Every 15 Seconds, Someone In the United States Suffers a Traumatic Brain Injury

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1 Every 15 Seconds, Someone In the United States Suffers a Traumatic Brain Injury Background: Traumatic injury is the leading cause of death among persons between the ages of 1-44 years, accounting for 2.5 million hospitalizations and 180,000 deaths each year. 1 Traumatic brain injury (TBI) is a traumatically induced physiologic disruption of brain function, which can lead to permanent or temporary impairments to cognitive, physical and psychosocial functions. 31 Classically TBI has been classified into broad categories of mild, moderate and severe. This division is solely based upon clinical criteria as it relates to level of consciousness and defined by the Glasgow Coma Scale (GCS). While use of GCS has been demonstrated to be extremely helpful in the clinical management and prognosis of TBI, limitations exist. The GCS does not take into account the heterogeneity of individual cerebral physiology nor does it provide specific information about the pathophysiologic mechanisms responsible for the associated neurological deficits of TBI. The SFGH Neurotrauma Program supports the use of a multidimensional classification system which considers duration of loss of consciousness, post-traumatic amnesia, presenting level of consciousness, technologically advanced imaging, sensitive biomarkers and bioinformatics, and recognition of individual symptomatology variation. 31,32 Traumatic Brain Injury (TBI) Incidence Causes and Outcome The CDC estimates that annually, over 1.7 million Americans sustain a traumatic brain injury (TBI). 2 Of those individuals, approximately 275,000 will be hospitalized and 52,000 will die as a result of their injury. 2 Concussion or mild TBI accounts for 75% 3 of this population and approximately million individuals will be treated and released from the emergency department with a mild TBI. 3 The nationally recognized age, gender, and mechanism of injury stratification is consistent with that of San Francisco General Hospital and Trauma Center. Traditionally, in San Francisco the incidence of males sustaining a traumatic brain injury is greater than that of females. San Francisco is the fourteenth-most populous city in the country with an estimated population of 825,111. While 5% of this population is under the age of 5, those aged 65 and older make up 14% 33. Consistent with such statistics are the average ages of those evaluated and treated for TBI at SFGH, with 5% of patients being ages 1-17 and 27% of patients being >65 years of age. The top five mechanisms of injury, in order, for sustaining a Traumatic brain injury in San Francisco include; falls, assault, pedestrian accidents (struck by or against), and motor vehicle collisions. 1

2 TBI-related Disability and Cost to Society Every 5 minutes someone becomes permanently disabled as a result of a traumatic brain injury 4. Traumatic brain injury contributes to 1/3 of all injury-related deaths in the United States 2. 70,000-90,000 of those who survive will have lifelong disabilities and 2,000 more will live in a persistent vegetative state. 4 Neurological impairments following TBI include coma, paralysis or motor loss, speech and swallowing difficulties, emotional problems, memory difficulties and seizures. The severity varies, but even patients with mild traumatic brain injures can have significant cognitive impairments which can impact their lives. Many patients remain permanently disabled requiring long-term nursing care and remaining at high risk for medical complications such as pneumonia, urinary tract infections, pressure ulcers, muscle wasting and frozen joints. A TBI not only impacts the life of an individual and their family, but it also has a large societal and economic toll. The estimated economic cost of TBI in 2010, including direct and indirect medical costs, is estimated to be approximately $76.5 billion. Additionally, the cost of fatal TBIs and TBIs requiring hospitalization, many of which are severe, account for approximately 90% of the total TBI medical costs. 5,6 Two thirds of all TBI survivors will live a normal lifespan, but will require life long services and support. SFGH Traumatic Brain Injury Program San Francisco General Hospital and Trauma Center is the only Level-I Trauma center in the San Francisco Peninsula receiving all trauma patients from the City and County of San Francisco as well as Northern San Mateo County. SFGH provides care to approximately 3600 critically injured patients annually. Of those, approximately 800 have sustained a Traumatic Brain Injury. In an ongoing effort to provide high-end, state-of-the-art Neurotrauma care, the SFGH TBI program provides a framework for the development of comprehensive multidisciplinary TBI treatment guidelines spanning from the pre-hospital setting, through the Emergency 2

3 Department, Intensive Care Unit, acute care unit, and culminating in programs focused on neurological recovery in the community. The goal of this program is to maximize return of neurological function and to provide avenues for community re-integration through intensive rehabilitation and vocational retraining (where possible) and in the process, to instill in our patients a sense of purpose, pride, self-esteem and confidence. The SFGH TBI Program also provides an infrastructure for the development of clinical research programs aimed at critically assessing current clinical practices and developing cutting-edge treatment protocols for TBI patients. The final mission of the SFGH/TBI Program is to develop educational programs for patients, their families, the community at large and health-care professionals. These may take the form of safety education and prevention programs for elementary school, junior and high school students or educational materials such as literature and videos for patients and their families. Educational programs for health-care professionals include regularly scheduled TBI in-services at SFGH, as well as continuing medical education courses within the UCSF/SFGH community. The educational process naturally extends to presentations at national and international neuroscience conferences, and mainly focuses on researchrelated activities. The following SFGH/TBI Program document is intended to be comprehensive yet flexible, designed as a work-in-progress, to be modified as our knowledge of TBI expands. It was created with input and support from anaesthesia, critical care medicine, the emergency department, hospital administration, neurology, neurosurgery, nursing, nutrition, occupational therapy, orthopedics, physical therapy, psychiatry, radiology, rehabilitation medicine, social work, speech therapy, and the trauma service. 3

4 References 1. NCIPC: Web-based Injury Statistics Query and Reporting System (WISQARS) M, Xu L, Wald MM, Coronado VG. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control. Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. Atlanta (GA): Centers for Disease Control and Prevention; Finkelstein E, Corso P, Miller T and associates. The Incidence and Economic Burden of Injuries in the United States. New York (NY): Oxford University Press; Coronado, McGuire, Faul, Sugerman, Pearson. The Epidemiology and Prevention of TBI (in press) Guerrero J, Thurman DJ, Sniezek JE. Emergency department visits association with traumatic brain injury: United States, Brain Injury, 2000; 14(2): Thurman DJ, Guerrero J. Trends in hospitalization associated with traumatic brain injury. JAMA, 1999; 282(10): Unpublished data from Multiple Cause of Death Public Use Data from the National Center for Health Statistics, Methods are described in Sosin DM, Sniezek JE, Waxweiler RJ. Trends in death associated with traumatic brain injury, JAMA 1995;273(22): Analysis by the CDC National Center for Injury Prevention and Control, using data obtained from state health departments in Alaska, Arizona, California (reporting Sacramento County only), Colorado, Louisiana, Maryland, Missouri, New York, Oklahoma, Rhode Island, South Carolina, and Utah. Methods are described in: Centers for Disease Control and Prevention. Traumatic Brain Injury -- Colorado, Missouri, Oklahoma, and Utah, MMWR 1997;46(1): Thurman DJ, Sniezek JE, Johnson D, Greenspan A, Smith SM. Guidelines for Surveillance of Central Nervous System Injury. Atlanta: Centers for Disease Control and Prevention, Thurman DJ, Alverson CA, Dunn KA, Guerrero J, Sniezek JE. Traumatic brain injury in the United States: a public health perspective. J Head Trauma Rehab, 1999; 14(6): Kraus JF. Epidemiology of head injury. In: Cooper, PR, ed. Head Injury, Third Edition. Baltimore: Williams and Wilkins, 1993; Annegers JF, Grabow HD, Kurland LT, et al. The incidence, cause and secular trends in head injury in Olmstead County, Minnesota, Neurology 1980;30: Kalsbeek WD, McLaurin RL, Harris BS, Miller JD. The national head and spinal cord injury survey: Major findings. Journal of Neurosurgery 1980; 53:S19-S24. 4

5 References 13. Klauber MR, Barrett-Connor E, Marshall LF, Bowers SA. The epidemiology of head injury: A prospective study of an entire community--san Diego County, California, American Journal of Epidemiology 1981; 113: Jagger J, Levine JI, Jane JA, Rimel RW. Epidemiologic features of head injury in a predominantly rural population. Journal of Trauma 1984; 24: Fife D, Faich G, Hollinshead W, Wentworth B. Incidence and outcome of hospitaltreated head injury in Rhode Island. American Journal of Public Health 1986;76: Whitman S, Coonley-Hoganson R, Desai BT. Comparative head trauma experience in two socioeconomically different Chicago-area commmunities: A population study. American Journal of Epidemiology 1984; 4: Cooper KD, Tabaddor K, Hauser WA, et al. The epidemiology of head injury in the Bronx. Neuroepidemiology 1983;2: Kraus JF, Black MA, Hessol N, et al. The incidence of acute brain injury and serious impairment in a defined population. American Journal of Epidemiology 1984; 119: MacKenzie EJ, Edelstein SL, Flynn JP. Hospitalized head-injured patients in Maryland: Incidence and severity of injuries. Maryland Medical Journal 1989:38: Thurman DJ, Jeppson L, Burnett CL, et al. Surveillance of traumatic brain injuries in Utah. West J Med 1996; 165: Centers for Disease Control and Prevention. Traumatic brain injury -- Colorado, Missouri, Oklahoma, and Utah, MMWR 1997; 46(1): Gabella B, Hoffman RE, Marine WW, Stallones L. Urban and rural traumatic brain injuries in Colorado. AEP 1997;7(3): Thurman DJ, et al. Traumatic brain injury in the United States: A report to Congress. Atlanta, Centers for Disease Control and Prevention, Sosin DM, Sniezek JE, Waxweiler RJ. Trends in death associated with brain injury, JAMA 1995;273: Max W, MacKenzie EJ, Rice DP. Head injuries: costs and consequences. Journal of Head Trauma Rehabilitation 1991;6(2): Thurman DJ, Sniezek JE, Johnson D, Greenspan A, Smith SM. Guidelines for Surveillance of Central Nervous System Injury. Atlanta: Centers for Disease Control and Prevention, National Committee for Injury Prevention and Control. Injury Prevention: Meeting the Challenge. New York: Oxford University Press, Pope AM, Tarlov AR, editors. Disability in America: Toward a National Agenda for Prevention. Washington, DC: National Academy Press,

6 References 29. Saatman, KE, Duhaime, AC, Bullock, R. (2008). Classification of traumatic brain injury for targeted therapies. Journal of Neurotrauma 25: Menon, D.K., Schwab, K., Wright, A.I., et al. Position statement: Definition fo traumatic brain injury. Archives of physical Medicine and Rehabilitation. 91:11, World population statistics: San Francisco Population Retrieved February 17, 2014 from 6

7 Introduction: TBI Guidelines Traumatic brain injury (TBI) results in an alteration of cerebral physiology which may be amenable to interventions directed at limiting the injury cascade and, therefore, secondary injury. It has been recognized that, both nationally and locally, approaches to the management of the head injured patient vary significantly. This has led to the formation of evidence-based Guidelines for the Management of Severe Head Injury, which were published by the Brain Trauma Foundation in and revised in Purpose The purpose of this document is to provide standardized guidelines for the acute care management of the head injured patient at San Francisco General Hospital and Trauma Center. These guidelines are based generally on the Guidelines for the Management of Severe Head Injury, which were published by the Brain Trauma Foundation in 1995 and revised in They have been modified and expanded to address issues specific to San Francisco General Hospital and reflect approaches to certain issues not addressed in the Guidelines for the Management of Severe Head Injury. These guidelines do not replace the physician s judgment in individual cases, but may be considered reasonable and current approaches to the management of the critically ill adult head injury patient. While this document does not address specific guidelines for the management of pediatric head injury patients, many of the same principles are applicable. These guidelines are intended to foster a coordinated, cooperative environment within the multidisciplinary team caring for head injured patients, which includes but is not limited to, the Neurosurgery and Neurology Services, the Critical Care Service, the Trauma Surgery Service, Critical Care Nursing, Rehabilitation and Social Services. 7

8 Emergency Department Evaluation Background The early identification of a patient with suspected traumatic brain injury allows for appropriate triage and rapid treatment, thereby preventing secondary brain injury. The most established tool used to assess the level of consciousness or brain function after a head injury is the Glasgow Coma Scale (GCS). The GCS was first established in 1974 by Teasdale and Jennett and has since become the gold standard for rapid assessment and triage of the patient with suspected traumatic brain injury. The GCS is scored out of 15 and is comprised of three categories: best eye response, best verbal response, and best motor response. The best score attainable is 15 and the worst score is 3, which indicates a comatose state. Additional physical exam findings alerting the examiner that the patient is experiencing severe intracranial hypertension requiring immediate intervention include alterations in pupillary size and response, and impairment in the brainstem reflexes (corneals, cough, gag, and respirations). Goals Early identification and triage of the patient with suspected traumatic brain injury Rapid detection of neurological impairment and/or neurological decline allowing for prompt intervention and treatment Prevention of secondary brain injury Guidelines The initial neurological exam should be performed prior to administration of sedation, analgesics, or paralytics. The exam should include: Glasgow Coma Scale (Adult/Pediatrics) Pupil assessment using the pupillometer or flashlight. Significant findings: - Asymmetry: 1mm or more difference in size of pupils - Fixed pupil with no reactivity Pupillometer NPI <3 <1mm response to bright light - Left and right distinction and duration of the following Unilateral or bilateral fixed pupil(s) Unilateral or bilateral dilated pupil(s) Fixed and dilated pupil(s) Brainstem reflexes: assessment for absence of one or more of the following; - Unilateral or bilateral corneals - Cough reflex - Gag reflex - Respiratory drive 8

