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• W2316491792 abstract "Introduction: Traumatic brain injury (TBI) constitutes a major cause of death and disability in developed countries. Acute respiratory distress syndrome (ARDS) is not an uncommon feature in patients with traumatic brain injury. ARDS and TBI can not only worsen but trigger each other. The management for ARDS may require permissive hypercapnia while in contradiction normocapnia or hypocapnia is needed for patients with intracranial hypertension. The use of inhaled nitric oxide in ARDS is not uncommon but its role in TBI has so far not been established. We report a case of acute intracranial hypertension (ICH) and ARDS treated with INO following TBI. A 13 years old boy was brought to the emergency room with multiple traumatic injuries and a low GCS (5/15) following a motor vehicle accident. He was resuscitate with mechanical ventilation, IV fluids, broad spectrum antibiotic, inotropes, blood and blood products. The trauma x-ray series showed multiple rib fractures, inter-trochanteric hip fracture and fracture of pelvis. CT trauma survey showed bleeding from external iliac vessels which was angioembolized and patient was transferred to intensive care unit. Repeat CT head was done as the patient developed anisocoria. It showed right temporoparietal epidural hematoma. Evacuation of hematoma was done and intracranial pressure monitoring device was inserted. Initial ICP and cerebral perfusion pressure (CPP) were 17 mm Hg and 60 mm Hg respectively. ICU course was complicated with ARDS, disseminated intravascular coagulation and rhabdomyolysis. Lung protective ventilation strategy (permissive hypercapnia) was initiated which lead to further increase in ICP with concomitant decrease in CPP. Patient's condition kept on worsening with rising ICP and PaCO2 in spite of measures which included sedation, paralysis and osmotherapy. Inhaled nitric oxide (INO) was started with the notion to improve the blood gas exchange and reduction of high ventilatory requirements. Initial dose of INO was 10 ppm which was gradually built up to 35 ppm. The ICP dropped from 28to 18 mmHg whereas CPP improved from 45 to 70 mmHg. 24 hours later ICP and blood gases improved to normal with reduction in FiO2 and PEEP (Table I). Variables Before INO 2 hours post INO 12 hours post INO 24 hours post INO PH 7.24 7.37 7.39 7.42 PaCO2 53 40 39 38 PaO2 58 128 80 88 HCO3 18 21 24 24 ICP 28 18 5 3 FIO2 100% 100% 60% 50% PEEP 16 16 10 8 INO was tapered and eventually patient weaned off from the ventilator. Repeat CT head revealed nothing of significance. Further course remained uneventful with no neurological deficit. Patient was transferred to the ward for further convalescence. The management protocol for raised ICP relies on keeping PaO2 around 100mmHg, PaCO2 between 30 to 35 mmHg and cerebral perfusion pressure (CPP) between 50–70 mmHg 4. This management plan is in contradiction with the practice guideline for ARDS which relies on permissive hypercapnia. It has been shown in studies that increase in PaCO2 induces cerebral vasodilatation and raised ICP. Nitric oxide (NO) is increasingly used in intensive care units (ICU) for the treatment of refractory hypoxemia in ARDS but its use in traumatic brain injury patients is not yet defined. The use of INO is still experimental in traumatic brain injury. Early and appropriate use of INO in TBI could save the patient from the catastrophic effects of ARDS and raised ICP. More scientific evidences are still awaited to define the role of INO in raised ICP. Keywords: Traumatic brain injury, raised intracranial pressure, ARDS and INO" @default.
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• W2316491792 date "2013-12-01" @default.
• W2316491792 modified "2023-09-26" @default.
• W2316491792 title "1211" @default.
• W2316491792 doi "https://doi.org/10.1097/01.ccm.0000440443.23453.b1" @default.
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