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April/June 2005, Volume :16 Number 2 , page 212 - 231 [Free]
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acute neurological injury,
critically ill child,
ICP management,
increased intracranial pressure,
neurological assessment
Increased intracranial pressure reflects the presence of mass effect in the brain and is associated with a poor outcome in children with acute neurological injury. If sustained, it has a negative effect on cerebral blood flow and cerebral perfusion pressure, can cause direct compression of vital cerebral structures, and can lead to herniation. The management of the patient with increased intracranial pressure involves the maintenance of an adequate cerebral perfusion pressure, prevention of intracranial hypertension, and optimization of oxygen delivery. This article reviews the neurological assessment, pathophysiology, and management of increased intracranial pressure in the critically ill child who has sustained an acute neurological injury.
Children may have increased intracranial pressure (ICP) for a variety of reasons. The most common etiologies of increased ICP in the pediatric intensive care unit (PICU) are due to severe traumatic brain injury (TBI), hydrocephalus, brain tumors, infections (ie, meningitis, encephalitis), metabolic encephalopathy, hypoxic/ischemic brain injury, cerebral infarction, and intraparenchymal blood due to a ruptured arteriovenous malformation or aneurysm. The mechanism by which ICP increases varies depending on the specific etiology (Table 1). The increased ICP can be due to either an increase in tissue volume, cerebral blood volume, or cerebrospinal fluid (CSF) volume. Examples of these are listed in Table 2. One or more of these factors occurring alone or simultaneously can increase ICP. The pathophysiology and management of increased ICP is based on the Monro-Kellie doctrine.
Intracranial pressure is defined as the total pressure exerted by the brain, blood, and CSF in the intracranial vault. The Monro-Kellie doctrine states that the cranium is a fixed vault made up of 3 components: the brain ([almost equal to]80%), blood ([almost equal to]10%), and CSF ([almost equal to]10%). When there is an increase in any one of these components, one or more of the other components must decrease to keep the total volume the same. The blood and the CSF are the only compartments that can compensate. The CSF compensates by displacing CSF from the ventricles and the cerebral subarachnoid space through the foramen magnum to the spinal subarachnoid space. The production of CSF can also be decreased, as well as the absorption increased, to decrease the total CSF. In addition, venous blood compensates by being displaced by the dural venous sinuses. For instance, if there is an intracranial mass (eg, brain tumor), the brain and the arterial volume will remain static while the CSF and the venous volumes will decrease until they can no longer compensate, at which point the ICP will increase (Figure 1).1 However, infants and children with open fontanels and sutures (usually less than 18 months old), may be able to compensate longer to chronic changes in the intracranial vault, but will still be susceptible to acute increases in ICP. It is crucial to understand the Monro-Kellie doctrine because management of increased ICP revolves around this basic principle.
Other key concepts of intracranial dynamics include autoregulation, compliance, cerebral blood flow, cerebral metabolic rate, and cerebral perfusion pressure (CPP). Autoregulation is the maintenance of a steady cerebral blood flow (CBF) by vasoconstriction and vasodilatation of the cerebral vessels despite fluctuations in systemic blood pressure. If autoregulation is impaired, CBF and cerebral blood volume (CBV) will become dependent on changes in systemic blood pressure. Compliance is an indicator of the brain's tolerance to increases in ICP. It is defined as a change in pressure resulting from a change in volume. Each patient has varying degrees of compliance even with similar injuries. The exact factors contributing to this are still unknown. When the patient's compliance is exhausted, there is a dramatic increase in the pressure/volume curve, leading to a rapid elevation in ICP.
In an uninjured brain, cerebral blood flow is regulated to supply the brain with adequate oxygen and substrates to meet its demands. The main physiologic influences on CBF are the partial pressure of arterial carbon dioxide (PaCO2), arterial oxygenation, pH, CPP, and cerebral metabolic rate. The PaCO2 is directly proportional to CBF and is the most potent chemical mediator of CBF. An increase in PaCO2 will cause vasodilatation, which will increase CBF and, thereby, potentially increase ICP. Likewise, acidosis and hypoxemia will also increase CBF by causing vasodilatation. CBF in excess of tissue demand will lead to hyperemia. Normal CBF in an adult is approximately 50-70 mL/100 g/min, and CBF of healthy children was found to be as high as 108 mL/100 g/min.2 CBF <20 mL/100 g/min is usually indicative of cerebral ischemia and has been associated with a poor outcome in children with TBI.3
Seizure activity and fever will increase CBF and cerebral metabolic rate. Methods to decrease the cerebral metabolic rate, such as hypothermia and barbiturates, will also decrease CBF. Cerebral metabolism is dependent on glucose to meet the body's energy demands. The brain functions via adenosine triphosphate (ATP) and the Krebs cycle to maintain aerobic metabolism. If there is hypoxia, the Krebs cycle cannot be activated and anaerobic metabolism will ensue. This will lead to the production of pyruvate and lactate, which will decrease the amount of ATP available for the cells and, thereby, decrease the amount of energy available.4
Cerebral perfusion pressure (CPP) is the pressure at which cells are perfused and is an important indicator of CBF. Sufficient CPP is necessary to prevent the development of secondary cerebral ischemia. CPP provides an indirect measurement of CBF and is calculated by measuring the difference between the mean arterial pressure (MAP) and the ICP as demonstrated by the following equation: CPP = MAP - ICP. Normal CPP values for children are not clearly established, but the following values are generally accepted as the minimal pressure necessary to prevent ischemia: adults CPP >70 mm Hg; children CPP >50-60 mm Hg; infants/toddlers CPP >40-50 mm Hg.5 Research has shown that a CPP <40 mm Hg is a significant predictor of mortality in children with TBI.6 Furthermore, in a study of 17 comatose children with severe central nervous system (CNS) infections, a CPP <30 mm Hg was associated with universal mortality.7
Normal ICP values are estimated at 2-6 mm Hg for infants and 3-7 mm Hg for young children. The normal ICP for older children and adults is 0-10 mm Hg.8 Intracranial hypertension is defined as an ICP >20 mm Hg for more than 5 minutes, although a lower number may be used for infants and young children. One suggestion for pediatric patients has been to maintain the ICP <20 mm Hg for children aged 8 years to adults, <18 mm Hg for children aged 1-8 years, and <15 mm Hg for infants.5
An ICP >20 mm Hg has been found to be a powerful predictor of poor neurological outcome in adults with TBI.9,10 ICP normally increases with activities such as suctioning, painful stimuli, and coughing and does not warrant intervention unless it does not return to baseline within about 5 minutes. However, interventions to minimize the ICP response to these activities, such as lidocaine prior to suctioning, should be instituted. It is important to distinguish "normal" or expected increases in ICP versus intracranial hypertension because the latter requires immediate intervention based on a tiered management approach.
In addition to the primary injury caused by TBI, a space-occupying lesion, or an intra-cerebral bleed, etc., cerebral edema is often a major cause of increased ICP. Cerebral edema can be categorized as vasogenic, cytotoxic, or interstitial. However, rarely does one occur in isolation; rather, the patient with cerebral edema may have a combination of all 3 mechanisms. Vasogenic cerebral edema is due to increased capillary permeability around the area of injury or inflammation. It can be local or diffuse and occurs around mass lesions (eg, brain tumors, abscesses, intracerebral hematomas) and inflammatory processes (eg, meningitis, encephalitis). Cytotoxic cerebral edema is due to cerebral ischemia and hypoxia, causing irreversible cell death. The cells affected may include neurons and astrocytes, and occurs in diffuse axonal injury, cerebral infarction, and near drowning. Interstitial cerebral edema is often seen in patients with obstructive hydrocephalus or excessive CSF production and is due to an increase in the hydrostatic pressure of CSF. Cerebral edema begins to occur immediately after TBI, intracerebral hemorrhage, and other cerebral insults, and increases for 72 hours post-insult.11
The initial assessment of the neurologically injured child consists of assessment of ABCs (airway, breathing, and circulation), Glasgow Coma Scale (GCS) score, cranial nerve function, signs and symptoms of increased ICP, temperature, and cardiorespiratory assessment. Astute observation of any abnormal respiratory patterns is crucial, since this may be the first vital sign change indicating neurological dysfunction. Abnormal respiratory patterns that may be detected include Cheyne-Stokes, central neurogenic hyperventilation, apneustic, ataxic, and cluster breathing. All, except for Cheyne-Stokes, indicate brain stem abnormality. Cheyne-Stokes is less specific and indicates a cerebral, cerebellar, or brainstem impairment.
The most ominous cardiorespiratory abnormality is Cushing's triad. Cushing's triad occurs when there is cerebral ischemia causing peripheral vasoconstriction. This vasoconstriction leads to increased systolic blood pressure to improve cerebral perfusion. Cardiac baroreceptors sense this increased blood pressure, resulting in a vagal response manifested as bradycardia. Abnormal or irregular respirations are the final component of Cushing's triad and occur due to brainstem compression. It is important to note earlier signs of increased ICP (see Table 3) because Cushing's triad is a very late sign in neurologically injured children and usually indicates impending herniation.
