The document discusses renal anatomy and physiology, effects of anesthesia on renal function, and perioperative management of patients with renal disease. It notes that anesthesia can decrease renal blood flow and glomerular filtration rate through various direct and indirect mechanisms. Factors that increase risk of perioperative acute kidney injury are described. Assessment of renal function includes history, exam, labs, and urine analysis. Management involves maintaining perfusion and fluid balance, using appropriate anesthetic agents, and monitoring for complications in the postoperative period.
Effects of anesthesia and surgery on renal functionHASSAN RASHID
THIS PRESENTATION DISCUSSES IN BRIEF THE VARIOUS EFFECT OF ANAESTHESIA AND SURGERY ON RENAL FUNCTIONS. IT ALSO DISCUSSED THE PROTECCTIVE EFFECTS OF ANAESTHETIC AGENTS ON KIDNEY DURING THE PERIOPERATIVE PERIOD,
This document provides an overview of acute and chronic renal failure. It defines renal failure as loss of kidney function and describes how acute renal failure has a sudden onset and is potentially reversible, while chronic failure progresses slowly over months or years. The major causes, symptoms, and metabolic consequences of both acute and chronic renal failure are discussed. Laboratory findings and management approaches for acute renal failure are also outlined. The document contrasts the features of acute versus chronic renal failure and describes problems related to end-stage renal disease as well as dialysis options.
The Medical Assessment and Management of OliguriaLuis Daniel Lugo
The document discusses the medical assessment and management of oliguria. It defines oliguria as urine output less than 400 mL per day in adults. Oliguria can result from prerenal, intrinsic renal, or postrenal causes. The assessment of oliguria involves urine analysis and blood tests to evaluate electrolytes, BUN, creatinine, and acid-base balance. Medical management focuses on treating the underlying cause, managing fluid balance and hyperkalemia, and considering dialysis for complications like volume overload or refractory acidosis. Identifying and treating reversible causes is important for prognosis, which depends on etiology and comorbidities.
This document summarizes the pathophysiology of acute kidney injury (AKI). It describes AKI as an abrupt reduction in kidney function that can be diagnosed through changes in creatinine, BUN, and urine output levels. The pathophysiology of AKI is categorized into pre-renal, intrinsic, and post-renal forms. Pre-renal AKI is due to reduced blood flow to the kidneys, intrinsic AKI involves direct kidney damage, and post-renal AKI is caused by urinary outflow obstruction. The goals of treatment are to minimize injury, reduce complications, and restore kidney function through supportive care, fluid management, and renal replacement therapies like hemodialysis in severe cases
This document discusses renal failure, including acute kidney injury (AKI) and chronic renal failure. It defines AKI as the sudden loss of kidney function over hours to days, causing a buildup of waste products. AKI can be caused by decreased blood flow, direct kidney damage, or obstruction of urine flow. The stages of AKI are initiation, oliguria, diuresis, and recovery. Treatment involves fluid management, electrolyte control, infection prevention, and possibly dialysis. Nursing care focuses on monitoring fluids and electrolytes, reducing the metabolic rate, providing skin care, and preventing infections.
The document discusses renal system considerations for anesthesia. The kidneys play a vital role in fluid, electrolyte and acid-base balance. Patients with renal failure are at risk of fluid imbalance, electrolyte disturbances and acid-base abnormalities. Anesthesiologists must carefully manage fluids, monitor for hypotension, and use appropriate drugs that are metabolized by the liver rather than the kidneys to avoid further renal injury.
This document discusses acute kidney injury (AKI) in pediatrics. It defines AKI and describes its causes, pathophysiology, clinical features, evaluation, and management. The most common causes of AKI in children include acute tubular necrosis, sepsis, nephrotoxic agents, hemolytic uremic syndrome, and glomerulonephritis. Evaluation involves history, labs, ultrasound, and sometimes biopsy. Management focuses on fluid balance, nutrition, treating complications like fluid overload and electrolyte abnormalities, and initiating dialysis in severe cases.
Acute kidney injury (AKI) is a deterioration of renal function over hours to days resulting in failure to excrete waste and maintain homeostasis. [1] There are over 35 AKI definitions showing its complexity. [2] It can be classified as oliguric/non-oliguric or prerenal, renal, postrenal. [3] Prerenal and acute tubular necrosis account for most hospital AKI cases. [4] Management involves diagnosis through tests and imaging, and treatment focusing on fluid balance, electrolytes, and potentially renal replacement therapy. [5] The prognosis remains poor especially in critically ill patients, as currently the condition can only be supported but not cured. [6
Effects of anesthesia and surgery on renal functionHASSAN RASHID
THIS PRESENTATION DISCUSSES IN BRIEF THE VARIOUS EFFECT OF ANAESTHESIA AND SURGERY ON RENAL FUNCTIONS. IT ALSO DISCUSSED THE PROTECCTIVE EFFECTS OF ANAESTHETIC AGENTS ON KIDNEY DURING THE PERIOPERATIVE PERIOD,
This document provides an overview of acute and chronic renal failure. It defines renal failure as loss of kidney function and describes how acute renal failure has a sudden onset and is potentially reversible, while chronic failure progresses slowly over months or years. The major causes, symptoms, and metabolic consequences of both acute and chronic renal failure are discussed. Laboratory findings and management approaches for acute renal failure are also outlined. The document contrasts the features of acute versus chronic renal failure and describes problems related to end-stage renal disease as well as dialysis options.
