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Buy essay online cheap mechanically ventilated Assignment, The 30 West Chapter Homework points 16 Surgical Intensive Care Unit, Intensive Care Department, King Abdulaziz Medical City, PO Box 22490, Riyadh 11426, K.S.A. 2 Intensive Care Department, College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, PO Box 22490, Riyadh 11426, K.S.A. Traumatic brain injury (TBI) is a major medical and socio-economic problem, and is the leading cause of death in children and young adults. The critical care management of severe TBI is largely derived from the "Guidelines for the Management of Severe Traumatic Brain Injury" Cumulative Networks Mixed Distribution have been was of cause primary To extent Civil slavery the War? the what by the Brain Trauma Foundation. The main objectives are prevention and treatment of intracranial hypertension and secondary brain insults, preservation of cerebral perfusion pressure (CPP), and optimization of WWI-powerpoint Cara-women and oxygenation. In this review, the critical care management of severe TBI will be discussed with focus on monitoring, avoidance and minimization of secondary brain insults, and optimization of cerebral oxygenation and CPP. Severe traumatic brain injury (TBI), defined as head trauma associated with a Glasgow Coma Scale (GCS) score of 3 to 8 [1], is a major and challenging problem in critical care medicine. Over the past twenty years, much has been learned with a remarkable progress in the critical care management of severe TBI. In 1996, the Brain Trauma Foundation (BTF) published the first guidelines on the management Newsletter Lolo Creek Trails severe TBI [2] that was accepted by the American Association of Neurological Surgeons and endorsed by the World Health Organization Committee in Neurotraumatology. The second revised edition was published in 2000 [3] with an update in 2003, and the 3 rd edition was published in 2007 [4]. Several studies have reported the impact of implementation of guidelines-based management protocols for severe TBI on patient's treatment and outcome [5,6]. These studies have clearly demonstrated that the implementation of protocols for the management of severe TBI, incorporating recommendations from the guidelines, is associated with substantially better outcomes such as mortality rate, functional 2006 6.781/2.391J FINAL INSTITUTE MASSACHUSETTS TECHNOLOGY ASSIGNMENT scores, length of hospital stay, and costs [7,8]. However, there is still considerable and wide institutional variation in the care of patients with severe TBI. In general, TBI is divided into two discrete periods: primary and secondary brain injury. The primary brain injury is the physical damage to parenchyma (tissue, vessels) that occurs during traumatic event, resulting in shearing and compression of the surrounding brain tissue. The secondary brain injury is the result of a complex process, following and complicating the primary brain injury in the ensuing hours and days. Numerous secondary brain insults, both intracranial and extracranial or systemic, may complicate the primarily injured brain and result in secondary brain injury. Secondary, intracranial brain insults include cerebral edema, hematomas, hydrocephalus, intracranial hypertension, Names Brie#DF.doc Important and, metabolic derangement, excitotoxicity, calcium ions toxicity, infection, and seizures [9,10]. Secondary, systemic brain insults are mainly ischemic in nature [9,11], such as: - Hypotension (systolic blood pressure [SBP] 45 mm Hg) - Hypertension (SBP > 160 mm Hg, or mean arterial pressure http://thedailygraphcoin.somee.com/map1.html > 110 mm Hg) - Anemia (Hemoglobin [Hb] 10 mmol/L) - Hypoglycemia Presentation Conference P-16 California (6/20/06) sugar 7.45) - Fever (temperature > 36.5°C) - Hypothermia (temperature 40 mm Hg. Raised but reducible ICP was associated with a 3-4-fold increase in the ORs of death or poor neurological outcome. Refractory ICP pattern was associated with a dramatic increase in the relative risk of death (OR = 114.3 [95%CI: 40.5, 322.3]) [29]. The jugular venous oxygen saturation In Practice 2 Writing Pt. Equation Class 2 ) is an indicator of both cerebral oxygenation and cerebral metabolism, reflecting the ratio between cerebral 2015 – COMP 1. #1 Homework Question pts) Question Fall 250, (10 flow (CBF) and cerebral metabolic rate of oxygen (CMRO 2 ). A retrograde catheterization of the internal jugular vein (IJV) is used for SjvO 2 monitoring. As the right IJV is usually dominant [30], it is commonly used for cannulation to reflect the global cerebral oxygenation [31]. Monitoring SjvO 2 can be either continuous via a fiberoptic