This is a patient with a history significant for chronic thrombocytopenia with a baseline platelet count in the 90s and nasal septum deviation, who presented to the emergency department with complaints of intermittent midsternal chest pain that was not radiating, described as nonexertional, which lasted for an hour at a time. The chest pain was associated with shortness of breath. The patient described the pain as pressure-like, with no radiation or modifying factors. The pain was intermittent and lasted for approximately 1 hour. At the time of admission, the patient denied any sick contacts or long-distance travel. The patient noticed some exacerbation of the chronic nasal congestion in the last several days preceding the day of admission. She denied headaches, fever, cough, sputum production, neck stiffness, or photophobia.
The patient was not in acute distress, appeared anxious, head, eyes, ears, neck, throat (HEENT) exam was unremarkable. The cardiac exam was within normal limits. At the same time, the patient had mild chest wall tenderness that was reproducible. The rest of the physical exam was unremarkable.
The patient had an abdominal ultrasound that was interpreted as an unremarkable study without hepatosplenomegaly.
An electrocardiogram (EKG) did not demonstrate any evidence of acute coronary syndrome.
The patient was admitted to the hospital with a diagnosis of chest pain and no risk factors for coronary artery disease. It was mentioned in the history and physical exam note that the patient had no EKG changes and had a normal troponin. It was also mentioned that the patient was not hypoxic. The admitting physician suspected that the patient had a viral illness.
Another admitting diagnosis was non-anion gap metabolic acidosis that was improving; further monitoring of the laboratory results was planned at the time of admission.
The health plan's determination is upheld.
This patient presented to the hospital with complaints of chest pain. The chest pain was atypical, reproducible on physical exam, and not related to cardiac origin. The patient was hemodynamically stable, had a normal troponin level, and her chest x-ray was normal. There was a low probability of venous thromboembolism because of the lack of risk factors and a normal D-dimer level. Even though the patient's platelet count was lower than the baseline, there was no mention that the patient had active bleeding or any other clinical manifestations of thrombocytopenia.
The reason for the non-anion gap metabolic acidosis was not clear, but it improved quickly, and there were no clinical manifestations associated with this condition. There were no additional diagnostic tests or procedures required for the treatment of this condition.