StudentShare
Contact Us
Sign In / Sign Up for FREE
Search
Go to advanced search...
Free

Paramedic Intervention into Fluid, Electrolyte and Acid-Base Disturbances in Renal Failure - Case Study Example

Summary
The paper “Paramedic Intervention into Fluid, Electrolyte and Acid-Base Disturbances in Renal Failure”  is a motivating variant of a case study on nursing. The kidney is one of the major body organs involved in the regulation of body fluids and electrolytes. The homeostatic control of body fluids and electrolytes occur along the renal tubules in the nephron…
Download full paper File format: .doc, available for editing
GRAB THE BEST PAPER98.6% of users find it useful

Extract of sample "Paramedic Intervention into Fluid, Electrolyte and Acid-Base Disturbances in Renal Failure"

Fluid, Electrolyte and Acid-base Disturbances in Renal Failure Student’s Name Institutional Affiliation Fluid, Electrolyte and Acid-base Disturbances in Renal Failure The kidney is one of the major body organs involved in the regulation of body fluids and electrolytes. The homeostatic control of body fluids and electrolytes occur along the renal tubules in the nephron (Thomson & Macnab, 2009; Kraft, Btaiche, Sacks & Kudsk, 2005). A healthy functioning kidney usually excretes approximately 1500ml of water in addition to surplus electrolytes such as phosphate, potassium, sodium and magnesium (Thomson & Macnab, 2009). Therefore, renal failure, be it acute or chronic, may result in a substantial electrolyte and fluid derangements in the body in addition to acid-base imbalance. Occurrence of Chronic Renal Failure (CRF) CRF or Chronic kidney disease (CKD) can be described as a disease characterized by a decrease in "glomerular filtration rate (GFR) to less" than 60ml/min/1.73m2 for at least three months or a progressive loss in the functionality of the renal system that occurs over at least three months to years (Murpbree & Thelen, 2010). CKD's etiology may be a variety of diseases and factors that include hypertension, cystic kidney diseases, vascular diseases, diabetic kidney disease, recurrent kidney stone disease, tubulointerstitial diseases, glomerular diseases, urinary tract dysfunction or obstruction, unresolved episodes of acute kidney injury and congenital renal defects (Metcalfe, 2007; Nahas & Bello, 2005). Moreover, factors such as nephrotoxins, proteinuria, hyperlipidemia, smoking, systemic hypertension, impaired renal perfusion and hyperphosphatemia can aggravate the progress of CKD (Murpbree & Thelen, 2010). Exposure to the above risk factors drives the progressive destruction and loss of renal function. These factors cause cumulative physical damage to the kidney cells that results in the release of "inflammatory mediators, including cytokines, chemokines and growth factors" (Nahas & Bello, 2005). The latter, most notably transforming growth factor (TGF) beta 1, is a primary activator of intracellular signal transduction pathways in glomerular and tubolointerstitial cells. Initially, these pathways mediate healing of injured renal cells but repeated stimulation caused by persistent exposure to diseases or factors highlighted above ultimately results in progressive tubolointerstitial fibrosis and glomerulosclerosis (Nahas & Bello, 2005). The loss of renal function is initially asymptomatic as the kidney possesses innate activity that enables it to maintain a normal GFR due to compensatory hypertrophy and hyperfiltration in the nephron. However, progressive damage leads to persistent uremic symptoms typical of CKD (Thomas, Kanso & Sedor, 2008). Fluid Imbalance in Renal Failure As CKD progresses, fluid abnormalities begin manifesting as the compensatory mechanisms of the kidney get exhausted. This is common when the GFR falls to lower than 15ml/min/1.73m2 during stages 4-5 of the disease (Kovesdy, 2012). The impact of the “renin-angiotensin-aldosterone system” (RAAS) in fluid balances is blunted by sclerosis and fibrosis of the glomeruli and the tubulointerstitial cells (Wolf & Ruster, 2006). At this stage, the ability of the kidney to dilute or concentrate urine maximally has remarkably decreased, therefore, affecting the kidney's ability to respond to alteration in water intake. The dilution capacity is maintained for longer periods compared to the concentration capacity during the late stages of the disease ultimately resulting in a constant urine osmolality despite variation in water intake (Kovesdy, 2012). These changes are central to fluid overload and hypovolemia experienced in CKD (Thomson & Macnab, 2009). In the early stages of CKD, fluid overload may become apparent after an increased fluid intake either orally or parenterally during fluid therapy but this manifestation is overt in the