Exam 5 Study Guide - Neurological Disorders PDF

Exam 5 - Select Neurological Disorders Recorded Lecture Neurologic System ○ Structures: Central Nervous System → brain and spinal cord Peripheral Nervous System → cranial and spinal nerves Autonomic and Somatic Systems Basic functional unit is the neur...

Exam 5 - Select Neurological Disorders Recorded Lecture Neurologic System ○ Structures: Central Nervous System → brain and spinal cord Peripheral Nervous System → cranial and spinal nerves Autonomic and Somatic Systems Basic functional unit is the neuron can't replicate - ○ Function: Controls all motor, sensory, autonomic, cognitive, and behavioral activities ○ Brain Frontal lobe → cognitive function, concentration, storing memory, affect, judgment, personality, social behaviors, broca’s area Temporal → somatic, visual, auditory, interpretive, wernicke’s area Parietal → sensory function, shape, size, weight, texture, consistency, spatial perception of body Occipital → visual interpretation, eye reflexes Cerebellum → integration of sensory stimuli, movement and balance Thalamus → relay for sensory Hypothalamus → body temp, appetite, fluid balance, sleep and wake cycles Pituitary → “master gland”, controls many hormones Brainstem → where most cranial nerves originate, breathing, heart rate, BP, arousal, consciousness, attention, concentration ○ Spinal Cord Divided into four areas Cervical C1-C7 Thoracic T1-T12 Lumbar L1-L5 Sacral S1-S4 Sensory tracts carry impulses from periphery to brain Motor tracts carry impulses from brain/spinal cord to periphery ○ Peripheral Nervous System 31 pairs of spinal nerves → carry input between the dermatomes and the spine motor sensory > 12 cranial nerves Autonomic Nervous System Functions to regulate activities of internal organs and to maintain and restore internal homeostasis Regulated by centers in the spinal cord, brainstem, and hypothalamus Sympathetic NS → STIMULATES, fight or flight response, norepinephrine Parasympathetic NS → INHIBITS, controls mostly visceral functions Somatic Nervous System Nerves that go into the skin and muscles that are involved in conscious activity Responsible for transmitting sensory information for voluntary movement Contains two major types of neurons: ○ Motor (efferent): carried information FROM the CNS to produce physical action ○ Sensory (afferent): carries information TO the CNS to take in sensory information ○ Protective Structures Bones Skull, vertebrae  Meninges → connective tissues to support, protect, and nourish the brain and spinal cord Dura mater, arachnoid mater, pia mater Cerebrospinal Fluid → clear fluid produced in the choroid plexus that circulates in the subarachnoid space, ventricles, and spinal cord; supportive and protective Contains proteins and glucose Blood Brain Barriers → protects the brain from pathogens and toxins, supplied oxygen and glucose to the brain ○ Neurotransmitters: Communicate messages from one neuron to another or to a specific target tissue Can potentiate, terminate, or modulate a specific action Can excite or inhibit a target cell Many neurologic disorders are caused by an imbalance in neurotransmitters Acetylcholine → memory, learning, muscles Serotonin → feelings, sleep, intestinal movement Norepinephrine → contracts blood vessels, “vasopressor” Dopamine → happiness, addiction, motivation Endorphins → happiness, pain, exercise GABA & glutamate → cognition and development Neurologic Assessment ○ Past medical history of patient and family: Previous injury or cognitive problem Sleep disorders Chronic disease Previous neurological problems Lifestyle patterns ○ Current history and symptoms: Pain or headache Dizziness or vertigo Speech or swallowing difficulty Weakness or numbness Visual disturbances Bowel and bladder difficulties Seizures Disorientation, mental status Personality changes ○ Risk factors for cerebrovascular disease: Age (older than 55) Male African American HTN Cardiovascular disease High cholesterol Obesity Diabetes Oral contraceptive use Smoking, drug and alcohol use Routine Neurological Assessment  ○ 5 major components: 1. Consciousness → mental status, intellectual function 2. Cognition → emotional status, thought content, language ability 3. Motor System → muscle size, tone, and strength, coordination, balance, romberg test 4. Sensory System → tactile sensation, superficial pain, temperature, vibration and position sense 5. Reflexes → DTRs ○ Level of Consciousness THE MOST IMPORTANT PART OF A NEURO ASSESSMENT How awake and responsive the patient is Based on the amount of stimulation needed ott elicit a response Continuum: fully awake → coma ○ Pupillary Response Tests the integrity of the pathway between the sensory information and the motor responses in the brains stem Autonomic reflex, controlled by parasympathetic nervous system Normal: equal, round, reactive to light, accommodation ○ Glascow Coma Scale Eye opening, motor response, verbal response 13-15 → mild injury 9-12 → moderate injury 3-8 → severe injury ○ Gerontologic Considerations: Important to distinguish normal aging from abnormal changes Structural and physiological changes Motor and sensory alterations Temperature regulation and pain perception changes Determine previous mental status for comparison Distinguish delirium from dementia Diagnostics ○ Diagnostic Imaging: Types CT PET MRI Cerebral angiography Myelography Carotid ultrasound Transcranial doppler Electroencephalography Electromyography Nerve conduction studies Evoked potential studies ○ Nursing Care for Neurodiagnostic Procedures: Angiography, MRI, CT, PET/SPECT Assess for allergies Renal function Teach importance of not moving, metallic taste, warm sensation  Empty bladder, encourage fluids after Assess metal devices or implants for MRI Lumbar Puncture Position to stretch spinal cord Headache may indicate leakage at the site Lie flat, fluids, pain medications Electromyography and nerve conduction studies Small needles may cause bleeding and discomfort Nerve conduction involves placement of electrodes and low current electrical activity to determine muscle response Assess anticoagulant and muscle relaxant use → contraindicated Nuclear Medicine PET → assess blood sugar if diabetic SPECT → assess for allergic reactions ○ Laboratory Diagnostics: CBC > ↑ WBC BMP electrolytes > - Glucose Ammonia level ~ can carse ↓ LOC BUN alcohol/drug screen ABGs Cerebrospinal fluid analysis Infectious Neurological Disorders ○ Meningitis ○ Encephalitis Meningitis ○ Inflammation of the membranes and the fluid space surrounding the brain and spinal cord arachnoid pia > - mater ○ Types: - ear infections Pneumonia - aerosol contamination Septic caused by bacteria (streptococcus pneumoniae, Neisseria meningitidis) Aseptic caused by viral infection secondary to cancer or a weak immune system often pediatric & ○ Manifestations include: Headache, fever, changes in LOC, behavioral changes, n/v Nuchal rigidity (stiff neck), positive Kernig sign, positive Brudzinski sign & photophobia ○ CSF > 2300 Leukocytes, + gram stain, low CSF glucose ○ Medical Management: Prevention: no sharing utensils kissing > or Meningococcal vaccine to youth (11-12 years old); booster at age 16 (16 - 23 years old) First year college students and members of the military Pharmacological: Early administration of high doses of appropriate IV antibiotics for bacterial meningitis ○ VANCOMYCIN need trough levels > - Dexamethasone Treatment for dehydration, shock & seizures symptom related - ○ Nursing Management: Droplet precautions → until at least 24 hours on antibiotics  Assistance in lumbar puncture Positioning → help patient sit up and so they don’t move during procedure - arch back Medication