Acute Kidney Injury

Introduction of Acute Kidney Injury and the Impact of the Disease on Pediatrics and Adults

Acute kidney injury (AKI) is defined as a sudden but often reversible decrease in kidney function. The disease affects both children and adults, with the majority of cases being reported in children. The Kidney Disease Improving Global Outcomes (KDIGO) criteria for AKI are as follows: urine output of 0.5 ml/kg/hr for 6 hours, serum creatinine increase of >0.3 mg/dl or more for 48 hours, or serum creatinine increase of 1.5 times the baseline or more within the last 7 days (Kellum et al., 2021).

The Acute Kidney Injury Network (AKIN) has three stages of the disease, with the details as stated hereafter: stage 1: serum creatinine of 1.5-1.9 times the baseline or ≥0.3 mg/dl serum creatinine or <0.5 ml/kg/hr for 6-12 hours; stage 2: serum creatinine of 2-2.9 times the baseline or urine output <0.5 ml/kg/hr for ≥12 hours; stage 3: serum creatinine of 3 times the baseline or increase to ≥4.0 mg/dl or <0.3 ml/kg/hr for >24 hours or anuria for ≥12 hours (Kellum et al., 2021). Depending on the severity of the disease, its impact on the patients varies.

The disease has nearly identical effects on the pediatric and adult populations. First, the disease may necessitate a prolonged hospitalization, which the patients may not have anticipated. During hospitalization, patients spend a lot of money on care and interventions, and managing AKI becomes expensive in the long run (Olowu et al., 2018).

Furthermore, patients may contract hospital-acquired diseases during their stay, increasing morbidity and the cost of care. In some cases, the disease causes death, accounting for 23.3% of adult mortality and 13.8% of pediatric mortality (Olowu et al., 2018). The disease also contributes to significant psychosocial morbidity because hospitalization is stressful, and patients are away from their daily income-generating activities. Furthermore, the interventions that patients undergo during their hospitalization, such as phlebotomy and injections, are painful and cause discomfort.

Pathophysiology and Common Findings in History and Physical Examination

Numerous factors contribute to the disease. Etiology drives pathophysiology. However, the ultimate cause of acute tubular necrosis is either ischemia or toxins, which cause cell death, effacement of the brush border, and loss of tubular cell function (Goyal et al., 2022). The etiology of AKI is divided into three categories: prerenal, renal, and postrenal.

Hypovolemia caused by hemorrhage, burns, vomiting, or diarrhea; cardiac failure, sepsis, or drug-induced hypovolemia in the case of diuretics are examples of prerenal factors (Goyal et al., 2022). Renal factors include nephrotoxins such as aminoglycosides (Gentamycin), NSAIDS (Diclofenac), and iodinated contrast; infections and metal poisoning (mercury), myoglobinuria, and myeloma, among others (Goyal et al., 2022). Kidney stones, tumors, prostatic hypertrophy, and retroperitoneal fibrosis are all post-renal factors.

The history and physical examination are important in the diagnosis of AKI. Dehydration, decreased urine output, changes in urine color, thirst, nausea and vomiting, and confusion or drowsiness are common findings in history (Goyal et al., 2022). Dehydration-related findings in the physical examination include decreased capillary refill, weak or absent peripheral pulses, low blood pressures, cold extremities, temperature gradient, and skin pinch or >2 seconds.

Patients may also exhibit signs of obesity, as well as signs of cardiac failure such as lower limb edema and liver disease such as jaundice. In general, no single symptom or sign is pathognomonic of AKI. What is discovered is a constellation of symptoms and signs that necessitates a doctor’s clinical acumen to make a diagnosis of AKI.

Incidence and Prevalence of the Disease

It is estimated that 1% of patients admitted to hospitals in the United States have AKI at the time of admission. The estimated incidence rate of AKI during hospitalization is 2-5% (Hoste et al., 2018). It is further estimated that approximately 1% of general surgery patients develop AKI within 30 days of surgery, while it occurs in more than 50% of intensive care unit patients (Hoste et al., 2018).

According to Yadav et al. (2022), 21% of recipients of a solitary kidney transplant developed AKI within 6 months of the transplant. Harding et al. (2020) discovered that from 2000 to 2015, the admission rates of dialysis patients requiring AKI increased while mortality rates decreased significantly. Hospitalization rates for adults with diabetes increased from 26.4 to 41.1 per 100,000 population.

Those without diabetes increased from 4.8 to 8.7 per 100,000 people between 2000 and 2009 (Harding et al., 2020). Furthermore, statistics show that approximately 95% of nephrology consultations are due to AKI, demonstrating the magnitude of the disease and its impact on patients and healthcare in general.

