NURSING nur265 AdvMedSurgExam3MANAGEMENT OF CLIENTS WITH COMPLEX NEUROLOGICAL PROBLEMS Central Nervous System

- Brain and spinal cord - Meninges (protective covering for brain and spinal cord) o Dura matter (outside layer), arachnoid matter (middle layer), pia matter (inner layer), epidural space (between skull and duramatter) Brain - 3 main areas - Brainstem (basics, life sustaining) - Cerebellum (coordination) - Forebrain (includes relay station, memory, intelligence, creativity, emotions) Cerebral Cortex - Frontal lobe (front of head, controls voluntary movement, broca’s area for expressive, voluntary eye movement, judgment, reasoning, concentration) - Parietal lobe (understanding sensation, spatial relationships, perception of body parts, taste) - Temporal lobe (wernicke’s area for receptive, auditory center for sound interpretation, complicated memory patterns) - Occipital lobe (primary visual center) Cerebellum - Receives continuous information regarding the condition of muscles, joints, and tendons - Control is ipsilateral (controls same side) Head injuries - Injury to the scalp, skull, or brain. Most common cause of death from trauma. Blunt or penetrating. - Highest at risk are male’s age 15-24 r/t playing sports, being more active/impulsive and elderly r/t falls. Pathophysiology of TBI - Brain suffers traumatic injury  brain swelling or bleeding increases intracranial volume  rigid cranium allows no room for expansion of contents so intracranial pressure increases  pressure on blood vessels within the brain causes blood flow to the brain to slow  cerebral hypoxia and ischemia occur  intracranial pressure continues to rise, brain may herniate  cerebral blood flow ceases o If ICP goes up pt is at risk for brain herniation and pt will die Anatomy of Head Injuries - Scalp o Significant bleeding; portal of infections (direct route to brain) - Skull o Protective, rigid, fixed space. o Fractures at the base of the skull  Leaking CSF from nose, pharynx, or ears • CSF if it tests + for glucose, will cause yellow halo on sheets  Battle signs: ecchymosis behind the ear - Dura (protective covering) - Brain (direct, primary; indirect, secondary) Direct (Primary) Brain Injuries - Primary injury: due to initial damage (contusions, lacerations, damage to blood vessels, or foreign object penetration - Direct damage done to brain (being stabbed in the head), irreversible Indirect (Secondary) Brain Injury (Prevent, stop, slow down, or reverse) - Secondary injury is damage that evolves after the initial injury (Expanding mass, lesions, swelling, hydrocephalus (abnormal increase of CSF fluid) or bleeding. - Increased ICP and/or herniation - Diagnosis and treatments target minimizing the effects of the indirect injuries Brain Injury - Closed brain injury (blunt trauma): Acceleration/deceleration injury occurs when the head accelerates then rapidly decelerates, damaging brain tissue. (Car accident) - Open brain injury: Object penetrates brain or scalp and skull are opened from a traumatic injury. - Concussion (brain shakes): A temp loss of consciousness with no apparent structure damage. Manifestations of Brain Injury - Altered LOC (Earliest indicator) - Pupil abnormalities (Check pupils of TBI pts for size and reaction to light. Report any changes to provider immediately because they could indicate an increased ICP) - Sudden onset of neurological deficits and neurological changes; change in sense, movement, and reflexes o Flaccid limbs, drooping of face, cushing’s triad (severe HTN with widening pulse pressure, the difference between diastolic and systolic 40 or greater is widening pulse pressure. Look at trends can be moving towards cushing’s triad) - Changes in vital signs (cushing’s triad, bradycardia) - Headache, seizures (check nail bed pressure for pain) - Posturing (stimulate pain to see if they posture, pinch chest/sternal rub, if pt postures they are getting worse) o Decorticate (in towards core), decerebrate (out) Management of the Pt with a Head Injury - Always assume cervical spine injury until ruled out o Don’t move them, C-Spine collar o Log roll off slide board, log roll until Dr. clears pt with CT Scan - Preserve brain homeostasis and prevent secondary damage o Treat cerebral edema with mannitol o Maintain cerebral perfusion (keep HOB 30 degrees, neutral alignment) o Maintain oxygenation, cardiovascular, and respiratory function o Manage fluid and electrolyte balance. o Prevent seizures  Prophylactic Dilantin (Phenytoin) first 7 days o Monitor for SIADH and diabetes insipidus r/t damage to the pituitary gland Supportive Measures - Respiratory support; intubation (if they can’t maintain airway), and mechanical ventilation - Seizure precautions and prevention (pad side rails, have suction available) - NG to manage reduced gastric motility and prevent aspiration o To check placement test gastric content, air bolus, or x-ray - Fluid and electrolyte maintenance o Sodium level will be effected with brain injury - Pain and anxiety management - Nutrition o Feeding tube possible o If neurologically impaired check pts ability to swallow (sit pt up, give small amount of water) - Be careful not to over sedate to be able to check neuro function properly Intracerebral Hemorrhage (Tearing of small arteries or veins) - Bleeding into the substance of the brain  edema = increased ICP - May be due to trauma or a non-traumatic cause (HTN, infection, tumors) - Treatment o Supportive care (keep them breathing and heart beating) o Control of ICP (HOB 30 degrees, neutral alignment, mannitol, no straws, no coughing, no suctioning) o Administer fluids, electrolytes, and antihypertensive medication  Aneurysm – control B/P, monitor B/P o Craniotomy (burr holes), craniectomy (take out whole piece) to control bleeding Intracranial Pressure (ICP) - Decreased LOC = first sign, Cushing’s triad = late sign - 10-15 is normal ICP - Intracranial space contains brain, blood vessels, and CSF o If one increases another will compensate to decrease ICP, CSF easiest to compensate (Monroe-Kellie Hypothesis) - Severe headache, decreased LOC, restless, dilated pupils, pinpoint pupils - To decrease ICP give furosemide and mannitol - Dilantin (phenytoin) for seizures - Intraventricular catheter (IVC) o Allows accurate measurement of intracranial pressure o Allows drainage or sampling of cerebrospinal fluid Nursing management for IICP - Neuro assessment (pupils dilated, decreased LOC, strength) - Positioning (neutral position, HOB 30 degrees) - Vent support (ABG’s, watch CO2, keep CO2 @ 35-38 because CO2 is a vasodilator will raise ICP) - IVC assessments (measure hourly (drainage), check drsg for drainage/infection) o NEVER