This document discusses acute kidney injury (AKI). It notes that AKI is common in ICU patients and associated with increased mortality. Sepsis and postoperative/toxic causes are common. It defines AKI and discusses causes including prerenal, postrenal, and intrarenal. For intrarenal causes, it mentions glomerulonephritis, vasculitis, interstitial nephritis, acute tubular necrosis, and sepsis-induced AKI. It reviews diagnosis and novel biomarkers. Prevention and treatment sections discuss volume expansion, diuretics, vasopressors, vasodilators, sedation, hormonal manipulation, metabolic interventions, statins, and renal replacement therapy.
Management of acute kidney injury (AKI) involves several common principles including optimizing hemodynamics, correcting fluid and electrolyte imbalances, discontinuing nephrotoxic medications, and dose adjusting other medications. Treatment depends on the underlying cause of AKI and may involve managing life-threatening complications, diagnosing and treating the underlying condition, and renal replacement therapies like hemodialysis or peritoneal dialysis. Prevention efforts focus on recognizing at-risk patients and using preventive measures to avoid AKI. The prognosis of AKI depends on the specific cause and presence of other factors, with prerenal azotemia and postrenal azotemia generally having a better prognosis than other forms of intrinsic AKI.
AKI is defined as an increase in serum creatinine concentration within 48 hours or 1.5 times the baseline within 7 days. It can be prerenal, intrinsic, or postrenal. Prerenal AKI is reversible if renal perfusion is optimized through fluid resuscitation and vasopressors. Intrinsic AKI is commonly caused by sepsis, ischemia, nephrotoxins and has a worse prognosis. Treatment focuses on treating the underlying cause, managing complications like fluid overload, and starting renal replacement therapy for severe cases.
This document summarizes diabetic ketoacidosis (DKA), a life-threatening complication of diabetes caused by a lack of insulin. It discusses precipitating factors, cardinal features, pathophysiology, investigations, and treatment including fluid therapy with isotonic saline, insulin therapy via IV bolus and infusion, potassium replacement, and bicarbonate therapy if the pH is low. Monitoring of glucose, electrolytes, and vital signs is important. Treatment of underlying infections or other precipitating causes is also needed. Hyperglycemic hyperosmolar state, a similar condition without ketoacidosis, is also summarized.
This document discusses acute kidney injury (AKI), including its definition, diagnosis criteria, epidemiology, classification, pathogenesis, etiology, treatment, and management. AKI is defined as an abrupt reduction in kidney function, diagnosed by changes in serum creatinine, BUN, and urine output. Between 5-7% of hospitalized patients and a greater percentage of ICU patients develop AKI. Mortality from AKI exceeds 50% despite improvements in care. AKI is classified using criteria like RIFLE, AKIN, and KDIGO which consider risk, injury, failure, and loss of kidney function. Causes include prerenal issues like dehydration, intrinsic renal damage, and postrenal obstruction
Hyperkalemia is defined as a serum potassium level greater than 5.5 mmol/L. The severity can range from mild (<6.0 mmol/L) to moderate (6.0-7.0 mmol/L) to severe (7.0-8.0 mmol/L potentially causing ECG changes and above 8.0 mmol/L potentially causing cardiac arrest). Management involves stabilizing the membrane potential with calcium salts for ECG changes, shifting potassium into cells with insulin and glucose, removing potassium from the body with resins or dialysis, and preventing further increases by reviewing medications and diet.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterized by hyperglycemia, dehydration, and metabolic acidosis. It is diagnosed based on blood sugar over 14 mmol/L, presence of ketones, pH below 7.3, and bicarbonate below 18 mmol/L. Management involves rapid intravenous fluid resuscitation, gradual rehydration and electrolyte replacement, and insulin therapy to reverse hyperglycemia and ketosis while closely monitoring for complications. The goals are to correct estimated fluid deficits over 24 hours and lower blood glucose by 3-4 mmol/L per hour.
A 45-year-old man presented with headache, visual disturbances, and papilledema with a blood pressure of 200/115 mmHg. He was admitted to the CCU/ICU. This case represents a hypertensive emergency characterized by severe hypertension (grade 3) associated with acute hypertensive emergency organ damage (HMOD) including papilledema, which requires immediate but careful intervention to lower blood pressure, usually with intravenous therapy. Hypertensive emergencies typically present with severe hypertension, funduscopic changes, microangiopathy, and can be associated with encephalopathy, acute heart failure, and acute renal deterioration. The goal of treatment is to reduce blood pressure to prevent further organ damage.
This document provides an overview of acute kidney injury (AKI), formerly known as acute renal failure. It discusses the definition and epidemiology of AKI and describes the main causes as pre-renal, intrinsic renal, and post-renal. Pre-renal AKI is the most common type and is caused by reduced renal blood flow. The document outlines the diagnostic evaluation, complications, treatment approaches including dialysis indications, and outcomes of AKI. It emphasizes the importance of identifying and eliminating nephrotoxic agents to optimize management of this condition.
Management of acute kidney injury (AKI) involves several common principles including optimizing hemodynamics, correcting fluid and electrolyte imbalances, discontinuing nephrotoxic medications, and dose adjusting other medications. Treatment depends on the underlying cause of AKI and may involve managing life-threatening complications, diagnosing and treating the underlying condition, and renal replacement therapies like hemodialysis or peritoneal dialysis. Prevention efforts focus on recognizing at-risk patients and using preventive measures to avoid AKI. The prognosis of AKI depends on the specific cause and presence of other factors, with prerenal azotemia and postrenal azotemia generally having a better prognosis than other forms of intrinsic AKI.
AKI is defined as an increase in serum creatinine concentration within 48 hours or 1.5 times the baseline within 7 days. It can be prerenal, intrinsic, or postrenal. Prerenal AKI is reversible if renal perfusion is optimized through fluid resuscitation and vasopressors. Intrinsic AKI is commonly caused by sepsis, ischemia, nephrotoxins and has a worse prognosis. Treatment focuses on treating the underlying cause, managing complications like fluid overload, and starting renal replacement therapy for severe cases.
This document summarizes diabetic ketoacidosis (DKA), a life-threatening complication of diabetes caused by a lack of insulin. It discusses precipitating factors, cardinal features, pathophysiology, investigations, and treatment including fluid therapy with isotonic saline, insulin therapy via IV bolus and infusion, potassium replacement, and bicarbonate therapy if the pH is low. Monitoring of glucose, electrolytes, and vital signs is important. Treatment of underlying infections or other precipitating causes is also needed. Hyperglycemic hyperosmolar state, a similar condition without ketoacidosis, is also summarized.
