NURS 2450 - Exam 2 Edited

What is MS?

- a chronic, progressive, degenerative disorder of the CNS

- segmental demyelination of nerve fibers of the brain and spinal cord

- onset 20-50 years of age (middle age and younger)

- women 2-3x more than men

- 5x more prevalent in temperate climates (northern US, Canada, Europe)

- average life expectancy 20-25 years from diagnosis

Describe the physiological process in MS.

3 pathological processes:

- chronic inflammation

- demyelination (caused by antigen/antibody reaction)

- gliosis/scarring in the CNS

Primary neuropathologic condition:

- autoimmune process orchestrated by activated T cells

- can be triggered by environment and infection

- onset: insidious, vague Sx (months to years), and intermittent

insidious

proceeding in a gradual, subtle way, but with harmful effects.

What are the etiologies of MS?

- unknown, but unlikely that there is just one cause

- geographical and genetic factors

- genetic predisposition w/ infectious and immunologic factors

What are some triggering factors of MS and why?

infection, smoking, emotional stress, physical injury, excessive fatigue, pregnancy, poorer state of health

1st/2nd/3rd relatives w/ it

clinical manifestation of MS: motor

→ weakness/paralysis of limbs/trunk/head

→ diplopia (double vision)

→ scanning speech

→ muscle spasticity (interferes w/ speech, gait)

clinical manifestation of MS: sensory

→ numbness

→ tingling

→ blurred vision

→ vertigo (whirling & loss of balance)

→ tinnitus (rining & noise in one or both ears); decreased hearing

→ chronic neuropathic pain

→ Lhermitte's sign (transient sx described as electrical shock radiating down spine to limbs; can occur w/ neck flexion),

→ patchy blindness

→ pain in thoracic/abdominal regions

clinical manifestation of MS: Cerebellar

→ nystagmus

→ ataxia (gait instability)

→ dysarthria

→ dysphagia

clinical manifestation of MS: bowel & bladder

→ constipation (insufficient fluid, decreased activity, slow motility),

→ spastic bladder (most common; small capacity for urine; increase urgency & frequency)

→ flaccid bladder (large capacity for urine, but no sensation/pain/desire to void)

clinical manifestation of MS: sexual dysfunction & fatigue

usually assoc. w/ increased energy needs (heat, humidity)

→ erectile dysfunction r/t spinal cord dysfunction

→ decreased libido

→ decreased vaginal lubrication

→ painful intercourse

clinical manifestation of MS: emotional changes

→ depression, anger

- cognition??

Describe the clinical courses of MS.

- relapsing-remitting

- primary-progressive

- secondary-progressive

- clinically isolated syndrome (CIS)

Relapsing-remitting MS

relapses with either full recovery or some remaining neurological signs/symptoms and residual deficit on recovery;

periods between relapses characterized by lack of disease progression

aka flairs

85-90% initial dx

Primary Progressive MS

accumulation of disability from disease onset

slowly worsening neuro function from beginning, but no distinct relapse or recovery;

10%

Secondary Progressive MS

initially relapsing-remitting

sudden progression w/ or w/o relapse/remission;

50% w/ relapse-remitting develop this after 10 years

Clinically Isolated Syndrome (CIS)

first clinical episode that is suggestive of MS;

pt reported corresponding sx

objective findings that reflect demyelination;

develops acutely or sub-acutely w/ duration of at least 24 hrs

w/ or w/o recovery

would occur in absence of fever or infection,

resembles typical MS relapse;

no evidence of previous demyelination in PMH

What are some potential causes of pseudo-exacerbation/relapse/fair of MS?

Common triggers:

→ stress

→ fatigue

→ illness

→ heat

- does not cause new damage

- very distressing to patients

- must treat underlying cause

How is MS diagnosed?

- no definitive diagnostic test

- diagnosis of exclusion

→ based on hx

→ clinical manifestations

→ imaging studies

MRI: can show presence of either play inflammation | atrophy | tissue damage

CSF analysis: helps rule out other causes

→ evoked potentials

electrical events generated by peripheral stimulation

simple sensory, visual, brain stem auditory

50-90% have abnormal visual responses)

- McDonald's criteria:

1) lesions in 2 different locations

2) damage/attack interval (different time)

3) rule out other conditions

Management Goals for a patient w/ MS

- maximize neuromuscular function

- maintain independence

- fatigue management

- psychosocial wellbeing

- adjust to the illness

- decrease factors that precipitate exacerbations (ex. heat)

