Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition

Carney, Nancy; Totten, Annette M; O’Reilly, Cindy; Ullman, Jamie S.; Hawryluk, Gregory; Bell, Michael J.; Bratton, Susan L.; Chesnut, Randall M.; Harris, Odette A.; Kissoon, Niranjan; Rubiano, Andrés M.; Shutter, Lori; Tasker, Robert C.; Vavilala, Monica S.; Wilberger, Jack E.; Wright, David W.; Ghajar, Jamshid

doi:10.1227/neu.0000000000001432

Cited by 2,629 publications

(2,417 citation statements)

References 39 publications

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“…Although hypothermia has been successfully studied in many single clinical trials in patients after head injuries, larger, randomised multi-centre trials have not demonstrated any benefits associated with this form of treatment [50]. Moreover, the fourth edition of guidelines of the Brain Trauma Foundation on severe posttraumatic brain injury of 2017 does not recommend prophylactic hypothermia in patients with diffuse brain injury [51].…”

Section: Application Of Hypothermiamentioning

confidence: 99%

Zaburzenia termoregulacji pochodzenia ośrodkowego — jak diagnozować i leczyć

Zawadzka¹,

Szmuda²,

Mazurkiewicz-Bełdzińska³

2017

Anaesthesiol Intensive Ther

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Fever is a common symptom in the Intensive Care Unit. At least half of febrile episodes are caused by infection. Excluding infectious etiology and other non-infectious causes of fever, especially in patients with central nervous system (CNS) disorders, attention should be paid to disturbances of thermoregulatory centre. In particular, subarachnoid haemorrhage, cerebral trauma, along with ischaemic or haemorrhagic stroke are strongly associated with the development of central fever. Proper, speedy diagnosis of the cause of fever makes it possible to implement preventive measures against the harmful effects of hyperthermia on the CNS and to avoid the consequences of inappropriate treatment. The aim of this review is to present the current treatment options for the management of central fever and to analyze recent recommendations for the treatment of hyperthermia, including the use of hypothermia. The recommendations of American and European associations are inconsistent, mainly due to the lack of randomized clinical trials confirming the effectiveness of such treatment. The diagnosis of central fever is still made by the exclusion of other causes. The authors of the review intended to present the characteristic features of central fever, differentiating this state from infectious fever and also analyze the presence of central fever in particular neurological diseases. It seems particularly important to establish diagnostic criteria for central fever or to find diagnostic markers. It is also necessary to conduct further randomized clinical trials evaluating the indications for treatment of hyperthermia.

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Section: Application Of Hypothermiamentioning

confidence: 99%

Zaburzenia termoregulacji pochodzenia ośrodkowego — jak diagnozować i leczyć

Zawadzka¹,

Szmuda²,

Mazurkiewicz-Bełdzińska³

2017

Anaesthesiol Intensive Ther

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“…Сегодня установлено, что в основе вторичных повреждений мозга после травмы лежат гемодинамические факторы [5]. Очевидно, что и многие симптомы при травмах головы обусловлены также этими нарушениями.…”

Section: Cerebrovascularunclassified

Cerebrovascular reactivity in patients with cerebral contusion and its possible pharmacological correction

et al. 2016

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Aim. Evaluation of dimephosphone as a medication for correction of cerebrovascular reactivity damage in patients with acute traumatic brain injury of mild to moderate severity.Methods. The study included 40 patients with acute traumatic brain injury admitted to the Department of Neurosurgery of Kazan City Clinical Hospital №7. All patients were divided into 2 groups: patients who did not receive dimephosphone were included in group 1, in group 2 patients received drug therapy identical to that in group 1 but with additional 15% solution of dimephosphone 15 ml 3 times a day for 12 days. Evaluation of cerebral blood flow was conducted by transcranial Doppler with the use of analyzer of blood flow velocity «Sonomed 300M». Patients underwent daily functional tests (compression test, hypercapnic test, hypocapnic test) during the days 1 to 12 of hospital stay.Results. The conducted study confirms disorders of cerebrovascular reactivity in patients with acute traumatic brain injury. Also it was found that patients treated with dimephosphone as part of comprehensive therapy at a dose of 15 ml of 15% solution 3 times a day, cerebrovascular reactivity indices (index of vasomotor reactivity, overshoot coefficient) recovered significantly faster.Conclusion. All patients in the acute period of traumatic brain injury with cerebral contusion have disorders of cerebrovascular reactivity; recovery of cerebrovascular reactivity in patients with traumatic brain injury is accelerated by inclusion of dimephosphone in comprehensive treatment.

