Karen Patton Alexander, MD

https://medicine.duke.edu/faculty/karen-patton-alexander-md

In its classic form, patients with concussion experience a transient loss of consciousness followed by a rapid return to a normal state of alertness blood pressure symptoms purchase 50 mg atenolol. Both the supply and metabolic conversion of substrates, which are well matched under normal circumstances, can be significantly abnormal after head injury blood pressure chart diabetes atenolol 100 mg order on-line. Glucose is the primary energy substrate of the brain and can be metabolized aerobically or anaerobically blood pressure guidelines chart atenolol 50 mg without prescription. Of the total energy generated, 50% is used for neurotransmitter production, release, and uptake (synaptic activity); 25% is used for maintenance and restoration of ion gradients across the cell membrane; and the remaining 25% is used for molecular transport, biosynthesis, and other unidentified processes blood pressure medication when pregnant order atenolol 50 mg with visa. RegulationofCerebralBloodFlow Glucose and glycogen stores in astrocytes are extremely limited, and there is no significant storage capacity for oxygen in the brain blood pressure medication viagra buy atenolol 50 mg lowest price. Therefore, the brain depends on continuous blood flow to meet its glucose and oxygen needs. In general, substrate availability is determined by three factors: concentration of substrate in blood, flow volume, and the rate of substrate passage across the blood-brain barrier. The brain possesses several mechanisms to ensure substrate availability, both under normal circumstances and during times of physiologic stress. This is primarily accomplished through changes in caliber of resistance vessels, arterioles with a diameter of 30 to 300 µm. The effects of hypocarbia and hypercarbia are mediated by pH changes in the perivascular space. Most of the intracranial blood volume is present in vessels with diameters between 30 and 300 µm. Changes in vessel caliber primarily occur in arterioles (200 µm), whereas the diameter of venules remains more or less constant. Blood viscosity changes with variations in hematocrit, gamma globulin, and plasma fibrinogen. Although these pathways are not completely understood, key features include inappropriate release of excitatory neurotransmitters. This shift toward hyperglycolysis has been demonstrated in both animal and clinical studies after severe head injury. Although lactic acid is a byproduct of anaerobic metabolism, it may have neuroprotective effects in the injured brain. For example, acidosis shifts the hemoglobin-oxygen dissociation curve to the right, improving oxygen delivery to damaged tissue. Also, acidosis optimizes tissue pH for glycolysis and causes vasodilation, which maximizes available collateral flow to the damaged region. Despite these effects, however, the recovery potential of tissue in the presence of high lactate and resultant acidosis is poor. This was largely based on the work of Vink and coworkers,247 who demonstrated normal mitochondrial function after severe head injury. This mitochondrial damage appears to occur through calcium-mediated interference of respiratory chain­linked functions. This represents a significant mechanism of secondary injury that can dramatically worsen patient outcome. This is followed by membrane failure, sodium-potassium pump arrest, cell swelling and dysfunction, and eventual cell death. Langfitt and Obrist suggested three hypothetical states of brain dysfunction after head injury: brain regions that are irreversibly damaged, brain regions that are dysfunctional, and ischemic brain (Table 331-11). Derangements are often confined to local brain regions262-265 and may affect different mechanisms of cerebrovascular regulation in varying ways. Density of deep frontal white matter (expressed in Hounsfield units) during and after resolution of swelling was measured in 12 children in this study. Although there was a significant difference between these two time points, no density differences were found between children with edema and controls. Others have found that pressure autoregulation is always intact during the first 36 hours after injury, but then absent in 50% of patients between 36 and 96 hours after injury. Bouma and associates282 performed autoregulation tests in 117 severely head-injured patients. However, no specific temporal pattern or relation to clinical status could be determined. Endothelial damage may be responsible for the perturbation of pressure autoregulation. In experimental brain injury, endothelial lesions are often present with severe ischemia or trauma. In total, 38% of patients demonstrated impaired viscosity autoregulation after head injury. Reduced blood viscosity, as obtained with mannitol administration, results in vasoconstriction when viscosity autoregulation is intact. Reduced blood viscosity in the context of impaired viscosity autoregulation, however, does not induce a vascular response. Large artery vasospasm decreases the diameter of the macrocirculation, resulting in reduced perfusion pressure. Marmarou and associates plotted this curve on a semilogarithmic scale to create a straight line. Neurotoxic edema is caused by excessive release of excitatory amino acids, loss of calcium and potassium homeostasis, and generation of free radicals. In a series of experiments at the Medical College of Virginia, Barzo and colleagues325,326 investigated the role of vasogenic and cellular edema in a rodent model of diffuse brain injury. The apparent diffusion coefficient increased with vasogenic edema and decreased with cytotoxic edema. This increase in extracellular volume is thought to be the result of blood-brain barrier compromise. Total brain water remained increased, suggesting delayed intracellular fluid accumulation or cellular edema. This results in uncal and hippocampal herniation into the space between the midbrain and the tentorial edge (ambient and crural cisterns). This results in compression of the midbrain from side to side with resultant elongation of its anterior-posterior diameter. The ipsilateral cerebral peduncle and oculomotor nerve are compressed, resulting in contralateral hemiparesis, ipsilateral pupillary dilation, and decreased level of consciousness (due to distortion or deafferentation of the upper part of the reticular activating system). Brain herniation occurs in five major patterns, and each is associated with a characteristic clinical presentation (Table 331-14). This is often asymptomatic, but in severe cases, pericallosal arteries can be compressed, resulting in unilateral or bilateral frontal infarcts. Rather than herniating transtentorially, medial temporal structures herniate posteriorly or bilaterally, compressing the quadrigeminal plate at the level of the superior colliculi. Central (Axial) Herniation Central or axial herniation is defined as a downward shift of the brainstem toward the foramen magnum. Because of this downward progression, the brainstem is elongated in its anteriorposterior diameter, and central perforating branches of the basilar artery become stretched. This can result in brainstem ischemia and hemorrhage, the latter occasionally resulting from reversal of the displacement by operative decompression. Clinically, central herniation results in impaired consciousness and a Cushing response to brainstem ischemia (arterial hypertension, bradycardia, and respiratory irregularity). It should be noted that brainstem ischemia is not always present in patients with a Cushing response,328 and a Cushing variant response (tachycardia or systolic hypotension with absence of the classic Cushing triad) should not give a false sense of security in the presence of posterior fossa lesions. Tonsillar herniation causes obliteration of the cisterna magna and compression of the medulla oblongata, the latter resulting in apnea. The shape and size of the tentorial opening determine whether signs of tentorial or tonsillar herniation predominate with supratentorial mass lesions. When the opening is small, major symptoms are usually tentorial in nature; when the opening is large, tonsillar herniation may occur without any preceding signs of tentorial herniation. For example, in the acute injury phase, hypoxia is typically due to severe hypoventilation, airway obstruction, aspiration, or hemothorax and pneumothorax. Lower hemoglobin levels improve blood viscosity but may compromise oxygen delivery, whereas elevated levels provide better oxygencarrying capacity but cause the blood to become more viscous. Of note, some authors have reported improved tissue oxygenation with transfusion,358-360 whereas others have demonstrated better outcome with lower levels. For example, although severe skull fractures may occur with crush injuries, there is typically minor brain injury in these patients owing to minimal brain motion within the cranial vault. Basilar skull fractures are often caused by direct impact to the occiput, mastoid prominence, supraorbital area, or facial bones. Because of the thinness of the basilar skull, fractures may also occur as a result of stress waves propagating from a more remote site of impact. Resting energy expenditure and cardiac output decreased progressively between 37° C and 33° C, whereas mixed and jugular venous oxygen saturation remained normal. However, pooled data did not reveal an overall difference in mortality between normothermia and prophylactic hypothermia. Injuries to the Scalp and Skull Injures to the scalp can result in significant blood loss and hemodynamic instability and should be promptly addressed during trauma resuscitation. Injuries to the skull can result in fractures over the cortical surface (convexity fractures) or along the skull base (basilar fractures). Convexity fractures are often categorized as linear, depressed, or penetrating-perforating and are related to the nature of impact. For example, depressed skull fractures typically result from impact of small objects with surface area of less than 2 square inches; the resultant strain is concentrated immediately beneath the impact site. The resultant patterns of linear skull fractures are determined by bone density, local thickness, and presence of sutures. Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging. Biomechanics of traumatic brain injury: influences of the morphologic heterogeneities of the cerebral cortex. Elevated body temperature independently contributes to increased length of stay in neurologic intensive care unit patients. Relationship of early cerebral blood flow and metabolism to outcome in acute head injury. Measuring the burden of secondary insults in head-injured patients during intensive care. The diagnosis of head injury requires a classification based on computed axial tomography. Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm. Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike. Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 299 patients. Concussion was defined as an "immediate and transient posttraumatic impairment of neural function. This disturbance of brain function is typically associated with normal structural neuroimaging findings. Duration of symptoms is highly variable and may last from several minutes to days, weeks, months, or longer in some cases. Patients with risk factors of coagulopathy, history of neurosurgical procedures, history of epilepsy, drug or alcohol consumption, or age greater than 60 are included in the high-risk group regardless of the clinical presentation. These categories are based upon the risk of intracranial hematoma requiring surgical evacuation. Epidemiology Estimates of mild traumatic brain injury in child and adult populations vary greatly, and have ranged from 49% to 90%8,9 of traumatic brain injury in the literature. The long-term morbidity and mortality should be extremely low, for few of them sustain potentially serious intracranial injury. Nonetheless, the potential for major injury is omnipresent, and an organized and consistent approach serves well to ensure proper management. Cassidy and associates8 provide comprehensive descriptions of epidemiologic studies of mild traumatic brain injury from 19802000. Although estimated rates vary between studies, most studies find increased rates in males and young adults, with mixed results for race. By sport, American football,16 soccer, and ice hockey are often cited as having the highest concussion rates in the United States. In football, linebackers, wideouts, and safeties, respectively, sustained the greatest number of concussions in one study,21 with other studies rating quarterbacks,28 running backs, and defensive secondary players being more atrisk. In brief, concussion initially results in what has been described as a "metabolic mismatch," during which cerebral blood flow significantly decreases, yet demand for glucose increases. Increased excitatory activity caused by increased extracellular K+ is then followed by diffuse depression of neuronal activity. Recent experiments with radioactive tracers have shown the axonal injury may occur in a nonlethal concussive model, and that progressive axonal swelling and disturbance in axonal transport results in the hours and days following the injury. Recent autopsy studies suggest chronic traumatic encephalopathy, especially tauopathy, has been seen in case studies of modern professional football players. At times, patients who are experiencing postconcussion symptoms have been told they did not sustain a brain injury because they did not experience a loss of consciousness. A study of concussed athletes revealed a small subsample who did not experience symptom onset until about 14 to 15 minutes after injury (mean = 14. In this study, concussed athletes who endorsed any degree of mental fogginess had worse performance on memory, reaction time, and processing speed measures, as well as reporting an overall higher total symptom score. The duration of amnesia is documented as the time between the occurrence of injury and the time at which the individual regains normal, continuous memory functioning. In assessing retrograde amnesia, the on-field staff can ask the athlete questions regarding details occurring just before the trauma. Following injury, the duration of retrograde amnesia will tend to shrink over time.

Therefore, shock waves have been used to explain the formation of intermediate coup contusions (a name sometimes used to describe hemorrhages occurring on surfaces that are not convex), scattered deep intracranial hemorrhages, and traumatic intracerebral hematomas hypertension hypokalemia purchase atenolol on line amex. However, because these waves travel so rapidly and are quickly dissipated, this mechanism remains a matter of debate prehypertension 37 weeks pregnant buy atenolol online now. From a mechanical point of view, acceleration and deceleration are the same physical phenomena and differ only in direction heart attack low vs diamond order atenolol 100 mg line. For example, the effects of accelerating the head in the sagittal plane from the posterior to anterior direction act the same as decelerating the head from anterior to posterior arteria gastroepiploica atenolol 50 mg order on line. Similar to contact injuries, head motion results in strain within brain tissue that can cause either functional or structural damage blood pressure 10060 order 100 mg atenolol visa. First, differential movement of the skull and brain can be produced by head acceleration or motion. This relative movement occurs because the brain is free to move to some degree within the skull and the brain lags behind the skull for a brief moment after acceleration begins as a result of inertia. When combined, these factors allow the skull and dura to move relative to the brain surface, thereby potentially causing localized strain at the surface. Particularly susceptible in this situation are the parasagittal bridging veins between the brain surface and dura, which may tear if the strain exceeds the tolerance of the vessels, and such tears cause about 60% of acute subdural hematomas. Furthermore, movement of the brain away from the skull creates a region of low pressure that if sufficiently intense, causes contrecoup contusions. Second, head acceleration can produce strain within the brain parenchyma and therefore result in widespread disturbances in brain function or structures. This deformation is visualized with a superimposed grid pattern that deforms from the acceleration impartedduringimpact(shownasanarrow). In each type of injury, the severity and extent of damage are intimately linked to the magnitude, rate, duration, direction, and type of inertial loading. Types of Head Acceleration Three types of acceleration can occur: translational, rotational, and angular. Translational acceleration occurs when the center of gravity of the brain (which is approximately in the pineal region) moves in a straight line. Purely translational acceleration is uncommon because the physiologic articulation of the head and neck limits this pure movement. Exceptions occur when the head moves in a translational manner for brief periods or the head becomes arrested with other motions. An exception may be vertex impact, during which superior to inferior motions can occur. The brain motions that take place during translational acceleration are primarily due to the relative brain skull motions previously described and not to strain produced deep within the brain. Concussive injuries do not occur when the head experiences a purely translational acceleration. Therefore, translational acceleration does not cause diffuse brain injuries, but it can produce focal injuries, including contrecoup contusions and intracerebral and subdural hematomas. Rotational acceleration occurs when there is rotation about the center of gravity of the brain without the center of gravity itself moving. Because the center of gravity of the brain is in the pineal area, pure rotational acceleration is a virtual impossibility in nearly all clinical situations. For the brain to rotate around an axis that goes through the pineal area, the entire body would have to swing around it. A notable exception is when the head is rotated solely in the horizontal plane, in which case pure rotation may occur about a vertical axis running through the pineal area. Rotational acceleration is a very important and highly injurious mechanism because not only does it produce the high surface strain seen in translational motions but it is also the only mechanism capable of producing high levels of strain deep within the brain itself. However, because of the infrequency of pure rotational motions in clinical situations, the effects of rotational acceleration are usually seen after angular acceleration of the head. Angular acceleration occurs when components of translational and rotational acceleration are combined. The exact location of this rotation point, in conjunction with the magnitude of the impact force, determines the proportion of translation and rotation that the brain experiences. As the rotation point moves higher up the cervical spine, there is a proportionally greater rotational component; moving the rotation point lower introduces proportionally more translational acceleration. As might be expected, angular acceleration is the most damaging brain injury mechanism because it combines the injurious mechanism of both translational and rotational movements, especially the latter. Virtually every known type of head injury can be produced by angular acceleration, except for skull fracture and epidural hematoma. Several studies have now documented the in vivo motion of the brain during angular motions13,14 and have investigated the head motions associated with sports and concussive impacts. Itisraretofindinstances of pure translational or rotational acceleration in "real-world" injury situations. The angular motion leads to combined translational and rotational acceleration, thereby creating injury patterns that arise from both acceleration types. The amount of inertially induced damage depends not only on the type of acceleration imparted to the head but also on several other factors. The magnitude of acceleration can be viewed as being proportional to the amount of strain delivered to the brain, and the acceleration