Neurologic Problems and Traumatic Brain Injury Exam Review, Exams of Health sciences

Download Neurologic Problems and Traumatic Brain Injury Exam Review and more Exams Health sciences in PDF only on Docsity! Exam 3 Review FINAL. 45: NEUROLOGIC PROBLEMS MONITORING FOR INCREASED INTRACRANIAL PRESSURE • Most at risk for increased ICP resulting from edema during the first 72 hr. after onset of a stroke • May have worsening neuro changes starting within 24-48 after their endovascular procedure from increased ICP • Assess these pt. Q 1-4 hr. CHART 45-6 KEY FEATURES • Decreased LOC (lethargy to coma) • Behavior changes: restlessness, irritability, and confusion • HA • N/V (may be projectile) • Change in speech pattern/slurred speech: o Aphasia • Change in sensorimotor status: o Pupillary changes: dilated and nonreactive (“brown pupils”) or constricted and nonreactive o Cranial nerve dysfunction o Ataxia • Seizures (usually within first 24 hr. after stroke) • Cushing’s triad: o Severe HTN o Widened pulse pressure o Bradycardia • Abnormal posturing: o Decerebrate o Decorticate >> INTERVENTIONS • For increased ICP experiencing a stroke: o Elevate HOB – sitting them up is very important o O2 therapy (for O2 < 94%) o Maintain head in midline, neutral position – promotes venous drainage from the brain Exam 3 Review FINAL. o Avoid sudden and acute hip or neck flexion during positioning o Avoid the clustering of RN procedures – can elevate ICP even more ▪ Not for neuro pt. o Hyperoxygenate before and after suctioning o Provide airway management to prevent unnecessary suctioning and coughing that can increase ICP o Maintain quiet environment if pt. has a HA o Keep the room lights low to accommodate and photophobia o MT BP, heart rhythm, O2 sat, blood glucose, and body temp to prevent secondary brain injury and promote positive outcomes after stroke ▪ MD usually like BP to be slightly elevated after a stroke (SBP = 140-150) • CRITICAL RESCUE!! – Be alert for S/S of increased ICP in the head injury and report any neuro deterioration to the MD or Rapid Response Team immediately! o The 1st sign of increased ICP is a declining LOC Exam 3 Review FINAL. injury or arise later from vessel damage Exam 3 Review FINAL. • All hematomas are potentially life threatening because they act as space- occupying lesions and are surrounded by edema • 3 types of hemorrhage: o Epidural hematoma: arterial bleeding into the space between the dura and inner skull. ▪ Caused by a fracture of the temporal lobe ▪ “lucid intervals” awake and talking and a momentary moment of unconsciousness o Subdural hematoma (SDH): venous bleeding into the space beneath the dura and above the arachnoid ▪ From a tearing of the bridging veins and within the cerebral hemispheres or from a laceration of brain tissue ▪ Bleeding from this occurs more slowly than from an epidural hematoma ▪ Acute – presents within 48 hr. ▪ Subacute – between 48 hr. and 2 weeks ▪ Chronic – from 2 weeks to several months o Traumatic intracerebral hemorrhage (ICH): the accumulation of blood within the brain tissue caused by the tearing of small arteries and veins in the subcortical white matter ▪ From a blow to the back of the head or fractures > BRAIN HERNIATION • In the presence of increased ICP, the brain tissue may shift and herniate downward, trying to go thru the foramen magnum • S/S o Cheyne-Stokes respirations o Pinpoint o nonreactive pupils o potentially hemodynamic instability • Any of these S/S are life-threatening and you must call the MD immediately! ETIOLOGY • Most common causes of TBI are falls and motor vehicle accidents • Alcohol and drugs are a significant contributing factor • Summer and spring months, evenings, nights, and weekends have the greatest number of injuries • More common in males than females Exam 3 Review FINAL. >>> COLLABORATIVE CARE >>> ASSESSMENT > HISTORY • May be hard to obtain a hx. from the pt. due to amnesia from injuries o May be obtained from first responders or witnesses in this case • Did the pt. lose consciousness? For how long? • Differentiate confusion from head trauma and intoxication • Determine whether the pt. had fluctuating consciousness or seizure activity and whether there is a hx. of a seizure disorder. > PHYSICAL ASSESSMENT • Assess for: o S/S of increased ICP, hypotension, hypoxemia, hypercarbia (PaCO2 > 40-45), or hypocarbia (PaCO2 < 40-45) o Hypercarbia can contribute to ICP o Hypocarbia is caused by hyperventilation and can lead to vasoconstriction resulting in ischemia o EtCO2 or a capnography is used to detect CO2 levels in intubated pt. TABLE 45-4 DIFFERENCES AMONG MILD, MODERTE, AND SEVERE TBI’S TYPE CAUSED BY S/S MILD (MTBI) -- concussion ▪A blow to the head, transient confusion or feeling dazed or disoriented and 1 or more of these conditions: (1) Loss of consciousness for up to 30 min. (2) loss of memory for events immediately before or after the accident (3) focal neuro deficits that may or not be transient ▪LOC does not have to occur for a person to be dx. w/ MTBI ▪No evidence of brain damage on a CT or MRI imaging scan ▪HA ▪Dizziness ▪ Changes in behavior ▪Usually resolve within 72 hr. ▪ Lasting longer than 72 hr. Is considered “post-concussion syndrome” MODERATE ▪A period of LOC for 30 min. – 6 hr. and a GCS score of 9 – 12. ▪Often but not always, focal or diffuse brain injury can be seen with a dx. CT or MRI scan ▪Post-traumatic amnesia may last up to 24 hr. may occur with either closed or open brain injury ▪ Short acute or critical care stay may be needed to prevent secondary injury from brain edema, intracranial bleeding, or inadequate cerebral perfusion 10 Exam 3 Review FINAL. o Atropine causes fixed/dilated pupils • Late S/S of increased LOC: o Severe HA o Nausea o Vomiting (often projectile) o seizures • pt. with a brain injury is at risk for potentially devastating ICP elevations during the first hours after the event and up to 3-4 days after injury when cerebral edema can occur. • Assess for bilateral motor responses • The pt. motor loss or dysfunction usually appears contralateral (opposite side) to the site of the lesion • S/S of brainstem or cerebellar injury: o Ataxia (loss of balance) o Decreased or increased muscle tone o Weakness • Assess ears and nose for any signs of CSP leaks o Fluids are sent to the lab to be tested for glucose and electrolyte content • CSF placed on a white absorbent paper or linen can be distinguished from other fluids by the “halo” sign, a clear or yellowish ring surrounding a spot of blood • Raccoon’s eyes can mean a fracture of the skulls base > PSYCHOSOCIAL ASSESSMENT • Pt. may have personality changes after a TBI • May have memory loss or altered ability to communicate and understand language > LABS • No serum test to dx. a primary brain injury • Detection of the protein S-100B in serum may indicate some kind of injury to the brain > IMAGINING ASSESSMENT • CT • MRI • Functional MRI >>> ANALYSIS • Top problems for TBI o 1. Decreased cerebral tissue perfusion o 2. Decreased memory, sensation, and mobility 11 Exam 3 Review FINAL. >>> INTERVENTIONS > MAINTAINING CEREBRAL TISSUE PERFUSION GOAL: maintain adequate cerebral tissue perfusion with no evidence of secondary brain injury from cerebral edema and increased ICP • Cerebral perfusion is not usually affected by a mild TBI INTERVENTIONS: • Nonsurgical – o PRIORITY = ABC’s and then preventing secondary injury o Interventions are directed towards preventing or detecting secondary brain injury or the conditions that contribute to secondary brain injury such as: ▪ increased ICP ▪ promoting fluid and electrolyte balance ▪ monitoring the effects of treatments and drug therapy o Health teaching o Emotional support o VS 1-2 hr. o Report dysrhythmias, hypotension, and hypertension to the MD o Therapeutic hypothermia may be started, regardless of the presence of fever ▪ This is to rapidly cool the pt. to a core temp of 89.6*F and 93.2*F for 24- 48 hr. after the primary injury – this stops dead tissue from dying ▪ Rewarming must be done carefully, doing it too rapidly can cause cardiac dysrhythmias ▪ Goal = to reduce brain metabolism and prevent the cascade of molecular and biochemical events that contribute to secondary brain injury in moderate-to-severe TBI o Check ABG’s o Hyperventilation for the intubated pt. during the first 24 hr. after brain injury is usually avoided because it may produce ischemia by causing cerebral vasoconstriction o CO2 is a very potent vasodilator that can contribute to increases in ICP o Prevent intermittent and sustained hypoxemia o PaO2 levels are maintained between 80-100 to prevent secondary injury o If the pt. is intubated, provide 100% O2 before and after each pass of the endotracheal suction catheter. o Lidocaine given IV or endotracheally may be used to suppress the cough reflex; coughing increases ICP 12 Exam 3 Review FINAL. o ACTION ALERT!! – position the TBI pt. to avoid extreme flexion or extension of the neck and to maintain the head in the midline, neutral position ▪ Log roll when positioning ▪ HOB elevated at least 30* -- prevents aspiration • Unless this negatively affects the pt. – elevated BP • Avoid sudden elevation of HOB • DETERMINING BRAIN DEATH o Before brain death is declared, determine if the pt. consented to be an organ donor. o 4 things that must be met to establish brain death: ▪ 1. Coma of known cause ▪ 2. Normal or near normal core body temp (higher than 96.8*F) ▪ Normal SBP (higher than 100) ▪ At least one neuro exam • DRUG THERAPY o Mannitol (Osmitrol) – an osmotic diuretic ▪ Often used to treat cerebral edema by pulling water out of the extracellular space of the edematous brain tissue (reduces ICP) ▪ Most effective as a bolus (thru a filtered needle) rather than continuous infusion ▪ Furosemide (Lasix) – loop diuretic • Often given in adjunctive with Mannitol to reduce rebound effect and enhance the therapeutic action ▪ MT I/O’s, for severe dehydration, and indications for acute renal failure ▪ Measure electrolyte and osmolarity levels Q6H o Opioids (Morphine sulfate or fentanyl) – used for ventilated pt. to decrease agitation and restlessness > MAINTAINING COGNITION, SENSORY PERCEPTION, AND MOBILITY GOAL: to not have decreased memory, sensation, and mobility INTERVENTIONS: • Cognitive rehab: helps pt. regain function in areas that are essential for a return to independence and a good quality of life • Always introduce yourself before pt. interaction • Keep explanations short and simple and give them right before or during interactions • Have the family bring familiar objects into the