FLUSH A DRAIN!!!!!!!! - Maintain fluid restriction (r/t increased ICP) - Teach pt to avoid coughing, straining during BM, sneezing, blowing nose - Maintain quiet environment and limit stimuli (give rest periods) - Maintain normal temp (increased temp with increased ICP, put pt on cooling blanket) Cushing’s traid - Widening pulse pressure (rising systolic, declining diastolic) 40 difference, Severe HTN, Bradycardia Herniation - Damage to brain from trauma  increased ICP  displacement of the brain matter  results in herniation of the brainstem o PT will have cheyne-stokes respirations Diffuse Brain Injuries - Concussion (“mild to severe traumatic brain injury”, no significant imaging findings) o Headaches, irritable o Try to wake up q4hrs, bring back to ER if vomiting occurs or pt won’t wake up - Axonal Injury (Severe Injury caused by sheering of axons o No strenuous activity for 7 days or until headache free but @ least 7 days o No TV, no reading Focal Brain Injuries - Epidural Hematomas *EMERGENCY SITUATION* See this Pt first! o Blood collection in the space between the skull and dura. Usually caused by a tear of the middle meningeal artery. Brief loss of consciousness with return of lucid state; then, as hematoma expands, increased ICP will often suddenly reduce LOC (Lose consciousness  wake up  then out again) o Treatment = measures to reduce ICP o Pt needs monitoring and support of vital body functions and respiratory support - Subdural Hematomas o Slow venous bleed  can die r/t bleed going unnoticed o Blood beneath dura o Very common in elderly r/t falls o Acute/subacute  Acute: symptoms develop over 24 to 48 hours  Subacute: symptoms develop over 48 hours to 2 weeks  Requires immediate control of ICP o Chronic  Develops over weeks to months  Clinical signs and symptoms may fluctuate Diagnostic Evaluation - Physical and neurological exam, skull and spinal x-rays, CT scan, MRI, PET scan Pre-hospital Care of Head Injured Patients - ABC’s, spinal immobilization (anyone who falls assume they have neck injury, c-spine collar), initial resuscitation, rapid transport Head Injury Management - GOAL: Prevent of minimize secondary injuries to the brain ED Assessment of Head Injured Patients - ABC’s, history, clues to brain injury, physical exam (treat life threats first), the “D” of the ABC’s stands for neuro exam Glasgow Coma Scale (GCS) - Measures motor 1-6, verbal 1-5, eyes 1-4, 15 = best, 1 = bad - GCS scores o 13-15 – mild head injury o 9-12 – moderate head injurt o or = to 8 – severe head injury  5 or less call the life center! Collaborative problems/potential complications - Decreased cerebral perfusion  increased ICP - Cerebral edema and herniation  Cheyne-stokes resp  death - Impaired oxygenation and ventilation  intubate (check ABG’s) 35-38 for CO2 - Impaired fluid, electrolyte, and nutritional balance  Sodium levels - Risk of post-traumatic seizures  7 days after, antiepileptic dilatin (phenytoin) Major Goals - Patent airway, adequate CPP, fluid and electrolyte balance, adequate nutrition, normal body temperature, skin integrity, prevent secondary injury, prevent sleep deprivation, support the family, knowledge about rehab, no complications! Management Principles - Rapid imaging for definitive diagnosis - Early, rapid specialty care (neuro surgeons, trauma centers) - Temporizing measures o Hyperventilation (to decrease their CO2 on ventilator) o Mannitol to reduce ICP o Burr holes to relieve pressure on skull Nursing Interventions - Provide ongoing assessment and monitoring - Maintain airway o Elevate HOB 30 degrees o Suction with caution, this increases ICP o Prevent aspiration and respiratory insufficiency, check ability to swallow o Monitor ABG’s, ventilation, and mechanical ventilation. Monitor for pulmonary complications, potential ARDS. NURSING nur265 AdvMedSurgExam3MANAGEMENT OF CLIENTS WITH COMPLEX NEUROLOGICAL PROBLEMS Central Nervous System - Brain and spinal cord - Meninges (protective covering for brain and spinal cord) o Dura matter (outside layer), arachnoid matter (middle layer), pia matter (inner layer), epidural space (between skull and duramatter) Brain - 3 main areas - Brainstem (basics, life sustaining) - Cerebellum (coordination) - Forebrain (includes relay station, memory, intelligence, creativity, emotions) Cerebral Cortex - Frontal lobe (front of head, controls voluntary movement, broca’s area for expressive, voluntary eye movement, judgment, reasoning, concentration) - Parietal lobe (understanding sensation, spatial relationships, perception of body parts, taste) - Temporal lobe (wernicke’s area for receptive, auditory center for sound interpretation, complicated memory patterns) - Occipital lobe (primary visual center) Cerebellum - Receives continuous information regarding the condition of muscles, joints, and tendons - Control is ipsilateral (controls same side) Head injuries - Injury to the scalp, skull, or brain. Most common cause of death from trauma. Blunt or penetrating. - Highest at risk are male’s age 15-24 r/t playing sports, being more active/impulsive and elderly r/t falls. Pathophysiology of TBI - Brain suffers traumatic injury  brain swelling or bleeding increases intracranial volume  rigid cranium allows no room for expansion of contents so intracranial pressure increases  pressure on blood vessels within the brain causes blood flow to the brain to slow  cerebral hypoxia and ischemia occur  intracranial pressure continues to rise, brain may herniate  cerebral blood flow ceases o If ICP goes up pt is at risk for brain herniation and pt will die Anatomy of Head Injuries - Scalp o Significant bleeding; portal of infections (direct route to brain) - Skull o Protective, rigid, fixed space. o Fractures at the base of the skull  Leaking CSF from nose, pharynx, or ears • CSF if it tests + for glucose, will cause yellow halo on sheets  Battle signs: ecchymosis behind the ear - Dura (protective covering) - Brain (direct, primary; indirect, secondary) Direct (Primary) Brain Injuries - Primary injury: due to initial damage (contusions, lacerations, damage to blood vessels, or foreign object penetration - Direct damage done to brain (being stabbed in the head), irreversible Indirect (Secondary) Brain Injury (Prevent, stop, slow down, or reverse) - Secondary injury is damage that evolves after the initial injury (Expanding mass, lesions, swelling, hydrocephalus (abnormal increase of CSF fluid) or bleeding. - Increased ICP and/or herniation - Diagnosis and treatments target minimizing the effects of the indirect injuries Brain Injury - Closed brain injury (blunt trauma): Acceleration/deceleration injury occurs when the head accelerates then rapidly