Adult Health II Study Guide PDF

Risk factors: HTN, age, aortic diseases, genetics, trauma, tobacco use a. Clinical Manifestations Pain characterized as… - Sudden, severe pain in anterior part of chest, or interscapular pain radiating down spine to abdomen or legs...

Risk factors: HTN, age, aortic diseases, genetics, trauma, tobacco use a. Clinical Manifestations Pain characterized as… - Sudden, severe pain in anterior part of chest, or interscapular pain radiating down spine to abdomen or legs - Described as “sharp”, “worst ever”, “tearing”, “ripping” - May mimic that of MI Cardiovascular (hypotension, tachycardia, peripheral pulses), neurologic (altered LOC, dizziness, weakness, syncope, absent carotid and temporal pulses), and respiratory signs (SOB) may be present Older patients are more likely to have hypotension and vague symptoms b. Aorta may rupture: Hemorrhage may occur in mediastinal, pleural, or abdominal cavities Lead to occlusion of arterial supply to vital organs If ruptured, emergent surgical intervention required - 90% mortality with ruptured AAAs - Results in exsanguination and death c. Management: Bed rest (semi fowlers), pain relief, blood transfusion (if needed) Supplemental O2, maintain IV access, continuous ECG, labs, imaging studies, check pulses Drug therapy: antihypertensives and pain meds Surgical therapy Exam 3 Study Guide Ch 21 Emergency nursing Emergency Nursing 1. Emergency management: care given to patients with urgent and critical needs > 130 million people visit EDs each year, leading to overcrowding and long wait times - Number of patients admitted to the hospital is increasing - Older, sicker patients w more complex needs are being seen in the ED Most common reasons for ED visits  EMTALA (emergency medical treatment and labor act) - prevents any hospital ED that receives Medicare funds (which includes most US hospitals) from refusing to treat patients 2. Disaster nursing: another component of emergency nursing Includes mass casualty, terrorism, environmental disasters Assessment Triage (“to sort”): process of rapidly determining patient acuity; - Triage system identi es and categorizes patients so the most critically ill are treated 1st - 5 Level Emergency Severity Index: uses concepts of illness severity and resource use (ECG, lab tests, radiology, IV uids) to determine who we should treat rst Primary Survey: A, B, C, D, E Secondary Survey: F, G, H, I - Primary and secondary survey is used for all trauma pts, for nontrauma pts, primary survey is followed by a focused assessment Emergency Severity Index (ESI) ESI-1 and 2 will NOT have stable VS, while ESI-3 to 5 should have stable VS ESI-1 Unstable Obvious life threatening, seen immediately by physician I.e. cardiac arrest, intubated trauma pt, overdose w bradypnea, severe respiratory distress, anaphylactic shock ESI-2 Threatened Likely life threatening, continuous monitoring, seen within 10 min I.e. chest pain from ischemia, multiple trauma unless responsive, suicidal pt, immunocompromised pt w fever, acute stroke  ESI-3 Stable Possibly life threatening, multiple procedures and tests I.e. abdominal pain or gyno disorders unless in severe distress, hip fracture in older pt, vomiting, HTN ESI-4 Stable Not life threatening, requires exam and 1 diagnostic test I.e. closed extremity trauma, simple laceration, cystitis ESI-5 Stable Not life threatening, requires exam only Cold symptoms, minor burns, poison ivy, prescription re ll Primary Survey Focuses on identifying & stabilizing life-threatening conditions at each step A - Airway, B - Breathing, C - Circulation, D - Disability, E - Exposure - If there is uncontrolled external hemorrhage, the usual ABC may be ABC, C for catastrophic hemorrhage, this is controlled rst in this case A-Assessment of Airway (and alertness) Airway obstruction is cause of nearly all immediate trauma deaths - Results in hypoxia → death - S/S of compromised airway: dyspnea, inability to speak, gasping (agonal) breaths, foreign body in airway, trauma to face or neck Causes: saliva, bloody secretions, vomitus, laryngeal trauma, dentures, facial trauma, factures, and dentures Risks: seizures, drowning, anaphylaxis, foreign body obstruction, cardiopulmonary arrest Assessment Interventions - least to most invasive 1. Inspection Maintain cervical spine stabilization w 2. Auscultation airway management (also keep bed at) 3. Palpation: palpate face, neck, chest for 1. Oxygen tenderness, swelling, fractures or 2. Suction or remove any foreign bodies subcutaneous emphysema (crackly 3. Chin lift/jaw thrust maneuver opens sensation indicative of air trapping airway beneath the skin) 4. Insert oral/nasal airway 5. Intubate  Assessing alertness is important for right airway 6. Cricothyrotomy (if intubation is not interventions possible) Rapid-Sequence Intubation (RSI): preferred procedure for securing an unprotected airway - Use of sedation/anesthesia and paralytic: aid in intubation and reduce the risk for aspiration and airway trauma - Sedation (lowers anxiety, discomfort, awareness, gagging, resistance, and stress response) should be given prior to paralytic (unable to breath or move) B -Breathing & Ventilation/ Post RSI Adequate air ow thru upper airway does not ensure adequate ventilation Common causes: fractured ribs, pneumothorax, penetrating injury, allergic rxns, PE, asthma attacks Assessment Interventions 1. Inspection: spontaneous or assisted, rise and fall of O2 via non rebreather mask the chest (paradoxical mvmt, use of accessory or abd Bag valve mask (BVM) ventilation w muscles, visible wounds, color of nail beds, mucous 100% O2, needle decompression, membranes) intubation, and tx of underlying 2. Auscultation: bilateral breath sounds, diminished or cause absent breath sounds 3. Palpation: chest wall, clavicle and neck for tenderness, and SQ air C- Circulation and Control of hemorrhage Uncontrolled internal or external bleeding leads to risk for hemorrhagic shock Assessment Interventions 1. Palpation: quality and rate of pulses → 1. Insert two large bore IVs in upper carotid, radial, femoral (peripheral pulses extremities (unless contraindicated, may be absent bc of injury or other options: intraosseous or central vasoconstriction venous access)  2. Inspection: for skin for color, temp, 2. Start aggressive uid resuscitation using moisture NS or LR Assess for signs of shock: mental status, delayed 3. Packed RBCs if needed (O– type in cap re ll, VS emergencies) NO circulation → initiate CPR (C-A-B) Start compressions within 10 seconds of identifying cardiac arrest Compress chest at least 2 inches, 30 times on the lower half of the breastbone Compress 2-handed, with one hand on top of the other Compress at a rate of at least 100 compressions per minute Each set of 30 compressions should take 18 seconds or less Allow complete chest recoil after each compression Minimize interruptions in chest compressions to less than 10 seconds CPR ratio is 30 compressions to 2 breaths Ratio stays the same for one-person & two-person CPR D- Disability Brief neurological assessment - LOC: measure of the degree of disability - Glasgow coma scale (GCS) is used to determine LOC, not accurate for intubated or aphasic patients - Assess pupils for size, shape, equality, and reactivity  AVPU for alertness - Alert = speak to patient, if alert and responsive - Verbal = response to verbal stimuli - Pain = response to painful stimuli - Unresponsive = does not respond to painful stimuli E -Expose/Environmental Remove clothing to assess full body - Do NOT cut thru forensic evidence (i.e. sexual assault) Do not remove impaled objects Prevent heat loss w warming measures such as warm blankets, overhead warmers, and warm uids Maintain privacy Secondary Survey F -Full set of vital signs and Family presence Obtain VS: BP, pulse rate, RR, SpO2, temp, pain - BP in both arms may be necessary if there is chest trauma or abnormally high or low Determine family desire to be present during resuscitation and invasive procedures - Bene ts for patients, caregiver and sta : provide comfort, advocate, and reminds sta of the person behind the trauma - Serve as patient and sta helpers - Assign someone to explain care and answer questions G - Give Comfort and Get monitoring devices Pain management: nonpharm and pharm measures - Nonpharm/general comfort: adjusting lighting, warm blankets, ice or heat packs, positioning, distraction - Psychological support: acknowledge their pain and feelings Monitoring devices: lab