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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten clinically intact weaned piglets were experimentally intoxicated by intravenous injection of lipoproteide-free lipopolysaccharide endotoxin according to Westphal of E. coli O 127:B8. Severe endotoxin shock with all clinical manifestations of experimental coli-enterotoxaemia was induced in all animals and included circulatory disorder with tachycardia, intermittent pallor and/or cyanosis, symptoms of severe systemic intoxication, neurological symptoms, such as lack of coordination, hindleg staggering, spasm, paresis, paralysis, changes in respiration, such as rise in respiratory frequency and deepened breathing premortal deceleration of respiration and gasping for breath, temperature, variation, including hyperthermia and aggravating hypothermia, gastro-intestinal symptoms, such as temporary vomiting and persistent diarrhoea, leucopenia, eosinopenia, variation of haematocrit, edematisation, increased transudation, congestion, and gastro-intestinal shock lesions. Eight animals died. These experiments quite obviously have confirmed that endotoxin shock is the common pathogenetic principle behind all forms of coli-entertoxaemia (i.e, the forms of edematisation, cardiovascular failure, and gastro-intestinal processes.) Lipopolysaccharide endotoxin alone may be responsible for the development of both edemas and neurotoxic symptoms (edema disease) and diarrhoea (gastro-intestinal form of coli-enterotoxaemia). The pathogenetic relevance of additional toxins (neurotoxin and enterotoxin) is discussed under this aspect.
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PMID:[Experimental studies on the pathogenesis of Coli-enterotoxemia in swine. 4. Effect of lipopolysaccharide endotoxin on weaned piglets following parenteral administration]. 33 9

Three cases of jellyfish envenomation which occurred in the Indian Ocean and the Andaman Sea are reported. In each instance the stinging occurred on the upper extremities, and impaired the circulation to the stung limb(s), with absent distal arterial pulses, regional cyanosis, and the threat of distal gangrene. One of the patients is seriously and permanently handicapped, with bilateral upper-limb numbness and paresis; another patient has permanent sensory loss; the third patient, who also had brachial-artery narrowing that was demonstrated by angiography, made an uneventful recovery. The first two patients underwent surgical fasciotomy, whereas surgical exploration was performed on the third patient. Reduced blood flow in the major arteries of the limbs was observed directly in each case. Further, the arterial segment that primarily was affected, in each case, appeared to be that which underlay the actual site of the sting. All patients were young persons with no previous history of vascular disease. These cases corroborate the vascular and neurogenic injury, which previously have been reported in experimental animals and in human patients, that may result from jellyfish venoms.
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PMID:Acute regional vascular insufficiency after jellyfish envenomation. 290 46

The clinical, biochemical and pathological effects of the fresh shoots of Chrozophora plicata on Nubian goats and Desert sheep were investigated. The animals were given single or repeated daily doses of 10, 5, 1 and 0.5 g/kg of chrozophora shoots by stomach tube and died at various times post dosing. The main signs of Chrozophora poisoning in both species of ruminants were salivation, dyspnea, bloat, inappetence, dullness, diarrhea, paresis of the hind limbs, recumbency and lateral deviation of the head and neck. The main lesions were hemorrhage in the lungs, heart and kidneys, pulmonary cyanosis and edema, hepatic fatty change and depletion of glycogen, catarrhal enteritis, ascites, hydropericardium and serous atrophy of the cardiac fat and renal pelvis. An increase in the concentration of urea, ammonia and bilirubin and in the activity of GOT and a decrease in total protein were detected in the serum. Hematological changes indicated the development of anemia.
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PMID:Experimental Chrozophora plicata poisoning in goats and sheep. 318 65

