Effusion may be a result of
- trauma(bleeding, blood in effusion)
- systemic, blood vessel obstruction
- inflammation / infection
- tumors(circles in diagram) may invade the pericardium and rupture the wall or other layers
lymphoma caused mediatsinal mass in this case
necrosis was seen on pericardial wall with white/pale color
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Massive Circumferential MI
Myocardial Infarct
- stenosis -> ischemia
- coronary artery occlusion: LAD > RCA > circumflex
- hypoxia due to decreased oxygen supply
- hypotension (the cause of this case, 80/60)
- high metabolic demand (e.g. thyroid disease Graves)
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Lymphoma is a variety of cancer that originates in lymphocytes or, more rarely, of histiocytes. Collectively, these cell types form the reticuloendothelial system and circulate in the vessels of the lymphatic system. There are many types of lymphoma. Lymphomas are part of the broad group of diseases called hematological neoplasms.
In the 19th and 20th centuries the affliction was called Hodgkin's Disease, as it was discovered by Thomas Hodgkin in 1832. Colloquially, lymphoma is broadly categorized as Hodgkin's lymphoma and non-Hodgkin lymphoma (all other types of lymphoma). Scientific classification of the types of lymphoma is more detailed.
Hodgkin's lymphoma, also known as Hodgkin's disease, is a type of lymphoma first described by Thomas Hodgkin in 1832. Hodgkin's lymphoma is characterized clinically by the orderly spread of disease from one lymph node group to another and by the development of systemic symptoms with advanced disease. Pathologically, the disease is characterized by the presence of Reed-Sternberg cells. Hodgkin's lymphoma was one of the first cancers to be rendered curable by combination chemotherapy.Symptoms
Swollen but painless lymph nodes are the most common sign of Hodgkin's lymphoma, often occurring in the neck. The lymph nodes of the chest are often affected and these may be noticed on a chest X-ray.
Splenomegaly, or enlargement of the spleen, occurs in about 30% of people with Hodgkin's lymphoma. The enlargement, however, is seldom massive. The liver may also be enlarged due to liver involvement in the disease in about 5% of cases.
About one-third of people with Hodgkin's disease may also notice some systemic symptoms, such as low-grade fever, night sweats, weight loss, itchy skin (pruritus), or fatigue. Classically, involved nodes are painful after alcohol consumption, though this phenomenon is rare. Patients may also present with a cyclic high-grade fever known as Pel-Ebstein fever, although there is debate as to whether or not this truly exists [1]. Systemic symptoms such as fever and weight loss are known as B symptoms.
[edit] Diagnosis
Hodgkin's lymphoma must be distinguished from non-cancerous causes of lymph node swelling (such as various infections) and from other types of cancer. Definitive diagnosis is by lymph node biopsy (removal of a lymph node for pathological examination). Blood tests are also performed to assess function of major organs, to detect lymphoma deposits or to assess safety for chemotherapy. Positron emission tomography (PET) is used to detect small deposits that do not show on CT scanning. In some cases a Gallium Scan may be used instead of a PET scan.
[edit] Pathology
[edit] Macroscopy
Affected lymph nodes (most often, laterocervical lymph nodes) are enlarged, but their shape is preserved because the capsule is not invaded. Usually, the cut surface is white-grey and uniform; in some histological subtypes (e.g. nodular sclerosis) may appear a nodular aspect
[edit] Microscopy
Microscopic examination of the lymph node biopsy reveals complete or partial effacement of the lymph node architecture by scattered large malignant cells known as Reed-Sternberg cells (typical and variants) admixed within a reactive cell infiltrate composed of variable proportions of lymphocytes, histiocytes, eosinophils, and plasma cells. The Reed-Sternberg cells are identified as large often bi-nucleated cells with prominent nucleoli and an unusual CD45-, CD30+, CD15+/- immunophenotype. In approximately 50% of cases, the Reed-Sternberg cells are infected by the Epstein-Barr virus.
