Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 50-year-old female was admitted because of nausea, vomiting, and cerebellar ataxia. Computed tomography scan revealed an enhanced mass accompanied with a cyst in the right cerebellar hemisphere. The mass situated in the subcortical region was removed. Histologically, highly vascular tumor cells lined the cavities. Postoperative radio- and chemotherapy were administered and the clinical symptoms improved gradually. Two months later, the patient complained of dyspnea. Chest X-ray on second admission demonstrated cardiomegaly. Hemorrhagic pericardial effusion amounting to 1000 ml was aspirated by pericardial puncture. Papillary clusters of tumor cells were demonstrated in the pericardial effusion. The patient died of cardiac failure. At necropsy solid tumors were located in the heart, lung, left inguinal region, and cerebellum. Histological diagnosis was mesothelioma arising from the heart. Primary pericardial mesotheliomas are rare; approximately 106 cases have been reported. Pericardial mesothelioma frequently spreads to the adjacent pleura and mediastinum, but distant metastases are extremely rare because patients with pericardial mesothelioma tend to die early due to cardiac failure or cardiac tamponade.
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PMID:[Brain metastasis from primary pericardial mesothelioma. Case report]. 170 70

The patient presented in this paper had been stable for 3 months after the induction of hemodialysis, when nausea, vomiting and hepatomegaly suddenly developed. A chest film revealed rush cardiomegaly, and massive pericardial effusion was demonstrated by echocardiography. One liter of hemorrhagic fluid was removed by pericardiocentesis and subsequent pericardial drainage under echocardiography. The patient received chemotherapy against pulmonary tuberculosis 30 years ago and calcification on chest film was apparent. Although sputum smear and pericardial effusion was negative for acid-fast organisms, combination therapy was initiated for suspected tuberculosis. The patient recovered completely and 2 months later it was demonstrated that cultures of sputum grew mycobacterium tuberculosis. Tuberculin skin test (PPD), which was negative 2 months previously, converted to positive. Tuberculosis must be considered as a potential cause of pericardial tamponade in patients on regular hemodialysis, and prompt therapy for both cardiac tamponade and the occult infection is warranted.
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PMID:Tuberculosis on regular hemodialysis--a case of pericardial tamponade. 276 29

In a series of 250 consecutive open-heart operations, three cases of late cardiac tamponade were noted following the operation. This led the authors to review the literature pertaining to this complication. Ninety-nine cases were collected. The frequency of late tamponade associated with cardiac surgery was 0.62% and was fatal in 16.2% of those cases. The delay before the tamponade appeared varied from 3 days to 3 months (mean 14.5 +/- 7.8 days). The initial clinical picture is insidious and vague, and this constitutes the danger of late cardiac tamponade. The clinical signs are of the respiratory (dyspnea, chest pain), gastrointestinal (anorexia, vomiting) and central nervous (mental confusion, even coma) systems. Pallor with a drop in hematocrit in patients on anticoagulant therapy suggests occult bleeding. A definitive diagnosis depends on catheterization of the right side and on mono- and bidimensional echocardiography. The authors believe that computerized axial tomography represents an interesting noninvasive and reliable examination technique when it can be used during emergency treatment. Pericardial puncture, which is both a diagnostic and therapeutic technique, was useful in one third of the cases; it produced a false-negative result in 12%. The resulting differential diagnoses are pulmonary embolism, myocardial insufficiency and septic shock. Late cardiac tamponade may be produced by one of two mechanisms: hemopericardium due to overdosage of anticoagulants or an exacerbated form of the post-pericardiotomy syndrome. Emergency treatment is always necessary. Pericardiocentesis is a useful diagnostic aid and provides temporary stabilization preoperatively. A wide surgical approach is always indicated. The mortality in untreated patients is 100%. The frequency of immediate relapse or, occasionally, of delayed relapse is estimated to be 11%; relapse may be lethal.
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PMID:[Late tamponade after heart surgery: a dreadful diagnostic pitfall]. 634 35

