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Clinical 3 > AKI > Flashcards

AKI Flashcards

1
Q

What is AKI?

A

Sudden, acute drop in kidney function and GFR occurring over a period of
hours, days, or weeks

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2
Q

Is AKI reversible?

A

May be reversible depending on cause or may lead to permanent renal failure

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3
Q

What is AKI characterized by?

A

fluid, electrolyte and acid-base imbalances and wasting

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4
Q

How can AKI be defined in terms of numbers?

A
  • Increase in SCr by ≥ 0.3 mg/dl (≥ 26 μmol/l) within 48 hours
  • Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days;
  • Urine volume <0.5 ml/kg/h for 6 hours.
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5
Q

what are the 3 AKI classifications according to etiology?

A

prerenal
intrarenal
postrenal

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6
Q

Describe prerenal AKI

causes, dietary intervention

A

• Impaired blood flow to kidneys resulting in decreased urine output and retention of N waste products

Causes:
• Hypovolemia: hemorrhage, burns, diarrhea ,vomiting, inadequate fluid replacement
• Increased vascular capacity and leakiness:sepsis,anaphylaxis
• Heartis compromised: heart failure, cardiogenic shock after an MI
• Renal stenosis: Fibromuscular dysplasia, atherosclerosis causing stenosis

• Minimal dietary intervention required; reversible if underlying problem treated

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7
Q

Describe intrarenal AKI

causes, dietary intervention

A

Damage within kidney cells due to ischemia, toxins and tubular obstruction

Cause: acute tubular necrosis (ATN) = death of epithelial cells in the renal tubular that cause obstruction of the lumen and fluid back-up.
• Prerenal issue causing lack of blood flow
• Exposure to nephrotoxic exogenous compounds: (antibiotics), heavy metals, ethylene glycol
• Exposure to nephrotoxic endogenous compounds: myoglobin (released from muscle damage cells), uric acid (destruction of DNA/RNA re. chemotherapy), hemoglobin
• Interstitial nephritis and glomerulonephritis
• Nutrition management is critical

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8
Q 
Describe postrenal (obstructive) AKI
causes, dietary intervention
A
  • Obstruction in urine flow (urinary tract obstruction)
  • Causes: bladder cancer, benign prostate hyperplasia, strictures, blood clots, renal stones
  • Minimal dietary intervention and reversible if underlying problem corrected
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9
Q

what are the phases of AKI

A

• Onset: Kidney injury occurs (hours to days)
• Oliguric (or anuric) phase: Urine output decreases from renal tubule damage (8 – 14 days…)
• Diuretic phase: Healing and urine output increases (7 to 14 days)
- Decreasing BUN/Cr, potassium, phosphorus and Magnesium
• Recovery: Tub (Months ++)

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10
Q

what are the stages of AKI? at what stage is dialysis given?

A

1, 2, 3

dialysis is usually started in stage 2 or 3

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11
Q

is AKI hyper or hypo metabolic

A

hyper

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12
Q

Clinical manifestations of AKI

A
  • extremely low urine output
  • fluid and electrolyte disorders
  • azotemia
  • wasting, particularly if they are both oliguric and hypercatabolic (common complications of AKI)
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13
Q

AKI has a poor __ and a high __ rate associated with the degree of __ and __.

A

AKI has a poor prognosis and a high mortality rate associated with the degree of hypercatabolism and infection.

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14
Q

Symptoms and signs of AKI

A

•Fluid retention/overload

  • Swelling in the hands, face, or feet
  • SOB (worse during activity or when lying down)
  • Tachycardia and enlarged neck veins

• Electrolyte abnormalities (K, Mg, Na often high)

  • Muscle cramps
  • Irregular heartbeat
  • Neurological problems, (tingling, paralysis, confusion)

• Metabolic acidosis

  • Nausea, vomiting, and loss of appetite
  • Muscle fatigue
  • Rapid breathing
  • Headache
  • Confusion or lethargy

• Anemia

  • Paleness
  • Shortness of breath
  • Fatigue
  • Irregular heartbeat
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15
Q