decelerates, damaging brain tissue. (Car accident) - Open brain injury: Object penetrates brain or scalp and skull are opened from a traumatic injury. - Concussion (brain shakes): A temp loss of consciousness with no apparent structure damage. Manifestations of Brain Injury - Altered LOC (Earliest indicator) - Pupil abnormalities (Check pupils of TBI pts for size and reaction to light. Report any changes to provider immediately because they could indicate an increased ICP) - Sudden onset of neurological deficits and neurological changes; change in sense, movement, and reflexes o Flaccid limbs, drooping of face, cushing’s triad (severe HTN with widening pulse pressure, the difference between diastolic and systolic 40 or greater is widening pulse pressure. Look at trends can be moving towards cushing’s triad) - Changes in vital signs (cushing’s triad, bradycardia) - Headache, seizures (check nail bed pressure for pain) - Posturing (stimulate pain to see if they posture, pinch chest/sternal rub, if pt postures they are getting worse) o Decorticate (in towards core), decerebrate (out) Management of the Pt with a Head Injury - Always assume cervical spine injury until ruled out o Don’t move them, C-Spine collar o Log roll off slide board, log roll until Dr. clears pt with CT Scan - Preserve brain homeostasis and prevent secondary damage o Treat cerebral edema with mannitol o Maintain cerebral perfusion (keep HOB 30 degrees, neutral alignment) o Maintain oxygenation, cardiovascular, and respiratory function o Manage fluid and electrolyte balance. o Prevent seizures  Prophylactic Dilantin (Phenytoin) first 7 days o Monitor for SIADH and diabetes insipidus r/t damage to the pituitary gland Supportive Measures - Respiratory support; intubation (if they can’t maintain airway), and mechanical ventilation - Seizure precautions and prevention (pad side rails, have suction available) - NG to manage reduced gastric motility and prevent aspiration o To check placement test gastric content, air bolus, or x-ray - Fluid and electrolyte maintenance o Sodium level will be effected with brain injury - Pain and anxiety management - Nutrition o Feeding tube possible o If neurologically impaired check pts ability to swallow (sit pt up, give small amount of water) - Be careful not to over sedate to be able to check neuro function properly Intracerebral Hemorrhage (Tearing of small arteries or veins) - Bleeding into the substance of the brain  edema = increased ICP - May be due to trauma or a non-traumatic cause (HTN, infection, tumors) - Treatment o Supportive care (keep them breathing and heart beating) o Control of ICP (HOB 30 degrees, neutral alignment, mannitol, no straws, no coughing, no suctioning) o Administer fluids, electrolytes, and antihypertensive medication  Aneurysm – control B/P, monitor B/P o Craniotomy (burr holes), craniectomy (take out whole piece) to control bleeding Intracranial Pressure (ICP) - Decreased LOC = first sign, Cushing’s triad = late sign - 10-15 is normal ICP - Intracranial space contains brain, blood vessels, and CSF o If one increases another will compensate to decrease ICP, CSF easiest to compensate (Monroe-Kellie Hypothesis) - Severe headache, decreased LOC, restless, dilated pupils, pinpoint pupils - To decrease ICP give furosemide and mannitol - Dilantin (phenytoin) for seizures - Intraventricular catheter (IVC) o Allows accurate measurement of intracranial pressure o Allows drainage or sampling of cerebrospinal fluid Nursing management for IICP - Neuro assessment (pupils dilated, decreased LOC, strength) - Positioning (neutral position, HOB 30 degrees) - Vent support (ABG’s, watch CO2, keep CO2 @ 35-38 because CO2 is a vasodilator will raise ICP) - IVC assessments (measure hourly (drainage), check drsg for drainage/infection) o NEVER FLUSH A DRAIN!!!!!!!! - Maintain fluid restriction (r/t increased ICP) - Teach pt to avoid coughing, straining during BM, sneezing, blowing nose - Maintain quiet environment and limit stimuli (give rest periods) - Maintain normal temp (increased temp with increased ICP, put pt on cooling blanket) Cushing’s traid - Widening pulse pressure (rising systolic, declining diastolic) 40 difference, Severe HTN, Bradycardia Herniation - Damage to brain from trauma  increased ICP  displacement of the brain matter  results in herniation of the brainstem o PT will have cheyne-stokes respirations Diffuse Brain Injuries - Concussion (“mild to severe traumatic brain injury”, no significant imaging findings) o Headaches, irritable o Try to wake up q4hrs, bring back to ER if vomiting occurs or pt won’t wake up - Axonal Injury (Severe Injury caused by sheering of axons o No strenuous activity for 7 days or until headache free but @ least 7 days o No TV, no reading Focal Brain Injuries - Epidural Hematomas *EMERGENCY SITUATION* See this Pt first! o Blood collection in the space between the skull and dura. Usually caused by a tear of the middle meningeal artery. Brief loss of consciousness with return of lucid state; then, as hematoma expands, increased ICP will often suddenly reduce LOC (Lose consciousness  wake up  then out again) o Treatment = measures to reduce ICP o Pt needs monitoring and support of vital body functions and respiratory support - Subdural Hematomas o Slow venous bleed  can die r/t bleed going unnoticed o Blood beneath dura o Very common in elderly r/t falls o Acute/subacute  Acute: symptoms develop over 24 to 48 hours  Subacute: symptoms develop over 48 hours to 2 weeks  Requires immediate control of ICP o Chronic  Develops over weeks to months  Clinical signs and symptoms may fluctuate Diagnostic Evaluation - Physical and neurological exam, skull and spinal x-rays, CT scan, MRI, PET scan Pre-hospital Care of Head Injured Patients - ABC’s, spinal immobilization (anyone who falls assume they have neck injury, c-spine collar), initial resuscitation, rapid transport Head Injury Management - GOAL: Prevent of minimize secondary injuries to the brain ED Assessment of Head Injured Patients - ABC’s, history, clues to brain injury, physical exam (treat life threats first), the “D” of the ABC’s stands for neuro exam Glasgow Coma Scale (GCS) - Measures motor 1-6, verbal 1-5, eyes 1-4, 15 = best, 1 = bad - GCS scores o 13-15 – mild head injury o 9-12 – moderate head injurt o or = to 8 – severe head injury  5 or less call the life center! Collaborative problems/potential complications - Decreased cerebral perfusion  increased ICP - Cerebral edema and herniation  Cheyne-stokes resp  death - Impaired oxygenation and ventilation  intubate (check ABG’s) 35-38 for CO2 - Impaired fluid, electrolyte, and nutritional balance  Sodium levels - Risk of post-traumatic