introduction to emergency nursing concepts final_2
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Introduction toEmergency Nursing
ConceptsSandra H. Lewis, ARNP-BC-ADM
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Continued Full spinal mobilization is being challengedand reexamined:
Asking: Is full spinal mobilization
necessary in all trauma patients? How appropriate is the assessment ofprehospital assessment?
Concerns over the high false positive rate
that occurs with prolonged spinalimmobilization.
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Current Guidelines
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Objectives 1. Explain emergency care as acollaborative, holistic approach thatincludes patient, family and significant
others. Discuss priority emergency measures for
any patient with an emergency situation. 3. Discuss pre-hospital, emergency care
and resuscitation of the trauma patient.
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Objectives Discuss disaster triage concepts andcontrast with traditional triage
concepts.
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Trauma The fourth leading cause of death for ALLages.
Nearly of all traumatic incidents involvethe use of alcohol, drugs or othersubstance abuse.
Is predominantly a disease of the youngand carries potential for permanentdisability.
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Systems Approach to
Trauma An organized approach to traumacare that includes:
Prevention, access, acute hospitalcare, rehabilitation, and research.
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Trimodal Distribution of
Death First peak- seconds to minutes from timeof injury to deathsevere injuries:lacerations of the brain, brainstem, high
spinal cord, heart aorta, large bloodvessels. Second peak- minutes to several hours:
subdural, epidurdal hematomas,hemopneumothorax, ruptured spleen,
lacerated liver, pelvic fractures, otherinjuries associated with major blood loss.
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Third peak-occurs several days toweeks after the initial injury: most
often the result of sepsis andmultiple organ failure. At this stage,outcomes are affected by carepreviously provided.
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Levels of Trauma Care American college of SurgeonsCommittee on Trauma
Levels I-IV, Level ones are the mostsophisticated and care for all aspectsfrom prevention to rehabilitation.
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Trauma Triage Minor trauma: single system injurythat does not pose threat to life or
limb and can be appropriately treatedat a basic emergency facility.
Major trauma: serious multi system
injuries that require immediateintervention to prevent disability.
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Mechanism of Injury
Is vital to the initial assessment andmay raise suspicions about the
patients injury pattern. Blunt vs. penetrating injury
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Blunt Trauma Most often results from vehicularaccidents, but may occur in assaults,
falls from heights, and sports relatedinjuries.
May be caused by accelerating,
decelerating, shearing, crushing, andcompressing forces.
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Blunt Trauma, cont. Coup-contra coup injury Body tissues respond differently to
kinetic energylow density poroustissues and structures, such as lungs,often experience little damage
because of their elasticity.
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Blunt Trauma cont. The heart , spleen and liver are lessresilient often rupturing or fragmenting.
Often, overt external signs are notapparentmaking the mechanism of injurymost important to the practitionerperforming the physical examination.
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Penetrating Trauma Results from the impalement of foreignobjects into the body.
More easily diagnosed because of obvious
injury signs. Stab wounds are usually low velocitythedirect path, the depth and widthdetermine injury.
Women tend to have trajectories in adownward motion, men in an upward force.
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Penetrating Trauma cont. Ballistic trauma may be either low orhigh velocity injuries.
Missiles or bullets that come intocontact with internal structures thatproduce a change in in pathway
release more energy and result inmore injury than a direct pathway.
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Penetrating Trauma,
cont. Injuries sustained from penetratingobjects must be assessed for the
potential for infection from thedebris carried by the penetratingobject.
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Disaster / Mass Casualty
Triage Concepts Most severe injuries in mass traumaevents are fractures, burns,
lacerations, and crush injuries. Most common injuries are eye
injuries, sprains, strains, minor
wounds and ear damage. (CDCWebsite)
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Mass Casualty: Who is at
risk? Anyone in surrounding area. Rescue workers and volunteers.
