Air Embolism: Endovascular System

The clinical picture of acute pulmonary embolism (PE) is not similar from various aspect of its pathophysiological course presenting from minimal symptoms to variety of severity of disease like severe hypoxia, hypotension, right heart failure and death1. Massive pulmonary embolism is defined as obstruction of blood flow to a lobe or multiple segments of the lung, or for unstable hemodynamics, i.e. failure to maintain blood pressure without supportive measures.” This case highlights about aggressiveness of treatment and role of thrombolytic therapy for a severely hemodynamic unstable patient2.

The procedure was done emergently because of the patient’s critical condition. His right IJ area was prepped in the usual fashion. It was very difficult to visualize his right IJ vein, even though his habitus should have allowed us to do so, but the patient was, I believe, severely intravascularly volume depleted, and his vein was collapsing. I have attempted to access the right internal jugular vein multiple times, both under real-time ultrasound guidance and even later on blindly. I was able to get blood return and hit the vein; however, I was not able to advance the guidewire. I was able to advance it one time and put the catheter in, and it was nonfunctioning. I had to take the catheter out and tried multiple other times on the right IJ vein without success. That procedure was terminated. Pressure was applied. There was no cervical hematoma whatsoever. The patient was uncomfortable because of the length of the procedure but did well otherwise. Hemodynamically, he was unchanged, and his oxygen saturations remained stable.I prepped the IJ vein area in the usual fashion. One percent lidocaine was used for local anesthesia. Again, the left IJ vein was collapsing. With deep inspiration, the vein could be well visualized on the real-time and ultrasound guidance, after which I could get access to the left IJ vein. A wire was advanced without difficulty while the

A.W., a 52-year-old woman disabled from severe emphysema, was walking at a mall when she suddenly grabbed her right side and gasped, “Oh, something just popped.” A.W. whispered to her walking companion, “I can’t get any air.” Her companion yelled for someone to call 911 and helped her to the nearest bench. By the time the rescue unit arrived, A.W. was stuporous and in severe respiratory distress. She was intubated, an IV of lactated Ringer’s (LR) to KVO (keep vein open) was started, and she was transported to the nearest emergency department (ED).

The patient may have a hard time breathing because she is in pain after having surgery. Since they patient doesn’t want to breath due to the pain it can cause atelectasis and later sepsis if not treated in time. It would be important to teach the patient about splinting and to use an incentive spirometry in order to help her be able to breath. Another risk factor for the patient not being able to oxygenate would be hypovolemia since there is less blood volume which can also lead to less oxygen being able to travel in the blood or able to perfuse throughout the body.

Mr. S was driving when he experience a stabbing chest and back pain for the first time. The pain was so severe he immediately went to his local ER. Pulmonary ventilation and perfusion (VQ) scan and Computed tomography angiography (CTA) was done at his local ER. VQ scan was negative for pulmonary embolism (PE). CTA of the chest revealed

A tension pneumothorax occurs when the lung is punctured, but there is no outside opening for air to escape. The pressure that builds is put on internal organs, which decreases cardiac output and the lungs’

A Deep Venous Thrombosis (DVT) will propagate when there is either stasis of blood flow, endothelial injury, or if the patient is in a hypercoagulable state. Under physiological conditions, a dislodged DVT can predictably settle in the pulmonary arteries causing a pulmonary embolism. However, a DVT in the presence of a intracardiac shunt or PAVM can paradoxically cause an embolism in branches of the aorta. The pathophysiological mechanism varies depending on the etiology of the paradoxical embolism. For instance, in a paradoxical embolism due to a PFO, a DVT gets dislodged and enters the right atrium where a transient increase in right atrial pressure during a Valsalva maneuver can force the embolism through the PFO and into the left atrium

According to new research by Japan's Osaka University, binge watching sessions increase a person's chance of receiving a fatal pulmonary embolism.