tests, ECG, feeding tubes, O2 and/or ventilation H- History & Head-to-Toe Assessment SAMPLE - S = Symptoms from the injury or illness - A = Allergies - esp latex, contrast dye for possible diagnostics and procedures  - M = Medication history - P = Past medical history (PMH) - L = Last meal - if surgery/anesthesia is immediate - E = Events preceding illness or injury Physical head-to-toe assessment - Head, neck, face - Chest - Abdomen and anks - Pelvis and perineum - Extremities I- Inspect Posterior Surfaces Logroll patient (protect cervical spine) to inspect posterior surfaces - Requires 3-4 (or more) people, 1 person supports the head Inspect and palpate for deformities, bleeding, lacerations, bruising; palpate entire spine Abdomen and anks - evaluate frequently for subtle changes - Blunt or penetrating trauma, inspection of external signs of injury, auscultate bowel sounds, palpate masses, guarding, and femoral pulses - Focused abdominal sonography for trauma (FAST) for intra abdominal hemorrhage, CT scan for retroperitoneal bleeding Trauma Wound or injury in icted on a body from a mechanism in which the body cannot protect itself Consider forensic evidence Multiple Trauma: Priority Management Establish airway and ventilation Control hemorrhage - pressure, elevation, tourniquet Prevent and treat hypovolemic shock - aggressive uid resuscitation, blood products, maintain body temp Assess for head and neck injuries Evaluate for other injuries Splint fractures and reassess pulses and neurovascular status Perform more thorough assessment, and diagnostic studies after stabilization Types of Injuries  Intra-abdominal injuries a. Penetrating - gunshot or stab wounds b. Blunt - motor vehicle accidents (MVAs), falls, blows, explosions Internal bleeding Intraperitoneal injury (contamination, infection) Genitourinary (kidneys, ureters or bladder) Crushing injuries/ fractures FAST (focused abdominal sonography for trauma) Exam Rapid ultrasound assessment to identify blood in the peritoneal space and assess cardiac function Noninvasive, cannot rule out retroperitoneal bleed (so a CT may be needed) Gerontologic Considerations: Emergency Care People > 60 account for 20% of all ED visits - Regardless of age, aggressive interventions are warranted for all injuries or illnesses unless pt has a preexisting terminal illness, very low chance for survival, advance directive stating di erent course of action  Know normal aging processes and explore symptoms reports as many elderly patients dismiss S/S as part of aging Elderly are at high risk for injury → primarily from falls Causes: generalized weakness, environmental hazards, orthostatic hypotension, cardiovascular syncope - Determine if physical ndings caused the fall or if they are due to the fall - I.e. acute confusion from stroke caused the fall or head injury from tripping on rug Environmental Emergencies Heat Cold Submersion Stings/Bites Poisonings Violence Terrorism Heat Induced Illnesses: Heat Stroke Medical emergency, most severe form of heat stress Failure of the heat regulating (hypothalamic thermoregulatory) mechanisms - Increased sweating, vasodilation, increased RR deplete uid and electrolytes, esp Na+ Can be non-exertional (w/o signi cant physical activity) or exertional (during physical activity) Thermal injury at the cellular level → cerebral edema and hemorrhage - Death from heatstroke is directly related to amount of time that the body temp is high Assessment Management Profound CNS Stabilize ABCs: 100% O2, cardiac monitoring, correcting dysfunction: altered mental electrolytes and coagulation status, confusion, weakness Rapidly reduce the core temperature until it reaches 102℉ → coma Immersion in a cold water bath (most e ective) Body temp 105℉ or higher Remove clothing, cover with cool, wet sheets Hot, dry skin, no sweat Place in front of large fan Tachypnea, tachycardia Apply ice to neck, groin, chest and axillae Monitor for temp and control shivering (treat w chlorpromazine)  - Bc shivering increase core temp Monitor for rhabdomyolysis (risk for kidney injury), DIC Hypothermia Core temperature < 95℉ Occurs when heat produced by the body cannot compensate for heat lost to the environment a. Primary - environmental exposure b. Secondary - speci c condition that produces hypothermia Risk factors: environment, some meds, alcohol, traumatic injury, shock, DM Symptoms (mimic cerebral or metabolic disturbances) - Ataxia (cerebellum is esp sensitive to temp changes), shivering, lethargy, bradycardia, hypotension, metabolic and respiratory acidosis Mild 93.2 – 96.8℉ Moderate 86 – 93.2℉ Severe < 86℉ Shivering Rigidity, slow speech Appears dead, no shivering Lethargy Bradycardia HR, RR metabolic rate may not be Confusion Slowed RR detectable, very low BP, blue skin Behavior changes BP only obtainable by Absent re exes, pupils xed & Minor HR changes (↑ to doppler dilated compensate at rst) Acidosis Slow blood increases risk of MI, Hypovolemia PE, stroke, renal failure Management - ABCs - Remove wet clothing, rewarm the patient Active Internal Warming External Warming (active or passive) Heated Humidi ed O2 Warm blankets Warmed IVF Skin to skin Peritoneal Lavage Radiant Heat Lamps Cardiopulmonary Bypass  - Supportive care - Correct dehydration and acidosis - Cardiac monitoring and treat dysrhythmias – death usually caused by refractory V b → warm them to at least 86 before pronouncing death - Monitor for afterdrop (further drop in core temp), so rewarm gradually - Discontinue rewarming once the core reaches 90 -95℉ Submersion Injuries Result of hypoxia after submersion in a substance (usually water) Risk factors: inability to swim, substance use, poor judgment, trauma, seizures, hypothermia, stroke, child neglect Non-Fatal Drowning: survival for at least 24 hours after submersion that caused respiratory arrest - Aspiration of substance (i.e. water) → destruction of alveolar-capillary membrane → pulmonary edema → ARDS - Hypoxia → hypercapnia → resp acidosis - Bradycardia/ dysrhythmias Aggressive resuscitation e orts (airway, ventilation) improve survival esp in prehospital phase Do not abandon e orts to save the patient prematurely Treatment: - Mechanical ventilation w PEEP or continuous positive airway pressure can improve gas exchange across the alveolar-capillary membrane when pulmonary edema is present - Correct hypoxia and uid imbalances - Support basic physiologic functions - Rewarm patient if hypothermia is present Bites Dog bites management Cat bites management Human bites management Clean with irrigation Clean with irrigation Clean with irrigation Debridement Debridement Debridement Tetanus prophylaxis/rabies - Tetanus prophylaxis/rabies - Tetanus prophylaxis depending on last date of vaccines, same as dog bites Analgesics wound severity, behavior of dog Analgesics Antibiotics  Analgesics Antibiotics Take pictures for evidence Antibiotics Leave open puncture (esp for violence and SA) Loosely suture lacerations wounds (allows for Common sites - hands, ear, (allows room for swelling, drainage, ↓ risk of abscess nose, vagina, penis drainage, tension relief of wound formation) edges) Report to public health Report to public health authorities authorities Tick Spider Snake Lyme Disease Brown Recluse Envenomation (poisoning by Flu-like symptoms Non-painful venom): Bulls eye rash Fever, chills, N/V, Edema, ecchymosis Arthritis, meningitis, malaise, joint pain Necrosis neuropathies Reddish purple w Lymph node tenderness Rocky Mountain Spotted Fever necrotic center N/V Pink rash Black Widow Numbness Flu-like symptoms Pin prick feeling Metallic taste Tick Paralysis Systemic e ects within Can progress to coma Flaccid ascending paralysis 30 min Can be fatal Abdominal rigidity, N/V, Lie down HTN, tachycardia, Remove constrictive items Tick removal - use forceps or paresthesias, severe pain Cleanse & cover wound tweezers to grasp tick close to pt Immobilize the body part below of attachment, pull steadily Ice, elevate, analgesia, cardio- heart upward, clean w soap/water pulmonary monitoring, Antivenin (available for each Antibiotics antivenin species) Violence Acting out of emotions to cause harm Family and intimate partner violence (IPV), elder abuse Causes: organic disease (brain tumors, TBI, epilepsy, brain lesions, neurodegenerative diseases), psychosis, antisocial behavior, drug and alcohol use  Screen for family violence and IPV: “Do you feel safe at home?”, be sensitive when gathering information → could lead to increased risk for pt, report