Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 8-day-old male Angus calf was presented to the University of Illinois, Veterinary Teaching Hospital, Urbana, IL, for lethargy, weakness, and poor suckle reflex. Clinical evaluation revealed a strong left-sided heart murmur and a split S2 sound. The calf died within 48 hours. Necropsy revealed a combination of the following cardiac defects: left ventricular hypoplasia, high ventricular septal defect, left auricular atresia with mitral valve aplasia, patent foramen ovale, patent ductus arteriosus, and pulmonary trunk atresia. Mild suppurative pneumonia with pulmonary edema and congestion were also present. This combination of defects appears to be similar to the hypoplastic left heart syndrome in humans and is reported here for the first time in cattle.
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PMID:Atypical hypoplastic left ventricular syndrome in a calf. 1546 Mar 25

Acute carbon monoxide poisoning is the most common cause of poison-related deaths in the U.S. A 21-year-old white woman was referred to Ruby Memorial Hospital after exposure to carbon monoxide (CO) from a faulty furnace. She developed acute weakness, dyspnea, nausea and vomiting. An electrocardiogram revealed sinus tachycardia, non-specific ST-T wave abnormalities, and a prolonged QTc interval. The chest X-ray revealed pulmonary edema and the 2-D echocardiography revealed decreased left ventricular systolic function with an ejection fraction of 25%. She was treated with high-flow oxygen and supportive medical therapy with complete resolution of the left ventricular dysfunction six weeks later. She has been followed for over one year without medical therapy and without recurrence of her symptoms. This case illustrates that the depressant effect of CO poisoning on the myocardium can be reversed in the short term with supportive medical therapy and recovery sustained in the long term without medical therapy.
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PMID:Carbon monoxide poisoning: a case report of reversible cardiormyopathy. 1577 62

A 3-week-old Thoroughbred colt was presented for weakness and cyanosis. A pansystolic regurgitant murmur and other physical findings suggested that the foal developed pulmonary oedema as a consequence of congenital heart disease. A large atrial septal defect, a high ventricular septal defect and dysplasia of the atrioventricular valves were visualised echocardiographically. A persistent common atrioventricular canal was observed at necropsy.
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PMID:Common atrioventricular canal in a foal. 1603 29

Children who have heart disease may present to the emergency department (ED) in many stages of life with a range of cardiovascular manifestions, from minimally irritating palpitations to the life-threatening derangements of shock or lethal dysrhythmia. They can present with congenital heart disease, after a temporizing procedure has been performed or after their definitive repair. Children can also present with fever, weakness, dyspnea, syncope, or chest pain; alternatively, children may present to the ED with active dysrhythmia, pulmonary edema, or cardiogenic shock . These symptoms and presentations may result from Kawasaki disease,hypertrophic cardiomyopathy, or arrhythmia; therefore, emergency physicians must also be comfortable with the most common types of heart disease associated with these symptoms and presentations. The purpose of this article is to describe the physiology and presentation of undiagnosed congenital heart disease, to describe the complications that can occur after a staged or definitive repair,and to discuss acquired heart disease in children.
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PMID:Cardiovascular emergencies in the pediatric patient. 1619 47

Thallotoxicosis is described in an adult Pit Bull Terrier. The dog exhibited anorexia, emesis, weakness, conscious proprioceptive deficits, and a hemorrhagic diarrhea before death. A severe, acute necrotizing enterocolitis was evident upon histological examination, as was a multifocal to coalescing pulmonary edema. Liver and kidney thallium concentrations were 18 and 26 ppm, respectively. The source of the thallium was determined to be thallium sulfate obtained by a person with the intent to harm family members. Although thallium has not been produced in the United States for 20 years, this report demonstrates the need to consider thallium toxicosis as a differential diagnosis for animals presenting with vague and mixed gastrointestinal and neurological signs.
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PMID:Thallium toxicosis in a Pit Bull Terrier. 1656 74

