Accelerated Diagnosis Pathway Vs Traditional Diagnosis Pathway for Chest Pain Management in Emergency Department

Accelerated Diagnosis Pathway Vs Traditional Diagnosis Pathway for Chest Pain Management in Emergency Department

Having intense chest pain usually gets people to be admitted to the hospital quickly. However, research now suggests there should be reassessment of the guidelines currently used to evaluate likely severity of one’s pain conditions. According to the Australian Medical Journal, most patients’ chest pains do not have cardiac causes. Due to differences in symptoms, they may be assessed using different methods. Despite the hospital having to spend more time and significant resources in certain protocols of diagnosis, researches have to be done to identify those diagnosis techniques that can be used to identify patients who can be discharged without further engagements in acute pain investigations.

Accelerated Diagnosis Pathway (ADP) and Traditional Diagnosis Pathway (TDP) are two broad chest pain management protocols currently used in Monash health emergency departments. ADPs have generally been designed to identify and manage patients with low-risk chest pain in the emergency department (ED) (‘t Veld et al., 2017). On the contrary, TDP is more suited for patients with high-risk chest conditions and takes longer time and may involve more resources (‘t Veld et al., 2017). The National Heart Foundations of Australia (NHFA) and the Cardiac Society of Australia and New Zealand (CSANZ) have used recent 12-month clinical audits to recommend suitable guidelines and strategies of helping patients with chest pain conditions according to their severity (Chew et al., 2016). Therefore, the right protocol for patient chest pain therapy is determined by severity of one’s conditions. The severity is scaled as “low-risk”, “moderate-risk” and “high-risk”. This essay aims to explore the criteria for stratification of the severity of chest pain and the pathophysiology of the condition, in comparison with published research and current practice across Monash health.

Chest pain can appear in many forms, starting from dull aches to sharp stabs. However, one generally endures a feeling of burning or crushing in the chest. The pain can travel up the neck and into the jaw, and spread back or down in one or both arms. Heart-related pain is associated with heart disease and it can be described by pressure, burning, full or tight chest, crushing or searing pain to the back, jaw, neck, shoulders and arms, with associated cold sweat, shortness of breath, nausea or vomiting. However, other types of pain can be noted with trouble in swallowing, sour taste, intensified pain when breathing deeply, and so forth (Chew et al., 2016).

Essentially, chest pain in patients such as those with acute coronary artery disease is caused by myocardial ischemia or infraction, which results from imbalance between myocardial oxygen demand and blood supply. Specifically, myocardial ischemia results from three factors: reduction of coronary blood supply due to conductive effect of coronary artery, deficient relaxation or abnormal constriction of coronary microcirculation and reduced oxygen-carrying capacity of blood. When blood flow becomes inadequate to meet oxygen demands of myocardial cells, they will switch from aerobic to anaerobic functioning. This anaerobic metabolism would continuously impair mechanical, metabolic and electrical functioning of the myocardial tissue. Angina pectoris is a common clinical manifestation of the anaerobic functioning of the myocardial tissue. Studies have found that adenosine may be the major chemical mediator of pain related to angina pectoris. ATP is degraded to adenosine during ischemia (Alaeddini, 2018); the resulting adenosine would diffuse to extracellular spaces to cause arteriolar dilation and angina pain.Prevalence of chest pain increases with increase in age. It should be expected that the majority of cases and deaths related to chest pain will occur in individuals above 75 years. Troponin is released from the myocyte cytosolic pool during myocardial infarction (MI). Its isoforms are T and I, and are known to be specific for MI. When myocyte gets injured, troponin is released in a period of 2-4 hours and this may persist upto seven days. Its release is however expected to peak at the 12

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hour. Creatine Kinase (CK) is also expressed in the heart muscle when there is injury. Since it lasts in short duration, it may not be suitable for tests that occur after 2-3 days. Myoglobin is the muscle pigment that primarily carries oxygen. When muscle tissue is damaged, its production increases to respond to the increased need of oxygen (Alaeddini, 2018). Monash Emergency like most of hospitals in Australia use the troponin biomarker tests cTnI (cardiarc troponin I) to diagnose their patients as per both ADP and TDP. For ADP, the Radiometer AQT Flex analyser is used, and the limits of detection are 0.01 and 0.25 ng/mL. TDP uses laboratory testing of troponin and the cTnI has to have a lower limit of 0.01 ng/mL. Although both results are presented on a 99

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percentile, ADP has to show less variation coefficient of 0.04 ng/mL compared to TDP’s 0.06 ng/mL (Monash Emergency, 2017). Therefore, ADP tests have to show higher levels of troponins, but with less coefficients of variation.

