Trauma Flashcards
-Hypotension
-Bradycardia, fast cap refill
-Flushed warm skin
-Priapism
Neurogenic Shock
Sympathetic nerves originate from the T-spine, injury to the area can block the nerve pathways & inhibit the release of epi & norepi, which produces the typical tachycardia, pallor, & diaphoresis as seen in other types of shock
-Bradycardia caused by loss of sympathetic autonomic activity (T6 and above)
-Hypotension caused by loss of vasomotor control and peripheral vascular resistance
-Priapism (T6 and above)
-Loss of sweating and shivering
-Poikilothermia (impaired regulation of body temperature causing variation with ambient temperature)
-Loss of bowel and bladder control
Autonomic Dysfunction
-Aching
-Burning
-Tingling
-Inability to make small movements with your hands (fine motor skills)
-Numbness in your hands or arms
-Paralysis or weakness
-Muscle spasticity
-Difficulty walking
Central cord syndrome
Lack of nerve signals between your brain and your arms and hands (sometimes legs) is a hallmark indicator of central cord syndrome
-Decreased sensation of pain & temperature below the level of the lesion
-Intact light touch & position sensation
-Paralysis below the lesion
Anterior cord syndrome
An incomplete spinal cord syndrome that predominantly affects the anterior 2/3 of the spinal cord
- Weakness/Paralysis & Sensation loss on Affected Side
- Contralateral Pain & Temperature loss
HX:
- Knife or GSW Injury
Brown-Séquard syndrome
A functional hemitransection of the spinal cord resulting from a ruptured intervertebral disk or the pushing of a fragment of the vertebral body on the spinal cord
-Midfacial edema
-Unstable maxilla
-Lengthening of the face (Donkey face)
-Epistaxis
-Numb upper teeth
-Nasal flattening
-Cerebrospinal fluid rhinorrhea
Le Fort fractures
Le Fort fractures
Group of fractures involving partial or complete separation of the midface from the skull
Mainly pterygoid plates of the sphenoid bones
Fracture
Type I Le Fort
Horizontal; Alveolar Ridge
Fracture
Type II Le Fort
Pyramidal; Nasofrontal Suture
Fracture
Type III Le Fort
Horizontal; Craniofacial Dislocation
-80% of all fractures to the skull
-Usually not depressed
-Often occur without an overlying scalp laceration
Linear skull fracture
Seen as a straight line on the radiograph
Usually associated with major-impact trauma;
Commonly results from an extension of a linear fracture into the floor of the anterior and middle fossae;
Can cause a dural tear leading to a connection between the subarachnoid space, the paranasal sinuses, and the middle ear
Basilar skull fracture
-Nausea and vomiting
-Abnormal extraocular movements
-Hearing loss
-Facial palsies
-Battle signs
-Raccoon eyes
-Hemotympanum
-CSF leakage from the nose (rhinorrhea) or eyes (otorrhea) that can result in bacterial meningitis
Basilar skull fracture
-Occurs when a portion of the skull is pushed below the level of the adjacent skull
-Commonly associated with scalp lacerations causing an open fracture
-High risk for infection and seizures
-Often require surgical removal of the bone fragments (craniectomy)
Depressed skull fracture
Open vault fracture
Opening exists between a scalp laceration and brain tissue
-Often associated with trauma to other systems
-High mortality rate
-Exposure of brain tissue may lead to infection (meningitis)
-Surgical repair is required
TBI
An alteration in brain function, or other evidence of brain pathology, caused by an external force
Divided into 2 groups:
-Primary brain injury
-Secondary brain injury
Primary brain injury
Direct trauma to the brain and to the associated vascular injuries that occurred from the initial injury
Secondary brain injury
Results from intracellular and extracellular derangements that were either initiated at the time of the injury or result from a consequence of the initial injury
Secondary brain injury derangements
-Hypoxia
-Hypocapnia
-Hypercapnia from airway compromise
