0000000000973049
AUTHOR
Daniel Agustin Godoy
Diez mandamientos fisiológicos a lograr durante el traumatismo craneoencefálico grave
Resumen Los avances en la monitorizacion cerebral multiparametrica han permitido ahondar en el conocimiento de la fisiopatologia del traumatismo craneoencefalico, y en como la terapeutica disponible puede modularla. Para ello, se antoja imprescindible conocer e interpretar una serie de principios fisiologicos y fisiopatologicos basicos que propician, por un lado, un entorno metabolico cerebral adecuado para prevenir un incremento de la lesion cerebral primaria y favorecer su recuperacion, y por otro lado, permiten adaptar de forma individualizada los recursos terapeuticos a la situacion concreta del paciente. En el presente articulo se exponen, en forma de decalogo, sustentados en dichas no…
Extubation in neurocritical care patients: the ENIO international prospective study
Purpose: Neurocritical care patients receive prolonged invasive mechanical ventilation (IMV), but there is poor specific information in this high-risk population about the liberation strategies of invasive mechanical ventilation. Methods: ENIO (NCT03400904) is an international, prospective observational study, in 73 intensive care units (ICUs) in 18 countries from 2018 to 2020. Neurocritical care patients with a Glasgow Coma Score (GCS) ≤ 12, receiving IMV ≥ 24 h, undergoing extubation attempt or tracheostomy were included. The primary endpoint was extubation failure by day 5. An extubation success prediction score was created, with 2/3 of patients randomly allocated to the training cohort …
Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”
AbstractMaintaining an adequate level of sedation and analgesia plays a key role in the management of traumatic brain injury (TBI). To date, it is unclear which drug or combination of drugs is most effective in achieving these goals. Ketamine is an agent with attractive pharmacological and pharmacokinetics characteristics. Current evidence shows that ketamine does not increase and may instead decrease intracranial pressure, and its safety profile makes it a reliable tool in the prehospital environment. In this point of view, we discuss different aspects of the use of ketamine in the acute phase of TBI, with its potential benefits and pitfalls.
Additional file 4 of Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”
Additional file 4: Table S1. Comparative cost of 24 hours intravenous infusion of sedative and analgesic drugs. mg: milligrams; kg: kilograms; h: hour; min: minute; mcg: micrograms
Ten physiological commandments for severe head injury
Advances in multiparametric brain monitoring have allowed us to deepen our knowledge of the physiopathology of head injury and how it can be treated using the therapies available today. It is essential to understand and interpret a series of basic physiological and physiopathological principles that, on the one hand, provide an adequate metabolic environment to prevent worsening of the primary brain injury and favour its recovery, and on the other hand, allow therapeutic resources to be individually adapted to the specific needs of the patient. Based on these notions, this article presents a decalogue of the physiological objectives to be achieved in brain injury, together with a series of …
The effects of arterial CO2 on the injured brain: Two faces of the same coin
Serum levels of carbon dioxide (CO2) closely regulate cerebral blood flow (CBF) and actively participate in different aspects of brain physiology such as hemodynamics, oxygenation, and metabolism. Fluctuations in the partial pressure of arterial CO2 (PaCO2) modify the aforementioned variables, and at the same time influence physiologic parameters in organs such as the lungs, heart, kidneys, and the gastrointestinal tract. In general, during acute brain injury (ABI), maintaining normal PaCO2 is the target to be achieved. Both hypercapnia and hypocapnia may comprise secondary insults and should be avoided during ABI. The risks of hypocapnia mostly outweigh the potential benefits. Therefore, i…
Extubation strategies in neuro-intensive care unit patients and associations with outcomes
Background Prolonged invasive ventilation is common in patients with severe brain injury. Information on optimal management of extubation and on the use of tracheostomy in these patients is scarce. International guidelines regarding the ventilator liberation and tracheostomy are currently lacking. Methods The aim of 'Extubation strategies in Neuro-Intensive care unit patients and associations with Outcomes' (ENIO) study is to describe current management of weaning from invasive ventilation, focusing on decisions on timing of tracheal extubation and tracheostomy in intensive care unit (ICU) patients with brain injury. We conducted a prospective, international, multi-centre observational stud…
Additional file 5 of Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”
Additional file 5: Figure S5. Potential indications of ketamine continuous infusion in traumatic brain injury.
Additional file 1 of Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”
Additional file 1: Figure S1. Systemic and cerebral consequences of pain and agitation. SIRS: systemic inflammatory response syndrome; Tº: central temperature; HR: heart rate; pa02: oxygen arterial pressure; paCO2: carbon dioxide arterial pressure; coagul: coagulation alterations; IAP: intraabdominal pressure; UO: urinary output; Hypovol: hypovolemia; Hypergly: hyperglycemia; ICP: intracranial pressure; CBF: cerebral blood flow; CPP: cerebral perfusion pressure; CMO2: cerebral metabolic rate of oxygen; CMGl: cerebral metabolic rate of glycemia; CBV: cerebral blood volume.
Additional file 2 of Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”
Additional file 2: Figure S2. Sedation and Analgesia ideal level.
Additional file 3 of Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”
Additional file 3: Figure S3. Mechanisms of neuroprotection by ketamine. Ketamine is a “glutamate modulator.” It exerts its effect basically at two levels: a) presynaptic, inhibiting the release of glutamate and b) post-synaptic, acting as a competitive blocker of N-Methyl-D-Aspartate receptors, thereby excitotoxic injury through inhibiting the entry of calcium into cells, the formation of nitric oxide and oxygen free radicals. Modulates glucose metabolism and the generation of mitochondrial ATP. Inhibits the apoptotic phenomenon. Additionally, it inhibits spreading depolarizations and acts as an antithrombotic and anti-inflammatory by inhibiting platelet aggregation and the production and …