Acute kidney injury etc... Flashcards
Renal Function
Normal Renal Function
THE KIDNEY IS NOT JUST A FILTER
REGULATION, REMOVAL, HORMONAL
Anatomy
Kidney
Nephrons
Renal vein & renal artery
Ureters
Bladder
Urethra
Renal Function
Think uric the c or k as in makla and acid as in lemons or oranges
- Fluid balance (absorbs/reabsorbs water)
- BP control (renin
- Acid/base (hydrogen (H+) and bicarbonate (HCO3)
- Electrolyte balance (sodium, potassium, calcium & phosphorus)
- Removal of wastes (urea which is a waste product of proteins, metabolites, toxins, uric acid which is a waste product of food)
- Erythropoietin (promotes the formation of RBCs in the bone marrow)
- Vitamin D (activation)
Nephron Anatomy
Functional Unit
1-2 million in each kidney
Glomerulus within Bowman’s capsule
**Afferent arteriole –caries blood to the glomerulus to get filtered.
**Efferent arteriole – carries blood from the glomerulus
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Collecting duct
Renal Vasculature
The renal vasculature is responsible for supplying the kidneys with oxygen and nutrients to support their function. The kidneys receive a large percentage of cardiac output, about 20-25%, despite only comprising about 0.5% of the body’s total weight.
Renal blood flow (RBF) is about 1200 mL/min and is maintained by an intricate network of vessels that include the renal artery, interlobar arteries, arcuate arteries, and afferent and efferent arterioles that supply and drain the glomerulus, respectively. Capillaries surround all parts of the nephron, allowing for efficient exchange of solutes and fluids.
The afferent arteriole brings blood to the glomerulus, where it is filtered to form urine. The efferent arteriole then drains the glomerulus and supplies blood to the peritubular capillaries, which surround the renal tubules and allow for reabsorption and secretion of solutes.
Autoregulation of renal blood flow helps maintain a constant flow of blood to the kidneys despite changes in systemic blood pressure. The kidneys can increase or decrease resistance in the afferent and efferent arterioles to maintain perfusion pressure within a certain range. In particular, diastolic perfusion pressure (DPP), mean arterial pressure (MAP), and central venous pressure (CVP) are important parameters for maintaining renal perfusion and preventing acute kidney injury (AKI).
A decrease in DPP has been associated with an increased risk of AKI, while changes in MAP alone may not accurately reflect the risk of renal injury. Therefore, it is important to monitor and maintain adequate perfusion pressure to ensure proper kidney function.
Read slide 7 `
Monitoring Renal Function
Lab values:
Blood Urea Nitrogen (BUN) - BUN is a waste product generated from protein metabolism, which is filtered by the kidneys and excreted in urine. Elevated BUN levels can indicate hepatic or renal impairment, dehydration, high protein diet, infection, steroid use, GI bleed. Decreased BUN levels can indicate malnutrition, fluid volume excess, or severe hepatic damage.
Creatinine (Cr) - Creatinine is a waste product generated from muscle metabolism, which is also filtered by the kidneys and excreted in urine. Elevated creatinine levels can indicate chronic kidney disease (CKD), kidney obstruction, intense exercise, low muscle mass, pregnancy, or certain medications like cimetidine, trimethoprim-sulfamethoxasole (Bactrim), corticosteroids, vitamin D metabolites, salicylates, phenacemide, pyrimethamine. Creatinine levels are slightly higher in males than females due to their higher muscle mass.
BUN/Cr ratio - The BUN/Cr ratio is the ratio of BUN to creatinine levels in the blood. An increased ratio can indicate fluid deficit or hypoperfusion of the kidneys, while a decreased ratio can indicate fluid volume excess or malnutrition.
Glomerular Filtration Rate (GFR) - GFR is a measure of the amount of blood filtered by the kidneys per minute. It is considered the best indicator of renal function and is used to stage CKD. GFR can be estimated using equations based on serum creatinine, age, sex, and race.
Specific Gravity - Specific gravity is a measure of the concentration of solutes in urine, indicating the ability of the kidneys to concentrate urine. Low specific gravity can indicate diabetes insipidus or renal disease, while high specific gravity can indicate dehydration.
Urinalysis - Urinalysis involves a physical and chemical examination of urine, which can provide information about renal function and the presence of various conditions such as urinary tract infections, kidney stones, and proteinuria. The test may include evaluating the appearance, pH, glucose, protein, ketones, bilirubin, urobilinogen, leukocytes, nitrites, and microscopic examination of cells and casts in the urine.
Glomerular Filtration Rate (GFR)
-Normal GFR (glomerular filtration rate) is the amount of blood that is filtered by the glomeruli (tiny blood vessels in the kidneys) per minute. It is typically estimated based on the level of creatinine in the blood, and a GFR of 100-125 ml/min is considered within the normal range for healthy adults.
Creatinine clearance (CrCl) is a measure of how efficiently the kidneys are able to remove creatinine from the blood. It is often used as an estimate of GFR.
As people age, their GFR gradually decreases, typically by around 1 cc/min/year after the age of 40. This can be due to various factors, including changes in blood flow to the kidneys and a reduction in the number of functioning nephrons (the basic filtering units in the kidneys).
If there is an abrupt decrease in GFR, there may be a corresponding increase in creatinine levels in the blood, since the kidneys are less able to clear it from the body. Creatinine is a waste product produced by the muscles that is filtered out of the blood by the kidneys.
In contrast, if the decrease in GFR is gradual, there may be little change in creatinine levels, since the kidneys are able to compensate and maintain relatively stable levels of creatinine clearance.
It is true that around 40% of people with decreased GFR may have a serum creatinine within the normal range, since the kidneys are able to maintain relatively stable creatinine levels even as GFR declines. However, other markers of kidney function may be abnormal in these cases, such as albuminuria (an excess of protein in the urine).
Urinalysis
Color: This refers to the color of the urine, which can vary from pale yellow to dark amber. Urine color can be affected by a variety of factors, including hydration status, diet, medications, and medical conditions.
Clarity: This refers to the transparency of the urine, which can range from clear to cloudy. Cloudy urine may be a sign of infection or the presence of crystals or other particles in the urine.
Sediment: This refers to the solid particles or material that may be present in the urine, such as cells, bacteria, crystals, or mucus. The presence of sediment may indicate an underlying medical condition.
Specific gravity: This measures the concentration of particles in the urine and reflects the kidney’s ability to regulate the water balance in the body. A low specific gravity may indicate kidney dysfunction or overhydration, while a high specific gravity may indicate dehydration or a problem with the kidney’s ability to concentrate urine.
pH: This measures the acidity or alkalinity of the urine. Normal urine pH ranges from 4.5 to 8.0. Abnormal pH levels may be an indicator of certain medical conditions or dietary habits.
Bacteria and leukocytes: These are markers of a possible urinary tract infection or inflammation.
Protein: This measures the amount of protein present in the urine. The presence of protein in the urine may be a sign of kidney damage or other medical conditions.
Ketones: This measures the presence of ketones in the urine, which may be an indicator of diabetes or other metabolic disorders.