hospital • Pt. with brain injuries often lose their sense of smell 15 Exam 3 Review FINAL. o Loss of balance or dizziness (ataxia) o Weakness or paralysis in one part or one side of the body (hemiparesis or hemiplegia) o Difficulty thinking, speaking, or articulating words o Changes in cognition, mentation, or personality o Papilledema (swelling of the optic disc), indicating increased ICP • CHART 45-10 COMMON BRAIN TUMOR S/S CEREBRAL TUMORS BRAINSTEM TUMORS •Headache (most common) •Seizures •Vomiting unrelated to food intake •Changes in vision •Hemiparesis or hemiplegia •Hypokinesia (decreased motor ability) •Hyperesthesia, paresthesia, decreased tactile discrimination •Aphasia •Changes in personality or behavior •Hearing loss (acoustic neuroma) • Facial pain and weakness •Dysphagia, decreased gag reflex •Nystagmus •Hoarseness •Ataxia and dysarthria (cerebellar tumors) •Apnea •Bradycardia • hypotension >>> INTERVENTIONS • depend on the type, size, and location of the tumor > SURGICAL MANAGEMENT • Craniotomy: incision into the cranium to remove the tumor, improve S/S related to the lesion, or decrease the tumor size o Goal is to remove the tumor as much as possible w/o damaging normal tissue PRE-OP • No alcohol, NSAIDS, tobacco, or anticoagulants for the last 5 days before sx. o Some surgeons may require a week or longer • NPO for at least 8 hr. POST-OP • FOCUS = MT the pt. for changes in status and prevent complications, especially increased ICP • ACTION ALERT!! – assess neuro and VS Q15-30min. for the first 4-6 hr. after a craniotomy and then every hour. o If stable for 24 hr. checks are reduced to every 2-4 hr. 16 Exam 3 Review FINAL. o Report immediately if the pt. has a decreased LOC, motor weakness, or paralysis, aphasia, decreased sensation, and sluggish pupil reaction to light. Personality changes (agitation, aggression, or passivity) can indicate worsening neuro status. IMMEDIATE POST-OP CARE • Periorbital (around the eyes) edema and ecchymosis is not unusual and are treated with a cold compress to decrease the swelling – normal finding • Irrigate the affected eye with warm saline or artificial tears to improve pt. comfort • Continuous heart MT • Regardless of setting, ensure recording of the pt. intake and output for the first 24 hr. • Fluid restrictions of 1500 mL daily if pituitary is involved and SIADH develops • Repositioning and deep breathing Q2H • VTE precautions • Supratentorial - elevate the HOB 30*, position to avoid extreme hip or neck flexion, maintain head midline to prevent increased ICP • Infratentorial (brainstem) – lay flat or at 10*, side lying and alternating sides Q2H for 24- 48 hr. or until ambulatory, and remains NPO until awake and alert • Check the head dressing Q1-2H for signs of drainage o Small or moderate amount is expected • May have a Hemovac or Jackson-Pratt drain in place for 24-72 hr. after sx. o Measure the drainage Q8H and record the amount and color (normal = 30- 50 mL every 8 hr.) • CRITICAL RESCUE!! – after craniotomy, MT the dressing for excessive amounts of drainage. Report a saturated head dressing or drainage greater than 50 mL/8hr immediately to the surgeon! MT frequently for S/S of increased ICP. • Labs MT: o CBC o Electrolytes o Osmolarity o Coagulation o HCT and Hgb – may be low from blood loss during sx. or diluted from large amounts of IV fluids given during sx., or elevated if the blood was replaced. • Hyponatremia may occur as a result of fluid volume overload, syndrome of inappropriate antidiuretic hormone (SIADH), or steroid administration. • Hypokalemia may cause cardiac irritability • Hypernatremia = muscle weakness, restlessness, extreme thirst, and dry mouth. o Untreated can lead to seizures. 17 Exam 3 Review FINAL. • DI should be considered if the pt. voids large amounts of very dilute urine with an increasing serum osmolarity and electrolyte concentration • May be mechanically ventilated for the first 24-48 hr. after sx. • Suction when necessary o Remember to Hyperoxygenate before, during, and after suctioning. • Glucocorticoids (dexamethasone/Decadron) – reduces cerebral edema • Antibiotics are given for several days after sx. PREVENTING AND MANAGING POST-OP COMPLICATIONS • Main complication of supratentorial sx. is increased ICP from cerebral edema or hydrocephalus and hemorrhage. • S/S of increased ICP: o Severe HA o Deteriorating LOC o Restlessness o Irritability o Dilated or pinpoint pupils that are slow to react or nonreactive to light – late sign • Hydrocephalus (increased CSF in the brain)—caused by the obstruction of the normal CSF pathway from edema o Rapidly progressive – same S/S as increased ICP o Slowly progressive – HA, decreased LOC, irritability, blurred vision, urinary incontinence o Intraventricular catheter (ventriculostomy) may be placed to drain CSF during sx. or right after sx. o For log-term treatment – surgical shunt is inserted to drain CSF to another area of the body • Subdural and epidural hematomas S/S: o Severe HA o Rapid decreased LOC o Progressive neuro deficits o Herniation syndromes o Treatment = osmotic diuretics and ICP monitoring • Respiratory complications: o Atelectasis and pneumonia – prevent by turning and deep breathing every hour, incentive spirometer, and humidified air ▪ Suctioning may be helpful but can increased ICP • Wound infection: 20 Exam 3 Review FINAL. MENINGITIS >>> PATHO • An inflammation of the meninges of the brain and spinal cord, specifically the pia mater and arachnoid. • Bacterial and viral organisms are most often responsible for meningitis. • The organisms enter the CNS via the bloodstream or are directly introduced into the CNS o Direct routes – penetrating trauma, surgical procedures on the brain or spine, or a ruptured brain abscess • Pt. with an infection in the head or neck/throat has an increased risk for meningitis • Infections linked to meningitis include: o Otitis media o Acute or chronic sinusitis o Tooth abscess o Tongue piercing infection -- rare • The infecting organism may spread to both cranial and spinal nerves, causing irreversible neuro damage. • Increased ICP may occur due to the blockage of the flow of CSF, change in cerebral blood flow, or thrombus (blood clot) formation VIRAL MENINGITIS • Most common type • “aseptic meningitis” • Common viral organisms: o Enterovirus o Herpes simplex virus-2 (HSV-2) o Varicella zoster virus (VZV) – the chicken pox and shingles o Mumps virus o HIV • Treatment = antiviral agents 21 Exam 3 Review FINAL. BACTERIAL MENINGITIS 22 Exam 3 Review FINAL. • Most common is Streptococcus pneumoniae and meningococcal meningitis • Meningococcal meningitis is a medical emergency with a high mortality rate, often within 24 hr. o Highly contagious o Outbreaks of this are most likely to occur in areas of high population density, such as college dorms, military barracks, and crowded living areas >>> COLLABORATIVE CARE >>> ASSESSMENT • Do a complete neuro and neurovascular assessment • Assess for complications such as increased ICP o If left untreated, can lead to herniation of the brain and death. • Seizure activity may occur when meningeal inflammation spreads to the cerebral cortex • Inflammation can also result in abnormal stimulation of the hypothalamic area where excessive amounts of antidiuretic hormone (ADH) (vasopressin) are produced. o Excess vasopressin results in water retention decreased sodium o SIADH may lead to further increases in ICP • SIRS (systemic inflammatory response syndrome): a reaction to either endotoxin produced by infecting bacteria or activation of the immune cells by infecting organisms, can cause a rapidly falling BP and tachycardia. CHART 42-11 KEY FEATURES OF MENINGITIS • Decreased of change in LOC, confusion • Disoriented to person, place, year • Pupil reaction and eye movement: o Photophobia o Nystagmus o Abnormal eye movements • Motor response: o Normal early in disease process o Hemiparesis, hemiplegia, and decreased muscle tone possible late o Cranial nerve dysfunction • Memory changes: o Attention span (usually short) o Personality and behavior changes o Bewilderment 23 Exam 3 Review FINAL. ▪ Pt. should wear mask when outside of their room ▪ Teach visitors about these precautions ENCEPHALITIS >>> PATHO 24 Exam 3 Review FINAL. • Is an inflammation and infection of the brain tissue and often the surrounding meninges. • Usually a viral infection but can be bacteria, fungi, or parasites. • The virus travels to the CNS via the bloodstream • Viral encephalitis can be life threatening or lead to persistent neuro problems such as learning disabilities, epilepsy, memory deficits, or fine motor deficits. • After the virus invades the brain tissue, it begins to reproduce, causing an inflammatory response o Unlike in meningitis, this inflammation does not cause exudate (pus) formation o Demyelination of axons and destruction of white matter occurs. o This destruction leads to hemorrhage, edema, necrosis (cell death), and the development of small lacunae (hollow cavities) within the cerebral hemispheres. o Widespread edema can cause compression of blood vessels, leading to further increased ICP. ▪ Death may occur from herniation and increased ICP • Arboviruses – transmitted to humans thru the bite of an infected mosquito or tick o Most common = Eastern or Western equine encephalitis, St. Louis encephalitis, California encephalitis, and West Nile virus. • West Nile virus – o Infection is usually mild, and pt. is usually asymptomatic ▪ May have mild flu-like S/S – fever, body aches, N/V o Small percentage may develop serious disease ▪ S/S severe HA, high fever, decreased LOC, tremors, vision loss, seizures, muscle weakness or paralysis ▪ May last for several weeks and neuro deficits may be permanent o The incubation period is 2-15 days after being bitten by an infected mosquito o Other sources are blood products, breast milk, or an organ transplant >>> COLLABORATIVE CARE >>> ASSESSMENT • The typical pt. with encephalitis has high fever, and reports N/V, and a stiff neck. (flulike illness) • Assess for other S/S including: 25 Exam 3 Review FINAL. o Changes in mental status (agitation) o Motor dysfunction (dysphagia – difficulty swallowing) o Focal (specific) neuro deficits o Photophobia and phonophobia (noise sensitivity) o Fatigue o S/S of increased ICP (decreased LOC) o Joint pain o HA o Vertigo • Assess LOC using the Glasgow Coma Scale • Mental status changes are more severe in encephalitis than in meningitis o Changes include acute confusion, irritability, and personality and behavior changes • CRITICAL RESCUE!! – in