seizures  7 days after, antiepileptic dilatin (phenytoin) Major Goals - Patent airway, adequate CPP, fluid and electrolyte balance, adequate nutrition, normal body temperature, skin integrity, prevent secondary injury, prevent sleep deprivation, support the family, knowledge about rehab, no complications! Management Principles - Rapid imaging for definitive diagnosis - Early, rapid specialty care (neuro surgeons, trauma centers) - Temporizing measures o Hyperventilation (to decrease their CO2 on ventilator) o Mannitol to reduce ICP o Burr holes to relieve pressure on skull Nursing Interventions - Provide ongoing assessment and monitoring - Maintain airway o Elevate HOB 30 degrees o Suction with caution, this increases ICP o Prevent aspiration and respiratory insufficiency, check ability to swallow o Monitor ABG’s, ventilation, and mechanical ventilation. Monitor for pulmonary complications, potential ARDS. o Monitor I+O’s, daily weights. Monitor electrolytes and blood glucose (goes up with injury). Maintain adequate nutrition. Implement strategies to prevent injury.  Assess for constriction (swelling or bleeding) due to dressings and casts  Pad side rails incase pt has seizures  Prevent self-injury; avoid restraints (will stress them out) - Strategies to prevent injury o Reduce environmental stimuli, use adequate lighting to reduce visual hallucinations, implement measures to minimize disruption of sleep-wake cycles, provide skin care, implement measures to prevent infection - Maintain body temperatures o Maintain appropriate environmental temperature, use covers for warmth, administer acetaminophen for fever, use cooling blankets for high temp; prevent shivering. Nursing Focus for Pts with Head Injuries - Risk for ineffective airway clearance, altered cerebral tissue perfusion, altered nutrition, risk for injury, risk for increased ICP, altered thought process Delayed Problems for Patients with Head Injuries - Post-concussion syndrome  cluster of symptoms (weeks – months) o Headache, fatigue, loss of concentration, unable to carry on conversation, anxious, sleep disturbances, noise/light sensitivity - Delayed CSF leak, delayed seizure activity SPINAL CORD INJURY - Contusion, laceration, or compression of the spinal cored o Primary  direct injury o Secondary  results of ischemia, hypoxia, and/or hemorrhage  Usually reversible or preventable during the first 4 – 6 hours after injury o Complete  no sensation o Incomplete  partial sensation - Types of Injuries o Hyperflexion, hyperextension, compressions Etiology of Spinal Cord Injuries - Most common cause is trauma (auto accident, falls), most injuries occur at the mobile segments of the spinal cord: o C1-C2, C4-C6, T11-T12 - Edema occurs 1 hour after injury and peaks after 2-3 days; usually subsides after 7 days o Pt usually given Methylprednisolone to decrease inflammation Clinical Manifestation - Complete Transection: o Immediate paralysis, loss of function below level of injury, hypotension, loss of temperature control - Incomplete Injuries: o Partial losses - Cervical Injury: o Tetraplegia - Thoracic or Lumbar Injury: o Paraplegia - Injuries C3 – C5  r/t phrenic nerve o Causes problems with movement of the diaphragm for breathing Cervical Spine (C Spine) Injuries - Injury results from flexion, extension, rotation, compression, or a combination of forces - Mostly blunt, some penetrating - C Spine injuries range from stable to unstable o Falls  C Collar  CT, doc clears (log roll until Dr. clears) Evaluation of C Spine Trauma - ABC’s (top priority) - History (mechanism of injury)  get info from medics, EMT’s - Palpation, Neuro exam (GCS, motor, sensory, reflexes/tone) Halo Systems - Watch for infection and clean around all sites - Assess skin, pressure is avoided if one finger can be inserted easily between jacket and skin - Watch for osteomyelitis o Temperature, sites, WBC count (report changes to physician immediately) - Wear loose fitting cloths - Don’t drive while using the device - Use straws to drink with C Spine Imaging - Flexion and extension views assess for ligamentous injuries - CT Scan – study of choice in many trauma centers - MRI ED Management of C Spine Injuries - Immobilization, Neuro exam, Imaging (CT Scan), Appropriate consultation, Methylprednisolone protocol (to decrease inflammation) o Backboards are a transport device, not definite immobilization devices. Get pt off the backboard ASAP. Use C Spine collar, log roll pt off board. Spinal and Neurogenic Shock - Spinal shock (Spinal Shock Syndrome) o Occurs immediately as cords response to injury  Often lasts less than 48 hours but may continue for several weeks, resolves slowly o Flaccid below level of injury, no spinal reflexes, bowel/bladder dysfunction, difficulty regulating temp, won’t sweat below level of injury  Pt getting better when they start having spastic reflexes - Neurogenic Shock o Starts within 24 hours, most commonly seen in pt with injury at T6 or above o Potentially life-threatening problem that results from disruption in pathways between upper and lower motor neurons  Critical Rescue: Monitor the pt with acute SPC at least hourly for severe bradycardia, warm/dry skin, severe hypotension. Notify the physician immediately if these symptoms occur, because this problem is an emergency! Neurogenic shock is treated symptomatically by restoring fluids to the circulating blood volume and providing supportive care.  Hypotension  Dextran  Bradycardia below 50 – 60 beats  Atropine Sulfate  Muscle spasms  Intrathecal Baclofen • Monitor for common adverse effects which include sedation, fatigue, dizziness, and changes in mental status. Seizures and hallucinations may occur if ITB is suddenly withdrawn. Autonomic Dysreflexia *Life threatening* - Acute emergency that can occur with an injury above T6 - Characterized by severe HTN, bradycardia, severe headache, nasal stuffiness, flushing. SUDDEN INCREASE OF B/P is hallmark sign! - The cause of the syndrome is usually a distended bladder or constipation. - This is a neurologic emergency and must be promptly treated to prevent a hypertensive stroke! o Place pt in sitting position to lower B/P *FIRST PRIORITY* o Notify the health care provider then look for the issue. Loosen tight clothing, check urinary catheter for kinks, no catheter check for bladder distention, temp of room. o Label chart that pt is at risk for autonomic dysreflexia  more likely to occur again if it occurs once. o Pt may be given Hydralazine or nitrates Neck Trauma - May quickly become dangerous or fatal from associated CNS injury, hemorrhage, or airway compromise. - Blunt Neck Trauma o Difficult to assess o Top priority = Airway protection  