Trauma 1

HEAD INJURY (TRAUMA)  Involves injury to the scalp, skull, and brain tissues SCALP INJURY  isolated scalp trauma is generally classified as a minor head injury. Trauma may be result in abrasion, contusion, laceration or hematoma. Management  the area is irrigated before the laceration is sutured SKULL FRUCTURES OR INJURY  A break in the continuity of the skull caused by forceful trauma Assessment  Base of the skull- Hemorrhage from the nose  Battle’s sign – area of ecchymosis ( bruising ) seen over the mastoid  CSF Otorrhea – csf es cape from the ears ( basal skull fracture )  CSF Rhinorrhea – csf escape from the nose ( basal skull fracture )  Halo sign – a blood stain surrounded by yellowish stain seen on the bed linens or the head dressing Racoon Sign Management::  non depressed skull fx – no Tx is necessary  deformed skull fractures – Surgery is the mgt of choice • Bone grafting • Surgical debridement • Antibiotic treatment BRAIN INJURY Clinical manifestation  altered level of consciousness, confusion, pupillary abnormalities, sudden onset of neurologic deficits. Types of brain injury:  Concussions. Jarring of the brain and its sudden, forceful contact with the rigid skull. There is transient period of unconsciousness.  Contusion ( bruising ). A structural alteration characterized by extravasations of blood cell. A more severe injury in which the brain is bruised, with possible surface hemorrhage.

 Lacerations. Tearing of tissues caused by a sharp fragment or object or a shearing force. Hemorrhage is a serious complication. Hemorrhage may cause epidural hematoma, subdural hematoma, intracerebral or subarachnoid hemorrhage.  Compression of the brain. Result from depressed fracture causing edema and hemorrhage. Assessment;  S/Sx of increased ICP.  CSF leakage from the ears and nose.  Battle’s sign Management;  Care of the client with increased ICP.  Monitor drainage from ears and nose. ( Test the fluid for glucose with Tes- Tape; CSF is positive for glucose.  Monitor for S/Sx of meningitis, atelectasis, pneumonia, UTI SPINAL CORD INJURY  Damage to the spinal cord range from transient concussion ( from which the patient fully recover ) to contusion , laceration, to complete compression of the cord substance to complete transaction of the cord .  The most common cause of SCI is motor vehicle crashes following by violence related injuries and falls.  The predominant risk factor for SCI include the AGE, GENDER, and Alcohol and Drug use.  The vertebrae most frequently involved in SCI are the 5th, 6th, 7th cervical, the 12th thoracic, and the 1st lumbar vertebrae. These vertebrae are the most susceptible because there is a great range of mobility in the vertebral column in these areas. Pathophysiology:  Damage of the spinal cord 1. from transient concussion, to contusion and laceration 2. to compression of the cord substance 3. to complete transectional the cord 2 Categories of SCI 1. Primary injury – Result of the initial insult or trauma and are usually permanent. 2. Secondary - result of a contusion or a tear injury, nerve fibers disintegrate, ischemia, hypoxia, edema, hemorrhage lesions, destruction of myelin and axon > are the principal cause of SC degeneration at the level of injury. Manifestations:  A complete SC lesion can result in: • Paraplegia – paralysis of the lower body

• Quadriplegia – paralysis of all 4 extremeties  Acute pain – back and neck  Respiratory dysfunction – T1- T11 and the diaphragm

Assessment and diagnostic findings: Assessment: 1. Detailed neurologic exam is performed 2. Initially diagnostic X-ray and CT Scanning are performed. 3. MRI if a ligamentous injury is suspected 4. Further exam to the head and chest 5. Continuous ECG monitoring may be indicated if a cord injury is suspected since bradycardia and asystole are common in acute spinal injuries. Emergency Management:  at the scene of the injury, the patient must be in a neutral position, to prevent an incomplete injury from becoming complete, the patient must be immobilized on a spinal board.  Head. Prevent flexion, extension, or rotation  Body. When transferring the body, slide the victim carefully into a board and avoid any twisting movement that may damage the SC by causing a bony fragment to cut into, crash.  Extremities. The patient must always be maintained in an extended position.  Once the extent of the injury has been determined the patient may be placed on a rotating bed. or in a cervical collar . Management:: GOAL: to prevent further SCI and to observe for symptoms of progressive neurologic deficits.  High dose corticosteroids ( Methylprednisolone ) improve motor and sensory outcomes at 6th weeks, 6th months, and 1 year if given within 8 hours of injury.  Respiratory therapy  Skeletal fracture reduction and traction Surgical Management:  if cord compression is present  if vertebrae is unstable or fragmented  if the cord is penetrated  bony fragments are in spinal canal and neurologic status is decreasing.

HEAD TRAUMA

DEFINITION Head trauma may be defines as any injury to the scalp, skull or brain. ETIOLOGY Motor vehicle accidents are the foremost cause of head injuries. Other causes are assaults, falls and accidents. MECHANISMS OF INJURY a. Acceleration- occurs when the immobile head is struck by a moving object. b. Deceleration- if the head is moving and hits an immobile object c. Deformation- refers to injuries in which the force results in deformation and disruption of the integrity of the impacted body part (e.g., skull fracture). RISK FACTORS The major factor contributing to the occurrence of head injury is alcohol consumption. Primary prevention centers on the education of clients of all ages. Secondary prevention is not an issue in head trauma because other health conditions do not increase the incidence of head trauma. Tertiary prevention focuses on preventing or minimizing the complications of head trauma. PATHOPHYSIOLOGY a. Linear Skull Fractures- thin lines radiographically and do not require treatment.

b. Depressed Skull Fractures- may be associated with bone fragments penetrating into brain tissue. c. Basilar Skull fractures- occurs in bones over the base of the frontal and temporal lobes. They are rarely seen radiographically. d.

Concussions- is a head trauma that may result in loss of consciousness for 5 minutes or less. There is no break in the skull or dura.

e. Contusions- cause more extensive damage. It damages the brain substance itself, causing multiple areas of petichial and punctuate hemorrhage and bruised areas. SIGNS AND SYMPTOMS a. Subjective- Lethargy and indifference to surroundings b. Objective- signs of increased ICP, lack of orientation to time and place, paresthesia, labored respirations, (+) Babinski sign, coma and dilatation and fixation of pupils PHARMACOLOGIC MANAGEMENT a. Antiseizure medication- such as phenytoin b. Histamine antagonist- such as cimetidine are given to reduce the risk of stress ulcer. c. Mild analgesics and antibiotics may be prescribed. d. Osmotic diuretics may be required to reduce ICP. NURSING MANAGEMENT a. Observe for s/s of increased ICP. Institute neural checks every 15 minutes for several hours. b. Maintain airway.

c. Perform neurological assessment. Use Glasgow Coma Scale d. Institute seizure precautions, administer anticonvulsants if ordered. e. Provide care for the unconscious client 1. Observe for changes in vital signs. 2. Keep the client’s head slightly elevated to reduce venous pressure w/in cranial cavity. 3. Provide frequent oral hygiene. 4. Position the client to prevent pressure areas from forming decubiti. 5. Maintain adequate fluid balance. 6. Evaluate the client’s LOC at frequent intervals. 7. Provide auditory and tactile stimulation. f. Support natural defense mechanism. Encourage diet of nutrient-defense foods. g. Evaluate client’s response from time to time.