Acute Kidney Injury admission

Most of the times, Acute Renal Failure is noticed in patients who are admitted to ER with some other Acute illness like any infection, vomiting, diarrhea etc.

Potassium and / or Phosphorus are usually elevated.

ER:

IV Fluids-ER usually gives one or two liters of iv fluid boluses.

They check Urinalysis /UA

Foley Catheter-if there is urinary retention due to BPH

Hospitalist:

Order Urine for Electrolytes like Urine Sodium, Urine Creatinine so that FENA can checked.

Give IV Fluids-Most patients with mild AKI improve with iv fluids. NS or 1/2 NS depending on Na level. If patient has history of Heart Failure, make sure to put limited fluids and for limited time. e.g. order fluids for 6-12hrs and reevaluate.

If Potassium is slightly elevated, it may improve when IV fluids improved kidney function. If Potassium is more than 7, usually the patient gets admitted to ICU.

Order Input/Output monitoring. No need for Foley for every patient for this.

US of Kidney and Urinary Bladder–>Also, Urology Consult if there is bladder obstruction due to BPH or kidney stone in ureter leading to hydronephrosis.

Do not do any CT or MRI with IV contrast if patient is in AKI.

Discontinue ACEI/ARBs, diuretics like HCTZ, Lasix, Bumex and NSAIDs, also discontinue BP meds if there is hypotension.

Start Bicarbonate drip if severe Metabolic Acidosis [Low HCO3].

Nephrology consult if patient is in severe AKI. Mild AKI usually improves by next day with iv fluids and may not need Nephrology consult.

If AKI is not improving for more than 72hrs despite iv fluids, you may be dealing with ATN in which case you need to involve nephrologist for possibility of starting HD.

How do you document?

e.g. Acute Kidney Injury on CKD stage 3

What does Nephrologist do?

May start HD if needed depending on severity.

May start Phosphate binders if Phosphorus is very high with baseline CKD.

May adjust fluids.

Some theoretical concepts but most are not that challenging.

Causes of Metabolic Acidosis: [Mnemonic MUD PILES]

M – Methanol

U – Uremia

D – DKA

P – Paraldehyde

I – Isoniazid

L – Lactic Acid

E – Ethanol, Ethylene glycol

S – Salicylates

Metabolic Acidosis with a Normal Anion Gap:

Longstanding diarrhea (bicarbonate loss)

Uretero-sigmoidostomy

Pancreatic fistula

Renal Tubular Acidosis

Intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants

Renal failure

Consider RTA if patients have metabolic acidosis with a normal anion gap or unexplained hyperkalemia.

 Feature Type 1 Type 2 Type 4
Incidence Rare Very rare Common
Mechanism Impaired H+ excretion in the distal tubule Impaired HCO3 resorption in the proximal tubule Decrease in aldosterone secretion or activity
Plasma HCO3(mEq/L) Usually < 15, often < 10 Usually 12–20 Usually > 17
Plasma K Usually low but tends to normalize with alkalinization Usually low and decreased further by alkalinization High
Urine pH > 5.5 Treat with HCO3 > 7 if plasma HCO3 is normal < 5.5 if plasma HCO3 is depleted (eg, <15 mEq/L) Treat with NaHCO3/K Citrate/Thiazide < 5.5 Treat with Diuretic, Low K diet
*Type 3 is very rare.

Metabolic Acidosis with an Elevated Anion Gap:

  • Lactic acidosis
  • Ketoacidosis
  • Chronic renal failure (accumulation of sulfates, phosphates, uric acid)
  • Intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene, sulfates, metformin.
  • Rhabdomyolysis

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