to authorities, provide options to pt Poisonings Causes harm to the body through chemical action (can a ect every tissue and any body system) - May be accidental, occupational, recreational, or intentional - Can be ingested, inhaled, injected, splashed in the eye, absorbed thru the skin Severity depends on type, concentration, route of exposure Management depends on: 1. Decreasing absorption: a. Gastric lavage (stomach pumping) - may be intubated, most e ective if done within the hour of ingestion, monitoring for signs of distress - Contraindicated w caustic agents, co-ingested sharp objects b. Activated charcoal - most e ective intervention: administer PO or via gastric tube within 60 mins of poison ingestion - Contraindicated w diminished bowel sounds, paralytic ileus, ingestion of substance poorly absorbed by charcoal (i.e. iron, lithium, alcohol), signi cant intestinal bleeding, caustic agents (strong acid or base) 2. Enhance elimination: a. Cathartics (i.e. sorbitol) - give w 1st dose of charcoal to stimulate intestinal motility/increase elimination b. Whole bowel irrigation - cleanse entire GI tract, liquid solution used c. Hemodialysis can be an option for alcohols, aspirin, lithium 3. Implementing toxin-speci c interventions per poison control center Skin and eye poisoning management: dermal cleansing/eye irrigation - Skin and ocular decontamination: remove toxins from skin and eyes using water or saline for at least 15 min Exception: mustard gas; toxins can be removed w/ SALINE ONLY bc water mixes with mustard gas and releases chlorine gas - Skin: assess for burns, blisters, and systemic e ects; eye: assess vision acuity, damage Death in the Emergency Department Determine if patient could be candidate for non–heart beating donation Tissues and organs (e.g., corneas, heart valves, skin, bone, kidneys) can be harvested from patient after death  - Organ procurement organizations (OPOs) assist in screening potential donors, counseling donor families, obtaining informed consent, harvesting organs Must recognize importance of hospital/cultural considerations in preparing the bereaved to grieve Disasters and Emergencies If a mass casualty/ disaster situation occurs: the agency disaster preparedness plan where you work (emergency response plan) should be immediately activated Color tagging of patients: - Black = expected to die or are deceased, i.e. cardiac arrest, massive head trauma - Red = life threatening injury requiring immediate intervention, i.e. severe bleeding, airway obstruction, resp distress - Yellow = urgent, but not life threatening injuries, i.e. fractures, signi cant but stable injuries - Green = minor injuries, i.e. minor cuts, abrasions, sprains Ch 63 Chronic neurologic problems Objectives Di erentiate between epilepsy and seizure types Compare and contrast the pathophysiology and clinical manifestations of neurologic disorders Identify diagnostic tests, nursing priorities, client education, and possible treatment interventions associated with chronic Seizures A sudden abnormal, excessive, electrical discharge bw brain cells that causes temporary abnormalities in muscle tone or movements, behaviors, and sensations or states of awareness. Causes: - Stroke - direct, or indirect (scar tissue) - Metabolic impairment: uremia (toxins buildup due to kidney dysfunction), encephalopathy, poisoning - Blood sugar dysregulation (hyper and hypo) - High fever (esp in kids) - Drug or alcohol withdrawal (start 4-6 hrs after last drink), benzos, other illicit drug use - HTN (Malignant HTN)– esp in women of child bearing age - Idiopathic – sometimes have one and then never have another  - Genetics, CNS infection (meningitis) Depending on the type, a seizure may occur in 4 phases (not all pts have every phase): 1. Prodromal phase - sensations of behavior changes that precede a seizure by hours or days 2. Aural phase - sensory warning that is similar each time a seizure occurs and is part of the seizure activity 3. Ictal phase - from 1st symptoms to the end of seizure activity 4. Postictal phase - recovery period after the seizure → can last hours or several days Types: Generalized (both hemispheres of brain) Focal/Partial (only 1 hemisphere of brain) Tonic-clonic (grand mal) - loses consciousness; if Begin on 1 side or 1 area and e ects are based on upright, falls to the round which side is a ected Body sti ens (tonic) for 10-20 sec then extremities jerk (clonic) Simple partial (focal awareness) - conscious, Time: 30-40 secs to several min alert, unusual feelings or sensation (very emotional Cyanosis, excessive salivation, tongue or cheek experience), sensory changes, localized twitching biting, incontinence may occur Postictal: possible muscle soreness, feels tired, may Complex partial (focal impaired awareness) - sleep for hours, no memory of seizure loss of consciousness or change in awareness, Absence (petit mal) - often in children unresponsive, automatisms, may continue activity a. Typical: sudden onset, brief staring spell (“zoning before the seizure or do something normally out” look”), sudden recovery, 20 secs Myoclonic - rapid, irregular, brief jerking, 1-2 sec, many occuring in a short time Atonic (drop attack) or akinetic - brief, sudden loss of tone → collapse, great risk for head injury, < 15 sec  Epilepsy (seizure disorder) Group of neurologic diseases characterized by recurring seizures - 2 or more seizures > 24 hrs apart w/o and underlying problem = possible epilepsy - May or may not have clear triggers Seizures from systemic and metabolic problems are not seizure disorder if they stop when the underlying problem is corrected Causes: idiopathic for 70% of people, remaining 30% is due to: - Head trauma (seizures at time of trauma, increases risk of seizures occurring later on) - CNS infection, brain tumor, genetics - Lead poisoning - Prenatal disturbances (preeclampsia) (note causes of seizures above can be included here too) Status epilepticus (SE): seizure lasting for > 5 min OR more than 1 seizure in a 5 min period w/o return of normal LOC afterwards - Neurological emergency - The longer the seizure lasts, the less likely it is to stop w/o drug therapy Diagnostics Treatment CBC, CMP (any infectious causes), Most seizures are self-limiting and rarely cause injury, so med Procalcitonin (increase 3x the normal care is unnecessary value after seizure) - But if SE or injury occurs, or 1st time seizure, med care needed! Serum or urine drug screen (any overdose) Guidelines for seizure care: Lumbar puncture (collect CSF, measure Ensure patent airway, never force anything bw pt clenched pressures) teeth, NPO CT, MRI - done in any new onset seizure Safety: NO restraints, side rails up and padded, low position, to rule out structural lesion no pillows, clear objects near patient, loosen or remove tight EEG (Electroencephalogram) - done clothing within 24 hr of suspected seizure; tests for If standing, lay down (side lying position is best) Stay with pt until seizure has passed, note seizure length and brain waves like beta and alpha, assess the description patient like ECG if showing asystole Anticipate anti seizure meds and need for intubation Aware of seizure hx: ensure patent IV, have nasal cannula, tubing, ow meter, suction gauge, suction container already assembled; close to nurses station, 1:1 sitter Reassure and reorient pt after seizure Monitor VS, LOC, SpO2, GCS; patient education  Common medications - Anticonvulsants: levetiracetam - Benzodiazepines (tx status epi): diazepam (Valium), lorazepam, midazolam - Hydantoins: Phenytoin-Dilantin - High dose sedation: midazolam, propofol, fentanyl Antiseizure drugs - Abrupt withdrawal after long term use may cause seizures - Side e ects: CNS → vision changes, drowsiness, ataxia, mental slowness Multiple sclerosis (MS) Chronic, unpredictable, progressive, degenerative disorder of the CNS caused by the destruction of myelin in nerve tissue due to an in ammatory response - Remember myelin allows electrical impulses to travel quickly and efficiently Classi ed by: - Periods of exacerbation (in ammation continues → demyelination) and remission (in ammation ceases, myelin heals) - Or rapid progression of symptoms with increasing loss of function (myelin will eventually lose the ability to regenerate) - Incidence is highest in young adults ages 20-40, w onset of symptoms bw 20-50 yrs old - A ects females more than males; mainly in caucasians - More common in temperate climates; symptoms may change w the seasons Clinical