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Multiple sclerosis etiology

- unknown cause

- unlikely related to a single cause

- genetics and environmental related to infectious, immunologic, and genetic factors

- precipitating factors can turn on MS in someone with a genetic disposition

- precipitating factors: infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poorer state of health

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Multiple sclerosis classification scheme

Relapsing-remitting

- clearly defined relapses with full recovery or minimal residual

- 80+% are diagnosed with this type of relapse

Primary-progressive

- accumulation of disease

- no distinct relapse or recovery

- 10% of MS

Secondary-progressive

- start with relapse-remitting

- there is also progression

- 50% of patients diagnosed with relapse-remitting develop this within 10 years

Clinically isolated syndrome (CIS)

- episode that is indicative of MS

- clinical episode with symptoms similar to MS

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Multiple sclerosis diagnosis

- no definitive diagnostic test

- based on: history, clinical manifestations, and results of imaging studies

- diagnosis of exclusion

Imaging and tests that can assist in diagnosis

- MRI

- CSF analysis

- evoked potentials: electrical events generated in by peripheral stimulation of a sensory organ to measure response time (somatosensory, visual, or brainstem auditory) (patients with MS have delayed visual response 50-90% of the time)

3 Criteria for Diagnosis

- lesions in 2 different locations

- damage/attack interval (usually a month apart)

- rule out

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Multiple sclerosis clinical manifestations

Motor

- weakness or paralysis

- double vision

- scanning speech

- muscle spasticity (interferes with speech and gait)

Sensory

- Lhermitte's sign: electrical shock radiating down spine and neck

- numbness

- tingling

- blurred vision

- dizziness (vertigo)

- loss of balance

- patchy blindness

- reticular nerve root pain

Cerebellar

- nystagmus

- involuntary eye movement

- ataxia

- dysarthria

- dysphagia

- difficulty swallowing

Fatigue

- increased energy needs

- heat

- decreased fluids

Bowel and Bladder

- constipation

- spastic bladder: possible dribbling or incontinence

- flaccid bladder

Sexual dysfunction

- erectile dysfunction

- decreased libido

- decreased vaginal lubrication

- pain during intercourse

Emotional changes

Cognition

- 50% may experience short-term conversational or planning issues

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Multiple sclerosis pseudo relapse

- also known as pseudo-exacerbation or pseudo-flare

- common triggers: stress, fatigue, illness, and heat

- not causing new damage

- very distressing to patients

- treat underlying cause

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Impact of Pregnancy on a Patient with Multiple Sclerosis

- pregnancy can exacerbate symptoms and progression

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goals of disease modifying therapy

- 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

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Adjunctive pharmacologic treatment for multiple sclerosis

- acute exacerbations: glucocorticoids (methylprednisolone, prednisone, etc.) (reduces edema at the site of demyelination) and plasma exchange (for a bad reaction to glucocorticoids)

- anticholinergics: treating bladder symptoms, increasing the amount of urine that can be held

- CNS stimulants for fatigue

- muscle relaxants for spasticity

- nerve conduction enhancer - improves walking speed (cautioned in CKD and seizure disorder)

- tricyclic antidepressants for chronic pain

- antispasmodics for spasticity (baclofen)

- anti seizure for chronic pain

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Functional limitation in patients with multiple sclerosis

- impaired physical mobility

- impaired urinary elimination

- interrupted family processes

- risk for falls

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Multiple sclerosis patient teaching

- good balance of exercise and rest

- nutrition

- treatment regimen (medication management and adherence)

- self-catheterization if necessary

- adequate intake of fiber to aid in regular bowel habits

- emotional adjustments

- lifestyle changes

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ALS etiology-classifications

- sporadic: without family history, random, 90-95% of cases

- familial: one occurrence in family, dominant inheritance

- onset: 40-70 years of age

- men vs. women - 2:1 men to women

- 5000 people in US diagnosed annually

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ALS clinical manifestions UMN vs. LMN

Typical manifestations: muscle weakness, dysarthria, dysphagia

Other manifestations: pain, sleep disorders, spasticity, drooling, emotional lability, depression, esophageal reflux, constipation