A thorough neurological assessment must be performed as soon as the child is clinically stable because this will serve as the baseline for comparison of future examinations. After the cardiorespiratory status has stabilized, the GCS is determined. It is important to utilize a modified GCS for infants and young children in order to obtain the most accurate score (Table 4). In a study of 151 children, a GCS < 8 twenty-four hours after TBI, in addition to factors such as hypoxia and cerebral edema, was associated with a poor outcome.12 To obtain the best response, it is necessary to give the patient the maximal stimulation-this may include giving painful stimuli such as mandibular pressure, sternal rub, or supraorbital pressure. These tests are optimal because they assess the central nervous system response, whereas fingerbed pressure assesses peripheral pain response.
Cranial nerve (CN) testing is next and begins with an assessment of CN III to determine direct and consensual pupillary response including size, reactivity, and shape of each pupil. It is imperative to be aware of medications that were administered that may affect pupil response (eg, atropine, narcotics). At least 10 seconds should elapse between each eye exam to allow the consensual response to fade. Abnormal pupillary responses include pupils that are unequal, constricted, dilated, nonreactive, or have hippus (Table 5). Hippus is the abnormal dilation and constriction of the pupil in response to bright light. It may indicate pressure on CN III and be associated with transtentorial herniation or it may be insignificant and represent a normal variant.
If the patient is awake, the 6 fields of gaze are assessed to determine extra-ocular movements (EOMs). If the patient is unresponsive, EOMs can be assessed by oculocephalic testing (Doll's eyes) and oculovestibular testing (cold calorics). However, if the C-spine has not been cleared, the oculocephalic test should be deferred. An abnormal response to oculocephalic testing (as you turn the patient's head side-to-side, the eyes remain fixed and do not rotate) may indicate injury to the midbrain or pons, or that the patient is in a deep coma. An abnormal response to oculovestibular testing (after irrigating each external auditory canal with iced water, the eyes do not deviate toward the side of irrigation with nystagmus) may indicate injury to cranial nerves III, VI, or VIII, or brain stem injury. The fundus is examined for papilledema. Although the presence of papilledema indicates increased ICP, its absence does not indicate the absence of increased ICP. The fundus is also examined for retinal hemorrhages, which may indicate child abuse, sagittal sinus thrombosis, or coagulation abnormalities.
Further cranial nerve testing in the unresponsive or intubated child should include eliciting a gag or cough reflex, and assessment of swallowing. Impairment in CN IX and X can greatly affect the child's ability to manage their oropharyngeal secretions and protect their airway. Cranial nerves and their functions are summarized in Table 6.
Motor assessment includes recognition of any abnormal posturing (eg, extension, flexion, flaccidity), muscle symmetry, strength, and tone. Flaccidity indicates severe dysfunction of the lower brain stem. Deep tendon reflexes are elicited to assess for central and peripheral nervous system dysfunction.
Abnormalities that are detected in the neurological exam must be correlated with the patient's previous examination, diagnosis, and radiologic findings. The location of a mass lesion or hemorrhage, or presence of mass effect or hydrocephalus must be assessed immediately to accurately diagnose and respond to impending herniation.
The radiologic study of choice for immediate assessment of the child with acute neurological impairment or deterioration is a noncontrast CT scan. A contrast CT scan may be necessary for further diagnosis of space occupying and vascular lesions, and infections, but is not warranted in the initial assessment of the child with increased ICP. On a noncontrast CT, highly dense structures, such as blood, will appear white, and low density areas, such as air, CSF, and edema, will appear black. Initial inspection of the CT scan should proceed with observation of any intracranial mass lesion, midline shift, skull fracture, presence of hemorrhage (extra-axial, intraparenchymal, or intraventricular), ventricular size, symmetry, and patency of basal cisterns (Figure 2). CT findings consistent with increased ICP include a mass lesion, intracerebral hemorrhage, midline shift, loss of sulci, ventricular effacement, and cerebral edema (Figure 3).
ICP monitoring is indicated for children with TBI whose GCS <8 or for children with other acute neurological injuries who have clinical signs of increasing ICP, are status post resection of acute traumatic intracranial hematoma or other major neurosurgical procedures, or have a neurodiagnostic test indicative of a high probability of increased ICP (ie, cerebral edema, midline shift, cisternal compression, intracerebral hemorrhage).13,14 Children who do not usually benefit from ICP monitoring are children with hypoxic injuries (ie, near drowning) and some central nervous system infections (ie, encephalitis).
Although ICP monitoring has never been subjected to randomized controlled studies to evaluate its effectiveness, its use has been associated with decreased morbidity and mortality, and improved outcome in patients with TBI, intracerebral hemorrhages, and CNS infections.15-17 It is not the monitor itself that improves outcome, but the information gleaned from this modality that guides appropriate interventions. ICP monitoring is crucial to identify rapidly increasing pressure and to institute appropriate therapy to prevent intracerebral herniation and preserve cerebral perfusion. It is also necessary to monitor ICP in order to calculate the CPP.
The current gold standard for ICP monitoring is intraventricular catheter placement, preferably an implantable microtransducer (fiberoptic or strain-gauge). This method allows simultaneous monitoring of ICP and management of increased ICP by CSF drainage. Other methods of monitoring ICP include intraparenchymal, subdural, subarachnoid, and epidural catheter placement-although the latter locations are very rarely used. Depending on the type of catheter, care will vary. ICP monitors with intracranial transducers are zeroed at the time of placement and therefore do not require any further zeroing. However, extracranial transducers require frequent zeroing and leveling because they must be adjusted with changes in patient position and recalibrated to atmospheric pressure.
In the past, children at risk for increased ICP were managed primarily with interventions to decrease their ICP and maintain an adequate CPP. This remains true, but the role of cerebral oxygenation and the ability to monitor it has recently been incorporated into the care of these children. Adjunct monitoring modalities utilized to prevent cerebral ischemia and optimize the patient's outcome include transcranial doppler (TCD) ultrasonography, jugular venous oxygenation saturation (SjvO2) monitoring, brain tissue partial pressure oxygen monitoring (PbtO2), non-invasive cerebral oxygenation monitoring, and brain metabolism monitoring.
As mentioned previously, CPP monitoring involves calculating the difference between MAP and ICP. CPP can also be assessed via xenon computed tomography (CT) scan, perfusion CT, perfusion magnetic resonance imaging (MRI), and positron emission tomography (PET) scanning. These modalities offer excellent information regarding regional CBF but are limited to one point in time. Continuous monitoring of CBF would be ideal and allow for interventions aimed at optimizing cerebral perfusion. For instance, if CBF were low, interventions would be directed at increasing vasopressor support or fluid therapy, or by decreasing cerebral demand by increasing sedation. If the patient were hyperemic, then methods to decrease the CBF, such as hyperventilation, would be instituted.18
CBF can also be evaluated via TCD ultrasonography, which non-invasively determines CBF velocity in the proximal vessels of the Circle of Willis. This is particularly helpful when assessing for vasospasm and stenosis in a child with a stroke. The adequacy of CBF related to cerebral metabolic demand can be assessed by SjvO2 and PbtO2. SjvO2 is a continuous measurement of the oxygen saturation in the jugular vein after cerebral perfusion has occurred. The jugular mixed venous saturation is compared to the arterial oxygen saturation, and the arteriovenous oxygen content difference (AVDO2) is then calculated. Normal SjvO2 is 55% to 70%; <55% indicates cerebral hypoperfusion; <40% indicates cerebral ischemia, whereas >75% indicates luxury perfusion and possible cellular death. Although SjvO2 is helpful in assessing cerebral oxygenation, a more direct approach is the measurement of partial pressure brain tissue oxygenation.
PbtO2 is a more specific method of measuring cerebral oxygenation via a microprobe inserted directly into parenchymal tissue or the penumbra of an intracerebral lesion. There is controversy regarding the optimal insertion area. Some advocate for placement in uninjured brain tissue to assess global cerebral oxygenation, while others opt for placement in the penumbra of an intracerebral lesion to obtain information of cerebral oxygenation for the area most at risk.19 Ideally, either method allows for continuous monitoring of cerebral oxygenation and early recognition of cerebral ischemia. The various types of catheters currently available (eg, Neurotrend [Diametrics Medical Limited, St. Paul, MN], LICOX [Integra Life Sciences, Plainsboro, NJ]) may yield different values and interventions should be adjusted accordingly. PbtO2 is a more specific method of measuring cerebral oxygenation via a microprobe inserted directly into parenchymal tissue or the penumbra of an intracerebral lesion. There is controversy regarding the optimal insertion area. Some advocate for placement in uninjured brain tissue to assess global cerebral oxygenation, while others opt for placement in the penumbra of an intracerebral lesion to obtain information of cerebral oxygenation for the area most at risk.19 Ideally, either method allows for continuous monitoring of cerebral oxygenation and early recognition of cerebral ischemia. The various types of catheters currently available (eg, Neurotrend, [Diametrics Medical Limited, St. Paul, MN], LICOX [Integra Life Sciences, Plainsboro, NJ]) may yield different values, and interventions should be adjusted accordingly. Using the LICOX catheter, normal PbtO2 values in uninjured parenchyma are >=20 mm Hg and interventions to improve cerebral oxygenation are indicated if the value is <15 mm Hg.20 For non-injured brain tissue, normal values are between 20 to 35 mm Hg. A decrease in partial pressure of brain tissue oxygen can be seen with decreased PaCO2, hypoxemia, increased ICP, and decreased CPP. Most of the available research on the utility of brain tissue oxygenation is from adult TBI patients. There are a few studies from adult patients with brain tumors, arteriovenous malformations, and stroke demonstrating that the additional information obtained from this modality is beneficial.19 A decrease in partial pressure of brain tissue oxygen can be seen with decreased PaCO2, hypoxemia, increased ICP, and decreased CPP. Most of the available research on the utility of brain tissue oxygenation is from adult TBI patients. There are a few studies from adult patients with brain tumors, arteriovenous malformations, and stroke demonstrating that the additional information obtained from this modality is beneficial.19