This document discusses acute kidney injury (AKI), including its definition, diagnosis criteria, epidemiology, classification, pathogenesis, etiology, treatment, and management. AKI is defined as an abrupt reduction in kidney function, diagnosed by changes in serum creatinine, BUN, and urine output. Between 5-7% of hospitalized patients and a greater percentage of ICU patients develop AKI. Mortality from AKI exceeds 50% despite improvements in care. AKI is classified using criteria like RIFLE, AKIN, and KDIGO which consider risk, injury, failure, and loss of kidney function. Causes include prerenal issues like dehydration, intrinsic renal damage, and postrenal obstruction
Hyperkalemia is defined as a serum potassium level greater than 5.5 mmol/L. The severity can range from mild (<6.0 mmol/L) to moderate (6.0-7.0 mmol/L) to severe (7.0-8.0 mmol/L potentially causing ECG changes and above 8.0 mmol/L potentially causing cardiac arrest). Management involves stabilizing the membrane potential with calcium salts for ECG changes, shifting potassium into cells with insulin and glucose, removing potassium from the body with resins or dialysis, and preventing further increases by reviewing medications and diet.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterized by hyperglycemia, dehydration, and metabolic acidosis. It is diagnosed based on blood sugar over 14 mmol/L, presence of ketones, pH below 7.3, and bicarbonate below 18 mmol/L. Management involves rapid intravenous fluid resuscitation, gradual rehydration and electrolyte replacement, and insulin therapy to reverse hyperglycemia and ketosis while closely monitoring for complications. The goals are to correct estimated fluid deficits over 24 hours and lower blood glucose by 3-4 mmol/L per hour.
A 45-year-old man presented with headache, visual disturbances, and papilledema with a blood pressure of 200/115 mmHg. He was admitted to the CCU/ICU. This case represents a hypertensive emergency characterized by severe hypertension (grade 3) associated with acute hypertensive emergency organ damage (HMOD) including papilledema, which requires immediate but careful intervention to lower blood pressure, usually with intravenous therapy. Hypertensive emergencies typically present with severe hypertension, funduscopic changes, microangiopathy, and can be associated with encephalopathy, acute heart failure, and acute renal deterioration. The goal of treatment is to reduce blood pressure to prevent further organ damage.
This document provides an overview of acute kidney injury (AKI), formerly known as acute renal failure. It discusses the definition and epidemiology of AKI and describes the main causes as pre-renal, intrinsic renal, and post-renal. Pre-renal AKI is the most common type and is caused by reduced renal blood flow. The document outlines the diagnostic evaluation, complications, treatment approaches including dialysis indications, and outcomes of AKI. It emphasizes the importance of identifying and eliminating nephrotoxic agents to optimize management of this condition.
- The mortality rate for acute liver failure ranges from 56% to 80%. The main role of intensive care therapy is providing multi-organ support.
- Paracetamol toxicity is the most common cause of acute liver failure in the Western world. Hepatic encephalopathy is no longer the main cause of death, but its detection and management require sophisticated monitoring.
- Hepatorenal failure results from complex interactions between splanchnic, renal, and systemic circulation in response to liver failure. Terlipressin has been shown to help treat it.
- Novel hepatic replacement therapies are under development but definitive studies on their efficacy have not been published yet.
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its levels are regulated by the kidneys, sodium-potassium pump, and aldosterone. Causes of hyperkalemia include intracellular shifts, decreased excretion, and excess intake. Clinical features range from asymptomatic to muscle weakness to arrhythmias. ECG changes correlate with potassium levels and include peaked T waves, PR prolongation, and eventually a sine wave pattern. Treatment focuses on antagonizing cardiac effects with calcium, driving potassium intracellularly with insulin/beta-agonists, and removing it through cation exchange resins, diuretics, or hemodialysis.
This document discusses diabetic emergencies, specifically diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). It covers the pathophysiology, clinical presentation, diagnosis, treatment priorities of volume repletion, potassium replacement, and insulin administration, as well as complications, disposition, and pitfalls in management. The goal of treatment is to correct dehydration, electrolyte imbalances, and acidosis while gradually lowering blood glucose levels.
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.
Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.
Hypernatremia is defined as a plasma sodium level >145 mEq/L. It can be caused by primary sodium gain or water deficit when compensatory mechanisms are impaired. Clinical presentation depends on severity and chronicity. Treatment goals are correction rates of 0.5 mEq/L/hr for acute cases and 0.3 mEq/L/hr for chronic cases.
Hyponatremia is defined as a sodium level <135 mEq/L. It can be caused by disorders of water homeostasis or increased arginine vasopressin levels. Clinical presentation ranges from nausea and vomiting to seizures and death depending on severity. Diagnostic approach involves determining if the case is due to "osis"
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
The document provides information on the management of diabetic ketoacidosis (DKA). It discusses diagnosing DKA, including euglycemic DKA. Treatment involves three steps - correcting fluid deficits with isotonic saline, treating electrolyte abnormalities like potassium replacement, and administering insulin via continuous IV infusion. Monitoring of laboratory values is important to gauge resolution of ketoacidosis and switch to subcutaneous insulin when indicators are met. Complications can include hypoglycemia and hypokalemia.
This document discusses hypokalemia, defined as a serum potassium level below 3.6 mEq/L. It notes that potassium is critical for nerve impulse transmission and muscle function. The major causes of hypokalemia include decreased intake, intracellular shifts, non-renal losses like vomiting/diarrhea, and renal losses due to drugs like diuretics. Clinical features range from muscle weakness to cardiac arrhythmias. Diagnosis involves evaluating electrolytes, ECG changes, urine studies, and considering underlying causes. Treatment focuses on replacing potassium losses and correcting the underlying etiology.
Acute metabolic complications of diabetes mellitusPushpAnjali6
This document provides information on acute metabolic complications of diabetes mellitus, including diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state, hypoglycemia, and lactic acidosis. It defines DKA as hyperglycemia, ketosis, and acidemia and describes the pathogenesis involving unchecked ketogenesis in insulin deficiency. Precipitating factors, symptoms, signs, investigations, and treatment of DKA are outlined. Treatment involves fluid replacement, insulin administration, monitoring of electrolytes like potassium and phosphate, and ongoing monitoring of the patient. Complications of DKA include shock, cerebral edema, pulmonary edema, hypoglycemia, and electrolyte imbalances. Hyperosmolar hyperglycemic
- Correction insulin is preferable to sliding scale insulin for managing inpatient hyperglycemia as it treats current high blood sugars and prevents future highs through the use of basal, nutritional, and correctional insulin components.
- The case study patient should be started on correctional insulin therapy which includes initiation of basal insulin, nutritional insulin with meals, and additional correctional insulin for blood sugars over target.
- When initiating or adjusting insulin therapy in the hospital, consideration should be given to the patient's diabetes type and weight to determine the total daily insulin dose and regimen. Frequent monitoring and adjustments are important to achieve good glycemic control.
This document defines hypercalcemia and discusses its causes, evaluation, clinical presentation, and management. The main causes are parathyroid hormone dependent (primary hyperparathyroidism, tertiary hyperparathyroidism) and independent (malignancy, vitamin D related, endocrinopathies). Evaluation involves history, exam, and labs. Acute management is rehydration and medications to increase calcium excretion. Long term management depends on the underlying cause and may involve surgery, bisphosphonates, glucocorticoids, or ketoconazole.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes caused by low insulin levels and high levels of counter-regulatory hormones. This leads to hyperglycemia, lipolysis, ketogenesis, and metabolic acidosis. Common precipitants include infections, inadequate insulin treatment, and myocardial ischemia. Clinical features include nausea, vomiting, abdominal pain, dehydration, and Kussmaul breathing. Diagnosis involves measuring glucose, ketones, electrolytes, and acid-base status. Management consists of fluid resuscitation, insulin administration, electrolyte replacement, and treating any precipitating causes. Complications can include cerebral edema, cardiac dysrhythmias, and pulmonary edema. Pro
1. Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, ketonemia, and metabolic acidosis in patients with diabetes mellitus.