The Medical Assessment and Management of OliguriaLuis Daniel Lugo
The document discusses the medical assessment and management of oliguria. It defines oliguria as urine output less than 400 mL per day in adults. Oliguria can result from prerenal, intrinsic renal, or postrenal causes. The assessment of oliguria involves urine analysis and blood tests to evaluate electrolytes, BUN, creatinine, and acid-base balance. Medical management focuses on treating the underlying cause, managing fluid balance and hyperkalemia, and considering dialysis for complications like volume overload or refractory acidosis. Identifying and treating reversible causes is important for prognosis, which depends on etiology and comorbidities.
This document summarizes the pathophysiology of acute kidney injury (AKI). It describes AKI as an abrupt reduction in kidney function that can be diagnosed through changes in creatinine, BUN, and urine output levels. The pathophysiology of AKI is categorized into pre-renal, intrinsic, and post-renal forms. Pre-renal AKI is due to reduced blood flow to the kidneys, intrinsic AKI involves direct kidney damage, and post-renal AKI is caused by urinary outflow obstruction. The goals of treatment are to minimize injury, reduce complications, and restore kidney function through supportive care, fluid management, and renal replacement therapies like hemodialysis in severe cases
This document discusses renal failure, including acute kidney injury (AKI) and chronic renal failure. It defines AKI as the sudden loss of kidney function over hours to days, causing a buildup of waste products. AKI can be caused by decreased blood flow, direct kidney damage, or obstruction of urine flow. The stages of AKI are initiation, oliguria, diuresis, and recovery. Treatment involves fluid management, electrolyte control, infection prevention, and possibly dialysis. Nursing care focuses on monitoring fluids and electrolytes, reducing the metabolic rate, providing skin care, and preventing infections.
The document discusses renal system considerations for anesthesia. The kidneys play a vital role in fluid, electrolyte and acid-base balance. Patients with renal failure are at risk of fluid imbalance, electrolyte disturbances and acid-base abnormalities. Anesthesiologists must carefully manage fluids, monitor for hypotension, and use appropriate drugs that are metabolized by the liver rather than the kidneys to avoid further renal injury.
This document discusses acute kidney injury (AKI) in pediatrics. It defines AKI and describes its causes, pathophysiology, clinical features, evaluation, and management. The most common causes of AKI in children include acute tubular necrosis, sepsis, nephrotoxic agents, hemolytic uremic syndrome, and glomerulonephritis. Evaluation involves history, labs, ultrasound, and sometimes biopsy. Management focuses on fluid balance, nutrition, treating complications like fluid overload and electrolyte abnormalities, and initiating dialysis in severe cases.
Acute kidney injury (AKI) is a deterioration of renal function over hours to days resulting in failure to excrete waste and maintain homeostasis. [1] There are over 35 AKI definitions showing its complexity. [2] It can be classified as oliguric/non-oliguric or prerenal, renal, postrenal. [3] Prerenal and acute tubular necrosis account for most hospital AKI cases. [4] Management involves diagnosis through tests and imaging, and treatment focusing on fluid balance, electrolytes, and potentially renal replacement therapy. [5] The prognosis remains poor especially in critically ill patients, as currently the condition can only be supported but not cured. [6
This document discusses acute kidney injury (AKI), including its definition, causes, diagnostic approach, and management. It describes renal autoregulation and how various vasoconstrictors and vasodilators maintain renal blood flow. Prerenal, intrinsic, and postrenal causes of AKI are outlined. The diagnostic approach involves assessing history, physical exam, labs, and imaging to determine the etiology. Urine sediment analysis can provide clues about the underlying renal process. Management involves treating the underlying cause and preventing further injury.
Neonatal acute kidney injury (AKI) can result from prerenal, intrinsic renal, or postrenal causes. It is characterized by impaired kidney function and dysregulation of fluid, acid-base, electrolytes, and waste products. AKI is defined using modified KDIGO criteria of changes in serum creatinine and urine output. Prevention focuses on supporting circulation and avoiding nephrotoxins. Treatment involves careful fluid management, electrolyte replacement, and potentially renal replacement therapy. Outcomes depend on the severity and etiology of AKI, with prognosis generally worse than in adults.
