Organ Failure LP Sp18 (2).
Know lab values
BUN 10-20 mg/dL
Creatinine male: 0.6-1.2, Female: 0.5-1.1
WBC 5-10
RBC 4.2-5.4 (f), 4.7-6.1 (m)
Hgb 12-16 (f), 14-18(m)
Hct 37-47% (f), 42-52% (m)
Plt 150-400
Na 136-145
K+ 3.5-5.0
Ca+ 9.0-10.5
Mg 1.3-2.1
Phosphorus 3.0-4.5
Specific gravity 1.005-1.030
pH 7.35-7.45
PaCo2 35-45
Pao2 80-100
Hco3 21-28
Blood osmolarity 285-295
Albumin 3.5-5.0
24 hr urine for creatinine clearance -void 1st thing in am and discard the 1st specimen, then collect all urine in 24
hrs
ACUTE KIDNEY INJURY OR ARF
-Sudden onset, lasts weeks to <3mos, good prognosis if treated early
o Rapid loss in kidney function leading to the collection of metabolic wastes in the body.
o Can result from conditions that reduce blood flow to the kidneys(prerenal failure),
glomeruli/tissue/interstitial damage(Intrarenal failure), of obstruction of urine flow(postrenal
failure).
o If occurs in pts who already have reduced kidney function, it may lead to ESKD (end-stage
kidney disease)
o This acute syndrome may be REVERSIBLE. Reduced blood flow, toxins, tubular ischemia,
infections, and obstruction have different effects on renal system.
o With shock or other problems causing an acute reduction in blood flow to the kidneys
(hypoperfusion), the kidney compensates by constricting renal blood vessels, activating renin-
angiotensin-aldosterone , releasing ADH. This helps increase blood volume and improve kidney
perfusion but has other responses:
o Oliguria (less than 400 ml/day) and Azotemia(the retention and build up of nitrogenous wastes in the
blood). Obstruction anywhere within the urinary tract may result in reduced urine formation and full
or partial obstruction to urine outflow.
o If BUN rises faster than creatinine- cause usually r/t protein breakdown or dehydration
o When both BUN and creatinine rise and ration btwn them remains constant- kidney dysfunction
o Highest death rate is trauma (70%) and surgery. AKI caused by nephrotoxic substances has the
lowest rates of recovery.
CLASSIFICATIONS:
, Organ Failure LP Sp18 (2).
Risk, Injury, Failure, Loss, End-stage (1st 3 may be reversible, last 2 may not )
TYPES
Prerenal causes- decreased blood flow to kidneys from renal artery up to heart that deprives kidney of
nutrients; sudden/severe drop in BP (shock) or interruption of BF to kidneys
o most common causes are hypovolemic shock and heart failure.
o Occurs in 60-70% of cases
o Usually occurs w/volume depletion states
▪ Blood or fluid loss (surgery, trauma, shock)
▪ BP drugs resulting in hypotension
▪ MI= low CO
▪ Infection
▪ Severe burns, dehydration (hypovolemia)
o Results in hypoperfusion and decreased GFR
o *Can be corrected by correcting blood volume, increasing blood pressure, and improving CO.
Intrarenal causes- AKA oliguric AKI or ATN (acute tubular necrosis). Direct damage to kidneys
o damage to the renal structures
➢ Inflammation of glomeruli (glomerulonephritis) or tubules (vasculitis)
➢ Nephrogenic agents (such as aminoglycosides)
➢ Local infection (strep or pyelonephritis)
➢ Certain meds- NSAIDS, ACEI, ABX
4 Phases to intrarenal failure
1. Initiation period – begins with initial insult and ends with oliguria (begins with cause to kidney, ends with
S/S appear. Must find cause to correct, prevent long term damage.
2. Oliguric phase Occurs within 1 – 7 days of renal insult and can last a few days to several weeks. Average duration 10
– 14 days. We want this stage to be short as possible. Some skip this stage and go right to diuretic stage.