manifestations: - CNS: fatigue, cognitive impairment, depression, unstable mood - Hearing loss - Visual: nystagmus, diplopia, blurred vision - Speech/throat: dysarthria, dysphagia - Sensation: pain, numbness, paresthesias (numbness and tingling) esp in back, Lhermitte’s sign (electric shock felt down the spine w neck exion), dizziness - MSK: weakness, spasms, tremors, ataxia - Bowel/urinary: diarrhea, constipation, incontinence, frequency, retention - Reproductive: erectile dysfunction, decreased libido, decreased sensation Diagnostics Nursing care Neuro exam, careful history Symptom management, no cure, promote Lumbar puncture w CSF analysis - ↑ # of T independence cells, ↑ IgG Monitor motor movements for interference w ADLs Cerebral, spinal optic nerve MRI - shows Encourage activity balanced w rest periods multifocal lesions Assess cognitive function Evoked response testing of visual, auditory, Educate: somatosensory impulses show delayed - Bladder/bowel training conduction - Positioning (at risk for pressure ulcers) CT scan shows density of white matter or - Avoid temperature extremes plaque formation - Medication compliance (DMDs) - Increase uids, high ber diet - Risk of falls, teach safety Myasthenia gravis (MG) Chronic, autoimmune disorder a ecting the neuromuscular junction characterized by fatigue and severe skeletal muscle weakness - Antibodies destroy ACh receptors, preventing Ach from stimulating muscle ctx A motor disorder NOT a ecting sensation and coordination Occurs with remissions and exacerbations Manifestations Nursing care Hallmark: weakness of skeletal muscles esp Plan for plasmapheresis (removes AChR muscles engaged in repetitive mvmt like muscles antibodies → decreased S/S) used to move eyes, eyelids, chew, swallow, speak Prepare for intubation and breathe Implement aspiration precautions (soft diets, Ptosis (drooping of eyelids), diplopia NG or PEG tube may needed) Weakness in mouth muscles Frequent airway and speech assessments Muscles are weak, but DTRs are normal Patient teaching Weakness and fatigue are secondary to stress, Medication adherence fever, and overexertion Stress management Carry medical identi cation Complications Testing  Myasthenic Crisis: abrupt exacerbation of Tensilon (edrophonium) Test: di erentiates muscle weakness, severe decline in muscles bw the 2 crises by giving an AChE inhibitor that support resp system due to little If it's MG crisis → pt will improve for a stimulation in NMJ short time (needed the ACh) No ctx, no cough, no gag re ex, accidly, If its cholinergic crisis → condition will dilated pupils, tachy, HTN, incontinent worsen (too much ACh already) Cholinergic Crisis: overdose of AChE Have atropine (anticholinergic) ready for inhibitors → increased ACh cholinergic crisis and intubate SLUD: salivation, lacrimation, Serum Acetylcholine Test: an increase of Ach urination, defection; N/V, blurred is a positive exam for MG vision, muscle twitching, paralysis, hypotension, brady (PsNS e ects) Guillain barre syndrome (GBS) (ch 65) Acute autoimmune disorder, immune system attacks healthy nerve cells in peripheral nervous system (PNS) characterized by ascending paralysis (begins in the legs and progressively moves to trunk and arms) Unknown cause, but is usually triggered by an infectious illness or viral vaccination Manifestations: - Symmetric weakness beginning in the lower extremities and progresses into the upper extremities and torso - Paresthesia, aches, cramps, hyperesthesia, pain is often worse at night - Paralysis of the intercostals and diaphragmatic muscle – be prepared for intubation - Autonomic nervous system dysfunction - ortho hypotension, HTN, brady, heart block, asystole are possible, paralytic ileus, urinary retention, facial ushing, diaphoresis - Cranial nerve involvement - facial weakness, paresthesia, EOM issues, dysphagia - Symptom improvement beginning at the 4th week of onset of symptoms Testing Medications Hard to diagnose bc its similar to metal Medical management poisoning initially Tracheostomy Patient history and clinical assessment  Lumbar puncture - CSF analysis help exclude Plasmapheresis (plasma exchange helping other causes remove antibodies and other immune Electromyography (EMG) - nerve fxn factors) Pulmonary function tests (PFTs) – understand Enteral feeding lvl of pulmonary involvement Medications for supportive management Antibiotics Pain control Anticoagulation - risk for DVTs Nursing Considerations - Airway management - Pneumonia prevention - Communication – cannot speak, secretions - Pain control - Skin integrity – 2 hr positioning - VTE prophylaxis - Eye care – facial paralysis - I/O’s, nutrition – bowel sounds, EN or PN may be needed, assess for ileus - Decrease fear and anxiety Parkinson’s Disease (PD) Chronic, progressive neurodegenerative disorder due to an imbalance of two neurotransmitters dopamine (inhibitory) and Ach (excitatory); de cient in dopamine → greater e ects of Ach - Characterized by bradykinesia (slow movement), rigidity (increased muscle tone), tremor at rest, gait changes A ects older adults mostly, avg ~60 yrs old, more men than women Eventual complete debilitation Cardinal signs is the yellow boxes Treatment - no cure Nursing considerations Meds - manage symptoms Improve mobility - PT, OT can help Carbidopa, Levodopa - monitor for signs of dyskinesia, Provide nutrition education - eating 6 small e ects may be delayed for weeks to months, report any meals a day, use extra time to eat, bite sized uncontrolled movement of face, eyelids, mouth, Assess for aspiration risks tongue, arms, hands, or legs; mental changes; Provide e ective communication palpitations; and problems urinating (appropriate to mental cognition) Antidepressants - low dopamine Provide medication teaching Anticonvulsants - for excessive tremors Assess safety risks - remove rugs, excess Surgery: Deep brain stimulation – electrodes to brain and furniture, clear oors, higher toilet, etc connected to generator placed in the upper chest - programmed to deliver speci c current to targeted brain location Huntington’s Disease Progressive, degenerative brain disorder causing deterioration of physical, emotional and cognitive abilities - Chorea: abnormal and excessive involuntary movements → gets worse as disease progresses Genetically inherited, autosomal dominant disorder, idiopathic cause, no cure  Fewer than 200,000 cases in the U.S. per year 3 stages - slow progression Early Stage - mild Middle Stage Late Stage Forgetfulness Decision making di culty Bedridden Di culty concentrating Frequent outbursts & ts Uncontrollable eye movement Clumsiness Diet changes & weight loss Loss of bowel/bladder Depression Frequent falls Memory loss Mood swings Constant bodily jerking Can work and drive, need Non verbal Mostly independent help w eating, dressing Around the clock supervision and care, PEG tube, a bit of awareness Meds: some drugs can treat chorea and behavioral issues like neuroleptics and benzos, SSRIs can be used for depression, antipsychotics may be needed as well Nursing Care - no cure, symptom management - Support genetic counseling (ethical issue) - Provide emotional support - self harm and SI risk, discuss end of life care as well - Modify environment for safety - Provide respiratory needs - Provide padded side rails on beds (if policy allows) - Maintain patient dignity - Provide nutritional needs esp bc caloric intake is high due to chorea, EN or PN may be needed as disease progresses - Assess skin integrity often (Q2H turning) Amyotrophic Lateral Sclerosis (ALS) aka Lou Gehrig's disease Rare, progressive neuromuscular disorder marked by loss of motor neurons - Destroyed motor neurons can produce or transport signals to muscles - Half of all patients diagnosed will die within 2 to 5 years of onset of symptoms Manifestations: - Classic signs: progressive muscle weakness, atrophy w fatigue - Weakness may begin in the hands or limbs before progressing to other parts, ne motor skills (writing, typing) deteriorate rst  - Tripping and falling, di culty walking and doing ADLs - Muscle cramps and twitching in your arms, shoulders and tongue - Inappropriate crying, laughing or yawning - Loss of elimination control - Spastic, weak muscles with increased DTRs - Atrophy of the tongue and facial muscles result in slurred speech, impaired swallowing, and inability to maintain their airway → resp failure → death - Does not a ect intelligence, but may have problems w decision making and memory Testing Nursing care - no