This document provides an overview of acute kidney injury (AKI) in children. It defines AKI, discusses its classification, epidemiology, staging, etiology, pathophysiology, clinical features, investigations, treatment, and prognosis. AKI is diagnosed based on rises in serum creatinine and/or decreases in urine output. Common causes in children include sepsis, malaria, glomerulonephritis, and nephrotoxic medications. Treatment involves fluid management, treating the underlying cause, and potentially renal replacement therapy for severe cases. Outcomes depend on the severity and reversibility of the kidney injury.
Chronic renal failure of small animals.pptDr.hema hassan
This document discusses chronic renal failure (CRF). It defines CRF as when the kidneys can no longer maintain their excretory, regulatory, and endocrine functions. Common causes of CRF in dogs, cats and large animals are described. The document compares CRF to acute renal failure and outlines some of the clinical signs seen with uremia. It discusses concepts such as hyperfiltration in remnant nephrons and factors that can contribute to the progressive nature of renal disease such as dietary factors. Mechanisms by which the kidneys maintain solute and water balance during declining renal function are also described.
Brief Information regarding the disorders of the genitourinary system. This presentation involves the disorders of the urinary system including Chronic Kidney Disease, Congenital problems related to the urinary system, and renal cancers.
This document provides information about hepato-renal syndrome (HRS), which is a syndrome that develops in patients with liver cirrhosis and portal hypertension, characterized by impaired renal function. It discusses the pathophysiology, including splanchnic arterial vasodilation, renal arterial vasoconstriction, and cardiac dysfunction. It describes the four types of HRS based on time course and precipitating factors. It provides details on diagnostic criteria and management, including general management, renal vasodilators, systemic vasoconstrictors such as terlipressin, and contraindications for vasoconstrictor therapy.
This document discusses acute kidney injury (AKI) in intensive care unit patients. It provides definitions and criteria for AKI, including RIFLE and AKIN classifications. Mortality rates increase significantly with more severe AKI, from 5-10% with no renal dysfunction to 26-40% with renal failure. While decreased urine output can indicate decreased kidney function, urine output alone is a less severe marker. Multiple factors influence the relationship between renal blood flow, perfusion pressure, and glomerular filtration rate. Early markers like neutrophil gelatinase-associated lipocalin and cystatin C may help predict AKI and prognosis better than creatinine. Fluid management must balance resuscitation with avoiding overload,
1. Acute kidney injury (AKI) is the sudden deterioration of renal function that can range from mild to severe. It is a global problem associated with high morbidity and mortality.
2. AKI is classified based on location of injury (pre-renal, intrinsic, post-renal), urine output, and severity of decline in renal function. Common causes include sepsis, nephrotoxins, and decreased renal perfusion.
3. Management involves treating the underlying cause, maintaining fluid/electrolyte balance, and potentially renal replacement therapy for complications like fluid overload or severe electrolyte imbalances. Outcomes depend on factors like age, cause, and need for dialysis.
Elimination of drug Biopharmaceutics M.Pharm.pptxRameshwar Dass
Delve into the pivotal aspect of drug elimination in biopharmaceutics on our slides, offering insights into strategies and mechanisms aimed at optimizing drug disposition and refining therapeutic outcomes
ANAESTHESIA FOR PATIENTS WITH RENAL FAILURE.pptxSweetPotatoe1
The document discusses renal failure and its implications for anesthesia. It describes the functions of the kidneys and defines acute kidney injury and chronic kidney disease. For patients with renal impairment, pre-operative optimization is important, including fluid management and electrolyte correction. Regional anesthesia is preferred over general anesthesia when possible due to better hemodynamic stability. Careful monitoring is needed during and after surgery to watch for fluid overload, electrolyte abnormalities, and other complications.
Hepatorenal syndrome is a condition characterized by impaired renal function in patients with advanced liver disease and portal hypertension. There are two types - type 1 is rapid and progressive, leading to death within a month without treatment, while type 2 is less severe but still associated with worse prognosis. The pathogenesis involves splanchnic vasodilation triggering renal vasoconstriction. Treatment involves vasoconstrictors like terlipressin combined with albumin to increase mean arterial pressure and improve renal function. Achieving at least a 10 mmHg increase in MAP with vasoconstrictor therapy correlates with better renal outcomes in hepatorenal syndrome patients.
This document defines acute kidney injury (AKI) and describes its classification, diagnosis, and management. AKI is an abrupt deterioration in kidney function that is usually reversible. It is classified using criteria like RIFLE, AKIN, and KDIGO that stage AKI based on changes in serum creatinine and urine output. Biomarkers like cystatin C and NGAL can help detect early AKI. Treatment involves fluid resuscitation, removing nephrotoxins, and initiating renal replacement therapy if needed. Outcomes depend on the underlying cause and range from complete recovery to end-stage renal disease.