➢ UOP: < 400 ml/day is usually the first symptom
➢ Elevated BUN and Cr
➢ S/S:
• Neuro: lethargic, confused, itching, tired = low protein (safety)
• Hyperkalemia (restrict K+ foods, monitor, Kayexalate)
• High fluid in body (edema, HTN) (restrict fluids, strict I/O, daily wt.,
monitor BP, O2, lung sounds, RR)
➢ Metabolic acidosis (confused, Kussmaul’s), safety, respiratory status, Bicarb
➢ Mild hyponatremia (high phos, low Ca, high urine sp. Gr. >1.030)
(restrict phosphate)
3. Diuretic phase-nephrons on way to recovery, GFR starts to improve, patient more alert, urine sp. Gr <1.030 (diluted)
➢ Follows oliguric phase
➢ Gradual increase in UOP of 1 – 3 L/d (as much as 3-6L/d)
➢ F&E depletion is a major complication
➢ Monitor for hyponatremia, hypoK+, and dehydration
➢ May last 1 – 3 weeks
➢ Hypovolemia (I/O, daily wt.)
➢ Postural hypotension and tachycardia
➢ BUN decreases slowly
➢ Na+ and K+ loss in urine
➢ Increased mental status
➢ Increased activity tolerance
4. Recovery phase
➢ GFR back to normal and maintained
➢ BUN and CR stabilize and then decrease
➢ Can take up to 12 months
➢ Major improvements occur in the 1st 1 – 2 weeks
➢ Most common cause of death in ARF is infection
Postrenal causes-Factors outside kidney – below level of kidney
, Organ Failure LP Sp18 (2).
o Often related to obstructions of outflow within kidneys or urinary tract
• Stones, enlarged prostate, cervical/colon cancer
o Almost always treatable
HEALTH PROMOTION
• Avoid dehydration by drinking at least 2-3L of fluids daily. This is especially important for athletes.
Antibiotics are common drugs that have nephrotoxic side effects. NSAIDs can cause or increase the
risk for ARF.
• PRIORITY: preventing volume depletion. S/S of volume depletion (low UOP, Decreased SBP,
decreased pulse pressure, orthostatic hypotension, thirst, rising blood osmolarity)
HX:
• recent surgery, trauma, or transfusions might lead to reduced renal blood flow, drug use. Especially antibiotics, ace-
inhibitors, and NSAIDs, recent imaging procedures that used contrast dye, disease that impair renal function- DM,
lupus, long term HTN. Possible glomerulinephritis: ask about recent colds, influenza, gastroenteritis, and sore
throats. Extensive bowel preps, NPO status before surgery, and fluid loss during surgery can cause prerenal
azotemia.
ASSESSMENT:
• s/s are r/t to azotemia (retention of waste in body) & underlying cause;
• Prerenal azotemia: hypotension, tachycardia, decreased CO, decreased central venous pressure, decreased
UOP, lethargy
• Intrarenal and Post-renal azotemia: Oliguria (<400 ml/day) or anuria (<100 ml/day), edema, HTN, tachycardia,
SOB, distended neck veins, elevated CVP, weight gain, respiratory crackles, anorexia, nausea, vomiting, and
lethargy or changes in LOC. Electrolyte imbalances
LABS /DIAGNOSTICS/ IMAGING:
• Urine tests BUN, Cr.) If Cr is high=low kidney function
• X-rays (abdominal x-rays) is used to check the size of the kidneys.
• Renal ultrasonography- useful with urinary tract obstructions
• CT scans w/o contrast dye- obstruction or tumors
• Renal scan/ cystoscopy/ retrograde pyelogrpahy
• Kidney biopsy
NURSING INTERVENTIONS:
-What nursing interventions are important?
-heart monitor, VS, Vasopressins, safety, strict I/O, may be on fluid restrictions
-based on kidney function
-continuously monitor patient
-MAP=65 mm hg
-Oliguria (<400 ml/day of urine) anuria (<100 ml/day)
-Drug therapy
BP meds, diuretics, Kayexalate (lowers K+)
• What do we need to remember about drug therapy? Toxicity
• Cardiac glycosides
• Digoxin (watch for N/V and halos)
• Vitamins and minerals (monitor)
• Synthetic erythropoietin (monitor)
• Phosphate binders (low phosphate, high Ca+)
• Amphojel, AluCap
-IV therapy
-calcium gluconate, Insulin
-CVP/PAP catheters
-Calcium Channel Blockers
-increases blood flow to kidneys
-Monitor protein intake due to degree of AKI (increased breakdown=uremia or azotemia)
-Oral supplements of TF or
TPN Complications from AKI
• Metabolic (acidosis)
, Organ Failure LP Sp18 (2).
