Friday, July 26, 2013

Acute Kidney Injury

Today in subspecialty morning report (nephrology) we discussed an elderly patient who presented to the emergency department with a history of agitation, vomiting and a recent episode of dysuria treated with two courses of antibiotics. Referred for AKI and hyperkalemia.

Past history included alcohol use, depression, possible COPD, and spinal stenosis.

Medications included citalopram, quetiapine, and bisoprolol, as well as recent courses of TMP/SMX and Levofloxacin.

Automatically think of TMP/SMX when hyperkalemia is brought up. The TMP component blocks ENaC and so acts like a K sparing diuretic and can cause hyperkalemia. Beta-blockers as well can theoretically worsen hyperkalemia (by inhibiting shift of K into cells)

Given his history of a recent urinary symptoms and now clinical deterioration, there was discussion whether this person could be presenting with persistent infection.

If he truly had a urinary infection recently, then it would be important to not only treat, but investigate the reason why this 91 year old male now has a urinary infection.

Given his history of spinal stenosis, the possibility of bladder dysfunction was raised as well.

Clinically he was afebrile and hemodynamically stable, although elderly patients can present atypically, and he is on a betablocker that may mask tachycardia. His exam was significant only for abdominal tenderness. He had no asterixis.

Asterixis, a form of negative myolconus, and inbability to maintain sustained contraction, DDx:
- Hepatic encephalopathy 
- Uremic encephalopathy
- Hypercarbic encephalopathy

Labs were significant for a potassium of 7.1 and a creatinine of 1750 (baseline of 50). 

Remember that creatinine comes from muscle and so 'normal' depends on the person. Actively rising creatinine will overestimate GFR, and actively dropping creatinine will underestimate GFR.

The question was raised as to whether he has underlying CKD.
One way to determine would be to U/S looking for small kidneys.
Although, there are causes of CKD with large kidneys
- DM
- Amyloid
- HIV nephropathy

He also had a mild Anion gap metabolic acidosis.

AG = Na - (Cl + HCO3)
Normal depends on Albumin.
An albumin of 40, gives a normal AG of 12
The lower the albumin, the lower the normal AG (for every 10 decrease in albumin, ~ 2 lower AG)
Causes of AGMA (anion gap metabolic acidosis)
- Lactic Acidosis
- Ketoacidosis (diabetic, alcohol, starvation)
- Renal failure
- Toxins (methanol, ethylene glycol, ASA)

This is a classic example of the tried and true internal medicine approach to acute renal failure. Won't be discussed in detail here, but click here for a good CPC NEJM case that reviews the approach.

A bladder scan that revealed 1.5L of retained urine.

Treated for acute urinary obstruction and hyperkalemia

1. Hyperkalemia
- Calcium gluconate
- Shift with insulin and D50W (insulin to shift K into cells, D50W to avoid hypoglycemia)
- Facilitate excretion - treated his acute urinary obstruction

2. Obstruction
- With a foley inserted he diuresed and his creatinine fell 500 points within hours and ultimately improved to his baseline of 50. Gratifying case and he did not need dialysis.
- He is being investigated as to the cause of his obstruction.

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