One of the following 1. Increase in serum creatinine by >.3 mg/dL in 48 hours 2. Increase in serum creatinine 1.5X baseline within last 7 days 3. Urine output

L20: AKI Flashcards by Jeri Sheldon (AZ PA Mast 20)

Acute renal failure

refers to severe AKI which requires dialysis

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AKI diagnosis

One of the following

Increase in serum creatinine by >.3 mg/dL in 48 hours
Increase in serum creatinine 1.5X baseline within last 7 days
Urine output*

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Prerenal AKI

decreased renal perfusion

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Intrinsic renal AKI

acute tubular necrosis

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Postrenal AKI

obstructive

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Prerenal disease can be caused by

True volume depletion
Hypotension (Shock, Aggressive HTN tx)
Edema
Selective renal ischemia (Bilateral renal artery stenosis)
Medications affecting GFR

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Medications affecting GFR

NSAIDS

ACE-I

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Intrinsic renal disease can be caused by

Renal ischemia: from any severe prerenal disease

Sepsis: hypotension→ release of cytokines and activation of neutrophils

Nephrotoxins

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Risk of AKI from IV contrast

Pre-existing renal disease: rare in normal renal function

Volume depletion

Repeated doses of contrast

DM, CHF, age

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Nephrotoxic drugs to avoid for 48 hours after IV contrast

NSAIDS

Metformin

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Nephrotoxins that may cause AKI

Rhabdomyolysis→ Heme pigments
Cisplatin
HIV meds
IVIG
Mannitol
IV contrast
Aminoglycosides

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Causes of postrenal AKI

Bilateral obstruction:

Prostatic disease: hyperplasia or cancer

Metastatic cancer

Neurological disease: neurogenic bladder→ urinary retention

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Obstructive BPH tx

foley catheter

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Nonoliguric

> 400 mL/24 hours

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Oliguric

<400 mL/24 hours

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Anuric

<100 mL/24 hours

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Make sure urine from a urinalysis

Is at room temperature within 2 hours of collection (or refrigerated then rewarmed)

Foley catheter: get sample “fresh” from tubing, not bag

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Pathognomonic for acute tubular necrosis

muddy brown casts

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Normal serum creatinine levels by gender

Male: .6-1.2 mg/dL
Female: .5-1.1 mg/dL

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How is serum creatinine related to GFR?

Inverse relationship

ex: doubled serum creatine would represent a halved GFR

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Prerenal fractional excretion of sodium (FENa)

<1%

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Intrarenal fractional excretion of sodium (FENa)

> 2%

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fractional excretion of sodium (FENa) is between 1-2%

could be either prerenal or intrarenal causes

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when is fractional excretion of sodium (FENa) unreliable

diuretics

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fractional excretion of sodium (FENa) calculation

(Urine Na/Serum Na)/ (Urine Cr/Serum CR) x 100%

Would diagnose post-renal cause of AKI if seen on ultrasound

hydronephrosis

Indication for renal biopsy

To provide more definitive diagnosis when there is no clear explanation of AKI: Creatinine is markedly elevated/significantly worsens May allow therapeutic intervention to prevent end stage renal disease

Contraindications for renal biopsy

Bleeding diathesis Pyelonephritis Renal tumor Solitary native kidney

When is dialysis indicated for AKI?

Life-threatening complications Volume imbalance, metabolic acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia, uremia, AMS (severe AKI)

Fluid challenge

if fluid causes an increase in urine, the cause of AKI is prerenal

Signs/symptoms of volume depletion

History of fluid loss: N/V | Hypotension, tachycardia, oliguria

How to do a fluid challenge

1-3 L of .9 NS | Reassess

How might a patient become volume overloaded?

Initial presentation ~OR~ Fluid retention from IV therapy + decreased ability to secrete sodium and water

Volume overload treatment

Diuretics | I+Os

What can volume overload eventually cause?

Fluid retention→ pulmonary edema→ respiratory failure

If diuretics don't increase urine output in a volume overloaded patient

stop diuretics | start dialysis

Causes of metabolic acidosis

Excretion of acid and regeneration of bicarb impaired + Low GFR Diarrhea→ lost bicarb→ worsens Sepsis, trauma, multi-organ failure (lactic/keto acids)

For whom is dialysis the preferred treatment of metabolic acidosis?

Severe oligo-anuric AKI + volume overload + pH <7.1 (hemodynamically unstable)

For whom is bicarbonate administration not preferred in cases of metabolic acidosis?

volume overload: causes large sodium load that can contribute to volume overload

2 ways to manage metabolic acidosis

Dialysis | Bicarbonate administrations

When can bicarb be given for metabolic acidosis?

``` not volume overloaded and: Diarrhea pH <7.1 awaiting dialysis Rhabdomyolysis → prevent further renal injury by myoglobin → Falling out of favor ```

Hyperkalemia presentation

Has very few symptoms, but is fatal | Impaired neuromuscular transmission and cardiac conduction abnormalities

Hyperkalemia treatment

Medical therapy + dialysis | → Remove excess and drive extracellular K+ into cells

If a patient is asymptomatic, hypocalemic, and hyperphostphatemic

correct hyperphosphatemia

Why do Hypocalcemia and Hyperphosphatemia occur in AKI?

Reduced GFR→ increased phosphorus → decreased calcium Common

When is the total serum concentration of ionized calcium inaccurate?

Low albumin

Signs of hypocalcemia

paresthesia, tetany (carpopedal spasm) confusion seizures trousseau's sign (carpal spasm after occlusion of brachial artery) chvostek’s sign (tap facial nerve→ contraction) QT prolongation

Treatment of symptomatic hypocalcemia and hyperphosphatemia

IV calcium | → Severe hypocalcemia: given while awaiting dialysis regardless of risk of calcification

IV Calcium side effects

If severely hyperphosphatemic, IV calcium → calcium phosphate crystal deposition in vasculature/organs

Hyperphosphatemia >6 mg/dL treatment

dietary phosphate binders

If a hyperphosphatemic patient cannot tolerate oral intake

dialysis

Hyperphosphatemia >12 mg/dL treatment

dialysis → faster than binders → more effective in preventing injury to to crystal precipitation

Dietary phosphate binders if the patient is also hypocalcemic

Calcium acetate | Calcium carbonate

Dietary phosphate binders if the patient is not hypocalcemic

Aluminum hydroxide | Lanthanum carbonate

Severe uremia treatment

dialysis

Severe uremia symptoms

pericarditis neuropathy decline in mental status

When is severe uremia more common?

CKD

An episode of AKI

greater risk of CKD and ESRD

predictor poor prognosis for short term and long term mortality

serum creatinine increases by .3 mg/dL

If a patient gets AKI during their ICU stay

there is a 50% mortality rate

How many patients: Have AKI on admission? Develop AKI during hospitalization? Develop AKI in the ICU?

1% 25% 60%