Download 1 Every 15 Seconds, Someone In the United States Suffers a

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 1.365 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.
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TBI-related Disability and Cost to Society
Every 5 minutes someone becomes permanently disabled as a result of a traumatic brain
injury4. Traumatic brain injury contributes to 1/3 of all injury-related deaths in the United
States2. 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
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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.
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References
1. NCIPC: Web-based Injury Statistics Query and Reporting System (WISQARS)
http://www.cdc.gov/injury/wisqarsFaul 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; 2010
2. 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; 2003.
3. 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;
2006.
4. Coronado, McGuire, Faul, Sugerman, Pearson. The Epidemiology and Prevention
of TBI (in press) 2012
5. Guerrero J, Thurman DJ, Sniezek JE. Emergency department visits association
with traumatic brain injury: United States, 1995-1996. Brain Injury, 2000;
14(2): 181-6.
6. Thurman DJ, Guerrero J. Trends in hospitalization associated with traumatic
brain injury. JAMA, 1999; 282(10):954-7.
7. Unpublished data from Multiple Cause of Death Public Use Data from the
National Center for Health Statistics, 1996. Methods are described in Sosin DM,
Sniezek JE, Waxweiler RJ. Trends in death associated with traumatic brain injury,
1979-1992. JAMA 1995;273(22):1778-1780.
8. 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, 1990-1993. MMWR 1997;46(1):8-11.
9. 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, 1995.
10. 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):602-15. Kraus JF. Epidemiology of head injury. In: Cooper, PR, ed.
Head Injury, Third Edition. Baltimore: Williams and Wilkins, 1993; 1-25.
11. Annegers JF, Grabow HD, Kurland LT, et al. The incidence, cause and secular
trends in head injury in Olmstead County, Minnesota, 1935-1974. Neurology
1980;30:912-919.
12. 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.
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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, 1978. American Journal of Epidemiology 1981; 113:500-509.
14. Jagger J, Levine JI, Jane JA, Rimel RW. Epidemiologic features of head injury in a
predominantly rural population. Journal of Trauma 1984; 24:40-44.
15. Fife D, Faich G, Hollinshead W, Wentworth B. Incidence and outcome of hospitaltreated head injury in Rhode Island. American Journal of Public Health
1986;76:773-778.
16. 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; 4:560-580.
17. Cooper KD, Tabaddor K, Hauser WA, et al. The epidemiology of head injury in the
Bronx. Neuroepidemiology 1983;2:70-88.
18. 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; 119:186-201.
19. MacKenzie EJ, Edelstein SL, Flynn JP. Hospitalized head-injured patients in
Maryland: Incidence and severity of injuries. Maryland Medical Journal
1989:38:725-732.
20. Thurman DJ, Jeppson L, Burnett CL, et al. Surveillance of traumatic brain injuries
in Utah. West J Med 1996; 165:192-196.
21. Centers for Disease Control and Prevention. Traumatic brain injury -- Colorado,
Missouri, Oklahoma, and Utah, 1990-1993. MMWR 1997; 46(1):8-11.
22. Gabella B, Hoffman RE, Marine WW, Stallones L. Urban and rural traumatic brain
injuries in Colorado. AEP 1997;7(3):207-212.
23. Thurman DJ, et al. Traumatic brain injury in the United States: A report to
Congress. Atlanta, Centers for Disease Control and Prevention, 1999.
24. Sosin DM, Sniezek JE, Waxweiler RJ. Trends in death associated with brain injury,
1979-1992. JAMA 1995;273:1778-80.
25. Max W, MacKenzie EJ, Rice DP. Head injuries: costs and consequences. Journal of
Head Trauma Rehabilitation 1991;6(2):76-91.
26. 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, 1995.
27. National Committee for Injury Prevention and Control. Injury Prevention:
Meeting the Challenge. New York: Oxford University Press, 1989.
28. Pope AM, Tarlov AR, editors. Disability in America: Toward a National Agenda for
Prevention. Washington, DC: National Academy Press, 1991.
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References
29. Saatman, KE, Duhaime, AC, Bullock, R. (2008). Classification of traumatic brain
injury for targeted therapies. Journal of Neurotrauma 25:719-738.
30. 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,
1637-1640.
31. World population statistics: San Francisco Population 2013. Retrieved February
17, 2014 from http://www.worldpopulationstatistics.com/san-franciscopopulation-2013/.
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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 19951 and revised in 2007.1
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 2007. 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.
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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
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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 outcome4. 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.
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 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 (0.1-0.3
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 20-30 minutes with
neostigmine (20-70 mcg/kg) and glycopyrrolate (0.6 mcg/kg).
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 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
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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.
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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 death1.
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.
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• 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:S2-1-62.
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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
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
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
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
0
1
2
3
4
5
Strength
No contraction
Flicker or trace contraction
Active movement with gravity eliminated
Active movement against gravity
Active movement against resistance; (Subdivisions)
Normal strength
4 - slight resistance
4 moderate resistance
4 + strong resistance
Goal
 Performance of a complete neurological examination in order to rapidly detect
deviations from baseline thus preventing neurological disability.
18
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
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
 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
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 10-15 mmHg; ICP above 20 mmHg is considered elevated6.
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 Monitoring1
• 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
 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 catheters1.
•
•
•
•
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
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
•
•
In order to minimize the effect of head-of-bed (HOB) elevation on CPP, HOB
should be raised no more than 30o. This strategy also addresses the observation
that cerebral blood flow drops as the HOB elevation exceeds 30o – 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
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 trauma9. 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
 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 PaO2 95-105mmHg unless otherwise instructed (Goal 100mmHg)
 Maintenance of a PaCO2 35-45mmHg unless otherwise instructed (Goal 40mmHg).
Target PaCO2 for signs of herniation: 25 mm Hg.
 Maintenance of a PH of 7.35-7.45mmHg
 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
 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. 34:216-222.
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):5965.
28
FiO2§
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
ICP > 20 and/or Labile: PEEP & Other
Interventions
< 0.50
5 cmH2O
5 cmH2O
0.50-0.59
5-8 cmH2O
5 cmH2O
0.60-0.69
1.
10 cmH2O
5-8 cmH2O
2.
begin considering ARDS Net protocol
0.70-0.79
10-12
8 cmH2O
0.80-0.89
1.
12-16 cmH2O
1. 10-12 cmH2O
2.
PEEP titration evaluation*
2. PEEP titration evaluation*
3.
Consider aerosolized prostacyclin
3. Consider aerosolized prostacyclin
1.
> 16 cmH2O
1.
12 cmH2O
2.
PEEP titration evaluation
2.
PEEP titration evaluation
3.
Trial of aerosolized prostacyclin
3.
Trial of aerosolized prostacyclin
4.
Avoid FiO2 of 1.0 (de-nitrogen atelectasis)
4.
Avoid FiO2 of 1.0 (de-nitrogen atelectasis)
5.
Consider prone position
5.
Consider prone position
6.
Consider recruitment maneuvers
6.
Consider recruitment maneuvers
7.
Downgrade PaO2 goals to___?
7.
Down-grade PaO2 goals to___?
> 0.90
§
Denotes sustained FiO2 requirements > 24h
*
Incremental PEEP Trials should be done (perhaps Q-Day) to assess potential recruitment (degree
of improvements in PaO2/FiO2, compliance and Vd/Vt) balanced against potential adverse effects on
BP, ICP, CPP, SjvO2, PBRO2
29
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
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 propofol7, 8, 10. Many published protocols have
also used prophylactic neuromuscular blockade5, 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 25-50 mcg IV Q15’ or hydromorphone 0.4-0.8mg q1o 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
•
•
•
•
mechanical ventilation, line placement, endotracheal suctioning, patient safety
and restraint).
Propofol infusion at 10-80 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 recovery13.
 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
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 15-30 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 0.25-1.0 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
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 10-15 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
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 100-200.
 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
Hypothermia
Background
Hyperthermia, even of 1-2o 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 3233o C) decreases cerebral oxygen utilization and acts as a neuroprotectant. Despite reports
from small series of improved outcome after induced hypothermia5, 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 2nd or 3rd tier therapy for refractory elevated
ICP.
Guidelines
 Goal temperature (measured intravascularly or rectally) will be 36.0-38.0o C. (See
Fever Management for Critical Neurological Injury: Traumatic Brain Injury and
Stroke 2014).
 For T > 37.5o 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<38.3o 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 2014.
 Although intermittent doses of meperidine (12.5-50 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 32-33o C using nasogastric lavage may be
considered in cases of refractory elevated ICP.
36
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-0.25-1.0g/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 0.25-1gm/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
•
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
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 seizures12.
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 15-20 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
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 defined4
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 hypovolemia4. CSW is most likely to occur in
40
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.
Symptoms associated with hyponatremia
• Mild or gradual hyponatremia: Anorexia, headache, irritability, muscle
weakness
•
Goals
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 sequelae4.
 Modulate therapy as follows4:
• Stop if the change in Na+ is > 10mEq/L in 24 hours
• Do not exceed a rate of correction of 1.3 + 0.2mEq/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 0.1-0.2mg PO QD
- Demeclocycline 300mg PO BID
41
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
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.
Assessment characteristics of impaired oxygenation
• Confusion/Decreased mental acuity
• Somnolence
• Restlessness/Irritability
• Hypercapnea
• Hypoxia
• Dyspnea
• Cyanosis
• Tachycardia/dysrhythmias
• Anxiety
Goals
 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 medulla2. 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
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
TBI1. Most cases occur within two weeks of injury3. The most likely organisms are
S. aureus, Enterobacteriaceae, Pseudomonas sp., and pneumococci4. San Francisco
General Hospital and Trauma Center utilizes the CDC definition for hospitalacquired meningitis/ventriculitis9.