ADP was developed as an innovative measure of quickly and safely identifying chest pain patients that may not be at high-risk in Australian emergency departments. These involve those at low-risk or moderate-risk. Chest pain was noted as one of the most common conditions that lead Australians into EDs (Pash, 2015). It is estimated that about 500,000 cases of the condition are reported in the country’s emergency departments each year. However, although the number is significantly high, the majority of those admitted are not at risk of suffering from heart attack. For efficient identification of patients due to increasing number of presentations, ADP and its variant techniques have been developed (Pash, 2015; Cullen et al., 2017). Departments such as Queensland Emergency Departments use contemporary Troponins as preliminary biomarkers in their ADPs to identify those with low-risk conditions. Improved ADPs such as the IMProved Assessment of Chest pain Trial (IMPACT) are used to identify patients with low-risk to moderate-risk cases (Cullen et al., 2017). Troponin levels in the first diagnosis would determine if one has suspected conditions or not. However, since ADP is supposed to be more efficient, some hospitals in the Australasian region have opted for a combination of biomarkers. In this case, ADP can use point-of-care multi-marker assays to categorize a patient between 10minutes to 2 hours. The multi-markers can be cardiac Troponin I, creatine kinase and myoglobin. Although TDPs can use the same markers, they usually take longer (Chew et al., 2016). For instance in this case it could be 6 hours (Meek et al., 2012). This is because, the latter pathway is meant to identify individuals whose conditions are not readily manifested. In case the patient’s conditions present higher risk, the HEART scores 4+ test needs to be done within 10 hours of arrival, if earlier tests showed negative results (Monash Emergency, 2017). The Monash Emergency (2017) has also noted that manifestation of chest pain within 6 hours of arrival could be low-risk. However, there have to be no potentially unstable features, and the EDACS score has to be less than 16.

During presentation, ADP uses very sensitive biomarkers and test scores to identify patients that may have suspected symptoms of life-threatening chest pains. The risks are supposed to be quantified for another step to be taken to ensure the patient’s welfare (Munro et al., 2015). In this regard, the NHFA and the CSANZ have issued guidelines of initial steps that should be taken to ascertain whether ADP or TDP should be used for chest diagnosis (Chew et al., 2016). ST elevation MI (STEMI), acute coronary syndrome (ACS) and other life-threatening conditions such as pulmonary embolus and aortic dissection have to be considered. Obstructive coronary artery disease (CAD), major adverse cardiac events (MACE) and non-ST-elevation ACS have to be noted also (Chew et al., 2016). Nevertheless, the patient is assessed on whether he or she understands measures to be taken in case pain symptoms appear in future (Chew et al., 2016; Perera et al., 2018). As already noted, ADP usually uses high sensitive elements of biomarkers and test scores to get rapid results on whether the person under consideration has high-risk chest pain or not. However, it can be hard to rule out some patients in the first instance due to the fact that it creates anxieties in them, especially if they are used to traditional models of diagnosis, prognosis and treatment, whereby changes in the model have to be demonstrated by quality and justified by better outcome (Croft et al., 2015). Therefore, by TDP, when a person is presented in the ED complaining about chest pain, although the symptoms may not be confirmed by some scores and biomarkers, it is usually believed that they may take a longer time to be manifested. TDP is comprehensive, and can be used to diagnose those who need thorough examinations and possible hospitalization until they get well (Parsonage, 2017). The Monash Emergency (2017) mentions some abnormal signs about which the medical leader must be notified immediately for the chest pain assessment to follow the TDP. They are BP < 90 systolic, oxygen saturation < 90% and HR < 60 or > 130. The Monash Emergency Department has outlined further that any other ECG abnormality and prompt serial cTnI have to follow TDP (Monash Emergency, 2017). A patient is usually admitted for extensive investigations to be done about his or her condition (Cullen et al., 2013). He or she will be put under a program of testing intervals to ascertain possible conditions of chest pain. Clinicians are therefore tasked with conducting several tests to ascertain the risk level of one’s chest pain condition (Cullen et al., 2013). This determines the stratification one will undergo and the kind of treatment he will receive. The Monash Emergency (2017) has outlined that in case one is diagnosed with symptoms of likely acute coronary syndrome (ACS), more sensitive ADP tools such as those of EDACS should be used. The cut-off score has to be EDACS < 16 for one to remain under ADP. Any score above 16 will require TDP. Moreover, in case of unstable angina pectoris (UAP), whereby one’s conditions are unstable, it is needed that one uses the TDP (Monash Emergency, 2017). However this should be ascertained first by cTnI test as per ADP. Depending on the risk of one’s condition, one may undergo therapies such as pharmacotherapy, reperfusion, invasive management for Non ST segment elevation acute coronary syndrome (NSTEACS), and so forth (Chew et al., 2016). This are supposed to be done until one gets well. In case suspected symptoms emerge, the patient will be involved in medical therapies in the ED depending on the severity of his or her condition (Chew et al., 2016). Therefore, TDP therapy is more relevant for patients with high-risk or acute chest pains that require admission.

