Bronchospasm is acute narrowing of the airways of lungs, which gives rise to wheezing and shortness of breath. Commonly seen in obstructive lung disease, but a rare finding in patients with hypocalcemia. This is a case that outlines a rare presentation of hypocalcemia induced bronchospasm in a patient with no known history of asthma or chronic obstructive pulmonary disease (COPD). In this report, we present a case of a 57 years old male with no history of asthma or COPD who presented with intractable bronchospasm. Initial work-up for common entities was negative. Patient was found to be profoundly hypocalcemic and treatment provided resolution of symptoms. Early recognition of hypocalcemia induced bronchospasm is important in clinical practice to optimize management and provide improvement in symptoms.
The radiocontrast media(RCM) is widely used in the medical field. One of the most common side effects of RCM is nephropathy. Pulmonary complications are very rare (<0.04%), and 0.0001%-0.008% events are related to pulmonary edema. We describe a case of non-cardiogenic pulmonary edema (NCPE) as a result of RCM use during angiography for acute limb ischemia.Case: Our patient is a 38-year-old male with peripheral artery disease status post stent of the right superficial femoral artery (SFA), who presented to the hospital with right leg pain and right third toe gangrene. CTA showed occlusion of bilateral SFAs. Angiography via femoral approach using Visipaque 320 (iso-osmolar nonionic iodinated radiocontrast media) was complicated by SFA clot dislodgement which traveled distally. On day two, interventional radiology was able to revisit his case with successful angioplasty and stenting of the occluded vessels. An hour after, the patient developed dyspnea and desaturation on room air requiring new onset oxygen supplementation. Physical exam revealed bilateral rales and tachypnea. Chest x-ray (CXR) showed new bilateral diffuse airspace opacities [Figure 2]. Arterial blood gas (ABG) revealed hypoxemia with elevated A-a gradient on 4L nasal cannula. He was placed on NIPPV (non-invasive positive pressure ventilation) and given furosemide. ABG showed some improvement but repeat CXR showed persistent opacities. Methylprednisolone was started and 24hours later there was significant improvement in aeration on CXR [Figure 3] with de-escalation of oxygen therapy. Transthoracic echocardiography showed normal ejection fraction. After a 5-day course of steroids the patient's CXR improved and he was no longer dyspneic or hypoxic on room air. Discussion: Pulmonary edema is a rare complication in 0.001% to 0.008% of patients injected with RCM and can be life threatening. Although anaphylaxis is one of the most common adverse reactions of RCM, pulmonary edema can be easily missed in young patients. Our patient had normal cardiac function, no mucocutaneous manifestations, presence of patent airway, and had received RCM multiple times in the past making cardiogenic pulmonary edema or anaphylaxis unlikely. NCPE is characterized by endothelial injury to blood vessels, leading to extravasation of fluid into interstitium of the lungs, by vasoactive mediator release and complement activation. Diuretic use will not treat the underlying issue and corticosteroids have shown better resolution of symptoms. More cases need to be reported for earlier recognition and better management of these patients.
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