Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of vasospasm after subarachnoid hemorrhage remains a formidable challenge. The prompt recognition of this complication is essential to prevent ischemic damage. Initial orders should include adequate fluid and sodium supplementation to avoid volume depletion. Prophylactic hypervolemia is not effective in reducing the incidence of vasospasm and may be deleterious. Oral nimodipine (60 mg every 4 hours for 21 days) should be started on admission because it protects against delayed ischemic damage. Increasing blood flow velocities on serial transcranial Doppler studies are reliable indicators of early development of vasospasm. When symptomatic vasospasm occurs, hemodynamic augmentation therapy should be instituted. Crystalloids and colloids may be used to promote hypervolemia. Colloids may provide additional benefit by producing hemodilution. However, the rheological benefits of hemodilution may be offset by reduced oxygen carrying capacity when hematocrit drops below 28%. Hypertension may be induced by administering inotropic drugs and, in certain cases, cardiac output optimization using dobutamine also is necessary. When aggressive medical therapy fails to reverse ischemic deficits, prompt endovascular intervention is indicated. Focal vasospasm of larger vessels may be effectively treated with angioplasty and the benefits of this procedure are durable. Diffuse vasospasm involving smaller arterial branches may be treated with intra-arterial infusion of vasodilators, such as papaverine, verapamil, or nicardipine. Unfortunately, these dilatory effects tend to be short-lasting. In refractory cases, hypothermia may be considered, although value of this strategy remains largely unexplored.
 ...
PMID:Cerebral Vasospasm in Subarachnoid Hemorrhage. 1567 13

Delayed cerebral ischemia as a result of cerebral vasospasm is the most common cause of death and disability after aneurysmal subarachnoid hemorrhage (SAH). It leads to death or permanent neurologic deficits in over 17-40% of SAH patients. The initial and main symptom of cerebral vasospasm is diffuse headache and may be accompanied with a slight increase in discomfort from neck stiffness and fever. The clinical diagnosis of cerebral vasospasm is made when the patient experiences an altered level of consciousness or a new focal neurologic deficit. There has been a great progress in identifying the patients at risk, putative mechanisms, and possible treatment options for cerebral vasospasm. However, the problem is by no means solved, mainly due to a limited understanding of the pathologic mechanisms of this complex disease. The iatrogenic factors that can increase the risk of cerebral vasospasm include prolongation of the subarachnoid clot by antifibrinolytic drugs, hypotension, inappropriate treatment of hyponatremia, hypovolemia, hyperthermia and increased intracranial pressure. Nimodipine has been shown to improve neurologic outcome and decrease the incidence of cerebral vasospasm. Triple H therapy is a treatment designed to augment cerebral blood flow for patient with cerebral vasospasm. Hypervolemic hypertension is induced with intravenous volume expansion with crystalloid or colloid to increase cardiac output and raise blood pressure. However, small randomized trials showed no clear benefit. Recently, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators has emerged as the primary intervention for treating medically refractory ischemia from cerebral vasospasm and in many centers is being used as a first-line treatment or even prophylactically. In addition, promising new treatments for cerebral vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia; however, all still need further clinical trials. Newly recognized mediators of cerebral vasospasm after SAH include endothelium-derived mediators, vascular smooth-muscle-derived mediators, proinflammatory mediators involved in blood-brain barrier disruption, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Moreover, observations in the laboratory have, in many circumstances, matched those of reported small series. Larger, prospective, randomized trials are needed to verify several hypotheses of molecular pathophysiology and clinical treatment regimens.
 ...
PMID:Treatment of cerebral vasospasm after subarachnoid hemorrhage--a review. 1567 31

