final exam Flashcards
Fluid volume 1kg=
1 Liter
anuria
<50 mL/24hrs of urine output
(<1-2 mL/hr)
earliest clinical manifestation of AKI
oliguria
oliguria
less than 0.5mL/hr (400mL in 24hrs)
Pathophysiology of AKI
reduced blow flow to the kidneys (shunting)
hypovolemia
hypotension
reduced cardiac output & HF
Obstruction of kidney or lower urinary tract
bilateral blood flow obstruction
RIFLE
Severity Level
Risk- decreased U/O for 6hrs; Cr 1.5
Injury- decreased U/O for 12hrs; Cr 2x baseline
Failure- anuria >12 hours; Cr 3x baseline
Outcomes levels of loss
Includes utilization of some type of renal replacement therapy
Loss (> 4 weeks)
Persistent AKI
End-stage kidney disease
>3 months of AKI
Prerenal failure
reduced blood flow to the kidney
Intrarenal/Intrinsic Failure
damage the glomeruli, interstitial tissue, or tubules
Postrenal failure
obstruction of urine flow
Prerenal Failure causes
*hypoperfusion
*FVD- GI Loss/ Hemorrhage/ renal loss (diuresis)
*Impaired Cardiac Efficiency- Cardiogenic shock (pump failure)/ dysrhythmias/ HF/ MI
*Vasodilation- anaphylaxis, sepsis (distributive shock)/antihypertensive medications
Early AKI (levels R & I) can be reversed.
prerenal clinical characteristics
decreased urine output
increased BUN/creatinine
increased urine osmolality
increased serum K+ and mag
FVD- H&H high/low. trend MAP
Intrarenal Failure causes
*Parenchymal Damage
*Prolonged Renal ischemia (2 hypoxia)- hemoglobinuria (blood trans reaction)/ rhabdo/ blocked blood flow
*Nephrotoxic Agents- aminoglycosides, NSAIDS, contrast dye/poisons/ chemo
*Infectious Processes- acute pyelonephritis/glomerulonephritis
*Disease Process- acute tubular necrosis
Intrarenal Clinical Characteristics
increased BUN/Creatinine
increased K+ & mag
often decreased urine output
increased weight
FVE
Postrenal Failure causes
-ureter, bladder, or urethral cancer, cervical cancer
-Kidney, ureter, or bladder stones
-BPH or cancer
-bladder atrophy
-calculi
-blood clots
What happens in Postrenal Failure
-obstruction distal to kidney
-pressure rises in the kidney tubules and causes decreased GFR
Postrenal Clinical Characteristics
increased BUN/ creatinine
decreased or sudden anuria
Postrenal clinical treatmeants
early intervention
relieve obstruction- surgery, cystoscopy, catheter, flush
uremia s/s
pruritis, muscle cramps, change in mental status, n/f, fatigue, anorexia, wt loss, seizures, decreased LOC, and/or MI
hyperkalemia s/s
n/v. chest pain, muscle weakness, numbness, tingling, GI pain, short QTI, peaked T wave, QRS prolongation, short PRI
Phases of Intrarenal AKI
Initiation Phase:
Begins with the initial insult and ends when oliguria develops
Oliguric Phase:
Increase in substances that SHOULD be excreted by kidneys (potassium, creatinine, urea (BUN), magnesium
Uremia s/s and hyperkalemia s/s develop
10-14 days
400 ml in 24 hours (0.5ml/kg/hr) or less
Diuretic Phase:
Gradual increase in urine output, stabilized lab values, achieve normal or elevated urine output levels
Still an altered kidney function, abnormal GFR
Recovery phase:
Can take 3-12 months to achieve this state
GFR is 1%-3% less than what it should be
Normal lab value ranges
Metabolic acidosis s/s
change in mental status, tachycardia., n/v, h/a, anorexia, fatigue -compensatory: tachypnea
AKI assessment
- Determine AKI Cause
Address Fluid Volume Status
FVE or FVD
FVD: Prerenal
FVE: Intra/Post Renal - All AKI Types
Rising BUN and Creatinine
Increased serum potassium, and phosphorous, and magnesium
Decreased serum calcium - Electrolyte management:
Hyperkalemia - Perform EKG, Cardiac Monitor
Administer sodium polystyrene (Kayexalate)
Hypocalcemia and hyperphosphatemia
Phosphorus binders: sevelamer (Renagel), lanthanum carbonate (Fosrenol)
May require temporary HD
May require calcium replacements
Address Acid/Base Imbalances
Metabolic Acidosis s/s
AKI Diagnostic findings
EKG
Renal ultrasound
Renal CT or MRI
X-ray (KUB)
Cystoscopy
Labs:
BUN
Cr
BNP
ABG
BMP (electrolytes)
U/A
Urine electrolytes
AKI medical management
- Medical Management: restore normal chemical and fluid balance
- Fluid management
Prerenal- administer IV fluids
Intra/Post Renal- fluid restriction, diuretics - Treat metabolic acidosis
- Blood pressure management
Prerenal- increase
Intra/Post- avoid hypertension - Metabolic Acidosis
ABGs, Sodium Bicarbonate administration
Decreased serum CO2 levels and decreased pH. - Renal Replacement
