Introduction to the case study
Ms. Aziza, 52 years old, is transferred to the high-dependency unit from the medical ward with altered mental status, fever, hypotension, tachycardia, and desaturation. She was initially admitted to the cardiology ward with atrial fibrillation, nausea and vomiting, and poor oral intake. She is a known diabetic on diet control, hypertensive on amlodipine, and epileptic on levitiracetam. She also has gastroesophageal reflux disease, severe mitral valve regurgitation and tricuspid regurgitation, atrial fibrillation, and stage three chronic kidney disease. She is diagnosed with stroke secondary to infective endocarditis and septic shock. This paper will analyze the pathophysiology of the current acute condition, considering the vital signs, patient history, and investigation results. It will explain whether these findings are within the normal range or abnormal, supported by relevant literature. In addition, create a concise medical management plan and thoroughly evaluate the most recent evidence-based nursing practices for the chosen ailment, ensuring that you prioritize the care requirements. Lastly, explain how this acquired information will benefit your current or future professional practice.
Pathophysiology
Endocardium that is both intact and healthy usually withstands bacterial seeding. Infectious endocarditis often progresses after a prodromal endocardial damage and bacteremia phase. Initial endocardial damage can occur due to mechanical stress during catheter or electrode insertion, turbulent flow around damaged valves, or both (Yallowitz & Decker, 2023). The required damage is produced in the context of intravenous drug usage by recurrent valvular barrage by co-injected particulate particles. The propensity for vegetations to develop on the atrial and ventricular surfaces of the mitral and aortic valves demonstrates that hemodynamics is a critical player in the pathogenesis. The vegetation is concentrated just downstream of the regurgitant flow, which suggests that these areas are more likely to sustain endocardial injury due to hypoperfusion of the intima (Yallowitz & Decker, 2023).
Moreover, infectious endocarditis is more common in high turbulence lesions, such as tiny ventricular septal defects with jet lesions or stenotic valves, compared to defects linked to large surface areas or low flow. This is likely because high-pressure flow causes more localized damage. Platelet aggregation occurs in the injured endocardium, creating an environment favorable to the growth of sterile, non-bacterial thrombotic vegetation.
Colonization of the vegetation is after that made possible by subsequent bacteremia. The required bacteremia can originate from a long-term, distant infection or appear temporarily due to periodic hematogenous inoculation of the oral flora during dental or gingival manipulation (Yallowitz & Decker, 2023). It is still necessary for a pathogenic organism to be able to bind to and facilitate the formation of platelet-fibrin deposits, even in the presence of endocardial damage and bacteremia. As an example, it has been discovered that three different proteins produced by Staphylococcus aureus—clumping factors A, B, and serine-aspartate repeat protein—are responsible for mediating platelet aggregation (Yallowitz & Decker, 2023). Expansion of the once sterile platelet-fibrin deposits shields pathogens from the host’s immune response and paves the way for plant growth, scientifically speaking.
If left untreated, the infection can destroy the heart’s valves and prevent blood from flowing normally (Elsaghir & Al Khalili, 2023). Heart failure, in which the heart fails to pump enough blood throughout the body to satisfy the demands of the body adequately, is one of several potentially fatal consequences that could result from this. Septic emboli develop when an infection gets complex and spreads to the bloodstream—for example, vegetation on a heart valve or a significant bacterial inoculum on the susceptible vascular region. Due to the invasion of new territory, the vegetation breaks down into smaller particles that enter the bloodstream and obstruct a specific blood vessel, resulting in a double-whammy injury: an ischemia insult and an inflammatory/infectious insult. Ren vegetation from right-sided endocarditis commonly embolises the lungs, resulting in septic pulmonary emboli (Elsaghir & Al Khalili, 2023). One congenital heart defect that may facilitate paradoxical emboli is the patent foramen ovale (PFO), which is associated with cryptogenic strokes. Typically, emboli originating from left-sided endocarditis vegetations travel to the brain, where they obstruct cerebral arteries and cause strokes, such as in this case.