Hypothermia is currently considered as the most effective neuroprotective method. In recent years hypothermia has been more and more applied in clinical conditions. Hypothermia has been used with promising results in severe head trauma where it can evidently decrease the intracranial pressure, improve cerebral perfusion pressure and by its direct neuroprotective effect it diminishes the secondary ischemic brain damage. Hypothermia has been widely used also during complicated neurosurgical operations when cerebral vessels are manipulated (operations of cerebral aneurysms, arteriovenous malformations, scull base tumours). Hypothermia has been recently tested also in some types of stroke, mainly in subarachnoid haemorrhage and ischaemic stroke.
 ...
PMID:[The use of moderate hypothermia in neurosurgery]. 1578 77

Aneurysmal subarachnoid hemorrhage (SAH) remains a very prevalent challenge in neurosurgery associated with a high morbidity and mortality due to the lack of specific treatment modalities. The prognosis of SAH patients depends primarily on three factors: (i) the severity of the initial bleed, (ii) the endovascular or neurosurgical procedure to occlude the aneurysm and (iii) the occurrence of late sequelae, namely delayed ischemic neurological deficits due to cerebral vasospasm. While neurosurgeons and interventionalists have put significant efforts in minimizing periprocedural complications and a multitude of investigators have been devoted to the research on chronic vasospasm, the acute phase of SAH has not been studied in comparable detail. In various experimental studies during the past decade, hypothermia has been shown to reduce neuronal damage after ischemia, traumatic brain injury and other cerebrovascular diseases. Clinically, only some of these encouraging results could be reproduced. This review analyses results of studies on the effects of hypothermia on SAH with special respect to the acute phase in an experimental setting. Based on the available data, some considerations for the application of mild to moderate hypothermia in patients with subarachnoid hemorrhage are given.
 ...
PMID:Hypothermia as a neuroprotective strategy in subarachnoid hemorrhage: a pathophysiological review focusing on the acute phase. 1584 6

Laser Doppler fluxmetry (LDF) and electrocorticography (ECG) are techniques used to indicate successful occlusion of the middle cerebral artery (MCAO) in the intraluminal filament model of ischemic stroke. However, each method has several advantages and drawbacks. This article describes a simple technique to simultaneously and continuously monitor LDF and ECG over both cerebral hemispheres. We investigated the potential of this method to improve the reliability of the filament model. Thirty male Sprague-Dawley rats were subjected to transient MCAO under three different experimental conditions (n=10 each group): MCAO in [A] normothermic animals, in [B] animals treated with hypothermia and in [C] animals receiving barbiturate for induction of burst suppression. Cortical blood flow was continuously recorded bilaterally by LDF and the electrocorticogram was continuously recorded over both hemispheres. The results show that monitoring of cortical electrophysiological activity by ECG allows detection of subarachnoid hemorrhage (SAH) during normal electrophysiological status and provides continuous control of barbiturate induced burst suppression as well as information about postischemic electrophysiological recovery. ECG did not detect MCAO, premature reperfusion, or SAH during burst suppression induced by barbiturates. In contrast, MCAO, SAH and premature reperfusion were rapidly indicated by LDF. Our findings suggest that simultaneous bilateral LDF and ECG during MCAO are of complementary value, in particular if barbiturates are investigated.
 ...
PMID:Simultaneous bilateral laser Doppler fluxmetry and electrophysiological recording during middle cerebral artery occlusion in rats. 1643 28

Neuroprotective activity with magnesium associated with animal models of cerebral ischaemia, seizure, perinatal hypoxia/ischaemia, subarachnoid haemorrhage and traumatic brain injury has provided the justification for clinical stroke trials. However, the recent IMAGES stroke clinical trial found magnesium to be largely ineffective. Hence, due to the negative stroke trial outcome, current FAST-MAG trial and our own experience with magnesium in cerebral ischaemia animal models, we thought it prudent to review these preclinical and clinical studies. We reviewed nine studies describing the use of magnesium following global cerebral ischaemia and fourteen following focal cerebral ischaemia. Four global ischaemia and six focal ischaemia studies did not show a significant neuroprotective effect with magnesium. In the majority of positive magnesium studies animal body temperature was not monitored post-ischaemia. Thus the effects of post-ischaemic hypothermia cannot be ruled out as a confounding factor in positive magnesium cerebral ischaemia studies. Moreover, data from our own laboratory indicates that magnesium is only neuroprotective when combined with post-ischaemic hypothermia. These data provide a possible explanation of why the IMAGES trial was largely unsuccessful, as current stroke patient management does not involve hypothermia induction. Future preclinical and clinical cerebral ischaemia trials with magnesium should consider combining treatment with mild hypothermia.
 ...
PMID:Is magnesium neuroprotective following global and focal cerebral ischaemia? A review of published studies. 1695 24

