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High Acuity Exam 4 > AKI ppt (chap 26) > Flashcards

AKI ppt (chap 26) Flashcards

1
Q

Define AKI.

A

Abrupt reduction in kidney function that leads to elevated creatinine, elevated blood urea nitrogen (BUN), and usually decreased urine output (oliguria). AKI is potentially reversible

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2
Q

What is the most common cause of AKI?

A

Sepsis and MODS

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3
Q

Why is the goal of AKI early diagnosis and prevention?

A

Since the prognosis is often reversible it is best to recognize and treat (the nurse should keep in mind that AKI often occurs in hospitalized pts). AKI has a high morbidity and mortality and the risk for it increases in sepsis, bleeding, and cardiac events. AKI is expensive to treat due to prolonged hospital stays and the need for dialysis or other RRTs

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4
Q

What are the phases of oliguric AKI?

A

Initiation, oliguric, diuretic, recovery

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5
Q

Describe phase one of oliguric AKI.

A

Intiation: begins at time of renal insult and continues until signs and symptoms are apparent. It lasts from hours to days with minimal effect on the endocrine function of the kidneys

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6
Q

Describe phase two of oliguric AKI.

A

Oliguric: usually last 5 to 10 days but can last weeks. Functional changes such as decreases in glomerular filtration, urine formation, and renal clearance. ↑ in serum concentration of urea, creatinine, uric acid, K, Mg, and urine output is

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7
Q

Describe phase three of oliguric AKI.

A

Diuresis: usually last 1 to 3 weeks but can last for months. Starts with gradual increase in urine output but watch for signs of dehydration (initial UO being 1 - 3 L/d then, possibly 3 - 5 L/d). Pt is unable to concentrate urine. Labs, acid-base, BUN/Cr start normalizing

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8
Q

Describe phase four of oliguric AKI.

A

Recovery: usually last for months to 1 year. Starts with increasing GFR and maximal kidney functions start to return such as regulatory and excretory mechanism.
BUN/Cr plateau, then decrease

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9
Q

What are the normals for specific gravity, urine osmolality, cr clearance, serium cr, urea nitrogen (BUN), BUN to cr ratio.

A 
specific gravity - 1.010-1.025
urine osmolality - random; 50-1200 mOsm/kg H2O
cr clearance - 85-135 mL/min
serium cr - 0.6-1.2 mg/dL
urea nitrogen (BUN) - 5-25 mg/dL
BUN to cr ratio - about 10:1 or 15:1
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10
Q

Out of these serum lab values which ones will increase or decrease with AKI: BUN, cr, uric acid, K, Cl, P, Ca, albumin.

A

BUN, cr, uric acid, K, Cl, P - increase

Ca, albumin - decrease

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11
Q

Out of these urine lab values which ones will increase,decrease, or be postive with AKI: protein, glucose, cr clearance, uric acid

A

protein - increase
glucose - positve
cr clearance, uric acid - decrease

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12
Q

What will be some abnormal findings with ABG, CBC, urine analysis of electrolytes, urinalysis.

A

ABG: metabolic acidosis
CBC: low hcg & hct, WBC possibly increased
Urine analysis of electrolytes: not valued if on diuretics, valuable indicators of functioning renal tubules, fractional excretion of Na+ (FENa)
Urinalysis: renal epithelial or granular casts maybe present

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13
Q

What are the different types of AKI?

A

Pre-renal, intra-renal, post-renal

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14
Q

Describe pre-renal injury. What is the patho behind it?

A

Occurs above/before the kidneys which leads to reduced blood flow to the kidneys by evoking renal salt and water retention. Pathophysiology: hypoperfusion to the kidney leads to the release of renin
which activates RAAS. RAAS leads to peripheral vasoconstriction, increased sodium reabsorption, release of antidiuretic hormone, enhance vasoconstriction, water reabsorption, decrease urine output, and increased urea

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15
Q

What are causes of pre-renal injury?