cure Diagnosis of exclusion - rule out Promote activity and exercise (moderate intensity, endurance) other possibilities rst Provide ROM exercises Physical exam Assess Blood and urine Bowel function daily - use stool softeners CT/MRI Scanning Skin integrity → frequent repositioning EMG Nutrition - lots of uids, ber, prune juice, small Nerve conduction study frequent meals Muscle biopsy Swallow ability - reduce aspiration risk Respiratory - early identi cation Emotional support - they are fully aware of what is happening (discuss advance directives and resources) Skills related to neurological problems Risk Factors Trauma Hemorrhage Tumors Infection Metabolic disorders Hypoxic conditions Hypertension Cigarette smoking Stress Aging process Chemicals Diagnostic Tests Radiographs: - CT Scan - detects problems such as hemorrhage, tumor, cyst, edema, infarction, brain atrophy, structural abnormalities  - MRI - detects strokes, multiple sclerosis, tumors, trauma, herniation, and seizures Greater deatil than CT, improved resolution, takes longer time to complete - Cerebral angiography - maps out bl ow in the brain and can detect aneurysms, hematomas, blockages, stroke risk, tumors Lumbar puncture - used to collect CSF for analysis for conditions like meningitis, bleeding, in ammation, neuro disorders, cell counts, protein, glucose - Normal CSF: clear, colorless, odorless, free of RBCs, little protein Electroencephalography (EEG) - detects electrical brain activity changes, seizures, epilepsy Caloric testing - assess the vestibular system for vertigo, dizziness; can assess brainstem function Lumbar Puncture (spinal tap) procedure Position: side-lying, knees drawn up to the chest A hollow needle is inserted into the arachnoid space of the spinal canal, usually bw the L3-L4 or L4-L5 space to retrieve CSF for analysis Contraindicated in increased ICP Preprocedure: explain process, baseline VS, sedative and analgesia, empty bladder, position Postprocedure: - Monitor neuro and VS, HA, drainage from puncture site - Keep pt in at position for 1 hr or several hrs to reduce risk of spinal HA - Assess for possible complications: HA, temporary paresthesia. - Rare complications: spinal or epidural bleeding or nerve root trauma - Watch for weakness, loss of sensation, or paraplegia - Encourage uids w straw, give analgesia Assessment Findings – depends on the injury Manifestations result from increased ICP Changing neurological signs Level of consciousness (LOC) = most sensitive indicator of neuro status Airway & breathing pattern changes, VS changes Visual changes (pupils, papilledema - edematous optic disc), GCS Nuchal rigidity, meningeal irritation CSF drainage (clear drainage from nose or ears, use glucose strip test, if pos = CSF) Weakness/paralysis, decreased sensation Posturing, re ex changes, seizure activity Cranial nerves Level of Consciousness Terminology Conscious Confused – disoriented to person, place, or time Delirious – agitation, uctuating level of awareness Somnolent – slow response, small stimulation Obtunded – need intense stimulation Stuporous – deep state of unresponsiveness, super intense stimulation needed (sternal rub) Comatose – no response Cranial Nerves Respirations Cheyne-stokes – cycle of hyperventilation followed by apnea - HF, end of life, brain trauma Hyperventilation – sustained, regular rapid and deep breathing Apneustic – prolonged inhalation, brief exhalation Ataxic – deep and shallow breath w no pattern - Severe damage to brainstem – esp trauma and strokes Cluster – clusters of breaths follow each other w irregular pauses bw Posturing Decorticate – to the “core”, internal rotation and adduction of the arms with exion of the elbows, wrists, and ngers, extension of the legs may be seen Decerebrate – the arms are sti y extended, adducted, and hyperpronated; hyperextension of the legs with plantar exion of the feet - More serious than decorticate Re exes Babinski – pos (toes spread out when the sole is stroked) = abnormal in adults, damage to corticosteroid tract Corneal – absent = indicate dysfunction of trigeminal or facial nerve Gag – absent = impairment of glossopharyngeal nerve, risk of aspiration Meningeal Irritation General Findings Irritability Nuchal rigidity Headaches, photophobia, N/V, fever & chills Tachycardia Nystagmus, abnormal pupil reaction Brudzinki’s Sign, Kernig’s Sign  Motor response Memory changes Glasgow Coma Scale 3 areas assessed in the GCS are the patient’s ability to 1. Open the eyes when a verbal or painful stimulus is applied - opening of eyes 2. Speak - best verbal response 3. Obey commands - best motor response Fully alert, best score: 15 Coma: < 8 Unresponsive: 3 Ch 65 Spinal cord injury Overview Trauma to spinal cord causes disruption of the nerve tracts & neurons - Edema develops resulting in: loss of motor function, sensation, re ex activity, bowel and bladder control 1. Cervical – C5, 6, 7 2. Thoracic – T12 3. Lumbar – L1 Spinal Cord Injury (SCI) Causes: - 50% Motor vehicle accidents (MVA) - 24% Falls - 11% Violence - in large urban areas, gunshot wounds may surpass falls - 9% Sport injuries - 6% Other miscellaneous Classi cation of SCI: 1. Mechanisms of injury: a. Flexion b. Hyperextension c. Compression d. Flexion-rotation - most unstable 2. Level of injury - cervical, thoracic, lumbar or sacral a. Injury from C1–T1 can cause tetraplegia (quadriplegia) - paralysis of all 4 extremities b. Injury below T2 can cause paraplegia - paralysis and loss of sensation in the legs 3. Degree of injury a. Complete cord involvement - total loss of sensory and motor function below the level of injury b. Incomplete cord involvement - mixed loss of voluntary motor activity and sensation and leaves some tracts intact; 6 syndromes - Central Cord Syndrome - Anterior Cord Syndrome - Brown-Sequard Syndrome - Posterior Cord Syndrome - Conus Medullaris Syndrome - Cauda Equina Syndrome Spinal and neurogenic shock Spinal shock (NOT true shock) Neurogenic shock (TRUE shock) Complete, but temporary loss of motor, sensory, Massive vasodilation (happens from re ex (DTR and sphincter), and autonomic unopposed PsNS response due to loss of SNS function innervation) → tissue hypoperfusion Occurs immediately after injury S/S: Hypotension, bradycardia, temp Edema, “concussed” cord dysregulation Resolves over days to weeks Resolves over weeks Most common in injuries above T6 Autonomic Dysre exia (aka Autonomic Hyperre exia) Massive, uncompensated cardiovascular reaction mediated by the SNS Happens after spinal shock is resolved and occurs in injuries at T6 and higher, and cervical lesions Causes: distended bladder or rectum are common, but any sensory stimulation can be a cause (urinary retention, impaction, UTI, PI, tight clothing) Neurological emergency → uncorrected can lead to epilepticus, stroke, MI, death Assessment ndings Interventions Sudden severe HA Raise the HOB 45, or sit upright (lower BP) Severe HTN and bradycardia (30-40 bpm) Check for causes Flushing and sweating above the level of injury Notify HCP Pale Loosen tight clothing Nausea Bladder scanning/ in and out cath immediately Vision problems - blurred vision or spots to relieve bladder irritation Piloerection Digital rectal exam w anesthetic Apprehension Administer meds (nitroglycerin, hydralazine) Document, education Incomplete Cord Involvement Central Cord Syndrome Damage to central spinal cord  Occurs most commonly in cervical cord region More common in older adults Caused by hyperextension injury in people w degenerative disease Manifestations: motor weakness and sensory loss are present in both upper and lower extremities, but upper extremities is more pronounced - Burning pain in upper extremities Anterior Cord Syndrome Damage to anterior spinal artery from acute compression of anterior portion of spinal cord Results in compromised blood ow to anterior spinal cord Common w exion injury A ects: motor, loss of pain, loss of temperature (below level of injury) Posterior tracts are not injuried, so touch, position, motion, and vibration remain intact Posterior Cord Syndrome (rarer) Damage to posterior portion of gray & white matter Hallmark: motor function remains intact Loss of vibratory sense, crude touch, and position sensation Brown Sequard Syndrome Damage to one half of spinal cord usually from penetrating injury to spinal cord Manifestations: Ipsilateral (same side as injury) Contralateral (opposite side of injury) Loss of motor function, light touch, Loss of pain and temperature sensation