A 30-year-old man who died from brain metastasis of cardiac angiosarcoma is presented. His chest X-ray film showed cardiac tamponade and bilateral pleural effusion. His symptoms were improved only by drainage of the bloody pericardial and pleural effusion. During the course of the disease, multiple nodular infiltrates were seen on chest CT and hemoptysis occurred repeatedly. He presented to our hospital. On the first night of hospitalization, symptoms including headache, vomiting and disturbance of consciousness appeared and brain CT showed suspected brain metastasis. He died on the 20th hospital day with no definite diagnosis having been established. At postmortem examination, a hen's egg sized cardiac angiosarcoma was found infiltrating the right atrial wall. Metastatic foci were found in the epicardium and bilateral lungs. This case was considered to be angiosarcoma of the heart, manifesting various clinical symptoms because of bleeding from the metastatic foci.
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PMID:[A case of angiosarcoma of the heart with cardiac tamponade and repeated hemoptysis]. 827 23

Pericarditis is a frequent and serious complication of chronic uremia. The uremic pericarditis can get much improvement by aggressive heparin-free hemodialysis therapy. However, the presenting symptoms and signs are too nonspecific to identify at early stage. Cardiac tamponade is the late and fatal complication, and need the immediate & adequate management. A 35-year-old female patient suffered from nausea, vomiting and right upper quadrant dull pain in November 1993, and was admitted to a local hospital. Uremia (BUN: 210 mg/dl, serum Cr.: 13.2 mg/dl) and abnormal liver function (SGOT: 330 IU/L, SGPT: 449 IU/L) were found, then she received regular hemodialysis therapy. About 10 days later, acute exacerbation of liver function (SGOT: 2,488 IU/L, SGPT: 1,048 IU/L), consciousness disturbance and hypotension occurred during hemodialysis. She was referred to our ER immediately. At ER, she had been on comatous, shock state with pulseless electric activity. After resuscitation and serial evaluation, cardiac tamponade was diagnosed. Emergent pericardiocentesis and then bilateral partial pericardiectomy were done about 2 hours later. The pericardial effusion was bloody without evidence of malignancy, bacterial or TB infection. The pathology of pericardium revealed chronic inflammation only. HBsAg, Anti-HCV Ab, and anti-HAV IgM were undetectable. So the etiology of acute hepatitis was diagnosed as ischemic hepatitis. Her general condition and vital sign became stable thereafter. The liver function also improved rapidly. She was discharged one month later and received maintainance hemodialysis therapy and no evidence of recurrence till now.
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PMID:[Acute uremic pericarditis presented as cardiac tamponade with acute ischemic hepatitis: a case report]. 904 74

Carbohydrate-deficient glycoprotein syndrome type 1 (CDGS-1) is an autosomal recessive hereditary metabolic disorder, the gene locus of which is chromosome 16p13. The disorder is characterised by genetic heterogeneity, and by decrease in the gene product, phosphomannomutase 2, though the heterogeneity is far less manifest in affected Swedish families. Its incidence is 1/80,000 live births, and the under-5 mortality rate over 30 per cent. The causes of death are liver failure, cardiac tamponade, haemorrhaging, and severe infection. The characteristic biochemical aberration is the occurrence of deficient carbohydrate chains in many but not all circulating glycoproteins, and the serum and blood concentrations of some glycoproteins may be above or below normal. These changes may improve over time, but never normalise. The clinical picture is generally more problematic during the first years of life when psychomotor retardation is complicated by failure to thrive, liver dysfunction, pericardial effusions, and stroke-like episodes. In addition, strabismus, lipocutaneous anomalies, and gluteal fat pads are always present, and muscular hypotonia and restricted joint mobility are common. Failure to thrive is common, with vomiting and diarrhoea and subsequent slow growth. Inflammation is a constant finding in the liver, and very common in the small bowel. Pancreatic function is also affected. Pericardial effusion has been reported in 50 per cent of the youngest children, requiring pericardectomy in 30 per cent of cases. Haemorrhaging and thromboembolic complications may occur, and the serum concentrations of several factors and inhibitors are low, particularly those of factors V and XI, protein C and antithrombin. Stroke-like episodes occur in about 30 per cent of cases, often following an infection, with coma lasting for hours to several days. Such sequelae as hemiplegia, blindness, and other focal neurological pathology have been observed transiently. Diagnosis is based on the serum carbohydrate-deficient transferrin level, verified by isoelectric focusing. Molecular genetic procedures enable point mutations to be identified and prenatal diagnosis to be performed in many families.
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PMID:[CDGS-1--a recently discovered hereditary metabolic disease. Multiple organ manifestations, incidence 1/80,000, difficult to treat]. 988 93

