Phantom or vanishing tumor stands for a localized transudativeinterlobar pleural fluid collection in congestive heart failure. Pseudotumors commonly manifest as incidental radiographic findings in patients with disorders associated with pleural effusions, especially congestive heart failure. The name originates from its frequent resemblance to a tumor on the chest X- ray and from its tendency to vanish after appropriate management of heart failure [1].
A pseudotumor may serve as a marker of left heart failure, or another disorder associated with transudative pleural effusions. A correctly diagnosed pseudotumor is typically an incidental finding that has minimal impact on patient management; however, pseudotumors may be erroneously diagnosed
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He had shortness of breath increasing for the last two weeks. On review of symptoms, he denied cough and chest pain, but in last two days he had high temperature up to 38C. His medical history was significant for left ventricular failure with an ejection fraction of 30-35% measured by echocardiography. He undergone a bypass surgery 7 years ago, using ASA, ramipril, furosemide, spironolactone.He was a lifelong nonsmoker, using tiotropium bromide, fixed combination of inhaler corticosteroid/beta agonist and short acting beta agonist on …show more content…
The chest examination was remarkable for dull auscultatorysound at the right side. The remainder of the physical examination was unremarkable. The blood pressure was 110/70mmHg and heart rate was 85 beats/min.The peripheral blood leukocyte count was 23000 x 109/L, with neutrophils 89%.C reactive protein was 276ng/l, while other parameters were in normal range. The posteroanterior chest radiogram showed pleural effusion on right side and imflammatory changes on rest right lung apically [Figure 1A]. He was admitted to the hospital and receive two antibiotics- ciprofloxacin and ceftriakson and his chronic cardiac therapy. We performed pleural punction and its analysis showed that pleural effusion is transudative etiology. We got 2 liters of serous fluid. After 3 days, we made control chest radiogram and laboratory findings [Figure 2A]. Chest radiogram showed significant improvement in lung parenchyma as well as reduction of pleural effusion. Laboratory finding were: Le 12,7x109/L, Neutophils 80% and C reactive protein was 123ng/l. The patient was feeling better. We have done echocardiography which showed enlargement in left heart chamber, systolic dysfunction, ejection fraction 25%, moderate mitral and aortic regurgitation, pulmonary artery pressure (42mmHg). The patient introduced intensive IV loop diuretic therapy. 48 hours later, a significant decrease in the pleurlaleffusion was observed [Figure
Pathophysiology When Pulmonary Stenosis is present, resistant to blood flow cause right ventricular hypertrophy – right atrial pressure will increase – reopening of the foramen ovale, shunting of unoxygenated blood into the left atrium, systemic circulation. Clinical manifestation: Cyanosis, characteristic murmur , cardiomegaly . Treatment: Baloon angioplasty (neonate).
Thank you for reviewing Ronald Cocks, an 89 year old gentleman with an array of medical comorbidities. Ronald has a history of prior asbestos exposure and is an ex-smoker of approximately 20 pack years. He is quite frail, although still ambulates independently with a 4-wheel frame and is currently living at a retirement village. Ronald was referred to me just prior to Christmas with a two month history of sudden onset voice hoarseness. He was noted to have a 4.5cm left upper lobe cavitatory mass in close proximity to the left upper lobe pulmonary arteries and abutting the left upper lobe pleura.
Splenic Artery Aneurysm Splenic artery aneurysm is the third most common aneurysm in the abdomen and the most common type to affect the internal organs. The spleen is an abdominal organ that forms part of the immune system. It has a large artery that supplies blood to it. When a portion of this artery balloons or widens because of weakness in its walls, an aneurysm develops. Other more common intra-abdominal aneurysms affect the aorta and the iliac arteries.