Interdisciplinary management of MS: pharmacological therapy

- pharmacological therapy

→ to slow progression

→ provide symptomatic relief

→ tailored to disease pattern

- promoting function through rehabilitation

- providing emotional support

- complementary and alternative medicine (aerobic exercises)

Interdisciplinary management of MS: modifying disease therapy

- Injection, PO, IV

goals:

decrease relapse rate

slower accumulation of brain lesions on MRI

- will not heal scarring

- may not improve current functioning

- may have some effect on progression

- consideration of side effects

Interdisciplinary management of MS: Adjunctive Pharmacological Therapy

o Acute exacerbations: glucocorticoids (methylprednisolone, prednisone; at site of inflammation), plasma exchange

decreases edema

o Anticholinergics: bladder sx

o CNS stimulants: fatigue

o Muscle relaxants: spasticity (also Botox)

o Nerve conduction enhancer: improve walking speed (selective K+ channel blocker); caution w/ seizure disorder and CKD

o Tricyclic antidepressants, AEDs: chronic pain syndromes

o Antispasmodic (baclofen): also for muscle

o Anti-seizure

Nursing Assessment

subjective:

PMH

→ viral infections

→ geographic location for cold temp

→ pregnancy

→ vaccine

medications - corticosteroids?

functional health patterns:

→ malaise

→ weight loss

→ difficulty chewing

→ numbness

→ muscle tingling)

objective:

integumentary (pressure ulcers, etc)

neurological

musculoskeletal

diagnostic findings

Nursing diagnosis MS

→ impaired physical mobility

→ impaired urinary elimination

→ interrupted family processes

→ risk for falls

→ risk for infection

Nursing Management (MS)

- trigger identification

- support

- patient education

- good balance of exercise and rest

- nutrition

- tx regimen

- self-cath

- adequate fiber intake

- emotional adjustments

- lifestyle changes

What is ALS?

amyotrophic lateral sclerosis (Lou Gehrig's disease)

- rare and progressive disorder

- characterized by loss of motor neurons (degenerate, then unable to send impulses to muscle fibers)

- sporadic/random (90-95% of cases) or familial (dominant inheritance; 50% pass it on)

- onset at 40-70 years

- men 2x more than women

ALS name breakdown

A-myo-trophic → no muscle nourishment

lateral → are of spinal cord

sclerosis → hardening

Describe the pathophysiological process of ALS.

- unknown patho

- gradual degeneration of motor neurons

→ gradually die and cannot produce and transmit signals to muscles

- sensation and cognition are not affected

What are some potential causes of ALS?

- thought to be gene mutations, elevated glutamate levels, autoimmune

Clinical manifestation of ALS

typical:

→ muscle weakness

→ dysarthria

→ dysphagia

→ upper vs lower motor neuron

others s/sx:

→ pain

→ sleep disorders

→ spasticity

→ drooling

→ emotional lability

→ depression

→ esophageal reflux

→ constipation

- sequelae: muscle wasting, fasciculations

ALS clinical manifestations: upper motor neuron

→ Loss of dexterity or ability to coordinate movements

→ Weakness

→ Spasticity

→ Hyperreflexia

*affect movement rather than muscle itself

ALS clinical manifestations: lower motor neuron

*no signals arriving at muscle

Sx:

→ weakness

→ paralysis

→ hyporeflexia

→ fasciculations (twitching)

→ flaccidity

→ muscle cramps

- involuntary muscles affected: heart, GI tract, bladder; respiration (indirect r/t immobility)

claw hands

physical manifestation of ms

How is ALS diagnosed?

- difficult to dx;

- thorough neuro exam is key

- dx of exclusion:

→ electrodiagnostic test

→ blood and urine studies,

→ x-rays

→ spinal tap

→ MRI

→ myelogram of cervical spine

→ muscle/nerve biopsy

- El Escorial criteria

ALS Interdisciplinary Management

- PT, OT

- speech and swallow evaluatio

- neuro

- pharmacological

- nursing

ALS Pharmacological Management

- prognosis: no cure, death occurs secondary to respiratory tract infection 2-6 years post-dx (hospice vs ventilator)

- Riluzole (Rilutek):

→ inhibits glutamate (glutamate blocker)