Interpretation of Current Evidence-Based Treatment

AKI management requires a step-by-step approach. First, Sykes et al. (2018) recommend treating sepsis, if present, before moving on to other steps in the STOP AKI campaign. The following interventions are recommended for sepsis management: high flow oxygen, blood samples for culture, intravenous antibiotics, intravenous fluid resuscitation, checking hemoglobin and serial lactates and assessing the need for transfusion, and finally, hourly urine output measurement (Sykes et al., 2018).

Moore et al. (2018) elaborated well on the second step of STOP AKI: identifying, avoiding, and stopping potential nephrotoxins. The nephrotoxins at play are aminoglycosides like gentamycin, NSAIDs like Diclofenac, and iodinated contrast media (Moore et al., 2018). Ostermann et al. (2019) discuss the role of fluid therapy in AKI management in the third step. First, this step is tailored to the individual.

Before beginning fluid therapy, the patient’s volume status must be assessed, and key points in the assessment include capillary refill, pulse rate, blood pressure, respiratory rate, jugular venous pressure, edema (periphery and pulmonary), and the fluid balance chart (Ostermann et al., 2020). A crystalloid solution, such as Hartmann’s, lactated Ringer’s, or Plasma-Lyte 148, is preferred (Ostermann et al., 2020).

In some circumstances, such as AK secondary to rhabdomyolysis, 0.9% sodium chloride would be preferred (Ostermann et al., 2020). The STOP AKI interventions conclude with the prevention of harm and treatment of complications. Complications such as hyperkalemia, acidemia, fluid overload-induced pulmonary edema, and uremic encephalopathy are managed at this stage (Goyal et al., 2022; Negi et al., 2018). Furthermore, the potential etiologies of AKI are appropriately managed.

Role of a Registered Nurse in the Management of AKI and the Role of Pharmacological vs. Non-pharmacological Treatment

Nurses, as the majority of healthcare workers, interact with patients more frequently, including AKI patients. Nurses play an essential role in assessing patients’ vital signs, including heart rate, blood pressure, oxygen saturation, temperature, and respiratory rate. Furthermore, the RN evaluates the volume status of the patients using the parameters listed in the preceding paragraph.

Fluid therapy, nutrition, drug administration, patient education, and counseling are all examples of nursing interventions (Goyal et al., 2022). The importance of pharmacology in the treatment of AKI cannot be overstated. Antibiotics play an important role when there is a known source of infection.

Furthermore, the following drugs may be used to treat hyperkalemia, a complication of AKI: calcium gluconate, nebulized albuterol, insulin and dextrose, loop diuretics (Furosemide), potassium binders such as Kayexalate, and aldosterone analogs such as 9-alpha fluorohydrocortisone (Kellum et al., 2021).

In hypervolemic AKI patients who are not anuric, diuretics may be used to relieve hypervolemia (Kellum et al., 2021). Non-pharmacological interventions are also necessary, including fluid therapy, nutrition (restricting potassium-rich foods), bed head elevation in the case of fluid overload-induced pulmonary edema, patient education, and patient reassurance.

Cultural and Social Cultural Considerations and Impact on the Care Plan

Care is influenced by culture in a variety of ways. One, language barriers may impede communication between the care provider and the patient, thereby jeopardizing the therapeutic relationship between the patient and the care provider (Negi et al., 2018).

Two, some communities, such as the Jehovah’s Witnesses and Christian scientists, refuse medical treatment, claiming that God’s healing is sufficient (Swihart et al., 2021). Other social-cultural factors that harm care are patients’ beliefs in alternative medicines and their distrust of healthcare services or clinicians. To avoid sociocultural quandaries, it is critical to raise disease awareness to improve people’s health-seeking behavior.

Prognosis and Long-term Health Considerations

When AKI is well managed, the prognosis is generally favorable. However, factors such as advanced age, multiorgan failure, hypotension, oliguria, multiple blood transfusions, vasopressor support, and noncavitary surgery may have a significant negative prognostic impact (Fiorentino et al., 2018).

AKI is linked to the progression of chronic kidney disease in the long term; up to 20% of patients with an inpatient diagnosis of acute tubular necrosis progress to chronic kidney disease stage IV or higher within 18-24 months (Fiorentino et al., 2018). Furthermore, AKI can cause recurrent AKI episodes, increase the risk of cardiovascular events, and raise the risk of mortality.

Conclusion

AKI, a renal disease, is the leading cause of nephrology consultations. The disease has multiple contributory factors, which are classified as prerenal, renal, and postrenal. A high clinical index of suspicion is required for the diagnosis, which is derived from the history, physical exam, and laboratory tests.

If the diagnosis is confirmed, the STOP AKI approach is recommended for aggressive treatment. When the disease is aggressively managed, the prognosis is generally good. However, other patient factors, such as advanced age and comorbidities, may negatively prognosticate the disease.

References

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