severe cases of encephalitis, pt. may have increased ICP from cerebral edema, hemorrhage, and necrosis of brain tissue. Changes in VS that require an immediate notification of the MD are widened pulse pressure, new bradycardia, and irregular resp. effort. Pupils that become increasingly dilated and less responsive to light are also communicated urgently. Left untreated, increased ICP leads to herniation of the brain tissue and possibly death. > DIAGNOSTICS • Lumbar puncture (LP) is done to analyze the CSF for the specific offending organism. • Electroencephalogram is done to evaluate brain wave activity to detect seizures • CT scan (with or without contrast) to evaluate increased ICP >>> INTERVENTIONS • CHART 42-13 PROTECTING FROM WEST NILE VIRUS o Limit your time outside between dusk and dawn when mosquitos are out o Wear protective clothing, including long sleeves and pants o Use an insect repellant containing DEET when outdoors o Remove areas of standing water from flowerpots, trash cans, and rain gutters o Check windows and door screens for holes that need repair o Keep hot tubes and pools clean and properly chlorinated o Do not swim in lakes or ponds that are not designated for swimming • There is no curative treatment for West Nile viral encephalitis • Acyclovir (Zovirax) – antiviral drug of choice for treatment of herpes encephalitis and is associated with a significantly lower mortality rate than vidarabine (Vira-A) 28 Exam 3 Review FINAL. • Use SBAR when getting pt. from ER nurse >>> PHYSICAL ASSESSMENT • Airway, breathing pattern, circulation is PRIORITY!! • Pt. with a cervical SCI is at high risk for resp. compromise because the cervical spinal nerves control the diaphragm • Pulse, BP, and peripheral perfusion (pulse strength and cap refill) • Indications of intra-abdominal hemorrhage, or hemorrhage/bleeding around fracture sites • Level of consciousness: Glasgow Coma Scale (GCS) • Spinal shock (spinal shock syndrome) – occurs immediately as the cord’s response to the injury. o The pt. has complete but temporary loss of motor, sensory, reflex, and autonomic function that often lasts less than 48 hr. but may continue for several weeks o Spinal shock is NOT the same as neurogenic shock • Level of injury: o Tetraplegia – (Quadriplegia- paralysis or Quadriparesis- weakness) of all 4 extremities ▪ Seen with cervical cord and upper thoracic injury o Paraplegia- paralysis of the legs 29 Exam 3 Review FINAL. o Paraparesis – weakness of the legs SPINAL SHOCK! – (spinal shock syndrome) occurs immediately as the cord’s response to the injury. Pt. has complete but temporary loss of function that usually lasts less than 48 hours but may continue for several weeks. Spinal shock is NOT the same as neurogenic shock. > NEUROLOGIC SYSTEM • Hypoesthesia: decreased sensation • Hyperesthesia: increased sensation > CARDIOVASCULAR SYSTEM • If injury is above the 6th thoracic vertebra • Bradycardia, hypotension, hypothermia occurs because of loss of sympathetic input which may lead to dysrhythmias • Systolic BP below 90 requires emergency attention, lack of oxygen to spinal cord could worsen condition > RESPIRATORY SYSTEM • Breathing problems due to issues with respiratory muscles • Pulse oximetry every 8-12 hr. • O2 sat at 92 or less with adventitious breath sounds may indicate complications (pneumonia, atelectasis) > GI SYSTEM Autonomic dysreflexia (AD): “autonomic hyperreflexia” involuntary nervous system overreacts to external or bodily stimuli. (potentially life-threatening, TREAT ASAP TO PREVENT A HYPERTENSIVE STROKE) – occurs after spinal shock • Risk factors = o Bladder distention o UTI o Epididymitis or scrotal compression o Bowel distention or impaction from constipation o Irritation of hemorrhoids • Triggered by sustained stimuli at T-6 or below from: o Restrictive clothing o Full bladder, constipation, or UTI – most common o Pressure Areas o Fecal Impaction 30 Exam 3 Review FINAL. o Pain – from sharp objects, tight clothing, hot temperatures • S/S: o Severe HTN o Bradycardia o Severe headache o Nasal stuffiness o Flushing above level of lesion, pale below level o Heavy sweating above level of lesion o Goosebumps o Blurred vision or spots in vision • CHART 43-2 KEY FEATURES – AUTONOMIC DYSREFLEXIA o Sudden, significant rise in SPB and DBP accompanied by bradycardia ▪ Severe HTN is a hallmark sign!! o Profuse sweating above the level of lesion – especially in the face, neck, and shoulders; rarely occurs below the level of the lesion because of sympathetic cholinergic activity. o Goose bumps above or possibly below the level of the lesion o Flushing of the skin above the level of the lesion – especially in the face, neck, and shoulders o Blurred vision o Spots in the pt. visual field o Nasal congestion o Onset of severe, throbbing HA o Flushing about the level of the lesion with pale skin below the level of the lesion o Feeling of apprehension • Treatments o Dopamine (Dextran) – for hypotension o Atropine – for brady cardia 33 Exam 3 Review FINAL. o Dopamine – severe hypotension • Atropine sulfate – treats bradycardia below 50-60 • AD is a neurologic emergency and must be promptly treated to prevent a hypertensive stroke! • Measures to help prevent AD: o Prevent bladder and bowel distention o Manage pain and room temp o MT for early VS changes CRITICAL RESCUE! – (Neurogenic Shock) MT acute spinal cord injury at least Q1H and notify MD IMMEDIATELY if: - Pulse ox < 95% - Aspiration – intubation or bronchial endoscopy o Stridor, garbled speech, or inability to clear airway - Symptomatic bradycardia w/ ↓ LOC and ↓ urine output - Hypotension w/ systolic < 90 or MAP < 65 - If BP get too high = stroke Treatment: - Fluids - Vasopressor IV therapy - Supportive care CRITICAL RESCUE! – (AD) RN intervention: - Raise HOB immediately to help reduce BP (PRIORITY!) - Call MD for BP reducing meds - Determine the cause of AD and treat promptly o Make sure cath has no kinks o If bladder is distended = cath pt o Check room temp and blankets = adjust to comfortable for pt. o Check for UTI S/S o Check for fecal impaction o Check for pressure injuries o MT BP Q10-15min o Give nifedipine or nitrate to lower BP 34 Exam 3 Review FINAL. • CHART 43-3 AUTONOMIC DYSREFLEXIA – IMMEDIATE INTERVENTIONS o Place pt. in a sitting position (FIRST PRIORITY!), or return to a previous safe position o Notify the MD or rapid response team o Assess for and treat the causes: ▪ Check for urinary retention or cath. Blockage • Check the urinary cath tubing (if present) for kinks or obstructions ▪ If a urinary cath. Is not present, check for bladder distention and catheterize immediately if indicated: • Consider using anesthetic ointment on tip of cath before insertion to reduce urethral irritation o Determine if a urinary cath infection or bladder calculi (stones) are contributing to genitourinary irritation o Check the pt. for fecal impaction or other colorectal irritation, using anesthetic ointment at rectum. Disimpact if needed o Examine skin for new or worsening pressure injuries o MT BP every 10-15 min. o Give nifedipine or nitrate to lower BP as needed o Pt. with recurring AD may get an alpha blocker prophylactically >>> PREVENTING SECONDARY INJURY • Goal: adequate spinal cord stabilization • Priority is to immobilize the fracture (stabilize spine) to prevent further damage • Assess neurologic status, VS, pulse ox, and altered comfort Q1-4H • Carefully document changes in motor and sensory function • Keep spine in proper alignment while healing • Must have order to remove neck brace o Remove with another RN holding head once a day to check for skin breakdown • For airway intervention – jaw thrust maneuver over a head tilt • Log rolling when moving pt to side to keep head aligned • Halo fixator: most commonly used device for immobilization of the cervical spine. o Worn for 8-12 weeks o Affixed by 4 pins or screws into the outer aspect of the skull o NEVER turn pt. by holding or pulling on halo o Do not adjust the crews holding it in place o Check skin frequently to ensure no breakdown 35 Exam 3 Review FINAL. o 1 finger between jacket and skin o MT neuro status for changes in movement or decreased strength o Special wrench available if needed to remove in an emergency o Tape wrench to vest o Do not use sharp objects (wire hanger) to relieve itching o Keep pin site clean with saline and Vaseline dressings o MT VS for sings of infection o PT TEACHING: ▪ Be careful when leaning forward or backward ▪ Wear loose clothing with Velcro instead of buttons ▪ Bathe in bathtub of sponge bath ▪ Wash under vest and use powders and lotions sparingly ▪ Change liner if it starts to stink ▪ Support head with small pillow when sleeping ▪ Keep as active as possible but avoid contact sports or swimming ▪ Do NOT drive ▪ Use straws to drink ▪ Cut food into small bites ▪ Wrap pins in cloth when going out in cold temps ▪ Clean pin sites as instructed by MD ▪ Observe pin site daily for S/S of infection ▪ increase fluids and fiber to prevent constipation ▪ Use comfortable position during sex ▪ Keep wrench on chest > DRUG THERAPY • Tizanidine – muscle relaxer o May cause severe drowsiness and sedation • Intrathecal baclofen (ITB) (Lioresal) – implantable infusion pump or intrathecal cath o AE – sedation, fatigue, dizziness, changes in mental status o If suddenly withdrawn seizures and hallucinations may occur • Celecoxib (Celebrex) – prevents or treats heterotopic ossification (bony overgrowth) o AE – risk of myocardial infarction and stroke • Calcium and bisphosphonates – helps prevent osteoporosis from lack of weight bearing activities o Continues exercises if possible, to help prevent this 38 Exam 3 Review FINAL. 