A 78-year-old lady was found at her home after a fall earlier in the day by her daughter. Medication history is significant for aspirin, statin, glipizide, and acetaminophen use for chronic low back pain. She recently visited her primary care physician with significant weight loss and failure to thrive. She is currently admitted in the intensive care unit (ICU) for multiple rib fractures and flail chest. Her urine analysis and labs are as follows:
What is the most likely cause for her acid-base abnormality and hyperkalemia?
Correct Answer: B
This patient has high anion gap metabolic acidosis with resultant acidosis-induced hyperkalemia. One of the overlooked causes of metabolic acidosis is elevation of serum oxoproline levels, seen more commonly in undernourished patients taking acetaminophen regularly. The patient has no lactate or ketones in their lab workup. Isopropyl alcohol toxicity causes an osmolar gap only and no anion gap (choices A, C, and D are incorrect). Causes of high anion gap metabolic acidosis can be remembered with the mnemonic—GOLDMARK:
When a source of high anion gap metabolic acidosis is not obvious, elevated 5-oxoproline level (also called pyroglutamic acid) should be considered, especially if there is a history of acetaminophen use.
A 55-year-old male with a long-standing diabetes, heart failure with reduced ejection fraction, and open-angle glaucoma presents to the emergency room. He reports loose stools for last few days. His list of medications includes metoprolol, acetazolamide, atorvastatin, aspirin, and metformin.
The most likely cause of this patient’s acidosis is:
Correct Answer: A
The pH suggests acidosis. The anion gap is 10, which is appropriate for an albumin of 4. There is no respiratory-driven acidosis as denoted by the normal pCO2 of 40. Therefore, this patient has normal anion gap metabolic acidosis (NAGMA). The next step is to determine the etiology using a calculation of the urine anion gap (UAG)
Na + K - Cl = 56 + 10 - 76 = -10
A positive numerical value on UAG in NAGMA can be seen with renal tubular acidosis, spironolactone, and acetazolamide use. Diarrhea typically results in numerically negative UAG. Typically acidosis is associated with hyperkalemia unlike in this scenario, which can be explained by GI loss of potassium, resulting in hypokalemia in spite of academia.
A 59-year-old female with a history of hypertension and gout is admitted in the ICU for observation status post thrombolysis for ischemic stroke. Her outpatient medications include metoprolol, colchicine, aspirin, metformin, and meloxicam. Vitals are normal except for sinus tachycardia with a heart rate (HR) of 108 beats per minute. Low bicarbonate is noted on labs prompting an arterial blood gas (ABG), and patient is found to be mildly acidotic. Lab values are given below:
Which of the following can most likely be expected to be the cause of this?
Correct Answer: C
The blood gas suggests a metabolic acidosis. The anion gap is 12, which is appropriate for an albumin of 4. There is no respiratory-driven acidosis component as denoted by normal pCO2 of 38 mm Hg. This patient has NAGMA. The next step is to calculate the UAG
U.Na + U.K - U.Cl = 56 + 10 - 56 = 10
A positive numerical value on UAG in NAGMA can be seen in renal tubular acidosis (type 1 and type 4), spironolactone, and acetazolamide use. This patient has serum chemistry consistent with renal tubular acidosis type 4 with hyperkalemia not explained by any other etiology. Types of renal tubular acidosis with their respective differentiating features are depicted in the table below:
A 55-year-old female presents with headaches and generalized weakness. Her mental status is intact. Her vital signs are blood pressure (BP) 170/80 mm Hg, HR 120/min, respiratory rate (RR) 18/min, and temperature 36.8°C.
What is the next best test to determine the cause of this acid-base abnormality?
The patient has a pH of 7.48, with a bicarbonate level of 34 mEq/L, suggesting metabolic alkalosis as the acid-base disorder. Hypokalemia is also noted with potassium of 3.1 mEq/L consistent with metabolic alkalosis. In differentiating the cause of metabolic alkalosis, urine chloride levels can be utilized. Urine chloride level less than 10 mmol/L suggests volume responsive or contraction alkalosis that can be corrected with saline replacement. Urine chloride greater than 20 mmol/L is associated with alkalosis that is resistant to volume expansion such as excess aldosterone, severe potassium deficiency, diuretic therapy, or Bartter syndrome. Metabolic alkalosis can be a feature of Cushing syndrome, but ordering a serum cortisol level would not be the first-line investigation (choice A). Liver function tests and serum ionized calcium are not typically useful for the investigation of metabolic acidosis (choices C and D).
A 30-year-old male with history of alcohol abuse presents with nausea and vomiting. He is jaundiced, agitated, and endorsing visual hallucinations. Vital signs are as follows:
Labs and ABG values are shown below:
Which of the following best describes the acid-base disorder?
The patient has a significant anion gap of 36 [138−(22 + 80) = 36], which makes high anion gap metabolic acidosis as one of the acid-base derangements even though the pH is alkalotic. Using Winters formula, the patient’s CO2 to compensate for the acidosis should be
This value is more than the pCO2 of the patient which is 28, suggesting more CO2 washout, thus adding respiratory alkalosis as a component of the acid-base disorder. Additionally, the patient’s albumin is 4, making the normal anion gap for this patient as 12; the difference between the normal anion gap and patient’s anion gap is 36 − 12 = 24. This means the acid-base disorder has caused the original bicarbonate level to decrease by 24. So, by adding 24 to the patient’s current bicarbonate level of 22, we can get the original bicarbonate level this patient started out with, which would be 22 + 24 = 46, thus making the patient’s original acid-base problem as metabolic alkalosis. The patient has a combined respiratory alkalosis, metabolic acidosis, and metabolic alkalosis.
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