Idiopathic intracranial hypertension headache

Idiopathic intracranial hypertension (IIH) is a disorder of increased intracranial pressure that may have papilledema with normal imaging study results. Headache is the most frequent symptom. Although the headache characteristics are indistinguishable from the symptoms of migraine headache, accompanying symptoms of increased intracranial pressure, such as pulsatile tinnitus, transient visual obscurations, and radicular neck pain, may aid in the diagnosis. Magnetic resonance imaging, including venography, is essential for the diagnosis of the primary idiopathic intracranial hypertension. Medical treatment for the headache includes weight loss for obese patients, diuretic therapy, and migraine preventive medications. If medical therapy does not abolish the headache, surgical options should be considered. Because patients with IIH have a poor quality of life, patient education and supportive materials are important.     

Primer on medical management of severe brain injury

OBJECTIVE: To review the current understanding of the medical management of severe brain injury. DATA SOURCE: The MEDLINE database, bibliographies of selected articles, and current English-language texts on the subject. STUDY SELECTION: Studies related to management of intracranial hypertension, traumatic brain injury, and brain edema. DATA EXTRACTION: All studies relevant to the subject under consideration were considered, with a focus on clinical studies in adults. DATA SYNTHESIS: Basic rules of resuscitation must apply, including adequate ventilation, appropriate fluid administration, and cardiovascular support. The control of intracranial pressure can be considered in three steps. The first step should be initial slight hyperventilation with a target PaCO2 of 35 mm Hg and cerebrospinal fluid drainage for intracranial pressure of >15-20 mm Hg. The second step should be mannitol or hypertonic saline and hyperventilation to target PaCO2 of 28-35 mm Hg. The third step should be barbiturate coma or decompressive craniectomy. Additional management issues, including seizure prophylaxis, sedation, nutritional support, use of hypothermia, and corticosteroids, are also discussed. CONCLUSIONS: Brain injury is frequently associated with the development of brain edema and the development of intracranial hypertension. However, with a coordinated, stepwise, and aggressive approach to management, focusing on control of intracranial pressure without adversely affecting cerebral perfusion pressure, outcomes can be good.     

Benign intracranial hypertension.

Benign intracranial hypertension is a cause of progressive visual loss in children and young adults. Diagnosis is primarily clinical and requires radiographic exclusion of an intracranial mass and measurement of cerebrospinal fluid pressure. Treatment is directed at reducing intracranial pressure in idiopathic cases or correcting associated conditions. Carbonic anhydrase inhibitors, loop diuretics and steroids have been used for treatment. Adjunctive surgery may be indicated in cases of rapid vision loss or if medical treatment fails. Benign intracranial hypertension tends to be self-limited, with a course of less than 12 months in most cases.     

Cerebrospinal fluid physiology and the management of increased intracranial pressure

Increased intracranial pressure can result in irreversible injury to the central nervous system. Among the many functions of the cerebrospinal fluid, it provides protection against acute changes in venous and arterial blood pressure or impact pressure. Nevertheless, trauma, tumors, infections, neurosurgical procedures, and other factors can cause increased intracranial pressure. Both surgical and nonsurgical therapeutic modalities can be used in the management of increased intracranial pressure attributable to traumatic and nontraumatic causes. In patients with cerebral injury and increased intracranial pressure, monitoring of the intracranial pressure can provide an objective measure of the response to therapy and the pressure dynamics. Intraventricular, intraparenchymal, subarachnoid, and epidural sites can be used for monitoring, and the advantages and disadvantages of the various devices available are discussed. With the proper understanding of the physiologic features of the cerebrospinal fluid, the physician can apply the management principles reviewed herein to minimize damage from intracranial hypertension.     