Diuretics : Dr Renuka Joshi MD,DNB, (FNB )Renuka Buche
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, effects, dosages, and interactions. It covers loop diuretics like furosemide and bumetanide that act in the thick ascending loop of Henle; thiazide diuretics like hydrochlorothiazide that act in the distal convoluted tubule; and potassium-sparing diuretics like spironolactone and amiloride that act in the collecting duct. It provides recommendations for diuretic use and combinations in the treatment of heart failure and fluid overload.
Renal insufficiency occurs when the kidneys fail to remove waste and regulate fluids and electrolytes. It can be acute or chronic. Acute renal failure involves a rapid decline in function and is classified as prerenal, intrarenal, or postrenal based on cause. Chronic renal failure is a progressive loss of kidney function that eventually leads to death without treatment. It involves stages of initial damage, polyuria, oliguria, and terminal kidney failure. Treatment for chronic renal failure includes dialysis or kidney transplantation.
Effect of Anesthesia and Surgery on Renal System.pptxGanta Ranganath
Both anesthesia and surgery can affect renal function through hemodynamic changes and stress responses. Anesthetics like volatile agents can decrease glomerular filtration rate through effects on renal blood flow and perfusion pressure. Muscle relaxants may cause transient hypotension. Intravenous agents generally have minor direct renal effects. Colloids like albumin are renoprotective while hydroxyethyl starch and dextran can cause acute kidney injury. Drugs that alter hemodynamics like NSAIDs, ACE inhibitors, and positive pressure ventilation can also impact renal function. Surgery induces stress responses and fluid shifts that can lead to prerenal azotemia. Specific procedures like pneumoperitoneum, cardiopulmonary bypass, aortic cross
Acute kidney injury (AKI) is the abrupt reduction of renal function over a period of less than 3 months. It can be caused by decreased renal blood flow (prerenal), direct kidney injury (renal), or urinary tract obstruction (postrenal). AKI has systemic effects and increases the risk of complications like fluid overload, electrolyte imbalances, and metabolic acidosis. Treatment involves restoring renal perfusion, treating the underlying cause, managing complications supportively or with renal replacement therapy, and preventing further kidney injury. AKI increases mortality, hospital stay, and risk of progressing to chronic kidney disease.
This document discusses acute kidney injury (AKI), including its definition, causes, diagnostic approach, and management. It describes renal autoregulation and how various vasoconstrictors and vasodilators maintain renal blood flow. Prerenal, intrinsic, and postrenal causes of AKI are outlined. The diagnostic approach involves assessing history, physical exam, labs, and imaging to determine the etiology. Urine sediment analysis can provide clues about the underlying renal process. Management involves treating the underlying cause and preventing further injury.
Neonatal acute kidney injury (AKI) can result from prerenal, intrinsic renal, or postrenal causes. It is characterized by impaired kidney function and dysregulation of fluid, acid-base, electrolytes, and waste products. AKI is defined using modified KDIGO criteria of changes in serum creatinine and urine output. Prevention focuses on supporting circulation and avoiding nephrotoxins. Treatment involves careful fluid management, electrolyte replacement, and potentially renal replacement therapy. Outcomes depend on the severity and etiology of AKI, with prognosis generally worse than in adults.
This document provides an overview of acute kidney injury (AKI) in children. It defines AKI, discusses its classification, epidemiology, staging, etiology, pathophysiology, clinical features, investigations, treatment, and prognosis. AKI is diagnosed based on rises in serum creatinine and/or decreases in urine output. Common causes in children include sepsis, malaria, glomerulonephritis, and nephrotoxic medications. Treatment involves fluid management, treating the underlying cause, and potentially renal replacement therapy for severe cases. Outcomes depend on the severity and reversibility of the kidney injury.
Chronic renal failure of small animals.pptDr.hema hassan
This document discusses chronic renal failure (CRF). It defines CRF as when the kidneys can no longer maintain their excretory, regulatory, and endocrine functions. Common causes of CRF in dogs, cats and large animals are described. The document compares CRF to acute renal failure and outlines some of the clinical signs seen with uremia. It discusses concepts such as hyperfiltration in remnant nephrons and factors that can contribute to the progressive nature of renal disease such as dietary factors. Mechanisms by which the kidneys maintain solute and water balance during declining renal function are also described.
Brief Information regarding the disorders of the genitourinary system. This presentation involves the disorders of the urinary system including Chronic Kidney Disease, Congenital problems related to the urinary system, and renal cancers.
