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Can pulmonary infarction be asymptomatic?

Can pulmonary infarction be asymptomatic?



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I think it can because there are many parts in lungs. Like for some COPD patients. However, I am not sure if COPD patients can have infarction.

Lungs have parallel circulation. Red infarct is possible there. Blood can flow there. One symptom should be at least pain. So now, I think no asymptomatic possible. But still, I am not sure.

Can pulmonary infarction be asymptomatic?


No. Based on experience. Lungs are very active organs.


Pulmonary embolism as a cause of unexplained sinus tachycardia after right ventricular myocardial infarction

We present the case of a patient who developed new-onset asymptomatic sinus tachycardia after undergoing treatment for a right ventricular myocardial infarction. Even after excluding heart failure, infection and bleeding, the sinus tachycardia persisted. Computed tomography pulmonary angiography showed multiple bilateral pulmonary emboli. The vital sign abnormality resolved after treatment with an anticoagulant. We postulate that the pulmonary emboli originated from thrombi that were formed in the infarcted and dysfunctional right ventricle. Pulmonary embolism is a very rare complication of right ventricular myocardial infarction, and patients usually present with pleuritic chest pain. Our case highlights that asymptomatic sinus tachycardia could be a presenting feature of pulmonary embolism after the occurrence of a right ventricular myocardial infarction. A high index of suspicion is warranted in order to detect this potentially lethal complication.


Pulmonary Vein Thrombosis: A Recent Systematic Review

The pulmonary veins (PVs) are the most proximal source of arterial thromboembolism. Pulmonary vein thrombosis (PVT) is a rare but potentially lethal disease its incidence is unclear, as most of the literature includes case reports. It most commonly occurs as a complica-tion of malignancy, post lung surgery, or atrial fibrillation and can be idiopathic in some cases. Most patients with PVT are commonly asymptomatic or have nonspecific symptoms such as cough, hemoptysis, and dyspnea from pulmonary edema or infarction. The thrombi are typically detected using a variety of imaging modalities including transesophageal echocardiogram (TEE), computed tomography (CT) scanning, magnetic resonance imaging (MRI), or pulmonary angiog-raphy. Treatment should be determined by the obstructing pathological finding and can include antibiotic therapy, anticoagulation, thrombectomy, and/or pulmonary resection. The delay in diagnosing this medical entity can lead to complications including pulmonary infarction, pulmonary edema, right ventricular failure, allograft failure, and peripheral embolism resulting in limb ischemia, stroke, and renal infarction (RI).

Keywords: pulmonary vein thrombosis.

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1. The hypothesis of a thrombus…

Figure 1. The hypothesis of a thrombus in the pulmonary vein stump after lobectomy

Figure 2. CT scan of the chest…

Figure 2. CT scan of the chest with IV contrast

A thrombus (white arrow) in…

Figure 3. Baseline 2D transesophageal echocardiography

Figure 3. Baseline 2D transesophageal echocardiography

TEE demonstrating mobile echogenic thrombus within right superior pulmonary…


Complications

Complications of pulmonary embolism include the following:

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Figure 1: High-resolution CT scan of the lungs showed multiple sub-centimeter pulmonary nodules, most of which showed central cavitations, scattered throughout both lungs, largest measuring about 7 mm. There were also numerous blebs bilaterally in the upper lobes and superior segments of the lower lobes. No significant adenopathy was appreciated.

