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Temperature Management in Acute Stroke

2008-10-31T15:51:00.000-07:00

Research Applied to Clinical Practice
by Robert C. Knies, RN MSN CEN
Section Editor

Temperature Management in Acute Stroke:
Why does it matter ?

If you are like me, I am inquisitive when I obtain "different" outcomes or data on my assessments of patients. This was happening to me when I assessed stroke patients and obtained elevated temperatures, I presumed that the patient had infarcted near the hypothalamus and that was causing the hyperthermia. I also began to recognize that these patients (those with elevated temperatures) were usually the ones who were already very debilitated on their arrival in the ED, and progressed to negative outcomes.
Since the beginning of the 1990’s, when stroke research gained its strength, causes for progression of strokes were investigated. Amongst the most controversial are hyperthermia and how the brain temperature (or core temperature) affects the progression and ultimate outcome of a stroke.

The first discussion came in relation to the common association of fever to infection. So several studies evaluated the presence of fever in acute stroke patients and whether a source of infection could be identified (Georgilis, Plomaritoglou, Dafni, Bassiakos & Vemmos, 1999). The focus became whether the patient was febrile on arrival or within the first 48 after admission. Some of the first results were; those who develop fever are older, suffer more severe strokes, the fevers were associated with invasive techniques and these febrile patients had poor outcomes. Beamer, Coull, Clark, Hazel. & Silberger (1995) discuss how patients who have an infectious process in effect when a stroke occurs are at a higher risk for detrimental outcomes.

Other researchers (Ginsberg & Busto, 1998) studied the effects of hyperthermia and ischemia on rat brains and came to the following conclusions:

Hyperthermia increases release of neurotransmitters (e.g., Glutamate) which causes increase in neuron energy use, specifically in areas of the penumbra.
Hyperthermia increases oxygen radial production.
Hyperthermia causes an increase in the openings of the blood brain barrier.
Hyperthermia causes increases in ischemic depolarizations (periinfarct depolarizations). Which means there is an increase of extracellular potassium and intracellular calcium, and this imbalance requires significant increases in cellular energy to restore homeostasis, which ultimately deteriorates penumbra and extends the infarct.
To relate this back to humans, these same researchers summarized some small studies and one large study (Reith, Jogensen, Pedersen, Nakayama, Raaschou, Jeppesen & Olsen, 1996) to conclude that elevated cerebral temperature occurring during a stroke will detrimentally affect severity, outcome and mortality.

To further investigate how hyperthermia during a stroke causes detrimental outcomes, researchers are investigating brain chemicals and their respective antagonists elevation(s) that occur in relation to stroke or hyperthermia. Castillo, Davalos, & Noya (1997) have shown that the neurotransmitter glutamate has been associated with progression of strokes by its excitatory effects and energy use by neurons. Fibrinogen has also been evaluated as a predictor of stroke occurrence or re-occurrence (Beamer, Coull, Clark, Hazel, & Silberger, 1995).

Castillo, Davalos, & Noya (1999) have been investigating glutamate concentrations in the cerebral spinal fluid (CSF) and its levels related to hyperthermia. They initially evaluated the levels of glutamate and glycine in CSF and plasma and how their levels affect progression of a stroke (Castillo, Davalos, & Noya, 1997). They concluded that elevated glutamate levels correspond with progression of strokes and physiologic deterioration with in the first 48 hours. Their current research added on to their initial hypothesis that glutamate affects progression of strokes, and took it to the next step to evaluate the relationship of hyperthermia and glutamate levels.

Fibrinogen and other proteins are known to elevate with tissue injury or infection and that its action affects the thromobotic activity in the intravascular space. Research has shown that during a stroke fibrinogen and other protein(s) production increases, and that they increase with or without infection presence (Syrjanen, Teppo, Valtonen et al, 1989; Ameriso, Wong, Quismorio, Fisher, 1991; Fassbender, Rossol, Kramer, et al., 1994). Ultimately this leads to increases in thrombi development and subsequent new infarcts or extension of existing infarcts.

Beamer, Coull, Clark, Hazel, & Silberger (1995) investigated how cytokines (such as; Interleukin [IL] 1, 6, and 11; tumor necrosis factor -a ; and transforming growth factor -b ) interact to regulate hepatic synthesis of fibrinogen and other acute phase proteins. What they present is that Interleukin 1 is a potent proinflammatory cytokine, that causes the vasculature to increase the ‘stickiness" of leukocytes and activate neutrophils, which will affect thrombi development. However, no increase of peripheral levels of IL-1 was found in a series of acute stroke patients who had no active infectious process in place (Fassbender, Rossol, Kramer, et al. , 1994). Comparatively, that same study showed that there were elevated levels of IL-6, which is produced by many cells following stimulation by IL-1. What is significant is that these elevated levels were found within 4 hours after onset of stroke, and were significantly correlated with the infarct volume and patient outcomes.