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Bioterrorism
Agents/Diseases, Threats CDC Website ( see handout)
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Disaster Triage www.bt.cdc.gov/masstrauma/index.asp
www.nyerrn.com/simulators
http://www.bt.cdc.gov/masstrauma/index.asphttp://www.bt.cdc.gov/masstrauma/index.asphttp://www.nyerrn.com/simulatorshttp://www.nyerrn.com/simulatorshttp://www.bt.cdc.gov/masstrauma/index.asphttp://www.bt.cdc.gov/masstrauma/index.asp -
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Pre-Hospital Care and
Transport The time from injuryto definitive care is adeterminant of
survival. Careful attention is
given to C-spineimmobilization,
breathing andcirculation(ABCs)
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Current Guidelines on
C-Spine Immobilization Although it has been challenged, C-spine immobilization is still the
protocol for trauma patients untildiagnostically cleared (X-Ray)
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Additional Pre-Hospital
Measures Occlusive dressings to open chestwounds
Needle thoracotomy to relievetension pneumothorax
Endotracheal intubation
Cricothyrtomy
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Caveat!!! Research has indicated INCREASEDmortality with IV fluids BEFORE
hemorrhage control. Transport is not delayed to start IVaccess!
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Transport
How is it decided? Travel time Terrain
Availability of air or groundtransport
Capability of personnel
Weather
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Emergency Care Phase
Preparation Trauma team at receiving hospitalresponds before arrival of patient
Report has been transmitted Preparations are initiated based on
report.
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Initial Patient
Assessment Clinical presentation Physical assessment
History of traumatic event Pre-existing illness
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Primary Survey Most crucial assessment tool in traumacare
1-2 minutes MAX!
Designed to identify life threateninginjuries ACCURATELY
Establish priorities
Provide simultaneous therapeuticinterventions.
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Resuscitation Phase Secondary Survey:
Table18:2 page 647/648
32
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EFGHI = E- Expose the patient F- *Full set of vital signs, *five interventions
(cardiac monitor, pulse oximetry, urinary
catheter, NG if not contraindicated, lab studies) G- giving comfort measurespain control,reassurance to patient and family
H- history/ head to toe assessment I- inspect for hidden injuries-log roll patient to
inspect posterior aspect.
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Sequence of Diagnostic
Procedures Influenced by:
Level of consciousness Stability of patients condition
Mechanism of injury
Identified injuries
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Maintain Airway Patency Essential to trauma management EVERY trauma patient has potential for
airway obstruction
Most common obstruction: Tounge
Other common causes: blood or vomitus,secretions, structural impairment,
depressed sensorium, absent gag reflex
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Maintaining the airway Simple, simple!!
Nasopharyngeal airway
Oropharyngeal airways
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Definitive Nonsurgical
Airway Endotracheal intubation-Complete controlof the airway
Nasotracheal intubationINDICATED forthe spontaneously breathingpatient..CONTRAINDICATED in thepatient with facial, frontal sinus, basilar
skull or cribriform plate fractures.
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Choice of Airway
management Familiarity of procedure Clinical condition of the patient
Degree of hemodynamic stability
A PATENT AIRWAY IS THE
CORNERSTONE OF SUCCESSFULTRAUMA RESUSCITATION
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A LIFE THREATENING
CONDITION EXISTS Altered mental status (agitation) Cyanosis( nail beds and mucous membranes) Asymmetrical chest expansion
Use of accessory muscles/abdominal muscles Sucking chest wounds Paradoxical movements of the chest wall Tracheal shift
Distended neck veins Diminished or absent breath sounds
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Impaired Gas Exchange Follows airway obstruction as the nestmost crucial problem for the traumapatient.
Reasons: decreased inspired air, retainedsecretions, lung collapse or compression,atelectasis, accumulation of blood in the
thoracic space.
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Decreased Cardiac
Output/Hypovolemia Acute Blood lossMOST commoncause in acute trauma
May be external or internal
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Additional Causes of
Decreased Cardiac Output (impaired venous return to the heart) Tension Pneumothorax
Pericardial Tamponade (fromdecreased filling and ventricularejection fraction)
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Table 18-4 Pay attention to Class I through IV*EBL (estimated blood loss)
*Changes in pulse, BP, RR, UOP,mental status.
