Does Induce Therapeutic Hypothermia Impact Neurologic Function And Improve Patients Out - Research Paper Example

? Does Induce Therapeutic Hypothermia Impact Neurologic Function And Improve Patients Out Does Induce Therapeutic Hypothermia ImpactNeurologic Function And Improve Patients Out Introduction Therapeutic hypothermia has emerged as one of the most common medical practice used in dealing with neurologic outcomes especially patients experiencing cardiac arrest. The physiologic effects that involve pharmacologic and cooling effects of neuromuscular and sedatives blocking agents have been observed to affect the neurophysiologic findings as well as clinical examinations. The above may result in to unpredictable results in neurologic prognostication. This paper is going to conduct a review on past prognosis assessments on patients under therapeutic hypothermia treatment. The review is aimed at proving that therapeutic hypothermia does impact neurologic functions thus improving the conditions of patients. Over the years, therapeutic hypothermia has stood out as the most appropriate care that can be given to patients with neurologic outcomes one of them being cardiac arrest. History The use of induced hypothermia following a neurologic condition such as cardiac arrest was first reported between 1950’s and 1960’s. At this early stages of its discovery, the target temperature in the process were lower in comparison to those used in the current times as well as the duration and method used although the results are more so the same. Despite this realization, the findings in the past were inconclusive as well as higher complication rates being observed. Until 1990’s, there were no further hypothermia investigations as a resuscitative measure. After this juncture, laboratory studies were used to demonstrate the benefits associated with hypothermia. Value of this paper This study adds up to the many other studies that have been conducted on the role played by hypothermia in dealing with neurologic conditions and has been used in updating cardiopulmonary resuscitation guidelines and its findings used as recommendations for hypothermia in neurologic conditions especially patients suffering from cardiac arrest and don’t regain consciousness. The findings can also be used in the implementation of therapeutic hypothermia in patients suffering from pulseless electrical activity, asystole and in house cardiac arrest cases. The results can be used to guide and advice nurses to consider hypothermia to patients unable to follow verbal commands following spontaneous circulation. The study recommends that patients suffering from cardiac-arrest should be transported suing facilities that can offer therapeutic hypothermia together with advanced neurologic monitoring, coronary reperfusion and standardized care. Why is this topic important in the field of nursing Nurses have been identified as to play a significant role in detecting, preventing and treating adverse complications and effects of therapeutic hypothermia. With the information provided in this paper, the nurses will be better placed to deal with most of the adverse effects in intensive-care settings. In normal settings, care for patients under therapeutic hypothermia may require intensive massive following its complexity thus the information provided by this paper may be relevant in guiding nurses as they provide such services. The reduction in morbidity and mortality and the improvement of neurologic outcomes is mostly caused by Therapeutic hypothermia. More so the condition has also several effects on the outcome of a cardiac arrest survivor. New mechanism to analyze the impact of therapeutic hypothermia when it is used to treat patients with neurologic prognosis is reviewed in this paper. In the standard therapeutic hypothermia protocol the patients are subjected to cooling for about 24 hrs to a specific temperature of 33 and it ranges from 32-34 while applying the catheter-based cooling or the surface -based method. In the cooling process the patients are treated with agents like benzodiazepines, opioids ,propofol or even a combination of the agents. To prevent shivering, the patient is given Neuromuscular blockade that is given with a no depolarizing neuromuscular blocking agents like vecoronium (Peberdy, 2010). The paper is thus going to review prognosis on patients under therapeutic hypothermia treatment by making use of evidence from different studies and reports. Most of the studies have limited evidence on the prediction of poor prognosis. The findings of this study are crucial in the nursing field as with such information, the nurses will be better placed to apply therapeutic hypothermia while taking care of patients with neurologic outcomes. Literature Review Considering standard clinical neurologic examinations that include corneal reflexes, motor responses and papillary light responses on painful stimuli are normally conducted on patients facing neurologic conditions such as cardiac arrest resuscitated. ANN Practice parameters have that 72 hours following a cardiac arrest, corneal reflexes