Pulmonary Langerhans cell histiocytosis (PLCH), also known as histiocytosis X and eosinophilic granuloma, is an uncommon interstitial lung disease (ILD) that primarily afflicts young Caucasian cigarette smokers. The exact incidence and prevalence of this disease are unknown, but it probably represents 5% of all ILD (1). Young adults between the ages of 20 and 40 years old are usually affected, and the gender distribution varies among studies. Some studies report male predominance, others suggest that women are more frequently affected than men and others report equal distribution (1,2). The vast majority of patients are smokers (90% or more) and there are no known occupational exposures or known predisposing genetic factors (3). The most common symptoms are nonproductive cough and dyspnea, although patients may also complain of constitutional symptoms such as fatigue and weight loss. Twenty-five percent of the patients are asymptomatic and approximately 15% present with spontaneous pneumothorax (3). The chest radiograph is abnormal in most patients. Findings in the early stages of the disease include nodules in the upper and middle lung zones with sparing of the lung bases and costophrenic angles. As the disease progresses, a reticulonodular pattern predominates followed by cystic changes (2, 4). In end-stage PLCH, reticular areas of opacity in the upper and middle lung zones and honeycomb lung can be found (4). HRCT scan is more sensitive than radiography. Findings include nodules of varying size, some may have cavities like the ones seen in this patient, and they are usually found in the upper and middle lung zones with relative sparing of the lung bases(3, 4). Cystic lesions are the most common feature and usually measure less than 10 mm in diameter. The demonstration of nodules and cysts in a characteristic distribution is highly suggestive of PLHC (5). However, when only nodules or cysts are present, the specificity decreases and other diseases should be considered (4).

Centrilobular emphysema is less likely in this patient given the CT scan findings. Blebs can be seen in emphysema but not nodules. When cystic lesions predominate such as in advance PLHC, it may be difficult to distinguish from emphysema, but that is not the case in this patient (6). Other diseases to consider in predominantly cystic PLHC are lymphangioleioyomatosis, idiopathic pulmonary fibrosis and Pneumocystis jiroveci pneumonia (4). Lymphangioleiomyomatosis occurs almost exclusively in women of childbearing age and affects the lungs diffusely rather than the upper lung zones like in PLHC(4).  The cystic lesions of idiopathic pulmonary fibrosis have a subpleural and basilar distribution and patients have decreased lung volumes (4). Patients with Pneumocystis jirovecii pneumonia may also develop lung cysts that may be indistinguishable from cystic lesions of PLHC (4).

Respiratory bronchiolitis-associated interstitial lung disease is a rare disease that occurs in young smoking adults in their third through sixth decades of life such as this patient. The most common symptoms are chronic cough and dyspnea. CT scan findings include fine centrilobular nodules and areas of ground glass bilaterally. Both upper and lower lung fields are affected. Emphysematous changes can coexist (4, 6).

Silicosis is a lung disease caused by inhalation of mineral dust. Patients may be asymptomatic or present with exertional dyspnea and productive cough. Some patients may also have constitutional symptoms such as weight loss and malaise. CT scan manifestations include multiple small (<10 mm) nodules that are scattered diffusely throughout the lungs (but may be more prominent in the upper lung fields), and pleural thickening. The nodules in PLHC follow a centrilobular distribution whereas the nodules in silicosis have a perilymphatic distribution (7).

Multiple pulmonary nodules can be seen in metastatic cancer but they are usually localized in the better perfused lung bases and not the upper lobes like the nodules seen in this patient. Cavitation of metastatic lesions occurs in less than 5% of the cases (8). Patients with PLCH are at increased risk of developing malignant neoplasm but it does not seem to be related to tobacco exposure. Lymphoma, myeloproliferative disorders, lung, prostate and breast cancer and are some of the malignancies that have been described (9-11).

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Figure 2                                               Figure 3

The definitive diagnosis of PLCH requires lung biopsy. Transbronchial biopsy has a low yield, its sensitivity is approximately 10- 40% (3). Surgical lung biopsy has the highest yield. The histopathology findings of early stages of PLCH include an increase in the number of Langerhans cells and nodules composed of Langerhans cells, lymphocytes, fibroblasts, eosinophils (hence the former term eosinophilic granuloma), neutrophils, plasma cells and pigmented macrophages (from cigarette smoking). In the later stages the nodules are replaced by fibroblastic proliferation that results in the classic stellate lesions. Immunohistochemical staining for the CD1a antigen (a specific marker for Langerhans cells) and S-100 protein (Figures 2 and 3) is also recommended, especially in difficult cases. The finding of 5% or greater amounts of Langerhans cells in BAL is suggestive of PLCH (1,3). However, the mere presence of Langerhans cells is in BAL is not diagnostic since these cells can be found in other situations such as in current smokers and in other ILD (12).

