Prognostic Effects of Treatment Protocols for Febrile Convulsive Status Epilepticus in Children

Background: Febrile status epilepticus is the most common form of status epilepticus in children. No previous reports compare the effectiveness of treatment strategies using fosphenytoin (fPHT) or phenobarbital (PB) and those using anesthetics as second-line anti-seizure medication for benzodiazepine-resistant convulsive status epilepticus (CSE). We aimed to examine the outcomes of various treatment strategies for febrile convulsive status epilepticus (FCSE) in a real-world setting while comparing the effects of different treatment protocols and their presence or absence.Methods: This was a single-center historical cohort study that was divided into three periods. Patients who presented with febrile convulsive status epilepticus for ≥60 min even after the administration of at least one anticonvulsant were included. During period I (October 2002–December 2006), treatment was performed at the discretion of the attending physician, without a protocol. During period II (January 2007–February 2013), barbiturate coma therapy (BCT) was indicated for FCSE resistant to benzodiazepines. During period III (March 2013–April 2016), BCT was indicated for FCSE resistant to fPHT or PB. Results: The rate of EEG monitoring was lower in period I than period II+III (7.7% vs. 83.3%, p<0.01). Midazolam was administered by continuous infusion more often in period I than period II+III (84.6% vs. 25.0%, p<0.01), whereas fPHT was administered less often in period I than period II+III (0% vs. 27.4%, p<0.01). The rate of poor outcome, which was determined using the Pediatric Cerebral Performance Category scale, was higher in period I than period II+III (23.1% vs. 7.1%, p=0.03). The rate of poor outcome did not differ between periods II and III (4.2% vs. 11.1%, p=0.40).Conclusions: While the presence of a treatment protocol for FCSE in children may improve outcomes, a treatment protocol using fPHT or PB may not be associated with better outcomes.

Prediction of Glasgow Outcome Scale after Barbiturate Coma Therapy in patients suffering from Refractory Intracranial Hypertension after Brain Tumour Surgery: Incorporating Ensemble approach into automated Machine Learning

Ensemble approach is incorporated into Automated machine learning to predict Glasgow outcome scale and In-hospital mortality in patients receiving Barbiturate coma therapy for refractory intracranial hypertension post Brain tumour surgery.

Temporal effects of barbiturate coma on intracranial pressure and compensatory reserve in children with traumatic brain injury

Background The aim was to study the effects of barbiturate coma treatment (BCT) on intracranial pressure (ICP) and intracranial compensatory reserve (RAP index) in children (< 17 years of age) with traumatic brain injury (TBI) and refractory intracranial hypertension (RICH). Methods High-resolution monitoring data were used to study the effects of BCT on ICP, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and RAP index. Four half hour long periods were studied: before bolus injection and at 5, 10, and 24 hours thereafter, respectively, and a fifth tapering period with S-thiopental between < 100 and < 30 μmol/L. S-thiopental concentrations and administered doses were registered. Results Seventeen children treated with BCT 2007–2017 with high-resolution data were included; median age 15 (range 6–17) and median Glasgow coma score 7 (range 3–8). Median time from trauma to start of BCT was 44.5 h (range 2.5–197.5) and from start to stop 99.0 h (range 21.0–329.0). Median ICP was 22 (IQR 20–25) in the half hour period before onset of BCT and 16 (IQR 11–20) in the half hour period 5 h later (p = 0.011). The corresponding figures for CPP were 65 (IQR 62–71) and 63 (57–71) (p > 0.05). The RAP index was in the half hour period before onset of BCT 0.6 (IQR 0.1–0.7), in the half hour period 5 h later 0.3 (IQR 0.1–0.7) (p = 0.331), and in the whole BCT period 0.3 (IQR 0.2–0.4) (p = 0.004). Eighty-two percent (14/17) had favorable outcome (good recovery = 8 patients and moderate disability = 6 patients). Conclusion BCT significantly reduced ICP and RAP index with preserved CPP. BCT should be considered in case of RICH.

