TCRN

Kehr’s sign
Referred left shoulder pain, usually indicates a splenic injury
Base deficit
Base deficit more than -6 indicates the need for agressive resuscitation and determination of the etiology
CXR
Most important tool providing useful information in the early minutes. Can identify major sources of blood loss from injuries in the chest or elevated diaphragm with displacement of abdominal organs
Tracheobronchial injury
Should be suspected if after chest tube placement a significant air leak is present
Diagnostic Peritoneal Lavage
Alternative to FAST scan to detect abd bleeding. A urinary catheter and gastric tube should be in place prior to procedure.
FAST
Focused Assessment with Sonography in Trauma. Used to detect free fluid in peritoneum or hemoperitoneum. Free fluid appears “black” on the screen. Has replaced DPL when available.
Positive FAST scan
Hemodynamically unstable trauma patient with a positive fast are taken directly to the OR for laparotomy
Ultrasound abd exam
Not useful to detect injuries to the diaphragm, intestine and pancreas. In patients with obesity, ascites and/or subQ emphysema the accuracy is reduced.
CT scan
Hemodynamically stable patients may be taken to CT
Angiography
Embolization is useful in treating patient with unstable pelvic fractures, liver and splenic hemorrhage. Use of hybrid OR suites to allow for surgical and interventional radiology methods of treatment simultaneously.
Diagnostic laparoscopy
Can be used to detect or exclude finding so f hemoperitoneum, organ injury, intestinal spillage or peritoneal penetration. Most useful in evaluating possible diaphragmatic injuries, espectially in penetrating thoracoabdominal injuries on the left site
Diaphragmatic injuries
Usually resultant of penetrating throacoabdominal injuries on the left side, including 11-12 rib fractures on the left.
Small intestine injuries
Result from shearing forces in MVC or direct blows that crush intestine between force and the vertebrae. Most commonly intra-abd injury in penetrating trauma. Occurs often with spinal injury. Pancreatic/solid organ injury are predictive of increased risk for hollow viscus injury. Signs of peritonitis develop. Any blow to the abd/penetrating injury to the lower chest/abd should increase suspicion of injury
Treatment of small intestine injury
Control bleeding prior to exploration. Debridement and closure and ligation of bleeders. Resection for multiple defects. Observe for wound infection/abscess development
Cause of duodenum injuries
Penetrating trauma most frequent cause. Usually conconcurrent mult-organ injuries. Usually found intraoperatively, commonly missed during exlap. Blunt force injury cause by vetebral compression.
Duodenal injury treatment
Identification with CT scan. Commonly patients have midepigastric or back pain with evolving peritoneal signs 6-24 hrs after injury. Primary closure in OR, closed drainage system. Goals are to control hemorrhage, debride devitalized tissue and provide drainage. Non operative management requires close observation for expanding or ruptured hematomas causing bleeding or peritoneal contamination.
Jejunum and ileum injuries
Jejunum lies in umbilical region, ileum lies in the hypogastric/pelvice regions. Lap belt can cause bowel to be crushed between the vertebrae and a solid object. Incorrect wearing of seatbelt increases chance for injury
Stomach injury
Rare, more common in children. Penetrating trauma most common cause. May find free air on cxr/fua. Pain to epigastric/abd area, tenderness, signs of peritonitis. Bloody output from gastric tube. Surgical intervention, is gastric content leakage, copious peritoneal irrigation and delayed primary closure
Large intestine
Rectal injuries may be associated with severe pelvic fracture. Lethal due to sepsis related to fecal contamination. Most are due to penetrating trauma. Transverse colon most often injured. Most injuries are contusions. Laparotomy with primary repair and colostomy is performed when perforation to the colon or rectum is suspected. Abscesses can be percutaneously drained.
Liver injuries
Commonly injured due to size and location. Cause of injury is blunt and penetrating trauma. MVC most common cause. Greatest mortality risk is hemorrhage.
High velocity GSW cause more widespread damage that creates massive hemorrhage. Suspect liver injury in any patient with blunt injury to right side. FAST scan to rule out free fluid. CT scan in hemodynamically stable patient. Graded I to IV.
Treatment of liver injuries
Nonoperative in select patient. OR for complex lacerations/arterial blush. Angioembolization for patients with contrast pooling or arterial blush. Pack and stabilize bleeding and return to OR 24-36 hours later for removal of packing and definitive management of liver/possible closure. Aggressive intraoperative resuscitation to prevent hypothermia, coagulopathy and hemodynamic stability. Damage control surgery.