Noninvasive measurement of cerebral oxygenation can be done by near-infrared spectroscopy, which measures cerebral oxygen saturation via oximetry. This method has the advantage of being noninvasive and portable, but it is not commonly used in pediatrics.
Brain metabolism monitoring provides an individual assessment of brain chemistry after injury to guide treatment accordingly. Currently, it is not routinely used in most PICUs, but would allow for measurement of neurochemicals (ie, lactate, pyruvate, glucose, glutamate, urea, and glycerol) via an intraparenchymal microdialysis catheter.
Despite the etiology of the primary neurological injury, the main focus of management is to prevent and minimize secondary injury. Although primary injury and secondary injury most commonly refer to children with TBI, this terminology can also be applied to children with metabolic or hypoxic-ischemic encephalopathy and children with nontraumatic primary brain lesions, infections, and intracranial hemorrhage. The primary injury refers to the initial insult regardless of the mechanism of injury or illness. The secondary brain injury refers to the processes that occur within hours to days after the primary injury that can be prevented or minimized-such as cerebral ischemia, cerebral edema, and neurochemical alterations. Mitigating factors known to worsen secondary injury are hypoxia and hypotension.21 Other factors that may worsen secondary brain injury after TBI include the release of excitatory neurotransmitters, the formation of free radicals, and increased levels of intracellular calcium and potassium.4 The neurological devastation caused by the secondary injury is often worse than the underlying primary disorder. Therefore, management is directed at prevention of secondary injury.
Recently, recommendations on the management of increased ICP in children with TBI have been published.13,22 These recommendations are based on pediatric studies and extrapolated from adult TBI research. Since there are limited outcome studies to support the current management of children with increased ICP from etiologies other than TBI, this management is often instituted for these children also. A schematic of increased ICP management is provided in Figure 4. The reader is also referred to the "Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents"13 for an algorithm detailing escalation of therapy.
ICP management based on the Monro-Kellie doctrine includes interventions to decrease cerebral volume, control CSF volume, control CBV, and decrease cerebral metabolic rate (Table 7). The goal of these therapies is to maintain an age-appropriate CPP and an ICP <20 mm Hg or as appropriate for age. In adults with TBI, the maintenance of CPP >70 mm Hg is used in some centers based on research demonstrating that increasing the CPP, rather than decreasing the ICP, improves patient outcomes.23 However, there are limited data on the benefits of CPP-driven management in pediatrics,24 and it is not routinely implemented.
The initial management of the child with suspected increased ICP is assessment of airway, breathing, and circulation (ABCs). Even prior to a thorough neurological exam, if the patient is unarousable or having difficulty maintaining a patent airway, rapid sequence intubation should occur. Endotracheal intubation should also be considered if the child has a GCS <8, a CT scan consistent with diffuse cerebral edema, neurological injury at risk for decompensation, chest wall instability, abnormal respiratory pattern, loss of protective airway reflexes, or upper airway obstruction. Intubation should proceed with administration of medications to blunt the ICP during the procedure. Suggested medications to facilitate the intubation without increasing the ICP are thiopental, lidocaine, and a short-acting, nondepolarizing neuromuscular blockade agent (eg, vecuronium, atracurium).
Adequate oxygenation is necessary to prevent the sequelae of secondary insults and should be maintained with a PaO2 > 60 mm Hg, an oxygen saturation >90%, and physiologic positive end expiratory pressure (PEEP) of 5 cm H2O. Increasing the PEEP to 10 cmH2O has not been associated with a worse neurological outcome. The deleterious effects of hypoxemia are more significant than the possible venous congestion caused by PEEP >5 cm H2O.25,26
Age-appropriate blood pressure must also be maintained or restored to ensure adequate CPP and prevent further ischemia. The avoidance of hypotension is crucial since it has been associated with increased mortality in children with TBI.21,27-30 Hypotension in children is defined as systolic blood pressure below the fifth percentile for age or by clinical signs of shock.13 Median systolic blood pressure (50th percentile) can be estimated by using the following formula for children greater than 1 year of age: 90 + (2 x age in years).31 Children in hypovolemic shock can compensate fairly well and may not become hypotensive until they become profoundly hypovolemic. Other signs of decreased perfusion and shock include tachycardia, decreased urine output (<1 mL/kg/hr), weak/thready/absent peripheral pulses, prolonged capillary refill time (>2 seconds), and/or decreased mentation. Fluid boluses are administered as needed to the hypotensive child. The neurologically injured child must be fluid resuscitated the same as any other child presenting in shock. There is no indication for fluid restriction. Vasopressor support is initiated if the child remains hypotensive despite appropriate fluid resuscitation.
The patient's head is positioned midline to encourage jugular venous drainage and the head of the bed is elevated to 15[degrees] to 30[degrees]. These methods have been found to be effective in decreasing intracranial pressure and optimizing CPP in adult patients with TBI.32-34 Both increasing the head of the bed beyond 30[degrees] and decreasing the head of the bed below 15[degrees] have been associated with increased ICP and/or decreased CPP.33,35 In another study,36 CPP was found to be optimal with the bed in a flat position; however, ICP increased. A study of adult patients with cerebral lesions (ie, tumors, infections) recommended supine flat position due to a linear decrease in CBF with head of bed increased to 45[degrees].37 However, if ICP was elevated and CBF was normal or increased, positioning the head of bed 30[degrees] was recommended.37
Based on the available literature, the child's head should be maintained midline to prevent impairment in drainage from the external jugular veins and the head of bed should be maintained at 30[degrees] with alterations based on the child's response. The child must be euvolemic prior to placing in this position to avoid orthostatic hypotension.
CSF drainage provides an immediate, but transient, decrease in ICP due to reduction in CSF.38 Depending on the patient's status, it can be done either continuously or intermittently. The optimal method of continuously monitoring ICP and draining CSF simultaneously is via a ventriculostomy catheter. There is limited research on the effect of CSF drainage on ICP, CPP, CBF, and metabolic rate. One pediatric study39 revealed that children undergoing ventricular drainage had decreased ICP and improved outcome. Another study40 in adults compared ventricular drainage to mannitol and found that both treatments decreased ICP.
For refractory intracranial hypertension, lumbar drainage may be considered if the basal cisterns are open, and there is no evidence of midline shift or a significant mass lesion on neuroimaging.41
Mannitol has been a cornerstone of intracranial hypertension management for decades, but has not been compared to a placebo in randomized controlled studies. Its efficacy has been evaluated by comparison to other existing therapies for intracranial hypertension. When mannitol was compared to CSF drainage, it was found to be more effective in the management of increased ICP in adults with TBI.40 Boluses of mannitol were also found to be more effective than a continuous drip.42 Some have argued that administration of mannitol on a standard dosing regimen (eg, every 2 hours), instead of as needed for ICP >25 mm Hg, provides better ICP control.43
Mannitol has two mechanisms of action: (1) an osmotic diuretic that produces an osmotic gradient, drawing fluid from the brain tissue into the vascular space to be excreted via kidneys and (2) a rheological effect that decreases blood viscosity and hematocrit and increases CBF and cerebral O2 delivery.22 The rheologic effect occurs immediately and is responsible for decreased ICP within minutes of administration. This occurs due to increased plasma volume, which decreases blood viscosity and hematocrit, and increases CBF and cerebral oxygen delivery that leads to vasoconstriction and decreased ICP. The osmotic diuresis develops more slowly and lasts up to 6 to 8 hours. As such, mannitol is usually given as a bolus every 4 to 6 hours since its osmotic effect occurs 15 to 30 minutes after administration and its duration of action is 2 to 8 hours. Autoregulation of CBF must be intact for the effects of mannitol to work; however, autoregulation is often disrupted in brain injured patients.