rate is proportional to the strain rate. Both strain and the strain rate are factors contributing to the structural or functional limit of intracranial tissues. If the magnitude of acceleration is constant, the rate of acceleration varies inversely with the duration for which the acceleration is applied. Acceleration magnitude Blast-Induced Brain Injuries the effects of blast loading on humans originated with the term "shell shock" from World War I, which was used to describe a collection of symptoms that included a temporary altered mental state or confusion immediately after the blast. Despite being periodically addressed since its recognition as a clinical syndrome, only very recent studies have better described the conditions of blastinduced brain injury. The primary injury phase consists of the response of brain tissue to the blast wave (an intense overpressurization impulse component of the blast). The tertiary injury phase is due to head contact/acceleration as the body is moved by the "blast wind" (forced super-heated airflow). These groupings apply to the study of not only brain injuries but also other body regions susceptible to injury from blast. Primary blast injury is limited to injuries caused by the rapidly expanding blast wave. In air, the shock wave oscillates between overpressure and underpressure segments, but these waves dampen out quickly. The presence of structures and fluid interfaces complicates this pressure profile. For this reason, a large number of studies have focused on the fluid-air interfaces in the body because they are highly vulnerable to the passing pressure waves. Studies in these areas have generated injury thresholds for both the pulmonary system and the gut/bowel. Secondary blast injury covers both the penetrating and nonpenetrating injuries that occur when high-velocity projectiles/ fragments impact the head. Conversely, if the duration of acceleration is constant, the acceleration rate varies directly with the magnitude of the acceleration. If one applies a constant amount of acceleration and varies only the duration over which the acceleration occurs, three zones of clinical interest are encountered. The exact relationships between mechanical loading (magnitude, type, and direction of acceleration) and injury patterns are becoming increasingly more refined with computational models of the head/brain structure. Second, if the duration of acceleration is slightly longer, strain begins to appear within the brain but is primarily restricted to the periphery. Injuries produced in these circumstances are confined to the brain periphery and vessels. It is thus extremely complex to try to map acceleration profiles into exact patterns of damage within the brain. Several simple descriptors of acceleration-the amount and type of acceleration, its duration, and the rate at which the acceleration is applied to the head-are interrelated and together contribute to the pattern of injury observed within each individual. Certainly, these parameters are linked; for example, with a constant level of acceleration, as the duration increases, head velocity and movement also increase. A hard impacting object can cause a linear fracture, with most of the energy from the object being used to deform the skull locally. To prevent a more localized depressed skull fracture, the impacting object must be larger than approximately 2 square inches. However, if the impacting object or surface is considerably larger, the contact is distributed across a broad area of the scalp and the local bending effects necessary for fracture to occur may not be present. Acceleration injuries may occur in parallel with an impact that will cause a fracture because most impact situations will set the head in motion and therefore cause acceleration of the head superimposed on the contact loading effects. Management of the energy of the impact for a skull fracture occurs immediately beneath the impactor. If the impacting force is substantial, all bone under the impactor is damaged and skull perforation occurs. Nevertheless, the mechanics of these penetrating lesions is becoming clearer, given the frequency of gunshot wounds in the civilian population. This induces cavitation damage along the path of the projectile, as well as primary laceration damage along the path of the fragment. At the mechanistic level, these injuries are best modeled as a tissue laceration, with the obvious complicating mechanisms related to blood in the extracellular space and the potential for secondary brain injuries such as hypoxia. Tertiary blast injury occurs when the primary blast wind causes the victim to collide with fixed or mobile objects. These types of injuries share the most in common with contact/ acceleration injuries in civilians, where both the contact and acceleration forces can contribute to the different intracranial injuries that occur. Helmets worn by troops reduce the likelihood of injuries from direct contact for most of the head. However, current military helmets are not designed to specifically reduce rotational acceleration after a helmeted impact. As a result, the predominant mechanism of tertiary blast injuries in helmeted troops is the intracranial deformations caused by the head striking an object or the head being struck by an object with sufficient mass to cause a significant inertial load. In nonhelmeted victims, tertiary blast injuries can also include skull fracture or contusions from focal contact forces when the unprotected head strikes an object or surface. Basilar Fracture Caused chiefly by either direct impact or propagation of stress waves through the skull as a result of remote impact, basilar fractures may also occur as a consequence of the impact to facial bones. The thin anterior basilar skull is particularly susceptible to remote contact effects because the structure of this region is considerably weaker and not as effective in managing the local skull deformations initiated by remote impact. Common impact points for producing a basilar skull fracture include the skull base, facial or mandibular bones, and remote skull impact points. Fatal basilar skull fracture can also occur when the torso of a driver or passenger is adequately restrained in a vehicular crash but the head is allowed to move as a result of the impulsive forces in such a manner that the cervical spine is distracted from the base of the skull. Robert Hubbard and Jim Downing, was designed specifically to prevent this type of injury. Other similar restraining systems have been designed for use in motorcycle racing and equestrian events. It is clear that many of these injuries can occur in combination, and isolated occurrences of these types of damage, particularly after severe head injuries, are rare. As a result, it is common to find particular brain damage mechanisms associated primarily with motor vehicle accidents and other patterns of damage associated more frequently with falls or assaults or with pedestrianversus-vehicle accidents. Focal Brain Injury Epidural Hematoma Epidural hematoma can be considered a more complex case of linear skull fracture. Impact test without neck support Unrestrained head motions and injurious neck loads Impact test with neck support Head and helmet supported relative to torso period, vessels in the underlying dural membrane are torn and bleeding ensues into the epidural space. Subdural bleeding is also possible without skull fracture because the local skull bending caused by an impact may be sufficient to tear dural vessels without exceeding the failure limit of the bone. Coup Contusions Immediately under the impact point, coup contusions arise principally from the local skull bending or fracture caused by an impact from a relatively small, hard object. These phenomena in turn subject the underlying cortical and pial vascular network to strains that if excessive, cause bleeding at or near the brain surface. Damage is likely to occur when the skull is "rebounding" from the impact and the vessels are experiencing tensile strain. For cases of skull fracture, the localized strain from the skull contacting the cortical surface provides a means for the vascular damage noted in the pia and cortex. Contrecoup Contusions Two phenomena have been attributed to the pathogenesis of countercoup contusions: cavitation effects and inertial loading. Of the two, the more likely mechanism of contrecoup damage is translational or angular head motion. On impact, the brain moves toward the impact site and creates an area of negative pressure directly opposite the loading point. This negative pressure may in turn cause damage by exceeding the tensile strength of water or, alternatively, cause small gas bubbles to appear within the parenchyma. The return to normal or positive pressure will cause the small bubbles to collapse and is termed cavitation. However, it is difficult to conduct experiments that clearly support the cavitation mechanism, and this mechanism does not easily explain contusions located outside the region considered opposite the impact. Instead, it appears that the regions of vascular disruption and cortical damage and contrecoup regions are due primarily to acceleration effects and can result from either translation or angular head motions. Each head motion, particularly angular movement, is capable of producing tensile strain throughout the brain. If the tensile strain is greater than the vascular tolerance in a given region, contusion occurs. However, because these injuries are inertial and can therefore be caused by impulsive loading only, impact is not necessary for contrecoup contusions to occur. The term "contrecoup" can therefore be considered misleading because the critical mechanism is most often acceleration and not the contact effects from impact. In situations in which the head experiences impulsive loading, contrecoup contusions occur solely because of the strain generated in the cortical brain region during the acceleration period. Strain concentrations may occur in specific regions of the brain because of geometric effects and are responsible in part for the high incidence of frontal and temporal lobe contusions observed clinically.