In guinea-pigs, the oral and subcutaneous LD50 values were very similar (cf. 0,173 mg/kg over 48 h with 0,116 mg/kg over 24 and 48 h). When dosed subcutaneously, a cumulative effect was observed. Intravenous administration of cotyledoside to anaesthetized guinea-pigs resulted in: dyspnoea, increased heart rates and blood pressures, and electrocardiagraphic changes typical of cardiac glycoside poisoning. A positive cardiac inotropic effect was succeeded by a positive chronotropic one. In sheep, acute and subacute intoxication resulted in ruminal, respiratory and cardiac changes. The signs included ruminal stasis, cyanosis, cardiac arrhythmia, ectopic foci and AV dissociation, followed by hypotension and progressive respiratory and cardiac failure. The skeletal muscles were affected in only 1 sheep vide infra. In chronically intoxicated sheep typical clinical signs of "krimpsiekte" developed, e.g. weakness, reluctance to stand, unsteadiness on feet, tremor and paresis of hindquarter muscles, paresis of the neck, arching of the back and standing with the feet close together. Respiratory function was affected in all 3 cases; ruminal stasis, with concomitant loss of appetite occurring in one, and a transient change in heart function in another. The syndrome induced by acute cotyledoside poisoning is similar to that of other cardiac glycosides, but the paretic signs of chronic intoxication resemble "krimpsiekte", a disease associated only with intoxication with the plants of the family Crassulaceae.
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PMID:Studies on South African cardiac glycosides. II. Observations on the clinical and haemodynamic effects of cotyledoside. 718 41

The Sneddon's syndrome consists of neurologic manifestations associated to the presence of livedo reticularis and cyanosis of the extremities. The pathological process is an endothelial obliteration of arterioles, leading to a reticular appearance of the skin, despite the environment temperature. The authors present three new cases, caucasian males with 7, 16 and 54 years of age. The youngest started with hemilateralized motor seizures and showed a porencefalic area in the CT scan. The oldest had livedo reticularis, acrocyanosis and started with hemilateralized motor seizures, and a hemiparesis as sequela; CT scan with parasagittal infarct and occlusion presented of one anterior cerebral artery on angiography. The third patient started with hemifacial seizures, developed a labioglossolaringeal paresis and dysarthria as sequela; CT scan and MRI showed multiple infarcts, with multiple occlusions of cortical branches on angiography. The skin biopsies showed endothelial vascular hyperplasia in all cases. Only one (54 years old) patient had a positive IgG antiphospholipid antibodies. The Sneddon's syndrome seems not to be so rare and have to be considered in the etiological investigation of cerebral infarcts, mainly in young people.
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PMID:[Sneddon syndrome. Report of 3 cases]. 757 13

A 37-year-old woman with increasing dyspnoea over several months suddenly developed severe ortho- and tachypnoea as well as cyanosis of the lips and acrocyanosis. Pulmonary angiography revealed massive bilateral pulmonary emboli with a systolic pulmonary artery pressure of 75 mm Hg. Phlebography demonstrated a thrombotic occlusion of the deep veins of the left leg extending to the distal femoral vein. Thrombolysis treatment was started via an indwelling pulmonary artery catheter (500,000 IU urokinase and 10,000 IU heparin as bolus, then 1 mill. IU urokinase and 1,000 IU heparin per hour). After two hours an incomplete left-sided paresis occurred (involving ocular and facial muscles, dysarthria, left arm and left leg) and the thrombolytic infusion was stopped. But cerebral computed tomography (CT) did not demonstrate any intracerebral haemorrhage. The heparin infusion was restarted (partial thromboplastin time between 70 and 90 s). CT examinations during the next few days showed the development of an ischaemic infarction in the distribution of the right medial cerebral artery. Angiography demonstrated occlusion of the right internal carotid artery. The diagnosis of a paradoxical embolus was supported by easy cardiac catheter passage through a patent foramen ovale. Subsequent pulmonary angiography demonstrated a thrombus-free pulmonary arterial circulation with a normal pulmonary arterial pressure. There was gradual and extensive regression of the incomplete hemiparesis.
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PMID:[Paradoxical cerebral embolism during fibrinolysis therapy in deep vein thrombosis and pulmonary embolism]. 820 47