management → abx Frequent or continual assessment, including VS & LOC Neuro checks Pain & fever management Safety monitoring Seizure, airway, environment Monitor daily weight, serum electrolytes, urine: Volume, specific gravity & osmolality Prevent complications associated with immobility Supportive care & coping with hospitalization/family education Kernig Sign ○ What is a Positive Kernig Sign? A physical exam sign that indicates pain or resistance in the hamstrings when a patient’s knee is extended while lying supine with their hip flexed at a right angle Leg cannot be completely extended May also have back pain INDICATES A POSITIVE KERNIG’S SIGN!! ○ A positive Kernig’s sign raises suspicion for meningitis ○ A lumbar puncture should then be completed to promptly and accurately diagnose meningitis Brudzinski’s Sign ○ Severe neck stiffness that causes the patient’s hips and knees to flex up when neck is flexed INDICATES A POSITIVE BRUDZINSKI’S SIGN ○ Also raises suspicion for meningitis Post Lumbar Puncture Care ○ Generally, keep patient supine 1 hour post procedure Prone can help also ○ Monitor for bleeding/CSF leak ○ Promote fluids ○ Assess for headache ○ Treat pain/nausea ○ Severe headache that worsens when upright & patient is: Nauseous, + neck stiffness, photophobia, etc → post-dural headache May require “blood patch” ○ Patient’s blood injected to fill epidural space = seal CSF leak Encephalitis ○ Acute, inflammatory process of the brain tissue /S get worse over days to weeks starts as fir sls > , then progresses causing brain to swell Causes the brain to swell ○ Causes include viral infections & fungal infections Can be autoimmune > HSV : 2 1 MMR : varicell praccines reduce rate ~ ○ Manifestations may include: > - attacks brain Starts off as flu-like signs & symptoms then progresses Get worse over first few days to weeks  Headache, fever, confusion, hallucinations Stiff neck, photophobia, seizures Vector borne → rash, flaccid paralysis, parkinson-like movements ○ Medical Management: Zika WNL > , Neuroimaging (CT/MRI) Lumbar puncture EEG sseizures Blood, sputum, urine labs ○ Pharmacological Management: Acyclovir for HSV infection Amphotericin B or other antifungal agents Vaccinations → PREVENTION ○ Nursing Management: Frequent & ongoing assessment ICP monitoring Supportive care Ketogenic diet high fat low carbs < , - most common risk factor Guillain-Barré Syndrome flu infections diarrhea, respiratory illness - , ○ Autoimmune disorder with an acute attack of peripheral nerve myelin may last for > - weeks or years Rapid demyelination myelin becomesAffects ~ damaged: Nerve fiber is exposed Swan cells way signals: sent are Swan cells ○ Most often follows a viral infection Influenza Campylobacter dejuni ○ Manifestations are variable but symmetrical ○ Signs & symptoms (most common): Ascending weakness respiratory failure < Paresthesias weakness ; tingling in both leps ~ Hyporeflexia CV/respiratory effects if severe cant ventilate properly > ○ Does not affect cognitive function/LOC ○ Medical Management: Medical emergency traveling towards lungs > - Think AIRWAY Anticipate ICU level of care, continuous monitoring & respiratory support Mechanical ventilation, CV support, anticoagulation Plasmapheresis & IVIG Reduce circulating antibodies → improves outcomes ○ Nursing Care: problems w/ respiration talking swallowing bladder > - , , , Airway monitoring Mobility Nutritional support Assisting with communication Psychosocial support Assisting with ADLs Monitoring for complications ○ Complications:  Respiratory failure Pneumonia, ARDS Autonomic dysfunction Urinary & bowel retention Paralytic ileus VTE immobilized > - DVT, PE Fluid & electrolyte imbalance Sepsis Pressure injuries Degenerative Disorders ○ Degenerative Disk Disease ○ Amyotrophic Lateral Sclerosis (ALS) Degenerative Disk Disease ○ Most common neurological disorder ○ Causes lower back pain Acute vs chronic ○ Involves intervertebral disk between the vertebral bodies Cervical, lumbar, thoracic (rare) Herniation (ruptured disk) Lumbar most common Sciatica → pain, tenderness through thigh/leg - worsens with activity/movement Bulging ○ Back pain is a significant public health disorder - economic burden, psychosocial impacts conservative > - +X ○ Assessment: Patient health history Recent injury Age Occupational stresses Physical assessment Dependent on location, acute vs chronic, and effect on surrounding structures (nerves) Pain Extreme sensitivity to touch Changes in sensation and DTRs ○ Diagnostics: MRI Gold standard → best for lumbar CT with myelography Neuro exam Reflexes, sensory or motor impairment Electromyography (EMG) Skeletal muscle responses ○ Surgical Interventions: ONLY RECOMMENDED FOR SEVERE PAIN Non surgical treatments → pain meds, PT & injections Goal = to reduce pressure on nerve root  Spinal cord function monitored during surgery Minimally invasive Laminectomy → relieves compression - removes bone and facet junction (lamina) - creates space between vertebrae Spinal fusion → fuses vertebrae - thereby eliminating defective disc, stabilizes spine Amyotrophic Lateral Sclerosis (ALS) ○ “Lou Gehrig disease” ○ Loss of motor neurons in the anterior horn of the spinal cord and loss of motor nuclei of the lower brainstem ~no muscle nourishment, scarring or hardening Motor neurons degenerate over time until they eventually die > - brain can't control movement can'tspeak eat or breath ○ Unknown case survival-2-5yrs , , > Hypothesis: overexcitation of glutamate = cell injury/neuronal death ○ Manifestations: rate of progression varies ~ Onset: 40-60 years old, all social-ethic backgrounds, genetic component Progressive weakness and atrophy of muscle cramps, twitching & lack of coordination, fatigue Spasticity, DTRs brisk and over active Difficulty speaking, swallowing, breathing 25% of patients → weakness starts here (CN) Voice → nasal sound Bladder & bowel function remain intact May have some cognitive dysfunction late stage > ○ Diagnostic Studies: Based on clinical examination Signs & symptoms No test is specific to diagnosis Electrodiagnostic tests: Electromyography (EMG) and nerve conduction velocity (NCV) Blood & urine studies Serum protein ○ Electrophoresis ○ Thyroid & parathyroid hormone levels ○ 24 hour urine collection for heavy metals ○ Assessment: Clinical manifestations Individualized Symptoms depend on location of affected motor neurons Initial Gradual onset, painless, progressive muscle weakness or stiffness Tripping, dropping things Abnormal fatigue of the arms and/or legs Slurred speech, muscle cramps and twitches, and/or uncontrolled periods of laughing or crying Late Permanent ventilator assistance Sense of sight, touch, hearing, taste and smell are not affected For many, muscles of the eyes, bladder & rectum are generally not affected ○ Management:  No cure Focus on quality of life and maintaining function Riluzole, edaravone, PB-TURSO (newest) Medications to slow disease progression Different effects on the brain → neuroprotective properties Palliative medications Baclofen (Lioresal) & diazepam (Valium) for muscle speciosity Modafinil (Provigil) for fatigue Likely managed at home Mechanical ventilation & end of life decisions i.e., PEG ○ Nursing Interventions: Prevent aspiration: PEG tube management Positioning oral care ~ Maintain airway: Support airway Prevent injury: Aid with immobility Patient & family support Refer to ALS association Oncologic Neurologic Disorders ○ Brain Tumors ○ Spinal Cord Tumors Oncologic Tumors ○ Brain tumors Benign or malignant, 100+ types Primary or secondary Classification is based on location and histologic characteristics Incidences increases with age & prior cancer history ○ Types of