2. Risk factors include newly diagnosed diabetes, insulin omission, poor metabolic control, and infection.
3. Treatment involves intravenous fluid resuscitation, insulin therapy, electrolyte replacement, and treating any precipitating infections.
4. Complications of DKA treatment include cerebral edema, hypoglycemia, and hypokalemia. Careful monitoring during resuscitation is important.
This document discusses diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), two serious complications of diabetes. It defines DKA as hyperglycemia, ketosis, and acidosis, while defining HHS as hyperglycemia, hyperosmolarity, and altered mental status. It then provides further details on the pathogenesis, diagnostic evaluation, treatment, and monitoring of patients with DKA or HHS. Hypoglycemia is also briefly discussed.
This document discusses the management of hyperkalemia in chronic kidney disease (CKD). It notes that hyperkalemia is common in CKD patients, affecting 40-50% of those with end-stage renal disease, and is associated with increased mortality. The causes of hyperkalemia in CKD include increased intracellular shifting of potassium, decreased renal excretion, and medications that inhibit the renin-angiotensin-aldosterone system. The document outlines approaches for acute and chronic management of hyperkalemia in CKD, including calcium supplementation, insulin therapy, beta-agonists, cation exchange resins, and dialysis in severe cases. It emphasizes the importance of addressing both acute life-threatening rises in potassium as well
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
This document provides an overview of STEMI (ST-segment elevation myocardial infarction). It defines STEMI and lists its clinical features and complications. It discusses the important investigations for STEMI including electrocardiogram, cardiac markers, echocardiogram, and MRI. It also outlines the management of STEMI both in the emergency department and hospital, including reperfusion therapies, medications, monitoring for complications, and addressing issues like hypotension and hypovolemia.
Interface between renal disease and CADSumit Shanker
This document discusses the relationship between renal disease and cardiovascular illness. Some key points:
- The kidneys and heart communicate extensively through hormones and the sympathetic nervous system. Renal dysfunction increases cardiovascular risk.
- Risk rises when the estimated glomerular filtration rate (eGFR) drops below 60 mL/min/1.73m2. Microalbuminuria also predicts increased CVD risk regardless of diabetes status.
- Anemia due to chronic kidney disease is linked to worse heart failure outcomes and increased mortality. Treatment of anemia has risks that may outweigh benefits.
- Contrast-induced acute kidney injury is a risk for those with an eGFR <60 undergoing imaging with iodinated contrast
This document discusses acute kidney injury (AKI) in the intensive care unit (ICU). It defines AKI and describes its staging and epidemiology. It lists common risk factors for AKI and discusses biomarkers for risk stratification. The main causes of AKI in the ICU are sepsis, low blood pressure, and nephrotoxic medications. AKI can cause multiple organ dysfunction and increased mortality. Treatment involves fluid management, renal replacement therapy such as continuous renal replacement therapy, and managing complications of AKI and renal replacement therapy.
- The mortality rate for acute liver failure ranges from 56% to 80%. The main role of intensive care therapy is providing multi-organ support.
- Paracetamol toxicity is the most common cause of acute liver failure in the Western world. Hepatic encephalopathy is no longer the main cause of death, but its detection and management require sophisticated monitoring.
- Hepatorenal failure results from complex interactions between splanchnic, renal, and systemic circulation in response to liver failure. Terlipressin has been shown to help treat it.
- Novel hepatic replacement therapies are under development but definitive studies on their efficacy have not been published yet.
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its levels are regulated by the kidneys, sodium-potassium pump, and aldosterone. Causes of hyperkalemia include intracellular shifts, decreased excretion, and excess intake. Clinical features range from asymptomatic to muscle weakness to arrhythmias. ECG changes correlate with potassium levels and include peaked T waves, PR prolongation, and eventually a sine wave pattern. Treatment focuses on antagonizing cardiac effects with calcium, driving potassium intracellularly with insulin/beta-agonists, and removing it through cation exchange resins, diuretics, or hemodialysis.
This document discusses diabetic emergencies, specifically diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). It covers the pathophysiology, clinical presentation, diagnosis, treatment priorities of volume repletion, potassium replacement, and insulin administration, as well as complications, disposition, and pitfalls in management. The goal of treatment is to correct dehydration, electrolyte imbalances, and acidosis while gradually lowering blood glucose levels.
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.
Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.
Hypernatremia is defined as a plasma sodium level >145 mEq/L. It can be caused by primary sodium gain or water deficit when compensatory mechanisms are impaired. Clinical presentation depends on severity and chronicity. Treatment goals are correction rates of 0.5 mEq/L/hr for acute cases and 0.3 mEq/L/hr for chronic cases.
Hyponatremia is defined as a sodium level <135 mEq/L. It can be caused by disorders of water homeostasis or increased arginine vasopressin levels. Clinical presentation ranges from nausea and vomiting to seizures and death depending on severity. Diagnostic approach involves determining if the case is due to "osis"
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
The document provides information on the management of diabetic ketoacidosis (DKA). It discusses diagnosing DKA, including euglycemic DKA. Treatment involves three steps - correcting fluid deficits with isotonic saline, treating electrolyte abnormalities like potassium replacement, and administering insulin via continuous IV infusion. Monitoring of laboratory values is important to gauge resolution of ketoacidosis and switch to subcutaneous insulin when indicators are met. Complications can include hypoglycemia and hypokalemia.
This document discusses hypokalemia, defined as a serum potassium level below 3.6 mEq/L. It notes that potassium is critical for nerve impulse transmission and muscle function. The major causes of hypokalemia include decreased intake, intracellular shifts, non-renal losses like vomiting/diarrhea, and renal losses due to drugs like diuretics. Clinical features range from muscle weakness to cardiac arrhythmias. Diagnosis involves evaluating electrolytes, ECG changes, urine studies, and considering underlying causes. Treatment focuses on replacing potassium losses and correcting the underlying etiology.
Acute metabolic complications of diabetes mellitusPushpAnjali6
This document provides information on acute metabolic complications of diabetes mellitus, including diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state, hypoglycemia, and lactic acidosis. It defines DKA as hyperglycemia, ketosis, and acidemia and describes the pathogenesis involving unchecked ketogenesis in insulin deficiency. Precipitating factors, symptoms, signs, investigations, and treatment of DKA are outlined. Treatment involves fluid replacement, insulin administration, monitoring of electrolytes like potassium and phosphate, and ongoing monitoring of the patient. Complications of DKA include shock, cerebral edema, pulmonary edema, hypoglycemia, and electrolyte imbalances. Hyperosmolar hyperglycemic
- Correction insulin is preferable to sliding scale insulin for managing inpatient hyperglycemia as it treats current high blood sugars and prevents future highs through the use of basal, nutritional, and correctional insulin components.
- The case study patient should be started on correctional insulin therapy which includes initiation of basal insulin, nutritional insulin with meals, and additional correctional insulin for blood sugars over target.