We report a case of subarachnoid hemorrhage (SAH) and carotid cavernous fistula (CCF) caused by Le Fort I osteotomy. A 16-year-old boy was scheduled to undergo Le Fort I osteotomy for a cleft lip and palate. After down fracture was completed, more than 1000 ml of bleeding was observed. When he became concious, we found anisocoria and imcomplete paralysis in the left side of his body. CT and angiography showed CCF and SAH to be present. After coil embolisation for CCF and therapeutic hypothermia had been performed, he recovered without severe neurological deficits. We should remember that unexpected mass bleeding in this surgery would suggest the incidence of intracranial vascular injuries.
 ...
PMID:[Subarachnoid hemorrhage as a complication of Le Fort I osteotomy]. 1724 49

Hypothermia is generally defined as a core body temperature less than 35 degrees C (95 degrees F), and is one of the most common environmental emergencies encountered by emergency physicians. A 32-year-old male hunter was admitted to the hospital with altered mental status. He remained unconscious, Glasgow Coma Scale (GCS) score was recorded as 5/15, and pupils were dilated and unreactive. His vital signs showed a heart rate of 48 beats/min, respiratory rate of 10 breaths/min, blood pressure of 95/50 mm Hg, and rectal temperature of 31 degrees C. An electrocardiogram (ECG) was obtained and showed marked sinus bradycardia and J waves. His finger-stick glucose was 85. He was intubated. After 3 h of active rewarming, his temperature was 34 degrees C, and the repeat ECG showed near-complete resolution of the J waves and acceleration of the sinus rate to 68 beats/min. At the same time, emergency head computed tomography (CT) scan showed subarachnoid hemorrhage (SAH) and subdural hemorrhage. The patient died on the third day of admission. In this case we want to indicate that J waves and obtunded state could be due to either SAH or hypothermia, and SAH could have been missed if initial obvious hypothermia had been believed to cause all symptoms.
 ...
PMID:The Osborn wave in accidental hypothermia. 1739 90

This report describes the clinical characteristics, treatment, and pathologic mechanisms of neonatal ultrahyperpyrexia syndrome induced by improper care. Clinical data on 14 cases of neonatal ultrahyperpyrexia syndrome induced by improper care were retrospectively analyzed. All 14 neonates had become comatose with ultrahyperpyrexia or hyperpyrexia; 8 of these patients twitched, 12 had high muscular tension, 2 exhibited low muscle tone, and 9 had respiratory dysfunction. Computed tomography revealed a patched, low dense shadow in the frontal and parietal lobes of the cerebral cortex in 9 patients; local cerebral hemorrhage occurred in 3 cases, and subarachnoid hemorrhage was reported in 2. After systematic treatment was provided, 13 neonates survived, but 1 died. Dysfunction of the neural, respiratory, and circulatory systems was the main pathologic mechanism noted in these cases of neonatal ultrahyperpyrexia syndrome induced by improper care. Early treatment, acute hypothermia, and supplemental fluids are the keys to successful therapy.
 ...
PMID:Fourteen cases of neonatal ultrahyperpyrexia syndrome induced by improper care. 1752 66

The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications.
 ...
PMID:Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis. 1754 22


<< Previous 1 2 3 4 5 6 7 8 Next >>