Acute renal failure occurs when the kidneys are unable to excrete waste products from the body, causing them to accumulate in the blood. It can be caused by conditions that decrease renal blood flow or damage the kidneys. Patients are classified as oliguric, excreting less than 500mL of urine per day, or nonoliguric, excreting more than 500mL daily. Risk factors include advanced age, diabetes, heart or liver disease. Diagnosis involves urine and blood tests to check kidney function and imaging tests in some cases. Treatment focuses on treating the underlying cause, managing fluid balance and electrolytes, and dialysis in severe cases.
Acute and Chronic Renal Failure. Easy Slides.Anubhav Singh
The document provides information on acute and chronic renal failure. It discusses the etiology, pathophysiology, symptoms, diagnostic tests, and management of acute renal failure. It also covers the introduction, etiology, symptoms, stages, treatment, and prevention of chronic renal failure. The key differences between non-dialysis dependent chronic kidney disease and end-stage renal disease are also outlined.
This includes a comprehensive study of Renal Failure - both AKI & CKD (ESRD). It is very helpful for those who are managing the clients with renal failure.
1. Acute renal failure (ARF) is an acute, potentially reversible condition where the kidneys fail to maintain homeostasis. Causes include prerenal factors like shock, congestive heart failure, or intrarenal injury from toxins. Symptoms range from nonspecific like fever to specific kidney issues like electrolyte imbalances. Treatment focuses on fluid management, electrolyte replacement, and potentially dialysis.
2. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It is usually caused by congenital anomalies or acquired glomerular diseases. Symptoms emerge late and include fatigue, nausea, and cardiac/bone issues. Treatment manages complications and slows progression with a low protein
Chronic kidney disease (CKD) consists of a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).
Acute renal failure is a sudden reduction in kidney function that results in waste accumulating in the blood. It can be caused by problems affecting blood flow to the kidneys like dehydration, blood loss from major surgery or burns, or kidney problems preventing proper filtration. Symptoms include reduced urination, swelling, fatigue, and shortness of breath. Treatment focuses on fluid balance, electrolytes, nutrition, and preventing complications like infection that can further stress the kidneys.
This document provides information on acute kidney failure (ARF), including its definition, risk factors, pathophysiology, diagnosis, and nursing care considerations. ARF occurs when the kidneys are unable to excrete waste from the body due to high levels of toxins. It is characterized by three phases: onset, maintenance, and recovery. Nursing interventions focus on monitoring fluid balance, electrolytes, output, diet, and preventing infections to support the patient's recovery.
The document discusses drugs and their effects on the kidney. It covers normal kidney function, estimation of renal function, loop and thiazide diuretics, nephrotoxic drugs such as NSAIDs and aminoglycosides, and prescribing considerations in kidney disease. The ALLHAT trial found thiazide-type diuretics were superior to other antihypertensives in preventing cardiovascular disease due to their lower cost and greater efficacy.
This document defines and discusses acute renal failure (ARF), including its etiology, pathogenesis, investigations, management, and prognosis. ARF is a sudden, usually reversible loss of kidney function developing over days or weeks with reduced urine output. The etiology is divided into pre-renal, renal, and post-renal causes. Pre-renal ARF is due to decreased renal perfusion from conditions like heart failure or blood loss. Renal ARF includes acute tubular necrosis from ischemia or nephrotoxins. Post-renal ARF occurs from urinary tract obstruction. Management involves treating the underlying cause, fluid and electrolyte balance, and potentially renal replacement therapy. Prognosis depends on severity and
Acute and Chronic Renal Failure. Easy Slides.Anubhav Singh
The document provides information on acute and chronic renal failure. It discusses the etiology, pathophysiology, symptoms, diagnostic tests, and management of acute renal failure. It also covers the introduction, etiology, symptoms, stages, treatment, and prevention of chronic renal failure. The key differences between non-dialysis dependent chronic kidney disease and end-stage renal disease are also outlined.
This includes a comprehensive study of Renal Failure - both AKI & CKD (ESRD). It is very helpful for those who are managing the clients with renal failure.
1. Acute renal failure (ARF) is an acute, potentially reversible condition where the kidneys fail to maintain homeostasis. Causes include prerenal factors like shock, congestive heart failure, or intrarenal injury from toxins. Symptoms range from nonspecific like fever to specific kidney issues like electrolyte imbalances. Treatment focuses on fluid management, electrolyte replacement, and potentially dialysis.
2. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It is usually caused by congenital anomalies or acquired glomerular diseases. Symptoms emerge late and include fatigue, nausea, and cardiac/bone issues. Treatment manages complications and slows progression with a low protein
Chronic kidney disease (CKD) consists of a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).
Acute renal failure is a sudden reduction in kidney function that results in waste accumulating in the blood. It can be caused by problems affecting blood flow to the kidneys like dehydration, blood loss from major surgery or burns, or kidney problems preventing proper filtration. Symptoms include reduced urination, swelling, fatigue, and shortness of breath. Treatment focuses on fluid balance, electrolytes, nutrition, and preventing complications like infection that can further stress the kidneys.
This document provides information on acute kidney failure (ARF), including its definition, risk factors, pathophysiology, diagnosis, and nursing care considerations. ARF occurs when the kidneys are unable to excrete waste from the body due to high levels of toxins. It is characterized by three phases: onset, maintenance, and recovery. Nursing interventions focus on monitoring fluid balance, electrolytes, output, diet, and preventing infections to support the patient's recovery.
The document discusses drugs and their effects on the kidney. It covers normal kidney function, estimation of renal function, loop and thiazide diuretics, nephrotoxic drugs such as NSAIDs and aminoglycosides, and prescribing considerations in kidney disease. The ALLHAT trial found thiazide-type diuretics were superior to other antihypertensives in preventing cardiovascular disease due to their lower cost and greater efficacy.
This document defines and discusses acute renal failure (ARF), including its etiology, pathogenesis, investigations, management, and prognosis. ARF is a sudden, usually reversible loss of kidney function developing over days or weeks with reduced urine output. The etiology is divided into pre-renal, renal, and post-renal causes. Pre-renal ARF is due to decreased renal perfusion from conditions like heart failure or blood loss. Renal ARF includes acute tubular necrosis from ischemia or nephrotoxins. Post-renal ARF occurs from urinary tract obstruction. Management involves treating the underlying cause, fluid and electrolyte balance, and potentially renal replacement therapy. Prognosis depends on severity and
Acute renal failure and chronic renal failureNEHA BHARTI
This document provides information about acute renal failure. It begins by defining renal failure and its two types - acute and chronic. Acute renal failure is described as a sudden loss of kidney function over hours to weeks. Risk factors, phases, clinical manifestations, diagnostic evaluations, and management including pharmacologic therapy, fluid/electrolyte replacement, nutrition, and dialysis are summarized. Chronic renal failure is defined as a gradual loss of kidney function over months to years that progresses to end-stage renal disease requiring dialysis or transplant. Stages and uremic symptoms affecting multiple organ systems are outlined.
Pyelonephritis
It is the inflammation of the kidney & upper urinary tract that usually results from the bacterial infection of the bladder.
Pyelonephritis can be classified in several different catagories:
-acute pyelonephritis
-chronic pyelonephritis
-xanthogranulomatous pyelonephritis
This document provides an overview of renal failure and its nursing management. It begins with an anatomical and physiological overview of the urinary system, focusing on kidney structure and function. The two main types of renal failure discussed are acute kidney injury (AKI), previously called acute renal failure (ARF), and chronic renal failure (CRF). AKI is defined as a sudden decline in kidney function over 48 hours and can be caused by prerenal, intrarenal, or postrenal factors. CRF is a gradual loss of kidney function over months or years. The global and Indian burden of kidney disease is also reviewed.
The kidneys filter blood and regulate fluid levels in the body by selectively reabsorbing or secreting solutes. Urine passes from the kidneys through ureters into the bladder, then through the urethra. The kidneys contain nephrons which filter blood and reabsorb or excrete products. Hematuria, the presence of blood in urine, can indicate issues ranging from minor infections to serious conditions like cancer and requires medical evaluation.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure. It defines AKI and provides causes and characteristics of pre-renal, renal, and post-renal AKI. Pre-renal AKI is caused by decreased renal perfusion due to issues like volume depletion or heart failure. Renal AKI can be caused by issues affecting the glomeruli, interstitium, or tubules, such as acute tubular necrosis. Post-renal AKI is due to urinary tract obstruction. The document outlines evaluation of AKI including history, exam, urine and serum tests, imaging, and novel biomarkers. It also discusses complications of AKI and general management strategies.