Upper Motor Neuron manifestations

- loss of dexterity or ability to coordinate movements

- weakness

- spasticity

- hyperreflexia

Lower Motor Neuron manifestations

- weakness

- paralysis

- hyporeflexia

- fasciculations

- flaccidity

- muscle cramps

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ALS diagnosis

- difficult to diagnose

- thorough neurological examination is key

- diagnosis of exclusion: electrodiagnostic tests, blood and urine studies, spinal tap, x-rays, MRI, pyelogram of cervical spine, and muscle and/or nerve biposy

- El Escorial criteria

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ALS drug therapy

Riluzole

- decreases body's level of glutamate

- slows progression of disease

Edaravone

- slows functional deterioration

- prevents oxidative stress

- came out 2 years ago

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ALS nursing interventions

Facilitating communication: over articulation, limit distractions, sit face to face, yes/no systems, eye blinking, smartphone, letter board, speech generating devices

Aspiration precautions: honey or nectar thick food, coughing and deep breathing exercises, secretion management with coughalator and chest physiotherapy, incentive spirometry, suctioning

Falls precautions: bed alarm, bed in lowest position, lifts, wheelchair safety, promote safe mobility

Skin management: turn q2hr, promote adequate nutritional intake, avoid boney prominences, reposition in wheelchair, incontinence management

Nutrition: appropriate consistency, small bites, eat slowly, positioning after eating, small frequent meals, high fiber, hydration, G tube, parenteral nutrition as the disease progresses

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ALS prognosis

- no cure

- death typically occurs from a respiratory tract infection

- 2-6 years after diagnosis

- focus on symptom management

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SLE etiology

- unknown

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SLE risk factors

- potentially due to genetics, hormones, or environmental factors

- possible environmental factors: sun or UV exposure, stress, viruses, chemicals, toxins, medications

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SLE pathophysiology

- the immune system produces auto reactive B cells and T cells, which make a type of protein called autoantibodies

- these autoantibodies in turn attack the bodies' cells, leading to inflammation

- these autoantibodies target various components of the cell nucleus and result in a Type III hypersensitivity response

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SLE clinical manifestations

General

- fever

- weight loss

- joint pain

- excessive fatigue

Dermatologic

- malar/butterfly rash

- alopecia

- mouth ulcers

- photosensitivity

Musculoskeletal

- arthritis

- swelling

- pain

- stiffness

- deformity

- subluxation

- swan neck of finger

- ulnar deviation

Pulmonary

- pleurisy: inflammation of tissue that lines the lungs

Cardiac

- pericarditis

- myocarditis

- endocarditis

- fibrosis of sinoatrial and atrioventricular nodes (can lead to heart block)

- antiphospholipid syndrome: formation of abnormal blood clots

- Raynaud's phenomenon: narrowing of blood vessels

Renal

- mild proteinuria

- glomerulonephritis

Nervous System

- seizures

- headaches

- peripheral neuropathy

- cognitive problems: disordered thinking, disorientation, memory deficits

- depression

- anxiety

Hematologic

- anemia: low RBC

- leukopenia: low WBC

- thrombocytopenia: low platelets

- coagulation disorders: excess bleeding or clotting

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SLE diagnosis

Labs

- ANA test

- Anti-DSDNA test

- Anti-smith antibody

- antiphospholipid antibodies

X-ray

- can be used to assess affected joints

ECG

- can be used to access cardiac abnormalities

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SLE pharmacologic treatment

- NSAIDS: reduce inflammation

- antimalarial agents: decrease autoantibody production

- corticosteroids: decrease inflammation (should be limited to the lowest dose)

- steriod-sparing medications: suppress immune system; control inflammation

- anticoagulants: increases blood clotting time

- monoclonal antibodies: target B-cells

- respiratory corticotropin injection: contains naturally occurring hormone ACTH, stimulates body to produce cortisol, helps reduce inflammation

- immunosuppressive medications: suppress the immune system

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SLE non-pharmacologic treatment

Nutrition

- no special diet

- consider: alcohol use, fat & salt intake, and calcium intake

- avoid alfalfa and garlic

Exercise

- low impact: walking, swimming, yoga, pilates, cycling

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SLE complications

- infections

- end-stage renal disease

- stroke

- heart attack

- pregnancy complications

- skin scarring

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SLE nursing management

- pain management

- patient education

- maintain optimal role function

- positive self-image

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Primary prevention of abdominal trauma

- seatbelts: most effective way to reduce injury with MVC and reduces serious injury in crash by 50%

- helmets: most effective way to reduce injury in MCC; estimated to prevent 37% of fatal motorcycle injuries