Dialysis
AKI prevention
AKI early identification
Prevent dehydration
Avoid hypotension
Limit exposure to nephrotoxins
Adequate fluid administration:Avoid over diuresis, maintain MAP, caution with nephrotoxic agents & IV contrast
Preserve renal function
Prevent complications
Balance FVE and FVD
Nutrition Therapy in AKI
High carbohydrate diet (limit fat intake d/t ketone production)
So carbs are used for energy, then protein can be used for tissue and muscle needs
Protein- very individualized
Limited to needed only, then increased when in diuretic phase
Nursing Management of AKI
- All Types
Monitor urine output and total I/O
Weigh daily
Cardiac monitoring
ABG interpretation - Prerenal
Administer IVF, blood products - Intrarenal
Restrict fluids, renal diet
Limit nephrotoxins (NSAIDs, chemo, contrast, aminoglycosides, etc.) - Postrenal
Perform bladder scans, administer urine flow medications (tamsulosin, finasteride)
Rhabdomyolysis
- Toxic syndrome caused by the release of myoglobin from skeletal muscle
Causes AKI
Can cause intra-renal injury or ATN - Traumatic
Crush injuries, burns, electrocution, falls with long down time - Non-traumatic
Illicit drugs, heat stroke, medications (i.e. statins), malignant hyperthermia
Rhabdomyolysis clinical characteristics
- Muscle cramps, weakness and dark (tea-colored) urine
- Increased serum creatine kinase
Indicative of muscle injury or disease - Increased myoglobin
- Increased BUN/Creatinine, potassium
- AKI
Rhabdomyolysis treatment & nursing management
-IVF, dialysis
-Monitor lactate Levels, CK, BUN/Creat, potassium
-Cardiac monitor, frequent VS, I/O
Acute Tubular Necrosis causes
- Ischemia:Pre-renal causes (shock)
- Nephrotoxins:
Antibiotics
Heavy metals
Poisons
Anesthetics
Radiopaque Contrast Dye
Heme pigments:
Myoglobin Rhabdomyolysis: Released from muscle tissue caused by damage
Hemoglobin Intravascular hemolysis:blood transfusion reactions
Acute Tubular Necrosis (ATN) characteristics
- ATN is an AKI caused by damage to the kidney tubules
-Damaged cells of epithelial tubules, kidney structures are damaged/ destroyed
Tubules=tiny ducts that filter blood
Epithelial cells take 7-21 days to regenerate - Most Common intrinsic AKI
- ATN impairs release of ADH
- U/A- Muddy brown casts present
ATN Acute Tubular Necrosis treatment and Nursing management
Same as intrarenal failure
-Support, IVF, avoid nephrotoxins, treat complications
Contrast Induced AKI
Contrast (IV, PO, PR) is used in a wide variety of diagnostic imaging.
Contains Iodine or gadolinium (gad) Molecular structure (3 ring) for tissue differentiation
Agents higher than blood osmolality (275-299 mOsm/kg) are hyperosmolar and can cause shifts of both solutes and water in a variety of organs – especially the KIDNEYS
Renal Replacement Therapy
Needed when the pathologic changes of stage 4 and 5 CKD are life threatening or pose continuing discomfort to the patient
When conservative therapies such as diet, drugs, and fluid restrictions are no longer effective alone
Transplantation may be discussed at anytime
HD/CRRT or PD
Hemodialysis (HD)
Most common renal replacement therapy used with ESKD & renal failure
Dialysis removes excess fluids and waste products and restores chemical and electrolyte balance
Passes patient blood through an artificial semipermeable membrane to perform the filtering and excretion functions of the kidney
HD Vascular Access: Permanent
AV Fistula: An internal anastomosis of an artery to a vein– located in Forearm– needs to mature for 2-4 months or longer
AV Graft: Synthetic vessel tubing tunneled beneath the skin, connecting and artery and a vein– Located in forearm, upper arm, inner thigh– needs to mature for 1-2 weeks
HD Vascular Access: Temp
- HD Catheter: Dual or Triple Lumen- Inserted in Subclavian, internal jugular, or femoral vein: can be used immediately after insertion- need chest x-ray to confirm placement
- Subcutaneous Device: An internal device with two metallic access ports and two catheters inserted into large central veins: Located in Subclavian– Can be used immediately after insertion
HD Vascular Access nursing concerns
Limb alert
assessments: Bruit (swish heard)
Thrill (vibration felt)
HD Nursing Care
- Medications can be dialyzed out with HD and should not be administered just before or during HD
- Vasoactive drugs can cause hypotension during HD (nitroglycerin, nitroprusside, etc.)