-Aspiration of gastric contents
-Thoracic injury
-Anemia and hypotension from external and internal hemorrhage
-Hyperglycemia or hypoglycemia that can further injure ischemic brain tissue
Classifications of brain injuries
Diffuse
Focal
Diffused brain injury
Usually caused by acceleration–deceleration forces
-Diffuse axonal injury (DAI)
-Hypoxic–ischemic damage
-Meningitis
-Vascular injury
Major cause of damage in diffuse brain injuries
Disruption of axons – the neural processes that allow one nerve to communicate with another
Concussion (mild DAI)
-Function of the brainstem or both cerebral cortices are temporarily disturbed
-Altered level (or loss) of consciousness is followed by periods of drowsiness, restlessness, and confusion, with a fairly rapid return to normal behavior
-Amnesia
-Vomiting
-Combativeness
-Transient visual disturbances
-Defects in equilibrium and coordination
-Changes in blood pressure, pulse rate, and respiration (rare)
2 types of amnesia in mild DAI
Retrograde amnesia: no recall of the events before the injury
Antegrade amnesia: after recovery of consciousness
Moderate DAI
Head injury that results in minute petechial bruising of the brain tissue
-Often accompanied by basilar skull fracture
-Most patients will survive; however, permanent neurologic impairment is common
-Patient is initially unconscious, followed by persistent confusion, disorientation, and amnesia of the event
Recovery from Moderate DAI
During recovery, patients often experience:
*Inability to concentrate
*Frequent periods of anxiety
*Uncharacteristic mood swings
*Sensorimotor deficits
Severe DAI
Severest form of brain injury and involves severe mechanical shearing of many axons in both cerebral hemispheres extending to the brainstem
Severe DAI S/S
Often unconscious for prolonged periods
Patients may exhibit abnormal posturing and other signs of ICP
Focal brain injury
Generally caused by contact;
Specific, grossly observable brain lesion concentrated in one region of the brain
-Scalp injury
-Skull fracture
-Surface contusions
-Brain hemorrhage
Cerebral contusion S/S
-Increased ICP =
-Headache
-Nausea/vomiting
-Seizures
-Loss of consciousness (maybe coma)
-Hemiparesis
-Aphasia
-Personality changes
Cerebral blood flow
Mean arterial pressure (MAP) - ICP
Normal MAP
85 - 95 mm Hg
Normal ICP
10 - 15 mm Hg or less (5-10)
Normal CPP
70 and 80 mm HG
(60 mm Hg is the minimum threshold to adequately perfuse the brain)
When ICP increases
CCP decreases
When CCP decreases
Vessels in the brain dilate, which results in increased ICP
Early signs and symptoms of increased ICP
Headache
Nausea and vomiting
Altered level of consciousness
S/S of Increased ICP
Cushing triad:
-Increased SBP
-Bradycardia
-Irregular respiratory pattern
-Decorticate or decerebrate posturing
Respiratory changes as Increased ICP rises
Hypoventilation
Cheyne-Stokes breathing
Central neurogenic hyperventilation
Ataxic breathing
Brain hemorrhages
-Epidural
-Subdural
-Subarachnoid
-Cerebral (intraparenchymal)
Epidural hematoma
Between the cranium and the dura in the epidural space
Usually a rapidly developing lesion
Commonly associated with a laceration or tear of the middle meningeal artery
S/S Epidural hematoma
Early stages: Headache & drowsiness
-Transient loss of consciousness, followed by a lucid interval (6-18 hrs); others have variable presentation or never regain consciousness
Common causes of Epidural hematoma
Low-velocity blows to the head
Violent altercations
Deceleration injuries
Subdural hematoma
Between the dura and the arachnoid mater in the subdural space
Usually results from bleeding of the veins that bridge the subdural space
Associated contusion or laceration of the brain often is present
Classifications of Subdural hematomas
Depends on the time lapse between the injury and the development of symptoms:
-Acute: if symptoms occur within 24 hours
-Subacute: if symptoms occur between 2 and 10 days