Glucose: This measures the amount of glucose present in the urine, which may be an indicator of diabetes or other metabolic disorders.
Nitrites: This measures the presence of nitrites in the urine, which may be a sign of a urinary tract infection.
Bilirubin/urobilinogen: These are markers of liver function and may be elevated in the presence of liver disease or other medical conditions.
Toxins: A urinalysis does not usually include a direct measurement of toxins in the urine. However, some drugs or other substances may be detected in the urine as part of a drug screening or toxicology analysis.
Affects of Aging on the Renal system
Loss of skeletal muscle mass: The loss of muscle mass that occurs with aging is in proportion to the loss of glomerular filtration rate (GFR), so serum creatinine levels don’t change much. This can make it difficult to detect early kidney disease in older adults.
Loss of renal mass: As a person ages, there is a gradual loss of renal mass, which can affect the kidney’s ability to filter and excrete waste products. The reduction in renal mass is most profound in the renal cortex.
Changes in nephrons: The number of nephrons in the kidney decreases with age, which can lead to a decrease in renal function. Additionally, the remaining nephrons may undergo hypertrophy and hyperfiltration, which can lead to glomerular sclerosis.
Changes in hormonal regulation: The renin-angiotensin-aldosterone system (RAAS) becomes less efficient with age, leading to a decrease in renin and aldosterone production. This can affect blood pressure regulation and electrolyte balance.
Changes in bladder function: Aging can also affect bladder function, leading to urinary incontinence, retention, or frequency. In women, cystoceles (prolapse of the bladder into the vagina) may occur due to weakened pelvic muscles. In men, benign prostatic hyperplasia (BPH) can cause urinary retention, but androgen deprivation therapy can slow the progression of chronic kidney disease (CKD) associated with BPH.
Other factors: Other factors that can affect the renal system with aging include decreased cardiac output, hypertension, decreased thirst sensation, and changes in medication metabolism.
Overall, these changes can lead to a decreased ability to regulate fluid and electrolyte balance, excrete waste products, and maintain acid-base balance, which can increase the risk of kidney disease and other health problems in older adults.
Declining Renal Function
Renal function decline is a continuum that can progress from renal insufficiency to acute kidney injury, chronic renal failure, and end-stage renal disease. In renal insufficiency, the kidneys can still function to some degree, but nephrons compensate, and toxins may accumulate, leading to symptoms such as nocturia, polyuria, anorexia, nausea/vomiting, weakness, fatigue, and mild anemia. The BUN rises, and creatinine (Cr) is less than 2, and the glomerular filtration rate (GFR) decreases. Without intervention, renal insufficiency may progress to renal failure.
Acute kidney injury (AKI) is a sudden decline in renal function, often due to a decrease in blood flow to the kidneys or damage to the kidneys themselves. AKI can lead to a sudden rise in BUN and Cr, and a decrease in GFR. It can also cause oliguria (low urine output), volume retention, and hypertension. Treatment for AKI often involves addressing the underlying cause, such as fluid and electrolyte imbalances, and sometimes requires renal replacement therapy.
Chronic renal failure (CRF) occurs when the kidneys can no longer meet the body’s demands for waste removal and fluid and electrolyte balance. In the early stages of CRF, there may be an increase in urine output (polyuria), but the quality of the urine may be poor. As CRF progresses, the BUN increases with Cr greater than 5, and GFR continues to decrease. This can lead to oliguria (low urine output) or anuria (no urine output), volume retention, and hypertension. Other symptoms of CRF can include azotemia (an excess of nitrogenous waste products in the blood), acidosis (a buildup of acid in the body), anemia (a deficiency of red blood cells), and imbalances in electrolytes such as potassium, sodium, and calcium.
End-stage renal disease (ESRD) is the final stage of renal failure, where the kidneys have permanently failed, and dialysis or kidney transplant is necessary to sustain life. In ESRD, there is a severe elevation in BUN and Cr, with a GFR less than 15. There may also be imbalances in electrolytes such as high potassium, sodium, and phosphate levels, and low calcium levels, as well as acidosis. In addition to the renal symptoms, ESRD can cause systemic impairments, such as uremic syndrome, which can affect multiple organ systems in the body.
Kidney Disease Stages
Kidney disease is divided into 5 stages, based on filtration
Manifestations of impaired kidney function are not often seen until GFR is < 50%
Acute Kidney Injury (AKI)
AKI (Acute Kidney Injury) is a sudden and rapid decrease in kidney function, characterized by an abrupt decline in glomerular filtration rate (GFR). The etiology of AKI can be prerenal, intrarenal or postrenal. Prerenal causes include systemic hypoperfusion resulting from conditions such as hypovolemia, hypotension or sepsis. In response to systemic hypoperfusion, the renin-angiotensin-aldosterone system (RAAS), antidiuretic hormone (ADH) and sympathetic nervous system (SNS) are activated to increase vascular tone and reabsorption of sodium and water. However, this time-limited response can result in ischemia and infarction of nephrons if systemic pressures continue to fall. If the decrease in GFR persists, acute tubular necrosis (ATN) may develop.
The most common cause of AKI is prerenal volume depletion from loss of body fluids. Other causes of AKI include acute glomerulonephritis, acute interstitial nephritis, acute tubular necrosis, post-renal obstruction, and drug-induced nephrotoxicity. AKI can progress to chronic kidney disease (CKD) if not managed properly. The mortality rate for AKI with RRT (renal replacement therapy) can be as high as 50%.
AKI
Usually starts by oliguria but now always and marked increase in BUN & Cr and/or azotemia
The term “azotemia” refers to an accumulation of nitrogen-containing waste products in the blood that are normally excreted by the kidneys. In the context of AKI, azotemia is often used as a synonym for an increase in blood urea nitrogen (BUN) levels.
AKI: S & Sx
Increased BUN and Cr: As the kidney function decreases, the BUN and Cr levels in the blood will increase.
Decreased GFR: GFR is a measure of the rate at which blood is filtered by the kidneys. In AKI, the GFR will decrease.
Increased specific gravity or fixed: In AKI, the urine specific gravity may be increased or fixed at 1.010 despite fluid intake. The specific gravity of normal urine ranges from 1.002 to 1.035, with higher values indicating more concentrated urine. A fixed specific gravity of 1.010 despite fluid intake may indicate a problem with the kidneys’ ability to concentrate urine, which can be seen in conditions such as AKI or chronic kidney disease.
Anemia: AKI can cause a decrease in the production of erythropoietin, which can lead to anemia.
HTN and CHF: AKI can lead to the retention of fluid and electrolytes, which can cause hypertension and congestive heart failure.
A,N,V: AKI can cause symptoms of nausea, vomiting, and abdominal pain.
Puritis: AKI can cause itching due to the buildup of uremic toxins in the bloodstream.
AKI Acid-base, fluid & electrolytes, toxins
pH depends on number of functioning nephrons
Metabolic acidosis. it’s called metabolic because the problem is in the kidneys and their lack of production of bicarbonate. It’s not a lungs problem..
pH of the blood becomes more acidic than normal (less than 7.35). The severity of metabolic acidosis depends on the number of functioning nephrons, as the kidneys are responsible for regulating acid-base balance in the body.