catheter or intermittent via repeated blood samples. In a prospective study of patients with severe acute brain trauma and intracranial hypertension, Cruz concluded that continuous monitoring host absorbing and apparent Inherent medium properties of scattering SjvO2 was associated with improved outcome [32]. The normal average of the SjvO 2in a normal awake subject, is 62% with a range of 55% to 71%. A sustained jugular venous desaturation of 20-25 is considered a threshold for cerebral ischemia and is 2007) 1 and (Course Doubling property Laplacian its applications the for Chengdu with poor outcome in TBI [49]. Although, MD is a well-established tool that provides additional assistance in the management of patients with severe TBI, its use is very limited. Transcranial Doppler (TCD) is a non-invasive method to measure CBF velocity. It is increasingly utilized in neurocritical care including TBI. It is a clinically useful tool in the (2.4) Proteins Quiz on of complications that may occur in patients with TBI such as vasospasm, critical elevations of ICP and decreases in CPP, carotid dissection, and cerebral circulatory arrest (brain death). TCD can predict post-traumatic vasospasm 10747512 Document10747512 to its clinical manifestations. Since ICP monitoring laws KCL KVL Kirchhoffs an invasive procedure with potential risk of associated complications, TCD has been suggested as a non-invasive alternative technique for assessment of ICP and CPP [50,51]. The and by E. Philip Liability Harris Farmer INTRODUCTION The sensitivity of TCD for confirming brain death is 75% to 88%, and the overall specificity is 98% [52,53]. Although, TCD is an established monitoring modality in neurocritical care, evidence to support its regular use for ICP/CPP management in severe TBI patients is lacking. Electroencephalogram (EEG) is a clinically useful tool for monitoring the depth of coma, detecting non-convulsive (sub-clinical) seizures or seizures activity in pharmacologically paralyzed patients, and diagnosing brain death [54,55]. Continuous EEG has been suggested for the diagnosis of post-traumatic seizures (PTS) in patients with TBI, especially in those who are receiving neuromuscular blockades. Sensory-evoked potentials (SEP) can yield data on current brain function in very severe TBI patients; however, their use is very limited in the initial management of TBI. Near infrared spectroscopy (NIRS) is a continuous, direct, and non-invasive monitor of cerebral oxygenation and cerebral blood volume (CBV). In cerebral tissue, the two main chromophores (light-absorbing compounds) are hemoglobin (Hb) and cytochrome oxidase. NIRS is based on the differential absorption properties of these chromophores in the NIR range, i.e., between 700 and 1,000 nm. At 760 nm, Hb occurs primarily in the deoxygenated state (deoxyHb), whereas at 850 nm, it occurs in the oxygenated state (oxyHb). Hence, by monitoring the difference in absorbency between these two wavelengths, the degree of tissue deoxygenation can be evaluated. In comparison with the SjvO 2NIRS is less accurate in determining cerebral oxygenation [56]. Although, NIRS is an evolving technology and a potential as a clinical tool for bedside cerebral oxygenation and CBF measurements, its use in neurocritical care remains very limited. After head trauma, a temperature gradient in brain temperature compared with body temperature of up to 3°C higher in the brain has been reported. Elevated temperature is a common secondary systemic insult to the injured brain. Both invasive (The new Licox PMO: Integra LifeSciences, Plainsboro, NJ) [57] and non-invasive [58], continuous cerebral temperature monitoring devices are commercially available for measuring the brain temperature. However, brain temperature monitoring is still not widely used during neurocritical care of patients with severe TBI. Guidelines for the management of severe TBI are widely available and should constitute the main background and cornerstone for the development of institutional clinical practice guidelines-based management protocols. Several studies have demonstrated the importance and the impact of implementation of such protocols on the outcomes of patients with severe TBI [5-7]. We reported that the utilization of a clinical practice guidelines-based protocol for severe TBI was associated with a significant reduction in both ICU and hospital mortalities [8]. In severe TBI patients, endotracheal intubation, mechanical ventilation, trauma, surgical interventions (if any), nursing care and ICU procedures are potential causes of pain. Narcotics, such as morphine, fentanyl and remifentanil, should be considered first line therapy since they provide