Recently hypertonic saline (HS) administration has been shown to decrease ICP and improve outcome in pediatric TBI patients. 44-47 Hypertonic solutions have the advantage of decreasing ICP and decreasing cerebral volume by producing an osmotic gradient in the brain, while also supporting intravascular volume. Pediatric studies in children with TBI have found that HS is effective in decreasing ICP and improving CPP with no adverse reactions, including children with refractory intracranial hypertension.44-47 Hypertonic saline has also been reviewed in children with diabetic ketoacidosis and presumed cerebral edema. The use of 10 mL/kg bolus dosing of HS was found to correlate with an improvement in the child's GCS and level of consciousness.48 HS is usually administered as a continuous infusion, starting at 0.1 to 1.0 mL /kg/hr. Serum sodium and neurological status must be closely monitored during therapy due to the possibility of osmotic demyelination syndrome (central pontine myelinosis), which can occur with a rapid increase in serum sodium. 49 This destruction of the white matter, often to the pons, can cause significant neurological devastation due to rapid osmotic shifts. In addition, the formation of organic osmolytes (idiogenic osmoles), which are osmotically active molecules that accumulate intracellularly in the brain during hyperosmolar states to maintain cerebral volume and prevent cellular dehydration, may contribute to cerebral edema upon abrupt discontinuation of hyperosmolar therapy. As such, when HS therapy is no longer indicated, serum sodium should be slowly corrected to normal values (0.5 to 1.0 meq/L/hour) to avoid complications associated with osmotic shifts. Other potential complications of HS therapy include rebound increase in ICP50 and renal insufficiency.44 In addition to decreasing cerebral edema, advantages of HS may include improved hemodynamic status by expansion of plasma volume, as well as vasoregulatory effects and immune modulation that may contribute to prevention of secondary injury.49
Regardless of which osmotic therapy is instituted, the patient must be maintained euvolemic with an indwelling catheter measuring urine output throughout therapy. Maintenance and bolus intravenous fluids are administered to maintain euvolemia. Serum osmolality must also be monitored to prevent renal tubular dysfunction. With mannitol, the maximum recommended serum osmolality is 320 mOsm/L. However, a serum osmolality of 365 mOsm/L has been well tolerated in children receiving HS.44,45 It is unclear whether this disparity is due to inherent differences between mannitol and HS, current management aimed at euvolemia versus fluid restriction, or differences between adults and children with regard to nephrotoxicity susceptibility.13 Recently, some concern was expressed regarding increased renal dysfunction when serum sodium is > 160 meq/L in euvolemic children with intracranial hypertension;51 however, these findings have not been reported in randomized controlled trials.
In the past, prophylactic hyperventilation was a mainstay of therapy for increased ICP management. It was thought that children after TBI were hyperemic, which led to cerebral edema and increased ICP and that hyperventilation decreased CBF and improved outcome.52 However, the role of hyperemia was challenged when a study2 revealed that children normally have higher resting CBF than adults, not just children after TBI. Further studies3,53 revealed that children may actually have decreased CBF after TBI.
Hyperventilation was employed to decrease ICP by causing vasoconstriction, which decreased CBF and CBV. However, recent studies have demonstrated that aggressive hyperventilation dramatically decreases CBF, which may give rise to or exacerbate cerebral ischemia, thus enhancing rather than decreasing secondary injury.54-57 Patients that have received hyperventilation have also been found to have a worse outcome.58,59
Hyperventilation is currently only recommended in the initial management of increased ICP for acute, significant increases in ICP.60,61 It is not recommended for prophylactic treatment of increased ICP because of the potential for worsening cerebral ischemia. Furthermore, it depletes the brain tissue interstitial bicarbonate buffering capacity, which may lead to a loss of local vasoconstrictor effects.62 Normally, alkalosis causes arteriolar constriction, but with loss of this buffer system, it can no longer respond appropriately and may not cause vasoconstriction to decrease CBF. Mild hyperventilation (PaCO2 30 to 35 mm Hg) may be implemented if increased ICP continues despite CSF drainage, appropriate sedation and analgesia, head position, and osmolar therapy. Significant hyperventilation (PaCO2 <30 mm Hg) should be reserved for patients with refractory intracranial hypertension unresponsive to initial therapies.58 Intermittent hyperventilation should be instituted for acute, sharp increases in ICP or signs of impending herniation.63,64
Maintaining the patient normothermic (T = 37[degrees]C) is the goal to prevent complications of both hypothermia (T <35[degrees]C) and hyperthermia (T >38.5[degrees]C). Patients who have acute neurological injury may have temperature fluctuations due to infection, sepsis, intracranial blood, and hypothalamic disturbances. A core temperature greater than 37.5[degrees]C is associated with increased ICP and increased cerebral metabolic rate of oxygen. In experimental models of brain injury, hypothermia has been found to be neuroprotective by decreasing cerebral metabolism, extracellular glutamate release, mobilization of calcium, production of free radicals, and nitric oxide synthesis.65 However, in studies of adults with TBI, hypothermia has been associated with increased systemic complications and no improvement in patient outcomes.66-68 Potential side effects of hypothermia include increased risk of pneumonia, skin breakdown, electrolyte imbalances, hypotension, coagulopathy, and shivering.
Given the potential benefits of hypothermia, moderate hypothermia (33[degrees]C) has been researched for its role in the management of increased ICP. Adult studies have shown that moderate hypothermia may improve outcome.69,70 Recently, very mild hypothermia (35-35.5[degrees]C) was studied65 in adult head injured patients and was found to decrease intracranial hypertension and maintain sufficient CPP. This study65 also found that decreasing the body temperature below 35[degrees]C did not improve intracranial hypertension and actually decreased CPP. A recent pediatric study71 instituted moderate hypothermia within 6 hours of TBI and continued it for 48 hours. This study71 demonstrated a decrease in the severity of intracranial hypertension and was tolerated without any side effects, although there was no significant difference in mean ICP and CPP.
Children with increased ICP should be normothermic with interventions aimed at prevention of fever and shivering. Ideally, core or brain temperature is measured. Core temperatures can be measured via a Swan Ganz catheter or a bladder or rectal probe. Brain temperature can be monitored via SjvO2 or PbtO2 catheters. Moderate hypothermia is reserved for children with refractory intracranial hypertension not responsive to initial therapies. Upon discontinuation of hypothermia treatment, the patient must be rewarmed slowly to prevent complications, such as electrolyte imbalances (particularly potassium), an increase in cerebral edema, acidosis, and hypotension.
Children with acute brain injury who are mechanically ventilated should be appropriately sedated and receive adequate pain management to prevent pain and anxiety, which will increase the cerebral metabolic rate and ICP. There are no randomized controlled studies comparing sedation methods in children with acute neurological injury. The most common agents used are opiods, benzodiazepines, and/or barbiturates. Administration of neuromuscular blockade agents (NMB) may be necessary to facilitate mechanical ventilation and control PaCO2, prevent shivering, and prevent movement that may increase ICP. Use of NMB will limit physical examination findings of increased ICP to assessment of the pupillary response; no other assessments will be accurate while the patient is pharmacologically paralyzed. An ICP monitor is usually necessary in these patients. Additional monitoring may include the Bispectral Index (BIS) to provide an objective measure of cerebral electrical activity and assign a numerical value to the level of sedation.
Since the use of NMB will eliminate motor activity associated with seizures, but not brain epileptiform activity, children at high risk for seizures may require continuous electroencephalograph (EEG) monitoring. Indications for NMB must be weighed against obscuring the neurological examination, as well as a possible increase in patient complications. In a study of adults with TBI,72 the use of NMB was associated with increased intensive care unit (ICU) length of stay and nosocomial pneumonia.
Children who have sustained a significant head injury are more likely than adults to have seizures, possibly due to their lower seizure threshold.13 Patients with GCS <8 have an increased risk of early seizures after TBI.73 If the child presents with seizure activity, initial treatment with a benzodiazepine (eg, lorazepam) and/or phenytoin (or fosphenytoin) should be instituted, followed by anti-epileptic medication (eg, phenytoin, fosphenytoin) for at least 2 weeks. The etiology of the seizure (ie, temporal lobe tumor, intraparenchymal bleed) and the patient's clinical status will ultimately determine the duration of antiepileptic treatment.
Children who have significant parenchymal injury after TBI or are less than one year old are at increased risk of seizure activity and should be considered for seizure prophylaxis to prevent early posttraumatic seizures.13 In children with TBI, seizures most commonly occur within the first 24 hours after injury.5 Regardless of the seizure etiology, seizure activity must be terminated immediately in the child with increased ICP. Seizures increase the metabolic rate, which will increase CBF and CBV leading to an increase in ICP. If the metabolic demands exceed the supply, cerebral ischemia will ensue, leading to irreversible neurological damage.
There is limited research on the use of anti-epileptic medications after traumatic brain injury. Studies in adults have shown that anti-epileptic medications for long-term prophylaxis did not improve outcome74 and are only effective in the first week after TBI to decrease the incidence of early onset seizures.75 In children, anti-epileptic medications are recommended for short-term use, unless deemed otherwise by the child's seizure activity.