Bleeding, tracheal/pharyngeal injury, aspiration - Neck Trauma Assessment and Management o Airway protection, CT scan evaluation, Esophagram, Esophagoscopy, Trauma surgeon experienced with management of neck trauma. - Nursing Focus for Neck Injuries o Ineffective airway clearance, inadequate ventilation, impaired gas exchange, risk for aspiration, risk for hypotension - Take home points o Top priority = ABC’s + Cervical immobilization  C Collar o Early recognition of injuries, rapid initiation of treatment, rapidly transfer to appropriate trauma facility o Goal: prevent secondary injury Meningitis - Highly contagious, happens in places that you have close living quarters - Inflammation of the meninges that surround the brain and meninges - Bacterial, viral, or on rare occasions fungal - Causes: o Bacterial  LIFE THREATENING  standard precautions  Put in droplet precautions until confirm (private rooms, doors closed)  Risk factors: head trauma w/ basilar skull fx, otitis media, sinusitis, neurosurgery, pneumonia o Viral (Not as severe, doesn’t last as long)  “aseptic meningitis”, caused by herpes simplex, herpes zoster, Epstien-Barr virus, measles, mumps o Fungal  Cryptococcus neoformas most common - Manifestations o Nuchal rigidity (inability to flex neck forward), positive Brudzinski’s sign, Kernig’s sign, fever, chills, headache, back and abdominal pain, photophobia (sensitivity to light), IICP, decreased LOC/confusion, seizures. - Diagnostics/Labs o Lumbar puncture  Keep flat after, may develop spinal headache, watch for CSF leak, watch for signs and symptoms of infections. Clear  good, Cloudy  bad  Get informed consent  Get blood culture before starting the antibiotics o CT Scan, CBC, Electrolytes, CXR - Nursing Interventions o Follow ABC’s, take VS and perform neuro check every 2-4 hours, manage pain, record I/O’s carefully to prevent fluid overload, monitor body weight to detect fluid retention early, ROM every 4 hours, decrease environmental stimuli (quiet environment, minimize bright light exposure, maintain bed rest with HOB @ 30 degrees), maintain transmission based precautions (standard/droplet), monitor for and prevent complications (IICP, vascular dysfunction, fluid/electrolyte imbalance, seizures, shock) Trigeminal Neuralgia - Affects the trigeminal/5th cranial nerve, occurs more often 50 years old, more women than men. Sudden, intense facial spasms, often brought on by dental procedures, unilateral, familial. o r/t impaired inhibitory mechanisms in the brainstem caused by excessive firing or irritated fiber in the trigeminal nerve. Trauma and infection of the teeth, jaw, or ear may be contributing factor. - Manifestations o Sharp/excruciating, shooting, piercing, burning bursts of pain. Continuous burning sensation that involves entire face, may or may not have remission periods o Pain will lead to twitching, pain last from several weeks to months o If pt has intermittent episodes the older then get the shorter the remissions are - Diagnosis o CT/MRI - Treatment o Pain management, radio surgery to destroy nerve fibers o Baclofen to relax muscles, Gabapentin an antiepileptic drug Bell’s Palsy - Acute paralysis of cranial nerve VII, More often in young adults. Caused by inflammatory process triggered by dormant herpes Type 1 - Manifestations o Pain behind the ear or face prior to paralysis, paralysis of all facial muscles on the affected side, cannot close eyes, wrinkle forehead, smile, whistle, or grimace, face appears masklike and sags, taste may be impaired - Treatment o Corticosteroids (short, 1 week), antiviral meds (cyclovir drugs) o Teach pt to manually close eye to protect cornea  patch/tape closed at bedtime  close eyelid at intervals and instill artificial tears o As muscle tone improves teach the pt to grimace, wrinkle the brow, force the eyes closed, whistle, and blow air out of the cheeks three or four times daily for 5 minutes in front of a mirror o Surgery (reserved for pt’s with complete/severe bell’s palsy Encephalitis *see this pt first!* - Inflammation of brain tissure and meninges (affects cerebrum, brainstem, and cerebellum) - Etiology o Viral (usually life-threatening), bacterial, fungal, parasitic - Manifestations o High fever, photophobia, fatigue, changes in mental status (more severe than w/ meningitis), dysphagia, IICP, joint pain, headache, N/V, stiff neck  Watch for signs and symptoms of IICP (pupils, widening pulse pressure) - Diagnosis o Lumbar puncture, EEG, CT Scan - Nursing Interventions o Elevate HOB (unless pt just underwent lumbar puncture), dark room/ quiet environment, will end up in rehab (goal is to get better) Guillain-Barre Syndrome - Acute inflammation syndrome, demyelination of peripheral nerves, peaks after 55, euro-Americans most often affected - Manifestations o Ascending paralysis (begins in legs and spread to the arms/upper body), decreased/absent deep tendon reflexes, respiratory compromise, loss of bowel and bladder, ataxia, paresthesias, pain, dysphagia, diplopia, difficulty speaking, facial weakness, labile BP, dysrhythmias, tachycardia  As they get worse they have ascending paralysis, their symptoms usually resolve from head down - Diagnosis o Health history, manifestations – sudden onset, LP, MRI, CT Scan - Treatment o Plasmapheresis (removes the circulating antibodies), IVIG – Immunoglobulin Myasthenia Gravis - Autoimmune disease of neuromuscular junction. Attacks acetylcholine receptors decreasing nerve stimulation and decreasing muscle contraction - Remissions and exacerbations (mornings are their best time) - Manifestations o Fatigue, ptosis (drooping eyelids), diplopia, dysphagia (difficulty chewing/swallowing), muscle weakness, inability to close eyes completely - Diagnosis o AChR antibodies, Enlarged thymus  chest x-ray o Tensilon test  they get better o Possible complications during Tensilon test:  Cholinergic crisis (too much cholinesterase inhibitor drugs)  sudden increase of muscle weakness, inability to clear secretions hard time swallowing • Have atropine ready just in case pt goes into cholinergic crisis  Myasthenic Crisis (too little cholinesterase inhibitor drugs), can be caused by an infection as the body increases metabolic needs. • If Myasthenic crisis occurs pt drugs will be withheld due to increased secretions created by the drugs. When drug restarted they will start them on low dose and slowly titrate them back up. - Treament o Cholinesterase inhibitor drugs  pyridostigmine (expect day to day changes with patients symptoms and administer with small amount of food to help alleviate GI side effects). Corticosteroids, plasmapheresis o Frequent rest periods, small frequent meals (soft diet), artificial