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Alterations in Perception

Jan 25, 202513 min read2514 words

References

This discussion is based on Dr. Rotairo’s presentation on alterations in perception.

Traumatic Brain Injury

The leading cause of death and disability from ages 1 to 44, at an annual rate of ~52,000 deaths due to TBI, with two-thirds of that population being men. It is caused by an external mechanical force and may result in permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness. These forces may occur from falls, collisions (vehicles, other moving objects such as a baseball), violence (gunshots, abuse, shaken baby syndrome), sports injuries, etc.

Types of TBI

  1. Closed: the skull is not broken; the brain is not exposed. This may be due to rapid movement such as in sudden accelerations or decelerations. Depending on which region the brain hits, this may be considered as a coup (frontal) contusion from deceleration or sudden hyperextension of the head, or contrecoup (occipital) contusion from acceleration or sudden hyperflexion of the head.
  2. Open: a penetrating head injury which may be focal (isolated to one area) or diffuse (widespread).

The damage caused by a traumatic brain injury, i.e. it’s pathophysiology, begins with the primary injury, literally the damage caused by the trauma at the moment of injury. The secondary injury is the damage produced after the initial trauma, such as rebound contusions (the brain bounces back onto the contrecoup after hitting the coup), swelling, increased ICP, hypoxia, etc.

  1. Primary Brain Damage: due to two main mechanisms (a) contact, e.g. an object striking the head producing fractures or contusions, and (b) change in momentum, i.e. sudden acceleration and deceleration producing shear, tensile, and compressive strains on the brain. These may result in intracranial hematoma (most common cause of death in TBI), diffuse vascular injury, and injury to the cranial nerves and pituitary stalk.

Intracranial Hemorrhage

An intracranial hemorrhage is classified according to its location:

  1. Epidural Hematoma: bleeding from a fracture of the temporal bone and rupture of the middle meningeal artery.
  2. Subdural Hematoma: bleeding from ruptured bridging veins in the subdural space.
  3. Subarachnoid Hemorrhage: bleeding from damage to blood vessels in the posterior fossa stalk.
  4. Intracerebral Hemorrhage: bleeding within the brain
  5. Intraventricular Hemorrhage: bleeding into the ventricles of the brain
  1. Secondary Brain Injury: occuring hours or days after the initial injury, this may result from impairment in cerebral blood flow due to local edema, hemorrhage, increased intracranial pressure such, shock, disturbance of pulmonary ventilation (aspiration, chest wall instability, neurogenic disturbance), etc.
    • Decreased perfusion results in cellular destruction, causing neuronal death.

Clinical Manifestations

  1. Cognitive Changes: change in level of consciousness (loss of consciousness, speech, lethargy, attention deficit, mood disturbances), memory, learning, problem-solving, speed of mental processing, judgment, and decision-making.
    • Attention deficits, changes in sleep habits, and mood disturbances may be found in children with TBI, along with changes in eating habits and persistent, inconsolable crying.
  2. Physical Changes: weakness or numbness in the extremities; persistent, potentially worsening headache, spasticity, physical paralysis, chronic pain, changes in sensorium, loss of stamina, and loss of control of the bowel and bladder.

Categorized into severity of TBI:

  1. Mild TBI: loss of consciousness for seconds to minutes, problems with memory or concentration, headache, dizziness/loss of balance, nausea/vomiting, and difficulty sleeping
  2. Moderate to Severe TBI: loss of consciousness for minutes to hours, problems with speech, inability to awaken from sleep, weakness or numbness in the extremities or digits, loss of coordination (ataxia), and persistent, worsening headache.

Posturing

Individuals with severely injury may experience decorticate or decerebrate posturing:

  1. Decorticate: the arms are rigidly flexed at the elbows and wrists, with the legs possible flexed with the toes rigidly pointed. This indicates a lesion in the brain, and may sometimes be produced by applying a painful stimulus to a comatose patient. In Glasgow’s coma scale, this finding would be rated as a 3/6 on the motor scale.
  2. Decerebrate: the arms are rigidly straight and internally rotated. The legs are extended with the toes rigidly pointed. This is usually observed in patients afflicted by compression of the brain stem at a low level. In Glasgow’s coma scale, this finding would be rated as a 2/6 on the motor scale.

The progression of a patient from a decorticate posture to a decerebrate posture indicates worsening of their condition, as reflected by Glasgow’s coma scale.

