SG IM FO RUM 2015; 38 (9 ) SHARE MORNING REPORT Is it Really Just a Number? Sara Haque , MD; Javeria Haque , MD; and Michele Fang, MD

Drs. Haque and Haque are residents at the Presence Saint Francis Hospital Department of Internal Medicine in Evanston, IL, and serve as the presenter and discussant. Dr. Fang is editor of Morning Report and can be reached at [email protected].

77-year-old woman presents to soft nontender abdomen without corrected bicarb is more than 30, Athe emergency department with hepatosplenomegaly, and no edema then there is a primary metabolic al - altered mental status. There is no of the extremities. She has bruises kalosis. If the correct bicarb is 23 to immediate family member available on her forehead and knees. Her 30, then there is no additional disor - for further history. The patient does neurological exam is nonfocal. der. If the corrected bicarb is less not know what medical conditions There is clear evidence of altered than 23, then a hidden metabolic she has, what medications she is alertness in this patient. Her exam is acidosis exists. In our case, the bi - taking, or the details of her social nonfocal, making stroke or tumors carb is 16 and the (Na-

and family history. less likely. She does have tachyp - (Cl+HCO 3 )) is 6, so the corrected bi - The differential diagnosis for al - nea, which especially in the elderly carb is 10. Therefore, our patient tered mental status is broad. It in - can be a sign of sepsis syndrome has a respiratory alkalosis with a cludes infectious causes, such as even without fever. Tachypnea can non-anion gap metabolic acidosis. urinary tract infection, pneumonia, also be present in pulmonary em - The differential diagnosis for a meningitis, and endocarditis; meta - bolism, hyperthyroidism, anxiety, normal anion gap metabolic acidosis bolic conditions, such as hypo - and respiratory acidosis. is divided into two groups: GI glycemia, hyper/hyponatremia, and metabolic abnormalities, espe - losses, such as diarrhea, fistulae, or hypercalcemia, hypoxia, hypercap - cially with the tachypnea, will need ileal loop, and renal causes, such as nia, hepatic encephalopathy, uremic to be ruled out. I would recommend renal tubular acidosis, carbonic anhy - encephalopathy, drug intoxication or a full , com - drase inhibitor use, or post hypocap - withdrawal, and Wernicke en - plete count, and arterial blood nia. The differential diagnosis of cephalopathy; intracranial events, gas if the basic metabolic panel is respiratory alkalosis includes hypox - such as cerebrovascular accident, abnormal. The bruises on the fore - emia, stimulation of pulmonary or intracranial hemorrhage, primary or head and knees could indicate a pleural receptors (i.e. pneumonia, metastatic tumors, and encephalitis; problem with platelets or abnormal pulmonary embolism, pulmonary cardiac events, such as arrhythmias, coagulation (e.g. from warfarin, liver edema, asthma), psychogenic hyper - 1 heart failure, and hypertensive disease), so a head CT to rule out ventilation, medications (e.g. theo - emergencies; and vasculitis. The bleed and INR, PT, and PTT should phylline, catecholamines, salicylates, differential diagnosis of altered be obtained. and progesterone), CNS disorders, mental status is based on historical The patient’s labs are as follows: fever, early sepsis, and increased and physical findings. It is especially sodium 138, potassium 3.7, chloride minute ventilation secondary to ven - important to distinguish delirium 116 (H), 16 (L), creati - tilator management. The differential from dementia. tine 0.8, bun 26; CBC, AST, ALT, diagnosis can be narrowed if both Unfortunately, in this case, no col - , albumin, and respiratory alkalosis and metabolic laborative information is available, and PT/INR/PTT are normal. Arterial acidosis are present, and it includes

the patient is not able to provide any blood gas reveals a pH 7.45, pCO 2 gram-negative sepsis, acute car - additional history. Therefore, physical 26.1 (L), calculated HCO 3 16.0 (L), diopulmonary arrest, severe pul - exam and laboratory and radiology and pO 2 97. monary edema, and salicylate data will have to play a more critical The patient has a mixed-acid intoxication. role in this patient assessment . base picture with a pH in the normal This patient has a negative On physical exam, the patient is range but with a low bicar - head CT. Urine toxicology is nega -

drowsy and oriented to self only. bonate and low serum CO 2. With tive. Salicyclate level is high at 88

The patient is afebrile with a pulse the PCO 2 less than 40, this patient mg/dL. (Therapeutic level is 10 to of 80, blood pressure of 130/70, res - has a respiratory alkalosis. However, 30 mg/dL.) When the patient’s fam - pirations of 25, and oxygen satura - in order to determine if there is a ily arrives, they explain that the tion of 97% on room air. She has secondary disorder, we need to cal - patient was consuming 20 baby moist mucus membranes, clear culate the corrected bicarbonate, aspirins a day for three months for

lungs to auscultation, a regular heart which is equal to the actual HCO 3 osteoarthritis. rate and rhythm without murmurs, a plus the anion gap minus 12. If the continued on page 2 SHARE

MORNING REPORT continued from page 1

The patient is transferred to ICU. Aspirin is a commonly used els in the presence of elevated sali - A bicarbonate drip is started to alka - medication and is frequently associ - cylate levels. 2 linize the urine; however, the salicy - ated with intentional and suicidal in - late level continues to increase to a gestion. The classic presentation of Take Home Points peak of 98 mg/dL. Emergent he - salicylate toxicity is anion gap meta - 1. Aspirin toxicity can present as modialysis is initiated. After two ses - bolic acidosis secondary to salicyclic non-anion gap metabolic acidosis. sions of hemodialysis, the salicylate acid, , and ketones in ad - 2. Lab results can “over-measure” levels normalize. dition to respiratory alkalosis and serum chloride, explaining Management of salicyclate toxic - respiratory acidosis. Our patient had “pseudo-normal” anion gap in ity consists of: 1) detoxification with an anion gap of 6 with hyper - the setting of salicylate toxicity. activated charcoal; 2) alkalinization of chloremia (116). Renal, central, and urine, although hypokalemia must be other causes of References corrected in order for alkalinization to were ruled out with history, physi - 1. Jacob, J, Lavonas, EJ. Falsely be effective; and 3) hemodialysis cal, and labs. On review of prior normal anion gap in severe when the patient has altered mental case reports, similar elevation of salicylate poisoning caused by status, pulmonary or cerebral edema, serum chloride has been reported laboratory interference. J Ann renal insufficiency, fluid overload, a and is a lab error due to high con - Emerg Med 2011; 58(3):280-1. serum salicylate level greater than centration of salicylate. 1 Our lab 2. Mori L, Waldhuber S. Salicylate 100 mmol/L in acute overdose, or uses the Roche Cobas Integra ana - interference with the Roche clinical deterioration despite aggres - lyzer, which has been known to Cobas Integra chloride electrode. sive supportive care. cause falsely elevated chloride lev - Clin Chem 1997; 43:1249-50. SGIM

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SG IM FO RUM 2015; 38 (9 )