Case report
A 12-year-old boy, weighing 114 kg and 170 cm in height, admitted to our pediatric intensive care unit (PICU) due to severe chlorine gas poisoning. He inhaled chlorine for about 3 minutes due to the burst of disinfection pipe in a swimming pool 4.5 hours before admission, and showed extra breathing effort, shortness of breath and white foamy sputum when evacuated the toxic environment. Four hours before admission, he arrived at a local hospital and received budesonide atomization and oxygen inhalation, but gradually deteriorated to cyanosis, irritability and confusion. Thirty minutes before admission, he arrived at the emergency department of our hospital. The monitoring showed heart rate (HR) 130 bpm, respiration rate (RR) 30 pm, transcutaneous oxygen saturation (SPO2) 80%, blood pressure (BP) 130/80 mmHg. Physical examination showed unconsciousness, shortness of breath but regular rhythm, extensive wet rales in both lungs and warm extremities. Immediately endotracheal intubation and bag-mask positive pressure ventilation was done with pure oxygen inhalation, his SP02 gradually increased to 85%. Large amount of pink foam was sucked from tracheal cannula. He was transferred to PICU immediately after tracheal intubation.
Main auxiliary investigation after PICU admission included:
1. Chest X-ray: diffuse parenchyma and interstitial lesions in both lungs (Fig1-1).
2. Blood routine: 21.19×109/L of leukocytes, 88.6% of neutrophils.
3. C reactive protein 8 mg/L, procalcitonin is normal.
4. Venous blood gas: PH7.169, PCO2 60.3 mmHg, PO2 37.2 mmHg, SO2 57.8%, lactic acid 4.5 mmol/L.
5. The electrolytes, liver and kidney function and blood coagulation function were nearly normal. He was diagnosed as severe chlorine poisoning, severe ARDS and inhaled toxic gaseous pneumonia. Normal frequency MV was initiated with inspired oxygen fraction (FiO2) 100%, positive end-expiratory airway pressure (PEEP) 20 cmH2O, RR 15 pm, tidal volume (VT) 500ml, peak inspiratory pressure monitored was 48 cmH2O. Methylprednisolone 2 mg/kg/d was given intravenously for anti-inflammation, midazolam/fentanyl for analgesia and sedation, and rocuronium muscle relaxation. Under such support, themonitoring heart rate was around 110 bpm, SPO2 92%, BP 100/80 mmHg. We calculated oxygen saturation index (OSI) 27.3 instead of oxygen index (OI) due to the difficulty of arterial blood collection.
Three hours after admission, the child’s BP suddenly dropped to 72/50 mmHg, SPO2 75%, with HR rose to130 bpm, adrenaline 0.8 ug/kg/min was given to increase blood pressure, but with poor effect. Bedside transthoracic echocardiography was done immediately by some senior PICU doctors, but we failed to get a clear image, which may be related to the higher condition of MV, extreme obesity and operators’ experience. Since the child’s oxygenation couldn’t be maintained under routine treatment and combined with unstable circulation, we prepared to undergo V-AECMO life support.
Seven hours after admission, the catheterization through the right internal jugular vein and jugular artery was completed by cardiac surgeon due to difficulty of catheterization in the femoral vein, and the VA-ECMO was initiated with rotational speed 3000 rpm, blood flow 3L pm, airflow 5L pm, FiO2 100%. The SPO2of the child rose to 98%, then we successfully down-regulated the MV parameters to FiO2 60%, PEEP 12 cmH2O, RR 20 pm, VT 300 ml. X-ray showed pulmonary transmittance was greatly elevated (figure 1-2). The circulation condition was improved significantly to BP 116/80 mmHg and stable pulse pressure gap. Bed side cardiac ultrasound performed by our certified ultrasound doctor showed normal left ventricular systolic function and the adrenaline was successfully withdrawn within 2 hours. 15 hours after admission, the patient presented with continuous oliguria accompanied by progressive increase of urea nitrogen and creatinine, and was dealt with continuous renal replacement therapy (CRRT).
On the second day of admission, MV’s FiO2 was down-regulated to 40%. On the 3rd day of admission, the urine output recovered and urea nitrogen and creatinine decreased gradually, we stopped CRRT successfully. On the 5th day of admission, the chest X-ray showed that the pulmonary lesions were mostly absorbed (figure 1-3), and the vital signs were stable. The ECMO was removed when the ventilator was set to FiO2 60%, PEEP 12 cmH2O, VT 450 ml, RR 20/min. After the removal of ECMO, the child presented a transient aggravation of pulmonary exudation (figure 1-4) with SPO2 decreased to 90%, his oxygenation gradually stabilized after the PEEP was increased to 16cmH2O and furosemide intravenous injected at a dose of 1mg/kg.
On the 7th day after admission, we down-regulated the PEEP to 6 cmH2O, FiO2 to 40%. The child’s OI was 3.68 with normal spontaneous breath and clearconscious, and the pulmonary exudation was nearly absorbed (Fig. 1-5). After MV was successfully removed, he was supported by bi-level non-invasive positive pressure ventilation for 12 hours, and then we gave him nasal catheter. Fiberoptic bronchoscopy was performed before withdrawing the ventilator, which showed inflammation of tracheobronchial intima and poor ventilation in some subbranches of the left lower basal segment. Enteral feeding was started from 5% glucose on the same day.
From the 8th day of admission, the child gradually weaned off oxygen inhalation and could get out of bed and do some physical exercise. The lung CT showed exudation lesion was absorbed (Fig 1-6 and 1-7), while the pulmonary function showed mild mixed ventilatory dysfunction may be due to his extreme obesity. The transcranial doppler, brain magnetic resonance image, cervical vascular ultrasound and cardiac ultrasound were all normal. During the recovery period of enteral feeding, a transient pancreatic injury occurred with amylase and lipase increased to 18U/L and 195.5 U/L respectively, they all returned to normal after several days’ somatostatin infusion. During the 2nd-4th day after admission, the child was given nitroprusside and nicardipine pump successively due to the increase of BP (up to 170/100 mmHg) for unknown reason. His BP returned to normal on the 5th day of admission with no reliance on long-term oral antihypertensive drugs.
The child hospitalized in our hospital relatively longer due to the incision fat liquefaction and discharged one month after admission. The lung CT in the 2 month’s follow-up showed no abnormality (Fig.1-8). There were no sequelae in the follow-up 3 months after admission, his physical ability returned to the basic level, and could do physical exercise as before.