Categories of Renal Injury
Prerenal injury:
Prerenal injury is caused by decreased blood flow to the kidneys, which leads to reduced renal perfusion and ischemia. This can happen due to various conditions such as hypovolemia, sepsis, hypotension, heart failure, liver failure, and renal artery stenosis. The decreased blood flow causes a reduction in filtration pressure, because less fluid means less pressure in the hose and eventually, glomerular filtration pressure falls. However, no structural damage to the kidney has yet occurred, and the condition is reversible. If not addressed, prerenal injury can progress to acute kidney injury (AKI). (One of the primary mechanisms is the reduction in effective circulating volume. People with advanced liver disease often have a reduced effective circulating volume due to increased vasodilation, increased capillary permeability, and decreased plasma oncotic pressure. This can lead to a reduction in renal perfusion pressure, which can cause renal vasoconstriction, reduced glomerular filtration rate (GFR), and eventually AKI.)
Intrinsic renal injury:
Intrinsic renal injury, also called intrarenal injury, is caused by problems within the renal tissue itself. This can result from a wide range of conditions such as ischemia, toxins, infections, autoimmune disorders, and genetic disorders. Intrinsic renal injury is categorized based on the primary site of injury, which includes acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vascular damage. ATN, one of the most common causes of intrinsic renal injury, is characterized by the death of renal tubular epithelial cells due to ischemia, toxins, or sepsis. Nephrotoxicity, another cause of intrinsic renal injury, can be caused by medications like aminoglycosides, contrast media, and non-steroidal anti-inflammatory drugs (NSAIDs). Rhabdomyolysis, a condition that occurs when muscle tissue breaks down and releases toxic substances, can also cause intrinsic renal injury. Hepatorenal syndrome, a complication of liver cirrhosis, is another cause of intrinsic renal injury.
Postrenal injury:
Postrenal injury occurs when there is obstruction in the urinary outflow tract, which prevents the urine from leaving the kidneys. This can be caused by mechanical or functional issues, such as tumors, kidney stones, benign prostatic hyperplasia (BPH), and urethral strictures. The obstruction can lead to an increase in pressure within the renal system, causing damage to the kidney’s tissues and impairing renal function. The severity of the injury depends on the duration and degree of obstruction.
It is essential to identify the type of renal injury accurately to initiate appropriate treatment and prevent further damage. Diagnostic tests like urine tests, blood tests, and imaging studies can help identify the underlying cause of renal injury. Treatment may include addressing the underlying cause, providing supportive care, and in severe cases, renal replacement therapy may be needed.
Causes of AKI slide 19
The list you provided outlines various causes and types of acute kidney injury (AKI). Here is a brief explanation of each:
Intrinsic AKI: This refers to damage to the kidney tissue itself, such as the glomeruli, tubules, or interstitium. Causes include ischemia, nephrotoxins (both exogenous and endogenous), infections, and systemic conditions like vasculitis and malignant hypertension.
Prerenal AKI: This is caused by a decrease in blood flow to the kidneys, which can be due to hypovolemia (low blood volume), decreased cardiac output, congestive heart failure, liver failure, or impaired renal autoregulation.
Postrenal AKI: This occurs when there is an obstruction of urine flow out of the kidneys or bladder. Causes include bladder outlet obstruction, bilateral pelvoureteral obstruction, or unilateral obstruction of a solitary functioning kidney.
Some specific examples of AKI causes listed in your statement are:
NSAIDs (nonsteroidal anti-inflammatory drugs) and ACE-I/ARB (angiotensin converting enzyme inhibitors/angiotensin receptor blockers) can cause prerenal AKI by affecting renal blood flow and vasoconstriction.
Cyclosporine, a medication used to prevent transplant rejection, can cause intrinsic AKI by damaging the renal tubules.
Hemolysis (the breakdown of red blood cells), rhabdomyolysis (the breakdown of muscle tissue), and intratubular crystals can all cause intrinsic AKI by obstructing or damaging the renal tubules.
Prerenal Causes of AKI
Prerenal causes of acute kidney injury (AKI) refer to conditions that lead to a decrease in renal blood flow, which subsequently results in a reduction in glomerular filtration rate (GFR) and impaired kidney function. These causes are typically reversible if promptly identified and managed. Common prerenal causes of AKI include:
Reduced effective circulating volume (ECV): This can result from volume depletion due to factors such as dehydration, diuretic use, third-spacing (i.e. fluid accumulation in body cavities or interstitial spaces), blood loss or gastrointestinal losses such as vomiting or diarrhea.
Cardiovascular causes: Conditions that affect cardiac output or blood pressure can lead to prerenal AKI. These may include myocardial infarction (MI), heart failure (HF), cardiac tamponade, tension pneumothorax, cardiac dysrhythmia, valve dysfunction or abdominal aortic aneurysm (AAA).
Shock states and sepsis: In conditions such as sepsis, the body’s inflammatory response can lead to decreased blood flow to the kidneys, resulting in prerenal AKI.
Obstructed renal blood flow: Any condition that obstructs blood flow to the kidneys, such as renal artery stenosis or thrombosis or obstruction of the inferior vena cava, can result in prerenal AKI.
Medications: Certain medications can cause prerenal AKI by affecting blood flow to the kidneys. These may include drugs that lower blood pressure, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and nonsteroidal anti-inflammatory drugs (NSAIDs).
Causes of Renal Hypoperfusion
When PVR is increased, the resistance to blood flow in the peripheral blood vessels is higher. This means that the heart has to work harder to pump blood through the vessels, and there is a decrease in blood flow to the organs and tissues of the body. This can lead to a decrease in perfusion, which can cause ischemia (a lack of oxygen) in the affected organs and tissues.
In the kidneys, decreased perfusion due to increased PVR can lead to renal hypoperfusion, which can cause kidney damage or failure over time. Conditions that increase PVR, such as sepsis, hepatorenal syndrome, drug overdose, and the use of vasodilators, can all lead to renal hypoperfusion.
Therefore, it is important to identify and treat the underlying cause of increased PVR to prevent damage to the organs and tissues of the body due to decreased perfusion. Treatment may involve medications to reduce PVR (such as vasodilators), or addressing the underlying condition that is causing the increased PVR.
Intrarenal Causes of AKI
Interstitial nephritis: Inflammation of the kidney’s interstitial tissue can cause AKI. Causes of interstitial nephritis include drug reactions (e.g., antibiotics, NSAIDs), infections (e.g., pyelonephritis), and autoimmune diseases (e.g., lupus).
Glomerulonephritis: Inflammation of the glomeruli (the kidney’s filtering units) can cause AKI. Causes of glomerulonephritis include infections (e.g., streptococcal), autoimmune diseases (e.g., lupus), and certain medications.
Vasculitis: Inflammation of the blood vessels in the kidney can cause AKI. Causes of vasculitis include autoimmune diseases (e.g., lupus), infections (e.g., hepatitis B and C), and certain medications.
Nephrotoxins: Certain substances can be toxic to the kidneys and cause AKI. Examples of nephrotoxins include contrast media, heavy metals (e.g., lead), and certain medications (e.g., aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, and cimetidine/ranitidine).
