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

Bone marrow necrosis (BMN) is a relatively rare entity and has been associated with a poor prognosis. It is most commonly found in patients with neoplastic disorders, severe infections and sickle cell anemia. An unusual case of antiphospholipid syndrome (APS) with extensive bone marrow necrosis is described in a 27 year old woman. The patient presented with severe pancytopenia, some cognitive impairment resulting from a previous cerebrovascular accident, fever, hypertension, dyspnoea, tachycardia, hepatosplenomegaly, and vaginal bleeding. Her laboratory findings included a strongly positive Coombs' test (anti-IgG and anti-C3d), a prothrombin time of 23 seconds and an activated partial thromboplastin time of 45 seconds. Anticardiolipin antibody tests were positive. Antinuclear and anti-DNA antibodies were negative but the anti-SM test was positive. A bone marrow biopsy specimen was reported as showing extensive necrosis. The patient was treated with steroids, transfusion, and plasma exchange with some clinical improvement but her pancytopenia did not respond and necessitated frequent transfusions. This case lends further support to the association between APS and BMN.
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PMID:Bone marrow necrosis in antiphospholipid syndrome. 915 83

Preoperative acquired clotting parameters such as prothrombin time, activated partial thromboplastin time, antithrombin III, platelet concentration, and fibrinogen show coagulopathy caused by insufficiency of the diseased liver. Intraoperative determination of clotting factors or parameters is not helpful to direct intraoperative transfusion of blood, blood components, or platelets because transfusions performed solely for correction of clotting data do not correlate with the real intraoperative requirements and increase the costs of orthotopic liver transplantation. However, the use of antihyperfibrinolytic drugs seems to reduce intraoperative blood loss. Patients with cirrhotic disorders caused by portalvenous hypertension show extensive collaterals and increased intravascular blood volume. Thus it is plausible that especially overcorrection of blood loss during the surgical preparation in the preanhepatic phase of the operation results in extensive blood loss. Therefore, to avoid blood loss we attempt to keep volume substitution to a minimum during the preanhepatic phase of the operation. In contrast, during the anhepatic and postanhepatic phases we attempt to reestablish normovolemia by transfusing red packed blood cells and fresh-frozen plasma. Strictly confined use of blood products in the preanhepatic phase, followed by later correction of intravascular blood volume, may reduce intraoperative blood loss; it also seems to ensure adequate substitution of clotting factors.
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PMID:Coagulation techniques are not important in directing blood product transfusion during liver transplantation. 940 72

The association between coagulation abnormalities and pregnancy outcome was investigated in a case-control study conducted at Lady Hardings Medical College and Associated Hospitals in New Delhi, India, in 1991-92. Enrolled were 30 neonates born to mothers with pregnancy-induced hypertension (PIH) and 30 infants of normotensive mothers. Compared with control infants, infants of mothers with PIH had significantly elevated levels of prothrombin time (PT), partial thromboplastin time with kaolin (PTTK), thrombin time (TT), and fibrinogen and fibrinogen degradation products (FDP) and significantly reduced platelet counts and fibrinogen. PTTK and TT were significantly higher in neonates born to mothers with hypertension of more than 1 month's duration, but the difference in PT, fibrinogen, and platelet count was not significant. Also observed was a significant correlation between decreasing gestational age and derangement in all coagulation parameters and between decreasing birth weight and an increase in FDP level. The incidence of disseminated intravascular coagulation was higher in preterm than term neonates. 43.3% of neonates required admission to the neonatal intensive care unit and the perinatal mortality rate was 3.3%.
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PMID:Correlation of coagulation abnormalities with clinical outcome in neonates of mothers with pregnancy induced hypertension. 983 64

