Kaplan- Neuro – Flashcards
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what is the most common cause of TBI
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falls then MVC
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what is the primary injury with a TBI
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initial damage to the brain- contusion/laceration
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what is the secondary injury with a TBI
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evolves hours or days after, results from inadequate delivery of nutrients and oxygen
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what is the monroe-kellie hypothesis
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cranial vault is non expandable therefore is one of the volumes increases it will displace another volume
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what makes up the cranial vault
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brain(80%), blood(10%), and cerebral spinal fluid(10%)
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what happens when there is an increase in ICP
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Blood is decreased. Brain may be shifter down
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what is the problem with scalp laceration
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the scalp is very vascular which can cause profuse bleeding
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what is a complication of a scalp laceration
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infection
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what are types of skull fractures
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linear, depressed, simple, open or closed
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what are clinical manifestations of scalp injuries and skull fractures
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hemorrhage from nose/ears, ecchymosis over mastoid (battle sign), CSF otorrhea/rhinorrhea(basilar skull fracture)
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what is the glasgow coma scale
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Standardized tool for assessing LOC in brain injury patients; use for anyone you suspect to have a brain injury; Highest score- 15; Lowest-3
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what is the medical management for scalp injuries and skull fractures
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usually don't require surgical treatment, close observation, check for associated brain injury, cervical collar
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what does the brain not store
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oxygen or glucose
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when can cell death/brain damage happen
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when the blood supply is interrupted, even for a short time
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what is a contusion
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the brain is bruised
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what is a common s/s of a contusion
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confusion/stuor
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what determines patient outcome with a contusion
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area of the injury and the severity
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when does hemorrhage and edema usually peak with contusions
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18-36 hours
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what is a concussion
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temporary loss of neurologic function what changes the LOC
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what is used to care for concussion patients
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overnight observation
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what is a diffuse axonal injury
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swelling & degeneration of axons in white matter
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when does an axonal injury occur
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after a TBI takes 12-24 hours to develop
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what are s/s of a diffuse axonal injury
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decreased LOC, increased ICP, global cerebral edema
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what is an epidural hematoma
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bleeding between the skull and the dura
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what is the sequence of symptoms seen with an epidural hematoma
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decrease in LOC, lucid interval, with increasing restlessness/agitation, followed by coma
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how does the brain try compensate with an epidural hematoma
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rapid absorption of CSF to maintain normal ICP
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what is the treatment of an epidural hematoma
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burr holes, clot removal, bleeding control, may require craniotomy, drain placement to prevent re-accumulation
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whats a subdural hematoma
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occurs from bleeding between the dura mater and the brain
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what is the usual origin of a subdural hematoma
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venous
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what are causes of a subdural hematoma
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trauma, coagulopathy, or ruptured aneurysm
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is a subdural hematoma acute or chronic
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both
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what is the usual cause of an acute subdural hematoma
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major head injury
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when do symptoms develop with an acute subdural hematoma
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24-48 hours
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what are s/s of acute subdural hematoma
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change in LOC, pupillary changes, hemiparesis, increas in BP and respirations, decrease in heart rate
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who is most effected by chronic subdural hematoma
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elderly
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when do symptoms present with chronic subdural hematoma
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weeks to months from a minor injury
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what are the s/s of a chronic subdural hematoma
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headache, personality changes, focal seizures
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what is a chronic subdural hematoma sometimes mistaken for
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psychiatric condition
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what is the treatment for a chronic subdural hematoma
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burr holes, craniotomy
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where is the bleeding in an intracerebral hematoma
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in the parenchyma
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what are causes of a intracerebral hematoma
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systemic HTN, ruptured aneurysm, intracranial tumor, bleeding disorders, complication of anticoag therapy
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what is the treatment for a intracerebral hemorrhage
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supportive care, management of ICP, manage fluid and electrolytes, manage HTN, craniotomy
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what are s/s of a penetrating head trauma
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altered LOC, confusion, pupillary abnormalities, altered gag reflex, sudden neuro deficits, headache, seizures
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what are the changes in vitals for a penetrating head trauma
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altered respiratory, widened pulse pressure, bradycardia, tachycardia, hypo/hyperthermia
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what is decerebrate position
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arms extended with wrists rotated; feet are turned in
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what is decorticate position
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Arms flexed and held close to body, toes pointed.
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what is glasgow coma scale
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scoring system used to quantify the level of consciousness following traumatic brain injury
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what are the categories of glasgow coma scale
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eye opening response, verbal response, motor response
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what is the lowest glasgow coma scale
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3
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what is the highest glasgow coma scale
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15
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what is the CT scan used for with head trauma
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presence, nature, extent, and location of injury- helpful for ongoing management
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what is the MRI used for with head trauma
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more accurate picture of the injury- pt has to be stable
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when is a PET used in head injury
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determines brain function
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what is the management for brain injuries
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physical examination, neuro exam, CT, MRI, monitor cervical spine- cervical collar, prevent secondary injury, monitor vitals
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what is the management of brain injuries
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preserve brain homeostasis, prevent secondary injury,
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what are causes of secondary injuries in the brain
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cerebral edema, hypotension, respiratory depression, hypoxemia, electrolyte disturbance
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what factors influence ICP
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arterial pressure, venous pressure, intraabdominal pressure, posture, temperature, blood gases(CO2/O2)
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what are causes of increased ICP
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brain tumors, sub arachnoid hemorrhage, toxic encephalopathy
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what is a normal ICP
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0-15
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what does increase ICP do to cerebral blood flow
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decreases blood flow causing ischemia and cell death
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what is compensation with ICP evidenced by
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slow bounding pulse, irregular respiration rate
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what effects cerebral blood flow
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carbon dioxide
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what does increased PaCO2 cause
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vasodilation- increased cerebral blood flow, and ICP
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what does decreased PaCO2 cause
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vasoconstriction- decreased cerebral blood flow
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what is cerebral edema
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abnormal accumulation of water or fluid in the intracellular space, extracellular space or both
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how does cerebral edema cause increased ICP
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as brain tissue swells the brain attempts to compensate
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what is cerebral perfusion pressure
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it is the pressure it takes for the heart to provide the brain with blood
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what is the cushings triad
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bradycardia, hypertension, bradypnea
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what are complications of increased ICP
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shifting of the brain tissue to an area of lower pressure, interferes with blood supply,
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what can happen when there is no blood flow
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cerebral ischemia, infarction, brain death
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what do the nurse need to monitor with increased ICP
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I/O, fluid and electrolytes, weight, lab results, ABG results, vitals, function level prior to injury, oral care, ROM
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what is involved in a neuro assessment
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pupil movement, eye movement, GCS, vitals, motor assessment
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what is the medical management for increased ICP
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decrease cerebral edema (limit fluids), maintain temp, reduce CSF(ventriculostomy), reduce intracranial blood volume, maintain oxygenation, reduce metabolic demands
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what is the pharmacologic management of increased ICP
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osmotic diuretics(mannitol), lasix, antiseizure meds, corticosteroids, proton pump inhibitor, levophed, tylenol
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what are nursing actions that increase ICP
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suctioning, PEEP, coughing, positioning, environmental stimuli, cluster nursing care
