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

Hypotension following traumatic brain injury (TBI) is recognized as an important secondary insult that is associated with adverse outcome. We aimed to describe the relationship between actual levels of admission blood pressure and Glasgow Outcome Scale (GOS) at 6 months. Individual patient data from the IMPACT database were available on systolic (N = 6801) and mean arterial (N = 6647) blood pressure. Regression models with restricted cubic spline functions were used to explore the shape of the relationships between blood pressure and outcome in unadjusted and adjusted analyses. Proportional odds methodology was applied to quantify the strength of the associations across the full range of the GOS. Analyses were performed to search for threshold values. A smooth U-shaped relationship was observed between systolic (SBP) and mean arterial (MABP) blood pressures and outcome, without any evidence of an abrupt threshold effect. Best outcomes were observed for values of SBP of the order of 135 mm Hg and for values of MABP of the order of 90 mm Hg. Both lower (OR 1.53; 95% CI: 1.31-1.80) and higher levels (OR 1.42; CI: 1.20-1.68) of SBP and lower (OR 1.30; CI 1.12-1.51) and higher levels of MABP (OR 1.45; CI 1.19-1.76) were associated with poorer outcome. These findings were consistent across studies. The relationship between high blood pressure level and poorer outcome largely disappeared on adjusted analysis. Current guidelines for the management of blood pressure in TBI focus on the avoidance of hypotension as defined by SBP < 90 mm Hg. Our finding of a smooth relationship with improving outcome as SBP increases up to 135 mm Hg, while not supporting a strong causal inference, does suggest that current guidelines need to be reconsidered.
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PMID:Prognostic value of admission blood pressure in traumatic brain injury: results from the IMPACT study. 1737 94

A 60-year-old woman with hypertension was seen for a routine examination. Her best-corrected visual acuity was 20/20 bilaterally. Intraretinal hemorrhages were found in the parafoveal region of the right eye. A fundus fluorescein angiography evaluation identified the hemorrhages as arterial macroaneurysms. The following day, the patient returned complaining of blurred vision that had developed the previous evening. Best-corrected visual acuity was counting fingers in the right eye. A subhyaloid hemorrhage approximately three optic disks in size was found in the macular region. The hemorrhage was drained with an Nd:YAG laser.
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PMID:Retinal arterial macroaneurysm rupture following fundus fluorescein angiography and treatment with Nd:YAG laser membranectomy. 1739 98

Transfusion-related acute lung injury (TRALI) is defined as new acute lung injury (ALI) that occurs during or within six hours of transfusion, not explained by another ALl risk factor. Transfusion of part of one unit of any blood product can cause TRALI. The mechanism may include factors in unit(s) of blood, such as antibody and biologic response modifiers. In addition, yet to be described factors in a patient's illness may predispose to the condition. The current incidence is estimated to be 1 in 5000 units. Patients present with acute dyspnea, or froth in the endotracheal tube in intubated patients. Hypertension, hypotension, acute leukopenia have been described. Management is similar to that for ALI and is predominantly supportive. When TRALI is suspected, Blood banks should be notified to quarantine other components from the same donation. No special blood product is required for subsequent transfusion of a patient who has developed TRALI.
Best Pract Res Clin Anaesthesiol 2007 Jun
PMID:TRALI--definition, mechanisms, incidence and clinical relevance. 1765 Jul 71

Despite a significant improvement in the US maternal mortality ratio since the early 1900s, it still represents a substantial and frustrating burden, particularly given the fact that - essentially - no progress has been made in most US States since 1982. Additionally, the US Centers for Disease Control and Prevention has stated that most cases are probably preventable. Two disheartening issues within this topic include a gross underestimation of the magnitude of maternal mortality - particularly before 1987, but which likely persists to a lesser degree today - and the continued significant racial disparity in maternal mortality. Explanations for the plateau in maternal mortality include the recent trend of delayed childbearing, with the potential accompanying complications associated with older reproductive age (particularly over 35 years) and multiparity. The impressive increase in multifetal pregnancies related to delayed childbearing and assisted reproductive technology also plays a role. Finally, peripartum cardiomyopathy has become an increasingly recognized source of maternal mortality. Pregnancy-related mortality is largely accounted for by thromboembolic disease, hemorrhage, hypertension and its associated complications, and infection. However, since the inclusion of maternal deaths occurring after 42 days post-delivery as pregnancy related, traumatic injuries - including homicides and suicides - are an alarming source of maternal mortality. An especially important contemporary issue to consider within this topic is cesarean delivery "on maternal request", opponents of which cite concerns not only for immediate morbidity and mortality increased over that associated with a vaginal birth, but also for potential morbidity and mortality associated with future pregnancies. One particularly appealing opportunity to reduce maternal mortality is to recognize, examine, and learn from so-called "near-miss" cases.
Best Pract Res Clin Obstet Gynaecol 2008 Jun
PMID:Maternal mortality in the United States. 1818 28