The Normal Tone feature uses a proprietary algorithm that will provide pulse tones during non motion and adequate perfusion conditions prehypertension prevalence buy discount atenolol 50 mg on-line. Oxyhemoglobin (oxygenated blood), deoxyhemoglobin (non-oxygenated blood), carboxyhemoglobin (blood with carbon monoxide content), methemoglobin (blood with oxidized hemoglobin) and blood plasma constituents differ in their absorption of visible and infrared light (using spectrophotometry, see figure below) prehypertension occurs when 100 mg atenolol order with mastercard. The amount of arterial blood in tissue changes with your pulse (photoplethysography) blood pressure chart emt cheap atenolol 100 mg on-line. Therefore, the amount of light absorbed by the varying quantities of arterial blood changes as well blood pressure chart young adults discount atenolol 50 mg overnight delivery. The detector receives the light, converts it into an electronic signal and sends it to the Rad-57 for calculation arterial nicking cheap atenolol 100 mg. The maximum of the skin surface temperature is measured at an ambient temperature of less than 106º F (41º C). Fractional Saturation the Rad-57 is calibrated to measure and display functional saturation (SpO2): the amount of oxyhemoglobin expressed as a percentage of the hemoglobin that is available to transport oxygen. Note that carboxyhemoglobin is not capable of transporting oxygen, but is recognized as oxygenated hemoglobin by conventional pulse oximetry. As blood samples are usually taken over a period of 20 seconds (the time it takes to draw the blood) a meaningful comparison can only be achieved if the oxygen saturation, carboxyhemoglobin and methemoglobin concentration of the patient are stable and not changing over the period of time that the blood gas sample is taken. Additionally, drawn, whole-blood testing can be affected by sample handling methods and time elapsed between blood draw and sample testing. Conventional pulse oximeters assume that arterial blood is the only blood moving (pulsating) in the measurement site. During patient motion, however, the non-arterial blood also moves, causing conventional pulse oximeters to read low values, because they cannot distinguish between the arterial and venous blood movement (sometimes referred to as noise). Adaptive filters are powerful because they are able to adapt to the varying physiologic signals and/or noise and separate them by looking at the whole signal and breaking it down to its fundamental components. However, because of the changes in the physiological parameters such as blood volume, arterial-venous coupling, etc. All pulse oximetry measurement information, as well as instrument status data, is displayed on the front panel of the instrument. All user input is handled by control buttons on the front panel and the sensor cable connection is located at the top edge of the instrument. Rad-57 supports the full line of Masimo sensors (see Section 8, Sensors and Patient Cables). A Direct Connect Rainbow reusable sensor or patient cable or a Direct Connect Red reusable sensor or patient cable attaches to the patient cable connector on the top of the Rad-57 Instrument. Used to enter the setup menus and to select/activate certain entries within the menu/setup system. Ensure the speaker is not covered or the Instrument is placed face-down on bedding or other sound absorbing surface. Displays parameter/measurement numeric values and indicates parameter/measurement label. The Perfusion Index provides an indication of the percentage of pulsatile signal to non pulsatile signal. Push a second time to return the Instrument to standard alarm monitoring During saturation monitoring, use these buttons to adjust the volume of the pulse beep tone. Within the menu/setup system, these buttons are used to select values within each menu option. Do not use any other type of batteries or 5 10 15 20 25 power source to run the instrument. To install the batteries first remove the battery cover by depressing the small 10 15 20 25 the rectangular button at the bottom15 the cover, and sliding the 25 down off the bottom of the of cover 5 10 20 instrument. All four indicators will be lit when the batteries are full, with fewer indicators being lit as the batteries lose their charge. When the battery life is low, the battery indicator will begin to flash and an audible alarm will sound. Unpacking and Inspection Remove the instrument from the shipping carton and examine for signs of shipping damage. The contact address and phone numbers are listed in Section 9, Service and Maintenance. Configure the Instrument for your regional power line frequency (50 or 60 Hz) if needed. Refer to Section 4, General Setup and Use for additional steps to verify proper functioning of the Instrument. Understand its status and alarm messages (see Section 5, Alarms and Messages and Section 6, Troubleshooting). If utilizing a patient cable, select a sensor that is compatible with the Instrument and the patient before connecting it to the cable. If using a single patient adhesive or disposable sensor, check that the emitter (red light) and the detector are properly aligned. Verify all front-panel indicators momentarily illuminate and an audible tone is heard 8. Verify the front-panel display is free of alarm and system failure messages (see Section 5, Alarms and Messages) and the battery indicator shows sufficient charge (see Section 4, Battery Level Indicator). Verify that the patient alarms are functional by setting the high and low SpO2 and pulse rate alarm limits beyond the patient readings. Verify the sensor alarms are functional by removing the sensor from the sensor site. Create an alarm condition by lowering the SpO2 or pulse rate high alarm limits beyond the patient readings. Verify the sensor is applied correctly and that the measured data is appropriate, see Section 4, Successful SpO2 Monitoring. After monitoring is complete, remove the sensor from the patient and store or dispose of the sensor according to governing rules. Adjustments made by the user will be retained after a power cycle for all values except alarm silence. Tissue damage can be caused by incorrect application or use of a sensor, for example by wrapping the sensor too tightly. Numeric Display - SpO2 Stability of the SpO2 readings may be a good indicator of signal validity. Although stability is a relative term, experience will provide a good feeling for changes that are artifactual or physiological and the speed, timing, and behavior of each. The stability