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)

High cardiac output failure/state (HCOF) is regular feature of some illnesses e.g. thiamine deficiency, hyperthyroidism, severe anemia, Paget's disease or arteriovenous fistulae. HCOF in multiple myeloma is reported quite rarely. 31-year-old man was admitted because of fatigue, dyspnea and subfebrilities. Heart rate was 116/min, sinus rythm blood pressure 110/60 mmHg. Chest film showed cardiomegaly with sings of interstitial pulmonary edema, echocardiography mild dilatation of the left ventricle with hyperkinetic wall motion and small pericardial effusion. Hemoglobin was 104 g/l, leukocyte count 13.5 x 10(9)/l with 30% of plasmatic cells. Serum protein electrophoresis demonstrated a monoclonal gammapathy, X ray studies of the skelet multiple osteolytic lesions. Diagnosis of plasmocytic leukemia-form of multiple myeloma was established and chemotherapy (vincristine + adriamycine + dexamethason) was started. Patient cardiac status deteriorated. Cardiac catheterisation demonstrated mean righ atrial pressure of 25 mmHg, mean pulmonary artery pressure of 28 mmHg and pulmonary artery wedge pressure of 24 mmHg. Co was 20.0 l/min (C.I. 11.5 l/min/m2). In continuing of chemotherapy and symptomatic therapy for heart failure patients status gradually improved and complete remission of the myeloma and normalisation of cardiac parameters was achieved. Heart failure in multiple myeloma patients has been attributed to amyloidosis of myocardium, hyperviscosity syndrome, co-existing CAD or anthracycline toxicity. HCOF should be considered in patients with clinical evidence of heart failure and normal left ventricular function.
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PMID:[Hypercirculatory heart failure in a patient with plasmacytic leukemia]. 855 97

Shoshin beriberi, a uncommon cause of hemodynamic instability (or cardiac shock) and acute heart failure may go undiagnosed in Western countries where prevalence is low. This severe heart condition due to thiamine deficiency is rapidly fatal unless specific therapy is given. The most frequent cause in France is chronic alcoholism. There are no specific signs on the electrocardiogram in a patient with acute heart failure due to shoshin beriberi. The chest x-ray simply shows signs of pulmonary edema and heart enlargement. The echocardiography may be normal although hypokinesia and/or dilatation of the left ventricle (due to thiamine deficiency) are sometimes noted. Diagnosis is suspected in patients with chronic alcoholism who develop acute global heart failure with lactic acidosis. Right catheterism confirms low cardiac output resulting from arteriovenous shunts. Blood tests (red cell transacetolase activity, measurement of effect of pyrophosphatase, plasma and intraerythrocyte thiamine) confirm the diagnosis a posteriori. Clinical improvement is rapid after intravenous infusion of vitamin B1. The danger of fulminant beriberi heart failure in undernourished alcoholic patients emphasizes the need for regular prescription of vitamin B1.
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PMID:[Shoshin beriberi. A rapidly curable hemodynamic disaster]. 1160 66

(1) When people who are physically dependent on alcohol stop drinking, they experience an alcohol withdrawal syndrome. The symptoms generally resolve spontaneously within a week, but more severe forms may be associated with generalised seizures, hallucinations and delirium tremens, which can be fatal. (2) We carried out a literature review in order to obtain answers to the following questions: how to predict or rapidly diagnose a severe alcohol withdrawal syndrome; how to prevent and treat this syndrome; how to manage severe forms; and how to deal with the risk of vitamin B1 deficiency. (3) The main risk factors for severe withdrawal syndrome are: chronic heavy drinking; a history of generalised seizures; and a history of delirium tremens. (4) Anxiety, agitation, tremor, excessive sweating, altered consciousness and hallucinations are signs of a severe withdrawal syndrome. (5) Individual support and effective communication seem to reduce the risk of severe withdrawal syndrome. (6) Oral benzodiazepines are the best-assessed drugs for preventing a severe alcohol withdrawal syndrome, particularly the risk of seizures. When given for a maximum of 7 days, the adverse effects are usually mild. (7) Clinical trials of other antiepileptics suggest they are less effective than benzodiazepines, and their addition to benzodiazepine therapy offers no tangible advantage. (8) Betablockers increase the risk of hallucinations, and clonidine increases the risk of nightmares, and the efficacy of these two drugs is not well documented. Neuroleptics increase the risk of seizures. There are no convincing data to support the use of magnesium sulphate or meprobamate (the latter carries a risk of serious adverse effects). Acamprosate, naltrexone and disulfiram are not beneficial in alcohol withdrawal. (9) Gradual withdrawal, i.e. ingestion of decreasing amounts of alcohol, has not been compared with other methods but is generally not recommended. (10) There are no specific recommendations on hydration. Note that excessive water-sodium intake carries a risk of pulmonary oedema in patients with heart disease. (11) As vitamin B1 deficiency is frequent and can lead to serious complications in alcohol-dependent patients, oral vitamin B1 supplementation is widely recommended, despite the absence of comparative trials. High doses must be used to compensate for poor absorption. Intravenous administration is best if patients have very poor nutritional status or severe complications such as Gayet-Wernicke encephalopathy (a medical emergency), even though rare anaphylactic reactions have been reported after vitamin B1 injection. (12) Planned alcohol withdrawal in specialised hospital units has been extensively studied. Outpatient withdrawal may be more appropriate for patients who are at low risk of developing severe withdrawal syndrome. (13) A large proportion of alcohol-dependent patients were excluded from trials of withdrawal strategies. These include elderly patients, patients with serious psychiatric or somatic disorders, and patients who are also dependent on other substances. (14) An oral benzodiazepine is the best-assessed treatment for a single episode of generalised seizures or hallucinations during alcohol withdrawal. (15) In randomised comparative trials benzodiazepines were more effective than neuroleptics in preventing delirium-related mortality. Currently, with appropriate fluid-electrolyte support, continuous monitoring of vital signs, and respiratory support if necessary, the mortality rate for delirium tremens is under 3%. (16) In practice, patients who are attempting to stop drinking alcohol need close personal support and communication, and a reassuring environment, as well as regular monitoring for early signs of a withdrawal syndrome; the latter may require benzodiazepine therapy.
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PMID:Alcohol withdrawal syndrome: how to predict, prevent, diagnose and treat it. 1732 38

