medsurg 2.2 Flashcards by SOPHIA ANNE MANUBAY

Major cause of disability and death

TRAUMATIC BRAIN INJURY

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Major causes: MVA and falls in elderly
○ Violence cause closed head injury 7-10% of cases
○ Penetrating Injury - firearms
○ Blast Injury
● Occur in all ages but peak in young adults
○ Leading cause of death in 25 y/old
○ M>F
● MVA common in young adolescence

TBI

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Violent shaking or jarring of the brain and resultant transient functional Impairment
● Mild TBI defined by transient appearance af neurologic signs and symptoms following either a direct or indirect rapid movement in the brain causing extreme rotational or translational brain acceleration or deceleration injury (sudden change in the momentum of the head)

concussion

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Core features: immediately after trauma and largely reversible
○ Occurs immediately, does not wait for days
● Loss of consciousness at impact is not required for diagnosis
● No evidence of structural brain injury using conventional neuroimaging
○ Physiologic injury to brain

concussion

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Brief Period of Disorientation, staggering, or amnesia
● Appears Normal
● First manifestations
→ (next bullet)
● Immediate loss of consciousness suppression of supporting reflexes, transient respiratory arrest, brief tachycardia, and fall in BP following a momentary rise

Clinical Manifestation CONCUSSION

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● “Concussive convulsions” - may occur immediately after LOC and confer an increased risk of later seizures
○ Tinamaan head → if there is injury in
cerebral cortex (neurons are found in our gray matter) → sometimes, they become hyperexcitable → seizures
● Retrograde amnesia
● Anterograde amnesia

Clinical Manifestation Concussion

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● Athletes who have had a concussion are more likely than others to have another concussion in the same playing season
● There is a decline in reaction time and in other neuropsychological tests after concussion,

which returns to baseline over several days or weeks

Concussion in Athletes

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The number of recollected concussions is proportional to the degree of impairment on neuropsychological tests
● Increased risk of dementia and other neurodegenerative disorders
● Medical evaluation with imaging and neuropsychological tests
● Physical and cognitive rest followed by graduated physical and mental activity.

Concussion in Athletes

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Based on clinical suspicion - neurological symptoms without significant focal neurologic findings
● No rigorously studied or FDA approved medial or physical therapies that Led are clearly proven to hasten recovery.

Diagnosis and TX Concussion

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● 80-90% of persons with single uncomplicated concussions fully recover within 2 -weeks
● Recurrent concussions - more prolonged recovery with decreasing threshold to injury
● Likely to express migraine headaches, mood disorders, BPPV
● Post-concussive pts are susceptible to Recurrent concussions increased risk of developing major neuropsychiatric disorder associated with aging, including depression dementia, PD, ALS and erratic psychosocial behavior

Outcome Concussion

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most common at the temporoparietal region,

Linear 80%

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one or more bony fragments are displaced inward, compressing the underlying brain, 85% are open and prone to infection and CSF leakage;

Depressed

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multiple, shattered bony fragments

Comminuted

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over fracture is lacerated

open or compound scalp

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Depressed and comminuted fractures require surgical management for debridement, elevation of bone fragments and repair of dural
lacerations

Skull Fx

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May be missed by skull X-ray where cranial nerve sits or enters
● Best identified by ?
● May have cranial nerve injury or dural tear
○ Bc it is open, pt is high risked for Delayed meningitis

Basal skull fx - NCCT Bone Window

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tympanic perforation hearing loss, CSF otorrhea, PFP, Battle sign

petrous portion of the temporal bone

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anosmia, bilateral periorbital ecchymosis(both eyes may dark circles; aka racoon’s eyes), CSF rhinorrhea
(csf comes out of nose)

sphenoid frontal ethmoid bone

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● Traumatic coma lasting >6 hrs caused by multiple small lesions in the white matter tracts
○ Occurs in the whole brain
○ Axons are white matter
● Widespread micro-and macroscopic axonal-shearing injury
● Diffuse degeneration of white matter

diffuse axonal injury

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Mild =
● Moderate/Severe ->

mild = 6-24
Moderate/Severe -> 24 hrs

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● Single most important cause of persistent disability after traumatic brain damage

diffuse axonal injury

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Swollen, beaded and varicose upon release
○ If axon was to rupture, the proximal stub
would become a mass of axoplasm called
retraction balls

cajal 1928

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● Initial axonal stretch causes temporary ondulation and cytoskeletal misalignment associated with mechanical injury of the Na channels, causing massive Na influx