9 Initial Resuscitation of Blood Pressure and Oxygen Background In head injured patients, both hypotension (defined as a systolic BP < 90 mmhg) and hypoxia (defined as apnea, cyanosis, or a PaO2 < 60 mmhg) are associated with worsened clinical outcome 4. This occurs presumably because hypotension and hypoxia cause secondary injury in vulnerable brain tissue. While these insults may occur at any point in the clinical course of a patient with head injury, they often occur in the pre-hospital setting or during Emergency Department (ED) resuscitation. Patients with severe TBI may mask hypovolemic hypotension because of the Cushing s response to intracranial hypertension (hypertension with bradycardia and irregular breathing pattern). As such, patients may benefit from central venous monitoring during the period of acute fluid resuscitation to adequately assess their intravascular volume. A gradual increase in blood pressure associated with a gradual decrease in pulse (even if both are within normal limits) should suggest the development or progression of intracranial hypertension. Goals Avoid hypotension and hypoxia in patients with severe head injury Urgently treat hypotension and hypoxia, thus minimizing exposure of vulnerable brain tissue to these secondary insults Guidelines Hemodynamic resuscitation should begin in the ED with the placement of two largebore (14 or 16 G) IV s when possible. A groin Cordis may be placed in lieu of a peripheral IV. A subclavian central line should be placed when possible for volume-status assessment. The groin Cordis may be used to place a long central venous pressure line as long as two large-bore IV s are available for fluid resuscitation. Internal jugular lines are not practical in the ED setting since most patients will be wearing cervical collars. A temperature-sensing Foley catheter should be inserted during the initial resuscitation. This will help assess the patients fluid status as well as core body temperature. Systemic blood pressure should be recorded every five minutes during the initial resuscitation (ED) via automated sphygmomanometer. An arterial blood-pressure catheter (radial) should be placed as soon as possible to allow for continuous blood pressure readings. This procedure should be performed by a senior-level resident or an attending to ensure efficiency. 9

10 Volume resuscitation with 0.9%NS or blood (when appropriate) is the first intervention. Plasmalyte may be considered as an alternative resuscitation fluid, especially in patients with metabolic acidosis. Strict avoidance of hypotonic (0.45% and 0.225% NaCl) and D5-containing solutions should be observed during acute resuscitation and as routine maintenance fluids in the intensive care unit (ICU). At a minimum, systolic BP should be maintained above 90 mmhg. Ideally, mean arterial pressure (MAP) will be maintained above 80 mmhg, since a systolic blood pressure of 90 mmhg may be inadequate in the setting of elevated ICP. Systemic hypertension generally should not be treated in the acute setting of TBI, since this may reflect the body s natural response to intracranial hypertension. Antihypertensive medications may be administared if the systolic blood pressure is greater than 180 mm Hg. Beta blockers are the drug of choice in the absence of bradycardia. The first line beta blocker for use is labetolol, followed by metoprolol. Alternatives to beta blockers include calcium channel blockers such as nicardipine. Hydralazine should be avoided since it is thought to uncouple cerebral blood flow from metabolism. Pressors may be necessary in addition to volume resuscitation, especially in the setting of acute spinal cord injury (SCI). Phenylephrine, Norepinephrine, Epinephrine, or Dopamine are the pressors of choice. Phenylephrine may induce bradycardia in SCI and is generally reserved for use in TBI. The use of pressors in the acute setting should be agreed upon by ED, Trauma, Anesthesia and Neurosurgery attendings as applicable. Early intubation may be necessary to avoid hypoxemia in patients with severe head injury. While there is theoretical concern about pulmonary oxygen toxicity in patients receiving an FiO2 > 0.6, concerns of systemic and cerebral hypoxia take precedence. Treatment with supplemental oxygen will be initiated in the field and continued after arrival to ED. 100% FiO2 will be given prior to intubation and continued during the initial post-intubation period. FiO2 will be adjusted according to the the post-intubation arterial blood gas (ABG) to maintain PaO2 > 100. Rapid-sequence induction (RSI) should be carried out using Etomidate ( mg/kg) and succinylcholine or rocuronium as the agents of choice. Succinylcholine may theoretically increase ICP by depolarizing skeletal muscle, though patient outcome is unlikely affected by its use. Rocuronium, on the other hand is longer acting than succinylcholine a concern if intubation is not readily accomplished. Furthermore, it prevents the neurological examination of patients for a longer time than succinylcholine. Rocuronium may be reversed after minutes with neostigmine (20-70 mcg/kg) and glycopyrrolate (0.6 mcg/kg). 10

11 Due to the possibility of hypotension as a side effect, use of propofol in the intubated patient within the Emergency Department should be avoided, unless the patient has an arterial line in place and continuous monitoring of the blood pressure can be performed. Sedation should be provided to a medically paralyzed patient. Ventilation rate should be controlled to maintain adequate oxygenation. Because of the significant effects of ventilation on cerebral blood flow, hyperventilation during the acute resuscitation phase should be reserved for use only as a temporizing measure for patients with evidence of acute brain herniation. Hyperventilation can decrease venous return, cardiac output, and blood pressure, thereby increasing the incidence of secondary brain injury. Thus, hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow is often critically reduced. Initial serological studies must include the following: Post-resuscitation Arterial Blood Gas Chem-7 (Electrolytes, BUN, Creatinine and Glucose) CBC with platelets Coagulation panel (PT/PTT/INR) Serum Osmolarity Type and Screen (cross # of units as necessary) Serum alcohol level and Urine toxicology 11

12 Head Computed Tomographic Imaging in the Patient with Suspected TBI Background Worldwide, traumatic brain injury (TBI) is a leading cause of death and permanent disability, affecting approximately 1.7 million Americans annually. 1 Goal The purpose of this guideline is to correctly diagnose those patients with suspected traumatic brian injury, allowing early intervention and treatment and to ensure consistency in obtaining computed tomographic (CT) radiographic examination in the patient who presents with altered mentation. Guidelines A non-contrast head CT scan is indicated in head trauma patients with loss of consciousness or post-traumatic amnesia only if at least one of the following is present: 2 Headache Vomiting Age >60 years Drug or alcohol intoxication Deficits in short-term memory Physical evidence of trauma above the clavicle Post-traumatic seizure GCS <15 Focal neurologic deficit Coagulopathy (INR >1.4) A non-contrast head CT should be considered in head trauma patients with no loss of consciousness or post-traumatic amnesia if there is: 2 Focal neurologic deficit Vomiting Severe headache Age >65 years Physical signs of a basilar skull fracture GCS <15 Coagulopathy (INR >1.4) Dangerous mechanism of injury (ejection from a motor vehicle, pedestrian vs auto, fall from height >3 feet or 5 stairs) Any patient with an intitial positive head CT finding (acute intracranial blood or cranial fracture) is required to have a subsequent scan within six hours to assess for evolution of the intracranial bleed. 12

13 Neurosurgical Operative Intervention for the Patient with Traumatic Brain Injury Background The most significant complication of TBI is the development of an intracranial mass lesion(s). Without effective and timely surgical intervention, an intracranial lesion can exacerbate intracranial hypertension. Prolonged delay in the diagnosis or evacuation thereof may produce permanent cognitive impairments, vegetative survival or death 1. Goal Provide effective and timely surgical intervention for patients with posttraumatic intracranial mass lesions in accordance with the National Guidelines for the Surgical Management of Traumatic Brain Injury. Guidelines Management of acute epidural hematomas (EDH) EDH >30cc should be surgically evacuated regardless of GCS EDH <30cc and with <5mm midline shift with a GCS >8 without focal deficit can be managed non-operatively with serial CT scans and neurological observation - The first serial CT should be performed within 6-8 hours after injury. Management of acute subdural hematomas (SDH) SDH with a thickness >10mm or MLS >5mm should be surgically evacuated, regardless of GCS. All patients with a SDH and a GCS <9 should undergo ICP monitoring. GCS <9 with a SDH <10mm in thickness and MLS <5mm should undergo surgical evacuation of the lesion if the GCS decreased between the time of injury and admission by >2 points and/or the ICP is >20mmHg. Management of traumatic parenchymal lesions Parenchymal mass lesions with signs of progressive neurologic deterioration referable to the lesion, medically refractory intracranial hypertension, or signs of mass effect on CT should be treated operatively. GCS 6-8 with frontal or temporal contusions >20cc in volume with MLS >5mm and/or cisternal compression on CT scan, and patients with any lesion >50cc in volume should be treated operatively. Parenchymal mass lesions without evidence of neurologic compromise, controlled ICP, and no significant mass effect on CT may be managed nonoperatively with intensive monitoring and serial imaging. Management of posterior fossa mass lesions Lesions which create mass effect on CT or with neurological dysfunction or deterioration referable to the lesion should undergo operative intervention Lesions with no significant mass effect on CT and without signs of neurologic dysfunction may be managed with close observation and serial imaging. 13

14 Mass effect on CT is defined as: - Distortion, dislocation, or obliteration of the fourth ventricle - Compression or loss of visualization of the basal cisterns - Presence of obstructive hydrocephalus Management of depressed skull fractures Open (compound) fractures depressed greater than skull thickness should undergo operative intervention to prevent infection Open (compound) depressed skull fractures may be treated non-operatively if: - No clinical or radiographic evidence of dural penetration - No significant intracranial hematoma - No depression>1cm - No frontal sinus involvement - No gross cosmetic deformity - No wound infection - No pneumocephalus - No gross wound contamination Closed (simple) depressed skull fractures may be managed non-operatively or operatively depending on the degree of fracture displacement, extent of comminution, presence or absence of frontal sinus involvement and cosmetic considerations. References 1. Bullock, M.R., Chestnut, R., Ghajar, J., et al. (2006). Guidelines for the Surgical Management of Traumatic Brain Injury. Neurosurgery. 58:S

15 Timing of Non-Neurosurgical Operative Procedures Background Patients with severe head injury often have other injuries that require operative intervention. Strategies designed to treat non-neurologic injuries may be at odds with the guidelines for management of severe head injury if hypovolemia or hypotension is tolerated. Issues related to non-neurosurgical operative procedures may exacerbate secondary brain injury if attention is not taken to avoid hypotension and aggressive volume resuscitation, especially with hypotonic fluids. Goal To allow safe and successful treatment of non-neurologic injuries, while avoiding secondary brain injury. Guidelines In general, neurologic management issues will take precedence in patients with severe head injury and multi-system trauma. If a non-neurologic injury is immediately life-threatening, urgent medical and surgical intervention will be undertaken as appropriate, with attention to maintaining a minimum systolic BP > 90 mmhg (MAP > 90 mmhg strongly recommended) with volume and pressors, and PaO2 > 100 mmhg. ICP monitoring will be considered during the non-neurosurgical operative intervention with the threshold CPP of 70 mmhg being preferred. For non-life threatening non-neurologic injuries requiring operative management, timing of surgery will be at the discretion of the Neurosurgery Attending, with input from the appropriate surgical service(s). In general, these procedures should be deferred until at least 1 week post-trauma. Discussion will be undertaken between the surgical, neurosurgical, and anesthesia services prior to operative intervention in order to ensure accurate communication regarding goals of intraoperative neurologic management. 15

