Acute Renal Failure
Prepared By
Naomi Budha
Introduction
• Renal failure is temporary or permanent damage to the
kidneys that results in loss of normal kidney function. (Types
include AKI and CKD)
• Acute Renal failure is a sudden, usually reversible reduction
in glomerular filtration rate resulting in an increase in blood
concentration of urea and creatinine and disturbed fluid and
electrolyte homeostasis.
• It is a common life threatening condition in children, need
urgent and adequate treatment.
Incidence
• The incidence of any AKI was 26% and that of moderate-severe AKI
was 14%. The incidence of AKI was similar in high-income 27% (23–
32), low-middle-income 25%, and low-income 24% countries.
• Overall, AKI-associated mortality was observed in 11% of the
pediatric population. AKI-associated mortality rate was highest at 18%
and 22% in low-income and low-middle-income countries,
respectively (Meena et al., 2023 ).
• AKI accounts for 1.5-2% admission of the children in hospital.
Etiology
• The causes of AKI can be broadly divided into pre-renal, renal and post-
renal causes. Overlap exists and a patient may have more than one cause
foe their renal failure.
Pre-renal cause:- associated with conditions that ↓se renal blood
supply
Fluid Volume depletion resulting from
• Hemorrhage,
• Renal loses (diuretics, osmotic diuresis)
• Gastrointestinal loses (vomiting, diarrhea, nasogastric suction)
• Burn (fluid loss through damaged skin)
• Overuse of diuretics (excessive urination)
Etiology contd….
• Impaired cardiac output eg. Congestive heart
failure ,impaired cardiac efficiency, myocardial infraction,
heart failure, dysrhythmias and cardiogenic shock.
• Vasodilation resulting from sepsis, anaphylaxis and
antihypertensive medication (eg ACE inhibitors)
Renal cause:- causing decrease glomerular filtration rate
(GFR)
1. Prolonged renal ischemia
• Pigment nephropathy
• Trauma, injury, burns
• Transfusion reaction, hemolytic anemia
2. Nephrotoxic agents
• Aminoglycoside antibiotics(gentamycin, amikacin, tobramycin, streptomycin)
• Radiopaque contrast agent
• Heavy metals
• NSAIDs
• ACE inhibitors
Renal cause contd…
3)Infectious process
• Acute pyelonephritis (Bilateral Pyelonephritis)
• Acute glomerulonephritis
4) other conditions :- Tumour Lysis syndrome, Renal artery vein
thrombosis
Post renal cause:- obstruction to urine flow & prevent elimination
of urine
Renal calculi, obstructive uropathy, neurogenic bladder, tumors,
rhabdomyolysis, wilm’s tumor , strictures, blood clots and
developmental structural anomalies.
Pathophysiology
• For pre- renal cause (diarrhea) /fluid volume decrease due to vomiting,
trauma
• Severe reduction in glomerular blood flow
• Reduction in GFR
• Results in elevation of blood urea nitrogen(BUN) & decreased tubular
reabsorption of Na from proximal tubules.
• Increased concentration of Na in distal tubules.
• Stimulation of renin mechanism
• Vasoconstriction of afferent arterioles
• Subsequent decrease in GFR and prevents urinary losses of Na
Pathophysiology contd…
• If condition persists for long time cortical or tubular necrosis
• Intrinsic damage of renal parenchyma occurs (if renal perfusion is not
restored)
• Acute real failure
Phases of acute renal failure
There are four clinical phases of ARF
• Initial phase –begins with initial insult & end when oliguria develops and
lasts from hours to days.
• Oliguria phase- is accompanied by rise in the serum concentration of
waste substances. Urine output decreases from renal tubules damage.
• Last for 5-15 days (shorten in infant and children 3-5days and 10-14 days
in older children)and can persists for weeks where > 3weeks of this phase
results in irreversible renal damage.
Phases contd….
• Diuretic phase- the kidney try to heal & urine output increases but
tubule scarring & damage occur. But there is still risk of dehydration
& electrolyte imbalance so close monitoring is needed. Lasts for few
days.
• Recovery phase- tubular edema resolves & renal functions improves,
final resumption of normal urine osmolarity and blood electrolytes . It
may takes 3-12 months
Clinical manifestations
• Almost every system of the body is affected when there is failure of the normal renal
regulatory mechanism.
