Cases reported "Hypotension"

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1/51. Fatal cardiac ischaemia associated with prolonged desflurane anaesthesia and administration of exogenous catecholamines.

    PURPOSE: Four cardiac ischaemic events are reported during and after prolonged anaesthesia with desflurane. CLINICAL FEATURES: We have evaluated desflurane in 21 consecutive patients undergoing advanced head and neck reconstructive surgery. Four deaths occurred which were associated with cardiac ischaemic syndromes either during or immediately after operation. All patients in the study received a similar anaesthetic. This comprised induction with propofol and maintenance with alfentanil and desflurane in oxygen-enriched air. Inotropic support (either dopamine or dobutamine in low dose, 5 micrograms.kg.min-1) was provided as part of the anaesthetic technique in all patients. Critical cardiovascular incidents were observed in each of the four patients during surgery. These were either sudden bradycardia or tachycardia associated with ST-segment electrocardiographic changes. The four patients who died had a documented past history of coronary heart disease and were classified American Society of Anesthesiologists (ASA) II or III. One patient (#2) did not survive anaesthesia and surgery and the three others died on the first, second and twelfth postoperative days. Enzyme increases (CK/CK-MB) were available in three patients and confirmed myocardial ischaemia. CONCLUSION: These cases represent an unexpected increase in the immediate postoperative mortality for these types of patients and this anaesthetic sequence.
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2/51. Reversal by vasopressin of intractable hypotension in the late phase of hemorrhagic shock.

    BACKGROUND: Hypovolemic shock of marked severity and duration may progress to cardiovascular collapse unresponsive to volume replacement and drug intervention. On the basis of clinical observations, we investigated the action of vasopressin in an animal model of this condition. methods AND RESULTS: In 7 dogs, prolonged hemorrhagic shock (mean arterial pressure [MAP] of approximately 40 mm Hg) was induced by exsanguination into a reservoir. After approximately 30 minutes, progressive reinfusion was needed to maintain MAP at approximately 40 mm Hg, and by approximately 1 hour, despite complete restoration of blood volume, the administration of norepinephrine approximately 3 micrograms . kg(-1). min(-1) was required to maintain this pressure. At this moment, administration of vasopressin 1 to 4 mU. kg(-1). min(-1) increased MAP from 39 /-6 to 128 /-9 mm Hg (P<0.001), primarily because of peripheral vasoconstriction. In 3 dogs subjected to similar prolonged hemorrhagic shock, angiotensin ii 180 ng. kg(-1). min(-1) had only a marginal effect on MAP (45 /-12 to 49 /-15 mm Hg). plasma vasopressin was markedly elevated during acute hemorrhage but fell from 319 /-66 to 29 /-9 pg/mL before administration of vasopressin (P<0.01). CONCLUSIONS: Vasopressin is a uniquely effective pressor in the irreversible phase of hemorrhagic shock unresponsive to volume replacement and catecholamine vasopressors. Vasopressin deficiency may contribute to the pathogenesis of this condition.
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3/51. Is MAST in the past? The pros and cons of MAST usage in the field.

    Initially, MAST was viewed as a panacea for hypovolemic trauma patients. Through decades of study, this has not panned out. However, MAST seems to stabilize and decrease bleeding in pelvic and long-bone fractures of the lower extremities. It also appears useful in anaphylaxis and in non-traumatic intra-abdominal hemorrhage. The suit has proven deleterious to trauma victims with moderate hypotension (systolic BP 50-90 mm Hg) who face only a short ride to a hospital, especially those with thoracic injuries. Its role in patients with severe hypotension or long prehospital transport times remains unclear. In severely hypotensive patients, the improvement in BP and oxygenation to the heart and brain may override any negative effects of continued hemorrhage. We must wait for further studies to resolve these issues.
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4/51. Repeated hypotensive episodes due to hepatic outflow obstruction during liver transplantation in adult patients.