The administration of high dose barbiturates (eg, pentobarbital) is reserved for intracranial hypertension refractory to the aforementioned interventions. Barbiturates decrease ICP by decreasing cerebral metabolic rate, which decreases glucose utilization and oxygen demand, but may cause significant hemodynamic instability. Although there are limited pediatric studies examining barbiturate effectiveness and role in outcome, some studies have shown that intractable ICP may improve and in some lead to a good outcome.76 However, many patients require vasopressor support during therapy.77 Adult studies have also reported pentobarbital as an effective treatment to decrease ICP.78 However, some have shown no benefit in outcome,79 while others have shown an association with worse neurological outcome due to jugular venous desaturation.80
Monitoring of the child in a barbiturate coma should include burst suppression via EEG, invasive hemodynamic monitoring (eg, arterial blood pressure, central venous pressure, SjvO2), and frequent assessment of oxygenation status. Because of the significant side effects of barbiturate therapy and the limited data supporting its use, barbiturate therapy is only recommended for children with refractory intracranial hypertension.
Initial surgical management includes the immediate evacuation of a mass lesion (eg, brain tumor, epidural hematoma) and placement of ICP monitor as indicated, preferably a ventriculostomy. Decompressive craniectomy to increase intracranial compliance is reserved for patients with refractory intracranial hypertension, although some studies81,82 have advocated its use early after TBI before secondary injury occurs.
The use of corticosteroids is not indicated in the management of increased ICP after TBI. However, steroids may be indicated in decreasing swelling and stabilizing the cell membrane in patients with increased ICP due to mass lesions, such as brain tumors and abscesses, inflammation, and infections.
The main goals of fluid therapy are to maintain the patient euvolemic, normoglycemic, and prevent hyponatremia. In a recent pediatric study83 of 170 children with TBI, mean serum glucose >200 mg/dL was associated with poor neurological outcome, and serum glucose >300 mg/dL on admission was associated with 100% mortality. Although the exact mechanism of hyperglycemia after TBI is multifactorial and not completely understood, the detrimental effects of hyperglycemia on the injured brain have been repeatedly demonstrated.83-86 Current treatment in adults with TBI includes stringent glycemic control with insulin therapy.
Parenteral dextrose is avoided for at least 48 hours after acute neurological injury due to the increased risk of lactic acidosis, unless the patient is hypoglycemic-which requires prompt treatment. Enteral feedings may and should be instituted within 72 hours after injury. Early enteral feeding in adult patients with TBI has been associated with a dramatic decrease in ICU days and complications.87 Children with TBI have been found to have caloric needs 30%-60% greater than their basal metabolic expenditure88,89 and should be supplemented accordingly with the appropriate formula and rate. Unless contraindicated, the preferred method of delivering nutrition is via the enteral route. Due to potential impairments in the protective airway reflexes, it may be prudent to administer feedings via a postpyloric feeding tube to decrease the risk of aspiration.
Children with increased ICP should receive fluids at a daily maintenance rate, as well as fluid boluses as indicated for hypovolemia, hypotension, or decreased urine output. Since dextrose is usually avoided for the first 48 to 72 hours after injury, maintenance fluids usually consist of normal saline with the daily requirements of potassium chloride based on body weight. All fluids administered must be isotonic or hypertonic (eg, hypertonic saline) and hypotonic fluids must be avoided. In addition, hyponatremia must be prevented since it will worsen cerebral edema. If hyponatremia occurs, it must be corrected slowly to prevent central pontine myelinosis that can occur with rapid correction of sodium.
In addition to the nursing and medical interventions outlined above, care of the child and family is an important component in providing optimal patient care. In pediatrics, the child is cared for within the context of the family, and the child with increased ICP is no exception. It is important to encourage the caregivers and siblings (as appropriate) to touch and speak to the child. Studies in children and adults have found that ICP did not increase significantly or actually decreased with family presence90,91 or with physical touch.92,93 During these interactions, the child's ICP and hemodynamic status are monitored and care modified accordingly for any significant change.
There is limited research on whether clustering patient care activities (ie, bathing, suctioning, procedures, etc.) or providing rest periods in between activities is more beneficial to the patient.91,93,94 It is recommended to monitor the patients ICP, MAP, heart rate, central venous pressure, and CPP and continue or abort care accordingly. Additional sedation and analgesia should also be provided prior to any procedure that may cause pain, anxiety, or increased ICP, although the research in this area is lacking.
Research on the use of lidocaine prior to endotracheal suctioning to attenuate the ICP response in pediatric patients is scant and dated. Based on the available research, lidocaine (via endotracheal tube or intravenously) is usually recommended prior to suctioning to blunt the ICP response.95-97 One study95 demonstrated a more significant suppression of ICP elevation with 2 mL of 4% lidocaine administered intratracheally due to its anesthetic effect on the tracheobronchial mucosa. Lidocaine 1.5 mg/kg is the recommended dose for IV administration prior to suctioning.97,98 Regardless of the method of administration, the patient's response must be monitored and care adjusted accordingly.
Neuro-critical care of children with increased ICP revolves around the basic tenet of the Monro-Kellie doctrine and aims to decrease one or more of the intracranial compartments. The goal of management is to control CSF volume, brain volume, and blood volume. This control is achieved by proper patient positioning, normocarbia, CSF drainage, euvolemic osmolar therapy, sedation and analgesia, optimal cardiorespiratory status, normothermia, and seizure prophylaxis based on the patient's condition and response (Table 8). Implementation of hyperventilation, moderate hypothermia, and barbiturate therapy is reserved for patients with refractory intracranial hypertension. The best neurological outcome is associated with control of ICP <20 mmHg (or age appropriate) and a CPP >50 (or age appropriate), as well as prevention of hypoxia and hypotension. Much research is still needed to optimize management strategies for children with acute increased intracranial hypertension, particularly nursing interventions that may ultimately improve patient outcomes.
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Cross the dream of flight off your bucket list with a tandem skydive! At Skydive Awesome!, we feel your first skydive should be more than just a joy ride, and believe in a higher level of personalized service. You deserve to experience what it feels like to fly as a skydiver! From the moment you arrive until the time you leave we truly hope you depart feeling you're part of our awesome skydiving family!
Tandem Level I Skydive: $200
Video and Pictures : $75
Tandem Level II Skydive: $200
(If you do your Tandem Level I with us, you can get your Tandem Level II for $175).
Group Discounts:
- Requires reservation with deposit ($25 per person)
- 6-9 people: $10 off each tandem skydive
- 10 or more people: $20 off each tandem skydive
(May not be combined with any other promotional offers.)
Military Discount
- $20 off any tandem skydive
- Must have valid US Military issue ID
(May not be combined with any other promotional offers.)
Your first Tandem Skydive includes:
- Personalized instruction from one of our certified tandem instructors where you'll learn the correct body position for aircraft exit and freefall.
- A scenic flight to altitude with a bird's eye view of the Cascade Mountain peaks including the Three Sisters and Mt Hood.
- Approximately 45 seconds of freefall from 10,000 feet.
- A sensational 5-7 minute scenic parachute flight from 5,000 feet above Sisters, Oregon.
- A first jump certificate.
Video and Pictures package information:
- Your video and pictures will include footage of you geared up, including loading the plane, your ride to altitude, aircraft exit, freefall, your parachute flight, ending with your awesome reaction once you've returned to Earth.
- Videos of your entire experience.
- Pictures and videos shared on Google Drive.
Your Tandem Level II skydive:
- Your instructor will provide you with an altimeter.
- You will be educated about freefall body position, altitude awareness, practice parachute deployment handle touches, and parachute deployment. You and your instructor will follow a specific freefall dive flow and perform those maneuvers in the sky.
- You will be educated about parachute piloting by practicing altitude awareness, parachute control check, heading control, and parachute landing. You and your instructor will follow a specific parachute dive flow and perform those maneuvers in the sky.
Important information:
- Must be 18 years old (No exceptions) with a valid photo ID (driver's license, military, passport).
- There are some physical limitations to skydiving. Some individuals may require instructor and/or doctor approval to jump. Please contact us for additional information.
- Some medical conditions may prohibit your participation in skydiving. Please consult your doctor and/or call our staff before you arrive if you have any concerns.
- Students over 200lbs please contact us for additional information.
- Wear casual, seasonal-appropriate clothing. You can choose to put on a provided jumpsuit to wear over your clothes.
- Wear close-toed shoes with no hooks to hold the shoe laces. Please do not wear heels or sandals.
- You will not be allowed to jump if under the influence of drugs or alcohol.
- Contacts and glasses are ok, we have special goggles to fit over glasses.
- Reservations are recommended (required for groups larger than 6).
- Walk-ins are welcome, however our reservation schedule fills up, a wait could be expected.
- We require a credit card to hold a reservation. A $50 fee will be charged if you fail to cancel or show up.
- You may cancel your appointment up to 24 hours in advance at no charge.
- Your reservation time is your arrival time. On average your whole experience takes about 2-3 hours.
- We fly a Cessna 182 that can take 2 tandems at a time. It's not the size of the plane that matters, it's how you use it!