→ slows progression of disease

- Edaravone (Radicava): neuroprotective agent; antioxidant

→ prevents oxidative stress damage

→ slows functional deterioration

ALS nursing interventions: facilitating communication

→ have pt slow down and over-articulate,

→ limit distractions

→ sit face-to-face in well-lit room, yes/no systems

→ letter board

→ eye blinking

→ speech generating devices

→ smartphone

ALS nursing interventions: aspiration precautions

→ appropriate food consistency (honey),

→ coughing and deep breath exercises

→ secretion management (coughalator, chest physiotherapy),

→ Incentive Spirometer, suctioning

- early identification of respiratory insufficiency

- pain management

ALS nursing interventions: falls precaution

→ bed alarm

→ bed in lowest position

→ lifts

→ wheelchair safety (esp to transfer pt)

→ promote safety mobility

ALS nursing interventions: skin management

→ Turn q2hours (helps redistribute pt's weight)

→ Promote adequate nutritional intake

→ Avoid boney prominences → Reposition in wheelchair →Incontinence management

ALS nursing interventions: nutrition

→ small bites

→ appropriate food consistency

→ eat slowly

→ positioning after eating

→ small frequent meals

→ high fiber

→ hydration

→ G tube

→ PN as disease progresses

- diversional activities

MS summary

What is occurring?

Demyelination of nerve fibers r/t autoimmune

Classification:

Relapse-remitting, primary progressive, secondary progressive

Neurological Sequela

Sensory & Motor impact

Treatment

Non-curative; DMTs & Adjunctive Therapy

Prognosis

Longevity with appropriate management

ALS summary

What is occurring?

Motor neurons degeneration

Classification

Sporadic or familial

Neurological Sequela

Motor impacted; sensory and cognition are intact

Treatment

Non-curative

Prognosis

2-6 years post diagnosis

What are the different types of Lupus? How would you differentiate between each type?

- systemic lupus erythematosus (SLE)

- cutaneous lupus: only affects skin (rashes, photosensitivity)

- drug-induced lupus:

→ mimics S/Sx of SLE but no organ involvement

→commonly caused by hydralazine and procainamide,

→ takes months/years to develop

→ S/Sx disappear within months of stopping med

- neonatal lupus:

→ rare but present at birth

→ Abs passed from mother to baby

→ NOT the infant form of SLE

→ generally a skin rash is present, sometimes heart block

What is Systemic Lupus Erythematosus (SLE)?

an autoimmune disease that occurs when your body's immune system attacks your own tissues and organs

Describe the pathophysiology of SLE.

- in healthy immune system, B and T cells work together to attack Ags and defeat the body both directly and concurrently

- in SLE, autoreactive B and T cells are produced (autoantibodies) and attack the body's own cells → type III hypersensitivity response

→ inflammation

→ body cannot differentiate between healthy and non healthy cells.

- tissue damage occurs secondary to Ag-Ab response

- reactions can be local or systemic

What is the etiology of SLE?

exact caused is unknown

but risk factors are:

- genetics

- hormones (estrogen)

- environmental:

→ sun/UV exposure

→ stress

→ viruses

→ chemicals/toxins (pesticides, asbestos)

→ medications (Bactrim can cause photosensitivity)

SLE clinical manifestations: general

fever

→ greater than 100 w/ no other symptoms of illness

weight loss

joint pain

excessive fatigue

generally experienced on daily basis

but also w/ exacerbations (flares)

most common involved tissue in SLE clinical manifestations

skin and muscle

lining of lungs

heart

nervous system

kidneys

SLE clinical manifestations: dermatological problem

→ mallar/"butterfly" rash

red rash on their face thatstarts on the nose and expands onto the cheeks

→ alopecia (hair loss w/o scalp lesions)

→ mouth ulcers (folic acid helps)

→ photosensitive rashes (use zinc oxide; protects against UVA and UVB)

SLE clinical manifestations: musculoskeletal problem

arthritis

→ swelling

→ pain

→ stiffness,

→ deformity

→ subluxation

ulnar deviation

swan neck of fingers (flexion of outermost joint)

SLE clinical manifestations: cardiopulmonary problem

pleurisy → inflammation of lungs' pleura

pericarditis → inflammation of the pericardium

myocarditis → middle heart

endocarditis → inner heart

fibrosis of SA and AV nodes

→ sinus bradycardia

→ heart attack

antiphospholipid syndrome

→ proteins in blood are attacked by immune system,, leading to blood clots in arteries, veins, organs

Raynaud's phenomenon fingers, toes, ears, tip of nose affected when blood vessels spasm and block blood flow; → appear white, blue, red

SLE clinical manifestations: renal problem

40-50% develop

glomerulonephritis

→ tubular damage

→ interstitial inflammation

→ fibrosis

→ mild proteinuria

→ dec urine production

→ hematuria

→ edema (puffy face)

→ weight gain

SLE clinical manifestations: nervous system problems

→ seizures

→ headaches

→ peripheral neuropathy

→ cognitive problems disordered thinking, disorientation

memory deficits

→ depression, anxiety (may be related to stress of having chronic illness, rather than actual disease)

SLE clinical manifestations: hematological problems

anemia - low blood cells

leukopenia - low white blood cells

thrombocytopenia - low platelets

coagulation disorders - excessive bleeding or clotting

formation of antibodies against blood cell

List some triggers that cause lupus flares.

stress, temperature changes, infections, sun exposure

How is SLE diagnosed? What lab and diagnostic tests are used?

