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 Table of Contents  
Year : 2021  |  Volume : 3  |  Issue : 1  |  Page : 11

Diffusion-Limited Brain PtiO2 of the Penumbra in Periclot Area after Intracerebral Hemorrhage

1 Department of Neurology, Critical Care Unit, Regions Hospital, Saint Paul, MN, USA
2 Center of Biomedical Research (CIB), Universidad de Cartagena, Cartagena, Colombia

Date of Submission05-Nov-2020
Date of Acceptance23-Jul-2021
Date of Web Publication09-Nov-2021

Correspondence Address:
Dr. Luis Rafael Moscote-Salazar
Universidad de Cartagena, Cartagena
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jtccm.jtccm_22_20

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How to cite this article:
Janjua T, Moscote-Salazar LR. Diffusion-Limited Brain PtiO2 of the Penumbra in Periclot Area after Intracerebral Hemorrhage. J Transl Crit Care Med 2021;3:11

How to cite this URL:
Janjua T, Moscote-Salazar LR. Diffusion-Limited Brain PtiO2 of the Penumbra in Periclot Area after Intracerebral Hemorrhage. J Transl Crit Care Med [serial online] 2021 [cited 2023 Mar 31];3:11. Available from: http://www.tccmjournal.com/text.asp?2021/3/1/11/330191

The preservation of brain tissue after brain injury is the mainstay of neurocritical care management. From the primary lesion, the blood flow is disrupted, altering the supply of glucose and oxygen to the brain tissue. Monitoring brain oxygenation using direct and continuous techniques has been a reliable tool to provide information in real time regarding cerebral hypoxia.[1] Oxygen delivery and consumption can be evaluated by evaluating brain tissue partial tension of oxygen (PtiO2) level.

A 52-year-old right-handed male patient was brought to the emergency department with a sudden loss of consciousness, right-sided weakness, and severe hypertension. He was not awake but able to protect his airway and moving left side. An emergent computed tomography (CT) head was done showing right basal ganglia intracerebral hemorrhage with 6 mm shift. While shifting back to ED, he declined and required emergent intubation. Due to 6 mm shift, the intracranial pressure (ICP) monitor (Neurovent-Pto, Raumedic) was placed to follow both ICP and PtiO2. The next day his PtiO2 was 5 mmHg. A repeat CT head showed the placement of the tip of the catheter in the penumbra area. At that stage, 100% FiO2 challenge was given to confirm the location of the tip in the penumbra. After 10 min, PtiO2 went to 31 mmHg and stayed there confirming that the tip was in the vulnerable part of the area next to the collection of blood and PtiO2 was diffusion limited rather than perfusion [Figure 1].
Figure 1: Change of PtiO2 from 5.4 mmHg to 30.2 mmHg after 10 min of 100% FiO2 challenge, confirming diffusion limitation in the penumbra area

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The evaluation of the PtiO2 reflects the diffusion of oxygen in the brain tissue. This is reflective of driving pressure of oxygen to neuronal mitochondria. PtiO2 monitoring is an additional component for multimodal monitoring in the neurocritical patient.[2] Obviously, it is a technique that helps us establish treatment guidelines. Neuromonitoring is not a treatment and there is no strong evidence to support that its implementation improves the outcome. The diffusion of oxygen in the cerebral parenchyma, the consumption of cellular oxygen, and the cerebral perfusion maintain a balance that can be evaluated by employing PtiO2. Alterations of this parameter can be identified even in the context of ICP and normal cerebral perfusion pressure. In patients with brain injury, the presence of critical PtiO2 values is associated with a worse outcome. The location of the PtiO2 catheter is done by locating it in the healthy tissue or the nearby twilight area while avoiding areas of bleeding and contusion to limit the measurements altered by artifacts.[3] Diffusion-limited hypoxia associated with low PtiO2 values is related to cerebral edema. Our case reflects the relevance of understanding the pathophysiological events that occur at the perilesional level. The unfavorable neurologic outcome has been observed in patients with long-term low PtiO2 that represents an alteration of the global supply of glucose and oxygen.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

  References Top

Kett-White R, Hutchinson PJ, Czosnyka M, Boniface S, Pickard JD, Kirkpatrick PJ. Multi-modal monitoring of acute brain injury. Adv Tech Stand Neurosurg 2002;27:87-134.  Back to cited text no. 1
De Georgia MA. Brain tissue oxygen monitoring in neurocritical care. J Intensive Care Med 2015;30:473-83.  Back to cited text no. 2
Tran-Dinh A, Depret F, Vigué B. Brain tissue oxygen pressure, for what, for whom? Ann Fr Anesth Reanim 2012;31:e137-43.  Back to cited text no. 3


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