Abstract

We are describing the case related to previously healthy 40- year-old Female with a known medical history of essential hypertension (HTN) and without previous history of Diabetes Mellitus(DM). She was taking for her HTN – Amlodipine 5 mg once a day. The patient presented in our Emergency Department with abdominal pain, pleuritic chest pain, nausea and vomiting. She also complained of shortness of breath, generalized weakness and had low grade fever. On review of systems she was also found to be diaphoretic and having Kussmaul respiration. After the laboratory studies were obtained she was found to have severe metabolic acidosis and was admitted to the Intensive care unit. The differential diagnosis of her metabolic acidosis was broad, but she did not have DM – her HbA1c was 5.2% and she was not drinking alcohol. The screening for Methanol and ethylene glycol was negative. The patient did not have underlying kidney or liver disease. Also she did not have sepsis with lactic acidosis to explain her severe metabolic acidosis. She did not have also prolonged starvation. The drug screen of the patient was negative and she was not taking any medication to explain her metabolic acidosis. We are describing this case with severe metabolic acidosis, because we have found that the cause was severe acute pancreatitis. The cause of the acute pancreatitis was not found. It was not related to alcohol, increased triglycerides or any medications. Her ultrasound of the gall bladder was negative for gall bladder stones but mildly elevated ALT and AST might have been related to passed gall bladder sludge as a cause of her acute pancreatitis. The severe metabolic ketoacidosis due to acute pancreatitis is the challenging diagnosis and only few cases were described in the literature. The mechanism of acute pancreatitis causing severe metabolic acidosis seems to be related to the lipolytic action of elevated lipase as well as increased glucagon and relatively decreased Insulin in the scenario of acute pancreatic damage.

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