We report the results of a feasibility study using intravenous magnesium sulphate for deliberate hypotension in 16 ASA 1 patients undergoing major oral and maxillofacial surgery. All the patients received a standard nitrous oxide, oxygen, isoflurane, opioid and muscle relaxant anaesthetic. Magnesium sulphate was infused at 40 g/h until the mean arterial pressure reached 55 +/- 5 mmHg, followed by a maintenance dose of 5 g/h until 30 minutes prior to the end of surgery. The mean arterial pressure was significantly (P < 0.01) reduced by the magnesium sulphate when compared to baseline values. Control of the mean arterial pressure was satisfactory. No patient had reflex tachycardia, cardiac arrhythmia or rebound hypertension. In 14 patients the surgeons thought that the blood loss was less than when using other hypotensive anaesthetic techniques. In 2 patients the surgeons thought the blood loss was excessive. In another 2 patients, the surgeons thought that there was excessive facial swelling on completion of surgery. Postoperative muscle weakness and sedation were not problems clinically. Fourteen patients were extubated immediately after surgery and another 2 patients an hour later in the recovery room. Intraoperative urine output was well maintained. On completion of surgery, the prothrombin time was significantly increased (P < 0.05), and the partial thromboplastin time significantly decreased (P < 0.05) in all the patients (when compared to preoperative values); the clinical significance of this is unclear. The use of intravenous magnesium sulphate for deliberate hypotension is feasible in ASA 1 patients using a standard nitrous oxide, oxygen, isoflurane, opioid and muscle relaxant technique. This study forms the basis for a larger controlled study where the issues of postoperative sedation and weakness and coagulopathy can be dealt with in greater detail.
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PMID:Is it feasible to use magnesium sulphate as a hypotensive agent in oral and maxillofacial surgery? 1010 49

During an 8-year period, 32 consecutive patients with chronic renal failure on maintenance hemodialysis were diagnosed to have cerebral hemorrhage. The outcome was determined using the activity of daily life (ADL) at 6 months after hemorrhage. The overall mortality was 64%. Of the 12 surviving patients, no one made a good recovery (back to normality), 5 recovered to ADL grade II, 4 to grade III, 1 to grade IV, and 2 to grade V. Up to 91% of the patients had a history of hypertension. On admission, Glasgow coma scale (GCS) was 15 in 8 cases, 8-14 in 10, and below 8 in 14. The poor prognostic factors showing statistical significance included a poor admission GCS, age above 65 years, and blood sugar level of more than 200 mg/dl. Other factors which apparently were not related to the outcome included sex, history of stroke, acute myocardial infarction, hypertension, and diabetes mellitus, the locations of hemorrhage, the duration of hemodialysis, treatment modality (surgery vs non-surgery), and the laboratory data (blood urea nitrogen, creatinine, platelet count, hemoglobin, prothromin time, and partial thromboplastin time). This study confirmed a poor prognosis for hemodialysis patients with cerebral hemorrhage. More attention should be paid to the control of blood sugar in this group to improve the outcome of cerebral hemorrhage in hemodialysis patients, especially in elderly patients with poor admission GCS.
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PMID:Prognosis of spontaneous intracerebral hemorrhage in hemodialysis patients. 1051 65

In the present study, thromboviscometry was used to analyse the dynamic coagulation of blood in patients with severe systemic hypertension. Fibrinogen levels and whole blood viscosity, corrected for 45% haematocrit, were also monitored. The efficacy of thromboviscometry as an adjunct diagnostic tool, for determination of thrombogenic potential, was compared with that of detection of fibrinogen levels in the blood. Twenty-five cases of severe systemic hypertension (HT) in the 40 to 50-year age group were compared with 50 age and sex-matched normal controls (NC). The changes in whole blood viscosity were monitored with time at a constant shear rate, in a concentric cylinder viscometer, during the clotting process. The total thrombus formation time was significantly less in the HT group when compared with NC (238.9 +/- 38.72 s vs 315.1 +/- 32.93 s, P < 0.0005). The time required for a sudden increase in viscosity during clotting was also significantly lower in the HT group (205.9 +/- 34.37 s vs 272.9 +/- 28.83 s, P < 0.0005) and the overall rate of increase of thrombus viscosity was significantly higher in HT (245.2 +/- 36.44 centiPoise/s vs 183.6 +/- 16.32 centiPoise/s, P < 0.0005). There was, however, no significant change in the fibrinogen levels of the two groups. Thus, thromboviscometry was a more sensitive indicator of the thrombogenic potential of blood in HT than fibrinogen levels. The increased thrombogenic potential of hypertensive blood could be due to acceleration of the initial part of the coagulation process during the activation of factor Xa and the formation of thrombin.
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PMID:Thromboviscometry as a tool for evaluation of thrombotic risk in systemic hypertension. 1072 16

