PGY2 Stefan Nguyen presented an great case of a 65 year old Vietnamese man presenting with 2 weeks of worsening shortness of breath, lower extremity edema and weight loss. He was found to have a large pericardial effusion without clinical or echocardiographic evidence of tamponade, had a pericardiocentesis done and pericardial fluid cultures were positive for Mycobacterium Tuberculosis!

Pericardial effusions 
– Common infectious causes of pericardial effusions include Staph/Strep, Coxsackievirus, echovirus and don’t forget HIV!
– Malignancy should also be considered, in particular lung/breast cancer and Hodgkin lymphoma, though any malignancy can metastasize to the pericardium.
– Other etiologies include post-MI pericarditis, drug induced, rheumatologic (lupus/RA), uremia and idiopathic

Tuberculous Pericarditis: In the case today, Tuberculosis was suspected early on given that the patient was from Vietnam and presented with leukopenia and an elevated Alkaline phosphatase.
– When analyzing pericardial fluid, the most important studies include cell count (should be lymphocyte predominant in Tb), gram stain, culture and cytology. The yield of AFB smear is low from pericardial fluid and will generally be negative.
– There are no clear parameters for distinguishing transudative v exudative pericardial effusions.
– The utility of ADA in pericardial effusions is controversial, and generally the diagnosis of Tb depends upon clinical suspicion, lymphocyte predominant fluid and positive AFB culture. The Official American Thoracic Society and Infectious Diseases Society of America do recommend checking an ADA level, however this is a conditional recommendation with low-quality evidence.
**Remember that ADA is falsely elevated in PMN predominant pericardial or pleural fluid, and should only be in lymphocyte predominant fluid analysis.
– The use of steroids in the treatment of Tb Pericarditis was studied in a large trial in NEJM in 2014. The results showed that steroids did not decrease mortality, however did reduce the incidence of constrictive pericarditis. In patients with HIV, steroid use was associated with HIV-related cancer, specifically Kaposi’s Sarcoma. (https://www.nejm.org/doi/10.1056/NEJMoa1407380)

 

Today’s intern morning report presented by Percy Genyk involved a case of a 59 year old female presenting with oral bleeding and petechiae, found to have a platelet level<5 and is diagnosed with primary ITP.

When approaching a patent with bleeding, think about whether it is more likely related to platelet problem or the coagulation cascade. Coagulation disorders are more likely to present with large ecchymoses and soft tissue hematomas whereas platelet disorders present with epistaxis, gingival bleeding, superficial ecchymoses and petechiae.

Remember that ITP is a diagnosis of exclusion and other causes of thrombocytopenia need to ruled out first.
– A thorough history is necessary to search for medications, infections or other systemic conditions (rheumatologic, chronic liver disease) that may cause thrombocytopenia. Although history/exam/labs would be suggestive, always keep in mind the more emergent causes associated with thrombocytopenia such as thrombotic microangiopathies and DIC.
– A peripheral smear should be ordered in all patients with thrombocytopenia, which will also help evaluate for pseudothrombocytopenia.
– Broad routine work-up of ITP is not needed and guidelines recommend ordering peripheral smear, HIV and HCV only unless history is suggestive of other underlying conditions. Routine bone marrow biopsy is not recommended.
– Routine bone marrow biopsy is not recommended in the work up of ITP.

**Platelet transfusion is not indicated unless the patient is actively bleeding or has severely low platelets.
**Treatment of ITP is not indicated in all patients and is generally reserved for those with bleeding or platelet count less than 30,000. First line therapy includes glucocorticoids and IVIG.

Here is a quick reference with some important pearls on thrombocytopenia!

Today’s case involved a 62 yo M presenting with constipation, fatigue and lower extremity weakness. His labs are significant for severe hypercalcemia with a normal phosphorus. He is diagnosed with hypercalcemia due to PTHrP secretion, with no known history of malignancy. After a CT scan of his chest, abdomen and pelvis, he is found to have multiple liver lesions as well as a large pancreatic mass and biopsy of a liver lesion reveals well differentiated neuroendocrine carcinoma, likely pancreatic primary.

Take home points from today’s case:
– The first test to order for hypercalcemia is a PTH level, as primary hyperparathyroidism is the most common cause.
– If the PTH is low, should order PTHrP as humoral mediated hypercalcemia is the most common cause of non PTH mediated hypercalcemia.
– If PTHrP is not elevated, can consider other causes such as osteolytic lesions, vitamin D toxicity (can see hyperphosphatemia), increased production 1,25-dihydroxyvitamin D.
– In a patient with bone pain, renal failure and hypercalcemia, should think of Multiple Myeloma. Remember that MM can present with a low anion gap.
– In the presented patient, the PTHrP was elevated, prompting evaluation for a malignancy. Common malignancies associated with PTHrP production include squamous cell carcinomas, renal carcinoma, and breast carcinomas.

Pancreatic neuroendocrine tumors (NET) can be functioning (insulinoma, gastrinoma, glucagonoma, VIPoma) or nonfunctioning (do not present clinically with a hormonal syndrome). There are a few case reports of patients with pancreatic NET presenting with PTHrP secretion. Despite the presentation of hypercalcemia with imaging consistent with a pancreatic NET tumor, biopsy is still necessary to confirm the diagnosis.
**In a younger patients presenting with pancreatic NET, consider referral for genetic testing for hereditary endocrinopathies such as MEN 1, Von Hippel Lindau, and NF1.

Thank you Jaehoon for teaching us about pancreatic NETs and hypercalcemia!