This document provides information about hepato-renal syndrome (HRS), which is a syndrome that develops in patients with liver cirrhosis and portal hypertension, characterized by impaired renal function. It discusses the pathophysiology, including splanchnic arterial vasodilation, renal arterial vasoconstriction, and cardiac dysfunction. It describes the four types of HRS based on time course and precipitating factors. It provides details on diagnostic criteria and management, including general management, renal vasodilators, systemic vasoconstrictors such as terlipressin, and contraindications for vasoconstrictor therapy.
This document discusses acute kidney injury (AKI) in intensive care unit patients. It provides definitions and criteria for AKI, including RIFLE and AKIN classifications. Mortality rates increase significantly with more severe AKI, from 5-10% with no renal dysfunction to 26-40% with renal failure. While decreased urine output can indicate decreased kidney function, urine output alone is a less severe marker. Multiple factors influence the relationship between renal blood flow, perfusion pressure, and glomerular filtration rate. Early markers like neutrophil gelatinase-associated lipocalin and cystatin C may help predict AKI and prognosis better than creatinine. Fluid management must balance resuscitation with avoiding overload,
1. Acute kidney injury (AKI) is the sudden deterioration of renal function that can range from mild to severe. It is a global problem associated with high morbidity and mortality.
2. AKI is classified based on location of injury (pre-renal, intrinsic, post-renal), urine output, and severity of decline in renal function. Common causes include sepsis, nephrotoxins, and decreased renal perfusion.
3. Management involves treating the underlying cause, maintaining fluid/electrolyte balance, and potentially renal replacement therapy for complications like fluid overload or severe electrolyte imbalances. Outcomes depend on factors like age, cause, and need for dialysis.
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The document discusses renal failure and its implications for anesthesia. It describes the functions of the kidneys and defines acute kidney injury and chronic kidney disease. For patients with renal impairment, pre-operative optimization is important, including fluid management and electrolyte correction. Regional anesthesia is preferred over general anesthesia when possible due to better hemodynamic stability. Careful monitoring is needed during and after surgery to watch for fluid overload, electrolyte abnormalities, and other complications.
Hepatorenal syndrome is a condition characterized by impaired renal function in patients with advanced liver disease and portal hypertension. There are two types - type 1 is rapid and progressive, leading to death within a month without treatment, while type 2 is less severe but still associated with worse prognosis. The pathogenesis involves splanchnic vasodilation triggering renal vasoconstriction. Treatment involves vasoconstrictors like terlipressin combined with albumin to increase mean arterial pressure and improve renal function. Achieving at least a 10 mmHg increase in MAP with vasoconstrictor therapy correlates with better renal outcomes in hepatorenal syndrome patients.
This document defines acute kidney injury (AKI) and describes its classification, diagnosis, and management. AKI is an abrupt deterioration in kidney function that is usually reversible. It is classified using criteria like RIFLE, AKIN, and KDIGO that stage AKI based on changes in serum creatinine and urine output. Biomarkers like cystatin C and NGAL can help detect early AKI. Treatment involves fluid resuscitation, removing nephrotoxins, and initiating renal replacement therapy if needed. Outcomes depend on the underlying cause and range from complete recovery to end-stage renal disease.
Diuretics : Dr Renuka Joshi MD,DNB, (FNB )Renuka Buche
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, effects, dosages, and interactions. It covers loop diuretics like furosemide and bumetanide that act in the thick ascending loop of Henle; thiazide diuretics like hydrochlorothiazide that act in the distal convoluted tubule; and potassium-sparing diuretics like spironolactone and amiloride that act in the collecting duct. It provides recommendations for diuretic use and combinations in the treatment of heart failure and fluid overload.
Renal insufficiency occurs when the kidneys fail to remove waste and regulate fluids and electrolytes. It can be acute or chronic. Acute renal failure involves a rapid decline in function and is classified as prerenal, intrarenal, or postrenal based on cause. Chronic renal failure is a progressive loss of kidney function that eventually leads to death without treatment. It involves stages of initial damage, polyuria, oliguria, and terminal kidney failure. Treatment for chronic renal failure includes dialysis or kidney transplantation.
Effect of Anesthesia and Surgery on Renal System.pptxGanta Ranganath
Both anesthesia and surgery can affect renal function through hemodynamic changes and stress responses. Anesthetics like volatile agents can decrease glomerular filtration rate through effects on renal blood flow and perfusion pressure. Muscle relaxants may cause transient hypotension. Intravenous agents generally have minor direct renal effects. Colloids like albumin are renoprotective while hydroxyethyl starch and dextran can cause acute kidney injury. Drugs that alter hemodynamics like NSAIDs, ACE inhibitors, and positive pressure ventilation can also impact renal function. Surgery induces stress responses and fluid shifts that can lead to prerenal azotemia. Specific procedures like pneumoperitoneum, cardiopulmonary bypass, aortic cross
Acute kidney injury (AKI) is the abrupt reduction of renal function over a period of less than 3 months. It can be caused by decreased renal blood flow (prerenal), direct kidney injury (renal), or urinary tract obstruction (postrenal). AKI has systemic effects and increases the risk of complications like fluid overload, electrolyte imbalances, and metabolic acidosis. Treatment involves restoring renal perfusion, treating the underlying cause, managing complications supportively or with renal replacement therapy, and preventing further kidney injury. AKI increases mortality, hospital stay, and risk of progressing to chronic kidney disease.
