Nur 265 Exam 3 Study Guide 2023-2024, Exams of Nursing

Download Nur 265 Exam 3 Study Guide 2023-2024 and more Exams Nursing in PDF only on Docsity! [Date] Nur 265 Exam 3 Study Guide 2023-2024  Normal ICP 10-15 mmHg , pressures >20 mmHg impair cerebral circulation  IICP is leading cause of death from head trauma in pts who reach the hospital alive.  Cerebral Perfusion Pressure (CPP) o Blood flow required to provide adequate oxygenation & glucose for brain metabolism o Maintenance above 70 mmHg o CPP= MAP-ICP ▪ MAP= (2xD) + S MAP NEEDS TO BE ATLEAST 80 3  Compensation o First Response – CSF is shunted or displaced into the spine (compliance) o Next – Reduction of blood volume in the brain (autoregulation) o As ICP continues to increase cerebral perfusion decreases leading to brain tissue ischemia, edema, vasodilation then acidosis which causes further increases ICP o In edema remains untreated the brain may herniate into spinal canal – death from brain stem compression  Assessment Findings o Changes in LOC – First sign of IICP is declining LOC & includes restlessness or confusion to Stuporous ▪ W/o glucose & 02, brain shuts down. Ex. Pt knew who you were in am & now don’t remember o Headache – Quite environment may have photophobia so keep room lights very low. o Change in speech pattern – Aphasia, Slurred Speech o Changes in pupil size – 2 cm change in either direction is significant, dilated or constricted, Notify Dr ▪ Normal is 6 mm. Getting better if going back toward normal from dilated or constricted ▪ Uneven pupils tx as IICP until proven otherwise; pinpoint - brain stem (pons) dysfunction o Abnormal Posturing – Decorticate (flexion) or Decerebrate (extensor) ▪ Decorticate – arms drawn to core, legs straight ▪ Decerebrate – arms straight and stiff, pts rarely survive o Hyperthermia – followed later by hypothermia ▪ When hypothermic – BE CONCERNED, pressure on hypothalamus located next to brain stem o Cardiac & respiratory rate/rhythm changes ▪ Tachy first – Increased HR & RR before brady HR & RR o N/V – Common in IICP o Cushing’s Triad – Severe HTN, Widened Pulse Pressure, Bradycardia ▪ Late response & indicates severe IICP w/loss of autoregulation, Imminent death ▪ Systolic BP increases bc decreased blood flow to brain ▪ Pressure on Vagus nerve and brainstem = bradycardia [Date]  Managing IICP o Elevate HOB 30-45 degrees (unless contraindicated) ▪ If hypotension, elevate HOB where CPP >70 o Maintain head in a midline neutral position o Avoid sudden and acute hip or neck flexion during positioning – Log roll pt o Avoid clustering of care (bath followed by linen change) o Coughing and suctioning increase ICP o Decrease cerebral edema – osmotic diuretics (mannitol) & fluid restriction ▪ Mannitol is hypertonic- pulling fluid into vascular space- will inc. fluid output & monitor BP for HTN ▪ Furosemide used in adjunct to reduce incidence of rebound from mannitol. Helps reduce edema & blood volume, decrease Na uptake by the brain, & decrease production of CSF at choroid plexus. o LOW CSF using intraventricular drain system o Control fever w/antipyretics or cooling blanket – do not allow pt to shiver as will increase ICP ▪ ▪ ▪ ▪ ▪ ▪ When febrile every cell in body needs more 02 and glucose o Oxygenation – Hyperventilate on a vent to decrease CO2 which causes vasodilation o Reduce cellular metabolic demands – barbiturates (-bital, -barbital) and/or sedation (coma) Traumatic Brain Injury (946-957)  Primary Brain Injury o Occurs at time of injury o Open – Head fractured or penetrated; Closed – Blunt trauma, shaken baby o Open Head Injuries ▪ Skull Fractures  Linear Fx – thin line on x-ray, no tx unless underlying brain tissue damaged  Depressed Fx – Brain damage from bruising (contusion), laceration from bone fragments  Basilar skull Fx – Fx of bones of the base of skull & results in CSF leak from nose & ears. o May not be seen on plain x-ray, R/F Infection w/ CSF leak o Manifested by bruises around eyes(raccoon eyes) or behind ears (Battle’s sign) o Has potential for hemorrhage if it damages the internal carotid o Closed Head Injuries ▪ Caused by blunt force trauma ▪ Contusion – Bruising to brain tissue @ site of impact (coup) or opposite (contercoup) [Date] o Falls most common in older adults.  Assessment/Interventions o Hx – Did pt lose consciousness? Drug or alcohol consumption? All screened for abuse/neglect o Physical ▪ First priority is assessment of ABCs - Report any sign of respiratory problems immediately! ▪ Suspect neck injury until proven otherwise, stabilize w/ C-Collar and backboard  Skin breakdown & pressure ulcer formation are concern with spine board & c-collar  Once board removed, spinal precautions maintained until HCP indicates it is safe o (1) Bedrest; (2) No neck flexion with a pillow or roll; (3)No thoracic or lumbar flexion w/HOB elevation (reverse T acceptable); (4) Manual control of C spine anytime collar removed; (5) Log roll ▪ Prevent secondary brain injury – O2 & lowering ICP, Vent if needed, do not want CO2 to rise as it causes vasodilation & IICP. o Vital Signs ▪ Monitor VS Q 1-2 hrs – May be hypotensive or hypertensive (IV fluids to maintain above 90) ▪ Central fever caused by hypothalamic damage – no sweating, high, last days-weeks  Responds better to cooling (sponge bath, cool air)  Fever from any cause is associated w/higher mortality rates ▪ Cushing’s Triad – HTN, Wide PP, & Bradycardia – late sign of IICP and indicates imminent death ▪ Hypotension and tachycardia indicate hypovolemic shock o Neuro ▪ GCS ▪ Most important variable to assess w/any brain injury is LOC ▪ Dec or change in LOC is first sign of deterioration (behavior changes, restlessness, disorientation) ▪ Assess pupils  Pinpoint - & nonresponsive – Brainstem dysfunction @ level of ponds  Asymmetric, loss of light reaction, unilateral or bilateral dialed – herniation o Late signs of IICP – severe HA, N/V, seizures, papilledema - always sign of IICP ▪ Motor response - Decorticate or Decerebrate posturing o Psychosocial ▪ Personality changes – temper outbursts, depression, risk-taking, denial, talkative, outgoing o Therapeutic Hypothermia ▪ Rapidly cool pt to 89.6 – 93.2 for 24-48 hrs after primary injury to reduce brain metabolism and reduce secondary brain injury. o Mechanical ventilation ▪ Maintain PaCO2 at 35 to 38 to prevent IICP from vasodilation from CO2 ▪ Maintain PaO2 between 80-100 to prevent secondary injury ▪ Lidocaine given IV or endotracheally to suppress cough reflex; coughing increases ICP [Date] o Drug Therapy ▪ Mannitol through a filter  Reduces edema and blood volume, dec Na uptake by brain & dec CSF production  Used with furosemide to reduce rebound from Mannitol & enhances therapeutic action  Foley catheter for strict I&O, check serum (want 310-320) and urine osmolarity daily. ▪ NO Steroids are effective ▪ Propofol & dexmedetomidine – sedative agents with short ½ life ▪ Morphine or fentanyl in vented pts to dec agitation & restlessness if caused by pain.  Fentanyl is safer. Both reversed with naloxone. ▪ Antiepileptic drugs – phenytoin to prevent seizures ▪ Acetaminophen or aspirin for fever >101 if not from central fever (cooling only) ▪ Barbiturate Coma  Pentobarbital or thiopentone - For IICP that can’t be controlled  Dec metabolic demands of brain, requires vent, hemodynamic & ICP monitoring.  Complications – dec GI motility, dysrhythmias from hypokalemia, hypotension, fluctuations in body temp  Surgical Management o Insert ICP monitoring through burr hole (key hole craniotomy) - maintain w/strict sterile technique ▪ Be sure to provide head to toe assessment even though pt ICP being invasively monitored o Decompressive Craniotomy ▪ Removal of section of the skull – allows space for edema w/o Increasing ICP ▪ DO NOT LAY PT ON THE SIDE WHERE THE SKULL FRAGMENT WAS REMOVED. ▪ Pt must wear helmet when out of bed  Pt & Family Education for self-management – MILD BRAIN INJURY o Acetaminophen for HA Q 4 hrs o Avoid sedatives, alcohol, sleeping pills for at least 24 hrs o No strenuous activity for 48 hrs o Monitor or assist movement due to balance disturbances o If these sx occur bring back to ER ▪ Severe HA; Worsening HA; Persistent or severe N/V; Blurred vision; Drainage from ear or nose; Weakness; Slurred speech; Progressive sleepiness; Unequal pupil size  Interdisciplinary Care o Rehab specialists o Speech & Language Pathologists (SLP) o Dietitian o Rehab therapists o Severe brain injury requires lone-term case management & ongoing rehab o OT, PT, SLP, & home evaluations after discharge for severe [Date] Cerebral Aneurysm (chart 940) ● Intracranial aneurysm – weakness in a cerebral blood vessel wall, Saccular or berry most common in the head ● AV Malformations – Tangled arteries and veins, blood shunted from artery to a vein, can bleed or thrombose o Pt. present with HA, seizures, or focal deficits o Once bleeds, has 25% chance of bleeding again ● Surgery o Surgical ligation or resection (Open) ▪ Surgical removal of AVM or aneurysm, care same as craniotomy o Clip (Open) ▪ Clamp over aneurysm base to isolate, movement can occur ▪ Close attention on neuro to detect early rebleeding or migration of the clip. Changes in cognition or new focal neurologic deficits must be communicated urgently to the surgeon. o Coil: with stent assist; with balloon assist ▪ Detachable coils placed under fluoroscopy to occlude aneurysm w/o interrupting main vessel flow. 10[Date] o Provide reassurance that the surgeon will spare vital parts of brain while removing tumor o Check that the pt has not had alcohol, tobacco, anticoagulants, or NSAIDS for at least 5 days b4 surgery o NPO status for at least 8 hrs b4 surgery  Post-Operative Care o Focus is to monitor pt to detect changes in status & prevent or minimize complications (IICP) o Assess neurologic and VS @ 15-30 min for the first 4-6 hrs then Q 1 hr. If pt stable for 24 hrs checks decrease to Q 2-4 hrs. o Immediately report new neurologic deficits – Dec LOC, motor weakness or paralysis, aphasia, dec sensation, & reduced pupil reaction to light. Personality changes (agitation, aggression) can indicate worsening status o Periorbital edema and ecchymosis of one or both eyes is normal, tx w/cold compress o Irrigate affected eye w/warm saline solution or artificial tears to improve pt comfort. o Record I&O for the 1st 24 hrs & anticipate fluid restriction to 1500 mL a day if there is pituitary involvement o Do NOT reposition pt on the operative site o Supratentorial surgery – elevate HOB 30 degrees, avoid extreme hip or neck flexion & midline neutral position to prevent IICP o Infratentorial (Brainstem) craniotomy – Flat and side-lying, alternating sides Q2 for 24-48 hrs. ▪ Pt to remain NPO for 24 hrs due to edema around medulla causing vomiting and aspiration. o Check head dressing @ 1-2 hrs & mark, small or moderate amount expected (30-50 mL Q 8hrs) ▪ Report saturated head dressing or drainage > 50mL/8hrs immediately to surgeon! o Drugs Given routinely ▪ Antiepileptic drugs, H2 Blockers or PPIs for stress ulcer prophylaxis, and glucocorticoids (dexamethasone) to reduce intracranial edema ▪ Acetaminophen for fever or mild pain  Preventing Post-op Complications o IICP ▪ Severe HA, dec LOC, restlessness, irritability, & dilated or pinpoint pupils slow to react or