Cases reported "Hypotension"

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1/224. Primary percutaneous transluminal coronary angioplasty performed for acute myocardial infarction in a patient with idiopathic thrombocytopenic purpura.

    A 72-year-old female with idiopathic thrombocytopenic purpura (ITP) complained of severe chest pain. electrocardiography showed ST-segment depression and negative T wave in I, aVL and V4-6. Following a diagnosis of acute myocardial infarction (AMI), urgent coronary angiography revealed 99% organic stenosis with delayed flow in the proximal segment and 50% in the middle segment of the left anterior descending artery (LAD). Subsequently, percutaneous transluminal coronary angioplasty (PTCA) for the stenosis in the proximal LAD was performed. In the coronary care unit, her blood pressure dropped. Hematomas around the puncture sites were observed and the platelet count was 28,000/mm3. After transfusion, electrocardiography revealed ST-segment elevation in I, aVL and V1-6. Urgent recatheterization disclosed total occlusion in the middle segment of the LAD. Subsequently, PTCA was performed successfully. Then, intravenous immunoglobulin increased the platelet count and the bleeding tendency disappeared. A case of AMI with ITP is rare. The present case suggests that primary PTCA can be a useful therapeutic strategy, but careful attention must be paid to hemostasis and to managing the platelet count.
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2/224. Combined lung and liver transplantation in a girl with cystic fibrosis.

    PURPOSE: To describe the anesthetic considerations of a combined lung and liver transplant in a 14-yr-old girl with cystic fibrosis. CLINICAL FEATURES: A 14 yr-old girl with cystic fibrosis presented for combined liver and lung transplantation. Anesthetic management was complex in that the pulmonary, hemodynamic, and hematological changes after cardiopulmonary bypass and lung transplantation made the management of the subsequent liver transplant unique. We used a moderate dose fentanyl and isoflurane anesthetic with invasive monitoring including a pulmonary artery catheter. Upon reperfusion of the new liver our patient exhibited severe pulmonary hypertension that was associated with a decrease in cardiac output and systemic hypotension. Utilizing a pulmonary artery catheter, this episode was treated with an increase of prostaglandin E1 (PGE1) infusion to 0.025 microg x kg(-1) x min(-1) and the initiation of 3 microg x kg(-1) x min(-1) dobutamine. The pulmonary hypertension resolved and the cardiac output and blood pressure returned to baseline levels. CONCLUSION: The anesthetic considerations for a combined lung and liver transplant are complex because of the interactions and alterations in cardiovascular, pulmonary and hemostatic systems. The use of a pulmonary artery catheter was critical to the management of our patient because it allowed us to accurately treat an episode of hypotension occurring during liver transplantation. This episode was secondary to acute pulmonary hypertension which is common after pulmonary transplantation but unusual during liver transplantation. It is also critical that a team approach is used to consider all of the concerns of the multiple services managing these complex patients.
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3/224. intracranial hypotension with parkinsonism, ataxia, and bulbar weakness.

    OBJECTIVE: To describe a case of spontaneous intracranial hypotension with a previously unreported constellation of presenting features. DESIGN: Case report. SETTING: Tertiary care center. MAIN OUTCOME AND RESULTS: We describe a patient with intracranial hypotension who presented with a parkinsonian syndrome and later development of ataxia and prominent bulbar symptomatology. headache was not a feature of her initial presentation and was only reported after repeated questioning during later evaluations. magnetic resonance imaging of the patient's head revealed findings characteristic of intracranial hypotension. An [18F]fluoro-m-tyrosine positron emission tomographic scan showed normal striatal activity, suggesting intact presynaptic nigrostriatal function. Opening pressure on lumbar puncture was reduced at 40 mm H2O. A source of cerebrospinal fluid leakage was not identified on nuclear cisternography and the patient underwent lumbar epidural blood patching, which resulted in complete resolution of her signs and symptoms as well as in a marked improvement in her imaging findings. CONCLUSIONS: The clinical spectrum of intracranial hypotension can be broadened to include parkinsonism, cerebellar ataxia, and prominent bulbar dysfunction. As with more common manifestations of the disorder, these features may resolve after appropriate treatment.
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4/224. 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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5/224. Hypotensive ischemic optic neuropathy and peritoneal dialysis.

    PURPOSE: To report anterior ischemic optic neuropathy associated with systemic hypotension in a patient undergoing continuous ambulatory peritoneal dialysis. methods: Case report. A 58-year-old man undergoing continuous ambulatory peritoneal dialysis developed painless blurred vision in both eyes and bilateral optic disk swelling with an altitudinal field defect in the left eye. Twenty-four-hour ambulatory blood pressure monitoring was requested in addition to other routine investigations. RESULTS: Routine blood pressure measurement in the clinic was 130/86 mm Hg, but ambulatory blood pressure monitoring demonstrated pronounced early morning hypotension with individual readings as low as 91/41 mm Hg. CONCLUSIONS: renal dialysis can render patients hypotensive, and this may be associated with anterior ischemic optic neuropathy. The overnight drop in blood pressure may not be appreciated with routine blood pressure measurement. Therefore, 24-hour ambulatory blood pressure monitoring should be considered when investigating patients with suspected anterior ischemic optic neuropathy who are undergoing renal replacement.
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6/224. Possible venous argon gas embolism complicating argon gas enhanced coagulation during liver surgery.