- When initiating or adjusting insulin therapy in the hospital, consideration should be given to the patient's diabetes type and weight to determine the total daily insulin dose and regimen. Frequent monitoring and adjustments are important to achieve good glycemic control.
This document defines hypercalcemia and discusses its causes, evaluation, clinical presentation, and management. The main causes are parathyroid hormone dependent (primary hyperparathyroidism, tertiary hyperparathyroidism) and independent (malignancy, vitamin D related, endocrinopathies). Evaluation involves history, exam, and labs. Acute management is rehydration and medications to increase calcium excretion. Long term management depends on the underlying cause and may involve surgery, bisphosphonates, glucocorticoids, or ketoconazole.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes caused by low insulin levels and high levels of counter-regulatory hormones. This leads to hyperglycemia, lipolysis, ketogenesis, and metabolic acidosis. Common precipitants include infections, inadequate insulin treatment, and myocardial ischemia. Clinical features include nausea, vomiting, abdominal pain, dehydration, and Kussmaul breathing. Diagnosis involves measuring glucose, ketones, electrolytes, and acid-base status. Management consists of fluid resuscitation, insulin administration, electrolyte replacement, and treating any precipitating causes. Complications can include cerebral edema, cardiac dysrhythmias, and pulmonary edema. Pro
1. Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, ketonemia, and metabolic acidosis in patients with diabetes mellitus.
2. Risk factors include newly diagnosed diabetes, insulin omission, poor metabolic control, and infection.
3. Treatment involves intravenous fluid resuscitation, insulin therapy, electrolyte replacement, and treating any precipitating infections.
4. Complications of DKA treatment include cerebral edema, hypoglycemia, and hypokalemia. Careful monitoring during resuscitation is important.
This document discusses diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), two serious complications of diabetes. It defines DKA as hyperglycemia, ketosis, and acidosis, while defining HHS as hyperglycemia, hyperosmolarity, and altered mental status. It then provides further details on the pathogenesis, diagnostic evaluation, treatment, and monitoring of patients with DKA or HHS. Hypoglycemia is also briefly discussed.
This document discusses the management of hyperkalemia in chronic kidney disease (CKD). It notes that hyperkalemia is common in CKD patients, affecting 40-50% of those with end-stage renal disease, and is associated with increased mortality. The causes of hyperkalemia in CKD include increased intracellular shifting of potassium, decreased renal excretion, and medications that inhibit the renin-angiotensin-aldosterone system. The document outlines approaches for acute and chronic management of hyperkalemia in CKD, including calcium supplementation, insulin therapy, beta-agonists, cation exchange resins, and dialysis in severe cases. It emphasizes the importance of addressing both acute life-threatening rises in potassium as well
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
This document provides an overview of STEMI (ST-segment elevation myocardial infarction). It defines STEMI and lists its clinical features and complications. It discusses the important investigations for STEMI including electrocardiogram, cardiac markers, echocardiogram, and MRI. It also outlines the management of STEMI both in the emergency department and hospital, including reperfusion therapies, medications, monitoring for complications, and addressing issues like hypotension and hypovolemia.
Interface between renal disease and CADSumit Shanker
This document discusses the relationship between renal disease and cardiovascular illness. Some key points:
- The kidneys and heart communicate extensively through hormones and the sympathetic nervous system. Renal dysfunction increases cardiovascular risk.
- Risk rises when the estimated glomerular filtration rate (eGFR) drops below 60 mL/min/1.73m2. Microalbuminuria also predicts increased CVD risk regardless of diabetes status.
- Anemia due to chronic kidney disease is linked to worse heart failure outcomes and increased mortality. Treatment of anemia has risks that may outweigh benefits.
- Contrast-induced acute kidney injury is a risk for those with an eGFR <60 undergoing imaging with iodinated contrast
This document discusses acute kidney injury (AKI) in the intensive care unit (ICU). It defines AKI and describes its staging and epidemiology. It lists common risk factors for AKI and discusses biomarkers for risk stratification. The main causes of AKI in the ICU are sepsis, low blood pressure, and nephrotoxic medications. AKI can cause multiple organ dysfunction and increased mortality. Treatment involves fluid management, renal replacement therapy such as continuous renal replacement therapy, and managing complications of AKI and renal replacement therapy.
This document defines and provides guidelines for the diagnosis and management of acute kidney injury (AKI). It discusses definitions of AKI based on increases in serum creatinine and decreases in urine output. The causes of AKI should be determined when possible to guide management. Patients should be stratified by risk and monitored closely based on their risk factors. Renal replacement therapy may be needed for life-threatening fluid, electrolyte and acid-base imbalances. Prevention and treatment strategies are aimed at identifying and treating reversible causes while avoiding nephrotoxic medications when possible.
Hypertension , crf post renal transplant patient for surgeryDr Kumar
1. Chronic renal failure occurs when glomerular filtration rate is reduced to less than 10% of normal function for over 3 months. It is caused by conditions like diabetes, hypertension, glomerulonephritis.
2. It leads to fluid, electrolyte and acid-base imbalances, anemia, bone disease, neuropathy, impaired drug handling and increased risk of infections.
3. Anesthesia management includes preoperative correction of abnormalities, modified drug dosing and strict asepsis to prevent infections in the immunocompromised patient.
This document discusses hypertension (high blood pressure), including its causes, symptoms, diagnosis, and treatment. It defines hypertension and describes its classification. It also outlines lifestyle modifications and medications that are used to treat hypertension. The goals of treatment are to lower blood pressure and prevent target organ damage to the heart, brain, kidneys and eyes. Nursing care focuses on educating patients, monitoring for side effects, ensuring compliance with treatment, and evaluating treatment effectiveness.
download link : https://www.dropbox.com/s/a8ug16pfkvv1bzp/Cardiorenal%20syndrome.ppt?m
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Manejo de hemoderivados y anticoagulacion
objetivos
-Monitoria de la coagulación
-Manejo de la anemia y el sangrado
-Manejo de la coagulación
-Terapia anticoagulante y antiplaquetaria
Hypertension is a major health problem affecting 25% of adults and 50% of those over 60. It causes dangerous complications like heart attack, heart failure, stroke, and renal failure. The causes are mostly unknown except for 5% of secondary cases. Lifestyle modifications like reduced salt and fat intake, weight loss, exercise, and stopping smoking are beneficial for reducing blood pressure and complications. There are several classes of antihypertensive drugs that work through different mechanisms like reducing blood volume and pressure, blocking nerve signals, dilating blood vessels, and inhibiting hormone systems. The choice of drugs depends on individual patient factors and risks.
- Tissue factor binding to factor VII initiates the extrinsic blood coagulation cascade and contributes to activation of the intrinsic cascade. Tissue factor is normally not expressed in blood vessels but is expressed by macrophages and smooth muscle cells in atherosclerotic vessels, initiating arterial thrombosis.
- All blood-borne markers of inflammation have been shown to predict coronary artery disease or acute coronary syndrome except interferon alpha.
- The final common pathway of platelet aggregation is mediated through the GPIIb/IIIa receptor.