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
Goals
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
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
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 39.
6. 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
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
•
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 are4
• 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
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
 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 109
- 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
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
1. General Pain
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.
Goal
 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
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
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
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
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 PTSD23
• 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
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
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 68.
57
References
1. Baltas I, Tsoulfa S, Sakellariou P, et al.: Posttraumatic meningitis: Bacteriology,
hydrocephalus, and outcome. Neurosurgery 35: 422-7, 1994.
2. Brian JE, Jr.: Carbon dioxide and the cerebral circulation. Anesthesiology 88:
1365-86, 1998.
3. Eljamel M S M, Foy P M: Post-Traumatic CSF fistulae, the case for surgical repair.
Br J Neurosurgery 4: 479-83, 1990.
4. Greenberg M S.: Handbook of Neurosurgery (5th 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, 1988.
6. 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 75:731-739, 1991.
7. Palmar J D, Sparrow O C, Iannotti F I.: Postoperative heamatoma: A 5 year survey
and identification of avoidable risk factors. Neurosurgery 35: 1061-5, 1994.
8. Management and Prognosis of Severe Traumatic Brain injury
9. Center for Disease Control and Prevention. (2013). CDC/NHSN Protocol
Clarifications. Retrieved from http://www.cdc.gov
10. Chastre J, Fagon J-Y. Ventilator-associated pneumonia. Am J Respir Crit Care Med
2002;165:867.
11. Anon. National Nosocomial Infections Surveillance (NNIS) System Report, data
summary from January 1992 through June 2004, issued October 2004. Am J
Infect Control 2004;32:470.
12. Association for Professional in Infection Control and Epidemiology. Guide to the
elimination of ventilator- associated pneumonia; 2009.
13. Anon. Medicare fact sheet : proposals for improving quality of care during
inpatient stays in acute care hospitals in the fiscal year 2011. Notice of Proposed
Rule making. 2010.
14. 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) 438e443
15. Saint, S., Chenowith, C.E., (2003). Biofilms and catheter-asociated urinary tract
infections. Infectious Disease Clinics of North America. 17(411-432).
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-S50.
17. CDC: Guideline for Prevention of Catheter-associated Urinary Tract Infections,
2009 1-67.
18. 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;323:497-502
19. 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), 43-57.
58
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):453-463.
22. American Psychiatric Association. (2000). Diagnostic Statistical Manual of Mental
Disorders-IV-TR. Washington, D.C: Author.
23. National center for PTSD: http://www.ptsd.va.gov
59
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 formula @30 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
•
•
•
agent unless contraindicated, +/- TF hold and notify the team. If residuals
persist >400 mL, see ICU Enteral Nutrition Feeding Guideline, pg 67.
Day 2-3
- 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 1-6
- 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 2-6
- 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
-
•
•
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 2-3
- 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
Appendix B-1
SAN FRANCISCO GENERAL HOSPITAL TRAUMA CENTER
DEPARTMENT OF FOOD & NUTRITION SERVICES
POLICY & PROCEDURE MANUAL
Policy No:
Adopted:
Reviewed:
Revised:
CL003
11/05/98
7/18/2012
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
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
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
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
Work Process
Departmental Form
Timeliness
Documentation
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
•
•
•
DTR/NT
Nutrition Screening Form
•
Screening Form initiated within 24 hours
of identification of criteria and
documented within 48 hours.
DEPARTMENTAL:
• Screening, Assessment, and Activity Log
(SAA)
• Nutrition Screening Form
MEDICAL RECORD:
• Progress Notes & IPOC
Nutrition Screen within 72 hours
MDS documentation within 7 days of
SNF-SFBHC admission
Nutrition assessment documented within
14 days of admission
Registered Dietitian (RD)
Adult or Neonatal Nutrition Care Plan
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
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
Cognitive Dysfunction and Maladaptive Behavior Following TBI
Background for Cognitive Dysfunction and Maladaptive Behavior
Patients with TBI often exhibit cognitive and behavioral dysfunction either as a result of
the 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. 4 Moreover, their presence and severity may vary
over time and in an unpredictable fashion. Because of this, reassessment must be frequent
and treatment adaptable to changing patient conditions.
The interplay between cognitive dysfunction and behavioral issues is complex and their
interdependence can complicate patient management. For example, patients may have
short-term memory loss in addition to reduced safety awareness and lack of insight. 10 As
such, their inability to understand the implications of their deficits combined with their
inability to remember instructions may lead to unsafe situations. This may lead to the
imposition of behavioral limits by hospital staff – a situation that may unintentionally
increase patient frustration and possibly lead to aggressive behavior.
In order to avoid a cycle of increasingly stricter limits culminating in physical restraints
and sedation, therapeutic strategies should rather re-direct patient behavior and diffuse
situations that might otherwise escalate. These strategies should address a patient’s
emotional state and cognitive limitations, and focus on optimizing physical environment
and personal interactions and minimizing the use of psychoactive medications.
The use of the Rancho Los Amigos Levels of Cognitive Functioning8 is considered standard
practice in the field of TBI recovery. Levels I to VIII are used to characterize behaviors and
levels of cognitive functioning. Although an individual with TBI may show behaviors from
more than one level, the best-fit classification guides our interdisciplinary team to facilitate
recovery, family education, and patient care (See Appendix B Rancho Los Amigos scale).
Goals of Therapy: Cognitive Dysfunction
Optimize patient function through early cognitive/behavioral intervention.
Provide an environment that minimizes patient agitation and is conducive to learning.
Minimize the use of physical restraints.
Minimize the use of psychoactive medications.
Include both patient and family in the rehabilitation process through education and
involvement in the treatment plan, with particular attention to behavioral issues and
management.
 Develop an interdisciplinary approach to cognitive and behavioral dysfunction in
patients with TBI. The Interdisciplinary Team (IDT) includes, but is not limited to,
Neurosurgery, Nursing, Neuropsychology, Occupational Therapy (OT), Physical
Therapy (PT), Speech Therapy (ST), Psychiatric Clinical Nurse Specialist (CNS) &
Psychiatry.





68
 Utilize protocols detailing the manner and frequency of cognitive/behavioral
assessment.
 Utilize protocols for disseminating information amongst the appropriate clinical
services.
 Build performance improvement systems within the guidelines.
Guidelines: Cognitive Dysfunction
 Evaluation of cognitive dysfunction
• On admission, Neurosurgery & Nursing will screen the patient for cognitive
deficits and determine the need for/timing of consultation of the various
services mentioned above as the patient becomes more medically stable. These
services will evaluate physical, cognitive, behavioral and functional deficits.
•
•
•
Once the patient is medically appropriate for rehab therapies, they will undergo
evaluation. These evaluations will address the patient’s response to stimuli –
specifically the patient’s level of arousal/attention, ability to verbalize,
localization to sound, and response to tactile, auditory and olfactory stimulation.
The depth and breadth of this evaluation is paced in accordance with the
patient’s ability to tolerate and respond. Responses should be documented and
used to determine the current Rancho Level. Implications of other medical
conditions (ie: hyponatremia, infection, withdrawal, ICP, medication effects) will
be taken into account. Deterioration of mental status will be reported
immediately to the primary team.
Formal/standardized assessment may be initiated when a patient is cognitively
and behaviorally appropriate. Assessment is completed by the Speech
Pathologist and/or the Neuropsychologist. Common areas of impairment
addressed in the multidisciplinary cognitive and behavioral evaluation are:
- Orientation
- Attention/concentration/information processing
- Memory
- Visual-spatial/perceptual skills
- Expressive and receptive language
- Motor skills and sequencing
- Executive function (insight, problem solving, multitasking, judgment,
safety awareness, etc)
- Emotional functioning
Patient’s cognitive, behavioral and psychiatric issues will be addressed with
diagnostic treatment regularly by relevant services. Documentation of patient’s
status and limitations will be addressed in the patient’s medical record on a
regular basis.
69
•
•
•
•
•
•
Patient’s cognitive, behavioral and psychiatric issues will be discussed at the
weekly IDT meeting. Safety awareness, restraint usage, medication regimen, and
capacity will be addressed as indicated. ST, OT and Neuropsychology will
provide key cognitive and behavioral therapeutic assessments with input from
the IDT. The Rancho Scale will be used as a framework to guide these
assessments and intervention efforts, as well as for documentation.
Individualized cognitive therapy will be initiated pending the results of the
evaluation. Treatment will address the cognitive/behavioral impairments with
the goal of optimizing patient function as it relates to basic and community level
activities.
The Rehabilitation Service will assist the IDT in assessing the patient’s
safety/safety awareness, and the need for supervision in the prevention of falls,
elopement, self-injurious and assaultive behavior, as well as the optimal
environment for recovery. The goal is to manage unsafe and care-interfering
behaviors in the least restrictive manner.
The IDT will provide ongoing teaching to caregivers and family, with both
written and verbal instruction, regarding cognitive deficits specific to the patient
and suggestions to maximize cognitive function and reduce agitation.
The IDT will monitor the use of psychotropic medications for sedation and
neurostimulation. Adjustments to the medication regimen may be made by the
primary team to optimize overall level of functioning.
Substance abuse guidelines will be instituted if this is an identified patient issue.
