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IBUPROFEN TOXICITY AS A CAUSE OF RENAL TUBULAR ACIDOSIS TYPE 2 LEADING TO A

NONANION GAP METABOLIC ACIDOSIS S. SHACKOUR1; M. AKHTARI1;


K.NEWMAN;V.SARVANAN; B.C. KOLLA1; H. FRIEDMAN2. 1St Francis Hospital, Evanston, IL; 2St.
Francis Hospital, Evanston, IL. (Tracking ID # 171498)
LEARNING OBJECTIVES: 1-Recognizing Ibuprofen Toxicity as a cause of Renal Tubular Acidosis Type 2,
leading to a nonanion gap metabolic acidosis. 2-Recognizing the possible complications of Ibuprofen Toxicity.
CASE: A 33 year old female (with the PMHx of depression, and asthma) was found confused lying on the floor,
holding a bottle of motrin in her hand, and her breath smells alcohol. Upon admission, the patient seemed to be
deeply comatose with a GCS of 5/15. Significant physical exam findings on day1 include: BP of 76/32, HR of
92,Pupils that are sluggishly reactive but symmetric, all 4 limbs were flaccid and DTRs were not elicited.
Significant labs include: BUN of 9 on day1, and 45 on day4, 77 on day7. Cr of 0.74 on day1, 3.63 on day4, 6.39 on
day7. Ionized Calcium of 0.82 on day2, 0.95 on day 4, 1.19 on day7. Anion Gap of 12 on day1 and a non elevated
lactic acid level. AST of 665, ALT of 822 on day4, INR of 1.4 on day8. On day1, Alcohol level was 175, Ethylene
Glycol and Methyl Alcohol were not detected, Ibuprofen level was greater than 360 mg/L. Her ABGs were as
following: On day 1, 7.31/74/27.6/14 On day 2, 7.23/85/22.3/11 On day 3, 7.27/86/29/14 On day 4, 7.36/77/33.7/19
On day 5, 7.36/85/38.5/22 On day 6, 7.35/104/42.2/23 She developed the following complications during her
hospital course: 1-Metabolic Acidosis 2-Renal Failure 3-Hepatic impairment 4-ARDS 5-Hypocalcemia 6-
Hypotension 7-DIC Bicarbonate drip was started on day 2, and stopped on day 5. Hemodialysis was started on
day7, and stpped after 3 weeks. She was intubated on day10, and extubated on day15.
DISCUSSION: An increased anion gap metabolic acidosis may be seen after large ingestions of Ibuprofen. This
acidosis may represent a combination of lactic acidosis(caused by cellular hypoxia, seizures and impairing
intrahepatic gluconeogenesis from lactate) and weakly acidic NSAIDs metabolites. Ibuprofen toxicity can cause
proximal renal tubular acidosis (type 2), leading to a nonanion gap metabolic acidosis. Proximal renal tubular
acidosis is a hypokalemic hyperchloremic metabolic acidosis due to a selective defect in the proximal tubule´s
ability to adequately reabsorb filtered bicarbonate. Causes include multiple myeloma and nephrotoxic drugs like
ibuprofen. Acute forms of renal failure are rare in NSAID overdose. NSAID-induced renal injury most likely results
from inhibition of vasodilatory prostaglandins. Ibuprofen induced hepatic toxicity may manifest as an
asymptomatic elevation of transaminases, cholestasis, inhibition of albumin synthesis and fulminant hepatic failure.