CHRONIC RENAL FAILURE (CRF) or CHRONIC KIDNEY DISEASE (CKD)
Chronic or irreversible renal failure is a progressive reduction of functioning of renal tissue such that the remaining kidney mass can no longer maintain the body’s internal environment.
The document summarizes renal physiology and kidney function. It discusses:
1) The structure of the kidney including nephrons, collecting ducts, and microvasculature. Nephron number is established prenatally and cannot be replaced if lost.
2) Urine formation through selective retention and elimination of solutes and water by different nephron segments including the glomerulus, proximal tubule, loop of Henle, and collecting ducts.
3) Causes, types (prerenal, intrarenal, postrenal), phases, prevention and management of acute renal failure and end-stage renal disease where dialysis or transplantation is needed for survival.
The document discusses renal failure, including acute kidney injury (AKI) and chronic kidney disease (CKD). It covers the epidemiology and burden of kidney disease globally and in India. It describes the anatomy and physiology of the kidney and nephron. It defines AKI and its stages, causes including prerenal, intrarenal and postrenal factors. Signs, symptoms, diagnosis and management of AKI are summarized. CKD is defined and its stages, signs and symptoms, and diagnosis are outlined. Risk factors for CKD are also mentioned.
Chronic kidney disease, also called chronic kidney failure, describes the gradual loss of kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then excreted in your urine.
End-stage renal disease is a condition in which the kidneys no longer function normally and required excellent medical and nursing care for the managing this condition.
Chronic renal failure is a gradual loss of kidney function over time that cannot be reversed. It affects approximately 290,000 people in the United States. The kidneys gradually lose their ability to filter waste and excess fluid from the blood. Chronic renal failure is caused by conditions like hypertension, diabetes, kidney infections, and can lead to complications that affect many organ systems if not managed properly through treatments like dialysis and kidney transplantation. Proper management includes monitoring fluid and electrolytes, reducing metabolic rate, preventing infections, and providing nutritional therapy and skin care.
Chronic renal failure is the progressive loss of kidney function over time that can lead to end-stage renal disease. It is caused by conditions like diabetes, hypertension, and glomerulonephritis. As kidney function declines, patients experience complications from fluid and electrolyte imbalances, metabolic acidosis, anemia, renal osteodystrophy, and uremia. Treatment aims to prevent further deterioration of kidney function through controlling blood pressure, blood glucose, proteinuria, and other risk factors. Medications like ACE inhibitors, ARBs, diuretics, and statins are used and dosages may need adjustment based on level of kidney function.
This document discusses liver cirrhosis, including its types, causes, pathophysiology, clinical manifestations, complications, nursing diagnoses, and interventions. Liver cirrhosis is a chronic, degenerative disease characterized by replacement of normal liver tissue with fibrosis that disrupts liver structure and function. Common types are alcoholic cirrhosis and postnecrotic cirrhosis resulting from viral hepatitis. Complications include ascites, hepatic encephalopathy, and esophageal varices, which can lead to life-threatening bleeding if ruptured. Nursing care focuses on reducing metabolic demands, providing adequate nutrition and hydration, preventing infection, and protecting patients from injury and further complications.
Liver cirrhosis is a chronic, progressive disease characterized by widespread fibrosis and scarring of the liver that results in loss of liver function. It is caused by chronic liver injury from conditions such as hepatitis, alcohol abuse, or other chronic liver diseases. As cirrhosis progresses, it leads to hepatic insufficiency, portal hypertension, and other complications such as ascites, variceal bleeding, hepatic encephalopathy, and eventual liver failure. Treatment focuses on managing complications, slowing disease progression, and preventing further liver damage.
Renal failure is divided into acute renal failure (ARF) and chronic renal failure (CRF). ARF is characterized by rapid onset of renal dysfunction and increased waste products in the blood. It can be caused by issues with blood flow (pre-renal), the kidneys themselves (intra-renal), or urine outflow (post-renal). CRF is a progressive loss of renal function that eventually leads to end-stage kidney disease. It is caused by damage to the glomeruli or tubulointerstitial tissues and develops over four stages with declining kidney function and increasing symptoms of uraemia.
End stage renal disease and its managementShweta Sharma
This document provides information on the management of patients with end stage renal disease (ESRD). It discusses the pathophysiology and progression of chronic kidney disease to ESRD, clinical manifestations of ESRD, assessment and diagnostic findings, complications, and medical management including nutritional therapy, medications to treat complications, and dialysis. The main goals of management are to control fluid, electrolyte and acid-base imbalances and symptoms caused by kidney failure through dietary modifications and medications or renal replacement therapies like dialysis.
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
Acute kidney injury (AKI) is a critical condition where the kidneys rapidly decline in function over hours or days, causing waste and water to accumulate. It affects millions worldwide annually. AKI can be pre-renal from decreased blood flow, intra-renal from direct kidney damage, or post-renal from urinary tract obstruction. It is diagnosed through medical history, lab tests, and imaging and treated by addressing underlying causes, fluid/electrolyte management, and sometimes dialysis or transplantation. Risk factors include age, vascular diseases, diabetes, and previous kidney injuries.
This document discusses glomerulonephritis, which is inflammation of the glomeruli in the kidneys. It begins by reviewing kidney anatomy and the nephron. Acute glomerulonephritis is then defined as inflammation of the glomeruli caused by an antigen-antibody reaction, usually following a streptococcal infection. Clinical manifestations include edema, proteinuria, hematuria, and decreased kidney function. Chronic glomerulonephritis develops from repeated or unresolved acute attacks and results in irreversible scarring of the glomeruli. Nursing care focuses on fluid management, nutrition, infection prevention, and emotional support for the patient.
Acute renal failure is a sudden loss of kidney function over hours to days that results in oliguria or anuria and the buildup of waste products like BUN and creatinine in the blood. It can be caused by prerenal factors like decreased blood flow or direct kidney damage. Treatment focuses on restoring blood flow and removing waste until the kidneys can recover. Chronic kidney disease is progressive and irreversible, resulting in permanent kidney damage and uremia if untreated with dialysis or transplant.
Acute renal failure and chronic renal failureNEHA BHARTI
This document provides information about acute renal failure. It begins by defining renal failure and its two types - acute and chronic. Acute renal failure is described as a sudden loss of kidney function over hours to weeks. Risk factors, phases, clinical manifestations, diagnostic evaluations, and management including pharmacologic therapy, fluid/electrolyte replacement, nutrition, and dialysis are summarized. Chronic renal failure is defined as a gradual loss of kidney function over months to years that progresses to end-stage renal disease requiring dialysis or transplant. Stages and uremic symptoms affecting multiple organ systems are outlined.
Pyelonephritis
It is the inflammation of the kidney & upper urinary tract that usually results from the bacterial infection of the bladder.
Pyelonephritis can be classified in several different catagories:
-acute pyelonephritis
-chronic pyelonephritis
-xanthogranulomatous pyelonephritis
This document provides an overview of renal failure and its nursing management. It begins with an anatomical and physiological overview of the urinary system, focusing on kidney structure and function. The two main types of renal failure discussed are acute kidney injury (AKI), previously called acute renal failure (ARF), and chronic renal failure (CRF). AKI is defined as a sudden decline in kidney function over 48 hours and can be caused by prerenal, intrarenal, or postrenal factors. CRF is a gradual loss of kidney function over months or years. The global and Indian burden of kidney disease is also reviewed.
The kidneys filter blood and regulate fluid levels in the body by selectively reabsorbing or secreting solutes. Urine passes from the kidneys through ureters into the bladder, then through the urethra. The kidneys contain nephrons which filter blood and reabsorb or excrete products. Hematuria, the presence of blood in urine, can indicate issues ranging from minor infections to serious conditions like cancer and requires medical evaluation.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure. It defines AKI and provides causes and characteristics of pre-renal, renal, and post-renal AKI. Pre-renal AKI is caused by decreased renal perfusion due to issues like volume depletion or heart failure. Renal AKI can be caused by issues affecting the glomeruli, interstitium, or tubules, such as acute tubular necrosis. Post-renal AKI is due to urinary tract obstruction. The document outlines evaluation of AKI including history, exam, urine and serum tests, imaging, and novel biomarkers. It also discusses complications of AKI and general management strategies.
CHRONIC RENAL FAILURE (CRF) or CHRONIC KIDNEY DISEASE (CKD)
Chronic or irreversible renal failure is a progressive reduction of functioning of renal tissue such that the remaining kidney mass can no longer maintain the body’s internal environment.
