Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. It continues to be one of the most common causes of death in adults across all countries. It is found to be relatively lower in North America. When aerosol droplets that contain Mycobacterium tuberculosis are inhaled, it can deposit in the respiratory tract, particularly in the patient's lungs. Following this deposition, one of the four outcomes can take place. These include clearance of the organism immediately, primary disease, latent infection, and reactivation disease. Unhindered bacterial growth after primary infection can lead to a hematogenous spread of bacilli to produce disseminated TB. Esophageal involvement causing esophageal TB can be primary or secondary esophageal TB.We present a unique case of secondary esophageal TB with symptoms of dysphagia and odynophagia with primary TB focus on the lung. Computed tomography (CT) of the chest noted diffuse bilateral miliary lung disease. TB QuantiFERON gold and sputum culture were positive for TB. Mycobacterial culture for identification with high-performance liquid chromatography showed isoniazid-resistant TB. The patient was started on antitubercular therapy with rifampin, ethambutol, moxifloxacin, and pyrazinamide for a total of nine months. Esophagogastroduodenoscopy (EGD) reported severe ulcerations of the oropharynx and focal ulceration in the proximal to the mid esophagus. Histopathology revealed active ulcerative and granulomatous esophagitis with mycobacterial organisms. After EGD she was started on a full liquid diet and advanced as tolerated. After discharge, she followed with the Health Department and had three negative sputum cultures after the completion of therapy.

Neurological manifestations are common in SARS-CoV-2 infection, including life-threatening acute muscle weakness, due to neuromuscular disorders such as acute transverse myelitis (TM) and Guillain-Barré syndrome (GBS). These syndromes can rarely coexist and present as an overlap syndrome. Here, we report a patient who developed acute symmetrical proximal lower limb weakness 5 days after diagnosis of COVID-19. GBS was diagnosed due to the presence of motor signs, albumin-cytological dissociation in cerebrospinal fluid examination and axonal damage according to nerve condition tests. However, abnormal areas on MRI of the thoracic spine and lack of improvement with intravenous immunoglobulin supported a diagnosis of TM. Therefore, a possible overlap between GBS and TM was established. To our knowledge, this is the third case report of GBS/TM overlap syndrome after COVID-19. The patient’s full and rapid recovery with intravenous corticosteroids and plasmapheresis supports our diagnosis.

Renal tubular acidosis (RTA) is defined as inadequate excretion of acids via the kidneys to maintain the acidbase balance. In RTA type 4, there is either deficiency or resistance to aldosterone leading to impaired regulation of electrolytes and hydrogen ions. This leads to hyponatremia, hyperkalemia, and acidemia. We present an unsuspecting etiology to RTA type 4 in a critically ill. SARS-CoV-2 patient as noted by heparin use for VTE prophylaxis. [1,2] CASE PRESENTATION: A 72-year-old male with history of chronic kidney disease, leukemia in remission presents with 6-day history of flu-like symptoms including intermittent diarrhea, fevers, decreased appetite, shortness of breath and generalized malaise with exposure to several known sick contacts with SARS-CoV-2. The patient was admitted to the ICU for acute hypoxic respiratory failure and started on Decadron, Remdesivir, Azithromycin, Ceftriaxone, Lovenox, Zinc, and vitamin C and subsequently intubated on day 10. Creatinine up trended and peaked at 3.51 mg/dL on hospital day 14. He developed hyperkalemia initially presumed to be secondary to acute kidney injury. His platelet counts declined by >50%, >10 days after hospitalization. Due to concern for HIT, argatroban was started but stopped due to bleeding. As fondaparinux is contraindicated in renal failure, he was restarted on heparin when HIT ab (-) result was obtained. Serum potassium peaked at 6.7 mmol/L on day 21. He was treated with calcium gluconate, insulin D50, Patiromer 8.4 g with no significant improvement in potassium levels. Due to concerns that use of heparin may be causing hyperkalemia by suppressing aldosterone, heparin was discontinued. Subsequently, serum potassium levels improved to normal range. DISCUSSION:In RTA type 4, either low levels of aldosterone or from kidneys not responding to aldosterone, impaired sodium reabsorption and potassium secretion occurs. [2]. Persistent hyperkalemia in whom there is no apparent cause such as potassium supplements or a potassium-sparing diuretic or renal failure, hypoaldosteronism must be considered [3][4][5].In COVID-19, there exists a higher propensity for thromboembolic disease and often prevention with heparin can serve as the best treatment. Heparin has a direct toxic impact on the adrenal zona glomerulosa cells, which may be facilitated by a drop in the number and affinity of adrenal angiotensin II receptors [4,6]. This reduction in aldosterone can lead to severe hyperkalemia [6].CONCLUSIONS: This case is unique because hyperkalemia was noted to be refractory to the typical standard treatment given the etiology was hypoaldosteronism likely secondary to heparin use. Most patients with RTA if treated adequately in the early stages do not develop permanent kidney failure, have better mortality and morbidity outcomes and necessitate a broad etiologic differential.