Priti Vijay1, Bikrant Bihari Lal1, Vikrant Sood1, Rajeev Khanna1, Yashwant Patidar1, Seema Alam2. 1. Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, 110070, India. 2. Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, 110070, India. seema_alam@hotmail.com.
Abstract
BACKGROUND AND AIMS: The objectives were to evaluate the role of optic nerve sheath diameter (ONSD) to detect raised intracranial pressure (ICP) in pediatric acute liver failure (PALF), study the variations in ONSD with ICP-lowering measures and to evaluate its prognostic role. METHODS: PALF with clinical evidence of raised ICP were enrolled as cases, while those without raised ICP were control group A. ONSD was measured at admission and repeated regularly. It was also measured at time of each new episode of raised ICP and 2 h after the management of such episode. RESULTS: 31 PALF with raised ICP were included as cases and 15 without as control group A. ONSD was significantly higher in cases: 5 mm (IQR: 4.7-5.4) as compared to control group A: 3.8 mm (IQR: 3.3-4). ONSD greater than 4.55 mm at baseline diagnosed clinically raised ICP with 87.5% sensitivity and 100% specificity. The mean ONSD was 5.44 ± 0.49 mm during a total of 90 events of acute raised ICP. Clinical responders had a decrease in ONSD by 0.59 ± 0.24 mm by 2 h, whereas non-responders showed a decrease of 0.18 ± 0.23 mm, p < 0.0005. ONSD persisting more than 4.6 mm by 24 h of management predicted poor outcome with sensitivity and specificity of 83.3% and 72.7%. CONCLUSION: ONSD is a simple, bedside, inexpensive, reproducible and repeatable modality to assess ongoing change in ICP in PALF. ONSD more than 4.55 mm suggests raised ICP. The goal should be to bring ONSD down to less than 4.6 mm within 24 h by aggressive anti-ICP therapy to achieve favourable outcome.
BACKGROUND AND AIMS: The objectives were to evaluate the role of optic nerve sheath diameter (ONSD) to detect raised intracranial pressure (ICP) in pediatric acute liver failure (PALF), study the variations in ONSD with ICP-lowering measures and to evaluate its prognostic role. METHODS: PALF with clinical evidence of raised ICP were enrolled as cases, while those without raised ICP were control group A. ONSD was measured at admission and repeated regularly. It was also measured at time of each new episode of raised ICP and 2 h after the management of such episode. RESULTS: 31 PALF with raised ICP were included as cases and 15 without as control group A. ONSD was significantly higher in cases: 5 mm (IQR: 4.7-5.4) as compared to control group A: 3.8 mm (IQR: 3.3-4). ONSD greater than 4.55 mm at baseline diagnosed clinically raised ICP with 87.5% sensitivity and 100% specificity. The mean ONSD was 5.44 ± 0.49 mm during a total of 90 events of acute raised ICP. Clinical responders had a decrease in ONSD by 0.59 ± 0.24 mm by 2 h, whereas non-responders showed a decrease of 0.18 ± 0.23 mm, p < 0.0005. ONSD persisting more than 4.6 mm by 24 h of management predicted poor outcome with sensitivity and specificity of 83.3% and 72.7%. CONCLUSION: ONSD is a simple, bedside, inexpensive, reproducible and repeatable modality to assess ongoing change in ICP in PALF. ONSD more than 4.55 mm suggests raised ICP. The goal should be to bring ONSD down to less than 4.6 mm within 24 h by aggressive anti-ICP therapy to achieve favourable outcome.
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