tears, thymectomy Amyotrophic Lateral Sclerosis (ALS) A.K.A Lou Gehrig’s Disease - Upper/lower motor neuron disease, no known cause. Characterized by progressive weakness, muscle wasting and spasticity leading to paralysis. Death within 3 years of diagnosis. No specific treatment. Affects 40-60 year olds, more common in men. - Riluzole for symptoms management, extends period of survival, take on empty stomach  drug is toxic to liver, monitor liver enzymes - Pt will need hospice and they are at high risk for aspiration CARE OF PATIENTS WITH SHOCK Shock (Abnormal cellular metabolism, decreased O2) - Any problem that impairs oxygen delivery to body tissues and organs can start the “syndrome of shock”. Inadequate oxygenation results in anaerobic metabolism and accumulation of waste products. Shock affects ALL body systems. Classifications of Shock - Hypovolemic (decreased BP, urine output, LOC, MAP. Increased HR. Pt pale) o Burn or surgery patient - Cardiogenic (heart not adequately pumping, pt could have pulmonary congestion) o Heart failure, MI, V tach, V fib - Distributive o Septic – Infection that systemically stimulates o Neurogenic – Imbalance of para/sympathetic (sustained vasodilation) o Anaphylactic – Severe allergic reaction - Obstructive o Cardiac tamponade, pericarditis, tension pneumothorax (fluid squeezing heart) Pathophysiology of Shock - Manifestations usually the same in all types of shock. Inadequate perfusion and oxygenation  oxygenation and perfusion problems lead to anaerobic metabolism  effects are temporary and reversible if the cause is corrected within 1-2 hours from onset Recognizing Shock in the Elderly - Beta Blockers can mask tachycardia o Their HR may only be 85 when they go into shock - Myocardial dysfunction may be misinterpreted as old age, immune system may not be able to develop a febrile response due to aging (watch for low grade temp), confusion and changes in mental status may be interpreted as demetia. Stages of Shock - Initial stage o Compensating starts here so everything may be WNL o Baseline MAP is decreased (total blood volume and cardiac output are directly related to MAP) o A heart and respiratory rate increased from the patient’s baseline level or a slight increase in diastolic blood pressure may be the only objective manifestation of this early stage of shock. o Lactic acid is produced  request labs if shock is suspected - Compensatory Stage (Non-progressive) o MAP decreases 10-15 from baseline o Vasoconstriction, increased HR, and increased heart contractility. Body shunts blood from skin, kidneys, and GI tract. Results in cool clammy skin, hypoactive bowel sounds, and decreased urine output. Perfusion of tissues is inadequate. All of these manifestations are expected manifestations. o Patient will be in metabolic acidosis, their respiratory rate will increase to blow off the extra CO2 (kussmaul respirations). Confusion may occur and Na and glucose levels will be elevated. o Decreased pH, decreased CO2, decreased Bicarb  partially compensated acidosis o Compare changes to values and manifestations obtained earlier to check if patient’s condition is progressing. Stopping the conditions that caused the shock at this stage and providing supportive interventions can prevent shock from progressing. - Progressive Stage o Mechanisms that regulate BP can no longer compensate, BP decreases, and MAP decreases 20 or more from baseline. (normal MAP is above 60) o All organs suffer from hypoperfusion. Vasoconstriction continues, further compromising cellular perfusion. Mental status further declines as a result of decreased cerebral perfusion and hypoxia. May not even be responsive. o The progressive stage of shock is a life-threatening emergency. Immediate interventions are needed to reverse the effects of this stage of shock. The patient’s life usually can be saved if the conditions causing shock are corrected within 1 hour or less of the onset of the progressive stage. o Lungs begin to fail as CO2 goes up, pt may be intubated, and have dysrhythmias. As MAP falls below 70, GFR cannot be maintained and they will show an increased in BUN/Cr (showing dehydration). o Patient will have weak, thready pulse. May be blue, cyanotic. Decreased LOC, pt may express sense of “impending doom”. Very low BP, anuria, and decreased pH. - Refractory Stage (Irreversible) o Pt is going to die at this stage  will need hospice on board o Organ damage is so severe that the patient does not respond to treatment and cannot survive  Therapy is not effective in saving the patient’s life, even if the cause of shock is corrected and MAP temporarily returns to normal. o BP will remain low, renal and liver functions continue to fail, acidosis will increase, multiple organ dysfunction progresses to complete organ failure. o Pt will be on CRRT dialysis, pulse may be hard to find, slow shallow breaths, you won’t be able to get O2 stat r/t decreased perfusion to fingers. For ALL types of Shocks - Early identification and timely treatment is necessary for survival. Identify and treat the underlying cause Clinical Manifestations of Shock - Early: decreased LOC, increased HR, increased Diastolic BP, increased thirst. - Late: non-responsive, lethargic, sluggish pupils, decreased reflexes, cool cyanotic extremities (see this patient first!) Nursing Alert - By the time BP drops, damage has already been done at the cellular and tissue levels. The patient who is at risk for shock must be assessed and monitored closely before BP falls. o Surgery, burns, MI, heart failure, trauma, severe dehydration, immunocompromised r/t septic shock. Distributive Shock - Septic shock (must have infection and classified as SIRS) o Pt will have refractory hypotension (nothing will bring BP up)  Give vasopressor in central line for refractory hypotension and pt must have A line to measure MAP o SIRS (systemic inflammatory response syndrome)  Burn patient, trauma, severe infection  Exists if abnormalities occur in 2 of the following parameters: • Body temp (below 96.8, above 100.4) • Heart rate (above 90) • RR (above 20) • WBC (above 12,000, below 4,000)  Notify rapid response for any patient who has vital signs or other conditions that meet the sepsis with SIRS criteria o Sepsis Bundle  Measure serum lactate levels  Obtain blood cultures before giving antibiotics  Administer broad-spectrum antibiotic within 1 hour of diagnosis  If pt has hypotension start giving fluids (if BP does not respond to fluid resuscitation give pt vasopressor therapy) - Neurogenic Shock o Spinal Cord Injury - Anaphylactic Shock Management of All Types of Shock - Position in reverse trendelenburg first! - Fluid replacement to restore