pressure, position and vibration sense Losses are below level of the lesion Vasomotor paralysis Conus Medullaris Syndromeand Cauda Equina Syndrome Damage to very lowest portion of spinal cord (conus medullaris) and lumbar and sacral nerve roots (cauda equina) Manifestations: accid paralysis of lower limbs and are exic ( accid) bladder and bowel Cauda equina: complete loss of sensation bw legs, over buttocks, inner thighs and back of legs (saddle area) Assessment of Spinal Cord injuries Depends on level of injury (lowest spinal cord segment with intact function) - Higher level of injury = greater loss of function Respiratory complications at C3-5 or above Motor & sensory status Re exes Bowel and bladder (be wary of autonomic dysre exia) Pain Fear Skin integrity (no sensation to skin wounds) Nutrition/ hydration Emergency Interventions Improper movement can cause further damage! Assess respiratory status & maintain airway (ABCs) Prevent head exion, rotation or extension (assume head trauma unless proven otherwise) and spine motion w rigid cervical collar and supportive backboard w straps Maintain traction Logroll (keep the spine intact) Supine or reverse Trandelenburg, NO sitting position General Interventions Post Emergency Stabilization Respiratory System Assess respiratory status (pattern, sounds, secretions) Monitor ABGs Encourage deep breathing, incentive spirometer Monitor for S/S of infection Maintain mechanical ventilation if needed Cardiovascular System Monitor for cardiac dysrhythmias (avoid vagal stimulation, pacemaker may needed, tx symptomatic bradycardia) Assess for S/S of shock (neurogenic) Assess for DVT (tenderness may not be present) Monitor for orthostatic hypotension Neuromuscular System Assess neuro status, motor & sensory status Monitor for autonomic dysre exia & spinal shock Immobilize Assess pain Operative care Exercise techniques & accessories for prevention of problems Gastrointestinal System Assess abdomen Prevent bowel retention (enema, digital removal) Initiate bowel control program (esp no sensation) PPI and H2 blockers may be used to prevent stress ulcers Maintain adequate nutrition (begin within 72 hrs after injury) - EN or PN may be needed - high protein, high calorie Renal System Prevent urinary retention (foley or self cath) Neurogenic bladder Bladder control program Maintain F & E balance Monitor for infection Integumentary System Assess skin integrity (esp bony prominences) Turn every 2 hours Daily bathing  O oading (from wheelchair) Psychosocial Assess psychosocial status Prevent sensory deprivation (convos, music, reading, watching tv), and promote good sleep and rest Encourage expression, discuss concerns Promote rehabilitation, community resources Educate family/caregivers Cervical Level Injuries Injury at C2 to C3 is fatal C4 – Diaphragm a ected Injury above C4 – respiratory di culty & paralysis x 4 Injury C5-C8 – may have movement of shoulder Interventions for Cervical Injuries:Spine Traction Skull Tongs Halo Traction Traction applied Headpiece with 4 pins inserted in skull Weights attached to tongs Metal halo attached to vest/jacket Monitor neuro status (LOC, motor, Monitor neuro status sensation) Increased ICP - N/V, changes in neuro Increased ICP - N/V, changes in neuro Never move the client using Halo Ensure weights hang freely Assess for tightness Maintain body alignment Assess skin integrity Turn Q2 Provide pin care (2x cleaning w CHG, Assess pin insertion sites antibiotic ointment) Pin care Thoracic Level Injuries Loss of movement depends on the level of injury Leg paralysis may occur Autonomic dysre exia may occur in those with above T6 injuries Lumbar & Sacral Level Injuries  Loss of movement & sensation may occur Injury below S2-S3 results in neurogenic bladder Injury above S2 - male erection, but no ejaculation Injury between S2-S4 damages SNS and PsNS response - No erection and ejaculation Interventions for Thoracic/Lumbar/Sacral Bed rest Immobilization Assess for respiratory problems Use brace when OOB Surgical Interventions for Thoracic/Lumbar/Sacral Decompression laminectomy (relief of cord pressure) - removes part or all of the lamina (roof of the spinal canal) Spinal fusion - permanently joins two or more vertebrae Post-op care: - Monitor respiratory status - Monitor VS, neuro checks - Encourage deep breathing, IS (preventing atelectasis, pneumonia) - Assess for F & E imbalance, I & O - Assess for immobility problems, keep at as Rx, log rolling - Cast care - Pain meds - Fracture bedpan (designed w those injured in mind) - NPO then progress diet (liquids, soft, solids) Medications Dexamethasone (corticosteroid) Dextran (plasma volume expander) Dantrolene (for malignant hyperthermia and also chronic spasticity) Pain medication (avoid opioids if possible bc of constipation concerns) Antidepressants Inotropes (dobutamine) Gabapentin (may help w paresthesias, sensations) Ch 61 Acute intracranial problems Unconscious Patient Abnormal state of complete or partial unawareness of self or environment, unresponsive to stimulation Causes: head trauma, toxins, shock, hemorrhage, tumor, infection Assessment ndings: - Unarousable - Altered response to painful stimuli and altered respirations - Decreased cranial nerve activity Interventions: - Airway, VS, assess neuro status, lung sounds - Positioning - Monitor uid status and nutrition (i.e. NG, G tube) - Monitor elimination patterns (foley, any constipation complications, etc.) - Skin integrity (turning Q2H, careful cleaning) - Eyes, ears, nose, mouth - Seizure precautions, DVT prophylaxis - Prevent musculoskeletal issues (ROM exercises) Intracranial regulation Skull: enclosed space w 3 essential volume components: brain tissue blood and cerebrospinal Brain tissue - 78% Blood - 12% CSF - 10% Intracranial pressure (ICP): hydrostatic force measured in the brain CSF compartment - Normal = 5-15 mmHg - Abnormal = > 20 mmHg → notify HCP - Factors in uencing ICP: 1. Aerial and venous pressure 2. Intra-abdominal and intrathoracic pressure 3. Posture 4. Temperature 5. Blood gases (esp CO2 levels)  - ICP can be measured in the ventricles (ventriculostomy); subarachnoid, subdural, or epidural space; or brain tissue with a pressure transducer - Monro-Kellie doctrine - 3 components must stay at a relatively constant volume within the closed skull, if 1 of the 3 parts increases within the skull and the volume from another part is displaced, the total intracranial volume will not change Normal compensatory adaptations: applies the Monro-Kellie doctrine, the body can adapt to volume changes within the skull for a short time to maintain a normal ICP → when this mechanisms fail it results in compression and ischemia 1. Changes in CSF by altering CSF absorption or production, displacing CSF into the spinal subarachnoid space 2. Reduced blood volume – collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, changes in venous out ow 3. Distention of dura or compression of brain tissue – herniation Cerebral blood ow: amount of blood in mL passing thru 100 g of brain tissue in 1 min - 1/3 of the cardiac output, brain utilizes 20% of body’s O2 and 25% of its glucose - Total of 750-900 mL of bl ow to the brain per min - Autoregulation system - automatically adjusts cerebral bl vessel diameter to maintain constant bl ow w changes in arterial BP, helps maintain CPP WNL - Cerebral perfusion pressure (CPP) - pressure needed to ensure blood ow to the brain (good CPP = good cerebral blood ow) Required to meet brain’s metabolic and O2 demands Estimation of adequacy of cerebral circulation If ICP increases, CPP decreases CPP = MAP – ICP Ex/ BP 122/84, MAP = 97 mmHg Normal CPP = 60-100 mmHg ICP = 12 mmHg Ischemia, neuron death = < 50 mmHg CPP = 85 mmHg Increased ICP Medical emergency - potentially life threatening situation that results from an increase in any or all 3 components within the skull - ↑ ICP → ↓ CPP → ↑ risk for brain ischemia/infarction → poor prognosis Can impede circulation to the brain and absorption of CSF, a ect nerve cell functioning, lead to brain stem compression → herniation → resp arrest (compression of the resp control center in the medulla) →death  Common causes: mass (hematoma, contusion, abscess, tumor) and cerebral edema Assessment ndings Interventions Altered LOC ( at a ect, change in orientation, Monitor respiratory status (altered patterns or low level of attention, unconscious, or coma) snoring) Headache - nocturnal or morning HA is Prevent hypoxia concerning Mechanical ventilation