primary tumors Gliomas Meningiomas Acoustic neuromas Pituitary adenomas ○ Angiomas: masses of abnormal blood vessels ○ Metastatic tumors Brain Tumors ○ Classification ○ Benign/malignant Primary Secondary (metastatic) Location Gliomas (most common type of primary) Meningiomas (slow growing) Neuromas  Adenomas Angiomas ○ Glial Grading systems are used to indicate severity Glial tumors treated with combination therapy Surgery, radiation, chemotherapy - depends on size and location ○ Meningiomas Slow growing Preferred treatment surgery ○ Neuroma Rare - affect CN8 Radiotherapy Hearing loss ○ Adenomas Pituitary Common older adult - women Endocrine imbalances i.e., amenorrhea, Cushing’s disease ○ Symptoms depend on the location and size of the lesion and the compression of associated structures ○ Manifestations: Localized or generalized neurologic symptoms Symptoms of increased ICP Headache Vomiting Visual disturbances Seizures ○ Hormonal effects with pituitary adenoma ○ Loss of hearing, tinnitus, and vertigo with acoustic neuroma ○ Assessment: Headache - (severe, especially upon awakening) N/V Papilledema (swelling of the optic disc) Hemiparesis Seizures Altered mentation/personality Depend on location Ex. cerebellar tumor causes dizziness, parietal tumor causes decreased sensation on opposite sides of the body ○ Diagnostic Testing: Neurological evaluation CT scan MRI (preferred) PET (Positron Emission Tomography) EEG Lumbar puncture CSF to cytology Biopsy ○ Nonsurgical Management: Radiation therapy  Cornerstone of treatment for many brain tumors Chemotherapy Increase survival time not currative > - Blood-brain barrier challenge ○ Hard for drug to penetrate brain Pharmacologic therapy Dexamethasone (Decadron) ○ Decrease in edema & ICP ○ Use in acute patients Dilantin (anti-seizure) Mannitol (osmotic diuretic) ○ Decreases ICP ○ Medical Management: Goal is removal of tumor without increasing neurologic symptoms or to relieve symptoms by decompression Surgical types: Craniotomy open biopsy - Transsphenoidal surgery Stereotactic procedures small tumors, targeted radiation - Gamma knife (radiotherapy) ○ Not a knife at all ○ Complications: Increased cerebral edema/ICP Herniation/Ischemia Rupture/Hemorrhage Seizures/Hydrocephalus SIADH/DI/Pituitary dysfunction FLuid/Electrolyte imbalances ○ Nursing Interventions: Frequent neuro checks Monitor VS Pain management Positioning: upright unless indication Decrease stimuli Relieve anxiety → fear of death Reorient as needed check glucose levels Administer medications - Pain meds, corticosteroids, anticonvulsants Prevent ICP Risk for aspiration Prevent injury Ataxia Decreased sensation/numbness Weakness/fatigue Nutrition consult Physical/OT therapy Symptoms that may cause distress to the patient:  Pain, respiratory symptoms, bowel & bladder function, sleep, skin integrity, fluid balance, and temperature regulation Gliomas ○ Most common primary tumor in the CNS ○ Classified according to histopathologic features ○ Adult type vs pediatric types Spinal Cord Tumors ○ Classified according to their anatomic relation to the spinal cord Intramedullary: within the cord Extramedullary: extradural; outside the dural membrane (secondary - more common) ○ Manifestations: Pain Weakness loss of motor function loss of reflexes loss of sensation ○ Treatment: depends on the type of tumor and location Surgical removal Measures to relieve compression: dexamethasone combined with radiation improve symptoms - Nursing Process: The Care of the Patient with Cerebral Metastases or Inoperable Brain Tumors ○ Assessment: Focus = palliation Eliminate severe/distressing symptoms Chemotherapy & radiation may still be used for symptom reduction Pain management KEY! Must obtain baseline neurologic exam → can recognize change Assist with ADLs Nutrition: antiemetics, parenteral Psychosocial needs Family support/self-care ○ Interventions: Encourage independence for as long as possible Measures to improve cognitive function Allow patient to participate in decision making Allow patient to express fears and concerns Presence of family, friends, spiritual advisor, and healthcare personnel may be supportive Referral to counselor, social worker, home health care, support groups Referral; for hospice care ○ Improving Nutrition: Oral hygiene before meals Plan meals for times when patient is comfortable and well rested Measures to make mealtimes as pleasant as possible Ogger preferred foods Dietary supplements  Daily weight Record dietary intake  Select Neurological Disorders In Person Lecture Traumatic Brain Injuries (TBI) ○ Open Head Injuries ○ Closed Head Injuries ○ Intracranial Hemorrhage/Hematomas Brain Circulation ○ The brain receives ~ 15% of cardiac output or 750 mL of blood/minute ○ Collateral circulation achieved via circle of Willis largest pathway of blood to the brain > - Largest pathway of blood to the brain ○ Blood vessels in the brain only have 2, not 3 layers = more susceptible to injury/trauma Internal carotid arteries & vertebral arteries ○ Cerebral veins do NOT have valves to prevent backflow - must rely on gravity and blood pressure Brain Injury → Assessment ○ Health history Focus on the immediate injury, time, cause, and the direction and force of the blow Multisystem assessment ○ Baseline neuro assessment LOC first ! - LEVEL OF CONSCIOUSNESS = MOST IMPORTANT ASSESSMENT ○ LOC - Glasgow Coma Scale sensitive to KP ~ ○ Pupillary assessment PERRLA> ○ Motor/Sensation assessment squeeze > - push pull flex lift arms close eyes and tell me , , where im touching , , , ○ Cranial nerves advanced assessment - ○ Frequent and ongoing neurologic assessment call provider w/ changes ~ Are there deviations/changes from your last assessment? ALWAYS DO SERIAL ASSESSMENTS check reflexes for brain Stem function > Head Injury ○ A broad classification that includes injury to the scalp, skull, or brain ○ Most common cause of brain trauma is falls ○ Groups at the highest risk for brain trauma include: Males of all age groups Children 0 to 4 years old Adolescents ages 15 to 19 years Adults 65 years and older ○ Prevention is the best approach Traumatic Brain Injuries (TBI) ○ Global term to describe an alteration in brain function - rather than “head” injury ○ Causes disability and often mortality ○ Occurs when a sudden trauma damages the brain and disrupts normal brain function ○ TBI may have significant physical, psychological, cognitive, emotional, and social effects ○ Situations that often result in TBI: The head being struck by an object The head striking an object acceleration/deceleration of the brain without direct external impact  Foreign body penetrating the brain The force form a blast/explosion ○ Manifestations of Brain Injury: Altered LOC Pupillary abnormalities Sudden onset of neurologic deficits and neurologic changes; changes in sense, movement, reflexes Changes in vital signs HEADACHE Seizures ○ TBI Facts: Fall is the highest cause of TBI’s → age 0-4 & > 75 years at risk Highest rate of TBI hospitalizations occurs in ages 75 years + High cases of TBI in United States military Risk for TBI: Lower socioeconomic status, alcohol & drug use, and underlying psychiatric and cognitive disorders ○ Pathophysiology of Brain Damage: Series of events that can be classified as a primary or secondary injury Primary injury: ○ The initial mechanical damage caused by the impact, such as stretching or rupturing cell membranes ○ Consequence of direct contact to head/brain Secondary injury: management is as important as preventing primary injury > - ○ The additional damage that occurs after the primary injury, often as a result of a cascade of complex processes ○ Damage evolves over ensuing days and hours after the