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.