absence, papillary responses absence or motor responses absence predictions on prognosis are poor and have high uncertainty in the when it comes to prognosis of patients undergoing therapeutic hypothermia treatment. Some of the clinical examinations carried out in the past show that during motor testing, no extensor posturing or movement with regards to noxious stimulation can be considered as ineffective motor response as posturing or flex have been seen as to result in admirable incomes. The data that is available on clinical examinations from different sources indicate that patients under therapeutic hypothermia have reduced accuracy when it comes predicting poor prognosis (Abella, 2008). In one of the studies on 37 patients, the findings of the study had it that 2 of every 14 patients who showed poor motor responses after 72 hours following a cardiac arrest were able to regain their consciousness but both showed poor motor responses until the 6th day after the recovery (Polderman, 2010). In this case however, nerve functions on upper cranial still had their predictive value now that of the 6 patients, none of those suffering from corneal reflexes absence or papillary reactivity absence regained their consciousness after 72 hours. In another study involving 44 patients, none of the patients who lacked papillary light responses managed to regain their consciousness after 72 hours. However, 2 patients having poor motor responses and one who lacked corneal reflexes managed to regain their consciousness (Qadar, 2010). A similar study was also conducted on 45 patients and the findings showed that 2 of the 45 patients who lacked corneal reflexes or papillary response between 36 and 72 hours following the cardiac arrest achieved good outcomes after regaining their consciousness. 11 patients in the same study showed poor motor responses after 72 hours and went ahead to survive while 4 patients managed to have good outcomes (Chopp, Chen, Dereski and Garcia 2010) Taking into consideration the use of SSEP in the prognosis assessment following neurological conditions in relation to the existing AAN practice parameters, N20 response bilateral absence within 24 to 72 hours following a cardiac arrest, poor prognosis can be accurately predicted in patients who have not been given therapeutic hypothermia. A study on the same showed that one of the patients having severe N20 amplitudes bilateral reductions managed to survive and attained cognitive functioning (Peberdy, 2010). In this case, SEEP was carried out 2 days following the institution of rewarming. When it comes to the use of EEG in the assessment of neurologic prognosis, several time intervals and classification systems of recording following a resuscitation have baffled the EEG utility to predict prognosis accurately. The common background patterns that are normally observed following a cardiac arrest include discontinuous suppression-burst pattern, extremely low voltage or electrographic status epillepticus (Colbourne and Corbett, 2009). However, in this case, EEGs with very low-voltage are common during therapeutic hypothermia. This may come second to the effects of the pharmaco-logic of the opioids, propofol and benzodiazepines applied in sedation or owing to the reduction in the rate of cerebral metabolism and in genera electrical activity. Hypothermia has been identified as being protective against seizures independently (Colbourne and Corbett, 2008). In one of the studies using aEEG on 34 patients having continuous recording on EEG during therapeutic hypothermia, the results of the study showed that 2 of the total number of patients were observed to exhibit SB patterns, 1 of the patients showed alpha coma pattern but none of the three managed to regain their consciousness. Seven of the remaining patients had clinical seizures that were correlated with ESE, none of them managing to regain their consciousness. All the patients that had continuous EEG from the beginning regained consciousness, while the results were mixed in 24 patients with an initial pattern, 11 of whom evolved to some pattern that was not continuous when subjected to normothermia with none of them regaining consciousness. A similar study was also conducted on patients subjected to therapeutic hypothermia (Colbourne, Sutherland and Auer 2009). In this study, 100 patients were observed in an 8 hours median following a cardiac arrest. During therapeutic hypothermia, 14 of the patients showed an initial SB pattern and they all consequently died before they regained their consciousness. An initial therapeutic hypothermia pattern proved not to be predictive of prognosis while a continuous pattern showed pre-dictive value that was positive for regaining consciousness of around 91% (Nunnally, 2010). Therapeutic hypothermia was met at a 36 hours median following a cardiac arrest. In this case, 7 of the patients under study showed SB patterns, 17 of them had ESE while 24 of them died while being hospitalized. The 17 patients who had ESE were given an anticonvulsant standard treatment. In the initial stages, 9 of the patients showed a flat