Characteristics of classic Reed-Sternberg cells include large size (20–50 micrometres), abundant, amphophilic, finely granular/homogeneous cytoplasm; two mirror-image nuclei (owl eyes) each with an eosinophilic nucleolus and a thick nuclear membrane (chromatin is distributed at the cell periphery). Variants: Hodgkin's cell (atypical mononuclear RSC) is a variant of RS cell, which has the same characteristics, but is mononucleated. Lacunar RSC is large, with a single hyperlobated nucleus, multiple, small nucleoli and eosinophilic cytoplasm which is retracted around the nucleus, creating an empty space ("lacunae"). Pleomorphic RSC has multiple irregular nuclei. "Popcorn" RSC (lympho-histiocytic variant) is a small cell, with a very lobulated nucleus, small nucleoli. "Mummy" RSC has a compact nucleus, no nucleolus and basophilic cytoplasm. [2]
Hodgkin's lymphoma can be sub-classified by histological type. The cell histology in Hodgkin's lymphoma is not as important as it is in non-Hodgkin's lymphoma: the treatment and prognosis in Hodgkin's lymphoma depend on the stage of disease rather than the histotype.
Treatment
Patients with early stage disease (IA or IIA) are effectively treated with radiation therapy or chemotherapy. The choice of treatment depends on the age, sex, bulk and the histological subtype of the disease. Patients with later disease (III, IVA, or IVB) are treated with combination chemotherapy alone. Patients of any stage with a large mass in the chest are usually treated with combined chemotherapy and radiation therapy.
Currently, the ABVD chemotherapy regimen is the gold standard for treatment of Hodgkin's disease. The abbreviation stands for the four drugs Adriamycin, bleomycin, vinblastine, and dacarbazine. Developed in Italy in the 1970s, the ABVD treatment typically takes between six and eight months, although longer treatments may be required. Another form of treatment is the newer Stanford V regimen, which is typically only half as long as the ABVD but which involves a more intensive chemotherapy schedule and incorporates radiation therapy.
Another form of treatment, mainly in Europe for stages > II is BEACOPP.
With appropriate treatment, over 85% of Hodgkin's lymphoma cases are curable.
The high cure rates and long survival of many patients with Hodgkin's lymphoma has led to a high concern with late adverse effects of treatment, including cardiovascular disease and second malignancies such as acute leukemias, lymphomas, and solid tumors within the radiation therapy field. Most patients with early stage disease are now treated with abbreviated chemotherapy and involved-field radiation therapy rather than with radiation therapy alone. Clinical research strategies are exploring reduction of the duration of chemotherapy and dose and volume of radiation therapy in an attempt to reduce late morbidity and mortality of treatment while maintaining high cure rates.
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Pericardial effusion ("fluid around the heart") is an abnormal accumulation of fluid in the pericardial cavity. Because of the limited amount of space in the pericardial cavity, fluid accumulation will lead to an increased intrapericardial pressure and this can negatively affect heart function. When there is a pericardial effusion with enough pressure to adversely affect heart function, this is called cardiac tamponade. Pericardial effusion usually results from a disturbed equilibrium between the production and re-absorption of pericardial fluid, or from a structural abnormality that allows fluid to enter the pericardial cavity. Normal amount of fluid present in the pericardium - 15 to 50 mL.Types
It may be transudative(Congestive heart failure, Myxoedema, Nephrotic Syndrome), exudative(tuberculosis, spread from empyema) or haemorrhagic(trauma, rupture of aneuryms, malignant effusion).
[edit] Symptoms
Chest pain, pressure symptoms. A small effusion may have no symptoms.
Pericardial effusion is also present after a specific type of heart defect repair. An Atrial Septal Defect Secundum, or ASD, when repaired will most likely produce a pericardial effusion due to one of the methods of repair. One repair method of an ASD is to take a piece of the peridcardial tissue and use it as a patch for the hole in the atrial cavity.