 Treatment of cognitive dysfunction
• Once the assessment has been completed by IDT, cognitive behavioral diagnostic
information is utilized to understand Rancho Level of functioning which further
guides patient care, including interactions with RN staff. The goals of treatment
and the techniques used to manage the cognitively impaired patient vary
according to their Rancho level of functioning. Therapy addresses the
impairments noted during the evaluation to work towards optimizing function
in a variety of domains.
•
Individualized education is a crucial part of the recovery process, and must
occur at every level. The IDT will provide ongoing teaching to the individuals
involved in a patient’s care, with both written and verbal instruction, regarding
cognitive deficits specific to the patient and suggestions to maximize cognitive
function and reduce agitation. Instructions for interacting with the patient will
be communicated to ensure an optimal environment for recovery. This
communication will be dependent on the patient’s level of functioning.
70
 Cognitive dysfunction and Post-traumatic amnesia
• Anterograde and retrograde amnesia
- Anterograde amnesia or posttraumatic amnesia (PTA) is the inability to form
consistent day-to-day memories secondary to a brain injury.11 Retrograde
amnesia is the inability to remember occurrences prior to and including the
injuring event. During posttraumatic amnesia, patients with traumatic brain
injuries typically having waxing and waning mentation, distractibility, short
term and long term memory deficits, and agitation and restlessness.
-
-
The use of cognitive assessment can assist in tracking recovery and
determine appropriate compensatory strategies. Therapeutic treatment at
this point is designed to optimize recovery such as environmental
interventions, and family caregiver education.1
As the patient recovers, memories leading up to the traumatic event may
return. However, many patients who endure posttraumatic amnesia never
regain memory of the actual injuring incidence. In recovery, improvement
from retrograde amnesia typically follows resolution of anterograde
amnesia.11
 Cognitive dysfunction and stress disorders
• Acute Stress Disorder (ASD)
- Acute stress disorder is a result of exposure to a traumatic event, to oneself
or surrounding others, in which the patient experiences intense fear, horror,
or a sense of helplessness. This anxiety disorder develops within one month
after a severe traumatic incident. 2 The experience must involve a threat of
death, serious injury, or threat to physical integrity and the person’s
response must involve intense fear, helplessness, and horror. Symptoms can
effect any age group and include:
 Distressing dissociative symptoms
 Feelings of emotional detachment
 Reduced awareness of surroundings
 Derealization
 Depersonalization
 Dissociative amnesia



Persistently re-experiencing trauma related images
Avoidance of trauma related stimuli
Anxiety and increased arousal (hypervigilance, restlessness, and
exaggerated startle)
71
-
•
Patients with acute stress disorder will avoid reminders of the trauma and
frequently relive the event in the form of dreams, nightmares, or painful
memories. As a result of the above symptoms the patient suffering from
acute stress disorder may be misdiagnosed as having cognitive deficits and
behavioral issues. Individuals diagnosed with ASD are a high risk for
developing Post-traumatic Stress Disorder.5
Post-traumatic Stress Disorder (PTSD).
- Symptoms of PTSD are like those of an acute stress disorder but must persist
longer than 4 weeks following the traumatic event. Please refer to “Postconcussive Syndrome and Management of the 6 Most Common Symptoms” on
pp57-58.
 Cognitive dysfunction and safety
The nursing service will assist the Interdisciplinary Team (IDT) in assessing the
patient’s safety/safety awareness. This will include issues regarding restraint use,
supervision in the prevention of falls, elopement and assaultive behavior, as well as,
engineering an optimal environment to reduce the presence of potentially
hazardous behaviors.7 Institutional police should be called if the patient is violent
and a threat to him/herself or others or if uncontrolled escalating behavior
develops. IDT members should instruct the institutional police in management of
the patient.
Goals for Maladaptive Behavior
Optimize patient function through early cognitive/behavioral intervention.
Provide an environment that minimizes patient agitation.
Minimize the use of physical and chemical restraints.
Include both patient and family in the rehabilitation process through education and
involvement in the treatment plan, with particular attention to behavioral issues and
management.
 Develop a multidisciplinary approach to cognitive and behavioral dysfunction in
patients with TBI.
 Regularly disseminate information amongst the appropriate clinical services.
 Regularly engage in performance improvement projects to enhance patient care.




Guidelines for Maladaptive Behavior
 Evaluation of maladaptive behavior
• The interdisciplinary team (IDT) must evaluate maladaptive behaviors (e.g.,
agitation, pulling tubes, attempting to climb out of bed, striking out) during the
weekly IDT case conference, and more frequently, if needed. A focused progress
note outlining the evaluation of the problem and plan for intervention should
include:
- Identification of the behavior to be modified.
72
-
Identification of the triggers leading to the behavior. This may include who
might trigger the behavior, what situations trigger the behavior, and what
environmental conditions are present when the behavior occurs.
Identification of the treatment goal (e.g., decrease fall risk, limit agitation,
decrease striking out).
Determination of a plan for intervention and implementation. This should
include assignment of roles to IDT members.
Determination of a follow-up date to evaluate the success of intervention(s)
used. The follow-up date may be the next IDT case conference, or at an
earlier date, as needed.
 Interventions for maladaptive behavior
• Physical restraints
- Definition: Refer to SFGH Policy and Procedure 18.9 regarding restraint use.
- Types:
 Wrist and ankle restraints
 Mittens
 Waist restraints
 Vests (Poseys)
 Bed enclosures
-
Use:
 While the use of a restraint is often initiated to protect intravenous sites or
tubes or decrease risk of fall, utilization of a restraint is not without risk.
Examples of injuries related to restraint use may include, but are not limited
to: entanglement, pressure ulcers, fractures related to falls caused by
climbing over a side rail. A full assessment by the IDT of the risks and
benefits of restraint use will be assessed weekly at the IDT meeting. The risks
and benefits must also be discussed with the patient’s family; documentation
of such discussion must be evident in the medical record.

•
Careful monitoring (as per Nursing policy) of the use of the restraint, its
efficacy, and ongoing behaviors necessitating its continued use must be
documented. Discussion of the need to continue use of the restraint must be
discussed at the weekly IDT meetings or more frequently, as needed.
Environmental interventions for maladaptive behavior
- For all TBI patients, limiting excessive environmental stimulation is crucial.
Consideration of the environment may also be helpful in both limiting future
behavioral problems, as well as facilitating the recovery process. As patients
recover, a gradual increase in the degree of stimulation that patients receive may
begin, for example, by introducing exposure to light and other elements of one’s
surroundings. This may assist patients in becoming more aware of day and
night, and staff and family members, thereby improving orientation and sleep.
Family and caregivers are provided education regarding the degree of
73
•
stimulation appropriate for a patient’s level of recovery. Environmental
Stimulation Precautions: Please see Appendix C-4.
Behavioral interventions for maladaptive behavior
- Agitation: Excessive restlessness often associated with over-stimulation or
mental distress.
 Acknowledge the patient’s discomfort and reassure him of your desire to
help.
 Address the patient in a calm and soothing manner.
 Keep the lights low in the room.
 Minimize or omit television.
 Keep statements simple and concise when addressing the patient, as detailed
explanations and instructions tend to increase agitation.
 Cluster therapeutic care when appropriate.
 Limit the number of people in the room; step out of the room to address
others.
-
-
•
Combativeness: Striking out intentionally or unintentionally.
 Maintain your awareness of your position relative to the patient. Stand back
to avoid being hit or kicked. Do not crowd the patient; give the patient his
“space.”
 Address the patient in a calm and soothing manner.
 Acknowledge the patient’s discomfort.
 Let the patient know that you will be calling for additional help if needed.
 Avoid backing self into a corner when leaving the room. Always keep facing
the patient.
 If possible, remove any objects that may potentially harm the patient.
Impulsivity: The tendency to become active suddenly and spontaneously without
planning the activity or thinking about the consequences of the actions.
 Always assess the environment for safety before asking the patient to initiate
an activity.
 Inform the patient in a gentle but firm manner when an unsafe or impulsive
behavior is observed. Call attention to the consequences and suggest
alternative behaviors.
 Increase nursing supervision as needed to ensure safety
 Maintain spatial distance when setting limits until a sense of the patient’s
response is obtained.
 Cue the patient to slow down and think out loud before responding.
 Orient patient to use of call light.
Psychopharmacological interventions
- Psychotropic medications play a role in facilitating the recovery process in areas
such as limiting agitation, improving attention and concentration, and promoting
regular sleep-wake cycles. However, with any use of psychotropic medications,
as with the use of restraints, the risks and benefits must be weighed.
74
75
Symptom
Anxiety and Agitation
Evaluation
1.
Before using any medication to treat anxiety and/or agitation felt to be due primarily to the
TBI, other diagnoses that may result in such behavior must be ruled out. This includes
evaluation for the presence of metabolic dysfunction, sympathetic hyperactivity, thyroid
disease, drug or alcohol withdrawal, or any pre-morbid psychiatric illness, physical
discomfort, thirst, hunger, constipation, oxygen desaturation.
2.
Eliminate medications that may exacerbate anxiety, if possible. These medications may
include benzodiazepines, certain SSRIs, antidepressants, narcotics, albuterol, and H2
blockers.
3.
Evaluate for the presence of situational or environmental factors that might contribute to
increased anxiety and intervene accordingly. Such factors may include limiting overstimulation, assessing if particular visitors incite increased anxiety, and developing a
regular toileting program.