The document summarizes renal physiology and kidney function. It discusses:
1) The structure of the kidney including nephrons, collecting ducts, and microvasculature. Nephron number is established prenatally and cannot be replaced if lost.
2) Urine formation through selective retention and elimination of solutes and water by different nephron segments including the glomerulus, proximal tubule, loop of Henle, and collecting ducts.
3) Causes, types (prerenal, intrarenal, postrenal), phases, prevention and management of acute renal failure and end-stage renal disease where dialysis or transplantation is needed for survival.
The document discusses renal failure, including acute kidney injury (AKI) and chronic kidney disease (CKD). It covers the epidemiology and burden of kidney disease globally and in India. It describes the anatomy and physiology of the kidney and nephron. It defines AKI and its stages, causes including prerenal, intrarenal and postrenal factors. Signs, symptoms, diagnosis and management of AKI are summarized. CKD is defined and its stages, signs and symptoms, and diagnosis are outlined. Risk factors for CKD are also mentioned.
Chronic kidney disease, also called chronic kidney failure, describes the gradual loss of kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then excreted in your urine.
End-stage renal disease is a condition in which the kidneys no longer function normally and required excellent medical and nursing care for the managing this condition.
Chronic renal failure is a gradual loss of kidney function over time that cannot be reversed. It affects approximately 290,000 people in the United States. The kidneys gradually lose their ability to filter waste and excess fluid from the blood. Chronic renal failure is caused by conditions like hypertension, diabetes, kidney infections, and can lead to complications that affect many organ systems if not managed properly through treatments like dialysis and kidney transplantation. Proper management includes monitoring fluid and electrolytes, reducing metabolic rate, preventing infections, and providing nutritional therapy and skin care.
Chronic renal failure is the progressive loss of kidney function over time that can lead to end-stage renal disease. It is caused by conditions like diabetes, hypertension, and glomerulonephritis. As kidney function declines, patients experience complications from fluid and electrolyte imbalances, metabolic acidosis, anemia, renal osteodystrophy, and uremia. Treatment aims to prevent further deterioration of kidney function through controlling blood pressure, blood glucose, proteinuria, and other risk factors. Medications like ACE inhibitors, ARBs, diuretics, and statins are used and dosages may need adjustment based on level of kidney function.
This document discusses liver cirrhosis, including its types, causes, pathophysiology, clinical manifestations, complications, nursing diagnoses, and interventions. Liver cirrhosis is a chronic, degenerative disease characterized by replacement of normal liver tissue with fibrosis that disrupts liver structure and function. Common types are alcoholic cirrhosis and postnecrotic cirrhosis resulting from viral hepatitis. Complications include ascites, hepatic encephalopathy, and esophageal varices, which can lead to life-threatening bleeding if ruptured. Nursing care focuses on reducing metabolic demands, providing adequate nutrition and hydration, preventing infection, and protecting patients from injury and further complications.
Liver cirrhosis is a chronic, progressive disease characterized by widespread fibrosis and scarring of the liver that results in loss of liver function. It is caused by chronic liver injury from conditions such as hepatitis, alcohol abuse, or other chronic liver diseases. As cirrhosis progresses, it leads to hepatic insufficiency, portal hypertension, and other complications such as ascites, variceal bleeding, hepatic encephalopathy, and eventual liver failure. Treatment focuses on managing complications, slowing disease progression, and preventing further liver damage.
Renal failure is divided into acute renal failure (ARF) and chronic renal failure (CRF). ARF is characterized by rapid onset of renal dysfunction and increased waste products in the blood. It can be caused by issues with blood flow (pre-renal), the kidneys themselves (intra-renal), or urine outflow (post-renal). CRF is a progressive loss of renal function that eventually leads to end-stage kidney disease. It is caused by damage to the glomeruli or tubulointerstitial tissues and develops over four stages with declining kidney function and increasing symptoms of uraemia.
End stage renal disease and its managementShweta Sharma
This document provides information on the management of patients with end stage renal disease (ESRD). It discusses the pathophysiology and progression of chronic kidney disease to ESRD, clinical manifestations of ESRD, assessment and diagnostic findings, complications, and medical management including nutritional therapy, medications to treat complications, and dialysis. The main goals of management are to control fluid, electrolyte and acid-base imbalances and symptoms caused by kidney failure through dietary modifications and medications or renal replacement therapies like dialysis.
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
Acute kidney injury (AKI) is a critical condition where the kidneys rapidly decline in function over hours or days, causing waste and water to accumulate. It affects millions worldwide annually. AKI can be pre-renal from decreased blood flow, intra-renal from direct kidney damage, or post-renal from urinary tract obstruction. It is diagnosed through medical history, lab tests, and imaging and treated by addressing underlying causes, fluid/electrolyte management, and sometimes dialysis or transplantation. Risk factors include age, vascular diseases, diabetes, and previous kidney injuries.
This document discusses glomerulonephritis, which is inflammation of the glomeruli in the kidneys. It begins by reviewing kidney anatomy and the nephron. Acute glomerulonephritis is then defined as inflammation of the glomeruli caused by an antigen-antibody reaction, usually following a streptococcal infection. Clinical manifestations include edema, proteinuria, hematuria, and decreased kidney function. Chronic glomerulonephritis develops from repeated or unresolved acute attacks and results in irreversible scarring of the glomeruli. Nursing care focuses on fluid management, nutrition, infection prevention, and emotional support for the patient.
Acute renal failure is a sudden loss of kidney function over hours to days that results in oliguria or anuria and the buildup of waste products like BUN and creatinine in the blood. It can be caused by prerenal factors like decreased blood flow or direct kidney damage. Treatment focuses on restoring blood flow and removing waste until the kidneys can recover. Chronic kidney disease is progressive and irreversible, resulting in permanent kidney damage and uremia if untreated with dialysis or transplant.
This document provides information on acute and chronic renal failure, including causes, pathophysiology, assessment, diagnosis, complications, nursing diagnoses, and nursing care. Acute renal failure can be pre-renal, intra-renal, or post-renal and is caused by decreased blood flow or obstruction. Chronic renal failure is a progressive loss of kidney function over time due to various injuries and diseases. Common complications include fluid imbalance, electrolyte abnormalities, nutritional deficits, and increased risk of infection or cardiovascular issues. Nursing focuses on monitoring fluid status, diet, nutrition, and treating related symptoms and complications.
1) Acute renal failure is a sudden reduction in kidney function that results in waste accumulating in the blood and is categorized as pre-renal, renal, or post-renal based on the underlying cause.
2) Pre-renal acute renal failure is caused by problems affecting blood flow to the kidneys such as dehydration, blood loss, or heart issues. Renal acute renal failure involves direct damage to the kidney itself from issues like acute tubular necrosis. Post-renal acute renal failure is caused by problems blocking urine flow out of the kidneys.
3) Symptoms can include weakness, fatigue, edema, and electrolyte imbalances. Treatment involves addressing the underlying cause, maintaining
Acute kidney injury (AKI) is the rapid loss of kidney function that can be caused by physical injury, infection, toxins, or decreased blood flow to the kidneys. AKI leads to cell damage and loss of renal function. Treatment focuses on correcting the underlying cause, controlling complications through fluid management and dialysis, and allowing the kidneys time to recover. Nursing care involves close monitoring for changes in urine output, fluid balance, and laboratory values to guide treatment and detect early signs of complications.
Acute renal failure (ARF), also known as acute kidney injury (AKI), is a rapid loss of kidney function that can have several causes. It is classified as prerenal, renal, or postrenal depending on whether reduced blood flow, direct kidney damage, or urinary tract obstruction is responsible. Symptoms are non-specific but diagnosis involves testing for increased waste products and reduced kidney function. Treatment focuses on treating the underlying cause and managing complications, while prevention emphasizes hydration, shock treatment, monitoring of at-risk patients, and infection control. ARF carries risks of metabolic abnormalities and fluid/electrolyte imbalances if not properly managed.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure, in pediatrics. It defines AKI, describes the causes and pathophysiology, presents approaches to evaluation and management, and outlines treatment of complications. The key points are:
- AKI is defined as an abrupt reduction in kidney function over 48 hours, seen as a rise in creatinine or decrease in urine output.
- Common causes include prerenal failure from hypovolemia, intrinsic renal failure like acute tubular necrosis, and postrenal failure from urinary tract obstruction.
