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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HELLP syndrome is a severe complication of pre-eclampsia characterised by hemolysis, elevated liver enzymes and a low platelet count. It is associated with an increased risk of adverse outcome for both the mother and the fetus. Patients with HELLP syndrome are also at greater risk of pulmonary edema, adult respiratory distress syndrome, abruptio placentae, intracerebral hemorrhage, eclamptic convulsions, disseminated intravascular coagulation, ruptured liver hematomas and acute renal failure. Perinatal mortality is equally high. Before delivery, aggressive obstetric management is directed toward stabilization of the affected organ systems, if possible, and interruption of the pregnancy in the early phase of the accelerated disease progression. Definitive therapy is delivery. Parturients HELLP syndrome often require general anesthesia for Cesarean section delivery. The anesthetic technique is critical for these patients with a high risk of uncontrollable hypertension, bleeding and multiple organ failure. Remifentanil is increasingly used as a very short analgesic agent providing cardiovascular stability in high-risk patients. We report the management of a patient presenting in labor with HELLP syndrome, and describe the successful use of remifentanil as part of the anesthetic technique for her subsequent Cesarean section.
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PMID:General anesthesia with remifentanil for Cesarean section in a patient with HELLP syndrome. 1575 13

The impact of hypertension on left ventricular (LV) structure, pump function, and heart failure in Dahl salt-sensitive rats is poorly characterized but hypothesized to yield insights into the pathophysiology of heart failure with normal or preserved ejection fraction. Eighty Dahl salt-sensitive rats were fed either a high-salt (HS) or low-salt (LS, controls) diet starting at age 7 weeks. Ventricular properties were measured by echocardiography, hemodynamics and end-systolic and end-diastolic pressure-volume relationships (ESPVR and EDPVR, respectively). Compared with LS controls, HS rats developed severe hypertension and LV hypertrophy. At week 12, HS rats developed passive diastolic dysfunction (leftward/upward shifted EDPVR, increased chamber stiffness) with reductions in end-diastolic volume. However, the ESPVR also shifted upward (enhanced end-systolic function) so that overall pump function was enhanced compared with LS, and there was no change in end-diastolic pressure (EDP). At 16 and 20 weeks, HS hearts enlarged so that end-diastolic volumes and EDPVRs became similar to the respective age-matched LS controls. Concomitantly, the ESPVRs and overall pump function curves also moved toward controls, and ejection fraction declined. Despite normal or enhanced overall pump function at these times, EDP and wet lung weight increased, indicative of development of heart failure. In the Dahl salt-sensitive rat, which pathophysiologically retains salt and water, the development of heart failure (increased EDP and wet lung weight) is dissociated from changes in passive diastolic and active systolic properties. These observations suggest that a volume overload sate plays an important pathophysiological role in development of heart failure despite preserved overall ventricular pump function in this model of chronic hypertension.
Hypertension 2006 May
PMID:Development of heart failure in chronic hypertensive Dahl rats: focus on heart failure with preserved ejection fraction. 1658 20

Acute respiratory distress syndrome (ARDS) is a clinical-radiological diagnosis. Clinical diagnosis comprises severe hypoxemia assessed by arterial oxygen tension/fraction of inspired oxygen ratio of less than 200 and bilateral infiltrate on a chest radiograph in the absence of left atrial hypertension. The sensitivity and specificity of the clinical diagnosis vary based on the underlying etiology for ARDS. Except for presence of bilateral infiltrate on chest radiograph and severe hypoxemia on arterial blood gas, most diagnostic studies are used to exclude mimics of ARDS and potentially modify treatment. Computerized tomography of the chest is helpful in understanding the extent of the disease and is more sensitive in identifying pneumomediastinum and pneumothoraces seen frequently in patients with ARDS, which can be missed on a chest radiograph, especially if they are small in size. Measurements of alveolar dead space ventilation fraction can be helpful in determining the prognosis in individuals with ARDS. Bronchoalveolar lavage, transbronchial lung biopsy, and open lung biopsies can be safely performed in patients with ARDS. Bronchoalveolar lavage fluid in patients with ARDS shows neutrophil predominance with increased edema fluid to serum protein ratio. Diffuse alveolar damage, a pathognomic of ARDS, is seen on histopathology on transbronchial lung biopsy or open lung biopsy. Most common complications of these procedures include transient hypoxemia, respiratory acidosis, and pneumothorax with occasional persistent air leak. The potential risk of diagnostic studies should be balanced against the possible foreseeable benefits of the diagnostic studies.
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PMID:Diagnostic studies in patients with acute respiratory distress syndrome. 1676 46

