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NEURO END

NEURO END. MR OGUNDELE. HEAD INJURY. Head injury is a frequent cause of death and accidents are the most common cause of head injury with MVA being the leading cause. It includes injury to the scalp, skull, or brain.

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NEURO END

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  1. NEURO END MR OGUNDELE

  2. HEAD INJURY • Head injury is a frequent cause of death and accidents are the most common cause of head injury with MVA being the leading cause. It includes injury to the scalp, skull, or brain. • When there is traumatic injury to the skull, it may lead to depressed skull fracture leading to contusion or laceration of the underlying brain tissue.

  3. HEAD INJURY • A minor head injury might lead to CONCUSSION. Concussion is the term used to describe a closed head injury in which there is brief disruption in the level of consciousness, amnesia regarding the occurrence and headache. • In contusion, the brain tissue is bruised, blood from broken vessel accumulates, edema develops causing increased ICP

  4. HEAD INJURY • A closed injury is one in which the scalp and the skull are intact but the underlying brain tissue is damaged whereas in an open injury there is laceration of the scalp, fracture of the skull with damage to brain tissue. • Coup Countercoup injury or acceleration deceleration injury occurs when head is moving rapidly and hit a stationary object. The content within the cranium will hit the inside of the skull (Coup) and bounce back to hit the opposite area causing second injury (Counter Coup).

  5. HEAD INJURY • Severity of brain damage from head injury varies and this depends on the symptoms, neurological assessment, loss of consciousness etc. • Outward symptoms can be bruises, swelling, laceration, bleeding. Ecchymoses, rhinorrhea, otorrhea can be present. • Hematoma is a blood filled swelling that usually occurs after traumatic head injury and it can be subdural hematoma, epidural hematoma or intracerebral hematoma.

  6. S/S • Headache due to direct trauma and/or increasing intracranial pressure • Disorientation or cognitive changes • Changes in speech • Changes in motor movements • Nausea and vomiting due to increased intracranial pressure • Diminished or absent pupil reaction due to neurologic compromise • Decreased level of consciousness or loss of consciousness • Amnesia

  7. MANAGEMENT • Medical management of traumatic brain injury involves control of ICP and support of body functions. • Brain-injured patients may be partially or completely dependent for maintenance of respiration, nutrition, elimination, movement, and skin integrity.

  8. MANAGEMENT • Resuscitation including intubation and ventilation as required. • If neck injury is suspected, the patient should be immobilized until a spinal cord injury or unstable cervical spine has been excluded. • Surgical interventions may be necessary (craniotomy): • Removal of hematoma • Ligation of bleeding vessel • Burr holes (drilling holes) for decompression

  9. MANAGEMENT • Administer antibiotics for open head injuries to prevent infection. • Administer low-dose opioids for restlessness, agitation, and pain in ventilator dependent patients. • Administer osmotic diuretics to reduce cerebral edema:mannitol

  10. MANAGEMENT • Administer analgesics:acetaminophen (Tylenol) • High-protein, high-calorie, high-vitamin diet. • Platelet and packed RBC transfusions—if blood counts warrant transfusion.

  11. NSG MGT • Monitor vital signs for stability—SUSPECT "increased intracranial pressure" if blood pressure increases with widening pulse pressure and slow pulse. • Monitor neurologic status for changes—use Glasgow Coma Scale • Check for signs of infection at wound site in post-operative patients

  12. NSG MGT • Monitor signs for diabetes insipidus—increased risk due to injury to the pituitary gland. • Monitor intake and output. • Monitor urine specific gravity, serum, and urine osmolarity

  13. SPINAL CORD INJURY • Fracture, disclocation or subluxation(partial dislocation) of the vertebral column often results in spinal cord damage. • Cord injury is caused by compression, pulling and twisting or tearing of the cord. • The damage to the cord may involve the entire thickness of the cord (complete), or only a partial area of the spinal cord (incomplete)

  14. SPINAL CORD INJURY • A complete spinal cord injury means that there is no motor or sensory function below the level of the injury.  • An incomplete lesion means that there is some function remaining. This does not necessarily mean that the remaining function will be useful to the patient. • Spinal cord injury can be caused by penetrating trauma, extreme flexion or hyperextension (falling on buttocks), tumor growth etc

  15. SPINAL CORD INJURY • Whatever the cause of the injury, nerve transmission to the brain or from the brain may no longer occur below the level of the damage resulting in paralysis • Microscopic bleeding occurs in the gray matter immediately after spinal cord injury.