Medications
While minimizing agitation and/or anxiety is the goal, caution should be exercised in the
administration of these medications to avoid over sedation. Worsening of the patient’s mental
status due to over sedation may mask the presence of a true neurological decline or confound
the neurologic examination, thus necessitating a neurologic work up. Further, over sedation
limits the patient’s ability to safely participate in therapies and attend to tasks. Any neuroleptic
use may result in tardive dyskinesia or neuroleptic malignant syndrome. AIMS testing when
appropriate may be used to rule out dystonia. Monitor medications for possible paradoxical
effects such as agitation.
1. Anxiety / Agitation Related to
Benzodiazepines such as lorazepam and
Drug Withdrawal
diazepam may be of benefit, but present the risks
of negative side effects including excess sedation
and adverse effect on cognition.
2.
Anxiety / Agitation Not Related
to Drug Withdrawal
If a sleep disturbance is felt to be contributing to
the patient’s level of anxiety, consult with
psychiatry for drug choice and dosing. Melatonin
and low doses of Trazadone may be initiated and
increased until nighttime sleep is achieved.
Anticonvulsants (e.g., tegretol and valproic acid)
have demonstrated benefit in the control of
agitation.
3.
Imminent Danger to
Self/Others or Agitation
Limiting Ability to Render
Medical Care
Agitation Associated With
Inattention or Distractibility
Judicious use of short-acting benzodiazepines or
neuroleptic agents may be helpful in these cases.
Agitation Associated With
Sympathetic Hyperarousal
Beta blockers may be utilized in this setting, when
other etiologies for the symptoms of sympathetic
hyperarousal are ruled out. Of note, beta blockers
may cause CNS side effects (e.g., nightmares,
hallucinations, and insomnia) and may be
contraindicated in patients with COPD and
diabetes.
4.
5.
Stimulants (e.g., methylphenidate and amantidine)
have been useful in these instances. These
medications have also been helpful in patients who
demonstrate a lack of initiation, mimicking
depression, with respect to participating in tasks.
76
Symptom
Anxiety and Agitation
Agitation Related to Anxiety
(Continued)
Sleep Disturbance
6
Agitation Related to Psychotic
Symptoms, Including Delusions,
Hypervigilance, and Hallucinations
Evaluation and intervention
Buspirone has been used with some success in
this setting. Of note, buspirone has demonstrated
little sedative effect or adverse impact on cognition.
Risperadone may be considered. It has minimal
central nervous system effects, such as sedation,
as compared to other psychotropic medications.
1.
Use of a sleep chart can be helpful in tracking for the presence of a sleep disturbance.
This may include checking the patient at intervals of 30 minutes.
2.
Evaluate for the presence of situational or environmental factors that may adversely affect
the patient’s sleep patterns. This may include noise within the room or hallway, or
frequent medical interventions (e.g., vital signs, neuro checks, respiratory treatments).
Environment will be modified accordingly and integration of sleep hygiene principles
should be a focus of patient education and applied as appropriate (avoid stimulating
activities prior to sleep, avoid caffeine and large meals late at night, encourage napping
earlier in the day if daytime napping is interfering with nighttime sleep, avoid TV prior to
bedtime, keep a consistent bedtime routine).
3.
Evaluate for physiological factors that may affect sleep. These factors may include
posttraumatic stress disorder, sleep apnea, premorbid history of insomnia, or age >60
years.
Medications
The goals of therapy should be to assist in re-establishing the sleep/wake cycle. Different
medications affect the sleep cycle in different ways; certain agents may be selected based on
these interactions. None are without potential side effects that may adversely affect a
patient’s recovery.
•
Antidepressants: Trazadone increases slow wave sleep and improved REM sleep
latency. Amitryptiline may increase total sleep time, improve sleep quality, and
decrease number of awakenings. Anticholinergic Psychosis is a frequent?
4
complication of antidepressant administration.
•
Melatonin: Melatonin has been shown to help regulate the sleep/wake cycle
through its actions on melatonin receptors in the brain. It causes neither withdrawal
effects nor dependence, though it can cause daytime sleepiness and contribute to
14
irritability.
•
Benzodiazepines (middle acting): Clonazepam may decrease the number of
awakenings and increase Stage 4 sleep. Abrupt withdrawal may result in seizure or
death. The side effects of paranoia may complicate the recovery process.
Sedation, anterograde amnesia, impaired motor performance with increase risk of
falls, paradoxic agitation, and abuse potential are side effects inherent to all
15
benzodiazepines.
Hypnotics: Ambien and Restoril have been shown to assist with sleep. Sedation
and impaired motor performance are risk factors that need to be considered.
•
Based on information from the Behavior Management Program, Policy and Procedure Manual, Santa Clara
Valley Medical Center, and on Pharmacology and Brain Rehabilitation, Physical Medicine and Rehabilitation
Clinics of North America, 8:4, November 1997, AANN guidelines on the care of the patient with mild traumatic
brain injury, and Castriotta, Atanasov and Kuna. Treatment of Sleep Disorders after Traumatic Brain Injury,
Journal of Clinical Sleep Medicine, 5(2), 2009: 137.
77
References
1. Ahmed, S., Bierley, R., Sheikh, J. I., & Date, E. S. (2000). Post-traumatic amnesia after
closed head injury: a review of the literature and some suggestions for further
research. Brain Injury, 14(9), 765-780.
2. American Association of Neuroscience Nurses. (2012). Nursing management of
patients with mild traumatic brain injury. AANN Clinical Practice Guidelines.
3. American Psychiatric Association. (2000). Diagnostic Statistical Manual of Mental
Disorders-IV-TR. Washington, D.C: Author.
4. Arciniegas, D. B., Held, K., & Wagner, P. (2002). Cognitive impairment following
traumatic brain injury. Current Treatment Options in Neurology, 4(1), 43-57.
5. Bryant, R. A. (2006). Acute stress disorder. Psychiatry, 5(7), 238-239.
6. Castriotta, Atanasov and Kuna. (2009). Treatment of Sleep Disorders after
Traumatic Brain Injury, Journal of Clinical Sleep Medicine, 5(2),137.
7. Flannery, J. (1998). Using the levels of cognitive functioning assessment scale with
patients with traumatic brain injury in an acute care setting. Rehabilitation Nursing,
23(2), 88-94.
8. Hagen, C. (1998). The Rancho Los Amigos Scale Revised. Rancho Los Amigos: Author.
9. Meyer, M., Megyesi, J., Meythaler, J., Murie-Fernandez, M., Aubut, J., Foley, N., Salter,
K, Bayley, M, et. Al. (2010). Acute management of acquired brain injury part III: An
evidenced-based review of interventions used to promote arousal from coma. Brain
Injury, 24 (5), 722-729.
10. Prigatano, G. P. (2005). Disturbances of self-awareness and rehabilitation of patients
with traumatic brain injury: a 20-year perspective. The Journal of Head Trauma
Rehabilitation, 20(1), 19-29.
11. Stuss, D. T., Binns, M. A., Carruth, F. G., Levine, B., Brandys, C. E., Moulton, R. J., &
Schwartz, M. L. (1999). The acute period of recovery from traumatic brain injury:
posttraumatic amnesia or posttraumatic confusional state?. Journal of
Neurosurgery, 90(4), 635-643.
12. Tomlin, K. (2007). Workbook of Activities of Language and Cognition. East Moline,
IL: Linguisystems.
13. Jamora, C. W., Young, A., & Ruff, R. M. (2012). Comparison of subjective cognitive
complaints with neuropsychological tests in individuals with mild vs. more severe
traumatic brain injuries. Brain Injury, 26(1), 36-47.
14. Kemp, S., Biswas, R. et al. (2004). The value of melatonin for sleep disorders
occurring post-head injury: a pilot RCT. Brain Injury, 18(9), 911-919.
15. Rao, v., Rollings, P. (2002). Sleep disturbances following traumatic brain injury.
Current Treatment Options in Neurology, 4(1), 77-87.
16. National center for PTSD: http://www.ptsd.va.gov
17. Rothbaum, B., Astin, M., Marsteller, F. (2005). Prolonged exposure versusts eye
movement desensitization and reprocessing (EMDR) for PTSD rape victims. Journal
of Traumatic Stress, 18(6), 607-616.
78
Mobility Management Following TBI
Background
Individuals with TBI frequently exhibit a broad spectrum of physical and cognitive
impairments with varying levels of dysfunction. Impairments and disabilities frequently
include difficulty with mobility, performance of self-care/activities of daily living (ADLs),
perceptual ability, dysphagia, cognition, and communication.
Lack of early intervention leads to complications and prolonged morbidity, with
subsequent delay of return to maximal function. Early intervention facilitates the recovery
process and smooth transition to home or the next appropriate level of rehabilitative care
(e.g., Acute Rehabilitation).
Goals
 Prevent loss of ROM.
 Address issues related to abnormal muscle tone, in conjunction with medical
management.
 Prevent contractures and skin breakdown.
 Maximize strength/endurance.
 Improve motor control.
 Maximize ADL’s including feeding, grooming, dressing, and toileting.
 Maximize mobility including changing body position, balancing, transferring, walking,
and climbing stairs.
 Provide the appropriate level of stimulation to achieve treatment goals.
 Facilitate cognitive and perceptual recovery.
 Minimize risk of infection or medical complications.
 Increase the patient and caregivers’ awareness of deficits and their implications on the
patient’s recovery and return to the community.
 Educate patients and caregivers on compensatory techniques to facilitate ongoing
functional improvement.