initial injury ○ Positioning: Decorticate Arms are like “C’s” moves in toward the core Problems with cervical spinal tract or cerebral hemisphere Deceberate Arms are like “E’s” Problems within midbrain or pons ○ Open vs Closed Head Injuries: Open Penetrating trauma Object penetrates the brain or trauma is so severe that the scalp and skull are opened Exposed brain matter ○ High Risk of Infection meningitis > Skull fractures Scalp injuries Closed Blunt trauma Acceleration/deceleration injury occurs when the head accelerates and then rapidly decelerates damaging brain tissue ○ Coup-contrecoup Interferes with norma; functioning Concussion  Contusion Intracranial hemorrhage Coup-contrecoup ○ Coup = same sided injury Object impacts stationary head ○ Contrecoup = opposite side of injury Whiplash Contusion seizure risk ! > - ○ Bruising/damage to the surface of the brain - frontal temporal common ○ Result of acceleration/deceleration or blunt trauma – possible surface hemorrhage subdermal epidermal - , ○ Loss of consciousness (LOC) & stupor/confusion Symptoms and recovery depend on the amount of damage and associated cerebral edema Longer period of unconsciousness = more symptoms of neurologic deficits and changes in vital signs ○ Hemorrhagic necrosis of brain tissue ○ Effects peak 18-36 hours repeat assessment ~ ○ Care focused on secondary injury & supportive care, removing/stopping the bleeding craniotomy burr holes > , Concussion ○ A temporary loss of neurological function with no apparent structure damage May be with or without loss of consciousness ○ Usually caused by blunt trauma & rapid acceleration/deceleration Leads to chemical & energy deficits ○ TBI - Traumatic Brain Injury → mild, moderate, severe ○ Repeated concussions can lead to Chronic Traumatic Encephalopathy - CTE ○ Manifestations: Presentation depends on severity of the injury Microscopic changes that can’t be seen on a CT or MRI Can cause a variety of physical, cognitive and emotional symptoms Changes in LOC Memory difficulties Difficulty in awakening, lethargy Dizziness Confusion, irritability, behavioral changes Difficulty in speaking or movement Severe or worsening headache Vomiting Seizures ○ Concussion Evaluation: imaging only to look for bleeds - History of event → loss of consciousness, timing, injury details MSE → mood or behavioral changes? Neurologic Exam → GCS, balance, coordination, memory, seizures, s/s of increased ICP? Immediate post-concussion assessment and cognitive test (imPACT) good to have baseline test > - before injury Classification: Mild TBI Moderate TBI  Severe TBI ○ Cervical Spine Always assume a patient with a head injury also has a cervical spine injury until proven otherwise Need to stabilize cervical spine to prevent paralysis Place appropriately sized neck collar to immobilize cervical immobility - Minimize movement Keep head in neutral alignment Don't let them walk around Cervical injuries are cleared by imaging and/or physician exam ○ Management: Patient may be admitted for observation or sent home Observation of patients after head trauma → report immediately! Changes in LOC Difficulty awakening, lethargy, dizziness, confusion, irritability, anxiety Difficulty speaking or moving Severe headache Vomiting Patients should be aroused and assessed frequently Monitor airway patency Adequately oxygenate Suctioning nearby HOB 30 degrees Monitor mechanical ventilation closely Monitor ABGs Frequent reassessments Prevention of secondary injury Seizure precautions and prevention ○ IV Keppra works i n 15 mins > - NG tube to reduce gastric motility and prevent aspiration (not all patients) Fluid and electrolyte management potassium hypertonic fluids > , Pain and anxiety management Nutrition ○ Concussion Treatment at Home: no TV no class Physical and cognitive rest for 24 hours minimum N No electronics until no further symptoms, then progress to minimal activity and thinking ○ Short duration of TV, walking, etc. Exposure to bright lights, loud sounds, and movement may worsen symptoms No medications that will increase risk of bleeding TYLENOL No NSAIDs or aspirin Complete physical rest for 24-48 hours may need accomodations Once symptoms lessen → light aerobic activity N Return to learn → once 30-45 minutes of concertation is tolerated ○ Post Concussive Syndrome Concussion symptoms last beyond expected recovery time >3 months, can last years Profound physical, social, and emotional effects Can respond to treatment  Does typically get better with time and resolve NOT A TYPE OF CTE!!! ○ PREVENTION OF CONCUSSIONS IS KEY Vulnerable populations Avoid head injuries Seat belts Helmets Prevent falls Diffuse Axonal Injury ○ Widespread axon damage in the brain ○ Common with shaking of the brain ○ Shearing of the white matter occurs ○ Continuum of severity ○ When severe: Immediate coma Posturing Global cerebral edema Poor outcomes MRI ○ Treatment: Mostly supportive Treatment of increased ICP Scalp Wounds ○ Manifestations depend on the severity and location of the injury, often minor ○ Scalp wounds Tend to bleed heavily due to poor constriction of vessels Portals for infection especially penetrating · ○ Large avulsion = emergency Forcible tearing off of skin Skull Fracture ○ Classified by type & location, can be open or closed ○ With or without damage to the brain, symptoms depend on severity ○ Diagnosed by CT ○ Types: Linear: Most common, lower impact Usually benign and requires no intervention Depressed: High energy force causes the skull to be depressed inward Open depressed fracture: scalp is lacerated to the bone Closed depressed fracture: the scalp is intact TBI risk high in this type of injury Diastatic: along suture lines - Most often in infants Basilar:  High impact injury involving bones at the base of the skull Most concerning bruising around eyes : behind ears > Basilar Skull Fractures ○ Periorbital ecchymosis bruising around eyes late sign · , ○ Halo sign used to check for CSF leaks > - ○ Battle sign → retroauricular ecchymosis LATE FINDING ○ Hemotympanum blood in eardrum - Most frequent finding ○ Most tend to heal on their own - over time! ○ May require hospitalization depending on neurologic compromise! ~ monitor for this ! Intracranial Bleeding ○ Epidural hematoma worst requires immediate attention - , Space between the skull and the dura mater Arterial bleed high pressure, notdlot of space · ○ Subdural hematoma Between the dura mater and the brain Venous bleed lower pressure < Acute, subacute, chronic common in older adults > - ○ Subarachnoid hematoma Located between the pia and arachnoid membranes ○ Intracerebral hemorrhage chronic HIN trauma - penetrating Within the brain aneurysm issue Vascular Intracranial Bleeding ○ Physical & neurological exam rule out cervical spine · injury ○ Skull and spinal radiography ○ CT scan quick > - ○ MRI ○ PET Assess brain function ○ EEG brain wave testing > - ○ Lumbar puncture rule out meningitis, encephalitis ~ ○ Labs NEVER w/41CI > ABGs, urine tox screen, glucose, electrolytes Epidural Hematoma ○ Blood collection in the space between the skull and the dura ○ Patient may have: A brief loss of consciousness with return of lucid state As hematoma expands, increased ICP will often suddenly reduce LOC s/s of herniation ○ An emergency situation!! ○ Treatment Measures to reduce ICP, remove the clot, and stop bleeding Burr holes or craniotomy release pressure ~  ○ Patient will need monitoring and support of vital body functions need sedation Respiratory support s Subdural Hematoma ○ Collection of blood between the dura and the brain ○ Acute or subacute: Acute: symptoms develop over 24 - 48 hours Subacute: symptoms develop over 48 hours to 2 weeks Requires immediate