intravascular volume - Vasoactive medications to restore vasomotor tone and improve cardiac function (vasopressor, dopamine, dobutamine) - Nutritional support to address metabolic requirements o Depends on if GI has motility o Listen to bowel sounds, no bowels sounds then give TPN Medical management of Shock - Optimize intravascular volume - Maintain perfusion - Provide circulatory and ventilator support - Early enteral nutritional support - Control hyperglycemia  monitor especially w/ TPN - Prevent renal failure - Prevent GI irritation/bleeding  PPI (protonix, Pepcid), subQ heparin  to prevent secondary problems Nursing Alert - Tight glycemic control has been shown to reduce morbidity and mortality of acutely ill patients - Keep blood glucose levels at 80-100 mg/dl Nursing Management - Continuous patient assessment (every hour), monitor oxygenation, perfusion, control pain and anxiety, cardiac monitoring r/t hyperkalemia - Primary nursing focus: Adequate Tissue Perfusion and Oxygenation o MONITOR VITAL SIGNS Monitor Tissue Perfusion - Observe and assess patients for changes in the following: o LOC, VS, pulse pressure, urinary output, cap refill, skin conditions, lab values (CBC, CK/troponin, lactate, metabolic panel Fluid Replacement - 0.9% NaCl; lactated ringers (do not give lactated ringers with blood products) - Albumin (pulls fluid into vascular space), dextran (volume expander), Blood components - Complications of fluid replacement include fluid overload and pulmonary edema o Watch for JVD, CVP (over 12 might be bad) Vasoactive Medications - Used when fluid therapy alone does not maintain MAP o Nitroprusside  Improves blood flow to the myocardium by dilating the coronary arteries  Protect drug from light, light degrades drug  Assess BP q15mins, causes hypotension o Norepinephrine  Improves blood flow by increasing venous return (vasoconstrictor)  Assess pt for chest pain, monitor urine output, assess BP q15mins, o Dobutamine  Simulates heart to improve heart contraction  Assess for chest pain, assess BP q15mins - Give through central line, dosages are titrated to patients response. - Nursing Alert: o Vasoactive medications should NEVER be stopped abruptly as this could cause severe hemodynamic instability and perpetuate the shock state (titrate up/down) Nutritional Therapy - Nutritional support is needed to meet increased metabolic and energy requirements o Increased calories/protein, decreased glucose - Support with parenteral (w/o bowel sounds) or enteral (w/ bowel sounds) - GI system should be used if it is possible to support its integrity - Administration of H2 blockers or proton pump inhibitors Psychological Support of Patients and Families - This patient needs palliative care if it progresses - Anxiety, support for coping, patient and family education, communication, end of life care, grief processes. Multiple Organ Dysfunction Syndrome (MODS) - A progression of shock - Altered organ function that requires medical intervention to support continued organ function - High mortality rate 75-100% - The body’s response to MODS (last stage) o Increased HR, increased cardiac contractility and output, increased O2 consumption, increased release of catecholamine’s, cortisol, antidiuretic hormone, and glucagons. - Goals of treatment o Identify the underlying cause, maintain tissue perfusion and oxygenation, provide nutritional support, individual organ support (mechanical ventilation, dialysis, blood product transfusions, pharmacological support), avoid additional complications. MANAGING PATIENTS WITH BURNS Classification of Burns - Superficial partial-thickness (1st degree) o Pink/red in color, mild to moderate edema, painful, will blister o Entire epidermis, example sunburn - Deep partial-thickness (2nd degree) o Red/white, moderate edema, not as painful r/t burned nerve endings, no blister o Epidermis and into dermis, 3 weeks to heal with scarring, blood flow to area reduced - Full-thickness (3rd degree) o Black, leathery, hard, waxy, eschar, no pain o Epidermis, dermis gone, may be able to see tendons, possibly need debridement and skin graft Factors in Determining Burn Depth - How the injury occurred - Causative agent o Chemical, get it off! Electrical, put on cardiac monitor. - Temperature of agent - Duration of contact with the agent - Thickness of skin o Farmer may have thicker skin than a business man Classification of Burns by Extent of Injury - Minor burn 15% TBSA - Moderate burn 15-25% TBSA - Major burn 25% TBSA Methods to Estimate TBSA - Rules of 9’s  used to calculate resuscitation o Head and arms = 9% each, 27% combined. Ant/Post chest, legs = 18% each, 72% combined. Pubic are 1%. - Lund and Browder method  kids (shriners) - Palm method  1% for each are burned the size of their palm Pathophysiology of Burns - Burns are caused by a transfer of energy from a heat source to the body Physiologic Changes - Burns 25% TBSA = local response - Burns 25% TBSA = local and systemic response (inflammatory process, causes third spacing which leads to hypovolemic shock) - Local and systemic responses can depend on how long patient was in contact with certain agent, the temp of the agent, and the health of the patient prior to the burn. Effects of Major Burn Injuries - Metabolic Acidosis  bodies response to changing out K+ for hydrogen ions - Fluid and electrolyte shifts  hypovolemic, decreased albumin/sodium (r/t leaking out into vascular space with fluid), hyperkalemia (r/t cells bursting and releasing K+), increased H+H (increased viscosity r/t fluid shifts) - Cardiovascular  viscosity of blood increased, HR increased, decreased cardiac output, slow cap refill, weak/absent peripheral pulses, decreased BP - Pulmonary injury  Hot steam, hypoxic, burns to the upper chest, can causes respiratory problems (ET tube possible) o Carbon monoxide poisoning: Indoor fires, patient will be tired with cherry red face. Check blood for carboxyhemoglobin level - Renal/GI alterations  decreased blood flow, rabdomylosis r/t protein circulating through blood from tissue breakdown, shunting blood to vital organs, gut not vital - Thermoregulation  skin is gone Phases of Burn Injury - Emergent or Resuscitative Phase (Injury to completion of fluid resuscitation) - Acute of Intermediate Phase (Beginning of diuresis to wound closure) - Rehabilitation Phase (Would closure to optimal physical and psychosocial adjustment) Emergent or Resuscitative Phase (On-the-scene care) - Prevent injury to rescuers - Stop injury: extinguish flames, cool the burn, irrigate chemical burns - ABC’s: Establish airway, breathing, and circulation - Start oxygen and large-bore IV’s (14)  then triple lumen central line - Remove