Note the fluid/blood needed to
replace: 3:1 rule
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Priority Interventions Patent airway Maintaining adequate ventilation
Adequate gas exchange Then: Control hemorrhage, replace
circulating volume, restore tissueperfusion
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Control of External
Hemorrhage Direct Pressure Elevation
Compression of pressure points(arteries, veins)
AVOID tourniquetscan compromise
loss of circulation and loss of limb
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Control of Internal
Hemorrhage Identification and correction ofunderlying problem.
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Fluid Resuscitation Venous Access and Volume infused are key. Two large bore IVs 14-16 gauge. (never
less that 18, that is the smallest to give
blood through rapidly and not havehemolysis) Forearm and anti-cubital veins are
preferred Central lines are more beneficial as
resuscitation MONITORING tools
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Fluid Resuscitation Cont A pulmonary artery catheter may beinserted in the critical care unit tomonitor volume.
RULE: Venous access with largest borecatheter possible. Isotonic fluids are used INITIALLY Ringers Lactate is first choice followed by
Normal Saline
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Fluid Resuscitation Cont Large bore catheters, short tubing, rapidinfuser devise that warms fluids and blood.
An initial bolus of 2 liters of fluid is used
unless there is contraindication 3:1 rule= 3mls of crystalloid for each 1mlof blood loss.
INITIAL response to fluid challenge isurine output..should =50 ml in adult, LOC,heart rate, BP and capillary refill.
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Three Response Patterns Rapid Response- respond quickly to fluid challengeand remains stable at completion of bolus.
Transient Response- responds quickly but declineswhen fluids are slowed
(indicates continued blood loss)**Non Response- fail to hemodynamically respond
to crystalloid and bloodrequire immediatesurgical intervention.
See table 18-5 on page 652
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Decision to give Blood Based on patients response to initialfluid.
** if unresponsive to fluid, typespecific blood is given, IF LIFETHREATENINGmay give O positive.
***Crossmatched, type specific
should be given as soon as possible.
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Auto-transfusion Collection of blood from the patientsintra-thoracic injuries is anti-
coagulated and filtered andadministered to the patient.
SAFE, carries no compatibilityproblems, no risk of transmitteddisease.
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During resuscitative
phase Imperative to locate etiology ofhemorrhage:
Chest and pelvis, extremity X-rays
Abdominal ultrasound
Abdominal CT can be used but in the caseof hemodynamic instability Peritoneal
lavage is the quick, invasive test of choice
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Peritoneal Lavage Insertion of lavage catheter directly intothe abdomen
Aspiration of greater than 10 mls blood
and patient goes directly for surgery. If less than 10 mls of blood, 1 liter ofwarmed NS is infused into peritonealcavity, then drained and sent for cellcounts, amylase, bile, food particles,
bacteria, fecal matter.
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Hypothermia Defined as a core temp of 35 degrees Centigrade Can occur year round More susceptible person: older, using alcohol or sedatives,
severe injury, massive transfusions. In presence of cooler atmospheric temps Submersion in water Rapid infusion of room temp. IV fluids Effects the myocardium and the coagulation system. Can result in bradycardia, atrial and ventricular fibrillation.
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Treatment Warm fluids Warming blankets
Overhead warmers
O i i d
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Ongoing Signs and
Symptoms of Shock Decreased Hgb &Hct Deterioration of PaO2 and pH
Rising base deficits Diminished UOP (less than
>.5ml/kg/hr)
Increasing Lactate levels
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Unreliability of H&H Can take up to 4 HOURS!! To re-equilibrate, therefore cannot gauge
degree of shock.
O i M b li
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On-going Metabolic
acidosis Result of hypovolemia and hypoxia Indicates inadequate tissue perfusion
Indicates anaerobic metabolismvery inefficient cellular metabolism. Must be interrupted or cellular
dysfunction results in cellular
swelling, rupture and death.
M i Fl id
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Massive Fluid
Resuscitation Greater than 10 units of PRBCs over24 hours or the replacement of the
patients total blood volume in lessthan 24 hours.
It is associated with VERY pooroutcomes.
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Continued.. Purpose is to restore oxygentransport to the tissues, stop the
progression of shock, preventcomplications.
