Metabolism and nutrition
Principle Investigator: Torbjörn Karlsson
Background: The scientific background and evidence for nutritional efforts after severe head trauma is weak, but observational studies show that many of these patients (68% in our material) suffer malnutrition according to specific criteria during the course of treatment. We have observed that this affects the rehabilitation of this group of patients.
We aim to explore the course of energy balance the first months after head injury and to develop a clinical method to measure and predict energy expenditure after traumatic brain injury.
We have used daily indirect calorimetry and the doubly labeled water technique to assess energy expenditure in a group of TBI patients. We are using repeated CT scans to study the effects on muscle and fat catabolism and preliminary results show different effects on peripheral fat and intraabdominal fat deposits, while muscular catabolism seem to be more general.
SAH can give rise to an intracerebral metabolic crisis and we have observed that changes in the blood glucose by insulin injection (aiming at a tight glucose control) might give rise to a potentially to low intracerebral glucose concentration. We have also observed an increased level of non-transmittor amino acids 3-4 days after the onset of SAH, with a difference between non-awake patients with less affected consciousness. Possibly as a result of the intracerebral repair process.
Questions: What is the EE in the acute phase after SAH and how does it change over time?Is there a relation between EE and the severity of SAH as measured with Fisher, WFNS and the development of delayed ischemic neurologic deficits? Is there a relation between EE and the brains metabolism as measured with intracerebral microdialysis?Is there a relation between the EE, the endocrinological reactions and systemic complications?Is there a relation between the EE and the cerebral blood flow as measured with Xe-enhanced CT?
We are using clinical data, hormonal analyses, intracerebral microdialys and general hemodynamic monitoring completed with indirect calorimetry and radiology to answer the above questions. Preliminary results from an ongoing study (n 83 SAH patients) show increased p-NT-proBNP after SAH, probably both from the heart and the brain, and, the results indicate that p-NT-proBNP could be used as a marker of more severe SAH disease.
Members in the group 2013
Torbjörn Karlsson, MD, PhD
Elisabeth Ronne-Engström, MD, PhD
Jörgen Borg, Professor Karolinska Intitutet
Karolina Krakau, RN, PhD
Maria Zetterling, MD, PhD
Christoffer Nyberg, MD, PhD student
In collaboration with
Anders Magnusson, Professor Radiology Uppsala
Lars Ellegård, MD, PhD Gothenburg
Dissertations during 2012
Elisabet Nilsen, Associate Professor, Pharmacometry, Department of Pharmaceutical Biosciences