nonreactive o Hydrocephalus – caused by obstruction of the normal CSF pathway from edema ▪ HA, decreased LOC, irritability, blurred vision, urinary incontinence o Subdural or Epidural Hematoma ▪ Severe HA, rapid dec in LOC, progressive neurologic deficits, & herniation o Respiratory complications ▪ Atelectasis, PNA, & neurologic pulmonary edema (sx same as pulmonary edema but not associated w/cardiac problem) o Wound Infections ▪ Pts w/hx of DM, long-term steroid use, obesity, and previous infections ▪ Pt may or may not be febrile, wound reddened and puffy o Meningitis 11[Date] o Hyponatremia - from fluid overload from SIADH or steroids (weakness, change in LOC & confusion) ▪ UOP <20 mL/hr, decreased serum Na due to dilutional effect ▪ Conivaptan and tolvaptan for severe hyponatremia <118 o Hypernatremia – Caused by meningitis, dehydration, or DI (muscle weakness, restlessness, extreme thirst, and dry mouth). Untreated can lead to seizures. ▪ Suspect DI if pt voids lg amounts of very dilute urine w/inc serum osmolarity & electrolyte concentration. Urine specific gravity <1.005, urine osmolarity dec ▪ May need vasopressin if UOP >6L/24 hrs, desmopressin for long term replacement o Cerebral Salt Wasting (CSW) ▪ Primary cause of hyponatremia in neurosurgical pts. ▪ Hyponatremia, dec serum osmolarity, and dec blood volume ▪ Vasopressin and ANF levels differentiate CSW and SIADH ▪ Tx w/ replacement of Na and isotonic fluid volume  Community Based Care/IDC o Managed at home if possible, if have hemiparesis make sure home is accessible and safe o Rehab if needed, psychologist, dietitian (if radiation or chemo) o Teach seizure precautions as can have risk for up to 1 year after surgery 12[Date] Brain Abscess (962-964)  Purulent infection of the brain in which puss forms  Organisms from the ear, sinus, or mastoid area enter the bran by traveling along the wall of the cerebral veins.  Lung infection, ear infection, sinus infection, bullet, knife wound, or neurosurgery  Streptococci are most common organisms, Escherichia coli, Toxoplasma gondii (opportunistic infection in AIDS)  Assessment o Manifestations begin slowly – Fever, HA, Pain, hemiplegia, Ataxia, Sensory impairment, Aphasia, Seizures o Temporal field blindness – decrease in peripheral vision laterally o Severe – S/s of IICP ( Dec LOC, severe HA, bradycardia & widened pulse pressure) o Pupils respond normal in early stages o Inflammatory process is responsible for much of the clinical presentation  DX o WBCs and ESR elevated indicating presence of infection. IF ENCAPSULATED WBC COUNT NORMAL  Interventions o Combination antibiotics and maximum dosing o Antiepileptic drugs – phenytoin to prevent seizures Meningitis (863-865)  Inflammation of the meninges ( pia matter and arachnoid matter)  Caused by – penetrating trauma, surgery, ruptured brain abscess, basilar skull fx (ear or nose drainage of CSF), if have infection in the head (ear, nose, mouth, neck) has inc r/f meningitis  Otitis media, acute or chronic sinusitis, tooth abscess, tong piercing  Immunocompromised (w/o spleen) receiving tx for cancer, taking immunosuppressant drugs to manage autoimmune disease or solid organ transplant & older adults have an inc r/f  Viral Meningitis (most common) o Enterovirus, herpes simplex virus-2, varicella zoster virus (causes chix pox & shingles), mumps virus, & HIV  Bacterial Meningitis o Streptococcus pneumoniae (pneumococcal disease), H. Influenza, and Neisseria meningitides (meningococcal meningitis) o Meningococcal meningitis is a medical emergency! o Highly contagious – Outbreaks in high population density (college dorms, military barracks) o Vaccine available for meningococcal meningitis (Meactra & Menomune) o People ages 16-21 years have the highest risk of infection from meningococcal. First vaccine between 11-12 with a booster at 16. Adults should get an initial or booster when living in shared residence or a country where the disease is common or if they are immunocompromised. 15[Date] o In severe cases the pt may have IICP from cerebral edema, hemorrhage, & necrosis of tissue. Monitor for widened pulse pressure, bradycardia and irregular respirations (Cushing’s Triad – late sign of increase ICP)  Dx o LP – Clear fluid w/ INC protein, INC WBCs, & NORMAL Glucose o CT scan b4 LP to prevent herniation  Interventions/Management o Drugs ▪ Acyclovir or Vidarabine– antiviral drug for tx of herpes encephalitis ▪ NSAIDS for sx relief o Maintain patent airway to prevent PNA or atelectasis which leads to further brain hypoxia o Turn, cough deep breath Q2h; Assesse VS and neuro Q2 hr o Perform deep tracheal suction even with presence of increased ICP is respiratory status is compromised o HOB 30-45 degrees after LP o Keep room darkened and quite o Neuro deficits may be permanent 16[Date] o Prevention of West Nile Virus ▪ Insect repellant with DEET ▪ Vaccines for equine encephalitis Myasthenia Gravis (MG) (917-923)  Autoimmune disease that worsens with exercise and improves with rest.  