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Potential Complications ofMassive Fluid Resuscitation
Acid base imbalances Electrolyte imbalances
Hypothermia Dilutional coagulopathies Volume overload SIRS (systemic inflammatory response syndrome)
ARDS (acute respiratory distress syndrome) MODS (multi-organ dysfunction syndrome)
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Oxygen Debt Result of metabolic acidosisshift
from aerobic to anaerobicmetabolism resulting in accumulationof lactic acidhencelactic acidosis.
MUST REVERSE to prevent cellular
death
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Electrolyte Imbalances Hypocalcemia Hypomagnesemia Hyperkalemia
May lead to changes in myocardialfunction, laryngeal spasm, neuromuscularand central nervous systemhyperirritability
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Third Spacing
Vessels become more permeable tofluids and molecules, leading a changein movement from the intravascularspace to the interstitial space.
Patients become more hypovolemic
requiring more fluid replacement.
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Dilutional Coagulopathy Dilutional thrombocytopenia Reduced fibrinogen Reduced factor V, FactorVIII and other clotting
components
High levels of citrate in blood products reducecalciumleading to an ineffective clotting cascade(calcium is a necessary co-factor for thisprocess).
Platelet dysfunction can occur secondary to
hypothermia or metabolic acidosis
T t t f Dil ti l
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Treatment of DilutionalCoagulopathy
Improve tissue perfusion
Resolve hypothermia
Administer clotting factors (FFP,cryoprecipitate, platelets)
Monitor labs (H&H, PLT count,
fibrinogen, PT, PTT
Ch i th
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Changes in theCoagulation Cascade
Initially helpfulrelease ofinflammatory mediatorsover time
(can be a fairly short time) can resultin SIRS, ARDS, MODS
ssessment anM f f
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mManagement of specific
Organ Injuries Chest Injuries
Spinal Cord Injuries
Head Injuries Musculoskeletal Injuries
Abdominal Injuries
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Chest Injuries Tension Pneumothorax- is rapidly fatal Easily resolved with early recognition and
intervention Air enters the pleural cavity without a route of
escape, with each inspiration, additional air entersthe pleural space, INCREASING intrathoracicpressure causing collapse of the lung.
The increased pressure causes pressure on the
heart and great vessels compressing themTOWARD the unaffected side.
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Tension Pneumo cont.. Physical evidence: Mediastinal Shift & distended neck veins. RESULTS in: decreased Cardiac Output
and alterations in gas exchange Manifested by: severe resp. distress,chest pain, hypotension, tachycardia,absence of breath sound son affectedside, and tracheal deviation
Cyanosis is a LATE manifestation.
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Tension Pneumo cont Diagnosis based on CLINICAL presentation not
Chest x-ray Treatment is never delayed to confirm by X-ray Immediate decompression with a 14 gauge needle
(thoracostomy)..inserted at the 2ndintercostalspace at the midclavicular line on the INJUREDside.
This converts a tension pneumo to a simplepneumo.
Definitive treatment then requires placement of achest tube.
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Hemothorax Collection of blood in the pleural space
From injuries to the heart, great vessels,or pulmonary parenchyma
Signs and symptoms: decreased breathsounds, dullness to percussion on affectedside, hypotension, respiratory distress.
Treatment: Placement of chest tube.
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Open Pneumothorax Results from penetrating trauma that allows air to
pass IN AND OUT of the pleural space. Patient presents with hypoxia and hemodynamic
instability
Management: Three sided occlusivedressingfourth side is LEFT OPEN to allow forexhalation of air from the pleural cavity.
IF the dressing is occluded on all four sides thepatient may develop a tension pneumothorax.
Treatment: Chest tube placement
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Cardiac Tamponade Life threatening condition caused by RAPID accumulation of
fluid (usually blood) in the pericardial sac.
As intra-pericardial pressure increases, cardiac output isimpaired because of decreased venous return.
Classic signs are: BECKs Triad: muffled or distant heartsounds, hypotension, elevated venous pressureand may notpresent until the patient is hypovolemic and hypotensive.
Pulsus paradoxus= a decrease in systolic blood pressureduring spontaneous respiration.