Trauma: Physical injury to the kidney can cause AKI. Examples of trauma that can cause AKI include blunt trauma (e.g., from a car accident) and penetrating trauma (e.g., from a gunshot wound).
Acute tubular injury: Injury to the renal tubules can cause AKI. Causes of acute tubular injury include ischemia, nephrotoxins, and infections.
Contrast-Induced Acute Kidney Injury (CI-AKI)Contrast Inducted Nephropathy (CIN)
Contrast-induced acute kidney injury (CI-AKI) and contrast-induced nephropathy (CIN) are both conditions that can occur as a result of exposure to contrast agents used in medical imaging procedures such as CT scans and angiography.
CI-AKI typically occurs 24-48 hours after contrast administration, while CIN has a slower onset, typically taking 3-5 days to develop. CI-AKI is associated with a peak in creatinine levels in 3-4 days and has a mortality rate of around 34%.
There are several strategies that can be used to minimize the risk of CI-AKI/CIN, including pre-contrast prophylaxis, hydration with normal saline, hemofiltration, bicarbonate, and the use of non-ionic, low molecular weight contrast agents. However, patient factors such as hydration and hemodynamic status, underlying kidney disease or compromise, volume of contrast administered, and repeated doses within 48 hours, as well as the use of vasopressors, can also impact the risk of developing CI-AKI/CIN.
N-acetyl cysteine has been studied as a potential prophylactic agent for CI-AKI/CIN, but a 2016 meta-analysis found that oral administration did not offer much benefit. Overall, the prevention of CI-AKI/CIN requires a multifactorial approach that takes into account both patient and procedural factors.
Postrenal Causes of AKI
Stones, clots, hypertrophy (BPH), tumors leading to obstruction and backup or stasis
Bilateral ureteric obstruction (Bilateral ureteric obstruction refers to the blockage or obstruction of both ureters)
Bladder outlet obstruction
Urethral obstruction
Obstruction of a single functioning kidney
When postrenal AKI occurs, urine flow is blocked from both kidneys or from a single functioning kidney, causing urine to back up into the kidneys and damaging them. It’s important to identify and treat the underlying cause of postrenal AKI as soon as possible to prevent permanent damage to the kidneys.
Common Causes of Renal Injury
Prerenal: Excessive fluid loss, Decreased renal perfusion, Increased vascular capacity, Vascular obstruction, Drugs that alter renal hemodynamics
Intrarenal: Ischemia, Nephrotoxicity, Rhabdomylosis, Intratubular obstruction
Postrenal: Mechanical: blood clots calculi, tumors, prostatic hypertrophy, prostate CA, urethral strictures. Functional: Diabetic neuropathy, neurogenic bladder, drugs
Factors Affecting Renal Excretion
Blood flow to the kidneys: The kidneys receive about 20% of the cardiac output, which allows for proper filtration and waste removal. Any conditions that affect blood flow to the kidneys, such as arterial blockages or constriction, can cause renal injury.
Urine flow rate: The rate of urine flow is determined by several factors, including blood pressure, volume status, and hormone levels. A low urine flow rate can be a sign of kidney disease, obstruction, or dehydration.
Urine pH and pKa: Urine pH is a measure of the acidity or alkalinity of urine. The lower the pH, the more acidic the urine. pKa is a measure of the strength of an acid. In the kidneys, urine pH and pKa can affect renal fluid secretion and the formation of kidney stones.((protein kinase-attaches phosphates to proteins))
Physicochemical properties: The physicochemical properties of drugs can impact their absorption, distribution, metabolism, and excretion. These properties can also affect their interactions with the kidneys and their ability to be eliminated from the body.
Distribution and binding: The distribution and binding of drugs within the body can affect their concentration in the kidneys and their ability to interact with renal transporters and enzymes.
Drug interactions: Many drugs can interact with each other and affect their pharmacokinetics and pharmacodynamics. These interactions can also impact renal function and lead to adverse effects.
Biological factors: Biological factors such as age, gender, genetics, and body weight can affect drug metabolism, renal function, and drug interactions.
Disease states: Various disease states such as hypertension, diabetes, and kidney disease can affect renal function and drug metabolism, leading to altered drug effects and interactions.
AKI/ARFTwo Phases pretty much the same they can be used interchangeably.
AKI stands for Acute Kidney Injury, while ARF stands for Acute Renal Failure. These two terms are often used interchangeably to describe a sudden and rapid decline in kidney function.
There are two phases of AKI/ARF:
A) Oliguric phase: (1-3 weeks) During this phase, urine output decreases to less than 400 milliliters per day. The fluid volume in the body increases due to fluid retention, which can lead to edema (swelling) in various parts of the body. Potassium levels in the blood may increase, which can lead to life-threatening cardiac arrhythmias.
B) Diuretic phase: During this phase, urine output increases to more than 400 milliliters per day. The excess fluid that was retained during the oliguric phase is excreted in the urine, and as a result, the fluid volume in the body decreases. Potassium levels may also decrease due to increased urine output.
It is important to note that not all patients with AKI/ARF will progress through both phases, and some may skip the oliguric phase entirely. The duration of each phase can also vary depending on the underlying cause of AKI/ARF and the individual patient’s response to treatment.
RIFLE Classification System for Acute Kidney Injury. Don’t go deep !
The RIFLE classification system is a widely used system to classify and stage Acute Kidney Injury (AKI) based on changes in serum creatinine (Cr) levels and urine output. The acronym RIFLE stands for Risk, Injury, Failure, Loss, and End-stage kidney disease (ESKD). The classification criteria for each stage are as follows:
GFR Criteria:
Risk: Increase in serum creatinine by 1.5 times or GFR decrease by 25%
Injury: Increase in serum creatinine by 2 times or GFR decrease by 50%
Failure: Increase in serum creatinine by 3 times or GFR decrease by 75% or serum creatinine at or above 4 mg/dL
Urinary Criteria:
Risk: Urine output < 0.5 mL/kg for six hours
Injury: Urine output < 0.5 mL/kg for 12 hours
Failure: Urine output < 0.3 mL/kg or anuria for 12 hours
Loss: Complete loss of renal function for at least 4 weeks
End-stage kidney disease (ESKD): Need for renal replacement therapy (RRT) for more than 3 months.
It is important to note that AKI is a serious condition and requires prompt diagnosis and treatment to prevent further kidney damage and associated complications. The RIFLE classification system helps to identify and stage the severity of AKI and guide appropriate treatment and management strategies.
The clinical approach to a patient with Acute Kidney Injury (AKI)
The clinical approach to a patient with Acute Kidney Injury (AKI) involves several evaluation processes and responses. These are as follows:
Evaluate volume status: This involves performing a physical examination, measuring weight, central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), and administering a fluid challenge to assess for fluid responsiveness.
Rule out obstruction: A physical examination should be performed to assess the patency of catheters, and a renal ultrasound may be ordered to rule out obstruction. Foley catheterization may also be performed to obtain urine output measurements.
Renal function tests: These tests include measuring blood urea nitrogen (BUN), creatinine, electrolytes, hemoglobin, calcium, and phosphorus to evaluate kidney function and electrolyte balance.
