This case involves an 18-year-old female patient who presented with diarrhea, vomiting, fever and drowsiness. Upon examination, she was found to be febrile, tachycardic and had some dehydration. Laboratory tests revealed she had cholera infection as well as acute kidney injury, with rising serum creatinine and electrolyte imbalances. She was treated for cholera, sepsis, seizures and fluid imbalances. Her kidney function deteriorated over 11 days before beginning to recover. The lack of a proper medical history made diagnosis and management more challenging for this unconscious and unattended patient suffering from acute renal failure.
Acute renal failure can occur rapidly over hours to days and is characterized by abnormal water, electrolyte and solute balance. It is usually associated with oliguria. The causes can be pre-renal, intrinsic renal, or post-renal. Pre-renal causes involve reduced renal perfusion due to factors like volume depletion, hypotension, cardiovascular issues, or medications. Intrinsic renal causes include vascular, tubular, glomerular or interstitial disease. Post-renal causes involve urinary tract obstruction. Evaluation involves blood and urine tests to identify the specific cause and guide treatment.
The document discusses acute kidney injury (AKI), formerly called acute renal failure (ARF). It defines AKI as a sudden decrease in glomerular filtration rate (GFR) over hours to days. Serum creatinine is commonly used to assess renal function but is not an ideal marker as it rises after GFR drops and is affected by non-renal factors. The causes and types of AKI are described including pre-renal, renal (intrinsic), and post-renal. Acute tubular necrosis (ATN) is the most common cause of intrinsic AKI. Management involves identifying and correcting underlying causes, monitoring fluid balance, and treating complications like hyperkalemia. Dialysis is indicated for refractory
This document discusses acute renal failure (ARF), also known as acute kidney injury (AKI). It defines ARF, discusses its epidemiology and causes. The main causes of ARF are pre-renal (decreased blood flow/volume), renal (damage within the kidneys), and post-renal (obstruction of urine flow). The most common form of intrinsic ARF is acute tubular necrosis, often due to ischemia or nephrotoxins. Diagnosis involves lab tests of kidney function and urine analysis. Treatment focuses on identifying and reversing the underlying cause, maintaining fluid/electrolyte balance, and potentially initiating renal replacement therapy like dialysis.
Acute renal failure, also known as acute kidney injury, is defined as an abrupt loss of kidney function that develops within 7 days. It is characterized by a decrease in creatinine clearance and increases in blood urea nitrogen and creatinine levels. Acute renal failure can be caused by pre-renal issues that decrease blood flow to the kidneys, intrinsic renal issues that damage the kidneys, or post-renal issues that obstruct urine flow. The condition is diagnosed through blood and urine tests and imaging and treated by addressing the underlying cause, giving intravenous fluids, and providing renal replacement therapies like hemodialysis in severe cases.
An abrupt (within 48hr) reduction in kidney function currently defined as an absolute increase in serum creatinine of either >0.3 mg/dL or a percentage increase of >50% or a reduction in UOP (documented as oliguria of <0.5 ml/kg/hr for >6hr)
08 Al Ghonaim Approach To Acute Renal Failureguest2379201
The document discusses acute renal failure (ARF), including its definition, epidemiology, etiology, diagnosis, and treatment. ARF can be pre-renal, renal, or post-renal in etiology. The most common cause is acute tubular necrosis, often from hypotension, sepsis, or nephrotoxins. Diagnosis involves lab tests of kidney function and urinalysis. Treatment focuses on fluid management, avoiding nephrotoxins, and possibly dialysis.
Acute renal failure (ARF) is defined as a rapid reduction in kidney function resulting in build-up of waste products. It can be prerenal (functional), renal (structural), or postrenal (obstruction). Common causes include decreased blood flow, nephrotoxins, and urinary tract obstruction. Patients may present with edema, electrolyte abnormalities, and uremic symptoms. Diagnosis involves urine and blood tests. Treatment focuses on treating the underlying cause, fluid management, and sometimes dialysis.
The document discusses renal failure including definitions of acute renal failure (ARF), chronic renal failure (CRF), and end-stage renal disease (ESRD). It covers classifications and common causes of renal failure. Key points include that ARF can be pre-renal, renal, or post-renal in origin and has many potential causes. CRF is a slow, progressive loss of kidney function that is irreversible and can be caused by diabetes, hypertension, glomerulonephritis, and other conditions. Monitoring of renal function includes tests of serum creatinine and clearance rates.
Acute renal failure can occur rapidly over hours to days and is characterized by abnormal water, electrolyte and solute balance. It is usually associated with oliguria. The causes can be pre-renal, intrinsic renal, or post-renal. Pre-renal causes involve reduced renal perfusion due to factors like volume depletion, hypotension, cardiovascular issues, or medications. Intrinsic renal causes include vascular, tubular, glomerular or interstitial disease. Post-renal causes involve urinary tract obstruction. Evaluation involves blood and urine tests to identify the specific cause and guide treatment.
The document discusses acute kidney injury (AKI), formerly called acute renal failure (ARF). It defines AKI as a sudden decrease in glomerular filtration rate (GFR) over hours to days. Serum creatinine is commonly used to assess renal function but is not an ideal marker as it rises after GFR drops and is affected by non-renal factors. The causes and types of AKI are described including pre-renal, renal (intrinsic), and post-renal. Acute tubular necrosis (ATN) is the most common cause of intrinsic AKI. Management involves identifying and correcting underlying causes, monitoring fluid balance, and treating complications like hyperkalemia. Dialysis is indicated for refractory
This document discusses acute renal failure (ARF), also known as acute kidney injury (AKI). It defines ARF, discusses its epidemiology and causes. The main causes of ARF are pre-renal (decreased blood flow/volume), renal (damage within the kidneys), and post-renal (obstruction of urine flow). The most common form of intrinsic ARF is acute tubular necrosis, often due to ischemia or nephrotoxins. Diagnosis involves lab tests of kidney function and urine analysis. Treatment focuses on identifying and reversing the underlying cause, maintaining fluid/electrolyte balance, and potentially initiating renal replacement therapy like dialysis.
Acute renal failure, also known as acute kidney injury, is defined as an abrupt loss of kidney function that develops within 7 days. It is characterized by a decrease in creatinine clearance and increases in blood urea nitrogen and creatinine levels. Acute renal failure can be caused by pre-renal issues that decrease blood flow to the kidneys, intrinsic renal issues that damage the kidneys, or post-renal issues that obstruct urine flow. The condition is diagnosed through blood and urine tests and imaging and treated by addressing the underlying cause, giving intravenous fluids, and providing renal replacement therapies like hemodialysis in severe cases.
An abrupt (within 48hr) reduction in kidney function currently defined as an absolute increase in serum creatinine of either >0.3 mg/dL or a percentage increase of >50% or a reduction in UOP (documented as oliguria of <0.5 ml/kg/hr for >6hr)
08 Al Ghonaim Approach To Acute Renal Failureguest2379201
The document discusses acute renal failure (ARF), including its definition, epidemiology, etiology, diagnosis, and treatment. ARF can be pre-renal, renal, or post-renal in etiology. The most common cause is acute tubular necrosis, often from hypotension, sepsis, or nephrotoxins. Diagnosis involves lab tests of kidney function and urinalysis. Treatment focuses on fluid management, avoiding nephrotoxins, and possibly dialysis.
Acute renal failure (ARF) is defined as a rapid reduction in kidney function resulting in build-up of waste products. It can be prerenal (functional), renal (structural), or postrenal (obstruction). Common causes include decreased blood flow, nephrotoxins, and urinary tract obstruction. Patients may present with edema, electrolyte abnormalities, and uremic symptoms. Diagnosis involves urine and blood tests. Treatment focuses on treating the underlying cause, fluid management, and sometimes dialysis.
The document discusses renal failure including definitions of acute renal failure (ARF), chronic renal failure (CRF), and end-stage renal disease (ESRD). It covers classifications and common causes of renal failure. Key points include that ARF can be pre-renal, renal, or post-renal in origin and has many potential causes. CRF is a slow, progressive loss of kidney function that is irreversible and can be caused by diabetes, hypertension, glomerulonephritis, and other conditions. Monitoring of renal function includes tests of serum creatinine and clearance rates.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
This document provides an overview of acute renal failure (ARF). It defines ARF as a sudden decline in renal function associated with increased BUN and creatinine and oliguria. ARF can be pre-renal, post-renal, or intra-renal in origin. Clinical manifestations include fluid overload, electrolyte imbalances, and declining kidney function. Treatment involves addressing the underlying cause, fluid hydration, diuretics, and possibly dialysis. Nursing care focuses on monitoring fluid balance and labs, preventing complications like infection, and supporting the patient.
Acute renal failure is characterized by rapid deterioration of renal function over hours or days, usually associated with oliguria or anuria. It can be caused by pre-renal factors like hypovolemia, renal factors like acute tubular necrosis, or post-renal factors like bilateral obstruction. Treatment involves correcting underlying causes, managing fluid balance and electrolyte abnormalities, and potentially initiating dialysis for severe cases or complications. Full recovery may take weeks to months.
Acute renal failure can be prerenal, intrarenal, or postrenal in origin and progresses through onset, diuretic, oliguric, and recovery phases which may be reversible with treatment. Chronic renal failure is progressive and irreversible, leading to azotemia, uremia, and electrolyte imbalances. Treatment options include diet therapy, dialysis like hemodialysis and peritoneal dialysis, and renal transplantation. Nursing care focuses on managing complications and symptoms of renal failure like fluid imbalance, infection risk, fatigue, and anxiety.
This document discusses acute renal failure (ARF), including its causes, classification, pathophysiology, clinical features, investigations, and management. ARF is defined as the rapid onset of renal impairment resulting in the accumulation of nitrogenous waste products. It can be prerenal, intrinsic, or postrenal. Management involves prevention through proper fluid balance and monitoring, as well as conservative treatment and renal replacement therapy if needed. Symptoms include dyspnea, hypertension, arrhythmias, and neurological symptoms like confusion.
This document provides an overview of acute kidney injury (AKI). It discusses the definition, epidemiology, etiology, pathophysiology, diagnosis and treatment of AKI. Some key points:
- AKI accounts for 5-7% of acute care hospital admissions and 30% of ICU admissions, with mortality rates as high as 50%. It can worsen chronic kidney disease and increase the risk of end-stage renal disease.
- Causes include pre-renal issues like hypovolemia, renal issues like acute tubular necrosis, and post-renal issues like obstruction. Diagnosis involves history, physical exam, lab tests of kidney function and imaging.
