Shih-Yun Lan1, Jainn-Jim Lin2, Shao-Hsuan Hsia3, Huei-Shyong Wang1, Cheng-Hsun Chiu4, Kuang-Lin Lin5. 1. Division of Pediatric Neurology, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan; Chang Gung Children's Hospital Study Group for Children with Encephalitis/Encephalopathy Related Status Epilepticus and Epilepsy (CHEESE), Taoyuan, Taiwan. 2. Division of Pediatric Neurology, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan; Chang Gung Children's Hospital Study Group for Children with Encephalitis/Encephalopathy Related Status Epilepticus and Epilepsy (CHEESE), Taoyuan, Taiwan; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan; Division of Pediatric Critical Care and Emergency Medicine, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan. 3. Chang Gung Children's Hospital Study Group for Children with Encephalitis/Encephalopathy Related Status Epilepticus and Epilepsy (CHEESE), Taoyuan, Taiwan; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. 4. Molecular Infectious Disease Research Center, Division of Pediatric Infection, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Taoyuan, Taiwan; Chang Gung University College of Medicine, Taoyuan, Taiwan. 5. Division of Pediatric Neurology, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan; Chang Gung Children's Hospital Study Group for Children with Encephalitis/Encephalopathy Related Status Epilepticus and Epilepsy (CHEESE), Taoyuan, Taiwan. Electronic address: lincgh@adm.cgmh.org.tw.
Abstract
BACKGROUND: Acute pediatric encephalitis with fulminant cerebral edema can rapidly become fatal or result in devastating neurological sequelae. METHODS: All cases coded with the discharge diagnosis of acute encephalitis between January 2000 and December 2010 were reviewed. Of the 1038 children with acute pediatric encephalitis, 25 were enrolled in our study with ages ranging from 5 months to 16 years. RESULTS: The major neurological symptoms included an altered level of consciousness (72%), vomiting (60%), and headache (48%). The onset of neurological symptoms to signs of brain herniation ranged from 0 days to 9 days. Nineteen (76%) patients had a seizure 24-48 hours prior to showing signs of fulminant cerebral edema, and 12 (48%) patients developed status epilepticus. Sixteen patients died, and no survivors returned to baseline. Risk factors for seizures and status epilepticus were compared between the fulminant cerebral edema group (n = 25, 19 seizures, including 12 status epilepticus) and control group (nonfulminant cerebral edema) (n = 1013, 444 seizures, including 141 status epilepticus; p = 0.001 for seizures and p < 0.001 for status epilepticus). CONCLUSION: Our findings indicate that preceding seizures and status epilepticus are significant risk factors for fulminant cerebral edema in children with acute encephalitis.
BACKGROUND: Acute pediatric encephalitis with fulminant cerebral edema can rapidly become fatal or result in devastating neurological sequelae. METHODS: All cases coded with the discharge diagnosis of acute encephalitis between January 2000 and December 2010 were reviewed. Of the 1038 children with acute pediatric encephalitis, 25 were enrolled in our study with ages ranging from 5 months to 16 years. RESULTS: The major neurological symptoms included an altered level of consciousness (72%), vomiting (60%), and headache (48%). The onset of neurological symptoms to signs of brain herniation ranged from 0 days to 9 days. Nineteen (76%) patients had a seizure 24-48 hours prior to showing signs of fulminant cerebral edema, and 12 (48%) patients developed status epilepticus. Sixteen patients died, and no survivors returned to baseline. Risk factors for seizures and status epilepticus were compared between the fulminant cerebral edema group (n = 25, 19 seizures, including 12 status epilepticus) and control group (nonfulminant cerebral edema) (n = 1013, 444 seizures, including 141 status epilepticus; p = 0.001 for seizures and p < 0.001 for status epilepticus). CONCLUSION: Our findings indicate that preceding seizures and status epilepticus are significant risk factors for fulminant cerebral edema in children with acute encephalitis.
Authors: Siddharth Ninan; Peyton Thompson; Timothy Gershon; Natalie Ford; William Mills; Valerie Jewells; Leigh Thorne; Katherine Saunders; Thomas Bouldin; Jason R Smedberg; Melissa B Miller; Eveline Wu; Alyssa Tilly; Jeremy Sites; Daniel Lercher; Katherine Clement; Tracie Walker; Paul Shea; Benny Joyner; Rebecca Smith Journal: Child Neurol Open Date: 2021-06-14