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Antithrombin III (AT III) is a critical component of the coagulation cascade that functions primarily to inhibit activated coagulation factors IIa and Xa. AT III deficiency is a disorder that predisposes patients to thromboemboli. Antiphospholipid syndrome (APS) is an autoimmune disorder that predisposes patients to vascular and microvascular thrombosis, which can often be devastating and lead to multiorgan involvement. The mainstay of treatment for both conditions involves the use of lifetime vitamin K antagonists. Recent studies suggest that patients with APS refractory to warfarin therapy may benefit from the addition of aspirin, statin, or hydroxychloroquine; low weight molecular heparin; or a combination regimen. Studies have also suggested that patients with AT III deficiency refractory to warfarin therapy may see improvement with use of a novel oral anticoagulant. This case report describes the recurrent hospitalizations of a 45-year-old patient who presented with multiorgan thrombosis involving the descending aorta, deep lower extremity veins, superior mesenteric artery and artery of the brain. This led to mesenteric ischemia, limb necrosis and a subacute frontal cortex infarct. Initial anticoagulation therapy was refractory to the use of warfarin. Enoxaparin therapy was initiated, resulting in no further thrombotic events. Clinicians should consider poor gastrointestinal absorption of warfarin in patients who fail to reach therapeutic anticoagulation goals. In addition, a thorough workup for hereditary and acquired thrombophilias should be performed in patients who present with recurrent thromboemboli, as these disorders increase the risk of poor patient outcomes if left untreated.

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Urinary tract stones are found in many locations, such as in the kidney or ureter, and, less commonly, in the bladder. Bladder stones are solid calculi that are usually composed of calcified material, most commonly uric acid, and typically weigh less than 100 g. There is a higher prevalence of bladder stones in males than in females, which can be explained by the pathophysiology of how these stones are formed. Namely, bladder stones tend to form secondary to urinary stasis, such as in the setting of benign prostatic hyperplasia (BPH). However, bladder stones can form in otherwise healthy individuals without anatomic defects (e.g., urethral strictures) or urinary tract infections (UTIs). Foley catheters or any foreign bodies in the bladder can predispose to stone formation. Renal calculi, most commonly calcium oxalate or calcium phosphate in composition, can also travel through the ureter and get trapped in the bladder. The most significant risk factors for bladder stones include the presence of BPH and UTIs, both of which favor the development of additional layers of stone material. In exceptionally rare cases, bladder stones measure more than 10 cm in diameter and weigh more than 100 g. These entities have been referred to as giant bladder stones within the limited literature. Minimal data exist on the etiology, epidemiology, composition, and pathophysiology of giant bladder stones. We present the case of a 75-year-old male with a giant bladder stone composed of 100% carbonate apatite, measuring 10 cm × 6 cm and weighing 210 g.

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