advanced nursing exam 3

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Prerenal Causes of Renal Failure:

o Factors that reduce systemic circulation leading to a reduction in renal blood flow and decreased glomerular perfusion; prolonged leads to intrarenal AKI

o Common causes-

- decreased cardiac output (cardiogenic shock, dysrhythmias, heart failure, MI)

- Decreased peripheral vascular resistance (anaphylaxis, neurologic injury, septic shock)

- Decreased renovascular blood flow (embolism, renal artery thrombosis)

- Hypovolemia (burns, dehydration, GI losses, hemorrhage)

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Intrarenal Causes of Renal Failure:

o Conditions that cause direct damage to the kidney tissue, resulting in impaired nephron function

o Common causes-

- #1 in hospitalized patients is atubular necrosis – ischemia, nephrotoxins, sepsis

- Interstitial nephritis (allergies, antibiotics, NSAIDS, infections)

- Nephrotoxic injury (chemical exposure, contrast media, hemolytic blood transfusion reaction)

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Postrenal Causes of Renal Failure:

o Post renal: involves mechanical obstruction to the outflow of urine. When flow is obstructed urine refluxes into the renal pelvis.

o Common causes-

BPH, Bladder cancer, Renal calculi, Prostate cancer, Trauma

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Phases of Renal Failure: Oliguric

· Urinary changes—*oliguria – output < 400 mL/day

· Occurs within 1 to 7 days after injury

· Lasts 10 to 14 days

· Urinalysis shows casts, RBCs, WBCs, protein

· Specific gravity 1.010

· 50% patients non-oliguric; greater than 400 mL urine/day

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Phases of Renal Failure: Diuretic

· Daily urine output is 1 to 3 L; up to 5 L

· Osmotic diuresis from high urea and inability of tubules to concentrate urine

· Monitor for hypovolemia, hypotension, hyponatremia, hypokalemia, and dehydration

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Phases of Renal Failure: Recovery

· Increased GFR, decreased BUN and creatinine (return to normal)

· Influenced by the severity of injury and complications

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Lab values with acute renal failure:

o Lab Values: increase creatinine, increase BUN, decrease GFR, decreased specific gravity, azotemia (nitrogen in blood), hypokalemia/hyperkalemia, hyponatremia

o Monitor potassium closely

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Symptoms of Renal Failure:

o Fluid retention - edema, weight gain, crackles in the lungs

o Metabolic acidosis - tachycardia, HA, diarrhea, vomiting, Kussmaul breathing

o Normal or decreased serum Na+ - nausea, HA, weakness, seizures, coma

o Hyperkalemia - fatigue, weakness, dysrhythmias

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Solutions to Hyperkalemia:

o 1. calcium gluconate IV – increases threshold for cellular excitation so potassium moves back into cells (can cause arrhythmias, so give over 10 minutes in ICU)

o 2. Regular insulin IV – GIVE WITH DEXTROSE; given to drive potassium back into the cell

o 3. Sodium bicarbonate – exchanged hydrogen ions for potassium to neutralize pH

o 4. Kayexalate – excreted through the GI tract

o 5. Loop Diuretics – excretes through the urinary tract

o 6. Hemodialysis

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Continuous Renal Replacement Therapy (CRRT):

o Toxins and fluids are removed while acid-base status and electrolytes are adjusted slowly

o Used in hemodynamically unstable patients

o Patient is 1:1

o do not use AV fistulas for CRRT! use CVDC

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Common Complications of CRRT:

o #1: clotting

o Others: infection, bleeding, hypotension, electrolyte imbalance

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Sustained Low-Efficiency Daily Dialysis (SLEDD):

o Hybrid between intermittent HD and CRRT

o Managed strictly by an RN

o uses a CVDC

o Runs for 6-12hrs/day

o Patient does not have to be 1:1

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What is Hemodialysis?

o Rapid fluid removal, effective in potassium removal, temp access can be placed at bedside

o Restrictive, vascular access, expensive

o uses fistula

o if patient is hypotension (SEE THIS PATIENT FIRST)