Smoking cessation is the first line therapy. This intervention results in regression or stabilization of the disease and even in radiological improvement in some patients. Other patients develop progressive disease in spite of smoking cessation. For those patients corticosteroid therapy is often used, but this recommendation is based on case reports and expert opinion rather than prospective studies (1, 3).

Other experimental therapies with immunosuppressive agents such as vinblastine, cytarabine, chlorodeoxyadenosine, cyclophosphamide and methotrexate have also been used to treat patients with progressive disease (1, 3).

Lung transplantation should be considered in patients who do not respond to smoking cessation or aggressive medical therapy, although there is evidence that the disease may recur after transplantation (1, 3).

Most patients with PLCH have a good prognosis especially after successful smoking cessation. According to a retrospective analysis by Vassallo et al, patients with PLCH have a shorter long-term survival compared with the general population. The median survival time from the time of diagnosis is 12.5 years with a 5-year survival of 74.6% and 10-year survival of 63.9% (11).

References

  1. Vassallo R, Ryu JH, Colby TV, et al. Pulmonary Langerhans'-cell histiocytosis. N Engl J Med 2000 342:1969-1978.
  2. Attili AK, Kazerooni EA, Gross BH, et al. Smoking-related interstitial lung disease: radiologic-clinical-pathologic correlation. RadioGraphics 2008 28:1383-1398.
  3. Vassallo R, Ryu JH. Pulmonary Langerhans’cell histiocytosis. Clin Chest Med 2004 25: 561-571.
  4. Abbott GF, Rosado-de-Chritenson ML, Franks TF, et al. From the archives of the AFIP: Pulmonary Langerhans cell histiocytosis. RadioGraphics 2004 24:821-841.
  5. Kulwiec EL, Lynch DA, Aguayo SM, et al. Imaging of pulmonary histiocytosis X. Radiographics 1992 12:515-526.
  6. Vassallo R, Ryu JH. Tobacco smoke–related diffuse lung diseases. Semin Respir Crit Care Med 2008 29:643-650.
  7. Akira M. Imaging of occupational and environmental lung diseases. Clin Chest Med 2008 29: 117-131.
  8. Rusch VW. Lung metastasis. In: Abelloff M, Armitage J, Niederhuber J, Kastan M and McKenna W, editors. Clinical oncology, 4th ed. Philadelphia, PA: Churchill Livingstone Elsevier 2008. p 873-884.
  9. Tomashefski JF, Khiyami A, Kleinerman J. Neoplasms associated with pulmonary eosinophilic granuloma. Arch Pathol Lab Med 1991 115:499-506.
  10. Egeler RM, Neglia JP, Puccetti DM, et al. Association of Langerhans cell histiocytosis with malignant neoplasm. Cancer 1993 71:865-873.
  11. Vassallo R, Ryu JH, Schroeder DR, et al. Clinical outcomes of pulmonary Langerhans’-cell histiocytosis in adults. N Engl J Med 2002 346: 484-490.
  12. Auerswald U Barth J Magnussen H. Value of CD-1-positive cells in bronchoalveolar lavage fluid for the diagnosis of pulmonary histiocytosis X. Lung 1991169:305-309.

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Treatment of PVCs in Absence of Structural Heart Disease

In the presence of symptoms without structural heart disease, reversible causes of increased ectopy should be addressed. Treatment includes correcting electrolyte abnormalities (hypokalemia, hypomagnesemia, hypercalcemia), improving respiratory status (hypercapnea, hypoxia), treating hyperthyroidism, and avoiding medications that may precipitate ectopy such as digoxin, sympathomimetics, and tricyclic antidepressants. Avoidance of alcohol, amphetamines, caffeine, cocaine, and tobacco is also recommended. As anxiety can result in an increase in catecholamines resulting in increased ectopy, reassurance and treatment of underlying anxiety disorder may help. Daily magnesium supplementation with potassium supplementation has also been shown in a randomized clinical trial to decrease the occurrence of PVCs.13 While this trial did not demonstrate any improvement in symptoms, daily magnesium and potassium supplementation may be beneficial by promoting electrical stability and may be considered given the few side effects of additional electrolytes.