Available findings
Patient History
Ms. Aziza was initially admitted to the cardiology ward with atrial fibrillation, nausea and vomiting, and poor oral intake. She is a known diabetic on diet control, hypertensive on amlodipine, and epileptic on levitiracetam. She also has gastroesophageal reflux disease, severe mitral valve regurgitation and tricuspid regurgitation, atrial fibrillation, and stage three chronic kidney disease. The patient is also on furosemide for chronic kidney disease stage three and digoxin and endoxaban for atrial fibrillation.
Vital signs
The patient has a temperature of 36.6 degrees, blood pressure of 127/87mmHG, and a respiratory rate of 20 beats per minute, which were all within the normal limit. The patient, however, has an elevated heart rate of 110 beats per minute, which can be attributed to the need for the body to increase the demand for oxygen in the cells, which is not met as the patient has heart failure.
Lab results
Arterial blood gasses lab results show that the patient’s Bicarbonate is 30mEq/L, which is a high, elevated partial pressure of carbon dioxide (90 mmHg), elevated pH of 7.2, and low partial pressure of oxygen (64mmHg). This lab shows respiratory acidosis. Patel and Sharma (2023) explain that when breathing stops and carbon dioxide builds up in the blood, a condition known as respiratory acidosis occurs. Elevated arterial PCO2 mainly causes a drop in the arterial Bicarbonate to arterial PCO2 ratio, lowering the pH. Hypercapnia and respiratory acidosis are two symptoms that often accompany alveolar hypoventilation. The kidneys respond to an imbalance in Bicarbonate (HCO3-) and carbon dioxide (CO2) by increasing the excretion of acid (hydrogen and ammonium) and the reabsorption of base (Bicarbonate). This adjustment aids in restoring a normal pH.
The patient’s labs also show a low hemoglobin level of 6g/dl, which is indicative of severe anemia (Maitland et al.., 2019). The patient has an elevated blood urea level of 70mg/dl, which shows that the patient had kidney injury due to altered excretion. The patient’s electrolyte profile also shows hypokalemia (2.5 mmol/L). Insufficient potassium levels can impact vital bodily functioning. Prolonged potassium deficiency can lead to adverse consequences such as irregular cardiac rhythms, muscular debility, and potentially even paralysis. Staphylococcus aureus was positive on blood culture, while on urine culture, the Enterococcus faecalis was positive. Staphylococcus aureus is the most likely causative organism of Infective endocarditis. Enterococcus faecalis is the most likely organism to cause urinary tract infections in the patient.
The Echocardiography shows an ejection fraction of 60-65%, right ventricle dilatation, severe regurgitation, and mobile and tiny linear structures attached to both mitral valve leaflets and poorly coapting mitral valve. According to Coneybeare and Gordon (2022), patients experiencing cardiac arrest have been found to have dilatation of the right ventricle (RV). Typically, this occurrence is predominantly associated with a significant pulmonary embolism. Nevertheless, recent progress has unveiled numerous alternative factors contributing to the right ventricle’s expansion during cardiac arrest. Severe regurgitation necessitates more cardiac effort to circulate blood throughout the body adequately—the additional exertion results in hypertrophy of the left ventricle. If left untreated, the myocardium experiences a decline in strength. This can lead to cardiac failure. The mobile and tiny linear structures attached to both mitral valve leaflets and poorly coapting mitral valve indicate infective endocarditis, leading to vegetation and accumulations of diseased material on the valve leaflets.
The X-ray shows bilateral opacities. (Türk & Kökver, 2023)Some possible causes of opacity on chest X-ray images include parenchymal edema, inflammation, thickening of lung tissue, thickening of air space walls and fluid in air spaces, blood vessel damage and bleeding, malignant growth, fibrosis, and damaged or broken blood vessels. An MRI of the brain showed the presence of multiple infarcts and septic emboli, which are the causative agents of the stroke the patient is experiencing.
Medical Management Plan
The patient’s respiratory distress and acute respiratory acidosis will be managed by bi-level positive air pressure (BIPAP) and gradually escalated to intubation and mechanical ventilation. Respiratory acidosis treatment focuses on the underlying pathophysiologic mechanism or condition. Oxygen treatment may be necessary since many individuals with hypercapnia are also hypoxemic. The consequences of persistent hypoxemia can be avoided with the help of oxygen treatment. (Lone, 2023) It is essential to proceed cautiously while correcting chronic hypercapnia, as metabolic alkalemia can occur if it is corrected too quickly. When CSF becomes too alkaline, it can cause seizures. The requirements for being admitted to the intensive care unit (ICU) differ from one facility to another. However, they could encompass symptoms such as patient disorientation, lack of energy, exhaustion of the breathing muscles, and a low pH level (<7.25).