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Dialysis access sites:

o Venous access sites: common include subclavian & femoral

o Red: pulls patient blood

o Blue: pushes filtered blood back to the patient

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RN Responsibilities for Dialysis:

o Monitor flowsheets hourly

o Q8HRS labs

o Maintain line patency

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Chronic Kidney Disease (CKD):

o Defined as GFR < 60 for 3 months+

o S/S: fluid retention, peeing at night, insomnia

o Most die due to CVD (manage HTN)

o Do not be concerned if a patient with CKD comes in with a creatinine of 3 or a slightly low Hbg or RBC (this is normal for them) - high potassium and HTN are still a concern

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Management of CKD:

o Correct fluid volume issues, RRT, lower potassium

o Give calcium supplements, antihypertensives, erythropoietin, lipid-lowering drugs

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End Stage Renal Disease (ESRD):

o GFR < 15

o Symptoms usually begin here

o Dialysis or renal transplant is required for survival

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What education would you give a patient on peritoneal dialysis?

o Less complicated, portable system, less cardiovascular stress

o High infection risk, catheter migration

o Peritonitis is main concern with PD due to the catheter in abdomen – use strict aseptic technique

o PD patients have dialysis daily so missing an appointment is a concern

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Main differences between patient populations on hemodialysis vs peritoneal vs CRRT:

o Hemodialysis: usually 3 appointments per week, can be done through a catheter or fistula

o Peritoneal: belly filled with fluid where peritoneum is used as a natural filter, fewer restrictions, patients often need to be healthier

o CRRT: critically ill patients who are hemodynamically unstable

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Care for AV fistulas:

o Most CKD patients have a fistula

o Limb alert on that side; feel the thrill, listen for bruit (both are good)

o Post-Op: do not lift heavily

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Contraindications for kidney transplantation:

Advanced cancers, untreated heart disease, chronic respiratory failure, extensive vascular disease, chronic infection, unresolved psych issues

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Renal transplants and the use of immunosuppressive drugs cause increased mortality primarily due to what?

o Immunosuppressive drugs are required for life after transplant

o Increased mortality due to infection and cancer risk

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Are NSAIDs used for CKD patients?

No, because of the increased risk for renal damage and GI bleeding

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What is the Romberg test?

o Test of proprioception

o Have patient stand with feet together and close eyes

o (+) if sways or falls with eyes closed

o Indicates vestibulocochlear dysfunction or spinal cord disease

o Risk for falls

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Nerve regeneration in PNS vs CNS:

o PNS is more likely to regenerate than SNS

o PNS nerve fibers regenerate within the myelin sheath

o If the axon of the nerve is damaged, the cell will attempt to repair itself by growing back to its original destination through branches at the damaged end

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What does GABA do? What does that mean?

o GABA is the main inhibitory neurotransmitter, like serotonin and dopamine

o Block chemical messages to prevent their actions

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Function & assessment of the 1st cranial nerve:

o Olfactory nerve (smell) - purse sensory nerve

o Occlude one nostril and as the patient to identify specific smells

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Function & assessment of the 2nd cranial nerve:

o Optic nerve - pure sensory nerve

o Snellen assessment, one eye at a time

o Confrontation of visual fields

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Function & assessment of the 3rd cranial nerve:

o Oculomotor nerve - pure motor nerve

o Innervation of pupil and lens, upper eyelid, and visual tracking muscles

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Function & assessment of the 4th cranial nerve:

o Trochlear nerve - pure motor nerve

o Innervation of muscle used to move eye down and shift from side to side

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Function & assessment of the 5th cranial nerve:

o Trigeminal nerve - mixed nerve

o Facial sensation test

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Function & assessment of the 6th cranial nerve:

o Abducens nerve - pure motor nerve

o Innervates the muscle used to abduct the eye

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Function & assessment of the 7th cranial nerve:

o Facial nerve - mixed nerve

o Check for symmetrical movements of the face

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Function & assessment of the 8th cranial nerve:

o Auditory nerve - pure sensory nerve

o Hearing test & vestibular function tests (watch for nystagmus)