Loss of Acetylcholine receptors in the neuromuscular junctions  Some cases have hyperplasia (abnormal growth) of the thymus gland due to a thymoma (thyroid tumor)  Initially pts present with reports about vision from disturbances of the ocular muscles  Signs and Symptoms o Progressive muscle weakness that worsens w/repetitive use and improves w/rest o Dysphagia, Poor posture, Ocular palsies, Fatigue ▪ Increased r/f lung infections from aspiration of foods, fluids, or saliva o Ptosis (drooping eyelid), diplopia, flat affect, tendency for the mouth to hang open, drooling o Respiratory weakness and compromise o Loss of bowel & bladder function o Muscle aches, Paresthesias, dec sense of smell or taste o Smile transformed into a snarl o Weight loss from difficulty chewing and swallowing and regurgitation of fluids through the nose. o More difficulty eating after talking o Voice weaker or nasal twang after extended conversations o Consciousness NOT altered  Dx o Immediately confirmed by pt response to cholinergic drugs o Endrophonium (Tensilon) Test & Neostigmine (Prostigmin) Test ▪ Inhibits the breakdown of Ach ▪ Pt w/ MG will show IMPROVEMENT ▪ Atropine antidote o EMG – Electromyography helps confirm the dx  Medical Management/Treatments o Pyridostigmine(Mestinon) – Cholinesterase Inhibitor drug, prevent decrease of Ach ▪ Take 45 min to 1 hr before meals(to prevent aspiration) with a snack, to alleviate GI distress ▪ Keep meds and glass H2O at bedside if you are week in the am ▪ Set timer (watch) to take meds on time, post drug schedule so others know it. ▪ Plan strenuous activities when drug peaks ▪ Avoid drugs containing Mag, morphine, hypnotics or sedatives to avoid increased weakness 17[Date] o Plasmapheresis – antibodies removed from plasma to dec sx, for short-term mgmt of an exacerbation o Immunosuppressants – corticosteroids, methotrexate, rituximab o IV immunoglobulin (IVIG) – for acute management or long-term mgmt. for disease refractory to other tx o Thymectomy ▪ Have w/i 2 years of onset, not always immediately effective, some may have no change at all ▪ Immediately b4 surgery give pyridostigmine to keep pt stable during surgery ▪ Antibiotics given immediately b4 or during surgery. ▪ Sterile technique for wound care ▪ Observe for signs of pneumothorax or Hemothorax  Sudden SOB, Chest pain 20[Date]  More common in males peaking after age 55  Some pts require intubation  Healing occurs in reverse  Results from o Bacterial infection (Campylobacter jejuni) o Viral infections (Influenza, Epstein-Barr, and cytomegalovirus) o Live vaccines 1-3 weeks prior to sx o Trauma, surgery  Stages o Acute or initial (1-4 weeks) – Onset of first sx and ends when no further deterioration occurs o Plateau (several days to 2 weeks) o Recovery Stage (gradually over 4-6 mon, up to 2 y) – Re-myelination and axonal regeneration  Signs and Symptoms o Ask pt to describe sx in chronological order o Motor–ascending symmetric muscle weakness to flaccid paralysis, falls, clumsiness ▪ Dec DTR’s, Respiratory compromise, Loss of bowel & bladder control, & Ataxia o Sensory – Paresthesias & Pain (cramping) o Cranial nerve – Facial weakness, Dysphagia, Diplopia & Difficulty speaking o Autonomic manifestations – Labile BP (low or poor control), Cardiac dysrhythmias (tach), Tachycardia o Does NOT affect level of consciousness, cognition, or pupillary constriction or dilation o PARALYSIS IS ONLY TEMPORARY!  Interventions o Priority is airway management as inability to maintain an airway is a high risk ▪ Monitor closely for s/s respiratory distress (dyspnea, air hunger, adv breath sounds, dec O2 sat, & cyanosis), rate rhythm and depth Q 1-2 hrs. Decline in mental status indicated hypoxia ▪ Keep intubation equipment at bedside  Dec in vital capacity to < 15-20 mL/kg & inability to clear secretions – need to intubate ▪ Monitor ABGs o Implement aspiration precautions – HOB 45 degrees, test for dysphagia b4 restarting oral anything, suction o Tx w/either plasmapheresis or IV immunoglobulin (IVIG) – no benefit in combining them ▪ 1st - IVIG is safer and immediately available, doesn’t need shunt access  Complications range from mild discomfort ( chills, mild fever, myalgia, and HA) to major complications ( anaphylaxis, aseptic meningitis, retinal necrosis, acute renal failure) ▪ NO steroids used ▪ Plasmapheresis  Need a shunt – check for patency (bruit & thrill) Q 2 hrs & Keep double dog clamps bedside 21[Date] o Report loss of thrill or bruit, uncontrolled bleeding & redness, drainage or swelling  Monitor electrolytes b4 & after tx, anticipate Ca replacement  Diphenhydramine or corticosteroid as premedication when urticarial (skin react) present b4  R/f coag depletion, CBC & coag panel b4 & after tx  R/f Infection from immunoglobulin depletion, v/s w/temp 3x daily  Monitor fluid status during tx and 2x in 1st hr after tx  Colloid substitute of albumin after if needed, NO FFP o Cardiac monitor due to r/f dysrhythmias o HTN tx w/ BB (-olol) or nitroprusside (vasodilator for HTN) o Hypotension tx w/ IV fluids and putting pt in supine position (unless in resp distress) or Atropine o Encourage max independence, active or passive ROM exercises daily o Weigh pt 3x and monitor serum prealbumin each week to evaluate nutritional status o VTE prophylaxis – Enoxaparin, SCDs, Teds, and ensure documentation o Pain management (worse at night), paresthesia or hyperesthesia (sensitivity to touch) 22[Date] ▪ Severe and requires opioids, gabapentin, or TCAs (not older adults) ▪ Opioids given initially for severe pain bc TCAs & gabapentin take a while to become therapeutic. o Promote communication ▪ Difficulty communicating due to weak muscles of being vented ▪ Speech therapist needed to develop communication system ▪ Blinking, moving finger, Board, Flash cards, or computer device to communicate  Interdisciplinary Care o Respiratory therapist to improve gas exchange o Physical, Occupational, Speech & Dietitian to prevent complications of immobility & address self- care deficits. o Refer to a Social Worker, Chaplin or psychologist for further psychosocial support o Interdisciplinary health team needed for supportive devices for home use Spinal Cord Injury (SCI) (892-902)  Most common sites for injury are C1-C2, C4-C6, & T11-L2 as they are the most