This document summarizes the pharmacology of medications used to treat hypertension, including ACE inhibitors, ARBs, and CCBs. It reviews their mechanisms of action, efficacy, and safety profiles. It also discusses the renin-angiotensin system and its role in hypertension, current treatment guidelines, lifestyle modifications, and algorithms for antihypertensive drug selection and combination therapy.
The document discusses renal transplantation, including indications, donor criteria, preoperative workup, surgical procedure, anesthesia management, and postoperative care. Key points include: renal transplantation is indicated for end stage renal disease; donor criteria include age 5-49 years and good renal function; extensive preoperative testing is required; surgery involves vascular anastomoses of donor kidney; anesthesia goals include hemodynamic stability and adequate analgesia/relaxation; and postoperative monitoring focuses on graft function and complications like rejection.
This document discusses angina pectoris, also known as stable angina. It defines angina as chest pain or discomfort that occurs due to decreased blood flow to the heart muscle. It then describes the different types of angina and their causes. The main causes are atherosclerosis, coronary artery spasm, traumatic injury, and embolic events which can all restrict blood flow to the heart. The document outlines the goals of treatment which are to prevent heart attacks and death while reducing angina symptoms. It then discusses the various pharmacological treatments used including nitrates, beta blockers, calcium channel blockers, antiplatelet agents, ACE inhibitors, and ranolazine. Non-pharmacological options like percutaneous coronary
Angiotensin Converting Enzyme Inhibitors (ACE-I) are a class of drugs that inhibit the angiotensin converting enzyme and are often used as first-line treatment for congestive heart failure and hypertension. They work by inhibiting angiotensin converting enzyme, reducing stimulation of AT1 receptors and increasing bradykinin levels, leading to vasodilation. Common side effects include hypotension, dry cough, and hyperkalemia. ACE-I have various clinical uses including treatment of hypertension, heart failure, and diabetic nephropathy.
This document discusses inotropic agents, which are drugs that affect the strength of contraction of the heart muscle. It describes positive inotropes that increase contraction and negative inotropes that decrease contraction. The choice of inotrope depends on its pharmacological effects and the specific cardiovascular condition. Positive inotropes discussed include calcium, calcium sensitizers like levosimendan, catecholamines, cardiac glycosides, and others. Negative inotropes include beta blockers, calcium channel blockers, and antiarrhythmics. The mechanisms and effects of various catecholamines like dopamine, dobutamine, epinephrine, and dopexamine are also outlined.
This presentation deals with the most common antihypertensive drugs used in our day-to-day practice. The common 4 ABCDs (Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers, diuretics)
Clinical use of ACEI and ARB in cardiovascular diseases.pptxJabbar Jasim
This document discusses antihypertensive medications including angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). It outlines their indications, mechanisms of action, dosing, cautions, contraindications and side effects. ACE inhibitors are first-line for heart failure, hypertension, diabetic nephropathy and post-MI. ARBs are an alternative for those who cannot tolerate ACE inhibitor side effects like cough. Both need monitoring in renal impairment and caution in renovascular disease.
This document provides information on hypertension (high blood pressure), including its types, classification, pathophysiology, diagnosis, and treatment. It discusses the mosaic theory of hypertension and factors involved in fluid volume regulation. It outlines the clinical presentation of hypertension and diagnostic evaluation. Finally, it provides details on non-pharmacological and pharmacological treatment approaches for hypertension, describing specific drug classes like diuretics, beta-blockers, ACE inhibitors, and others.
This document discusses antihypertensive drugs. It describes 7 classes of antihypertensive drugs: diuretics, beta blockers, calcium channel blockers, ACE inhibitors, ARBs, sympatholytics/alpha blockers, and direct vasodilators. It provides details on the types, mechanisms of action, advantages, indications, side effects and considerations for each class. It also discusses patient compliance with antihypertensive medications and strategies to improve compliance.
This document discusses mechanical ventilation and the weaning process. It outlines the 7 stages of weaning and indicators for readiness to wean, including parameters like respiratory rate, tidal volume, rapid shallow breathing index, and maximum inspiratory pressure. It describes methods for spontaneous breathing trials and criteria for weaning failure. Difficult weaning can be caused by respiratory, cardiac, psychological, ventilator or nutritional factors. Daily assessment is important to evaluate readiness and avoid complications from prolonged mechanical ventilation.
PC mode uses pressure control ventilation where the ventilator controls the inspiratory pressure and the patient controls the respiratory rate and inspiratory time. The tidal volume depends on the inspiratory pressure set, lung compliance, and airway resistance. Key settings include inspiratory pressure, respiratory rate, inspiratory time, and PEEP. Plateau pressure and driving pressure should be monitored to avoid overinflation and volutrauma. PEEP is used to prevent alveolar collapse and improve oxygenation but can impact hemodynamics at higher levels by decreasing venous return and cardiac output.
This document discusses nutrition guidelines for critically ill patients. It recommends starting enteral nutrition within 24-48 hours of admission to provide 25 kcal/kg/day and over 1.2 g/kg/day of protein. Enteral nutrition is preferred over parenteral nutrition when possible. Guidelines suggest not stopping nutrition without a definite medical cause and consulting nutrition support teams.
1. The patient is a 75-year-old male admitted to the EICU for septic shock due to pneumonia and colitis. He received TPN for nutrition support from admission until signs of bowel recovery were seen.
2. Enteral nutrition was started with 500 kcal/day of tube feeding once bowel sounds returned, but was reduced due to distension. IV fluids were given initially until TPN was started providing over 1300 kcal per day.
3. Laboratory findings and the patient's clinical status including hemodynamics, mottling, and ventilator settings are discussed to determine the adequacy and progression of nutrition support and management of septic shock. Further suggestions may be considered.
This document discusses different types of mechanical ventilation and ventilation modes. It begins by outlining four types of respiratory failure that may require mechanical ventilation. It then discusses goals of mechanical ventilation related to oxygenation and ventilation. The document goes on to explain various ventilation modes including volume control, pressure control, pressure support, and APRV. It provides details on settings for tidal volume, minute ventilation, and initial mechanical ventilation settings. Overall, the document provides an overview of mechanical ventilation types, goals, modes, and initial settings.
1. Mechanical ventilation settings like PEEP aim to reduce ventilator-induced lung injuries from atelectrauma and overdistension while improving oxygenation.
2. The optimal PEEP level can be determined through methods like the ARDSnet table, transpulmonary pressure measurements, lung compliance curves, and stress indexes. Higher PEEP recruits more alveoli but may affect hemodynamics.
3. Pressure-volume curves can help identify the lower inflection point and lower deflection point to guide PEEP setting, along with recruitment maneuvers. Slow-flow curves more accurately detect inflection points.
1. Mechanical ventilation can be associated with significant morbidity and mortality if prolonged. Weaning patients from mechanical ventilation in a timely manner is important.
2. There are seven stages of weaning which include assessing patient readiness, conducting spontaneous breathing trials, and using various ventilator modes like pressure support to gradually reduce support.
3. Spontaneous breathing trials for 30 minutes to 2 hours are generally preferred for weaning but gradual reduction over days may be better in some cases. Daily assessment of readiness and trials are recommended with prompt reintubation if trials fail.