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Function & assessment of the 9th cranial nerve:

o Glossopharyngeal nerve - mixed nerve

o Stimulate the gag reflex

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Function & assessment of the 10th cranial nerve:

o Vagus nerve - mixed nerve

o Have patient say "ah" and inspect for symmetry of the palate

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Function & assessment of the 11th cranial nerve:

o Spinal accessory nerve - pure motor nerve

o Have patient turn head against resistance and elevate shoulders against resistance

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Function & assessment of the 12th cranial nerve:

o Hypoglossal nerve - pure motor nerve

o Have patient stick out their tongue and look for deviation

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How to perform a somatic sensory exam for pain, temperature, and touch:

o Touch with eyes closed

o Sharp dull, symmetrical, etc.

o Used to assess cranial nerve 5

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What role does the cerebellum play?

o Controls voluntary movement and stability

o If a patient has damage to the cerebellum, they are a high fall risk

<p>o Controls voluntary movement and stability</p><p>o If a patient has damage to the cerebellum, they are a high fall risk</p>
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Lumbar Puncture:

- halo sign - indicates clear fluid is CSF

- Contraindications: suspected increased ICP, trauma, infection at site

- Pre: have patient void, assess for pain, explain procedure

- During: lateral recumbent position

- Post: monitor neuro status and VS, HA, nuchal rigidity

<p>- halo sign - indicates clear fluid is CSF</p><p>- Contraindications: suspected increased ICP, trauma, infection at site</p><p>- Pre: have patient void, assess for pain, explain procedure</p><p>- During: lateral recumbent position</p><p>- Post: monitor neuro status and VS, HA, nuchal rigidity</p>
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Tests for the nervous system: CT, CT angiography

o CT Scan: provides rapid images of the brain with or without contrast

- Ask about allergies to shellfish, iodine, or contrast dye before

o CT angiography: noninvasive image of the vascular system in the brain

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Tests for the nervous system: cerebral angiography

- catheter inserted into femoral artery into aortic arch into carotid, contrast inserted, radiographic images are taken as contrast flows through vessels

- Assess for stroke risk before procedure due to risk of thrombi dislodgement

- After, monitor every 15-30 min for first 2 hours, every hour for next 6 hours, and every 2 hours for next 24 hours. Maintain bedrest for 6 hours.

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Tests for the nervous system: electroencephalography, electromyography, electromyography, evoked potentials

o Electroencephalography: electrical activity in the brain is recorded via scalp electrodes

o Electromyography: electrical activity associated with innervation of skeletal muscle determined via needle electrodes

o Electroneurography: measures conduction velocity of peripheral nerves

o Evoked potentials: recordings of electrical activity of nerve conduction after a stimulus via electrodes placed on the scalp

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Definition of nystagmus:

o Eyes make repetitive, uncontrolled movements resulting in reduced vision and impaired coordination

o Monitor for in testing the 3rd cranial nerve

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Definition of normal tracking:

o Patient should look at and follow a target with their eyes as the tester moves horizontally, vertically, and rotates

o Track should be smooth and brisk

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Definition of convergence:

o Eye moves towards the midline of the face

o Tested through holding an object away from the face and bringing it towards the nose

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Definition of accommodation:

Adjustment of the optics (lens & pupil) of the eye to keep an object in focus at different distances from the eye

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What is the cerebrum?

o Frontal lobe - cognitive, behavior, memory, movement

o Temporal lobe - language

o Parietal lobe - special information, sensory

o Occipital lobe - vision

<p>o Frontal lobe - cognitive, behavior, memory, movement</p><p>o Temporal lobe - language</p><p>o Parietal lobe - special information, sensory</p><p>o Occipital lobe - vision</p>
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What factors influence cerebral blood flow?