- Management involves treating complications, maintaining fluid/electrolyte balance, and considering dialysis for issues like fluid
Acute renal failure (ARF) is the sudden loss of kidney function, causing a build up of waste products in the blood. It can be oliguric or non-oliguric depending on urine output. ARF has three main causes - prerenal from low blood flow, intrinsic kidney damage, or postrenal from urinary obstruction. Management involves fluid management, electrolyte control, antibiotics for infection, and possibly dialysis. Nurses monitor patients closely and prevent complications through infection control and skin care.
This document provides an overview of nephrology and kidney diseases. It discusses the structure and function of the kidneys and nephrons. It also describes various kidney diseases including chronic kidney disease, acute renal failure, chronic renal failure, nephrotic syndrome, kidney stones, bladder cancer, and more. Treatment options and management of these diseases are also summarized.
Genitourinary disorders are conditions that affect the genitourinary system, which includes the urinary and reproductive systems. Some are congenital, and others are acquired later in life.
Large numbers of patients suffer from a variety of diseases in the genitourinary system, which is composed of kidneys, ureters, bladder, urethra, and genital organs. Genitourinary diseases include congenital abnormalities, iatrogenic injuries, and disorders such as cancer, trauma, infection, and inflammation.
Acute kidney failure happens when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and waste materials from the blood. Acute kidney failure is also called acute kidney injury or acute renal failure. It's common in people who are already in the hospital. It may develop rapidly over a few hours.
The kidneys are located retroperitoneally and filter waste from the blood to form urine. Kidney failure occurs when the kidneys cannot adequately remove waste or regulate fluids and electrolytes. Acute kidney injury is a sudden decrease in function while chronic kidney disease is long-term damage. Causes include decreased blood flow, direct damage, and obstruction. Treatment focuses on treating reversible causes and managing complications like anemia and bone disease. Dialysis or transplantation may be needed for late-stage disease.
The kidneys perform several important functions including removing waste, regulating electrolytes and blood pressure, activating vitamin D, and stimulating red blood cell production. Acute renal failure refers to a sudden, usually reversible loss of kidney function over days or weeks and is commonly caused by decreased blood flow to the kidneys (pre-renal) or direct kidney damage (intrinsic). Pre-renal acute renal failure, which accounts for 60-70% of cases, is often due to low blood volume from causes like bleeding, burns, or diarrhea. It can typically be reversed by restoring blood volume and pressure through fluid resuscitation.
Guideline, management of acute kidney injuryvita madmo
This document provides guidelines for the management of acute kidney injury (AKI). It defines AKI and outlines stages of severity based on the RIFLE, AKIN and KDIGO criteria. Management of AKI focuses on treating underlying causes, maintaining fluid and electrolyte balance, and considering renal replacement therapy for complications like fluid overload or severe azotemia. Dialysis modalities and anticoagulation options are discussed. The guidelines recommend supportive care including diet modification and avoiding nephrotoxic drugs.
Renal failure occurs when the kidneys are unable to remove waste and regulate fluids and electrolytes. This leads to the accumulation of waste in the blood and disruption of other body functions. There are two main types - acute renal failure, which develops rapidly over hours to days, and chronic kidney disease, which progresses over months to years. The main symptoms include leg swelling, fatigue, vomiting and confusion. Treatment focuses on fluid balance, electrolyte control, and renal replacement therapy such as dialysis. Prognosis depends on age and treatment.
This document provides an overview of acute kidney injury (AKI). It defines AKI and notes its worldwide epidemiology. The main causes of AKI are discussed as pre-renal, renal, and post-renal. The pathophysiology of each type is explained. Clinical presentation depends on the cause but may include elevated creatinine and reduced urine output. Staging of AKI is outlined using KDIGO criteria. Investigations and management aim to identify and treat the underlying cause while maintaining fluid and electrolyte balance. Complications include fluid overload and metabolic disturbances. Prognosis depends on severity and comorbidities.
Acute kidney injury (AKI), previously known as acute renal failure, is characterized by a sudden decrease in kidney function and the retention of waste products. It can be prerenal, renal, or post-renal in origin. Prerenal causes are due to decreased blood flow to the kidneys, renal causes involve damage to the kidneys themselves, and post-renal causes result from obstruction of urine flow. Diagnosis involves evaluating urine output, laboratory tests of kidney function, urine analysis, and occasionally imaging tests or kidney biopsies. Prompt diagnosis and treatment of the underlying cause is important to prevent further kidney damage and other complications of AKI.
This document provides information about strokes, including types, symptoms, risk factors, diagnosis, and treatment. It discusses the two main types of strokes: ischemic, caused by blockage of blood vessels in the brain, and hemorrhagic, caused by bleeding in the brain. Symptoms of stroke can include weakness, numbness, vision problems, dizziness, and confusion. Risk factors include age, high blood pressure, atrial fibrillation, diabetes, smoking, obesity, and family history. Diagnosis involves physical exams, imaging tests like CT scans and MRIs, and blood tests. Treatment focuses on preventing future strokes through medications like blood thinners, statins, and blood pressure medications as well as rehabilitation therapies.
Telemetry monitoring allows cardiac patients to move freely while their heart is monitored. It is used for patients who need continuous EKG monitoring but do not require intensive care. A diagnostic information system can aggregate over 5,000 different patient test results into a standardized, easy to read format. This increases efficiency and accuracy of patient care. Mechanical ventilators deliver gas into a patient's airways to support breathing. Modes include time cycled, volume cycled and flow cycled ventilation. Intensive care units aim to reduce stress and promote recovery through factors like natural lighting, family involvement and reduced noise.
Telemetry allows for remote cardiac monitoring of patients who do not require intensive care unit placement but still need monitoring. It transmits data from a patient's heart to monitoring staff while allowing the patient mobility. An ideal intensive care unit environment focuses on reducing stress for patients through access to natural light, views, family involvement, and other therapeutic elements. Laboratory tests aim to be precise, accurate, sensitive and specific to reliably determine medical conditions and distinguish those with a condition from those without.
1. Congestive heart failure occurs when the heart muscle is unable to pump blood efficiently, often due to conditions that stiffen or weaken the heart such as high blood pressure or coronary artery disease.
2. As the heart pumps less effectively, blood moves more slowly through the body and the heart has to work harder. The heart chambers may enlarge and fluid can build up in the lungs and other organs, causing congestion.
3. Treatment focuses on managing fluid levels, improving heart function, and treating the underlying cause. Medications target the renin-angiotensin-aldosterone system and sympathetic nervous system, while diuretics help remove excess fluid.
This document provides information on cardiac failure or congestive heart failure (CHF). CHF occurs when the heart muscle is too weak or stiff to pump blood efficiently. As a result, blood moves through the heart and body more slowly and pressure in the heart increases. The heart cannot pump enough oxygen and nutrients to meet the body's needs. Risk factors include hypertension, diabetes, dyslipidemia, coronary artery disease, and sleep disorders. Diagnosis involves physical exam, blood tests, chest x-ray, echocardiogram, and other cardiac tests. Treatment focuses on managing symptoms through lifestyle changes, medications like ACE inhibitors, beta blockers, diuretics, and devices or procedures for severe cases. Nursing care addresses
The document defines acute respiratory failure as abnormal gas exchange resulting from dysfunction of the respiratory system that is potentially life-threatening. It can be caused by issues in the lungs, chest wall, or central nervous system control of breathing. Signs include altered mental status, cyanosis, increased work of breathing, and abnormal blood gases. Diagnostic tests may include blood gases, chest x-ray, and pulmonary function tests. Risk factors include smoking, age, infection, and chronic lung disease. Treatment involves addressing the underlying cause, supplemental oxygen, bronchodilators, diuretics, and vasodilators. Nursing care focuses on monitoring respiratory status, clearing secretions, managing oxygen needs, and patient education.
Acute pulmonary failure occurs when abnormal gas exchange results from dysfunction of the respiratory system that threatens life. Risk factors include smoking, infections, lung disease, and neurological or muscular disorders. Symptoms include altered mental status, cyanosis, respiratory distress, and abnormal blood gases. Treatment focuses on stabilizing the patient, treating the underlying cause, and supporting respiratory function through oxygen, ventilation, suctioning, and positioning. Nursing care aims to maintain the airway, enhance gas exchange and nutrition, prevent complications, and provide education to the patient.
An acute myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow to the heart is blocked causing damage to heart muscle. Diagnosis involves ECGs, blood tests of cardiac markers, and symptoms like chest pain. Treatment focuses on restoring blood flow through medications and preventing further complications. Nursing interventions for an MI aim to support cardiac output and tissue perfusion, manage pain and activity levels, and provide education on lifestyle changes and medication management upon discharge.