- labs:

→ antinuclear antibody (ANA)

→ anti-double stranded DNA (anti-DSDNA)

→ anti-smith Ab, antiphospholipid Abs

→ x-ray (can be used to asses suspected joint)

→ ECG if suspected cv abnormalities

→ SLE diagnostic criteria: confirmed if score of 10 or greater

What is glomerulonephritis or lupus nephritis?

tubular damage caused by interstitial

inflammation/fibrosis; leads to decreased urine production, hematuria, proteinuria

- can cause intravascular volume expansion, edema, and systemic HTN

List potential complications that are associated with SLE.

→ infections

→ end-stage renal disease

→ stroke (interruption of blood supply to brain d/t antiphospholipid syndrome or htn)

→ heart attack (50x greater risk in ages 35-44 d/t CVD, atherosclerosis, etc.),

→ pregnancy complications

stillbirth

spontaneous abortion

placental abruption (immune complexes are deposited in placenta)

*must wait 6 months inactive SLE on meds compatible w/ pregnancy before getting pregnant

→ skin scarring (discoloration; photosensitivity d/t sun and rashes)

Why do complications occur during pregnancy?

immunocomplexes deposited in placenta can cause spontaneous abortions, stillbirth, intrauterine growth restriction;

disease should be inactive for at least 6 months prior to pregnancy

Describe the interprofessional care involved in SLE.

drug therapy, nutrition, exercise

goal is to prevent damage to inflamed joints/muscles while maintaining muscle strength;

low-impact activities such as walking, swimming, yoga, pilates, cycling

What dietary considerations should be included in patient teaching for someone with SLE?

- no special diet

- mild-moderate alcohol use

- monitor fat and salt intake (cholesterol, BP)

- important calcium intake to offset corticosteroids

- avoid alfalfa and garlic (assoc. w/ lupus-like flares; muscle pains, etc)

Discuss the pharmacologic treatment used in SLE. What class of medications are used and how do they work?

- NSAIDs reduce inflammation

- antimalarial agents (hydroxychloroquine, chloroquine) decrease autoantibody production

- corticosteroids treat inflammation

- immunosuppressants (methotrexate) suppresses the immune system

- anticoagulants increases blood clotting time; used in the presence of Antiphospholipid Syndrome

- monoclonal

antibodies (rituximab, belimumab) target B cells

- respiratory corticotropin injection (acthar) contains naturally occurring hormone ACTH

stimulates cortisol production for inflammation control

SLE and corticosteroids

should be limited to the lowest dose for the shortest possible time

Long term effects include:

• wt. gain & peripheral edema

• HTN

• Slow wound healing

• Increase in rate of infections

• Osteoporosis

• Increase in total cholesterol levels

additional SLE meds for chronic pain mngmnt

• Opioids

• Medical marijuana

• CBD

• Vitamin D b/c of shown deficiency

List the overall goals of nursing management.

- pain mgmt (should be tolerable)

- patient education (awerness and things to avoid)

- maintain optimal role function (independence)

- positive self-image

What is the leading cause of death in individuals 5 - 34 years of age?

motor vehicle crashes

Why is early intervention key in the care of a trauma patient?

- the golden hour: the first hour after injury will largely determine a critically injured person's chances for survival

- platinum 10 minutes: no more than 10 minutes of on-scene stabilization prior to initiation of transport

Describe the steps in the trauma primary survey.

A - airway maintenance (with cervical spine protection)

patent?

B - breathing (and ventilation)

inspection & auscultation

C - circulation (w/ hemorrhage control; STOP THE BLEED!)

responsiveness; skin color

D - disability (euro status)

E - exposure and environmental control; (completely undress patient to ensure no injuries are missed, avoid hypothermia)

What is the role of the nurse in the trauma bay during the primary survey?