mobile  Inflammation and swelling up and down the cord immediately after injury leads to loss of sensation & function  Cord edema peeks in 2-3 days and subsides in 7 days, not easy to determine degree of damage in this time  Assessment/Manifestations o First priority us to assess pt’s ABCs, Cervical SCI high r/f respiratory compromise (below C5 stay alive) ▪ Injury above C4 causes tetraplegia and pt can’t breathe independently o Below level of injury functions are lost ▪ Voluntary movement ▪ Sensation of pain, temp, pressure and proprioception ▪ Bowel and bladder function ▪ Spinal and autonomic reflexes (touch something hot, message doesn’t get to spinal cord) o Injury to C7 – pt can lift shoulders, elbows, wrists, and has some hand function. o Injuries to thoracic or lumbar spine can cause paraplegia- lower extremities are paralyzed o Sensory and Motor ▪ New loss of motor function in a pt w/recent SCI is an emergency, notify neurosurgeon! ▪ Reflexes and all movement or sensation absent immediately after due to spinal shock ▪ Reflexes may return if lesion is incomplete ▪ Muscle spasms can follow complete cord transection, NOT purposeful movement o Cardio & Respiratory ▪ Problems if injury is above T6 ▪ Bradycardia, Hypotension, & Hypothermia due to loss of sympathetic input ▪ Systolic BP <90 requires tx ▪ O2 sat <92% & advent. breath sounds indicate atelectasis or PNA, Hypercarbia means worse o GI & GU ▪ Assess for internal bleeding, distension, or paralytic ileus (dev w/i 72 hrs of hospitalization) 25[Date] ▪ Severe, throbbing HA o Causes ▪ Bladder or bowel distension ▪ Pressure ulcers ▪ Pain, muscle spasms, ingrown toe nails, uterine contraction (labor) o Immediate Interventions ▪ Place pt in sitting position (First priority!) ▪ Assess and tx the cause  IF pt has a catheter be sure it is not kinked as this is a common cause  Check sheets for wrinkles  Examine skin for new or worsening pressure ulcers  Give antihypertensive (nifedipine [CCB] or Nitrate) as prescribed ▪ Notify Dr after if can’t find the cause with quick assessment  Interventions o Injuries to lumbosacral area have flaccid bladder and bowel – Valsalva maneuver o Bowel program – stool softeners, fluids, high fiber, consistent time for elimination ▪ Rectal stimulation only if requested by HCP bc can cause vagal response (severe brady & syncope) o Teaching 26[Date] ▪ Mobility skills, pressure ulcer prevention, ADL skills, Bowel and bladder program, referral for sexual health counseling, Autonomic Dysreflexia prevention  Interdisciplinary Care o Respiratory therapist to improve gas exchange o PT and OT for splints to prevent contractures o Dietitian for assessment to initiate early nutrition, & speech therapy to assess swallowing b4 oral intake o Dietitian, Speech therapy, & OT to plan meals o Promote self-management w/regular communication w/pt , family, & interdisciplinary health care team o PT, OT, Rehab (goal is to prevent further loss of function), and home care for discharge Amyotrophic Lateral Sclerosis (ALS) (910-911)  Upper & lower motor neuron disease characterized by muscle weakness, muscle wasting (atrophy), & spasticity that eventually leads to paralysis.  Fatal paralytic disorder – Death w/i 3 years of diagnosis due to respiratory failure  Affects 5 in 100K people, common in men ages 40-60  Early Manifestations o Tongue atrophy o Weakness & beginning muscle atrophy of hands and arms o Fasciculations (twitching) of face or tongue o Difficulty controlling crying or laughing (emotional incontinence) o Nasal quality of speech o Dysarthria (slurred speech) & Dysphagia o Decreased vital capacity (<2L) o Fatigue while talking o Stiff or clumsy gait & abnormal reflexes o Sensory and cognition NOT affected o Bowel and bladder NOT effected  Dx o No specific test but Creatine Kinase (CK) will be increased  Interventions o No cure – INTERDICIPLINARY approach needed for maintaining optimum functioning and end-of-life care o Riluzole only drug approved for ALS pts to extend survival time (not a cure) ▪ Take drug on empty stomach ▪ Teach sx of liver toxicity (vomiting, jaundice) & have frequent liver enzyme tests o INTERDICIPLINARY health care team collaborates w/pt and family to develop individualized plan of care and palliation of sx o Referral to palliative care for sx management (pain fatigue, and dyspnea), not just at the end. 27[Date] o Pt and OT evaluate pt home and recommend modifications as the disease progresses o Special equipment obtained as needed to help w/ADLs and mobility o Prevent complications of immobility and promoting comfort o Speech therapist evaluate for speech and swallowing, techniques to speak louder & more clearly and develop communication system when pt can no longer communicate. o Nutrition consultant for planning meals pt can swallow when dysphagia occurs o Symptomatic tx of dyspnea or pain ▪ Opioids alone or in combo w/benzos if anxiety is present ▪ For palliation of terminal restlessness and confusion bc of hypercapnia, neuroleptics used (chlorpromazine) o Intermittent positive-pressure ventilation (IPPV) or BiPAP to aid breathing o Diaphragmatic pacing – electrical impulses to diaphragm, resulting in inhalation o Teach Pt the need for advanced directives, such as a living will b4 speech is severely impaired Trigeminal Neuralgia (TN) (926-927)  Irritation of the trigeminal (5th cranial) nerve (motor and sensory nerve)  More often in women >50  Intermittent episodes of SUDDEN INTENSE FACIAL PAIN 30[Date] Shock (739-756)  Decreased blood flow to the tissues – causes cellular dysfunction – leads to organ failure  Decreased tissue perfusion is the hallmark of the shock state and is seen in all types of shock  Tx focuses on return of tissue perfusion (MAP >65) & oxygenation  Hypovolemic o To little circulating blood volume decreases MAP from… ▪ Hemorrhage: Trauma, Ulcer, Surgery, & Inadequate Clotting ▪ Dehydration : Vomiting, Diarrhea, Diuretics, NG suctioning, DI, Hyperglycemia (polyuria) o Leads to anaerobic cellular metabolism and buildup of lactic acid causing metabolic acidosis.  