An acute myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow to the heart is blocked, injuring the heart muscle. Risk factors include previous cardiovascular disease, older age, smoking, high cholesterol, diabetes, high blood pressure, obesity, and chronic kidney disease. Treatment involves restoring blood flow through procedures like angioplasty or thrombolysis, along with medications like aspirin, nitroglycerin, and statins. Recovery involves cardiac rehabilitation with exercise training and lifestyle changes to manage risk factors and prevent future heart attacks.
A 58-year-old male was admitted to the hospital on June 22, 2014 with abdominal pain and was placed under the care of Dr. Mark Cacho and Dr. Brandt Lojo. Over the next three days, the doctors ordered various tests, medications, and procedures for the patient, including a complete blood count, plain saline solution, antibiotics, and an endoscopy with biopsy, which was performed on the third day. The patient was advised to rest after the endoscopy procedure and follow a diet of small, frequent meals while avoiding acidic foods.
The document outlines a treatment plan for ulcers, including medications to take (ranitidine, omeprazole, amoxicillin), avoiding certain exercises and foods, quitting smoking, following up with a doctor, and seeking immediate care for severe symptoms like abdominal pain or bloody vomit. Exercise is recommended but to avoid straining the abdomen. The patient should reduce stress, not stop medications without consulting their doctor, and contact their doctor if symptoms worsen or new ones arise.
Smoking and aging are major risk factors for duodenal ulcers. Smoking decreases the secretion of bicarbonate from the pancreas and increases the secretion of hydrochloric acid and pepsin into the stomach and duodenum. This increases the concentration and activity of acid and pepsin in the digestive tract. The duodenal mucosa cannot withstand the digestive action of hydrochloric acid and pepsin, damaging the mucosa and preventing it from secreting enough mucus to act as a protective barrier against hydrochloric acid. This decreases the resistance of the mucosa and destroys blood vessels, leading to further erosion of the mucosa and pain and bleeding in the abdomen.
The physical assessment examines the head, scalp, hair, face, eyelids, eyes, ears, mouth, neck, skin, nails, upper extremities, lower extremities, thoracic cavity, and abdomen. For each area, normal findings and actual findings are described and analyzed. The assessment found abnormalities in the skin, with black and blue areas on the lower back, and the abdomen, which was distended with tenderness on palpation. Otherwise, the physical exam was normal with no alterations noted.
The document contains multiple sections from nursing notes on different patients. It includes assessments of patients' symptoms and concerns, nursing diagnoses, objectives for interventions, details of interventions provided and their rationales, and evaluations of outcomes. Key information includes patients presenting with anxiety about their health, pain, knowledge deficits, and weight gain related to changes in diet. Nurses addressed these issues through monitoring, education, and lifestyle counseling aimed at reducing anxiety and pain levels, increasing knowledge, and identifying unhealthy eating habits within 8 hours of interventions.
Patient X, a 58-year-old grocery store manager, was experiencing abdominal pain several nights a week and occasional discomfort in the afternoon. An endoscopy revealed a peptic ulcer and infection with Helicobacter pylori bacteria. He was prescribed medication to reduce stomach acid and instructed to return for another endoscopy in 6 months. Peptic ulcer disease is common in the Philippines and a leading cause of death, especially among those with poor lifestyles. The duodenum is responsible for digesting food using enzymes secreted by the pancreas and bile from the liver and gallbladder.
This document summarizes four drugs used in combination to treat Helicobacter pylori infection and duodenal ulcers: clarithromycin, omeprazole, amoxicillin, and bismuth subsalicylate. It provides the classification, indication, contraindications, side effects, and important nursing considerations for each drug. The drugs are commonly administered together to eradicate H. pylori bacteria and treat associated gastritis and duodenal ulcers. Nurses should monitor patients for anticipated responses and side effects and educate them about proper administration and potential symptoms like black stools.
Patient X, a 58-year-old man, has been hospitalized since June 27th. During his hospitalization, he has reminded his daughters to focus on their education and advised his son to live a healthy lifestyle without drinking or smoking. As a person in middle adulthood, Patient X is experiencing the developmental task of generativity versus stagnation, which involves establishing stability and transmitting cultural values to younger generations. An endoscopy found ulceration in Patient X's duodenal area and tested positive for H. pylori infection and damage to the stomach lining.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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Assessment and Planning in Educational technology.pptxKavitha Krishnan
In an education system, it is understood that assessment is only for the students, but on the other hand, the Assessment of teachers is also an important aspect of the education system that ensures teachers are providing high-quality instruction to students. The assessment process can be used to provide feedback and support for professional development, to inform decisions about teacher retention or promotion, or to evaluate teacher effectiveness for accountability purposes.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
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How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
BÀI TẬP BỔ TRỢ TIẾNG ANH 8 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2023-2024 (CÓ FI...
Acute renal failure
1. Acute Renal Failure
Is the rapid breakdown of renal (kidney) function that occurs when high levels of uremic
toxins (waste products of the body's metabolism) accumulate in the blood. ARF occurs when the
kidneys are unable to excrete (discharge) the daily load of toxins in the urine.
Basedon the amountof urine that is excreted over a 24-hour period, patients with ARF are
separated into two groups:
Oliguric: patients who excrete less than 500 milliliters per day (< 16 oz/day)
Nonoliguric: patients who excrete more than 500 milliliters per day (> 16 oz/day)
In nonoliguric patients, the urine is of poor quality (i.e., contains little waste) because the blood
is not well filtered, despite the fact that an adequate volume of urine is excreted.
Both kidneys are failing when ARF occurs. One normally functioning kidney can maintain
adequate blood filtering.
Risk Factors
Acute kidney failure almost always occurs in connection with another medical condition or
event. Conditions that can increase your risk of acute kidney failure include:
Being hospitalized, especially for a serious condition that requires intensive care
Advanced age
Blockages in the blood vessels in your arms or legs (peripheral artery disease)
Diabetes
High blood pressure
Heart failure
Kidney diseases
Liver diseases
PA
A detailed and accurate history is crucial for diagnosing acute kidney injury
(AKI) and determining treatment. Distinguishing AKI from chronic kidney
disease is important, yet making the distinction can be difficult. A history of
chronic symptoms—months of fatigue, weight loss, anorexia, nocturia, sleep
disturbance, and pruritus—suggests chronic kidney disease. AKI can cause
identical symptoms, but over a shorter course.
It is important to elicit a history of any of the following etiologic factors:
Volume restriction (eg, low fluid intake, gastroenteritis)
Nephrotoxic drug ingestion
Trauma or unaccustomed exertion
Blood loss or transfusions
Exposure to toxic substances, such as ethyl alcohol or ethylene glycol
Exposure to mercury vapors, lead, cadmium, or other heavy metals, which
can be encountered in welders and miners
2. People with the following comorbid conditions are at a higher risk for
developing AKI:
Hypertension
Chronic heart failure
Diabetes
Multiple myeloma
Chronic infection
Myeloproliferative disorder
Connective tissue disorders
Autoimmune diseases
Urine output history can be useful. Oliguria generally favors AKI. Abrupt
anuria suggests acute urinary obstruction, acute and severe
glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing
urine output may indicate a urethral stricture or bladder outlet obstruction due
to prostate enlargement.
Because of a decrease in functioning nephrons, even a trivial nephrotoxic
insult may cause AKI to be superimposed on chronic renal insufficiency.
Acute kidney injury (AKI) has a long differential diagnosis. History can help to
classify the pathophysiology of AKI as prerenal, intrinsic renal, or postrenal
failure, and it may suggest some specific etiologies.
Prerenal failure
Patients commonly present with symptoms related to hypovolemia, including
thirst, decreased urine output, dizziness, and orthostatic hypotension. Ask
about volume loss from vomiting, diarrhea, sweating, polyuria, or hemorrhage.
Patients with advanced cardiac failure leading to depressed renal perfusion
may present with orthopnea and paroxysmal nocturnal dyspnea.
Elders with vague mental status change are commonly found to have prerenal
or normotensive ischemic AKI. Insensible fluid losses can result in severe
hypovolemia in patients with restricted fluid access and should be suspected
in elderly patients and in comatose or sedated patients.
Intrinsic renal failure
Patients can be divided into those with glomerular etiologies and those with
tubular etiologies of AKI. Nephritic syndrome of hematuria, edema, and
hypertension indicates a glomerular etiology for AKI. Query about prior throat
or skin infections. Acute tubular necrosis (ATN) should be suspected in any
3. patient presenting after a period of hypotension secondary to cardiac arrest,
hemorrhage, sepsis, drug overdose, or surgery.