late stages of the disease. Failure of the kidney to excrete free water and excess sodium results in accumulation of fluid in the intracellular and extracellular spaces resulting in edema and hypertension (Thomson & Macnab, 2009). Electrolyte imbalance in RF The predominant electrolyte changes in CKD especially stage 5 of the disease include hyperphosphatemia, hypocalcemia and hyperkalemia. Hyperphosphatemia occurs due to a decrease in phosphate excretion precipitated by impaired glomerular filtration (Karmarkar & Macnab, 2012). Hyperphosphatemia inhibits formation of active calcitriol resulting in diminished calcium absorption in the intestines leading to hypocalcemia (Thomas, Kanso & Sedor, 2008). At GFR of less than 15 ml/min/1.73m2, potassium excretion is decreased resulting in hyperkalemia (Mahaldar, 2012). Serum sodium concentration may vary depending on the water volumes. Hypernatremia is common in hypovolemic states while hyponatremia – dilutional hyponatremia, is common in water overload or after increased fluid intake (Arrovo, 2008). Table 1: Summary table of electrolyte changes in advanced CKD Electrolyte Changes in advanced CKD Potassium ions Increased Phosphate ions Increased Calcium ions Decreased Sodium ions Increased/decreased Acid-base Imbalances in RF The epitome of acid-base imbalance in end-stage RF is uremic acidosis characterized by an anion gap metabolic acidosis (Cibulka & Racek, 2007). With GFR of below 20 ml/min, a normal anion gap metabolic acidosis is common. The kidney regulates blood pH through excretion of excess H+ and production or reabsorption of hydrogen carbonate ions (Mahalder, 2012). This regulation is effected via transporters present in renal tubular cells that are progressively impaired as CKD advances. Ineffective renal bicarbonate and ammonia buffer system ultimately results in accumulation of acidic hydrogen ions due to inability of the kidney to generate and reabsorb sufficient bicarbonate and form ammonia (NH3) buffer (Cibulka & Racek, 2007). The anion gap is precipitated by accumulation of nonvolatile and organic acids. Below is a flow chart of the occurrence of metabolic acidosis in CKD. Signs and Symptoms of RF In the early stages 1-3 of CKD, there are limited or no symptoms despite a higher creatinine or blood urea nitrogen (Snyder & Pendergraph, 2005). In stages 4-5, GFR is less than 30ml/min/1.73m 2 manifesting as deranged metabolic, endocrine, water and electrolyte disturbances (Nahas & Bello, 2005). Inability of the kidney to concentrate urine as the disease progresses may manifest as nocturia. The earliest signs of uremia in renal failure include anorexia, fatigue, lassitude and a reduction in mental acuity (Snyder & Pendergraph, 2005). Metabolic acidosis in stage 5 of the disease presents with signs such as protein-energy malnutrition as a result of renal loss of proteins and essential amino acids, loss of lean body mass and increasing muscle weakness (Cibulka & Racek, 2007). As the kidney’s capacity to handle water and salt decreases as the disease advances, accumulation of fluid – hypervolemia, may result in pulmonary edema, peripheral edema, and hypertension. The latter may aggravate an already existing hypertension since hypertension is a risk factor for CKD (Arrovo, 2008). Anemia resulting from insufficient synthesis of erythropoietin in a deranged kidney manifests as fatigue, reduced exercise tolerance, impaired immunity and cognitive capacity and development of diseases of the cardiovascular system (Murpbree & Thelen, 2010). Occasionally, inability to excrete urea by the kidney results in accumulation and crystallization of urea on the skin after excretion alongside sweat. This manifests as uremic frost on the skin (Mahaldar, 2012). Paramedic Intervention Patient assessment is among the initial steps when handling patients manifesting with acute exacerbation of RF. The patient's history, a physical assessment, fluid and mental status assessment, and cardiac rhythm are all important in identifying pathologies or problems affecting the patient. Treatment at the pre hospital level may be specific depending on the priority after assessment, but it includes providing oxygen to the patient in addition to establishing an IV access (Middleton & Patel, 2014). Endotracheal intubation may be necessary for patients experiencing respiratory distress in addition to positive pressure ventilation (Ho & Wong, 2006). Carefully controlled IV fluids are applicable to patients with hypotension and dehydration signs. The fluids are provided in small – about 200ml-250ml as the dose is increased appropriately with a frequent assessment of alteration in blood pressure and breath sounds (Middleton & Patel, 2014). The latter is instrumental in