o Autoregulated via adjustment in diameter of cerebral blood vessels

o Factors include CO2, O2, and blood pH

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Head injury assessment:

o LOC

o Glasgow Coma Scale (< 8 is very concerning)

o Cranial nerve testing

o Motor strength - push/pull, pronator drift (insert picture)

o Vital signs

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How to measure CPP:

o Cerebral perfusion pressure (CPP) = MAP - ICP

o Normal is 60-100

o If CPP is low, blood flow is low

<p>o Cerebral perfusion pressure (CPP) = MAP - ICP</p><p>o Normal is 60-100</p><p>o If CPP is low, blood flow is low</p>
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How to measure ICP:

o Normal ICP is 5-15 (elevated is > 20 sustained)

o Measured as a mean pressure via catheter and transducer (must be level)

o Can drain intermittently or continuously; ventricular can be controlled by nurse

o Immediately report ICP elevation

o Inaccurate readings caused by leaks, obstructions, unlevel system, air in system

<p>o Normal ICP is 5-15 (elevated is &gt; 20 sustained)</p><p>o Measured as a mean pressure via catheter and transducer (must be level)</p><p>o Can drain intermittently or continuously; ventricular can be controlled by nurse</p><p>o Immediately report ICP elevation</p><p>o Inaccurate readings caused by leaks, obstructions, unlevel system, air in system</p>
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What are signs of increased intracranial pressure?

o change in LOC

o change in VS – Cushing’s triad

o compression of CNII – ipsilateral pupil dilation, sluggish pupils, eyelid ptosis

o decrease in motor function – hemiplegia, posturing

o headache that is worse in the morning

o projectile vomiting not preceded by nausea

o Will eventually lead to herniation, death of the brainstem, and loss of respiratory function

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Decorticate Posturing:

o "coming to the core"

o Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities

o Interruption of the voluntary motor tracts in the cerebral cortex

<p>o "coming to the core"</p><p>o Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities</p><p>o Interruption of the voluntary motor tracts in the cerebral cortex</p>
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Decerebrate Posturing:

o Worse to see

o All 4 extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet

o Interruption of the motor fibers in the midbrain and brainstem

<p>o Worse to see</p><p>o All 4 extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet</p><p>o Interruption of the motor fibers in the midbrain and brainstem</p>
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Stages of increased ICP:

o Stage 1: total compensation

o Stage 2: decreased compensation, risk for increased ICP

o Stage 3: failing compensation, cushing's traid

o Stage 4: herniation & imminent death

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What is Cushing's Triad?

o Change in VS: systolic HTN w/ widening pulse pressure, bradycardia, irregular respirations

o Ominous sign before moving into stage 4

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Nursing considerations for patients with an increased ICP:

o No lumbar punctures! Can cause cerebral herniation

o Maintain PaO2 > 100

o Maintain PaCO2 35-45 (will likely need mechanical ventilation)

o Begin feeding within 3 days of injury due to hypermetabolic state - will need glucose

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Mannitol indication and therapeutic response:

o Indicated for cerebral edema or increased ICP

o ICP should decrease as fluid is removed

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What does hypertonic saline do for patients with an increased ICP?

o Moves water out of cells and into blood

o Monitor BP and serum sodium levels

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What is cerebral herniation? What causes it?

o when brain tissues move from one part of the brain to another adjacent part of the brain

o Inadequate cerebral perfusion -> Cerebral herniation

o Death is imminent

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What is the Glasgow Coma Scale and how do you use it?

o Describes the consciousness of patients through assessing eye-opening, motor function, and verbal responses

o Mild/normal = 13-15, moderate = 9-12, severe = 3-8

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Considerations for head & spine injuries (times of main concern, hallmark S/S, what should nurses be monitoring):

o Primary prevention is key

o Mortality increased immediately, 2hrs after, and 3 weeks after

o Hallmark S/S: raccoon eyes (periorbital edema), battle's sign (postauricular ecchymosis & otorrhea)

o Nurse should monitor LOC

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Acute care of head injuries:

o Maintain HOB > 30*

o Daily weights

o Monitor for DI or SIADH

o keep head midline, avoid neck flexion, avoid hip flexion

o restraints and sedatives to prevent self-injury

o Seizure precautions

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Complication of head injuries - epidural hematoma:

o bleeding between dura and inner surfaces of the brain

o present with unconsciousness, brief period of consciousness, then decreased LOC again w/ nausea and vomiting

o requires immediate surgery

<p>o bleeding between dura and inner surfaces of the brain</p><p>o present with unconsciousness, brief period of consciousness, then decreased LOC again w/ nausea and vomiting</p><p>o requires immediate surgery</p>
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Bacterial meningitis (causative agents, s/s, complications):

o Acute inflammation of the meningeal tissue caused by Streptococcus pneumoniae and Neisseria meningitidis – (NM requires droplet precautions)

o Bacterial is a medical emergency

o S/S: fever, severe HA, n/v, nuchal rigidity, photophobia, decreased LOC, seizures

o Complications: increased ICP, changes in vision, cerebral edema (seizures, CNII palsy, bradycardia, HTN, death)

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Nursing actions for a patient with meningitis:

o Offer cooling blankets for a fever

o Administer sedatives to prevent shivering

o Initiate seizure precautions; have O2 and suction in room

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Define subdural hematoma:

o Accumulation of blood on the surface of the brain

o Often after a head injury

<p>o Accumulation of blood on the surface of the brain</p><p>o Often after a head injury</p>
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Define brain death:

o Function of the cerebral cortex of the brainstem is used to declare brain death as it controls respiratory, vasomotor, and cardiac functions

o If there is no electrical functioning in the brainstem, the patient is considered brain dead

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Directions of injury for the spine:

o Flexion – chin to chest

o Hyperextension – head pushed too far back

o Extension-rotation

o Compression – spine is compressed leading to vertebrae being crushed

o Flexion-rotation - most unstable because ligaments that stabilize the spine are torn; most often contributes to severe neurologic deficits

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Damage to anterior vs posterior spine:

o Damage to anterior spine - motor deficits

o Damage to posterior spine - sensory deficits

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Immediate care of SCI:

o Maintain airway

o Place patient in C-collar

o Permissive HTN: increases SBP is higher intentionally to ensure good blood flow to the cord; maintain SBP >90 and MAP >85

o Watch for increased medication interactions due to altered drug metabolism

o Encourage surgery within 24 hours

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Primary injury SCI:

Initial mechanical disruption of axons as a result of stretch or laceration

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Secondary injury SCI:

o Ongoing, progressive damage that occurs from inflammation after the initial injury

o Vessels dilate -> increased blood flow to spinal column -> increased pressure -> further damage

o Apoptosis occurs for weeks after the injury and may cause post-injury demyelination leading to scar tissue formation and neuro deficit

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Skeletal vs neuro levels of injury:

o Skeletal level of injury is main point at which the most vertebrae have sustained damage - includes cervical, thoracic, lumbar & sacral

- Cervical & lumbar most common

o Neurologic level is the lowest segment of the spinal cord that is fully intact. The level of injury may be cervical, thoracic, lumbar, or sacral.

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Complete vs Incomplete injury:

o Complete: total loss of sensory and motor function below level of injury

o Incomplete: mixed loss of voluntary motor activity and sensation; some tracts intact

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Incomplete SCI - Central cord syndrome:

o Commonly seen in cervical region

o Common in older adults

o Leads to motor weakness and sensory loss w/ dysesthesia pain in UEs

<p>o Commonly seen in cervical region</p><p>o Common in older adults</p><p>o Leads to motor weakness and sensory loss w/ dysesthesia pain in UEs</p>
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Incomplete SCI - anterior cord syndrome:

o Anterior spinal artery is damaged -> decreased blood flow

o Results from flexion injury

o Leads to motor paralysis and loss of sensation below injury

<p>o Anterior spinal artery is damaged -&gt; decreased blood flow</p><p>o Results from flexion injury</p><p>o Leads to motor paralysis and loss of sensation below injury</p>
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Incomplete SCI - Brown-Séquard Syndrome