Diffuse axonal injury

● Depolarization of the axonal openings for voltage gated Ca channels causing massive Ca influx
● Activation of various metabolic pathways and cytoskeletal changes, including activation of calpain, a protease that degrades microtubule proteins.

diffuse axonal injury

● Axon shearing injury is most severe at regions that are anatomically predisposed to maximal stress from rotational forces ● Macroscopic tears occur in midline structures (dorsolateral midbrain and pons, posterior corpus callosum parasagittal white matter, periventricular regions and internal capsule)

diffuse axonal injury

● Diffuse microscopic damage occurs as manifested by axonal retraction bulbs throughout the white matter of the cerebrum following microporation of membranes, leakage of ion channels, stearic conformational changes of proteins

diffuse axonal injury

Diffuse or focal ● Mechanisms: ○ Mass lesion (ie hematoma) ○ Cerebral edema ○ Increase cerebral blood volume due to abnormal vasodilation ■ Hyperfusion, increased vascular permeability causing plasma leakage and vasogenic

cerebral swelling

Delayed inflammatory response or dysfunction of cerebral vasomotor regulatory centers in the brainstem ■ During first 24 hours, there is cerebral hypoperfusion followed by hyperemia in 1-3 days after severe followed by arterial vasospasm in day- 4-7 ■ Hyperemia: dadami blood in 1-3 days → later on vasospasm ● The magnitude of swelling does not always correlate with the severity of injury

cerebral swelling

Focal parenchymal hemorrhage that result from "scraping" and "bruising" of the brain as it moves across the inner surface of the skull

cerebral contusions

cerebral contusion most common

inferior frontal and temporal lobes

● Small and multiple and cortical in location ● Bruised and bloodied brain ● May appear in delayed fashion > 1 day after trauma ● Frequently enlarge over 12-24 hrs

cerebral contusions

Tearing of small or medium sized vessels within the brain parenchyma ● Focal blood collection that displace brain structure ● traumatic and non traumatic; pero ito is non traumatic muna daw didiscuss ● NCCT: Traumatic ICH of the left frontal lobe with edema and mass effect

intracerebral hematoma

● Symptomatic within 72 hrs after injury ● More common after falls or assaults ● May lose consciousness as SDH enlarges ● Ipsilateral pupillary dilation with contralateral hemiparesis

Acute SDH

Symptomatic after 21 days (3 weeks) ● More common in >50yo ● 25-50% does not recall injury ○ Di na maalala how the injury happened kasi matagal na siya or chronic ● After 2 weeks, there is encapsulation of theclot and eventually liquefies into a hygroma

Chronic SDH

Rare complication of head injury ● Occurs in <1% of all cases but is found in 5-15% of autopsies

epidural H

Mortality rate: 100% in untreated, 5-30% in treated ● Treatment: Surgical evacuation (craniotomy, drainage and ligation of bleeding vessel)

epidural H

● No or short period of LOC ● Aka "talk and die" syndrome ● Late deterioration because of expansion of subdural or epidural hematoma, worsening edema around a contusion or delayed appearance of epidural clot

SERIOUS CEREBRAL DAMAGE FOLLOWING A LUCID INTERVAL

Blood is distributed over the convexities ○ Vs SAH secondary to aneurysmal rupture - over the basal cisterns

TRAUMATIC SUBARACHNOID HEMORRHAGE

Mortality from GSW to head is >95% ● Amount of tissue damage is dependent on kinetic energy and velocity of the missile, angle of entrance, number of bony fragments affected structures and configuration of secondary bullet tracts due to ricochet

penetrating injury

● Explosive missiles initiate overpressure waves that translate mechanical, thermal and electromagnetic energy to the brain by spallation, implosion and inertia directly through the cranium and indirectly through oscillating pressure in the fluid-containing large vessel

blast injury

Damage to BBB and to gray-white matter junction with deafferentations of the cortical columnar structure Loss of consciousness and altered mental status ○ Our cortex have vertical lamellations that are around 3 Million which are attributed to one function only (sensory or motor), if overpressure passes here, it is disrupted (tatagilid siya then babalik to upright position) 30% have long term neurologic deficits 11% PTSD Secondary blast injury due to debris resulting in penetrating or