pattern while 3 managed to gain their consciousness. In another study on 45 patients, continuous BIS monitoring was carried out for the initial 72 hours following a cardiac arrest. The findings of this study showed that 14 of the patients had a 0 BIS score in the first 24 hours. After a period of 6 months, a total of 11 patients had died while 1 survived but was in a vegetative state as 2 had neurologic deficits that were severe but managed to regain their consciousness (Katz, 1995). A study involving 100 patients had it that 3 of the patients had ESE during therapeutic hypothermia but later recovered and attained a good outcome after being aggressively treated using anticonvulsants. It was observed during this study that the 3 patients had EGG backgrounds that were reactive. In this study, 3 of the patients who lacked EEG background reactivity managed to regain their consciousness but still had neurologic impairments that were severe. In the past, MSE has been continuously proposed as one of the clinical features suggestive of poor prognosis (Heire 2009). MSE refers to one of the clinical entities that are normally observed following a cardiac arrest. Such observations may result in various EEG patterns that include SB, fat and ESE. MSE generally appears as repetitive, unrelenting, spontaneous, multifocal myoclonus and generalized involving the limbs, face and axial musculature in coma presence. There are a number of case reports on normothermic patients having MSE who managed to regain their consciousness. Myoclonus mostly affects patients with a primary hypoxic event, even in the absence of perfusion loss and in this condition Myoclonus is normally associated with admirable outcomes. In a study that had 44 patients undergo therapeutic hypothermia, the outcome of the study showed that 2 of the patients developed MSE in a span of 72 hours with neither of them managing to regain their consciousness (Chamorrow, 2010). In a different study involving a sample of 181 patients, the findings had it that 3 of the patients that developed MSE while undergoing therapeutic hypothermia managed to regain their consciousness. The 3 patients were identified as to be having corneal reflexes and papillary, reactive EEG backgrounds and N20 intact bilateral responses. The three were treated with anticonvulsants, benzodiazepines and propofol (Petito, 2010). There are reports from other studies that show evidence of isolated patients who got MSE during therapeutic hypothermia and later managed to regain their consciousness with admirable outcome. A part from neurophysiologic tests and clinical examinations, biochemical markers can also be applied in the prognosis prediction. Nuron-specific enolase (NSE) found in neutrons as well as neuronal injury can be easily located by the use of NSE increased levels presence in the blood or cerebrospinal fluid. NSE is also found in red blood cells and platelets and hemolysis may increase the value of serum NSE. A number of studies conducted on normothermic cardiac arrest patients show that high levels of serum NSE are related to poor outcome. The NSE levels usefulness in prognosis prediction in patients under therapeutic hypothermia has been studied. Different NSE levels are normally attenuated in hypothermic patients in comparison to the normothermic patients. Cut-off values of serum for NSE as well as NSE levels trends have been under investigation over time. Normally, hypothermia treatment may lead to a rapid decrease in NSE serum levels as well as decreased values on NSE over time related to consciousness recovery, reduced mortality and good neurologic outcome (Centers for Disease Control and Prevention 2011). In one of the studies carried out on serum levels, it was observed that an increase in the level of serum NSE within 24 to 48 hours was invariably related with poor results. In the same study, it was identified that about 31.2 mg/l serum level after 24 hours had a percentage of about 96 specificity for the prediction of poor results and a 25.0 mg/L level after 48 hours having a percentage of about 96 for the prediction of poor results. Problem Analysis In therapeutic hypothermia, the reduction in morbidity and mortality and the improvement of neurologic outcomes is mostly caused by Therapeutic hypothermia. More so the condition has also several effects on the outcome of a cardiac arrest survivor. New mechanism to analyze the impact of therapeutic hypothermia when it is used to treat patients with neurologic prognosis is reviewed in this paper. In the standard therapeutic hypothermia protocol the patients are subjected to cooling for about 24 hrs to a specific temperature of 33 and it ranges from 32-34 while applying the catheter-based cooling or the surface -based method. In the cooling process the patients are treated with agents like benzodiazepines, opioids ,propofol or even a combination of the agents. To prevent shivering, the patient is given Neuromuscular blockade that is given with a no depolarizing neuromuscular blocking agents like vecoronium (Peberdy, 2010). Controlled warming is later done to the patient