1. (43-2) A pt. who sustained a recent cervical spinal cord injury reports feeling flushed. The pt. BP is 180/100. What is the RN best action at this time? a. Perform a bladder assessment b. Insert an indwelling urinary cath. c. Turn on a fan to cool the pt. d. Place the pt. in a sitting position 2. (43-3) A RN is caring for a pt. who has a hard cervical collar for a complete cervical spinal cord injury. Which assessment finding will the RN report to the MD? a. Purulent drainage from the pin sites on the pt. forehead b. Painful pressure injury under the collar c. Inability to move legs or feet d. Oxygen sat of 95% on room air 44: PROBLEMS OF THE PERIPHERAL NERVOUS SYSTEM 39 Exam 3 Review FINAL. GUILLAIN-BARRE SYNDROME (GBS) >>> PATHO • An acute inflammatory disorder that affects the axons and/or myelin of the PNS causing impaired mobility and sensory perception as a result of altered immunity • Uncommon disorder affecting males slightly more than females • May be referred to as “acute idiopathic polyneuritis, acute inflammatory demyelinating polyneuropathy (AIDP)” • In demyelination GBS, symptoms typically begin in the legs and spread to the arms and upper body. o Ascending paralysis o Paralysis can increase in intensity until the muscles cannot be used at all and the pt. is almost totally immobile • As a result, some pt. requires mechanical ventilation because of a weak or paralyzed diaphragm and accessory muscles for respiration • GBS is likely the result of alter immunity • Antibodies attack the myelin sheath that surrounds the axons of the peripheral nerves o This destruction slows the transmission of impulses from node to node o Damaged motor neurons result it impaired mobility • Myelin sheath helps with electrical impulses ETIOLOGY • GBS is often associated with bacterial infection • In countries where the recent Zika virus has emerged, the number of GBS cases has increased, suggesting that the Zika virus may be a trigger >>> COLLABORATIVE CARE 40 Exam 3 Review FINAL. >>> ASSESSMENT > PHYSCAL ASSESSMENT • Have pt. explain GBS symptoms in chronologic order • Ask about altered comfort, numbness, and paresthesias (unpleasant sensation such as burning, stinging, and prickly feeling) • Typically, LOC, cognition, and pupillary constriction or dilation is not affected • Assess ability to frown, smile, whistle, or drink from a straw • Assess ability to cough, gag, and swallow • MT closely for varying BP • CHART 44-1 KEY FEATURES – GUILLAIN-BARRE SYNDROME MOTOR MANIFESTATIONS AFFECTING MOBILITY CRANIAL NERVE MANIFESTATIONS Ascending symmetric muscle weakness  Facial weakness flaccid paralysis without muscle atrophy Dysphagia Decreased or absent deep tendon reflexes Diplopia (DTRs) Difficulty speaking Resp. compromise and resp. failure Blurred or double vision Loss of bowel and bladder control (less common) Ataxia Loss of reflexes in the arms and legs – most common Clumsiness SENSORY PERCEPTION MANIFESTATIONS AUTONOMIC MANIFESTATIONS Paresthesias Labile (low) BP Pain (cramping) Cardiac dysrhythmias Tachycardia Palpitations > DIAGNOSTICS • No single lab study confirms GBS • Lumbar puncture is done to test CSF o An increase in CSF protein level can occur from inflammatory plasma proteins, myelin breakdown, and damage to nerve roots o High proteins may not occur until 1-2 weeks into illness, and peak at 4-6 weeks • MRI or CT to rule out other causes >>> ANALYSIS • Priority problems: 43 Exam 3 Review FINAL. MYASTHENIA GRAVIS (MG) • Fatigue and weakness in muscles innervated by cranial nerves • Muscle weakness that increases when the pt. is fatigued and limits their mobility and ability to participate in activities • Acquired autoimmune disease • 2 types: o Ocular o Generalized • Common first S/S: o Vision issues due to ocular muscle weakness • Can lead to death from resp. failure due to chest muscle weakness • More common among men • MG is caused by distorted acetylcholine receptors (AChRs) in the muscle motor end plate membranes. – inhibits muscle contraction o Antibodies are attached to the AChRs o As a result, nerve impulses are reduced at the neuromuscular junction; they do not result in muscle contraction ASSESSMENT >>>PHYSICAL ASSESSMENT • Airway = PRIORITY! • Quick onset can be caused by pregnancy, infection, and anesthesia • Ask pt. about specific muscle weakness • Temporary increase in weakness may be noted after vaccination, menstruation, and exposure to extreme environmental temps. • May have periods of exacerbation • Does it affect ADLs? • S/S worsen with repetitive muscle use • Hx of ptosis (dropping eyelids), diplopia (double vision), dysphagia (difficulty chewing or swallowing) 44 Exam 3 Review FINAL. • S/S: o Progressive muscle weakness (proximal) that worsens with repetitive use and usually improves with rest o Poor posture o Ocular palsies o Paralysis = muscle weakness o Ptosis; incomplete eyelid close o Diplopia o Resp. compromise o Loss of bowel and bladder control o Fatigue o Muscle achiness o Paresthesias o Decreased sense of smell and taste o Dysphagia o Facial muscles affected – chewing, swallowing, speech, and smile changes, jaw hangs open ▪ (bulbar involvement) o Shoulder weakness ▪ Ask about any difficulty holding up the head, brushing teeth, combing hair, or shaving • Talking may exhaust pt. • Tongue ulcers • Eaton-Lambert syndrome – muscle weakness around lungs, trunk, pelvic, and shoulder >>> DIAGNOSTIC ASSESSMENT • MG may be immediately confirmed by the pt. response to cholinergic drugs • Test the thyroid function (thyrotoxicosis) • Test positive for antibodies • Repetitive nerve stimulation (RNS) – selected nerves are electrically stimulated, which results in progressive decline in the strength of the associated innervated muscle o Most common test • Electromyography (EMG) – recording electrode placed in skeletal muscle to monitor similar to ECG o Progressive decrease in the amplitude of the waveform is a classic sign of MG o Done by technician at bedside • Single fiber EMG (SFEMG) – newer and more sensitive form of EMG test the difference of nerve firing between different muscles, variability is called “jitter” 45 Exam 3 Review FINAL. • edrophonium chloride (Enlon, Tensilon) (cholinesterase inhibitor) – given to pt. if improved muscle tone within 30-60 sec. usually signals the pt. has MG. muscle tone usually lasts 4-5 min. • edrophonium can also be used to determine whether increasing weakness in the MG pt. is from cholinergic crisis (too much cholinesterase inhibitor drug) or a myasthenic crisis (too little cholinesterase inhibitor drug) o if it is a cholinergic crisis – muscle tone does not improve after drug, weakness may increase and muscle twitching (fasciculations) around the eyes and face DRUG ALERT! – edrophonium can cause cardiac dysrhythmias and cardiac arrest. Antidote = atropine sulfate INTERVENTIONS • MG is one of the most treatable neurologic disorders • 2 main goals: o Treat S/S – anticholinesterases or cholinergic drugs o Inducing remission – immunosuppressive, corticosteroids, plasmapheresis, thymectomy >>> NONSURGICAL MANAGEMENT • RESPIRATORY GAS EXCHANGE ASSESSMENTS ARE PRIORITY! > PROVIDING RESPIRATORY RESPONSE • Both myasthenic and cholinergic crisis increases muscle weakness and pt. risk for resp. compromise • Increase risk for lung infections due to decreased ability to cough o May require suctioning o Assisted cough technique (like quadriplegic pt.) o CRITICAL RESCUE! – keep a bag valve mask setup for O2 and suctioning equipment at bedside for all MG pt. in case of resp. distress • Mechanical ventilation is applied while waiting on medications to come > PROMOTING MOBILITY • Assess muscle strength before and after periods of activity • Schedule for tests, treatments, etc. early in the day or during energy peaks • During max weakness help with positioning and activity o Assess for skin breakdown 48 Exam 3 Review FINAL. o Impaired fine-motor control and shoulder weakness cause difficulty raising the arms o Plan activities to follow the administration of meds o Periods of rest – repetitive movement can cause a crisis • Assist with communication (weakness in facial muscles) o Speak slowly and lip read o Repeat back what they say to ensure it is correct o Yes or no questions and hand gestures are helpful • Nutritional support – difficulty maintaining adequate intake of food and fluids o Muscles for chewing and swallowing are weakened o High calorie snacks o Calorie count, daily weight o Feeding tube if pt. cannot swallow o Assess gag reflex and ability to chew and swallow o Freq. oral hygiene o Cut food into small bites or use soft foods o Eat slowly o Observe for choking o HOB elevated during meals and 30-60 min. after o Thickening liquids to prevent choking o MT serum prealbumin levels o Give anticholinesterase 45-60 min. before meals • Eye protection o Inability to completely close eyes may lead to problems o Artificial tears during day to keep moist o Lubricant gel and shield at bedtime o Diplopia – cover eye with patch for 2-3 hr. at a time o May tape eyes shut at night >>> SURGICAL MANAGEMENT • Thymectomy (removal of the thymus gland) – usually done early in the disease o Sx within 2 years of disease onset have the best outcomes o Pyridostigmine (Mestinon) given with small amount of water immediately before Sx o If on steroids, give before Sx but tamper down after Sx o Plasmapheresis before and after Sx o Antibiotics before and during Sx o Most required gradual weaning from ventilator o Turn, cough, deep breathing 3-6x every 15-30 min. and use incentive spirometer 49 Exam 3 Review FINAL. CRITICAL RESCUE! – thymectomy pt. MT resp effort. If resp distress give O2 and elevate HOB at least 45* and call MD ASAP! CARE MANAGEMENT • Managed at home unless requiring new assistive devices • Little preparation of home setting is needed • Wheelchair changes to home if needed • Risk for exacerbations – infection, stress, Sx, hard physical exercise, sedatives, enemas, heat, alcohol, rheumatoid arthritis, seasonal temp changes • Avoid overheating, crowds, overeating, erratic changes in sleeping habits, emotional extremes • Teach warning signs of exacerbations –increased weakness, increased diplopia, ptosis, problems with chewing or swallowing • Plan activities with rest periods • Drugs are usually taken before activities • Drug therapy teachings: o Keep drugs and a glass of water at bedside if weak in mornings o Wear watch with alarm to remind you to take meds o Post your drug schedule so others know it o Plan strenuous activities when drug peaks o Keep a supply in car or at work o Check with MD before using OTC ACTION ALERT! – teach family CPR and have resuscitation bag, suctioning, and O2 available in home. TRIGEMINAL NEURALGIA (TN) 50 Exam 3 Review FINAL. • “tic douloureux” • Trigeminal nerve has 3 branches: o 1. Controls sensation in a person’s eyes, upper eyelid, and forehead o 2. Controls sensation in the lower eyelid, cheek, nostril, and upper gum o 3. Controls sensation in the jaw, lower lip, lower gum, and some of the muscles used for chewing • TN has these characteristics: o Affects the trigeminal (5th cranial) nerve o Occurs more often in people older than 50 and in women more than men o Causes a specific type of facial pain, which results in sudden, intense facial spasms o Is usually provoked by minimal stimulation of a trigger zone (such as dental procedures) o Is unilateral and confined to the area innervated by the trigeminal nerve, most often the 2nd and 3rd branches o Is familial due to an inherited pattern of blood vessel formation • The cause of TN is thought to be form excessive firing of irritated fibers in the trigeminal nerve. • Trauma and infection of the teeth, jaw, or ear may be contributing factors >>> COLLABORATIVE CARE >>> ASSESSMENT • TN is a chronic syndrome causing impaired comfort, most often severe pain. o 2 types of pain: classic and atypical • When describing TN pain, pt. use terms such as excruciating, sharp, shooting, piercing, burning, and jabbing • Atypical pain descriptions may include migraine like HA • Bursts of pain that lasts seconds to minutes long • Pain can be initiated by light touch, a change in facial expression (smiling), or chewing • The fear of precipitating agonizing attacks often causes pt. to avoid talking, smiling, eating, or attending to hygiene needs. • Something is pushing on the trigeminal nerve  only pain experienced is in the face. • The pain can cause uncontrollable facial twitching • Attack free periods tend to grow shorter as the pt. becomes older • Will usually have a CT or MRI to see if there is a reversible cause of trigeminal compression or inflammation 53 Exam 3 Review FINAL. 