The true role of IL-6 in strokes is still undefined, but because of its anti-inflammatory functions and how it opposes the effects of IL-1 and stimulates production of their antagonists (IL-1RA), appear to be a key that needs further research.

There is significant controversy amongst practitioners regarding site selection for measuring temperature. The truest site for measuring core temperature is the hypothalamus. However, because access to that site is impractical, the next best is the tympanic, because it measures form the internal carotid artery, which supplies the hypothalamus. But many emergency practitioners do not trust the accuracy of the tympanic thermometer, and prefer oral or rectal. These two sites also have their disadvantages and inaccuracies. The issue with tympanics is technique not accuracy (Knies, 1999). Many of the studies reviewed use the axilla as their measuring site (Georgilis, Plomaraitoglou, Dafni, Bassiakos & Vemmos, 1999; Castillo, Davalos, & Noya, 1999; Castillo, Davalos, Marrugat,, & Noya, 1998; Azzimondi, Bassein, Nonino, Fiorani, Vignatelli, Re, &D’Alessandro, 1995). One study (Reith, Jogensen, Pedersen, Nakayama, Raaschou, Jeppesen & Olsen, 1996) used tympanic as their site of measurement. Schwab, Spranger, Aschoff, Steiner, & Hacke (1997) discuss how cerebral temperature can exceed core body temperature by 1.0° C to 2.1° C. Which supports the use of tympanic temperature even more.

Castillo, Davalos, Marrugat & Noya (1998), concluded that the greatest detriment from hyperthermia to an evolving stroke occurs within the first 24 hours. The outcomes were evaluated at 3 months post infarct. An important point in this study is that the hyperthermia was not related to an identified infection. The need for effective body temperature management during the first 12 hours was reinforced in a study by Jorgensen, Reith, Pedersen, Nakayama, & Olsen (1996).

Where does this take us next? Obviously, hyperthermia prior to or during a cerebral infarct lead to poor outcomes, so, do we work on markers and agents that control the effects of neurotransmitters and proteins that are stimulated by hyperthermia? Or do we just focus on the hyperthermia? Well, researchers are tackling both ends of the spectrum. There are agents being tested which try to arrest the effects of free radicals, interrupt the ion exchange and the energy required for it, and many others. An area that is now being tapped with human research is that of cooling of the brain, even down to 33° C. There have been some research studies done on this and the outcomes have been promising, however there is significant cost related to this and it is labor intensive.

In summary, research has shown that:

Hyperthermia (>37.5° C), either prior to or during a stroke negatively affects outcomes.
There are several chemicals and proteins that are released during hyperthermia and affect clotting action.
There are several neuro transmitters that are activated during a stroke that can expend energy and affect the extension of the infarct.
Hypothermia (33° C) has been shown in research to be beneficial to prevent further brain damage post insult.
Aggressive body and cerebral temperature management during the first 24 hours has been shown to be the most effective in preventing detrimental outcomes related to hyperthermia.
What does this mean to nursing? We need to incorporate regular temperature assessments in the plan of care for stroke patients. Some suggest every 2 hours (during first 24 hours) for those stroke patients who present normothermic. And for those who present hyperthermic, aggressive initial interventions (anti-pyretics, cooling measures, etc.) and Q1 hour subsequent assessments.

As we are learning more and more about the brain itself and how insults (strokes, trauma, disease, etc.) affect it immediately and potential outcomes, we will continue to see more and more research on these and other issues. We only need to keep our eyes open.

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References:

Ameriso, S.F., Wong, V.L.Y., Quismorio, F.P., & Fisher, M. (1991). Immuno-hematologic characteristics of infection –associated cerebral infarction. Stroke, 22, 1004-1009.

Azzimondi, G., Basasein, L., Nonino, F., Fiorani, L., Vignatelli, L., Re, G., & D’Alessandro, R. (1995) Fever in acute stroke worsens prognosis. Stroke, 26, 2040-2043.

Georgilis, K., Plomaritoglou, A., Dafni, U., Bassiakos, Y., & Vemmos, K. (1999). Aetiology of fever in patients with acute stroke.
Journal of Internal Medicine, 246,. 203-209.

Beamer, N.B., Coull, B.M., Clark, W.M., Hazel, J.S., & Silberger, J.R. (1995). Interleukin-6 and Interleukin-1 receptor antagonist in acute stroke. Annals of Neurology, 37 (6), 800-805.

