Hydrocarbon aspiration (HA) is known to cause significant pulmonary disease by inducing an inflammatory response, hemorrhagic exudative alveolitis, and loss of surfactant function. We describe a pediatric case of HA which caused hypoxia and pulmonary hypertension that improved after administration of inhaled nitric oxide (iNO).
A previously healthy 18-month-old girl was found by her parent coughing and gagging, and had a bottle of “ultra-pure” lamp oil in her hand. She was taken to the emergency department, quickly became obtunded, was intubated, and then transported to the PICU for further management.Upon arrival, her weight was 9kg, temperature 37.3°C, pulse 191, blood pressure 103/51, respirations 48, and oxygen saturations 90% on 100% FiO2. On examination, she had tachypnea, coarse breath sounds with inspiratory and expiratory crackles throughout, and no wheezing. We suctioned copious bloody secretions from her endotracheal tube. On cardiac exam, she had tachycardia, no murmur, 5 second capillary refill, and 1+ peripheral pulses. The remainder of her exam was unremarkable Due to persistent hypoxia using conventional ventilation (maximum settings on pressure regulated volume control mode were tidal volume 100, peep 14, rate 24, and FIO2 100%), we switched to high frequency oscillator ventilation (HFOV) with initial settings of Hz 9, MAP 35, deltaP 38, and FIO2 100%. On HFOV she continued to have a PaO2/FiO2 ratio <100. She developed hypotension and coagulopathy, requiring fluid boluses, pressor support, fresh frozen plasma, and cryoprecipitate. We started stress dose hydrocortisone for hypotension refractory to escalating pressor support. We also started her on prophylactic antibiotics. ECMO was contraindicated because of pulmonary hemorrhage.On hospital day 2, we administered inhaled surfactant. Her PaO2 increased from 63 to 71 and FiO2 decreased from 97% to 95%. An echocardiogram showed mild left ventricular dysfunction and mild right ventricular enlargement with a tricuspid regurgitation (TR) gradient of 30 - 35 mmHg. To support her blood pressure she required epinephrine at 0.8mcg/kg/min and dopamine at 15mcg/kg/min. Her urine output was 1.5ml/kg/hr on a furosemide infusion at 1mg/hr. On hospital day 3, we started iNO at 10ppm. Her oxygenation improved immediately as demononstrated by a change in PaO2 from 56 to 172 and ability to wean FiO2. Within the next 24 hours we weaned her dopamine to 10mcg/kg/min and epinephrine to 0.1mcg/kg/min. Her urine output improved to 6ml/kg/hr. An echocardiogram on hospital day 4 demonstrated trivial TR. By hospital day 5, we were able to stop the dopamine and epinephrine infusions. A repeat echocardiogram on day 23 showed trivial TR and lack of systolic septal wall flattening consistent with resolution of pulmonary hypertension. We continued the iNO until hospital day 35. She also developed a pneumothorax and pneumatoceles which required no intervention. We switched her to conventional ventilation within a month, extubated her within 6 weeks, and ultimately discharged her without any oxygen therapy.
HA main toxicity is a chemical pneumonitis which can progress to acute respiratory distress syndrome (ARDS). The mainstay of HA is supportive therapy. The use of steroids is not fully supported in the literature. Surfactant has been demonstrated to be helpful in experimental animals, but not in humans. The use of iNO in adult patients with ARDS is controversial. We demonstrate the successful treatment of a pediatric case of ARDS secondary to HA using iNO. In this patient, iNO was effective in improving oxygenation and pulmonary hypertension with subsequent improvement in hemodynamics. Further studies are needed to determine if this specific subset of patients with ARDS from HA have a unique therapeutic benefit from iNO.
iNO may be effective for management of pediatric patients with ARDS and refractory hypoxemia secondary to HA.
Pallavi Patwari, None.