• Though symptoms can vary from person to person and depends upon underlying
cause and duration of illness.
• Someone in early stage kidney disease may not feel sick or notice symptoms as they
occur.
Specific features
-Severe oliguria (urine output <1ml/kg/hour) but in some cases urine output may not
be reduced. Anuria in some cases(uncommon)
-Azotemia, hyperkalemia, hypocalcaemia
-Metabolic acidosis manifested by tachycardia.
Clinical manifestations contd…
Nonspecific features
• May appear clinically ill & lethargic
• Persistent nausea & vomiting
• The skin & mucous membranes are dry from dehydration .
• Breath may be odor of urine
• Drowsiness, headache, muscle twitching & seizures.
• Swelling of the legs, ankles, feet, face and/or hands
• Shortness of breath due to extra fluid on the lungs
Nonspecific features contd…
• Abnormal heart rhythms, Muscle paralysis due to hyperkalemia
• Appetite loss, a bad taste in the mouth
• Difficulty sleeping, changes in mental status/ mood seizures ,
drowsiness due to electrolyte imbalances
• Darkening of the skin
• Excess protein in the blood
• In later stage weight loss
Diagnostic Evaluation
• History :- history of massive bleeding, severe diarrhea, shock and onset of s/s
eg oliguria (urine output < 0.5ml/kg/hour).
• Physical examination :- edema, signs and symptoms,
-Changes in urine – scanty to normal urine volume, may be hematuria, & low
urine specific gravity
• Urinary electrolytes :- Increased BUN & creatinine levels (azotemia) in
monitoring kidney function & disease progression. Hyperkalemia and Na
level, Calcium & phosphorus abnormalities.
• Urine culture to rule out infective organism(in case of UTI)
• ABG test to rule out metabolic acidosis
Diagnostic Evaluation contd…
• Hematology to rule out anemia
• Creatinine Phosphokinase (if rhabdomyolysis is suspected)
• Renal biopsy in cases of suspected RPGN or if AKI cause in uncertain
in case of rapidly rising creatinine.
• Anti- nuclear antibody, anti double- stranded DNA, c3, c4 , anti-
nuclear cytoplasmic antibody (ANCA), anti glomerular basement
membrane antibody (antiGBM) if patient has history, s/s consistent
with glomerulonephritis.
Therapeutic Management of ARF
• The kidney has a remarkable ability to recover from insult. Mgmt
should be planned according to underlying causes. Treatment includes:
- Treatment of underlying causes
- Management of complications
- Supportive care
Correction of dehydration , treatment of hyperkalemia and shock are
primary concerns of management.
Pharmacotherapy (Emergency management)
• For hyperkalemia :- administering cation- exchange resins (Kayexalate ) – works by
increases fecal potassium excretion through binding of K+ in the lumen of GI tract.
• For widen QRS complexes or peaked T waves
- Injection HCO3 1meq/kg IV to cause intracellular shift of potassium, this maneuver
dose not reduce total body K+ stores.
- Insulin and glucose IV:- this maneuver dose not reduce total body K+ stores
• Hypocalcaemia:- Calcium chloride 20mg/kg IV, this maneuver stabilizes the cardiac
myocyte membrane and prevents dysthymias.
• Volume overload:- Furosemide 1mg/kg IV with repeated doses as necessary.
• Low dose dopamine is often used to dilate the renal arteries through stimulation of
dopaminergic receptors.
• The elevated serum phosphate level may be controlled with phosphate-binding
agents (aluminum hydroxide).
Therapeutic Management of ARF contd…
• Maintenance of fluid balance is based on daily body weight, vital signs especially
BP, serial measurement of serum & urine concentrations (I/O), fluid losses, blood
pressure & the clinical status of the child.
• Insertion of foleys catheter to rule out urine retention, to collect urine and
monitor the effects of diuretics.
• Monitor sign of fluid excesses such as dyspnea, tachycardia, & distended neck
vein regularly.
• The lungs are auscultate for moist crackles.
• Pre-renal causes of ARF may be restored by IV fluid & blood product transfusion
& transfuse albumin for hypoproteinemia.
• Dialysis may be initiated to prevent from serious complications as hyperkalemia,
severe metabolic acidosis, and pericarditis.
• Counselling for renal transplant if needed.