craniotomy and control of ICP ○ Acute s/s: Changes in LOC may just be confused ~ Pupillary changes sone slow pupil Hemiparesis numbness tingling may be subtle ~ , , s/s of increased ICP one sided headache · Requires immediate craniotomy to evacuate clot ○ Chronic: Develops over weeks to months Causative injury may be minor and forgotten Clinical signs and symptoms may fluctuate Treatment is evacuation of the clot seizure precautions > - ○ Bleeding located between the pia and arachnoid membranes Sudden, severe HA, “worst headache” “Thunderclap” Manifestations of increased ICP Risk factors: Aneurysm Bleeding of AVM ○ Treatment: SCT MRI, Measures to reduce ICP, remove the clot, and stop bleeding Burr holes, craniotomy Monitor and support of vital body functions Strict blood pressure control Respiratory support Intracerebral Hemorrhage ○ Hemorrhage occurs into the parenchyma of the brain ○ May caused by trauma or a nontraumatic cause Systemic hypertension → ruptured of vessel Aneurysm, tumors, bleeding disorders Medication side effects, TPA, anticoagulation ○ Treatment: Supportive care Control of ICP Administration of fluids, electrolytes, and antihypertensive medications Surgical Craniotomy or craniectomy to remove clot and control hemorrhage, if possible Intracranial Pressure (ICP) ○ Amount of pressure created in the skull due to limited space Compensation to keep pressure normal ○ Normal ICP = 10 - 15 mmHg 15 - 20 = elevated ICP 20 - 25 increased ICP needing immediate tx ○ Increase brain tissue, blood, CSF will cause a change in the volume of the others Monroe-kelli doctrine = because of limited space in the skull, an increase in any one of components of the skull (brain tissue, blood, CSF) will cause a change in the volume of others ○ Increased ICP → decreased cerebral perfusion and causes ischemia, cell death, and (further) edema ○ Brain tissues may shift through the dura and result in herniation ○ Autoregulation: fro cl an Brain’s ability to change the diameter of blood vessels to maintain cerebral blood flow Baroreceptors and chemoreceptors ○ CO2 plays a role Decreased CO2 = vasoconstriction Increased CO2 = vasodilation ○ THE EARLIEST SIGN OF INCREASING ICP IS A CHANGE IN LOC!!! ○ Manifestations of Increased ICP: EARLY: ***CHANGES IN LOC*** Change in condition (ANY) Restlessness, confusion, increasing drowsiness, increased respiratory effort, purposeless movements Pupillary changes and impaired ocular movements Weakness in one extremity or one side Headache → constant, increasing in intensity, or aggravated by movement or straining ○ Manifestations of Increased ICP: LATE: Vital sign changes Increased BP, decreased HR Increased body temperature Widening pulse pressure Cushing’s triad = bradycardia, hypertension, bradypnea SBP increases → tries to overcome low CPP and combat high ICP = reflex slowing of HR NO intervention = brain herniation! This requires immediate intervention!! Projectile vomiting Decreased LOC; stupor to coma Posturing Hemiplegia, decortication, decerebration, or flaccidity Respiratory pattern alterations Cheyne-Stokes breathing and arrest Loss of brainstem reflexes Pupil, gag, corneal, and swallowing Pupils fixed and dilated Absence of oculocephalic reflex or “dolls eyes” ○ Nursing Assessment: Obtain history of events leading to illness Evaluate mental status, LOC Assessment of selected cranial nerves  Assess cerebellar function, reflexes, motor and sensory function Glasgow Coma Scale, pupil checks Frequent vital signs Assessment of intracranial pressure Strict I&O ○ Management: Diagnostics help determine underlying cause → CT SCAN AVOID LUMBAR PUNCTURE (LP) Goal is to avoid herniation, worsening increases in pressure, normalize pressure and neurologic functioning Monitoring Intracranial pressure (ICP) monitoring device Epidural bolt monitors ICP ~ Medications Hyperosmolar agents for cerebral edema: mannitol, 3% NaCl Barbiturates (phenobarbital) ↓ICP > Antiseizure medications (Levetiracetam) ~Keppra Sedatives protect brain time to heal > - , Maintain CPP Maintain hemodynamic stability → vasodilators vs vasopressors Head of the bed (HOB) to 30° or 45° smoving head ↑CP Stabilize CSF levels Draining cerebrospinal fluid External Ventriculostomy drain Maintaining normothermia (normal body temperature) shiveringI brain workload > fevers will not be Use of coverings: sheets, blankets to patient needs neurogenic effected by antipyretics “Neurogenic” fever → damage to hypothalamus ○ Antipyretics won’t work ○ Dantrolene, propranolol Administration of acetaminophen for true infectious fever ○ NOT RECTAL → stimulation increased ICP Increased temperature due to metabolic demand Cooling blankets or cool baths; avoid shivering Surgery Craniotomy or decompressive craniectomy ○ Complications of Increased ICP: Brainstem herniation SIADH → high ADH Will not diurese Diabetes insipidus → low ADH Kidneys cannot prevent excretion of water Cerebral Perfusion Pressure (CPP) ○ Net pressure gradient that drives oxygen delivery to cerebral tissue ○ Difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP), measured in millimeters of mercury (mmHg) Needs to be between 60 - 70 MINIMUM CPP = MAP - ICP  MAP = SBP + (2 x DBP)/3 What is Ventriculostomy Therapy? ○ Allows fluid trapped within the brain to escape into a drainage system ○ The system also lets us monitor pressures within the skull ○ The amount of cerebrospinal fluid (CSF) in a healthy brain is always the same: this fluid is produced and absorbed at rates that keep its total amount constant ○ Problem arises with: Obstruction - of drainage system Reabsorption Intracranial Surgery ○ Ventriculostomy drain ○ Craniotomy: opening of the skull Purposes: remove tumor, relieve elevated ICP, evacuate a blood clot, control hemorrhage ○ Craniectomy: excision of portion of skull ~ replace later HELMET for Safety , ○ Cranioplasty: repair of cranial defect using a plastic or metal plate ○ Burr holes: Circular openings for exploration or diagnosis to provide access to ventricles or for shunting procedures, aspirate a hematoma or abscess, or make a bone flap Complications of Increased ICP ○ Brainstem herniation → life threatening emergency that occurs when brain tissue shifts from one part of the skull to another due to increased pressure inside the skull Often leads to irreversible damage → respiratory and cardiac arrest Brain tissue pushed sideways and downward through small openings Common s/s: posturing, abnormal breathing pattern, absence of pupil response to light, decreasing LOC, decreasing GCS Treatment: reduction of ICP ○ SIADH → syndrome of inappropriate antidiuretic hormone, can not diurese (soaked inside!!) ○ Diabetes insipidus → low ADH, kidneys cant prevent excretion, low vasopressin (dry inside!!) Drug Therapy ○ Osmotic diuretics → mannitol ○ Corticosteroids → dexamethasone ○ Barbiturates → phenobarbital, thiopental, propofol ○ Neuromuscular blocking agents → pancuronium ○ Anti Seizure medications → phenytoin ○ Desmopressin Spinal Cord Injuries ○ PREVENTION IS KEY! ○ The result of concussion, contusion, laceration, or compression of the spinal cord ○ Causes: MVAs Falls Violence Sports injuries  ○ Risk factors: Alcohol and drug use Age (younger) Gender (male) ○ Incomplete vs Complete Injuries Incomplete → maintains some functioning, messages not completely lost Complete → no sensory or motor functioning below the level of injury ○ Primary injury Result of initial trauma May cause permanent loss of function Treatment is needed to prevent primary injury from developing into more extensive and permanent damage ○ Secondary injury Resulting from SCI → ischemia, hypoxia, hemorrhage Thought to be reversible or preventable during the first 4-6 hours