- Treatment focuses on optimizing
The document discusses the anatomy and physiology of the nephron, the functional unit of the kidney. It describes how nephrons filter blood to form urine via glomerular filtration. Damage to nephrons or decreased blood flow can cause acute kidney injury (AKI), also called acute renal failure (ARF). The causes, types (prerenal, intrinsic renal, postrenal), diagnosis and treatment of ARF are explained in detail. Early dialysis is important for managing complications of severe ARF like fluid overload, electrolyte abnormalities and uremia.
Copyright by Dr. Thuzar Win
Department of Medicine
University of Medicine - 2, Yangon
Feel free to request to take it down this slide if you are copyright owner.
This document provides an overview of acute renal failure (ARF), including its definition, symptoms, risk factors, anatomy and physiology of the renal system, diagnostic criteria, stages, classification, causes, and treatment. ARF is defined as a rapid decline in kidney function over hours to weeks that results in the buildup of waste products and fluid retention. The document discusses the key functions of the kidney in maintaining fluid, electrolyte, and acid-base balance. It classifies ARF into pre-renal, intrarenal, and post-renal types based on the underlying cause and describes the pathophysiology of each type. Treatment involves addressing the underlying cause, managing complications, and potentially dialysis in severe cases.
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.
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
This document discusses kidney injury and renal failure. It begins by defining acute renal failure and its causes, including pre-renal, renal, and post-renal factors. Features of different types of acute renal failure are outlined. Chronic kidney disease is also discussed, including causes, stages based on glomerular filtration rate, and complications involving bone disease, cardiovascular system, and other organ systems. Management of both acute and chronic kidney disease is described. The document concludes with an overview of urinary tract infections, risk factors, diagnosis, and treatment approaches.
Chronic renal failure is caused by various etiologies and leads to progressive loss of kidney function. It is characterized by fluid and electrolyte abnormalities, bone disease, cardiovascular complications, anemia, and other systemic effects. Treatment focuses on slowing progression through blood pressure control and protein restriction, and managing complications through treatment of mineral metabolism disorders, anemia, and other issues.
11 Turman Management Of Acute Renal Failure In PicuDang Thanh Tuan
This document provides an overview of the definition, causes, risk factors, evaluation, and management of acute renal failure (ARF) in pediatric intensive care unit patients. It discusses the importance of differentiating between pre-renal, renal, and post-renal causes of ARF. Key factors that influence outcomes like oliguria, multi-organ failure, and late initiation of dialysis are outlined. Fluid management and treatment of complications such as hypertension, electrolyte abnormalities, and anemia are also reviewed. Emerging potential new treatments for ARF are described but many have not proven effective in clinical trials.
02 Sperati Prevention And Management Of Acute Renal Failureguest2379201
This document provides an overview of acute renal failure (ARF), including its causes, diagnosis, and management. It discusses evaluating ARF through markers like fractional excretion of sodium and urea, and differentiating prerenal from intrinsic renal causes. Treatment involves supportive care and potentially renal replacement therapy, though the optimal modality and dose of therapy remain unclear from clinical trials.
Acute Kidney Failure is a sudden reduction in kidney function that results in nitrogenous wastes accumulating in the blood.
Chronic renal failure is a Progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic, fluid and electrolyte balance fails resulting in Uremia and Azotemia.
Definition, Etiology, Risk Factors, Stages, Clinical Manifestations, Management, Surgical Management, Prevention, Complications. Nursing Management
Acute Renal Failure 2* to Rhabdomyolysis 2* to Motor Vehicular AccidentDJ CrissCross
The document presents a case study of a 20-year-old male who developed acute renal failure secondary to rhabdomyolysis caused by a motorcycle accident. He was admitted with abdominal pain and distension. His creatinine levels increased significantly over his hospital stay, indicating acute kidney injury. He received various treatments including IV fluids, medications, and multiple hemodialysis sessions. His condition gradually improved and he was discharged after three weeks with instructions for outpatient follow up and medication.
This patient has been diagnosed with renal failure due to decreased glomerular filtration rate and sodium retention. Objective findings include edema, hypertension, weight gain, pulmonary congestion, oliguria, distended jugular veins, and changes in mental status. The nursing diagnosis is fluid volume excess related to decreased glomerular filtration rate and sodium retention impairing the kidneys' ability to filter fluids and excrete excess sodium. Short term goals are for the patient to demonstrate behaviors to monitor fluid status and reduce recurrence of fluid excess within 4-8 hours. Long term goals are for the patient to have stabilized fluid volume as evidenced by balanced intake/output, normal vital signs, stable weight, and freedom from edema signs within 3 days with nursing
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, hemorrhage, and asphyxia in newborns. Intrinsic renal failure can be caused by tubular diseases, interstitial diseases, glomerular diseases, or vascula diseases. Acute tubular necrosis is described as the most common cause. Post-renal ARF can result from urinary tract obstruction. Laboratory findings that can aid in diagnosis are also summarized.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
This document provides an overview of acute renal failure (ARF). It defines ARF as a sudden decline in renal function associated with increased BUN and creatinine and oliguria. ARF can be pre-renal, post-renal, or intra-renal in origin. Clinical manifestations include fluid overload, electrolyte imbalances, and declining kidney function. Treatment involves addressing the underlying cause, fluid hydration, diuretics, and possibly dialysis. Nursing care focuses on monitoring fluid balance and labs, preventing complications like infection, and supporting the patient.
Acute renal failure is characterized by rapid deterioration of renal function over hours or days, usually associated with oliguria or anuria. It can be caused by pre-renal factors like hypovolemia, renal factors like acute tubular necrosis, or post-renal factors like bilateral obstruction. Treatment involves correcting underlying causes, managing fluid balance and electrolyte abnormalities, and potentially initiating dialysis for severe cases or complications. Full recovery may take weeks to months.
Acute renal failure can be prerenal, intrarenal, or postrenal in origin and progresses through onset, diuretic, oliguric, and recovery phases which may be reversible with treatment. Chronic renal failure is progressive and irreversible, leading to azotemia, uremia, and electrolyte imbalances. Treatment options include diet therapy, dialysis like hemodialysis and peritoneal dialysis, and renal transplantation. Nursing care focuses on managing complications and symptoms of renal failure like fluid imbalance, infection risk, fatigue, and anxiety.
This document discusses acute renal failure (ARF), including its causes, classification, pathophysiology, clinical features, investigations, and management. ARF is defined as the rapid onset of renal impairment resulting in the accumulation of nitrogenous waste products. It can be prerenal, intrinsic, or postrenal. Management involves prevention through proper fluid balance and monitoring, as well as conservative treatment and renal replacement therapy if needed. Symptoms include dyspnea, hypertension, arrhythmias, and neurological symptoms like confusion.
This document provides an overview of acute kidney injury (AKI). It discusses the definition, epidemiology, etiology, pathophysiology, diagnosis and treatment of AKI. Some key points:
- AKI accounts for 5-7% of acute care hospital admissions and 30% of ICU admissions, with mortality rates as high as 50%. It can worsen chronic kidney disease and increase the risk of end-stage renal disease.
- Causes include pre-renal issues like hypovolemia, renal issues like acute tubular necrosis, and post-renal issues like obstruction. Diagnosis involves history, physical exam, lab tests of kidney function and imaging.
- Treatment focuses on optimizing
The document discusses the anatomy and physiology of the nephron, the functional unit of the kidney. It describes how nephrons filter blood to form urine via glomerular filtration. Damage to nephrons or decreased blood flow can cause acute kidney injury (AKI), also called acute renal failure (ARF). The causes, types (prerenal, intrinsic renal, postrenal), diagnosis and treatment of ARF are explained in detail. Early dialysis is important for managing complications of severe ARF like fluid overload, electrolyte abnormalities and uremia.
Copyright by Dr. Thuzar Win
Department of Medicine
University of Medicine - 2, Yangon
Feel free to request to take it down this slide if you are copyright owner.
This document provides an overview of acute renal failure (ARF), including its definition, symptoms, risk factors, anatomy and physiology of the renal system, diagnostic criteria, stages, classification, causes, and treatment. ARF is defined as a rapid decline in kidney function over hours to weeks that results in the buildup of waste products and fluid retention. The document discusses the key functions of the kidney in maintaining fluid, electrolyte, and acid-base balance. It classifies ARF into pre-renal, intrarenal, and post-renal types based on the underlying cause and describes the pathophysiology of each type. Treatment involves addressing the underlying cause, managing complications, and potentially dialysis in severe cases.
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.
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
This document discusses kidney injury and renal failure. It begins by defining acute renal failure and its causes, including pre-renal, renal, and post-renal factors. Features of different types of acute renal failure are outlined. Chronic kidney disease is also discussed, including causes, stages based on glomerular filtration rate, and complications involving bone disease, cardiovascular system, and other organ systems. Management of both acute and chronic kidney disease is described. The document concludes with an overview of urinary tract infections, risk factors, diagnosis, and treatment approaches.
Chronic renal failure is caused by various etiologies and leads to progressive loss of kidney function. It is characterized by fluid and electrolyte abnormalities, bone disease, cardiovascular complications, anemia, and other systemic effects. Treatment focuses on slowing progression through blood pressure control and protein restriction, and managing complications through treatment of mineral metabolism disorders, anemia, and other issues.
11 Turman Management Of Acute Renal Failure In PicuDang Thanh Tuan
This document provides an overview of the definition, causes, risk factors, evaluation, and management of acute renal failure (ARF) in pediatric intensive care unit patients. It discusses the importance of differentiating between pre-renal, renal, and post-renal causes of ARF. Key factors that influence outcomes like oliguria, multi-organ failure, and late initiation of dialysis are outlined. Fluid management and treatment of complications such as hypertension, electrolyte abnormalities, and anemia are also reviewed. Emerging potential new treatments for ARF are described but many have not proven effective in clinical trials.
02 Sperati Prevention And Management Of Acute Renal Failureguest2379201
This document provides an overview of acute renal failure (ARF), including its causes, diagnosis, and management. It discusses evaluating ARF through markers like fractional excretion of sodium and urea, and differentiating prerenal from intrinsic renal causes. Treatment involves supportive care and potentially renal replacement therapy, though the optimal modality and dose of therapy remain unclear from clinical trials.
Acute Kidney Failure is a sudden reduction in kidney function that results in nitrogenous wastes accumulating in the blood.
Chronic renal failure is a Progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic, fluid and electrolyte balance fails resulting in Uremia and Azotemia.
Definition, Etiology, Risk Factors, Stages, Clinical Manifestations, Management, Surgical Management, Prevention, Complications. Nursing Management
Acute Renal Failure 2* to Rhabdomyolysis 2* to Motor Vehicular AccidentDJ CrissCross
The document presents a case study of a 20-year-old male who developed acute renal failure secondary to rhabdomyolysis caused by a motorcycle accident. He was admitted with abdominal pain and distension. His creatinine levels increased significantly over his hospital stay, indicating acute kidney injury. He received various treatments including IV fluids, medications, and multiple hemodialysis sessions. His condition gradually improved and he was discharged after three weeks with instructions for outpatient follow up and medication.
