Case Presentation by Dr. Cameron Kyle-Sidell
CHIEF COMPLAINT(S): “My mother keeps throwing up”
HISTORY OF PRESENT ILLNESS: This is an 84-year-old woman who was brought in by her daughter and granddaughter. They report that she’s been throwing up constantly for 3 days, approx 10 times per day. Unable to tolerate food or water. Reports having some lightheadedness when she walks. No fevers, cough, rashes, or sick contacts. No abdominal pain. No recent trauma. She did fall several weeks ago hurting her elbow and her left, but came to the emergency room and got a CT of the head which showed no bleed. Patient medical history includes only hypertension treated with lisinopril. Previous cesarean section.
VITAL SIGNS: Systolic blood pressure 105, heart rate 71, oral temperature 35.1. Pulse oximetry is 98% on room air.
PE: No pertinent findings
Course in the ED:
CBC, electrolytes, lipase, and ALP ordered. IV established and patient received 1 L NS. Abd X-ray ordered. First thing to come back were the electrolytes. Patient’s creatinine is 6.4. Per CIS, patient’s baseline creatinine was 1.3 on November 28, 2010, two months previous. BUN is 108. All other labs WNL. Patient currently awaiting abdominal x-ray.
1. Regardless of the type, what is the final common pathway leading to all ARF?
- Reduced renal blood flow
- Decreased urine output
- Rising BUN and creatinine
- Increased urine output
2. Prerenal Failure is characterized by all except:
- BUN/Cr ratio greater than 10:1
- Decreased specific gravity
- Urine sodium concentration less than 20 mEq/dl
- FENa less than 1%
3. Our patient’s extremely elevated creatinine level of 6.4 tells us that she is experiencing:
- Prerenal azotemia only
- Intrinsic azotemia only
- Prerenal and intrinsic azotemia
- Impossible to tell
AND THE BONUS MILLION DOLLAR QUESTION:
After treatment, the patient’s creatinine…?:
- who cares, we lost the patient
- remained super high, like, because, the patient is on dialysis
- came down to, like, 2-something
- returned to baseline
1. Answer: a
The common pathway leading to all forms of renal failure is decreased renal blood flow. Patients can be oliguric or non-oliguric. Decreased urine output, if present, is a result of decreased GFR. Rising BUN and creatine is the hallmark of ARF and encompassed in the definition of it, but is a result of, not a cause of renal failure. The cause, regardless of the type of renal failure, is decreased renal perfusion. In prerenal, failure, this is due to decreased blood flow to vessels supplying the kidneys. In intrinsic renal failure, various disease state are associated with release of renal afferent vasoconstrictors and or/ direct ischemic renal injury. In post-obstructive renal failure, the increase in tubular pressure decreases the filtration driving force. As the pressure gradient equalizes, the maintenance of a depressed GFR is dependent upon renal efferent arteriole vasoconstriction, again leading to ischemia of the distal arterioles supplying the renal parenchyma.
2: Answer: b
In prerenal failure, the diminished renal perfusion causes activates the renin-angiotensin-aldosterone system, stimulated the increased absorption of sodium from the proximal tubules of the kidney. In pre-renal failure, the parenchyma of the kidney is not damaged and so the concentrating capacity of the kidney remains intact. Prerenal kidney will therefore lead to increased sodium reabsorption (and the resulting fluid reabsorption) and concentrating of the urine. One can therefore expect to see a FENa <1 and urine sodium concentration < 20 mEq/dl (body retaining sodium), and increased specific gravity (concentrated urine). Because BUN, as opposed to creatinine, can be freely filtered and absorbed by the kidneys, when the concentrating ability of the kidney’s remain intact, one can expect BUN levels to rise faster than creatinine (BUN absorbed while creatinine is not), leading to a BUN/Cr ratio greater than 10:1.
3: Answer: d
A single creatinine measurement cannot be used to determine between either the kinds of acute renal failure, or to distinguish between acute and chronic renal failure. Rising creatinine is a result of decreased GFR, and does not indicate whether or not injury to the kidney parenchyma has occurred. This is especially important to note when dealing with prerenal and intrinsic azotemia, as at some point, prolonged prerenal azotemia, or diminished renal perfusion, will lead to ischemic injury of the renal parenchyma. As Emergency physicians, we currently have no way now of knowing “when that line has been crossed,” and so we can only hope that our early intervention will be performed before such insult has occurred. It is important to note that if, when after rehydrating the patient, we do not witness sufficient increased urine output, we should be careful in further hydration, since we may be “too late,” (ie. the patient is now oliguric due to intrarenal damage) and further hydration can lead to complications from volume overload. There are some researches currently trying to develop assays that will can accurately and quickly determine the extent of active intraparenchymal renal damage (ie would be like looking forward elevated kidney “troponins.”)
Patient was admitted to hospital, where after three days of rehydration w/ careful observation of urine output, patient creatinine levels gradually decreased from 6.4 to 2.2. Three months later at an outpatient visit, patient creatinine had reduced further to her baseline of 1.3.
Filed under: Intern Report |