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trauma primary survey

A - airway (with cervical spine protection)

B - breathing (and ventilation)

C - circulation (with hemorrhage control - stop the bleed)

D - disability (neurological status)

E - exposure and environmental control (completely undress patient but avoid hypothermia)

- vital signs, IV's, drugs, transfusions, foley, gastric tube, documentation

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trauma secondary survey

- History: AMPLE (allergies, medications, PMH, last meal, and events surrounding injury)

- physical examination: neurologic, head and skull, maxillofacial, neck, chest, abdomen, perineum/rectum, musculoskeletal, and tubes/fingers

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common injuries in blunt trauma

- liver laceration

- splenic laceration

- renal laceration

- bowel hematoma

- pelvic hematoma

- retroperitoneal hematoma

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pre-op nursing management of abdominal trauma

- prep for surgical intervention (pending diagnostic data)

- fluid resuscitation

- protection of ABC's

- management of pain

- frequent abdominal assessments (observe for abdominal distention and palpate for pain and firmness)

- prevention of lethal triad

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post-op nursing management of abdominal trauma

Respiratory

- protect and monitor airway and breathing

- ensure latency of airway

- monitor vital signs

- position patient to ensure optimal lung expansion

- monitor color and character of secretions (suction as needed)

Cardiovascular

- maintain hemodynamic stability

- monitor VS

- frequent assessment of peripheral vascular system

- monitor mental status

- provide fluid resuscitation

- crystalloid: lactated ringers or normal saline(20-30 mL/kg)

- colloids

- monitor I/O

- vasopressors: study at Penn showed that vasopressin along with crystalloid and colloid resuscitation had no mortality benefit but did show statistically significant benefit of less overall fluid resuscitation

Hematologic

- prevent trauma triad of death

- stop the bleed

- keep the patient warm: keep patient covered as much as possible, apply warm blankets, keep room temp. high

- administer fluids, both crystalloid and colloid

- ensure they are warm

- monitor and maximize oxygenation

Gastrointestinal

- abdominal assessment: observe for increasing abdominal distention, auscultate for bowel sounds, and palpate to assess for pain or tenderness as well as firmness of abdominal wall

- trend bladder pressure: measures the intra-abdominal pressure and considered reliable only when patient is heavily sedated or chemically paralyzed

- nutrition: early involvement of nutrition team, advocate for 1.5-2.5g/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

Surgical Site

- incision assessment

- midline incision with full abdominal closure

- partial closure (such as a fascial closure where the skin remains open)

- open abdomen with ABThera, VAC, or other closure device

- indications 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)

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Neurologic exam

- glasgow coma scale

- pupils: CN II and III = midbrain

- not unilateral or bilateral dilated pupils (can be signed of increased ICP or herniation)

- extremity movement (equal?)

- in a comatose patient, checking protective reflexes such as blink (corneal reflex), gag, and cough are used to determine presence or absence of brain death

- observe for signs of trauma: lacerations, CSF rhinorrhea, peri-orbital hematoma, battles sign (bruising behind ear), raccoon eyes

- note PMH

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TBI classification and types of injury

Penetrating Injury

- a head injury in which the dura mater (outer layer of the meninges) is breached

- less common than closed head trauma but worse prognosis

- penetrating: foreign object penetrate and remains lodged

- tangential: foreign objects glances off skulls driving bone fragments into the brain

- perforating: through and through

- most common is GSW

Concussion

- low velocity injury resulting in functional deficit without pathological injury

- most common symptoms is headache

- neuroimaging is typically normal

- recovery from symptoms within 7 days to 6 weeks

- balance and coordination may be affected

- concussion clinics and outpatient therapy are useful for symptom management (which can affect QOL)

Acceleration and Deceleration Injuries

- coup: site of impact with blunt object

- contrecoup: opposite the area of impact

Diffuse Axonal Injury

- long connecting fibers in the brain (axons) are sheared as the brain accelerates and decelerates

- causes injury to many places in the brain

- patients are often in a coma without obvious lesion on CT scan; punctate hemorrhages can be seen on MRI

- supportive care

- poor outcomes

Subdural Hematoma

- bleeding between dura and arachnoid membranes

- elderly are prone d/t fragile vessels and brain atrophy

- can occur with relatively low impact or be spontaneous

- typically venous (tearing of bridging veins)

- close near observation/serial near exams: gradually increasing headache and confusion can indicate expansion