of the readings over time is affected by the averaging mode being used. This is due to a dampened response as the signal is averaged over a longer period of time than during shorter averaging times. There may also be a discrepancy between cardiac electrical activity and peripheral arterial pulsation. Inaccurate measurements may be caused by Intravascular dyes such as indocyanine green or methylene blue Arrhythmias Intra-aortic balloon support Numeric Display - SpHb (upgraded Instrument) A stable SpHb reading is associated with correct sensor placement, small physiological changes during the measurement and acceptable levels of arterial perfusion at the measurement site. Physiological changes at the measurement site are mainly caused by fluctuations in the arterial oxygen saturation, blood concentration and perfusion. Inaccurate measurements may be caused by: Elevated levels of bilirubin Motion artifact Low arterial oxygen saturation levels including altitude induced hypoxemia Numeric Display - SpMet (upgraded Instrument) A stable SpMet reading is associated with correct sensor placement, small physiological changes during the measurement and acceptable levels of arterial perfusion at the measurement site. Physiological changes at the measurement site are mainly caused by fluctuations in the oxygen saturation, blood concentration and perfusion. It is a calculated percentage between the pulsatile signal and nonpulsatile signal of arterial blood moving through the site. Extreme changes in the display number are due to changes in physiology and blood flow. The sensor must be well secured to the site for the Rad-57 to maintain accurate readings. For example, as may occur while lifting or crossing their legs during a diaper change. Low Perfusion Low Perfusion is indicated when the arterial pulsations are very low (weak perfusion). Actions to be Taken If the SpO2 readings show significant differences, do the following: Make sure the emitter and photodetector are aligned directly opposite each other. Select a site where the distance between the emitter and photodetector is minimized. Wipe the sensor site with a 70% isopropyl alcohol pad or rubefacient cream (10-30% methyl salicylate and 2-10% menthol) and allow to dry for 20-30 seconds. If possible, remove electrical noise sources such as electrosurgical units or other electrical/ electronic equipment. If artificial nails or excessive fingernail polish are present, select another site or remove the polish/artificial nails. If possible, ensure that the sensor is placed in a location with low ambient light. They are as follows: Normal Sensitivity ­ this is the recommended mode for typical monitoring purposes. It is also the suggested mode for care areas where patients are not visually monitored continuously. This mode delivers enhanced protection against erroneous pulse rate and arterial oxygen saturation readings when a sensor becomes inadvertently detached from a patient due to excessive movement. This mode is not recommended for care areas where patients are not monitored visually, such as general wards. It is designed to interpret and display data at the measuring site when the signal may be weak due to decreased perfusion. The operator should monitor these indicators periodically to determine remaining battery life and if the batteries should be replaced. Low Battery Audible Alarm If a low battery condition occurs during patient monitoring, a medium priority alarm will sound, and can be acknowledged by pressing the Alarm Silence Button. If a low battery condition occurs while not monitoring a patient, pressing the Alarm Silence Button will suspend the the alarm until the power is cycled or patient monitoring begins. If a low battery condition occurs, immediately discontinue patient monitoring and replace the batteries. During normal patient monitoring, the "Up" and "Down" Arrow keys control the Pulse Tone volume. In the setup/menu system, the "Up" and "Down" Arrow keys select among the options for each setting. Page 1 of 1 Setup Menu this section gives an overview of the Rad-57 menu selections available. The Enter key is used to enter the menu system and to move through the different menu levels. The parameter/measurement is set/selected when either the Enter or Next keys are pressed. On, Off Program 4/1/05 *available in upgraded ration, Rainbow, Buttons, 6/05 Adobe Illustrator 10. Pressing Display during an alarm condition will enable the display of other parameters for 10 seconds. To navigate through the menu, use the Power, Next, Up and Down keys located on the front panel of the oximeter. Turn the Rad-57 on and wait for the displays to scroll through the current settings. Trend data is stored in non-volatile memory, so it is not erased when the Instrument is shut off or when the batteries are replaced. Refer to Section 10 Accessories and contact Masimo to acquire these optional items. Erasing Trend Memory To erase (clear) the trend memory, turn the trend off and back on again. It requires a Masimo sensor and needs to acquire some clean data for this flag to be set. It is recommended that the operator be within a minimum of 10 feet from the Instrument. An audible alarm will accompany the display unless the oximeter has been set to Alarm Silence Mode. If the high alarm limit is set below the low alarm limit, the low alarm limit will automatically adjust to the next setting below the newly entered high alarm limit. SpMet* Low Limit SpMet* High Limit the SpMet high alarm limit can be set to "-" (Off) or anywhere between 1% and 99. The SpO2 low alarm limit can be set anywhere between 1% and 98%, with a 1% step size. The SpHb low alarm limit can be set to "-" (Off) or anywhere between 1 g/dl and 24 g/dl. When SpHb is placed in the "-" (Off) setting, the SpHb Low Limit alarm is disabled. The SpHb high alarm limit can be set to "-" (Off) or anywhere between 2 g/dl and 24. When SpHb is placed in the "-" (Off) setting, the SpHb High Limit alarm is disabled. If the user has not adjusted the alarm limits, then they will be set back to the factory defaults. Push Once ­ Alarm is silenced for 120 seconds and Alarm Silenced Indicator flashes. Alarm Silenced Indicator the Alarm Silenced Indicator provides visual feedback regarding the audible alarm status. The audible alarms are muted when the indicator is flashing or continuously illuminated. While monitoring a patient, acknowledging an alarm condition by pressing the Alarm Silence Button (one time) will silence the alarm tone for 120 seconds and the Alarm Silenced Indicator will flash.