A careful search for exposure to nephrotoxins should include a detailed list of
all current medications and any recent radiologic examinations (ie, exposure
to radiologic contrast agents). Pigment-induced AKI should be suspected in
patients with possible rhabdomyolysis (muscular pain, recent coma, seizure,
intoxication, excessive exercise, limb ischemia) or hemolysis (recent blood
transfusion). Allergic interstitial nephritis should be suspected with fevers,
rash, arthralgias, and exposure to certain medications, including NSAIDs and
antibiotics.
Postrenal failure
Postrenal failure usually occurs in older men with prostatic obstruction and
symptoms of urgency, frequency, and hesitancy. Patients may present with
asymptomatic, high-grade urinary obstruction because of the chronicity of
their symptoms. A history of prior gynecologic surgery or abdominopelvic
malignancy often can be helpful in providing clues to the level of obstruction.
Flank pain and hematuria should raise a concern about renal calculi or
papillary necrosis as the source of urinary obstruction. Use of acyclovir,
methotrexate, triamterene, indinavir, or sulfonamides implies the possibility
that crystals of these medications have caused tubular obstruction.
DX:
If your signs and symptoms suggest that you have acute kidney failure, your doctor may
recommend tests and procedures to verify your diagnosis. These may include:
Urine output measurements. The amount of urine you excrete in a day may help your doctor
determine the cause of your kidney failure.
Urine tests. Analyzing a sample of your urine, a procedure called urinalysis, may reveal
abnormalities that suggest kidney failure.
Blood tests. A sample of your blood may reveal rapidly rising levels of urea and creatinine —
two substances used to measure kidney function.
Imaging tests. Imaging tests such as ultrasound and computerized tomography (CT) may be used
to help your doctor see your kidneys.
Removing a sample of kidney tissue for testing. In certain situations, your doctor may
recommend a kidney biopsy to remove a small sample of kidney tissue for lab testing. To
remove a sample of kidney tissue, your doctor may insert a thin needle through your skin and
into your kidney.
Meds:
4. Drugs that are renally excreted may need to have their doses reduced in
patients with renal insufficiency or end-stage renal disease:
For prescribing purposes renal impairment is usually divided into three
grades:
Mild: GFR 20-50 ml/minute; serum creatinine approximately 150-
300 µmol/l.
Moderate: GFR 10-20 ml/minute; serum creatinine approximately
300-700 µmol/L.
Severe: GFR less than 10 ml/minute; serum creatinine>700 µmol/L.
Patients with a GFR above 50 ml/min do not usually require any
dosage adjustment.
Nephrotoxic drugs should, if possible, be avoided in patients with
renal disease because the consequences of nephrotoxicity are likely
to be more serious when the renal reserve is already reduced.
The situation may change if a patient begins dialysis, since some drugs
will be removed by the dialysis. Dialysis may lead to the loss of
therapeutic effect for some drugs.
Drugs to which particular attention must be given include many
antibiotics, histamine H2-receptor antagonists, digoxin, anticonvulsants
and non-steroidal anti-inflammatory drugs (NSAIDs).
nursing interventions
Excess Fluid VolumeMay be relate to
Compromised regulatory mechanism (renal failure)
Possibly evidenced by
Intake greater than output, oliguria; changes in urine specific gravity
Venous distension; blood pressure (BP)/central venous pressure (CVP) changes
Generalized tissue edema, weight gain
Changes in mental status, restlessness
Decreased Hb/hematocrit (Hct), altered electrolytes; pulmonary congestion on x-ray
Record accurate intake and output (I&O).
Include “hidden” fluids such as IV
Low output (less than 400 mL/24 hr) may be first indicator
of acute failure, especially in a high-risk patient. Accurate
5. antibiotic additives, liquid medications, ice
chips, frozen treats. Measure
gastrointestinal (GI) losses and estimate
insensible losses, e.g., diaphoresis.
I&O is necessary for determining renal function and fluid
replacement needs and reducing risk of fluid
overload. Note: Hypervolemia occurs in the anuric phase
of ARF.
Monitor urine specific gravity.
Measures the kidney’s ability to concentrate urine. In
intrarenal failure, specific gravity is usually equal to/less
than 1.010, indicating loss of ability to concentrate the
urine.
Weigh daily at same time of day, on same
scale, with same equipment and clothing.
Daily body weight is best monitor of fluid status. A weight
gain of more than 0.5 kg/day suggests fluid retention.
Assess skin, face, dependent areas for
edema. Evaluate degree of edema (on
scale of +1–+4).
Edema occurs primarily in dependent tissues of the body,
e.g., hands, feet, lumbosacral area. Patient can gain up
to 10 lb (4.5 kg) of fluid before pitting edema is detected.
Periorbital edema may be a presenting sign of this fluid
shift because these fragile tissues are easily distended by
even minimal fluid accumulation.
Monitor heart rate (HR), BP, and
JVD/CVP.
Tachycardia and hypertension can occur because of (1)
failure of the kidneys to excrete urine, (2) excessive fluid
resuscitation during efforts to treat hypovolemia/
hypotension or convert oliguric phase of renal failure,
and/or (3) changes in the renin-angiotensin system. Note:
Invasive monitoring may be needed for assessing
intravascular volume, especially in patients with poor
cardiac function.
Auscultate lung and heart sounds.
Fluid overload may lead to pulmonary edema and HF
evidenced by development of adventitious breath sounds,
extra heart sounds.
Assess level of consciousness;
investigate changes in mentation,
presence of restlessness.
May reflect fluid shifts, accumulation of toxins, acidosis,
electrolyte imbalances, or developing hypoxia.
Plan oral fluid replacement with patient,
within multiple restrictions. Intersperse
desired beverages throughout 24 hr. Vary
offerings, e.g., hot, cold, frozen.
Helps avoid periods without fluids, minimizes boredom of
limited choices, and reduces sense of deprivation and
thirst.
6. Correct any reversible cause of ARF,
e.g., replace blood loss, maximize cardiac
output, discontinue nephrotoxic drug,
relieve obstruction via surgery.
Kidneys may be able to return to normal functioning,
preventing or limiting residual effects.
Monitor laboratory/ diagnostic studies,
e.g.:
BUN, Cr;
Assess progression and management of renal
dysfunction/ failure. Although both values may be
increased, Cr is a better indicator of renal function
because it is not affected by hydration, diet, and tissue
catabolism. Note: Dialysis is indicated if ratio is higher
than 10:1 or if therapy fails to correct fluid overload or
metabolic acidosis.
Urine sodium and Cr;
In ATN, tubular functional integrity is lost and sodium
resorption is impaired, resulting in increased sodium
excretion. Urine creatinine is usually decreased as serum
creatinine elevates.
Serum sodium;
Hyponatremia may result from fluid overload (dilutional)
or kidney’s inability to conserve sodium. Hypernatremia
indicates total body water deficit.
Serum potassium;
Lack of renal excretion and/or selective retention of
potassium to excrete excess hydrogen ions leads to
hyperkalemia, requiring prompt intervention.
Hb/Hct;
Decreased values may indicate hemodilution
(hypervolemia); however, during prolonged failure,
anemia frequently develops as a result of RBC loss/
decreased production. Other possible causes (active or
occult hemorrhage) should also be evaluated.
Serial chest x-rays.
Increased cardiac size, prominent pulmonary vascular
markings, pleural effusion, infiltrates/ congestion indicate
acute responses to fluid overload or chronic changes
associated with renal and heart failure.
Administer/restrict fluids as indicated.
Fluid management is usually calculated to replace output
from all sources plus estimated insensible losses
7. (metabolism, diaphoresis). Prerenal failure (azotemia) is
treated with volume replacement and/or vasopressors.
The oliguric patient with adequate circulating volume or
fluid overload who is unresponsive to fluid restriction and
diuretics requires dialysis. Note: During oliguric phase,
“push/pull” therapy (push IV fluids and diurese with
diuretics) may be tried to stimulate kidney function.
Administer medication as indicated:
Diuretics, e.g., furosemide (Lasix),
bumetanide (Bumex), torsemide
(Demadex), mannitol (Osmitrol);
Given early in oliguric phase of ARF in an effort to
convert to nonoliguric phase, flush the tubular lumen of
debris, reduce hyperkalemia, and promote adequate
urine volume.
Antihypertensives, e.g., clonidine
(Catapres), methyldopa (Aldomet),
prazosin (Minipress);
May be given to treat hypertension by counteracting
effects of decreased renal blood flow and/or circulating
volume overload.