1. Mechanical ventilation troubleshooting involves identifying the cause of a patient's sudden respiratory distress by analyzing monitor alarms, physical signs, and ventilator graphs.
2. Common causes include ventilator issues like leaks, circuit blocks, or setting errors as well as patient issues such as pneumonia or pneumothorax.
3. The document outlines steps for troubleshooting including disconnecting the patient to manually bag and assess response, then treating the most likely problem by procedures like suctioning, adjusting settings, or emergency thoracostomy.
This document provides an overview of electrolyte disorders including hypernatremia, hyponatremia, hyperkalemia, hypokalemia, and hyperglycemia. It discusses the etiology, clinical effects, and approaches to management. Specifically, it covers how these disorders disrupt osmotic balance and cell volume, outlines factors that influence electrolyte concentrations, and provides guidelines for treatment including shifting electrolytes between intra and extracellular compartments or removing excess amounts. The document compares US and European guidelines for hyponatremia and concludes by thanking the reader.
Cardiogenic shock is a serious condition where the heart cannot pump enough blood to vital organs, causing hypotension and end-organ damage. The most common cause is acute myocardial infarction with left ventricular dysfunction. In-hospital mortality from cardiogenic shock is high, around 27-51%. Treatment involves stabilization, vasopressor support, mechanical circulatory support if needed, and identifying and treating the underlying cardiac cause, such as through coronary angiography and PCI. Despite aggressive treatment, cardiogenic shock remains a medical emergency with high mortality.
1. The document discusses definitions of sepsis, severe sepsis, septic shock from 1992, 2001, and 2016. It describes the criteria for systemic inflammatory response syndrome, sepsis, and septic shock.
2. Guidelines for management of sepsis from the Surviving Sepsis Campaign are summarized, including early goal directed therapy, resuscitation bundles, and antimicrobial therapy recommendations.
3. Key aspects of the updated 2018 Surviving Sepsis Campaign guidelines are highlighted, such as initial fluid resuscitation, hemodynamic support, antimicrobial administration, and duration of therapy.
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This document provides an overview of acid-base principles and disorders. It discusses the normal ranges for pH, PCO2, and HCO3 and defines acid-base disorders. Primary acid-base disorders are classified as respiratory or metabolic based on changes in PCO2 or HCO3. Secondary responses to primary disorders and mixed acid-base disorders are also covered. Evaluation of acid-base disorders follows a stepwise approach identifying the primary disorder and any secondary responses. Metabolic acidosis is further evaluated using anion gap, delta gap, and urine anion gap. Causes and treatments of various acid-base disorders are outlined.
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The Fascinating World of Bats: Unveiling the Secrets of the Nightthomasard1122
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Bats, the mysterious creatures of the night, have long been a source of fascination and fear for humans. With their eerie squeaks and fluttering wings, they have captured our imagination and sparked our curiosity. Yet, beyond the myths and legends, bats are fascinating creatures that play a vital role in our ecosystem.
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2. Epidemiology
• AKI is common complication occurring up to 1/3 of ICU
patients and is usually a manifestation of multiorgan failure
syndrome.
• Sepsis is the one of the most common causes, and
postsurgical, toxic causes are also common.
• Increasing AKI severity is associated with increased mortality,
and AKI patients have worse renal function at the time of
hospital discharge.
12. Prevention and treatment
Volume expansion
1. We recommend controlled fluid resuscitation in volume depletion,
while, however, avoiding volume overload (Grade 1C).
2. We recommend against the use of starches (Grade1A) as harm
has been shown and suggest not using gelatine or dextrans for
fluid resuscitation (Grade 2C).
3. We recommend correction of hypovolemia/dehydration using
isotonic crystalloids in patients receiving intravascular contrast
media (Grade 1B).
4. We recommend regular monitoring of chloride levels and acid–
base status in situations where chloride-rich solutions are used
(BPS).
13. Prevention and treatment
Volume expansion
5. We suggest the use of balanced crystalloids for large volume
resuscitation (Grade 2C).
6. We suggest using human serum albumin if a colloid is deemed
necessary for the treatment of patients with septic shock (Grade
2C).
7. We suggest prophylactic volume expansion with crystalloids to
prevent AKI by certain drugs (specified below) (BPS).
8. We suggest not delaying urgent contrast-enhanced investigations
or interventions for potential preventative measures (BPS).
14. Prevention and treatment
Diuretics
1. We recommend against loop diuretics given solely for the prevention of
acute kidney injury (Grade 1B).
2. We suggest using diuretics to control or avoid fluid overload in patients
that are diuretic-responsive (Grade 2D).
Loop diuretics
• Theoretical effect
• Inhibition of active Na transport reduces tubular O2 consumption decrease ischemic
injury (protection)
• Washing out necrotic debris blocking tubules, inhibiting PG dehydrogenase
reduce renovascular resistance, increase renal blood flow
• Evidence
• No evidence that the use of diuretics reduces the incidence or severity of AKI.
15.
16. Prevention and treatment
Vasopressor
1. We recommend titrating vasopressors to a mean arterial pressure (MAP)
of 65–70 mmHg (Grade 1B) rather than a higher MAP target (80–85
mmHg) in patients with septic shock. However, for patients with chronic
hypertension we recommend aiming for a higher target (80–85 mmHg)
for renal protection in septic shock (Grade 1C).
2. We recommend lowering systolic pressure to 140–190 mmHg rather
than to 110–139 mmHg in patients with acute cerebral hemorrhage with
severe admission hypertension (Grade 1C).
3. If vasopressors are needed for treatment of hypotension, we recommend
norepinephrine (along with correction of hypovolemia) as the first-choice
vasopressor to protect kidney function (Grade 1B) and suggest
vasopressin in patients with vasoplegic shock after cardiac surgery
(Grade 2C).
4. We suggest individualizing target pressure when premorbid blood
pressure is available (BPS).
17. Prevention and treatment
Vasodilator
1. We recommend against low-dose dopamine for protection against AKI
(Grade 1A).
2. We recommend not using levosimendan for renal protection in patients
with sepsis (Grade 1B) and recommend against its use for renal
protection in cardiac surgery patients with poor preoperative left
ventricular function or needing postoperative hemodynamic support
(Grade 1B).
3. We suggest not using fenoldopam or natriuretic peptides for renal
protection in critically ill or cardiovascular surgery patients at risk of AKI
(Grade 2B).
18. Prevention and treatment
Sedation
1. On the basis of current data no recommendation can be given, although
it appears that shorter sedation using propofol or dexmedetomidine may
have several advantages, possibly reducing the rate of AKI. (BPS)
Hormonal manipulation
1. We suggest targeting a blood glucose level at least below 180 mg/dL for
the prevention of hyperglycemic kidney damage in the general ICU
population (Grade 2B).
2. We suggest not using erythropoietin (Grade 2B) or steroids (Grade 2B)
for prevention of acute kidney injury.
19. Prevention and treatment
Metabolic intervention
1. We recommend not using high-dose IV selenium for renal protection in critically
ill patients (1B).
2. We suggest not using N-acetylcysteine to prevent contrast-associated AKI in
critically ill patients because of conflicting results and possible adverse effects
(Grade 2B).