as Rx Vomiting not preceded by nausea or projectile Maintain body temp, prevent shivering vomiting is possible Decrease environmental stimuli Abnormal VS ICP monitoring/drains Pupil changes - xed, unilateral, dilated = Monitor electrolyte & acid base emergency I & O, uid limitation Late Signs: Avoid vagal (bc it can lead to brady = ↑ ICP) VS changes - Cushing’s Triad: Position - head midline, avoid extreme exion of 1. Irregular ↓ respirations neck, elevate HOB no more than 30°, avoid 2. Bradycardia extreme hip exion; slow and gentle when 3. Systolic HTN w widening pulse moving pt pressure Medications Changes in motor function - Surgical post-op care contralateral hemiparesis or hemiplegia See care of the unconscious patient slides Posturing - decorticate or decerebrate Medications Surgical Interventions Use sedation carefully - NO morphine Ventriculoperitoneal shunt (VP shunt) for Opioids, sedatives cause N/V, can chronic increased ICP exacerbate high ICP Post-op care: IV propofol - rapid onset, short half life - - Position supine good for anxiety and agitation, but - Turn from back to allows for accurate neuro assess after non-operative side stopping - Monitor for S/S of shunt failure Hypotension can lower CPP, be wary - Monitor for S/S infection Anticonvulsants - barbiturates Craniotomy - incision through cranium to Antipyretics remove blood or tumor Muscle relaxers Complications: BP meds - Increased ICP Corticosteroids – depends on the situation, if - Hemorrhage used at all - CSF ow obstruction IVF - Hematomas Hyperosmotic agent – shrinks cells, moves water - Hypovolemic shock outside the cell - DI, SIADH Post-Craniotomy Care Monitor Positioning VS & Neuro Status Q 30-60 Varies with type of surgery & HCP preference For increased ICP ALWAYS check HCP orders for positioning Maintain mechanical ventilation Removal of bone ap Positioning Turn only to the non operative side Quiet environment Bedside recognition Monitor dressing and drains Posterior fossa surgery Notify HCP for drainage >50 On side with pillow under head mL/shift Not on the back Fluid restriction Infratentorial Surgery Monitor electrolyte levels Flat or HOB 30-45 degrees Apply ice packs Do not elevate HOB immediately post-op Administer medications without HCP order Supratentorial Surgery HOB 30 degrees Do not lower HOB immediately post-op without HCP order ICP Monitoring Devices Gold standard: monitoring ICP w ventriculostomy - specialized catheter is inserted into the lateral ventricle and coupled to an external transducer - Directly measures pressure within the ventricles, facilitates removal and/or sampling of CSF, and allows for intraventricular drug admin - Monitor for infection and leaking, assess color and clarity of uid LICOXBrain Tissue Oxygen Monitoring Measures intracranial tissue oxygen; keep Pbt O2 = 20-40 mmHg Intracranial pressure, and brain tissue temperature Indicated for patients at risk for cerebral ischemia Intended to assist with providing additional data to support clinical practice in cases where cerebral hypoxia and ischemia are a concern Cerebral Edema Abnormal accumulation of uid in the intracellular or extracellular spaces of brain tissue, associated with increased volume of brain tissue Types: 1. Vasogenic (most common type) - disruption of BBB, occurs mainly in white matter Tx: diuretics, steroids 2. Cytotoxic - disruption of cell membranes, direct uid build up in the cells (intact BBB) 3. Interstitial - ventricular enlargement due to excess CSF production, obstruction of ow, inability to reabsorb CSF Usually a result of hydrocephalus (buildup of uid in the brain) Causes: mass lesions, head injuries and surgery, infections, vascular insult, toxic or metabolic conditions Herniation  An abnormal protrusion of the brain through a defect or opening; the brain becomes compressed from shifting of greater pressure to a space of lesser pressure - Late sign of increased ICP Head Injury Injury or trauma to the scalp, skull, or brain Serious form of head injury = traumatic brain injury (TBI) Complications: cerebral bleed, hematomas, increased ICP, infections, seizures, personality changes, cranial nerve damage Types: - Scalp lacerations - external head trauma Complications: blood loss, infection - Skull fractures complications: intracranial infections, hematoma, meningeal and brain tissue damage - Head trauma - di use (generalized) or focal (localized) - Hematoma (epidural or subdural), hemorrhage (intracerebral or subarachnoid) Skull Fractures Location of fracture determines the manifestations - Raccoon eyes: periorbital bruising - Battle sign: postauricular bruising - Halo sign: uid on white gauze pad → blood coalesces into the center w yellowish ring around the blood (due to the presence of CSF)  - Rhinorrhea (CSF leakage from the nose) or otorrhea (CSF leakage from the ear) → con rms a fracture has traversed the dura Test uid w Dextrostix → if no blood and glucose is pos = presence of CSF Basilar Anterior Fossa Middle Fossa Posterior Fossa Location: base of the skull Frontobasilar Temporal lobe Cervical spine injury Involves the frontal and Raccoon eyes Battle sign Vertebral artery injury temporal lobes Halo sign, rhinorrhea Otorrhea or rhinorrhea Damage to lower cranial Monitor for CSF leaks Partial/total loss of vision, Watch for cranial nerve nerve Altered LOC, HA smell injury Anterior and middle fossa Eye movement defects Conductive hearing loss involvement Drips pads Loss of balance No nose blowing Focal Brain Injury Laceration: tearing of the cortical surface of the brain - Severe tissue damage, often occurs in open fractures and penetrating injuries - Management: antibiotics (until meningitis is ruled out), preventing secondary injury from increased ICP Contusion: bruising of the brain tissue within a focal area, usually associated w closed head injury, often occurs at a fracture site  - Coup-contrecoup: injury occurs at the site of the direct impact of the brain (coup) and at a 2nd area of damage on the opposite side away from injury (contrecoup), leading to multiple contused areas Complications: Epidural Hematoma Subdural Hematoma Intracerebral Hematoma Extradural hematoma Bleeding bw the dura and Bleeding within brain tissue, Bleeding bw the skull and dura arachnoid space deep, large mater Acceleration-deceleration Associated with contusions Associated with temporal or injury Can be caused by an evolving parietal skull fractures. Most common type hematoma or a delayed Arterial bleeding: commonly Venous bleeding hemorrhage middle meningeal artery Size and location of hematoma are key in determining the patients outcome Di use Brain Injury: Concussion  Sudden transient mechanical head injury w disruption of neural activity and a change in LOC Mild Classic Brief disruption in LOC upon + LOC/ transient impact + Memory loss Amnesia (retrograde), HA N/V, HA, dizziness, confused/disoriented Confused, disoriented, drowsy Post Concussion Syndrome - may develop 2 weeks to 2 Possible seizure activity months after injury - persistent HA, lethargy, personality and behavior changes, shortened attention span, decreased short term memory, changes in intellectual ability Di use Brain Injury: Di use Axonal Injury (DAI) Widespread axonal damage occurring after a mild, moderate or severe TBI - Trauma changes function of axon → axon swelling and disconnection Injury involves the entire brain tissue The brainstem and reticular activating system can be involved = prolonged coma S/S: decreased LOC, increased ICP, decortication or decerebration, global cerebral edema Chronic Traumatic Encephalopathy Progressive, neurological degenerative disorder Likely caused by repeated head injuries, i.e. football players Mood changes, memory loss, motor defects Diagnosed after death Brain Tumors Grows within the cranium Cause: Unknown, heredity, cranial irradiation, chemical exposure Manifestations are based on tumor location Types: Primary Secondary Arising from tissues within brain Resulting from metastasis of cancer from Intracerebral: gliomas elsewhere – most often lungs or breast  astrocytoma, blioblastoma multiforme, Most common brain tumors ependymoma, oligodendroglioma, astroblastoma Extracerebral Medulloblastoma, meningioma, acoustic neuroma Congenital Hemangioblastoma, craniopharyngioma Pituitary adenomas Chromophobic, eosinophilic, basophilic Wide range of manifestations Diagnostic tests CT scan, MRI HA is common – worse at night Cerebral angiography, EEG Seizures – common in gliomas and brain mets Endocrine