Reply to this discussion use referencesBe sure that the responses to the  Post of peers include 2 peer reviewed references with content that demonstrates critical analysis and synthesis of references used.In the case study presented, a combination of symptoms was presented along with clinical findings. This includes unresponsiveness mediated by Narcan administration, single sided pain and necrotic tissue, and abnormal EKG findings with elevated serum potassium. A history was also given of substance abuse.The initial symptom of unresponsiveness can most likely be caused by an opioid overdose due to the reversal by Narcan administration. Narcan is an opioid antagonist, which is used to reverse the effects of opiates by binding to opioid receptors to block opioid uptake (U.S. Department of Health & Human Services, 2021).The single sided pain and tissue necrosis most likely could be the result of overdose compartment syndrome, which is caused by tissue damage resulting from the constant pressure exerted on the side or limbs the unconscious person is laying on, and due to the altered mental status a lack of repositioning (Miller, 2021).The necrosis results in increased skeletal muscle breakdown resulting in Rhabdomyolysis which is characterized by circulation of components of necrotized muscle tissue (Miller, 2021). One cause of rhabdomyolysis is direct tissue injury, which in this case would be due to the necrotized tissue from the overdose compartment syndrome. Overdose compartment syndrome occurs when the cells, in this case skeletal muscle cells, are damaged from the patient laying on them for a prolonged period of time (Jones et al., 2020). Because of the prolonged injury, the cells have undergone cell death via necrosis due to the prolonged direct damage to the membrane of the cell. When cell swelling occurs, an acute oxygen deficit causes the cell to switch from aerobic to anerobic energy production resulting in an inevitable decrease in ATP production due to anaerobic energy production being less efficient (Miller & Zachary, 2017). If this is not corrected, the sodium/potassium pumps fail, leading to loss of control of volume control for the cell which results in the cell bursting and leaking intracellular contents extracellularly (Miller & Zachary, 2017). In part this results in increased serum potassium due to the displacement of the intracellular potassium.Normal potassium ranges from 3.5-5.0 (Weiss et al., 2017). The conduction system in muscles as well as the conductive cells of the heart rely on potassium going through the membrane (Weiss et al., 2017). The positive potassium leaving the cell will make the cell more negative (Weiss et al., 2017). If the serum is hyper concentrated with positive potassium, the potassium will leave the cell slower and the cell will be less negative (Weiss et al., 2017). This will result in a depolarized cell, which will be more excited (Weiss et al., 2017). The first sign of conduction issues is the peaked t waves and then prolonged PR interval EKG changes(Weiss et al., 2017).Regarding genetics and rhabdomyolysis, 11 genes have been identified that make a patient more likely to have an episode of rhabdomyolysis (Kruijt et al., 2020). A retrospective cohort of reviewed demographics as well as causation for cases of rhabdomyolysis, of which all three found external triggers to be the most common cause, however more recently data has shown that a combination of said external events as well as genetic predisposition increases risk (Kruijt et al., 2020).Additionally, predisposition to addiction also may have a genetic component. For example, research is being conducted to explore the association of the number of dopamine receptors a person has and the predisposition to become addicted to alcohol (American Psychological Association, 2008). By identifying genetic components that make a person more likely to be addicted, clinicians can educate and treat patients more appropriately to prevent situations such as initial overdose.If characteristics were changed, such as no history of substance abuse and a history of exercise intolerance or muscle weakness the response would change (Lahoria & Milone, 2016). If this were the case it would be more appropriate to investigate metabolic myopathies such as muscular dystrophy (Lahoria & Milone, 2016).In conclusion, the case study suggests the patient is in a state of rhabdomyolysis due to skeletal muscle damage from prolonged pressure exerted on the left side while unconscious from opioid abuse as it resolved with an opioid antagonist, with electrolyte changes of hyperkalemia due to the increased serum potassium from the breakdown of the muscle cells resulting in EKG changes. Genetic factors can play a factor in substance abuse as well as increased risk of rhabdomyolysis but are typically seen in repetitive cases of rhabdomyolysis with history of muscle weakness or exercise intolerance.

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