Complex analysis of intracranial hypertension using approximate entropy

OBJECTIVE: To determine whether decomplexification of intracranial pressure dynamics occurs during periods of severe intracranial hypertension (intracranial pressure >25 mm Hg for >5 mins in the absence of external noxious stimuli) in pediatric patients with intracranial hypertension. DESIGN: Retrospective analysis of clinical case series over a 30-month period from April 2000 through January 2003. SETTING: Multidisciplinary 16-bed pediatric intensive care unit. PATIENTS: Eleven episodes of intracranial hypertension from seven patients requiring ventriculostomy catheter for intracranial pressure monitoring and/or cerebral spinal fluid drainage. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We measured changes in the intracranial pressure complexity, estimated by the approximate entropy (ApEn), as patients progressed from a state of normal intracranial pressure (<25 mm Hg) to intracranial hypertension. We found the ApEn mean to be lower during the intracranial hypertension period than during the stable and recovering periods in all the 11 episodes (0.5158 +/- 0.0089, 0.3887 +/- 0.077, and 0.5096 +/- 0.0158, respectively, p < .01). Both the mean reduction in ApEn from the state of normal intracranial pressure (stable region) to intracranial hypertension (-0.1271) and the increase in ApEn from the ICH region to the recovering region (0.1209) were determined to be statistically significant (p < .01). CONCLUSIONS: Our results indicate that decreased complexity of intracranial pressure coincides with periods of intracranial hypertension in brain injury. This suggests that the complex regulatory mechanisms that govern intracranial pressure may be disrupted during acute periods of intracranial hypertension. This phenomenon of decomplexification of physiologic dynamics may have important clinical implications for intracranial pressure management.     

Hypertension after brain injury: case report

Hypertension after brain injury requires comprehensive evaluation and management. Focal brain injury to centers of blood pressure regulation, high levels of circulating catecholamines from generalized trauma or intracranial lesions, increased intracranial pressure, pheochromocytomas unmasked after trauma, and occult spinal cord injury with hyperreflexia represent possible causes of hypertension after brain injury. This case of a brain-injured patient who had episodes of hypertension and diaphoresis with catecholamine elevations in plasma and urine, and evidence of hypothalamic-pituitary dysfunction, demonstrates the importance of a thorough neuroendocrine evaluation in brain-injured patients with hypertension. When high levels of catecholamines are found, without further evidence of a pheochromocytoma, treatment with a beta blocker is appropriate.     

Hyperosmolar therapy in the treatment of severe head injury in children: mannitol and hypertonic saline

Traumatic brain injury is the result of a primary, acute injury and is complicated by the development of secondary injury due to hypotension and hypoxia. Cerebral edema due to brain injury compromises the delivery of essential nutrients and alters normal intracranial pressure. The Monroe-Kellie Doctrine defines the principles of intracranial pressure homeostasis. Treatment for intracranial hypertension is aimed at reducing the volume of 1 of the 3 intracranial compartments, brain tissue, blood, and cerebrospinal fluid. Hyperosmolar therapy is one treatment intervention in the care of patients with severe head injury resulting in cerebral edema and intracranial hypertension. The effect of hyperosmolar solutions on brain tissue was first studied nearly 90 years ago. Since that time, mannitol has become the most widely used hyperosmolar solution to treat elevated intracranial pressure. Increasingly, hypertonic saline solutions are being used as an adjunct to mannitol in basic science research and clinical studies. Hyperosmolar solutions are effective in reducing elevated intracranial pressure through 2 distinct mechanisms: plasma expansion with a resultant decrease in blood hematocrit, reduced blood viscosity, and decreased cerebral blood volume; and the creation of an osmotic gradient that draws cerebral edema fluid from brain tissue into the circulation. The pediatric section of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies adapted previously published guidelines for the treatment of adult brain injury into guidelines for the treatment of children with traumatic brain injury. These guidelines offer recommendations for the management of children with severe head injury, including the use of mannitol and hypertonic saline to treat intracranial hypertension. Acute and critical care pediatric advanced practice nurses caring for children with severe head injury should be familiar with management guidelines and the use of hyperosmolar solutions. The purpose of this article is to assist the advanced practice nurse in understanding the role of hyperosmolar therapy in the treatment of pediatric traumatic brain injury and review current guidelines for the use of mannitol and hypertonic saline.     