Probable cause for renal dysfunction: Nephrotoxic (drug) exposure such as NSAIDs, aminoglycosides, and hypotension, among other causes, should be evaluated and addressed.
Urine routine and microscopy: A urine sample should be obtained for routine and microscopy evaluation, which includes assessing specific gravity, protein, glucose, blood, casts (granular and/or cellular), cells, and crystals. A spot urine sodium and creatinine may also be obtained.
Urinary indices: The fractional excretion of sodium (FeNa) may be calculated to evaluate for tubular function and distinguish between prerenal and intrinsic AKI.
The approach to AKI should be individualized based on the patient’s clinical status and underlying cause of kidney injury. Treatment and management strategies may involve addressing the underlying cause, fluid and electrolyte management, and renal replacement therapy, among others.
AKI check slide 30
Focused Renal Assessment
Risk factors for the development of AKI include:
Advanced age
Chronic kidney disease (CKD)
Diabetes
Hypertension
Cardiovascular disease
Liver disease
Sepsis
Surgery
Trauma
Nephrotoxic medications
Contrast dye
Dehydration
Hypovolemia
Obstruction
Physical assessment:
Neurologic: Assess for altered mental status, confusion, seizures, or coma. These symptoms can be indicative of uremic encephalopathy, which is a potential complication of AKI.
CV: Monitor blood pressure, mean arterial pressure (MAP), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), preload, afterload, cardiac output (CO), ejection fraction (EF), coronary artery disease (CAD), and myocardial infarction (MI). These factors can impact renal perfusion and contribute to the development of AKI.
Pulmonary: Assess for signs of respiratory distress, hypoxemia, and pulmonary edema. These symptoms can be indicative of fluid overload and can contribute to the development of AKI.
GI: Monitor for nausea, vomiting, diarrhea, constipation, appetite, calorie intake, protein intake, and sodium intake. These factors can impact fluid balance and electrolyte balance and contribute to the development of AKI.
Hematologic and immune system: Monitor for anemia, leukocytosis, and thrombocytopenia. These factors can impact renal function and contribute to the development of AKI.
Integumentary: Assess for skin turgor and mucous membranes. These factors can be indicative of hydration status and can impact renal function.
Skeletal: Assess for bone pain and fractures. These factors can be indicative of underlying metabolic bone disease and can impact renal function.
Laboratory: Monitor blood urea nitrogen (BUN), creatinine (Cr), glomerular filtration rate (GFR), osmolality, and electrolyte imbalances. These factors can be indicative of renal function and can contribute to the development of AKI.
Remember all the reasons for an altered urine output, including decreased oral fluid intake and excess fluid loss, as these can contribute to the development of AKI.
AKI Preoperative Risk Assessment Tool
Check slide 32
AKI Medication
- Loop diuretics such as Furosemide (Lasix) are commonly used in the management of AKI to increase water excretion and improve fluid balance. Furosemide works by interfering with the chloride binding cotransport system in the Loop of Henle, which in turn inhibits the reabsorption of sodium and chloride ions. This results in increased urinary output and decreased fluid volume.
The peak action of Furosemide is typically reached about 60 minutes after administration, and its duration of action is approximately 6-8 hours. However, the actual onset and duration of action can vary depending on factors such as the patient’s renal function, hydration status, and co-administration of other medications.
AKI Medication. Inotropes (increase HR)
Dopamine is a medication that can be used in the management of AKI as an inotrope, which is a medication that increases myocardial contractility and cardiac output. In addition to its inotropic effects, dopamine can also cause selective dilation of the renal vasculature at low doses (1-5 mcg/kg/min) due to its activity on specific dopamine receptors in the renal vasculature.
By increasing renal blood flow and enhancing renal perfusion, dopamine can improve urine flow and help to prevent or treat AKI.
AKI Medication. Vasodilators
Fenoldopam
is a medication that belongs to a class of drugs known as vasodilators. It is a selective dopamine receptor agonist that has minimal adrenergic effects and is 6 times more potent than dopamine.
Fenoldopam is primarily used to treat severe hypertension, including patients with renal compromise, by causing vasodilation of the peripheral blood vessels and increasing renal blood flow. It is administered intravenously and is typically used in a hospital setting.
While fenoldopam is effective at lowering blood pressure, it can also cause some side effects, including headaches, flushing, nausea, and hypotension. It is important to monitor patients closely for these side effects and adjust the dosage as needed to minimize the risk of adverse events.
In summary, fenoldopam is a vasodilator that is used to treat severe hypertension in patients with renal compromise. While it is an effective medication, it can cause side effects and requires close monitoring when used in a hospital setting.
AKI Medication. Calcium channel blocker
Calcium channel blockers are a class of medications that work by blocking the entry of calcium ions into smooth muscle cells, leading to vasodilation and relaxation of blood vessels. One of the calcium channel blockers that is used in the treatment of acute kidney injury (AKI) is nifedipine.
Nifedipine is used to enhance the function of transplanted kidneys by improving blood flow and oxygenation to the organ. The vasodilation effect of nifedipine is thought to be mediated through the relaxation of smooth muscle in blood vessels.
In summary, nifedipine is a calcium channel blocker that is used to enhance the function of transplanted kidneys in patients with AKI. It works by producing vasodilation and improving blood flow and oxygenation to the kidneys.
Chronic Renal Insufficiency (CRI)
In summary, CRI and CKD are both terms used to describe the gradual loss of kidney function over time. CRI is often used interchangeably with early-stage CKD and refers to a mild decrease in kidney function that may not be associated with symptoms or complications. CKD is a broader term that includes more advanced stages of kidney disease and is associated with a range of complications. The stage of CKD is determined by the GFR.
Reduction of blood flow to the kidneys often caused by renal artery disease (HTN, diabetes)
Defined as decline in renal function to approximately 25% of normal
Risks include: Older age, gender, family history, race or ethnicity, genetic factors, hyperlipidemia, HTN, smoking, diabetes
Stages
Usually symptomatic when <50% “kidney function” is left.
Renal Diet
Limit the 3 P’s and Sodium
A renal diet is a special diet that is designed to help individuals with kidney disease maintain good health and manage their symptoms. The diet typically involves limiting certain nutrients that can be harmful to the kidneys, such as protein, potassium, phosphorus, and sodium.
The “3 P’s” refer to the nutrients that individuals with kidney disease should limit in their diet: potassium, phosphorus, and protein. High levels of these nutrients can be harmful to the kidneys and can exacerbate symptoms of kidney disease.
Potassium is a mineral that is found in many foods, including fruits, vegetables, nuts, and legumes. In individuals with kidney disease, high levels of potassium can cause muscle weakness, irregular heartbeats, and other complications. Therefore, individuals with kidney disease may need to limit their intake of high-potassium foods.
Phosphorus is a mineral that is found in many foods, including dairy products, meat, fish, and nuts. In individuals with kidney disease, high levels of phosphorus can cause bone disease and other complications. Therefore, individuals with kidney disease may need to limit their intake of high-phosphorus foods.