Calcium channel blockers;
Given early in nephrotoxic ATN to reduce influx of
calcium into kidney cells, thereby helping to maintain cell
integrity and improve GFR.
Prostaglandins.
Vasodilatory effect may improve circulating volume and
reestablish renal blood flow to aid in clearing nephrotoxic
agents from nephrons.
Insert/maintain indwelling catheter, as
indicated.
Catheterization excludes lower tract obstruction and
provides means of accurate monitoring of urine output
during acute phase; however, indwelling catheterization
may be contraindicated because of increased risk of
infection.
Prepare for dialysis as indicated, e.g.,
hemodialysis, peritoneal dialysis, or
continuous renal replacement therapy
(CRRT).
Done to correct volume overload, electrolyte and acid-
base imbalances, and to remove toxins. The type of
dialysis chosen for ARF depends on the degree of
hemodynamic compromise and patient’s ability to
withstand the procedure.
2. Risk for Decreased Cardiac Output
Risk factors may include
8. Fluid overload (kidney dysfunction/failure, overzealous fluid replacement)
Fluid shifts, fluid deficit (excessive losses)
Electrolyte imbalance (potassium, calcium); severe acidosis
Uremic effects on cardiac muscle/oxygenation
Possibly evidenced by
[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Monitor BP and HR.
Fluid volume excess, combined with hypertension (often
occurs in renal failure) and effects of uremia, increases cardiac
workload and can lead to cardiac failure. In ARF, cardiac
failure is usually reversible.
Observe ECG or telemetry for
changes in rhythm.
Changes in electromechanical function may become evident in
response to progressing renal failure/ accumulation of toxins
and electrolyte imbalance. For example, hyperkalemia is
associated with peaked T wave, wide QRS, prolonged PR
interval, flattened/absent P wave. Hypokalemia is associated
with flat T wave, peaked P wave, and appearance of U waves.
Prolonged QT interval may reflect calcium deficit.
Auscultate heart sounds.
Development of S3/S4 is indicative of failure. Pericardial friction
rub may be only manifestation of uremic pericarditis, requiring
prompt intervention/possibly acute dialysis.
Assess color of skin, mucous
membranes, and nailbeds. Note
capillary refill time.
Pallor may reflect vasoconstriction or anemia. Cyanosis is a
late sign and is related to pulmonary congestion and/or cardiac
failure.
Note occurrence of slow pulse,
hypotension, flushing, nausea/
vomiting, and depressed level of
consciousness (central nervous
system [CNS] depression).
Using drugs (e.g., antacids) containing magnesium can result
in hypermagnesemia, potentiating neuromuscular dysfunction
and risk of respiratory/cardiac arrest.
Investigate reports of muscle
cramps, numbness/tingling of
fingers, with muscle twitching,
hyperreflexia.
Neuromuscular indicators of hypocalcemia, which can also
affect cardiac contractility and function.
Maintain bedrest or encourage
adequate rest and provide
assistance with care and desired
Reduces oxygen consumption/cardiac workload.
9. activities.
Monitor laboratory studies, e.g.:
Potassium;
During oliguric phase, hyperkalemia is present but often shifts
to hypokalemia in diuretic or recovery phase. Any potassium
value associated with ECG changes requires
intervention. Note:A serum level of 6.5 mEq or higher
constitutes a medical emergency.
Calcium;
In addition to its own cardiac effects, calcium deficit enhances
the toxic effects of potassium.
Magnesium.
Dialysis or calcium administration may be necessary to combat
the CNS-depressive effects of an elevated serum magnesium
level.
Administer/restrict fluids as
indicated.
Cardiac output depends on circulating volume (affected by both
fluid excess and deficit) and myocardial muscle function.
Provide supplemental oxygen if
indicated.
Maximizes available oxygen for myocardial uptake to reduce
cardiac workload and cellular hypoxia.
Administer medications as
indicated:
Inotropic agents, e.g., digoxin
(Lanoxin);
May be used to improve cardiac output by increasing
myocardial contractility and stroke volume. Dosage depends
on renal function and potassium balance to obtain therapeutic
effect without toxicity.
Calcium gluconate;
Serum calcium is often low but usually does not require
specific treatment in ARF. Calcium gluconate may be given to
treat hypocalcemia and to offset the effects of hyperkalemia by
modifying cardiac irritability.
Aluminum hydroxide gels
(Amphojel, Basalgel);
Increased phosphate levels may occur as a result of failure of
glomerular filtration and require use of phosphate-binding
antacids to limit phosphate absorption from the GI tract.
Glucose/insulin solution;
Temporary measure to lower serum potassium by driving
potassium into cells when cardiac rhythm is endangered.
Sodium bicarbonate or sodium
citrate;
May be used to correct acidosis or hyperkalemia (by increasing
serum pH) if patient is severely acidotic and not suffering from
10. fluid overload.
Sodium polystyrene sulfonate
(Kayexalate) with/without sorbitol.
Exchange resin trades sodium for potassium in the GI tract to
lower serum potassium level. Sorbitol may be included to
cause osmotic diarrhea to help excrete potassium.
Prepare for/assist with dialysis as
necessary.
May be indicated for persistent dysrhythmias, progressive HF
unresponsive to other therapies.
3. Risk for Imbalanced Nutrition
Nursing Diagnosis
Nutrition: imbalanced, risk for less than body requirements
Risk factors may include
Protein catabolism; dietary restrictions to reduce nitrogenous waste products
Increased metabolic needs
Anorexia, nausea/vomiting; ulcerations of oral mucosa
Assess/document dietary intake.
Aids in identifying deficiencies and dietary needs. General
physical condition, uremic symptoms (e.g., nausea,
anorexia, altered taste), and multiple dietary restrictions
affect food intake.
Provide frequent, small feedings.
Minimizes anorexia and nausea associated with uremic
state/diminished peristalsis.
Give patient/SO a list of permitted
foods/fluids and encourage
involvement in menu choices.
Provides patient with a measure of control within dietary
restrictions. Food from home may enhance appetite.
Offer frequent mouth care/rinse with
dilute (0.25%) acetic acid solution;
provide gum, hard candy, breath mints
between meals.
Mucous membranes may become dry and cracked. Mouth
care soothes, lubricates, and helps freshen mouth taste,
which is often unpleasant because of uremia and restricted
oral intake. Rinsing with acetic acid helps neutralize
ammonia formed by conversion of urea.
Weigh daily.
The fasting/catabolic patient normally loses 0.2–0.5 kg/day.
Changes in excess of 0.5 kg may reflect shifts in fluid
balance.
Monitor laboratory studies, e.g., BUN,
prealbumin/albumin, transferrin,
sodium, and potassium.
Indicators of nutritional needs, restrictions, and necessity
for/effectiveness of therapy.
Consult with dietitian/nutritional support Determines individual calorie and nutrient needs within the
11. team. restrictions, and identifies most effective route and product,
e.g., oral supplements, enteral or parenteral nutrition.
Provide high-calorie, low-/moderate-
protein diet. Include complex
carbohydrates and fat sources to meet
caloric needs (avoiding concentrated
sugar sources) and essential amino
acids.
The amount of needed exogenous protein is less than
normal unless patient is on dialysis. Carbohydrates meet
energy needs and limit tissue catabolism, preventing
ketoacid formation from protein and fat oxidation.
Carbohydrate intolerance mimicking DM may occur in
severe renal failure. Essential amino acids improve nitrogen
balance and nutritional status, stimulate repair of tubular
epithelial cells, and enhance patient’s ability to fight
systemic complications.
Restrict potassim, sodium, and
phosphorus intake as indicated.
Restriction of these electrolytes may be needed to prevent
further renal damage, especially if dialysis is not part of
treatment, and/or during recovery phase of ARF.
Administer medications as indicated:
Iron preparations;
Iron deficiency may occur if protein is restricted, patient is
anemic, or GI function is impaired.
Calcium carbonate;
Restores normal serum levels to improve cardiac and
neuromuscular function, blood clotting, and bone
metabolism. Note: Low serum calcium is often corrected as
phosphate absorption is decreased in the GI system.
Calcium may be substituted as a phosphate binder.
Vitamin D;
Necessary to facilitate absorption of calcium from the GI
tract.
B complex and C vitamins, folic acid;
Vital as coenzyme in cell growth and actions. Intake is
decreased because of protein restrictions.
Antiemetics, e.g. prochlorperazine
(Compazine), trimethobenzamide
(Tigan).
Given to relieve nausea/vomiting and may enhance oral
intake.
