Neurogenic Fever Management

Topics: Traumatic brain injury, Intracranial pressure, Cerebral blood flow Pages: 5 (1781 words) Published: April 1, 2009
Developing Adult Critical Care (GM6314) Neurogenic fever management following traumatic brain injury patients Word count: The measurement of body temperature and treatment of fever have long been considered to be within the domain of nursing practice. Intensive care unit (ITU) nurses are well positioned to lead the way to best practices for fever management '' grounded in current evidence for their vulnerable patients with TBI. Introduction On the other hand, fever in the early stage of TBI might be of infectious cause rather than neurogenic(Thompson,2003) Progress in neuroscience over the past decade has enabled a better understanding of the neurobiological basis of fever. Apart from being a symptom, NF is also associated with neurologic complications, which are considered to be triggered mainly as a result of increased local cytokines activity which sets in motion a cascade of pathophysiological changes (inflammation, release of excitotoxic amino-acids, and production of free radicals) with delayed clinical presentation. Knowledge regarding these dynamic events is essential for a better understanding of fever management (new pharmacological avenues and non-pharmacological strategies), which are being developed to improve the outcome of this silent devastating condition. Physiology The hypothalamus and preoptic regions play a crucial role in integrating and initiating autonomic thermoregulatory mechanisms such as skin vasomotor responses, sweating, salivation, and shivering. On the other hand,there are cortical and subcortical areas that influence the activity of the hypothalamus includes: the orbito-frontal, anterior temporal, insular regions, amygdale (particularly the central nucleus), the periaqueductal gray, and the nucleus of the tractus solitarius, along with cerebellar nucleus. Damage to these areas due to the primary injury or from the secondary processes, releases the control of vegetative functions and results in disruption of overall autonomic balance. ( Kisner et al., 2006) Based on Monroe-Kelly hypothesis of intracranial pressure dynamics describes the skull as a closed system with 3 components: brain (80%), blood (12%) and CSF (8%) which coexists in a state of volume equilibrium ( Hickey 1997).The combination of these three volumes creates a pressure within the skull known as the ICP. Cerebral edema or any volume increase in one of the cranial constituents must be compensated by a decrease in volume of another, in order to maintain a constant ICP between o- 15 mmHg. {draw:frame} (Della Corte) Small increases in brain volume do not lead to immediate increase in ICP due to the ability of the CSF to be displaced into the spinal canal, as well as the slight ability to stretch the “falx cerebri” between the hemispheres and the tentorium, as well as between the hemispheres and the cerebellum. However, once the ICP has reached around 25 mmHg, small increases in brain volume can lead to marked elevations in ICP. CPP and CBF are directly related to ICP and are normally closely controlled through autoregulatory mechanisms (pressure and metabolic), in order to provide oxygen and nutrients to the brain. Hickey (1997) consider these mechanisms “the intrinsic ability of cerebral blood vessels to dilate or constrict in response to changes in the brains environment” despite fluctuating blood pressure and intracranial volumes. Also, these mechanisms are influenced by carbon dioxide (CO2), hydrogen (H+) and oxygen (O2) concentrations. Changes in these concentrations will alter the CBF due to changes in the cerebral blood vessels. (Guyton2000). A raised ICP not only impairs the CBF and CPP, but will interfere with the thermoregulatory role of hypothalamus and inhibits the body ability to regulate its own temperature, leading to NF. (Sherman, 1990) A rised fall in CPP below 12ml/mg/min produces irreversible damage to the neuronal cells. Physiological manifestations of fever include increased oxygen...

References: Agrawal, A., Timothy, J., Thapa, A.,(2007) Neurogenic fever. Singapore Med J_._ 48 (6), pp.492-495 http://www.ferne.org/Lectures/bis01%20pathophysiology%20intro.htm, visited on March 2008 Chen, F,W,H. (2000) Prevention of secondary brain injury. Crit Care Nurs. 20. pp.18 ' ' 27. Geffroy, A., Bronchard, R., Merckx, P., et al. (2004) Severe traumatic head injury in adults: which patients are at risk of early hyperthermia? Intensive Care Medicine.30. pp.785-790. Hickey, J,V., (1997). Craniocerebral injuries. The clinical practice of Neurological and Neurosurgical Nursing, (4th ed). Philadelphia: Lippincott. pp.314-323. Guyton, A,C., Hall, J,E., (2000) Cerebral blood flow, the cerebral spinal fluid and brain metabolism. Textbook of medical physiology, Elsevier, Philadelphia. pp. 663 ' ' 677. Kishner, S., Augustin, J., Strum, S., Post head injury autonomic complications. Available at: http://www..emedicine.com/pmr/topic108.htm. Accessed on March , 2008. Natale, J, E., Joseph, J,G., Helfaer, M, A., Shaffner, D, H., (2000).Early hyperthermia after traumatic brain injury in children: risk factors, influence on length of stay, and effect on short-term neurologic status. Critical Care Medicine. 28. pp.2608-2615. Schmutzhard, E., Engelhardt, K., Beer, R., Brossner, G., Pfausker, B.,Spiss, H., Unterberger, I., Kampfl, A. (2002) Safety and efficacy of a novel intravascular cooling device to control body temperature in neurologic intensive care patients: a prospective pilot study_. Critical Care Medicine._ 30. pp. 2481 ' ' 2488. Marion, D,W. (2001) Therapeutic moderate hypothermia and fever. Curr.Pharmaceutical Design 7. pp. 1533 ' ' 1536. Thorley, R,R., Wertsch, J, J., Klingbeil G, E.(2001) Acute hypothalamic instability in traumatic brain injury: a case report. Arch Phys Med Rehabil.;82:246 ' ' 249. Zauner, A., Daugherty, W, P., Bullock, M, R., Warner, D, S. (2002) Brain oxygenation and energy metabolism: part I—biological function and pathophysiology. Neurosurgery. 51. pp. 289 ' ' 301 Schwartz, S., Hδfner, K., Med, C., Aschoff, A., Schwab, S., (2000) Incidence and prognostic significance of fever following intracerebral hemorrhage. Neurology. 54. pp. 354-61. Appendix I: Terms related to the neurogenic fever management following TBI Pressure regulation: Dynamic state of vasoconstriction and vasodilatation to maintain constant CBF CBF remains constant despite a wide range of Mean arterial pressure Metabolic regulation: CO2 is most potent vasodilator affecting the brain Hyperthermia increases use of oxygen and glucose High hydrogen concentration Venous outflow: Cerebral veins have no valves, thin walls and little muscle coat Susceptible to compression Increases in intra-abd or thoracic alter venous return Cerebral perfusion pressure: CPP = MAP ' ' ICP CPP: 70 ' ' 100 mmHg
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