This patient has been diagnosed with renal failure due to decreased glomerular filtration rate and sodium retention. Objective findings include edema, hypertension, weight gain, pulmonary congestion, oliguria, distended jugular veins, and changes in mental status. The nursing diagnosis is fluid volume excess related to decreased glomerular filtration rate and sodium retention impairing the kidneys' ability to filter fluids and excrete excess sodium. Short term goals are for the patient to demonstrate behaviors to monitor fluid status and reduce recurrence of fluid excess within 4-8 hours. Long term goals are for the patient to have stabilized fluid volume as evidenced by balanced intake/output, normal vital signs, stable weight, and freedom from edema signs within 3 days with nursing
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, hemorrhage, and asphyxia in newborns. Intrinsic renal failure can be caused by tubular diseases, interstitial diseases, glomerular diseases, or vascula diseases. Acute tubular necrosis is described as the most common cause. Post-renal ARF can result from urinary tract obstruction. Laboratory findings that can aid in diagnosis are also summarized.
This document provides information on electrolytes and electrolyte imbalances. It defines electrolytes as compounds that conduct electric current when dissolved in solution. The major electrolytes in the body are potassium, sodium, calcium, phosphorus, chloride, and bicarbonate. Potassium is mainly found inside cells while sodium is mainly outside cells. Imbalances can occur when there are changes in the concentrations of these electrolytes, causing water to move in and out of cells. Common electrolyte imbalances discussed include hypernatremia, hyponatremia, hyperkalemia, and hypokalemia. Causes, signs/symptoms, and treatment approaches are described for each imbalance.
Tubulointerstitial nephropathy can be acute or chronic and is characterized by inflammation and scarring of the kidney tubules and surrounding tissue. Acute causes are often toxins or ischemia while chronic causes include obstructive uropathy, vesicoureteral reflux, analgesics, and heavy metals. Polycystic kidney disease is a common hereditary condition where numerous cysts develop in the kidneys, often leading to end-stage renal disease. Medullary sponge kidney is a benign condition present from birth that causes kidney cysts and issues like hematuria, urinary tract infections, and kidney stones.
The document discusses acute renal failure (ARF), which refers to a sudden and usually reversible loss of renal function that develops over days or weeks. ARF can be pre-renal, intrinsic renal, or post-renal in cause. Reversible pre-renal ARF occurs when haemodynamic disturbances like hypotension produce acute dysfunction that can be rapidly reversed by treating the underlying cause and restoring renal perfusion. Left untreated, pre-renal ARF can progress to established acute tubular necrosis. Proper diagnosis involves assessing the cause, signs of poor perfusion, and urine and blood tests. Management focuses on correcting the underlying problem and restoring blood volume through fluids.
La insuficiencia renal aguda es el cese brusco de la función renal, que puede ser reversible. Puede ser causada por factores prerrenales como deshidratación, hipoperfusión o nefrotóxicos, o por daño directo al riñón. Los síntomas incluyen edema, aumento de peso, presión arterial elevada y alteraciones electrolíticas y metabólicas. El tratamiento se enfoca en controlar las causas subyacentes y mantener un adecuado volumen circulante y oxigenación tisular.
Acte kidney injury-advances in diagnosis & management.Suneth Weerarathna
This document discusses advances in the diagnosis and management of acute kidney injury (AKI). It begins with objectives and outlines of topics including AKI definitions, classification systems, biomarkers for early detection, and management strategies. Novel biomarkers such as Kim-1, NGAL, and cystatin C allow detection of AKI earlier than serum creatinine. While renal replacement therapy is important for established AKI, prevention and treatment of underlying causes are priorities. Overall, awareness of AKI is increasing worldwide and standardized criteria along with new diagnostics and therapies can lead to better outcomes.
Proteinuira & Glomerular Disease, Dr. Sara Arnold, 11/8/14upstatevet
This document provides an overview of glomerular disease and proteinuria in dogs. It begins with a discussion of laboratory evaluation of proteinuria including urinalysis and urine protein to creatinine ratio testing. Pathophysiology of proteinuria is then reviewed including mechanisms in the glomerulus, tubules, and factors causing extra-renal proteinuria. Common causes of pathologic renal proteinuria are listed. The diagnostic workup for proteinuria is outlined including recommendations for additional testing based on urinary protein levels and presence of azotemia. Renal biopsy indications and contraindications are reviewed. Treatment options including ACE inhibitors, diet, immunosuppression, and managing hypertension are summarized. Factors impacting prognosis like severity
Internal Medicine Board Review - Dermatology Flashcards - by KnowmedgeKnowmedge
Internal Medicine Board Review Flashcards - This eBook contains 50 Dermatology Flashcards. The Flashcards are review questions and can be used to study for medical board exams including the USMLE Step Exams and the ABIM Internal Medicine Exam. More questions can be found at www.knowmedge.com
Internal Medicine Board Review - Neurology Flashcards - by KnowmedgeKnowmedge
This document contains a 50 question neurology flashcard set from Knowmedge for medical board exam preparation. Knowmedge is an online medical education platform that provides over 900 internal medicine questions, 4000 flashcards, and 1500 mnemonics to help learners prepare for exams. The flashcard set covers topics like migraines, seizures, multiple sclerosis, strokes, Parkinson's disease, and more. It encourages the user to sign up for Knowmedge's full internal medicine learning platform online for more practice questions and flashcards.
Internal Medicine Board Review - Oncology Flashcards - by KnowmedgeKnowmedge
Internal Medicine Board Review Flashcards - This eBook contains 50 Oncology Flashcards. The Flashcards are review questions and can be used to study for medical board exams including the USMLE Step Exams and the ABIM Internal Medicine Exam. More questions can be found at www.knowmedge.com
Internal Medicine Board Review - Hematology Flashcards - by KnowmedgeKnowmedge
This document provides a summary of a 50-question hematology flashcard set from Knowmedge, an online medical education platform. It includes flashcards on topics like types of anemia, electrolyte abnormalities, porphyrias, hemolytic diseases, thalassemias, and treatments for conditions like myelodysplasia, aplastic anemia, and sickle cell disease. The document encourages the user to visit Knowmedge.com for more flashcards and medical education resources to help prepare for board exams. It notes that passing board exams is an important step on the journey to becoming a physician.
This document provides information on metabolic acidosis and alkalosis. It discusses the importance of hydrogen ions in determining cell membrane permeability and pH. It defines metabolic acidosis and alkalosis and describes causes such as lactic acidosis, ketoacidosis, renal tubular acidosis. It explains the anion gap and factors that influence it. It also discusses evaluation of metabolic acid-base disorders using the anion gap, serum lactate and osmolality. Treatment of metabolic acidosis with sodium bicarbonate is described. Causes and clinical effects of metabolic alkalosis are also summarized.
Internal Medicine Board Review - Nephrology Flashcards - by KnowmedgeKnowmedge
The document is an introduction to a set of 50 nephrology/urology flashcards for medical board exam preparation provided by Knowmedge, an online medical education platform. It describes Knowmedge's resources including over 900 internal medicine questions, 4,000 flashcards, and 1,500 mnemonics. The flashcards cover topics in nephrology and urology and are intended to help users study for their medical board exams. Users are encouraged to visit Knowmedge's website and social media pages to learn more about their internal medicine learning tools and board review materials.
Internal Medicine Board Review - Infectious Disease Flashcards - by KnowmedgeKnowmedge
Internal Medicine Board Review Flashcards - This eBook contains 50 Infectious Disease Flashcards. The Flashcards are review questions and can be used to study for medical board exams including the USMLE Step Exams and the ABIM Internal Medicine Exam. More questions can be found at www.knowmedge.com
Renal Tubular Acidosis is a condition characterized by a normal anion gap metabolic acidosis due to impaired kidney function. There are different types of RTA defined by the location of the defect in the kidney tubules. Type 1 RTA involves a defect in distal tubules resulting in decreased secretion of hydrogen ions and inability to maximally acidify urine. Patients experience metabolic acidosis, hypokalemia, nephrocalcinosis, and in some cases hearing loss or growth issues. Treatment focuses on correcting electrolyte abnormalities and metabolic acidosis with alkali solutions.
Internal Medicine Board Review - Gastroenterology Flashcards - by KnowmedgeKnowmedge
Internal Medicine Board Review Flashcards - This eBook contains 50 Gastroenterology Flashcards. The Flashcards are review questions and can be used to study for medical board exams including the USMLE Step Exams and the ABIM Internal Medicine Exam. More questions can be found at www.knowmedge.com
Chronic Kidney Disease (CKD) is defined as a progressive loss of kidney function over months or years. Patients with early stage CKD are generally asymptomatic, while later stages can cause nausea, vomiting, fatigue, and other symptoms. CKD is staged based on glomerular filtration rate, with stage 5 being severe kidney failure requiring dialysis or transplant. Risk factors include diabetes, high blood pressure, smoking, and family history. Screening helps detect CKD in at-risk groups. Treatment focuses on lifestyle changes, medications, and dialysis or transplant for kidney failure.
Hematuria for undergraduates
this is a presentation i prepared for medical students about hematuria, hope u like it
for more urology resources visit:
www.uronotes2012.blogspot.com
Internal Medicine Board Review - Endocrinology Flashcards - by KnowmedgeKnowmedge
Internal Medicine Board Review Flashcards - This eBook contains 50 Endocrinology Flashcards. The Flashcards are review questions and can be used to study for medical board exams including the USMLE Step Exams and the ABIM Internal Medicine Exam. More questions can be found at www.knowmedge.com
The document discusses a case of a 23-year-old female with a history of ketamine abuse who presented with abdominal and flank pain and was found to have bilateral hydronephrosis, pyuria, and acute on chronic kidney disease. She was admitted multiple times for intravenous antibiotics and underwent placement of percutaneous nephrostomy tubes for her hydronephrosis. Her hospital courses involved monitoring of her declining renal function and electrolyte abnormalities related to her chronic ketamine-induced cystopathy.
