No abstract

BACKGROUND Coronavirus patients demonstrate varying degrees of respiratory insufficiency; many will progress to respiratory failure with a severe version of acute respiratory distress syndrome refractory to traditional supportive strategies. Providers must consider alternative therapies to deter or prevent the cascade of decompensation to fulminant respiratory failure. METHODS This is a case-series of five COVID-19 positive patients who demonstrated severe hypoxemia, declining respiratory performance, and escalating oxygen requirements. Patients met the following criteria: COVID-19 positivity, worsening respiratory performance, severe hypoxemia (Pao 2 ≤ 80) despite traditional supportive measures, escalating supplemental oxygen requirements, and D-dimer greater than 1.5 μg/mL. All patients received protocol directed thrombolytic therapy with tissue plasminogen activator (tPA). RESULTS All five patients improved without deleterious effects of thrombolytic therapy. Patient one was on maximum ventilator support, paralytics, and prone positioning without improvement. During tPA administration his Pao 2/FIO2 ratio improved from 69 to 127. Ventilator support was weaned immediately on posttreatment day 1, and he was extubated on posttreatment day 12. Our second through fifth patients were not intubated at time of initiation of tPA therapy. These patients each required significant oxygen supplementation trending toward intubation. After tPA therapy, all patients demonstrated a noticeable increase in Pao 2 values overtime. Three of these patients avoided intubation due to COVID-19–associated respiratory failure. CONCLUSION Administration of thrombolytics was followed by overall improvement in patients' oxygen requirements, and in three cases, prevented progression to mechanical ventilation, without deleterious effects. Clinical trials of thrombolytic therapy would further serve to underscore the efficacy and utility of this therapy. LEVEL OF EVIDENCE Case series of therapeutic effect, Level V.

With the development of endovascular therapy, treatment for hepatic artery aneurysm (HAA) has evolved from open excision and repair to include endovascular approaches. We reviewed our recent experience with HAA to help define the treatment of HAA. From 2002 to 2010, five patients underwent treatment of HAA, all men with a median age of 63.2 years (range, 41-75). The median diameter of HAA was 5.8 cm (range, 2.4 cm-11 cm). Four lesions involved the extrahepatic portion of the hepatic artery, and one was an intrahepatic HAA that involved the right hepatic artery. Three were true aneurysms and two were pseudoaneurysms associated with trauma. Four of the five HAA patients were symptomatic, three with nonspecific abdominal pain, and one with free hemorrhage from a ruptured intrahepatic pseudoaneurysm. All five underwent computed tomography and selective arteriography. Two patients underwent open surgical aneurysmectomy and revascularization because of aneurysm location and concerns of the potential lack of collateral flow. Three patients underwent an endovascular coil embolization because obliteration of a saccular aneurysm could be achieved without compromising arterial flow of the native hepatic vessel. Re-embolization was necessary in the intrahepatic aneurysm because of recanalization of a feeding vessel. Endovascular embolization is an important minimally invasive approach in the treatment of HAA. Depending on HAA location and the adequacy of collateral arterial flow around the lesion, open aneurysmectomy and revascularization may be required.