Hemobilia
In patients with liver injury RUQ pain and jaundice may present days and weeks post injury so follow up care is important
Splenic injuries
Most commonly injured intra-abd organ. 25% of all blunt visceral injuries. LUQ trauma, lower rib fractures to left. Kehr’s sign is caused by blood irritation to the phrenic nerve that causes referred pain to the left shoulder. CT scan is the imagining of choice for stable patients.
Acute splenic rupture triad
left hemidiaphragm elevation, left lower lobe atelectasis and pleural effusion not commonly present and not a reliable sign
Treatment of splenic injury
Nonoperative management, splenectomy/partial splenectomy, possible damage control. More focused on salvage of spleen. If patient has a splenectomy patient must receve vaccinations prior to discharge for H influenza/meningococcal/pneumococcal vaccine
Overwhelming Postsplenectomy Sepsis
Rare, more common in children. 1-5 years after surgery. Flu like symptoms, shock from sepsis and DIC followed by death. Preventative measures include vaccinations and education.
Pancreas
uncommon injury. If ductal tears, digestive enzymes invade. Major therapeutic challenge for clinical team. Most are associated with intra-abdominal injury and are found intraoperatively. GSW/Stab wounds are frequently the cause.
Retroperitoneal injury
Associated with blunt trauma involving pelvic fractures
Abdominal vascular injury
Usually occur with pelvic, thoracic or visceral injury. Retroperitoneal hematoma in conjunction with pelvic or spine trauma can contain up to 4 L of blood.
Pitfalls of abdominal trauma
failure to suspect intra-abdominal injury from mechanism of injury, failure to fully evaluate complaints of abdominal pain following blunt abdominal injury, failure to perform timely operative intervention, failure to recognize hemodynamic compromise and delay surgery for further diagnostic tests
Blood loss hypovolemia: class I
Blood loss hypovolemia: class II
750-1500/15-30%, >100, normal BP, decreased PP, RR 20-30, Mildly anxious
Blood loss hypovolemia: class III
1500-2000/30-40%, HR >129, decreased b/p, decreased PP, RR 30-40, anxious/confused
Blood loss hypovolemia: class IV
>2000/>40%, HR > 140, decreased b/p, PP decreased, RR >35, confused and lethargic
Compartment syndrome
Common areas for compartment syndrome include: lower leg, forearm, foot, hand, gluteal region and thigh
Burn formula
Adult and Chemical burns > 20% TBSA resuscitate at 2 ml LR x kg x TBSA in the first 24 hrs.
High voltage electrical injuries
4 ml LR x kg x % TBSA in the first 24 hours
Peds Burn formula (14 and under and
3 ml LR x kg x % TBSA in the first 24 hours
Inhalation injury
Do not wait to intubate, swelling will increase then increase the difficulty of placing an ETT. Stridor or horseness is a late sign.
Compartment syndrome signs and symptoms
Pain out of proportion for the injury, weak or absent distal pulses, delayed cap refil, firmness on palpation of muscle/soft tissue in surrounding area, distal skin cool to touch, distal skin pale or cyanotic, decrase in patient sensation
Hypovolemia in childresn
children can be hemodynamically stable up to a 40% blood loss but only have a blood volume of 7-8% of their body weight
Hypovolemic shock
chaning mentation, tachycardia, >120 HR greatest concern, cool, clammy skin, prolonged cap refill, narrowed pulse pressure (normal 40-50), decrased urine output, hypotension
Hypotension in shock
Systolic blood pressure does not fall until 30% blood loss in adults
SIRS
Systemic Inflammatory Response Syndrome. Severe physiologic reaction to injury characterized by systemic release of inflammatory cytokines and chemokines. Two or more of the following: temp > 38 or 90, RR > 20 or PaCO 12 or 10% bands
MODS
After SIRS becomes stage 3 and severe hypotension refractory to fluid and ionotropic support ischemic insult progresses. Dysfunction of at least two organ systems from inflammatory insult, trauma or sepsis.