A 29-year-old male was admitted to our hospital for further evaluation of left sided paresis, cyanosis, clubbing finger. The laboratory data revealed polycythemia and hypoxemia. Cerebralarteriogram showed right middle cerebral artery occulusion. Cardiofunctional test showed atrial fibrillation, lower left ventricular function. Cardiac catheterization, pulmonary arteriography and three dimensions CT were performed. Right to left shunt rate was 20.4%. A single large pulmonary arteriovenous fistura with a feeding artery (A10) and a draining vein (V10) was found clearly. In this cases, arteriovenous fistula was large, blood flow was thought to be rapid. We thought transcatheter embolization was not useful. And we performed right lower lobectomy. Postoperative course was not eventful. Cyanosis disappeared, clubbing finger was cured.
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PMID:[A case of arteriovenous fistula of the lung]. 1038 Apr 83

The comparative effects of diazinon and malathion on Najdi sheep were described in sheep allotted as untreated controls, diazinon-treated at 25 mg/kg/d or 50 mg/kg/d, and malathion-treated at 25 mg/kg/d or 50 mg/kg/d. Although serum cholinesterase (ChE) activity was reduced, neither significant clinical signs nor severe pathological changes were produced in sheep dosed orally with 25 or 50 mg diazinon/kg/d for 21 d. Both oral dose levels of malathion were lethal to sheep between 1 and 6 d and caused, prior to death, hyperexcitability, tremors, clonic convulsions, salivation, nasal discharge, incoordination of movement, paresis of the limbs and recumbency. Lesions were widespread congestion and hemorrhage, patchy pulmonary cyanosis, gastroenteritis and hepatonephropathy. These changes were accompanied by increases in the activities of serum SDH and AST, in the concentrations of urea, triglyceride and cholesterol, and decreases in ChE activity and in RBC, PCV and Hb values.
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PMID:Comparative effects of diazinon and malathion in Najdi sheep. 1050 28

The acute toxicity of dried Nerium oleander leaves to Najdi sheep is described in 12 sheep assigned as untreated controls, N. oleander-treated once at 1 and 0.25 g/kg body weight and N. oleander-treated daily at 0.06 g/kg body weight by drench. Single oral doses of 1 or 0.25 g of dried N. oleander leaves/kg body weight caused restlessness, chewing movements of the jaws, dyspnea, ruminal bloat, incoordination of movements, limb paresis, recumbency and death 4-24 hr after dosing. Lesions were widespread congestion or hemorrhage, pulmonary cyanosis and emphysema, hepatorenal fatty change and catarrhal abomasitis and enteritis. The daily oral doses of 0.06 g dried N. oleander leaves/kg body weight caused less severe signs and death occurred between days 3 and 14. In these animals, the main lesions were hepatonephropathy and gelatinization of the renal pelvis and mesentry and were accompanied by significant increases in serum AST and LDH activities, in bilirubin, cholesterol and urea concentrations and significant decreases in total protein and albumin levels, anemia and leucopenia.
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PMID:Acute toxicity of various oral doses of dried Nerium oleander leaves in sheep. 1178 96

Early recognition of limb ischemia may allow prompt, effective therapy for peripheral arterial injuries. A review of cases of peripheral arterial trauma at the Toronto General Hospital since 1953 revealed that 50% of the injuries were not immediately recognized. An expanding hematoma, pulsatile hemorrhage or the onset of a bruit and thrill signifies arterial damage in penetrating wounds. Ischemia may be difficult to recognize in patients with soft tissue or skeletal trauma, but the presence of distal pallor, coolness, paresis, cyanosis, anesthesia, poor capillary refill and disproportionate pain indicates significant arterial damage and necessitates surgical exploration. The diagnosis of arterial "spasm" in such instances is untenable and can only be made after direct inspection, or on the return of pulses after reduction of a fracture or release of a tight cast. Restoration of arterial continuity by end-to-end anastomosis is the recommended technique for all arterial injuries, since after ligation of even minor vessels, ischemia may ensue, and amputation may occasionally be necessary.
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PMID:THE RECOGNITION AND MANAGEMENT OF PERIPHERAL ARTERIAL INJURIES. 1428 3


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