Acute respiratory distress syndrome is a secondary acute respiratory insufficiency caused by an inflammatory syndrome which is characterized by an increased of permeability pulmonary edema, associated with many other clinic anomalies, radiological and pathophysiological not directly caused by, but with which it could coexist, a left atrial hypertension. The illness, characterized by refractory hypoxemia, recognizes several causes, which have direct or indirect harm on the cells of the membrane alveolus-capillary. In spite of the improvements in the therapeutic approach, during these last 40 years, represented by the aid of the mechanical ventilation and the use of selective pulmonary vasodilators, this condition is life threatening and often lethal: 90% of mortality rate amongst those older than 65 years.
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PMID:[Acute respiratory distress syndrome: definitions, mechanisms and treatment]. 1691 78

Thrombotic thrombocytopenic purpura (TTP) has been associated with scleroderma renal crises (SRC) in the past. However such reports markedly diminished after the onset of ACE inhibitor use. Recently, reports again have surfaced that describe scleroderma patients presenting with clinical evidence of TTP. We describe a 50-year-old female with longstanding limited cutaneous scleroderma who presented with hematochezia and thrombocytopenia along with other findings suggesting TTP. A colon biopsy revealed thrombi within the lumen. Her course was complicated by renal failure and hypertension that did not respond to ACE inhibitor therapy alone. She improved after a course of plasma exchange. She was discharged home only to return 2 months later with grand mal seizures and hypertension. During her course she developed adult respiratory distress syndrome. She again responded to plasma exchange and she was discharged home. She has remained stable for 2 years. This report emphasizes the importance of fully evaluating patients with longstanding limited cutaneous scleroderma who present with renal failure, hypertension, and thrombocytopenia in association with multiorgan complications. All possible etiologies, including SRC, TTP, vasculitis, and sepsis should be considered. Tissue biopsies (in this case, a colon biopsy revealed thrombi within the vessel lumen) may prove beneficial in assisting with the diagnosis. For such patients who fail treatment with ACE inhibitors, plasma exchange may be considered.
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PMID:Thrombotic thrombocytopenia purpura in a patient with systemic sclerosis. 1703 6

Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are clinical syndromes characterized by the sudden onset of severe hypoxemia and diffuse bilateral pulmonary infiltrates in the absence of left atrial hypertension. Although advances have been made in the understanding of the etiology, pathophysiology, and epidemiology of both entities, many questions remain regarding their incidence, diagnosis, and outcomes. This article reviews the currently used definition of ARDS and ALI, different studies that have advanced the understanding of the epidemiology and outcomes of these entities, and several diagnostic issues that are important for both clinicians and researchers.
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PMID:Clinical epidemiology of acute lung injury and acute respiratory distress syndrome: incidence, diagnosis, and outcomes. 1708 44

We are reporting a case of catastrophic antiphospholipid syndrome (CAPS) in an adult female manifested with severe hypertension followed by adrenal haemorrhagic infarction and adult respiratory distress syndrome. Adrenal involvement appears to be exceedingly high in CAPS and adult respiratory distress syndrome (ARDS) is the prevailing pulmonary manifestation in this condition, compared with these impediments in patients with simple antiphospholipid syndrome (APS). Even though the above manifestations are well recognized, their combination as an initial presentation of CAPS is uncommon.
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PMID:Catastrophic antiphospholipid syndrome presented with severe hypertension, adult respiratory distress syndrome and unilateral adrenal haemorrhagic infarction. 1743 1