Management and Challenges of Severe Traumatic Brain Injury

Traumatic brain injury (TBI) is the leading cause of death and disability in trauma patients, and can be classified into mild, moderate, and severe by the Glasgow coma scale (GCS). Prehospital, initial emergency department, and subsequent intensive care unit (ICU) management of severe TBI should focus on avoiding secondary brain injury from hypotension and hypoxia, with appropriate reversal of anticoagulation and surgical evacuation of mass lesions as indicated. Utilizing principles based on the Monro–Kellie doctrine and cerebral perfusion pressure (CPP), a surrogate for cerebral blood flow (CBF) should be maintained by optimizing mean arterial pressure (MAP), through fluids and vasopressors, and/or decreasing intracranial pressure (ICP), through bedside maneuvers, sedation, hyperosmolar therapy, cerebrospinal fluid (CSF) drainage, and, in refractory cases, barbiturate coma or decompressive craniectomy (DC). While controversial, direct ICP monitoring, in conjunction with clinical examination and imaging as indicated, should help guide severe TBI therapy, although new modalities, such as brain tissue oxygen (PbtO2) monitoring, show great promise in providing strategies to optimize CBF. Optimization of the acute care of severe TBI should include recognition and treatment of paroxysmal sympathetic hyperactivity (PSH), early seizure prophylaxis, venous thromboembolism (VTE) prophylaxis, and nutrition optimization. Despite this, severe TBI remains a devastating injury and palliative care principles should be applied early. To better affect the challenging long-term outcomes of severe TBI, more and continued high quality research is required.

Intracranial pressure–based barbiturate coma treatment in children with refractory intracranial hypertension due to traumatic brain injury

OBJECTIVERefractory intracranial pressure (ICP) hypertension following traumatic brain injury (TBI) is a severe condition that requires potentially harmful treatment strategies such as barbiturate coma. However, the use of barbiturates may be restricted due to concerns about inducing multiorgan system complications related to the therapy. The purpose of this study was to evaluate the outcome and occurrence of treatment-related complications to barbiturate coma treatment in children with refractory intracranial hypertension (RICH) due to TBI in a modern multimodality neurointensive care unit (NICU).METHODSThe authors conducted a retrospective cohort study of 21 children ≤ 16 years old who were treated in their NICU between 2005 and 2015 with barbiturate coma for RICH following TBI. Demographic and clinical data were acquired from patient records and physiological data from digital monitoring system files.RESULTSThe median age of these 21 children was 14 years (range 2–16 years) and at admission the median Glasgow Coma Scale score was 7 (range 4–8). Barbiturate coma treatment was added due to RICH at a median of 46 hours from trauma and had a median duration of 107 hours. The onset of barbiturate coma resulted in lower ICP values, lower pulse amplitudes on the ICP curve, and decreased amount of A-waves. No major disturbances in blood gases, liver and kidney function, or secondary insults were observed during this period. Outcome 1 year later revealed a median Glasgow Outcome Scale score of 5 (good recovery), however on the King’s Outcome Scale for Childhood Head Injury, the median was 4a (moderate disability).CONCLUSIONSThe results of this study indicate that barbiturate coma, when used in a modern NICU, is an effective means of lowering ICP without causing concomitant severe side effects in children with RICH and was compatible with good long-term outcome.

Barbiturate-induced dyskalaemia in patients with traumatic brain injury patient

A young man with severe traumatic brain injury and refractory intracranial hypertension was treated with a barbiturate coma. A rare side effect of barbiturates is dyskalaemia. The dyskalaemia presented with acute hypokalaemia that quickly became hyperkalaemia. Both electrolyte disturbances can have serious physiological complications. The cellular cause of the dyskalaemia is not well understood. The correct diagnosis and treatment of barbiturate dyskalaemia is essential in providing care. Clinicians treating patients with barbiturates need to be aware of this rare side effect. Our patient was quickly and correctly treated for the dyskalaemia and suffered no complications related to this side effect.