assessing for pulmonary edema that may be managed by employing "bi-level positive airways pressure [BiPAP]" (Ho & Wong, 2006). Pharmacologically the patient may be treated using diuretics such as furosemide to relieve any edema. Calcium, insulin, 50% dextrose and bicarbonate can manage hyperkalemia. Dosage of these medication may vary but common adult doses include 25 grams of 50% dextrose, 1 mEq/kg of an 8.4% sodium bicarbonate solution, 10 units of subcutaneous insulin and 8-16mg/kg of calcium chloride (Kraft et al., 2005). However, these management measures only serve to support the patient's vital systems and prompt transport to dialysis centers, or a hospital environment should be facilitated for definitive therapy. Conclusion RF may present as either acute renal failure or CKD. The former may occur superimposed on the latter. Paramedics need to identify and understand the presentation of both conditions to guide appropriate emergency interventions. CKD is a chronic condition that progresses through five stages culminating in end-stage renal failure. The initial first three stages may be asymptomatic, but its symptoms in later stages of the disease may be severe if not rapidly and aptly managed. Such symptoms include acid-base imbalances such as metabolic acidosis, and electrolyte disturbances such as hyperkalemia, hyperphosphatemia, and hypocalcemia. Therefore, the paramedics should carry out blood or urine tests to determine the severity of electrolyte and acid-base disturbances before instituting appropriate therapeutic interventions. While managing such patients, paramedics should prioritize their interventions by following the basic ABC where the airways are attended to first stabilizing them before making sure that the patient is in proper breathing condition and that the circulation is intact (Thim, Krarup, Grove, Rohde & Lafgren, 2012). Prioritization of interventions enables the paramedics to attend to vital patient parameters before normalizing any other dysfunction resulting from the disease. Once the patient has stabilized, transport should be urgently provided to the nearest appropriate hospital for further management in a hospital setup. This may include scheduling the patient for dialysis to restore normal homeostatic physiological state of the body. References Arrovo, A.R. (2008). Electrolyte and acid-base balance disorders in advanced chronic kidney disease. Nefrologia, 28(Suppl 3), 87-93. Cibulka, R. & Racek, J. (2007). Metabolic disorders in patients with chronic kidney failure. Physiological Research, 56, 697-705. Ho, K.M. & Wong, K. (2006). A comparison of continuous and bi-level positive airway pressure non-invasive ventilation in patients with acute cardiogenic pulmonary edema: a meta-analysis. Critical Care, 10(2), 1-8. Karmarkar, S. & Macnab, R. (2012). Fluid and electrolyte problems in renal dysfunction. Anaesthesis & Intensive Care Medicine, 13(7), 332-335. Kovesdy, C.P. (2012). Significance of hypo- and hypernatremia in chronic kidney disease. Nephrology Dialysis Transplant, 27, 891-898. Kraft, M.D., Btaiche, I.F., Sacks, G.S. & Kudsk, K.A. (2005). Treatment of electrolyte disorders in adult patients in the intensive care unit. American Journal Health System Pharmacy, 62, 1663-1682. Mahaldar, A.R. (2012). Acid-base and fluid electrolyte disturbances in chronic kidney disease. Clinical Queries: Nephrology, 1(4), 295-299. Metcalfe, W. (2007). How does early chronic kidney disease progress? Nephrology Dialysis Transplantation, 22(suppl 9), ix26-ix30. Middleton, J.P. & Patel, U.D. (2014). Comanaging cardiovascular and kidney diseases. Advances in Chronic Kidney Disease, 21(6), 453-508. Murpbree, D.D. & Thelen, S.M. (2010). Chronic kidney disease in primary care. Journal of American Board of Family Medicine, 23(4), 542-550. Nahas, A.M. & Bello, A.K. (2005). Chronic kidney disease: the global challenge. The Lancet, 365(9456), 331-340. Ruster, C.& Wolf, G. (2006). Renin-Angiotensin-Aldosterone system and progression of renal disease. Journal of the American Society of Nephrology, 17(11), 2985-2991. Snyder, S. & Pendergraph, B. (2006). Detection and evaluation of chronic kidney disease. American Family Physician, 72(9), 1723-1732. Thim, T., Krarup, N.H., Grove, E.L., Rohde, C.V & Lafgren, B. (2012). Initial assessment and treatment with the airways, breathing, circulation, disability, exposure (ABCDE) approach. International Journal of General Medicine, 5, 117-121. Thomas, R., Kanso, A. & Sedor, J.R. (2008). Chronic kidney disease and its complications. Primary Care. Clinics in Office Practice, 35(2), 329-344. Thomson, H. & Macnab, R. (2009). Fluid and electrolyte problems in renal dysfunction. Anaesthesia & Intensive Care Medicine, 10(6), 289-292. Read More

