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Iatrogenic Paradoxical Air Embolism in Pulmonary Hypertension: Case Reports3,4

Iatrogenic Paradoxical Air Embolism in Pulmonary HypertensionCase 3
A 44-year-old white man with a history of idiopathic pulmonary fibrosis and chronic atrial fibrillation presented to our institution with worsening dyspnea and hypoxia, thought to be due to progressive fibrosis, and subsequently underwent pretransplantation evaluation. He was receiving long-term oral anticoagulation for atrial fibrillation. The evaluation included a right-heart catheterization, which revealed mild-to-moderate PH (Table 1). An ASCE was performed to evaluate whether an intracardiac shunt was contributing to progressive hypoxemia, and this revealed a right-to-left shunt across a PFO, which was more pronounced during a Valsalva maneuver (Fig 2). There was no evidence of an atrial or ventricular defect. After the Valsalva maneuver, the patient experienced sudden onset of left-lower-extremity numbness and bilateral central blindness. Symptoms slowly improved over 30 min before completely resolving. Head CT findings were normal, and the patient denied any previous episodes of focal neurologic symptoms. mycanadianpharmacy.com

Physical examination findings were significant for an irregular pulse at 72 beats/min, Sa0£ of 90% on 3 L/min of oxygen via nasal cannula, bibasilar crackles, and significant digital clubbing. Neurologic examination findings were normal, including visual acuity testing. Laboratory studies were significant only for a therapeutic INR of 2.5. The patient experienced no further neurologic symptoms and underwent unilateral lung transplantation in April, 1998.
Case 4
A 53-year-old white woman presented to Vanderbilt Medical Center in August, 1994 for further evaluation and management of suspected PPH. As part of her evaluation, ASCE was performed, which revealed a PFO during a Valsalva maneuver. After ASCE, the patient experienced acute onset of right-lower quadrantan-opia, as well as left-hand numbness and ataxia. Head CT as well as MRI were performed, with normal findings for both. The patient denied any previous episodes of focal neurologic deficits.
Physical examination findings were significant for a resting Sa0£ of 92% on room air, a 2/6 tricuspid regurgitation with a prominent P2, and an RV heave. Extremity examination findings were negative for cyanosis or clubbing. Neurologic examination findings revealed right temporal lower-field quadrantanopia, without deficits in strength, sensation, or cerebellar function. Laboratory study results were remarkable only for mild renal insufficiency, with a serum creatinine level of 1.5 mg/dL.
Over the next 24 h, the patient’s visual deficits completely resolved, and subsequent neurologic examination findings were normal. Additional workup revealed no secondary causes of PH, and subsequent right-heart catheterization confirmed the diagnosis of PPH (Table 1). Despite intensive therapy with multiple vasodilators, the patient developed severe cor pulmonale and died 3 weeks after presentation.
Figure 2. ASCE in patient 3, demonstrating bubbles instantly traversing a PFO. See Figure 1 legend for expansion of abbreviations.