o Occurs from penetrating injury

o Ipsilateral loss of motor function from injury

o contralateral loss of pain and temperature sensation from injury

<p>o Occurs from penetrating injury</p><p>o Ipsilateral loss of motor function from injury</p><p>o contralateral loss of pain and temperature sensation from injury</p>
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Conus Medullaris Syndrome:

o Damage to lowest portion of the spinal cord

o Motor function can be preserved, weak, or flaccid

o Decrease in sensation and function in the perianal area

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Cauda Equina Syndrome:

o Asymmetrical distal weakness w/ flaccid paralysis of Les

o Loss of sensation in saddle area

o Areflexic bladder and bowel

o Severe pain

<p>o Asymmetrical distal weakness w/ flaccid paralysis of Les</p><p>o Loss of sensation in saddle area</p><p>o Areflexic bladder and bowel</p><p>o Severe pain</p>
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Timeline for SCI:

o Within 24 hours, permanent damage may occur because of edema

o Extent of damage and prognosis for recovery most accurately determined 72 hours or more after injury

o Greatest improvement occurs in first 3 to 6 months following injury

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Spinal shock:

o s/s: decreased reflex, loss of sensation, absent thermoregulation, flaccid paralysis below level of injury

o lasts days to weeks

o may mask post-injury neuro function

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What is neurogenic shock?

o s/s: hypotension, bradycardia, peripheral vasodilation, lowered cardiac output

o generally seen with T6 or higher injuries leading to uninhibited PNS

o treat with norepinephrine to supplement SNS depression

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Discuss findings of spinal cord injury at C5 & what functioning the patient will have intact:

o Partial paralysis of the hands and arms as well as the lower body

o Potential quadriplegia

o Bowel and bladder flaccidity

o Diaphragmatic breathing & respiratory insufficiency

o May need help managing secretions

o SNS dysfunction - neurogenic shock

o Poikilothermism - inability to sweat or shiver below level of injury (common with high cervical injuries)

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Discuss findings of spinal cord injury at C8 & what functioning the patient will have intact:

o Damage to nerves between C7 and T1

o Potential quadriplegia

o Bowel and bladder flaccidity

o More function in hands & arms

o SNS dysfunction - neurogenic shock

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Discuss findings of spinal cord injury at T1 & what functioning the patient will have intact:

o Partial or full paralysis of the lower part of the body

o SNS dysfunction - neurogenic shock

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Discuss findings of spinal cord injury at T10 & what functioning the patient will have intact:

Partial or full paralysis of the lower part of the body

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What is the highest injury that you can expect a patient to have full function of their UEs?

T6

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Autonomic dysreflexia:

o Seen in patients with injuries higher than T6

o Massive uncompensated cardiovascular reaction mediated by sympathetic nervous system

o SNS responds to stimulation of sensory receptors - parasympathetic nervous system unable to counteract these responses.

o S/S: HTN, bradycardia, throbbing headache, flushing above point of injury

o MEASURE PAITENT BP WHEN COMPLAINING OF HEADACHE

o Elevate HOB to 45*, notify HCP, assess for & remove stimulus, treat BP

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Care of neurogenic bowel:

o Bowel program started during acute care

o Daily rectal stimulant @ regular time or manual evacuation

o NG suctioning (monitor for metabolic alkalosis - monitor sodium & potassium)

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Care of the neurogenic bladder:

o Bladder dysfunction due to absent or decreased bladder innervation

o Acute Phase: urinary retention -> insert foley

o Post-Acute Phase: failure to store urine -> straight cath regimen

o Straight Cath regimen:

- 4-6x/day (Q4HRS)

- Keep urine residuals < 500mL

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Care of traction pin site:

o Cleansing with ½ strength peroxide and normal saline twice a day

o Applying antibiotic ointment

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Leading cause of death to SCI patients:

pulmonary embolism

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A patient presents with back pain that worsens with activity. What condition does the nurse connect this symptom to?

spinal cord tumor