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2. BASIC FUNCTIONS OF THE KIDNEY
Glomerulus –
• filtration and subsequent excretion of nitrogenous wastes.
Tubules – Selective reabsorption or secretion of
• water and ions to maintain fluid balance
• hydrogen ions to maintain acid–base homeostasis.
Endocrine –
• The production of renin
• the release of prostaglandins
• activation of both erythropoietin and vitamin D.
3. Main Functions Of The Kidneys
A WET BED
• Acid-Base Balance
• Water Balance
• Electrolyte Balance
• Toxin Removal
• Blood pressure Control
• Erythropoietin Production
• Vitamin D Metabolism
4. Effects of Anesthesia on Normal Renal Function
• General anesthesia is associated with a decrease of renal
blood flow, GFR, urinary flow, and electrolyte excretion
• Anesthesia may alter renal function by direct or indirect
effects
• Drugs associated with catecholamine release lead to
vasoconstriction, an increase in renal vascular resistance,
a decrease in renal blood flow, and a decrease in renal
function (indirect effects)
5. • High levels of spinal or epidural anesthesia can impair
venous return, diminish cardiac output, and reduce renal
perfusion.
• In most cases, changes in renal function are transient and
reversible.
• If they persist into the postoperative period, the cause is
often a combination of factors such as preexisting renal or
cardiovascular disease, or severe fluid imbalance, and the
importance of the anesthetic effects is decreased
Effects of Anesthesia on Normal Renal Function
6. VOLATILE ANESTHETICS AND RENAL FUNCTIONS
• Volatile anesthetics cause a decrease in GFR by
decreasing renal perfusion pressure either by
decreasing systemic vascular resistance (isoflurane
or sevoflurane) or cardiac output (halothane).
• This decrease in GFR is exacerbated by hypovolemia
and the release of catecholamines and antidiuretic
hormone as a response to painful stimulation
during surgery
7. SEVOFLURANE AND ITS RENAL EFFECTS (THEORETICAL)
• Sevoflurane is degraded in basic carbon dioxide
absorbents (Barium Hydroxide and Soda lime) into a
vinyl ether called compound A.
• Compound A has been implicated to cause renal injury
through fluoride toxicity (animal studies).
• High intra-renal fluoride concentrations impair the
concentrating ability of the kidney and may theoretically
lead to non-oliguric renal failure
8. Methoxyflurane And Its Effects On Kidneys
• Methoxyflurane causes vasopressin-resistant
polyuria, serum hyperosmolality, hypernatremia,
increased concentrations of serum urea nitrogen
and inorganic fluoride, and decreased urinary
potassium, sodium, osmolality, and urea nitrogen
concentrations.
• Therefore, clinically it is no longer used
10. OPIOIDS AND ITS RENAL EFFECTS
• Opioid are may decrease renal blood flow, GFR and
urine output which is minimal and transient.
• Remifentanil pharmacokinetics are unaffected by
renal functions due to rapid ester hydrolysis.
• With the exception of morphine and meperidine,
significant accumulation of active metabolites do not
occur.
11. OPIOIDS AND ITS RENAL EFFECTS
• The renal toxicity appears in the context of inappropriate use:-
either higher than needed doses, in the presence of other
toxins, chronic use of opioids (accumulation of metabolites),
deranged renal functions or with pre-existing dehydration.
• The accumulation of morphine metabolite (morphine-6-
glucuronide) and meperidine metabolite(normeperidine) has
been reported to prolong respiratory depression in patients
with kidney failure.
• Increased level of normeperidine has been associated with
seizures.
12. EFFECTS OF MUSCLE RELAXANT ON RENAL FUNCTIONS
• Upon administering histamine releasing muscle relaxants
(mivacurium, atracurium, succinylcholine, d-tubocurarine),
there is transient fall in blood pressure, renal blood flow
and cardiac output.
• Based on clinical and experimental data, it appears that
muscle relaxants have only a modest impact on RBF and no
meaningful adverse influence on postoperative Renal
functions when Blood Pressure and Cardiac Output are
adequately maintained
13. Effect Of Positive Pressure Ventilation On Kidneys
• Positive-pressure ventilation used during general
anesthesia can decrease venous return, cardiac output,
renal blood flow, and GFR.