16 Neurological Assessment in Acute Care Background Performance of serial neurological examinations by the interdisciplinary team is an essential component in the care of TBI patients. Serial examination allows for detection of not only drastic but also subtle changes in neurological status, thus allowing for prompt intervention to prevent further neurological disability and possibly death. Glasgow Coma Score The GCS was first established in 1974 by Teasdale and Jennett as a way to alleviate some of the ambiguities in exam and treatment that were occurring in patients presenting in an unconscious or comatose state. It provides a method for rapid and repetitive assessment of the head injured patient. The scale allows for appropriate triage, assists in guiding therapy and provides us with a basis for observing the depth of coma and degree of brain dysfunction. The scale assesses three components: eye opening, verbal response and motor response. The examiner should note the BEST score in all areas of testing. (See Appendix C-1) Pupillary Assessment One of the most important parameters for early evaluation of increasing intracranial pressure in the neurologically injured patient is pupillary size and reaction to light. The pupillary examination can be assessed in an unconscious patient or in a patient receiving neuromuscular blocking agents and sedation. Pupillary response should be obtained during initial resuscitation and every hour or as indicated thereafter. Size: The normal diameter of the pupil is between 2 and 5 mm, with the average pupil measuring 3.5 mm. Although both pupils should be equal in size, a 1-mm discrepancy is considered a normal deviation (anisocoria). Shape: Round: The normal shape of the pupil is round. Irregular: Irregular-shaped pupils may be the result of ophthalmological procedures such as cataract surgery or lens implants. Oval: A pupil that is oval in shape may indicate the early compression of cranial nerve III due to increased intracranial pressure. Reaction to Light: Brisk: Normally, pupils should constrict briskly in response to light. Sluggish: Slow pupillary response may indicate increased ICP. Nonreactive: Fixed pupils are often associated with extreme increases in ICP. This is well known to be related to a poor prognosis, especially when present bilaterally. If not caused by local trauma or drug action, this symptom indicates injury or compression of the third cranial nerve (oculomotor) and the upper brain stem, usually caused by an intracranial mass lesion or by diffuse brain injury. 16

17 Pupillometer: The pupillometer is used to obtain accurate, objective and consistent pupillary assessments. The most significant data obtained from the quantitative analysis obtained by the pupillometer is the Neurological Pupillary Index (NPI). The NPI is determined by extrapolating information, and includes pupillary size prior to light stimulation (MAX), pupillary size after light stimulus (MIN), % change of pupil, and constriction velocity (CV). Pupillometer measurements are obtained based on the patient s acuity per the following guidelines: GCS <12 and non-ventilated, Q1-2 hours or as indicated GCS <9 and ventilated, Q1-2 hours or as indicated Any neurological patient with multi-modality monitoring Q1-2 hours or as indicated - If the patient has an ICP monitor and the ICP has been stable (<20mmHg) and the patient has required no medical or surgical intervention for 48 hours, the pupillometer can be done once every shift Any neurologic assessment decompensation Per RN discretion when patient has dark irises, pupils that are difficult to assess, or RN has any questions about pupil reactivity. Brainstem reflexes Brainstem reflexes are reflective of the functional status of the brainstem. The brainstem reflexes that are easy, quick, and safe to evaluate at any time during the workup of a TBI patient include corneal reflex, cough/gag reflex, and respiratory drive assessment. These reflexes will be impaired or unreliable if the patient has received a neurological-muscular blocking agent or is on high levels of sedation or analgesia. In a patient who is awake, talking, and breathing with no difficulty, it can be assumed that these reflexes are intact. Corneal reflex: When an object is placed near or in an eye there should be an involuntary blink. This can be assessed with a drop of saline; if there is no blink when a drop of saline is instilled into the eye, the examiner should use a piece of gauze or cotton to gently touch the patients cornea and assess for a blink. Cough/ gag reflex: When the throat/trachea is irritated with an endotracheal tube or other object, there should be an involuntary gag/cough. Respiratory drive: This can be assessed by the presence of spontaneous respiration in a patient who is not intubated. In an intubated patient, this is evident by over-breathing a set rate on a ventilator. When a patient is intubated and sedated, it may be necessary to work with the respiratory therapist and bedside nurse to evaluate if spontaneous breathing is present. 17

18 Orientation Orientation assessment is reflective of cognitive impairment. The statement A&O X3 does not imply performance of an appropriate exam. It fails to identify specific components which may influence cognitive interventions. Components of a complete orientation exam: Person (First and Last name) Place (Hospital, City, State) Date (Year, Month, Day) Event and/or circumstances If the patient is unable to appropriately respond, the examiner should rule out the possibility of aphasia. A quick assessment tool to use is repetition of a familiar phrase, such as No if ands or buts. An inability to accurately repeat this statement implies the presence of an aphasia and requires detailed work-up by Speech Therapy. (See Cognition and Behavioral Guidelines) Motor When assessing the motor response of a head injured patient it is imperative that a focused motor exam be performed. In the unresponsive patient, the motor exam is incorporated into the GCS evaluation. If the patient is cooperative, motor strength should be tested in all four extremities with comparisons made bilaterally. The following muscle groups should be tested: Upper Extremities Deltoids Wrist Extensors Biceps Hand Grip Triceps Interossei Lower Extremities Quadriceps Tibialis Anterior Hamstrings Gastrocnemius Iliopsoas Extensor Hallucis Longis Grade Strength No contraction Flicker or trace contraction Active movement with gravity eliminated Active movement against gravity 4 - slight resistance Active movement against resistance; (Subdivisions) 4 moderate resistance Normal strength 4 + strong resistance Goal Performance of a complete neurological examination in order to rapidly detect deviations from baseline thus preventing neurological disability. 18

19 Guidelines Perform routine serial neurological examinations every 1-4 hours as appropriate. Brainstem reflexes should be evaluated in the initial workup, and as part of the routine serial neurological examinations in patients who are neurologically impaired. Pupillometry should be utilized with each serial neurological examination. MD notification of subtle or major neurological changes from baseline. Repeat Head CT for changes in neurological status, as indicated. Neurosurgical intervention as appropriate based upon findings. 19

20 Multi-Modal Monitoring Background Despite advances in understanding and treatment of severe head injury, significant morbidity and mortality remain. Monitors aimed at determining the metabolic and functional status of the brain are indispensable for state-of-the-art evaluation of posttraumatic cerebral pathophysiology. Current tools for the evaluation of cerebral metabolic status include: intracranial pressure (ICP) monitoring, jugular venous saturation (SJVO2) monitors, cerebral blood flow (CBF) monitors, brain tissue oxygen monitors (PbtO2), and microdialysis catheters. Current electophysiological monitors include electroencephalography (EEG), motor evoked potentials (MEP), somatosensensory evoked potentials (SSEP), brainstem auditory evoked response (BAER), and higher cognitive/executive responses such as the P300. Current imaging technologies also include CT perfusion scans (CTP), diffusion weighted imaging (DWI), diffusion tensor imaging (DTI), diffusion-perfusion MRI, and magnetic resonance spectroscopy (MRS). Goal To comprehensively monitor cerebral metabolic and functional endpoints in order to determine the physiological, functional, and metabolic status of the brain to allow for targeted therapy for each patient. Guidelines Based on physician discretion, patients with severe TBI requiring ICP monitoring may have one or more brain tissue monitors to assess the brain tissue oxygen levels and cerebral metabolism. Based on physician discretion, patients with ICP monitors may have jugular bulb catheters placed to help determine mixed venous cerebral oxygen extraction, and metabolic state. Based on physician discretion, some patients may also have parenchymal CBF monitors placed as part of the metabolic monitoring array. Based on physician discretion, patients with severe TBI may have 24-hour electrophysiological (EEG) monitoring started as close to admission to the ICU as possible. MEP, SSEP, BAER, and P300 responses may also be evaluated at regular intervals. Electrophysiological monitoring and assessment will continue until it is deemed no longer necessary by the Neurosurgery attending in consultation with the Neurocritical Care team. Based on physician discretion, patients will have CT perfusion scans and MR perfusion/diffusion scans as needed for quantitative and qualitative determination of cerebral blood flow and perfusion. 20

21 Based on physician discretion, MR spectroscopy may be obtained as needed to determine the patients cerebral metabolic picture as a function of neuroanatomical geography. Based on physician discretion, patients in whom diffuse axonal injury (DAI) is suspected may have an anatomical MRI and DTI to evaluate the integrity of the white matter tracts. 21

22 Intracranial Pressure (ICP) Monitoring Background ICP is frequently elevated in patients with severe head injury. Mechanisms causing elevated ICP include cerebral edema, intracranial hematoma formation, and hydrocephalus. While there is no prospective randomized controlled trial showing that treatment of elevated ICP improves outcome from severe head injury, there is a large body of evidence suggesting that monitoring of ICP and its subsequent treatment impact head injury outcome. Normal ICP is from mmhg; ICP above 20 mmhg is considered elevated 6. Goals Detect elevated ICP in order to allow surgical and medical management to lower ICP and maintain cerebral perfusion pressure (CPP). Allow for drainage of CSF (when available) as a means for treating elevated ICP. Guidelines Indications for ICP Monitoring 1 ICP monitoring is appropriate for patients with severe TBI (GCS 3-8) with an abnormal admission head CT scan. ICP monitoring is appropriate for patients with severe TBI (GCS 3-8) with a normal head CT scan if two or more of the following are present: - Age > 40 - Unilateral or bilateral motor posturing - Systolic blood pressure < 90 mmhg ICP monitoring may also be considered in patients with head injury who are undergoing non-neurosurgical operative procedures early in their hospital course, during which time neurologic examination will be unavailable. Technology for ICP Monitoring Placement of a ventricular catheter is the preferred method for ICP monitoring as it allows CSF drainage for the treatment of elevated ICP. When placement of a ventricular catheter is not deemed appropriate (i.e. slit ventricles, coagulopathy with INR > 1.7 or platelet count <50,000), then use of a parenchymal fiberoptic monitor (e.g. Camino) is preferred over other methods such as subdural monitoring. Threshold for Treatment of ICP ICP treatment should be initiated at an upper threshold of 20 mmhg. 1 ICP treatment should be taken in context of clinical examination and CPP data. 22

23 Methods of CSF Drainage: intermittent and continuous. Intermittent drainage for elevated ICP is the preferred method for traumatic brain injury patients. When intermittent drainage is used, the opening and closing pressures and volume of CSF drained should be recorded, as this may give an indication of intracranial compliance. Continuous CSF drainage at a specified pressure-height is an alternative, with the recognition that this method may interfere with continuous monitoring of ICP, unless an additional monitor is placed. Infection Control Emperic antibiotics will not be used for prophylaxis against infection after routine ICP monitor placement, including ventricular catheters 1. Great attention will be paid to sterile placement and maintenance of ICP monitors, especially ventricular catheters, as conditions during placement and instrumentation are the greatest risks for inducing infection. CSF will be sent for analysis from ventricular catheters as needed for infection surveillance and diagnosis. CSF will be withdrawn directly from the ventricular catheter using sterile technique. CSF sampling will be performed only by Neurosurgical team members who have undergone instruction, evaluation, and clearance by one of the Neurosurgical Attendings. CSF will be sent for the following: - cell count - glucose - protein - gram stain - culture - Concurrently, a serum glucose should be sent for comparison. Antibiotic coverage will be initiated for treatment of suspected or confirmed ICP monitor (esp. ventricular catheter) infection. Antibiotic coverage will be tailored to bacteriologic isolates and their sensitivities. 23

24 Cerebral Perfusion Pressure (CPP) Background Cerebral perfusion pressure (CPP) = MAP ICP. Cerebral ischemia may be the most important secondary event affecting outcome after severe traumatic brain injury. Cerebral perfusion pressure therapy is designed to prevent secondary ischemic insults to vulnerable traumatized brain tissue. 11 While the optimal CPP may vary from individual to individual, evidence from studies using transcranial Doppler ultrasound (TCD) and from the Traumatic Coma Data Bank suggest that a threshold CPP of at least 70 mmhg is an appropriate goal. 3, 6 More recent data suggests that a CPP of > 60 mmhg is preferred, though this target may vary according to the patient s individual autoregulatory set point. 1 Goals Avoid secondary cerebral ischemia of traumatized brain by ensuring adequate cerebral perfusion. Maintain euvolemia or slight hypervolemia, in order to ensure adequate cerebral and systemic organ perfusion. Guidelines CPP Management A CPP of > 60 mmhg will be maintained using volume and pressors as necessary. Threshold CPP will be tailored to individual patients using cerebral monitoring tools such as ICP, TCD, jugular venous oxygen saturation (SJVO2), and EEG. Patients will be assessed for the presence or absence of intact cerebral autoregulation and CPP goals will be adjusted accordingly. Hemodynamic Monitoring Insufficient evidence exists currently to recommend one method of hemodynamic monitoring in the brain injured patient over another. Therefore, we will recommend that all patients undergoing ICP monitoring receive a central venous catheter to measure CVP preferably via a subclavian route (to avoid possible IJ thrombosis, carotid artery puncture, and to reserve the IJ for SJVO2 monitoring). Patients will also receive an arterial catheter, preferably at the radial site. By convention, the arterial pressure transducer will be placed at the level of the right atrium. This group acknowledges that some published protocols have used arterial pressures at the level of the cerebral ventricles for CPP calculations. 24