• Management of other complications such as anemia through blood transfusion.
Therapeutic Management of ARF contd…
• ARF causes severe nutritional imbalances so calorie intake should be
encouraged acc. to requirement.
• Dietary proteins are limited to minimize protein break down & to prevent
accumulation of toxic end products.
• Calorie requirements are met with high carbohydrate meals because
carbohydrates have a protein sparing effect.
• Foods & fluid containing potassium & phosphorus (banana, citrus fruits &
juices, coffee dairy products) are restricted.
• Low sodium diet (avoid processed food, additional food intake).
• Vitamins and minerals supplementations.
Others
Prevent from injury during convulsion.
Provide care during dialysis.
Nursing management
Nursing assessment:- includes detail history of illness, drug therapy,
exposure to toxic substances, allergy, fever etc.
• Physical examination :- I/O, vital signs, urine specific gravity, daily
weight, hydration status and nutritional status
• Review of laboratory status: RFT
• ECG and Echocardiogram
• Chest x- ray to rule out pulmonary edema.
Nursing diagnosis
• Fluid and electrolyte imbalance related to altered kidney function.
• Imbalanced nutrition less than body requirement related to protein
catabolism, anorexia , nausea and vomiting.
• Risk of infection related to invasive procedures and malnutrition.
• Risk of injury related to metabolic abnormalities(uremia and
hyperkalemia).
• Knowledge deficit related to disease condition
Nursing intervention
Maintain fluid & electrolyte balance
• Strictly record of intake & output, daily weight(same scale and same
cloth), maintaining drip if fluid loss, monitor laboratory electrolytes
regularly & careful & regular monitor of edema and auscultation of
chest for crackles .
• Maintain fluid restriction as prescribed.
• Administer diuretics as prescribed.
• Promptly report signs of heart failure eg bounding pulse, shortness of
breath and adventitious breath sounds.
• Give oxygen if the patient is dyspnea.
Maintain nutrition
• Assess and document dietary intake and weight daily.
• Monitor blood electrolytes eg BUN, albumin Na and K.
• Restrict sodium, potassium and phosphorus intake as indicated.
• Provide small and frequent feedings
• Offer frequent mouth care .
• Provide hard candy and breath mints between meals.
• Consult with dietician support team
• Provide high calorie, low to moderate protein diet. Avoid concentrated
sugar sources
Infection prevention
• Assess edema, purulent drainage and skin changes.
• Hand hygiene maintain
• Avoid invasive procedures whenever possible and use aseptic
technique when doing invasive procedures.
• Provide routine line cares eg. catheter care and perineal care, sponge
bath.
• Remove indwelling catheter as possible.
• Encourage for deep breathing, coughing and frequent position change.
• Monitor WBC count regularly.
• Treatment of infections with antibiotics if culture is positive according
to report.
Injury Prevention
• Monitor blood test results (creatinine, BUN, electrolytes, calcium) and
promptly notify and manage the abnormalities.
• Watch for signs of hyperkalemia (weak , irregular pulse, abdominal
cramps and muscle weakness)
• Do not administer IV fluids with potassium while renal function is
impaired.
• Maintain low protein, low potassium, low Na and high carbohydrate
diet.
• Treat hyperkalemia (administer HCO3, IV glucose and insulin)
• Watch for signs of hypocalcaemia (muscle twitching and tetany) and
manage it timely.
Family education
• Explain the disease process and prognosis.
• Explain the level of renal function after the acute episode is over.
• Explain all steps of the diagnostic and treatment process to family
• Educate about the prompt medical treatment for the illness that may cause
renal injury.
• Discuss renal dialysis or transplantation if these are likely options for the
future.
• Provide emotional support to the child and family.
• Review the use of medication and explain the possible side effects
• Educate about the regular follow up and diet restriction
Complications
• Fluid buildup. AKI may lead to a buildup of fluid in your lungs, which can
cause shortness of breath.
• Chest pain. If the lining that covers your heart (pericardium) becomes
inflamed, child may experience chest pain.
• Muscle weakness. hyperkalemia may cause muscle weakness.
• Permanent kidney damage. Occasionally, acute kidney failure causes
permanent loss of kidney function, or end-stage renal disease (ESRD).
• Death. Acute kidney failure can lead to loss of kidney function and,
ultimately, death.