Acute kidney injury (AKI), previously called acute renal failure, is characterized by a reversible increase in blood creatinine and waste products and the kidney's inability to regulate fluids and electrolytes. AKI is defined as an abrupt loss of kidney function within hours to days resulting in fluid retention and electrolyte dysregulation. Causes of AKI include prerenal issues like low blood flow, intrinsic renal damage from toxins or infections, and postrenal issues causing urinary blockage. AKI is diagnosed through history, physical exam, tests of kidney function and urine analysis, imaging, and sometimes renal biopsy. Biomarkers like NGAL, IL-18 and KIM-1 show promise in early AK
This document provides an overview of acute kidney injury (AKI) in neonates. It discusses the definition, incidence, pathophysiology, risk factors, clinical features, management and outcomes of AKI. The presentation covers neonatal renal physiology, the classification of AKI, common causes of pre-renal, intrinsic renal and post-renal AKI. It also describes the challenges in diagnosing AKI in neonates and the approach to evaluating a neonate with suspected AKI, including relevant laboratory and imaging tests.
1) Acute kidney injury (AKI) is common, affecting up to 7-50% of ICU patients. It can be caused by prerenal, intrinsic renal, or postrenal factors.
2) The AKIN criteria is commonly used to stage AKI based on changes in serum creatinine and urine output. Stage 1 AKI involves a mild increase in creatinine or decrease in urine output.
3) Intrinsic renal AKI includes acute tubular necrosis, acute interstitial nephritis, and glomerulonephritis. These can be differentiated based on urine and microscopy findings as well as clinical context.
<SUMMARY>
The document provides an overview of acute kidney injury (AKI), including definitions, classification, epidemiology, etiology, diagnosis, management, and prevention strategies. It defines AKI according to the KDIGO criteria and discusses the RIFLE and AKIN classification systems. Prerenal, intrinsic, and postrenal causes of AKI are outlined. Diagnosis involves establishing baseline kidney function, identifying potential causes, and evaluating volume status, laboratory tests, and imaging studies. Management focuses on treating the underlying cause, optimizing hemodynamics, and preventing complications. Prevention emphasizes recognizing risk factors and avoiding nephrotoxic exposures.
</SUMMARY>
New microsoft office power point presentationGiri Dharan
This document describes the case of a 68-year-old woman presenting with chest pain and shortness of breath who was found to have hyponatremia. On examination, she had mild edema but normal vital signs. Tests found euvolemic hyponatremia with normal kidney function. She developed altered mental status after thrombolytic therapy for her heart attack. Hyponatremia was classified as SIAD based on lab results. Management focused on slow correction and monitoring for complications.
Dr. Ahmed Elberry provides an overview of acute kidney injury (AKI) including its definition, classification systems, causes, mechanisms, and clinical manifestations. AKI can be caused by prerenal, renal, or postrenal factors and results in a abrupt decrease in kidney function over hours to days. Common causes include ischemia, infections, drugs like NSAIDs, contrast media, and aminoglycosides. Patients with AKI may experience oliguria, azotemia, fluid overload, and electrolyte abnormalities.
Renal cell carcinoma after kidney transplantation 2017CHAKEN MANIYAN
This case discusses a patient who underwent a living related kidney transplant and subsequently developed increased creatinine levels and CMV viremia. Further workup revealed an enhancing nodule in the patient's native right kidney. The patient underwent surgery where a 3x3cm solid mass was removed from the right lower pole of the native kidney. A review of literature on renal cell carcinoma after kidney transplantation showed it can develop through transmission from donor, de novo occurrence in recipient, or recurrence in recipient. Immunosuppression places transplant patients at higher risk for developing various cancers.
This case involves a 7-year-old female presenting with acute renal failure, facial swelling, and hematuria. She had been treated for malaria and pneumonia in the past month. Her creatinine was elevated at 1711 umol/L, indicating severe acute renal injury. Possible causes of her acute renal failure include an allergic reaction to antibiotics like gentamicin or cephalosporins, or nephrotoxicity from multiple antibiotic exposures over the past month. Her renal failure should be managed by discontinuing any nephrotoxic medications, aggressive hydration, and monitoring of her renal function.
Wilson’s disease an update on diagnosis &Sarath Menon
Wilson disease is a genetic disorder of copper metabolism that can affect the liver, brain, eyes, and other organs. The document discusses Wilson disease in depth, covering copper metabolism, clinical presentation, diagnosis, and treatment approaches including medications, diet, monitoring, and prognosis. Treatment involves chelating excess copper from the body using medications like zinc, penicillamine, or trientine to control symptoms and prevent organ damage.
The document discusses acute kidney injury (AKI), defining it as an abrupt reduction in kidney function over a period of less than 3 months and outlining approaches to diagnosis and treatment. Common diagnostic markers for AKI include laboratory tests and urinalysis to identify abnormalities. Management of AKI depends on the underlying cause and severity, and may include intravenous fluids, diuretics, or renal replacement therapies like dialysis.
Acute kidney injury (AKI) is a common condition characterized by a sudden decline in kidney function. It affects 5-7% of hospital admissions and 30% of intensive care unit admissions. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Treatment focuses on optimizing fluid status and hemodynamics, removing nephrotoxins if possible, and initiating renal replacement therapy as needed based on the underlying cause and severity of AKI.
The document discusses hepatorenal syndrome (HRS), a type of kidney failure seen in patients with cirrhosis and ascites. It provides details on three patient case studies, including their histories, examinations, investigations and management considerations. Key points covered include definitions of acute kidney injury (AKI) and HRS, pathophysiology of renal dysfunction in cirrhosis, evaluation of patients, biomarkers for distinguishing HRS from other causes of AKI, and general management approaches including use of albumin infusion.
1. The document provides an overview of renal anatomy and physiology, clinical manifestations of renal diseases, methods for estimating renal function, and common renal disease syndromes.
2. Key aspects of renal anatomy discussed include the structure and function of nephrons, the glomerular filtration barrier, and countercurrent exchange mechanisms.
3. Common clinical signs of renal diseases include edema, hypertension, flank pain, urinary abnormalities, and changes in estimated glomerular filtration rate.
4. Major renal disease syndromes covered are nephrotic syndrome, nephritic syndrome, acute renal failure, and chronic renal failure.
Acute Kidney Injury; A case study with detailed etiology and managementkiyingiedison
- A 57-year-old female presented with decreased consciousness, decreased urine output, and vomiting. She was diagnosed with severe malaria and acute kidney injury.
- Laboratory tests showed acute kidney injury with a creatinine of 987umol/L. She received hemodialysis, IV antibiotics, and supportive care.
- Acute kidney injury is defined as an abrupt decrease in kidney function causing retention of waste and electrolyte dysregulation. It involves increased creatinine and decreased urine output. Management focuses on treating the underlying cause, maintaining fluid balance, and correcting biochemical abnormalities.
Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.It's most common in those who are critically ill and already hospitalized.
The document summarizes a patient's medical report during hemodialysis treatment. It includes information on the patient's medical history, physical examination findings, lab results, dialysis monitoring, diagnosis of end stage renal disease due to diabetes and hypertension, and treatment plan to address issues like intradialytic hypotension and anemia management through diet, medication, and ensuring adequate dialysis.
Hyponatremia is a common electrolyte disorder in diverse fields of medicine. A sound understanding of Physiology is essential for its management. Real life clinical examples are described
Similar to 19 Shoeb Bin Islam Acute Renal Failure (20)
1) Procedural sedation is used for many medical procedures and aims to provide analgesia, amnesia, and reduce anxiety while maintaining airway reflexes and spontaneous breathing.
2) While pulse oximetry became standard in the 1980s, capnography has emerged as the new gold standard for monitoring procedural sedation as it can detect respiratory issues that oximetry may miss.
3) Overlake Hospital implemented capnography monitoring for all procedural sedations after reviewing evidence and determining it was more effective for patient safety than relying on respiratory therapists to continuously monitor each procedure.
The evolution of pediatric mechanical ventilatorsDang Thanh Tuan
1. Mechanical ventilators have evolved from simple analog machines to sophisticated microprocessor-controlled devices with advanced modes of ventilation.
2. Early ventilators were open-loop controlled while modern ventilators use various closed-loop and dual-loop control schemes to better match ventilation to patient needs.
3. The newest generations of ventilators use proportional assist, automatic tube compensation, adaptive support ventilation, and other advanced modes that aim to provide more patient-synchronized support and facilitate weaning. However, further research is still needed to fully understand the outcomes of these newer ventilation strategies.
The document discusses various methods of patient monitoring during anesthesia, including their purposes, advantages, and limitations. It covers monitoring vital signs, standards for basic anesthesia monitoring according to the ASA, techniques like non-invasive blood pressure monitoring, ECG, pulse oximetry, capnography, and invasive arterial line monitoring. Key aspects emphasized are integrating multiple monitoring methods to evaluate oxygenation, ventilation, and circulation.
The document discusses the introduction and clinical applications of volumetric capnography (VCO2) at one hospital. It provides an agenda for the topics covered, which include VCO2 management, clinical applications, and data from the University of Tennessee Medical Center's experience using VCO2. Key applications discussed are ventilation management, monitoring changes in perfusion, optimization of positive end-expiratory pressure, and assisting with ventilator weaning trials. The University of Tennessee Medical Center saw decreases in length of mechanical ventilation, ventilator days, and re-intubation rates after implementing VCO2 monitoring.
18 basics of pediatric airway anatomy, physiology and managementDang Thanh Tuan
The document provides an overview of pediatric airway anatomy, physiology, and management. It discusses the differences between pediatric and adult airways, including a more rostral larynx, relatively larger tongue, angled vocal cords, differently shaped epiglottis, and funneled larynx in children. It also reviews normal airway management techniques like bag-mask ventilation and various airway devices, as well as complications from intubation. The goal is to protect, adequately ventilate, and oxygenate the pediatric airway.
The document discusses the use of capnography for non-intubated patients experiencing trouble breathing. It describes how capnography can help identify and monitor conditions like bronchospasm from asthma or COPD by examining patterns in exhaled carbon dioxide levels. Specific capnographic signatures are presented for different respiratory conditions including asthma attacks, COPD exacerbations, congestive heart failure, and hypoventilation states. Case studies demonstrate how capnography can track changes in a patient's condition before and after treatment.
Capnography can be used to summarize 3 key applications for intubated patients:
1) It can confirm correct endotracheal tube placement and detect displacement. Characteristic waveforms indicate proper vs displaced placement.
2) During CPR, it can assess the effectiveness of chest compressions by correlating end-tidal CO2 levels with cardiac output and blood flow.
3) It provides an early indicator of return of spontaneous circulation through a rapid rise in CO2 levels, earlier than other signs like pulse or blood pressure. It also aids the decision to cease resuscitation efforts based on CO2 levels.
Capnography measures exhaled carbon dioxide (CO2) to provide real-time monitoring of ventilation, unlike pulse oximetry which monitors oxygen saturation in the blood and is slower to detect changes. A normal capnographic waveform has four phases: 1) dead space, 2) ascending, 3) alveolar plateau, and 4) descending. The end-tidal CO2 value reflects the highest CO2 concentration in exhaled air and typically ranges from 35-45mmHg. Capnography can immediately detect conditions that impact ventilation such as hypoventilation, hyperventilation, and bronchospasm based on changes to the waveform shape, frequency, and CO2 values.