Causes of secondary brain injury
hypoxia, hypotension, hypocapnea or hypercapnea
Secondary brain injury
Leads to cerebral edema, mass effect, ischemia, cellular death
Optimizing oxygenation, ventilation and hemodynamics
Intubate with RSI, maintain O2 sat > 90%, optimally 98%, ETCO2 monitoring to keep around 35 – provides information about adequacy of circulatory flow, hyperventilation causes vasoconstriction and reduces PaCO2 and causes ischemia, PaCo2
Monroe-Kellie doctrine
Pressure volume relationships within the intracranial cavity, the craium is a non-expandable vault, increasing iCP is a warning that contents under pressure will try to relieve pressure by finding an exit in the area of least resistant – brain herniation
Normal ICP
0-15, > 20 requires intervention
8 Cranium bones
ethmoid, parietal, sphenoid, temporal, occipital
Dura
Outermost layer-firmly adhered to the inner skull with fixed attachments of the cranial sutures
Arachnoid
Loosely adhered to the pia mater, which makes the potential arachnoid space
Pia
closely associated with grey matter of the brain, is the innermost layer
CSF circulates
Between the pia and the arachnoid in the subarachnoid space, cushions and protects the brain and spinal cord
Middle meningeal artery
Key cause of epidural bleeds
cerebrum
right and left hemispheres of the brain
ventricular system
approx 500 ml of CSF is produced in the choroid plexus of the lateral ventricles each day
third cranial nerve
brainstem is the origin for the CNIII – CNX and CNXII
GCS 10
Eye opening to voice, confused verbal response, withdraws to pain
GCS
intubate, accepted definition of coma – categorized as severe brain injury
GCS 9-12
moderate brain injury
GCS >12
minor brain injury
CPP
cerebral perfusion pressure, maintain 60-70 mmHg
Avoid hypotension in ICH
Solitary and multiple episodes of hypotension have been shown to increase the morbidity and mortality associated with brain injury
Cushings Triad
hypertension, bradycardia and irregular respirations – ominous signs of herniation and require immediate attention and possible surgical intervention
ICP monitoring
Placed in all salvageable head injury patients with GCS
CPP/brain tissue oxygenation
assessed through the use of devices such as the brain tissue oxygen monitoring catheter to monitor cerebral perfusion, oxygenation and oxygen carrying capacity
Cerebral contusion
capillaries within the brain tissue are damaged and cause hemorrhage infarction or necrosis
Intracerebral
deeper in the brain tissue, may be single or multiples, can create mass effect, increased ICP, neurologic deterioration, headache, incrased ICP, pupil changes, abn posturing, hemiparesis, hemipalegia
SDH
Venous bleeding, acute
Herniation
Abdnormal protrusionof brain tissue through an opening when there is incrased intracranial pressue
Brown-Sequard
Hemisectionof cord from penetrating injury, loss of motor on side of injury, loss of sensation on opposite side
Temporal lobe herniation
oculomotor nerve runs along the edge of the tentorium and may becomme compressed against it during temporal lobe herniation, compression can cause a blown pupil
Uncal herniation
common herniation through the tentorial notch is the medial part of the temporal lobe the motor tract crosses the opposite side of the foramen magnum and results in contralateral hemiparesis
GCS that is assymetric
take the highest score
Neurogenic shock
results from impairment of the descending sympathetic pathways, results in loss of vasomotor tone and in sympathetic innervation to the heart. Rare in injury below T6. Loss of vasomotor tone cause vasodilation of lower extremities, visceral organs, blood pools in lower extremities. Bradycardia. Vasopressors are required, atropine for symptomatic bradycardia
Inability to perceive pain in the spinal cord injured patient
can mask a potentially serious injury elsewhere in the body, such as the usual signs of an acute abd
Bony level of injury
the veterbra at which the bones are damaged, causing injury to the spinal cord
Neurologic level of injury
determined primarily by clinical exam. Frequently discrepancy between the bony and neurologic levels because of the nerve innervation points
Central cord syndrome
disproportionately greater loss of motor strength in the upper extremities than in the lower extremities, with varying degress of sensory loss. Common with hyperflexion injury
Anterior cord syndrome
parapalegia and a dissociated sensory loss with a loss of pain and temporature sensation
C 1 – C 4
require intubation, below C 4 consider for increased work of breathing secondary to muscle innervation changes
Poikilothermic
Thermoregulartion is impaired and patient will take the temp of the room, adversely impacts bradycardic patients
Spinal Shock
flaccid paralysis, loss of autonomic function, abscence of cutaneous and/or proprioceptive sensation, cessation of all reflex activity below site of injury
C2 dens fracture
Common in geriatric patients, hyperextension injury
Compression fractures
axial loading injury, degree of compression affects stability, thoracic and lumbar spine usually affected
Burst fracture
fracturing in outward pattern, may impinge cord, can have compression and cord compression
Chance fracture
Usually L1-2, teardrop fracture, may result in paraplegia, and small bowel injury from lap belt compression and lumbar spine
SCIWORA
spinal cord injury without radiographic abnormality, common in PEDS, dislocation with spontaneous relocation, cord injury evident, imaging negative
Autonomic dysreflexia
uncontrolled, massive sympathetic reflex to noxious stimuli, below level of lesion
Hyphema
blood in anterior chamber of eye, prevent rebleeding, bedrest, limited activity, HOB elevated, cycloplegic agents – atropine gtts, may need patch
Open Globe
minimize additional damage, shield w/o pressure, eye patches contraindicated, anticipate need for OR
Orbital blowout fracture
Diplopia, can cause eye to look upward secondary to muscle/nerve impigement, emergency surgical repair indicated, delays increase risk of vision loss
LeFort I
transverse fx between maxillary and orbital floor, may include maxillary sinuses. Lower maxilla and teeth are mobile or floating but nose and midface stable. May have trismus, malocclusion. Check for mandible fx.