- potential surgery for evacuation

- seizure prophylaxis (presenting symptom can be seizure)

- possible drain

Epidural Hematoma

- bleeding between skull and dura layer

- typically arterial

- close near observation/serial near exams: lucid initially to unconsciousness (can happen quickly)

- potential surgery

- seizure prophylaxis

Subarachnoid

- bleeding between the Pia mater and the arachnoid membrane

- trauma is most common cause of SAH

- seizure prophylaxis

- occurs in 35% of TBI, typically in combination with other hemorrhage

- rarely causes vasospasm

- medical management only

Intracerebral Hemorrhage

- intraparenchymal hemorrhage: blood in brain tissue

- intraventricular hemorrhage: blood in ventricles

- seizure prophylaxis

- surgery: possibly

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Potential complications of head injury

- cerebral edema and herniation

- seizures

- hydrocephalus

- alternations of neuroendocrine function of hypothalamus and pituitary system (diabetes isipidus and syndrome of inappropriate anti-diuretic hormone)

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Cushing's triad

- increased BP (sympathetic response to cerebral ischemia, worsening problem)

- decreased HR (HTN is detected and stimulates vagus nerve)

- decrease RR or irregular respiratory pattern (compression or respiratory center)

means acute herniation (near emergency)

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TBI nursing management

Neuro

- serial neurologic exams (Q15min-Q4hours)

- monitoring/managing ICP; ICP

- manage pain/agitation

- EVD management

- repeat imaging - urgency

- seizures (clinical vs sub-clinical)

- HOB elevated (unless contraindicated)

- management of paroxysmal sympathetic hyperactivity

CV

- BP goals: avoid HTN in bleed; avoid hypotension to optimize CPP

- monitor HR: high risk of arrhythmias d/t sympathetic surge

- treat shock (fluid/vasopressors)

Respiratory

- monitor status; GCS

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SCI: traumatic vs. non-traumatic

Traumatic

- flexion/extension/compression

- fractures

- hematomas

Non-Traumatic

- tumors

- infection

- stenosis

- ischemic injury

- AVMs

- neuromuscular disease can present with weakness

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SCI major cause of death

- aspiration and shock

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ASIA scoring

A - complete; no motor or sensory function is preserved in the sacral segments S4-S5

B - incomplete; sensory but not motor function is preserved below the neurological level and includes sacral segments S4-5

C - incomplete; motor function is preserved below the neurological level and more than half of key muscles below the neurological level have a muscle grade less than 3

D - incomplete; motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more

E - norma; motor and sensory function are normal

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types of SCI injuries

Complete

- no residual function more than three levels below the injury affecting both sides equally

Incomplete

- any residual sensory or motor function below the injured level

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spine syndromes

Central Cord Syndrome

- most common type of incomplete injury

- injury to the center portion of the cervical cord - cervical motor fibers are located towards the center of the cord

- results in weakness in arms (loss of fine motor) more than legs

- surgical treatment remains controversial

- commonly found in hyperextension injury: older persons with cervical spondylosis/stenosis and younger persons with traumatic injury

- recovery is possible but variable

Brown-Sequard syndrome

- rare

- ipsilateral loss of motor and contralateral loss of sensation

- damage to half of the spinal cord; can be seen in patients with spinal cord tumor, trauma, infection and inflammatory disease, as well as disc herniation

Anterior Cord Syndrome

- complete motor paralysis and loss of temp. and pain perception distal to the lesion with preserved light touch, vibration, and proprioception

- caused by compression of the anterior spinal artery

- associated with burst fractures

Cauda Equina Syndrome

- nerve roots of the caudal equine are compressed (herniated disc, tumor, abscess)

- symptoms: weakness, difficulty urinating, loss of rectal tone, saddle anesthesia

- medical emergency

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Management of cardiogenic shock

- restore blood flow

- oxygen supply and demand

- thrombolytics

- angioplasty with senting

- coronary revascularization

- reduce workload of the heart with intra-aortic balloon pump (IABP) or ventricular assistive device (VAD)

- airway and oxygenation management

- drug therapy: positive inotropes (dopamine and dobutamine) ventodilation (nitroglycerin), and vasodilation (sodium nitroprusside), diuretics, and beta blockers

- supportive therapy

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common problems experiences by people who shift work

- characterized by insomnia, sleepiness, and fatigue

- sleep debt grows

- complications: mood, impact work performance, testosterone, higher accident risk, and substance use