A

HYPOVOLEMIA - which can be caused by hemorrhage, burns, shock, excessive sweating, peritonitis, nephrotic syndrome, gastrointestinal losses, renal losses (e.g. diuretics, diabetes insipidus, malignancies), or systemic vasodilation (e.g., sepsis,* neurogenic shock)

ALTERED PERIPHERAL VASCULAR RESISTANCE/ VASODILATION - which can be caused by sepsis, antihypertensive medications, drug overdose, anaphylactic reactions, neurogenic shock, or NSAIDs)

CARDIAC DISORDERS/ DECREASED OUTPUT - which can be caused by CHF, MI, cardiac tamponade, or arrhythmias)

RENAL ARTERY DISORDERS - which can be caused by emboli, thrombi, stenosis, aneurysm, occlusion, or trauma

HEPATORENAL SYNDROME

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16
Q

What will be the volume, specific gravity, urine Na, osmolality, urine cr, and sediment when doing a urine test for pre-renal injury?

A 
volume - decreased to normal
specific gravity - high
urine Na - low
osmolality - high
urine cr - normal
sediment - normal
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17
Q

Describe intra-renal injury. What is the patho behind it?

A

Injury to renal tissue. Damage to one or more parenchymal structure(s) which can lead to acute tubular necrosis (causes 45-58% of all renal failure). Usually associated with intrarenal ischemia, toxins, or both. Pathophysiology: vasoconstriction from ischemia and SNS stimulate RASS which causes further vasoconstriction, ischemia diminishes cellular metabolism and tubular transport causing anaerobic metabolism and acidosis which leads to tubular cell swelling and necrosis

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18
Q

What are causes of intra-renal injury?

A

Nephrotoxic agents, inflammatory processes (bacterial, viral, toxemia of pregnancy), immune processes (autoimmunity, hypersensitivity, rejection), trauma, radiation nephritis, obstruction (neoplasm, stones, scar tissue), intravascular hemolysis (transfusion reaction), and systemic and vascular disorders (renal vein thrombosis, malaria, myeloma, sickle-cell disease, DM, SLE)

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19
Q

Name some nephrotoxins.

A

Drugs (anesthetics, antimicrobials, anti-inflammatories like NSAIDs, chemo,) contrasts media, biologic substances (tumor products, heme pigments such as hemoglobin, myoglobin), environmental agents (pesticides, fungicides, organic solvents such as diesel fuel, phenol), heavy metals (lead, mercury, gold, arsenic, bismuth, uranium, cadmium), plant and animal substances (mushrooms, snake venom)

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20
Q

What will be the volume, specific gravity, urine Na, osmolality, urine cr, and sediment when doing a urine test for intra-renal injury?

A 
volume - oliguria/nonliguria
specific gravity - low
urine Na - high
osmolality - low
urine cr - low 
sediment - casts present
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21
Q

Describe post-renal injury. What is the patho behind it?

A

Obstruction of urine flow which leads to increases in intranephronal pressure and
impairment in tubular function. Pathophysiology: bilateral obstruction results in anuria, urine congestion backflows which leads to slow tubular flow and GFR.
Prolonged, collecting system dilates and compress tissues which damages nephrons, leading to dysfunction in concentrating and diluting mechanism

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22
Q

What are causes of post-renal injury?

A

Ureteral, bladder neck, or urethral obstruction (calculi, neoplasms, sloughed papillary tissue, strictures, trauma, blood clots, congenital abnormalities, foreign object, surgical ligation), prostatic hypertrophy, retroperitoneal fibrosis, abdominal and pelvic neoplasms, pregnancy, neurogenic bladder, bladder rupture, drugs (antihistamines, ganglionic blocking agents)

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23
Q

What will be the volume, specific gravity, urine Na, osmolality, urine cr, and sediment when doing a urine test for post-renal injury?

A 
volume - oliguria to anuria 
specific gravity - normal to varies
urine Na - normal to varies
osmolality - normal to varies
urine cr - normal to varies
sediment - normal to varies
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24
Q

Name the systemic manifestations of AKI.

A

Cardiovascular: heart failure, dysrhythmias, peripheral edema, HTN

Hematological: anemia, altered coagulation, susceptibility to Infection

Acid-Base Balance: metabolic acidosis

Respiratory: pulmonary edema, potential for pneumonia

GI: anorexia, N/V, gastritis, bleeding

Neuromuscular: drowsiness, confusion, irritability, coma
tremors, twitching, convulsions

25
Q

What are the major treatment goals of AKI?