They may be surrounded by larger areas of low density from associated vasogenic edema heart attack 5 fragger generic atenolol 50 mg on-line. As the contusion evolves, the characteristic "salt and pepper" pattern of mixed areas of hypodensity and hyperdensity becomes more apparent blood pressure causes discount atenolol 50 mg buy on-line. Nonhemorrhagic contusions appear as low attenuation areas and can be difficult to detect initially until the development of sufficient edema hypertension 2006 buy atenolol 50 mg amex. Again, because contusions involve the surface of the brain, they may have a "gyral" morphology arteria3d full resource pack discount atenolol online visa. An old contusion commonly evolves into a wedge-shaped area of peripheral encephalomalacia with the broad base facing the skull heart attack jack look in my eyes order atenolol 100 mg on-line. The intracerebral hematoma may result from expansion and coalescence of adjacent cortical contusions or it may result from microcavitation or shear-induced hemorrhage of small intraparenchymal blood vessels. The bleeding is more well-defined and tends to have less surrounding edema than the cortical contusion. Intracerebral hematomas are located deeper in the brain than cortical contusions and frequently involve the frontotemporal white matter. Involvement of the basal ganglia has been described; however, hemorrhage in the basal ganglia should alert the clinician that an underlying hypertensive bleed may be the culprit. B, T2-weighted image shows abnormal bright signal within the splenium (arrow) of the corpus callosum. E, 3-D color tractography demonstrates disruption of the commissural fibers at the posterior inferior margin of the splenium of the corpus callosum. The intracerebral hematoma is the most common cause of clinical deterioration in patients who have experienced a lucid interval after the initial injury. Delayed hemorrhage is the most common cause of clinical deterioration during the first several days after head trauma. As the hematoma evolves, a low-density rim, due to edema and pressure necrosis, can be observed. Ring enhancement can be seen within a subacute hematoma because of the proliferation of new capillaries lacking a complete bloodbrain barrier. The proposed pathogenesis is due to reperfusion hemorrhage secondary to vasospasm with subsequent vasodilation and hypotension, and subsequent hypertension exacerbated by an underlying coagulopathy. Associated low attenuation (vertical arrow) posterior to the acute contusion represents either vasogenic edema and/or nonhemorrhagic contusion. Traumatic vascular injuries include arterial dissection, pseudoaneurysm, and the arteriovenous fistula. Vascular injuries are often related to skull base fractures, and the internal carotid artery is the most commonly affected vessel. The injury usually occurs at sites of relative fixation, where the internal carotid artery enters the carotid canal at the base of the petrous bone and at its exit from the cavernous sinus beneath the anterior clinoid process. An arterial dissection occurs when there is incomplete disruption of the vessel wall with formation of a subintimal or intramural hematoma. Other imaging findings include an irregular and small caliber of the affected vessel. A watershed and/or embolic parenchymal infarction supplied by the injured vessel may also be seen. Conventional catheter angiograms have long been thought to be the "gold standard" for confirmation and delineation of the vascular dissection, and they can also show vasospasm and pseudoaneurysm formation. Nevertheless, the wall of the pseudoaneurysm provides little support, and hence it has a propensity to hemorrhage. The size of a partially thrombosed pseudoaneurysm is underestimated on conventional angiography because the angiogram only depicts the patent portion of the lesion. In the absence of thrombosis or turbulent flow, the pseudoaneurysm appears as a round area of signal void on both T1- and T2-weighted images. A, Sagittal noncontrast T1-weighted image shows an area of low signal with a high-intensity rim within the frontal lobe (arrow). B, Axial postcontrast T1-weighted image shows minimal ill-defined enhancement adjacent to the methemoglobin rim. B, the 6-hour follow-up study reveals interval development of multiple large left frontal hematomas with fluid-fluid levels (arrows) and a small right frontal hematoma. The right frontoparietal scalp soft tissue swelling has also increased (arrowhead). The traumatic arteriovenous fistula is a direct communication between an artery and a vein. Note how the total size of the aneurysm is much larger than the residual patent lumen. The chronicity of the lesion is demonstrated by the remodeling of the central skull base. Other imaging findings include enlarged extraocular muscles, proptosis, retrobulbar fat stranding, preseptal soft tissue swelling, and an ipsilateral convex cavernous sinus. However, the findings may be bilateral and symmetric because venous channels connect the cavernous sinuses. In severe cases, intracranial venous hypertension can lead to brain edema and hemorrhagic venous infarction. Skull base fractures, especially those involving the sphenoid bone, should alert the clinicians to search for associated cavernous carotid injury. It is most often caused by laceration of the middle meningeal artery with resultant meningeal artery to meningeal vein fistulous communication. Cerebral edema can be further divided into five major subtypes: vasogenic, cytotoxic, hydrostatic, hypo-osmotic, and interstitial. Hyperemia is thought to be the result of cerebral dysautoregulation, and cytotoxic edema is believed to occur secondary to ion channel leakage, mitochondrial failure, and tissue hypoxia. Interstitial edema occurs from movement of fluid into the periventricular space secondary to obstructive hydrocephalus. Hydrostatic edema occurs from a sudden increase in intravascular pressure and can be seen with a sudden decompression of a focal mass. Hypo-osmotic edema is caused by a decrease in serum osmolality, with a subsequent efflux of fluid from the intravascular to the extravascular space. In cytotoxic edema, the gray-white differentiation is typically lost, which is in contrast to hyperemia where the gray-white differentiation is preserved. With cytotoxic edema associated with circulatory arrest, the cerebellum and brainstem are usually spared and may appear hyperintense relative to the affected cerebral hemispheres. Traumatic brain herniation refers to displacement of brain tissue from one compartment to another secondary to the mass effect produced either by primary or secondary injuries. In subfalcine herniation, the most common form of herniation, the cingulate gyrus is displaced across the midline under the falx cerebri and above the corpus callosum. Compression of the ipsilateral ventricle because of mass effect and enlargement of the contralateral ventricle because of obstruction of the foramen of Monro can be seen on imaging. In uncal (medial transtentorial) herniation, the medial temporal lobe is displaced over the free margin of the tentorium. Effacement of the lateral aspect of the suprasellar cisterns is an important early clue of the presence of uncal herniation. In transtentorial herniation, the brain herniates either upward or downward because of lesions within the posterior fossa or supratentorium, respectively. Upward herniation occurs when portions of the cerebellum and vermis displace through the tentorial incisura. In posterior fossa downward herniation, the cerebellar tonsils displace through the foramen magnum. Downward herniation of the cerebrum manifests as effacement of the suprasellar and perimesencephalic cisterns. Inferior displacement of the calcified pineal gland is another clue for the presence of downward herniation. This type of herniation is being seen more often because of an increased use of decompressive craniectomies. With all types of brain herniation, the underlying culprit must be timely corrected to prevent additional secondary injury. Tonsillar herniation can cause ischemia in the territory of the posterior inferior cerebellar artery. B, Corresponding "bone window" image shows a fracture of the squamosal portion of the left temporal bone (arrow). C and D, Images from an external carotid artery catheter angiogram in the lateral projection show an abnormal blush of contrast because of filling of the middle meningeal vein via the middle meningeal artery. Mass effect from brain herniation or a hematoma can also cause noncommunicating hydrocephalus via compression of the aqueduct, foramen of Monro, or ventricular outflow foramina. On imaging, the ventricles are dilated, the sulci may be effaced, and there may be periventricular transependymal edema. The leptomeningeal cyst, an almost exclusively pediatric lytic calvarial lesion commonly referred to as a "growing fracture," is also caused by a tear in the dura. For the management of acute head trauma, the goal of imaging is to identify treatable injuries to prevent secondary damage. Severe holohemispheric cerebral (cytotoxic) edema with relative sparing of the basal ganglia is now evident. Persistent right-toleft midline shift (arrows) and left frontal ischemia (#) are also identified. The dilation of the lateral ventricles is due