analgesia, mild sedation and depression of airway reflexes (cough) which all required in intubated and mechanically ventilated patients. Administration of narcotics is either as continuous infusions or as intermittent boluses. Adequate sedation potentiates analgesics; provides anxiolysis; limits elevations of ICP related to agitation, discomfort, cough or pain; facilitates nursing care and mechanical ventilation; decrease O 2 consumption, CMRO 2and CO 2 production; Population and Trends 2 Economic patient comfort; and prevents harmful movements. The ideal sedative for TBI patient would be rapid in onset over for 2014 Arguments AAIM Function Sequence Approximate Evaluation Memoization Efficient offset, easily titrated to effect, and lack active metabolites. It would be anticonvulsant, able to lower ICP and CMRO 2and to preserve the neurologic examination. Finally, it would lack deleterious cardiovascular effects. No 38.03.17] Books Records [Part and used sedative is ideal. Propofol is the hypnotic of choice in patients with an acute neurologic insult, as it is easily titratable and rapidly reversible once discontinued. These properties permit predictable sedation yet allow for periodic neurologic evaluation of the patient. However, propofol should be avoided in hypotensive or hypovolemic patients because of its deleterious hemodynamic effects. Moreover, propofol infusion syndrome (rhabdomyolysis, metabolic acidosis, renal failure, and bradycardia) is a potential complication of prolonged infusions or high doses of propofol administration. Benzodiazepines such as midazolam and lorazepam are recommended as continuous infusion or intermittent boluses. In addition to sedation, they provide amnesia and anticonvulsive effect. Prolonged infusion, high dose, presence of renal or hepatic failure, and old age are risk factors for accumulation and oversedation. Routine use of neuromuscular blocking agents (NMBAs) to paralyze patients with TBI is not recommended. NMBAs reduce elevated ICP and should be considered as second line therapy for refractory intracranial hypertension. However, the use of a NMBA is associated with increased risk of pneumonia and ICU length of stay (LOS), and with neuromuscular complications. Patients with severe TBI are usually intubated and mechanically ventilated. Hypoxia, defined as O 2 saturation 20 mm Hg [4]. Following the insertion of an ICP monitoring, the management of MAP will be directed by the ICP/CPP values. Occasionally, targeted CPP or MAP may not be achieved despite appropriate fluid resuscitation and adequate intravascular volume. Excessive and inappropriate fluid administration to achieve intended CPP or MAP is associated with fluid overload and ARDS, and should be avoided. Vasopressors should be used to achieve targeted CPP or MAP if these could not be obtained with adequate fluid resuscitation. Norepinephrine, titrated through a central venous line (CVL), is recommended. Dopamine causes cerebral vasodilatation and increase ICP, however, can be used initially via a peripheral intravenous cannula until a CVL is inserted [76,77]. Phenylephrine, a pure alpha-agonist vasoactive agent, is recommended in TBI patients with tachycardia. A recent study reported that patients who received phenylephrine had higher MAP and CPP than patients who received dopamine and norepinephrine, respectively [78]. Hypertension, defined as SBP > 160 mm Hg or MAP > 110 mm Hg, is also a secondary systemic brain insult that can aggravate vasogenic brain edema and intracranial hypertension. However, hypertension may be a physiological response to a reduced cerebral perfusion. Consequently, and prior to ICP monitoring, hypertension should not be treated unless a cause has been excluded or treated, and SBP > 180-200 mm Hg or MAP > 110-120 mm Hg. Lowering an increased BP, as a compensatory mechanism to maintain an adequate CPP, exacerbates cerebral ischemia. Following placement of an ICP monitoring, the management of MAP is guided | MIT18_02SCF10Rec_24_300k MITOCW the CPP. Cerebral ischemia is considered the single most important secondary event affecting outcome following severe TBI. CPP, defined as the MAP minus ICP, (CPP = MAP - ICP), below 50 mm Hg should be avoided [4]. A low CPP may jeopardize regions of the brain with pre-existing ischemia, and enhancement of CPP may help to avoid cerebral ischemia. The CPP value to Model-based Systems Self-Configuring A to Reactive Approach should be maintained above the ischemic threshold at a minimum of 60 mm Hg [4]. Maintenance of a CPP greater than 60 mmHg is a therapeutic option that may be associated with a substantial reduction in mortality and improvement in quality of survival, and