Guidelines
 Rehabilitation Referral Process in the acute setting. This includes early assessment and
intervention by Rehabilitation Services, which is critical in the treatment of patients
with TBI to facilitate early improvement and to prevent complications.
 Assessment and treatment
• Comprehensive evaluation of the patient with TBI is crucial in the development of
treatment plans. Rehabilitation Services will identify the need for, and facilitate
planning of, ongoing interventions. Assessment will include identification of a
patient’s prior level of function in order to develop realistic treatment goals. All
assessments will include:
a) Tone
79


Tone will be assessed by observation, handling, and the modified Ashworth
scale if appropriate. Physical interventions may include positioning,
splinting, and/or neuromuscular techniques for inhibition/facilitation to
temporarily manage tone/prevent negative implications of abnormal tone.
Medical interventions will be considered when increased spasticity limits
function/places patient at risk of skin breakdown. Interventions may include
initiation of baclofen, tizanidine, dantrolene, and/or benzodiazepines.
Baseline and follow-up laboratory evaluations may be necessary, depending
on the agent used. Botulin toxin injections or motor point blocks may be
used if a more focused approach to a particular joint is needed.
b) Strength
 Strength will be assessed by observation, handling, and manual muscle
testing. It will be graded on a scale of zero to five (0-5) for patients who do
not exhibit spasticity. Neuromuscular facilitation techniques to maximize
return of strength/motor control will be employed. A therapeutic exercise
program will be developed for each patient to address his or her individual
needs.

Patients who are medically paralyzed and/or sedated, or who have sustained
motor impairments as a result of their injury, are at risk for pressure ulcers
due to immobility. The use of multipodus splints, specialized mattresses or
beds, specialized wheelchair cushions, and/or special positioning programs
may be recommended by Rehabilitation Services and carried out by
nursing/nursing assistants to prevent pressure ulcer formation. If a pressure
ulcer is identified, a wound care Clinical Nurse Specialist (CNS) will also be
consulted to provide recommendations and follow the patient as indicated.
c) Range of motion (ROM)
 ROM measurements will be performed and documented when appropriate.
A therapeutic exercise program will be developed to prevent ROM deficits
and contractures, and to maximize functional ROM. This may include use of
splinting or special positioning programs to maintain functional ROM. This
may include a component to be carried out by nursing staff/family members
when appropriate.

Heterotopic ossification (HO) may result in significant losses of ROM that
may adversely affect function. Special attention must be paid to any warm,
painful joint, even if the joint has no apparent relation to the patient’s
injuries. Initial evaluations may include plain films of the affected joints
(although this may be insensitive to early HO), and/or triple phase bone scan.
Alkaline phosphatase may be elevated in patients with HO, however, alkaline
phosphatase may often be elevated in TBI patients for other co-morbid
conditions. Treatment is controversial and may include active or activeassisted ROM and the use of didronel. In the late stages of HO (often when
the bone scan is negative), surgical excision may be considered.
80
d) Activities of daily living (ADLs)
 Assessment of ADL function/self care for each patient will include:
 Basic ADL’s:
• Dressing
• Grooming
• Feeding
• Bathing
• Toileting
• Functional Mobility (transfers, wheelchair mobility, household
distance ambulation)
 Cognitive Skills (Please see Cognitive/Behavioral Guidelines p68)
• Mental flexibility
• Executive functioning
• Problem-solving
• Memory
• Safety Awareness
• Attention
 Instrumental Activities of Daily Living (IADLs)
• Safety awareness/judgment for household and community level
activities
• Component skills required for cooking, cleaning, shopping, child
care etc
• Medication management
• Visual/perceptual skills for household and community level
activities
 Community Reintegration
• Basic Community Life Skills (i.e. keeping appointments, managing
transportation)
• Basic budgeting/money management skills
• Navigation/path-finding skills

A treatment plan will be developed and implemented for each patient based
on his or her individual needs to maximize or improve ability to perform
basic ADLs, IADLs, and community re-integration tasks in an independent-aspossible manner. Appropriate assistive devices will be obtained for each
patient to maximize functioning. Such equipment may include self-feeding
utensils, dressing aides, bathroom durable medical equipment, medi-sets,
assistive technology, etc.
e) Mobility
 Assessment of mobility will be performed on each patient. A therapeutic
program will be developed and implemented for each patient based on his or
her individual specialized needs. The following levels of mobility will be
assessed:
 Sitting/standing balance
81

 Bed mobility (scooting, rolling, sidelying to sit)
 Transfers (Bed-to-wheelchair, wheelchair-to-toilet, wheelchair-tobath, wheelchair-to-mat, car, etc)
 Wheelchair mobility (level surfaces, community surfaces, on to buses,
and into taxi’s)
 Gait (household, community, with/without distractions, level/uneven
surfaces, curbs, ramps, stairs, hills)
 Fall recovery
Appropriate assistive devices will be obtained for each patient to maximize
functional mobility. These may include orthotics, walking aides, specialized
wheelchairs, and wheelchair cushions.
f) Dysphagia
 When appropriate, Speech Therapy (ST) will evaluate patients to determine
if swallowing is within functional limits. ST will recommend appropriate diet
levels, and/or recommend tube feedings, if appropriate, to ensure adequate
nutrition and safety. Recommendations will be made regarding the level of
supervision needed at mealtimes and any compensatory techniques
necessary to facilitate safe swallowing. ST may recommend exercises for
patients and caregivers to carry out and will work with the patient as
indicated. ST may recommend video fluoroscopy for detailed evaluation of
the patient’s ability to swallow, if indicated.
g) Activity level for nursing/staff assistance
 Each component of the Rehabilitation Team’s assessment will include a plan
with therapeutic interventions to maximize function. The plan may include
instructions to nursing staff to assist the patient in an appropriate and safe
manner when the level of assistance for safe mobility/activity does not
require the skilled intervention of the rehabilitation team. Specific
instructions will be provided to the nursing staff, individualized to each
patient.
 Mobility interventions and Rancho Los Amigos Scale of Cognitive Functioning
• The Rancho Scale is a tool designed to identify patterns of recovery in people after
head injury. It is used to guide treatment interventions and strategies to optimize
the recovery of persons with TBI and to allow staff and caregivers a common
language to discuss a patient’s progression. See Appendix B for a detailed
description of the Rancho Scale and appropriate interventions.
 Positioning
• A positioning program should be implemented early in the course of treatment of
the patient with TBI, to be implemented by all staff that are involved in any physical
manipulation of the patient. This should also include the patient’s family and
friends.
82
•
•
Proper positioning is critical in the prevention of:
- Contractures.
- Abnormal patterns of muscle tone.
- Dysfunctional postures and positions of the head, trunk and pelvis,
particularly:
- Abnormally forward head.
- Protracted scapula.
- Posterior pelvic tilt.
- Trunk tightness.
Positioning in Bed
 Sidelying (or semiprone) is preferable to supine
 Head: neutral, aligned with spine.
 Bottom upper extremity: scapular protraction, humeral external rotation,
and flexed to approximately 90 degrees; elbow is flexed.
 Top upper extremity: scapular protraction and slight shoulder flexion,
resting on a pillow, with elbow extended.
 Wrists/hands: maintain wrist in extension (with use of splinting as needed),
maintain palmar arches.
 Lower extremities: pillow between knees, and under lower leg if needed, to
maintain alignment with the thigh and to prevent pressure ulcers; flex knee
and hips slightly.



•
If supine is required:
Shoulders: place small pillow underneath scapula, shoulders in slight
abduction and external rotation.
Upper extremities: elbows extended, forearms supinated, splinting for wrist
extension/digits as needed.
Lower extremities: slight knee flexion with the use of pillows, alternated
with knees in extended position.
Positioning in Wheelchairs
 The following positions may be achieved with shoulder straps, trunk
supports, seat belts, and/or lap boards as indicated.
 Pelvis: neutral or slight anterior pelvic tilt.
 Trunk: symmetrical and midline.
 Shoulders: slight external rotation, flexion, abduction.
 Upper extremities: elbow in comfortable flexion, forearms neutral, wrists
in slight extension, neutral radial-ulnar deviation, fingers in functional
position, thumbs radially abducted.
 Lower extremities: knees and ankles flexed at 90 degrees (splinting,
positioning devices may be necessary to achieve feet in a neutral
position).
 Head: midline.
83
 Passive range of motion (PROM)
• Perform PROM within the limits of pain to minimize contractures from heterotopic
ossification, muscle shortening, and joint capsular tightening. Patients should be
regularly assessed for subluxation at shoulders with appropriate precautions
instituted as needed.
• Avoid sudden stretches or overstimulation with range of motion.
• Instruct family members simple PROM exercises/precautions to avoid subluxation.
 Splinting and casting
• Splints may assist with positioning of flaccid patients. They also may temporarily
reduce tone by providing maintained pressure and stretch to targeted tendons, and
reduce complications related to abnormal tone.
•
Serial Casting:
- May be indicated for severe spasticity.
- May provide more neutral warmth and even skin pressure than splints.
- May be more effective than PROM, stretching, or splinting.
- Types:
 Drop out casts
 Bivalved casts
 Weight-bearing inhibitory casts
 Neuromuscular treatment
• Neurodevelopmental Treatment (NDT) is a therapy in which positions, weight
shifting, movements are utilized to increase or decrease muscle tone or elicit
righting motions. Principles are incorporated into bed mobility, transfers,
positioning etc.