to a combination of global volume loss and superimposed communicating hydrocephalus. A, Lateral skull film from a 6-month old infant who was unconscious shows a slightly diastatic fracture of the parietal bone (arrows). Follow-up films at (B) 2 weeks and (C) 6 weeks show progressive widening of the fracture. D, the chronic leptomeningeal cyst appears as a lobulated lytic lesion with scalloped margins (*). Acknowledgements We thank the residents, fellows, and attendings from the Neuroradiology Section of the University of California, San Francisco for their continuing effort in submitting interesting cases to the teaching file server tfserver. Evidence for cellular damage in normal-appearing white matter correlates with injury severity in patients following traumatic brain injury: a magnetic resonance spectroscopy study. This is followed by a more delayed phase of injury, which is mediated by intracellular and extracellular biologic pathways and can be present for minutes, hours, days, and even weeks after the primary insult. Overall, 90% of patients experienced one or more secondary insults, with 50% sustaining an insult of highest severity grade. Secondary insults were most common in the severely injured group (67 of 68) and occurred less frequently in moderate (7 of 36) and mild (3 of 20) injury groups. The authors found that 50% of patients sustained a secondary insult during transport within the hospital, and repeat secondary insults were common even during intensive care management. It is important to note, however, that none of these protocols have proved effective in a randomized clinical trial. In this chapter, we discuss the pathogenesis of closed head injury and the effect of trauma on cerebral metabolism and circulation. Basic concepts of therapeutic intervention, as they pertain to these processes, are reviewed. High-speed filming of gel-filled skulls36,47 and high-speed biplanar radiography of cadaveric brains48 have shed additional light on brain deformation after head injury. For example, Bayly and associates have studied the effects of mild linear50 and angular51 head acceleration on brain deformation in healthy volunteers. Their data suggest that mechanical responses are mediated by divisions between brain regions. Contact forces occur when the head is prevented from moving after impact, whereas inertial forces occur upon acceleration or deceleration of the head, resulting in differential motion of the brain relative to the skull. In 1966, Goldsmith defined three physical processes causing head injury52: collision of the head with a solid object at an appreciable velocity, an impulsive load producing sudden motion of the head without significant physical contact, and a static or quasistatic load compressing the head with gradual force. Collision typically results in brain injury through a combination of contact and inertial forces,53 whereas impulsive forces cause inertial loading to the head. Although mild injuries such as concussion may result from this process, impulsive forces typically occur in conjunction with a collision or impact mechanism. In this scenario, the contribution of inertial forces is negligible, and damage is caused by gradually increasing contact forces trapping the head against a rigid structure. Contact forces typically result in focal injuries such as coup contusions and skull fractures. Rotational injuries are particularly concerning because they cause injury to both the cortical surface and deep brain structures. The resultant magnitude of rotation that occurs with this injury depends on the distance between the center of gravity and the center of angulation: the smaller the distance, the larger the rotational component of angulation. In an experimental model of angular acceleration, the influence of duration of the acceleration force, the time to peak acceleration, and the magnitude of acceleration were tested; a threshold value was established below which the impact resulted in concussion rather than a subdural hematoma. In contrast, a brief, high-velocity impact often results in tearing of superficially located bridging veins and pial vessels, causing subdural hematoma. The former mechanism is typically seen with motor vehicle collisions, whereas the latter occurs in falls or assaults in which the head strikes a broad, hard surface, and inertial loading is the predominant mechanism. This scale has been universally adopted for grading the clinical severity of head injuries and other pathologies that impair consciousness. For example, most patients arrive to the hospital by ambulance unresponsive because of sedation and neuromuscular blockade. Diffuse axonal injury in severe traumatic brain injury visualized using high-resolution diffusion tensor imaging. Furthermore, intubation and concomitant injuries resulting in orbital swelling can significantly interfere with accurate eye opening and verbal scoring.

If this is the case, the patient is best hyperventilated to a Paco2 of 30 to 32 mm Hg and given 1 g/kg of mannitol immediately while being taken to the operating room hypertension icd 9 code 2013 atenolol 100 mg purchase fast delivery. The frequent use of anticoagulant and antiplatelet drugs, often for marginal indications, can generate dangerous operative conditions heart attack zing mp3 100 mg atenolol buy mastercard. Qualitative platelet disorders have been described in those with chronic alcoholism and chronic aspirin ingestion blood pressure norms order atenolol 100 mg line. Consideration of thromboelastography if available and if coagulopathy is suspected v arrhythmia grand rounds purchase generic atenolol canada. Radiographs of the chest and cervical spine (or keep the cervical spine immobilized in a collar) 3 blood pressure medication make you cough generic 100 mg atenolol otc. Two large-bore peripheral intravenous lines or one peripheral and one central line (while maintaining central venous pressure >5 cm H2O) 6. Both lower extremities placed in sequential compression devices to minimize the risk for deep vein thrombosis 10. In general, the head is placed on a horseshoe or "doughnut" headrest, turned to the opposite side while avoiding any constriction of the neck veins, and elevated above the level of the heart. A sandbag placed beneath the ipsilateral shoulder makes turning the head easier and also relaxes the tissues in the neck. Unless deterioration is rapid, the scalp should be shaved and prepared as for any other neurosurgical procedure. Similarly, the use of volatile agents (halothane, enflurane, sevoflurane, desflurane, and isoflurane) has had its drawbacks. Use of halothane for surgery on intracranial lesions has decreased in recent years, although it may be safe in low concentrations (0. Sevoflurane and desflurane have cerebrovascular effects similar to those of enflurane and should also be avoided. Because of its depressive effect on cerebral metabolism, isoflurane may be neuroprotective and is a more desirable anesthetic for neurosurgical procedures among the inhaled anesthetic agents. Barbiturates also attenuate the cerebral vasodilation produced by volatile anesthetics. A newer agent currently under intense scrutiny for use in neurosurgery is dexmedetomidine. It is an 2-agonist that has been promoted as a sedative that does not cause respiratory depression. More studies are needed to establish the cost-effectiveness and utility of dexmedetomidine versus older agents, such as propofol. They should generally be avoided or used in small amounts during anesthesia for acute central nervous system trauma because of their long duration of action and the availability of other agents. A small incision (<3 cm) is made in the midpupillary line, 4 cm from the midline and 2 cm in front of the coronal suture on the right side. The incision is carried down to the underlying bone, and the periosteum is elevated. If the coronal suture cannot be felt easily under the scalp, a distance of approximately 10 cm is measured upward and posteriorly from the superior orbital margin in the midpupillary plane. Next, a twist drill is used to make an opening in the skull perpendicular to the plane of the skull. The twist drill hole is cleaned of any bony fragments with a small curet, and the underlying dura is pierced with a blunt stylet. A ventriculostomy catheter is placed with use of the standard landmarks while keeping the trajectory of the cannula in the coronal plane of the coronal suture and aiming at the medial canthus of the ipsilateral eye. A distinct "popping" sensation is usually felt as one reaches the frontal horn of the lateral ventricle. This should occur when the tip of the ventricular catheter is 7 to 10 cm from the surface of the skull, which usually means that it is at the opening of the foramen of Monro of the ipsilateral frontal horn. The catheter should not be advanced more than 10 cm from the skull because of the risk for damage to the diencephalic structures. The ventriculostomy catheter is tunneled for a few centimeters in the subgaleal space. It is then secured firmly to the skin with sutures and connected to the pressure transducer system. No more than three passes should be made to reach the ventricles before placing intraparenchymal pressure monitoring devices. For the placement of intraparenchymal monitoring devices, the twist drill