This document provides an overview of capnography, which is a technology that objectively measures ventilation by detecting exhaled carbon dioxide. It can be used for both intubated and non-intubated patients to continuously monitor ventilation and the patient's ABCs. The document reviews the history of capnography, from its initial use in operating rooms to new portable technologies suitable for emergency medical services. It also outlines the clinical applications of capnography such as verifying endotracheal tube placement and monitoring treatment effectiveness.
Dr. Ajmal Eusuf discusses the importance and benefits of capnography monitoring in the ICU. Capnography can be used to confirm proper endotracheal tube placement, monitor ventilation, and detect various respiratory issues. While capnography is standard practice in operating rooms and recommended by guidelines, only about half of UK ICUs currently use it as a mandatory monitoring tool. Adopting capnography as routine bedside monitoring in the ICU would help compliance with protocols and better patient care, especially for critically ill patients who are sicker than those in operating rooms.
The document discusses two options for capnography monitoring from ZOLL - the CAPNOSTAT 3 mainstream CO2 sensor and the LoFlo sidestream CO2 module. It provides details on the benefits of each, such as the CAPNOSTAT sensor's accuracy and resistance to contaminants, and the LoFlo module's interchangeability and low 50ml/min sampling rate. The document emphasizes that both provide reliable, accurate CO2 monitoring and waveforms for assessing patient ventilation.
Applications of NMR in Protein Structure Prediction.pptxAnagha R Anil
This presentation explores the pivotal role of Nuclear Magnetic Resonance (NMR) spectroscopy in predicting protein structures. It delves into the methodologies, advancements, and applications of NMR in determining the three-dimensional configurations of proteins, which is crucial for understanding their function and interactions.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) CosmeticsMuskanShingari
Acne is a common skin condition that occurs when hair follicles become clogged with oil and dead skin cells. It typically manifests as pimples, blackheads, or whiteheads, often on the face, chest, shoulders, or back. Acne can range from mild to severe and may cause emotional distress and scarring in some cases.
**Causes:**
1. **Excess Oil Production:** Hormonal changes during adolescence or certain times in adulthood can increase sebum (oil) production, leading to clogged pores.
2. **Clogged Pores:** When dead skin cells and oil block hair follicles, bacteria (usually Propionibacterium acnes) can thrive, causing inflammation and acne lesions.
3. **Hormonal Factors:** Fluctuations in hormone levels, such as during puberty, menstrual cycles, pregnancy, or certain medical conditions, can contribute to acne.
4. **Genetics:** A family history of acne can increase the likelihood of developing the condition.
**Types of Acne:**
- **Whiteheads:** Closed plugged pores.
- **Blackheads:** Open plugged pores with a dark surface.
- **Papules:** Small red, tender bumps.
- **Pustules:** Pimples with pus at their tips.
- **Nodules:** Large, solid, painful lumps beneath the surface.
- **Cysts:** Painful, pus-filled lumps beneath the surface that can cause scarring.
**Treatment:**
Treatment depends on the severity and type of acne but may include:
- **Topical Treatments:** Such as benzoyl peroxide, salicylic acid, or retinoids to reduce bacteria and unclog pores.
- **Oral Medications:** Antibiotics or oral contraceptives for hormonal acne.
- **Procedures:** Such as chemical peels, extraction of comedones, or light therapy for more severe cases.
**Prevention and Management:**
- **Cleanse:** Regularly wash skin with a gentle cleanser.
- **Moisturize:** Use non-comedogenic moisturizers to keep skin hydrated without clogging pores.
- **Avoid Irritants:** Such as harsh cosmetics or excessive scrubbing.
- **Sun Protection:** Use sunscreen to prevent exacerbation of acne scars and inflammation.
Acne treatment can take time, and consistency in skincare routines and treatments is crucial. Consulting a dermatologist can help tailor a treatment plan that suits individual needs and reduces the risk of scarring or long-term skin damage.
This presentation gives information on the pharmacology of Prostaglandins, Thromboxanes and Leukotrienes i.e. Eicosanoids. Eicosanoids are signaling molecules derived from polyunsaturated fatty acids like arachidonic acid. They are involved in complex control over inflammation, immunity, and the central nervous system. Eicosanoids are synthesized through the enzymatic oxidation of fatty acids by cyclooxygenase and lipoxygenase enzymes. They have short half-lives and act locally through autocrine and paracrine signaling.
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)MuskanShingari
Skin is the largest organ of the human body, serving crucial functions that include protection, sensation, regulation, and synthesis. Structurally, it consists of three main layers: the epidermis, dermis, and hypodermis (subcutaneous layer).
1. **Epidermis**: The outermost layer primarily composed of epithelial cells called keratinocytes. It provides a protective barrier against environmental factors, pathogens, and UV radiation.
2. **Dermis**: Located beneath the epidermis, the dermis contains connective tissue, blood vessels, hair follicles, and sweat glands. It plays a vital role in supporting and nourishing the epidermis, regulating body temperature, and housing sensory receptors for touch, pressure, temperature, and pain.
3. **Hypodermis**: Also known as the subcutaneous layer, it consists of fat and connective tissue that anchors the skin to underlying structures like muscles and bones. It provides insulation, cushioning, and energy storage.
Skin performs essential functions such as regulating body temperature through sweat production and blood flow control, synthesizing vitamin D when exposed to sunlight, and serving as a sensory interface with the external environment.
Maintaining skin health is crucial for overall well-being, involving proper hygiene, hydration, protection from sun exposure, and avoiding harmful substances. Skin conditions and diseases range from minor irritations to chronic disorders, emphasizing the importance of regular care and medical attention when needed.
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...Donc Test
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
Selective alpha1 blockers are Prazosin, Terazosin, Doxazosin, Tamsulosin and Silodosin majorly used to treat BPH, also hypertension, PTSD, Raynaud's phenomenon, CHF
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
Spontaneous Bacterial Peritonitis - Pathogenesis , Clinical Features & Manage...Jim Jacob Roy
In this presentation , SBP ( spontaneous bacterial peritonitis ) , which is a common complication in patients with cirrhosis and ascites is described in detail.
The reference for this presentation is Sleisenger and Fordtran's Gastrointestinal and Liver Disease Textbook ( 11th edition ).
2. Case History
Name : x
Age : 18 years
Sex : Female
D/A : 20/04/09
D/D : 02/05/09
Admission problems :
(Partial History at the beganing)
1) Diarrhoea - 1 days
2) Vomiting - 1days
3) Fever - 1days
4) Drowsy – 1 hour
(Actually patient had no real attendant, we collected information from a person who did not give proper history and after than he left away )
3. ON EXAMINATION
On Examination
Patient was Drowsy followed by Unconciousness and febrile
Pulse : 100 / min, regular, moderate volume
R/R : 22 / min, no chest in drawing.
Temperature : 39`C
Blood Pressure : 100/65mmHg
Pallor, cyanosis, jaundice, oedema - Nil
Dehydration :Some DH
4. Nervous sytem Examination-
patient unconcious
Kernig`s Sign - Negative
Pupil – normal in size and reacting to light
After 10-12 hours patient developed repeated convulsion
Urination- Urine Passed ?7-8 hour prior to admission (scanty)
Other systems(CVS,RESPIRATORY,GIT) revealed nothing abnormalities
•*Actually patient had no real attendant, we collected information
from a person who did not give proper history and after than he left
away .
5. PROBLEM LIST
*ACUTE WATERY DIARRHOEA
*SOME D/H
*FEVER
*UNCONCIOUSNESS (? MENINGITIES )
*?RENAL FAILURE( Uremic Encephalopathy)
*SEPTECEMIA
* LACK OF PROPER HISTORY
6. LABORATORY INVESTIGATIONS
CBC:-
Hemoglobin-10.9gm/dl
Hct – 33.6%,
TC- 12.97 / 10^u,
Poly – 83.8%,
Lymp – 12.7%,
Band – 00%,
Monocytes – 3.4%,
Eosinophil – 00%
Basophil- 0.1%
ESR - 48 mm/1st hour
R/S for Cholera:- Vibrio Cholera01 E1 Tor Ogawa
CXR- Normal study
Blood C/S No Growth
USG and Urine R/M/E WBC cast and Epithelial cell-7-8 Protein-+
9. MANAGEMENT
Tab.Azythromycin for Cholera
Some D/H - I/V Acetate
Septicemia – Inj. Ceftriaxone
Convulsion - Inj. Diazepam + Inj. Phenoberbitone
For Hypokalamia – Syp Kcl through NG Tube
For Fluid over load - Inj Frusemide
Changing position Frequently
Proper Nursing care
Maintain urine input &output chart and fluid Intake accordingly
We had a plan to Refer the patient to Kidney hospital but we could not
manage any attendant .
10. RENAL FAILURE
DIAGNOSIS & MANAGEMENT
OF
AN UNCONCIOUS & UNATTENDENT
PATIENT
11. Anatomy: The Renal System
• Kidneys
• Ureters
– Enter at oblique angle
– Peristalsis
• Both prevent reflux
• Bladder
– Capacity 300–500 ml
• Urethra
– Excretion; outside of body.
– In Males surrounded by
prostate
12. How Do We Proceed?
Reduce Urine output/Anuria /urine abnormality
?Renal failure
?Acute or Chronic Renal Failure
If Acute renal Failure
Prerenal Renal Postrenal
ATN Develop or Not
ATN cause by Ischemia ATN caused by Nephrotoxic
Drugs
Fig: Algorithm for diagnosis and causes of renal failure of a unconscious
patient where proper history cannot elicited .
13. Classification system for AKI
Classification system for AKI
GFR Criteria Urine Output criteria
Risk
High
Sensitivity
Injury
Failure
High
Specificity
Loss
EKSD
14. RIFLE criteria for diagnosis of AKI
Increase in SCr Urine output
Risk of renal injury 0.3 mg/dl increase < 0.5 ml/kg/hr for > 6 h
Injury to the kidney 2 X baseline < 0.5 ml/kg/hr for >12h
Failure of kidney 3 X baseline OR Anuria for >12 h
function > 0.5 mg/dl increase if
SCr >=4 mg/dl
Loss of kidney Persistent renal failure
function for > 4 weeks
End-stage disease Persistent renal failure
for > 3 months
15. DEFINATION
Definition:
Means an abrupt deterioration of renal function within hours, leading to
retention of water, crystalloids and nitrogenous products.