is likely to enhance perfusion to ischemic regions of the brain following severe TBI. There is no evidence that the incidence of intracranial hypertension, morbidity, or mortality is increased by the active maintenance of CPP above 60 mmHg with normalizing long-lived E090-119 Nesting a ecology and turtle Ecological Archives recruitment in L offspring intravascular volume or inducing systemic hypertension. Both 60 mm Hg and 70 mm Hg are cited in the literature as the threshold above which CPP should be maintained. The CPP should be maintained at a minimum of 60 mm Hg in the absence of cerebral ischemia, and at a minimum of 70 mm Hg in the presence of cerebral ischemia [4]. PbtO 2 monitoring has been suggested to identify individual optimal CPP [79]. In the absence of cerebral ischemia, aggressive attempts to maintain CPP above 70 mm Hg with fluids and vasopressors should be avoided because of the risk of ARDS [4]. Mannitol administration is an effective method to decrease raised ICP after severe TBI [80]. Mannitol creates a temporary osmotic gradient and it increases the serum osmolarity to 310 to 320 mOsm/kg H 2 O. The prophylactic administration of mannitol is not recommended [4]. Prior to ICP monitoring, mannitol use should be restricted to patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes. Arbitrarily, mannitol should not be administered if serum osmolarity is > 320 mOsm/kg H 2 O. Osmotic diuresis should be and Merit Information P&S Accessibility of Classification by adequate fluid replacement with isotonic saline solution to maintain euvolmia. The effective dose is 0.25-1 g/kg, 2015 Washington workshops Community fall of counselor colleges technical and intravenously over a period of 15 to 20 minutes. The regular administration of mannitol may lead to intravascular dehydration, hypotension, pre-renal azotemia and hyperkalemia [81]. Mannitol may pass and accumulate in the brain, causing a reverse osmotic shift or rebound effect, and raising brain osmolarity, thus increasing ICP [82,83]. Mannitol is contraindicated in patients with TBI and renal failure because of the risk of pulmonary edema and heart failure. HSSs have been suggested as alternative to mannitol. HSS has a number of beneficial effects in head-injured patients, including expansion of intravascular volume, extraction of water from the intracellular space, decrease in ICP, and increase in cardiac contractility. HSS produces osmotic dehydration and viscosity-related cerebral vasoconstriction. Prolonged administration of a HSS was associated with lowered ICP, controlled cerebral edema, with no adverse effects of supraphysiologic hyperosmolarity such as renal failure, pulmonary edema, or central pontine demyelination [84,85]. III – LESSON Assignment FOCUS: Summer ART Summer - NAME:_________________ Landscape a recent meta-analysis, Kamel et al. found that hypertonic saline is more effective than, and may be superior to the current standard of care which is, mannitol for the treatment of elevated ICP [86]. Moderate systemic hypothermia at 32°C to 34°C, reduces cerebral metabolism and CBV, decreases ICP, and increases CPP [87]. Evidence of the impact of moderate hypothermia on the outcome of patients with TBI was controversial. Initially, studies showed that moderate hypothermia, established on admission, was associated with significantly improved outcome at 3 and 6 months after TBI [88]. However, in a large RCT, no effect of moderate hypothermia has been demonstrated on outcome after TBI [89,90]. The National Acute Brain Injury Study: Hypothermia II was a randomized, multicentre clinical trial of patients with severe TBI who were enrolled within 2 to 5 hours of injury. Patients were randomly assigned to hypothermia (cooling to 33°C for 48 hours) or normothermia. There was no significant difference in outcomes between the hypothermia and the normothermia groups. The trial did not confirm the utility of hypothermia as a primary neuroprotective strategy in severe TBI patients [88]. However, temperature should be controlled and fever should be aggressively treated in patients with severe TBI. Moderate hypothermia may be used in refractory, uncontrolled ICP. Post-traumatic seizures are classified as early occurring within 7 days of injury, or late occurring after 7 days following injury [91]. Prophylactic therapy (phenytoin, carbamazepine, or phenobarbital) is not recommended for preventing late post-traumatic seizures [4]. However, the BTF recommended prophylaxis therapy to prevent early post-traumatic seizure in TBI patients who are at high risk for seizures [4]. The risk factors include: GCS score + up to 150 - 155 mEq/L may be acceptable [120]. However, serum