restrictive objects/clothing and cover wounds o Remove jewelry, take off clothes  wrap them in sterile blanket - Quick assessment of injuries and details of burn incident o Electrical burn, cardiac monitor - Note: treat pts with falls and electrical injury for potential C Spine injury Emergent of Resuscitative Phase (Emergency Dept. Care) - Start fluid resuscitation o Improves cardiac output, amount determined by TBSA - Insert foley catheter o Strict I+O’s - Insert NG tube and place to suction (burns 25% TBSA) o Flush to keep patent, suck out gastric contents - Monitor ECG o r/t increased in K+ - Control pain o Only IV medication should be administered  may not be able to swallow and IV is quicker acting. Gut may not be working. Management of Shock (fluid resuscitation) - Increased HR, increased RR, cool, clammy, decreased BP - Start IV fluids immediately (NS, 0.9%) - Goals of fluid resuscitation o BP above 100 mm Hg systolic, MAP above 60-65 o Maintain urine output at 30-50 mL/hr o Maintain serum sodium levels, might go up really fast from fluid shift back into vascular space. Guides for Fluid Resuscitation - Consensus Formula *Need to know this for test* o 4 ml x wgt in kg x %TBSA burned  Don’t use .45 if 45% use 45! o Infused ½ of the total fluid in the first 8 hours from the time of injury o Infuse the remainder over the next 16 hours Fluid and Electrolyte Shifts (Emergent phase) - Dehydration (increased BUN/Cr r/t kidneys not working), reduced blood volume and hemoconcentration, decreased urine output, release of K+ from cells bursting resulting in hyperkalemia, sodium traps in edema fluid and shifts into cells as potassium is released causing hyponatremia. Care of the Patient in the Emergent Phase of Burn Care: Nursing Focus - Impaired gas exchange (burn on the neck or smoke inhalation) - Ineffective airway clearance (incentive spirometer to clear airway) - Fluid volume deficit (hypovolemia r/t burn), hypothermia, anxiety - Acute pain (IV meds only, around the clock schedule pain meds w/ PRN) Acute of Intermediate Phase - 48-72 hours after injury  until wound is closed - Continue frequent assessment, maintain respiratory and circulatory support, prevent infection, provide wound care, control pain - Provide nutritional support (increased calories, increased protein) o Swallowing ability, LOC o Bowel sounds, NG tube. No bowel sounds, TPN. - Watch for hypervolemia (JVD, pulmonary edema) r/t fluids given during initial phase Fluid and Electrolyte Shifts (Acute Phase) - Fluid re-enters the vascular space from the interstitial space - Hemodilution - Increased urinary output - Sodium is lost with diuresis: pt goes from hyponatremic initially from third spacing  hypernatremic with fluid shifts during intial fluid resuscitation  hyponatremic again with diuresis - Potassium shifts from extracellular fluid back into the cells: hypokalemia Care of the Patient in the Acute Phase of Burn Care: Nursing Focus - Excessive fluid volume r/t fluid resuscitation - Risk for infection r/t open wound - Imbalanced nutrition r/t increased metabolic needs - Acute pain r/t burn - Impaired physical mobility r/t burn - Ineffective coping r/t deformities from the burn or psychosocial - Interrupted family and lifestyle processes r/t taking care of the patient - Deficient knowledge r/t caring for burn wounds Rehabilitation Phase - Starts in the emergent phase and extends for a long period after the injury - Focus of rehabilitation o Wound healing o Psychosocial assessment  possible PTSD, depression r/t disfigurement or decreased ability to take care of self o Self-image and lifestyle changes o Vocational counseling o Support groups - Primary Goal o Restore maximum functional abilities Burn Wound Care - Wound cleaning  hydrotherapy - Use of topical agents  silver to promote healing o Watch WBC, if allergic to silver WBC will have sudden decrease - Wound debridement o Natural – leeches o Mechanical – wet to dry dressings o Surgical – removing dead skin with surgery - Wound dressing, dressing changes, and skin grafting  sterile, medicate IV prior to dressing changes Compartment syndrome - Occurs when tissue pressure within a confined body space becomes elevated and restricts blood flow. The resulting ischemia can lead to tissue damage and eventually tissue death. Assess the motor and sensory function of the affected extremity. Monitor for increasing pain, swelling, and tenseness. Report any of these symptoms to the health care provider immediately. Fasciotomoy may be necessary to prevent further injury and save the limb. Assess peripheral pulses. Biobrane dressing - You can see through the dressing to see if patient is getting an infection Wound Vac - Purpose is to pull out infection Pain Management - Burn pain has been described as one of the most severe forms of acute pain. Pain accompanies all burn care and treatments. - Types of burn pain: o Background or resting: Pain that never goes away o Procedural: dressing changes o Breakthrough: Around the clock and PRN pain meds - Analgesics o Morphine o Fentanyl  Patch for continuous relief o Anxiety can make pain worse. Pain can cause lack of sleep. o Non-pharmacologic measures  Reposition patient, use distraction Nutritional Support - Burn injuries produce severe metabolic abnormalities - Patients with burns have increased nutritional needs r/t stress and wound healing (increased protein/calories) - Nutritional support is based on patient’s pre-burn status and % of TBSA burned Other Major Care Issues - Pulmonary care, psychological support for patients and family, patient and family education, restoration of function Potential complications - Acute respiratory failure  chest burns - Acute renal failure  decreased blood flow to kidneys - Compartment syndrome  peripheral pulses, full circumference burns - Paralytic Ileus  No bowel sounds, abdominal distention, N+V - Gastric Ulcers/Curling’s Ulcer  Pantoprazole - Shock  hypovolemic and septic - Visceral damage (electrical burns)  organ damage - Acute respiratory failure  inhalation burns - Sepsis  Infections - Pulmonary edema  heart failure, fluid volume overload Home Care Instructions - Pain management  take on a schedule, don’t wait for pain to get out of control - Skin and wound care - Exercise and activity - Nutrition  increased calories/protein - Thermoregulation  appropriate clothing, may need jacket even if it is warm outside - Mental health  PTSD, depression Contractures - Portions of the skin that scar badly, can happen over time - Do ROM exercises to prevent decreased ROM from contractures that limit movement Pressure garments - Decreased edema, prevent hypertrophic scarring - Need to wear 23 hours a day