Protein is an essential nutrient that is needed for growth and repair of the body. However, in individuals with kidney disease, high levels of protein can cause damage to the kidneys and exacerbate symptoms. Therefore, individuals with kidney disease may need to limit their intake of high-protein foods, such as meat, poultry, fish, and dairy products.
Sodium is a mineral that is found in many foods and is often added to processed foods. In individuals with kidney disease, high levels of sodium can cause high blood pressure and fluid retention. Therefore, individuals with kidney disease may need to limit their intake of high-sodium foods, such as processed foods, fast food, and salty snacks.
In summary, a renal diet is a special diet that is designed to help individuals with kidney disease manage their symptoms and maintain good health. The diet typically involves limiting certain nutrients, such as protein, potassium, phosphorus, and sodium, to reduce the risk of complications associated with kidney disease.
Renal Diet
Potassium: Limit or avoid foods such as organ meats (liver, kidney), fish (salmon, tuna, halibut), dried fruits (raisins, prunes), beef, chicken, pork, milk, yogurt, dark green leafy vegetables (spinach, kale), and salt substitutes (potassium chloride).
Phosphorus: Limit or avoid foods such as milk, cheese, yogurt, nuts, seeds, beans, lentils, whole grains, bran cereals, chocolate, and dark sodas.
Protein: Calculation of protein needs and restriction is based on body weight and dialysis. For non-dialysis patients, protein intake is usually limited to 0.6-0.8 grams per kilogram of body weight per day. For dialysis patients, protein intake is usually higher, at 1.2 grams per kilogram of body weight per day.
Sodium: Limit or avoid processed foods, fast food, packaged meats (sausage, hot dogs), canned soups and vegetables, potato chips, pretzels, ham, bacon, and cheese.
It’s important to note that every individual’s nutritional needs may vary, depending on their specific condition and stage of kidney disease. A registered dietitian who specializes in renal nutrition can provide personalized recommendations for a renal diet.
Chronic & End-Stage Renal Failure (CRF & ESRD)
Systemic affects are wide ranging:
Chronic renal failure (CRF) and end-stage renal disease (ESRD) are serious medical conditions that affect the function of the kidneys. CRF refers to a gradual and irreversible loss of kidney function over time, while ESRD is the complete and permanent failure of the kidneys.
Both conditions have systemic effects that are wide-ranging, affecting multiple body systems. These effects include cardiovascular, hematologic, gastrointestinal, and neurologic symptoms. Patients with CRF or ESRD often require palliative interventions to manage their symptoms and maintain their quality of life.
Fluid and electrolyte imbalances are also common in CRF and ESRD patients. The kidneys play a crucial role in regulating the balance of sodium, potassium, calcium, and phosphorus in the body. In these conditions, there may be sodium and fluid retention, leading to edema and hypertension. The kidney is the primary organ responsible for potassium balance, so patients may experience hyperkalemia if the kidneys are not functioning properly. Additionally, imbalances in calcium and phosphorus levels can lead to hypocalcemia and bone disease.
Treatment for CRF and ESRD typically involves managing symptoms, addressing fluid and electrolyte imbalances, and supporting kidney function through dialysis or kidney transplantation. Dietary modifications, medications, and lifestyle changes may also be recommended to slow the progression of the disease and improve quality of life.
ESRD
ESRD can lead to various complications such as acid-base imbalances, anemia, hypertension, and heart failure. Treatment is aimed at managing these complications and improving quality of life. Also hypotension if rennin is not produced or released.
In terms of acid-base imbalances, ESRD can result in metabolic acidosis due to the loss of nephrons, which are responsible for regulating the body’s acid-base balance. Treatment may involve the use of sodium bicarbonate to correct the acidosis.
Other complications of ESRD include fluid and electrolyte imbalances such as hyperphosphatemia, hypocalcemia, and hyperkalemia. Management involves restricting fluid intake and limiting dietary intake of phosphorus, potassium, and sodium. Increasing calorie intake through fats and carbohydrates may also be recommended to help maintain muscle mass.
Overall, management of ESRD requires a multidisciplinary approach involving nephrologists, dietitians, and other healthcare professionals to optimize patient outcomes and improve quality of life.
ESRD
ESRD stands for End-Stage Renal Disease, which is a condition in which the kidneys fail to function adequately, and the patient requires either dialysis or a kidney transplant to survive.
The Social Security Administration (SSA) considers ESRD as a disability, and a person may qualify for Social Security disability benefits if they are unable to perform gainful activity for 12 consecutive months due to ESRD.
Medical management of ESRD includes controlling hypertension, managing volume overload, ensuring adequate nutrition, and monitoring electrolytes and toxins. Pharmacological interventions may also be necessary to manage the symptoms and complications of ESRD. These interventions may include folic acid and ferrous sulfate supplementation, phosphate binders (taken with meals), calcium sources and supplements, and stool softeners and laxatives.
Regular monitoring and management of these factors can improve the patient’s quality of life and help them to live longer with ESRD. Additionally, kidney transplantation is considered the most effective treatment for ESRD and offers the best chance for a patient to return to a normal life.
Renal Replacement Therapy - Hemodialysis
This process relies on the principles of osmosis and diffusion, which involve the movement of molecules from an area of higher concentration to an area of lower concentration.
Hemodialysis requires a large vascular access, typically in the form of an arteriovenous fistula or graft, to allow for adequate blood flow through the dialysis machine. This access is created by surgically connecting an artery and a vein in the arm or leg, or by placing a synthetic graft between an artery and a vein.
Hemodialysis is considered the most efficient and effective form of clearance for end-stage renal disease. It can remove large amounts of waste products and excess fluids from the body, helping to maintain a patient’s electrolyte balance and fluid levels.
However, hemodialysis is associated with several potential complications. These can include disequilibrium syndrome, muscle cramps, hemorrhage, air embolus, and hemodynamic flux, which can manifest as hypotension, dysrhythmias, and anemia.
Hemodialysis (HD)
Components include
Access: Hemodialysis requires access to the patient’s bloodstream, which is usually obtained through a surgically created arteriovenous fistula, arteriovenous graft, or central venous catheter.
Dialyzer: The dialyzer, also known as the artificial kidney, is the central component of the hemodialysis machine. It contains a semipermeable membrane that allows waste products and excess fluids to pass from the patient’s blood into the dialysate.
Filter: The filter, also called the membrane or screen, is located in the dialyzer and removes waste products and excess fluids from the patient’s blood.
Dialysate: Dialysate is a solution that is circulated through the dialyzer and helps to remove waste products and excess fluids from the patient’s blood. The composition of the dialysate can be adjusted to meet the specific needs of each patient.
During hemodialysis, the patient’s blood is drawn from the access site and pumped through the dialyzer, where it is filtered and cleaned by the dialysate. The cleaned blood is then returned to the patient’s bloodstream through the access site. This process usually takes several hours and is performed several times a week, depending on the patient’s individual needs.
Hemodialysis process
These are the different components of a typical hemodialysis machine, which work together to filter the blood of patients with end-stage renal disease:
Blood pump: The blood pump is responsible for drawing blood from the patient’s access site and circulating it through the hemodialysis machine.