CHECK THESE SAMPLES OF Paramedic Intervention into Fluid, Electrolyte and Acid-Base Disturbances in Renal Failure

Evidenced-Based Analysis of a Clinical Competency: Fluid and Electrolyte Balance of the Neonate

The author of the paper "Evidenced-Based Analysis of a Clinical Competency: Fluid and electrolyte Balance of the Neonate" will begin with the statement that clinical competency in the fluid and electrolyte balance of the neonate is an important clinical skill to develop in pediatric care.... 2) have paid attention that disorders of fluid and electrolyte are prevalent among neonates, and understanding the physiological changes in the neonate's body water and solute after birth is crucial in securing an efficient shift from the aquatic in-utero environment....
12 Pages (3000 words) Essay

The Acid Base Disturbance

However, ammonium chloride must not be administered to patients with known conditions of liver such as liver failure because the drug is likely to cause brain failure and damage in these patients (Lehne, 2010).... Consequently, renal replenishment is not very effective.... The volume substitution decreases renal capability to reabsorb Na+ and chloride ions.... Consequently, breathing above normal rate causes retention of CO2, increased renal excretion of bicarbonate and buildup of organic acids....
2 Pages (500 words) Essay

Fluid Hydration Support

From the paper "fluid Hydration Support", the human body has been provided with the ability to control and maintain its requirement for water and electrolytes along with other essentials.... Calculations for fluid requirements in the pediatrics category are strictly based on body weight as compared to rough estimation in adults.... Similarly, monitoring fluid intake and output may need some judicious efforts as compared to healthy and adult individuals....
9 Pages (2250 words) Essay

Acute renal failure

To ascertain the presence of acute renal failure in patients, the following diagnostic tests are required: Blood tests that include "CBC, blood urea nitrogen (BUN), creatinine, electrolytes (including Ca and PO4).... To ascertain the presence of acute renal failure in patients, the following diagnostic tests are required: Blood tests that include "CBC, blood urea nitrogen (BUN), creatinine, electrolytes (including Ca and PO4)Urine tests include Na and creatinine concentration and microscopic analysis of sediment; acidosis, hyperkalemia, hyponatremia, and anemia....
4 Pages (1000 words) Essay

Drug-Drug Interaction: the Relevance of Application of Orlistat

hen the diagnosis of metformin-associated lactic acidosis with cardiovascular collapse and acute prerenal renal failure was made, it was discovered that she needed She required vigorous rehydration, infusion of sodium bicarbonate, support of inotropic, and the therapy of renal replacement.... he study aims at answering the question of what initiates MALA in patients who previously had normal renal functions.... Though the approach of handling this condition is unknown, the available options have been supportive and usually focus on stopping the drug, correcting the acidosis, and treating the coexisting conditions which in most instances are renal impairment....
17 Pages (4250 words) Essay

Preventing Renal Failure in Patients with Rhabdomyolysis

This paper 'Preventing renal failure in Patients with Rhabdomyolysis' reviews the incidence, pathophysiology, clinical characteristics, diagnostic methods, advanced practice methods and research implications of rhabdomyolysis.... More serious cases may present with severe symptoms such as renal failure.... The author states that rhabdomyolysis has many causes, including cocaine abuse, trauma, strenuous exercise, infections, hyperthermia and other conditions that alter electrolyte balance or disrupt the integrity of the plasma cell membrane....
14 Pages (3500 words) Assignment

Renal Failure with Dialysis

The focus of this paper "renal failure with Dialysis" is on renal failure (RF) as a prevalent chronic disease that inflicts an enormous burden on the healthcare system not only in the United States but also in other developed and developing countries across the world (Matavinovic, 2009, p.... renal failure (RF) is a condition in which 'the kidneys fail to remove metabolic end-products from the bloodstream and regulate the fluid, electrolyte, and pH balance of the extracellular fluids'....
4 Pages (1000 words) Essay

Fluid Imbalances Caused by Renal Failure

The focus of the paper ''renal failure" is on how chronic renal failure occurs, fluid imbalances caused by renal failure, electrolyte imbalances caused by RF, including changes in potassium, calcium, phosphate, sodium, normal blood levels of electrolytes.... The symptoms the person experiences, or which can be measured and observed by medical staff, will vary according to the severity of the kidney failure, the underlying condition which causes it, and the rate at which the failure progresses....
6 Pages (1500 words) Essay
sponsored ads
We use cookies to create the best experience for you. Keep on browsing if you are OK with that, or find out how to manage cookies.
Contact Us