• Give bicarb and kayexalate to lower K+
• Cardiopulmonary
• Arrhythmias, overload, BP, HF, HTN, pericarditis, MI
• Neuro
• Lethargy, confusion, weakness
• Immune/infection
• #1 cause of death, pneumonia, sepsis
• GI
• N/V, ulcer, low peristalsis
• Hematologic
• Low RBC, anemia, bleeding
• Renal
• CKI, permanent kidney damage
• GFR should be >90; if it is lower = low UOP =more H20 in body (HTN, edema).
• Other
• Hiccups, low thyroid hormone
Manifests as:
-Increase in serum creatinine
-Increase in BUN
-Urinary volume change (usually low)
-What else?
-Ph low, electrolytes
NUTRITION:
Pts who have AKI have a high rate of protein breakdown; specified amnts of protein, sodium, and fluids. For patient
who does not require dialysis: 0.6 g/kg of body weight or 40 g/day of protein. For patients who DO require dialysis: 1-
1.5 g/kg; amount of sodium ranges from 60 to 70 mEq. Amt of fluid is generally calculated to be equal to urine
volume plus 500 ml. TPN may be necessary if their appetite is poor. Constantly monitor serum electrolytes to indicate
when TPN sol needs to be changed. IV fat emulsion (intralipid) infusions can provide a nonprotein source of calories.
In uremic patients, fat emulsions are used in place of glucose to avoid excessive sugars
Treatment
Dialysis therapies: when in critical care: some type of filtration is used to pull off fluid
• HD and PD are used in patients with L and E levels of AKI.
• Dialysis- indications for dialysis- uremia, persistent high K levels, acidosis, fluid volume excess,
uremic pericarditis, and encephalopathy. When HD is expected for several wks the catheter is usually
placed in the subclavian or internal jugular vein. If only one or two HD txs are needed, a femoral site
may be used. Longer use of femoral site is avoided bc the pts mobility is restricted and complications
like hematomas, and infection are common. Repeated access is impossible.
• The subclavian vein is used when possible, instead of femoral site bc the longer the femoral
catheter stays in place the greater risk for infection. Subclavian catheter can be placed in at
bedside.
• Monitor for s/s of procedure complications like pneumothorax(reduction breath sounds, tracheal
deviation away from midline, prominence and poor movement of one side of the chest) or
subcutaneous emphysema.
• If HD is needed long term, a long term catheter is placed. A tunneled HD catheter is inserted through the
tunnel and into the jugular vein.
• HD catheters have two lumens, one for outflow and one for inflow. A triple lumen has an extra lumen
for drawing venous blood or giving drugs and fluid w/o interrupting dialysis.
• PD- may also be used, although some patients such as those being mechanically ventilated, may not
be able to tolerate the abdominal distention that occurs with PD.
Continuous renal replacement therapy
• standard tx for ARF. Form of hemofiltration. Similar to HD but temporary and often better tolerated
• Continuous arteriovenous hemofiltration(CAVH) is used for pts with fluid volume overloads, resistant
to diuretics, and have unstable blood pressures and CO. requires the placement of both arterial and
venous catheters and an MAP of 60mmHg. The typical adult MAP is 100. CAVH continuously removes
large amounts of plasma water, wastes, and electrolytes. Electrolytes are replaced through prescribed
amounts of IV solutions. A major disadvantage of AV filtration is the risk for bleeding caused by
anticoagulants used to prevent clotting.