AKI complications

A

• Hematuria
• Reduced urine output (oliguria)
• Dehydration: may lead to excess thirst, dizziness, weak rapid pulse
• Uremia (high levels of urea in the blood): may affect the digestive system, brain, heart, lungs, and other parts of
the body.
• Side or lower back pain: If obstruction in urinary tract
• HYpercatabolism, high levels of protein breakdown

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16
Q

metabolic complications of AKI

A
  • Hypertension
  • hyperglycemia
  • insulin resistance
  • high cholesterol
  • high triglycerides
  • decreased protein synthesis
  • increased protein breakdown
  • azotemia
  • changes in electrolytes up or down
  • hypocalcaemia
  • metabolic acidosis
  • anaemia
17
Q

AKI: Nutritional goals

A
  • Minimize uremia and maintain the chemical composition of the body as close to normal as possible
  • Preserve body protein stores until renal function returns
  • Maintain fluid, electrolyte, and acid-base homeostasis
  • Nutritional support
18
Q

AKI: General Dietary Guidelines

A
  • Controlled protein, PO4, Na, K, fluid
  • Energy to meet requirements and minimize lean body mass breakdown
  • Consider: clinical condition, lab values, fluid status, type/frequency of dialysis
  • Supplementation of water soluble vitamins due to losses in dialysis
  • IBW vs actual weight vs dry weight
19
Q

does AKI require dialysis?

A

AKI often requires RRT

• Continuous renal replacement therapy (CRRT)

20
Q

Energy reccs for AKI

A

20-30 kcal/kg/d

Based on actual body weight (ideal body weight if obese)

21
Q

Protein reccs for AKI

A
  • 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis
  • 1.0–1.5 g/kg/d in patients with AKI on RRT
  • up to a maximum of 1.7 g/kg/d in patients on continuous renal replacement therapy (CRRT) and in hypercatabolic patients.
22
Q

Minerals, electrolytes, trace elements reccs for AKI

A

Maintain serum level

23
Q

Fluid reccs for AKI

A

Output + 400-500 ml

24
Q

what should be monitored in AKI?

A

Daily intake and output Serum electrolytes levels Blood pressure
Weight
TSF/MAMC (Triceps skinfold /midarm muscle circumference): Useful in stable patients–affected by hydration status

25
Q

what is the sign of fluid retention in AKI?

A

• Gain> 0.5-1kg/day suggests fluid retention

26
Q

what does weight loss suggest in AK

A

Loss (compared to dry weight) suggests LBM loss

27
Q

Which biochemical data should we assess in AKI patients

A 
• GFR
• BUN/serum creatinine
• Serum
• Serum albumin
• Serum cholesterol and lipid
profile
• Serum calcium
• Serum phosphorus
• Intake and output
28
Q

components of nutrition history that should be assessed

A
  • Usual food intake
  • Special diet instructions
  • Chewing/swallowing ability
  • Assessment of GI issues
29
Q

alimentation indicators that should be assessed

A

• Decreased P.O. intake
• TPN, PPN, TF (new order, sudden
discontinuation of, inappropriate composition/rate)
• Nausea, vomiting, anorexia, ileus

30
Q

medical history components that should be assessed

A
  • Disease or condition leading to AKI
  • Treatment modality
  • Concurrent medical conditions
  • Medical conditions with potential nutritional implications
  • Medications with food/drug interactions
31
Q

should AKi patients receive ONS?

A

When possible, patients with AKI should receive oral nutrition.
If a patient cannot eat adequately, other forms of nutrition support should be provided. Enteral nutrition support with standard formulas should be considered first for patients with AKI.
If necessary, specialized formulas with lower electrolyte levels can be considered

32
Q

Should protein be restricted in AKI?

A

no!

33
Q

ASPEN statement about all patients in ICU and PN calories

A

ASPEN: In all ICU patients receiving PN, mild permissive underfeeding should be considered at least initially. Once energy requirements are determined, 80% of these require- ments should serve as the dose of parenteral feeding

34
Q

preferred route of nutrition administration according to KDOQI

A

We suggest providing nutrition preferentially via the enteral route in patients with AKI.

Clinical 3 (17 decks)

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