新型隐球菌脑膜炎53例临床分析

目的总结分析新型隐球菌性脑膜炎的临床特征。方法分析53例新型隐球菌脑膜炎患者的临床表现、实验室检查、治疗及转归。结果新型隐球菌脑膜炎的临床表现以颅内压增高、脑膜刺激征为主。有基础性疾病者30例(占56．6%)。发病前有鸽子、禽类接触史者30例。脑脊液压力升高51例,其中49例超过200 mmH_2O。30例患者应用两性霉素B与氟康唑联合治疗。53例患者治愈4例,好转27例,死亡5例,自动出院17例。结论新型隐球菌性脑膜炎的主要临床表现是进行性颅内压增高。对进行性颅内压增高、脑膜刺激征阳性的患者反复进行脑脊液墨汁染色查新型隐球菌,有助于减少该病的误诊和误治。两性霉素B联合氟康唑静滴治疗隐球菌脑膜炎仍然安全、有效。     

Perioperative management of intracranial catastrophes

The management and evaluation of neurosurgical intracranial catastrophes require a multidisciplinary approach to optimize outcome. Intracranial pathology must be rapidly evaluated. Clinically, the patient's mental status, the degree and extent of focal neurologic deficits, and the dynamic nature of any changes in clinical status are assessed. The CT scan is invaluable for diagnosing and monitoring the progress and extent of intracranial pathology. Medical therapy for the control of intracranial hypertension must be undertaken simultaneously. This begins with provision of an adequate, protected airway and support of cardiopulmonary function. Specific measures to control intracranial hypertension include hyperventilation, osmotherapy, CSF removal, seizure control, autonomic control, sedation (primarily thiopental), muscle relaxation, mild hypothermia, and, if indicated, steroids. The goal of intraoperative management is physiologic support of systemic and cerebral hemodynamics. There should be a smooth transition from the discovery of the patient in extremis through the period of medical stabilization, operative intervention, and ultimate delivery of the patient to the intensive care facility for extended treatment.     

Compartment syndromes

Body compartments bound by fascia and limited by bony backgrounds are found in the extremities, buttocks, abdomen and thoracic cavity; conditions that cause intracompartmental swelling and hypertension can lead to ischemia and limb loss. Although compartment syndromes are described in all body regions from head to toe, the etiology, diagnosis, treatment, and prevention are best characterized for three key body regions: the first is extremity, the second is abdominal, and the third is thoracic compartment syndromes. Thoracic compartment syndrome usually occurs as a result of pathological accumulation of air, fluid or blood in the mediastinum and has traditionally been described in trauma. As the intracranial contents are confined within a rigid bony cage, any increase in volume within this compartment as a result of brain oedema or an expanding traumatic intracranial haematoma, leads to a reciprocal decrease in the volume of cerebrospinal fluid and intracranial venous blood volume. Limb compartment syndromes may present either in acute or chronic clinical forms. Intra-abdominal pressure can be measured by direct or indirect methods. While the direct methods are quite accurate, they are impractical and not feasible for routine practice. Indirect measurement is done through inferior vena cava, gastric, rectal and urinary bladder. Indirect measurement through urinary bladder is the simplest and is considered the method of choice for intra-abdominal pressure measurement. The management of patients with intra-abdominal hypertension is based on four important principles: the first is related to the specific procedures aiming at lowering intra-abdominal pressure and the consequences of intra-abdominal hypertension and abdominal compartment syndrome; the second is for general support and medical management of the critically ill patient; while the third is surgical decompression and the fourth is optimization after surgical decompression.     

Clinical review: Critical care management of spontaneous intracerebral hemorrhage

Intracerebral hemorrhage is by far the most destructive form of stroke. The clinical presentation is characterized by a rapidly deteriorating neurological exam coupled with signs and symptoms of elevated intracranial pressure. The diagnosis is easily established by the use of computed tomography or magnetic resonance imaging. Ventilatory support, blood pressure control, reversal of any preexisting coagulopathy, intracranial pressure monitoring, osmotherapy, fever control, seizure prophylaxis, treatment of hyerglycemia, and nutritional supplementation are the cornerstones of supportive care in the intensive care unit. Dexamethasone and other glucocorticoids should be avoided. Ventricular drainage should be performed urgently in all stuporous or comatose patients with intraventricular blood and acute hydrocephalus. Emergent surgical evacuation or hemicraniectomy should be considered for patients with large (>3 cm) cerebellar hemorrhages, and in those with large lobar hemorrhages, significant mass effect, and a deteriorating neurological exam. Apart from management in a specialized stroke or neurological intensive care unit, no specific medical therapies have been shown to consistently improve outcome after intracerebral hemorrhage.     