    We report two cases of unusual repeated hypotension, decreased cardiac output, decreased mixed venous oxygen saturation, decreased central venous pressure, pulmonary artery pressure, and pulmonary wedge pressure after the completion of all vascular anastamoses of liver transplantation. These unstable hemodynamics appear to reflect a clinically relevant picture of hypovolemia. However, the real cause was partial hepatic outflow obstruction. The obstruction was suspected because hypotension was alleviated by elevating the full-sized liver graft ventrally and to the left. Doppler ultrasound examination confirmed that the flow velocity of the hepatic vein outflow was insufficient when the liver fell to its resting position in the right hepatic fossa. An additional side-to-side cavo-caval anastomosis resolved the problem in one patient, whereas the other required not only the additional anastomosis, but also application of a tissue expander filled with 770 mL normal saline beneath the liver to eliminate the obstruction. We emphasize that obstruction of the hepatic outflow causes only temporal hypovolemia because of a decrease of venous return and that treatment of this complication should be surgical intervention to relieve the obstruction. Blind resuscitation with fluids will not solve the problem and, in fact, may result in fluid overload with subsequent complications.
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5/51. amniotic fluid embolism.

    amniotic fluid embolism is a rare occurrence, with no single pathognomonic clinical or laboratory finding. diagnosis is based on clinical presentation and supportive laboratory values. We describe the case of a 17-year-old nulliparous woman at 27 weeks' gestation who had uterine bleeding, hematuria, hemoptysis, hypotension, dyspnea, and hypoxemia within 30 minutes of vaginal delivery. Laboratory values revealed diffuse intravascular coagulation. Chest films were consistent with adult respiratory distress syndrome. pulmonary artery catheterization revealed moderately increased pulmonary capillary wedge pressure. Supportive measures, including oxygenation, fluid resuscitation, and plasma, were administered. Central hemodynamic monitoring and inotropic support were necessary. Our patient recovered uneventfully and 6 weeks later was living an unrestricted life-style.
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6/51. Persistent arterial hypotension after bilateral nephrectomy in a 4-month-old infant.

    A patient with congenital nephrotic syndrome underwent bilateral nephrectomy at the age of 4 months. She showed persistent hypotension from the fourth postoperative day until death at the age of nearly 5 months. No cause for the hypotension could be found. It is postulated that, especially in young infants, a deficiency of renin after bilateral nephrectomy may cause persistent hypotension. An explanation for the putative increased risk of this complication in young infants may be their need for a highly active renin-angiotensin system. Until more is known about the incidence of this complication and its predisposing factors, reluctancy towards the performance of bilateral nephrectomy in children under the age of 6 months is warranted.
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7/51. Familial corticosteroid-binding globulin deficiency due to a novel null mutation: association with fatigue and relative hypotension.

    Corticosteroid-binding globulin is a 383-amino acid glycoprotein that serves a hormone transport role and may have functions related to the stress response and inflammation. We describe a 39-member Italian-Australian family with a novel complete loss of function (null) mutation of the corticosteroid-binding globulin gene. A second, previously described, mutation (Lyon) segregated independently in the same kindred. The novel exon 2 mutation led to a premature termination codon corresponding to residue -12 of the procorticosteroid-binding globulin molecule (c.121G-->A). Among 32 family members there were 3 null homozygotes, 19 null heterozygotes, 2 compound heterozygotes, 3 Lyon heterozygotes, and 5 individuals without corticosteroid-binding globulin mutations. plasma immunoreactive corticosteroid-binding globulin was undetectable in null homozygotes, and mean corticosteroid-binding globulin levels were reduced by approximately 50% at 18.7 /- 1.3 microg/ml (reference range, 30-52 microg/ml) in null heterozygotes. Morning total plasma cortisol levels were less than 1.8 microg/dl in homozygotes and were positively correlated to the plasma corticosteroid-binding globulin level in heterozygotes. Homozygotes and heterozygote null mutation subjects had a high prevalence of hypotension and fatigue. Among 19 adults with the null mutation, the systolic blood pressure z-score was 12.1 /- 3.5; 11 of 19 subjects (54%) had a systolic blood pressure below the third percentile. The mean diastolic blood pressure z-score was 18.1 /- 3.4; 8 of 19 subjects (42%) had a diastolic blood pressure z-score below 10. Idiopathic chronic fatigue was present in 12 of 14 adult null heterozygote subjects (86%) and in 2 of 3 null homozygotes. Five cases met the Centers for disease Control criteria for chronic fatigue syndrome. fatigue questionnaires revealed scores of 25.1 /- 2.5 in 18 adults with the mutation vs. 4.2 /- 1.5 in 23 healthy controls (P < 0.0001). Compound heterozygosity for both mutations resulted in plasma cortisol levels comparable to those in null homozygotes. Abnormal corticosteroid-binding globulin concentrations or binding affinity may lead to the misdiagnosis of isolated ACTH deficiency. The mechanism of the association between fatigue and relative hypotension is not established by these studies. As idiopathic fatigue disorders are associated with relatively low plasma cortisol, abnormalities of corticosteroid-binding globulin may be pathogenic.
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8/51. sodium and water disturbances in patients with Sheehan's syndrome.