3. We suggest that all patients with or at risk of acute kidney injury have adequate
nutritional support preferably through the enteral route (BPS).
Statin
1. We recommend against the perioperative use of high dose statins to prevent
postoperative AKI in cardiac surgery (Grade 1A).
2. We suggest the short-term use of atorvastatin or rosuvastatin to prevent
contrast-associated AKI in high-risk patients undergoing coronary contrast
angiography (Grade 2B)
21. reference
• Jean-Lous Vincent, Textbook of critical care, 7th edition, Elsevier
• Michael Joannidis, Prevention of acute kidney injury
and protection of renal function in the intensive care unit: update 2017,
intensive care Med., 2017
• KDIGO-2012- AKI guideline
• Eric AJ Hoste, Epidemiology of acute kidney injury in critically ill
patients: the multinational AKI-EPI study, intensive care Med., 2015
Editor's Notes
AKI abrupt GFR 감소로 따른 nitrogen waste 의 retention 및 body fluid/electrolyte의 dysregulation 을 말함.
RIFLE crteria는 (ADQI acute dialysis quality initiative 에서 제안) 은 7일이내 baseline에서 Scr 이 50%이상 증가했을 때로 정의하고
Hospital mortality에 근거하여 Scr/GFR의 7일이내 base line 변화 정도에 따라 RIFLE 로 나누었음.
AKIN (AKI network) 에서는 RIFLE이 small Cr change 를 놓칠 수 있어 이를 보완하기 위해 제안된 기준으로
Scr 절대값 증가 (0. 3이상)를 넣음으로써 개정. RIFLE과 다른 점이 시간은 48시간 이내
KDIGO는 AKIN + RIFLE 두가지를 합하여서 48이내 0.3 이상 증가 혹은 7일 이내 50% 이상 증가로 정의.
UO 으로는 6시간동안 kg당 0.5cc미만.
유효순환용적의 regulatio을 담당하는 RAAS
안지오텐시노겐 이 간에서 분비 -> kidney에서 renal perfusion이 떨어지면 레닌이 분비되는데,
안지오텐시노겐이 AT1으로 전환, 폐에서 분비되는 ACE에 의해 ATII로 전환됨.
ATII는 tubular Na, Cl 재흡수시키고, K 분비 촉진, 물 retention
cortex aldosterone ->
소동맥 vasoconstriction 시켜 BP 높임.
pituitary gland 에서 ADH 분비, 물 재흡수
결국은 물, salt를 retention시켜 유효순환용적을 증가 시키고 , renin 분비에 negative feedback을 준다.
Prerenal AKI는 cell injury없이 renal perfusion이 감소해서 생기게되고
그 원인으로는 dehydration, hemorrhag로 인한 blood volume 감소나/ HF,LC와 같이 유효순환용적이 감소해서 발생할수 있다.
Prerenal cause에 의한 AKI발생시 RAAS 가 활성화되어 유효순환용적을 늘리는 역할을 함.
치료는 underlying cause교정으로 volume replacement 나 offending agent (RAAS inhibitor ) 를 끊는 것임.
Post renal cause는 urine flow가 막혀서 intratubular P가 증가함으로써 GFR이 떨어지게되어 발생한다.
그원인 중에서도 prostatic dz나 pelvic malig에 의한 obstrction인 extrarenal 가 있고
crystal depostion에 의한 intrarenal cause가 있음.
그원인으로는 tumor lysis syn. EG 섭취에 의한 uric acid생성 이나 MM같은 light chain dz에 의한 cast formatio에 의할수 있음.
신장 초음파를 통해서 진단할수 있음.
신장자체 문제 의한 Intrarenal cause로는 anatom에 따라 G,V,I,T 로 나뉘고
GN,Vasculitis 는 특징적으로 Urine redcell sediment 검출
Interstitial nephritis의 경우 WBC 가 있으며서 RBC가 있을수도 있고 없을수도 있다. NSAID/anti -> 약제 끊고 PD short term사용
ATN 이 가장 흔함.
hemodynamic ustablity에 의한 ATN은 지속되는 prerenal azotemia, hypoT, sepsis에 발생.
Toxin 약제 contrast media에 의해 발생.
Sepsis induced AKI는 그 메커니즘이 온전히 밝혀지지 않았는데, 이전에는 renal global ischemia에 의한 macro-circulatio의 문제로 생각되었으나
최근에는 Hypoperfusion이 없는 상태에서 AKI진행이 된다는 evidence들이 밝혀지고 있어,
micro-circulation dysfunction, inflammation, injury에 의한 adaptive bioenergetics 에 의한 것으로 생각
ATN 과 prerenal azotemia 의 구분 : index 들을 통하여
ATN에서 tubule 기능이 망가져 Na 재흡수가 제대로 이루어지 않고, Urine Nz이 40 이상, FENA 2% 이상 + 소변 농축 기능도 망가져 Osm 350미만
하지만 rhabdo- 나 contrast mediated AKI, sepsi에서도 FENA 낮게 나올 수 있다.
이뇨제 복용중인 환자에서 Prerenal azotemia 는 FENA 는 영향을 받기 때문에 FE urea 혹은 urine to plasma Cr 을 확인한다.
-> FE urea<35%, u/p Cr >15 일시 prerenal 일 가능성 높음. 하지만 FE urea도 specificity 낮다
CIN ; toxic effect로 ATN 도 일으키지만 renal vasoconstriction을 일으켜 medullary ischemia일으킴.
AKI 를 감시하여 early intervention 및 monitoring 을 할수 있게 하는 biomarker들이 있다.
Cystatic C는 GFR change를 반영하는 반면, NGAL은 tubular stress or injury 와 관계.
IL-18, L-FABP KIM-1 도 존재
2017년 intensive care medicine에 서 발표한 Prevention of acute kidney injury and protection of renal function in the intensive care unit: update
Volume depletion이 의심되는 환자는 volume overload에 유의하여 fluid resuscitation 을 하고 starch는 피한다.
Contrast media 사용시에는 hypovolemia를 cystalloid 로 교정한다.
Euvolemic 환자에서 prophylactive volume expansion은 권장되지 않는다.
Fluid resuscitation시에는 acid-base 및 Cl 레벨은 모니터링한다.
Crystalloid를 줄 때에는 balanced crystalloid를 주는 것으로 제안한다.
NS만 주었을 때 balanced sln에 비해서 AKI risk 및 RRT, mortality 증가 한다는 observation study가 있었으며,
Serum alubmin은 colloid가 필요한 septic shock환자에서 줄수 있다.
20% 알부민이 AKI/ need for RRT in severe sepsis 에는 큰 효과가 없으나 postivie fluid balanc를 줄이는데 효과 가 있게 나온 연구 있음.
Hypovolemia가 drug induced renal injury를 악화 시킬수 있기 때문에 AKI유발할수 있는 약물 (예를 들면 amphotericin B나 antivirals) 을 줄 때에는 prophylactic 하게 volume expansion을 시행한다.
contrast사용한 검사나 시술은 urgent한 경우에는 예방을하느라 늦추지 말라.