青岛地区中老年高血压人群的综合干预研究

目的研究高血压的综合干预措施,为高血压的防治提供依据。方法采用前瞻性的对照研究方法,对干预组实施包括标准化治疗、健康教育、血压管理在内的为期2年的综合干预措施,对比干预组与对照组的差别,率的比较采用卡方检验,均数比较采用t检验。结果研究发现干预组人群干预后高血压的控制率、血脂的达标率、BMI的达标率、高血压知识的知晓率均高于干预前及对照组(P0.05);干预组干预后人均门诊医疗费用增加1 254.6元/年(其中人均自付部分为307.2元),人均交通费增加90.0元/年,人均住院费降低3 389.7元/年,人均日常伙食费下降556.8元/年,与干预前及对照组比较,差异有统计学意义(P0.05)。结论针对中老年高血压患者采取综合干预措施可以有效地提高血压的控制率、血脂及BMI的达标率、高血压知识的知晓率,改善患者的生活方式。尽管综合干预增加了高血压患者的门诊费用和医疗相关的交通费,但也降低了住院费和日常伙食费,实际上减少了生活必须支出和医保支持,应当加强高血压患者的综合干预,加大相关投入。     

Intracranial pressure: dynamics and nursing management.

Patients suffering from traumatic or nontraumatic cerebral injury often develop intracranial hypertension. Accurate monitoring and prompt management are necessary to prevent deleterious and sometimes fatal effects of intracranial hypertension. This article reviews dynamics of intracranial pressure as well as compensatory and autoregulatory mechanisms. Essential management principles focusing upon prevention are presented to promote thorough and adequate nursing care for patients at risk for intracranial hypertension.     

SECONDARY HEADACHES

Background: The high pressures documented in the intracranial venous sinuses in idiopathic intracranial hypertension (IIH) could be the result of focal stenotic lesions in the lateral sinuses obstructing cranial venous outflow.
Objective: To explore the relation between venous sinus disease and IIH.
Methods: 12 patients with refractory IIH had dilatation and stenting of the venous sinuses after venography and manometry had shown intracranial venous hypertension proximal to stenoses in the lateral sinuses. Intrasinus pressures were recorded before and after the procedure and correlated with clinical outcome.
Results: Intrasinus pressures were variably reduced by stenting. Five patients were rendered asymptomatic, two were improved, and five were unchanged.
Conclusions: The importance of venous sinus disease in the aetiology of IIH is probably underestimated. Lateral sinus stenting shows promise as an alternative treatment to neurosurgical intervention in intractable cases.
Comment: This is one of the hot topics, that is, whether idiopathic increased intracranial pressure is usually due to a cortical sinus thrombosis, stenosis, or other anomaly. When more advanced techniques in magnetic resonance venography become more widely available and utilized, answers on the frequency of secondary idiopathic intracranial hypertension should become available. SJT     

Mechanical ventilation

The central goal in the management of a patient with acute encephalopathy and encephalitis is the prevention of hypoxemic of hypoxic secondary insults. It is recommended that partial pressure of arterial oxygen should be more than 80 mmHg with mechanical ventilation and supplemental oxygen. About carbon dioxide tension, it is standard practice to ventilate to normocapnia instead of routine setting of hypocapnia. Hyperventilation therapy is limited to specialized conditions with intracranial hypertension which is refractory to other therapy and induces neurological deteriorations. And it is presumed that increasing positive end-expiratory pressure could be related to increase intracranial pressure and decrease cerebral perfusion pressure in these patients especially with low blood pressure. To avoid unfavorable sequelae in brain, lung, and all other organs, we consider that under multimodal brain monitoring, ventilator setting should be decided on a case-by-case basis.     