25 In order to minimize the effect of head-of-bed (HOB) elevation on CPP, HOB should be raised no more than 30 o. This strategy also addresses the observation that cerebral blood flow drops as the HOB elevation exceeds 30 o even in the setting of a constant CPP, and with the ICP monitor zeroed at the foramen of Monro. Pulmonary artery catheters will be used at the discretion of the treating physician, particularly in patients who cannot be managed via other methods (CVP line, clinical evaluation, cardiac echo). Pressor and Volume Therapy CVP will be maintained at 5-10 mmhg, which is slightly hypervolemic. If a PA catheter is used, then PCWP will be maintained at 8-12 mmhg. Because these pressure measurements may be altered by changes in intra-thoracic pressure which accompany PEEP, ARDS/lung injury, and increased intra-abdominal pressure, attention must be made to correlate intravascular pressures with other measures of volume status such as urine output and heart rate in order to ensure euvolemia or slight hypervolemia. When pressors are used for CPP management, attention will be made to ensure that the patient is adequately fluid resuscitated before instituting a pressor infusion. Initial pressor of choice is phenylephrine (5-200 mcg/min), with dopamine (5-20 mcg/kg/min) an alternative choice. Norepinephrine is considered a second-tier choice and if considered, great attention must be paid to volume status in order to avoid precipitating systemic metabolic acidosis. 25

26 Respiratory Care Background Hypoxia is major contributor to the development of cytotoxic edema and thus is one of the most lethal of all secondary insults that a TBI patient can experience. Literature demonstrates that approximately 70% of all TBI patients will experience at least one episode of hypoxia during the early phases of care. A single episode of hypoxia, defined as a PaO2 <60 or oxygen saturation of <90%, can lead to a two-fold increase in TBI mortality. 1 Additionally, we know cerebral blood flow is often critically reduced following traumatic injury. Hyperventilation further decreases blood flow by causing vasoconstriction within the cerebral vascular system. Thus, the recommendation for early intubation and effective oxygenation for the TBI patient is crucial for prevention of secondary brain injury. The principal purpose of mechanical ventilation in severe brain injury is to ensure adequate systemic and cerebral oxygenation. Airway protection with endotracheal intubation is also important to avoid upper airway obstruction and aspiration. In the past, aggressive hyperventilation had been a cornerstone of brain injury management because of the ability to decrease ICP by decreasing cerebral blood volume via hypocapnic cerebral vasoconstriction. Recent evidence has demonstrated, however, that aggressive prophylactic hyperventilation actually worsens outcome after severe head trauma 9. The presumed mechanism for this is exacerbation of cerebral ischemia from the hypocapnic vasoconstriction, and the resulting acidosis. Hyperventilation should be reserved for use as a short-term strategy for lowering ICP until other measures can be instituted. In patients with normal lungs, a normal ABG is 7.40/40/100. In patients with acidosis or alkalosis, it is unknown how cerebral blood flow is affected, thus a normal ph will be the goal. Goals Ensure optimal oxygenation and ventilation, including mechanical ventilation in patients who require airway protection via intubation. Prevent secondary injury from hypoxia following TBI. Maintain normoventilation, as evidenced by a normal ABG. Optimize ICP control by fine-tuning ventilator control. Guidelines Rapid evaluation of respiratory and ventilatory status upon arrival to the Emergency Department Emergent tracheal intubation for the patient presenting with a GCS <8 26

27 Placement of an end-tidal CO2 (ETCO2) monitor on all intubated patients and/or patients with ICP monitoring. The goal ETCO2 is 1-5 points below pco2 as determined by correlating the patient s ABG to ETCO2. Initial ventilator settings will involve volume-controlled ventilation (AC or SIMV) with PEEP of 5. Recognizing that patients set their own minute ventilation via their medullary respiratory drive, patients that exhibit neurogenic hyperventilation will be allowed to do so. Changing the mode of ventilation will not affect this and it is currently unclear if neurogenic hyperventilation is deleterious or compensatory. PEEP of < 10 cm H2O will be tolerated without concern for exacerbation of ICP. On a case by case basis, the effect of PEEP on ICP will be considered. Because ventilation is a primary ICP-management modality, all changes in ventilation parameters in patients with ICP monitors must be cleared by the Neurosurgery Chief Resident or Attending. Any changes in ventilator-controlled respiratory rate to correct PaCO2 will occur slowly in a stepwise fashion and be instituted over a period of 1-2 hours. Hyperventilation may be used as an acute strategy to temporarily lower ICP in patients with evidence of acute brain herniation while the patient is being transported to CT, OR, or while other interventions such as ventriculostomy placement are being instituted. If hyperventilation has been used, it will be withdrawn slowly in a stepwise fashion over 2-4 hours to avoid a rebound increase in ICP. Maintenance of a PaO mmHg unless otherwise instructed (Goal 100mmHg) Maintenance of a PaCO mmHg unless otherwise instructed (Goal 40mmHg). Target PaCO2 for signs of herniation: 25 mm Hg. Maintenance of a PH of mmHg Ventilation rates are to be changed by 1 breath per hour unless otherwise instructed. Note: TBI patients with severe ARDS (high dead-space fraction) may need larger and/or more frequent rate changes to reach PaCO2 targets. An FiO2 challenge will be conducted every shift for any patient with brain tissue oxygen monitoring. An ABG will be obtained for any patient who experiences a PbtO2 drop to 15mmHg or below, a PbtO2 rise of >100mmHg for >30 minutes, or a increase/decrease in PbtO2 by 50%. ABGs and venous blood gases will be obtained every shift in any patient with SjvO2 monitoring for recalibration purposes; they will also be obtained after a noted SjvO2 decline to <55% or increase to >75%. 27

28 ABGs will be obtained on every intubated patient daily and PRN. Intubated patients will receive daily CXRs to assess ETT placement and assess pulmonary status. Patients will receive nebulizer treatments as indicated to to assure effective ventilation. Early mobilization will be considered for all TBI patients in an effort to promote pulmonary toileting, effective oxygen exchange, and prevention of ventilatorassociated pneumonia. Pneumonia will be diagnosed based upon accepted CDC criteria and antibiotic admistration will be tailored to organism sensitivity. Patients with suspected or diagnosed ARDS will be started on the SFGH ARDS protocol (see attached). Management of severe oxygenation/ventilation problems associated with ARDS (or other conditions) includes higher levels of PEEP, pulmonary recruitment maneuvers, aerosolized prostacyclin, use of neuromuscular blocking agents and/or prone positioning. Use of these therapies (as well as the order and combination) should be addressed in a multidisciplinary discussion weighing the risk/benefit ratios at any particular time point in a patient s disease progression. Intubated patients will be considered for early tracheostomy by hospital day 7. References: Chestnutt, R.M, Marshall, L.F, Klauber, M.R. et.al. (1993). The role of secondary brain injury in determining outcome from severe head injury. J. Trauma. 34: Rosenthal, G., Hemphill, J.C., Sorani, M., et.al. (2008). The role of lung function in brain tissue oxygenation following traumatic brain injury. J.Neurosurg. 108(1):

29 Fi O2 Appendix: 1 Proposed Guidelines for Respiratory Management of Severe Hypoxemia in Patients on Traumatic Brain Injury Protocol. ICP < 20 and Non-Labile: PEEP & Other Interventions < cmh 2 O 5 cmh 2 O cmh 2 O 5 cmh 2 O cmh 2 O 2. begin considering ARDS Net protocol ICP > 20 and/or Labile: PEEP & Other Interventions 5-8 cmh 2 O cmh 2 O cmh 2 O 2. PEEP titration evaluation* 3. Consider aerosolized prostacyclin > > 16 cmh 2 O 2. PEEP titration evaluation 3. Trial of aerosolized prostacyclin 4. Avoid Fi O2 of 1.0 (de-nitrogen atelectasis) 5. Consider prone position 6. Consider recruitment maneuvers 7. Downgrade Pa O2 goals to? Denotes sustained Fi O2 requirements > 24h cmh 2 O 2. PEEP titration evaluation* 3. Consider aerosolized prostacyclin cmh 2 O 2. PEEP titration evaluation 3. Trial of aerosolized prostacyclin 4. Avoid Fi O2 of 1.0 (de-nitrogen atelectasis) 5. Consider prone position 6. Consider recruitment maneuvers 7. Down-grade Pa O2 goals to? * Incremental PEEP Trials should be done (perhaps Q-Day) to assess potential recruitment (degree of improvements in Pa O2 /Fi O2, compliance and Vd/Vt) balanced against potential adverse effects on BP, ICP, CPP, Sjv O2, PBR O2 29

30 Appendix 2: Estimating Minute Ventilation Adjustments for PaCO2 in Patients with Severe ARDS with Elevated Dead-Space Ventilation or Hypermetabolism (VCO2 > 300 ml/min). Target Population: Patients with minute ventilation demand > 12 L/min to maintain normal range PaCO2. 1. Assess degree of disparity between measured vs. target PaCO2 2. Target minute ventilation = measured minute ventilation x (Measured PaCO2/ Target PaCO2) 3. Assess how quickly PaCO2 should change/hr to achieve target ICP. 4. Adjust RR change/hr to achieve minute ventilation adjustment/hr Example: VT x RR (VE) = 500 x 25 (12.5L/min) PaCO2 = 50 mmhg VE target = 12.5 x (50 40) VE target = 12.5 x 1.25 VE target = 15.6 L/min Total VE adjustment = 3.1 L/min for PaCO2 = 10 mmhg Target PaCO2 change/hr 5 mm Hg Strategy: 2 hrs to increase VE by 3.1 L/min Total RR increase of 6 breaths in 2 hrs: 3 breaths/hr Formula is clinically valid when VT (dead-space) and metabolic rate are relatively constant. This strategy can be used to adjust minute ventilation and PaCO2 in either direction. 30

31 Sedation and Analgesia Background Sedation and analgesia in patients with severe TBI are important aspects of patient care that influence patient comfort, ability to tolerate mechanical ventilation and critical care procedures, and ICP management. The use of sedatives can improve ICP control, but may obscure the neurologic examination. Protocols for the use of sedatives in brain injured patients vary widely, but most published series use significant doses of various agents including opiates, benzodiazepines, and propofol 7, 8, 10. Many published protocols have also used prophylactic neuromuscular blockade 5, 11. While the value of detailed serial neurologic examination in the patient with severe brain injury (GCS 3-8) is debated, a sedation protocol that maximizes patient comfort and ICP control, while allowing accurate neurologic examination is the ideal. Goals Ensure patient comfort after severe TBI in the setting of critical care interventions. Serve as an adjunct for ICP management and perhaps to decrease secondary brain injury by decreasing cerebral oxygen utilization. Avoid interfering with clinical neurologic assessment as feasible. Guidelines Analgesia and sedation are considered separate issues which must be addressed individually in each brain injured patient. Because sedation and paralysis are primary ICP-management modalities, any changes in sedation or paralytics in patients with ICP monitors must be cleared by the Neurosurgery Chief Resident or Attending. Analgesia: Patients will first be assessed for pain. For pain management, initial doses to be considered are fentanyl mcg IV Q15 or hydromorphone mg q1 o in bolus form. (Refer to Adult ICU Pain and Sedation 2014 for more detailed dosage and dosing interval information.) If initial attempts at analgesia are ineffective, then sedation (as described below) may be instituted. Sedation in ICP Control: Sedation will be used in conjunction with other ICP control measures such as CSF drainage and mannitol. Patients will first be assessed for the need for sedative agents Sedative usage will be avoided unless ICP remains elevated despite other ICP control measures, or as needed to tolerate critical care interventions (e.g. 31

32 mechanical ventilation, line placement, endotracheal suctioning, patient safety and restraint). Propofol infusion at mcg/kg/min is the preferred sedative. Patients must undergo continuous blood pressure monitoring while receiving a propofol infusion. - Propofol will be tapered over 30 minutes QAM for morning rounds, neurologic examinations and at other times when deemed necessary. - Use of Propofol for sedation should be avoided in the child weighing <40kg (see ICU Pediatric Pain/Sedation/Neuromuscular Blockade Ordersets 2014). - Triglyceride levels will be checked at baseline and every Monday with routine nutrition serology. If > 800, a lipase level will be obtained and Propofol will be discontinued if this is elevated. - Patients with >2 risk factors for Propofol-related infusion syndrome (PRIS) will undergo routine monitoring for PRIS per the High-Dose Propofol Infusion Protocol. - Any dose rates >80mcg/kg/hr must be approved by the primary service Attending physician. Alternative sedative infusions include dexmedetomidine, benzodiazepines (midazolam, lorazepam) or opiates (morphine, fentanyl). These infusions may have less reliable offset than propofol, making neurologic assessment less reliable. In patients receiving sedation, ongoing need for analgesia will be assessed and analgesia will be held if no indications of ongoing pain are present. If longer-acting sedatives are required for highly agitated patients, quetiapine is the preferred agent. Haloperidol is contraindicated due to its negative impact on long-term cognitive recovery 13. Neuromuscular Blockade Neuromuscular blockade may be used in patients with severe TBI at the discretion of the treating physician. Indications for usage include uncontrolled elevated ICP and severe pulmonary disease, such as ARDS. Paralytics should be monitored with peripheral nerve stimulator to maintain at least 1 of 4 twitches, if tolerated. - Atracurim and cisatracurium are alternatives to pancuronium and vecuronium in order to avoid concern of prolonged paralysis from impaired paralytic metabolism. Sedative and/or opiate infusions will continue in all patients receiving neuromuscular blockade. 32