• A double lumen dialysis catheter is inserted into a large vein(subclavian, jugular) for
CAVHD(continuous arteriovenous hemodialysis and filtration). A dialysate delivery system is used to
Know lab values
BUN 10-20 mg/dL
Creatinine male: 0.6-1.2, Female: 0.5-1.1
WBC 5-10
RBC 4.2-5.4 (f), 4.7-6.1 (m)
Hgb 12-16 (f), 14-18(m)
Hct 37-47% (f), 42-52% (m)
Plt 150-400
Na 136-145
K+ 3.5-5.0
Ca+ 9.0-10.5
Mg 1.3-2.1
Phosphorus 3.0-4.5
Specific gravity 1.005-1.030
pH 7.35-7.45
PaCo2 35-45
Pao2 80-100
Hco3 21-28
Blood osmolarity 285-295
Albumin 3.5-5.0
24 hr urine for creatinine clearance -void 1st thing in am and discard the 1st specimen, then collect all urine in 24
hrs
ACUTE KIDNEY INJURY OR ARF
-Sudden onset, lasts weeks to <3mos, good prognosis if treated early
o Rapid loss in kidney function leading to the collection of metabolic wastes in the body.
o Can result from conditions that reduce blood flow to the kidneys(prerenal failure),
glomeruli/tissue/interstitial damage(Intrarenal failure), of obstruction of urine flow(postrenal
failure).
o If occurs in pts who already have reduced kidney function, it may lead to ESKD (end-stage
kidney disease)
o This acute syndrome may be REVERSIBLE. Reduced blood flow, toxins, tubular ischemia,
infections, and obstruction have different effects on renal system.
o With shock or other problems causing an acute reduction in blood flow to the kidneys
(hypoperfusion), the kidney compensates by constricting renal blood vessels, activating renin-
angiotensin-aldosterone , releasing ADH. This helps increase blood volume and improve kidney
perfusion but has other responses:
o Oliguria (less than 400 ml/day) and Azotemia(the retention and build up of nitrogenous wastes in the
blood). Obstruction anywhere within the urinary tract may result in reduced urine formation and full
or partial obstruction to urine outflow.
o If BUN rises faster than creatinine- cause usually r/t protein breakdown or dehydration
o When both BUN and creatinine rise and ration btwn them remains constant- kidney dysfunction
o Highest death rate is trauma (70%) and surgery. AKI caused by nephrotoxic substances has the
lowest rates of recovery.
CLASSIFICATIONS:
, Organ Failure LP Sp18 (2).
Risk, Injury, Failure, Loss, End-stage (1st 3 may be reversible, last 2 may not )
TYPES
Prerenal causes- decreased blood flow to kidneys from renal artery up to heart that deprives kidney of
nutrients; sudden/severe drop in BP (shock) or interruption of BF to kidneys
o most common causes are hypovolemic shock and heart failure.
o Occurs in 60-70% of cases
o Usually occurs w/volume depletion states
▪ Blood or fluid loss (surgery, trauma, shock)
▪ BP drugs resulting in hypotension
▪ MI= low CO
▪ Infection
▪ Severe burns, dehydration (hypovolemia)
o Results in hypoperfusion and decreased GFR
o *Can be corrected by correcting blood volume, increasing blood pressure, and improving CO.
Intrarenal causes- AKA oliguric AKI or ATN (acute tubular necrosis). Direct damage to kidneys
o damage to the renal structures
➢ Inflammation of glomeruli (glomerulonephritis) or tubules (vasculitis)
➢ Nephrogenic agents (such as aminoglycosides)
➢ Local infection (strep or pyelonephritis)
➢ Certain meds- NSAIDS, ACEI, ABX
4 Phases to intrarenal failure
1. Initiation period – begins with initial insult and ends with oliguria (begins with cause to kidney, ends with
S/S appear. Must find cause to correct, prevent long term damage.
2. Oliguric phase Occurs within 1 – 7 days of renal insult and can last a few days to several weeks. Average duration 10
– 14 days. We want this stage to be short as possible. Some skip this stage and go right to diuretic stage.