subset: commoncrawl


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This resource is no longer available
Dell EqualLogic: Scale-Out Storage for a Virtualized World
In this exclusive ESG report, examine how your organization can leverage cost-effective scale-out storage to combat the ever increasing demands of your virtual environment. Learn about the key storage challenges organizations face today, and the pros and cons of adopting scale-up versus scale-out storage in your data center. Explore the unique features of a scale-out storage platform, including:
- Single shared storage service to hosts and applications with a single management view
- Scales seamlessly from small to very large configurations without impacting business operations
- Automates repetitive management tasks such as RAID configuration and sparing
- And more


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From direct care staff to program managers to clinicians, our employees make a difference every day. Our talented team helps individuals with intellectual and developmental disabilities thrive in the communities they call home. And as part of The MENTOR Network— a national network of local health and human services providers—REM's employees are part of a growing organization that's been at the forefront of providing innovative, community-based care for more than 30 years
CaregiverApply Now Job ID 17000N0U
Primary Location: United States-MN-MNApple Valley
Function:Direct Support Professional (Care Givers)
REM River Bluffs has Part-time, Overnights (Asleep or Awake), and weekend shifts available throughout the Apple Valley area.
REM River Bluffs is a great place to gain experience in: Human Services, Social Work, Psychology, Nursing, Alcohol and Drug Counseling, Education, Sociology, Criminal Justice, or Mental Health. If you are looking for CNA, DSP, or PCA experience, this is the job for you!
Whether you have previous experience in a role like this, or this just sounds like the type of impact you want to make… we want to hear from you! Join our team as a Caregiver/Direct Support Professional today! We have openings in Lakeville, Burnsville, Shakopee, Prior Lake, Eagan, South St Paul, and Rosemount.
Bring the right attitude; we'll train you for success!
REM Minnesota offers:
Flexible, consistent schedules. Full and Part time schedules available
A rewarding work environment with some of the best co-workers you could ask for
Family-oriented environment, casual dress, employee events
A chance to make a difference in people's lives on a daily basis
Competitive pay rates, paid time off, and benefits for 30+ hour work week
Paid training; Holiday pay
Career development, and advancement opportunities throughout the nation-wide Network
Access to employee discounts with various vendors
A dynamic work environment where no day is ever the same as the next
By joining the REM Minnesota team as a Caregiver/Direct Support Professional (DSP), you will work with individuals with a range of challenges including intellectual and developmental disabilities, severe and persistent mental health, children's behavioral health and individuals with medically complex challenges. You will work to restore and retain basic health functioning, independent living and community skills.
We offer residential services with supports tailored to the needs of each individual, including assistance with daily activities such as meal preparation and planning; medication administration; and personal cares. DSPs may also facilitate community involvement by accompanying individuals on outings in their community or providing transportation to work or other activities. In addition, DSPs support therapeutic and behavioral plans in partnership with clinical staff to encourage individuals to be as independent as possible and enhance the quality of life for those we support.
Must be 18 years of age
Valid driver's license in good standing
Successful clearance of local and/or state background checks
REM Minnesota is a partner of The MENTOR Network, a national network of local human services providers offering quality, community-based services. With ~30,000 employees serving ~30,000 people in 36 states, you'll have career opportunities from coast to coast. When you join The MENTOR Network, you'll make a difference every day and help to provide quality of life enhancing services to individuals across the country.
Come join our team of dedicated and caring professionals. Apply Today!


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Conference hears of progress in HIV/AIDS fight
HIV/AIDS researchers have announced progress towards new ways of treating and preventing infection, and have found some new clues to the virus's origins.
The findings were presented last week at the 13th Conference on Retroviruses and Opportunistic Infections in Denver, United States.
Researchers described how a candidate drug called MK-0518 substantially reduced virus levels in 80 per cent of HIV-infected people in a trial in Brazil.
In another study, a drug called tenofovir, which is already used to treat people with HIV, is being combined with another called FTC to see if it can also protect people from being infected in the first place.
The conference also heard new evidence supporting the theory that HIV evolved from the simian immunodeficiency virus that infects chimpanzees (SIVcpz).
Earlier research had suggested this but too few infected chimpanzees were found to investigate it further. Now, researchers have discovered that there are more than 30 strains of SIVcpz, and were stunned to find that in some areas the virus infects up to 35 per cent of the chimpanzee population.The researchers say two of these strains are genetically closer to HIV than any other known virus.
Link to full article in Science


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Milano, Italy
In 1988 DJ Molteni chose to follow his passion and threw himself into the "art of mixing". As he played in small prestigious clubs and venues throughout Italy his experience grew and he became a highly sought after DJ in the Club scene of the time. In 1996 he began working in collaboration with some private radio stations and Clubs in Northern Italy and over the next few years grew his experience to incorporate post production audio, jingles and dubbing specifically for Radio and TV Commercials. During this time he was retained by several prestigious Studios until 2006 when he was invited to produce the radio show "Ondesonore" for InBlu Network. This production included a dynamic program of electronic dance vibes with intricate musical technicality and great musical appeal. His work on this production was greatly acclaimed. DJ Molteni works with precision and great attention to detail, with dedication and first and foremost his greatest attribute, Passion!.
- Billie Ray Martin1,311 followersBerlin, Germany
- DamianMike26 followersBrescia, Italy
- Bob Sinclar4,505 followersParis, France


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We guarantee that when you book with us directly, we will offer you the lowest available rate.
Unfortunately we incur a minumum charge of 15% when you book through a third party website such as Expedia, HRS or Booking.com. Our best-price guarantee ensures we will match or offer a cheaper rate than advertised by third party websites.
We appreciate your custom and look forward to welcoming you to Zurich.


