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Weekly UpdatesABSTRACT
Neuromonitoring with the microdialysis technique is now being utilized at the bedside. Cerebral metabolism monitoring enables identification of clinical events hours or even days before clinical examination changes, providing clinical staff an opportunity for earlier intervention. Cerebral microdialysis also allows clinicians to evaluate the impact of therapeutics on cerebral metabolism and certain metabolic patterns, which can trigger specific alerts and/or clinical protocols. Cerebral metabolism monitoring through microdialysis can guide clinicians to institute therapeutic measures that prevent the occurrence of secondary injury. This article focuses on the state-of-the-art application of cerebral microdialysis, the rationale for its use, and the nursing implications of this technique.
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Patients experiencing neurological injury and diseases often have poor outcomes. Much of the care currently provided to these patients in the intensive care unit (ICU) is supportive in nature. Currently, serial neurological examinations are the primary method of identifying changes in the patient's neurological condition. Unfortunately, by the time a patient exhibits a neurological deficit, brain tissue may have already sustained irreparable damage. Newer methods of identifying secondary complications that jeopardize at-risk brain tissue are vital to improving outcomes from brain injury and diseases.
Basic neuromonitoring is commonplace in neurointensive care units in which traditional methods include monitoring intracranial pressure (ICP) via a parenchymal bolt or external ventricular drain and cerebral perfusion pressure (CPP). In the last 10 years, brain tissue oxygen ([P.sub.bt][O.sub.2]) monitoring and continuous electroencephalogram have become much more common in the neurocritical care setting. In 2002, CMA/Mcrodialysis received Food and Drug Administration (FDA) approval for the application of cerebral microdialysis, which made clinical cerebral metabolism monitoring available in the United States for the first time. CMA/Microdialysis has supported cerebral metabolism monitoring in Europe since 1995 and is currently the only company with FDA approval for cerebral microdialysis.
Microdialysis allows online monitoring of the extracellular environment and, in particular, bedside monitoring of the substrates of cerebral energy metabolism. These additional physiological data, along with other monitoring parameters, provide clinicians with information regarding impending episodes of neurological events, which is critical in patients whose underlying neurological status is unclear or who are experiencing varying degrees of coma. The aim of microdialysis monitoring is to identify signals of cellular disturbance before clinical symptoms are manifest. This identification may provide an opportunity for earlier intervention and prevention of secondary injury. This article is meant to provide an overview of the cerebral application of the microdialysis technique and its nursing implications.
Principle of Microdialysis
After more than three decades of developing, refining, and perfecting microdialysis, the technique is being adopted as a bedside tool for patients in various clinical settings (Klaus, Heringlake, & Bahlmann, 2004; Pojar & Mand'ak, 2006). As a technique, it is applicable to any clinical situation in which it is relevant to monitor organ metabolism. In addition to cerebral metabolism monitoring, recent literature outlines its application in myocardial (Mantovani et al., 2006; Poling et al., 2006), liver (Meybohm et al., 2006), pancreas (Esmatjes et al., 2003), intestinal (Krejci et al., 2006), intraperitoneal (Jansson, Strand, & Jansson, 2006), splanchnic (Knuesel et al., 2006), rectal (Solligard et al., 2007), and intraoral monitoring (Jyranki, Suominen, Vuola, & Back, 2006).
Bedside cerebral microdialysis allows frequent sampling of specific molecular substances within the interstitial fluid including but not limited to markers of energy metabolism (glucose, lactate, and pyruvate), excitotoxicity (glutamate), and phospholipid degradation (glycerol). Monitoring of molecular substrates, together with frequent clinical assessment, and other physiological and hemodynamic parameters provides information regarding cellular processes that can alert clinical staff to pathophysiological processes that may lead to secondary brain injury (Hillered, Vespa, & Hovda, 2005; Ungerstedt & Rostami, 2004).
