Pericardial edema

A consistent pericardial edema in chickens gave rise to the term chick edema disease (chick edema factor) (I). Two known outbreaks of the disease in the broiler industry resulted in a great loss of chickens. A lipid residue from the manufacturing fatty acids, being used as a feed ingredient, was a principal source of the toxic substance. Contamination of the lipid component with polychlorodibenzo-p-dioxins was attributed as the causal agent. 

Embryos >1500 At 96 h, some midgut malformations and pericardial edema 83... 

Embryonic zebra fish model was employed to study fullerene toxicity. This model is quite convenient because the embryos are transparent in the first week of life and their rate of development is rather fast. C60, C70, and C60(OH)24 have been tested on early embryogenesis (Usenko et al., 2007), presenting effects on this process with malformations, pericardial edema, and mortality. The results for fullerols are milder, but it is difficult to attribute this effect to the presence of the functionalizations themselves or to the easier solubilization, implying diminished cluster formations and avoiding the use of solvents as toluene or THF, the presence of which can play an important role in toxicity, as already demonstrated. 

One of the pollutants known to interfere with cardiovascular development is 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a persistent, bioaccumulative environmental contaminant, as well as a potent developmental toxicant and human carcinogen [30]. Piscine, avian, and mammalian cardiovascular systems are sensitive to TCDD toxicity, with effects including cardiac enlargement, edema, and several dysfunctions. In zebrafish embryos, these effects include areduction in cardiomyocyte number at 48 hpf, decreased heart size, altered vascular remodeling, pericardial edema, and decreased ventricular contraction culminating in ventricular standstill [31-34]. 

Fig. 5 Typical deformations detected in 96 hpf zebrafish embryos exposed at the indicated concentrations of the carcinogenic polycyclic aromatic hydrocarbons Benzo[a]Pyrene (b) and Benazo [k]Fluoranthene (c), or to the reportedly nontoxic AhR-ligand (3-naphthofiavone (d). A nonexposed, normal specimen is shown in (a). Arrows indicate (a) pericardial edema, (b) malformation of the lower jaw, (c) malformation of the tail, (tf) color of the yolk, and (e) coagulation...

Monkey 3 mo Cardio 12 M (pericardial edema) Allen and Norback 1973 Allen etal. 1973... 

Studies carried out by Incardona et al. (2006), about induction of alterations in zebrafish embryos by PAHs constituted by four aromatic rings, pointed out that chrysene did not show any embryotoxic and teratogenic effect in these embryos. The exposition to benzo[b] anthracene resulted in mortality in all the concentrations between 8 and 10 pM and defects in the development as a failure of head straightening, lack of finfold development and poor cardiac looping with pericardial edema hemorrhage, for concentrations between 2 and 6 pM. The continuous expositions to doses superior to 5 pM of pyrene resulted in systemic toxicity that occurred in the initial phases of the larval development, including dorsal curvature of the body axis, reduction in the peripheral circulation, anemia and pericardial edema. 

Toxic compounds should be excluded from the analysis. Typical signs of drug-induced toxicity are a deflated swim bladder, pericardial edema, or morphological malformations. 

Chick Edema Bioassay. Chick edema was produced in groups of birds treated with 1 and 10 /xg/kg/day of 2,3,7,8-TCDD and 10 and 100 /xg/kg/day of HCDD (Table V). The mean logarithm for pericardial fluid volume of the negative control groups was greater than 1.1460 and... 

The gross lesions seen in chicks treated with chlorodibenzodioxins are summarized in Table VI. The most consistent gross lesions were increased pericardial and peritoneal fluid, subcutaneous and pulmonary edema, hepatomegaly, and a mottled appearance of the liver. 

VS Blood pressure 160/85 mm Hg, pulse 70 beats per minute, temperature 36.8°C (98.2°F), Wt 150 lb (68.2 kg) Chest Regular rate and rhythm, normal S1r S3 and S4 both present slight pericardial friction rub Exts 3+ bilateral lower extremity edema which is present half-way up her calf... 

Adverse reactions may include Stevens-Johnson syndrome pericardial effusion T-wave changes rebound hypertension (following gradual withdrawal in children) decreased initial hematocrit, hemoglobin and erythrocyte counts nausea vomiting temporary edema alkaline phosphatase/serum creatinine/BUN increase, hypertrichosis. 

In adults, the signs and symptoms of hypothyroidism include somnolence, slow mentation, dryness and loss of hair, increased fluid in body cavities (e.g., the pericardial sac), low metabolic rate, tendency to gain weight, hyperlipidemia, subnormal temperature, cold intolerance, bradycardia, reduced systolic and increased diastolic pulse pressure, hoarseness, muscle weakness, slow return of muscle to the neutral position after a tendon jerk, constipation, menstrual abnormalities, infertility, and sometimes myxedema (hard edema of subcutaneous tissue with increased content of proteoglycans in the fluid). A goiter (i.e., enlargement of the thyroid gland) may be present. 