BPS는 grade는 없는 best practice statements (BPSs),
Loop diuretics는 prevention을 위해서 쓰면 안되며 이뇨제는 fluid 이뇨제에 반응이 있는 overload시에만 사용하도록 제안한다.
최근 연구에서는 oliguric환자에서 test dose Lasix 1-1.5mg/kg 에 시간당 100cc이상의 UO을 보이면 higher stage AKI로 진행하는 것이 감소함을 예측할수 있다고 한다.
-----
이론적으로는
Loop diuretics 는 Na transporter를 inhibition해서 산소 요구량을 낮춤으로 신장의 허혈손상을 막아 신장을 보호할수 있고
Necrotic debris를 wash out하고 PG Dehydrogenas를 억제하여 renal blood flow를 증가 시킴.
그러나 이것에 대한 뒷받침하는 data부족하다. Diureteics가 AKI 발생/중증도를 줄인다는 evidence가 없다.
2020 critical care에서 발표한 연구에서는
Furosemide의 AKI management outcome을 밝힌바 있는데
ICU의 14154 AKI 환자들을 propensity score에 따라 matching 해서 (이뇨제를 전혀투여 안받은군)/ (furosemide 를 투여받은군) 으로 나누어 4427 pairs of patients 를 LOS, renal functio회복, 90일 mortatliy 를 비교했고
Furosemide를 사용한 군에서 short term survival/ renal function 향상됨.
하지만 이런 결과들은 AKI U/O 기반한 stage 0-1 이나, Scr 기반 stage 2-3 인경우는 관련이 없었다.
따라서 … 특히 U/O stage 2-3 oliguria가 있는 환자에서 더 효과가 가 있으며, CKD환자나 cr 에 근거한 stage 2-3 환자는 효과가 없다.
Renal perfusion을 유지하기 위해서는 이론적으로 fluid resuscitatio이나 inotropics를 통해서 Cardiac output을 어느정도는 유지를 해야 함
승압제는 MAP 65-70 사이로 유지하는 것을 권장하며, 고혈압 환자에서는 high targe 80-85 사이를 유지한다.
뇌출혈 환자에서는 140-90 사이의 systolic pressure를 낮추는 것으로 권장하며
저혈압이 있는 경우 hypovolemia를 교정하면서 NE를 1st 초이스로 사용하여 kidney를 보호하며, vasopression은 cardiac surgery 후 vasoplegic shock환자에서 사용한다.
Large RCT 에서 NE 와 dopamine 의 mortalit차이가 없다고 되어 있으나 NE 가 첫1시간동안 tachycardia 를 덜 유발하고, cardiogenic shock환자에서는 survival에서 우위에 있고, RRT free day가 더 긴것으로 확인되었다.
Vasopression은 NE refractory shock에 쓸수 있고 post glomerular vas constriction을 기켜 GFR를 증가 시킬수있는 것으로 알려져 있으나, largest RRT in septic shock 연구에서 RRT free day에 특별히 영향을 주지 않으며, mortality향상도 전체 populatio이 아닌 subgroup에서 보였다고 함.
환자에 따라서 target pressure를 다르게 조정할수 있다.
Renal blood flow는 sympathetic stimulatio에 의해서 안지오텐신2 나 엔도텔린, vasocontrictive PG에 의해 vasocontriction이 일어나 줄어들게 된다.
Renal protectio을 위해 Vasodilater를 사용했을 때 몇가지 생각해볼점이 있는데 첫째는 hypotension을 유발하기 때문에 renal perfusion이 compromising 될수 있고, timing 역시 중요할수 있는
지연된 투여는 microcircuation이 이미 occlusion된 상태여서 effect가 적을수 있다.
AKI protection을 위해 저용량 도파민을 권장하지 않는다.
levosimendan (HF에 쓰이는 Ca sensitizer, inodilator, cardiopretective) 의 사용하지 않을 것으로 권장하며,
Fenoldopam 및 natriuretic peptide로 AKI risk있는 환자에서 사용하지 않는다.
renal dose dopamine이 selective renal vasocontricton을 예방한다고 알려져 이전에는 쓰엿으나 여러 meta analysis에서 renal dose dopaime이 AKI예방에 benefi이 없다고 결론지었따.
Fenoldopam 은 puredopamine A1 receptor agonist 로 systemic, renal vasodilation 하는 역할을 하였고 이전 연구에서는 AKI incidence를 낮추는 것으로 알려져 있었으나
최근 meta analysis 연구에서 cardiac/major surgery 시행한 AKI 위험은 낮추지만 RRT 나 사먕률을 낮추지는 하는 것으로 밝혀졌고,
또 post cardiac surgery에서는 renal protection기능이 없으면서 hypotension 유발 한다고 하였음.
Atrial natriuretic peptide는 atricum stretch/pressur에 의해 증가해서 renal afferent dilation/efferenct vasconstriction시켜서 GFR를 높이는것으로 알려져 있으나
최근 연구에서 prlphylactic low dose ANP 가 post op 의 peak Cr과 RRT need를 줄이는것으로 알려졌으나 case가 작고 AKI가 생긴 이후에는 effect가 없으며 high dose에서는 부정맥이나 저혈압등의 adverse effect가 빈번하게 일어났다.
Recommendation은 아니지만 propofol이나 dexmedetomidine과 같은 약물이 AKI를 줄일수 있다고 함.
Propofol은 신장에서 Oxidative stress 를 줄이고 dexmedetomidein은 vasopression분비를 줄여 diuresis를 유도하여 renal blood flow를 증가 시킬수 있는 것으로 알려져 있다.
혈당은 hyperglycemic kidney damage를 예방하기 위해 180미만으로 유지하고 EPO 나 steroi를 AKI예방을 위해 사용하지 않는다.
고혈당이 oxidative stress유발하고, 혈관과 면역학적 기능부전을 유도한다.
Steroid의 antiinflammatry effec가 AKI pathogenesis중 inflammatory componen를 억제하고 EPO는 apoptosis 및 inflammation 를 줄여 tissue regeneration을 촉진하는 것으로 알려져 있으나
AKI incindence를 줄이는데 효과는 없는 것으로 알려졌다.
Iv selenium을 AKI 보호를 위해 쓰지 않는 것을 권유한다.
NAC 을 CIN를 위해 사용하지 않는다. 왜냐하면 result 가 상충되는 것들이 있고, adverse effect가 있기 때문에 (allergic rxn 및 cardiac output 감소등)
장관을 통하여 nutiritional support하는 것을 모든 환자에서 권장.
Starvation은 신장에서 단백질 합성을 방해하고 분해를 일으켜 단백질 및 아미노산 투여하는 것은 신기능 향상시키지만 . Early parenteral nutritio은 urea level을 높여 RRT duration을 늘릴수 있음.
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Statin 은 antioxidant및 anti-inflammatory, antithrombotic effec가 있어 : 심장 수술 후 AKI를 방지하기 위해 statin쓰는 것으로 권장하며
coronary angiography 전에 contras에 의한 AKI high risk 환자에서 atorvastatin, rosu를 쓰는 것으로 제안.
Renal recovery를 기대하기 때문에 RRT 시기를 늦추는 경우가 많고 RRT 를 시작하는 적절한 시기는 정의된바 없다.
Prospective multicenter ICU cohort study