SESSION K8. Acute Kidney Injury

37th Annual Advanced Practice in Primary and Acute Care Conference: October 9-11, 2014 3:55 SESSION K8 Acute Kidney Injury Christopher K. Johnson, M...
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37th Annual Advanced Practice in Primary and Acute Care Conference: October 9-11, 2014

3:55

SESSION K8 Acute Kidney Injury Christopher K. Johnson, MD

Session Description: Acute kidney injury is a very common occurrence in hospitalized patients, and significant contributor to patients' morbidity and mortality. Come learn to "think like a nephrologist" and understand our approach to the diagnosis of acute kidney and how we manage it. Learning Objectives: Following my presentation, participants will be able to: 1. Devise a differential diagnosis of likely causes of AKI in the hospitalized patient. 2. Interpret blood and urine studies to support a likely diagnosis, including prerenal azotemia, acute tubular necrosis, and acute intersitital nephritis. 3. Comprehend the indications for and modalities of acute dialysis.

S E S S I O N K8

9/23/2014

Acute Kidney Injury Advanced Practice in Primary and Acute Care Christopher Johnson, MD October 10, 2014

OR HOW TO THINK LIKE A NEPHROLOGIST

Outline I have no financial interests to disclose.

I. Definitions II. Diagnosis III. Management IV. Renal Replacement Therapy

Preamble: Anatomy Review

100ml/min x 1440min/day = 144000ml/day = 144L /day

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Why AKI?

DEFINITIONS

AKI in the ICU is bad

Acute kidney injury is surprisingly common and a powerful predictor of mortality in surgical sepsis. White, Laura; Hassoun, Heitham; Bihorac, Azra; Moore, Laura; Sailors, R; McKinley, Bruce; Valdivia, Alicia; Moore, Frederick

RIFLE criteria Stage

Creatinine

Urine output

Risk

Increase > 50 % (or increase > 0.3 mg/dl)

6 hours

Injury

Increase > 100%

< 0.5 ml/kg/hr for > 12 hours

Failure

Increase > 200%

< 0.3 ml/kg/hr for > 12 hours or anuria

Loss

Need for RRT > 4 weeks

End-Stage

Need for RRT > 3 months

Journal of Trauma and Acute Care Surgery. 75(3):432-438, September 2013.

URINE OUTPUT IS CRITICAL

BUT IT IS A SIGN, NOT A GOAL

70kg x 0.5ml/kg/hr = 35ml/hr = concerning 70kg x 0.3ml/kg/hr = 21ml/hr = worrisome anuria = bad

There is no “goal urine output.” Those values are diagnostic, not directive.

It’s like temperature, not blood pressure.

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AKI in the ICU is bad

Acute kidney injury is surprisingly common and a powerful predictor of mortality in surgical sepsis. White, Laura; Hassoun, Heitham; Bihorac, Azra; Moore, Laura; Sailors, R; McKinley, Bruce; Valdivia, Alicia; Moore, Frederick Journal of Trauma and Acute Care Surgery. 75(3):432-438, September 2013.

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Classic Approach PRERENAL aka Perfusion - volume down - blood loss - cardiorenal - hepatorenal - ACE-inhibitors - NSAIDs - (contrast)

DIAGNOSIS

Suggested Approach in the ICU 1. Rule-out (most) postrenal: Urinary Catheter Also, this will give you real-time urine output

2. Make assessment of volume status Blood pressure, CVP, Urine Na, Physical Exam

3. If dry, give a fluid challenge A real fluid challenge (unless heart failure)

4. Evaluate medication list carefully Both for causes and troublesome meds

INTRARENAL aka Kidney - ATN - ischemic - toxic

-

AIN contrast rhabdo emboli TMA acute GN

POSTRENAL aka Drainage - prostate - bladder - neurogenic

- ureters - malignancy

- tubules - crystals

Urine Tests • Urinalysis – High specific gravity  concentrated urine – Leukocyte esterase  infection or AIN

• Urine microscopy – Granular casts  ATN – WBC  infection or AIN

• Urine electrolytes – Low Urine Na or Cl  Prerenal

Low Urine Sodium

Volume Down

Increased RAS

Increased sodium reabsorption

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Back to the Tubule! PRERENAL State of decreased perfusion Reversible with volume Can improve in hours Low urine sodium Bland urine sediment Additive risk with other renal toxins

ISCHEMIC ATN Death of kidney tubule cells Irreversible with volume Can improve in days to weeks High urine sodium “Muddy brown” granular casts Protective (?) from other renal toxins

PRERENAL AZOTEMIA AND ATN EXIST ON A SPECTRUM

BUT YOU STILL NEED TO TRY AND TELL THEM APART

Patients progress from temporary poor perfusion to cell damage over hours to days. It can be tough to tell where they are in the process.

Your management, particularly volume status, and expected course are quite different.

First, do no harm • “Avoid nephrotoxins” – Contrast, tubular toxins

• Maintain Adequate Perfusion – Blood pressure, Volume

• Evaluate All Medications

MANAGEMENT

– Antibiotic dosing – Electrolyte replacement orders – Blood pressure medications – ACE-I, diuretics

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Diuretics are Value Neutral

Diuretics Block Na reabsorption

In prerenal states (intravascular volume depletion), diuretics are harmful, exacerbating the underlying problem, and can worsen AKI. In heart failure, they can be curative. In ATN, they probably don’t matter.

Contrast is Usually Bad DIURETICS (AND FLUIDS) SHOULD BE GIVEN TO TREAT VOLUME EXCESS (DEFICIT) They should not be given to target a certain urine output, just to achieve that output. There are times when diuretics can forestall dialysis by converting to nonoliguria.

Unwanted Squeeze

Iodinated contrast (for CT scans) causes renal vasoconstriction. This effect is additive with other prerenal states, hypotension, diuretics. In these situations the risk is highest. Severe ATN may be in some ways protective – further contrast may not cause further damage. Contrast administration is not an indication for dialysis.

Caution with ACE-Inhibitors

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A little bit of math

Beware the estimated GFR

A 68-year-old man with chronic kidney disease and a baseline creatinine of 1.4 (eGFR = 44) presents acute-on-chronic heart failure with anuric acute renal failure with a creatinine of 2.8. What is his estimated GFR currently?

Classic Indications

RENAL REPLACEMENT THERAPY

Alphabet Soup

Acidosis Electrolytes Ingestion / Toxin Overload Uremia

Dialysis = Diffusion

Acronym

Stands For

IHD

Intermittent Hemodialysis

Meaning Usual dialysis

CRRT

Continuous Renal Replacement Therapy

General Term

CVVH

Continuous Veno-Venous Hemofiltration

Clears through convection using replacement fluids

CVVHD

Continuous Veno-Venous Hemodiafiltration

Adds dialysis to the CVVH circuit

SLED

Slow Low Efficiency Dialysis

Usual dialysis, but run with slower flows

SCUF

Slow Continuous UltraFiltration

Just volume removal without any clearance

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SCUF

CVVH

Continuous renal replacement therapy. Amlani GS. JPMA 2012; 62(3). Continuous renal replacement therapy. Amlani GS. JPMA 2012; 62(3).

CRRT / SLED

CVVHD(F)

Continuous renal replacement therapy. Amlani GS. JPMA 2012; 62(3). Continuous renal replacement therapy. Amlani GS. JPMA 2012; 62(3).

How much dialysis?

VA/NIH Acute Renal Failure Trial Network. NEJM 2008 258(1): 7-20.

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