Hypothermia for the management of intracranial hypertension in acute liver failure

Increased intracranial pressure in patients with acute liver failure remains a major cause of mortality. Treatment options are limited, and without urgent liver transplantation, mortality rates of up to 90% are common in those who fulfill criteria for poor prognosis. Several studies in animal models of acute liver failure set the stage for the clinical application of moderate hypothermia in humans. Few patients are treated with hypothermia for increased intracranial pressure. However, data indicate that moderate hypothermia is a safe and effective method of treatment for increased intracranial pressure that is unresponsive to other medical therapies, and that this treatment can be used as a successful bridge to liver transplantation. Recent data also suggest that increases in intracranial pressure can be prevented during the dissection and reperfusion phases of liver transplantation for acute liver failure if patients are kept hypothermic during the surgical procedure. This article focuses on the use of moderate hypothermia for the treatment of increased intracranial pressure in patients with acute liver failure.     

BLIND OVERNIGHT: A case of fulminant idiopathic intracranial hypertension

Idiopathic Intracranial Hypertension (IIH) is a syndrome seen predominantly in obese women of reproductive age group, characterized by signs and symptoms of increased intracranial pressure due to an unknown cause. Some individuals have a more malignant form of disease called fulminant idiopathic intracranial hypertension with rapid worsening of symptoms over days. We report a case of 33 year-old obese female (BMI 36.9) who presented with a severe headache and blurred vision for one week, found to have idiopathic intracranial hypertension with rapid worsening of symptoms suggestive of a fulminant course of disease. She was managed with prompt surgical intervention. In patients with fulminant idiopathic intracranial hypertension, surgery such as cerebrospinal fluid shunting or optic nerve sheath fenestration should not be delayed to prevent vision loss.     

Decreased adaptive capacity, intracranial: a proposal for a nursing diagnosis

A new nursing diagnosis is proposed related to failure of normal intracranial compensatory mechanisms manifested by repeated disproportional increases in ICP in response to noxious and nonnoxious stimuli. This diagnosis, decreased adaptive capacity--intracranial, occurs in patients with intracranial hypertension. It is not synonymous, however, with increased intracranial pressure (ICP). Rather, its use in the patient with intracranial hypertension allows the nurse to identify who is at high risk for disproportionate increase in ICP and decrease in cerebral perfusion pressure (CPP) secondary to ordinary activities of nursing care. The diagnosis can guide nursing management to reduce adaptive demands and increase adaptive capacity in those patients.     

Hypertonic saline,not mannitol,should be considered gold-standard medical therapy for intracranial hypertension

Hyperosmolar therapy is the principal medical management strategy for elevated intracranial pressure. Mannitol has been the primary hyperosmolar agent for nearly a century and remains the de facto gold standard for medical management of intracranial hypertension. Over the past 25 years, however, hypertonic saline (HTS) has become a progressively more common alternative to mannitol, and several recent studies have suggested its relative superiority. These findings have prompted calls for large-scale comparator trials of mannitol and HTS, but such trials would only be necessary if the designation of mannitol as the gold standard is appropriate and if current evidence suggests its therapeutic equipoise with HTS. Mounting evidence supporting HTS suggests that neither of these conditions is necessarily true and, instead, mandates reassessment of the actual gold-standard agent for hyperosmolar therapy. In the present article I make the case that current evidence supports HTS, not mannitol, as the better choice for gold-standard therapy for medical management of intracranial hypertension. This is accomplished first by examining the evidence on which the apparent designation of mannitol as the presumed gold-standard is based, then by reviewing the recent comparative efficacy data for HTS versus mannitol, and finanally by discussing additional clinical considerations for appropriate designation of a gold-standard agent for hyperosmolar therapy. This assessment has important implications both for patient care and for clinical trial design.     

“高血压俱乐部”对高血压的防治效果

目的探讨“高血压俱乐部”对高血压的防治效果。方法通过创建“高血压俱乐部”对高血压患者进行系统管理和教育。比较131例高血压患者加入“高血压俱乐部”前与加人后6个月动脉硬化程度[颈动脉一股动脉脉搏波速度（CF—PWV）]、用药依从性、血压控制率、生活方式中的不良行为及对医护人员满意度的变化情况。结果高血压患者加入“高血压俱乐部”后6个月CF—PWV值及生活方式中的不良行为均明显降低（P〈0．01）,用药依从性、血压控制率及对医护人员的满意度均明显升高（P〈0．01）。结论“高血压俱乐部”对高血压有较好的防治效果。