With significant, persistent symptoms in the absence of structural heart disease and after failure to identify an underlying cause, medical therapy is indicated with a beta blocker, a class II antiarrhythmic. A beta blocker is started at a low dose and titrated until symptoms are alleviated or better tolerated. Amiodarone, a class III antiarrhythmic agent, can also be used if beta blockade is unsuccessful in suppressing the symptomatic PVCs. During treatment with amiodarone, thyroid, hepatic, and pulmonary function needs to be closely monitored given the side effects of long term amiodarone use. Other antiarrythmics such as flecainide and propafenone may be considered these agents are associated with increased mortality due to their proarrhythmic potential. Ablation of the responsible ectopic focus may be useful in frequent, symptomatic, monomorphic PVCs refractory to medical therapy.14 Ablation is not recommended for treatment of asymptomatic PVCs.14


TREATMENT

In hemodynamically stable patients, without contraindications to systemic anticoagulation, parenteral anticoagulation with subsequent conversion to vitamin K antagonists is the mainstay of therapy. Early initiation is paramount as patients may quickly decompensate. Patients who present to the emergency room with acute PE have decreased mortality if anticoagulation treatment commences in the emergency room, rather than waiting until after admission.[17] Supportive care of hypoxemia and hemodynamic instability should be instituted. Hemodynamically unstable patients may benefit from fibrinolytic therapy. However, the role for fibrinolysis is limited, with significant bleeding occurring in up to 13% of patients. The use of bolus thrombolytics during cardiopulmonary arrest may have some benefit when PE is strongly suspected[18,19] and the patient does not respond to resuscitation. Mechanical thrombolysis with catheter-directed embolectomy and fibrinolytic therapy can also be used. Systemic heparin, either in the form of unfractionated heparin or low-molecular-weight heparin (LMWH), is the mainstay of treatment. LMWH is advantageous in ease of administration, monitoring, lower potential for heparin-induced thrombocytopenia. However, it is not an appropriate choice for patients with renal failure or for patients at significant risk of bleeding, because of its longer half-life and lack of reversibility. Newer options for anticoagulation include oral factor Xa inhibition with agents under investigation, such as rivaroxaban.[20,21] If patients continue to have PEs despite therapeutic anticoagulation, experience bleeding events, or have other contraindications to anticoagulation, permanent or temporary inferior vena cava filters (IVCF) may be used. IVCF can prevent further pulmonary emboli in patients with lower extremity deep venous thrombosis, but do not reduce mortality. Propagating iliofemoral venous thrombus while on anticoagulation is another indication for IVCF placement.


Short Communication

Faisal AH *

Department of Medicine, University Kebangsaan Malaysia Medical Centre, Malaysia

*Address for Correspondence: Dr. Mohamed Faisal Abdul Hamid, MBBS (IIUM), Doctor of Internal Medicine (UKM), Respiratory Unit, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latiff, Bandar Tun Razak, 56000, Cheras, Kuala Lumpur, Malaysia, Tel: +603-91455555, Fax: +603-91456679 Email: [email protected]

Dates: Submitted: 04 March 2017 Approved: 22 March 2017 Published: 23 March 2017

How to cite this article: Faisal AH. Cardiac Manifestations on Anti-Phospholipid Syndrome. J Clini Nephrol. 2017 1: 011-013.DOI: 10.29328/journal.jcn.1001002

Copyright: © 2017 Faisal AH. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


A fifth of asymptomatic COVID patients develop long COVID: study

Credit: Pixabay/CC0 Public Domain

Almost a fifth of COVID patients without symptoms went on to experience conditions consistent with long COVID a month after their initial diagnosis, according to a huge study published Tuesday.

The analysis by non-profit FAIR Health encompassed insurance claims from 1.96 million Americans—the largest population of patients ever studied for long COVID—from February 2020 to February 2021.

"Even as the COVID-19 pandemic wanes, long-haul COVID persists as a public health issue affecting many Americans," said FAIR Health's president Robin Gelburd.