A

Supportive therapy to maintain homeostasis until kidney heals.Prevent life-threatening complications fluid & electrolyte imbalance, and acid-base imbalance. Manage base on etiology and degree of injury: removal of cause or contributing factor, conservative intervention such as rest, volume management and dietary restrictions, aggressive interventions such as dialysis

26
Q

How do you treat fluid overload?

A

Fluid restriction & diuretics

27
Q

How do you treat metabolic imbalance?

A

Protein intake needed, but there are limits

28
Q

How do you treat hyperkalemia imbalances?

A

Stabilize cardiac system by giving IV calcium, move K into cells via cocktail, remove K from Body through diuretics, GI excretion, hemodialysis

29
Q

What is Calcium Gluconate used to treat? How does it work? What is the usual dosage? When does it start to take effect?

A

Calcium gluconate is used to treat hyperkalemia. It works by antagonism of membranes. The usual dose is 10-30 ml of 10% solution over 2 min. It starts to take effect after 5 minutes

30
Q

What is Insulin and Glucose used to treat? How does it work? What is the usual dosage? When does it start to take effect?

A

Insulin and Glucose are used to treat hyperkalemia. They work by increasing K entry into the cells. The usual dose is 10 U IV bolus with 0.5 mU/kg of body weight per minute in 50 ml of 20% glucose. It starts to take effect around 30 – 60 min

31
Q

What is Sodium Bicarbonate used to treat? How does it work? What is the usual dosage? When does it start to take effect?

A

Sodium Bicarbonate is used to treat hyperkalemia. It works by increasing K entry into the cells. The usual dose is 44-50 mEq IV over 5 min; can be repeated within 30 min. It starts to take effect around 30 – 60 min

32
Q

What is Albuterol used to treat? How does it work? What is the usual dosage? When does it start to take effect?

A

Albuterol is used to treat hyperkalemia. It works by increasing K entry into the cells. The usual dose is 20 mg, nebulized. It starts to take effect around 30 – 60 min

33
Q

What is Kayexalate used to treat? How does it work? What is the usual dosage? When does it start to take effect?

A

Kayexalate is used to treat hyperkalemia. It works by removing excess K. The usual dose is 20 g of resin with 100 ml of 20% sorbitol. It starts to take effect around 2 – 4 hours

34
Q

What is dialysis used to treat? How does it work? What is the usual dosage? When does it start to take effect?

A

Dialysis is used to treat hyperkalemia. It works by removing excess K. The usual dose is variable. It starts to take effect around 1 – 3 hours

35
Q

How do you treat sodium imbalances?

A

IV fluids, prevent hypernatremia with more free water or IV fluids (0.45% Saline), diuretics

36
Q

How do you treat calcium imbalances?

A

Vitamin D supplementation (IV or PO)

37
Q

How do you treat acid base imbalances?

A

If it’s metabolic acidosis you can treat with dialysis,

IV Fluids, or bicarbonate infusion

38
Q

Describe nursing management of AKI.

A

Monitoring fluid & electrolyte status, fluid management & restrictions, reduction of metabolic rate, manage dietary needs, prevention of infection, skin care, protect from exposure to nephrotoxic agents

39
Q

What are the renal causes for renal replacement therapy (RRT)?

A

AKI with: ARDS, septicemia, cerebral edema, or CV instability.

40
Q

What are the non-renal causes for renal replacement therapy?

A

SIRS, crush syndrome, lactic acidosis, CHF

41
Q

What are specific indications for renal replacement therapy?

A

Refractory fluid overload, hyperkalemia, metabolic acidosis, azotemia, signs of uremia (pericarditis, neuropathy, unexplained AMS), hyperthermia, overdose of dialyzable drugs

42
Q

g

A

g

43
Q

What are different access points for dialysis?