A 75-year-old female, exhibiting epigastric pain and vomiting, underwent treatment for acute gastritis. She also experienced incontinence of urine and chest pain. A diagnosis of acute myocardial infarction was made upon examination of electrocardiographic findings and the patient was transferred to our hospital. Diffuse infarction of the left ventricle and acute aortic dissection (Stanford type A) were diagnosed by electrocardiographic and echo-cardiography. An emergency operation was performed. After induction of anesthesia, elevation of pulmonary artery pressure and fall of pulse pressure were observed, indicating acute cardiac tamponade. Transesophageal ultrasonography disclosed the entry of dissection in the descending aorta. Dissection of the aorta extended proximally up to the annulus of the aortic valve and the right and left coronary arteries were compressed by its aneurysm. As aortic insufficiency was mild, only reconstruction of the ascending aorta was carried out. The patient was discharged in fair condition one month after operation under use of postoperative long-term administration of catecholamines.
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PMID:Stanford type A acute dissection developing acute myocardial infarction. 1071 24

This report describes a long-term survival case of left ventricular free wall rupture treated with percutaneous intrapericardial fibrin-glue fixation therapy. A 82-year-old woman was admitted to the emergency room because of vomiting and syncope diagnosed as acute posterolateral myocardial infarction complicated by cardiac tamponade. After her hemodynamic condition was stabilized by drawing off the bloody pericardial effusion, fibrin-glue was injected into pericardial space with the expectation that the glue would cover the oozing site of the left ventricular epicardium. After this therapy, the patient recovered and did not have any no recurrent cardiac events for 1 year. Serial echocardiographic studies revealed a preserved left ventricular function and no development of left ventricular restriction. This case suggests that percutaneous intrapericardial fibrin-glue fixation therapy is an effective treatment for the oozing type of left ventricular free wall rupture and that there is no risk of left ventricular restriction during long-term follow-up.
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PMID:Long-term usefulness of percutaneous intrapericardial fibrin-glue fixation therapy for oozing type of left ventricular free wall rupture: a case report. 1213 43

We present 2 children who developed postpericardiotomy syndrome (PPS) and the rare complication of cardiac tamponade after cardiac surgery, each requiring life-saving pericardiocentesis in the emergency department (ED). Each child presented with vomiting as a chief complaint, an initial sign that has not been reported previously. As the frequency of orthotopic heart transplants and other cardiac surgeries among children increases, it is likely that ED physicians will encounter PPS and cardiac tamponade with greater frequency, and it is imperative that it be recognized promptly and treated appropriately. We review PPS, cardiac tamponade, and the proper performance of a pericardiocentesis.
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PMID:Cardiac tamponade complicating postpericardiotomy syndrome. 1297 28

Cardiac tamponade is an infrequent but potentially lethal complication related to use of central venous catheters (CVC). We present the case of a 16-year-old female with Diamond-Blackfan anemia (DBA) who developed pericardial tamponade secondary to superior venous caval obstruction caused by CVC thrombosis. The patient presented 3 months after line placement with vomiting, abdominal pain, and cardiomegaly on chest X-ray (CXR). Her condition quickly decompensated with cardiac arrest and subsequent death despite immediate pericardiocentesis. As a result of this case, our center has developed a protocol for the management of CVC problems as a means of facilitating rapid recognition of central line clots.
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PMID:Central venous catheter thrombosis as a cause of SVC obstruction and cardiac tamponade in a patient with Diamond-Blackfan anemia and iron overload. 1576 84


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