Rapid decline in the GFR over days to weeks-
Cr increases by >0.5 mg/dL
GFR <10mL/min, or <25% of normal
Documented oliguria of <0.5 ml/kg/hr for 12 hrs
Acute Renal Insufficiency-
Deterioration over days-wks
GFR 10-20 mL/min
16. Definition
•Acute renal failure is • Chronic renal failure
sudden loss of the is a gradual and
ability of the kidneys to progressive loss of
excrete the ability of the
wastes, concentrate kidneys to excrete
urine, and conserve wastes, concentrate
electrolytes. ("Acute" urine, and conserve
means sudden, "renal" electrolytes.
refers to the kidneys.) – Kidney Damage for > 3
– Rapid decline in GFR months
(Over Hours To Days) – Irreversible
– Usually Reversible – 75-60% of function can
be lost before its
noticeable
17. Differentiating ARF vs. Chronic Renal Failure (CRF)
1) History
2) Oliguria = ARF; acute CRF decompensation
3) Renal ultrasound
• Normal or large = acute
• CRF – small (unless PKD, diabetes, amyloid)
4) ARF =Unstable azotemia (↑ or ↓ over days)
5) Anemia – unreliable for ARF vs. CRF
6) ↑PO4, ↑K+, metabolic acidosis, ↑uric acid –little diagnostic value
7) Urinalysis – no value unless normal
suggesting pre-renal azotemia .
18. CLASSIFICATION OF RENAL FILURE
Classification GFR (mls/min/1.73m2) Serum Creatinine
(mol/L)
Mild 20 to 50 150 to 300
Moderate 10 to 20 300 to 700
Severe < 10 > 700
Appendix 3 : BNF
20. STAGES
Onset – 1-3 days with ^ BUN and creatinine and possible
decreased UOP
Oliguric – UOP < 400/d, ^BUN,Crest, Phos, K, may last up
to 14 d
Diuretic – UOP ^ to as much as 4000 mL/d but no waste
products, at end of this stage may begin to see
improvement
Recovery – things go back to normal or may remain
insufficient and become chronic
21. Definitions
Anuria: No UOP or urine output less
than 50cc/24hr.
Oliguria: UOP<400-500 mL/d
Azotemia: Incr Cr, BUN
• May be prerenal, renal, postrenal
• Does not require any clinical findings
Ureamia : Azotemia + Clinical Menifastation
22. Prerenal ARF
• It occurs when renal blood flow is decreased before
reaching the kidney, causing ischemia of nephrons.
– ↓ Renal Perfusion = ↓ GFR leading to Oliguria
– Most common type of ARF
– Common Causes:
• Hypotension (severe and abrupt)
• Hypovolemia
• Low Cardiac Output States
– Treatment to correct cause, if not corrected it may
lead to permanent renal damage.
THE KIDNEYS ARE NORMAL
24. Intrinsic Renal Failure
Intrinsic Renal Failure
I. Renovascular obstruction (bilateral, or unilateral in the setting of one kidney)-
A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissection aneurysm, large
vessel vasculitis .
B. Renal vein obstruction: thrombosis or compression
II. Diseases of the glomeruli or vasculature -
A. Glomerulonephritis or vasculitis
B. Other: thrombotic microangiopathy, malignant hypertension, collagen vascular diseases (SLE)
III. Acute tubular necrosis -
A. Ischemia: causes are the same as for prerenal ARF, but generally the insult is more severe and/or
more prolonged
B. Infection, with or without sepsis syndrome
C. Toxins:
1. Exogenous: radiocontrast, calcineurin inhibitors, antibiotics (e.g., aminoglycosides),
2. Endogenous: rhabdomyolysis, hemolysis 27
25. IV. Interstitial nephritis –
A. Allergic: antibiotics ( -lactams, sulfonamides, quinolones, rifampin), nonsteroidal anti-
inflammatory drugs, diuretics, other drugs
B. Infection: pyelonephritis (if bilateral)
C. Infiltration: lymphoma, leukemia, sarcoidosis
D. Inflammatory, nonvascular: Sjögren's syndrome, tubulointerstitial nephritis with uveitis
V. Intratubular obstruction –
A. Endogenous: myeloma proteins, uric acid (tumor lysis syndrome), systemic oxalalosis
B. Exogenous: acyclovir, gancyclovir, methotrexate, indinavir
26. Prerenal Azotemia and Ischemic tubular necrosis
Prerenal azotemia - Intact Tubular Function
ATN - Renal Tubule Epithelium ( also Basement Membrane) Destruction.
There are two major histiologic changes that take place in ATN: -
(1) tubular necrosis with sloughing of the epithelial cells
(2) occlusion of the tubular lumina by casts and by cellular debris.
Prerenal Azotemia is the main factor that predisposes patients to ischemia- induced acute
tubular necrosis (ATN)
Most cases of ischemic ARF are reversible if the underlying cause is corrected.
27. In addition of the tubular obstruction, two other factors appear to contribute
to the development of renal failure in ATN:-
across the damaged tubular epithelia backleak of filtrate and
a primary reduction in glomerular filtration.
The decrease in glomerular filtration
results both from arteriolar
vasoconstriction and from mesangial
contraction.
The decline in renal function begins
abruptly following a hypotensive
episode,
rhabdomyolysis, or the administration of
a radiocontrast media.
When aminoglycosides are the cause,
the onset is more insidious, with the first
rise in creatinine being at seven or more
days.
28. AIN From Drugs
Renal damage is NOT dose-dependent
May take wks after initial exposure to drug
• Up to 18 mos to get AIN from NSAIDS!
But only 3-5 d to develop AIN after second exposure to drug
• Fever (27%)
• Serum Eosinophilia (23%)
• Maculopapular rash (15%)
• Bland sediment or WBCs, RBCs, non-nephrotic proteinuria
• WBC Casts are pathognomonic!
• Urine eosinophils on Wright’s or Hansel’s Stain
– Also see urine eos in RPGN, renal atheroemboli...
29. Difference Between Ischemic and Nephrotoxic ATN
Ischaemic ATN Nephrotoxic ATN
(Due to Hypovolumia)
Background History Diarrhoea,Vomitting,heart failure,Shock Drugs,Toxin
Kidney Invilvement 3rd Segment of proximal tubule Mostly proximal convoluted
(proximal tubule – Reabsorb 65% of tubule
Sodium) and Assending Loop of henlee
(Reabsorb 25% of Sodium)
FeNa Usually >3% Usually >1% ( 2-3%)
Clinical Triat Fever ,Rash ,Eosinophilia nit associated Mostly Present
UNa Usually Greater >40 Comperatively low(>20)
(Gradually Increasing from >20)
Urinary Protein Absent/+ +/++
WBC Cast Absent pathognomic
Eosinophiluria on Wrights Absent Mostly present
or Hansels Strain
Treatment Restore renal function Usually Fluid And Stop Offending
drugs and sometimes Steroid
31. How Do We Proceed
Reduce Urine output/Anuria /urine abnormality
?Renal failure
?Acute or Chronic Renal Failure
If Acute renal Failure
Prerenal Renal Postrenal
ATN Develop or Not
ATN cause by Ischemia ATN caused by Nephrotoxic
Drugs
Fig: Algorithm for diagnosis and causes of renal failure of a unconscious
patient where proper history cannot elicited .
32. MINIMUM STEPS FOR DIAGNOSIS
History Taking
General and Systemic Examination
Laboratory investigation
Serum Electrolyte Urine R/M/E USG OF ABDOMAN
Serum Creatinine Urinary Electrolyte
BUN Urinary Creatinine
Urinary Urea
Urea - Is the By-product of Protein metabolism
Creatinine- Is the By-product of Muscle metabolism
33. Some Important Formula
GFR = F (140 – age [yrs]) Ideal Body Wt (kg)
Serum creatinine (mol/L)
Where:
F = 1.23 for males and 1.04 for females
FeNa = (urine Na x plasma Cr) x100
(plasma Na x urine Cr)
BUN: Cr = blood urea nitrogen:creatinine ratio
Pre-renal=Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20
UNa = urinary concentration of sodium;
34. Predicting GFR using serum and urine
creatinine concentrations.
Cockcroft and Gault Equation
GFR = F (140 – age [yrs]) Ideal Body Wt (kg)
Serum creatinine (mol/L)
Where:
F = 1.23 for males and 1.04 for females
IBW = 50 kg + 2.23 kg for every 1” > 5 feet in height (male)
IBW = 45.5 kg + 2.3 kg for every 1” > 5 feet in height (female)
35. Assessing the patient with acute renal
failure – Laboratory analysis
• Fractional excretion of sodium:
(UrineNa+ x PlasmaCreatinine)
FENa= ______________________ x 100
(PlasmaNa+ x UrineCreatinine)
It is the Simple measurement of Tubular Excretory function
– FENa < 1% → Prerenal
– FENa > 2% → Epithelial tubular injury (acute tubular necrosis),
obstructive uropathy
– If patient receiving diuretics, can check FE of urea.
36. FeNa = (urine Na x plasma Cr)
(plasma Na x urine Cr)
FeNa <1%
1. PRERENAL
• Urine Na < 20. Functioning tubules reabsorb lots of filtered Na
2. ATN (unusual)
• Postischemic dz: most of UOP comes from few normal
nephrons, which handle Na appropriately
• ATN + chronic prerenal dz (cirrhosis, CHF)
3. Glomerular or vascular injury
• Despite glomerular or vascular injury, pt may still have well-
preserved tubular function and be able to concentrate Na
37. More FeNa
FeNa 1%-2%
1. Prerenal-sometimes (eg-Related with Sepsis)
2. ATN-sometimes
3. AIN-higher FeNa due to tubular damage
FeNa >2%-3%
1. ATN Damaged tubules can't reabsorb Na.usually
nephrotoxic ,Sepsis
FeNa >3%
Goes in Favour of Ischaemic ATN
38. Guide To The Differential Diagnosis of intrinsic ARF
Eosinophiluria Present:
Acute Interstitial
nephritis likely
Eosinophiluria Absent:
Acute interstial
nephritis possible
Muddy Brown Granular Casts
39. Assessing patient with acute renal failure –
Urinary Casts
Red cell casts Glomerulonephritis
Vasculitis
White Cell casts Acute Interstitial
nephritis
Fatty casts Nephrotic
syndrome, Minimal
change disease
Muddy Brown casts Acute tubular
necrosis
41. Classification and differential diagnosis of acute renal failure
Intrinsic Renal Disease
Prerenal Azotemia Postrenal Azotemia Acute Tubular Acute Acute
Necrosis Glomerulonephritis Interstitial
(Oliguric or Polyuric) Nephritis
Etiology Poor renal Obstruction of the Ischemia, Poststreptococcal; Allergic
perfusion urinary tract nephrotoxins collagen-vascular reaction; drug
disease reaction
Serum BUN:Cr ratio > 20:1 > 20:1 < 20:1 > 20:1 < 20:1
Urinary indices
UNa (mEq/L) < 20 Variable > 20 < 20 Variable
FENa (%) <1 Variable >1 <1 < 1; > 1
Urine osmolality > 500 < 400 250–300 Variable Variable
(mosm/kg)
Urinary sediment Benign or Normal or red cells, Granular Dysmorphic red cells White cells,
hyaline casts white cells, or crystals (muddy brown) and red cell casts white cell
casts, renal tubular casts, with or
casts without
eosinophils
BUN: Cr = blood urea nitrogen:creatinine ratio;
UNa = urinary concentration of sodium;
FENa = fractional excretion of sodium
42. ATN Prerenal
Cr increases at increases
0.3-0.5 /day slower than
0.3 /day
U Na, UNa>40 UNa<20
FeNa FeNa >2% FeNa<1%
UA epi cells, Normal
granular casts
Response to Cr won’t Cr improves
volume improve much with IVF
BUN/Cr 10-15:1 >20:1
The FENa tends to be high in ischemic ATN but is often low in patients with sepsis-induced,
pigment-induced, and some forms of nephrotoxic ATN (e.g., contrast-associated).