•
Proprioceptive Neuromuscular Facilitation (PNF) is a method of promoting or
hastening the response of the neuromuscular mechanism through stimulation of
proprioceptors.
 Axial rotation of the trunk may be needed to inhibit tone with the comatose
patient who is posturing.
 Hip and knee flexion must be maintained, avoiding the supine position and
resistance to the back of the head, to assist in lessening extensor tone.
 Immediately after achieving successful inhibition of tone, more normal
movement in a functional pattern should be attempted.
84
Patient and Family Education and Psychosocial Support
Background
A wide body of literature has demonstrated that comprehensive patient and family
education and psychosocial support improve health outcomes. For the traumatically
injured, education that focuses on expected symptoms, natural history and expectations of
recovery are particularly germane.5 Consistent with the mission and vision of San Francisco
General Hospital, education is delivered to patients and their families in a culturally,
educationally and linguistically appropriate manner. The educational and patient/family
support process recognizes that patients and their families are an integral part of
treatment and goal setting. Through this, they are more likely to cope positively with the
injury sequelae, have improved outcomes, and are less likely to sustain repeated injury and
secondary functional decline.3
The educational plan will be based on the following five aspects of care: disease process,
recovery process, symptom and medication management, lifestyle and risk modification,
and follow up care and support. As the patient and family have a greater understanding of
the five aspects of care, individuals can begin to take an active role in managing their health
and that of their loved ones.
Goals
 Allow patients and their families to be more informed of their disease process and
its management through education, thus playing an active role in the recovery
process.
 Ensure that patient and family support are integrated into the plan of care both in
the inpatient and outpatient settings, in an interdisciplinary and collaborative
way.
Guidelines
 It is the responsibility of all IDT members to assess the readiness of patients and
families for educational content and the need for family support. The patient’s
educational plan will be individualized and anchored in the aforementioned five
aspects of care. SFGH patient education documentation standards will be followed
(SFGH P&P 5.14, Nursing P&P 11.2- Addendum II Interdisciplinary Patient
Education Record).
 The Social Worker will conduct an ongoing psychosocial assessment of family needs
including the grieving process, practical and emotional support systems, coping
skills, and financial resources (SFGH P&P 1.17,sec. IV). The IDT will monitor
changes in coping and family needs throughout the recovery continuum, adapt the
treatment plan and make necessary referrals.
85
 Patient/Family educational barriers, preferences, motivation and stressors will be
assessed by all IDT members upon admission and at regular intervals throughout
the hospital stay. Interdisciplinary rounds will include the development of an
individualized educational care plan for each patient/family. The IDT in their
weekly meeting will focus on ways to address the barriers, enhance motivation,
reduce stressors, and fill in knowledge gaps. Family and, to the extent possible, the
patient will be included in goal setting.
 Individualized educational materials will be determined by patient condition and
provided along the recovery spectrum. Family and patient educational resources
include the TBI education folder, BASIC website, Krames patient education
handouts, outside consultants, and the Patient Education Resource Center (PERC)
located in the medical Library.
 At times, the complexity of the patient’s acuity, psychosocial, and disposition issues
are such that additional coordination and collaboration are necessary. Patient and
family centered care meetings may be called by any member of the IDT for
coordination of the recovery process, educational issues, family support, and
development of a comprehensive discharge plan. The IDT will meet prior to discuss
the patient’s status and to appoint a “team leader” for the family meeting.
 As individuals recover from their injuries, they and their families need a
tremendous amount of support. To assist in this, the IDT helps the family to identify
existing supports (physical, financial, and psychosocial), community programs, and
refer to the monthly TBI support group facilitated by members of the IDT.
 Evaluation of financial resources for the patient and family are an integral
component of treatment planning and family education. The eligibility worker
explores these resources, verifies insurance coverage and distributes pertinent
information to the Social Worker and the Utilization Management Nurse. If the
patient does not have coverage, and is eligible for Medi-Cal, the eligibility worker
will refer to the Medi-Cal worker who will assist the patient/family in the
completion of the application. Should the patient also need monetary assistance, the
Social Worker will assist with applications to SDI, SSI, or General Assistance (GA).
The SFGH SSI worker may be consulted to assist the SW with new applications or
verification of existing cases. Medical insurers are contacted and kept appraised of
patient’s ongoing recovery, level of care, medical and rehabilitation needs by the
Utilization Management Nurse.
 The IDT will assess patient’s readiness for discharge as determined by medical
stability, functional ability, fiscal resources and family input. A collaborative effort
by the IDT is made to determine a viable discharge plan. The patient and family are
educated about options for rehabilitation needs, and the decision is ultimately
theirs. The MS will arrange transportation and discharge referrals. The IDT will
support the family during the decision making process and through the transition to
the appropriate level of care.
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References
1. Junque, C., Bruna, O, Mataro’, M. (1997). Information needs of traumatic brain injury
patients' family members regarding the consequences of the injury and associated
perception of physical, cognitive, emotional and quality of life changes. Brain Injury,
11(4), 251-258.
2. Kim, Y. (2011). A systematic review of factors contributing to outcomes in patients
with traumatic brain injury. Journal of Clinical Nursing, 20(11-12),1518-1532.
3. Moore, M., Winkelman, A., Kwong, S., Segal, S., Manley, G.T. & Shumway, M. The
Emergency Department Social Work Intervention for Mild Traumatic Brain Injury
(SWIFT-Acute): A Pilot Study. Brain Injury. May 2014, Vol. 28, No. 5-6 : Pages 517878.
4. Pegg, P., Auerbach, S., et. Al. (2005). The Impact of Patient-Centered Information on
Patients' Treatment Satisfaction and Outcomes in Traumatic Brain Injury
Rehabilitation. Rehabilitation Psychology, 50(4), 366-374.
5. Ponsford, J., Draper, K., Schonberger, M. (2008). Functional outcome 10 years after
traumatic brain injury: It’s relationship with demographic, injury severity, and
cognitive and emotional status. Journal of the International Neuropsychological
Society, 14(2), 233-242.
87
Management of Substance Abuse in the Patient with TBI
Background
Many people who incur a traumatic brain injury have a substance abuse problem prior to
their injury. In fact, studies reveal substance use in 30-80% of patients at the time of
injury.3,5 The presence of substance use/abuse has been associated with poorer outcomes,
a more complicated course of treatment, increased utilization of the healthcare system,
decreased quality of life, decreased functionality and decreased treatment compliance.
After their injury, patients often experience persistent symptoms of chronic pain, cognitive
deficits, sleep disturbances, and psychological symptoms such as irritability, frustration,
anxiety and depression. In fact, literature reports depression rates of TBI patients to be as
high as 50%.2,5 These symptoms combined with a long recovery process place the TBI
patient at risk for new or ongoing substance use/abuse. 1,4,6,7
Goals
 Detect and manage substance withdrawal.
 Educate patient and family about substance use disorders and their interaction with
TBI.
 Support patient through the use of motivational interviewing and by facilitating
attendance at appropriate patient support groups.
 Promote integrated treatment of substance use disorders at all levels of care.
Guidelines
 Detection and management of substance withdrawal
• A team effort to gather substance use history from collateral sources and
laboratory information is necessary to screen for the risk of substance
withdrawal, as the patient may not be able to provide a complete history.
• Substance withdrawal will be included in the differential diagnosis of TBI
patients with at risk substance use who develop agitation and/or delirium.
 Patient and family education
• Culturally appropriate patient and family education materials on substance
use disorders will be available.
• Team members will have an adequate knowledge of the interaction of
substance use disorders and TBI, so that the patient will have multiple brief
educational interventions.
 Patient Support
• Team members will be knowledgeable about patient support and twelve step
programs available to hospitalized patients.
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References
1. Bjork, J., Grant, S. (2009). Does traumatic brain injury increase risk for substance
abuse? Journal of Neurotrauma, 26: 1077-1082.
2. Bombardier, C., Fann, J., et al. (2010). Rates of major depressive disorder and clinical
outcomes following traumatic brain injury. JAMA,303(19): 1938-1945.
3. Chen, C., Yi, H., et. al. (2012). Alcohol use at the time of injury and survival following
traumatic brain injury: Results from the National Trauma Data Bank. Journal of
Studies on Alcohol and Drugs, 73(4): 531-541.
4. Corrigan, J. D. (1995). Substance abuse as a mediating factor in outcome from
traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 76 (4), 302309.
5. Kolakowsky-Hayner, S., Gourley, E., et.al. (1999). Pre-injury substance abuse among
persons with brain injury and persons with spinal cord injury. Brain Injury, 13(8),
571-81.
6. Kreutzer, J., Seel, R., Gourley, E. (2001). The prevalence and symptom rates of
depression after traumatic brain injury: a comprehensive examination. Brain Injury,
(15(7): 563-567.
7. Miller, S., Baktash, S., et al. (2013). Risk for addiction-related disorders following
mild traumatic brain injury in a large cohort of active-duty U.S. Airmen. American
Journal of Psychiatry, 170: 383-390.
8. Ponsford, J. , Whelan-Goodinson, R., Bahar-Fuchs, A. (2007). Alcohol and drug use
following traumatic brain injury: A Prospective study. Brain Injury, 21(13-14), 13851392.