opening is made as described earlier. After opening the dura with a blunt stylet, the transducer tip is placed directly in the brain parenchyma at a distance of 2 to 3 cm. CraniotomyTechnique Scalp Incision the superficial temporal artery should be palpated and marked and the vertical limb of the incision placed between the artery and the tragus. The skin incision is started at the zygomatic arch and then curved backward to the parietal eminence and upward above the auricle to reach 2 cm from the midline. It is then carried forward to the frontal region and curved across the midline just behind the hairline. In balding patients, the frontal part of the incision may be carried into the forehead, but it should be closed with 5-0 nylon suture for a good cosmetic result. The incision can be made with a scalpel, although use of a needle-tipped (Colorado) Bovie may minimize scalp bleeding. Then, using a Bovie cutting diathermy device, an incision is made in the superficial temporal fascia and in the temporalis muscle down to the bone, close to the margin of the skin opening. Ideally, the margins of the bony craniotomy should be approximately 15 by 12 to 15 cm in size. The patient is placed supine with the head preferably in a head holder, which also gives wide access to both sides. The whole head is shaved, prepared, and draped to allow access to the frontal, parietal, and temporal areas. The bur holes are typically placed on the side of localizing neurological findings- ipsilateral to a dilated pupil, contralateral to the most abnormal motor response, and ipsilateral to a skull fracture. It must be stressed that none of these signs are absolute and that if no hematoma is found on the suspected side, the other side should be explored in all cases. After diagnosis of either an acute subdural or extradural hematoma or no hematoma, two additional bur holes can be placed appropriately in the parietal and frontal regions. The skin incisions must be made in such a manner that if a formal craniotomy is required, they can be joined to form the skin flap. This opening is then rapidly extended with Leksell rongeurs to form a limited craniectomy about 3 cm in diameter. If the hematoma is in the subdural space, the dura is opened, and the underlying hematoma is promptly evacuated. Because adequate decompressive operations may require débridement of these lesions, the frontal and temporal lobes (especially the poles) should be accessible in the field of exposure. The inferior part of the frontal lobe should also be accessible down to the floor of the anterior fossa because the orbital gyri are frequently involved. Once the tamponade effect of the blood clot is released after craniotomy, these veins may start bleeding and can be better visualized if the craniotomy is close to the midline. These venous structures are especially vulnerable in the elderly, in whom the dura is usually thin and tightly adherent to the more irregular inner surfaces of the skull. The bur holes are then enlarged with a Kerrison bone punch and undermined to allow a Penfield No. If the dura is torn during this step, it is desirable to drill extra bur holes to prevent inadvertent lacerations of the dura by the craniotome. If greater medial exposure is needed, it can be carried out more safely with Leksell rongeurs under direct vision. Further exposure of the middle fossa is obtained with the use of Leksell rongeurs to remove parts of the lateral sphenoid wing and the temporal bone in piecemeal fashion, as low as needed, for temporal tip access. The first goal after removing the bone flap is decompression of any mass lesions that may be present. Commonly described techniques include a C-shaped durotomy based on the sagittal sinus, a cruciate opening, and a "basal" or "reversed U-shaped" durotomy. A second durotomy is begun over the lowest part of the temporal lobe so that the temporal tip may be removed, if major brain swelling ensues, after any subdural clots are removed. The dura should not be cut near the midline to avoid damage to the parasagittal bridging veins. The incision is carried low across the middle meningeal artery toward the temporal lobe to fashion the reversed U-shaped dural opening. Care is taken to protect the underlying brain tissue with a cottonoid pad if indicated. This durotomy technique permits good access to the basal frontal and temporal lobes and prevents parasagittal herniation of the frontal lobe and occlusion of bridging veins against the dural edge. Next, smaller slit incisions may be made circumferentially around the craniotomy (although not parasagittally) to grant additional access for removing the hematoma. Once the hematoma is removed, the surgeon may decide to connect and complete the full extent of the durotomy, depending on the amount of swelling present or how much visualization is needed to adequately address the surgical goals. Bleeding can also originate from the middle meningeal vein, the diploic veins, or the venous sinuses. One study reported an arterial source of bleeding in only 36% of adults and 18% of children. As the hematoma enlarges, the dura is progressively stripped from the inner table. To maximize intracranial relaxation, the patient may be given mannitol and mildly hyperventilated (Paco2 30 mm Hg). The slash incision, which typically runs vertically, should be fashioned so that it can be extended to the larger "trauma flap" if necessary. The incision is made with a scalpel or a Colorado needletipped Bovie and taken directly down to the bone. After the skin incision, hemostasis is obtained with the help of Raney clips or electrocautery. The periosteum is then rapidly stripped to fully expose the cranium in the region of the hematoma. More bur holes can be created as necessary depending on the size or location of the clot. With such a vertical incision, removal of the hematoma may be achieved within about 5 minutes of beginning the incision. A Kerrison punch and a curved curet can be used to enlarge and undercut the bur holes to allow a Penfield No. The blood, which is usually clotted, is removed with the help of suction, irrigation, and cup forceps. The bleeding source, typically a branch of the middle meningeal artery, can generally be controlled with bipolar diathermy. Occasionally, the main trunk of the middle meningeal artery is bleeding because of a fracture involving the petrous bone. In these cases, adequate low temporal exposure is facilitated by the vertical incision advocated here. The foramen spinosum can be packed with bone wax or a combination of bone wax and Surgicel. After evacuation of the hematoma, meticulous hemostasis is obtained in the epidural space with Surgicel and Gelfoam, and bone wax is applied to the bone edges. Central dural tack-up sutures are also placed in the center of the bone flap to obliterate the central dead space under the bone flap. Bur hole covers should always be placed over the frontal bur holes for the best cosmetic result. The superficial temporal fascia and then the galea are approximated with 2-0 Dexon or similar suture. Skin staples are placed on the skin margins, the wound is dressed, and a head bandage is placed. Rarely, intradural "reperfusion" hematomas develop rapidly under a removed extradural hematoma. After evacuation of the extradural hematoma, if the underlying dura becomes tense, a limited opening should be made in the dura and any hematoma removed with gentle suction and bipolar diathermy. A larger dural opening must be made rapidly if persistent subdural bleeding is seen to visualize and coagulate the source, which may be a bridging vein. A ventriculostomy may be needed in unconscious patients, especially if an intraparenchymal mass lesion is present. Occasionally, the craniotomy will need to be enlarged to expose the bleeding point. In such cases, both the incision and the craniotomy can be expanded to a more traditional frontotemporoparietal craniotomy. Emergency angiography has demonstrated bleeding points and traumatic tears in the middle meningeal artery, which can be embolized with coils or Onyx. Mortality has been reported to be between 50% and 60% in various series and between 57% and 68% in patients initially seen in coma. Therefore, surgical planning should consider the need to contend with concomitant lesions or parenchymal injuries. In a retrospective study, 34 patients older than 65 years were compared with a similarly treated younger patient population (33 patients aged 18 to 40 years); mortality rates were more than 4 times higher in the older patients. In a study of 68 consecutive patients with warfarin-related intracranial hemorrhages, Mathiesen and associates reported that traumatic hematomas were found in 26 patients. However, lower mortality rates of 48% and 16% have been reported after warfarin-related intracranial hemorrhages. As with all trauma craniotomies, it is customary to takes measures to maximize intracranial relaxation. Such measures include the administration of mannitol and the institution of mild hyperventilation. The subdural space should be widely inspected for additional hematoma, bleeding, and surface contusions. Achieving and maintaining hemostasis at the operative site is the most difficult and most important aspect of trauma neurosurgery.

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