Complications

An altered level of consciousness is highly representative of worsening conditions in the brain for a patient with traumatic brain injury. These may appear in varying degrees:

  1. Coma: the person is fully unconscious, resulting from widespread damage to all parts of the brain. It may take days to weeks for a person to emerge from a coma, after which they may still remain in a vegetative state.
  2. Vegetative State: a potentially permanent state wherein individuals are physically awake, but show no signs of cognition.
  3. Minimally Conscious State: a severely altered level of consciousness but with some evidence of self and environmental awareness.
  4. Locked-In Syndrome: a condition where an individual’s consciousness is intact, but they are unable to speak or move, often only being able to communicate with eye movement or blinking.

Other complications include :

  1. Infections, a consistent problem in patients with skull fractures or other openings or entry points.
  2. Blood Vessel Damage from the injury, which can result in strokes or clotting.
  3. Nerve Damage, specifically the cranial nerves that arise directly from the brain, can result in facial paralysis, loss of vision, and dysfunction related to other cranial nerves.

Management

Operative management is not used to correct brain injury. It is only used to address (a) the need for ICP monitoring with a bolt or other device, (b) bleeding within the brain; surgical removal or drainage may be necessary, and (c) removal of skull bone fragments/damaged tissue and repair of skull fractures if present in open head injuries.

Pharmacologic management may be used for the following:

IndicationTreatment
Increased intracranial pressureDiuresis
Seizure activityAnti-seizure drugs. This is used prophylactically during the first week of management.
Medical induction of a comaDone to reduce the oxygen demands of the brain, reducing the potential for cell death in hypoperfusion.
Problems with attention and concentrationAmantadine, Methylphenidate, Bromocriptine, Antidepressants

Cerebrovascular Accident

Any functional abnormality of the cerebral nervous system, also called a “brain attack”, cerebral infarction, cerebral hemorrhage, ischemic stroke, or simply a stroke. This is caused by an interruption of the blood supply to the brain, often from an aneurysm or an obstruction, resulting in damage to the brain tissue.

Etiology

  1. Ischemic Stroke: 85% of strokes; this is a stroke resulting from obstruction of blood vessels, often due to atherosclerosis. Atherosclerosis is a deposition of fatty substances, cholesterol, and cellular waste products, calcium, and other substances in the inner lining of an artery. Collectively, this build-up is referred to as “plaque”.
  2. Hemorrhagic Stroke: 15% of strokes; this is a stroke resulting from bleeding into the surrounding brain tissue (intracerebral, intraventricular, subarachnoid) from a ruptured blood vessel. These are primarily caused by uncontrolled hypertension. This may also be caused by an arteriovenous malformation.
  3. Cerebral Thrombosis: clotting in an artery that supplies a vital brain center.
  4. Cerebral Hemorrhage: an artery bursts as the aneurysm wall bursts potentially from a severe rise in blood pressure, causing hemorrhage and ischemia.
  5. Cerebral Embolism: a blood clot travels into the brain’s blood vessels, shutting off blood supply.

The risk factors for cerebrovascular accidents vary, but many are related to lifestyle factors. These are divided between modifiable and non-modifiable risk factors:

  1. Non-modifiable: age, gender, race, heredity
  2. Modifiable: hypertension, diabetes, transient ischemic attacks (modified with aspirin use), hyperlipidemia, obesity, heart disease, oral contraceptive use (risk for emboli formation), physical inactivity, stenosis, hypercoagulability, cigarette smoking, and alcohol abuse.

Stages of a CVA

  1. Transient Ischemic Attack (TIA): short-lived obstructions of blood flow. These are “mini strokes” and are a warning sign for a progressive cerebrovascular disease.
    • Temporary loss of neurologic function may occur, but only last less than one day and often less than even fifteen minutes. Most of these resolve within three hours.
  2. Reversible Ischemic Neurologic Deficit (RIND): these are TIAs that begin to produce symptoms that last up to a week.
  3. Stroke In Evolution (SIE): gradually worsening symptoms of brain ischemia
  4. Completed Stroke (CS): the symptoms of the stroke stabilize and rehabilitation can begin.