➢ UOP: < 400 ml/day is usually the first symptom
➢ Elevated BUN and Cr
➢ S/S:
• Neuro: lethargic, confused, itching, tired = low protein (safety)
• Hyperkalemia (restrict K+ foods, monitor, Kayexalate)
• High fluid in body (edema, HTN) (restrict fluids, strict I/O, daily wt.,
monitor BP, O2, lung sounds, RR)
➢ Metabolic acidosis (confused, Kussmaul’s), safety, respiratory status, Bicarb
➢ Mild hyponatremia (high phos, low Ca, high urine sp. Gr. >1.030)
(restrict phosphate)
3. Diuretic phase-nephrons on way to recovery, GFR starts to improve, patient more alert, urine sp. Gr <1.030 (diluted)
➢ Follows oliguric phase
➢ Gradual increase in UOP of 1 – 3 L/d (as much as 3-6L/d)
➢ F&E depletion is a major complication
➢ Monitor for hyponatremia, hypoK+, and dehydration
➢ May last 1 – 3 weeks
➢ Hypovolemia (I/O, daily wt.)
➢ Postural hypotension and tachycardia
➢ BUN decreases slowly
➢ Na+ and K+ loss in urine
➢ Increased mental status
➢ Increased activity tolerance
4. Recovery phase
➢ GFR back to normal and maintained
➢ BUN and CR stabilize and then decrease
➢ Can take up to 12 months
➢ Major improvements occur in the 1st 1 – 2 weeks
➢ Most common cause of death in ARF is infection
Postrenal causes-Factors outside kidney – below level of kidney
, Organ Failure LP Sp18 (2).
o Often related to obstructions of outflow within kidneys or urinary tract
• Stones, enlarged prostate, cervical/colon cancer
o Almost always treatable
HEALTH PROMOTION
• Avoid dehydration by drinking at least 2-3L of fluids daily. This is especially important for athletes.
Antibiotics are common drugs that have nephrotoxic side effects. NSAIDs can cause or increase the
risk for ARF.
• PRIORITY: preventing volume depletion. S/S of volume depletion (low UOP, Decreased SBP,
decreased pulse pressure, orthostatic hypotension, thirst, rising blood osmolarity)
HX:
• recent surgery, trauma, or transfusions might lead to reduced renal blood flow, drug use. Especially antibiotics, ace-
inhibitors, and NSAIDs, recent imaging procedures that used contrast dye, disease that impair renal function- DM,
lupus, long term HTN. Possible glomerulinephritis: ask about recent colds, influenza, gastroenteritis, and sore
throats. Extensive bowel preps, NPO status before surgery, and fluid loss during surgery can cause prerenal
azotemia.
ASSESSMENT:
• s/s are r/t to azotemia (retention of waste in body) & underlying cause;
• Prerenal azotemia: hypotension, tachycardia, decreased CO, decreased central venous pressure, decreased
UOP, lethargy
• Intrarenal and Post-renal azotemia: Oliguria (<400 ml/day) or anuria (<100 ml/day), edema, HTN, tachycardia,
SOB, distended neck veins, elevated CVP, weight gain, respiratory crackles, anorexia, nausea, vomiting, and
lethargy or changes in LOC. Electrolyte imbalances
LABS /DIAGNOSTICS/ IMAGING:
• Urine tests BUN, Cr.) If Cr is high=low kidney function
• X-rays (abdominal x-rays) is used to check the size of the kidneys.
• Renal ultrasonography- useful with urinary tract obstructions
• CT scans w/o contrast dye- obstruction or tumors
• Renal scan/ cystoscopy/ retrograde pyelogrpahy
• Kidney biopsy
NURSING INTERVENTIONS:
-What nursing interventions are important?
-heart monitor, VS, Vasopressins, safety, strict I/O, may be on fluid restrictions
-based on kidney function
-continuously monitor patient
-MAP=65 mm hg
-Oliguria (<400 ml/day of urine) anuria (<100 ml/day)
-Drug therapy
BP meds, diuretics, Kayexalate (lowers K+)
• What do we need to remember about drug therapy? Toxicity
• Cardiac glycosides
• Digoxin (watch for N/V and halos)
• Vitamins and minerals (monitor)
• Synthetic erythropoietin (monitor)
• Phosphate binders (low phosphate, high Ca+)
• Amphojel, AluCap
-IV therapy
-calcium gluconate, Insulin
-CVP/PAP catheters
-Calcium Channel Blockers
-increases blood flow to kidneys
-Monitor protein intake due to degree of AKI (increased breakdown=uremia or azotemia)
-Oral supplements of TF or
TPN Complications from AKI
• Metabolic (acidosis)
, Organ Failure LP Sp18 (2).