    We report a case of a major venous argon embolism during argon beam coagulation of a liver biopsy. The essential signs were an abrupt reduction in end-tidal carbon dioxide partial pressure, in SpO2 and in systolic arterial pressure, at the time of coagulation. Spontaneous recovery was observed within 10 min. Precautions in respect of usage are highlighted.
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7/224. Intravenous valproate associated with significant hypotension in the treatment of status epilepticus.

    Intravenous valproate has been suggested for the treatment of status epilepticus in part because of its relatively good cardiovascular safety profile. We report a case of severe hypotension associated with intravenous valproate used to treat status epilepticus in an 11-year-old girl. Valproate 960 mg (30 mg/kg) was infused over 1 hour. The patient's blood pressure decreased from a baseline of 130/80 mm Hg to 70/55 mm Hg, 39 minutes into the infusion. Although her seizures stopped, her blood pressure fluctuated between 90/60 mm Hg and 60/30 mm Hg over the next several hours, requiring treatment with intravenous fluids and pressor therapy. Endotracheal intubation eventually was performed. Once her blood pressure stabilized, the patient improved clinically. To our knowledge, this is the first report of significant hypotension associated with intravenous valproate in the treatment of status epilepticus in the pediatric population.
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8/224. Abolished nocturnal blood pressure fall in a boy with glucocorticoid-remediable aldosteronism.

    Glucocorticoid-remediable aldosteronism (GRA) is a rarely recognised cause of arterial hypertension. We report the features of a 13-year-old boy with hypertension (casual blood pressure (BP) 140-180/95-110 mm Hg) discovered during a routine paediatric check. Ambulatory BP monitoring (ABPM) revealed significant hypertension with an abolished nocturnal BP fall (mean daytime BP 155/108 mm Hg, mean night-time BP 156/104 mm Hg, nocturnal BP fall 0/4%) which was indicative of secondary hypertension. Despite triple antihypertensive drug therapy the hypertensive control was unsatisfactory. Laboratory tests revealed hypokalaemia (3.0 mmol/l), suppressed plasma renin activity (0.012 nmol/l/h) and high plasma aldosterone (1.190 nmol/l). The diagnosis of primary hyperaldosteronism was established and GRA was further confirmed by the presence of the chimaeric GRA-gene and dexamethasone therapy was initiated. During the next 2 months of dexamethasone therapy all three antihypertensive drugs were discontinued and BP remained under control with restoration to a normal nocturnal BP fall (mean daytime BP 129/77 mm Hg, mean night-time BP 113/64, nocturnal BP fall 12/17%). A change of therapy from dexamethasone to spironolactone was necessary due to the side effects of corticosteroids after 3 months. spironolactone alone (0.8-2 mg/kg/day) was able to control the BP sufficiently. In conclusion, to our knowledge, this is the first reported case of abolished nocturnal BP fall in a patient with genetically proven GRA. This study indicates that GRA can cause severe hypertension even in children, associated with an abolished nocturnal BP fall. GRA thus should be excluded in all hypertensive patients with circadian BP rhythm disturbances.
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9/224. Hypotension with dobutamine: beta-adrenergic antagonist selectivity at low doses of carvedilol.

    OBJECTIVE: To report a case of marked hypotension resulting from the concomitant use of low-dose carvedilol and intravenous dobutamine. CASE SUMMARY: A 54-year-old white man with severe heart failure was placed on carvedilol 3.125 mg orally twice a day; three days later the dosage was increased to 6.25 mg orally twice a day. His symptoms of heart failure worsened with increasing fluid retention, orthopnea, paroxysmal nocturnal dyspnea, and elevated blood urea nitrogen and creatinine. He was admitted for treatment of decompensated heart failure with intravenous dobutamine. With each increase in intravenous dobutamine, systolic blood pressure fell. dobutamine was discontinued when systolic blood pressure reached 56 mm Hg. In a subsequent admission for decompensated heart failure, when the patient was not taking carvedilol, he was treated with intravenous dobutamine and systolic blood pressure increased. DISCUSSION: Although carvedilol is a nonselective beta-adrenergic antagonist, at low doses it is a selective beta1-adrenergic antagonist. dobutamine is a beta1-, beta2-, and alpha1-adrenergic agonist. Typically, patients with heart failure treated with intravenous dobutamine have a small increase in systolic blood pressure. We propose that the drop in blood pressure with dobutamine in this patient was caused by a fall in systemic vascular resistance due to vascular beta2-adrenergic receptor activation. The normal increase in cardiac output was partially blocked by selective beta1-adrenergic blockade at low doses of carvedilol. CONCLUSIONS: Beta-adrenergic blockade with carvedilol is now common therapy for patients with congestive heart failure. Intravenous dobutamine is often used when these patients have worsening heart failure. Recognition that treatment with dobutamine in patients taking low doses of carvedilol may result in hypotension is important for appropriate monitoring and therapy.
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10/224. Cardiovascular collapse associated with extreme iatrogenic PEEPi in patients with obstructive airways disease.

    Chronic obstructive pulmonary disease (COPD) is commonly associated with positive alveolar pressure at end-expiration (intrinsic PEEP or PEEPi) caused by a prolonged expiratory time constant. Positive pressure ventilation (PPV) with large tidal volumes and high ventilatory frequencies may cause pulmonary hyperinflation, with increases in intrathoracic pressure and cardiopulmonary effects. We report two cases, one of fatal pulseless electrical activity, the other of life-threatening hypotension, both during vigorous manual PPV, in patients with severe COPD. This phenomenon has been well-recognized by intensivists but is reported poorly more widely.
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