Clinical Manifestations - Warning Signs

  1. Sudden weakness, paralysis, or numbness of the face, arm, or leg especially on one side of the body.
  2. Sudden dimness or loss of vision in one or both eyes, potentially including uncontrollable eye movements or eyelid drooping (ptosis).
  3. Sudden loss of speech/comprehension, confusion, or difficulty speaking or understanding speech.
  4. Unexplained sudden dizziness, unsteadiness, loss of balance, or coordination.
  5. Sudden, severe headache.
  6. Swallowing difficulties or drooling may also occur.
  7. Loss of memory during the attack may occur.
  8. Personality changes, mood changes, and changes in the level of consciousness may occur.

Left-Sided Cerebrovascular Accident

  1. Right-sided hemiplegia
  2. Impaired speech and language
  3. Slow performance and impaired comprehension
  4. Visual field deficits
  5. Aware of deficits, depression, and anxiety may occur

Right-Sided Cerebrovascular Accident

  1. Left-sided hemiplegia
  2. Spacial-perceptual deficits
  3. Short attention span, impaired concept of time
  4. Impaired judgment, impulsive
  5. Unaware of problems; minimizes problems

Diagnosis

  1. An ultrasound can show blood flow in the head via carotid doppler studies.
  2. A CT Scan is the primary method of diagnosis, being able to identify the size and location of the CVA, and differentiates between ischemic and hemorrhagic type of strokes. Furthermore, a CT Angiography can visualize the vasculature of the brain.
  3. An MRI is also able to visualize the brain.

The FAST Method

In a pre-hospital setting, the F.A.S.T. method may be used:

  1. Face: ask the person to smile. Is one side or both sides of the face droopy?
  2. Arms: ask the person to raise both arms. Are one of the arms drifting downward or not equal to the other?
  3. Speech: ask the person to repeat a simple sentence. Is their speech slurred, strange, or slow?
  4. Time: time is highly important in caring for a patient undergoing a stroke. Get help and emergency services as soon as possible once the presence of a stroke is suspected.

Complications

  1. Re-bleeding
  2. Cerebral Vasospasm, which may produce/worsen cerebral ischemia
  3. Acute Hydrocephalus if the ventricular system of the brain becomes dysfunctional
  4. Seizures
  5. Motor, sensory, cranial nerve, cognitive, and other functional deficits

Management

IndicationTreatment
HypoglycemiaD50 Infusion
Hyperglycemia (>200 mg/dL)Insulin
HypertensionLabetalol 10-20 mg IVP repeated q10-20min
Nicardipine 5 mg/h, titrate by 2.5 mg/h q5-15min max. 15 mg/h, lower to 3 mg/hr once target BP is reached
Enalapril 1.25 mg IVP
Sodium nitroprusside (0.5 mcg/kg/min)
Possible Ischemic Changes or Atrial FibrillationContinuous cardiac monitoring, thrombectomy (removal of thrombus), anticoagulant therapy, and antiepileptic therapy
IVF TherapyIsotonic sodium chloride (NSS) at 50 mL/hr unless otherwise indicated; avoid D5W and excess administration
AspirationNPO status until swallowing is assessed.
HypoxiaOxygenation therapy if SaO2 is <94%.
HyperthermiaAntipyretics: rectal or oral acetaminophen and cooling blankets as needed
PositioningLying flat or head elevated (30 degrees)
Aneurysm (hemorrhagic stroke)Surgery is used to secure a blood vessel at the base of the aneurysm.
Correct/prevent obstructionThe gold standard thrombolytic used is Alteplase IV r-tPA via IV. This is used within three to four and a half hours of a stroke.

Nursing Management

  1. Assessment: ABCs, VS, Neurologic Screening, 12-lead ECG, CBG monitoring, admittance to the stroke unit if no surgery will be done.
  2. Management: oxygen therapy (if hypoxic), blood glucose correction if indicated, and general supportive therapy.

Nursing Diagnoses

  • Ineffective tissue perfusion r/t decreased cerebrovascular blood flow
  • Ineffective airway clearance r/t level of consciousness
  • Impaired physical mobility
  • Impaired verbal communication
  • Impaired swallowing r/t loss of reflux
  • Unilateral neglect r/t visual field cut and sensory loss
  • Impaired urinary elimination
  • Situational low self-esteem r/t actual or perceived loss of function
  1. Interventions:
    1. Maintain skin integrity
    2. Encourage PROM to affected extremities, and AROM to the unaffected extremities every two hours.
    3. Elevate the affected extremities to promote venous return and to reduce swelling
    4. Maintain a safe environment to reduce risk of injury
    5. Teach the scanning technique: turning the head side-to-side when eating and ambulating to compensate for hemanopsia.
    6. Provide care to prevent deep vein thrombosis: sequential compression stockings, frequent position changes, mobilization
    7. Educate the client on the prevention of a stroke: lifestyle changes (diet, weight control, exercise, avoid alcohol and smoking, and other risk factors), routine health assessment (check cholesterol levels (LDL <70 mg/dL), blood pressure control, blood glucose)