1. (44-1) The RN is caring for a pt. diagnosed with GBS. Which assessment findings require nursing action? Select all that apply. a. BP of 80/42 b. RR of 24 c. Shallow breathing pattern d. Peripheral O2 Sat of 85% e. Diminished breath sounds in all lung fields 2. (44-3) the RN is caring for a pt. with trigeminal neuralgia. Which pt. problem is the priority for the RN? a. Facial twitching b. Problems with communication c. Ptosis and diplopia d. Severe facial pain INTRO TO BURN INJURY 26: BURNS >>> PATHO • Tissue destruction caused by a burn injury leads to local and systemic problems that affect fluid and electrolyte balance and lead to protein losses, sepsis, and changes in the body’s function • PRIORITY = prevention of infection and closure of the burn wound SKIN CHANGES 54 Exam 3 Review FINAL. > ANATOMIC CHANGES • When burn injuries occur, skin can regrow as long as parts of the dermis are present > FUNCTIONAL CHANGES • No protective barrier – increased risk for infection • Massive fluid loss thru excessive evaporation • Can destroy sweat glands – reducing excretory ability • With partial-thickness burns, nerve endings are exposed – increased sensitivity and pain • Harder time maintaining normal body temp. > DEPTH OF BURN INJURY • Severity of a burn is determined by how much of the body surface area is involved and the depth of the burn o Differences in skin thickness in various parts of the body also affect burn depth o Skin is thinner in older adults • Burn wounds are classified as: o Superficial-thickness ▪ Desquamation (peeling of dead skin) occurs 2-3 days after the burn ▪ Usually heals without a scar o Partial-thickness ▪ Superficial partial-thickness • A good blood supply remains • Wounds are pink and moist and blanch when pressure is applied • Small vessels bringing blood to this area are injured, resulting in the leakage of large amounts of plasma, which in turn lifts the heat-destroyed epidermis, causing blister formation o Small blisters are left intact o Large blisters are opened and debrided to promote healing ▪ Deep partial-thickness • No blisters • Red and dry skin with white areas • When pressure is applied the skin blanches slowly or not at all • Less pain than superficial due to destruction of nerve endings • Deeper injury can occur from hypoxia and ischemia • Skin grafts can decrease haling time o Full-thickness ▪ This wound does not regrow, and areas not closed by wound contraction require grafting 55 Exam 3 Review FINAL. ▪ Hard, dry, leathery eschar ▪ The eschar is dead tissue, it must slough off or be removed from the wound before healing can occur ▪ Edema is severe under eschar ▪ When the injury is circumferential (completely surrounds an extremity or the chest), blood flow and chest movement for breathing may be reduced by tight eschar ▪ Escharotomies (incisions through the eschar) or fasciotomies (incisions through eschar and fascia) may be needed to relieve pressure and allow normal blood flow and breathing ▪ Healing time depends on establishing a good supply of blood supply in the injured areas (can range from weeks to months) o Deep full-thickness ▪ Extend beyond the skin and damage muscle, bone, and tendons ▪ Flame, electrical, or chemical injuries ▪ Wound is blackened and depressed with no sensation ▪ Need early excision and grafting ▪ May need amputation (extremities) • Burn severity – depends on depth, extent, and location of injury o Minor o Moderate o Major CHARACTERISTIC S SUPERFICIAL SUPERFICIAL PARTIAL- THICKNESS DEEP PARTIAL- THICKNESS FULL- THICKNESS DEEP FULL- THICKNESS COLOR Pink to red Pink to red Red to white Black, brown, yellow, white, red Black EDEMA Mild Mild to moderate Moderate Severe Absent PAIN Yes Yes Yes Yes and no Absent BLISTERS No Yes Rare No No ESCHAR No No Yes, soft and dry Yes, hard and inelastic Yes, hard and inelastic HEALING TIME 3-6 days About 2 weeks 2-6 weeks Weeks to months Weeks to months GRAFTS REQUIRED No No Can be used if healing is prolonged Yes Yes 58 Exam 3 Review FINAL. • Fluid remobilization starts at about 24 hr. after injury, when the capillary leak stops. o The diuretic stage begins at about 48-72 hr. after the burn injury as capillary membrane integrity returns and edema fluid shifts from the interstitial spaces into the intravascular space. o Blood volume increases, leading to increased kidney blood flow and diuresis unless kidney damage has occurred. o Body weight returns to normal over the next few days as edema subsides o Hyponatremia – due to increased Na secretion from the kidney and loos of Na from wounds o Hypokalemia – from potassium moving back into cells and being excreted in urine o Blood transfusions are only needed when the pt. Hct is less than 20-25% and has S/S of hypoxia o Metabolic acidosis – due to loss of bicarbonate in the urine and the increased rate of metabolism > CARDIAC CHANGES • ↑ HR and ↓ Cardiac output – from the initial fluid shifts and hypovolemia that occurs after a burn injury • Cardiac output may remain low until 18-36 hr. after the burn injury o It improves with fluid resuscitation and reaches the normal levels before plasma volume is restored completely. • ↓ Na = seizures • ↑ K+ = cardiac • NI = fluid resuscitation and O2 > PULMONARY CHANGES • Resp. problems are usually caused by superheated air, steam, toxic fumes, or smoke o Major cause of death in burn pt. and most likely when burns occur indoors • Resp. failure form burn injuries can result from airway edema during fluid resuscitation, pulmonary capillary leak, chest burns that restrict chest movement, and carbon monoxide poisoning • The upper airway is affected when inhaled smoke or irritants cause edema and obstruct the trachea • The ciliated membrane lining the trachea normally traps foreign materials. o Smoke and gases slow this activity, allowing particles to enter the bronchi o The lining of the trachea and bronchi may slough 48-72 hr. after injury and obstruct the lower airways 59 Exam 3 Review FINAL. • Lung tissue injuries result from toxic irritant damage to the alveoli and capillaries o Leaking capillaries cause alveolar edema, which can occur immediately or up to a week after the injury o The fluid that diffuses into the lung tissue spaces contains proteins ▪ Progressive pulmonary failure develops ▪ Pulmonary edema and ↓ O2 and CO2 > GI CHANGES • Fluid shifts and decreased cardiac output decreases blood flow to the GI tract • The sympathetic nervous system stress response increases secretion of epinephrine and norepinephrine – inhibits GI motility and blood flow • Peristalsis decreases, and a paralytic ileus may develop • Secretions and gases collect in the GI tract, causing abd. distention • Curling’s ulcer: acute gastroduodenal ulcer that occurs with the stress of severe injury o May develop within 24 hr. after a severe burn due to reduced GI blood flow and mucosal damage o H2 histamine blockers, proton pump inhibitors. And early enteral feedings can help prevent ulcers > METABOLIC CHANGES • ↓ acid in gut • Serious burn injury increases metabolism by increasing secretion of catecholamines, antidiuretic hormone, aldosterone, and cortisol o Pt. O2 use and calorie needs are high • Catecholamines – activate the stress response o This rapidly uses up the body’s glucose and calorie supply • The heat and water loss from the burn increases metabolic rate and calorie needs o May double or triple normal calorie needs depending on the extent of the injury o Elevated needs peak at 4-12 days after the burn and can last for months until wounds are closed • The hypermetabolic condition also increases core body temp. – low-grade fever o Body knows it is losing heat thru the wound and is trying to compensate for that. > IMMUNOLOGIC CHANGES • Increased risk for infection due to damage of the protective layer or the skin • Inflammatory response is activated, and immune function may be suppressed o Worsened by ABX therapy 60 Exam 3 Review FINAL. ETIOLOGY • Dry heat injuries – open flame in house fires and explosions • Moist heat (scald) injuries – contact with hot liquids or steam • Contact burns – when hot metal, tar, or grease contacts the skin, often leading to a full- thickness injury • Chemical burns – usually at home or industrial accidents, or assault. Chemicals come in direct contact with skin or are ingested • Electrical injuries – burns from an electrical current entering the body o “grand masquerader” of burns because the surface injury may look small, but the internal injuries may be severe o Electrical energy is converted to heat energy inside the body o to test for damage = put them on a monitor o organs in the path of the current may become ischemic and necrotic • radiation injuries – when exposed to large doses of radioactive material HEALTH PROMOTION • Assess water temp before bathing • Set hot water tanks below 140*F • Enforce use of potholders • Never add a flammable substance to an open flame • Sunscreen and protective clothing to avoid sunburns • No smoking in bed, around alcohol, or while taking drugs that induce sleep • Keep lighters and matches away from children • Keep clothing, bedding, and flammable objects away from space heaters • Keep screens and doors closed on fireplaces and have chimneys swept each year • No smoking or open flames around O2 tanks • Check home smoke detectors • Have a planned escape route