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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to the United States Food and Drug Administration, untoward reactions to capillary hemodialyzers occur at a rate of 3.5 of every 100,000 dialyzers sold. Allergic symptoms immediately after initiation of dialysis consist of burning retrosternal pain, sensation of diffuse heat, cold perspiration, periorbital and facial edema, flushing, laryngeal stridor, bronchial hypersecretion, hypotension, bradycardia, and loss of consciousness. In 1982 Popli et al. reported four patients suffering from such allergic manifestations; three were successfully managed after being taken off dialysis. These investigators thought that inadequate rinsing of cuprammonium cellulose capillary dialyzers was responsible for the reactions, and recommended rinsing the blood compartment with 2 liters of normal saline, and the dialysate compartment with 10 liters of dialysate, both in a single-pass fashion over 20 minutes. Nichols and Platts (1982) (3) reported 15 patients with urticaria, severe bronchospasm, and shock occurring immediately after the blood had been returned from the dialyzer. These authors suggested that the sterilizing agent, ethylene oxide (ETO), was responsible. Poothullil et al. (1975) (4) described a patient with pruritus, severe dyspnea, and hypotension during dialysis. On the basis of a positive skin prick test (dermal reaction to ETO-exposed human albumin) and of antigen-induced histamine release from peripheral leucocytes, these workers suggested that ETO was responsible for the allergic reactions. Marshall et al. (1984) (5) reported that 8.9% of hemodialysis patients had positive skin tests to ETO and that 12.1% were ETO-radioallergosorbent test (RAST) positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Three cases of hemodialysis-associated hypersensitivity reactions. 405 93

A 60-year-old woman suffered from recurrent episodes of fever, hypertension, facial flushing, vomiting, stridor, slowly progressive symptoms of hypohidrosis, and orthostatic hypotension. The episodes were synchronous with elevated catecholamine concentration in plasma and urine. This is an example of paroxysmal autonomic hyperreflexia in a setting of pure progressive autonomic failure.
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PMID:Autonomic hyperreflexia in pure progressive autonomic failure: a case report. 841 40

The symptoms that result from compression of the superior vena cava are known as superior vena cava syndrome. The syndrome was originally described as secondary to infection such as tuberculosis or syphilitic aortic aneurysm. Currently, the origin is generally cancer or thrombotic events. Adenocarcinoma of the lung is the most common cause. Thrombotic causes are increasing because of the rise in use of pacemakers and central venous catheters for access or treatment purposes. Symptoms may include a feeling of fullness in the head, dyspnea, and cough. Clinical findings may include facial and neck swelling; dilated venous channels over the trunk, upper extremities, and neck; facial flushing; cyanosis; respiratory stridor and distress; and neurologic signs. Primary symptoms are in the neck and head. Treatment of superior vena cava syndrome will depend on the cause of the compression. If thrombosis is found, thrombolysis and anticoagulation may be indicated. With carcinoma or infection, specific drugs or radiation may be used. In cases of compression, dilation and stenting of the superior vena cava may be performed. In some cases a bypass of the superior vena cava may be indicated.
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PMID:Superior vena cava syndrome. 1732 62

Three mixed-bred raptors (Falco rusticolus x Falco cherrug) from a German falcon breeder were presented with a history of respiratory distress. In one bird a laryngeal stridor was noted, and oral examination revealed an epiglottal swelling. In the other two birds, nasal discharge and sneezing were the main clinical symptoms. Nasal flushing samples and biopsies were collected for pathologic, bacteriologic, and parasitologic examination. Results confirmed a cryptosporidial infection. Polymerase chain reaction (PCR) and DNA analysis identified the causative agent to be Cryptosporidium baileyi. No cryptosporidia were detected in fecal samples, indicating the infection was confined to the respiratory system. Analysis of prey animals (pigeons, quail) failed to identify the source of infection. Treatment was initiated with paromomycin in all three birds, whereas in two birds an additional therapy with azithromycin was given. However, no clinical improvement was seen after several weeks of treatment, and the birds either died or were euthanatized. To the authors' knowledge, these are the first confirmed cases of disease caused by cryptosporidia in the order of Falconiformes.
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PMID:Upper respiratory tract infection caused by Cryptosporidium baileyi in three mixed-bred falcons (Falco rusticolus x Falco cherrug). 1864 71

Idiopathic anaphylaxis (IA) is defined as anaphylaxis without any identifiable precipitating agent or event. The clinical manifestations of IA are the same as allergen-associated (immunologic) anaphylaxis and include urticaria, angioedema, hypotension, tachycardia, wheezing, stridor, pruritus, nausea, vomiting, flushing, diarrhea, dysphagia, light-headedness, and loss of consciousness. Patients usually tend to have the same manifestations on repeated episodes. IA is a prednisone-responsive disease that is ultimately a diagnosis of exclusion. Approximately 40% of patients are atopic. Serum tryptase (or urine histamine or its metabolite) will be elevated acutely but if elevated in the absence of anaphylaxis, should suggest alternative diagnoses including indolent systemic mastocytosis. A focused history, examination, and follow-up will dictate whether a patient's symptoms may be attributable to disorders that mimic anaphylaxis, such as indolent systemic mastocytosis, carcinoid syndrome, pheochromocytoma, hereditary angioedema acquired C1 esterase inhibitor deficiency, or panic attacks. The presence of urticaria may help limit the differential because they do not usually accompany any of the aforementioned disorders, except for indolent systemic mastocytosis. IA is classified according to the symptoms as well as the frequency of attacks. Patients who experience six or more episodes in a year or two or more episodes in 2 months are classified as IA-frequent (IA-F). Patients who experience fewer episodes are classified as IA-infrequent (IA-I). This distinction is important because IA-F patients initially will require prednisone as disease-modifying therapy whereas most IA-I patients will not. Patients with IA must carry and know when and how to self-administer epinephrine.
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PMID:Chapter 25: Idiopathic anaphylaxis. 2279 98

Idiopathic anaphylaxis (IA) is defined as anaphylaxis without any identifiable precipitating agent or event. The clinical manifestations of IA are the same as allergen-associated (immunologic) anaphylaxis and include urticaria, angioedema, hypotension, tachycardia, wheezing, stridor, pruritus, nausea, vomiting, flushing, diarrhea, dysphagia, light-headedness, and loss of consciousness. Patients usually tend to have the same manifestations on repeated episodes. IA is a prednisone-responsive disease that is ultimately a diagnosis of exclusion. Approximately 40% of patients are atopic. Serum tryptase (or urine histamine or its metabolite) will be elevated acutely, but, if elevated in the absence of anaphylaxis, should suggest alternative diagnoses, including indolent systemic mastocytosis. A focused history, examination, and follow-up will dictate whether a patient's symptoms may be attributable to disorders that mimic anaphylaxis, such as indolent systemic mastocytosis, carcinoid syndrome, pheochromocytoma, hereditary angioedema or acquired C1 esterase inhibitor deficiency, or panic attacks. The presence of urticaria may help limit the differential diagnosis because urticaria does not usually accompany any of the above-mentioned disorders, except for indolent systemic mastocytosis. IA is classified according to the symptoms as well as the frequency of attacks. Patients who experience six or more episodes in a year, or two or more episodes in 2 months are classified as having IA-frequent (IA-F). Patients who experience fewer episodes are classified as having IA-infrequent (IA-I). This distinction is important because patients with IA-F will initially require prednisone as disease-modifying therapy, whereas most patients who with IA-I will not require prednisone. Patients with IA must carry and know when and how to self-administer epinephrine.
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PMID:Idiopathic anaphylaxis. 3169 Mar 94