Blast Injury

Violent shaking of the body or head of an infant, resulting in rapid acceleration and deceleration of the cranium ○ Galaw siya ng galaw and najajar head sa skull ● Combination of subdural and retinal hemorrhages ● High risk of slowing of cognitive development, acquired microcephaly (brain atrophy)

Shaken Baby Syndrome

Assessment and stabilization of airway, breathing and circulation ● Resuscitation, history taking and examination ○ Done fast; not done step by step, rather can be done simultaneously ● Spine immobilization ● Imaging studies ● Management of coagulopathies ● Management of increased ICP

IMMEDIATE CLINICAL EVALUATION

CT – emergency imaging of choice for head and cervical spine injury ○ Bone ○ Hematoma or hemorrhages ○ Cerebral edema ○ Pneumocephalus (air inside brain cavity) ○ Mass effect and brain tissue displacement ○ Compression obliteration of the mesencephalic cisterns or midline shifts ● MRI – focal lesions related to DAI but not for emergency evaluations; may be done later on if there is suspect of DAI ○ Acute DAI – hyperintense E on DWI and hypointense on ADC

RADIOGRAPHY AND IMAGING

○ Tearing of dura and arachnoid membranes ○ Usually associated with fractures of ethmoid, sphenoid or orbital plate of the frontal bone ○ CT: pneumocephalus ■ Kita na may pumasok na air within skull sa CT ○ Sx: CSF lead from scalp laceration. nase (CSF rhinorrhea – runny nose but CSF), ear (CSF otorrhea) ■ Test for glucose or tau (+) CSF, (-) mucus ■ Mucus will leave the material stiff ○ Tx: head elevation (35%), lumbar drain: if > 2 weeks. surgical repair

CSF Fistula

- collection of air in the cranial cavity ○ Pneumatocele or pneumocephalus ○ Pocket of air in the epidural or subdural space over the convexities, between hemispheres ■ There is air within cranial cavity ○ Small collection of air is absorbed without incident but large volume may produce a mass effect (tension pneumocranium) and may need surgical aspiration

aerocele

○ Result from traumatic laceration of the ICA within the cavernous sinus ■ ICA is napunit ■ Blood goes out and went to cavernous sinus ○ Pulsating exophthalmos, ocular chemosis, orbital bruit

carotid caverous fistula

■ Blood enters the sinus and distends the superior and inferior ophthalmic veins ■ Tight and painful ■ Partial or completely immobile

carotid cav fistula

Distended orbital and periorbital veins and paralysis of the CN III, IV, V, VI as they pass through or within the walls of the cavernous sinus ○ Risk: permanent visual loss caused by venous retinal infarction ○ Dx: Angiography bc ICA is affected ○ Tx: Endovascular balloon placement through the defect in arterial wall into the venous side of the fistula

carotid cavernous fistula

Traumatic arterial dissection and vascular injuries (thrombosis and thromboembolism) ● Secondary subfalcine herniation with ACA infarction or PCA pressed against the tentorium ● Cranial nerve injuries ● Infections - extradural (osteomyelitis), subdural (empyema), subarachnoid (meningitis) or intracerebral (abscess)

carotid cav fistula

○ 40% ○ Cranial pain, dizziness, fatigue, insomnia, irritability, restlessness and inability to concentrate ○ Overlap with depression and anxiety ○ May persist for years ○ Duration of symptoms is not related to severity of injury ■ Even if mild lang injury ng patient, nagkakapost concussive syndrome ○ Tx: psychotherapy, antidepressants or anxiolytics

PCS

treatment of choice for massive acute and chronic subdural, epidural or parenchymal hematoma with mass effect

CT scan

liquified chronic subdural hematomas;

burr hole or twist drill

Gsw

surgical exploration and repair

cerebral edema and intracranial hypertension

Decompressive hemicraniectomy