- take vitals signs

- IVs and drugs

- transfusions

- foley, gastric tube etc

- documentation

can also be responsible for:

removing clothing

blood and labs

patient transport

Describe the trauma secondary survey.

AMPLE (allergies, medications, PMH, last meal, events surrounding injury) for quick focused history; perform in series and in parallel w/ primary survey

rapid head to toes

front and back

What is the role of the nurse during the secondary survey?

attempts to obtain pertinent info and to evaluate/treat injuries not found during primary survey

List potential causes of blunt abdominal trauma.

MVC, MCC, pedestrian vs car, assault w/ blunt force, fall

List potential causes of penetrating abdominal trauma.

stab wound, GSW

*piercing skin entering body and creating a wound

Identify common injuries associated with blunt abdominal trauma.

1. liver/splenic/renal laceration

2. bowel/pelvic/retroperitoneal hematoma

emergent management of abdominal trauma

unstable pt → FAST → + → operating room

stable pt → FAST → + → CT

stable pt → FAST → - → stop, repeat FAST, CEUS, CT or observation

The Focused Assessment with Sonography in Trauma (FAST)

•An ultrasound protocol developed to assess for peritoneal bleeding.

Indications for the exam:

•Blunt and/or penetrating abdominal trauma

•Thoracic trauma

•Hypotension

Describe the pre-operative nursing management priorities of abdominal trauma.

- prep for surgical intervention (awaiting dx data)

- fluid resuscitation

- protection of ABCs

- pain management

- frequent abdominal assessment

(observe for distention, palpate for pain and firmness → could be sign of abdominal hypertension → abdominal compartment syndrome)

Explain the trauma triad of death.

coagulopathy, hypothermia, and acidosis

- begins and ends w/ bleeding: stop bleeding, administer warm fluids, monitor and maximize oxygenation

- hypothermia (core temp < 95F) leads to decreased coagulation

- coagulopathy occurs d/t losing clotting factors (through hemorrhage)

- acidosis (arterial pH < 7.35) largely caused by poor tissue perfusion

increased lactic acid in blood

What is the significance of intraabdominal pressure monitoring?

- normal pressure should be b/w 0-5 mmHg

- use of indwelling urinary cath is only reliable if pt is heavily sedated or chemically paralyzed

- intraabdominal HTN (> 12 mmHg) can lead to abdominal compartment syndrome

- abdominal compartment syndrome is a medical emergency that requires immediate exploratory laparotomy and relief of pressure

Post-op nursing management associated with abdominal trauma: respiratory

• Protect & monitor the patient's airway & breathing

• Ensure patency of airway

• Monitor vital signs

• Position patient to ensure optimal lung expansion

• Monitor color and character of secretions

• Suction as needed

signs of decreased perfusion

- CNS/brain: restlessness/anxiety, then agitation/confusion

- cardiac: increased HR, decreased BP

- GI: decreased motility, then ileus, then mesenteric ischemia

- renal: decreased urine output, then oliguria, then anuria

- skin: decreased cap refill, cold extremities, then mottled, cyanotic, cold extremities

Post-op nursing management associated with abdominal trauma: surgical site

incision assessment

- surgical site incision can be:

a) midline incision w/ full abdominal closure

b) partial closure (fascia closed, skin open)

c) open abdomen w/ ABThera VAC

Post-op nursing management associated with abdominal trauma: surgical site indication for the open abdomen

•Damage control surgery

•Abdominal compartment syndrome

•Massive fluid replacement

•Requirement for second-look surgery

→ To assess bowel viability or to evaluate and treat continued intra-abdominal contamination

Post-op nursing management associated with abdominal trauma: Cardiovascular

Maintain hemodynamic stability

•Monitor VS

•Frequent assessment of peripheral vascular system

•Monitor mental status

•Provide fluid resuscitation

→ Crystalloid

→→ IV fluids: Lactated Ringers (LR) or Normal Saline (NSS)

→→ 20-30mL/kg

→ Colloid

•Bleeding? → Give them back what they’re losing!

