Navigating Acute Kidney Injury: Uncovering the Pathophysiology and Management of Renal Calculi

Abstract

Assessment 2: Case study essay [University] NUM2306 Adult Health Care 1 [Name] October 11th, 2021 1319 words Table of Contents Introduction3 Pathophysiology3 Management5 Medications6 Conclusion7 References8 Assessment 2: Case study essay Introduction Obstruction to the bladder, ureters and/or kidney can cause Acute Kidney Injury (AKI), and if not treated, can lead to renal failure (Goldfrap, 2016). AKI decreases the functioning abilities of the kidney and the body’s homeostasis, due to the decline in Glomerular Filtration Rate (GFR) (Craft et al., 2019). Kidney stones, also known as renal calculi, are a known cause of postrenal AKI and cause of urinary obstruction (Nevo et al., 2019). In Australia, 10% of the population will experience a kidney stone (Thia & Saluja, 2021). Annually 12,000 hospital admissions are due to renal calculi, noting that 75-90% of incidences pass spontaneously without surgical attention (Cunningham et al., 2016). Key risk factors include poor diet, dehydration, hypercalciuria, PH imbalances, humid climates, and presence of supersaturation in urine (Srivastava et al., 2019). This case study is focussed on patient Sally Jones, a 56-year-old lady, who has a 6mm stone in her right ureter. The pathophysiology of renal calculi and the clinical manifestations that Sally presents will be discussed, along with recommended nursing management and medical interventions that would be put in place for Sally. Pathophysiology Acute Kidney Injury (AKI), previously known as acute kidney failure, is classified by the location of the obstruction/trauma (Goldfrap, 2016). The three classifications are prerenal, intrarenal and postrenal (Craft & Gordon, 2020). Kidney stones are an example of postrenal AKI (Zeimba & Matlaga, 2015), and are characterised by their mineral composition (Shadman & Bastani,2017). Evidence states there are four types of renal calculi, the most being calcium stones, accounting for up to 75% of calculi incidences (Solo et al., 2017). The less common are uric acid stones, struvite stones (Also known as ‘infection stones’, caused by UTIs) and cystine calculi, which are traced to genetic or secondary to a metabolic disorder (Shadman & Bastani, 2017). Moreover, precipitation of these minerals forms small hard crystals due to decrease of urine volume, supersaturation of urine or change in the PH levels (Srivastava et al., 2019). A stone may continue to grow once attached to the urothelium, due to additional organic matter forming around the nidus (Craft et al., 2019). Renal calculi are generally asymptomatic until they enter the ureter (Solo et al., 2017). Sally may have had an UTI first, that has led to a struvite stone. By consideration of the urinalysis (UA), which displays blood, nitrates, proteins, and a cloudy appearance which is a diagnosis of infection in the bladder (Trimarchi, young & Lombi, 2015). The common symptoms of acute pyelonephritis (caused by a UTI and struvite stone) are fever, chills, cloudy urine, voiding and flank pain, which are all clinical manifestations Sally is experiencing and secondary to kidney stones (Grasso & Goldfrap, 2014). The right sided flank pain that Sally is experiencing is called renal colic, this occurs due to the stone passage causing spasming and contracting of the smooth muscle in the ureter (Cunningham et al., 2016). Additionally, the obstruction due to the calculus in the ureter, initiates the release of prostaglandins and the inflammatory response (Afshar et al., 2015). Prostaglandins generate vasodilation that increases urinary flow, intra-ureteral pressure, oedema, vascular permeability and uretic spasming and hyperperistalsis (Afshar et al., 2015). Moreover, prostaglandins are what causes Sally to feel continuous pain and nausea (Steinberg & Chang, 2016). The presence of haematuria and higher than normal serum creatinine and BUN levels indicate AKI and the decline in kidneys function and glomerular filtration rate (GFR) (Craft et al., 2020). The decline in the GFR means retention of waste products such as creatine and BUN that are otherwise excreted in a normal functioning kidney (Jennette et al., 2015). Moreover, this will also signal the brain centres that the renal BP has decreased, which will initiate a negative feedback response increasing Sally’s heart rate (108bpm), BP (124/87), and respiratory rate (22) to compensate and work to restore the homeostasis (Craft et al., 2019). Immediate medical attention is needed to relieve pain and smooth muscle spasming in the ureter (Thia & Saluja, 2021). Management Renal calculi require immediate nursing management and medical expulsion therapy (MET), to relieve Sally of renal colic (Thia et al., 2021). Sally presents to ED with a pain score of 8 out of 10, which classifies as severe pain (Royal Perth Bentley Group, [RPBG], 2020). The World Health Organisation Pain management guidelines suggest collecting subjective data, pain score, and reduce fear (Berman, 2017). The first step is to offer Sally non-pharmalogical treatment, deep breathing exercises and encouragement of fluid consumption to reduce further stone formation (Cunningham et al., 2016). The use of intravenous (IV) fluids should be implemented to work towards urinary dilution, to prevent further stone growth (Ziemba & Matlaga, 2015). The second step is dependant on the level of pain andchoosing a medication that will limit side effects and have the most rapid effect (Royal Perth and Bentley Group [RPBG], 2020). Evidence suggests that the use of non-steroid anti-inflammatory drugs (NSAIDS), adjuvant medications (co-analgesics) and alpha blockers, are the most effective relief for renal colic, then that of opioid medications (Watt et al.,2018). NSAIDs decrease...