33 Mannitol and Hypertonic Saline therapy for ICP Control Background Mannitol is effective for treatment of elevated ICP after severe brain injury. It is thought that an intact blood-brain barrier is necessary for maximal effectiveness of mannitol. Effects within minutes are observed due to rheologic effects on blood volume. Osmotic effects are seen within minutes. Mannitol may be more effective when administered as intermittent boluses, rather than continuous infusion. Recent data also suggests that hypertonic saline solutions (3%, 7% or 23.4% NaCl) effectively reduce ICP. These solutions can be used as a primary treatment for increased ICP or as an adjunct to mannitol. Hypertonic saline (HTS) may also be effective as a salvage treatment in patients for whom mannitol therapy has failed. Goals To treat acutely elevated ICP or diminished CPP, while avoiding hypovolemia. To treat clinical signs of cerebral herniation prior to ICP monitoring or if ICP does not reflect focal tissue shifts (e.g. focal temporal lobe pathology). Guidelines Mannitol dosing is gm/kg IV bolus, given on a prn basis. Consideration may be given to regular interval dosing (Q6 hrs), but this is generally avoided. Serum osmolality should be checked 1 hour after mannitol dose, and kept below 320 mosm, especially if renal function is a concern. Mannitol will not be given if serum osmolality is >320. Hypertonic saline solution (23.4% NaCl) may be used at the discretion of the treating physician and will be administered as a slow IV push only by Neurosurgical or Neurocritical Care team members who have undergone instruction, evaluation, and clearance by one of the Neurosurgical or Neurocritical Care Attendings. Vital signs will be monitored Q 5 mins during administration and Q 15 mins after for 1 hr to ensure hemodynamic stability. (refer to HTS protocol 2014) Serum sodium should be checked 1 hour after HTS administration. Infusions of HTS should be held for Na+>155. Fluid replacement, usually with NS, will be undertaken to maintain appropriate volume status, usually euvolemia. Plasmalyte is an alternative fluid replacement solution, especially in patients with metabolic acidosis (which may be exacerbated by large volumes of NS or HTS). 33

34 Barbiturates Background The use of high-dose barbiturate therapy ( pentobarb coma ) for the control of intractable intracranial hypertension is controversial. While barbiturates do lower ICP by decreasing cerebral metabolism and altering vascular tone, significant data regarding improved outcome is lacking. Additionally, high-dose barbiturates have significant systemic complications, most notably hemodynamic compromise and possibly increased infection risk. Therefore, barbiturate therapy in severe head injury is a second-line treatment, usually reserved for potentially salvageable patients with refractory intracranial hypertension. Goal To treat refractory intracranial hypertension, while avoiding systemic cardiovascular complications which may diminish CPP. Guidelines Barbiturate therapy may be considered in patients with persistently elevated ICP, especially if CPP remains diminished despite maximal medical and surgical treatment. Consideration can be given to earlier institution of barbiturates in individual situations. Barbiturate therapy consists of pentobarbital with a loading and maintenance dose. Loading dose: 10mg/kg over 30 minutes or 5 mg/kg Q 1hr x 3 Maintenance dose: Initially 1 mg/kg/hr, adjusted hourly based on ICP and EEG Monitoring with EEG for burst suppression is mandatory. Initial interburst interval goal is seconds, to be modified based on ICP control. Pentobarbital loading should not be delayed for EEG placement or for PA catheter placement. Pulmonary-artery (PA) catheter placement may be useful. Pressor and inotropic support are usually needed for patients undergoing barbiturate therapy. Weaning of pentobarbital infusion will be initiated after 24 hours of acceptable ICP control. Decrease pentobarbital dose by 50% each day. Discontinue pentobarbital 48 hours after wean initiated, if tolerated. In individual situations, more rapid weaning of pentobarbital infusion may be considered. 34

35 Glucocorticoids Background Glucocorticoids have been used in the past for treatment of brain edema in a variety of neurologic conditions, including head trauma, stroke, brain tumor, and cerebral abscess. Although currently used for vasogenic edema in tumor and abscess, they have been shown ineffective in lowering ICP or improving outcome in patients with head trauma and stroke. Goal Minimize the adverse effects of glucocorticoid therapy in TBI patients who require it for other conditions. Guidelines Glucocorticoids will not be used for the treatment of head trauma. Glucocorticoid treatment for other indications may be provided in patients with head trauma. These indications include asthma, prior outpatient corticosteroid use, stress induced adrenal insufficiency. In patients with head trauma who are receiving glucocorticoids for other indications, insulin infusion will be used to maintain serum glucose from In patients with head trauma who are receiving glucocorticoids for other indications, non-depolarizing neuromuscular blocking agents will be avoided if at all possible, because of concerns of persistent paralysis from muscle damage induced by the combination of the two agents. 35

36 Hypothermia Background Hyperthermia, even of 1-2 o C, worsens brain injury after experimental trauma in animal subjects. It is thought to worsen secondary brain injury after stroke, intracranial hemorrhage, and trauma in human patients as well. Hypothermia has been considered a neuroprotective strategy in all of these diseases. Theoretically, hypothermia (usually to o C) decreases cerebral oxygen utilization and acts as a neuroprotectant. Despite reports from small series of improved outcome after induced hypothermia 5, larger clinical trials have consistently shown no benefit. Also, there are concerns about systemic effects of hypothermia including coagulopathy, increased infection risks, and cardiac arrhythmias. At present, a strategy of avoiding hyperthermia is essential, with the role of induced hypothermia being less certain. Goals Avoid hyperthermia-induced secondary brain injury. Consider induced hypothermia as a 2 nd or 3 rd tier therapy for refractory elevated ICP. Guidelines Goal temperature (measured intravascularly or rectally) will be o C. (See Fever Management for Critical Neurological Injury: Traumatic Brain Injury and Stroke 2014). For T > 37.5 o C, antipyretics such as acetaminophen will be initiated. Scheduled antipyretics will be considered for patients with recurrent fever spikes. Mechanical measures such as cooling blankets, ice packs, and fans will be used to keep T<38.3 o C. Appropriate measures will be taken to identify and treat infectious sources. Patients with shivering from fever or hypothermia measures will be treated as needed, per the order sets for Fever Management for Critical Neurological Injury: Traumatic Brain Injury and Stroke Although intermittent doses of meperidine ( mg) may be considered for rigors/shivering in patients who cannot tolerate propofol, in general, meperidine is to be avoided because of concerns that it may lower seizure threshold. More aggressive hypothermia to o C using nasogastric lavage may be considered in cases of refractory elevated ICP. 36

37 Integrated Approach to ICP and CPP Management Background ICP is a global measure that can be related to a number of intracranial processes. These indclude intra- and extracellular edema, venous outflow obstruction, hyperemia, mass effect, and CSF disturbances. Additional neuromonitoring may be necessary, and assessment of autoregulation will be employed to direct individualized therapy. A tiered approach will be used to target therapies more specifically to different mechanisms of elevated ICP. Failure to control ICP within on etier prompts rapid progression to the next tier; higher tiers reflect more intensive management strategies, and include higher risk of complications. Tier 1 Maintain neutral head position, and remove cervical collar if C spine clear Head of bed to be placed at >30 degrees Avoid circumferential ETT taping Assure patient is on a bowel regimen. Increased abdominal pressure can lead to increased ICP. Maintain temperature <37.5 C Seizure prophylaxis Sedation and analgesia using recommended agents (propofol, fentanyl, and versed) in intubated patients Ventricular drainage performed intermittently. Drain EVD to 10cmH2O for ICP >20 sustained for >5min. The preferred method for ICP monitoring and drainage is to leave the ICP device to the transducer for continuous monitoring and to drain only for elevations above the threshold (20mmHg). Mannitol g/kg IV bolus x 1 dose Repeat CT imaging for neurologic changes, and hourly neuro exams Tier 2 Hyperosmolar Therapy Mannitol should be administered as intermittent boluses of gm/kg body weight. It is important to maintain a euvolemic state when when osmotic diuresis is instituted with mannitol. The serum sodium and osmolality must be assessed frequently (every 6 hours) and additional doses should be held if the serum osmolality exceeds 320mOsm/L, or Na exceeds 160. Mannitol may be held if there is evidence of hypovolemia. 37

38 Hypertonic Saline: boluses of 23.4% sodium chloride solution (30cc) may be used. Serum sodium and osmolality must be assessed frequently (every 6 hours) and additional doses should be held if the serum sodium exceeds 160mEq/L. PaCO2 Goal 30-35mmHg, as long as brain hypoxia is not encountered. Neuromuscular Paralysis: pharmacologic paralysis with a continuous infusion of a neuromuscular blocking agent should be employed if the above measures fail to adequately lower the ICP and restore CPP. The infusion should be titrated to maintain at least two twitches (out of a train of four) using a peripheral nerve stimulator. Adequate sedation must be utilized if pharmacologic paralysis is employed. Tier 3 Decompressive hemi-craniectomy or bilateral craniectomy should only be performed if Tiers 1 and 2 are not sufficient. (Excluding cases meeting the Guidelines for Surgical Management of Traumatic Brain Injury). Barbiturate or Propofol (anesthesia dosage) induced coma is an option for those patients who have failed to respond to aggressive measures to control malignant intracranial hypertension. However, it should only be instituted if a test-dose of barbituates or Propofol results in a decrease in ICP, thereby identifying the patient as a responder. Hypotension is a frequent side effect of high dose therapy. Therefore, meticulous volume resuscitation should be insured. A phenylephrine infusion may also be required. 38

39 Seizure Prophylaxis Background Posttraumatic seizures may occur early, within 7 days of injury, or late, after 7 days. Seizures may worsen ICP control and worsen secondary brain injury, especially if status epilepticus occurs. Prospective, randomized trials have shown that prophylactic anticonvulsants may prevent the occurrence of early, but not late, posttraumatic seizures 12. Goal Prevent seizures in patients with traumatic brain injury Guidelines Anticonvulsants will be administered to any patient with intracranial hemorrhage, excluding those with isolated traumatic subarachnoid hemorrhage, at the discretion of the Neurosurgery Team. Dosing of phenytoin: IV load mg/kg and initial maintenance 100 mg IV TID. Once a patient is able to take PO medications, it will be changed to PO route for the remainder of the course to prevent thrombophlebitis and infiltration into soft tissues. Fosphenytoin as a loading agent is preferred as hypotension may be less prominent. Intravenous preparations of loading and maintenance (fos)phenytoin are preferred as PO/NG preparations may have less reliable absorption. Levetiracetam, carbamazepine or phenobarbital will be considered if phenytoin cannot be tolerated. Use of phenobarbital for seizure prophylaxis will be considered in all children <1 year of age. In general, prophylactic anticonvulsants will be discontinued after seven days. For patients with early posttraumatic seizures, anticonvulsants will be continued beyond the 7 day period and up to 3-6 months post-injury. Consideration of an alternative anticonvulsant will be given when a patient has a history of HIV, liver dysfunction, renal dysfunction or other factors that may interfere with medication effect or metabolism. Care should be taken in the administration of phenytoin to monitor for signs of cardiovascular effects: bradycardia, hypotension, AV heart block. Phenytoin and albumin levels should be drawn 48 hrs after bolus. The patient should be monitored for signs of toxicity. A phenytoin level of 10-20, corrected for albumin level, will be considered therapeutic. 39

40 Seven Causes of Acute Neurological Decline Background Acute neurological decompensation following a TBI can occur in a matter of minutes, or up to weeks after the initial insult. The seven major causes for neurological decline in the traumatic brain injured patient include: metabolic derangement, toxicity, respiratory insult, infection, seizures, hydrocephalus or a new hemorrhage. Each of these contributing factors will be detailed in the following sections. Goal Early detection, causality identification and intervention for the TBI patient with an actue neurological decline Guidelines Perform routine serial neurological examinations every 1-4 hours as appropriate. Examination shall include but is not limited to the following elements: GCS, pupillary exam, brainstem reflexes, cognitive testing, motor strength testing and sensory examination. Noted changes in the GCS of >2 points, or observed changes to the neurological exam will necessitate an immediate notification to the Neurosurgical team. 1. Metabolic derangement: Hyponatremia Hyponatremia in the TBI patient is usually the result of cerebral salt wasting (CSW) or syndrome of inappropriate antidiuretic hormone secretion (SIADH). The differentiation of hyponatremia due to CSW versus SIADH is essential. Failure to distinguish CSW from SIADH in a hyponatremic patient with TBI will lead to inappropriate therapy and potentially exacerbate morbidity and mortality. Restricting fluids in the setting of CSW may result in vasospasm-induced ischemia. SIADH defined 4 Release of Antidiuretic Hormone (ADH) in the absence of physiologic (osmotic) stimuli resulting in elevated intravascular volume or hypervolemia and hyponatremia (Na + <134). The primary cause for SIADH in the TBI patient is excessive intravenous fluid resuscitation. The treatment for SIADH is fluid restriction. Cerebral Salt Wasting defined Renal loss of sodium as a result of brain injury producing hyponatremia (Na + <134) and a decrease in extracellular fluid volume hypovolemia 4. CSW is most likely to occur in 40