after injury Spinal Cord Injury Assessment ○ Rapid assessment: Immobilization Spinal backboard Cervical neck collar ○ Prevent secondary injury Positioning ○ Cardiovascular Stability ○ Diagnostic Evaluations ○ Incomplete spinal cord lesions Sensory or motor fibers (or both) are preserved below the lesion Bladder or bowel dysfunction paralysis/paresis Loss of sweating ability - hypothalamic dysfunction ○ Complete spinal cord lesion Total loss of sensory and motor fibers below the lesion Paraplegia → lower two extremities Tetraplegia → all extremities ○ Loss of: Motor function Sensation Reflex activity Bowel and bladder control Changes in body image Role performance self -concept ○ THINK ABOUT NEUROGENIC SHOCK S/S Decreased blood pressure Decreased heart rate Need vasopressors! ○ Location: Injuries above C4 → paralysis of respiratory muscles and all four extremities  AIRWAY RISK!! The higher the injury the greater the loss of function Cervical C3, C4, C5 → KEEPS THE DIAPHRAGM ALIVE! Need mechanical ventilatory support Support for head control Support for eating Fully to maximally dependent May have some limited shoulder or elbow mobility Thoracic Loss of thoracic muscles → shallow breathing May lose abdominal muscle control Likely requires wheelchair Short distances with assistance Lumbar Normal to impaired bladder Normal to impaired sexual function Likely can ambulate with or without assistance ○ Nursing Assessment in Spinal Cord Injury: Respiratory → note effort or lack Mental status/mood Motor sensory function (especially early on) Bladder distension Temperature management Spinal Cord Injury Management - Acute Phase controversial ○ Prevent secondary injuries > - ○ Pharmacologic → corticosteroids, anticoagulation, support HR/BP ○ Respiratory support SDVT riSk ○ Positioning → LOG ROLL ○ Surgical intervention ○ Crutchfield Tongs and Traction: Reduction and traction for dislocations Neck in neutral position Weights are gradually added Weights hang freely Site care to minimize infection Specialized bed ○ Halo Vest Traction: Monitor for neuro changes with movement Keep wrench at bedside at all times Assess skin Sterile pin care Clean daily Foam linen helps with breakdown Sponge Baths only Never pull on device Notify MD if bolts loosen  Shampoo hair only → no other products! Roll onto side with arms out to get out of bed High protein/calcium diet ○ Braces: TLSO → thoracic lumbar sacral orthosis Single piece that opens in the front CTLSO → cervical thoracic lumbar sacral orthosis Stabilized head and neck Both stabilize after surgery SCI Management ○ Medication therapy: Methylprednisolone Anticoagulation therapy Pain management therapy Stool softeners ○ Surgical Treatment: Usually reserved for thoracic and lumbar injuries Indication for compression of spinal cord ○ Airway Management: Maintain high PaO2 Mechanical ventilation if neededPrevent complications of immobility ○ Prevent complications of immobility ○ Nursing Interventions: Monitor respirations and breathing pattern Lung sounds and cough Monitor for changes in motor or sensory function → report immediately! ~ prevent secondary injury Assess for spinal shock Monitor for bladder retention or distension, gastric dilation, ileus Temperature management poikilothermia can't regulate temp ~ , Maintain skin integrity, appliance care Assess for complications Sensory aids → glasses, hearing aids Body positioning, passive ROM, collars Psychosocial support Spinal Cord Injury Complications ○ Spinal shock Neurologic response to SCI Sudden depression of reflex activity below the level of spinal injury Bladder paralysis and distension Muscular flaccidity, lack of sensation and reflexes Usually temporary May occur months after injury ○ Neurogenic Shock Vascular response to SCI Loss of sympathetic nervous system Blood pressure, heart rate, and cardiac output decrease  Venous pooling occurs because of peripheral vasodilation Paralyzed portions of the body do not perspire ○ Other DVT Skin breakdown Sexual dysfunction Pain syndromes Spasticity Bowel dysfunction Autonomic dysreflexia Autonomic Dysreflexia ○ MEDICAL EMERGENCY ○ Occurs after spinal shock has resolved and may occur years after the injury ○ Occurs in persons with SC lesions above T6 ○ Autonomic nervous system responses are inappropriate → exaggerated and abnormal response to a stimuli ○ Symptoms: severe pounding headache sudden increase in blood pressure profuse diaphoresis nausea nasal congestion bradycardia ○ Triggering stimuli: distended bladder distension or contraction of visceral organs (constipation) stimulation of the skin ○ STROKE AND SEIZURE RISK ○ Remove stimuli immediately! ○ Interventions: Recognize Report Correct cause Educate ○ Nursing Interventions: Place patient is seated position - HIGH FOWLERS rapid assessment to identify and eliminate the cause Empty bladder with catheter Examine rectum for mass Examine skin Examine any other stimulus Administer ganglionic blocking agent → HYDRALAZINE Label chart or medical record if patient is at risk Educate patient in prevention and management  Burn Injuries Anatomy of the Skin ○ Layers of the Skin: body's first layer of defense ~ Epidermis → outer layer of the skin no vessels ~ Dermis → connective tissue = hair folicies Subcutaneous → most protective layer; connective & adipose tissue ○ Function of the Skin: Protection Thermoregulation Metabolism of nutrients and wastes Sensation ○ Gerontologic Considerations: Increased risk of skin breakdown > - Diminished mobility, postural stability, strength, coordination, sensation, visual acuity, and declining memory Increased mortality with burns Increased complications Pneumonia, sepsis, dysrhythmias Skin integrity changes Thinner & less elastic = deeper wounds = delayed healing Pulmonary, cardiac, kidney & hepatic changes Fluid resuscitation issues Medication clearance Cognitive impairments Pathophysiology of Burns ○ Burns are caused by: understand type to treat properly · Heat one source of heat to another - Chemical may be internal - Electrical 4 risk of arrhythmias > - Radiation ○ Physiologic Changes: Severe burns induce response that affects almost every organ system Burns more than 30% may produce a local and systemic response and are considered major burns Systemic response includes release of cytokines and other mediators into systemic circulation Fluid shifts and shock result in tissue hypoperfusion and organ hypofunction L ↓ body in high alert State third spacing Local Response redness Swelling > - , hypovolemic shock ○ Zone of coagulation (ischemia) Deepest layer → POINT OF MAXIMUM DAMAGE permanent tissue damage > Treatment is surgical debridement ○ Zone of stasis (edematous) PREVENT SECONDARY INJURY potentially salvageable tissue , want to increase perfusion ~ Decreased tissue perfusion Potentially salvageable Nurses have the most impact here  ○ Zone of hyperemia not cellulitis ! > - Redness & inflamed tissue Increased tissue perfusion Minimally damaged tissue Most likely heals in 7-10 days Systemic Response → 30% of body or more burned ○ Cytokine release ○ Cardiovascular changes Hypotensive & hypoperfusion Increased capillary permeability Decreased intravascular protein & fluid Third spacing Decreased contractility Peripheral & splanchnic (organ) vasoconstriction AKI Decreased LFTs Decreased LOC Paralytic ileus ○ Respiratory changes Bronchoconstriction ARDS ○ Metabolic changes Increased BMR Increased blood glucose Feed the gut ○ Immunological changes Decreased immunity Increased infection risk Heat ○ Contact with heat/heated objects or fluids ○ Proteins denature and break down causing cell damage ○ The amount of tissue destruction is determined by: Temperature & duration show not ? how