Cardiogenic o Direct pump failure from MI, Cardiac Arrest, Ventricular Dysrhythmias, Cardiomyopathies o Decreased CO, Tissue Hypoxia but sufficient blood volume (backed up), o S/S – JVD, Hypotension (S<90, DEC CO, DEC UOP, cool extremities (vasoconstriction), altered mentation, INC PAWP. o Inotropic Agents – Dobutamine, Amrinone, Amniodarone  Distributive o Blood volume lost from distribution to the interstitial tissues where it cannot perfuse organs. o Caused from vasodilation (warm), pooling of blood, and increased capillary leak. Decrease MAP o Neural-induced – Pain, Anesthesia, Stress, SCI, Head trauma o Chemical-induced – Anaphylaxis, Sepsis, Capillary leak o Neurogenic Shock ▪ Loss of blood vessel tone (dilation) after severe cord injury resulting in hypoperfusion ▪ Manifestations occur w/i 24 hrs after injury, most common above T6 o Septic Shock ▪ Infectious organisms present in the blood, massive vasodilating from body’s immune response o Anaphylactic Shock ▪ Allergic reaction w/results in vasodilation, DEC BP, DEC CO; due to histamine o Capillary Leak Syndrome ▪ Capillaries response to chemicals that enlarge pores and allow fluid to shift into interstitial tissues ▪ From: Burns, Liver impairment, Ascites, Peritonitis, Hypoproteinemia, Excessive Trauma (large wounds), & Kidney Disease  Obstructive o Impair the ability of the normal heart to pump effectively – Non cardiac factor, total body fluid not effected o Cardiac Tamponade – JVD, Paradoxical pulse, Hypotension, Bradycardia – pressure on the heart o PE – Sudden dyspnea, Chest pain, Restlessness, Cough, Tachycardia, Tachypnea, Desat, Crackles, PF Rub o Pericarditis – Substernal pain radiates shoulder, worse supine, pericardial friction rub, HTN, JVD, 31[Date] Edema o Tension pneumothorax – RBS, Asymmetrical thorax, Tracheal deviation, JVD, Tachypnea, kinked aorta o Thoracic tumors (obstruct outflow); Arterial Stenosis; Pulmonary Hypertension  *Stages of Shock* o Initial – MAP decreases by <10 mm/Hg ▪ Compensatory mechanisms effective at returning SBP to normal O2 perfusion to organs maintained  Mild vasoconstriction & Increased HR from SNS stimulation ▪ Difficult to detect at this stage, usually pts who were NPO b4 surgery ▪ Post-op pts who are tachycardic w/o pain & cold extremities from vasoconstriction ▪ HR & RR increase or slight increase in DBP may be only manifestation of this stage o Non Progressive – MAP DEC 10-15 mm/Hg ▪ Hypoperfusion begins & cells do not receive enough O2 to meet needs – Anaerobic Metabolism ▪ Lactic acid production causes mild acidosis and hyperkalemia – Hyperventilation to compensate 32[Date] ▪ SNS compensation – Moderate vasoconstriction, INC HR, DEC PP ▪ Kidney compensation – Release ADH, aldosterone, epi & norepi. DEC UOP, INC Na absorption  Epi & Norepi cause vasoconstriction, INC contractility, & INC BS ▪ Tissue hypoxia occurs in NONVITAL organs – Skin, GI, & kidneys but not enough to cause damage  Baroreceptors sense dec BP and cause shunting of blood to vital organs ▪ S/S – Thirst, Anxiety, Restlessness, Tachycardia, Tachypnea, DEC UOP, DEC SBP, INC DBP, Narrow PP, cool extremities, 2%-5% DEC in O2 sat o Progressive (Decompensated) – MAP DEC >20 ▪ Compensatory mechanisms begin to fail, blot clots form from blood sludging ▪ Hypoxia of vital organs – Anoxia (no oxygen)of vital organs ▪ Acidosis progresses – Low pH w/rising lactic acid and potassium levels, Inc anaerobic metabolism ▪ S/S – Rapid weak pulse, Hypotension, Pallor to cyanosis of oral mucosa & nail beds, Cool & moist skin, Anuria, 5%-20% DEC in O2 sat ▪ Life-threatening emergency! Pt can be saved if corrected in 1 hr or less from onset of this stage o Refractory (Irreversible) – DEATH ▪ Too much cell death & tissue damage result from too little O2 reaching the tissues. ▪ Vital organs have extensive damage and cannot respond to interventions ▪ Severe tissue hypoxia w/ischemia and necrosis ▪ Multiple Organ Dysfunction Syndrome (MODS) – 2 or more organ systems fail  Massive release of toxic metabolites and enzymes  Trigger small clots to form which block perfusion more and damage more cells  Liver, heart, brain, and kidney function lost first. Most profound is damage to heart  Mortality 90-100% when 3+ organ systems fail  S/S – Rapid loss of consciousness, non-palpable pulse, cold dusky extremities, slow shallow respirations, unmeasurable O2 sat,  Therapy not effective at saving life, even if cause of shock corrected & MAP temp normal  Assessment Findings o Assign an RN not an LPN or UAP to assess VS of a pt at r/f or suspected of having hypovolemic shock o Cardiovascular Changes ▪ Dec MAP – Assess pulses for rate and quality, initial stage pulse increases  Increased HR is the first manifestation of shock! ▪ Hypotension – Drop in DBP, changes in SBP not always present in initial stage  When assessing BP, consider pt/s baseline, 90/50 may be normal in a healthy an adult ▪ Vasoconstriction – raises DBP while SBP stays same resulting in narrow PP  SBP decreases as shock progresses ▪ O2 Sat decreases w/each stage – Any value below 70% is emergency, refractory stage o Renal Changes 35[Date]  Early detection of sepsis b4 progression to septic shock is a nursing priority  Sepsis With SIRS