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insomnia etiology

- behaviors

- lifestyle

- diet

- medical conditions

- medications

- stressful life events

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prevention of organ rejection

- both the donor and recipient are tested to identify HLA antigen variations, which minimizes rejection

- activation of lymphocytes are cellular rejection

- activation of antibodies are humoral rejection

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treatment of organ rejection

- calcineurin inhibitors

- corticosteroids

- antimetabolites

- antibody products

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diabetes insipidus clinical manifestations

- polydipsia

- polyuria

- excretion of large quantities of urine (2-20L/day, very low specific gravity, very low urine osmolality, serum osmolality is elevated)

- nocturia

- generalized weakness

- dehydration

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acute thyrotoxicosis management

- medical emergency

- propylthiouracil

- beta blockers

- IV fluids

- cardiac monitoring

- adequate oxygenation

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Cushing's syndrome etiology

- iatrogenic administration of exogenous corticosteroids

- ACTH-secreting pituitary adenoma: large cause of endogenous cases

- adrenal tumors: less common

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Hyperparathyroidism diagnosis

- serum PTH levels

- serum Ca

- serum P+

- bone density measurements

- urine

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Hyperparathyroidism management

Surgical

- partial vs. complete (outpatient)

- auto transplantation of normal parathyroid tissue

Calcium supplementation for life if surgical interventions fail

Conservative approach if asymptomatic or mild symptoms

- labs

- annual x-rays or DEXA scans

- drug therapy

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Multiple sclerosis pathophysiology

Three Characterizing Pathologic Processes

- chronic inflammation

- demyelination

- gliosis in the CNS: scarring, nonspecific reaction-like changes

Primary Neuropathologic Condition

- autoimmune process orchestrated by activated T cells

- T cells migrate to the CNS, causing a blood-brain disruption

Onset

- insidious

- vague symptoms

- intermittent

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Golden hour vs. platinum 10

Golden hour

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

Platinum 10

- later coined to restrict the time of pre-hospital care of critically injured trauma patients to no more than 10 minutes of on-scene stabilization time prior to initiation of transport

- resulted in a scoop and run approach to encourage rapid transport to the local trauma center

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Etiology: blunt vs. penetrating

Blunt

- MVC

- MCC

- pedestrian vs car

- assault with blunt force

- fall

Penetrating

- stab wound

- gunshot wound

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abdominal trauma complications

Abdominal compartment syndrome

- condition caused by abnormally increased pressure within the abdomen that is associated with organ dysfunction

- risk factors: trauma, surgery, infection

- intra-abdominal hypertension can impair the function of nearly every organ system

- clinical manifestations: abdominal distention worsening to tense, rigid abdomen; abdominal pain out or proportion to injury; tachypnea and/or dyspnea

- treatment: relief the pressure; emergency that needs to go to the OR immediately for exploratory laparotomy

Renal injury

- causes: pre-renal and intra-renal (secondary to prolonged hypotension; toxins such as antibiotics and IV contrast dye)

- monitor urine output

- inform provider if patient produces less than 0.5mL/kg/hr

- obtain labs as ordered

- monitor creatinine, BUN, and electrolytes

Infection

- prevent and treat

- monitor for sepsis (shivering, extreme pain or general discomfort, pale or discolored skin, sleepy/confused, "I feel like I might die" statements, shortness of breath

- antibiotics (prophylaxis and treatment)

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Trauma triad of death

- hypothermia

- coagulopathy

- acidosis

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Motor strength scaling

- musculoskeletal strength graded out of 5

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TBI signs

- use GCS

- decorticate (flexor) posturing: damage to cerebral hemispheres

- decerebrate (extensor) posturing: deeper brain structures, including midbrain, pons, brain stem

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TBI symptoms: mild vs. severe

Mild

- LOC for secs to min or none but state of being dazed/disoriented

- headache

- N/V

- fatigue

- speech problems

- dizziness

Moderate to Severe

- LOC for several mins to hours

- headache

- repeated N/V

- seizures

- dilation of one or both pupils

- clear fluids from nose or ears

- weakness

- agitation

- slurred speech

- come (GCS

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SCI etiology

- fractures

- dislocation

- masses such as tumors

- hematomas

- abscesses

- ischemic injuries (spinal stroke)

- penetrating injuries to the spine accounts for about half of spinal injuries in urban centers