long ? ○ Injury diminished outwards as heat dispersed around central site ○ Treatment: Rinse burned skin with cool water until the pain stops → NOT COLD!!! - take of jewelry and tight clothing DO NOT break the blisters ↑ infection risk > - Seek treatment if more than superficial burn Chemical → caustic burns ○ Exposure to corrosive substances was it ingested ? ~ ○ Acids, bases, oxidizing/reducing agents, solvents, alkylants, chemical weapons ○ Severity Alkali > Acid damage - moreproteins to Warmer temperature, greater volume, concentration, contract duration Specific mechanism of chemical action, degree of tissue penetration  ○ Occur immediately on contact may progress for some time ○ May not be immediately evident ○ May diffuse deeper into structure without initial damage to skin surface > - neutralize : rinse control call poison Electrical high risk for arrhythmias ~ ○ Passage of electricity through tissue = rapid injury DO NOT TOUCH PATIENT IF ELECTRICITY IS STILL INSIDE THEM!!! Look for entry & exit wounds ○ Subdermal damage significantly greater than superficial injury ○ Flash, conductive or lightening ○ Extent of injury determined by: Current → higher force = increased lethality/tissue damage Voltage → higher voltage = more damage Frequency → very high frequencies = tissue burning Duration → longer duration = more tissue damage Pathway → current flowing through the heart = lethal Tissue resistance Pathway, depth dependent Skin vs bone less resistant more resistant Radiation ○ Excessive exposure to radiation ○ Ultraviolet (UV) light Sunlight, most common cause of radiation, superficial burns ○ Ionizing radiation Radiation therapy, X-Rays, radioactive fault ○ Thermal burns Electromagnetic radiation Microwave, cell phone, IR, x-ray, MRI, OR Classification of Burn Depth ○ First-degree (superficial) ○ Second-degree (partial thickness) ○ Third-degree (full thickness) ○ Fourth-degree (full thickness with deep burn necrosis) Depths of Burns: First-Degree (Superficial) ○ Superficial injuries that involve outermost layer of skin; sunburn ○ Skin layers involved: Epidermis ○ Clinical features: hypersensitivity < Sensation intact, pain, erythema, blanchable, hair follicles present ○ Healing 5-10 days, no scarring, heals completely may peel ~ ○ Treatment: Oral pain medication Cool compresses, skin lubricants Depths of Burns: Second-degree (Partial Thickness) ○ Skin layers involved: Extends from ENTIRE epidermis into PARTIAL dermis ○ Clinical features: Sensation may be impaired hypersensitivity > Pain, erythema, minor blanching Blisters, containing serious, yellow to white fluid may weep s Some hair follicles intact ○ Healing: Depends on depth Superficial: 2-3 weeks spontaneously re-epithelializes ↑ of loss pigmentation Deep partial: 1-2 months, re-epithelializes, hypertrophic scars common, grafting may be recommended to expedite healing Depths of Burns: Third-Degree (Full Thickness) ○ Destruction of the epidermis, dermis, and underlying tissue, lack of sensation ○ Skin layers involved: Extends through ENTIRE epidermis & ENTIRE dermis ○ Clinical features: No sensation > nopain Stiff, leathery, eschar Black, gray, white, cherry red No hair follicles, thrombosed veins visible ○ Healing: Incomplete/months often needs grafting ~ Scarring decreases function Depths of Burns: Fourth-Degree (Full Thickness with Deep Burn Necrosis) ○ Full thickness that includes fat, fascia, muscle, and/or bone Deep burn necrosis ○ Clinical features: Black and charred ○ Healing: Requires debridement/amputation sescharotory Skin flap coverage Does NOT re-epithelialize, cannot graft Factors to Consider in Determining Burn Depth/Severity ○ How the injury occurred ○ Causative agent ○ Temperature of agent ○ Duration of contact (time) ○ Thickness of the skin at the site consider location > - Diagnosis of Burns Percentage: Estimated Total Body Surface Area (TBSA) Burned ○ Palmer Method Used to estimate extent of scattered burns Size of patient’s hand, including fingers is 1% TBSA  ○ Lund and Browder Method Recognizes % of TBSA of various anatomic parts ○ Rule of Nines Most common Based on anatomic regions Palmer Method ○ Simplest tool ○ By utilizing the patient’s palm ○ Ideal for small or scattered burns ○ Limited by user and patient variability Lund and Browder Method ○ Commonly used for infants and children ○ Account for variation in body shape with age young to old ○ Inability to accurately represent high BMI patients Wallace Rule of Nines ○ Each major body part assigned value corresponding to approximate proportion of body area ○ Clinically efficient ○ Calculated by dividing the body into percentages of 9 ○ Limitations: pediatric and obese patients Rule-of-9s Total Subdivision Head 9% Anterior Head = 4.5% Posterior Head = 4.5% Torso 18% Chest = 9% Abdomen = 9% Back 18% – Each Arm 9% Anterior Arm = 4.5% Posterior Arm = 4.5% Each Leg 18% Anterior Leg = 9% Posterior Leg = 9% Perineum 1% – Effects & Potential Complications of Major Burn Injury ○ Fluid & Electrolyte Shifts: Dehydration ~hemoconcentrated ↓ Blood volume, ↓ UOP ↑K, ↓ Na metabolic acidosis > - ○ Cardiovascular Effects: ↓ Cardiac output Hypovolemia Distributive shock Hypovolemic shock ○ Pulmonary Injury: Upper & lower airway CO poisoning Restrictive defects ARDS direct or fumes > - ○ Renal & GI: AKI srit hypovolemia, monitor output Curling ulcer stress ulcers protonix > , Paralytic ileus monitor output BS NG Tube > - , , Protein losses may cause brown urine ~ ○ Musculoskeletal: Compartment syndrome pressure build up in muscles > Pain Contractures #aresthesias Abnormal wound healing &oikilothermia ○ Immunologic Alterations: I allow Immunodepression Paralysis & uselessness Sepsis/Infection ○ Thermoregulation: Hypermetabolism Hyperglycemia Insulin resistance Hypothermia Inhalation Injury ○ Smoke inhalation Singed nasal hair, eyebrows, and eyelashes Hoarseness, nasal septal edema, wheezing, smoky breath ○ Can be DEVASTATING ○ Airway edema & mucosal sloughing = LOSS OF A PATENT AIRWAY sintubation ? Brassy cough, drooling, dysphagia, audible wheeze, crowing, and stridor ○ Hydrogen cyanide poisoning almond smell > ○ Carbon monoxide poisoning ○ Risk factors & symptoms: More common in the elderly, immobile, and children Fire in an ENCLOSED space Raspy or hoarse voice Facial burns (2nd degree or worse)  Singed facial hair Arterial PaCo2 < 60 mmHg > NO BIPAP ! Carboxyhemoglobin > 15% Bronchospasm or wheezing Metabolic acidosis Alcohol & drug use + fire Carbon Monoxide Poisoning ○ Symptoms: Dizziness Chest pain Confusion Blurred vision Headache SOB Nausea ○ Clinical Severity of CO Poisoning: Normal CO = < 2% Smoker CO = < 5% CO poisoning = > 9% NEED CO OXIMETER NOT SPO2!!! ○ Treatment: 100% FiO2 NRB!!!! Labs: BMP, ABG< carboxyhemoglobin (CHOb) TRANSFER to local burn center Hyperbaric treatment REMEMBER: SpO2 saturations CANNOT tell you if someone has CO poisoning Hydroxocobalamin to reverse cyanide toxicity Urine marone like red wine ↓ normal = 2% ○ DO NOT BE ALARMED! copoisoning >9 % = ○ Lab Testing and Diagnostics: Serum laboratory studies CMP ○ Potassium ○ Sodium CBC with differential ○ Hematocrit high uIt firid loss ~ Electrolytes k +, Na > Arterial Blood Gases ○ Metabolic acidosis Type and Screen Electrical Burns EKG Cardiac enzymes Urine myoglobin Head CT Respiratory Burns  Carboxyhemoglobin ABGs Cardiac Enzymes EKG CXR Phases of Burn Injury ○ Emergent/Resuscitative Phase Prevent injury to the rescuer Stop injury stop, drop, and roll Extinguish flames Cool the burn Irrigate chemical burns ABCs → establish airway, breathing, and circulation Start oxygen and large bore IVs Remove restrictive objects and cover the wound to prevent infection Clothes Jewelry Primary assessment