Adrenocortical carcinoma is a rare disease. A 32 years old lady presented with complaints of hypertension, abdominal swelling, weight gain, hirsutism and bone pains. She was found to have a large adrenocortical carcinoma with associated Cushing's and virilization syndromes. Radical adrenalectomy was done with subsequent plan for Mitotane and radio frequency ablation for hepatic metastasis. However, she succumbed to respiratory failure due to ARDS, a month after operation.
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PMID:Adrenocortical carcinoma with endocrine syndromes. 1807 May 81

Acute respiratory distress syndrome (ARDS) is the most devastating form of acute lung injury (ALI) or pulmonary edema (PE). We presented the experimental studies and clinical investigations of two serious forms of ALI. Drastic and severe PE could be induced by intracranial hypertension or cerebral compression (CC). The CC-induced PE was attributed to overactivation of the medullary sympathetic mechanism. Sympathetic vasoconstriction of the systemic and pulmonary resistance and capacitance vessels caused shift of blood volume from the splanchnic vascular beds to the lung. The hemodynamic changes led to systemic and pulmonary hypertension. Consequently, left ventricular failure as evidenced by dramatic decline in aortic flow with a slow decrease in pulmonary flow resulted in pressure and volume loading in the pulmonary circulation. These changes finally produced severe alveolar flooding and sudden death. Vasodilators such as sodium nitroprusside or nitroglycerin were capable of reducing the CC-induced pulmonary pathology and hemodynamic alterations. Fat embolism syndrome (FES) is a serious clinical problem in patients suffering from long bone fractures. ARDS may develop and cause mortality. Our laboratory reported a total of 14 subjects associated with FES and died of ARDS. We also developed a simple technique to produce FES. Corn oil was mixed with distilled water to form fatty micelles. Intravenous administration of or introduction of fatty micelles in anesthetized rats or isolated perfused lungs caused severe alveolar damage. Our clinical observation and animal experimentation revealed that infusion of fatty acids caused physical phase, resulting in microvascular obstruction accompanied by pulmonary hypertension and increased capillary permeability. Thereafter, the lipases in the lung hydrolyzed the neutral fat and released free fatty acids and biochemical mediators which were toxic to the lung. Our data have suggested that nitric oxide (NO), inducible NO synthase (iNOS), phospholipase A2, free radical and inflammatory cytokines (tumor necrosis factor alpha, interleukin-1beta and interleukin-6) are involved in the biochemical phase of FES with ARDS. The alveolar macrophages are the major source of iNOS. Later study also found that neutrophil elastase and myeloperoxidase were elevated following fat embolism. N-acetylcysteine (an antioxidant), and NOS inhibitors such as Nomega nitro-L-arginine methyl ester (L-NAME), S-methylisothiourea (SMT) or L-N6 (1-iminoethyl)-lysine (L-Nil) were able to abrogate the FES or the fat embolism-induced changes.
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PMID:From neurogenic pulmonary edema to fat embolism syndrome: a brief review of experimental and clinical investigations of acute lung injury and acute respiratory distress syndrome. 2035 24

Non-cardiogenic pulmonary oedema (NCPE) is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, and no evidence of left atrial hypertension/congestive heart failure/fluid overload. The diagnosis of drug-related NCPE relies upon documented exclusion of other causes of NCPE like gastric aspiration, sepsis, trauma, negative pressure pulmonary oedema, etc. We describe two cases (45-year male and 6-year male), who had undergone elective surgery under general anaesthesia. They developed NCPE within 3-5 minutes after administration of 'neostigmine-glycopyrrolate' used to reverse residual neuromuscular blockade. Both patients were treated successfully with mechanical ventilatory support, and adjuvant therapy, viz., frusemide, dopamine, steroids. This report emphasizes that this fatal complication may be seen with neostigmine, the pathogenic mechanism remains unknown, and it probably is a drug-related NCPE.
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PMID:Non-cardiogenic pulmonary oedema after neostigmine given for reversal: A report of two cases. 2088 79


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