cardiovascular-agents and Brain-Edema

The management of severe head injuries in general and that of high intracranial pressure (ICP) in particular are among the most challenging tasks in neurocritical care. One of the difficulties still faced by clinicians is that of reducing variability among centers when implementing management protocols. The purpose of this paper is to propose a standardized protocol for the management of high ICP after severe head injury, consistent with recently published clinical practice guidelines and other clinical evidence such as that provided by the systematic reviews of the Cochrane Collaboration. Despite significant advances in neuromonitoring, deeper insight into the physiopathology of severe brain trauma and the many therapeutic options available, standardized protocols are still lacking. Recently published guidelines provide sketchy recommendations without details on how and when to apply different therapies. Consequently, great variability exists in daily clinical practice even though different centers apply the same evidence-based recommendations. In this paper we suggest a structured protocol in which each step is justified and integrated into an overall strategy for the management of severe head injuries. The most recent data from both the preliminary and definitive results of randomized clinical trials as well as from other sources are discussed. The main goal of this article is to provide neurotraumatology intensive care units with a unified protocol that can be easily modified as new evidence becomes available. This will reduce variation among centers when applying the same therapeutic measures. This goal will facilitate comparisons in outcomes among different centers and will also enable the implementation of more consistent clinical practice in centers involved in multicenter clinical trials.

Topics: Adrenal Cortex Hormones; Analgesics; Anticonvulsants; Brain Edema; Brain Injuries; Calcium Channel Blockers; Cardiovascular Agents; Case Management; Combined Modality Therapy; Craniocerebral Trauma; Critical Care; Electrophysiology; Evidence-Based Medicine; Fluid Therapy; Hemodynamics; Humans; Hypnotics and Sedatives; Intracranial Hypertension; Monitoring, Physiologic; Neuromuscular Nondepolarizing Agents; Practice Guidelines as Topic; Seizures

Organophosphorus exposure affects different organs such as skeletal muscles, the gastrointestinal tract, liver, lung, and brain. The present experiment aimed to evaluate the effect of escin on cerebral edema induced by acute omethoate poisoning. Sprague-Dawley rats were administered subcutaneously with omethoate at a single dose of 60 mg/kg followed by escin treatment. The results showed that escin reduced the brain water content and the amount of Evans blue in omethoate-poisoned animals. Treatment with escin decreased the levels of tumor necrosis factor-alpha (TNF-α), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and prostaglandin E₂ (PGE₂) in the brain. Escin also alleviated the histopathological change induced by acute omethoate poisoning. The findings demonstrated that escin can attenuate cerebral edema induced by acute omethoate poisoning, and the underlying mechanism was associated with ameliorating the permeability of the blood-brain barrier.

Topics: Acute Disease; Animals; Blood-Brain Barrier; Brain; Brain Edema; Cardiovascular Agents; Cyclooxygenase 2; Dimethoate; Dinoprostone; Escin; Insecticides; Matrix Metalloproteinase 9; Permeability; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha

We describe a postpartum woman who, after an uneventful pregnancy, developed posterior reversible encephalopathy syndrome after spinal anesthesia, complicated by postdural puncture headache.

Topics: Adult; Anesthesia, Spinal; Brain Edema; Brain Ischemia; Cardiovascular Agents; Cesarean Section; Diffusion Magnetic Resonance Imaging; Female; Humans; Magnesium Sulfate; Magnetic Resonance Angiography; Post-Dural Puncture Headache; Postpartum Period; Pregnancy; Syndrome; Treatment Outcome; Vasospasm, Intracranial

Topics: Acute Disease; Brain Edema; Brain Ischemia; Cardiovascular Agents; Case Management; Combined Modality Therapy; Decompression, Surgical; Fever; Humans; Hyperglycemia; Hypertension; Hypoxia; Intracranial Hypertension; Pneumonia; Thrombolytic Therapy; Urinary Tract Infections; Water-Electrolyte Imbalance

Recent studies indicate that centrally released arginine vasopressin (AVP) facilitates brain water permeability in normal and pathological conditions. The effects of central administration of arginine vasopressin (AVP) receptor antagonists on vasogenic brain edema were studied in rats. V1 or V2 receptor antagonists were stereotactically injected into the lateral ventricle 10 min prior to or 1 h after cold brain injury. The injury resulted in significant increases in the mean water content of the lesion and the contralateral hemispheres by 1.15 and 0.38%, respectively. Twenty-four hours after injury, the brain water and sodium contents, the brain swelling, and plasma osmolality were measured. V1 receptor antagonist of 50 ng significantly decreased the brain water and sodium contents and the brain swelling in the adjacent cortex of the lesion without changes in serum osmolality. On the other hand, 5 ng of V1 receptor antagonist and V2 receptor antagonist had no effect on edema. The V1 receptor of AVP is thought to act predominantly on water permeability of the brain. Peptide therapy may become an additional tool for brain edema treatment.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Blood Pressure; Body Water; Brain Chemistry; Brain Edema; Cardiovascular Agents; Cerebrovascular Disorders; Cold Temperature; Injections, Intraventricular; Male; Rats; Rats, Sprague-Dawley

Topics: Brain; Brain Edema; Cardiovascular Agents; Muscle Relaxants, Central; Neurosurgery; Neurosurgical Procedures