- Coordinate meds with physician & HD RN
- Post HD:
- Monitor for s/s of side effects from treatment
- Most common problems include:
Hypotension
h/a
N/V
Malaise
Dizziness
Muscle cramps
Complications of HD
- Dialysis Disequilibrium Syndrome (fluid volume shifts)
-Cerebral edema and increased ICP
-Neurological symptoms (h/a, n/v, restlessness, decreased LOC, seizures, coma, or death)
-Hypotension (circulatory collapse)
Peritoneal Dialysis information
Allows exchange of wastes, fluids, and electrolytes to occur in the peritoneal cavity
Slower than HD
Less hazardous
CKD patients can select HD or PD
PD is great for patients who are difficult to obtain vascular access on, can’t tolerate anticoagulation, who are unstable, and those with a chronic infection
Not a treatment for AKI
Peritoneal Dialysis process
Sterile dialysate (1-2L) is introduced into the peritoneal cavity via an abdominal catheter and waste ducts are cleared by diffusion and osmosis
Contraindications to Peritoneal Dialysis (PD)
peritoneal adhesions
extensive intra-abdominal surgery
Complications of PD (peritoneal dialysis)
Peritonitis (inflammation of peritoneum)- most common
60-80% of long-term pts
Cloudy dialysate drainage, diffuse abdominal pain, and rebound tenderness
Tx: antibiotics, heparin, maybe removal of catheter
Stomach & small intestine are ___
acidic
Large intestine is ___
alkalotic
What makes up the small intestine?
Duodenum, jejunum, ileum
what makes up the large intestine
cecum, ascending colon, transverse colon, sigmoid
Reabsorbs water, passages of wastes, neutralizes contents
Large Intestine
an acute abdominal pain (non-traumatic), if not treated, is ____
life threatening
Causes for acute abdominal pain
bowel obstruction (large or small)
appendicitis
diverticulitis
Complications of acute abdominal pain
peritonitis
sepsis and septic shock
Primary peritonitis
spontaneous bacterial peritonitis (ie PD catheter)
Secondary peritonitis
perforated organs that leak contents (ie diverticulitis, trauma, infection. ingestion of sharp object)
tertiary peritonitis
immunocompromised infection (chemo/aids/hiv)
Peritonitis complications
Immediate hypermotility followed by paralytic ileus (consider bowel sounds)
* Peristalsis slows or stops in response to the inflammation
* Toxins and wastes enter the Abdominal cavity and can enter the blood stream
* Causing Sepsis and SEPTIC SHOCK
* Fluid backs up in the small intestine causing dilation and can leak into the abdominal cavity
* Air and Fluid collect in the Bowel
peritonitis causes
Bacteria or chemicals entering the abdominal cavity causing widespread inflammation
* Fluid shifts from intestinal ECF to abdominal cavity, causing hypovolemia -HYPOVOLEMIC
SHOCK (consider risks r/t FVD)
* Bowel or appendix perforation, peritoneal dialysis contamination, leaked pancreatic enzymes
Peritonitis clinical manifestations
Pain
* Mimics disorder causing the problem
* Begins as diffuse abdominal pain that transitions to constant, localized and increasing intensity
* Rebound tenderness and extremely distended abdomen
* Very Rigid, board like abdomen
* Anorexia, nausea and vomiting
* Increased abdominal pressure causing vena cava flattening, gut ischemia, ARF/anuria, worsening acidosis, difficulty ventilating
* Normal 0-5mmHg
* Diminished peristalsis with eventual Ileus
* Decreased or absent bowel sounds and absence of flatus and feces
* Tachycardia
* Hypotension (decreased CO)
* Fever
* Sepsis, hypovolemia, shock
Peritonitis assessment and dx
Radiology: Abdominal Xray and CT Scan showing free air, bowel dilation and distension, bowel inflammation or edema/fluid in
the abdomen, abscesses
* Labs: Increased WBCs, disturbances in potassium, sodium and chloride
Peritonitis Medical Management
- NPO
- Isotonic IVF-many LITERS
- Pain management
- Opioids
- Electrolyte replacement
- r/t AKI from decreased CO
- Antibiotics
- E.Coli, Klebsiella, Pseudomonas, Streptococcus
- Broad spectrum until causative agent determined
- Semi- Fowlers position
- NG/OG tube to decompress the abdomen
- Surgery: REPAIR CAUSE
- Laparotomy
- Pre/intra/post-op care needed
- Drains and wound care
Appendicitis pathophysiology
Inflamed and edematous appendix
* Occlusion caused by stool, foreign body or infectious material
* Causes ischemia and bacterial impedance
* Gangrene
* Perforation
* Appendix ruptures and contents can center peritoneum
* Occurs with 6 to 24 hours of appendicitis
* Most common complication: peritonitis
appendicitis clinical manifestations
Constant pain that progresses to RLQ pain (McBurney’s Point)
* Rebound tenderness
* Rovsing’s Sign- push on LLQ & pain occurs in RLQ
* n/v
* Anorexia
* Fever
Appendicitis assessment and dx
increased WBC, increased C-Reactive Protein (released from liver in response to
inflammation)
* Ultrasound showing enlarged appendix, CT scan
* Surgical Intervention (exploratory)
* Drainage of abscess
* Removal of appendix (appendectomy)
TPN- Total Parenteral Nutrition
Intensive and complete nutrition supplement
* Hypertonic Solution with dextrose, minerals,
electrolytes, protein
* Given via a central line
* Monitor I/O, monitor blood glucose
