Study of PbiO2 Variation by Body Temperature and Capnia in Severe Head Trauma Patients Treated With Targeted Temperature Control

2019-10-04 08:31:38 | BioPortfolio


Serious head trauma is a common and pathology and responsible of high morbidity and mortality. The major challenge, from the very first hours, is to limit cerebral ischemia by controlling secondary brain injury factors.

These parameters must be integrated early in order to guide the better cerebral resuscitation. Brain monitoring is multimodal:transcranial Doppler, intracranial pressure sensor, cerebral tissue pressure in O2.

In the case of refractory intracranial hypertension to well-conducted medical treatment, targeted temperature control showed its efficacy on the control of intracranial pressure.

There are few data in the literature on PbtO2 modifications during therapeutic hypothermia.

PbtO2 monitoring is now commonly used according to literature data, showing the benefit of the latter but the interpretation of its values during the phase of targeted temperature control is not known. Due to the lack of data on the variation of values of PbtO2 during the hypothermia phase, values falsely comfortable or falsely weak could lead respectively to a lack of support of an episode of tissue hypoxia or the introduction of unjustified aggressive therapeutics.


This is a prospective, non-interventional, mono-centric study at surgical intensive care unit at Brest medical university hospital.

This study will be conducted in a reference center for the management of patients with traumatic brain injury, who is used to collect prospective data.

The clinical research structure of Brest Medical University allows data analysis and the investigators have the clinical knowledge for their interpretation.

After verification of the inclusion and non-inclusion criteria and information of the family (parent or relative) or the holder of parental authority, patients will be included in order of arrival in the service.

The population studied is the trauma brain injured patients with an initial Glasgow coma scale of less than 8 at pre-hospital care or neurological impairment with Glasgow Coma Scaleless than 8 in the first 24 hours after admission to intensive care.

The installation of a intra-cranial pressure/ PbtO2 probe (INTEGRA Licox PtO2 monitor) is performed by the neurosurgeon according to the protocol service.

Approximately 30 patients were monitored with a PbtO2 sensor in 2018 in the Surgical intensive care unit at Brest Medical University Hospital.

After verification of inclusion and non-inclusion criteria, oral and written information will be given to parent or relative of the patient. A no-objection form will be sent to the patient as soon as possible to confirm his participation.

Follow-up of the patient is carried out until discharge of intensiv care unit. The duration of participation in the study is the duration of treatment by targeted temperature control, very variable depending on the clinical evolution of patients, from 1 day to more than one week. The management of the patients included in this study is not modified in relation to the treatment usually recommended in the intensiv care unit.(based on French recommendation).

In order to describe the variations of PbtO2 values, the PbtO2 values are collected at time T0 before induction of targeted temperature control, at time T1: the first hour of the targeted temperature control phase (<35 ° C) at time T2: during the phase of temperature stability (<35 ° C) defined as two successive hours of hypothermia, at time T3 defines as 6 hours at a stable temperature in hypothermia, then once a day up to the end of the targeted temperature control phase.

Then the values of PtiO2 are collected during the daily hypercapnia test during targeted temperature control phase.

Demographic data collected are age, sex, weight, height, and data on gravity at the entrance: IGS2 score, first Glasgow Coma scale score, time to CT-scan and IMPACT score.

Data on time to PbtO2 probe and ICP probe insertion and time to equilibration of PbtO2 value.

Data were collected at all times, T0, T1, T2, T3 (as defined above) and daily: the body temperature (collected by esophageal thermal probe), the cerebral perfusion pressure, the value of PtiO2 / PIC, FiO2 / etCO2, an arterial blood sample, a blood count and a daily ionogram,daily transcranial Doppler data, doses of amines, curares and sedation.

During the stay were collected: time to and nature of the surgical procedure and realization of a craniectomy or not, position of the PtiO2 probe on a control scanner, an at the discharge: prognosis score (GOS-E),lenght of stay in intensive care unit, death in intensive care unit.

Study Design


Severe Brain Injury






University Hospital, Brest

Results (where available)

View Results


Published on BioPortfolio: 2019-10-04T08:31:38-0400

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Medical and Biotech [MESH] Definitions

Prolonged unconsciousness from which the individual cannot be aroused, associated with traumatic injuries to the BRAIN. This may be defined as unconsciousness persisting for 6 hours or longer. Coma results from injury to both cerebral hemispheres or the RETICULAR FORMATION of the BRAIN STEM. Contributing mechanisms include DIFFUSE AXONAL INJURY and BRAIN EDEMA. (From J Neurotrauma 1997 Oct;14(10):699-713)

A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.

Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.

Conditions characterized by persistent brain damage or dysfunction as sequelae of cranial trauma. This disorder may result from DIFFUSE AXONAL INJURY; INTRACRANIAL HEMORRHAGES; BRAIN EDEMA; and other conditions. Clinical features may include DEMENTIA; focal neurologic deficits; PERSISTENT VEGETATIVE STATE; AKINETIC MUTISM; or COMA.

An injury in which the damage is located on the opposite side of the primary impact site. A blow to the back of head which results in contrecoup injury to the frontal lobes of the brain is the most common type.

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