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Cardiac Tamponade Causes: penetrating trauma to chest, blunt
trauma to chest. Diagnosed with FAST ( focused abdominal
sonography or pericardiocentesisdontwith 16 or 18 gauge cath over needle and35 ml syringe and 3 way stopcock)
Aspirated pericardial blood usually will not
clot unless the heart has been penetrated.
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Cardiac Tamponade cont.. Arterial BP can dramatically improve
with as little as 15-20 ml of bloodremoved.
Nurses should anticipate and preparefor pericardiocentesis in the eventof cardiac arrest.
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Pulmonary Contusion Results from blunt or penetrating
trauma to the chest One of the most common causes of
death after trauma Predisposes the patient to pneumonia
and ARDS.
Can be difficult to detect.
P l C t i t
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Pulmonary Contusion cont..
May not be seen on initial X-ray Infiltrates and hypoxemia may not occur
for hours of days.
Clinical presentation includes: chestabrasions, ecchymosis, bloody secretions,PaO2 of 60mmHG or less on room air.
Often associated with flail chest and rib
fractures
Pulmonary Contusion
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Pulmonary Contusioncont..
The bruised lung becomes edematous,resulting in hypoxia and respiratorydistress
Treatment is ventilatory support,careful fluid administration, painmanagement.
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Rib Fractures cont Treatment: Depends on ribs Fxd and
age of patient. Elderly with multiplerib fx may require hospitalization.
Patient Teaching is very important:
DO NOT restrict chest movement, pain
control, ambulation.
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Flail Chest Usually caused by blunt force trauma, EX: Chest
hits steering wheel. Three or more adjacent ribs are fractured. Flail section floats freely resulting in paradoxical
chest movement. Flail section contracts INWARD with inspirationand expands OUTWARD with expiration.
Treatment: Intubation/mechanical ventilation,frequent pulmonary care, aggressive pain
management.
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Aortic Disruption Produced by blunt trauma to the chest Ex: rapid deceleration from head-on MVA,
ejection, or falls.
Four common sites of dissection: the leftsubclavian artery at the level of theligamentum arteriosum, the ascendingaorta, the lower thoracic aorta above thediaphragm, and avulsion of the innominate
artery at the aortic arch.
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Aortic disruption cont.. Signs: weak femoral pulses, dysphagia,
dyspnea,hoarsness, pain. Chest x-ray shows wide
mediastinum(greater or equal to 8mm),tracheal deviation to the right, depressedmainstem bronchus, first and second ribfractures, left hemothorax.
CONFIRMATION is done with aortogram
Treatment is SURGICAL
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Spinal Cord Injury Mechanism of injury can be:
hyperflexion, hyperextension, axialloading, rotation, penetrating trauma
Initially: ABCs, immobilization
Triage to appropriate facility
Complete sensory &motor neuro exam
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Spinal Cord Injury Lateral C-Spine films, possible Spinal
CT to rule out occult fracture. Dislocations of the spine are reduced
ASAP Postural reduction with tongs, halo
traction or surgical fusion.
IV methylprednisolone within 8 hours
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Spinal Cord Injury Spinal Shock= loss of sympathetic
output=Neurogenic shock results arebradycardia, hypotension.
Need vasopressors to compensatefor loss of sympathetic innervationand resultant vasodilatation.
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Spinal Cord Injury cont. Potential Complications: GI dysfunction,
autonomic dysreflexia, DVT, orthostatichypotension, loss of bowel and bladder
function, immobility, spasticity, andcontractures.
THINK EARLY PREVENTION ANDINTERVENTION!!!!
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Head Injury Can be caused by blunt or
penetrating trauma.
Lacerations to the scalp produceprofuse bleeding.
Fractures of the skull may have
underlying brain injury
Heady Injury cont
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Heady Injury cont
Basilar skull fractures are located atthe base of the cranium andpotentially involve 5 bones that formthe base of the skull.
Are diagnosed based on the presenceof CSF in the nose (rhinorrhea) orears (otorrhea)
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Heady Injury cont.. Basilar Skull Fracture cont Ecchymosis over the mastoid
(Battles sign) Hemotympanium (blood in the middle
ear) Raccoon eyes or periorbital
eccymoses =cribiform plate fracture
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Head Injury cont. Potential complications of Basilar
Skull Fractures: Infection and cranialnerve injury.