"The findings in our new study shed significant light on this emerging issue for all individuals who have long-haul COVID, as well as for policy makers, providers, payors and researchers."

"Long COVID" refers to symptoms of the disease that persist more than four weeks after being diagnosed.

The study found that across all ages, the most common post viral conditions were in order of frequency: pain, breathing difficulties, high cholesterol, general discomfort and fatigue, and high blood pressure.

The odds of dying 30 days or more after initially being diagnosed with COVID were 46 times higher for patients who were hospitalized with COVID and discharged compared to those who weren't hospitalized.

Overall, 0.5 percent of COVID patients who were hospitalized then discharged died 30 days or more after their initial diagnosis.

Nineteen percent of asymptomatic COVID patients experienced long COVID symptoms 30 days out from their initial diagnosis the figure grew to 27.5 percent of COVID patients who were symptomatic but not hospitalized, and 50 percent of those who were hospitalized.

The order of most common long COVID conditions varied by age group—for example in the pediatric population, intestinal issues replaced high cholesterol as the third most frequent.

Most long COVID conditions were associated more with females than males—but some, such as cardiac inflammation, were more common in males, who accounted for 52 percent of cases against 48 percent for females.

A quarter of all such cases occurred among individuals aged 19-29.

Among the four mental health conditions evaluated after 30 days, anxiety was the most common, followed by depression, adjustment disorders and tic disorder.

The biggest drawback of the new study is it lacks a control group of people who never got COVID, which would help determine the extent to which COVID caused the conditions as opposed to being coincidental.

The causes of long COVID, which is also known as long haul COVID, post-COVID syndrome or post-acute sequelae of COVID, remain unknown.

"Theories include persistent immune activation after the acute phase initial damage from the virus, such as damage to nerve pathways, that is slow to heal and persistent presence of low-level virus," the study said.


Can pulmonary infarction be asymptomatic? - Biology

A recent study suggests about half of asymptomatic COVID-19 carriers may end up with damage to their lungs. /AP Photo

Scientists have made significant progress over the past few decades in understanding the role of hyaluronic acid in pulmonary health and disease – and now some suspect it could explain why some COVID-19 sufferers struggle with breathing.

Hyaluronic acid is a molecule of extracellular matrix that is naturally produced in the body. Its main function is to act as a thin protective layer or lubricant, but it is also a key regulator of inflammation and fibrosis in the lung.

Past studies have shown a correlation between high levels of hyaluronic acid and spots throughout the lungs in X-ray images, an observation that has also been made in seriously ill COVID-19 patients.

Daniel Jacobson, the lead researcher for computational systems biology at Oak Ridge National Laboratory in Tennessee, U.S., has been leading a study to understand how COVID-19 affects human body systems.

The research suggests that health risks to asymptomatic coronavirus carriers could be more significant than previously realised, with as many as half of them going on to develop varying degrees of damage to their lungs.

"There may be a fair amount of damage going on that they're completely unaware of. But they can go from asymptomatic to a 'long hauler' with long-term outcomes," adds Jacobson.

"If all that is true, that really should change how we think about this disease, even from a public health perspective," warns Jacobson. "Because an asymptomatic infection can lead to a long-term disability [and] that [can have] a radical impact on society."

Currently most countries are focusing their testing and treatment efforts on those suffering symptoms of the virus such as a fever or a cough.

Using samples taken from inside the lungs, Jacobson's team has found the virus affects the level of hyaluronic acid in the lungs.

"It can absorb over a thousand times its own weight in water. It becomes a hydrogel," Jacobson told CGTN's RAZOR program. "And so what we saw in COVID-19 patients is the three genes that are responsible for synthesizing hyaluronic acid were all significantly up-regulated, and two of the genes responsible for keeping it under control were significantly down-regulated.

"You're also letting a lot of plasma, a lot of water effectively, leak into that same space and [it is] going to form a hydrogel – it's like having Jell-O in your lungs. And those are the surfaces where you're trying to exchange oxygen and carbon dioxide, and that simply doesn't happen well through the hydrogel."

This could explain why some COVID-19 patients have suffocated even when on ventilator support.