Patients with acute interstitial nephritis may present with triad of fever, rash, and eosinophilia)
UA (1 - 2+ protein, renal tubular epithelial cells, wbc’s - eosinophils, wbc casts)
43. Intervention by Inj.Frusemide and its outcome of an ARF ( Develop ATN)
1st 2nd 3rd 4th 5th 6th Total
Duratio
n
Pt-1 6.9 9.45 6.09 2.7 2.0 1.4 6 Days
Pt-2 4.6 3.4 6.0 4.8 3.3 2.3 (day 6) 7 days
1.3(day 7)
Pt-3 6.5 8.7 9.9 10.3 5.1 1.4 11 Days
-Day -3 day-4 Day-5 Day-9 day-11
Patient develop ATN Due to Prerenal cause
Cholera patient-1 Cholera patient-2 Septicemia patient
FeNa 4.24% 3% 1.13%
GFR 7 ( Severe) 8 (Severe) 18.6 ( Moderate)
BUN/Cr 13.92 5.06 20
Urinary Na 44.7 17.9 34.6
Renal Index 5.46 3.7 1.5
USG Noraml Normal Suggestive of bilateral
parenchymal Diseases
46. Intrinsic renal injury Lovastatin, ethanol, codeine, Elevated CPK, ATN urine Drug discontinuation,
(rhabdomyolysis) barbiturates, diazepam sediment supportive care
Quinine, quinidine,
Intrinsic renal injury sulfonamides, hydralazine, High LDH, decreased Drug discontinuation,
(severe hemolysis) triamterene, nitrofurantoin, hemoglobin supportive care
mephenytoin
Penicillin, methicillin ampicillin,
rifampin, sulfonamides,
thiazides, cimetidine,
phenytoin, allopurinol,
Intrinsic renal injury Fever, rash, eosinophilia,
cephalosporins, cytosine
(immune-mediated urine sediment showing Discontinue medication,
arabinoside, furosemide,
interstitial pyuria, white cell casts, supportive care
interferon, NSAIDs,
inflammation) eosinophiluria
ciprofloxacin, clarithromycin,
telithromycin, rofecoxib,
pantoprazole, omeprazole,
atazanavir
Gold, penicillamine, captopril,
NSAIDs, lithium, mefenamate, Edema, moderate to severe
Intrinsic renal injury Discontinue medication,
fenoprofen, mercury, interferon- proteinuria, red blood cells,
(glomerulopathy) supportive care
, pamidronate, fenclofenac, red blood cell casts possible
tolmetin, foscarnet
Obstruction Aciclovir, methotrexate, Sediment can be benign
Discontinue medication,
(intratubular: crystalluria sulfanilamide, triamterene, with severe obstruction,
supportive care
and/or renal lithiasis) indinavir, foscarnet, ganciclovir ATN might be observed
Discontinue medication,
Methysergide, ergotamine,
Obstruction (ureteral; Benign urine sediment, decompress ureteral
dihydroergotamine,
secondary to hydronephrosis on obstruction by intrarenal
methyldopa, pindolol,
retroperitoneal fibrosis) ultrasound stenting or percutaneous
hydralazine, atenolol
47.
48. Result Interpretations
24/04/09 24/04/09
S.Na + -128.6mmol/L GFR -6.5 ml/min(SEVERE RENAL FAILURE)
S.K+ - 2.73 mmol/L FeNa -4% ( >2%) (ATN)
S.Cl - 93 mmol/L FENa - 35% ( Pre Renal )
TCO2 - 13.5mmol/L Urinary Na+ - 44.7 mmol/L ( <20mmol/L ATN)
Anion gap -24.83mmol/L Oliguria - Urine out put less than 500 cc
BUN - 138.94mg/dl Urinary Creatinine = 8.17% (<20% ATN)
UREA - 49.26 mmol/L Serum Creatinine
Serum Creatinine – 882.3u mol/L BUN/Creatinine = 14.03 ( <20% Renal)
URINARY ELECTROLYTE
Urine R/M/E - No Eosinophilurea, WBC cast and
U.Sodium - 44.7mmol/L
Epithelial cell-7-8 Protein-+
U.Potassium - 12.77mmol/L BUN: Cr = blood urea nitrogen:creatinine ratio;
UNa = urinary concentration of sodium;
U.Cl- - 33mmol/L FENa = fractional excretion of sodium
FeNa = (urine Na x plasmaCr) 100
TCO2 - 5mmol/L
(plasma Na x urineCr)
U.Creatinine (Random)-7211 umol/L
49. SO,PATIENT DEVELOPED-
-SEVERE RENAL FAILURE
- PRERENAL CAUSE AND
- DEVELOPED ACUTE TUBULAR NECROSIS (ATN)
50. Etiology of ARF among Inpatients
ATN (45%)
Prerenal (21%)
ARF on CKD (13%)
Obstruction (10%)
GN/vasc (4%)
AIN (2%)
Atheroemboli (1%)
KI 50:811-818, 1996
51. Etiology of ARF among Outpatients
P rerenal (70% )
Intrarenal (11% )
O bs truc tion(17% )
idiopathic (2% )
AJKD 17:191-198, 1991
52. Acute renal failure: Focused History
• Nausea? Vomiting? Diarrhea?
• Hx of heart disease, liver disease, previous renal disease,
kidney stones, BPH?
• Any recent illnesses?
• Any edema, change in
urination?
• Any new medications?
• Any recent radiology studies?
• Rashes?
55. Treatment of ARF
• Eliminate the toxic insult
• Hemodynamic support
• Respiratory support
• Fluid management
• Electrolyte management
• Medication dose adjustment
• Dialysis
56. Acute Renal Failure: Fluid Therapy
If patient is fluid overloaded
• fluid restriction (insensible losses)
• attempt furosemide 1-2 mg/kg
• Renal replacement therapy (see later)
If patient is dehydrated:
• restore intravascular volume first
• then treat as euvolemic (below)
If patient is euvolemic:
• restrict to insensible losses (30-35 ml/100kcal/24 hours) +
other losses (urine, chest tubes, etc) or
57. Management of ARF - Volume status
• Water balance
– "Maintenance" is IRRELEVANT in ARF!!!
– If euvolemic, give insensibles + losses + UOP
– If volume overloaded, they don't need anything
(except the minimum for meds and glucose)
• concentrate all meds; limit oral intake
– Need frequent weights and BP, accurate I/O
– Insensibles = 30 cc/100 kcal or 400cc/M2/day
– If has any UOP, Frusemide may help with fluid
overload
58. HYPERKALAMIA
• With ARF, K+ will increase and will be worsened by
infection, hemolysis, acidosis
• DON'T IGNORE A HIGH K+ just because the specimen is
hemolyzed especially in a patient who could easily be
hyperkalemic
• How can you tell if it is “real”?
-check EKG for peaked T waves, widened QRS
• It’s real. What’s the first thing to do?
- Restriction of dietary K+ intake
- Eliminate K+ supplements and K+-sparing diuretics
-Emergently stabilize membranes with calcium to prevent
arrhythmia
59. Hyperkalemia
• What’s next?
– Shift K+ intracellularly with:
• insulin + hypertonic dextrose: 1 unit of insulin/4 g
glucose
• bicarbonate infusion ((1-2 mEq/kg)
• Inhaled –B2 agonist therapy to promote intracellular
mobilization.
– Check IV fluids to ensure no intake
• What happens to ionized calcium level as you correct the
acidosis?
• Increases albumin binding so ionized calcium decreases
• What’s the third step?
– Remove from body with Lasix, dialysis
60. DIETARY MODIFICATION
• total caloric intake– 35~ 50 kcal/kg/day
to avoid catabolism
Salt restriction– 2~4 g/day
Potassium intake– 40 meq/day
• Phosphorus intake– 800 mg/day
• Uremia-nutrition
– Restriction protein is not necessary in ARF, maintain caloric intake
– Carbohydrate ≥ 100gm/day to minimize ketosis and protein catabolism
• Drug
– Review all medication, Stop magnesium-containing medication
– Adjusted dosage for renal failure, Readjust with improvement of GFR
61. Management of Ischemic and Nephrotoxic Acute Renal Failurea
Management Issue Therapy
Reversal of Renal Insult
Ischemic ATN Restore systemic hemodynamics and renal perfusion through volume resuscitation
and use of vasopressors
Nephrotoxic ATN Eliminate nephrotoxic agents
Consider toxin-specific measures: e.g., forced alkaline diuresis for rhabdomyolysis,
allopurinol/rasburicase for tumor lysis syndrome
Prevention and Treatment of Complications
Intravascular volume overload Salt and water restriction
Diuretics
Ultrafiltration
Hyponatremia Restriction of enteral free water intake
Avoidance of hypotonic intravenous solutions, including dextrose-containing
solutions
Hyperkalemia Restriction of dietary K+ intake
Eliminate K+ supplements and K+-sparing diuretics
Loop diuretics to promote K+ excretion
Potassium binding ion-exchange resins (e.g., sodium polystyrene sulfonate or
Kayexelate)
Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote
intracellular mobilization
Inhaled –B2 agonist therapy to promote intracellular mobilization
Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium
Dialysis
62. Metabolic acidosis Sodium bicarbonate (maintain serum bicarbonate >15 mmol/L or arterial pH
>7.2)
Administration of other bases, e.g., THAM
Dialysis
Hyperphosphatemia Restriction of dietary phosphate intake
Phosphate binding agents (calcium carbonate, calcium acetate, sevelamer
hydrochloride, aluminum hydroxide)
Hypocalcemia Calcium carbonate or gluconate (if symptomatic)
Hypermagnesemia Discontinue Mg++ containing antacids
Hyperuricemia Treatment usually not necessary if <890 mol/L or <15mg/dL
Allopurinol, forced alkaline diuresis, rasburicase
Nutrition Protein and calorie intake to avoid net negative nitrogen balance
Dialysis To prevent complications of acute renal failure
Choice of agents Avoid other nephrotoxins: ACE inhibitors/ARBs, aminoglycosides, NSAIDs,
radiocontrast unless absolutely necessary and no alternative
Drug dosing Adjust doses and frequency of administration for degree of renal impairment
63. Acidosis
• Maintain serum bicarbonate >15 mmol/L or
arterial pH >7.2
• Acidosis makes the kids feel terrible
• BUT...
