Ketogenic Diet Uptodate – Pharmacological management of neurogenic bowel dysfunction after spinal cord injury and multiple sclerosis: a systematic review and clinical implications
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Ketogenic Diet Uptodate
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Effect Of A Plant Based, Low Fat Diet Versus An Animal Based, Ketogenic Diet On Ad Libitum Energy Intake
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By Jason B. Katz 1, Kent Owusu 2, 3, Ilisa Nussbaum 2, Rachel Beekman 2, Nicholas A. DeFilippo 4, 5, Emily J. Gilmore 2, Lawrence J. Hirsch 2, McKenzie K. Cervenka 6 and Carolina B McKeel 1, 2, *
Epilepsy And The Ketogenic Diet
Department of Neurology, Division of Epilepsy, Johns Hopkins Hospital, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Received: 7 January 2021 / Revised: 4 February 2021 / Accepted: 13 February 2021 / Published: 22 February 2021
Background: Status epilepticus (SE) carries high mortality and morbidity, often requiring an intensive medical approach. Recently, the implementation of a ketogenic diet (KD) in adults with refractory and superrefractory CE has been shown to be effective and beneficial. Methods: We present our experience, including difficulties in achieving and maintaining ketosis, in an adult with newly diagnosed refractory status epilepticus (NORSE). Case vignette: A previously healthy 29-year-old woman was admitted with cryptogenic NORSIE following a febrile illness; The layer is reinforced with a long-lasting super fireproof SE. A complete examination was noted for mild cerebral spinal fluid (CSF) pleocytosis, high nonspecific serum inflammatory markers, and edematous hippocampi with limited diffusion on magnetic resonance imaging (MRI). CSF tests were normal and serial MRIs showed resolution of edema and dissociation with progressive hippocampal and diffuse atrophy. He required prolonged therapeutic coma with multiple anesthetic infusions, 16 trials of antiseizure drugs (ASD), empiric immunosuppression, and partial bilateral oophorectomy. The enteral ketogenic regimen was started on hospital day 28. However, stable beta-hydroxybutyrate levels > 2 mmol/L were achieved at 37 days after full adjustment of the treatment plan. KD was difficult to manage in the intensive care unit (ICU) and was discontinued due to poor nutrition and comorbidity. KD is restarted in a non-ICU unit to facilitate reduction of ASD without recurrence of SE. Discussion: There are unknown risks in common treatments for CE, including antibiotics, electrolyte replenishment formulations, different preparations of the same drug (ie, parenteral, tablet, or suspension), and solutions used for oral care—complicating internal use of KD. cancer. Comprehensive management and understanding of KD issues is essential to successfully implementing and maintaining ketosis.
Ketogenic diet; status epilepticus; relapse of refractory status epilepticus; arrest; critical care; ketogenic ketosis diet; status epilepticus; relapse of refractory status epilepticus; arrest; critical care; ketosis
The Role Of Mentorship And Collaboration In The Fall And Rebirth Of The Ketogenic Diet
Status epilepticus (SE) carries high mortality and morbidity, often requiring an intensive medical approach. Recently, the implementation of the ketogenic diet (KD) in adults with refractory and superrefractory CE has been shown to be effective and feasible [1, 2, 3, 4, 5]. Often used in childhood epilepsies, KD has emerged as an effective adjunctive therapy for pediatric SE [6, 7]. We present our experience with an adult with relapsed refractory status epilepticus (NORSE), focusing on the unexpected difficulty of achieving and maintaining ketosis. Appropriate advice as well as thorough evaluation of factors interfering with ketosis are often seen in the critical care setting and offered by others.
A previously healthy 29-year-old woman was admitted to another institution with recurrent refractory status epilepticus (NORSE) after a febrile illness complicated by long-term superrefractory SE. Three days prior to presentation, she had fever, headache, vomiting, and fatigue as a result of contact with her son with an upper respiratory tract infection. On the morning of the admission, her friend tried to wake her up for work and found her unresponsive and shaky. In the emergency room, he was lethargic and unresponsive. During her initial evaluation, she was diagnosed with a 45-second bilateral tonic-clonic seizure that resolved with 2 mg of lorazepam intravenously. Head count was unremarkable and analysis of cerebrospinal fluid (CSF) revealed mononuclear pleocytosis (2 RBC, 41 nucleated cells (57% mononuclear cells), glucose 93, protein 54)). A one-hour electroencephalogram (EEG) showed diffuse delta activity associated with sleep spindles and K complexes without epileptiform discharges. He was monitored at a lower level and treated with levetiracetam and acyclovir. On the second day in the hospital, he was comfortable but raised his voice; He was able to follow simple commands over the central line, say his name and the current president, but he wasn’t in time. He was found to be squinting, but no EEG was done at the time. On the third hospital day, he began having brief convulsive seizures that were relieved by intravenous lorazepam and were associated with recovery of consciousness. At that time, phenytoin (1 g loading dose, maintenance 100 mg q8h) was added to his antiseizure drug (ASD) regimen. On the fourth hospital day, he had multiple convulsive seizures without return to baseline, complicated by hypoxic acute respiratory failure requiring intubation. He was transferred to the intensive care unit (ICU) where he was started on propofol, and valproic acid (20 mg/kg loading dose, maintained at 750 mg Q8H) was added. A typical EEG revealed right frontal and centotemporal lesions associated with periods of eye twitching. He was started on pentobarbital infusion (5 mg/kg bolus, maintained at 1 mg/kg hourly) and transferred to our center for regular EEG monitoring.
According to the latest list compiled by the International League Against Epilepsy, CE is “a condition resulting from the failure of functions responsible for seizure termination or initiation mechanisms, for example, leading to chronic, prolonged seizures” . Although the definition of SE varies in terms of time domain depending on the type of seizure, it is generally accepted that seizure activity is greater than 5 minutes in duration, or two or more seizures may occur when the individual does not recover. to the boundary between seizures, indicating SE. . Gamma-aminobutyric acid (GABA) neurons in the pars reticulum of the substantia nigra play a key role in extinction . During status epilepticus, GABA metabolism is altered in this region and results in disinhibition of excitatory pathways: GABA synthesis slows down . GABA conversion time increases threefold,  and GABA receptors (first found on the surface of the cell membrane) move into the intracellular space within minutes of seizure activity to continue [11, 12, 13]. Early initiation of abortifacient drugs is crucial, as internalization of GABA receptors contributes to treatment refractoriness.
Early administration of a parenteral benzodiazepine (eg 0.1 mg/kg lorazepam) is considered the first treatment for SE . If the patient does not respond to a benzodiazepine and a second well-selected and prescribed ASD in appropriate doses, he is in refractory status epilepticus (RSE). It has been reported that one in five patients with RSE will go on to develop super-refractory status epilepticus (SRSE), defined as (1) seizures lasting 24 hours or more after initiation of the anesthetic (ie, propofol) or (2) recurrence . of SE during reduction or withdrawal of therapeutic anesthetic coma . Clinical presentation of RSE in patients without brain injury or remote, primary epilepsy or toxic/metabolic explanation according to New Start Refractory Status Epilepticus-NORSE . Epilepsy syndrome associated with febrile infection (FIRES) is a subgroup of NORSE, a febrile syndrome that precedes the onset of SE by 1–14 days [ 14 , 15 , 16 ]. Therefore, our patient is suitable for the diagnosis of FIRES and NOSE. Additionally, criteria for electroencephalographic status epilepticus in patients without known epileptic encephalopathy were established based on the Salzburg consensus: (1) recurrence of epileptiform discharge frequency greater than 2.5 Hz, or (2) recurrent epileptiform discharges.
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