Septic shock related to endocarditis will be managed using fluid resuscitation, albumin, and antibiotics. One course of antibiotic treatment may include giving a patient 2 grams of intravenous Naficillin or oxacillin every four hours for at least six weeks (Brusch, 2023). Restoring the amount of circulating fluids and optimizing cardiac output are the goals of administering a fluid bolus in septic shock. A central venous catheter should be inserted into the internal jugular or subclavian vein if fluids cannot be given quickly enough, or a 30-to-60-minute fluid bolus of 30 mL/kg (1-2 L) should be administered. There are two situations in sepsis when albumin is administered. To start, it is a standard tool for first aid. (Ye et al.., 2022) At this point, albumin infusion raises the plasma colloid osmotic pressure, and albumin’s propensity to expand in volume aids in keeping hemodynamic stability.
Chronic kidney injury in this patient will be managed through fluid resuscitation, while acute thrombocytopenia and coagulopathy will be managed using transfused FFP and platelets. Patients with coagulopathy can be treated with fresh frozen plasma by replenishing or supplanting plasma proteins that are either lacking or flawed. An increase of about 20% in factor levels can be achieved with a typical dose of 10–20 mL/kg (4–6 units in adults) (Khawar et al.., 2022). An increase of about 10% of several components is sufficient to achieve hemostasis. Additionally, each unit of fresh frozen plasma comprises about 250 ml, which means it can give some volume resuscitation. Patients with renal impairment require extra attention when it comes to fluid and electrolyte management because of the razor-thin margin of safety. Acute kidney damage (AKI) can occur with insufficient fluid administration, while congestive heart failure and pulmonary edema can result from excessive fluid transfusion.
Nursing Management
One nursing management is hemodynamic monitoring. Critically, sick patients’ care revolves around hemodynamic monitoring. Information regarding the efficiency of the pump, the capacity of the arteries and veins, the volume of blood, and the perfusion of tissues can be obtained using both invasive and non-invasive techniques. It is possible to determine whether a patient is experiencing distributive, hypovolemic, cardiogenic, or obstructive shock based on the accurate data collected via hemodynamic monitoring. Hemodynamic monitoring, in conjunction with clinical evaluation, aids in fluid delivery, vasoactive medication selection and titration, and the determination of whether mechanical support is required to treat refractory shock and other complications. It permits real-time assessment of treatment efficacy. Secondly, the VAP bundle, CLABSI, and CAUTI bundles were implemented. Negm et al. (2021) found that device-associated infections (DAIs) were reduced once care bundles were implemented.
Third, nursing management is the implementation of medical plans like medications, investigations, and transfusions as indicated. They are also responsible for preventing pressure injuries and addressing the nutritional requirements of the patients. Six essential components comprise pressure ulcer admission assessments, daily risk assessments, skin inspections, moisture management, nutrition and hydration optimization, and pressure minimization as pressure injury prevention measures.
Application
This case study has enabled me to improve my ability to provide comprehensive and effective patient care, and this is based on the knowledge gained of septic shock and infective endocarditis. It is crucial to enhance patient outcomes by identifying early warning signs, responding swiftly, and collaborating with the healthcare team based on my understanding of the etiology, clinical presentations, and evidence-based management strategies for these conditions. With this information, I can better evaluate and track patients’ progress, administer targeted treatments, and inform patients and their loved ones about ways to stay healthy. In conclusion, keeping up with the latest research on treatment and evidence-based practice enables me to give excellent, person-centered care to my patients and guarantees that I can adjust to new medical standards in my nursing career.
Conclusion
Sepsis is one of the leading causes of mortality among ICU patients. This study promotes critical analysis and knowledge skills that can be used in early detection and prevention of complications. It is essential to understand the cellular level mechanisms that occur in septic shock that have been discussed in the pathophysiology and interpretation of the patient results. Finally, the paper discussed Ms Aziza’s medical and patient management.
References
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