The clinical presentation of beriberi can be quite varied. In the extreme form, profound cardiovascular involvement leads to circulatory collapse and death. This case report is of a 72 year-old male who was admitted to the Neurology inpatient ward with progressive bilateral lower extremity weakness and parasthesia. He subsequently developed pulmonary edema and high output cardiac failure requiring intubation and blood pressure support. With the constellation of peripheral neuropathy, encephalopathy, ophthalmoplegia, unexplained heart failure, and lactic acidosis, thiamine deficiency was suspected. He was empirically initiated on thiamine replacement therapy and his thiamine level pre-therapy was found to be 23 nmol/L (Normal: 80-150 nmol/L), consistent with the diagnosis of beriberi. Cardiovascular magnetic resonance (CMR) showed severe left ventricular systolic dysfunction, markedly increased myocardial T2, and minimal late gadolinium enhancement (LGE). After 5 days of daily 100 mg IV thiamine and supportive care, the hypotension resolved and the patient was extubated and was released from the hospital 3 weeks later. Our case shows via CMR profound myocardial edema associated with wet beriberi.
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PMID:Cardiovascular magnetic resonance in wet beriberi. 2183 1

A 48-year-old man was brought to our emergency room with acute abdominal pain and systemic edema, indicating acute circulatory failure with lactic acidosis. Furosemide treatment paradoxically worsened the systemic edema and induced confusion. He had no drinking history but hardly ate legumes or meats containing thiamine. Administration of fursultiamine dramatically improved the symptoms and subsequently caused pulmonary edema. Thiamine deficiency may occur in nondrinkers with an unbalanced diet. In this condition, diuretic therapy can worsen the symptoms before thiamine supplementation by promoting the flushing of water-soluble vitamins but is needed for the management of secondary pulmonary edema after thiamine replenishment.
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PMID:Thiamine Deficiency in a Nondrinker and Secondary Pulmonary Edema after Thiamine Replenishment. 3153 90

Persistent pulmonary hypertension of the newborn (PPHN) is a syndrome of high pulmonary vascular resistance (PVR) commonly seen all over the world in the immediate newborn period. Several case reports from India have recently described severe pulmonary hypertension among infants in the postneonatal period. These cases typically present with respiratory distress in 1-6-month-old infants, breastfed by mothers on a polished rice-based diet. Predisposing factors include respiratory tract infection such as acute laryngotracheobronchitis with change in voice, leading to pulmonary hypertension, right atrial and ventricular dilation, pulmonary edema and hepatomegaly. Mortality is high without specific therapy. Respiratory support, pulmonary vasodilator therapy, inotropes, diuretics and thiamine infusion have improved the outcome of these infants. This review outlines four typical patients with thiamine-responsive acute pulmonary hypertension of early infancy (TRAPHEI) due to thiamine deficiency and discusses pathophysiology, clinical features, diagnostic criteria and therapeutic options.
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PMID:Thiamine-Responsive Acute Pulmonary Hypertension of Early Infancy (TRAPHEI)-A Case Series and Clinical Review. 3312 40