-Chronic: if symptoms occur after 2 weeks
S/S of subdural hematoma
Headache
Nausea and vomiting
Decreasing level of consciousness
Coma
Abnormal posturing
Paralysis
Bulging fontanelles, in infants
Subarachnoid hemorrhage
Intracranial bleeding into the CSF, resulting in bloody CSF & meningeal irritation;
-Bleeding may extend into the brain if the force from the broken vessel is sudden and severe
-Patients often report a sudden and severe headache that is initially localized and then spreads and becomes dull and throbbing
S/S subarachnoid bleeding
-Dizziness
-Neck stiffness
-Unequal pupils
-Vomiting
-Seizures
-Loss of consciousness
-Severe hemorrhage may result in coma and death
-Permanent brain damage is common in those who survive
Intracerebral hematoma
Collection of blood within the substance of the brain, most commonly in the frontal or temporal lobe
Signs and symptoms may be immediate or delayed, depending on size and location of the hemorrhage;
Once symptoms appear, the patient usually deteriorates rapidly
Moderate TBI GCS
9 - 13
Severe TBI GCS
8 or less
Categories of Spinal cord Lesions (transections)
Complete or incomplete
Autonomic Dysfunction Manifestations
-Bradycardia caused by loss of sympathetic autonomic activity (T6 and above)
-Hypotension caused by loss of vasomotor control and peripheral vascular resistance
-Priapism (T6 and above)
-Loss of sweating and shivering
-Poikilothermia (impaired regulation of body temperature causing variation with ambient temperature)
-Loss of bowel and bladder control
C2 through C4 dermatomes
Collar of sensation around the neck and over the anterior chest to below the clavicles
T4 dermatome
Sensation to the nipple line
T10 dermatome
Sensation to the umbilicus
S1 dermatome
Sensation to the soles of the feet
Autonomic hyperreflexia syndrome
(autonomic dysreflexia)
Resolution after spinal shock associated with chronic SCI in patients who have injuries at T6 or above
-Paroxysmal hypertension (up to 300 mm Hg)
-Pounding headache
-Blurred vision
-Sweating (above the level of injury) with flushing of the skin
-Increased nasal congestion
-Nausea
-Bradycardia (30–40 beats/min)
6 P’s of Compartment Syndrome
Pain
Pallor
Paresthesia (pins/needles sensation)
Pulselessness
Paralysis
Poikilothermia (body part normalizes its temp to the surrounding area)
Acute Compartment Syndrome
Build up of excessive pressure between the muscle & fascia which leads to tissue ischemia, infarction, & subsequent contracture. These results in an accumulation of myoglobin, potassium, & lactate. Once released, these by-products flood the body causing:
-Metabolic acidosis
-Renal failure
-Dysrhythmias
Acute Compartment Syndrome Causes & TX
Causes:
-Crush Injury
-Fracture/Contusion
-Casts/Dressings/Splints
-Burns
-Vascular Injury/bleeding disorders
-Seizures
-Snake bites
-Rhabdo
-Hypotension/Hypoxia
TX:
-XABC’s
-Fluids 1-2L (NS)
-EKG
-Pain management (Ketamine)
Prior to Release/Hyperkalemia
-Tourniquet extremity
-Calcium
-Albuterol
6 Priorities of Orthopedic Injuries
Pain
Deformity
Vascular Compromise
Nerve Compromise
Stability
Wounds
Pain
Where is your pain?
Is it painful at rest?
Only when it is moved?
Does it hurt to touch?
*Pain management
Deformity
*Any deformity merits some degree of immobilization
Vascular Compromise
*Control Hemorrhage
Is the (not amputated) extremity warm to the touch? Pale? Is there normal or delayed capillary refill to the extremity?
If an extremity is pulseless, this will require prompt management to avoid permanent damage from loss of blood flow
*Any splint or immobilization done in the prehospital setting should prompt rechecking of the pulse
Nerve Compromise
*Check C/M/S
Stability
*Splint extremities to prevent further damage/pain (especially prior to moving)
Wounds
Any wounds over a fracture site will be “open fracture”
Higher risk for infection
*Irrigate with saline and/or cover with saline soaked gauze to protect the bone, if possible