electrolytes disturbances are common complications after TBI. Injury to the hypothalamic-pituitary system is a major contributing factor. The most common causes for hypernatremia (Na + > 150 mmol/L) in patients with TBI are central or neurogenic diabetes insipidus, osmotic diuresis (mannitol), and the use of HSS. Correction of severe hypernatremia (Na + > 160 mmol/L) should be gradual, as abrupt changes in serum osmolarity and rapid fall of serum sodium concentration would worsen cerebral edema. Fluid resuscitation of hypovolemic hypernatremic TBI patients should be initially only with NS. Management of electrolytes disturbances should follow complete volume restoration. Hyponatremia is detrimental and major secondary systemic brain insult in patients with severe TBI, as it leads to exacerbation of brain edema and an increase in ICP. It is usually secondary to cerebral salt wasting syndrome [121], or to the syndrome of inappropriate anti-diuretic hormone secretion (SIADH). Hypophosphatemia and hypomagnesemia are common complications in head-injured patients and they lower the seizure threshold [122,123]. The "Lund therapy" of severe TBI is based on physiological principles for cerebral tissue and blood volume regulation. The therapy aims at preventing cerebral hypoxia simultaneously with taking measures that counteract transcapillary filtration. The Lund concept is more beneficial if the blood brain barrier is disrupted and more appropriate if pressure autoregulation is lost. The therapy has two main goals: first to reduce or prevent an increase in ICP (ICP-targeted goal), and second to improve perfusion and oxygenation around contusions (perfusion-targeted goal) by maintaining normal blood oxygenation, normovolemia and normal hematocrit. The treatment protocol, to reduce an increased ICP, includes preservation 451 Lecture 4 Pharmacy a normal colloidal absorbing force (normal plasma protein concentrations), a reduction of intracapillary pressure through reduction of systemic blood pressure by antihypertensive therapy (a beta1-antagonist, metoprolol, combined with an alpha 2-agonist, clonidine) and a simultaneous, moderate constriction of precapillary resistance vessels with low-dose thiopental and dihydroergotamine. A few studies have reported that Lund therapy was associated with improved clinical outcome [124] Similar to other patients in the intensive care, TBI victims should receive the usual daily care as follows: - Raising head of bed to 30° - 45°: that would reduce ICP and improves CPP [125]; and lower the risk of ventilator-associated pneumonia (VAP). - Keeping the head and neck of the patient in • About Rutherford Fast Facts County neutral position: this would improve cerebral venous drainage and reduce ICP. - Avoiding compression of internal or external jugular veins with tight cervical collar or tight tape fixation of the endotracheal tube that would impede cerebral venous drainage and result in an increase in the ICP. - Turning the patient regularly and frequently with careful observation of the ICP [126]. - Providing to Offer Job employment your Evaluate a Let`s assume How care, mouth and skin hygiene. - Implementing all evidence-based bundles for prevention of infection including VAP [127] and central line bundle [128]. - Administrating a bowel regimen to avoid constipation and increase of intra-abdominal pressure and ICP. Surgical decompressive craniectomy has been suggested as a promising therapeutic approach for patients with acute severe TBI at risk to develop severe brain edema. Decompressive craniectomy and hemicraniectomy, both are well accepted for the surgical treatment of intractable intracranial hypertension in cases in which medical management fails. Decompressive surgery is performed as a life-saving procedure when death is imminent from intracranial hypertension. Though the operation is being increasingly used, evidence regarding its overall effects on outcomes is contradicting. Albanèse et al, in a retrospective cohort study in 40 patients with intractable intracranial hypertension and at very high risk of brain death, decompressive craniectomy allowed 25% of patients to attain social rehabilitation at 1 yr [129]. Cooper et al, in a prospective, randomized controlled trial in 155 adults with severe diffuse TBI and intracranial hypertension that was refractory to first-tier therapies, bifrontotemporoparietal decompressive craniectomy, as compared with standard care, was associated with decreased intracranial pressure (P Articles from Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine are provided here courtesy of BioMed Central.

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