[edit] Treatment
Treatment depends on the underlying cause and the severity of the heart impairment. Pericardial effusion due to a viral infection usually goes away within a few weeks without treatment. Some pericardial effusions remain small and never need treatment. If the pericardial effusion is due to a condition such as lupus, treatment with anti-inflammatory medications may help. If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space. A drainage tube is often left in place for several days. In some cases, surgical drainage may be required
--------------------------------------------------------Cardiac tamponade, also known as pericardial tamponade, is a medical emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). The elevated pericardial pressure puts significant pressure on the heart, causing a decrease in diastolic filling of the ventricles, and hence in stroke volume. The end result is ineffective pumping of blood, shock and often death.
Pathophysiology
The outer pericardium is made of fibrous tissue (Thibodeau & Patton 2003) which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase (Mattson Porth 2005).
If fluid continues to accumulate, then with each successive diastole, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to decreased stroke volume (Mattson Porth 2005). This causes obstructive shock to develop, and if left untreated then Cardiac arrest may occur (in which case the presenting rhythm is likely to be Pulseless electrical activity)
[edit] Diagnosis
Initial diagnosis can be challenging, as there are a number of differential diagnoses, including Tension pneumothorax (Gwinnutt & Driscoll 2003), and accute heart failure[citation needed]
Classical cardiac tamponade presents three signs, known as Beck's triad. Hypotension occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid inside the pericardium (Dolan & Holt 2000).
Other signs of tamponade include pulsus paradoxus (a drop of at least 10mmHg in arterial blood pressure on inspiration) (Mattson Porth 2005), and ST segment changes on the electrocardiogram (Dolan & Holt 2000), which may also show low voltage QRS complexes (Longmore et al 2004), as well as general signs & symptoms of shock (such as tachycardia, breathlessness and decreasing level of consciousness).
Tamponade can often be diagnosed radiographically, if time allows. Echocardiography often demonstrates an enlarged pericardium or collapsed ventricles, and a chest x-ray of a large cardiac tamponade will show a large, globular heart (Longmore et al 2004)
--------------------------------------------------------Beck's triad is comprised of fall in the systolic pressure, rising jugular venous pressure and suppressed heart sounds. These findings are typical of cardiac tamponade.
1: The rising jugular venous pressure is evidenced by distended jugular veins while in a non-supine position. It is caused by reduced diastolic filling of the right ventricle, due to the outside pressure being exerted on it by the expanding pericardial sac. This results of a backup of fluid into the veins draining into the heart, most notably, the jugulars. In severe hypovolaemia, the neck veins may NOT be distended.
2: The fall in systolic pressure results when the fluid in the pericardial cavity accumulates to a degree that it impairs ventricular stretch, thus reducing stroke volume and cardiac output.
3: The suppressed heart sounds occur due to the muffling effects of the sounds passing through the fluid surrounding the heart.
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Symptoms of MI
- diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue, adrenergic symptoms
Dx of MI
- EKG - flipped T waves, ST elevation(transmural infarct), ST depression(subendocardial infarct), pathologic Q waves (transmural infarct, usually late), dysrhythmias(fibrilation, premature ventricular contraction, V tach)
- Cardiac isoenzymes (elevated CK mb fraction), troponin I, AST(nonspecific)
Treatment of MI
BEMOAN
- BEta-blocker
- Morphin
- Oxygen
- Aspirin
- Nitrates
Infarcts: red vs. pale
Red(hemorrhagic infarcts occur in loose tissues with collaterals, such as lungs, intestines, or following re-perfusion)
Pale infarcts occur in solid tissues with single blood supply such as brain, heart, kidney and spleen.
Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.[62]
Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers.[63] Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus.[64] The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar (which are typical steps in wound healing). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells.[62]
These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.[65]
Contraction band necrosis