Castillo, J., Davalos, A., & Noya, M. (1997). Progression of ischaemic stroke and excitotoxic aminoacids. Lancet, 349, 79-83.

Castillo, J., Davalos, A., Marrugat, J., Noya, M. (1998). Timing for fever-related brain damage in acute ischemic stroke. Stroke, 29, 2455-2460.

Castillo, J., Devalos, A., & Noya, M. (1999). Aggravation of acute ischemic stroke by hyperthermia is related to an excitiotoxic mechanism. Cerebrovascular Diseases, 9, 22-27.

Fassbender, K., Rossol, S., Kammer, T., Daffertshofer, M., Wirth, S., Dollman, M., & Hennerici, M. (1994). Proinflammatory cytokines in serum of patients with acute cerebral ischemia: kinetics of secretion and relation to the extent of brain damage and outcome of disease.
Journal of Neurological Science, 122 (2), 135-139.

Ginsberg, M.D. & Busto, R. (1998). Combating hyperthermia in acute stroke: A significant clinical concern. Stroke, 29, 529-534.

Knies, R. (1999). Temperature Measurement in Acute Care: The Who, What Where, When, How, Why and Wherefore’s.
Accepted for publication in Med-Surg Nursing. Publication date to be announced

Reith, J., Jorgensen, H.S., Pedersen, P.M., Nakayama, H., Raaschou, H.O., Jeppesen, L.L., & Olsen, T.S. (1996). Body temperature in acute stroke: Relation to stroke severity, infarct size, mortality, and outcome. Lancet, 347, 422-425.

Syrjanen, J., Teppo, A.M., Valtonen, V.V., Livanainen, M., & Maury, C.P. (1989). Acute phase response in cerebral infarction.
Journal of Clinical Pathology, 42 (1), 63-68.

Schwab, S., Spranger, M., Aschoff, A., Steiner, T., & Hacke, W. (1997). Brain temperature monitoring and modulation in patients with severe MCA infarction. Neurology, 48, 762-767.

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"Research Applied to Clinical Practice: Temperature Management in Acute Stroke: Why does it matter ?"
[http://ENW.org/Research-StrokeTemp.htm]
is a webarticle by Robert C. Knies, RN MSN CEN [bknies@stevenshealthcare.org]
©Robert C. Knies, RN MSN CEN
presented by Emergency Nursing World ! [http://ENW.org]
Tom Trimble, RN [Tom@ENW.org] ENW Webmaster
ENW name, logos, and layout ©Tom Trimble, RN

Retrieved from http://enw.org/Research-StrokeTemp.htm on October 31 2008

Invasive Hemodynamic Monitoring

2008-10-13T13:31:00.000-07:00

Cardiac Output
Cardiac Output (in liters/minute) is defined as the amount
of blood ejected from the ventricle (primarily the left
ventricle) in a minute. Cardiac output is the term that is
used when discussing the pumping effectiveness and
ventricular function of the heart – the cardiac performance.

Stroke Volume
Stroke volume (SV) is the amount of blood ejected from the
left ventricle each time the ventricle contracts. Stroke
volume is the difference between end-diastolic volume
(EDV), the amount of blood in the left ventricle at the end
of diastole, and end-systolic volume (ESV), blood volume in
the left ventricle at the end of systole. Normal stroke volume
is 60 to 100 ml/beat.
SV = EDV – ESV

Preload
Preload refers to the amount of myocardial fiber stretch at
the end of diastole. Preload also refers to the amount of
volume in the ventricle at this phase. It is very difficult to
actually measure fiber length or volume at the bedside. It
has been clinically acceptable to measure the pressure
required to fill the ventricles (LVFP) as a measure of left
ventricular end diastolic volume (LVEDV) or fiber length.

Afterload
Afterload refers to the resistance, impedance, or pressure
that the ventricle must overcome to eject its blood volume.
Afterload is determined by a number of factors, including:
volume and mass of blood ejected, the size and wall
thickness of the ventricle, and the impedance of the
vasculature. In the clinical setting, the most sensitive
measure of afterload is systemic vascular resistance (SVR)
for the left ventricle and pulmonary vascular resistance
(PVR) for the right ventricle. In reality, the resistance of the
vascular system is derived from the measurements of cardiac
output (CO) and mean arterial pressure (MAP). The
formulas for calculating afterload look at the gradient
difference between the beginning (inflow) of the circuit and
the end (outflow) of the circuit.

Review of Hemodynamic Monitoring

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Temperature Management in Acute Stroke

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Invasive Hemodynamic Monitoring