Acute renal failure.pptx for BNs 2nd year

Acute renal failure.pptx for BNs 2nd year

  • 1.
  • 2.
    Introduction • Renal failureis temporary or permanent damage to the kidneys that results in loss of normal kidney function. (Types include AKI and CKD) • Acute Renal failure is a sudden, usually reversible reduction in glomerular filtration rate resulting in an increase in blood concentration of urea and creatinine and disturbed fluid and electrolyte homeostasis. • It is a common life threatening condition in children, need urgent and adequate treatment.
  • 3.
    Incidence • The incidenceof any AKI was 26% and that of moderate-severe AKI was 14%. The incidence of AKI was similar in high-income 27% (23– 32), low-middle-income 25%, and low-income 24% countries. • Overall, AKI-associated mortality was observed in 11% of the pediatric population. AKI-associated mortality rate was highest at 18% and 22% in low-income and low-middle-income countries, respectively (Meena et al., 2023 ). • AKI accounts for 1.5-2% admission of the children in hospital.
  • 4.
    Etiology • The causesof AKI can be broadly divided into pre-renal, renal and post- renal causes. Overlap exists and a patient may have more than one cause foe their renal failure. Pre-renal cause:- associated with conditions that ↓se renal blood supply Fluid Volume depletion resulting from • Hemorrhage, • Renal loses (diuretics, osmotic diuresis) • Gastrointestinal loses (vomiting, diarrhea, nasogastric suction) • Burn (fluid loss through damaged skin) • Overuse of diuretics (excessive urination)
  • 5.
    Etiology contd…. • Impairedcardiac output eg. Congestive heart failure ,impaired cardiac efficiency, myocardial infraction, heart failure, dysrhythmias and cardiogenic shock. • Vasodilation resulting from sepsis, anaphylaxis and antihypertensive medication (eg ACE inhibitors)
  • 6.
    Renal cause:- causingdecrease glomerular filtration rate (GFR) 1. Prolonged renal ischemia • Pigment nephropathy • Trauma, injury, burns • Transfusion reaction, hemolytic anemia 2. Nephrotoxic agents • Aminoglycoside antibiotics(gentamycin, amikacin, tobramycin, streptomycin) • Radiopaque contrast agent • Heavy metals • NSAIDs • ACE inhibitors
  • 7.
    Renal cause contd… 3)Infectiousprocess • Acute pyelonephritis (Bilateral Pyelonephritis) • Acute glomerulonephritis 4) other conditions :- Tumour Lysis syndrome, Renal artery vein thrombosis Post renal cause:- obstruction to urine flow & prevent elimination of urine Renal calculi, obstructive uropathy, neurogenic bladder, tumors, rhabdomyolysis, wilm’s tumor , strictures, blood clots and developmental structural anomalies.
  • 8.
    Pathophysiology • For pre-renal cause (diarrhea) /fluid volume decrease due to vomiting, trauma • Severe reduction in glomerular blood flow • Reduction in GFR • Results in elevation of blood urea nitrogen(BUN) & decreased tubular reabsorption of Na from proximal tubules. • Increased concentration of Na in distal tubules. • Stimulation of renin mechanism • Vasoconstriction of afferent arterioles • Subsequent decrease in GFR and prevents urinary losses of Na
  • 9.
    Pathophysiology contd… • Ifcondition persists for long time cortical or tubular necrosis • Intrinsic damage of renal parenchyma occurs (if renal perfusion is not restored) • Acute real failure
  • 10.
    Phases of acuterenal failure There are four clinical phases of ARF • Initial phase –begins with initial insult & end when oliguria develops and lasts from hours to days. • Oliguria phase- is accompanied by rise in the serum concentration of waste substances. Urine output decreases from renal tubules damage. • Last for 5-15 days (shorten in infant and children 3-5days and 10-14 days in older children)and can persists for weeks where > 3weeks of this phase results in irreversible renal damage.
  • 11.
    Phases contd…. • Diureticphase- the kidney try to heal & urine output increases but tubule scarring & damage occur. But there is still risk of dehydration & electrolyte imbalance so close monitoring is needed. Lasts for few days. • Recovery phase- tubular edema resolves & renal functions improves, final resumption of normal urine osmolarity and blood electrolytes . It may takes 3-12 months
  • 12.