To check whether a patient’s chest pain is low-risk, moderate-risk or high-risk, ADP uses five variables: 12-lead electrocardiogram (ECG), risk factors, personal history, age factor and Troponin levels. Scoring usually ranges from 0 to 10 in all variables. Low –risk patients have to show a score of 3 or less. Those with 4-6 are considered to be moderately at risk (Munro et al., 2015). Those with 7-10 are at high-risk and would be considered for urgent interventions (Byrne, 2014). To ascertain whether one has low-risk, moderate-risk or high-risk pain condition, it is recommended that at least three of the scoring elements indicate the same or higher score (Chew et al., 2016; Meek et al., 2016). However, due to likely significant miss rates in some tests, some assessment procedures such as NHMRC Level of Evidence (LOE), GRACE, CRUSADE, HEART and IMPACT scores have been recommended (Chew et al., 2016; Brady & de Souza, 2018). These are considered more advanced protocols to diagnose this kind of pains. It is however important to mention that TDP may use the techniques used by ADP in additions to others. For instance, there have been TDP clinical studies using 12-lead electrocardiogram, troponin tests, and the other three techniques (Cullen et al., 2017). The Monash Emergency (2017) has recommended that practitioners follow the American guideline in scoring risks associated with patient history. In this regard, discomfort or pressures in chest, neck, and epigastric region, or acute chest pain without cardiac source have to be studied (Monash Emergency, 2017). The National Heart Foundation of Australia (NHFA) and the Cardiac Society of Australia and New Zealand (CSANZ) have put forward 3 kinds of tests that medical practitioners can use in case they have patients with identifiable high-risk symptoms and delaying identifiable symptoms. In this regard, firstly, diagnostic accuracy may be increased by using computer-assisted results from the ECG (Byrne, 2014). However, experienced personnel are needed in TDP since complex conditions are expected. ECGs tests and those that concern biomarkers such as the cardiac troponin have to be done in intervals recommended by a specialist. Secondly, chest X-ray is recommended for traditional pathways to assess conditions such as cardiac enlargements and identify other coronary conditions. Lastly, repeat radio-logical investigation is usually required in case a chest X-ray is not presented for review (Chew et al., 2016).

Although the National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand have not explicitly documented an agreement on the mutual functioning of ADP and TDP, it is evident that both pathways are necessary in the ED. ADP is more relevant in preliminary assessment of low-risk patients with chest pains that do not require inpatient investigation and hospitalization (Scott-Jones, et al., 2017). It is notable that most hospitals are using one kind of test only, especially the troponin I test. To increase efficiency and effectiveness of identifying patients according to their levels of risks, both ADP and TDP have to use combination of at least three tests: zero-and-two hour troponin levels, ECG, and TIMI (thrombolysis in myocardial infarction) scores to identify a patient with low-risk chest pain (Chew et al., 2016; Grant et al., 2014). However, other tests such as creatine kinase(CK) and myoglobin (Mb) tests can be used. However, the ADP protocol is well suited for patients in critical conditions or those in referral programs. In conclusion, the government and hospitals have to ensure that there are both multidisciplinary and interdisciplinary teams that can use both protocols to manage chest pains (Gatchel & Lippe, 2014). ADP can be used as primary health care measure for preliminary pain management (Scott-Jones, et al., 2017). TDP should however be reserved for patients with acute, very severe or hard-to-discover conditions. It should also be used for those admitted in referrals. There have to be staging arrangements whereby patients are stratified according to their conditions. Each stage has to have its special demands according condition complexity and severity as one progresses from the first stage to the last one(Parsonage, 2017). Practitioners such as those at The Monash Emergency (2017) recommend that more improved protocols such as EDACS, which do not include cTnI results, should be used for initial assessments to ascertain whether a person requires ADP or TDP. Additionally, the HEART score does not include findings on troponin and ECG levels and therefore it can also be considered a better stratifying tool between patients for ADP and those for TDP (Monash Emergency, 2017). Despite giving optimal cares to all patients according to their chest pain conditions, this strategy will reduce unnecessary costs due to readmissions, length of stays, follow-up works, pharmacotherapy, personnel and technology requirements, and infections and re-infections.

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