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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Water intoxication during or following oxytocin induced labor, albeit a rare event, can nevertheless cause potentially fatal complications or risk of neurological damage. Large doses of oxytocin plus large volumes of electrolyte-free solutions are the prime factors associated with water intoxication. Suggested treatment consists of hypertonic saline. Although circulatory overload and pulmonary oedema can occur from saline treatment it is believed that the risk of cerebral oedema is greater than risk from saline treatment. Prevention of water intoxication includes: 1) restriction of fluid intake; 2) monitoring of analgesia given; 3) interruption of continuous infusion; 4) fluid balance with control of serum electrolytes and osmolality; and 5) use of electrolyte-containing fluid as a vehicle for the oxytocin.
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PMID:Water intoxication after oxytocin-induced midtrimester abortion. 28 25

Preeclampsia is a disease of unknown etiology and a major contributor to maternal and neonatal morbidity and mortality. With severe preeclampsia, numerous factors including intravascular volume depletion and susceptibility of developing pulmonary edema complicate anesthetic management. Invasive monitors such as CVP or PA pressure measurements are often required for guiding fluid management. When possible, lumbar epidural blockade is the preferred method for providing analgesia and anesthesia. Under all circumstances, a collegial and collaborative approach between obstetrician and anesthesiologist facilitates optimum patient care.
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PMID:Anesthetic concerns in the patient with preeclampsia. 176 45

The aim of this study was to evaluate factors relevant to morbidity and mortality in 54 patients undergoing oesophagectomy at Royal Newcastle Hospital between 1985 and March 1989. There was a high incidence of concurrent medical problems. Significant anaesthetic complications occurred in 6 patients. There were 16 serious general medical complications and 10 surgical complications. Respiratory complications included basal collapse (19), sputum retention (6), pulmonary oedema (2), pleural effusion/haemothorax (5), and severe aspiration syndrome (5). Seven patients required mechanical ventilation for more than 3 days. Two deaths occurred postoperatively. As a result of this audit, changes have occurred in patient selection, management of chylothorax, epidural analgesia and timing of tracheal extubation.
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PMID:Peri-operative care for oesophagectomy patients. 187 43

Two patients with hypertrophic obstructive cardiomyopathy (HOCM) presented for delivery. The first had a repeat Caesarean section with general anaesthesia and the second gave birth vaginally with epidural analgesia. Both patients developed pulmonary oedema in the peripartum period. These cases highlight the delicate fluid requirements of the pregnant patient with HOCM. The fluid management of the parturient is discussed with particular emphasis on the pathophysiology of HOCM. The indications for invasive monitoring are presented.
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PMID:Pulmonary oedema in two parturients with hypertrophic obstructive cardiomyopathy (HOCM). 234 Jun 17

A case is described in which unusually high doses of intravenous ritodrine were used for 6 weeks to postpone premature labour. Treatment was complicated by tachydysrhythmias and pulmonary oedema. Epidural analgesia was used successfully for pain relief during labour and Caesarean section. The pathophysiology is discussed.
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PMID:Ritodrine-induced pulmonary oedema in labour. Successful management using epidural anaesthesia. 649 97

Naloxone (Narcan) is generally considered to be a narcotic antagonist devoid of pharmacologic activity except for its reversal of opioid (narcotic) effects. Case reports indicate that naloxone in its role of narcotic antagonist may induce hypertension, pulmonary edema, atrial and ventricular arrhythmias, or cardiac arrest in certain patients, particularly those with pre-existing cardiac abnormalities. These adverse effects of naloxone may be due to extreme sympathetic nervous system activity resulting from the reversal of narcotic analgesia, an effect of the drug on peripheral or central opioid receptors or a drug interaction with other anesthetic agents. Any patient given naloxone, particularly in the presence of surgical pain, should be closely monitored for adverse cardiovascular effects.
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PMID:Naloxone-associated morbidity and mortality. 703 51

A patient undergoing prostatectomy under epidural analgesia developed clinical signs of a severe TURP syndrome. During resuscitation, it was revealed that serum sodium was only moderately decreased. Plasma oncotic pressure was, however, markedly decreased and the pressure gradient between plasma oncotic pressure and pulmonary capillary wedge pressure (approximately hydrostatic pressure) was 1 mmHg (0.13 kPa) only, allowing almost free filtration of fluid through the pulmonary capillary wall, resulting in a non-cardiogenic pulmonary edema. The patient was successfully resuscitated with albumin and inotropic stimulation with prenalterol.
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PMID:Non-cardiogenic pulmonary oedema. A serious complication of transurethral prostatectomy. A case report. 732 25