– watch sodium and fluid overload
– watch lowering ionized calcium levels (by
increasing binding of calcium to albumin)
64. INDICATION FOR DIALYSIS
• Dialysis may not be necessary for all people, but is frequently lifesaving,
particularly if serum potassium is dangerously high.
• Common symptoms that require the use of dialysis include-
Uremia - Obtundation, asterxis, seizures,decreased mental
status,pericarditis increased potassium levels,
Urine Output -total lack of urine production,
Metabolic Acidosis – PH< 7.2mmol/L despite Sodium Bicarbonate
Therapy
Sodium Bicarbonate therapy not tolerate due to fluid
over load
65. Indications for renal replacement therapy
• Volume overload -
- Resistance to Diuretics ,Specially pulmonary oedema
– Pulmonary edema, CHF, refractory HTN
– NOT for peripheral edema, esp. with cap. leak
• Hyperkalemia - (S.Potassium >6.5mmol/L
S.Potassium>5.5 mmol/L with ECG change)
.waste products- uncontrolled accumulation of nitrogen waste products (serum
creatinine > 10 mg/dl and BUN > 120 mg/dl).
• Nutrition- Need to maximize nutrition
• Sodium imbalance - Severe dysnatremias (sodium concentration greater than
155 meq/L or less than 120 meq/L)
• Hyperthermia
• Drug overdose-Overdose with a dialyzable drug/toxin
67. Modes of renal replacement therapy
• Peritoneal dialysis - also gentle and don't need
heparinization but slow and catheter may leak or not
work.
• Hemodialysis - very fast, but need big lines and systemic
heparinization; causes hemodynamic instability and
uremic dysequilibrium symptoms
68. Complications of acute renal failure
Hyperkalemia.
Acute pulmonary edema.
Cardiac arrhythmia.
Convulsions.
Infections e.g. Pneumonia.
Deep venous thrombosis and pulmonary embolism.
Gastrointestinal bleeding.
69. ARF: Risk factors for mortality
• Multi-organ failure
• Bacterial Sepsis
• Fungal sepsis
• Hypotension/vasopressors
• Ventilatory support
• Initiation of dialysis late in hospital course
• Oliguria/anuria: with oliguric ARF, mortality is >
50% compared to < 20% with non-oliguric ARF
70. Causes of death in acute renal failure
• Infection e.g.pneumonia
• Hyperkalemia.
• Pulmonary edema.
• Cardiac arrhythmia.
• Deep venous thrombosis and pulmonary embolism.
• Acute pericarditis.
• Convulsions and coma.
71. Oliguria, renal failure.
Dehydration: Obstruction
•U.Na<20mmol/l. Renal failure
•U.Osmol.>500
Chronic -U.catheter
-Percutaneous nephrostomy.
-Rehydrate. -Ureteric catheter.
-Fluid and diuretic
challenge -Correct Reversible Factors.
-Mannitol -Dialysis.
-AGN, RPGN and, Acute Acute tubular necrosis
vasculitis
•C3,ANCA,,ANA,Ad -CVP, fluid balance, electrolyte balance,acid
sDNA… etc base balance, diet,dopamine infusion, high
•Consider dose diuretic dose, monitoring, treatment of
steroid,immunosuppr complications, and consideration of dialysis
essive and plasma
exchange.
Management of acute renal failure
72. Best cure is to prevent
• Have a high index of suspicion for
reversible factors - volume depletion,
decreasing cardiac function, sepsis, urinary
tract obstruction
• Be sure patient is well-hydrated when
exposing patient to nephrotoxic drugs
73. Anticipate Problems
• Avoid worsening the ARF
– Adjust medicines for renal insufficiency
– Avoid nephrotoxins if possible
– Think about to avoid less potent drug prescribtion
– Close observation of toxic effect of drugs.
– Early detection of toxic effect of drug.
– Avoid intravascular volume depletion (especially in
third-spacing or edematous patients)
74. Nursing Interventions
•Monitor I/O, including all body fluids
• Monitor lab results
• Watch hyperkalemia symptoms: malaise,
anorexia, paresthesia, or muscle weakness, EKG
changes
• watch for hyperglycemia or hypoglycemia if
receiving TPN or insulin infusions
75. • Maintain nutrition
• Safety measures-
Mouth care
Daily weights
• Assess for signs of heart failure
• GCS
• Skin integrity problems
76. Complications (ARF)
• Increased risk of infections
• Gastrointestinal loss of blood
• Chronic renal failure
• End-stage renal disease
• Damage to the heart or nervous system
• Hypertension
77. Patient / Family Education
• Call your health care provider if decreased
urine output or other symptoms indicate
the possibility of acute renal failure.
• Call your health care provider if nausea or
vomiting persists for more than 2 weeks.
• Call your health care provider if decreased
urine output or other symptoms of chronic
renal failure occur.
79. PROBLEM-1
X- 80 years old male presented with Cough for 7, Fever for 6 days , diarrhoea and vomiting for 1 day.
Patient was previously diagnosed as a case of COPD. On Examination Patient was drowsy, some D/H
present,Pulse-101/min BP- 75/35 mmHg , SPO2 without O2-90% R/R-30/min RBS-6.8 mmol/L..Patient
last pass urine 6 hour back (scanty).
S.Electrolyte- S.Na - 133.2mmol/L S.K - 4.36 mmol/L S.Cl – 98.5 Tco2-19.9 mmol/L Anion Gap-
19.9mmol/L S.Creatinine-223.4 umol/L ( 2.5 mg/dl)
BUN- 50.34mg/dl
U.Creatinine- 5103 umol/L (57.7mg/dl) U.Specific Grvity – 1.003 U.Na – 34.6mmol/L
Urine R/M/E – R.B.C- 1-2
Puss cell - 6-8
Epithelial Cell – 4-6
Cast - granular (1-2)
USG of Whole Abdoman-
Sugestive of bilateral paranchymal diseases.Kidney size is normal.
Bilateral Pleural Effusion (mild?)
Dilated portal vein But no spleenomegaly.
QUESTIONS
Q-1 In which stage patient is in RIFLE CRITERIA?
Q-2 Is patient acute or chronic renal failure?
Q-3 Is it Prerenal Renal or Post renal?
Q-4 ATN developed or not?
Q-5 What is the -daily raising of Creatinine?
FeNa - ?
U Na - ?
Important findings related with diagnosis?
Q-6 What is the final Diagnosis and Differential Diagnosis?
Q-7 Treatment Option for the patient ?
Q-8 Dialysis Needs or not?
80. PROBLEM-2
Y- 65years old male presented with diarrhoea and vomiting for 1 and half day.He Non Diabetic But Hypertensive.
On Examination Patient was Alart but feeling restless his pulse-92/min ,BP-105/70mmHg Some D/H was present ,
RBS-6.1mmol/L..Patient last pass urine 5-6 hour back (scanty)
1st Day – S.Cretinine- 610umol/L (6.9mg/dl)
S.Electrolyte- S.Na - 128.2mmol/L S.K - 3.6 mmol/L S.Cl – 90.5 Tco2-19 mmol/L Anion Gap- 22.4mmol/L
S.Creatinine-836 umol/L ( 9.45 mg/dl)
BUN- 50.34mg/dl
U.Creatinine- 3940.1 umol/L U.Specific Grvity – 1.018 U.Na – 19.8mmol/L
Urine R/M/E – R.B.C- 4-6
Puss cell - 15-20
Epithelial Cell – 4-6
Cast - granular (0-1)
USG of Whole Abdoman-Normal Study
QUESTIONS
Q-1 In which stage patient is in RIFLE CRITERIA?
Q-2 Is patient acute or chronic renal failure?
Q-3 Is it Prerenal Renal or Post renal?
Q-4 ATN developed or not?
Q-5 What is the -daily raising of Creatinine?
FeNa - ?
U Na - ?
Important findings related with diagnosis?
Q-6 What is the final Diagnosis and Differential Diagnosis?
Q-7 Treatment Option for the patient ?
Q-8 Dialysis Needs or not?
81. PROBLEM-3
Z- 18 years old Female presented with diarrhoea and vomiting for 1and half day, Fever since morning , For
Diarrhoea she took I/V Fluid and Some Medication from outside. On Examination Patient was drowsy follwed
by unconciousness, some D/H present,Pulse-98/min BP- 95/60 mmHg , SPO2 without O2-90% R/R-30/min
RBS-6.8 mmol/L..Patient last pass urine 5-6 hour back (scanty) Temp-39`C.No Pupil Dilated,No Neck rigidity,
After 10-12 hour patient develop repeated convulsion.
1st S.creatinine – 582.6 umol/L ( 6.5 mg/dl)
S.Electrolyte- S.Na - 132.6mmol/L S.K - 3.2 mmol/L S.Cl – 98.5 Tco2-14.9 mmol/L Anion Gap- 19.9mmol/L
S.Creatinine-882.3 umol/L ( 9.9mg/dl)
BUN- 138.94mg/dl
U.Creatinine- 7481 umol/L , U.Na – 26.7mmol/L
Urine R/M/E – R.B.C- 7-8 CBC – Hb%- 10 , TWBC -14700
Puss cell - 12-14 Nutrophil- 81.4% Poly-10%
Epithelial Cell – 4-6 monocyte- 0.2% ,Eosinophil-7.4%
Protien- ++
Cast - granular (2-4) Eosinophil-+
USG of Whole Abdoman- Normal Study.
QUESTIONS
Q-1 In which stage patient is in RIFLE CRITERIA?
Q-2 Is patient acute or chronic renal failure?
Q-3 Is it Prerenal Renal or Post renal?
Q-4 ATN developed or not?
Q-5 What is the -daily raising of Creatinine?
FeNa - ?
U Na - ?
Important findings related with diagnosis?
Q-6 What is the final Diagnosis and Differential Diagnosis?
Q-7 Treatment Option for the patient ?
Q-8 Dialysis Needs or not?