• Decreased cardiac output leads to release of
catecholamines, ADH, renin, and angiotensin II with
the activation of the sympathoadrenal system and
resultant decrease in renal blood flow
14. EFFECT OF REGIONAL ANAESTHESIA ON KIDNEYS
• Spinal and epidural anesthesia only slightly decrease GFR
and RBF in proportion to the decrease in mean arterial
pressure.
• The preexisting intravascular volume and the quantity of
intravenous fluids given strongly influence the renal
response to spinal and epidural anesthesia.
• There is also decreased diuresis and a marked fall in sodium
excretion.
• These trends are gradually reversed during recovery.
15. EFFECTS OF POSITIONING ON KIDNEYS?
Kidney Rest Position
Trendelenburg
Position
Lithotomy Position
16. EFFECTS OF POSITIONING ON KIDNEYS?
• Open procedures on kidney are carried out in ‘kidney
rest position’ – lateral flexed position.
• Dependant leg is flexed and the other is extended.
• Axillary roll – placed under dependant upper chect.
• Operating table is extended to achieve maximal
separation between iliac crest and costal margin.
• Kidney rest is elevated to raise the non dependant
iliac crest higher and increase surgical exposure.
17. EFFECTS OF POSITIONING ON KIDNEYS?
• This position is associated with adverse respiratory and
circulatory effects.
• It can significantly decrease the venous return to heart by
compressing the inferior vena cava.
• Also, the venous pooling in the legs potentiates anesthesia
induced vasodilation.
• Lithotomy and Trendelenburg position:-
• Elevation of leg drain blood into central circulation acutely,
mean BP and CO are increased
• Conversely, rapid lowering of legs from these positions acutely
decreases venous return and can result in hypotension.
18. Acute Kidney Injury And Acute Tubular Necrosis
• Acute kidney injury (AKI) is an acute decline in renal
function sufficient to result in the retention of
nitrogenous end-products of metabolism
• Causes :
• Pre-renal – Inadequate perfusion – 40%–70%
• Renal – Intrinsic renal disease – 10%–50%
• Post-renal – Obstructive uropathy – 10%
19. PREVENTION OF ACUTE TUBULAR NECROSIS (ATN)
PREOPERATIVE ASSESSMENT
• Factors known to be associated with increased risk for
AKI should be known and managed
PERIOPERATIVE MANAGEMENT
o Prevention of new AKI by:
• Maintain oxygenation
• Maintain normocarbia
• Optimize intravascular volume and cardiac output
20. ASSESSMENT OF RENAL FUNCTIONS
• Why is assessment of renal function important?
1. Preoperative renal dysfunction is associated with
greater risk of postoperative complications.
2. Certain well-defined risk factors for new AKI or
deterioration in renal function are detectable
preoperatively
21. Conditions
Associated With
Increased Risk Of
Perioperative
Acute
Kidney Injury
(AKI) OR (ATN)
1. Preoperative renal disease
2. Diabetes mellitus
3. Hypertension 4. Cardiac failure
5. Preoperative ‘shock’ states
6. Cirrhosis 7. Sepsis
8. Biliary obstruction
9. Multiple system trauma
10. Multiple organ failure
11. Extracellular fluid volume deficit
12. Elderly patients
13. Aortorenal vascular disease
22. HISTORY AND EXAMINATION
• SYMPTOMS
• In the early stages of renal disease there may be no symptoms.
• When symptoms do occur, they include:
• Fatigue, general malaise, headaches
• Nausea, weight loss, loss of appetite
• Pruritus, dry skin • Polyuria
• Polydypsia • Dysuria
24. INVESTIGATIONS
1- PLASMA
Electrolytes are increased early
oSodium, potassium, chloride and bicarbonate The changes in
their levels will exacerbate dysrhythmias and compromise
resuscitation
Frank renal failure results in hypocalcemia, hyperphosphatemia
and hypermagnesemia
25. INVESTIGATIONS
1- PLASMA
Urea and nitrogen
• Urea is produced by protein catabolism in the liver
Creatinine is a by-product of muscle metabolism and
production is related to muscle mass
• Serum creatinine is an insensitive indicator of renal
function – the value may be normal even if GFR is reduced
by 50%.
26. INVESTIGATIONS
2- URINE
APPEARANCE
• Gross – bleeding, infection
• Microscopic – casts, bacteria, cells
pH: Normally urine is acidic
SPECIFIC GRAVITY (SG)
• SG refers to the concentration of
solutes in urine; the ability to
concentrate is a measure of
tubular function. This is, however,
nonspecific .
Substances/conditions affecting SG
Protein
Glucose
Mannitol
Diuretics
Extremes of age
Antibiotics (carbenicillin)
Temperature
Hormonal imbalance (pituitary,
adrenal and thyroid disease)
27. OSMOLALITY
•The number of osmotically active particles per unit solvent (mOsm/L).