o Infection in blood stream & causes widespread inflammation (Systemic Inflammatory Response Syndrome) o Widespread vasodilation and blood pooling o Low-grade fever and mild hypotension are early signs o Suspected or identified infection w/ some of the following ▪ Temp > 101 (38.3C) or <96.8 (36C) ▪ HR >90 BPM ▪ RR >20 ▪ WBC >12,000 or <4,000 ▪ Arterial HYPOtension (SBP<90; MAP <70) ▪ UOP <0.5 mL/kg/hr ▪ Absent bowel sounds ▪ INR >105 or aPTT >60 ▪ Platelet count <100,000 ▪ Elevated Lactic Acid Levels ▪ Hyperglycemia (glucose >140) in absence of diabetes ▪ Unexplained change in mental status ▪ Significant edema or positive fluid balance 36[Date] o Clotting w/microthrombi forming causing hypoxia and reducing organ function. Will progress unless intervene ▪ If tx at this stage cycle of progression stops and good outcome. If not progresses to severe sepsis o Call RRT or HCP for any pt who has VS or other conditions that meet sepsis w/SIRS criteria  Severe Sepsis o Sepsis PLUS sepsis-induced organ dysfunction or tissue hypoperfusion – hypoxic tissues o Microthrombi formation widespread – uses up platelets & clotting factors (DIC) o Decreasing levels of activated protein C indicate beginning of severe sepsis o Plasma D-Dimer levels rise as fibrin in clots break down o Hyperglycemia, Anaerobic metabolism, Widespread capillary leak, Pooling of blood, & Warm extremities o WBCs no longer elevated (may be extremely low) due to bone marrow not keeping up w/demand o Manifestations – INC HR, INC SBP, Low O2 sat, Rapid RR, Dec to absent UOP, Change in pt cognition and affect o The stress of severe sepsis can cause adrenal insufficiency – IV hydrocortisone and oral fludrocortisone  Surviving Sepsis Care Bundle o Within the first 3 hrs of suspecting severe sepsis ▪ Serum lactate levels ▪ Blood cultures B4 antibiotics ▪ Broad-spectrum antibiotics ▪ HYPOtension OR serum lactate level is >4 mmol/L – 30 mL/kg crystalloids IV o Within 6 hrs of initial manifestations of suspected septic shock ▪ Vasopressors for HYPOtension that didn’t respond to fluid therapy to maintain MAP>65  Dopamine, Noreip, Phenylephrine ▪ If Arterial HYPOtension persists despite fluids (indicating septic shock) or lactic acid remains >4  Measure Central Venous Pressure (CVP)  Measure Central Venous Oxygen Saturation ▪ Re-measure lactic acid (lactate) level if initial value was elevated o Target outcomes of implementing sepsis bundle are obtaining and maintaining a Central Venous Pressure (CVP) of 8mm Hg or higher, central venous O2 sat of at least 70% and return of lactic acid levels to normal  Septic Shock o Sepsis-induced hypotension persisting despite adequate fluid resuscitation o Tachypnea and tachycardia are early s/s o MODS – Organ failure evident w/poor clotting w/uncontrolled bleeding (platelets & clotting factors gone) o Even w/interventions death rate is very high o Clinical Manifestations resemble late stage of hypovolemic shock 37[Date] o DIC - Bleeding from any area of non-intact skin o LOW Hct, Hgb, Platelets, Fibrogen levels, Activated protein C – from DIC  Factors Increasing R/F Sepsis o Malnutrition, Immunosuppression, Lg open wounds, GI ischemia, Invasive procedures, >80 Y, Infection w/ resistant organisms, Chemotherapy, Alcoholism, DM, CKD, Transplant recipient, Hepatitis, HIV/AIDS o Aspirin, corticosteroids, antibiotics and cancer therapy drugs  Assessment o Cardiovascular changes ▪ Early Sepsis & Septic Shock - CO and BP are low in early sepsis and very low in septic shock. ▪ Severe sepsis – INC CO, INC HR, & INC BP ▪ DIC – excessive clotting uses up clotting factors, leads to poor clotting & inc r/f hemorrhage in septic shock stage. Blood may ooze from gums, mucous membranes, IV sites, stick sites o Respiratory Changes ▪ First caused by compensatory mechanisms to try to maintain O2 w/rate increase ▪ ARDS may occur in septic shock from prolonged inflammatory response o Kidney/urinary changes ▪ If pt suddenly has low UOP be leery of severe sepsis or septic shock, INC serum creatinine levels o Psychosocial 40[Date]  Burn Classifications o Superficial-Thickness ▪ Epidermis only part injured – least damage ▪ From prolonged exposure to low-intensity heat (sunburn) or short (flash) exposure to high heat ▪ Desquamation – Peeling of dead skin occurs 2-3 days after the burn o Superficial Partial-Thickness ▪ Injury to upper 1/3 of dermis , leaving good blood supply ▪ Pink and moist and blanch when pressure applies, leaks plasma causing blisters ▪ Large blisters are opened and debrided to promote healing ▪ Increase pain sensation, nerve endings exposed, touch causes intense pain o ▪ Fewer healthy cells remain, red and dry w/white areas in deeper parts ▪ Soft dry eschar - Scab ▪ Blanches slowly or not at all and blood flow is reduced o FULL THICKNESS ▪ Hard, inelastic, dry, leathery eschar (dead skin) ▪ Some painful and some not ▪ Eschar mush slough off or be removed before healing can occur ▪ Circumferential – Completely surround extremity or chest, blood flow/chest movement reduced ▪ Escharotomy or Fasciotomies – to relief pressure & allow blood flow and breathing ▪ Waxy white, deep red, yellow, brown, or black ▪ Compression garments to minimize fluid loss while healing o Deep Full Thickness ▪ Damage to muscle, bone, and tendons w/NO sensation ▪ Black, hard and inelastic eschar, and depressed o Electrical Burns ▪ Surface injuries look small but internal injuries huge, with entrance & exit wounds & arch burns ▪ Airway and breathing intact – concerned with organs and HEART RHYTHUM ▪ Due to internal injuries – count anterior & posterior % for TBSA  System Changes 41[Date] o Vascular Changes ▪ Fluid shift – After initial vasoconstriction, result of vessels dilating & leaking fluids interstitially  Loss of plasma and proteins, decreasing blood volume & BP  Fluid shift w/excessive weight gain occurs in 1st 12 hrs & continues for 24-36 hrs ▪ Profound fluid, electrolyte and acid based imbalances  Hypovolemia o Hemoconcentration – INC blood osmolarity, Hct >52%, Hgb >18 bc dehydration o Increased blood viscosity, reducing blood flow & increasing tissue hypoxia  Metabolic acidosis  HYPERkalemia – from direct cell injury that releases large amounts of cellular K+  HYPOnatermia – Loss from wounds into interstitial spaces ▪ Fluid remobilization  24 hrs after injury, capillary leak stops  Diuretic stage begins 48-72 hrs after injury - HYPOnatermia, HYPOkalemia, & anemia o Cardiac Changes ▪ INC HR & DEC CO ▪ After 24 hrs CO will INC to 2-2.5x normal ▪ BP will vary w/fluid status o Pulmonary Changes ▪ Damage from inhalation injury (esp indoors), cause edema & obstruction of trachea o GI & GU Changes ▪ DEC blood flow to GI tract – paralytic ileus may develop causing abd distension  If have 25% burn or intubated, need NG tube to remove gastric secretions ▪ Curling’s Ulcer – acute GI ulcer from stress of severe injury (give PPI or H2 Blockers to prevent) ▪ UOP decreased during 1st 24 hrs from decreased blood flow, concentrated & INC specific gravity ▪ Damage to kidneys from myoglobin (lg molecules)release from muscle damage can cause AKI o Metabolic Changes ▪ Pt’s O2 use and caloric needs are high due to hypermetabolism ▪ Pt’s caloric needs 2-3x normal and peek 4-12 days after burn and remain elevated for months o Neuro ▪ NO DEC LOC from just a burn except w/prolonged smoke exposure ▪ Always look for cause for neuro changes o Hypothermia from loss of body heat through burn wound ▪ Shivering INC O2 & caloric needs & causes vasoconstriction, extremely harmful (keep room warm) ▪ Tx shivering with thorazine  Resuscitation Phase of Burn Injury o 1 – Secure patent airway ▪ Inspect for s/s of inhalation burn  Injured in a closed space, burns to face, singed hair, oral charcoal  Progressively hoarse, wheezing, stridor, brassy cough, audible breath sounds  Drooling or difficulty swallowing  Pt about to lose airway! Immediately apply O2 and call RRT IMMEDIATE INTUBATION ! ▪ Monitor carbon monoxide (CO) levels on pt w/sx on inhalation, sx of CO poisoning don’t occur until levels reach 15% (normal is <5%)  CO has high affinity for Hgb and takes place of O2, pulse ox reads 100%  Pt will be cherry red, warm, w/absence of cyanosis but tachycardic, tachypnic, & hypoxic  Need a carboxy hemoglobin test for accurate readings pulse ox will not be accurate ▪ Thermal (Heat) Injury  Steam or aspiration of hot liquids  Tissues rehydrate during fluid resuscitation and swell causing obstruction  Intubation early b4 obstruction occurs ▪ Pulmonary Fluid Overload  From fluid resuscitation may cause heart failure  Pt is SOB & has dyspnea in supine position & has crackles  Elevate HOB to 45 degrees, apply O2, and notify burn team or RRT ▪ Keep intubation equipment at bedside  PaO2 <60 need to intubate ▪ R/F ARDS  Coordinate w/Respiratory Therapy – PEEP needed on vent  Monitor ABGs and Pulse Ox  Immediately report s/s of respiratory distress or changes in respiratory patterns to burn & RT ▪ If pt is on a vent & high pressure alarm sounding escharotomy needed to reduce pressure on chest o 2 – Support circulation & organ perfusion by fluid replacement ▪ 4mL/kg/%TBSA of crystalloid (NS or LR) solution IV in 24 hrs 24 ▪ Topical antimicrobial ointments  Silver sulfadiazine, Sulfamylon, bacitracin – applied 1-2x daily  Acticoat, Mepilex Ag, & Aquacel Ag – Contain antimicrobials that release over days o Left on wound for up to 7 days ▪ Systemic Antibiotics only when pt has s/s of ACTUAL INFECTION ▪ Disposable items – Pillows, dishes, etc. as much as possible ▪ NO plants, flowers, raw foods, rugs, or upholstered articles o Minimizing Weight Loss ▪ Coordinate w/ registered dietitian ▪ Pt needs (25 kcal/kg) + 40 kcal x %TBSA in 24 hrs, can exceed 5000 calories a day ▪ High protein needed for heeling ▪ Encourage pts who can eat solid foods to ingest as many calories as possible whenever they can ▪ Offer frequent high-calorie, high-protein supplemental feedings ▪ Parental feedings as last resort, if GI tract not functional or needs not met orally o Maintaining Mobility ▪ Positioning  Prevent contractors - Maintain pt in neutral body position w/minimal flexion o Head and neck – No pillow, rolled towel under neck, Neck splint o Chest – Supine position, folded towel under spine between scapulae o Elbow – Keep joint in extended position o Wrists & fingers – Splint 25 o Ankles – padded foot board or splint o Legs – Pillow between knees o Hip – Supine, legs extended, trochanter roll, foam wedge along lateral aspect ▪ ROM exercises  3x a day; hand, thumb and fingers every hour awake ▪ Ambulation ASAP ▪ Compression Dressings  After grafts heal to prevent contractures & tight hypertrophic scars, which can inhibit mobility  Worn 23 hrs a day, every day, until scar tissue is mature (12-24 months)  Save mobility and reducing scaring  Rehabilitative Phase of Burn Injury o Reassure pt feelings are normal, coordinate w/ other health care team members to address issues o Discharge planning will involve many disciplines, interdisciplinary team meets regularly to evaluate o Needs to be addressed b4 discharge ▪ Financial assessment ▪ Family resources ▪ Psychological referral ▪ Pt & family teaching ▪ Training for wound care ▪ Speech therapy ▪ Rehab referral ▪ Home assessment ▪ Medical equipment ▪ Long-term care placement