of body systems blankets to maintain temp ~ Secondary assessment including history of the accident and pertinent history Treat patient with falls and electrical injuries as for potential cervical spine injury Patient is transported to emergency department Fluid resuscitation is begun Foley catheter is placed ↓ aspiration risk ; decompress NG tube inserted and placed to suction > - Patient is stabilized and condition is continually monitored ECG, continuous cardiac monitoring Address pain → ONLY IV PCA fentanyl > , Tetanus vaccine tetanus causes & airway risk be contraction causing mus Psychosocial consideration and emotional support Nursing Management of Emergent Phase: ABCs Vital signs Assess hemodynamic status invasive Bpline > - Monitor for fluid volume deficit Assess extent of burn Get central venous access Keep patient warm → warm room and fluids Fluid Resuscitation: Maintain SBP >100 mmHg Keep urine output 30-50 mL/hr (.5mL/kg/hr) → crucial to monitor, tells about perfusion! Maintain serum sodium → Parkland Baxter Formula ○ Parkland Baxter Formula Used to determine the amount of fluid to infuse for a burn patient ½ of total calculated volume given in the first 8 hours time starts at time ~ Durn of ½ of total calculated volume given over the following 16 hours  4mL x %TBSA x kg ALWAYS LR → closest fluid to normal body fluid monitor output ! > - tells perfusion Fluid and Electrolyte Shift: Dehydration > third spacing Decreased blood volume Hemoconcentration Decreased urine output Hyperkalemia Hyponatremia sfollows water Metabolic acidosis Complications of Emergent Phase: Acute respiratory failure Distributive shock Acute kidney injury Compartment syndrome Paralytic ileus Curling ulcer ○ Acute/Intermediate Phase 48-72 hours after injury Continue assessment and maintain respiratory and circulatory support, fluid and electrolyte balance, GI and renal function Goals Prevention of infection Burn wound care Pain management Modulation hypermetabolic response feed ! give insulin ! - Early positioning and mobility searly ROM Nursing Management of Intermediate Phase: Restoring fluid balance Preventing infection Modulating hypermetabolism Promoting skin integrity Relieve pain and discomfort Promoting mobility Strengthening coping strategies Supporting patient and family Monitoring and managing complications Fluid and Electrolyte Shifts: 48 hours post burn the vascular system is self repairing Fluid re enters the vascular space Hemodilution Increased urinary output SODIUM is lost with diuresis always hyponatremia > - POTASSIUM shifts from extracellular fluid into cells → hypokalemia Metabolic acidosis Complications in the Intermediate Phase Heart failure and pulmonary edema Acute respiratory failure  Sepsis Visceral damage (electrical burns) ○ Rehabilitation Phase Rehabilitation is begun as early as possible in the emergent phase and extends for a long period of time after the injury Reconstruction and rehabilitation Focus is on wound healing, psychosocial support, self image, lifestyle, and restoring maximal functional abilities ROM ! ~ The patient may need reconstructive surgery to improve function and appearance Counseling and support groups may assist the patient PTSD, anxiety, depression, sleep disturbance Burn Management ○ Medical Respiratory therapy → airway, oxygen, suctioning frequent reassessments - CXR ABG COHg BUN, Creatinine, GFR Mechanical ventilation prevent loss of airway > ○ Surgical Bronchoscopy Debridement Escharotomy Grafts ○ Pharmacological Fluid resuscitation IVF Pain management Analgesics Histamine 2 blockers Antimicrobial ointments ○ Nursing Strict I&O Wound care Airway patency ○ Pain Management Pain accompanies care and treatments such as wound cleaning and dressing changes Types of burn pain Background or resting Procedural Breakthrough Analgesics IV use during emergent and acute phases Role of anxiety in pain Effect of sleep deprivation on pain Nonpharmacologic measures ○ Burn Wound Care  Dressings Several layers of dry dressings Lighter over joints Facial OTA after cleansing Wound Cleaning Antimicrobial ointments for moisture and debridement Hydrotherapy Wound Debridement: Removal of devitalized tissue or burn eschar in preparation for grafting and would healing Removal of tissue contaminated by bacteria and foreign bodies, thereby protecting the patient from invasion of bacteria Documentation should include color, odor, size, exudate, signs of re-epithelialization, any changes, and other key characteristics Wound Grafting: Skin grafting Deep partial or full thickness burns Earlier functional ability and reduces scarring Types ○ Autografts: patients own skin ○ Homografts: from deceased donors ○ Xenografts: from animals Occlusive Dressings remain in place for 3-5 days post op Burn Shock ○ Inflammatory release of histamines and prostaglandins causing large fluid shifts leading to: Decreased cardiac output Increased vascular resistance vasodilation Hypovolemia Hypoperfusion ○ Management: Prevent or minimize Parkland Burn Formula ○ Complications: Acute renal failure Decreased perfusion Pulmonary edema Liver failure Cardiac failure Occlusion of arteries Permanent brain damage Death Nutritional Support Therapy ○ Burn injuries produce profound metabolic abnormalities and patients with burns have great nutritional needs related to stress response, hypermetabolism, and requirement for wound healing ○ Goals: balance and match nutrient utilization ○ Nutritional support is based on patient preburn status and percent of TBSA burned  ○ Enteral route is preferred → decrease aspiration risk ○ Supplementation Vitamin C Zinc Copper Vitamin E Selenium Vitamin D Burn Prevention ○ Matches, lighter, hot irons, curling irons kept out of reach of children ○ Never leave children unattended around fire or in the bathroom or bathtub ○ No smoking in bed, while using oxygen ○ Caution against throwing flammable liquids onto already burning fire ○ Avoid overhead electrical wires and underground wires when working outside ○ Caution against running and electrical cord under carpets or rugs ○ Caution when cooking; beware of loose clothing ○ Having a working fire extinguisher in the home and knowing how to use it  Critical Care Condition Chart Condition: __________________ meningitis 7 Pathophysiology Signs & Symptoms Risk Factors inflammation of membranes and the headache Dacterial infection fluid space surrounding brain : SC fever Cancer ↓ LOC Septic : BACTERIAL (Strepto neisseria behavioral ↓ immunity , changes unvaccinated a Septic : VIRAL (secondary to a immunity) n/v college students nuchal rigidity military + Kernig sign -Brudinski sign photophobia - Labs & Diagnostics Lumbar puncture - CSF > 2300 leukocytes + gram stain low CSF glucose 5 Nursing Interventions droplet precautions assist w/ lumbar puncture med management frequent vital signs ; neurochecks pain ? fever management Seizure,dirway environment , monitoring as ladmonitoring prevent complications from immobility supportive care Treatment treat dehydration , shock , seizures Medications Patient Education d examethisone > - ↓ inflammation droplet precautions > - no kissing or sharing drinks vancomycin > - bacterial  Critical Care Condition Chart Condition: __________________ encephalitis 7 Pathophysiology Signs & Symptoms Risk Factors starts as fir s/s then progresses viral infections a cute , inflammatory process of brain + issue autoimmune disorders headache viral HSV fever traveling unvaccinated : MMR varicella confusion fungal : , Vector : Zika west hile virus , hallucinations autoimmune Stiff neck Photophobia seizures rash vector borne paralysis : , , Parkinson like movements - Labs & Diagnostics CT/MRI lumbar puncture EEG 1 abs