A

Acute catheter which is usually placed in the neck or groin, chronic catheter which is usually tunneled and placed in the subclavian vein, AV fistula which is a surgical connection of artery & vein, AV Graft which is an implanted artificial tube to connect the artery and vein

44
Q

How do renal replacement (dialysis) machines work?

A

Ultrafiltration, hemofiltration, or hemodialysis

45
Q

Why do AKI pts in high acuity settings use continuous dialysis instead of intermittent or hybrid dialysis?

A

To dialyse patients in a more physiologic way, slowly, over 24 hours, just like the kidney. Intensive care patients are particularly suited to these techniques as they are, by definition, bed bound, and, when acutely sick, intolerant of the fluid swings associated with intermittent dialysis

46
Q

How does continuous veno-venous hemofiltration (CVVH) work?

A

Continuous venovenous hemofiltration, a form of convective dialysis. The ultrafiltration rate is high, and replacement electrolyte solution is required to maintain hemodynamic stability. This mode is also very effective for clearing mid sized molecules, such as inflammatory cytokines. It is hypothesized that removal of such mediators may play a role in improving outcome in sepsis

47
Q

How does continuous veno-venous hemodialysis (CVVHD) work?

A

Continuous venous venous hemodialysis– which is continuous diffusive dialysis, the dialysate is driven in a direction countercurrent to the blood. This provides reasonably effective solute clearance, although mostly small molecules are removed

48
Q

How does continuous veno-venous hemodifiltration (CVVHDF) work?

A

Continuous venous venous hemodiafiltration, which is the most popular method of dialysis in ICU, combines convective and diffusive dialysis. Both small and middle molecules are cleared, and both dialysate and replacement fluids are required

49
Q

How does slow continuous ultrafiltration (SCUF) work?

A

Slow continuous ultrafiltration, which is used for volume control in fluid overloaded patients. SCUF does not require the use of replacement fluid, and fluid removal is 300ml to 500ml per hour

50
Q

Define ultrafiltration.

A

The movement of fluid through a membrane caused by a pressure gradient. The higher the pressure the greater the movement of fluid

51
Q

What are the advantages of continuous RRT?

A

Improved CV stability, improved tolerance to ultra-filtration thereby enabling the removal of large fluids loads over time, ability to maintain azotemia, better solute control even in severely catabolic patients

52
Q

What are the disadvantages of continuous RRT?

A

Intensive nursing requirements, usage of more NHPPD, aggressive anticoagulation, immobility leading to longer LOS/debility, cost

53
Q

What are the advantages of intermittent RRT?

A

Same outcomes as CRRT, significantly less costly, precise achievement of UF goals without hypotension, able to start mobility program, unrestricted patient access - available for diagnostics surgery etc…

54
Q

What are the disadvantages of continuous RRT?

A

Training time is longer, staff perceive it as “dialysis”

55
Q

What are the advantages of hemodialysis?

A

High intra-dialytic solute clearances if patient can tolerate, works well with chronic patients, ideal for non acute patients

56
Q

What are the disadvantages of hemodialysis?

A

Not feasible for the hemodynamically unstable patients, high intradialytic solute clearances, disequlibrium and water shift may worsen brain edema and increase ICP

57
Q

What are general complications of RRT?

A

Bleeding, electrolyte imbalances, acid-base imbalances, infection inappropriate dosing of medications

58
Q

What are complications of RRT during treatment?

A

Seizure (excessive urea clearance especially during first tx), bleeding (excessive anticoagulant, accidental removal of needles, uncapped catheters), muscle cramps (excessive ultrafiltration), dialzer hypersensitivity (to materials in filter), fever (bacteremia, water born pyrogens, overheated dialysate), hypotension (excessive ultrafiltration, cardiac arrhythmia, air embolus hemorrhage, anaphylactoid rx), air embolism (defective machine detector, leak in the circuit, empty air-vented IV), cardiac arrest (electrolyte imbalance, hyperthermia, hemolysis)

59
Q

What is the prognosis of AKI?

A

Still poor even if AKI is treated w/ RRT. High mortality rates and 20% who survive remain dialysis dependent. AKI is not only a consequence of severe disease but also contributes to poor outcomes

High Acuity Exam 4 (7 decks)

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