Metformin is a biguanide. Due to its effects in suppressing the hepatic production of endogenous glucose and in increasing insulin sensitivity in adipose tissue and skeletal muscle, the agent is used particularly in type 2 diabetes mellitus and metabolic syndrome, in which insulin resistance is especially pronounced. Lactic acidosis is one of the most important side effects of metformin. A male patient, born in 1923, was admitted to the emergency unit of our hospital for sudden vertigo, weakness, dyspnea, cyanosis, and lethargy. His history data showed that the patient had been suffering from type 2 diabetes mellitus for 10 years and taking Glargin (insulin), 12 U/kg, once daily and Glucophage (metformin), 850 mg thrice daily. The patient's general condition was fair; stupor, time and spatial orientation were absent. Analysis of arterial blood gases showed the presence of metabolic acidosis, hypokalemia, hypoxemia, and hypercapnia. Thereafter the patient was transferred to the intensive care unit of the hospital; intubated and connected to a T-bird ventilation apparatus. On the following day, an analysis of arterial blood gases indicated the proximity of the results to their physiological parameters. Ventilation was stopped; and monitoring of the patient continued by following the T-shape type of ventilation discontinuation. There were no X-ray signs of pneumonia or pulmonary edema. On the same day, the patient was extubated and oxygen inhalation in a dose of L/min was continued through a mask. On day 4 since therapy was initiated, the patient's vital signs, serum sugar and lactate levels became normal. By determining a new treatment regimen, the patient was discharged from the intensive care unit. Dyspnea, acidosis, and hypoxia developed in the patient resulted from lactic acidosis caused by the use of metformin. It should be remembered that dyspnea, acidosis, and hypoxia, which suddenly developed in metformin-treated patients with type 2 diabetes mellitus, may be caused by lactic acidosis.
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PMID:[A clinical case of development of lactic acid acidosis in a diabetic patient taking metformin]. 1675 49

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.
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PMID:Two fatal cases of selenium toxicity. 1689 Oct 71

Hypoxic liver injury is defined as a massive, but transient, increase in serum transaminase levels due to an imbalance between hepatic oxygen supply and demand in the absence of other acute causes of liver damage. It typically occurs in elderly individuals with right-sided congestive heart failure and low cardiac output. Precipitating factors include arrhythmias or pulmonary edema. Symptoms include weakness, shortness of breath, and right upper quadrant pain. Less commonly, hypoxic liver injury is seen in patients with severe hypoxemia or septic shock. Characteristically, the transaminase level is elevated 20-fold but normalizes rapidly over several days. Imaging studies reveal hypoechoic or hypodense lesions that resolve completely with reversal of the initiating event. Treatment and prognosis depend on the underlyIng disease.
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PMID:Hypoxic liver injury. 1697 Feb 20