    Clinical manifestations • Almostevery system of the body is affected when there is failure of the normal renal regulatory mechanism. • Though symptoms can vary from person to person and depends upon underlying cause and duration of illness. • Someone in early stage kidney disease may not feel sick or notice symptoms as they occur. Specific features -Severe oliguria (urine output <1ml/kg/hour) but in some cases urine output may not be reduced. Anuria in some cases(uncommon) -Azotemia, hyperkalemia, hypocalcaemia -Metabolic acidosis manifested by tachycardia.
  • 13.
    Clinical manifestations contd… Nonspecificfeatures • May appear clinically ill & lethargic • Persistent nausea & vomiting • The skin & mucous membranes are dry from dehydration . • Breath may be odor of urine • Drowsiness, headache, muscle twitching & seizures. • Swelling of the legs, ankles, feet, face and/or hands • Shortness of breath due to extra fluid on the lungs
  • 14.
    Nonspecific features contd… •Abnormal heart rhythms, Muscle paralysis due to hyperkalemia • Appetite loss, a bad taste in the mouth • Difficulty sleeping, changes in mental status/ mood seizures , drowsiness due to electrolyte imbalances • Darkening of the skin • Excess protein in the blood • In later stage weight loss
  • 15.
    Diagnostic Evaluation • History:- history of massive bleeding, severe diarrhea, shock and onset of s/s eg oliguria (urine output < 0.5ml/kg/hour). • Physical examination :- edema, signs and symptoms, -Changes in urine – scanty to normal urine volume, may be hematuria, & low urine specific gravity • Urinary electrolytes :- Increased BUN & creatinine levels (azotemia) in monitoring kidney function & disease progression. Hyperkalemia and Na level, Calcium & phosphorus abnormalities. • Urine culture to rule out infective organism(in case of UTI) • ABG test to rule out metabolic acidosis
  • 16.
    Diagnostic Evaluation contd… •Hematology to rule out anemia • Creatinine Phosphokinase (if rhabdomyolysis is suspected) • Renal biopsy in cases of suspected RPGN or if AKI cause in uncertain in case of rapidly rising creatinine. • Anti- nuclear antibody, anti double- stranded DNA, c3, c4 , anti- nuclear cytoplasmic antibody (ANCA), anti glomerular basement membrane antibody (antiGBM) if patient has history, s/s consistent with glomerulonephritis.
  • 17.
    Therapeutic Management ofARF • The kidney has a remarkable ability to recover from insult. Mgmt should be planned according to underlying causes. Treatment includes: - Treatment of underlying causes - Management of complications - Supportive care Correction of dehydration , treatment of hyperkalemia and shock are primary concerns of management.
  • 18.
    Pharmacotherapy (Emergency management) •For hyperkalemia :- administering cation- exchange resins (Kayexalate ) – works by increases fecal potassium excretion through binding of K+ in the lumen of GI tract. • For widen QRS complexes or peaked T waves - Injection HCO3 1meq/kg IV to cause intracellular shift of potassium, this maneuver dose not reduce total body K+ stores. - Insulin and glucose IV:- this maneuver dose not reduce total body K+ stores • Hypocalcaemia:- Calcium chloride 20mg/kg IV, this maneuver stabilizes the cardiac myocyte membrane and prevents dysthymias. • Volume overload:- Furosemide 1mg/kg IV with repeated doses as necessary. • Low dose dopamine is often used to dilate the renal arteries through stimulation of dopaminergic receptors. • The elevated serum phosphate level may be controlled with phosphate-binding agents (aluminum hydroxide).
  • 19.
    Therapeutic Management ofARF contd… • Maintenance of fluid balance is based on daily body weight, vital signs especially BP, serial measurement of serum & urine concentrations (I/O), fluid losses, blood pressure & the clinical status of the child. • Insertion of foleys catheter to rule out urine retention, to collect urine and monitor the effects of diuretics. • Monitor sign of fluid excesses such as dyspnea, tachycardia, & distended neck vein regularly. • The lungs are auscultate for moist crackles. • Pre-renal causes of ARF may be restored by IV fluid & blood product transfusion & transfuse albumin for hypoproteinemia. • Dialysis may be initiated to prevent from serious complications as hyperkalemia, severe metabolic acidosis, and pericarditis. • Counselling for renal transplant if needed. • Management of other complications such as anemia through blood transfusion.