•Monitor intake & output

•Vasopressors

→ Sentinel study showed no mortality benefit but did show statistically significant benefit of less overall fluid resuscitation

Post-op nursing management associated with abdominal trauma: hematologic

• Prevent Trauma Triad of Death

• Remember, STOP THE BLEED

•Keep the patient warm

•Keep patient covered as much as possible

•Apply warm blankets or electric warming blanket

•Keep room temperature high

•Administer fluids, both crystalloid and colloid and ensure they are warm

•Monitor and maximize oxygenation

Post-op nursing management associated with abdominal trauma: GI

- abdominal assessment

•Observe for increasing abdominal distention

•Auscultate for bowel sounds (will likely be hypoactive or absent)

•Palpate to assess for pain or tenderness as well as firmness of abdominal wall

- Trend bladder pressures

•Measures the intra-abdominal pressure

•Considered reliable only when patient is heavily sedated or chemically paralyzed

- Nutrition

Post-op nursing management associated with abdominal trauma: GI Nutrition

•Early involvement of Nutrition Team

•Advocate for 1.5 – 2.5 g/kg/day of protein to start

•Monitor nutritional status with weekly labs (albumin, pre-albumin, c-reactive protein)

•Monitor and replace electrolytes

•Weigh patient daily

•If contraindications to TEN exist, advocate for patient to start TPN within 48 hours of initial damage control procedure.

Post-op nursing management associated with abdominal trauma: GI Bladder pressure

Negative pressure wound therapy or vacuum-assisted wound closure (VAC)

Closed suction removes excess fluid from the wound, allowing for:

•enhanced circulation

•removal of cellular waste

•reduced risk of bacterial contamination

Explain the potential complications in abdominal trauma.

in general

→ the longer the delay of abdominal closure, the greater the risk; abdominal viscera become immobilized and cocoon-like (frozen abdomen) within 14-21 days

1) abdominal compartment syndrome

2) renal injury

3) infection

Abdominal compartment syndrome

- abnormally increased pressure within the abdomen that is assoc. w/ organ dysfunction

- risk factors: trauma, surgery, infection

- causes (MODS):

→ brain swelling/ischemia

→ decreased cardiac output

→ IVC blood flow obstruction (diminished BF to LE)

→ arterial hypoxemia/hypercarbia, impaired venous damage (major cause of renal impairment)

→ hypoperfusion/ischemia of bowel d/t decreased mesenteric blood flow

- clinical manifestations:

→ abdominal distention/tense, rigid abdomen

→ disproportionate abdominal pain

→ tachypnea and/or dyspnea

Treatment:

- Emergency!! Immediately to OR for exploratory laparotomy, need to relieve pressure

What intra-abdominal pressure are concerning?

Renal injury (as a complication of abdominal trauma)

- causes:

→ pre-renal (secondary to impaired perfusion, e.g. hypovolemic shock)

→ intra-renal (secondary to prolonged hypotension; antibiotics, IV contrast dye)

- Nursing interventions:

→ monitor urine output (notify if < 0.5 mL/kg/hr)

→ monitor Cr, BUN, electrolytes

Infection (abdominal trauma complication)

major infections in 10-15% of abdo trauma patients

highest risk factor in hollow, viscous injury

- monitor for SEPSIS

•S – shivering, or fever

•E – extreme pain or general discomfort

•P - pale or discolored skin

•S – sleepy, difficult to arouse, confused

•I – statements such as “I feel like I might die”

•S – shortness of breath

- Abx:

→ prophylaxis (post-op; as caution)

→ tx (active or suspected infection; always look at culture data)

head injury assessment

• ABC…DE (disability, exposure/environment) if trauma

• Neurological Exam

→ GCS

→ Pupils: CN II & III = midbrain;

note unilateral or bilateral dilated pupils (can be signs of increased ICP or herniation)

→ Extremity Movement (Equal?)

→ In a comatose patient:

check protective reflexes such as blink (corneal reflex), gag, and cough to determine presence or absence of brain death

→ Observe for signs of trauma

Lacerations? CSF rhinorrhea, peri-orbital hematoma, Battles sign (bruising behind ear), Racoon eyes?

• Note patients PMH & Mechanism:

→ underlying disorder? Trauma? what came first? Headache then fall? Seizure then fall? Medications?

Head trauma GCS Assessment

Glasgow coma scale:

→ objective level of the patient's conscious state

→

head trauma motor exam

assessment: 0 (total paralysis) to 5 (active movement against full resistance)

posturing indicates severe brain damage

- decorticate (flexor) = damage to cerebral hemispheres

- decerebrate (extensor) = deeper brain structures, incl. midbrain, pons, brain stem

What is traumatic brain injury (TBI)?

an injury to the brain caused by an external force

→ penetrating

→ concussion

→ acceleration and deceleration

→ diffuse axonal injury

→ hematomas and hemorrhages

→→SDH

→→epidural hematoma

→→ ICH; SAH

What are classifications of TBI?

- open (penetrating) vs closed (closed-head)

- primary (moment of initial injury) vs secondary (complications)

- mild, moderate, or severe