for over 8 to 12 hours after the induction of hypothermia is over after 24 hours. After the patient is rewarmed the paralytic agents like the sedatives and analgesics are removed. To make the patient comfortable, sedation is minimized after the rewarming is over. However an anticonvulsant medication can be administered to patients who have developed conditions like seizures. Pharmacologic effects that deter clinical examination can arise due the sedation and neuromuscular blockade used in the hypothermia. Despite the fact that the medication is administered for 48 hours after the cardiac arrest, the sedatives are used in the body for as long as 72 hours or even more (Bernard, 2009). Hypothermia has mild effects on the pharmaco-kinetic and pharmacodynamic nature of the sedatives, neuromuscular blocking agents and analgesics. The renal and hepatic drug clearance can also be reduced by the hypothermia. However the hypothermia plays a role in the significant increase in serum midazolam, propofol and fentanyl concentrations. After conditions such as cardiac arrest, initial neurologic injury takes place following the impairment of the oxygen flow in the brain as a result of circulatory collapse. With the lack of oxygen, the brain changes to anaerobic metabolism which ends up in excessive glutamate and calcium excretion. The excess excites brain cells resulting in more hypoxemia which in the long run causes cellular and mitochondrial death. When circulation is resorted, reperfusion injury takes place while the death of cells initiates an inflammatory response where the immune system releases macrophages and neutrophils to eliminate the cells that are dead. This process leads to the production of free radicals that continues to damage the cells further worsening the inflammatory response. It is this cycle that causes in neurologic condition. The overall evidence from some of the studies reviewed in this paper indicate that the absence of motor response after 72 hours following a post arrest is not reliable in the prediction of poor prognosis in patients undergoing therapeutic hypothermia. Despite this realization, motor response presence can be taken to suggest a good result. Brainstem reflexes absence after 72 hours implies a poor prognosis but cannot be applicable with absolute certainty. The data from the studies reviewed also show that N20 response absence following rewarming or in some cases during therapeutic hypothermia is likely shows poor prognosis, but following the isolated recovery case, N20 response bilateral absence after 72 hours may not absolutely predict poor prognosis (Safar, 2010). EEG reactivity on the other hand may be of great assistance in the prognosis assessment and reactivity presence may be seen to imply good results. However, EEG have to be conducted as soon as possible during therapeutic hypothermia is the ESE assessment and also in the identification of background pattern. As SB pattern in the therapeutic hypothermia normally shows poor diagnosis. ESE can also be taken to show poor results. However, seizures have to be aggressively treated as poor results is not certain and no studies have yet to be conducted in examining aggressive anticonvulsant medication treatment efficacy (Milde, 2010). Incase MSE appears, then it has to be aggressively evaluated with EEG and anticonvulsants applied in the treatment of electrographic seizures now that MSE is not invariably associated with poor results. In addition, MSE is not likely to play any role as a sign that is prognostic in patients undergoing therapeutic hypothermia. It was also inferred from the study that a 0 BIS score is not a sure prediction of poor prognosis. Despite the ESE and EEG findings, therapeutic hypothermia does not have poor prognosis that are uniform. The results on near-normal or normal MRI following a cardiac arrest be followed by continued supportive care now that such patients can awaken with ultimately good results. Equally, the widespread diffusion-weighted abnormalities presence or depression associated with ADC may be taken as to mean poor outcome. However, MRI has so far not yet been considered as a valid predictive tool (Hypothermia after Cardiac Arrest Study Group 2012) Discussion Accurate prognostication following neurologic conditions has proved to be challenging. Neurologists are normally consulted to seek expertise on the meaningful recovery chances. Poor outcome criteria are expected to have high certainty degree before being employed routinely in clinical practices. The introduction of therapeutic hypothermia has made neurologic prognosis more difficult. Looking at the reviewed data, there appear to be several criteria that can be used in the absolutely prediction of recovery consciousness. This implies that prognosis now rests on the integration of results from different diagnostic or clinical tests. In case there are any uncertainties in the prognosis with a given patient following a neurologic condition, more time should be allowed to pass now that clinical features can recover neuroimaging showing delayed fashion injury, and normalized