RESUSCITATION PHASE OF BURN INJURY • Immediate care focuses on maintaining an open airway • Resuscitation phase: the first phase of a burn injury, begins at the onset of injury and continues for about 24-48 hr. • PRIORITIES for management during this phase is: o 1. Secure the airway o 2. Support circulation and organ perfusion by fluid replacement o 3. Keep the pt. comfortable with analgesics 63 Exam 3 Review FINAL. o Burns inside the mouth and singed nasal hairs also indicate possible inhalation injury. o Black particles of carbon in the nose, mouth, and sputum and edema of the nasal septum indicate smoke inhalation, as does a “smoky” smell to the pt. breath o A change in resp. pattern may indicate a pulmonary injury. The pt. may: ▪ Become progressively hoarse ▪ Develop a brassy cough ▪ Drool or have difficulty swallowing ▪ Produce sounds on exhalation that include audible wheezes, crowing, and stridor ▪ Any of these changes may mean the pt. is about to lose their airway o Upper airway edema and inhalation injury are most common in the trachea and mainstem bronchi ▪ Wheezes on auscultation – indicate partial obstruction o CRITICAL RESCUE!! – MT pt. resp. efforts closely, for a burn pt. in resuscitation phase – brassy cough, drooling, difficulty swallowing, audible breath sound on exhalation, respond by immediately applying O2 and notifying the Rapid Response Team o Pt. with severe inhalation injuries may have such rapid obstruction that, within a short time, they cannot force air thru the narrowed airways ▪ Wheezing is absent, intubate immediately o Many pt. are intubated when inhalation injury is first suspected instead of waiting until airway obstruction where intubation is very difficult • CARBON MONOXIDE POISONING o One of the leading causes of death from a fire o CO2 is rapidly transported across the lung membrane and binds tightly to hemoglobin in place of O2 to form carboxyhemoglobin (COHb), which impairs O2 unloading at the tissue level o PaO2 stays normal o The vasodilating action of carbon monoxide causes the “cherry red” color (or at least the absence of cyanosis) in these pt. ▪ S/S vary with the concentration of COHb o Edema is building = intubate • PULMONARY FLUID OVERLOAD o Pulmonary edema can occur even when the lung tissues have not been damaged directly o Circulatory overload from fluid resuscitation may cause congestive heart failure 64 Exam 3 Review FINAL. o The pt. is short of breath and has dyspnea in the supine position. ▪ Crackles heard on auscultation o CRITICAL RESCUE!! – MT pt. resp. efforts for pulmonary edema. When S/S of pulmonary edema are present, elevate the HOB at least 45*, apply O2, and notify the burn team or Rapid Response Team CARDIOVASCULAR ASSESSMENT • Hypovolemic shock is a common cause of death in the resuscitation phase in pt. with serious injuries • At first, cardiac S/S are caused by hypovolemia and decreased cardiac output • MT the degree of edema and assess cardiac status by measuring central and peripheral pulses, BP, cap refill, and pulse oximetry o Noninvasive BP readings are inaccurate in pt. with large burns of upper extremities, use invasive BP MT • S/S at first: o Tachycardia o Decreased BP o Decreased peripheral pulses o Slow cap refill or absent o With fluid resuscitation – peripheral edema and pt. weight increases • ECG changes can indicate damage to the heart as a result of electrical burn injuries or stress that induces a MI o Get ECG readings on admission and continue to MT throughout the resuscitation phase KIDNEY/URINARY ASSESSMENT • Changes in kidney function with burn injury are related to decreased blood flow and cellular debris • During the fluid shift, blood flow to the kidney may not be adequate for filtration o Urine output is greatly decreased ▪ Urine is very concentrated with high USG o Mimicking hypovolemic shock • Destroyed RBC release hemoglobin and potassium. o When muscle damage occurs from a major burn or electrical injury, myoglobin is released from damaged muscle and circulates to the kidney. o Most damaged cells release proteins that form uric acid o All of these large molecules in the blood may precipitate in the kidney tubular system 65 Exam 3 Review FINAL. o A “sludge” then forms that blocks kidney blood and urine flow and may cause kidney failure • Assess kidney function: o I/O’s hourly ▪ Urine output is decreased during the first 24 hr. of the resuscitation phase ▪ Fluid resuscitation is provided at the rate needed to maintain urine output at 30-50 mL per hour or 0.5 mL/kg/hr o MT USG, BUN, creatinine, sodium levels SKIN ASSESSMENT • Determine the size and depth of burn injury • Size is estimated in comparison with the total body surface area (TBSA) • Size is needed to calculate drug doses, fluid replacement volumes, and caloric needs • Use the “Rule of 9’s” to estimate burn percentage GI ASSESSMENT • Decreased blood flow and sympathetic stimulation reduced GI motility and promote development of a paralytic ileus. – N/V, abd. distention • Bowel sounds are usually reduced or absent in a pt. with severe burns • Pt. with burns of 25% TBSA or who are intubated generally require a NG tube inserted to prevent aspiration and remove gastric secretions • Examine stool and vomit for blood > LAB ASSESSMENT • Hgb – elevated from fluid volume loss • Hct – elevated from fluid volume loss • Glucose – elevated from stress responses and altered uptake across injured tissues • Na – decreased, trapped in edema fluid and lost thru plasma leakage • K+ - elevated, disruption of the sodium-potassium pump, tissue destruction, and RBC hemolysis • Chloride – elevated, fluid volume loss and reabsorption of chloride in urine • PaO2 – slightly decreased • PaCO2 – slightly increased from resp. injury • pH – low from metabolic acidosis • COHb – elevated, from inhalation of smoke and carbon monoxide 68 Exam 3 Review FINAL. ▪ Purpose is to prevent shock by maintaining blood fluid volume o Resuscitation for a severe burn requires large fluid loads in a short time to maintain blood flow to vital organs o All common formulas recommend that half of the calculated fluid volume for 24 hr. be given in the first 8 hr. after injury. o The other half is given over the next 16 hr. for a total of 24 hr. o Fluid boluses are avoided because they increase capillary pressure and worsen edema o In the second 24 hr. period after a burn injury, the volume and content of the IV fluids are based on the pt. specific fluid and electrolyte balance needs and their response to treatment o Fluid replacement formulas are calculated from the time of injury and not from the time of arrival at the hospital. ▪ Ex: if a burn injury occurred at 8 AM but the pt. was not admitted to the hospital until 10 AM, the first 8-hr. period would be completed at 4 PM (8 hr. after the injury) ▪ Thus, if resuscitation was delayed by 2 hr. until admission not the hospital, calculated fluids would need to be given over the next 6 hr. period rather than an 8 hr. period ▪ Burn resuscitation formulas are guides – the pt. response to therapy determines exact fluid requirement o The management of extensive burns requires a large-bore central venous catheter so massive fluid loads can be given ▪ Peripheral lines are less useful o MT pt. responses is critical to determine the adequacy of resuscitation for hydration and blood perfusion of the brain, heart, and kidneys. o Urine output is the most common and sensitive noninvasive assessment parameter for cardiac output and tissue perfusion o Regardless of the total amount of fluid calculated as needed for the pt., the amount of fluid given depends on how much IV fluid per hour is needed to maintain the hourly urine output of 0.5 mL/kg (about 30 mL/hr) o Burn pt. may develop severe hypovolemic shock and need invasive cardiac MT o MT ECG activity for large burn pt. o CHART 26-4 FLUID RESUSCITATION OF THE BURN PT. ▪ Initiate and maintain at least 1 large-bore IV line in an area of intact skin ▪ Determine appropriate fluid type and total volume to be infused over 24 hr. postburn 69 Exam 3 Review FINAL. ▪ Give ½ of the total 24 hr prescribed volume within the first 8 hr. postburn and the remaining volume over the next 16 hr. ▪ Assess IV access site, infusion rate, and infused volume at least hourly ▪ MT these VS at least hourly: • BP • HR • RR • Breath sounds • Voice quality (if not intubated) • O2 sat • End-tidal carbon dioxide levels ▪ Assess urine output at least hourly: • Volume • Color • USG • Character • Presence of protein ▪ Assess for fluid overload: • Formation of dependent edema • Engorged neck veins • Rapid, thready pulse • Presence of lung crackles or wheezes on auscultation ▪ Measure additional body fluid output hourly • DRUG THERAPY o For shock prevention o A common mistake in management is giving diuretics to increase urine output rather than changing the amount and rate of fluid infused. o Diuretics do not increase cardiac output; they actually decrease circulating volume and cardiac output by pulling fluid from the circulating blood volume to enhance diuresis ▪ Lasix’s can kill burn pt! ▪ Reduces blood flow to vital organs ▪ Increases the risk for severe hypovolemic shock ▪ Only burn pt. that MIGHT get diuretics is electrical burn pt. • SURGICAL o Escharotomy – sx. procedure for the treatment of inadequate tissue perfusion 70 Exam 3 Review FINAL. ▪ An incision thru the burn eschar relieves pressure caused by the constricting force of fluid buildup under circumferential burns on the extremity or chest and improves circulation ▪ A fix for Compartment syndrome > MANAGING PAIN AND ALTERATIONS IN COMFORT • The pain associated with burn injuries is both chronic and acute, with the causes being multifactorial. • Accurate assessment of the pt. pain and comfort level before and during procedures is an essential part of pain management GOAL: alleviated or reduced pain level INTERVENTIONS: • PRIORITY NI = continually assessing the pt. pain level, using appropriate pain- reducing strategies, and preventing complications • NONSURGICAL o Drug therapy – mostly for pain ▪ Opioid analgesics – morphine sulfate, hydromorphine (Dilaudid), fentanyl ▪ Nonopioid analgesics ▪ During resuscitation phase IV route is used for giving meds • IM meds go into the interstitial spaces and do not relieve pain • This will prevent delayed rapid reabsorption leading to lethal blood levels from meds > PREVENTING ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) GOAL: not experience ARDS, normal ABGs, maintain normal lung compliance INTERVENTIONS: • NI focus = increasing lung compliance