41 patients with large cerebral contusions, and time of onset is typically around post-injury day 5-7. The treatment for CSW is volume repletion with 0.9%NS, and sodium repletion with 3% hypertonic saline and/or oral NaCl tablets. Resistant cases may require the addition of fludrocortisone and/or Demeclocycline. Goals Symptoms associated with hyponatremia Mild or gradual hyponatremia: Anorexia, headache, irritability, muscle weakness Severe hyponatremia (<120mmol/L) or a rapid drop (>0.5mmol/hr) o Neuromuscular excitability o Seizures o Cerebral edema o Intracranial Hypertension o Muscle twitching and o Respiratory arrest cramps o Possibly permanent o Nausea/Vomiting neurologic injury o Confusion o Coma, death Early detection of sodium abnormalities and identification of cause. Performance of serial neurological examinations with interventions as necessary for confusion and agitation. Avoidance of rapid normalization or hypernatremia during correction, with frequent sodium checks to prevent central pontine myelinolysis. Slow sodium correction to normal. Guidelines Evaluate with strict monitoring of I & O, and with the following labs: Urine osmolality, serum osmolality, serum chemistry (sodium), Urine sodium. SIADH: First line treatment is fluid restriction (< 1 liter/day). CSW: Hydration with 0.9% NS and Na + replacement. Start with a 10% sodium correction per day in order to prevent neurologic sequelae 4. Modulate therapy as follows 4 : Stop if the change in Na + is > 10mEq/L in 24 hours Do not exceed a rate of correction of mEq/L/hr First line therapy: NaCl tabs 2-3gms PO TID. If hyponatremia persists despite NaCl tab administration, start 3% NaCl at 25-60cc/hr. Monitor Na + every 2-6 hours unless otherwise indicated. Resistant Cases: - Fludrocortisone mg PO QD - Demeclocycline 300mg PO BID 41

42 2. Toxicity: Recreational and Iatrogenic Drugs The use of alcohol and recreational drugs is common with TBI. Seventy-five percent of all TBI patients were drinking alcohol at the time of their injury. Serum ETOH >21.7mmol/liter can cause vestibular and cerebellar dysfunction, increased nystagmus, diplopia, dysarthria, and ataxia. 16 Alcohol and drug intoxication can decrease the GCS by >2 points. A daily review of the patient s medications is necessary for all TBI patients. This is especially true in the setting of acute neurological decompensation. Many frequently used drugs (narcotics, benzodiazepines, tricyclic antidepressants, anticonvulsants, etc.) may cause alterations in the neurological status of the TBI patient. Goals Early identification of alcohol and drug intoxication on presentation. Early identification of neurological altering substances within the inpatient setting. Minimize the use of neurological altering medications in the TBI patient population. Avoid abrupt discontinuation of narcotics and sedatives due to the possibility of acute withdrawal syndromes. Guidelines Daily reviews will be performed for all medications currently prescribed and administered to the TBI patient by the physicians and nurses. Pharmacological review for Central Nervous System (CNS) effects of medications prior to administration. All medications, both prescribed and administered, will be reviewed weekly by the Interdisciplinary team (IDT). Care will be taken to avoid narcotic and sedative weans by >10% per day. The Pain Management service will be consulted when indicated to assist with pain management and narcotic/sedative weans. 42

43 3. Respiratory See the Respiratory Care section on page 26 for a detailed discussion of this topic. It is well documented in the literature that the injured brain has increased metabolic demands. Primarily this involves an increase in glucose and oxygen requirements. During periods of hypoxia there is a decrease in tissue oxygenation to brain cells that may have been injured during the traumatic event. Hypoxia is defined as a PaO2 of < 60mmHg or oxygen saturation of <90%. Literature has shown that hypoxia occurs in >70% of all TBI patients and a single episode of hypoxia leads to a two-fold increase in mortality. Goals Assessment characteristics of impaired oxygenation Confusion/Decreased mental acuity Somnolence Restlessness/Irritability Hypercapnea Hypoxia Dyspnea Cyanosis Tachycardia/dysrhythmias Anxiety Ensure adequate oxygenation, ventilation, and airway protection. Prevent secondary injury from hypoxia and/or hypocapnia. Guidelines The initial goal in all patients will be normoventilation, recognizing that ph defines ventilatory status, as driven by the medulla 2. In patients with normal lungs, a normal ABG is 7.40/40/100. A CO2 of 35 in these patients represents mild hyperventilation. A goal PaO2 of 100 mmhg will be maintained. A goal pco2 of 35-45mmHg. 4. Infectious Processes The patient with TBI has an increased susceptibility to infectious processes. This can be attributed to impaired LOC, decreased mobility, prolonged ventilatory support, and invasive procedures such as line, drain and catheter insertions, neuromonitoring devices and operative interventions. The development of such infections leads to prolonged ICU and hospital stays. 43

44 Early indications of infectious processes include the development of altered mental status, a febrile response, hemodynamic change (tachycardia, hypotension, tachypnea), elevated white blood cell count, and/or elevated lactate. However, it is important to remember that these are less likely to occur in the elderly, in immune compromised patients, and in TBI patients with impaired thermoregulatory responses. The three most commonly identified sources of infection in the SFGH TBI patient population include meningitis, pneumonia, and urinary tract infections. Meningitis/Ventriculitis Post-traumatic meningitis occurs in 1-20% of patients with moderate to severe TBI 1. Most cases occur within two weeks of injury 3. The most likely organisms are S. aureus, Enterobacteriaceae, Pseudomonas sp., and pneumococci 4. San Francisco General Hospital and Trauma Center utilizes the CDC definition for hospitalacquired meningitis/ventriculitis 9. Classic symptoms for meningitis include: Headache Fever Sensorial disturbances Neck and back stiffness Positive Kerning sign Positive Brudzinski s sign CSF abnormalities Hospital Acquired/Ventilatory Associated Pneumonia Development of pneumonia following traumatic brain injury can be attributable to aspiration following an altered level of consciousness and/or intubation with ventilatory support. Literature demonstrates that the rate of developing ventilator associated pneumonia after 48 hours of ventilatory support is between 8-28% 10,11,12 and this rate increases in the TBI patient population due to longer ventilatory exposure. 11,13 San Francisco General Hospital and Trauma Center utilizes the Center for Disease Control (CDC) definition for ventilator associated pneumonia. 9 Urinary Infection Urinary tract infection is the most common hospital acquired infection; 80% of these infections are attributable to indwelling urethral catheters. 15 The daily risk of developing a urinary infection varies from 3-7% when an indwelling urethral catheter remains in place. 16 San Francisco General Hospital and Trauma Center utilizes the CDC definition for asymptomatic and symptomatic urinary tract infections. 9 Goals Early detection and work-up of potential infections processes. Involvement of General Medicine and Infectious Disease services when appropriate. Culture guided antibiotics with an identifiable duration of treatment. Removal of indwelling urinary catheters as soon as possible to begin bladder training. Early mobilization to improve respiratory status and prevent development of VTE. 44

45 Guidelines For temperatures > 38.5, obtain pan cultures to include sputum, urine, blood, and when appropriate, CSF. Obtain CXR to rule out presence of a respiratory source, when appropriate. Obtain duplex ultrasound evaluation in the presence of fever and swollen or tender extremity, to rule out DVT as a potential source. Administer antibiotic coverage tailored to bacteriologic isolates and their sensitivities; consider Infectious Disease involvement. 5. Seizures Posttraumatic seizures may occur early, within seven days of injury, or late, after seven days. Seizures may worsen secondary brain injury especially if status epilepticus occurs. Prospective randomized trials have shown that prophylactic anticonvulsants may prevent the occurrence of early, but not late posttraumatic seizures. 18 Goals Prevent seizures in patients with head trauma. Early identification and intervention for seizure activity. Guidelines See Seizure Prophylaxis Guidelines on page Hydrocephalus Hydrochephalus in the setting of TBI is due to the presence of blood products obstructing the flow of cerebrospinal fluid (CSF) in the subarachnoid space, and/or absorption of CSF in the arachnoid villi. The increasing accumulation of CSF creates pressure on the brain tissues preventing the nerve cells from functioning properly. Symptom development from hydrocephalus is dependent upon patient age, degree of ventricle enlargement, rate of hydrocephalus development and underlying medical condition. Symptoms include: Headache Nausea/Vomiting Visual disturbances (blurred or double vision) Downward gaze Cognitive difficulties Memory loss Lethargy Poor coordination Dizziness or imbalance Gait abnormalities Urinary incontinence 45

46 Goals Early identification of acute changes in neurologic status. Hydrocephalus management with drainage using an EVD or lumbar drain. Placement of a ventriculoperitoneal shunt for long-term hydrocephalus management. Guidelines The two basic methods for CSF diversion are external ventricular catheters (EVD) or Lumbar Drainage (LD). 19 See SFGH policy and procedure (Critical Care Policy 2.0) for CSF drainage for elevated intracranial pressure. See SFGH policy and procedure lumbar drain (LD) management (policy #). Indications for EVD and/or LD placement in the setting of hydrocephalus Obstructive hydrocephalus, including communicating and noncommunicating Subarachnoid hemorrhage (SAH) resulting in acute hydrocephalus due to obstruction of arachnoid villi Cerebral edema Surgical mass lesions Infections (meningitis) Continuous CSF drainage at a specified pressure-height and/or hourly CSF quantity (volume drainage) is identified and recorded every 1-2 hours as indicated. Infection Control Empiric antibiotics will not be used for prophylaxis against infection after EVD or LD placement. Great attention will be paid to sterile placement and maintenance of EVD s and LD s, especially ventricular catheters, as conditions during placement and instrumentation are the greatest risks for inducing infection. CSF will be sent for analysis from ventricular catheters and/or LD as needed for infection surveillance and diagnosis. CSF will be withdrawn directly from the catheter using sterile technique. CSF sampling will be performed only by Neurosurgical team members who have undergone instruction, evaluation, and clearance by one of the Neurosurgical Attendings. CSF will be sent for the following: cell count, glucose, protein, gram stain, culture. Concurrently, a serum glucose should be sent for comparison. 46

47 Antibiotic coverage will be initiated for treatment of suspected or confirmed infection. Antibiotic coverage will be tailored to bacteriologic isolates and their sensitivities. 7. Intracranial Hemorrhage Although rare, the risk of developing a post-operative hemorrhage following craniotomy exists; it is around 1%. The most common site for hematoma development is intraparenchymal at 43-60%, followed by epidural at 28-33%. Overall mortality following a post-craniotomy bleed is approximately 32% 5,7. Clinical findings suggestive of hemorrhage following craniotomy are 4 Depressed level of consciousness Focal neurological findings Seizures Goals Early identification of acute neurological changes and/or decompensation. Prompt neurosurgical intervention, as indicated, for new hemorrhage and/or hemorrhage re-accumulation. Guidelines STAT head CT in the presence of changes to baseline or new neurological decompensation. Immediate neurosurgical intervention for possible hematoma evacuation, or ICP monitoring and treatment. 47

48 General Acute Care Issues Background The overarching goals of TBI treatment are to prevent secondary injury and to optimize conditions of recovery. Patients with traumatic head injuries have multiple issues related to general acute care management. These include, but are not limited to, nutritional support, prevention of deep venous thrombosis and gastrointestinal ulcers, IV fluid and blood product management, and early initiation of rehabilitation. Goals Prevent complications of critical illnesses that may lead to secondary injury in the TBI patient. Ensure adequate nutrition in head injury patients. Maximize recovery potential following traumatic brain injury. Guidelines Nutritional Support (please see nutritional guidelines) Enteral feeding will commence as early as feasible, preferably within 24 hours post-trauma. 140% of resting metabolism will be supplied for most patients; 100% of resting metabolism for patients receiving neuromuscular blockade. Duodenal feedings are preferred over stomach feedings. For patients who cannot receive enteral feeding, TPN will be provided. VTE Prophylaxis Sequential compression devices (SCDs) will be the preferred method of DVT prophylaxis and will be initiated, if possible based on other injuries, at time of admission unless the patient is ambulating 3 or more times a shift. Consideration will be given for the initiation of Low-molecular weight heparin (enoxaparin 30 mg SQ bid or 40mg SQ daily) on post-injury day 2 (48 hours after admission). Ulcer Prophylaxis An H2-blocker or a PPI will be initiated at time of ICU admission and will continue until a method of enteral feeding is obtained Use of a PPI is encouraged in patients >65 years of age IV Fluids All infusions will be mixed in 0.9% NS. Plasmalyte is an alternative IV fluid, especially in patients with metabolic acidosis. Euvolemia is the goal for all patients. When possible a total hourly fluid rate will be identified and achieved. 48