The microdialysis catheter can be inserted emergently at the bedside in the ICU through a bolt via a burr hole or in surgery during an open craniotomy. It is typically inserted into the pericontusional brain tissue in patients with traumatic brain injury or in the region of the parent vessel at risk for vasospasm in patients with subarachnoid hemorrhage (Ungerstedt & Rostami, 2004). Perfusion fluid is pumped through the catheter, which has a 10-mm semipermeable membrane at the distal end which functions similar to a blood capillary, allowing molecules to diffuse into perfusion fluid, enabling collection. At a perfusion fluid flow rate of 0.3 [micro]l/min, the concentration of metabolites recovered represents approximately 70% of the tree concentration in the interstitial fluid. The standard catheter allows a molecular weight cutoff of 20 kDa or smaller to be collected into a microvial, which includes glucose, lactate, and pyruvate (see Fig 1). A catheter with a molecular cutoff of 100 kDa is available, allowing larger molecules to be collected, such as cytokines or inflammatory markers, and which is used as a part of an institutional review board research protocol. Metabolite concentration levels from hourly samples are calculated at the bedside using a colorimetric-based analyzer. Immediate bedside analysis alerts clinicians of perturbed cellular energy metabolism (Ungerstedt & Rostami, 2004).
[FIGURE 1 OMITTED]
Review of Cerebral Metabolism
For brain tissue to survive and retain function, it must first receive fuel from the bloodstream in the form of oxygen and glucose and then convert that fuel into the major cellular energy source, adenosine triphosphate (ATP). Neurons use energy to maintain ionic homeostasis, normal cellular metabolic functions, and synaptic communication. Adequate cerebral blood flow provides oxygen, glucose, and other nutrients for the brain. Glucose is extracted from the blood and delivered to neurons by astrocytes. At the cellular level, energy production occurs first through glycolysis, the process of converting glucose to pyruvate and/ or lactate, generating 2 ATP molecules for every mole of glucose. Oxygen availability enables pyruvate to enter the mitochondria where it generates 18 times as much energy (net 36 ATP) as glycolysis alone does through aerobic metabolism. This fact exemplifies the critical importance of proper oxygenation of brain tissue (Zauner, Daugherty, Bullock, & Warner, 2002).
By measuring interstitial glucose, pyruvate, and lactate concentration levels, microdialysis provides clinical insight related to altered or disrupted cerebral energy production (Ungerstedt & Rostami, 2004). Normal fluctuations in energy production lead to variations in lactate and pyruvate concentrations in the interstitial fluid. This makes it more difficult to determine when energy metabolism is faltering; therefore, it is common to also evaluate the ratio of lactate concentration to pyruvate concentration, which has the effect of normalizing these fluctuations and eliminating differences due to variation in metabolite recovery (Hillered et al., 2005). This calculation is commonly referred to as the lactate: pyruvate ratio (LPR), which is the most thoroughly evaluated metabolic ratio in the literature.
When the brain tissue does not have enough energy to perform cellular maintenance, it is unable to maintain normal homeostasis, and the membrane walls begin to breakdown. One of the byproducts of cell membrane degradation is the release of glycerol into the extracellular space (Ungerstedt & Rostami, 2004). Glutamate is the major excitatory neurotransmitter of the central nervous system. It is also an important component of cellular metabolism. Both glycerol and glutamate interstitial fluid concentrations can be monitored using microdialysis and have been used as clinical metabolic markers in Europe for many years (Ungerstedt & Rostami, 2004). At the time of this writing, both glycerol and glutamate measurements are under review by the FDA for clinical use in the United States. Under conditions of metabolic derangement, both elevations of glycerol and glutamate levels confirm that energy disruption is resulting in cellular damage. Some institutions use glycerol and glutamate under the auspices of research protocol approved by the institutional review board.
Nurses should be aware that the precise metabolic relationship of glucose, pyruvate, and lactate within the context of aerobic and anaerobic conditions is under scrutiny. More specifically, it has been proposed and supported by in vitro experimentation that glucose is always converted to lactate (Schurr, 2006; Schurr & Payne, 2007), contrary to the classical view that the conversion of glucose to lactate only occurs during anaerobic metabolism (Champe, Harvey, & Ferrier, 2005; Hillered et al., 2005; Ungerstedt & Rostami, 2004). This is not a trivial distinction to make because it has broad implications about what lactate elevations might mean clinically and what response(s) may be warranted. It has been understood for some time that lactate is the preferred cerebral fuel source after ischemia (Schurr, Dong, Reid, West, & Rigor, 1988; Schurr, Payne, Miller, & Rigor, 1997a, 1997b; Schurr, Payne, Miller, & Tseng, 2001). Astrocytes produce and shuttle lactate to neurons to support their high-energy demands, and therefore strict interpretation of lactate concentration changes is complicated (Magistretti, 2006; Magistretti & Pellerin, 1999, 2000; Magistretti, Sorg, Yu, Martin, & Pellerin, 1993). It has also been shown that the brain will extract systemic lactate circulating in blood (Glenn et al., 2003).
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