• Give bicarb and kayexalate to lower K+
• Cardiopulmonary
• Arrhythmias, overload, BP, HF, HTN, pericarditis, MI
• Neuro
• Lethargy, confusion, weakness
• Immune/infection
• #1 cause of death, pneumonia, sepsis
• GI
• N/V, ulcer, low peristalsis
• Hematologic
• Low RBC, anemia, bleeding
• Renal
• CKI, permanent kidney damage
• GFR should be >90; if it is lower = low UOP =more H20 in body (HTN, edema).
• Other
• Hiccups, low thyroid hormone
Manifests as:
-Increase in serum creatinine
-Increase in BUN
-Urinary volume change (usually low)
-What else?
-Ph low, electrolytes
NUTRITION:
Pts who have AKI have a high rate of protein breakdown; specified amnts of protein, sodium, and fluids. For patient
who does not require dialysis: 0.6 g/kg of body weight or 40 g/day of protein. For patients who DO require dialysis: 1-
1.5 g/kg; amount of sodium ranges from 60 to 70 mEq. Amt of fluid is generally calculated to be equal to urine
volume plus 500 ml. TPN may be necessary if their appetite is poor. Constantly monitor serum electrolytes to indicate
when TPN sol needs to be changed. IV fat emulsion (intralipid) infusions can provide a nonprotein source of calories.
In uremic patients, fat emulsions are used in place of glucose to avoid excessive sugars
Treatment
Dialysis therapies: when in critical care: some type of filtration is used to pull off fluid
• HD and PD are used in patients with L and E levels of AKI.
• Dialysis- indications for dialysis- uremia, persistent high K levels, acidosis, fluid volume excess,
uremic pericarditis, and encephalopathy. When HD is expected for several wks the catheter is usually
placed in the subclavian or internal jugular vein. If only one or two HD txs are needed, a femoral site
may be used. Longer use of femoral site is avoided bc the pts mobility is restricted and complications
like hematomas, and infection are common. Repeated access is impossible.
• The subclavian vein is used when possible, instead of femoral site bc the longer the femoral
catheter stays in place the greater risk for infection. Subclavian catheter can be placed in at
bedside.
• Monitor for s/s of procedure complications like pneumothorax(reduction breath sounds, tracheal
deviation away from midline, prominence and poor movement of one side of the chest) or
subcutaneous emphysema.
• If HD is needed long term, a long term catheter is placed. A tunneled HD catheter is inserted through the
tunnel and into the jugular vein.
• HD catheters have two lumens, one for outflow and one for inflow. A triple lumen has an extra lumen
for drawing venous blood or giving drugs and fluid w/o interrupting dialysis.
• PD- may also be used, although some patients such as those being mechanically ventilated, may not
be able to tolerate the abdominal distention that occurs with PD.
Continuous renal replacement therapy
• standard tx for ARF. Form of hemofiltration. Similar to HD but temporary and often better tolerated
• Continuous arteriovenous hemofiltration(CAVH) is used for pts with fluid volume overloads, resistant
to diuretics, and have unstable blood pressures and CO. requires the placement of both arterial and
venous catheters and an MAP of 60mmHg. The typical adult MAP is 100. CAVH continuously removes
large amounts of plasma water, wastes, and electrolytes. Electrolytes are replaced through prescribed
amounts of IV solutions. A major disadvantage of AV filtration is the risk for bleeding caused by
anticoagulants used to prevent clotting.
• A double lumen dialysis catheter is inserted into a large vein(subclavian, jugular) for
CAVHD(continuous arteriovenous hemodialysis and filtration). A dialysate delivery system is used to