and improving PaO2 levels • PRIORITY NI = coordinating respiratory therapy strategies and MT the pt. response to these interventions • In collaboration with MD team and RT, give PEEP to provide a continuous positive pressure in the airways and alveoli • Pt. usually on burn ICU ACUTE PHASE OF BURN INJURY • The acute phase begins about 36-48 hr. after injury, when the fluid shift resolves, and lasts until wound closure is complete 73 Exam 3 Review FINAL. • done by RN, PCA, and PT ▪ enzymatic debridement – naturally done by body’s own enzymes or a topical enzyme agent, such as collagenase (Santyl) is used for rapid wound debridement. • Applied during the once a day dressing change o Standard wound dressing – multiple layers of gauze applied over the topical agents and held in place by gauze bandages wrapped around ▪ Dressings are usually changed and reapplied Q12-24H after thoroughly cleaning the areas o Biologic dressing – are skin or membranes obtained from human tissue donors (homograft or allograft) or animals (heterograft or xenograft) ▪ When applied over open wounds, a biologic dressing adheres and promotes healing or prepares the wound for permanent skin graft coverage ▪ Used for temporary wound coverage and closure ▪ Allografts are human skin obtained from a cadaver and provided thru a skin bank • Disadvantages – high cost and risk for transmitting a bloodborne infection ▪ Heterografts are skin from another species • Pig skin (porcine) is the most common > MINIMIZING POTENTIAL FOR INFECTION • Burn wound infection occurs thru: o Auto-contamination – the pt. own normal flora overgrows and invades other body areas o Cross-contamination – organisms from other people or environments are transferred to the pt. • S/S of infection: o Foul smelling discharge o Fever o Blood culture/wound site colonization o WBC elevation GOAL: remain free from infection and not develop sepsis INTERVENTIONS: • Focus = preventing infection and removing infected tissue • NONSURGICAL 74 Exam 3 Review FINAL. o PRIORITY NI = using principles of infection control to prevent transmission, providing a safe environment, and MT for early detection of infection • DRUG THERAPY o All burn pt. are at risk for the growth of Clostridium tetani (a deadly infection) o Tetanus toxoid administration enhance immunity to C. tetani and is routinely given on administration into the hospital with a burn ▪ Acute phase = tetanus o Topical antimicrobial drugs are used for infection prevention in burn wounds TOPICAL DRUG NURSING INTERVENTIONS Silver sulfadiazine (Silvadene, Thermazene) - watch for allergic reaction causing a drop in WBC count - do not use if reaction to sulfonamide has occurred - use on deep partial-thickness or full- thickness wounds - MT wounds for infection Collagenase (Santyl) with Polysporin powder - apply once a day - use on partial-thickness wounds with eschar - MT wounds for infection - may be used with barrier dressing such as Xeroform Gentamicin sulfate (Garamycin, Gentamar) - nephrotoxic – MT kidney fx. closely, changes in creatinine and BUN - ototoxic – MT hearing weekly • Providing a safe environment: o Isolation therapy may be used o Asepsis techniques ▪ Change gloves when handling different parts of the body and when handling dirty to clean dressings o Equipment on burn units are not shared between pt. o Use disposable items as much as possible o Daily cleaning of equipment o Because Pseudomonas has been found in plants, no plants or flowers are allowed on the unit. o Some burn units do not let pt. eat raw foods (salad, fruits, peppers) to reduce exposure to organisms o Rugs and upholster articles harbor organisms, and their use is restricted o No visitors when the pt. is immunosuppressed 75 Exam 3 Review FINAL. o Ill people, small children, and other pt. should not come into direct contact with the burn pt. o Some burn units recommend that all visitors wear PPE in the pt. room ▪ No data supports the effectiveness of this > MAINTAINING MOBILITY GOAL: pt. will have minimal limitations in muscle movement, joint mobility, walking, and self- positioning INTERVENTIONS: • NONSURGICAL o Positioning ▪ Maintain the pt. in a neutral body position with minimal flexion to prevent contractures o ROM ▪ Performed at least 3x daily ▪ Burned hands – ROM every hour while awake o Ambulation ▪ Start ASAP as soon as the fluid shift is resolved ▪ Try to do 2-3x daily and progress over time o Compression dressings ▪ Applied after grafts heal to help prevent contractures and tight hypertrophic scars (can inhibit mobility) ▪ For best effectiveness, pressure garments must be worn 23 hr a day, every day, until the scar tissue is mature (12-24 months) ▪ They can be uncomfortable with itchiness and increased warmth ▪ Reinforce to the pt. and family that wearing pressure garments is beneficial in saving mobility and reducing scarring. QUESTIONS 1. (26-1) The pt. asks about ways to prevent carbon monoxide poisoning. Which teaching will the RN provide? a. “You can see black smoke when carbon monoxide is in the air.” b. “If you are experiencing carbon monoxide poisoning, your skin will begin to turn blue.” c. “The only way to get poisoned from carbon monoxide gas is if you are in the presence of a fire.” 77 Exam 3 Review FINAL. - cancer therapy degeneration - anaphylaxis pericarditis - anticoagulation (ineffective valve) - sepsis - thoracic tumors therapy - capillary leak – - tension - dehydration (ascites) pneumothorax - vomiting - burns - diarrhea - extensive trauma - heavy diaphoresis - liver impairment - diuretic therapy - hypoproteinemia - NG suction - diabetes insipidus CHART 37-1 SHOCK – KEY FEATURES CARDIOVASCULAR NEUROMUSCULAR - ↓ cardiac output - ↑ pulse rate - thready pulse - ↓ BP - narrowed pulse pressure - postural hypotension - low central venous pressure - flat neck and hand veins in dependent positions - slow cap refill - diminished peripheral pulses Early: --- anxiety --- restlessness --- ↑ thirst Late: --- ↓ CNS activity (lethargy to coma) --- generalized muscle weakness --- diminished or absent deep tendon reflexes --- sluggish pupillary response to light RESPIRATORY GI - ↑ RR - shallow depth of respirations - ↑ PaCO2 - ↓ PaO2 - cyanosis, especially around lips and nail beds - ↓ motility - diminished or absent bowel sounds - N/V - constipation KIDNEY SKIN - ↓ urine output - ↑ specific gravity - sugar and acetone present in urine - cool to cold - pale to mottled to cyanotic - moist, clammy - mouth dry, paste like coating present REVIEW OF GAS EXCHANGE AND TISSUE PERFUSION 78 Exam 3 Review FINAL. • Perfusion is related to MAP o 60-70 = potential for shock TYPES OF SHOCK • More than 1 type of shock can be present at the same time o EX: trauma caused by a car wreck may trigger hemorrhage (leading to hypovolemic shock) and a MI (leading to cardiogenic shock) • Hypovolemic shock – when too little circulating blood volume decreases MAP, resulting in inadequate total body perfusion and has exchange o From: dehydration, poor clotting with hemorrhage • Cardiogenic shock – when the heart muscle is unhealthy, and pumping is impaired o From: MI o Decreases cardiac output and MAP • Distributive shock – blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs o From: blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak o Decreases MAP and may be neural-induced or chemical-induced o Neural-induced – a loss of MAP that occurs when sympathetic nerve impulses are decreased and blood vessel smooth muscles relax, causing vasodilation and poor perfusion o Chemical-induced – occurs when certain body chemicals or foreign substances in the blood vessels start widespread changes in blood vessel walls ▪ (3 common origins) anaphylaxis, sepsis, capillary leak syndrome. ▪ Anaphylaxis – extreme type of allergic reaction • Skin rash  Benadryl • Flushing • airway obstruction  intubate, epi • MT even after epi/Benadryl has been given ▪ Sepsis – widespread infection that triggers whole body inflammation • “septic shock” ▪ Capillary leak syndrome – is the response of the capillaries to the presence of histamine and other chemicals that enlarge capillary pores and allow fluid to shift from the capillaries into the interstitial tissues • These fluids are stagnant, and no gas exchange occurs • Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, large wounds, kidney disease, hypoproteinemia, and trauma 79 Exam 3 Review FINAL. • Obstructive shock – (blockage) problems that impair the ability of the normal heart to pump effectively o Heart remains normal but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. o From: cardiac tamponade HYPOVOLEMIC SHOCK >>> PATHO • Problem = loss of vascular volume, resulting in a decreased MAP, and sometimes a loss of circulating RBC • Reduced MAP slows blood flow, decreasing tissue perfusion • The loss of RBC’s decreases the ability of the blood to oxygenate the tissue it does reach • “anaerobic cellular metabolism” 82 Exam 3 Review FINAL. - S/S = a sense of “something bad”, confused, increased thirst, rapid and weak pulse, low BP, pallor to cyanosis of oral mucosa and nail beds, cool and moist skin, anuria, 5-20% decrease in O2 sat - Labs = low pH with rising lactic acid and potassium levels - ACTION ALERT!! – this stage is a life-threatening emergency! Vital organs will only tolerate this for a short period of time, immediate interventions are needed. The pt. life usually can be saved if the conditions causing shock are corrected within 1 hr. or less of the onset of the progressive stage. REFRACTORY STAGE – the pt. dies - Occurs when too much cell death and tissue damage result from too little O2 reaching the tissues - Vital organs have extensive damage and cannot respond effectively to interventions, and shock continues. - So much damage has occurred with release of metabolites and enzymes that damage to vital organs continues despite interventions - Severe tissue hypoxia with ischemia and necrosis - Release of myocardial depressant factor from the pancreas - Buildup of toxic metabolites - Multiple organ dysfunction syndrome (MODS) – the sequence of cell damage caused by the massive release of toxic metabolites and enzymes - Once the damage has started, the sequence becomes a vicious cycle as more dead cells open and release metabolites – these trigger small clots to form (microthrombi) - Liver, heart, brain, and kidney functions are lost first - S/S = rapid loss of consciousness, nonpalpable pulse, cold and dusky extremities, slow and shallow respirations, unmeasurable O2 sat, - Therapy including fluid replacement is not effective