studies Nausea and vomiting Treatment Cognitive dysfunction – memory problems, Chemotherapy mood or personality changes Radiation therapy Muscle weakness Surgery Sensory losses Radiation therapy Aphasia May be primary treatment Visual – spatial dysfunction May be adjunctive therapy In ammatory conditions of the brain Brain Abscess: accumulation of pus within the brain tissue that can result in infection Bacterial Meningitis: acute in ammation of the meningeal tissues surrounding the brain and spinal cord Viral Meningitis: acute in ammation with clinical and lab evidence – negative cultures Encephalitis: an acute in ammation of the brain Bacterial Meningitis (meningococcal or pneumococcal) Acute in ammation of the meningeal tissues surrounding the brain and spinal cord - Medical emergency  Cause: bacteria - streptococcus pneumoniae, neisseria meningitidis Transmission: droplet thru resp tract or blood stream, or enter by direct extension from penetrating skull wounds or fractured sinuses in basilar skull fractures - Droplet precautions, respiratory isolation Risk Factors: - Living in a dormitory (college students, military personnel, prisoners) - Serious drug allergies - Recent exposure to someone with bacterial meningitis - Recent travel to areas known for meningococcal disease - History of injected drug use - Recent head trauma - Otorrhea or rhinorrhea - HIV infection or other immunocompromised conditions Manifestations: - Mild lethargy, fever, HA, N/V, sti neck (nuchal rigidity), red, macular rash - Altered LOC, photophobia → possible signs of increased ICP - Positive Brudzinski's or Kernig’s sign Brudzinski's Kernig’s Pt supine position. Place your hand Supine position, ex the patient’s hip under his neck and ex it forward, chin and knee to form a 90° angle. Then to chest. attempt to extend his leg. Pos = exes his ankles, knees, and hips Pos = exhibits pain or resistance to bilaterally. Painful when neck is exed extension and spasm of the hamstring Diagnostics: - Blood cultures, CBC, BMP, CT scan  - Lumbar puncture w CSF analysis - ↓ glucose concentration, purulent and turbid CSF, and WBC > 1000 Nursing care - Monitor VS & neuro status - Assess for increased ICP, cranial nerve assessment - Seizure precautions (phenytoin used) - Isolation precautions - Elevate HOB 30 degrees, avoid exion of neck or extreme hip exion - Decreased stimulation - Adequate hydration and nutrition (high protein, high calories diet) - Administer analgesics and antibiotics - Codeine for HA, tylenol or aspirin for fever, mannitol for diuresis, dexamethasone Viral Meningitis Lymphocytes in ltrate the pia-arachnoid tissue, but usually not as severely. No exudate forms, so it is self-limiting and usually requires only symptomatic treatment. Common causes: Enteroviruses, HIV, HSV - Others: Coxsackievirus, Poliovirus, Arboviruses, Mumps virus, Epstein-Barr virus, West Nile virus S/S: HA, fever, photophobia, sti neck Encephalitis In ammation of brain parenchyma and usually meninges, a ects cerebrum, brainstem & cerebellum Causes: viral, bacteria, fungi, parasites Transmission: mosquito, tick, herpes virus, mumps, chickenpox, freshwater ponds/lakes Assessment Interventions Cold sores Monitor VS & neuro Insect bites & swimming in fresh water, travel Assess LOC using GCS Fever, HA, N/V Assess for + Kernig’s or Brudzinski’s Nuchal rigidity Elevate HOB 30-45 degrees MSK changes - hemiparesis, tremors, seizures Administer acyclovir (Zovirax) for Neuro de cits - personality changes, impaired memory, encephalitis caused by HSV amnesia, dysphasia Initiate Rehab  Increased ICP Ch 42 Shock, SIRS Shock Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism - Insu cient circulation of oxygenated blood to meet metabolic demands - O2 demand > O2 supply - Secondary to injury (blunt trauma) and hemodynamics Hypoperfusion → hypoxia → anaerobic metabolism → lactic acid build up → cellular death → vital organ dysfunction → death Cause of shock, initial presentation, and management varies for each type of shock, but the physiologic response of the cells is similar Review hemodynamics in ch 35 Stages of Shock 4 overlapping stages of shock Initial stage Shock occurs at a cellular level Not clinically apparent: possible mild ↑ HR and RR, likely normal BP Compensatory stage ↓ CO and narrowing of pulse pressure → Activates compensatory mechanisms to baroreceptors in carotid and aortic bodies maintain CV dynamics and stabilize activate SNS → vasoconstriction and release of circulation/perfusion epi and norepi → blood ow to heart and brain is maintained, but blood ow to non Most reliable sign of poor perfusion = LOC vital organs is shunted → ↓ BP Restlessness, irritability, apprehension (subtle) Myocardium responds to SNS and ↑ O2 Mild ↑ HR , ↑ RR, possible ↓ urine output, bowel demand by ↑ HR and contractility sounds may be hypoactive ↓ blood ow to kidney activates RAS system, Possible hyperglycemia, and hypernatremia producing angiotensin II → stimulates aldosterone release (from adrenal cortex) → If caught at this stage, the patient will recover with Na+ retention → raises serum osmolality and little or no residual e ects stimulates release of ADH (posterior pituitary) → ↑ water reabsorption → ↓ urine and ↑ blood volume which improves preload, CO, and BP Progressive stage CO falls, tissue hypoxia occurs → cells switch Compensatory mechanisms begin to fail from aerobic to anaerobic metabolism → lactic acid builds up → metabolic acidosis Deterioration of LOC: confusion, apathy, ↓ Aerobic metabolism: glucose (primary energy response to painful stimuli source) is broken down to produce pyruvic BP < 25% from baseline (MAP 25% volume loss - correlates with irreversible phase - Hr > 130, BP markedly decreased, >30 RR, maxed out vent settings, anuric - Poor prognosis Treatment goals: - Restore intravascular volume: 3 ml of isotonics for every estimated 1 ml of uid loss - Prevent further volume loss by nding the cause and treating it - Keep MAP > 65 (correlates w perfusion) Nursing considerations: - Replace uid loss - if bleeding give blood, if GI/urinary loss give crystalloids or colloids (warm uids helps maintain body temp) - Vasoactive medications – dopamine, norepi – for patients who may not immediately respond to volume - Stop the bleeding if hemorrhagic Obstructive Shock Physical obstruction to blood ow occurs w decreased CO (impedes out ow or lling of the heart) Causes: cardiac tamponade, constrictive pericarditis, tension pneumothorax, massive PE, superior vena cava syndrome, abdominal compartment syndrome Hemodynamics: 1. Decreased CO: decreased blood to the heart 2. Variable preload: depends on the etiology of the obstruction 3. Increased afterload: due to nature of obstruction (PE) or bc of body’s compensatory mechanisms - Right ventricular afterload (PE), left ventricular afterload (cardiac tamponade) Treatment goals: relieve the obstruction - Pericardiocentesis for cardiac tamponade - Needle decompression for tension pneumothorax or chest tube insertion - Removal of the PE by surgery or with thrombolytic therapy Summary Chart Cardiac Output Preload Afterload Treatment (SVR) Cardiogenic ⇩ ⇧ ⇧ Improve pump function Distributive Normal or ⇧ Normal to ⇩ ⇩ Reverse peripheral vasodilation Hypovolemic ⇩ ⇩ ⇧ Replace lost volume Obstructive ⇩ Variable ⇧ Relieve the obstruction SIRS - Systemic In ammatory Response Syndrome Systemic, generalized, in ammatory response due to a variety of insults including infection (sepsis), ischemia, infarction, and injury - Tachycardia: > 90-100 bpm - Decreased BP - WBCs: > 12,000 or < 4,000 - Body temperature: > 100.4 or 65mm Hg SBP > 90mm Hg HR < 120 bpm *Arterial Line Emergent Phase - Wound Care Elevate burned extremities if no fractures present Fasciotomies/Escharotomies Cleansing Decontamination Debridement Coverage Prevent Infection Emergent Phase - Medications IV Analgesia Sedatives Tetanus Antibiotics Thromboembolism Prophylaxis *** Avoid IM or SC route Emergent Phase - Nutrition Hypermetabolic State Aggressive nutritional support Provided through enteral tube or parentally Diet high in protein, carbs, fats & vitamins High Calorie Acute Phase = Begins when hemodynamically stableGoal: Obtain wound closure through restorative therapy Wound Care Assessment Cleansing Debridement Dressing Skin Grafting Pulses Acute Phase Rehabilitative PhaseGoal: Gain independence and achieve maximal function Education Wound care Prevent Contractures Psychosocial Needs Emotions Fear Anxiety Anger Guilt Depression