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“…Although mannitol has been recommended as the first-choice hyperosmotic agent over hypertonic saline (10), recent recommendations have not found sufficient evidence to identify the optimal agent or their optimal method of administration (i.e. dose and bolus vs. continuous infusion) in patients with severe traumatic brain injury (11).…”

mentioning

confidence: 99%

The Complex Process of Haemostasis and Interactions due to Hyperosmotic Fluids

Granell¹,

Llau²

2017

Turk J Anaesth Reanim

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N atural haemostasis includes a variety of physiological events by which bleeding stops in case of vascular injury. Haemostasis is a complex process that involves several steps to achieve the final objective of haemorrhage cessation. Classically, the first step is the constriction of injured blood vessels to decrease local blood flow, leading to platelet adhesion and aggregation, which are referred to as 'primary haemostasis'. Afterwards, the process of fibrin formation and stabilisation begins, referred to as 'secondary haemostasis', which involves many intermediate enzymatic reactions with coagulation factors. These steps have a feedback restricting haemostasis to prevent thrombotic events through the activation of the fibrinolytic system that allows the beginning of the repair of the vascular and tissue defect (1).This course of haemostatic events has been explained by developing theories to elucidate all interactions between platelets, coagulation factors via the waterfall model, cofactors without enzymatic activity, antithrombotic mechanisms, and so on. In previous years, the cell-based model of haemostasis, in which the endothelium has a central role, has been accepted because of its best explanation of haemostasis. In this model, which was first proposed in 2001 (2), three overlapping phases can be differentiated. In the initiation phase, which is the first phase, coagulation starts when the vasculature is injured and subendothelial cells expose tissue factor (TF), which is the key initiator of haemostasis, that binds to coagulation factor VII, leading to its activation to FVIIa. The TF/FVIIa complex begins the activation of other coagulation factors, with the final objective of the formation of small amounts of thrombin (3). In the amplification phase, which is the second phase, thrombin activates platelets that have adhered to the site of injury and several coagulation factors. They bind to thrombogenic platelet surfaces and intensify and amplify prothrombinase activity (4). In the third phase (propagation phase) activated factors on catalytic platelet surfaces activate prothrombin (factor II) resulting in a massive generation of thrombin (factor IIa). The generated 'thrombin burst' converts fibrinogen into fibrin to form a sufficiently large clot. In the final step, thrombin-activated factor XIII (FXIIIa) catalyses the formation of crosslinks between fibrin fibres to form an elastic and stable fibrin clot (5).This 'perfect system' is disrupted in current clinical practice by the administration of several drugs. The most commonly known are antiplatelet and anticoagulant agents, but some others can also disturb coagulation. For example, if the infusion of large amounts of fluids is needed to restore intravascular volume and maintain tissue perfusion when an important blood loss occurs, a nonspecific coagulopathy due to the dilution of coagulation factors and platelets could impair the coagulation. It is related to the amount of infused fluid rather than to its type.Nevertheless, in addition to this dilut...

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Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition

Cited by 2,629 publications

References 39 publications

Zaburzenia termoregulacji pochodzenia ośrodkowego — jak diagnozować i leczyć

Zaburzenia termoregulacji pochodzenia ośrodkowego — jak diagnozować i leczyć

Cerebrovascular reactivity in patients with cerebral contusion and its possible pharmacological correction

The Complex Process of Haemostasis and Interactions due to Hyperosmotic Fluids

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