Dialyzer (Filter): The dialyzer is the central component of the hemodialysis machine. It contains a semipermeable membrane that allows waste products and excess fluids to pass from the patient’s blood into the dialysate.
Dialysate: Dialysate is a solution that is circulated through the dialyzer and helps to remove waste products and excess fluids from the patient’s blood. The composition of the dialysate can be adjusted to meet the specific needs of each patient.
Dialyzer inflow pressure monitor: This component monitors the pressure of the blood as it enters the dialyzer.
Venous pressure monitor: This component monitors the pressure of the blood as it leaves the dialyzer and returns to the patient’s bloodstream.
Arterial pressure monitor: This component monitors the pressure of the blood as it is pumped into the dialyzer.
Heparin pump: The heparin pump is used to prevent blood clots from forming in the dialyzer or the patient’s access site.
Air trap and air detector: These components are used to prevent air bubbles from entering the patient’s bloodstream during hemodialysis.
Air detector clamp: This component automatically clamps the tubing if air bubbles are detected.
After the blood has been filtered and cleaned by the dialyzer, it is returned to the patient’s bloodstream through the access site. The cleaned blood is then circulated through the patient’s body, carrying oxygen and nutrients to the organs and tissues. The hemodialysis process usually takes several hours and is performed several times a week, depending on the patient’s individual needs.
How HD Works 47
Hemodialysis (HD) works by using the principles of diffusion to remove waste products and excess fluids from the patient’s blood. Diffusion is the process by which molecules move from an area of high concentration to an area of low concentration until equilibrium is reached.
During HD, the patient’s blood is pumped through the semipermeable membrane of the dialyzer, where it is in close proximity to the dialysate solution. The dialysate contains a balanced solution of electrolytes, such as sodium and magnesium, and other substances that help to remove waste products and excess fluids from the patient’s blood.
As the blood flows through the dialyzer, metabolic toxins, urea, small proteins, and other waste products diffuse from the bloodstream across the membrane into the dialysate solution. At the same time, electrolytes and other substances that are needed by the body are allowed to pass from the dialysate into the bloodstream to maintain the body’s electrolyte balance.
Water molecules also move across the membrane in a process called ultrafiltration, which removes excess fluid from the patient’s bloodstream. The rate of ultrafiltration can be adjusted by altering the pressure and composition of the dialysate solution.
why is removing water called ultrafiltration ?
The process of removing water from the blood is called ultrafiltration because it involves the use of a filtering system that selectively removes water and certain dissolved solutes from the blood based on size and charge.
Renal Replacement Therapy - Hemodialysis Indications : Meaning when it is needed.
what does refractory mean in this context ?
In the context of the indications for hemodialysis, “refractory” means that the condition being referred to is not responding to conventional treatments or interventions. For example, refractory hyperkalemia means that the patient’s high potassium levels are not improving with medications or dietary changes alone. Refractory acidosis means that the patient’s acid levels are not being adequately managed with medications or other interventions. These refractory conditions may require hemodialysis to help remove the excess substances from the bloodstream and improve the patient’s health.
Refractory hyperkalemia: High levels of potassium in the blood that do not respond to medical treatment or dietary changes can lead to dangerous arrhythmias and other complications.
Refractory acidosis: A buildup of acids in the blood can cause severe symptoms such as confusion, lethargy, and seizures. Hemodialysis can help remove excess acids from the bloodstream.
Volume overload: Hemodialysis can help remove excess fluid from the body that can accumulate in patients with kidney failure and cause swelling in the legs, ankles, and other areas.
Elevated BUN with symptoms of complications: A high level of blood urea nitrogen (BUN) can indicate kidney failure and may cause symptoms such as fatigue, nausea, and vomiting.
Pericarditis: Inflammation of the sac surrounding the heart (pericardium) can occur in patients with kidney failure and may require hemodialysis to remove excess fluid and toxins.
Encephalopathy (hepatorenal syndrome/AMS, ALOC): Buildup of toxins in the bloodstream can cause neurological symptoms such as confusion, altered mental status, and even coma.
Pulmonary edema: Fluid buildup in the lungs can lead to shortness of breath, coughing, and other respiratory symptoms that may require hemodialysis to remove excess fluid and improve breathing.
Mnemonic = HAVEPEE
Hemodialysis
Hemodialysis can be performed in different settings, including inpatient units, dialysis centers, and at home. In the inpatient and dialysis center settings, patients are typically given a set schedule or time slot for their hemodialysis treatments, and there may also be a night-time option available.
However, home hemodialysis offers several advantages over inpatient or center-based hemodialysis. Patients on home hemodialysis have a more flexible schedule, and they may experience less nausea, more energy, and better sleep. Home hemodialysis also decreases the risk of complications and problems associated with inpatient or center-based hemodialysis, such as painful muscle cramps, high blood pressure, headaches, stroke, hypotension, high phosphate, and pruritus (itching).
Home hemodialysis treatments can last between 2-10 hours, depending on the type of treatment prescribed. There are several types of home hemodialysis, including standard home hemodialysis (3 times per week), short daily hemodialysis (5-7 days per week), and nightly home hemodialysis (3-6 times per week). Patients on home hemodialysis are trained to perform their own treatments at home or with the help of a caregiver.
Continuous Renal Replacement Therapy (CRRT)
Continuous renal replacement therapy (CRRT) is a form of renal replacement therapy that is primarily used for critically ill patients who are hemodynamically unstable. Unlike hemodialysis, which is done over a period of several hours, CRRT is more gradual and continuous. There are five main methods of CRRT: SCUF, CAVH, CAVH-D, CVVH, and CVVH-D.
SCUF (Slow Continuous Ultrafiltration) works by convection to pull off fluid, while CAVH (Continuous Arteriovenous Hemofiltration) works by convection to pull off fluid and waste using the patient’s blood pressure. CAVH-D (Continuous Arteriovenous Hemodialysis) and CVVH-D (Continuous Veno-Venous Hemodialysis) both use dialysate to remove waste in addition to convection. Finally, CVVH (Continuous Veno-Venous Hemofiltration) works by diffusion like a “slow” hemodialysis, but is still considered a form of CRRT due to its continuous nature.
CRRT is indicated for patients with multiple organ dysfunction syndrome (MODS), sepsis, acute renal failure (ARF), or those who are unable to tolerate hemodialysis or peritoneal dialysis.
Complications of CRRT can include fluid imbalance, hemorrhage, hemofilter occlusion, infection, thrombus, and vascular occlusion.
Indications for CRRT
Continuous Renal Replacement Therapy
A: Metabolic acidosis (pH <7.1) - CRRT can help to correct acid-base imbalances in patients with severe metabolic acidosis.
E: Electrolytes –Hyperkalemia (K > 6.5 or rapidly rising), hypermagnesemia - CRRT can help to remove excess potassium and magnesium from the body in patients with severe electrolyte imbalances.
I: Ingestion –Certain alcohol and drug intoxications - CRRT can be used as part of the management of certain types of poisoning, including salicylates, lithium, methanol, ethylene glycol, theophylline, and phenobarbital.