neurophysiology (Greer, 2009). In our own conclusion for a patient to undergo hypothermia, to detect that a patient has strong poor prognosis, some of the things that are normally taken into consideration include, the absence of a papillary light response or that show corneal reflexes at 72 hours after the arrest, the lack of the cortical N20 response, a rising NSE levels between 24 and 48 hours after the arrest, a SB EEG pattern or ESE during hypothermia and an important depressions of MRI ADC values 3 days after the arrest (Greer, 2010). The absence of motor function on clinical examination 72 hours after the cardiac arrest may result in the presence of myoclonic status epilepticus frequently ,a flat EEG pattern during hypothermia and a serum NSE level above 33 and 72 hours after the arrest. Such factors should not be considered in determining a patient that is to undergo hypothermia. The following features should be considered when predicting a good prognosis; the presence of a motor response of withdrawal within 48 hours after the arrest, absent or very little abnormalities on DWI 3 days after the cardiac arrest and a prolonging EEG pattern without epileptiform action during hypothermia. However the features have not be been ascertained, a more complex analysis should been done before drawing conclusions. A number of common bias trials should be done on the prognosis after the cardiac arrest. The study thus asserts that continued widespread use of therapeutic hypothermia following neurological outcomes calling for any interested party to always err on the caution side when it comes to prognosis assessment (Bernard, 2008). Implications for practice The studies reviewed above have demonstrated that therapeutic hypothermia mitigates brain damage following cardiac arrest. The exact mechanism to go about it is not yet clear but different approaches have been used like cerebral oxygen consumption reduction as well as multifactorial physical and chemical mechanisms, destructive enzymatic retardation, free-radical reactions suppression, intracellular acidosis reduction and biosynthesis inhibition. This study has proved that patients treated with therapeutic hypothermia following neurologic conditions have improved neurologic outcome without any side effects in comparison with the results of historical controls. Recommendations for Future Study Future studies should be carried out in an effort to confirm the ability of absolute prognostic of the corneal reflex and pupilary light response inpatients going through therapeutic hypothermia. In addition, pro-spective trails in future should be in such a manner that they are well positioned to evaluate the role played by neuroimaging when it comes to prognosis. In future, more comprising studies should be done to verify the accuracy of predictive tools especially to patients undergoing therapeutic hypothermia after the cardiac arrest. Such studies should be done when the prognosis process is not certain because the recovery can be delayed. In case of any delay measures like the establishment of time points with the current prognostic tools used (Wijdicks, 2008). In reference to the review of the all process, we suggest that the following practical advice: EEG should be undertaken as early as possible and should be persistent. The treating of electrographic seizures especially the ESE should be done aggressively 72 hours after the patient has achieved normothermia, the patient should be induced with papillary, motor responses and corneal. It is advisable to perform SSEP on patients 48 hours has received normothermia. The NSE should be induced 48 to 72 hours after the normothermia. Because it is hard to assess the utility of neuroimaging thus 24 to 48 hours after achieving the normothermia, the patient should get a CT for prognostication. After a period of 3 to 5 days following normothermia, the MRI should be performed (Wijdicks, 2008). References Abella B. (2008). “Intra-arrest cooling improves outcomes in a murine cardiac arrest model.”Circulation Benson et al. (2000). “The use of hypothermia after cardiac arrest.” AnaesthAnalg. 38:423-28 Bernard, S., et al. (2008). “Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia.” N Engl J Med. 21: 346(8): 5557-63 Bernard, S., et al. (2009). “Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia.” N Engle J Med. 346(8): 557-563 Centers for Disease Control and Prevention (2011). Healthcare-associated infections. www.cdc.gov/HAI. Accessed May 14, 2013 Chamorrow, C., et al. 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A case report and a brief review on the treatment of hypothermia. Amj Ther. 17(2):223-225 Safar, P. (2010). “Resuscitation from clinical death: Pathophysiologic limits and therapeutic The Hypothermia After Cardiac Arrest Study Group. (2010). Mid therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 346(8): 549-556 Wijdicks, M. (2008). The Comatose Patient. New York: Oxford University Press Zeiner, A., et al . (2008). “Hyperthermia after cardiac arrest is associated with unfavourable neurological outcome.” Arch Int med. 161;2007 -12 Read More