4. Risk for Infection
Risk factors may include
Depression of immunologic defenses (secondary to uremia)
Invasive procedures/devices (e.g., urinary catheter)
Changes in dietary intake/malnutrition
Possibly evidenced by
12. [Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Promote good handwashing by patient and staff. Reduces risk of cross-contamination.
Avoid invasive procedures, instrumentation, and
manipulation of indwelling catheters whenever
possible. Use aseptic technique when caring
for/manipulating IV/invasive lines. Change
site/dressings per protocol. Note edema, purulent
drainage.
Limits introduction of bacteria into body. Early
detection/treatment of developing infection may
prevent sepsis.
Provide routine catheter care and promote
meticulous perianal care. Keep urinary drainage
system closed and remove indwelling catheter as
soon as possible.
Reduces bacterial colonization and risk of
ascending UTI.
Encourage deep breathing, coughing, frequent
position changes.
Prevents atelectasis and mobilizes secretions to
reduce risk of pulmonary infections.
Assess skin integrity.
Excoriations from scratching may become
secondarily infected.
Monitor vital signs.
Fever (higher than 100.4°F) with increased pulse
and respirations is typical of increased metabolic
rate resulting from inflammatory process,
although sepsis can occur without a febrile
response.
Monitor laboratory studies, e.g., WBC count with
differential.
Although elevated WBCs may indicate
generalized infection, leukocytosis is commonly
seen in ARF and may reflect inflammation/injury
within the kidney. A shifting of the differential to
the left is indicative of infection.
Obtain specimen(s) for culture and sensitivity and
administer appropriate antibiotics as indicated.
Verification of infection and identification of
specific organism aids in choice of the most
effective treatment. Note: A number of anti-
infective agents require adjustments of dose
and/or time while renal clearance is impaired.
5. Risk for Deficient Fluid Volume
Risk factors may include
13. Excessive loss of fluid (diuretic phase of ARF, with rising urinary volume and delayed return of
tubular reabsorption capabilities)
Possibly evidenced by
[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]
Measure I&O accurately.
Weigh daily. Calculate
insensible fluid losses.
Helps estimate fluid replacement needs. Fluid intake should
approximate losses through urine, nasogastric/wound drainage, and
insensible losses (e.g., diaphoresis and metabolism). Note:Some
sources believe that fluid replacement should not exceed two-thirds
of the previous day’s output to prevent prolonging the diuresis.
Provide allowed fluids
throughout 24-hr period.
Diuretic phase of ARF may revert to oliguric phase if fluid intake is
not maintained or nocturnal dehydration occurs.
Monitor BP (noting postural
changes) and HR.
Orthostatic hypotension and tachycardia suggest hypovolemia.
Note signs/symptoms of
dehydration, e.g., dry mucous
membranes, thirst, dulled
sensorium, peripheral
vasoconstriction.
In diuretic or postobstructive phase of renal failure, urine output can
exceed 3 L/day. Extracellular fluid volume depletion activates the
thirst center, and sodium depletion causes persistent thirst,
unrelieved by drinking water. Continued fluid losses/inadequate
replacement may lead to hypovolemic state.
Control environmental
temperature; limit bed linens as
indicated.
May reduce diaphoresis, which contributes to overall fluid losses.
Monitor laboratory studies, e.g.,
sodium.
In nonoliguric ARF or in diuretic phase of ARF, large urine losses
may result in sodium wasting while elevated urinary sodium acts
osmotically to increase fluid losses. Restriction of sodium may be
indicated to break the cycle.
6. Deficient Knowledge May be related to
Lack of exposure/recall
Information misinterpretation
Unfamiliarity with information resources
Possibly evidenced by
Questions/request for information, statement of misconception
Inaccurate follow-through of instructions/development of preventable
Complications
Review disease process, prognosis, and
precipitating factors if known.
Provides knowledge base from which patient can make
informed choices.
14. Explain level of renal function after acute
episode is over.
Patient may experience residual defects in kidney
function, which may/may not be permanent.
Discuss renal dialysis or transplantation if
these are likely options for the future.
Although these options would have been previously
presented by the physician, patient may now be at a
point when options need to be considered/decisions
made and may desire additional input.
Review dietary plan/restrictions. Include
fact sheet listing food restrictions.
Adequate nutrition is necessary to promote
healing/tissue regeneration; adherence to restrictions
may prevent complications.
Encourage patient to observe
characteristics of urine and
amount/frequency of output.
Changes may reflect alterations in renal function/need
for dialysis.
Establish regular schedule for weighing. Useful tool for monitoring fluid and dietary status/needs.
Review fluid intake/restriction. Remind
patient to spread fluids over entire day and
to include all fluids (e.g., ice) in daily fluid
counts.
Depending on the cause/stage of ARF, patient may
need to either restrict or increase intake of fluids.
Discuss activity restriction and gradual
resumption of desired activity. Encourage
use of energy-saving, relaxation, and
diversional techniques.
Patient with severe ARF may need to restrict activity
and/or may feel weak for an extended period during
lengthy recovery phase, requiring measures to conserve
energy and reduce boredom/depression.
Discuss reality of continued presence of
fatigue.
Decreased metabolic energy production, presence of
anemia, and states of discomfort commonly result in
fatigue.
Determine/ prioritize ADLs and personal
responsibilities. Identify available
resources/support systems.
Helps patient manage lifestyle changes and meet
personal/family needs.
Recommend scheduling activities with
adequate rest periods.
Prevents excessive fatigue and conserves energy for
healing, tissue regeneration.
Discuss/review medication use. Encourage
patient to discuss all medications
(including over-the-counter [OTC] drugs)
and herbal supplements with physician.
Medications that are concentrated in/excreted by the
kidneys can cause toxic cumulative reactions and/or
permanent damage to kidneys. Some supplements may
interact with prescribed medications/contain electrolytes.
15. Stress necessity of follow-up care,
laboratory studies.
Renal function may be slow to return following acute
failure (up to 12 mo), and deficits may persist, requiring
changes in therapy to avoid recurrence/complications.
Identify symptoms requiring medical
intervention, e.g., decreased urinary
output, sudden weight gain, presence of
edema, lethargy, bleeding, signs of
infection, altered mentation.
Prompt evaluation and intervention may prevent serious
complications/progression to CRF.
Other Possible Nursing Care Plans
Fluid Volume, deficient (specify)—dependent on cause, duration, and stage of recovery.
Fatigue—decreased metabolic energy production/dietary restriction, anemia, increased energy
requirements, e.g., fever/
inflammation, tissue regeneration.
Infection, risk for—depression of immunologic defenses (secondary to uremia), changes in
dietary intake/malnutrition, increased environmental exposure.
Therapeutic Regimen: ineffective management—complexity of therapeutic regimen, economic
difficulties, perceived benefit.
Pathophysiology of Acute Renal Failure
The interaction of tubular and vascular events result in ARF. The primary cause of
ATN is ischemia. Ischemia for more than two hours results in severe and irreversible
damage to the kidney tubules. Significant reduction in glomular filtration rate (GFR)
is a result of (1) ischemia, (2) activation of the renin-angiotensin system , and (3)
tubular obstruction by cellular debris. As nephrotoxins damage the tubular cells and
these cells are lost through necrosis, the tubules become more permeable. This results
in filtrate absorption and a reduction in the nephrons ability to eliminate waste.
The clinical course of ARF is characterized by the following three phases:
Phase 1. Onset
16. ARF begins with the underlying clinical condition leading to tubular necrosis, for
example hemorrhage, which reduces blood volume and renal perfusion. If adequate
treatment is provided in this phase then the individual's prognosis is good.
Phase 2. Maintenance
A persistent decrease in GFR and tubular necrosis characterizes this phase.
Endothelial cell necrosis and sloughing lead to tubular obstruction and increased
tubular permeability. Because of this, oliguria is often present during the beginning of
this phase. Efficient elimination of metabolic waste, water, electrolytes, and acids
from the body cannot be performed by the kidney during this phase. Therefore,
azotemia, fluid retention, electrolyte imbalance and metabolic acidosis occurs. The
patient is at risk for heart failure and pulmonary edema during this phase because of
the salt and water retention. Immune function is impaired and the patient may be
anemic because of the suppressed erythropoietin secretion by the kidney and toxin-
related shorter RBC life.
Phase 3. Recovery
Renal function of the kidney improves quickly the first five to twenty-five days of this
phase. It begins with the recovery of the GFR and tubular function to such an extent
that BUN and serum creatinine stabilize. Improvement in renal function may continue
for up to a year as more and more nephrons regain function.