But the staff understood and Dr. Westwood got an ambulance and reached to ED. He presented with diaphoresis, motor dysfunction, paresthesia, nausea, and ascending paralysis from his leg to the upper body, arms, face and head. He became cyanotic and hyperventilating and it turned to be bradycardiac with a BP 90/50mmHg. After five hour long clinical treatment procedures were followed for tetrodotoxin poisoning, his vital signs were
5. Approach to the diagnosis. 5.1. Is it cardiac or not? 5.2.
Site of colostomy appears clean, dry and intact. Fecal material present inside colostomy pouch. Patient reports pain at 0 (Numeric scale
In more severe cases patients often suffer from hypovolemia due to massive blood loss into the pleural cavity or due to the increased severity of the pneumothorax
Then he was kept for observation for 3 days. The patient developed fever again (39oC) and parenteral paracetamol was able to decrease his temperature temporary for only 2 hours and kept rising again to 39oC. Parenteral antibiotics were started again for a week. However, the fever didn’t decline at all. Abdominal CT scan was performed but revealed nothing except cholelithiasis. A descion of removing the previously inserted plastic stent in CBD was made.
1281). Damage to the pulmonary endothelium triggers the release of neutrophils in a great amount, and the neutrophils stimulate the release of other inflammatory mediators such as tumor necrosis factor, prostaglandin, leukotrienes, histamine and platelet-activating factor (McKane, 2010, 1281). Consequently, capillary membrane becomes more permeable which further allows more fluids, proteins and red blood cells casts to flow into alveoli (McKane, 2010, p.1281). It later causes the lungs to collapse resulting in atelectasis and reduce the lungs compliance (McKane, 2010, p.1281). In addition, pulmonary vasoconstriction can result from platelet aggregation, atelectasis and inactivated surfactant (McKane, 2010, p. 1281).
The right TM is bulging with copious cerumen and questionable purulent fluid behind the TM, but the TM landmarks appear normal bilaterally. His throat is erythematous and the nares are draining thick, yellow mucus. Liam’s diagnosis is a right AOM, and the following paragraphs
I note she also underwent an echocardiogram, and this revealed normal LV size and systolic function with some diastolic dysfunction and elevated pulmonary artery pressures with a PAP of 35mmHg, assuming RA pressure of 3mmHg. There was mild aortic regurgitation. On review today, Glenys is much improved and believes that there is no ongoing dyspnooea. As mentioned, her restless legs symptoms are similar to
There is also a necessity to avoid venous stasis in the legs that may cause a pulmonary embolus. Head drop is more prevalent during this final stage of the disease and the patient’s ability to breath is also compromised. Breathing complications may require the use of a suction machine to assist the patient. Physical therapy techniques should be used to assist cardiopulmonary distress. Techniques include repositioning the patient so the body is able to exchange oxygen and blood adequately.
He had coughing fits (54) that were quite normal at first
In humans they are localized in the liver in most of the cases and in other organs of bodies such as spleen, brain heart and kidney. The disease occur with slow-growing mass this mass is called cysts. The patient may be asymptomatic even if cysts are peresent. But if they occur then include cough, shortness of breaths and pain in chest. It is diagnosed by different combination ofd tools and techniques i.e, histopathology,
Other physical examination findings were normal. The patient had no known chronic illnes. But he had history of taking alcohol 20-40 gr / daily and smoking 1-2 pockets / daily for 40 years. He had no special family history. Patient’s laboratory findings were ; creatinin: 1.02 mg/dl, albumin: 2.9 mg/dl, Total bilurubin: 4.0 mg/dl, ALT:22 IU/L AST:20 IU/L, hemoglobin:10.6 gr/dl, platelet: 232.000, protrombin time: 18.7 sn, INR: 1.37, serum protein elektrophoresis: beta-gamma bridging, serum-ascites albumin gradient: 2.1 gr/dl, AFP: 6000 IU/ml, CA 19.9-CA 125-CEA: negatif, HBsAg (+), HBeAg (-), HBV DNA: 61.700 IU/ml, HDV (-), AntiHCV (-), markers for otoimmun hepatites and other etiological tests were negative.