89
Prevention of Traumatic Brain Injury
Background
The CDC estimates that annually, over 1.7 million Americans sustain a TBI2. Of those
individuals, approximately 275,000 will be hospitalized and 52,000 will die as a result of
their injury2. Health promotion and injury prevention efforts have been shown to
successfully reduce the incidence of TBI and repetitive injury. San Francisco General
Hospital and Trauma Center (SFGH) is committed to saving lives, protecting people and
lowering the health and societal costs of deficits related to traumatic brain injury.
Goal
 Outline SFGH’s approach for raising TBI awareness and identify methods of TBI
prevention, through community outreach programs and patient and family
education.
Guidelines
 Identify high-risk populations1.
• Males are more likely to sustain a TBI.
• Adults 65 years and older have the highest rate of TBI deaths.
• Children under the age of one and adults 65 years and older are most likely
to sustain a TBI severe enough to require hospitalization; 15 to 19 year olds
have the third highest rate.
• Children under the age of one, followed by 1 to 4 year olds, are the most
likely to be treated in an emergency department for a TBI; 15 to 19 year olds
have the third highest rate.
 Identify leading causes of TBI1
• Nationally, falls continue to be the leading cause of TBI (35.2%)
- Falls account for 50% of the TBIs among children age 0-14 years and 61%
of all TBIs among adults >65
• Among all age groups, motor vehicle crashes are the seconding leading case
of TBI (17.3%), and account for the largest percentage of TBI-related deaths
(31.8%).
• Struck by/against events were the second leading cause of TBI among
children between the ages 0-14 years.
• Assaults produce 10% of TBIs in the general population and account for
2.9% in children aged 0-14 years and 1% in adults aged >65 years.
 The SFGH Neurotrauma Program works in conjunction with the National ThinkFirst
Program to raise TBI awareness, and to institute health promotion and prevention
efforts.
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 SFGH Neurotrauma Program efforts include but are not limited to the following
categories of prevention:
• Fall Prevention
• Violence Prevention
• Motor Vehicle Safety
• Pedestrian Safety
• Bicycle Safety
• Playground Safety
• Sporting Activities
 Early assessment and intervention for drug and alcohol use assists in the prevention
of high-risk activities and the potential for repetitive injury.
References
1. NCIPC: Web-based Injury Statistics Query and Reporting System (WISQARS)
http://www.cdc.gov/injury/wisqars
2. Faul 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;
2010.
3. American Association of Neurological Nurses. Care of the patient with mild
traumatic brain injury. 1-35; 2012.
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Appendix B: Rancho Los Amigos Scale of Cognitive Functioning
Rancho Level I–II Characteristics
I.
II.
Rancho Level I: No Response
Patients at this level demonstrate the following in response to auditory or tactile
stimulation:
1. No observable changes in behavior.
2. No movement, voluntary or involuntary, with the possible exception of spinal
cord reflexes.
3. No muscle tone changes.
4. No eye opening or pupillary reactions.
Rancho Level II: Generalized Response
Patients at this level respond to internal and external stimulation, such as loud
noises, pain, and quick position changes, in the following manner:
1. Decerebrate rigidity or extensor posturing
a) Hips and shoulders extended, adducted and internally rotated
b) Knees and elbows extended
c) Wrists and fingers flexed
d) Feet plantar-flexed and inverted
e) Trunk extended
f) Head retracted.
2. Intact pupillary reactivity.
3. Spinal and lower brainstem level reflexes, such as:
a) Asymmetrical tonic neck reflex (ATNR)
b) Tonic labyrinthine reflex (TLR)
c) Positive supporting reaction
d) Oculovestibular reflexes
e) Grasping and sucking reflexes
Rancho Level I-II Interventions
1. Always explain what is about to be done using a calm voice.
2. Provide controlled levels of stimulation to facilitate increased frequency of
motor response, without disrupting the patient’s homeostasis.
3. Supply each stimulus with an intended motor response, either verbally
requested or implied by the therapist’s handling of the patient.
4. As the patient responds more consistently, channel these responses into
more appropriate interaction with the environment.
5. Establish a coordinated rehabilitation treatment plan between Physical
Therapy, Occupational Therapy, and Speech Therapy.
6. Establish a positioning program, utilizing splinting/casting, as needed.
7. Begin treatment of oral motor dysfunction (see Dysphagia section).
8. Temporarily reduce extensor tone and increase flexor response.
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9. Maintain ROM by optimal positioning, stimulation, PROM, and facilitating
increasing amounts of voluntary movement.
10. Stimulation Therapy
a) The goal of stimulation therapy is to increase the patient’s response to
the environment.
b) When indicated, this therapy is typically performed by the family, in
coordination with a Speech Pathologist and other members of the IDT.9
11. Neuromuscular treatment
a) Neurodevelopmental Treatment (NDT) is a therapy in which positions,
weight shifting, movements are utilized to increase or decrease muscle
tone or elicit righting motions. Principles are incorporated into bed
mobility, transfers, positioning etc.
b) Proprioceptive Neuromuscular Facilitation (PNF) is a method of
promoting or hastening the response of the neuromuscular mechanism
through stimulation of proprioceptors.
c) Axial rotation of the trunk may be needed to inhibit tone with the
comatose patient who is posturing.
d) Hip and knee flexion must be maintained, avoiding the supine position
and resistance to the back of the head, to assist in lessening extensor
tone.
e) Immediately after achieving successful inhibition of tone, more normal
movement in a functional pattern should be attempted.
Rancho Levels III-IV Characteristics
III.
Rancho Level III: Localized Response
1. Patients at this level demonstrate decorticate rigidity or flexor posturing as a
response to stimulation, resulting in:
a) Shoulders: adducted, internally rotated, flexed.
b) Elbows: flexed, forearms pronated.
c) Hands: wrists and fingers flexed.
d) Hips: extended, adducted, and internally rotated.
e) Knee / Ankles: along with the hips may demonstrate a triple flexion
response
IV.
Rancho Level IV: Confused, Agitated
1. Patients at this level demonstrate a withdrawal response, in which the
shoulders abduct in more rapid movement than in prior levels.
2. Patients can easily become overstimulated and fluctuate to a lower Rancho
Level.
Rancho Levels III-IV Interventions
1. When localization is present, such as the patient pulling on tubes or lines, or
quickly focusing on people or objects, attempt to:
a) Obtain greater consistency in localizing responses and avoiding
stereotypic movements.
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b) Decrease interval between stimulation and response.
c) Increase the patient’s ability to follow simple commands, attend to an
activity, and use common objects, beginning with automatic responses.
d) Engage patient in assisting with range of motion activities, either by
performing formal exercises or incorporating activities into functional
tasks.
e) Allow as much movement as is safe/clinically indicated.
2. Continue to:
a) Identify more precisely any motor or sensory impairments by
observing bed positioning, response to stimuli, facial response.
b) Increase the consistency, variety, and quality of stimuli as tolerated.
c) Perform treatment in a quiet, controlled environment with limited
distractions and simple commands.
d) Manage muscle tone and encourage more functional patterns of
movement throughout the body.
e) Monitor for signs and symptoms of agitation with removal of stimuli
as needed.
f) Improve motor function.
g) Increase cognition and perception.
h) Utilize splinting/orthotics as necessary.
i) Incorporate family and friends into the treatment plan as patients
may respond more consistently to familiar people.
3. Work toward:
a) Channeling the patient’s responsiveness and alertness.
b) Increasing the patient’s ability to move independently
c) Increasing participation in basic activities of daily living.
4. Activities of daily living
a) Encourage patient in simplified ADL activities.
b) Utilize forward or backward chaining to break up task and facilitate
successful performance.
c) Adapt environment to decrease stimulation and provide salient visual
cues.
d) Structure ADLs into a routine that can be consistently carried out by
caregivers.
5. Neuromuscular treatment
a) Utilizing NDT, PNF, or other techniques in the facilitation of specific
muscles, introduce mat activities to elicit head and neck control,
rolling, and sitting. Neuromuscular techniques can also be utilized in
facilitating transitional movement, such as moving from prone to
prone-on-elbows, or from prone to sidelying, etc. Bilateral Movement
Training can be used within the context of mobility or basic ADLs to
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facilitate voluntary movements or refine motor control of the involved
limbs.
b) Begin to incorporate Motor Learning strategies in order to provide
patients with various types of practice under a variety of conditions to
encourage the relearning of previously held skills, and the transfer of
these skills to new environments.
6. Cognitive Support
a) Focus the patient’s attention on the external environment, by
engaging him/her in self care activities and other automatic tasks
b) If restraints are utilized, strive to remove restraints during periods of
supervision, such as therapy sessions, RN care, and close coach and
educated/trained family interactions.
c) Provide structure and predictability in the daily routine to reduce
confusion.
d) Soothe the patient by sustained touch, slow vestibular stimulation,
familiar voices and sounds, talking with the patient, physical activity
such as walking or being wheeled, and other repetitive techniques.
e) Monitor impact of intervention on increasing or decreasing targeted
behavior and titrate accordingly.
f) Give the patient frequent periods of rest or pauses during the activity.
g) Reduce environmental stimulation to reduce agitation, i.e. TV turned
off, no music, curtains drawn, 2 visitors at a time.
h) Educate family members regarding patient’s abilities and difficulties
and ways to optimize current level of functioning.
Rancho Level V-VI Characteristics
V.
Rancho Level V: Confused, Inappropriate
Patients at this level demonstrate localization as a response to stimulation. The
responses are quicker and more appropriate, such as pushing away a painful
stimulus, visual tracking, and blinking in response to a bright light. Patients may
require step-by-step instructions to carry out even familiar motor activities.
VI.