Spinal Cord Injury

A spinal cord injury damages the indwelling nerves running along the spinal column. This may be caused by motor vehicle accidents, falls, violence, sporting injuries, etc. that produce hyperextension, hyperflexion, vertical compression, and extreme rotation, among other forms of injury. Acceleration, deceleration, deformation, traction, shearing, sliding, fractures, and dislocation all may cause spinal cord injury.

The extent of damage depends on what part of the spinal column is damaged, with the most damage being caused by injury to the cervical spine, then the thoracic spine, then the lumbar spine. By frequency, the proportion of each type of injury is:

  1. Incomplete Quadriplegia (C6): 34.1%
  2. Complete Quadriplegia (C4): 18.3%
  3. Incomplete Paraplegia (L1): 18.1%
  4. Complete Paraplegia (T6): 23.0%

Clinical Manifestations

  1. Spinal Shock: 1 week to 3 months after injury, this affects skeletal muscles, the bladder, the bowel, sexual function, and autonomic control:
    • Skeletal Muscles: Paralysis and flaccidity; loss of sensation
    • Loss of bladder and rectal control
    • Drop in blood pressure
    • Poor venous circulation
    • Poor thermal control with an impaired sympathetic nervous system
    • Sweating and capillary dilation (autonomic control)
  2. Neurogenic Shock: a loss of sympathetic nervous system outflow will result in vasodilation, hypotension, bradycardia, and hypothermia.
  3. Autonomic Hyperreflexia occurs when blood pressure rises after spinal shock resolves or in regions above the level of injury. The cardiovascular system responds to teh return of sympathetic nervous system stimulation, overcompensating to produce:
    • Paroxysmal hypertension: pounding headache, blurred vision
    • Sweating, flushing of skin
    • Nasal congestion, nausea
    • Piloerection
    • Bradycardia
    • Bladder or rectal distention

Causes

This is a syndrome that may occur after spinal shock resolves, but it may also be due to the nervous system “overfiring” as it attempts to reach parts of the body that are below the level of injury, i.e., not receiving the appropriate signals by the brain. This results in a clinical image of pale, cool, lower extremities (if the injury is mid-thoracic; T6), while the upper half of the body experiences severe blood pressure, flushing, headaches, distended neck veins, bradycardia, sweating, etc.

The brain attempts to send these autonomic signals to parts of the body when they experience pressure (pressure areas), restrictive clothing, a full bladder (neurogenic bladder) and fecal impaction/rectal distention (neurogenic bowel).

Diagnostic Examination

  1. Physical Examination
  2. Radiologic Studies: chest and spine x-ray
  3. Myelographic Examination
  4. Somatosensory Evoked Potential Studies
  5. Pulmonary Function Tests
  6. Arterial Blood Gases
  7. CT Scans
  8. MRIs

Management

Nursing Diagnoses

  1. Ineffective breathing pattern (if respiratory muscles are affected)
  2. Risk for trauma
  3. Impaired physical mobility
  4. Disturbed sensory perception
  5. Acute pain
  6. Anticipatory grieving (loss of function/disability)
  7. Bowel Incontinence/Constipation
  8. Impaired urinary elimination
  9. Risk for autonomic dysreflexia/hyperreflexia
  10. Risk for impaired skin/tissue integrity
  11. Inadequate knowledge regarding condition, prognosis, complications, treatment, self-care, and discharge needs
  1. Immobilization
  2. Decompression
  3. Corticosteroids
  4. Nutrition
  5. Lung Function
  6. Skin Integrity
  7. Bowel and bladder management

Also Read: First Aid for AD

Seizure Disorders

Guillaine-Barre Syndrome

GBS is a demyelinating disease also known as Landry’s paralysis. It is an autoimmune disorder of the peripheral nervous system, which produces an acute, progressive, inflammatory demyelination of axons of the peripheral, sensory, and motor nerve roots.

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