Hypertensive disorders of pregnancy (HDP) are one of the most common direct causes of maternal mortality worldwide. Cerebral haemorrhage is the main final cause of hypertensive deaths and probably implies that doctors are reluctant to treat sustained high blood pressure effectively during pregnancy. Maternal deaths from HDP can probably be reduced markedly by: (1) promoting antenatal care and instituting a recall system for defaulters; (2) instituting regional centres and regional obstetricians to provide advice on, or care for, women with severe pre-eclampsia; (3) educating health professionals through continuing professional education and the use of clinical guidelines of management; and (4) informing the general public on complications associated with the pre-eclampsia/eclampsia syndrome.
Best Pract Res Clin Obstet Gynaecol 2008 Jun
PMID:Maternal deaths due to hypertensive disorders in pregnancy. 1828 11

Recovery from general anaesthesia is a period of intense stress for patients: there is sympathetic activation, catecholamine release, and increase in blood pressure or heart rate. Stressful events increase cerebral blood flow and cerebral oxygen consumption, potentially producing elevation of intracranial pressure and thus, favouring cerebral insults. Measures to prevent agitation, hypertension, shivering, and coughing are therefore very well justified in neurosurgical patients. The rationale for a "rapid-awakening-strategy" after craniotomy with general anaesthesia is that an early diagnosis of postoperative neurological complications is essential to limit potentially devastating consequences and finally improve patient outcome. A trial of early recovery may always be attempted to perform a neurological evaluation. An awake patient is the best and the cheapest neuromonitoring available. If, after surgery, a patient does not rapidly recover consciousness, or a focal neurological deficit becomes apparent, a head CT-scan should be performed as soon as possible to rule out a neurosurgical complication. Close monitoring during the first 24 hours after craniotomy is mandatory.
Best Pract Res Clin Anaesthesiol 2007 Dec
PMID:Recovery and neurological evaluation. 1828 30

The causes of postoperative cardiovascular disturbances in neurosurgical patients include direct cardiac neurogenic effects, clinical situations where brain tissue is underperfused, and hyperdynamic states. EKG and echographic abnormalities are common in subarachnoid hemorrhage where cardiac troponin I is the most useful predictor of cardiac risk after SAH. Neurogenic pulmonary edema is short lived and often resolves with resolution of the neurologic problem. In traumatic brain injury, where areas of ischemia co-exist with luxury perfusion, advanced hemodynamic monitoring and prevention of jugular venous desaturation best avoid secondary brain injury and achieve optimal neurologic outcome. Induced hypertension improves blood flow through vessels compromised by cerebral stenting, angioplasty, microcatheters, thrombolysis, carotid clamping, intracranial bypass and cerebral vasospasm. Hyperdynamic lesions include vascular breakthrough after elimination of cerebral arteriovenous malformations, but also emergence hypertension and hyperemia. Pharmacologic agents and adjunctive measures are effective in controlling both the systemic and the cerebral circulation.
Best Pract Res Clin Anaesthesiol 2007 Dec
PMID:Cardiovascular therapy of neurosurgical patients. 1828 33

Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. When ICP increases above 20 mmHg it may damage neurons and jeopardize cerebral perfusion. If such a condition persists, treatment is indicated. Control of ICP requires measurement, which can only be performed invasively. Standard techniques include direct ventricular manometry or measurement in the parenchyma with electronic or fiberoptic devices. Displaying the time course of pressure (high-resolution ICP tonoscopy) allows assessment of the validity of the signal and identification of specific pathological findings, such as A-, B- and C-waves. When ICP is pathologically elevated--at or above 20-25 mmHg--it needs to be lowered. A range of treatment modalities is available and should be applied with consideration of the underlying cause. When intracranial hypertension is caused by hematoma, contusion, tumor, hygroma, hydrocephalus or pneumatocephalus, surgical treatment is indicated. In the absence of a surgically treatable condition, ICP may be controlled by correcting the patient's position, temperature, ventilation or hemodynamics. If intracranial hypertension persists, drainage of CSF via external drainage is most effective. Other first-tier options include induced hypocapnea (hyperventilation; paCO2 < 35 mmHg), hyperosmolar therapy (mannitol, hypertonic saline) and induced arterial hypertension (CPP concept). When autoregulation of cerebral blood flow is compromised, hyperoncotic treatment aimed at reducing vasogenic edema and intracranial blood volume may be applied. When intracranial hypertension persists, second-tier treatments may be indicated. These include 'forced hyperventilation' (paCO2 < 25 mmHg), barbiturate coma or experimental protocols such as tris buffer, indomethacin or induced hypothermia. The last resort is emergent bilateral decompressive craniectomy; once taken into consideration, it should be performed without undue delay.
Best Pract Res Clin Anaesthesiol 2007 Dec
PMID:Prevention and treatment of intracranial hypertension. 1828 35

Postoperative nausea and vomiting (PONV) are the most frequent side-effects in the postoperative period, impairing subjective well-being and having economic impact due to delayed discharge. However, emetic symptoms can also cause major medical complications, and post-craniotomy patients may be at an increased risk. A review and critical appraisal of the existing literature on PONV in post-craniotomy patients, and a comparison of these findings with the current knowledge on PONV in the general surgical population, leads to the following conclusions: (1) Despite the lack of a documented case of harm caused by retching or vomiting in a post-craniotomy patient, the potential risk caused by arterial hypertension and high intra-abdominal/intra-thoracic pressure leading to high intracranial pressure, forces to avoid PONV in these patients. (2) There is unclarity about a specifically increased (or decreased) risk for PONV in post-craniotomy patients compared with other surgical procedures. (3) The decision whether or not to administer an antiemetic should not be based primarily on risk scores for PONV but on the likelihood for potential catastrophic consequences of PONV. If such a risk cannot be ruled out, a multimodal antiemetic approach should be considered regardless of the individual risk. (4) Randomized controlled trials with antiemetics in post-craniotomy patients are limited with respect to sample size and methodological quality. This also impacts upon the meaning of meta-analyses performed with trials that showed marked heterogeneity and inconclusive results. (5) No studies on the treatment of established PONV are available. This highlights the need to transfer knowledge about PONV treatment from other surgical procedures. (6) Despite the possibility that PONV in post-craniotomy patients can be triggered by specific conditions (e.g. surgery near the area postrema at the floor of the fourth ventricle with the vomiting centre located nearby), recommendations based on trials in post-craniotomy patients may be flawed. Thus, general knowledge on prevention and treatment of PONV must adopted for craniotomy settings.
Best Pract Res Clin Anaesthesiol 2007 Dec
PMID:Prevention and control of postoperative nausea and vomiting in post-craniotomy patients. 1828 38

Perioperative beta blockade or the use of alpha2 agonists remains a contentious and controversial area of perioperative medicine. Although there is no question that the liberal use of beta blockers (or alpha2 agonists) to prevent or reduce overt signs of sympathetic overactivity, particularly at known periods of stress (e.g. induction, incision, emergence, etc) is an important and routine part of the management of high risk patients, there remains considerable controversy in the literature regarding the efficacy of either short or long-term regimens on cardiac morbidity or long-term outcomes, particularly in those patients not previously receiving medication for known coronary artery disease or hypertension. The role of strict heart rate control (and its safety with regards to hypotension and possibly congestive heart failure) versus intermittent fixed dosing of beta blockers is particularly contentious. We consider the latest literature on this topic and identify areas of agreement and contention and present the latest recommendations of the American Heart Association/American College of Cardiology Perioperative Guidelines Group.
Best Pract Res Clin Anaesthesiol 2008 Mar
PMID:Beta blockers and alpha2 agonists for cardioprotection. 1849 91


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