Severe fluid retention (manifested as pleural effusion, pericardial effusion, pulmonary edema, and ascites) and hepatotoxicity occur rarely... 

Although the two growth factors have similar effects on neutrophil counts, G-CSF is used more frequently because it is better tolerated. G-CSF can cause bone pain, which clears when the drug is discontinued. GM-CSF can cause more severe side effects, particularly at higher doses. These include fevers, malaise, arthralgias, myalgias, and a capillary leak syndrome characterized by peripheral edema and pleural or pericardial effusions. Allergic reactions may occur but are infrequent. Splenic rupture is a rare but serious complication of the use of G-CSF for PBSC. 

A wide range of aldesleukin-induced adverse effects is associated with the capillary leak syndrome, which is characterized by an increase in vascular permeability with subsequent leakage of fluids and proteins into the extravascular space (4). This results in a third-space clinical syndrome, generalized or peripheral edema, weight gain, cardiovascular and pulmonary comphcations with hypotension, pericardial, and pleural effusions, ascites, oliguria, and prerenal azotemia. Symptoms usually resolve in a few days after aldesleukin withdrawal. Studies on the mechanism have raised a number of hypotheses, such as damage to the endothehal cells, release of secondary cytokines, and activation of the complement cascade (15). 

In acute promyelocytic leukemia arsenic trioxide can cause a syndrome similar to the retinoic acid syndrome (15), with fever, skin rash, edema, pleural effusion, pericardial effusion, and acute respiratory failure. 

Pleural and subsequent pericardial effusion developed in a woman treated with itraconazole 200 mg bd for a localized pulmonary infection with Aspergillus fumiga-tus (SEDA-18, 282). After more than 9 weeks of treatment she developed a pericardial effusion, which necessitated drainage. Itraconazole was withdrawn. Six weeks later, and 2 weeks after the resumption of itraconazole, she developed signs of pulmonary edema and cardiac enlargement. These signs disappeared rapidly on discontinuation of itraconazole. 

A 52-year-old man with a history of chronic hypertension presented with worsening dyspnea and leg edema. He had been taking minoxidil for 10 years. The cardiac silhouette was markedly enlarged. Echocardiography and computed tomography showed a large pericardial effusion. Minoxidil was withdrawn and the effusion resolved within 1 month. 

In dogs, high doses of BCNU resulted in severe bone marrow hypoplasia with delayed, reversible thrombocytopenia. The other major toxicides observed were cardiopulmonary (pulmonary edema, myocardial infarction, and pericardial hemorrhage), intestinal mucosal damage with hemorrhage, renal toxicity, and delayed hepatotoxicity. Similar toxicity was seen in monkeys except that cardiopulmonary toxicity did not occur. In rats, initially well-tolerated doses may cause death later. There is sufficient evidence for the carcinogenicity of BCNU in rats. BCNU is embryo-and fetolethal in rats and rabbits at doses nontoxic to the mother and can induce a variety of teratogenic effects in rats. 

Heart failure causes Kerley s B lines (edema of interlobular septa), which appear as thin, horizontal reticular fines in the costophrenic angles. At higher pressures, alveolar edema and pleural effusions appear in the pleural space or as blunting of the costophrenic angles. Pericardial effusions also may appear as a large heart, but because it usually occurs rapidly, there is no evidence of pulmonary venous congestion. 

The signs and symptoms are usually insidious in onset and may consist of anorexia, malaise, edema, anasarca, or ascites, and pericardial and pleural effusions may also be present. As a result of a hypercoagulable state, pulmonary embolism may develop, but rarely results in death. " The incidence of renal vein thrombosis varies from 5% to 62%, " and membranous nephropathy should be suspected when there is a sudden onset of hematuria loin pain pulmonary embolus fluctuating or worsening proteinuria or glomerular filtration rate renal tubular acidosis or an increase in leg edema. Hypertension is found in about 30% of patients and is more common in the presence of renal insufficiency or until the disease is advanced. 

Retention of sodium and water in progressive renal failure results in hypertension, edema, pleural and pericardial effusions, and pulmonary edema, the last being a life-threatening event requiring immediate dialysis. Hypertension may be severe, leading to heart failure or encephalopathy. Hyponatremia occurs if water is retained in excess of sodium. If severe, it may cause muscular twitching and convulsions (water intoxication). Dialysis is the treatment of choice (R14). 

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