  • 21.
    Therapeutic Management ofARF contd… • ARF causes severe nutritional imbalances so calorie intake should be encouraged acc. to requirement. • Dietary proteins are limited to minimize protein break down & to prevent accumulation of toxic end products. • Calorie requirements are met with high carbohydrate meals because carbohydrates have a protein sparing effect. • Foods & fluid containing potassium & phosphorus (banana, citrus fruits & juices, coffee dairy products) are restricted. • Low sodium diet (avoid processed food, additional food intake). • Vitamins and minerals supplementations. Others Prevent from injury during convulsion. Provide care during dialysis.
  • 23.
    Nursing management Nursing assessment:-includes detail history of illness, drug therapy, exposure to toxic substances, allergy, fever etc. • Physical examination :- I/O, vital signs, urine specific gravity, daily weight, hydration status and nutritional status • Review of laboratory status: RFT • ECG and Echocardiogram • Chest x- ray to rule out pulmonary edema.
  • 24.
    Nursing diagnosis • Fluidand electrolyte imbalance related to altered kidney function. • Imbalanced nutrition less than body requirement related to protein catabolism, anorexia , nausea and vomiting. • Risk of infection related to invasive procedures and malnutrition. • Risk of injury related to metabolic abnormalities(uremia and hyperkalemia). • Knowledge deficit related to disease condition
  • 25.
    Nursing intervention Maintain fluid& electrolyte balance • Strictly record of intake & output, daily weight(same scale and same cloth), maintaining drip if fluid loss, monitor laboratory electrolytes regularly & careful & regular monitor of edema and auscultation of chest for crackles . • Maintain fluid restriction as prescribed. • Administer diuretics as prescribed. • Promptly report signs of heart failure eg bounding pulse, shortness of breath and adventitious breath sounds. • Give oxygen if the patient is dyspnea.
  • 26.
    Maintain nutrition • Assessand document dietary intake and weight daily. • Monitor blood electrolytes eg BUN, albumin Na and K. • Restrict sodium, potassium and phosphorus intake as indicated. • Provide small and frequent feedings • Offer frequent mouth care . • Provide hard candy and breath mints between meals. • Consult with dietician support team • Provide high calorie, low to moderate protein diet. Avoid concentrated sugar sources
  • 27.
    Infection prevention • Assessedema, purulent drainage and skin changes. • Hand hygiene maintain • Avoid invasive procedures whenever possible and use aseptic technique when doing invasive procedures. • Provide routine line cares eg. catheter care and perineal care, sponge bath. • Remove indwelling catheter as possible. • Encourage for deep breathing, coughing and frequent position change. • Monitor WBC count regularly. • Treatment of infections with antibiotics if culture is positive according to report.
  • 28.
    Injury Prevention • Monitorblood test results (creatinine, BUN, electrolytes, calcium) and promptly notify and manage the abnormalities. • Watch for signs of hyperkalemia (weak , irregular pulse, abdominal cramps and muscle weakness) • Do not administer IV fluids with potassium while renal function is impaired. • Maintain low protein, low potassium, low Na and high carbohydrate diet. • Treat hyperkalemia (administer HCO3, IV glucose and insulin) • Watch for signs of hypocalcaemia (muscle twitching and tetany) and manage it timely.
  • 29.
    Family education • Explainthe disease process and prognosis. • Explain the level of renal function after the acute episode is over. • Explain all steps of the diagnostic and treatment process to family • Educate about the prompt medical treatment for the illness that may cause renal injury. • Discuss renal dialysis or transplantation if these are likely options for the future. • Provide emotional support to the child and family. • Review the use of medication and explain the possible side effects • Educate about the regular follow up and diet restriction
  • 30.
    Complications • Fluid buildup.AKI may lead to a buildup of fluid in your lungs, which can cause shortness of breath. • Chest pain. If the lining that covers your heart (pericardium) becomes inflamed, child may experience chest pain. • Muscle weakness. hyperkalemia may cause muscle weakness. • Permanent kidney damage. Occasionally, acute kidney failure causes permanent loss of kidney function, or end-stage renal disease (ESRD). • Death. Acute kidney failure can lead to loss of kidney function and, ultimately, death.