Rancho Level VI: Confused, Appropriate
Patients at this level demonstrate responses to stimulation that are more
appropriate, such as withdrawing from stimuli that is noxious or irritating, but
not to stimuli that produces no discomfort. Patients are able to carry out simple
requests and initiate purposeful activity.
Rancho Level V-VI Interventions
1. As the patient’s agitation decreases, he will respond more to the external environment,
initially confused and responding in inappropriate ways. Other deficits will become
more evident, including: poor short-term memory, difficulty learning new tasks,
persistent confusion, decreased attention, visual-spatial dysfunction, apraxia, and/or
inconsistent orientation. Given this, the Speech Pathologist and Occupational Therapist
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are primarily responsible for providing cognitive therapy and guiding the IDT’s plan of
care.
2. Goals for the patient are:
a)
b)
c)
d)
e)
Pay attention to tasks and specific stimuli.
Process sequential organization.
Improve immediate and short-term memory.
Analyze, associate and categorize tasks.
Work to improve neuromuscular skills, perceptual skills, and activities of daily
living (household and community level)
f) Structure the patient’s environment
g) Reduce complexity and duration of tasks to the patient’s ability.
h) Keep distractions at a minimum.
i) Keep the patient’s schedule and immediate environment as consistent as
possible.
j) Allow for frequent rest breaks.
k) Encourage the involvement of familiar people, items, and activities.
l) Improve selected movement through facilitation.
m) Increase fine motor control through manipulative activities and exercises for
specific muscles.
n) Improve cognitive ability to process and store information.
o) Incorporate compensatory strategies to increase carryover of skills.
p) Develop a home program that patient/caregivers can be carrying out outside of
formal therapy sessions.
3. Activities of daily living
a) Continue activities of daily living training as noted in Rancho Levels III–IV.
b) Incorporate assistive devices/equipment as indicated.
c) Incorporate compensatory strategies (ie. checklists, mental imagery, anchoring, selftalk etc) as appropriate.
d) In the performance of these activities, as the patient becomes more successful:
1) Decrease verbal and physical cuing.
2) Increase complexity and speed of the tasks.
3) Continue to provide assistance, and repeat or rephrase instructions, as needed.
4) Encourage task performance under a variety of conditions to increase
generalization.
4. Neuromuscular treatment
a) Continue muscle facilitation and strengthening exercises to improve stability,
mobility, and function.
b) Perform activities that combine trunk movements and rotation with upper
extremity reaching and functional pattern.
c) Coordinate weight shifting and weight bearing with upper- and lower-extremity
movements.
d) Incorporate body weight assisted treadmill training as appropriate.
e) Refine activities to emphasize higher level coordination tasks as needed.
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f) Emphasize both bilateral training and forced use of involved extremity.
g) Begin balance training on uneven surfaces in preparation for community level
activities.
5. Perception
Continue visual-perceptual assessment, incorporating activities such as:
a) Matching, sorting, and discriminating color, size, and shape.
b) Working 3–4 piece puzzles, tracing, and design copying.
c) Sequencing tasks, coding tasks, visually scanning tasks.
d) Completing forms/basic money management tasks
6. Cognitive Support
a) Therapy may be hampered by the patient’s irritability, lack of cooperation, lack of
insight, mood fluctuations, impulsivity, ease of frustration, dependence on family,
confusion, and disorientation.
b) Goals of therapy at this level are to:
1) Increase attention to more specific tasks
2) Increase process of sequential organization
3) Increase immediate and short-term memory
4) Increase analysis, association and categorization skills
5) Increase insight to deficits
6) Increase initiation and continuation of basic tasks
c) Staff should continue to:
1) Structure the patient’s environment
2) Reduce complexity and duration of tasks to the patient’s ability
3) Keep distractions to a minimum
4) Orient the patient regularly and when appropriate
5) Speak with the patient in a simplified but age appropriate manner
6) Introduce cognitive and behavioral compensatory strategies
7) Educate family members regarding patient’s abilities and challenges, and ways
to optimize current level of functioning
8) Change immediate environment and schedule as little as possible
Rancho Level VII - Characteristics
VII.
Rancho Level VII: Automatic, Appropriate. Patients at this level demonstrate fairly
consistent responses to the external environment. Responses are robot-like;
judgment and problem solving abilities are limited. Patients at this level can
complete routine tasks, but may have difficulty in distracting or stressful situations
and continue to require minimal assistance for routine daily living skills. They are
unable to think about the consequences of a decision or action, and may
overestimate their abilities. There is a superficial awareness of some disabilities, but
little to no awareness of the limits they place on the ability to safely and accurately
carry out household, community, work and leisure activities of daily living.
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Rancho Level VII - Interventions
1. When the patient demonstrates fairly consistent responses to the external
environment, attempt to:
a) Increase the patient’s purposeful, goal-directed behavior
b) Increase the initiation of activities of daily living
c) Increase performance of more complex tasks, responsibility for tasks and
consequences
2. Continue to improve neuromuscular skills, perceptual and cognitive skills, and
activities of daily living (emphasis on IADLs and community level activities).
3. Work toward:
a) Gradually decreasing external structuring of the patient’s environment.
b) Improving the patient’s ability to respond appropriately in social situations.
c) Assessing and addressing educational, avocational and vocational issues.
d) Increasing the patient’s awareness of deficits and functional implications.
4. Activities of daily living
a) Continue ADL training as noted in Rancho Levels III–VI.
b) Incorporate independent planning, sequencing, and initiation of ADLs into
routine.
c) Address underlying skills for IADLs and assess level of supervision that may be
required.
5. Neuromuscular treatment
a) Continue to address problems such as decreased strength, decreased sensation,
apraxia, ataxia, spasticity, and difficulty with fine motor control, and equilibrium
reactions. Incorporate mental imagery/practice when appropriate.
6. Community Reintegration
a) Community reintegration tasks should be introduced as the patient becomes
more consistent with performing activities of daily living and mobility tasks at a
household level.
b) Important skills to include in preparing for community reintegration:
1) Managing money, including check writing/ATM usage, shopping, and paying
bills.
2) Mobilizing within the community, including using private and/or public
transportation, handling architectural barriers, driver training as
appropriate.
3) Time management, including keeping a memory book, keeping track of
appointments
4) Discharge planning should begin early in the patient’s hospital course.
Rancho Level VIII- Characteristics
VIII. Rancho Level VIII: Purposeful, Appropriate
A. Patients at this level demonstrate adequate responses to the external
environment. Subtle impairments in cognition persist, especially in novel
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situations. They can now independently shift back and forth and complete
tasks accurately for at least two hours. He is aware of disabilities/deficits
when they interfere with task completion, and takes appropriate corrective
action, but may need assistance to anticipate a problem before it occurs. He
may continue to be depressed and irritable, but is able to self-monitor the
appropriateness of social interaction with stand-by assistance.
B. At this stage the patient can handle multiple tasks simultaneously in a
majority of environments, but may require periodic rest breaks. He is able to
independently develop and maintain assistive memory devices. The patient
is able to think independently and carry out steps to complete familiar and
unfamiliar personal, community, household, work and leisure tasks, but may
require more than the normal amount of time or compensatory strategies to
complete them. Social interaction behavior is consistently appropriate
Rancho Level VIII- Interventions
1. When the patient demonstrates increased insight into deficits and ability to
compensate for these deficits, increase the complexity of the task, environmental
stimulus and environmental level.
2. Continue to:
a) Decrease external structuring of the patient’s environment.
b) Improve the patient’s neuromuscular and cognitive skills.
c) Improve the patient’s ability to respond appropriately in social situations.
d) Assess and address educational, avocational and vocational issues.
3. Work toward:
a) Increasing the patient’s independent use of compensatory strategies.
b) Educating patient re: activities to avoid (e.g. Substance use, risk-taking
behaviors)
c) Increasing the patient’s purposeful goal-directed behavior and performance of
more complex tasks
d) Increasing initiation of independent living and daily skills
e) Increasing responsibility for tasks and consequences
f) Increasing awareness of physical and cognitive limitations
4. Neuromuscular treatment
a) Continue to address problems such as decreased strength, sensation, apraxia,
ataxia, spasticity, difficulty with fine motor control and equilibrium reactions as
discussed in previous sections.
5. Cognitive Rehabilitation
b) The goal at this stage is to increase the patient’s insight into their deficits and
effective compensatory strategies. The general focus is on enhancing the
patient’s ability to concentrate on specific tasks, organize, prioritize, and use
information, and to remember increasing amounts of information.
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c) Treatment plans are individualized according to the patient’s prior level of
functioning with the goal of helping the patient achieve their highest level of
ability. Skill acquisition is obtained through selection and teaching of cognitive
compensatory strategies, systematic practice, and generalization to their home
and community environments. Tasks include:
1) Complex reading, writing, and mathematical tasks
2) Tasks involving increasing analysis of information, such as summarizing
paragraphs, interpreting stories etc.
3) Deductive reasoning tasks
4) Community management such as: bill paying, grocery shopping,
transportation, household tasks
6. Community Reintegration
a) Continue to address skills noted in Rancho Level VII. Additional important skills
to include in preparing for community reintegration include recreational
activities, employment, parenting, driving, and navigation
7. Discharge Planning
a) At this level, patients may have deficits that are not immediately apparent to
people who did not know them pre-morbidly. Educate patient and caregivers on
how to address this issue, as well as additional issues to anticipate in the
home/community environment, with referrals to the TBI support group, followup to social work and psychological care as appropriate.
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