In the preceding pages we have submitted evidence which shows that a simple intratracheal injection of a solution in a normally breathing rabbit penetrates within a few seconds to the alveoli, chiefly those of the left lower lobe; that absorption is rapid and well maintained; and that the procedure may be repeated effectively a number of times even with a substance like adrenalin which decreases absorption. It was also shown that absorption of adrenalin from the lung could be obtained at a time when double the dose given intramuscularly exerted no blood pressure effect whatever, and that absorption could still take place after the development of pulmonary edema, when there was an undoubted dilution of the injected solution with a serum-containing liquid and when a diminution of the absorptive field had occurred. The solution injected, after reaching the alveoli, is probably largely taken up by the capillaries of the pulmonary veins. This is indicated by the great rapidity with which an intratracheal injection of adrenalin may cause a rise of blood pressure. In numerous instances, for example, the pressure began to rise less than 5 seconds after the completion of an injection, equaling and even surpassing in rapidity of effect an intramuscular injection. Absorption by the lymphatics probably plays a secondary part, an assumption rendered all themore likely if we consider that lymph nodes are interpolated in the lymphatic pulmonary path, where the bed of the lymph stream becomes greatly widened and the current slowed. Injection into the lungs, however, offers another advantage due to the vascular arrangement of the absorbing field which could be of value therapeutically. Absorption of liquids injected into the lung probably takes place largely through the capillaries of the pulmonary veins; to a slight extent possibly through the capillaries of the bronchial veins which empty partly into the pulmonary veins, partly into the azygos veins; and probably some absorption occurs also through the lymphatics. By far the larger proportion of the absorbed material will thus be rapidly delivered to the left auricle and then to the left ventricle. At each succeeding systole, as long as absorption continues, a fraction of the drug will be driven into the coronary arteries and be able to affect the musculature of the cardiac pump. This fact ought to render the procedure of intratracheal injection a valuable method when it becomes imperative to stimulate a suddenly failing heart as promptly as possible by drugs of the digitalis group. Intratracheal injection is perhaps better under the conditions mentioned than the intravenous route, for the surface veins cannot always be entered with promptness and certainty even under fairly normal conditions, and in cases of cardiac weakness the difficulties will be measurably increased, while an intratracheal injection can be carried out with ease. Moreover, it is legitimate to expect that some absorption will take place from the lung alveoli as long as the heart-lung circulation persists, no matter how feebly, and that thus some of the drug will reach the heart to act on this structure itself more promptly perhaps than when the drug is administered successfully through surface veins. As far as the intramuscular route is concerned, we have shown that the intratracheal injection of adrenalin gives prompt though diminished absorption at a time when double the dose intramuscularly exerts no blood pressure effect whatever. The technical difficulties of giving an intratracheal injection in animals are slight. Tracheotomy as practised by us in the present series of experiments is not necessary, for the injection may be given into the intact trachea without exposure of the trachea. The hypodermic needle is inserted through the skin about 1 cm. below the larynx in a slanting caudad direction; the entrance of the needle into the trachea is readily felt. The injection should not be so rapid that the injected solution fills the entire tracheal lumen, but it should flow down the sides of the trachea. If the lumen is entirely filled, an expiration may drive some of the injected liquid into the larynx causing cough. In our experiments each injection of about 0.5 cc. consumed approximately 5 seconds. In the human subject no data are available as far as our knowledge goes, but a priori it would seem that an intratracheal injection is almost as simple as in the lower animals. The free hypodermic needle could be inserted into the tracheal lumen immediately below the cricoid cartilage. The needle itself should preferably be connected with the syringe by a short length of rubber tubing to minimize the danger of breaking the needle by a sudden move of the patient. The amount of the solution should not be too small, so that at least a fraction of it may reach the alveoli as promptly as possible; 3 to 5 cc. probably would suffice. Insertion of the needle in the locality mentioned would puncture the isthmus of the thyroid, but this is of no significance, especially when the procedure is employed in cases of cardiac failure where the gravity of the condition would warrant incurring much heavier risks than a slight bleeding from the thyroidal isthmus. In conclusion it may be said that the incorporation of drugs by intratracheal injection, while not as generally applicable as other methods, nevertheless has advantages which warrant its use also in human therapeutics.
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PMID:THE ABSORPTION OF ADRENALIN AFTER INTRATRACHEAL INJECTION. 1986 21

1. Colloidal silver has no specific action on the bone marrow in dogs but is a systemic poison which may cause anorexia, weakness, loss of weight, anemia, and death. 2. Hemolysis can be demonstrated after large doses of colloidal silver and the anemia presumably is due in part at least to a destruction of red blood cells in the peripheral circulation. 3. The colloidal silver, injected intravenously, is deposited as granules almost exclusively in the cells of the reticulo-endothelial system after the manner of particulate substances. 4. Repeated injections of non-lethal amounts of this substance are invariably followed by hyperplasia of the bone marrow. In no case was aplasia found. 5. Large single doses of this material cause rapid death in 12 hours or less characterized by pulmonary edema and congestion. 6. An initial increase in the number of erythrocytes and leucocytes may occur following smaller amounts of silver, but repeated injections cause a considerable anemia, without a definite increase in the leucocytes and with no signs of blood platelet deficiency.
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PMID:I. EFFECTS OF THE INTRAVENOUS INJECTION OF COLLOIDAL SILVER UPON THE HEMATOPOIETIC SYSTEM IN DOGS. 1986 54


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