It is usually presented by a classic triad of symptoms: 1.) respiratory changes; 2.) neurological abnormalities; 3.) petechial rash. The client will normally present first with respiratory changes such as dyspnoea, tachypnoea, and hypoxemia and can progress to respiratory failure. One half of the clients with a fat embolism caused by a long bone fracture will develop severe hypoxaemia and respiratory insufficiency and will require mechanical ventilation. Neurological changes resulting from cerebral embolism produces signs in 86% of cases and often occur after respiratory distress. The changes vary from mild confusion to severe seizures. The most common being confusion with focal neurological signs such as hemiplegia, aphasia, apraxia, and anisocoria. The third in the triad the petechial rash will be the last to develop and it occurs in 60% of the cases. The rash is due to embolization of small dermal capillaries leading to extravasation of erythrocytes. The rash is in the conjunctiva, oral mucous membranes, and skin folds of the upper body. The rash appears within the first 36 hours and disappears completely within 7

Air embolism is a rare but potentially fatal consequence of air entering the vascular system. It can result from a wide range of procedures, including those related to vascular access in interventional radiology, in addition to open surgical procedures. We set out to review all cases of air embolism at our institution over a 25-year period, including analysis of cause, clinical signs and symptoms, treatment and prognosis.

Because patients who often have right ventricular hypertrophy and large pulmonary arteries, they’re at elevated risk for blood clots, especially if immobilized, polycythemic, or dehydrated-all of which can occur during an exacerbation. I start the client’s intravenous, using a #20 gauge needleless system, to his non-dominant left median cubital vein. I hung D5.45NS infusing via Alaris pump at 75cc/hr. And, also administered Solu Medrol (Methylprednisolone sodium succinate) via IVP. Nafcillin intravenous antibiotic therapy was also ordered and started as well. About 0300, I am doing my patient rounding, to check vital signs, change positioning, pain management, bowel/bladder needs and etc. I walk into the client’s room to find him waving his hand, extinguishing a match after lighting up a cigarette. He takes a puff of the cigarette with his oxygen at 2 liters/minute via nasal cannula still attached on his face. I approached him fast and request that he extinguish it, immediately! He does not and becomes verbally combative, “ No f-bomb blank, blank, blank is going to take my cigarette away!” He reaches to throw his box of tissues at me, that’s when his cigarette falls out of his mouth and onto the tile floor. And, yes, I step on it, and the cigarette extinguishes. I was fortunate to arrive early enough so that the room did not fill with

One day post op Ms Smith had clinical indications of a large flank hematoma and pelvic swelling. An abdominal ultrasound was ordered to check for possible internal bleeding. The ultrasound probe was placed on Ms. Smith and her entire abdomen appeared as nothing but dark shadow no matter what probe, frequency, or pressure was applied. To a new sonographer or someone who hasn’t seen this before it could be quite puzzling. Apparently during Ms. Smiths extended surgery the air that was put into her abdomen to for better visualization had not been completely removed. It is a rare complication of surgery, and is called subcutaneous emphysema. It additionally can be caused by a collapsed lung, blunt force trauma, and scuba diving. The air usually

Background: Occult Pneumothoraxes (OPTX) represents air within the pleural space that is not visible on conventional chest radiographs, but ultimately detected with CT . In a study comparing differences in pneumothoraces, while similar in size, patients significantly underwent tube thoracostomy compared with patients who had overt pneumothoraces1. While optimal management of occult pneumothoraxes has not been identified, the increased use of computed tomography has led to a rise in detection. Occult OPTX Extended focused assessment with sonography for Trauma, also known as eFAST, is screening test that has been shown to useful in identifying OPTX. Our aim of the present study is to identify if there are any differences in OPTX detections between

Pulmonary Enema can be identified in a PA and lateral chest radiograph, using a horizontal beam which is critical for the projection of air-fluid levels. It appears an increasingly diffuse in radiodensity in the hilar regions, interstitial spaces and the interlobar septa. Clinical indications or signs of the condition (pulmonary edema) include Signs of the condition include a rapid respiratory rate, heaving of the chest and abdomen, intercostal muscle retractions, and cyanosis. To improve the movement of air into and out of the chest, the patient will often sit upright to breathe and resist laying down. (Venes, D, 2005 p. 666 )

Capnography is the most feasible and safer method to monitor venous air embolism in children.