A 37-year-old parturient with severe preeclampsia accompanied by pulmonary edema underwent emergency cesarean section. Pulmonary artery (PA) catheter inserted while the patient was awake revealed hyperdynamic state with increased cardiac index and preload, and decreased systemic vascular resistance. Epidural anesthesia and analgesia were provided with a satisfactory outcome. Monitoring of PA pressure and cardiac index was continued postoperatively in ICU for fluid management. We conclude that preoperative PA catheterization provides useful hemodynamic information in severe preeclamptic patients associated with persistent oliguria, pulmonary edema and hyperdynamic state.
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PMID:[Pre- and post-operative management of cesarean section in a parturient with severe preeclampsia accompanied by hyperdynamic state]. 940 34

Coronary artery disease (CAD), arterial hypertension, chronic bronchitis and diabetes mellitus are the most frequently encountered diseases complicating the clinical course of the vascular patient. Clinical signs of cardiac or pulmonary disease are often absent in patients with decreased functional capacity due to claudication. For instance, clinical evidence of coronary artery disease was found in 36% of patients scheduled for different vascular surgical procedures, whereas coronary angiography revealed significant stenoses in as many as 53-68%. Patients with chronic hypertensive disease, coronary artery disease and increased impedance to left ventricular ejection due to atherosclerosis frequently develop impairment of left ventricular (LV) function. Even without clinical or radiological evidence, approximately 20-35% of vascular patients have a LV ejection fraction below 50% indicating impaired systolic LV function. The incidence of diabetes mellitus in vascular surgical patients is around 18%. When requiring insulin treatment, diabetes is an independent risk factor for postoperative ischemic events and congestive heart failure. Those with autonomic neuropathy are often asymptomatic as regards coronary artery disease. Coronary artery disease is responsible for over 50% of the immediate, medium- and long-term mortality and morbidity. Unstable myocardial ischemia, acute myocardial infarction which is detected by troponin I and ischemic pulmonary edema are the most common immediate postoperative cardiac complications. A large number of recent studies, using long-term ECG recording techniques, have allowed more accurate estimation of the incidence and time course of perioperative myocardial ischemia in vascular surgical patients. The highest incidence of ischemia when compared to daily life activities has been noted during the first two days after surgery but has been reported to remain elevated even 3-5 days after surgery. Interestingly, the incidence of intraoperative ischemia is lower than that observed during daily life. Knowledge of the etiology of perioperative myocardial infarction is essential if one is to improve cardiac outcome after vascular surgery. Many studies have addressed this important field in patients undergoing vascular surgery. They have documented a relationship between perioperative myocardial ischemia and postoperative myocardial infarction. Although postoperative myocardial infarctions are in most cases limited to endocardium (non Q wave infarction) they significantly reduce life expectancy of the vascular surgical patients. The reduction of cardiac risk following general surgery should focus on methods by which the incidence of myocardial ischemia, particularly during the postoperative period, could be reduced. These methods include intensive intraoperative analgesia or preventive administration of cardiovascular treatment which limit postoperative stress: alpha-2 agonists or betablocking agents. There are, at present, no studies which convincingly confirm an overall decreased mortality if coronary bypass surgery is performed prior to peripheral vascular surgery. Although it has been demonstrated that the mortality of the peripheral procedure is reduced to approximately one half, the mortality of a coronary bypass procedure in vascular surgical patients is five to eight times that recorded in a coronary artery bypass population without peripheral vascular disease. It remains to be shown if the use of coronary angioplasty prior to peripheral vascular surgery can provide a more satisfactory overall outcome. Several non-invasive techniques have been suggested to improve the identification of high-risk patients undergoing vascular surgery. These tests include exercise ECG, ambulatory ECG, dipyridamolethallium scintigraphy and determination of left ventricular ejection fraction by gated radionuclide imaging. (ABSTRACT TRUNCATED)
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PMID:[Physiopathologic introduction to anesthesia and resuscitation of the vascular patient]. 955 51

The pathophysiology of elevated intracranial pressure (ICP) is assessed from a three cerebral compartment model and from brain compliance. The mechanisms leading to elevated ICP (expanding process, cerebral edema, brain swelling, hydrocephalus) and their consequences (brain herniation, ischemia-anoxia phenomenon, Cushing reaction and neurogenic pulmonary edema) are overviewed. The causes of elevated ICP in children are reported with emphasis on traumatology. Diagnostic procedures include clinical assessment, fundoscopy, cerebral computerized tomography scan and specific problems of cerebrospinal fluid investigation. Methods and results of intracranial pressure monitoring are reported. The treatment of elevated ICP is based upon clinical follow-up and monitoring of ICP. General therapeutic rules consist of adequate position, suppression of any neck, skull and abdominal compression, stimuli limitation and fluid restriction. Specific treatments include mechanical ventilation, sedation and analgesia, barbiturates, anticonvulsant drugs, mannitol, corticosteroids, hypothermia, enteral nutrition, and antibiotics.
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PMID:[Intracranial hypertension in the infant: from its physiopathology to its therapeutic management]. 975 78


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