Lefort II
includs central maxilla, nasal area, ethmoid bones, tripod shape, grasping front teeth and palate causes movement to nose and upper lip w/o movement to orbital complex, caved in appearance, edema, subconjunctival hemorrhage and epistaxis, early intubation for airway protection. CSF presence – rhinorrhea suggests open skull fx
LeFort III
complete craniofacial dysfunction, associated with massive soft tissue, ocular injuries, TBI, skull injuries, cribiform plate and dural tears, rocking mxillar moves the entire face
Tripod fx
separation of all three major attachments of the zygoma to the rest of the face
Orbigozygomatic fracture
complex fractures of zygoma and orbital floor, pain, trismus, diplopia, numbness to upper lip, lower lid and bilateral nasal area, surgical repair indicated
Neck trauma
internal jugular vein and internal carotid artery most commonly injured
Zone I neck trauma
highest mortality, angle of mandible to base of skull, difficult to assess, and exploration can increase mortality
Zone II neck trauma
mid portion of neck, injuries apparent on exam, most carotid injuries occur here, manage by observation.
Zone III Neck trauma
clavicles and sternal notch to cricoid cartilage. hard to assess surgically as so high at skull base. Diagnosis essential as infection can occur and impact mortality after 24 hours. Embolization very valuable, exploration can damage cranial nerves. Angiography to delineate site of injury
S/S of emergency intervention in neck trauma
airway obstruction, pulsatile bleeding, expanding hematoma, unresponsive, extensive subcutaneous emphysema
s/s of neck trauma needing more diagnostics
voice change, wide mediatstinum, hemoptysis, hematemesis, dysphonia/dysphagia, drooling, bloody sputum, horner’s syndrome, pain with turning neck
Horner’s syndrome
a contracted pupil, drooping upper eyelid, and local inability to sweat on one side of the face, caused by damage to sympathetic nerves on that side of the neck
Neck trauma treatment
stabiltize airway, pressure control for bleeding, subclavial injury needs IV on opposite site, consider permissive hypotension, repair vs ligation, shunting, embolization, ligation, antithrombotic
Neck trauma diagnostic testing
CXR mandated for zone I, CT most accepted, CT angiogram – excellent for laryngeal and tracheal injuries, as reliable as arteriography. Arteriogram – considered gold standard, invasive with risk of complications, contast load but embolization can happen at the same time.
Associated injuries with neck trauma
LeFort fractures, basilar skull fracture involving carotid canal, diffuse axonal injury with GCS
Frontal impact
Suspected injuries: Capone do, anterior flail chest, myocardial contusion, pneumothorax, traumatic aortic disruption, fracturednspleennornkiver, posterior fracture/dislocation of hip and/or knee
Side impact
Suspect injuries: contra lateral neck sprain, Capone go, lateral flail chest, pneumothorax, traumatic aortic disruption, diaphragmatic disruptive, fractured spleen liver or kidney, fix
Pelvis or scetabulum
Rear impact
Cspine injury or soft tissue to neck
Pedestrian struck
Head injury, traumatic aortic disruption, and visceral injury, fractured lower extremity or pelvis