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David L. Givens, the former Tennessee Titans wide receiver who sued the team after a 2006 knee injury [1] ended his career again has filed a $25 million federal lawsuit against the team.
Givens joined the Titans in March 2006, signing a five-year deal worth $24 million. But Givens injured his knee that November, requiring multiple surgeries and preventing him from playing football again. The Titans eventually released him.
Givens is suing the team for $25 million in damages, claiming he has suffered physical and emotional pain, loss of income and loss of enjoyment of life.
The suit (which can be viewed here [2]) claims that an internal team memo showed that the Titans found out about "a large defect" on Givens' left knee through a team-contracted physician's examination of him the same month he joined the team.
That memo, according to Givens' suit, stated that the defect "may require surgery at some point," but no one from the team told Givens, who sustained the career-ending injury that season.
Robbie Bohren, director of media relations for the Titans, said the team had not yet received the new lawsuit filed on Tuesday and therefore did not yet have a comment on it.
Givens first filed suit in September 2009, but a federal judge dismissed it five months later, stating that Givens must first go through an arbitration process. Givens' most recent filing states that it has been six months since the last arbitration filings and a decision has yet be made in those proceedings.
Givens' attorney Daniel Warlick had not responded to a message seeking comment as of Tuesday night.
|GivensTitansLawsuit.pdf [2]
[1] http://nashvillecitypaper.com/content/sports/report-ex-titan-givens-sues-team
[2] http://nashvillecitypaper.com/files/citypaper/GivensTitansLawsuit_0.pdf


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What are you reading right now? A Moveable Feast and a M.F.K. Fisher book
How many books have you read so far? 2 children's picture books: Madeline and Babar
Are you getting tired yet? Oddly, no.
Do you have any tips for other Readers or Cheerleaders, something you think is working well for you that others may not have discovered? Two words: Readathon Lite...
Update: Hour 18 did me in. I got in a few pages of Time Was Soft There and fell asleep....But I'm back for the last thirty minutes. I've got my coffee going and I'm determined to read to the finish line.
This was my favorite Readathon. I only left the house once, to go to a wedding shower (that I discovered is actually for today, but that's another story!) I had the fun French music going...my husband zipped out and surprised me with croissants and gelato for snacks...and I finished four French-ish books! Happy Day!
"You didn't ask to be born, you didn't make the world as it is, you didn't make yourself as you are. Why torment yourself? Why not take life just as it comes?"
from Good Morning, Midnight by Jean Rhys


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In order to rout the hireling of the French bourgeoisie Baron Wrangel the Southern front needs to strengthen its cavalry units. I order each military district, immediately and with exceptional energy, to set about forming cavalry units: squadrons, troops and mounted machinegun troops (in accordance with the establishments laid down in the order of the Revolutionary War Council of the Republic 1919 No.465, p.1201/226).
There are to be converted into these formations:
For this same purpose, purchase of suitable horses from the population, on a voluntary basis, is to be undertaken on a large scale.
The Central Supply Administration is to take very urgent measures, disregarding all established priorities, to ensure that the units being formed receive arms and all other articles of supply.
Special attention is to be given to the successful formation of these units by the districts, with extensive agitation in the localities to point out the particular importance of the present measures for the defence of Soviet Russia.
Special attention will be paid to the district and provincial commissariats which distinguish themselves by their greater progress in carrying out this military order.
The formation of units is to be completed by September 1 of this year.
The order is to be transmitted by telegraph.
Last updated on: 26.12.2006


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German composer, violinist, conductor, music educator, and scholar Carl Venth (1860-1938) was a leading classical music figure in Texas in the first half of the twentieth century. After studying with Ferdinand Hiller at the Cologne Conservatory and Henry Wieniawski in Brussels, Venth became the concertmaster of the Flemish Opera House at age 18 and then became the concertmaster of the Opera Comique in Paris in 1879. In 1880 he immigrated to New York City, where he led and organized several orchestras and musical ensembles, such as the Venth College of Music and the Brooklyn Symphony Orchestra.
In 1908, Venth moved to Texas to work as violin director at the Kidd-Key College in Sherman. He also served as dean of the School of Fine Arts at Texas Woman's College (later Texas Wesleyan University) in Fort Worth from 1914 through 1931 and as head of the music department of Westmoorland College (now part of Trinity University) in San Antonio from 1931 through 1938. Furthermore, Venth directed the Frohsinn Chorus, conducted the Dallas Symphony Orchestra, and organized and served as the first conductor of the Fort Worth Symphony Orchestra. He served as president of the State Music Teachers' Association, receiving an honorary life membership. He also accepted honorary degrees from the Chicago Musical College and New York College.
On July 13, 1899, Venth married Norwegian-American Cathinka Firth Myhr (1867-1958).
The Carl Venth Papers, 1885-1959, primarily consists of printed and handwritten sheet music composed by Venth. The papers also include correspondence and memoranda, notes, legal documents, newspaper clippings, photographs, sound recordings, and programs concerning the career of Venth and his wife Cathinka.
Use of audio material by appointment only; please contact sound archivist.
Unrestricted use.
Carl Venth Papers, 1885-1959, Dolph Briscoe Center for American History, The University of Texas at Austin.
Some material has been separated to the Artifact Collection.
See also the Venth (Carl) Papers at the Fort Worth Library in Forth Worth, Texas.
This collection contains unprocessed materials.
This collection was processed by Chester V. Kielman and B.S., June-July 1964. Subsequent revisions were made by W.H. Richter, February 1966 June 1969; Sara Rumbo, February 1973; Laurel Rozema, May 2010; and Paloma Graciani, March 2016.
Basic processing and cataloging of this collection was supported with funds from the National Historical Publications and Records Commission (NHPRC) for the Briscoe Center's
(Please refer to separate Venth (Carl) Collection Checklist in Card Catalog - Section A for item-level description)


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This page lists all content tagged with the term
VIM: http://www.lagmonster.org/docs/vi.html
SVN: http://www.linuxfromscratch.org/blfs/edguide/chapter03.html
Getting an error similar to the following when doing a branch or commit in SVN?
svn: Commit failed (details follow):
svn: MKACTIVITY of '/svn/forms/!svn/act/ebcddac9-12da-4ae4-86d8-bdcfbccdc682': 403 Forbidden
Check the case! In this instance, the svn repo was actually called "Forms." Changing the case got rid of the error.
I'm a software tester, developer, and graphic designer living in Colorado Springs with my wife and son. I have five years of experience with automated testing, ten years of software engineering and development, and fifteen years in illustration and 3D graphics.


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Engagement: Skinner-Gatewood
Published 6:00 am, Sunday, February 6, 2011
Jim and Linda Skinner of Plainview announce the engagement of their son, Ross Edward, to Allison Nichole Gatewood, daughter of Scott and Sandy Wright and Mark and Shanda Gatewood, all of Belton.
Miss Gatewood is a 2005 graduate of Belton High School and received a bachelor's degree in communication studies in 2009 from Sam Houston State University.
She is employed by the university's registrar's office at Sam Houston State University.
Skinner is a 2004 graduate of Plainview High School and received a bachelor's degree in business administration in 2009 and will receive a master's degree in business administration/professional in human resource in May from Sam Houston State University. In addition, he has completed certification as a PHR.
He is employed by Sam Houston State University as an assistant project manager.
The couple will be married Oct. 1, 2011, at Tenroc Ranch in Salado.


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- Home >
- Hand Tools >
- Building Tools >
- Cold Chisels & Bolsters >
- Faithfull Fluted Plugging Chisel With Grip
Designed to remove mortar from between bricks prior to re-pointing or the removing of a brick. The cutting edge is wider than the blade to give clearance, and the flute allows faster clearance of debris. Size 230 x 5mm (9 x 3/16 in). Fitted with a plastic guard to protect the users hand.
|Chisel Length
|230 mm
|Chisel Width
|5 mm
Own it? Review it! Be the first to tell everyone what you think about this product...


