conclusions

Hydrocarbon aspiration is an important cause of pulmonary injury. The majority of cases will not have significant symptoms, but there is potential to develop severe pneumonitis causing respiratory failure and ARDS. In these two cases with ARDS, HFOV provided a superior means of oxygenation and ventilation, used either alone or in conjunction with ECMO, when CV was inadequate despite high-pressure settings and FiO2. Once discharged home, neither patient required any supplemental respiratory support. HFOV can be a beneficial mode of ventilation for patients with severe hydrocarbon pneumonitis, providing better oxygenation with lower pressures, resulting in less barotrauma and a lower risk of chronic lung disease.

References
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