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

We report 5 patients with intracerebral hemorrhage after orthotopic liver transplantation (OLT) and identify the possible risk factors. Between November 1991 and April 1999, 75 adult patients received 77 orthotopic liver transplants at Queen Mary Hospital, Hong Kong. Five patients (6.5%) developed intracerebral hemorrhage postoperatively. Clinical and laboratory data were reviewed, and potential risk factors were analyzed. The 5 patients developed intracerebral hemorrhage within 40 days (range, 1 to 37 days; median, 4 days) after OLT. The mortality rate was 80% (4 of 5 patients). The intraoperative blood transfusion volume (median, 17,200 mL; range, 15,750 to 30,360 mL) administered to patients who developed intracerebral hemorrhage postoperatively was significantly greater than that (median, 6,990 mL; range, 1,840 to 22,680 mL) for patients without the complication (P =.0008). Massive intraoperative transfusion (>15,000 mL) was required in all 5 patients (100%) with intracerebral hemorrhage but only 9 of 72 patients (12.5%) in the other group (P =.0001). Four of 5 patients (80%) with intracerebral hemorrhage had intraoperative hypotension compared with 7 of 72 patients (9.7%) in the other group (P =.001). No significant difference was found in age, prothrombin time (PT), activated partial thromboplastin time (APTT), incidence of hypertension, bleeding at extracerebral sites, cyclosporine A neurotoxicity, thrombocytopenia, hemodialysis, and sepsis between the patients with and without intracerebral bleeding. However, the median cumulative score of coagulation parameters (PT, APTT, platelet count) was significantly greater in the group with than without intracerebral bleeding (median score, 3 v 1; P =.023). Intracerebral hemorrhage is 1 of the most disastrous complications after OLT. Intraoperative hypotension, massive intraoperative transfusion, and coagulopathy may be correlated with this complication.
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PMID:Intracerebral hemorrhage after liver transplantation. 1082 37

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

Increased plasma fibrinogen levels and hemostatic abnormalities suggestive of a prothrombotic state are present in patients with end-stage renal failure and could contribute to increased cardiovascular morbidity in these patients. We investigated the relationship between abnormalities of the hemostatic system and the degree of renal failure and whether these abnormalities are associated with increased prevalence of cardiovascular events in patients with arteriolar nephrosclerosis. In 425 patients recruited at a hypertension clinic we assessed the renal function by creatinine clearance, urinary protein excretion, and microalbuminuria, the prevalence of atherosclerotic disease, and measured prothrombin time, activated partial thromboplastin time. fibrinogen, prothrombin fragment 1+2 (F1+2), D-dimer, and antithrombin. Early impairment of renal function (creatinine clearance, 30 to 89 ml/min per 1.73 m2 of body surface area) caused by arteriolar nephrosclerosis was found in 172 patients. Patients with early renal failure were significantly older and had significantly greater values of blood pressure, plasma fibrinogen, F1+2, and D-dimer than patients with normal renal function. Elevated D-dimer and fibrinogen levels were independently associated with the presence of decreased creatinine clearance. Log fibrinogen, log F1+2, and log D-dimer were inversely correlated with creatinine clearance. The prevalence of coronary artery, cerebrovascular, and peripheral vascular disease was significantly greater in patients with mild renal failure than in those with normal renal function. Elevated levels of fibrinogen and D-dimer were associated with the presence of atherosclerotic disease independent of renal function and other risk factors. In conclusion, changes in hemostatic parameters occur early in the course of renal failure in patients with arteriolar nephrosclerosis, suggesting a prothrombotic state that may contribute to the risk for atherosclerotic disease at all levels of renal function.
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PMID:Increased fibrinogen levels and hemostatic abnormalities in patients with arteriolar nephrosclerosis: association with cardiovascular events. 1105 51


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