A 59-year-old Thai man with a dry weight of 43.6 kilograms (kg) was transferred from the medical intermediate unit to the medical intensive care unit on the fourth day of admission because he suffered septic shock with candidemia requiring vasopressor (norepinephrine) and intensive monitoring to improve the hemodynamic instability. He came to the hospital with acute progressive dyspnea and new-onset ascites with a low albumin gradient (Serum to Ascites Albumin Gradient: SAAG < 1.1 g/dL) and high protein. He had the following underlying diseases: type 2 diabetes, hypertension, old pulmonary tuberculosis, end-stage renal disease with no residual urine output requiring hemodialysis three times a week, triple vessel disease with left ventricular ejection fraction (LVEF) 27%, and peripheral artery disease (PAD) with chronic limb ischemia with dry gangrene status post a left percutaneous transluminal angioplasty stent with femoral artery endarterectomy. On the third day of admission, he suffered from dyspnea and was referred for an emergency multidetector computed tomography (MDCT) angiography to evaluate the suspected acute pulmonary embolism. It was reported that a small thrombus (1.9 x 0.7 cm2) was seen in the right atrium (RA) adjacent to the tip of the central venous catheter. Then, he was prescribed an enoxaparin sodium prefilled syringe (Clexane  4000 IU (40 mg)/0.4 mL, Sanofi, Paris, France) 40 mg SC once daily (OD) with bodyweight 46.8 kg for RA thrombus treatment. The recommended dose of enoxaparin is generally determined by bodyweight and renal function. The administration was at the same time each day (5 p.m.) to avoid hemodialysis treatments, which were normally scheduled in the morning (8-9 a.m.). In this case, the anti-Xa level was evaluated 4 h after the dose at 9 p.m. on a non-hemodialysis day to assess the efficacy and safety of enoxaparin. In addition, the anti-Xa levels were monitored because the patient had impaired renal function and needed an optimal enoxaparin therapy for a right atrial thrombus. The anti-Xa level was measured 4 h after the sixth once-daily dose of 40 mg enoxaparin, which was administered to the abdominal wall, as illustrated in Figure 1. The anti-Xa level was 0.72 IU/mL, which was within therapeutic levels (0.5-1.0 IU/mL) for a right atrial thrombus. The clinician provided enoxaparin 40 mg SC OD, with the SC injection at the abdominal wall with local edema. During his ICU hospitalization, the patient had peripheral edema, developed ascites, and gained weight (6 kg) due to ascitic fluid accumulation, hence necessitating an abdominal paracentesis. Because the patient had an operation to change tunneled-cuffed catheters (TCC) on day 11 following a suspected infected TCC, the enoxaparin was held for 4 days from day 10 to 13. After surgery, the patient experienced bleeding and clots in the endotracheal tube, so the clinician decided to withhold the enoxaparin for another two days. Although anti-Xa was within the therapeutic range, there was a risk that bleeding could be partially attributable to LMWH. Yet, LMWH-related bleeding is generally systemic, that is, bleeding affecting multiple sites rather than an isolated airway. In this case, the more likely causes of bleeding from endotracheal tube were airway mucosal injuries associated with long-standing intubation, localized inflammation of trachea and bronchi, and the acquired platelet dysfunction from renal failure. Because of a persistent thrombus in the RA, the patient was further examined by a cardiologist with a repeated echocardiogram. The cardiologist recommended restarting enoxaparin 40 mg SC OD as before and monitoring anti-Xa levels on a regular basis. After the fifth dose of enoxaparin, the peak anti-Xa level was 0.3 IU/mL, which was subtherapeutic. In order to achieve the therapeutic peak level (0.5-1.0 IU/mL), the enoxaparin dose was then increased to 60 mg SC OD, which was determined as 1.17 mg/kg/dose (current bodyweight of 55 kg) Yet, the peak anti-Xa level lowered to 0.25 IU/mL from the augmented enoxaparin dose. Because the anti-Xa level declined as the dose increased and was considered subtherapeutic, ascites at the abdominal wall were suspected to interfere with the SC enoxaparin absorption. As a result, the patient's treatment continued with enoxaparin 60 mg SC OD as originally prescribed while switching the SC injection site from the abdominal wall to the deltoid to avoid any potential counter-intervention from the ascites. Figure 2 shows that the enoxaparin 60 mg SC OD administered to the deltoid arms without edema resulted in peak anti-Xa levels of 0.45 and 0.51 IU/mL, respectively. The anti-Xa peak levels were nearly within the therapeutic range (0.5-1 IU/mL) The physician chose to maintain the enoxaparin dose and did not increase it although the anti-Xa level appeared to be slightly subtherapeutic. This was due to the fact that the patient was still on hemodialysis and had previously experienced endotracheal tube bleeding. The dose, duration, anti-Xa level, site of enoxaparin injection, vasopressor dose, and relationship with hemodialysis were indicated in Table 1. The anti-Xa level at the deltoid site tended to increase twofold when compared to that at the abdominal wall. As a result, for this patient with massive ascites, the deltoid region was likely a more suitable SC site to provide an improved bioavailability of enoxaparin.