  16. SPINAL CORD INJURY • Irritation of the cell causes edema to develop and spread along the next one or two segment. Edema causes temporary loss of function; it reaches it peak between 2 to 3 days and subsides after 7 days. • The inflammatory process may injure the myelin covering the axon, and the chemical and electrolyte changes interrupt nerve impulse transmission.

  17. SPINAL SHOCK • Immediately after spinal cord injury, the cord below the injury stops functioning completely. • This causes a disruption of sympathetic nervous system function, resulting in vasodilation, hypotension, and bradycardia (neurogenic shock or spinal shock). • Dilation of the blood vessels allows more blood flow just beneath the skin. This blood cools and is circulated throughout the body, causing hypothermia.

  18. SPINAL SHOCK • The patient is unable to maintain control of body temperature and all reflexes below the level of the injury are lost, and retention of urine and feces occurs. • Spinal shock can last from a week to many weeks in some patients.

  19. S/S • Loss of motor control • Loss of reflexes due to damage of the spinal cord, • Flaccid paralysis • Lack of bowel and bladder control

  20. S/S • Altered sensation (tingling—paresthesia; diminished—hypoesthesia; increased hyperesthesia) • Bradycardia, hypotension, hypothermia due to problems with the autonomic nervous system

  21. MANAGEMENT • Immobilize the affected area of the spinal cord to decrease chance of further irritation. • Place the patient in a flat position to avoid flexion or misalignment of the spine. • Monitor traction or collar to prevent skin irritation. • Administer corticosteroid to decrease inflammation at point of injury: methylprednisolone

  22. MANAGEMENT • Administer a plasma expander (Normal saline) which increases blood flow in the spinal cord, increasing oxygenation to the tissue. • Assist respirations if indicated. • Place patient in a rotation bed for repositioning to prevent pressure on skin. • Surgical repair of vertebral fracture or decompression may be necessary

  23. NURSING CARE • Monitor respiratory status—assess for changes in rate, effort, use of accessory muscles, cyanosis, altered mental status, and pulse oximetry reading. • Monitor neurologic status for changes—assess sensation, temperature, touch, position sense, comparing right to left. • Monitor for spinal shock:

  24. NURSING CARE • Flaccid paralysis, loss of reflexes below the level of injury, hypotension, bradycardia, possible paralytic ileus. • Monitor pulse and blood pressure for changes—change in heart rate, hypotension, or hypertension. • Assess skin for signs of pressure (redness) or breakdown. • Assess abdomen and listen for bowel sounds.

  25. Cerebral palsy • Cerebral palsy (CP) is a heterogeneous group of conditions arising from a non-progressive lesion occurring in the developing brain.

  26. Cerebral palsy • As the lesion of CP arises early in development it interferes with normal motor development. • The child will have disordered movement and posture but it is often complicated by other neurological and cognitive problems.

  27. Cerebral palsy • CP is classified according to the clinical picture: • Spastic CP accounts for 70% involving damage to the cerebral motor cortex or its connections. It may result in hemiparesis or quadriparesis

  28. Cerebral palsy • Dystonic (athetoid) CP accounts for 10%, and is characterised by irregular involuntary movements of some or all muscle groups. These may be continuous or occur only on voluntary movement. • Ataxic CP accounts for 10% and is characterised by hypotonia, weakness uncoordination and intention tremor.

  29. CAUSES • Cerebral malformation. • Hypoxia in utero and or peripartum. • Stroke in the perinatal period – cerebral haemorrhage or infarction. • Infection – intrauterine or post-natal. • Trauma at birth or post-natal. • Prolonged convulsions or coma in infancy. • Kernicterus

  30. S/S • Infants may present with poor sucking ability, increased or decreased tone, abnormal reflexes, convulsions or drowsiness in the neonatal period.

  31. MGT • Medication may be needed to control fits and hyperactivity. • Physical therapy is started in the first year of life, before abnormal motor patterns have become established. • Persistent deformities may require corrective orthopaedic surgery with post operative physiotherapy • Neurosurgical techniques are occasionally used for severe deforming spasticity to reduce spasm

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