49 Rehabilitaiton Early consultation and treatment by the following services: - Physical Therapy - Occupational Therapy - Speech Therapy - Physical Medicine and Rehabilitation (PM&R) Hematology DIC may occur in the setting of severe head injury. In the absence of bleeding, CBC/plts, PT/PTT will be checked daily. A Rotem, or thromboelastogram (TEG), study may be obtained. Consideration will be given for administration of platelets in the setting of daily asprin use and intracranial hemorrhage. Consideration will be given for administration of Bebulin (Prothrombin Complex Concentrate [see SFGH order set 1-019]) in the setting of daily coumadin use and intracranial hemorrhage. Consideration will be given for administration of Recombinant Factor VIIa (see SFGH order set 1-063) in the setting of reaching step 3 in the massive transfusion algorithm (see massive transfusion algorithm in Trauma Appendix B to Admin policy 2.06), and when the following conditions are met: - Platelets >50 x Fibrinogen >100mg/dl - Arterial ph >7.2 INR will be maintained < 1.4 Platelet count will maintained above 75,000 at the discretion of the Neurosurgery Attending. RBC transfusion will be considered for hemoglobin <7, even in the absence of DIC. 49

50 Post-Concussive Syndrome and Management of the 6 Most Common Symptoms Background Ongoing symptoms are common following even mild TBI. The symptoms range in severity and the trajectory of recovery is variable. The six most common symptoms include generalized pain, headache, vertigo, sleep disturbances, cognitive deficits and posttraumatic stress. Each symptom will be addressed in the following sections and will be depicted by numerical digits. Goals Early patient and family education on post-concussive symptoms and the anticipated trajectory of recovery. Early diagnosis and intervention for the common symptoms following TBI. Guidelines Every TBI patient will be individually assessed for the six most common postconcussive symptoms. Every patient and/or family will receive education on post-concussive symptoms and the anticipated trajectory of recovery following TBI. Each patient will be assessed based upon the Rancho Los Amigos scale of TBI recovery, and care will be individualized according to the current stage of recovery. Consultation will be sought from the following services when indicated: Pain Management Physical Therapy Occupational Therapy Speech Therapy Physical Medicine and Rehabilitation Neuropsychology Social Work 50

51 1. General Pain Goal Inadequate pain management has been associated with poor outcome. Psychological and physiologic response to pain may produce profound pathophysiologic effects. These include sympathetic hyperactivity, vasoconstriction with increased blood pressure, tachycardia, regional ischemia, poor wound healing, hypoventilation, atelectasis, hypoxemia and thromboembolic complications. Pain assessment and management in the post-traumatic head injured patient is complex as it must be instituted during, and in association with, the ongoing diagnostic evaluation of the extent of neurological injury. Altered mental status, impaired cognition and/or communication may make patient self-report of pain an unavailable assessment tool. The IDT may be required to utilize biological markers such as heart rate, blood pressure, respiratory rate, and behaviors as key assessments in the TBI patient. Pain management in the TBI patient is directed toward providing adequate patient comfort for compliance with diagnostic assessment and rehabilitation efforts, while maintaining physiologic/hemodynamic stability and providing minimal CNS related side effects. Guidelines Daily reviews will be performed by the physicians and nurses for all medications currently prescribed and administered to the TBI patient. Pharmacologic review for central nervous system (CNS) effects of medications prior to administration. Care will be taken to avoid narcotic and sedative weans by >10% per day. The Pain Management service will be consulted when indicated to assist with pain management and narcotic/sedative weans. Please refer to SFGH pain management policy (16.23) 51

52 Post-concussive Syndrome and Management of the 6 Most Common Symptoms 2. Headache Headache is a common symptom in TBI patients. Headache symptoms are expected to gradually improve over time with complete resolution to occur within several months following injury. Goals Rule out development of a mass lesion or cerebral edema as a source for acute headache development (i.e. meningitis, new hemorrhage, hyponatremia). Preventive and abortive therapy for headaches following TBI. Guidelines Obtain a STAT head CT to rule out development of new mass lesion and/or cerebral edema in the setting of acute or worsening headache symptoms. Laboratory evaluation (serum sodium) for acute or worsening headache symptoms. Institute a low stimulation environment. Assess environment for triggers and abort or remove them when able. Consider around the clock acetaminophen administration. Use narcotics as indicated, with the understanding that they may cause rebound headache symptoms. Consider the addition of NSAIDS, gabapentin, tricyclics or prazosin when acetaminophen and narcotics are ineffective. 52

53 Post-concussive Syndrome and Management of the 6 Most Common Symptoms 3. Sleep Disturbance It is estimated that 30-70% of TBI patients experience a sleep-wake disturbance in some form following injury. Common sleep disorders include; insomnia, excessive daytime sleepiness, delayed sleep phase syndrome, and narcolepsy. Poor sleep quality can have a significant impact on cognitive recovery, psychological health, social interactions, and return to professional productivity. Goal Initiate and maintain healthy sleep patterns in the patient with TBI. Guidelines Institute low stimulation environmental precautions Lower room lights Decrease noise Turn off TVs and Radios Discourage visitation during periods of sleep When possible discontinue neurological and vital sign checks between the hours of 22:00 and 06:00. Ensure uninterrupted periods of rest during the evening hours. Discourage frequent napping throughout the day. Strategic placement of the TBI patient near a window to aid in identification of day/night wake cycle. Avoid stimulant-containing beverages and/or food after the hour of 16:00. Provide patient and family education on sleep hygiene. 32 Administer medications as required to alleviate sleep disturbances. Melatonin is the first-line therapy for sleep disturbances. Additional medications to consider include: - Trazadone - Tricyclic antidepressants - Modafinil 53

54 Post-concussive Syndrome and Management of the 6 Most Common Symptoms 4. Positional Vertigo Between 30-65% of people with TBI suffer from dizziness and disequilibrium at some point in their recovery. Dizziness includes symptoms such as lightheadedness, vertigo (the sensation that you or your surroundings are moving), and imbalance. Goals Improve patient tolerance and participation with rehabilitation services. Prevent inpatient falls secondary to vertigo. Improve ambulatory status. Guidelines Institute fall precautions for TBI patients with symptoms of vertigo. Patient instruction on Brandt-Daroff exercises for vertigo. Administration of medications for the treatment of vertigo as indicated Scopolamine patch Meclizine 54

55 Post-concussive Syndrome and Management of the 6 Most Common Symptoms 5. Post-traumatic Stress Disorder (PTSD) Research indicates that people with TBI are more likely to develop PTSD than those who have not incurred a brain injury. 21 Due to similar symptomatology, the incidence of TBI patients with PTSD is hard to determine but is thought to range from 7-20%. Posttraumatic stress disorder is a result of exposure to a traumatic event, or to oneself or surrounding others, in which the patient experiences intense fear, horror, or a sense of helplessness. This anxiety disorder can develop months or even years after a severe traumatic incident; a diagnosis usually means the patient has had symptoms that last over one month after the incident. 22 The experience must involve a threat of death, serious injury, or threat to physical integrity. The individual usually suffers from one or more of the following dissociative symptoms: Persistently re-experiencing the traumatic event in images, feelings, dreams, internal and external cues, or physiological reactivity. Avoidance of trauma-related stimuli such as thoughts, activities, recollection of the experience. Diminished interest, feelings of detachment, restricted affective range, and foreshortened future planning. Increased arousal such as sleep disturbance, irritability/anger, distractability, hypervigilance, and exaggerated startle. Goals Early screening and acute symptom management for patients with PTSD. Provide patient and family education on the symptoms associated with PTSD. Provide psychological and family support for patients with symptoms of PTSD. Guidelines It is the responsibility of the interdisciplinary team to possess a heightened awareness of PTSD, and to seek evaluation and intervention by neuropsychology and psychiatric services. Therapy for PTSD 23 Cognitive Processing Therapy (CPT) helps by providing the patient with a way to handle distressing thoughts and to gain an understanding of the event. There are four parts to CPT. Learning about PTSD symptoms and how treatment can help Awareness of thoughts and feelings. Learning skills to help the patient question or challenge his/her thoughts. Learning about the common changes in beliefs (safety, trust, control, self-esteem) that occur after going through trauma. 55

56 Prolonged Exposure Therapy (PE) works to decrease the patient s distress about the trauma, helping the patient approach trauma-related thoughts, feelings and situations that he/she may have been avoiding. Repeated exposure to these thoughts, feelings, and situations helps reduce the power they have. There are four parts to PE therapy. Education about the treatment, common trauma reactions and the symptoms of PTSD. Breathing retraining is a skill that helps with relaxation. Learning how to control breathing can help in the short-term management of stressful situations. Real world practice/vivo exposure. The goal of this part is for the patient to practice approaching situations that are safe, but which he/she may have been avoiding because they are related to the trauma. This type of exposure practice helps trauma-related distress to lessen over time and allow the patient to gain more control over his/her life. Talking about the trauma memory over and over is called imaginal exposure. This helps the patient gain more control over his/her thoughts and feelings about the trauma. It also teaches the patient to not be afraid of the traumatic memories. Family Therapy and Support. Family members may not understand why the patient becomes easily angered, feels frightful, guilty or stressed thus PTSD can affect the whole family. Family therapy allows each family member to be educated on PTSD and to express his/her fears and concerns. Eye Movement Desensitization and Reprocessing (EMDR). EMDR incorporates elements of exposure therapy with eye movements or other forms of rhythmic, left-right stimulation, such as hand taps or sounds. Eye movements and other bilateral forms of stimulation are thought to work by unfreezing the brain s information processing system and allowing the individual to reprocess the memory. Medications for the treatment of PTSD Selective Serotonin Reuptake Inhibitors (SSRIs) - Citalopram (Celexa) - Fluoxetine (Prozac) - Paroxetine (Paxil) - Sertraline (Zoloft) 56

57 Post-concussive Syndrome and Management of the 6 Most Common Symptoms 6. Agitation, Confusion, and Cognitive Deficits Patients with TBI often exhibit cognitive and behavioral dysfunction either as a result of their injury or from a pre-existing/pre-injury condition. Deficits may include memory loss, difficulty with executive function, reduced safety awareness, emotional lability, social disinhibition, agitation or impulsivity. The severity and duration of these symptoms vary depending upon the magnitude of injury. 20 Goals Optimize patient function through early cognitive and behavioral intervention. Provide an environment that minimizes patient agitation and facilitates patient cooperation, learning, and recovery. Minimize the use of physical restraints. Minimize the use of psychoactive medications. Guidelines Please refer to the Guidelines for Cognitive Dysfunction and Maladaptive Behavior Following TBI, which begin on page

58 References 1. Baltas I, Tsoulfa S, Sakellariou P, et al.: Posttraumatic meningitis: Bacteriology, hydrocephalus, and outcome. Neurosurgery 35: 422-7, Brian JE, Jr.: Carbon dioxide and the cerebral circulation. Anesthesiology 88: , Eljamel M S M, Foy P M: Post-Traumatic CSF fistulae, the case for surgical repair. Br J Neurosurgery 4: , Greenberg M S.: Handbook of Neurosurgery (5 th ed.). (2001). New York,NY: Thieme. 5. Kalfas I H, Little J R: Post-operative hemorrhage: A survey of 4992 intracranial procedures. Neurosurgery23: 343-7, Muizelaar J, Marmarou A, Ward J, et al: Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurgery 75: , Palmar J D, Sparrow O C, Iannotti F I.: Postoperative heamatoma: A 5 year survey and identification of avoidable risk factors. Neurosurgery 35: , Management and Prognosis of Severe Traumatic Brain injury 9. Center for Disease Control and Prevention. (2013). CDC/NHSN Protocol Clarifications. Retrieved from Chastre J, Fagon J-Y. Ventilator-associated pneumonia. Am J Respir Crit Care Med 2002;165: Anon. National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2004, issued October Am J Infect Control 2004;32: Association for Professional in Infection Control and Epidemiology. Guide to the elimination of ventilator- associated pneumonia; Anon. Medicare fact sheet : proposals for improving quality of care during inpatient stays in acute care hospitals in the fiscal year Notice of Proposed Rule making Hui, X. ; Haider, A., et.al. (2013) Increased risk of pneumonia among ventilated patients with traumatic brain injury: every day counts!. Journal of Surgical Research 184 (2013) 438e Saint, S., Chenowith, C.E., (2003). Biofilms and catheter-asociated urinary tract infections. Infectious Disease Clinics of North America. 17( ). 16. Lo, E., Nicolle, L., Classen, D., et. Al. (2008). Strategies to prevent catheterassociated urinary tract infections in acute care hospitals. Infection control and hospital epidemiology 29(1) S41-S CDC: Guideline for Prevention of Catheter-associated Urinary Tract Infections, Tempkin, N.R., Dikmen, S.S, Wilensky, A.J. et al. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N. England Journal of Medicine. 1990;323: AANN Care of pt undergoing ICP/EVD or LD 20. Arciniegas, D. B., Held, K., & Wagner, P. (2002). Cognitive impairment following traumatic brain injury. Current Treatment Options in Neurology, 4(1),