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SCI mechanisms of injury

- must always be presumed until it is excluded (a missed injury can have devastating consequences)

- compression

- flexion

- extension

- rotation

- lateral bending/stress

- distraction

- penetration

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SCI acute complications

Spinal Shock

- transient depression or loss of reflex activity below the level of an acute spinal cord injury

Neurogenic shock

- form of distributive shock

- a sudden loss of autonomic tone due to spinal cord injury causes hypotension and bradycardia - unopposed parasympathetic innervation

- usually occurs in patients with injury T6 and above but can happen in any injury above L2

- management: airway support if needed, fluids and vasopressor support as needed, to maintain MAP

- atropine for bradycardia vs pacing (temporary or permanent?)

Autonomic dysreflexia

- uncontrolled sympathetic response secondary to a stressor in patients with a SCI T6 and above (unlikely to occur with injuries below T10)

- life threatening HTN and bradycardia when there is a noxious stimulus below the level of injury

- initial complaint is headache - any patient with headache and SCI above T6 should have their BP checked immediately

- common triggers are bladder dissension, fecal impaction/constipation, pressure injury

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SCI nursing management

Neuro

- serial neurologic exams, especially motor strength and sensation

- maintain proper spinal precautions/alignment

- pain management (neuropathic pain)

- patient/family education and support

- encourage patient to be active participant in their care/recovery (give them back some control)

Respiratory

- close monitoring

- pulmonary toileting (cough assist, chest PT, quad cough)

- management of secretions

CV

- BP monitoring

- HR/telemetry

- optimize perfusion - patients may require MAP goals of >80 or higher in initial injury period to optimize spine perfusion

- manage shock

GI/GU

- bowel regimen (may need standing suppository/rectal stimulation)

- strict bladder training

Skin

- frequent turns and skin assessments - offload pressure

- mobilize

Heme

- DVT prophylaxis

Discharge planning

- early PT/OT/Speech

- SCI rehabilitation/PM&R

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Medical management of spinal injury

- stabilization of spin

- distributive shock management: fluid resuscitation, atropine for bradycardia, vasopressors PRN

- no current support for steroids

- intensive support care

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causes of spinal tumors

- viruses

- defective genes

- exposure to certain chemicals and hazardous materials

- immune system disorders

- genetic diseases, such as tuberous sclerosis

- exposure to radiation

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SCI clinical manifestations

- trouble waking (abnormal gait)

- numbness/tingling

- bowel/bladder dysfunction

- general midback pain

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SCI diagnostic approach

- can take weeks

- often other causes ruled out first

- usually first diagnosed on MRI

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Management of spinal tumors

- surgical resection and stabilization of spine if possible

- radiation therapy

- chemo

- steroids to reduce swelling

- serial neuro assessments and spine exams

- pain management

- incentive spirometry

- prevent atelectasis

- peri-op abx

- wound and drain care/monitoring

- bowel regimen

- monitor for urinary retention

- mobilize

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leading causes of death in spinal cord injury after initial injury

- pneumonia

- PE

- sepsis

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Classifications of shock

- cardiogenic

- hypovolemic (absolute and relative)

- distributive (neurogenic, anaphylactic, and septic)

- obstructive

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Clinical manifestations of cardiogenic shock

- problem with the pump

- early: tachycardia, hypotension, narrowed pulse pressure

- respiratory: tachypnea, crackles, cyanosis, rhonchi

- cardiovascular: tachycardia, decrease in BP, decrease in cap refill, chest pain may or may not be present

- integumentary: pallor, cool, clammy

- renal: increase Na&H2O retention, decreased renal blood flow and urinary output

- neuro: anxiety, confusion, agitation

- GI: decreased BS, nausea, vomiting

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Clinical manifestations of hypovolemic shock

- dependent on age, extent of injury or insult, and overall state of health

- respiratory: tachypnea and bradypnea (late)

- cardiovascular: decreased preload, SV, and cap refill

- integumentary: pallor, cool, clammy

- renal: decreased u/o

- neuro: anxiety, confusion, agitation

- GI: absent bowel sounds

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Clinical manifestations of neurogenic shock

- main symptoms: hypotension, bradycardia, inability to regulate body temperature that leads to poikilothermia