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Secondary Head Injury Refers to the systemic (hypotension,
hypoxia, anemia, hypocapnia,hyperthermia) or intracranial (
edema, intracranial hypertension,seizures, vasospasm) changes thatresult in alteration in the nervoussystem..page 657..read this!!! Veryimportant.
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Secondary Head Injury Prehospital MOST important Supplemental oxygen, often intubation Aggressive and careful volume replacement
ICP monitoring/ Goal is 20mm Hg Cerebral Perfusion Pressure=MAP(mean
arterial pressure) Minus Mean ICP andkeep at 70mm Hg to decrease neurologicaldisability.
Secondary Head Injury
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Secondary Head Injurycont..
Osmotic and loop diuretics, CSFdrainage, hyperventilation (results invasoconstriction of cerebral vesselsallowing more space for swelling braintissue), paralysis WITH sedation,pentobarbital induced coma is final
intervention when all else fails.
Nursing Care for
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Nursing Care forTraumatic Head Injury
Airway, adequate ventilation and gas exchange,clearance of pulmonary secretions, proper headalignment, close neurological function monitoring.
Pulmonary complications are common, aggressive
pulmonary hygiene HOB at 30 degrees Assess for intracranial hemodynamics(ICP and
perfusion pressure) and patient tolerance
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Musculoskeletal Injuries See Types of Fractures Table 18-7 on
page 658 Extremity Assessment= the 5 Ps
Pallor pain, pulses, parethesia, paralysis(describes the neurovascular status of theinjured extremity.
When possible the injured extremity if
compared with the non-injured extremity
Musculoskeletal Injury
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Musculoskeletal Injurycont..
Fracture wounds should be debridedand the fracture reduced within 18hours to prevent infection andnonunion.
If hemodynamically unstable, skeletaltraction to realign the extremity maybe used .
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MS Cont.. Unstable Pelvis fractures can be life
threatening secondary to potentialfor severe hemorrhage,exsanguination, damage togenitourinary system and sepsis.
Traumatic Soft Tissue
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Traumatic Soft TissueInjury
Categorized as: contusions, abrasions,lacerations, punctures, hematomas,amputations, and avulsions.
All wounds are considered contaminated. Tetanus Toxoid and antibiotics are always
CONSIDERED.
Complications of
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Complications ofMusculoskeletal Injuries
Rhabdomolysis-a complication ofcrush injuriesmarkedvasoconstriction and hypotension
followed by ARFResults from muscle destruction.Myogolobin and potassium are released
from the damage muscles
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Cont.Can result in life threatening hyperkaemia.
Myoglobin excreted through the urine,combined with hypovolemia, produces ARF
and ATN if not aggressively treated.Treatment= Aggressive saline replacement,
alkalinization of urine, osmotic diuresis.
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Compartment Syndrome Places the patient at risk for limb
loss. More common in the legs and
forearms but can occur other places. The closed muscle compartment
contains neurovascular bundles
tightly covered by fascia.
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Cont An increase in pressure within that compartment produces
the syndrome. Internal sources= hemorrhages, edema, open or closed
fractures, crush injuries External sources=PASGs, casts, skeletal traction, air
splints. The pain is described as throbbing appearingDISPROPORTIONATE TO THE INJURY. Increases withmuscle stretching. The affected area is firm to touch.Paresthesia distal to the compartment, pulselessness, andparalysis are LATE signs.
Treatment s immediate surgical fasciotomy.
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Fat EmbolismUsually associated with long bone, pelvis, and
multiple fractures.Usually develops within 24 to 48 hours after injury.Hallmark clinical signs: low grade fever, new onset
tachycardia, dyspnea, increased resp rate andeffort, abnormal ABGs, thrombocytopenia andpetechiae.
Development of lipuria (fat in the urine) indicates
severe fat embolism syndrome.
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Fat embolism cont.. Prevention is the best treatment. Treatment is directed at preserving
pulmonary function and maintenance
of cardiovascular function. Careful attention to EKG changes. See Box 18-2 on page 660
IMPORTANT!!!