in saving the pt.’s life, even if the cause of shock is corrected and MAP temporarily returns to normal - Death – too late for the pt! ETIOLOGY • Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease that prevents total body perfusion • Hypovolemic shock from hemorrhage is common after trauma or surgery o Internal hemorrhage occurs with blunt trauma, GI ulcers, and poor control of surgical bleeding INCIDENCE AND PREVALENCE 83 Exam 3 Review FINAL. • The exact incidence of hypovolemic shock is not known because it is a response rather than a disease. HEALTH PROMOTION • Recognizing hypovolemic shock is a major nursing responsibility • Identify pt. at risk for dehydration and assess for early S/S o Especially for NPO pt. • Assess all pt. with invasive procedures or trauma for obvious or occult bleeding from impaired clotting. • Compare urine output with fluid intake • Check VS for pt. who have persistent thirst • Assess for shock in any pt. with a change in mental status, increased pain, or increased anxiety • Teach pt. who have invasive procedures about the S/S of shock • Stress the importance of seeking immediate help for obvious heavy bleeding, persistent thirst, decreased urine output, light-headedness, or a sense of impending doom >>> COLLABORATIVE CARE >>> ASSESSMENT > HISTORY • Ask about risk factors related to hypovolemic shock • Ask about the use of drugs such as aspirin, other NSAIDs, and diuretics that may cause changes leading to hypovolemic shock • Ask about I/O’s for the last 24 hr. o Super important because urine output is reduced during the 1st stages of shock, even when fluid intake is normal • Examine areas for poor clotting and hemorrhage (gums, wounds, and sites of dressings, drains, and vascular accesses • Check under the pt. for blood • Observe for any swelling or skin discoloration that may indicate an internal hemorrhage. > PHYSICAL ASSESSMENT • First changes noticed are usually cardiovascular CARDIOVASCULAR CHANGES • Decreased MAP • Assess pulses for rate and quality 84 Exam 3 Review FINAL. • In the initial stage – HR increases to keep cardiac output and MAP at normal levels o Increased HR is the first sign of shock • DBP increases o Narrowed pulse pressure • SBP decreases – as shock progresses • O2 sat: o Nonprogressive stage = 90-95% o Progressive stage = 75-80% o Anything below 70% is considered a life-threatening emergency and may signal refractory stage of shock RESPIRATORY CHANGES • RR increases to ensure that O2 intake is increased so it can be delivered to critical tissues KIDNEY AND URINARY CHANGES • Occur with shock to compensate for decreased MAP by saving body water thru decreased filtration and increased water reabsorption • Assess urine for volume, color, USG, and the presence of blood or protein • Decreased urine output is a sensitive indicator of early shock o Measure urine output at least Q1H o In severe shock, urine output may be absent SKIN CHANGES • Reduced skin perfusion • Assess for temp, color, and moisture o With shock, it will feel cool or cold to the touch and moist • Color changes first appear in mucous membranes and then around the mouth > LAB ASSESSMENT TEST NORMAL RANGE ABNORMAL FINDINGS pH (arterial) 7.35-7.45 Decreased PaO2 80-100 Decreased PaCO2 35-45 Increased Lactic acid (lactate) 3-7 Increased (arterial) 0.3-0.8 Hct F = 37-47% Increased = fluid shift or M = 42-52% dehydration Decreased = hemorrhage 87 Exam 3 Review FINAL. blood vessels, such as nitroprusside, can cause systemic vasodilation and 88 Exam 3 Review FINAL. increase shock if the pt. is volume depleted. Drugs that increase heart muscle contraction increase heart oxygen consumption and can cause angina or infarction. o MT VS and LOC – A MAJOR NURSING ACTION ▪ MT these pt. responses Q15min until stable: • Pulse • BP • Pulse pressure • Central venous pressure (CVP) • RR • Skin and mucosal color • O2 sat • Cognition • Urine output ▪ Hemodynamic MT in critical care settings ▪ Insertion of a CVP catheter • A decreased CVP from baseline reflects hypovolemic shock ▪ Intra-arterial catheters allow continuous blood pressure monitoring and are an access for arterial blood sampling ▪ They are inserted into an artery (radial, brachial, femoral, or dorsalis pedis) CHART 37-3 NI FOR HYPOVOLEMIC SHOCK • Ensure a patent airway • Insert an IV catheter or maintain an established catheter • Administer O2 • Elevate the pt. feet, keeping their head flat or elevated to no more than 30* • Examine the pt. for overt bleeding • Administer drugs • Increase the rate of IV fluid delivery • Do not leave the pt. 89 Exam 3 Review FINAL. SEPSIS AND SEPTIC SHOCK >>> PATHO • Sepsis leading to septic shock is a complex type of distributive shock that usually begins as a bacterial or fungal infection and progresses to a critical emergency over a period of days. • As progression occurs, the problems occur faster and to a greater degree. o Thus, control of sepsis and prevention of severe sepsis and septic shock are easier to achieve early in the process • Failure to recognize and intervene in early sepsis is a major factor for progression to septic shock and death INFECTION • When infection is confined to a local area, it should not lead to sepsis and shock • WBC’s bring more WBC’s to inflamed areas and kill invading organisms • Capillary leak occurs, allowing plasma to leak into the tissue o Causes swelling (edema) • This inflammatory response stops when it is no longer needed o The pt. does not have fever, tachycardia, decreased O2 sat, or reduced urine output 92 Exam 3 Review FINAL. o Pt. extremities may feel warm, and there is little or no cyanosis • The WBC count at this time may no longer be elevated because prolonged sepsis may have exceeded the bone marrow’s ability to keep producing and releasing new mature neutrophils and other WBCs o WBC may be extremely low • The pt. “appears” stable but is NOT! • S/S = o Lower O2 sat o Rapid RR o Decreased – absent urine output o Change in cognition and affect • Appropriate and aggressive interventions at this stage can still prevent septic shock, although mortality after a pt. reaches this stage is much higher than for sepsis and SIRS • At this point, the downhill course leading to septic shock is extremely rapid • TABLE 37-3 SEPSIS WITH SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS) CRITERIA o Suspected or identified infection with some of the following: ▪ Temp of more than 101*F or less than 96.8*F ▪ HR of more than 90 ▪ RR of more than 20 ▪ Abnormal WBC count -- > 12,000 or < 4,000 ▪ Hypotension – SBP < 90, MAP < 70 ▪ Urine output < 0.5 mL/kg/hr for 2 hr. ▪ Creatinine increase -- > 0.5 ▪ INR > 1.5 ▪ Absent bowel sounds ▪ Platelet count < 100,000 ▪ Elevated lactic acid (lactate) levels ▪ Decreased cap. Refill ▪ Hyperglycemia >140 ▪ Unexplained change in mental status ▪ Significant edema or positive fluid balance SEPTIC SHOCK • Septic shock: id sepsis-induced hypotension persisting despite adequate fluid resuscitation • It is the stage of sepsis and SIRS when multiple organ dysfunction syndrome (MODS) with organ failure is evident 93 Exam 3 Review FINAL. • Even with appropriate intervention, the death rate among pt. in this stage of sepsis is very high. • Severe hypovolemic shock and hypodynamic cardiac function are present as a result of an inability of the blood to clot because the platelets and clotting factors were consumed earlier • The S/S resemble the late stage of hypovolemic shock ETIOLOGY • Major cause of sepsis is a bacterial infection that escapes local control • Common organisms = Escherichia coli • Pt. at risk for infection are reduced immunity and those with a central line • Central lines in place even for short periods create a potential direct access point for microorganisms and can lead to central line associated blood stream infections • Sepsis – has to have an opening into the body  E. Coli HEALTH PROMOTION AND MAINTENANCE • Prevention is the best management strategy for sepsis and septic shock • Removing indwelling urinary catheters and IV access lines as soon as they are no longer needed • Ensure that pt. receiving mechanical ventilation are weaned from the ventilator ASAP • Early detection of sepsis before progression to septic shock is a major nursing responsibility. • The RN is the health care provider most in contact with the pt. and is in a unique position to detect subtle changes in appearance and behavior that can indicate sepsis o S/S = change in VS, lab findings, appearance, and behavior o Check for these changes every shift • Teach pt. and family the S/S of infection and how to use a thermometer and to take their temp twice a week and when they are feeling well >>> COLLABORTAIVE CARE >>> ASSESSMENT • Sepsis and septic check differ from other types of shock in many ways o May occur over many hours or days and the S/S are less obvious o Chance for recovery is good when the pt. is recognized as having sepsis with SIRS and interventions are started within 6 hr. o Septic shock, has a rapid downhill course > PHYSICAL ASSESSMENT 94 Exam 3 Review FINAL. CARDIOVASCULAR CHANGES • Differ in the stages of sepsis and septic shock • Cardiac output and BP are low in early sepsis and very low in septic shock • In severe sepsis, cardiac output is higher with increased HR and BP • DIC reduces perfusion and gas exchange and decreases O2 sat, causing widespread hypoxia and ischemia • The huge number of small clots uses clotting factors and fibrinogen faster than they can be produced, which eventually leads to poor clotting o This leads to hemorrhage RESPIRATORY CHANGES • ARDS may occur in septic shock • ARDS in a pt. with septic shock has a high mortality rate SKIN CHANGES • Differ at different stages of sepsis • Hyperdynamic stage – warm and no cyanosis • Progression to septic shock – cool, clammy with pallor, mottling, or cyanosis • DIC – petechiae and ecchymoses o Blood may ooze from the gums, other mucous membranes, and venipuncture sites and around IV catheters KIDNEY/URINARY CHANGES • Low urine output compared with fluid intake indicates shock • When a pt. with no kidney issues suddenly starts having a low urine output be suspicious of severe sepsis or septic shock > LAB ASSESSMENT • Get blood culture before ABX • Hallmark of sepsis – rising serum procalcitonin level, increased lactate level, normal or low WBC count • The actual diagnosis of sepsis is difficult to make, yet the best outcome depends on an early diagnosis and the implementation of appropriate aggressive interventions within 6 hr. >>> ANALYSIS • Priority problems: o 1. Widespread infection