-respiratory: related to injury level

- cardio: decreased BP, bradycardia, increase/decrease in temperature

- integumentary: pallor, cool, clammy

- renal: bladder dysfunction

- neuro: flaccid paralysis below level of lesion, loss of reflex activity

- GI: bowel dysfunction

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Clinical manifestations of anaphylactic shock

- main symptoms: dizziness, chest pain, incontinence, swelling of lips and tongue, wheezing, stridor, flushing, pruritus, uticaria, angioedema, and sense of impending doom

- respiratory: SOB, edema of larynx and epiglottis, wheezing, stridor, rhinitis

- cardio: CP, third spacing of fluid

- integumentary: flushing, pruritus, urticaria, angioedema

- renal: incontinence

- neuro: anxiety, feeling of impending doom, decreased LOC

- GI: cramping, ABD pain, diarrhea, vomiting, nausea

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Clinical manifestations of septic shock

- pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression

- respiratory: hyperventilation, crackles, respiratory alkalosis leading to acidosis, hypoxemia, ARDS (acute respiratory distress syndrome), and pulmonary hypertension

- cardio: increase/decrease in temp, myocardial dysfunction, ventricular dilation, decrease in EF

- integumentary: warm and flushed and then cool and mottled (late)

- renal: decreased urine output

- neuro: altered MS, confusion, agitation

- GI: GI bleed, paralytic ileus

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Clinical manifestations of obstructive shock

- main symptoms: decreased CO, increased afterload, and variable left ventricular filling pressure

- respiratory: tachypnea, SOB, bradypnea (late)

- cardio: decreased BP and preload

- integumentary: pallor, cool, clammy

- renal: decreased urine output

- neuro: anxiety, confusion, agitation

- GI: decreased or absent bowel sounds

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Management of hypovolemic shock

- treat the underlying cause

- large bore peripheral IVs or central venous catheter (CVC)

- fill the tank with crystalloids (LR, normal saline) and colloids (PRBCs, FFP, albumin, plasma volume expanders like hetastarch and dextran)

- invasive hemodynamic monitoring

- airway and oxygenation management

- no specific drug therapy

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Management of neurogenic shock

- based on the cause

- spine stability

- vasopressors (phenylephrine)

- atropine

- fluids must be used cautiously as there is a risk of fluid overload (change in resistance, not volume)

- body temperature

- airway and oxygenation management

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Management of anaphylactic shock

- prevention

- removal of offending cause

- airway and oxygenation management (endotracheal intubation or cricothyroidotomy)

- fluid resuscitation

- drug therapy: epinephrine, Benadryl, bronchodilators, corticosteroids

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Management of septic shock

- blood cultures identifying the organism

- labs

- abx

- aggressive fluid resuscitation

- vasopressors (norepinephrine)

- inotrope (dobutamine)

- prophylactic anticoagulants

- stress ulcer prophylaxis

- airway and oxygenation management

- invasive hemodynamic monitoring

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Management of obstructive shock

- treat the underlying cause: pericardiocentesis, needle decompression, chest tube insertion, embolectomy

- fluid resuscitation (temporary)

- airway and oxygenation management

- no specific drug therapy

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SIRS criteria

- temp over 100.9

- heart rate over 90 bpm

- respiratory rate of 22 bpm or PCO2 less than 32 mmHg

- WBC over 12 or WBC less than 4

Sepsis

- 2 SIRS + infection

Severe sepsis

- sepsis + 1 sepsis induced organ dysfunction

Septic shock

- severe sepsis + hypotension without response to fluid resuscitation

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Stages of shock

1. Initial

- cellular level

- usually not clinical apparent

- metabolism changes (lactic acid build-up)

2. Compensatory

- attempt to equilibrilate

- activation of neural, hormonal, and biochemical mechanisms

3. Progressive

- begins as compensatory mechanisms begin to fail

- changes in mental status

- CV system profoundly affected

- pulmonary system

- aggressive interventions (key to preventing MODS)

4. Irreversible/Refractory

- decreased perfusion, which leads to anaerobic metabolism

- decreased CO

- increasing capillary permeability

- increasing dilation

- profound hypotension and hypoxemia

- unlikely recovery

- sequelae: cerebral ischemia, worsening cardiac depression, and failure of one organ system

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How SVR, CO, and CVP relate to the presentation of cardiogenic shock

- increase in CVP, PAWP, and SVR

- decrease in CO

- related to systolic dysfunction (ineffective forward movement of blood) or diastolic dysfunction (ineffective filling)

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