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Abdominal Injuries The Classic sign is PAIN. But may be obscured by AMS, drug
or alcohol intoxication, Spinal cord
Injury with impaired sensation The liver is the most commonly
injured organ from blunt or
penetrating trauma
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Cont Liver injuries are graded I through VI.
Splenic injury most commonly occurs fromblunt trauma but can be caused by
penetrating trauma. Presentation: LUQ tenderness, peritoneal
irritation, referred pain to the left
shoulder (Kerrs sign)
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Cont Graded I to V. Diagnosed with FAST, Abd. CT or
peritoneal lavage. Patients more at risk for
pneumococcal disease and shouldhave immunization with in first few
post op days after splenectomy
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ContKidney Injury Usually attributed to blunt trauma
Presentation may include CVA
tenderness, microscopic or grosshematuria, bruising, ecchymosis overthe 11thand 12thribs, hemorrhage orshock.
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Cont Diagnostic testing= IVP, CT scan,
angiography, cystoscopy.
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Critical Care Phase ABCc Post OP standard VS= q5min x3,
q15minx3, q30min X2, q1 hour
forward. Shivering is to be avoided=increase in
metabolic rate and increase in oxygen
demands.
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Damage Control Surgery = Staged laporaotmy
Trying to avoid hypothermia,
acidosis, coagulopathy Shown to improve outcomes ofcritically ill patients with sever intra-abdominal injuries.
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ARDS Chapter 13 fully covers
May occur 2 to 48 hours after
traumatic injury, however sometimesup to 5 days or more beforeRECOGNIZABLE clinical signs.
There are direct and indirect causes.
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Cont Clinical Manifestations: hypoxemia, rising
CO2 levels, tachypnea, dyspnea, pulmonaryhypertension, decreased lung compliance,new diffuse bilateral lung infiltrates.
Treatment: correction of underlyingcause---maximize O2 to the tissues,decrease pulmonary congestion, preventfurther lung damage, supportcardiovascular system.
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DVT Increased incidence of DVT= patients with
obesity, age, malignancy, pregnancy, heartfailure, SCI, recent surgery, extremity
fractures, pelvic fractures, history ofDVT, prolonged immobilization, resp.failure, # of transfusions,central venouscatheterization, vascular injury.
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Cont.. Clinical Manifestations= pain and
tenderness, swelling fever, venousdistention, palpable cord, discoloration, +
Homans sign Treatment= prevention, prophylaxis, early
ambulation, sequential compressiondevices, filter placement in the inferiorvena cava.
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Cont. Pulmonary embolism is an often fatal
complication of DVT Clinical manifestations of PE= sudden
onset dyspnea, sudden onset chest pain,rapid shallow resps, SOB, Auscultation ofbronchial breath sounds, pale, dusky orcyanotic skin, Anxiety, decreased LOC,signs of hypovolemic shock (decreased BP,narrowing pulse pressure, tachycardia)
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Infection Pulmonary
Catheter Sepsis
Sinusitis
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Acute Renal Failure From systemic effects of trauma
OR from actual injury to the renalsystem
There is a reduction in renal bloodflow in the trauma patient associatedwith shock or low cardiac output.
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Altered NutritionNutritional demands are increased in the
trauma patient by alterations inmetabolism
Metabolism is increased by activation of thesympathetic response.
Ebb (1st24-48 hours after injury) and FlowPhase (peaks 5-10 days after injury)
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Cont. Because of this increased need the
patient may demonstrated:decreased body mass, increased O2consumption, increased CO2production, delayed wound healing,and a weakened immune system
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Cont.. Anthropometric measurements
Nutrition replacement in 24 to 48hours.
Route based on individual status ofpatientcan be enteral, or parenteral
Multiple Organ
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Dysfunction Syndrome Immune, inflammatory, and hormonal responses
are underlying causes. Defined as presence of altered organ function in
the acutely ill.
There is incomplete understanding of itspathophysiology.
Management focuses on prevention, earlyidentification, elimination of sources of infection,maint. Of tissue oxygenation and nutritionalsupport.