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At least that's what Joe Benigno of WFAN says. This morning after his opening monologue, he made a good case for his assertion.
Why did Willie Randolph go out of his way to burn up Jose Reyes after the Cubs finale regarding the play where he threw the ball home and got an out?
Reyes might have been able to go for the double play, but he played it safe instead and threw the ball home and got the sure out and prevented a run from scoring. If Jorge Sosa didn't serve up a meatball to Ronny Cedeno, the inning would have been over. Case closed.
Did Jose Reyes really deserve the wrath of Willie Randolph when at least he made the play and got out?
It seems like Willie Randolph has no problem picking on Jose Reyes, and yet he never utters a word to Carlos Delgado. In that same game, Delgado committed what I thought was an even bigger gaffe than that of Jose Reyes and yet Willie simply passed it off as a missed opportunity and a bad judgment call.
A bad judgment call? That wasn't bad judgement… it was poor execution and a lack of basic fundamentals. The bad judgment call was that of Reyes because he had a choice of throwing home or throwing to second. Carlos Delgado had no such choice. Carlos Delgado failed to field his position and allowed the inning to continue.
Did we really need Willie to get back inside of Jose Reyes' head just when he was starting to have fun again?
Why doesn't Willie ever lay down the law with Delgado or any of the other veterans for that matter?
It seems like Oliver Perez and Jose Reyes are the objects of Randolph's ire and he never misses an opportunity to discipline them either in clear view of the cameras or through the press.
Some may say he disciplines his veterans in private inside the clubhouse. If that's true then why have a double standard? The fact is there has never been any evidence that Willie Randolph has disciplined Delgado for not running ground balls out which he frequently does.
Maybe Benigno is right… Maybe Willie Randolph is afraid of Carlos Delgado. It certainly would explain a lot…


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Leadership Summit: Our annual Leadership Summit, usually held in April, tackles current topics and gives answers every leader needs to know.
Legislative Receptions: Our Legislative Receptions are held annually and this past year simultaneously in February at four locations on Monday, February 13, 2017. We usually invite all northeastern Ohio members of the Ohio General Assembly to attend. We will give each legislator a moment of microphone time, and we will attempt to seat them with members from their area.
Megaconference: The name says it all–Megaconference features twelve simultaneous breakouts in three one-hour time slots. Topics offered fall into the following three themes: leadership development, personal development, and professional development. This year's Megaconference was Saturday, March 4. Details available at neoea.org/Mega.
Negotiations Conference: NEOEA and OEA will provide for local affiliates to attend the annual NEOEA Presidents Plus Two Negotiations Conference to be held Friday, October 13 (NEOEA Day).The Negotiations Conference will provide information of use to both teacher and ESP members. We encourage participating locals to send entire bargaining teams and negotiating committees.
Summer Leadership: Our largest conference of the year is two days and features intensive training in association leadership for new and experienced leaders. In 2017 it will be held on July 26-27.


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Mcleod Shelby GT500 RXT Street...
Mcleod 2010 GT500 RXT Street Twin Disc Clutch Kit (Street) Includes: Mcleod RXT Clutch Mcleod Lightened Steel Flywheel NOTE: The 2010 GT50...//Shop Now
877-2-LETHAL (877-253-8425) or (561) 753-8105 or EMAIL // M-F 9-6
E85 USERS: We recommend using the Walbro F90000267 465lph pumps as these are the only pumps sold by Walbro as a 100% E85/Flex Fuel compatible fuel pump. We also recommend using the DivisionX DX-0010MW fuel filter with wire mesh filter element as paper elements are not compatible with E85.NOTE: This system comes standard with Fragola PTFE fuel hose. PTFE fuel hose is more durable than the standard hose and prevents fuel smell typically found when using non PTFE hose.We have used the standard Fragola non-Teflon based fuel hose on several of our shop cars with both gasoline and E85 with excellent results and no fuel smell. If you would like the non PTFE hose please choose that option from the dropdown menu. If you decide to purchase this kit with the standard hose Lethal Performance will not be liable for claims of fuel smell after installation.
The Lethal Performance return style fuel systems are designed as a "dead head" setup. This places the regulator before the fuel rails which we've found works better than the traditional return style setup. We use this same exact system in several of our shop cars including our 1150rwhp E85 powered 2013 GT500 and 872rwhp E85 powered 03 Cobra.
The fuel lines in this system come pre-assembled. Due to this, the installation of the system becomes much easier as you will not need to install any hose ends. With that said, the system is designed to be installed one way. If you try and install the lines in any other configuration then the one we designed it for you won't be able to properly install the system.
Lethal Performance is not responsible for any additional hose or fittings required due to custom installation.
With the release of the DivisionX S197 fuel hat we're excited announce several different return style fuel systems for the 2005-2010 3V Mustang GT owner in need of more fuel.
These fuel system are designed to help safely support higher hp levels and come with everything needed for a complete installation. So whether you're looking to support 700rwhp or 1400hp we have a kit specifically designed just for you.
One of the major improvements these new systems offer are the single feed line. In the past our systems used a different fuel hat which required the use of a 3-into-1 y-block. That also created the need for more lines and fittings making the system cost more and more difficult to install. The new systems use the DivisionX Gen 3 hat which has a single outlet and single return eliminating the use of an external y-block. In addition to that the new fuel hat incorporates an OEM style connector both on the hat and the wiring harness. The advantages to this are that there's no more wires passed through the hat. Wires passed through the hat and sealed with epoxy have been know to leak fuel. The OEM connector guarantees a leak free setup. In addition the OEM connector makes this a true PLUG-N-PLAY setup between the hat and wire harness that doesn't require any soldering at the hat. Simply plug the connector at the end of the wire harness into the connector on the hat and you're done.
The DivisionX fuel hat is a direct replacement for your stock fuel hat. Simply remove the stock setup and the DivisionX hat drops right in. The DX hat uses the same OEM venturi setup and level sender as the stock pump system did so your fuel level will always read accurately.
Easy to Upgrade- If at any point you grow out of the system you're in and need to step up to the next system to support more hp all you need is the pumps as all of the systems are the same except for the pumps.
System Includes:
DivisionX S197 Dual Pump Return Style Fuel Hat
DivisionX 3V High Flow Fuel Rails - Black Anodized
DivisionX 10 Micron Fuel Filter
PTFE Teflon Lined fuel hose (pre-assembled)
Aeromotive Pro-Series 4 Port 1:1 Boost Reference EFI Fuel Pressure Regulator
(2) Walbro/TI Autmotive DCSS 465lph Fuel Pumps
Lethal Performance Dual Relay Wiring Harness
DivisionX 0-100psi Fuel Pressure Regulator
XRP and Fragola Fuel Fittings
Fragola Push-Lite Fuel Hose
OEM Level Sender
Loom Clamps, Self Tapping Screws and Zip Ties
Vacuum Hose and T- Fitting for Boost Reference
Complete Installation Guide with Diagram can be downloaded from the Installation Instruction section at the bottom of our home page.
NOTES: 2010+ GT's and GT500's use a different level sender than the 05-09 GT's and 07-09 GT500's.Due to that all 2010+ GT's and GT500's need to re-use their stock level sender with this hat. To properly install your stock level sender use the dropdown menu to add the 2010+ level sender bracket to your order.
|Free Shipping
|2005-2009 GT / GT500 Fuel System Diagram (Traditional Style) (Size: 2.1 MB)
|DivisionX S197 Dual Pump Return Style Fuel Hat DX-0700 (Size: 94.7 KB)
|DivisionX S197 Dual Pump Return Style Fuel Hat DX-0700
|Lethal Performance Dual Pump Return Style Wiring Harness LP-DUALRETURNHARNESS (Size: 183.9 KB)
|Lethal Performance Dual Pump Return Style Wiring Harness
|S197 GT / GT500 850-1400rwhp Fuel System Installation Diagram (Size: 303.7 KB)
|S197 GT / GT500 850-1400rwhp Fuel System Installation Diagram
|S197 GT / GT500 850-1400rwhp Return Style Fuel System Installation Instructions (Size: 333.9 KB)
|S197 GT / GT500 850-1400rwhp Return Style Fuel System Installation Instructions