O: Refractory fluid overload (postoperative) - CRRT can help to remove excess fluid in patients with refractory fluid overload, which can occur after surgery or in other clinical contexts.
U: Uremia –high catabolism of ARF (pericarditis, neuropathy, decline in mental status) - CRRT can help to remove uremic toxins and other waste products from the body in patients with AKI or other conditions that cause uremia.
In general, CRRT is recommended for patients who require renal support, even before the development of complications of AKI. It is important to individualize the indications and timing of CRRT based on the patient’s clinical condition and response to treatment.
Temporary Dialysis Vascular Access
Temporary dialysis vascular access refers to the use of catheters for hemodialysis (HD) in patients with acute kidney injury (AKI) or other conditions that require renal support. The following are some important considerations for temporary dialysis vascular access:
-Do not use for routine access or blood draw: Temporary dialysis catheters are designed for short-term use and should not be used for routine access or blood draws, as this can increase the risk of infection and damage to the catheter.
-HD team use only: Insertion, maintenance, and removal of temporary dialysis catheters should be performed by a qualified HD team, such as a nephrologist or dialysis nurse.
-Use only the 3rd port if present during an emergency: Some temporary dialysis catheters may have multiple ports. In an emergency situation, only the third port should be used for HD access, as the first two ports may be used for other purposes such as medication administration.
-Flush lock with sodium citrate (4%) versus heparin: To prevent catheter-related bloodstream infections, temporary dialysis catheters should be flushed with an anticoagulant lock solution after each use. Sodium citrate (4%) is preferred over heparin, as it has been shown to be more effective in reducing the risk of infection.
-Aspirate and discard: Before use, the catheter should be aspirated and the aspirated fluid discarded to ensure that there is no clot or other debris that could cause catheter-related complications such as thrombosis or infection.
Overall, proper use and maintenance of temporary dialysis vascular access is essential for the safe and effective delivery of hemodialysis in critically ill patients.
Arterial Venous (AV) Fistula
HD Standards of Care
The following are some general standards of care for patients receiving HD:
Pretreatment:
Medications, nutrition, fluids: Patients should take their medications as prescribed and follow any dietary or fluid restrictions given by their healthcare provider.
Vital signs, weight, labs, symptoms: Patients should have their vital signs checked, their weight measured, and blood tests done before each HD session to monitor their health status.
Post-treatment:
Handoff -VS, Labs, fluids in/out, weight changes, blood glucose: Healthcare providers should communicate important information such as vital signs, labs, fluid intake and output, weight changes, and blood glucose levels between shifts to ensure continuity of care.
Labs: Blood tests should be performed after HD sessions to monitor fluid and electrolyte levels and to adjust the patient’s treatment plan if necessary.
Fluid and electrolyte shifts: Healthcare providers should monitor for changes in fluid and electrolyte levels during and after HD sessions to prevent complications such as hypotension, cramping, or arrhythmias.
Site observations: The access site for HD should be monitored for signs of infection or other complications.
Medications, nutrition, rest: Patients should be given any necessary medications or nutritional support after HD sessions, and encouraged to rest.
Discharge, support services (transportation, groups): Patients should be discharged after HD sessions with appropriate support services in place, such as transportation or access to support groups.
Complications and stressors:
Healthcare providers should monitor for and manage common complications and stressors associated with HD, such as fluid and food limitations, muscle cramps, fatigue, sleep problems, peripheral neuropathy (in patients with diabetes), vacation limitations, social isolation, pruritus (itching), and long dialysis treatment times.
Overall, HD treatment should be individualized and tailored to the patient’s specific needs and goals, with careful attention paid to managing potential complications and ensuring patient comfort and well-being.
Case Study -Dialysis
- The patient is a 67-year-old male, who is 3 days postoperative after a CABG x 3 operation. The patient has a history of HTN, type 1 diabetes, CAD, and ESRD, which is treated with hemodialysis 3x/week. The patient has a left AV shunt.
He is taking the following medications:
evSevelamer (Renegel) 2 capsules with each meal
Vitamin D, B12 and iron supplements with each meal
Calcium carbonate (OS-Cal): 3 tablets with each meal
Procrit (epoetin alfa): 100U/kg dose subcutaneously every M, W, & F on dialysis days
70/30 NPH and regular insulin 30U twice daily and finger stick blood glucose taken before meals and at bedtime and regular insulin given as per CHO intake as per sliding scale
Coreg (carvedilol 12.5 mg twice daily
Lanoxin 0.125 mg every other day (on even days)
Acetaminophen with Codeine No.3 1-2 tabs every 6 hours PRN for pain
Diphenhydramine hydrochloride 25 mg ery 8 hours PRN for itching
DSS (Colace)100 mg twice daily
- The patient is ordered to have daily dialysis. What is the rationale for this?
- The patient is going to hemodialysis at 0900 on an odd day. Which medication(s) should the nurse hold before sending the patient? Why?
- What nursing management considerations should be made for this patient?
Case Study Dialysis Answers
The increased metabolic rate increases (due to the surgury) metabolic wastes, therefore wastes accumulate faster in those with ESKD –uremia develops, and they need daily dialysis to get rid of wastes.
Hold the beta blocker/antihypertensive
Sign for restrictive extremity,; assess AV fistula, assess VS for hypotension, Check IVF for rate, K+ & Mg++, assess for FVE (weight, etc), lung sounds, heart sounds, monitor for complications: pericarditis, pleural effusions, PNA, electrolytes, monitor diet, appetite, check pre/albumin. Check skin/skin care, wound healing, blood glucose, saturation, pain control.
In the case study provided, the nurse was instructed to hold the patient’s beta blocker medication (carvedilol, or Coreg) before sending the patient to dialysis. The reason for this is because beta blockers can lower blood pressure, and dialysis can also lower blood pressure. Therefore, holding the medication can help prevent further drops in blood pressure during the dialysis treatment.
Peritoneal dialysis (PD)
Peritoneal dialysis (PD) is a type of renal replacement therapy that involves using the peritoneal cavity as a semipermeable membrane for fluid and solute exchange. This process relies on both osmosis and diffusion to remove excess fluid and waste products from the body.
PD requires a prescribed volume of dialysate solution, which is warmed and infused into the peritoneal cavity by gravity. The dialysate solution is left in the peritoneal cavity for a prescribed dwell time, during which time it absorbs excess fluid and waste products from the bloodstream. After the dwell time, the solution is drained out of the peritoneal cavity and replaced with fresh solution.
Patients undergoing PD have specific dietary needs, as the process of dialysis can result in the loss of important nutrients. Dietary recommendations are typically made by a registered dietitian.
Complications of PD can include peritonitis (which is indicated by abdominal pain and cloudy effluent), anorexia, hernia, low back pain, altered body image and sexuality, and a constant sweet taste.
PD can be administered continuously or intermittently. Continuous ambulatory peritoneal dialysis (CAPD) involves the patient performing manual exchanges of dialysate four times a day, seven days a week. Continuous cycling peritoneal dialysis (CCPD) is an automated form of PD that uses a machine to perform exchanges at night. Nighttime intermittent peritoneal dialysis (NIPD) involves cycles of dialysate exchanges throughout the night.