    Sheehan's syndrome has been attributed to ischemic damage of the pituitary gland or hypothalamic-pituitary stalk during the peripartum period. Well-described clinical features of Sheehan's syndrome include hypothyroidism, adrenal insufficiency, hypogonadism, growth hormone deficiency, hypoprolactinemia, and different sodium and water disturbances. The occurrence of sodium and water disturbances associated with Sheehan's syndrome depends on the degree of pituitary damage, time of onset since the initial pituitary insult, and concurrent medical conditions that also may play a role in sodium and water balance. We present a patient with Sheehan's syndrome with severe chronic hyponatremia; discuss a potential problem in the patient's management; and review the literature for various sodium and water disturbances, including acute and chronic hyponatremia as well as overt and subclinical central diabetes insipidus. Although Sheehan's syndrome is more prevalent in developing countries, the increasingly large immigrant population within the united states warrants better awareness of this syndrome and its potential complicating sodium and water disturbances. Prompt diagnosis and an understanding of the pathogenic mechanisms of sodium and water disturbances associated with Sheehan's syndrome may avoid potential treatment-related complications.
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9/51. Anterior ischemic optic neuropathy and dialysis: role of hypotension and anemia.

    The pathogenesis of anterior ischemic optic neuropathy (AION) primarily involves interference with the posterior ciliary artery blood supply to the prelaminar optic nerve. Uremic patients often have coexisting pathology such as hypotension (decreased blood delivery), or hypertension, atherosclerosis (increased resistance to blood supply), and anemia (low blood oxygen carrying capacity), predisposing them to AION. We describe a 49-year-old patient on dialysis for many years. He had long-standing hypotension, worsened during each dialysis treatment. He awoke one morning at age 48 complaining of blurred vision in the left inferior field. Based on the clinical course, funduscopic and fluorangiographic examination and visual field defects, AION was diagnosed. Nine months after the loss of vision in the left eye, vision in the right eye became blurred and worsened over the next 24 hours. The diagnosis of AION in the right eye was made. At the last examination ten months later, the patient, still amaurotic, was given a very poor prognosis for further recovery of the visual defects. Surprisingly, very few cases of AION have been reported in chronic uremic patients on dialysis: to the best of our knowledge, only 12 including ours. Most of these cases share some features, including hypotension above all and anemia as common risk factors. Neither the type of dialysis treatment (hemo-, peritoneal dialysis) nor sex seem to have any influence on the occurrence of AION. Uremic children can be affected. What is striking in the three published pediatric cases is that they all had polycystic kidney disease. Treatment of AION in all 12 cases consisted of a combination of steroids, i.v. saline, blood transfusions and rhEpo. AION was more frequently bilateral and irreversible, ending in permanent amaurosis. In conclusion, this study aims to stress that most cases of AION occurring in chronic uremic patients on dialysis have some common features, including hypotension above all and anemia as common risk factors.
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10/51. Mucosal lesions in the human small intestine in shock.

    Characteristic mucosal lesions in resected small intestinal segments from seven patients are reported. Preoperatively, four patients were in shock and general hypotension while the three remaining cases showed signs of local intestinal hypotension. The microscopic appearance of the mucosal lesions was in all patients identical with that previously observed in the feline and canine small intestine after haemorrhage or local intestinal hypotension. It is proposed that an extravascular short-circuiting of oxygen in the mucosal countercurrent exchanger and an intravascular aggregation of blood cells might produce tissue hypoxia which makes the mucosa vulnerable to enzymatic degradation.
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keywords = hypoxia, oxygen
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