59 21. Hoge, C.W., McGurk, D., Thomas, J.L., Cox, A.L, Engel, C.C., and Castro, C.A. (2008). Mild Traumatic Brain Injury in U.S. Soldiers Returning from Iraq. New England Journal of Medicine. 358(5): American Psychiatric Association. (2000). Diagnostic Statistical Manual of Mental Disorders-IV-TR. Washington, D.C: Author. 23. National center for PTSD: 59

60 Nutritional Management in the TBI Patient Background TBI patients exhibit moderate to severe hypermetabolism immediately following trauma. Energy expenditure post-trauma has been reported as 75% to 250% of basal energy expenditure. Caloric requirements are directly related to motor activity, infection, fever, level of sedation, level of consciousness, alterations in ICP, and any additional injuries. TBI patients can remain hypermetabolic and hypercatabolic from one week to one year postinjury. Enteral or parenteral nutrition support is often required and should begin as soon as the patient is hemodynamically stable. When clinically feasible, enteral nutrition should be used since it offers economic and physiologic benefits without severe complications. If enteral nutrition is contraindicated because of nonfunctioning gastrointestinal tract, parenteral nutrition can be utilized. Nutritional intervention is necessary for optimal recovery of the TBI patient. Goals Provide adequate kilocalories and protein to prevent extensive muscle catabolism and to improve nitrogen balance Maintain tolerance to nutrition therapy. Re-consult nutrition services as needed to address problems promptly. Follow patient per department protocol (See Screening Process for Clinical Nutrition Appendix B-1, page 63). Guidelines Day 1-7 guidelines for the intubated patient, or patient with NPO status: Day 1 - Obtain and record a dry weight. - Insert feeding tube. Aim for small bowel placement. If not feasible, gastric placement is acceptable. Oral route is necessary in the presence of a basilar skull fracture. - Confirm feeding tube position via KUB xray. - Consult Nutrition Service (via LCR/Invision, CPOE, or call x68604). - Once hemodynamically stable and GI tract functional, begin infusing a high protein +/- fiber enteral ml/hr. If questionable gut perfusion, order a standard no fiber formula at 30 ml/hr. - Upon initiation of enteral feeding the maintenance IV fluid rate will be decreased, in an effort to maintain a total intake balance appropriate to the patient s fluid status. - Order comprehensive metabolic panel and triglycerides if on Propofol. - Monitor glucose - Monitor tolerance by noting GI symptoms. Check gastric tube feed residuals q 4 hours; if >400 ml; refeed up to 400 ml, consider motility 60

61 agent unless contraindicated, +/- TF hold and notify the team. If residuals persist >400 ml, see ICU Enteral Nutrition Feeding Guideline, pg 67. Day Review nutrition consultation. - Adjust feeding rate or formula according to Nutrition Services recommendations and patient tolerance. Tolerance gauged by absence of nausea, vomiting, diarrhea or constipation and low gastric residuals. Day Review kcal/protein intake and TF tolerance. - Consider parenteral nutrition support if patient is not tolerating enteral TF; confer with Dietitian for recommendations. - Obtain metabolic study (indirect calorimetry) from RT; confer with Dietitian to determine if needed. - Monitor triglycerides at baseline and Q Monday if patient is on Propofol. Day 7 and thereafter - Monitor weekly Routine Nutrition Labs* and nitrogen balance results as available. Note: Nutrition labs are likely to be negatively impacted by acute phase/inflammation, thus the trend is more important than any one value of prealbumin or nitrogen balance calculation. - Adjust TF rate or formula according to patient tolerance and Dietitian recommendations. Day 1-7 guidelines for the patient that is not intubated or is recently extubated. Day 1 - Speech Language Pathologist (SLP) consultation for swallow evaluation if patient not appropriate for bedside swallow screen with nursing. - Begin PO diet as appropriate per SLP. - Consult Nutrition Services if patient has poor baseline nutrition or is unsafe for PO intake. Day Advance diet texture per SLP. - If patient is on TF, can cycle feeds to allow for improved appetite at meals. Consult with Dietitian for cycle recommendations and need to start 72 hour calorie count. Consider need for supplements or alter therapeutic diet restrictions. Day 7 and thereafter - Continue to monitor nutrition labs, weights, and adequacy of PO diet. Day 1-7 guidelines for the pediatric patient Day 1 - Follow adult guidelines. - If patient <10 years old requiring TF, begin a pediatric tube feeding formula at 1mL/kg/hr or 10mL/hr, whichever is less. - Consult Nutrition Service and Pediatric MD. 61

62 - Upon initiation of enteral feeding or TPN the maintenance IV fluid rate will be decreased in an effort to maintain a total intake balance appropriate to the patient s fluid status. Day Review nutrition consultation. - Advance tube feeding per Dietitian recommendations. - If taking PO, confer with Dietitian on ways to optimize intake. Day 5 and thereafter - Follow adult guidelines. Routine Nutrition Labs* for all patients every Monday: 24 hour urine collection for urine urea nitrogen level Comprehensive Metabolic Panel (Lytes, BUN, Cr, Glu, Ca, Alb, TP, LFTs) Lipid panel Magnesium Phosphorous Zinc Pre-Albumin C-reactive protein (CRP) 62

63 Appendix B-1 SAN FRANCISCO GENERAL HOSPITAL TRAUMA CENTER DEPARTMENT OF FOOD & NUTRITION SERVICES POLICY & PROCEDURE MANUAL Policy No: CL003 Adopted: 11/05/98 Reviewed: 7/18/2012 Revised: 9/28/2012, pending further revision 2013 TITLE: NUTRITION CARE - SCREENING PURPOSE: To outline a timely and effective interdisciplinary process for identifying patients who are admitted with compromised nutritional status or are at risk for developing malnutrition during their hospitalization. STATEMENT OF POLICY: All hospitalized patients are screened for nutritional risk within 24 hours of admission by nursing while completing the Patient Admission Database. RESPONSIBILITY: Nursing staff identifies risk factors associated with malnutrition upon admission via the Patient Admission Database in the LCR hospital computer system, Nursing may make a nutrition referral at anytime during a patient s hospitalization if new nutrition related risk factors or need for diet education is identified after initial nutrition screen A Physician or other Licensed Individual Practitioner (LIP) may identify nutrition risk and order a Nutrition Consult at any time during a patient s hospitalization. Ancillary staff (e.g. Rehabilitative Services, Pharmacy, and Medical Social Services) may identify nutrition related risk factors and refer to Clinical Nutrition. Clinical Nutrition staff screen for nutrition related risk factors by reviewing available diet office reports (see Relevant Data), Nursing Kardex, and participation in patient care rounds. ATTACHMENTS: Screening Process for Clinical Nutrition Program SFGH Clinical Nutrition Consult Board Screening, Assessment and Activity Log (productivity log) Nutrition Comprehensive Screening form 63

64 CROSS REFERENCE: Invision/LCR Admission Database. Nursing Policy & Procedure 2.1 Admission of Patient RELEVANT DATA: Available Diet Office Reports: Clinical Nutrition Consult Board Parenteral Nutrition Report NPO/ Clear Liquid Diet Report (CBORD Diet Office computer system generated) CBORD Host Round Reports (patient s name, age, admit date and diet prescription). Abbreviations: CL Clear Liquid DTR Dietetic Technician, Registered IPOC Interdisciplinary Plan of Care LIP Licensed Individual Practitioner LOS Length of stay NPO Nothing per os NT Nutrition Technician RD Registered Dietitian PROCEDURE: Nursing Nurses assess patients upon admission and complete the Patient Admission Database within 24 hours. The Patient Admission Database contains a Nutrition Risk Screen that includes: GI Complaints Poor Po Intake Nutrition Support Weight Changes (per patient &/or caregiver) Significant diet restrictions/allergies Nutrition related diagnosis Select Nutrition Screening Criteria are discussed with and information obtained from the patient (unless patient is unable to participate) or family members whenever possible. Referrals are automatically generated to Food & Nutrition Services Diet Office if any nutrition risk factors are clicked on the Nutrition Screening checklist completed in the Invision/LCR Patient Admission Database; this is the 24 hour nutrition screen Nutrition screening and assessment is completed per Clinical Nutrition Program Policies. 64

65 Other: Physicians and other LIP s initiate diagnosis based diet orders.the diet order may be a screening indicator to the Department of Food and Nutrition. The diet order is listed on diet office Host Round reports (see CL014, Processing of Patient Diet Orders ) for RD review. Providers also order consults for assessments, education, calorie counts, enteral and parenteral nutrition. Consults are logged on the Clinical Nutrition Consult Board. Other services, such as Pharmacy, Rehab, and Medical Social Services, may identify nutrition risk factors in the course of their screening and assessment process and make referrals to Clinical Nutrition. Clinical Nutrition Program See Attachment entitled Screening & Documentation Process for the Clinical Nutrition Program of Food & Nutrition Services. Communication regarding nutrition risk factors is done via: Direct Communication with RD, DTR or NT Team & Patient Care Rounds Telephone/pager Hospital Computer System (LCR) generated requests and orders Documentation regarding patient nutrition screening can be located as follows: Medical Record Patient Admission Database (Invision/LCR hospital computer system) Interdisciplinary Plan of Care (IPOC) Progress Notes in the Patient Medical Record Diet Office Data Host Round reports Screening, Assessment and Activity Logs DTR/NT Screening Forms 65

66 SFGH Food & Nutrition Services: Screening Process for Clinical Nutrition Program Source DTR/NT responsible for: Registered Dietitian (RD) responsible Consult Board: Consults and Referrals CBORD REPORTS: Host Rounds (census) NPO/Clear Liquids Skilled Nursing Facility: 4A Skilled Nursing Facility: SNF-SFBHC Food preferences Implement Calorie Count Screen for Diet Education needs Psychiatry referrals (see exception in RD box) RD referrals for follow up of low or no risk patients. DIET ORDER: Carb Controlled: Hospital day 3 LOS acute Cardiac: Hospital day 3 LOS acute Cardiac & Carb Controlled on Psychiatry: 10 days LOS LENGTH OF STAY: Acute: 7 days Psychiatry: 30 days Comprehensive Nutrition Screen within 72 hours of admission (exception: TF by RD) for: All other consults & referrals including: MD/LIP Consults (except for Preferences & Psychiatry) Psychiatry: patients on therapeutic diets listed below (exception from DTR/NT) RN-RD Rounds generated referrals Nutrition Technician Referrals Interdisciplinary referrals DIET ORDER: New TPN/PPN: 24 hours New Tube Feeding: 24 hours By DAY 4 on the following diets: NPO/Clear Liquid Renal, Protein or Fluid restricted; Blenderized, Puree,Dysphagia, Thick Liquids ICU stay: Hospital Day 3 Pediatrics: By Hospital Day 4 Assessment within 7 days MDS documentation within 7 days of SNF admission Nutrition Screen within 72 hours MDS documentation within 7 days of SNF-SFBHC admission Nutrition assessment documented within 14 days of admission Work Process DTR/NT Registered Dietitian (RD) Departmental Form Nutrition Screening Form Adult or Neonatal Nutrition Care Plan Timeliness Screening Form initiated within 24 hours of identification of criteria and documented within 48 hours. Assessment initiated within 24 hours: Of Identification of criteria, or Of receipt of MD /LIP consult Assessment initiated within 48 hours: Of receipt of RN or Patient Admission Database referral All assessments documented within 48 hours of notification/identification of criteria Documentation DEPARTMENTAL: Screening, Assessment, and Activity Log (SAA) Nutrition Screening Form MEDICAL RECORD: Progress Notes & IPOC RD s review all DTR/NT completed screening forms daily for risk factors and evaluation of appropriate risk level assignment. RD s will assess all high risk within 48 hours and moderate risk patients referred by DTR/NT within 72 hours. DEPARTMENTAL: Screening, Assessment, and Activity Log (SAA) Nutrition Care Plan MEDICAL RECORD: Progress Notes & IPOC 66

67 67

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