Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of chest pain in a 31-year-old woman after vaginal delivery with epidural analgesia during sulprostone administration is described. Chest pain occurred shortly after sulprostone was started and disappeared when sulprostone was stopped. Ischaemia related data were negative. Angiographically coronary arteries were normal. Coronary artery spasm aetiology was retained. Sulprostone pharmacology is summarized. Coronary artery effects are compared with literature reports. Recommendations before sulprostone use are underlined.
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PMID:[Chest pain and sulprostone during postpartum hemorrhage]. 1247 87

The acute chest syndrome is a generic term for pulmonary complications of sickle cell diseases with heterogeneous etiologies that include pneumonia, vaso-occlusion of pulmonary arterioles, rib infarction, and fat embolism syndrome. My review summarizes these etiologies, the evidence, and pathophysiology supporting the hypothesis that infarction of segments of ribs by the same vaso-occlusive process responsible for the acute episodes of pain (characteristic of the sickle cell diseases) is often involved in the acute chest structure. Inflammation associated with the infarct then causes splinting, hypoventilation, and hypoxia and further vaso-occlusion. The relationship with adult respiratory distress syndrome and fat embolism is also discussed. Use of the incentive spirometer combined with effective analgesia when chest pain is present is advocated for prevention of the pulmonary infiltrates. Newer understanding of the role of nitric oxide in regulating oxygen transport and its relationship to blood transfusions used in therapy of the acute chest syndrome are discussed.
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PMID:The role of rib infarcts in the acute chest syndrome of sickle cell diseases. 1267 38

Acute coronary syndromes encompass a heterogenous group of patients with different clinical presentations, who have differences in both the extent and severity of underlying coronary atherosclerosis and who have different degrees of risk of progression to myocardial infarction. For each patient, the pre-hospital practitioner should make individual treatment decisions based on the history and examination, the ECG findings, the facilities and diagnostic equipment available and the transfer time to the nearest appropriate hospital. Patients with acute ischaemic chest pain should have oxygen, aspirin, nitrates and opioid analgesia. A 12 lead ECG should be performed within 5 minutes of initial assessment. If the ECG reveals ST-segment elevation or presumed new LBBB, this signifies acute myocardial infarction and in most cases immediate reperfusion therapy should be considered. The evidence of benefit in terms of mortality and morbidity following prompt anti-platelet and fibrinolytic therapy in such cases is unequivable. Pre-hospital fibrinolysis is now well established and should be undertaken in patients with acute infarction on clinical and ECG grounds if the transfer to hospital is likely to exceed 30 minutes and it is less than 12 hours since the onset of pain. Patients with no ECG evidence of infarction may still be at considerable risk and should still be conveyed to the nearest appropriate medical facility. Whilst en-route, they should receive aspirin, nitrates, low molecular weight heparin (LMWH) and beta blockers provided there are no contra-indications.
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PMID:Acute coronary syndrome. 1501 5

A primigravida with idiopathic hypertrophic subaortic stenosis, New York Heart Association Classification III, developed acute chest pain with significant ST segment depression together with a new Q-wave in chest lead V6 on the electrocardiograph following delivery under lumbar epidural analgesia. An intrapartum myocardial infarct was suspected because serial creatine phosphokinase and its muscle-brain isoenzyme levels were elevated in the postpartum period. However, the ST segment and the Q-wave changes returned to baseline within 4 h, thus eliminating the possibility of acute myocardial infarction. The uterus and placenta release creatine phosphokinase and its muscle-brain isoenzyme substantially during normal vaginal delivery, thus mimicking acute myocardial infarction. Consequently, the elevations of creatine phosphokinase and its muscle-brain fraction alone are not diagnostic of myocardial infarction in the postpartum period. The diagnosis of myocardial infarction must be based on the clinical picture, serial electrocardiogram recording and determination of lactate dehydrogenase and aspartate amino transferase.
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PMID:Post partum creatine phosphokinase and its muscle-brain isoenzyme elevation and transient Q-wave in a patient with idiopathic hypertrophic subaortic stenosis. 1532 Nov 57

Acute aortic dissection is an infrequent but important differential diagnosis of acute chest pain. The variability of presenting symptoms makes it difficult to diagnose correctly. Important clinical indicators - besides chest pain - are symptoms related to acute aortic insufficiency and/or pericardial tamponade, variable acute neurologic alterations, or signs of peripheral or visceral malperfusion. The spontaneous prognosis depends on the location and extent of the dissection, and left untreated dissection carries a high mortality. The key goal of preclinical treatment is stabilization with analgesia, mild sedation (opioids, benzodiazepines) and treatment of hypertension (beta-blockers) or hypotension (fluid administration). If the patient presents with a high probability of dissection, early transfer to a specialized center appears advisable. Initial clinical diagnostic studies include transthoracic echocardiogram and computed tomography. If the ascending aorta is involved (Stanford type A) immediate replacement of the proximal aorta is necessary. Isolated dissections of the descending aorta (type B) require aggressive blood pressure control, but can be managed conservatively in most cases. A high level of vigilance is necessary in all patients to detect and treat visceral ischemia.
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PMID:[Acute aortic dissection. Differential diagnosis of a thoracic emergency]. 1624 38

