Closed Head Injury Flashcards
What is a closed head injury?
- Skull is intact and there is no penetration of the skull
- Direct and indirect force can cause this type of injury
- Rotational and/or deceleration can be involved
What causes a secondary injury in a closed head injury?
- Swelling and release of chemicals that promote inflammation and cell injury or death
- Causes cerebral edema, increasing intracranial pressure (ICP) and preventing CSF from draining, further increasing pressure and causing brain damage.
- If not controlled can cause brain herniation and death
What are some examples of secondary injuries that can occur after a closed head injury?
- Intracranial hemorrhage
- Cerebral edema
- Increased ICP
- Hypoxia causing brain damage
- Infection- common with penetrating trauma
- Chemical changes leading to brain death
- Hydrocephalus
What is Cushing’s triad?
Only present in about 1/3 of population, indicates increased ICP and impending cerebral herniation
1. HTN- widening pulse pressure
- SBP increases attempting to maintain CPP
2. Decreased respiratory rate
3. Bradycardia
What is a Basilar skull fracture?
A fracture of the floor of the skull
What are the manifestations of a basilar skull fracture?
- ‘raccoon eyes’ – periorbital ecchymosis
- Battle sign- mastoid ecchymosis
- Otorrhea and/or rhinorrhea (+ dextrostix test result, halo or target sign and salty taste in mouth) DO NOT OBSTRUCT FLOW)
How do you manage a patient with a basilar skull fracture?
- Provide prophylactic antibiotic coverage
- Oral intubation and oral gastric tube ONLY are indicated in place of nasal intubation and nasal gastric tube
What are the symptoms associated with a closed head injury?
1. Cerebral Edema
- Decreased LOC
- Pupillary dilatation ‘blown’ pupil
- Cushing triad
2. Decreased LOC
3. Posturing
- Decorticate: flexion of arms, wrists, fingers, adduction of arm against thorax, extension, internal rotation and/or plantar flexion with lower extremities
- Decerebrate: stiff extension, adduction and internal rotation of upper extremities (clenched teeth and hyperextended back, more of brain stem involved)
4. Hyponatremia- MOST COMMON finding in a brain injury patient
- Syndrome of inappropriate antidiuretic hormone (SIADH)
- Cerebral salt wasting (CSW): differentiation of CSW from SIADH is imperative as the treatment differs significantly
How often do you assess a patient’s neuro status post brain injury?
- Ongoing, every 30-60 minutes first 24 hours post injury
- Pupil size and reaction
- Vital signs
- All patients with a head injury are presumed to have a cervical spine injury until proven otherwise.
- Avoid any condition (fever, pain, shivering) that increases metabolic rate and therefore increases demand for glucose and oxygen
How do you manage a patient with a closed head injury?
1. Consult Neurosurgery & limit secondary injuries
2. Prevent hypotension and hypoxemia
- Maintain SBO > 90 mm Hg and PO2 > 60 mm Hg
- Maintain hematocrit at 30-33%. Administer PRBC’s if warranted
3. Treat cerebral edema/elevated ICP
- Hyperventilation PCO2 25-30 mm Hg
- Causes cerebral vasoconstriction and thereby lowers ICP
- Cerebral vasoconstriction also causes cerebral ischemia
4. Sedation and analgesia
- Opioid sedatives lower ICP by reducing metabolic demand and relieving anxiety and pain
5. ICP Monitoring
- ICP monitoring is NOT routinely appropriate for patients with MILD or MODERATE head injuries
- If ICP > 20-25 mm Hg for > 5 minutes, then treatment should be instituted to lower ICP
6. Seizure/DVT PPX
- For patients at high risk for posttraumatic seizures, anticonvulsants, such as phenytoin or levetiracetam, should be initiated early and continued for a minimum of 7 days.
- Use graduated compression stockings or intermittent pneumatic compression stockings until patient is ambulatory
- Low molecular weight heparin or unfractionated heparin should be used in combination with mechanical prophylaxis