•Osmolality is more specific than SG:
• Oliguria + Osmolality > 500 suggests prerenal azotemia
• Oliguria + osmolality < 350 likely to be acute tubular necrosis
PROTEIN
• <150 mg/24 h: normal excretion (exercise and standing can increase
this)
• >750 mg/24 h: indicator of renal parenchymal disease
• Massive: glomerular damage
INVESTIGATIONS
2- URINE
28. INVESTIGATIONS
3- CREATININE CLEARANCE
Measures the glomerular filtration of creatinine (Cr) which approximates GFR
eGFR = 141 × min(Scr/κ, 1)α × max(Scr/κ, 1)-1.209 × 0.993Age × 1.018 [if female] × 1.159 [if black]
o Abbreviations / Units
• eGFR (estimated glomerular filtration rate) = mL/min/1.73 m2
• SCr (standardized serum creatinine) = mg/dL
• κ = 0.7 (females) or 0.9 (males)
• α = -0.329 (females) or -0.411 (males)
• min = indicates the minimum of SCr/κ or 1
• max = indicates the maximum of SCr/κ or 1
• age = years
29. INVESTIGATIONS
4- OTHER TESTS
Advanced renal disease affects most organ systems.
Additional tests that may be useful in patients with advanced renal
disease include
• chest radiography
• electrocardiography
• complete blood count, serum electrolytes, and acid-base studies
30. ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE
• PREMEDICATION
• The effects of premedication with sedative drugs and opioids are
unpredictable due to decrease plasma proteins and the effect of
altered blood pH
• Agents to reduce gastric acidity and volume.
• Antihypertensives should generally be continued in the
perioperative
31. INDUCTION
• The pharmocokinetics of propofol are usually unaltered
• Thiopental has an increased volume of distribution and decreased
plasma protein binding resulting in an increase in free drug
concentration
• Avoid suxamethonium if the serum potassium level is greater than
5mmol/L
• Atracurium, cisatracurium and mivacurium are the neuromuscular
blocking agents of choice because of their rapid elimination and
independence of renal metabolism and excretion
ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE
32. MAINTENANCE:
1-Monitoring:
• Standard Monitoring
• CVP monitoring or transesophageal Doppler is a useful guide to
volume status and systemic blood pressure.
• Urine output should be monitored.
• Invasive Monitoring if required only
ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE
33. 2- General Anesthesia:
Response to IV anesthetic is unpredicted due to
(1) volume of distribution (which is often increased)
(2) protein binding (which may be decreased)
(3) low pH
(4) dependence on renal excretion for the parent drug or metabolites.
Ketamine and benzodiazepines are less heavily protein bound,
but metabolites of ketamine depend on renal excretion
Propofol is accepted for both induction and maintenance
ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE
34. Inhalational Anesthetic:
• Isoflurane and desflurane are effective inhalational agents, with
minimal metabolism.
• Enflurane use is controversial due to the potential accumulation of
fluoride ions
Opioids:
• Patients with kidney disease can develop high levels of morphine-
6-glucuronide and resultant respiratory failure
• Remifentanil does not accumulate in CKD
• Meperidine metabolites can cause convulsions when present in
high concentrations, and cannot be removed by dialysis, and
should be avoided.
35. Technique Advantages Disadvantages
Regional •Minimal changes in renal
hemodynamics
•May shorten hospital stays
•Allows for earlier detection of
capsular tears and bladder
perforation
•Lower incidence of postoperative
nausea and vomiting
•Reduced amount of operative
blood loss and the incidence of
deep vein thrombosis with
transurethral resection of prostate
•Presence of peripheral
neuropathy
•Tendency for bleeding
•Patient anxiety
•Less suitable for
prolonged procedures
•Hypotension with
sympathetic block; may
cause reluctance to
expand volume
36. Technique Advantages Disadvantages
Intravenous
anesthetics
• Hemodynamic stability • Unpredictable response
Hypertension
• Greater need for N 2 O
and neuromuscular
blockers
Volatile
anesthetics
•Good airway control
•Blood pressure control
•Duration not dependent on
urinary excretion
•Less neuromuscular blocking with
drugs required
•Fi o 2 can be increased because
N 2 O not necessary
•Alterations in renal
hemodynamics
•Decreased cardiac output
•Hypotension
•Increased incidence of
postoperative nausea and
vomiting
37. POSTOPERATIVE MANAGEMENT
• Consider admission to HDU after major surgery or if
significant comorbidities exist.
• Reevaluate fluid balance and hydration regularly using
clinical assessment, CVP and urine output (if any).
• Give supplemental oxygen.
• Measure serum electrolytes regularly.
• Thromboembolic prophylaxis is important.