Pneumomediastinum can easily be mistaken for a pulmonary embolus or myocardial infarction. We describe herein a case of pneumomediastinum postpartum. A primigravida complained five-hours postpartum of acute chest pain and mild dyspnea. The initial (working) diagnosis was pulmonary embolus and the patient was treated with antithrombotic therapy. A CT scan revealed the real cause of the chest pain: pneumomediastinum. The patient was given adequate analgesia and two days later was able to leave the hospital in good clinical condition. We suggest that in the case of acute chest pain during or shortly following labor, pneumomediastinum should be considered.
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PMID:Pneumomediastinum as a cause of acute chest pain postpartum. 1685 99

We observed consecutive hospital admissions for acute painful crisis (APC) among adults with Sickle Cell Disease (SCD) over a 6-month period in Trinidad and Tobago. Episodes (111) of APC resulted in 82 admissions of 59 patients. The most common site for pain was the trunk. Patients ranged in age from 17 to 53 years (median: 25). Median length of hospital stay was 4 days. Total dose of Pethidine given per admission ranged from 100 to 1650 mg (median: 525). The mean dose of morphine was 70 mg. Six (7%) of patients were readmitted within 10 days of discharge. Twenty-five (30%) of patients had chest pain at presentation of whom 10 (12%) had consolidation on chest X-ray, defining the acute chest syndrome (ACS). There was one death caused by biliary sepsis. The study revealed seemingly low opiate usage for in-hospital treatment of APC with acceptable rates of readmission. The BCSH 2003 guidelines seemed applicable apart for the choice and route of fluid for rehydration and opiate analgesia.
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PMID:Hospital admissions for acute painful crisis in Trinidad and Tobago. Are the British Committee for Standards in Haematology (BCSH) guidelines applicable? 1699 18

The case is reported of a 30-year-old multigravida, with insignificant history and stable vital signs, admitted to the labour room for normal vaginal delivery of twins. She received combined spinal epidural analgesia (bupivacaine plus fentanyl) for 3 h. Following uneventful delivery she received 0.2 mg methylergonovine maleate, intramuscularly. Nausea and vomiting occurred 70 min after placenta delivery, heart rate decreased, arterial blood pressure increased and there was chest pain. After excluding cardiac ischaemia, 0.5 mg atropine sulphate was administered intravenously. Chest pain improved but heart rate and blood pressure increased more than expected. The patient had mild headache and nausea, and antiemetic 4 mg ondansetron was given intravenously. Continuous monitoring for 4 h showed spontaneous chest pain relief and blood pressure improvement. In conclusion, serious delayed side-effects arising from methylergonovine maleate can occur in young, normal patients and close monitoring is required. Intravenous atropine sulphate following methylergonovine maleate administration may lead to severe hypertension and tachycardia.
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PMID:Postpartum severe sinus bradycardia following methylergonovine administration. 1883 11

Coronary heart disease is the major cause of death worldwide and is affecting millions of people in both developed and developing countries. Patients with myocardial ischemia typically experience chest pain (angina pectoris). Traditional viewpoint of ischemic cardiac pain might be related to "mechanical hypothesis" in early time and "chemical hypothesis" in modern time. However, perception of cardiac ischemic pain is still not well understood. The previous studies suggested that neurogenic mechanisms including neurogenic inflammation and neurogenic activity might participate in the pathophysiological processes following myocardial ischemia. Therefore, we raise "neurogenic hypothesis", that is, neurogenic mechanisms might play a pivotal role in myocardial ischemic injury. Analgesia intervention, rivalry of neurogenic inflammatory reactions and electrostimulatory therapy, etc. could not only relieve the pain symptoms, but also block nociception of body and neurogenic reaction induced by ischemia. Thereby ischemic myocardial injury would be extenuated and myocardial protection be produced. Attempts to confirm this hypothesis may lead to new theory of pathophysiologic mechanisms and provide potential intervention strategy for cardiac ischemic pain.
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PMID:Neurogenic hypothesis of cardiac ischemic pain. 1913 Nov 76

Acute coronary syndrome (ACS), encompassing unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI), is often the result of an acute thrombotic occlusion of the coronary vessels, associated with atheromatous plaque rupture or erosion. ACS is associated with a severely impaired prognosis and requires prompt and efficient specialist treatment. The clinical presentation may be identical across all three components of ACS. Establishing an accurate diagnosis without delay is of paramount importance to start treatment promptly. Patients with suspected ACS need to be referred immediately to A&E. Prehospital treatment, which includes aspirin, nitrates, morphine and oxygen (if hypoxic), should be initiated rapidly. Important features pointing towards a diagnosis of ACS include: typical characteristics of chest pain, presence of risk factors, and ECG changes suggestive of myocardial ischaemia. Chest discomfort in patients with ACS typically occurs at rest, is anginal in character and can range from mild tightness to central crushing chest pain. It may be associated with nausea, dyspnoea or diaphoresis. The chest pain may radiate to the arms, back or jaw and is often >20 minutes in duration. An accurate clinical history and a detailed examination are vital. Initial investigations are the same for all ACS events, with the need for urgent serial ECGs and the measurement of cardiac troponin levels, to assess myocardial damage. In NSTEMI, ECG changes suggestive of ischaemia are often present and associated with elevated cardiac troponin. In UA, there is a considerable reduction in myocardial perfusion leading to symptoms; but there is no rise in cardiac troponin. Risk stratification is imperative in assessment of ACS to allow efficient delivery of specialist care. Treatment includes: antiplatelets; antithrombotic agents; angina drugs; analgesia, and PCI.
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PMID:Managing unstable angina and non-ST elevation MI. 2066 21


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