Trauma

Front 1

Pneumothorax

Back 1

-Tracheal shift on external exam is a late sign pre-arrest sign of tension pneumo
-Kinking of the vena cava with acute preload decrease is the primary mechanism which precipitates cardiovascular collapse
-Positive pressure ventilation can exacerbate a pneumothorax by placing pressure on the vena cava and decreasing venous return
-Tube thoracostomy is the definitive treatment

Front 2

Needle decompression

Back 2

-Treatment of a tension pneumothorax includes immediate needle decompression
-an 18- to 20-gauge over-the-needle catheter (angiocatheter) is inserted into the second intercostal space just over the top of the third rib at the midclavicular line.
-a 5- to 10-mL syringe should be attached to the angiocatheter.
-The syringe is aspirated gently as the needle is advanced.
-A loss of resistance or a rush of air will be apparent as soon as the pleural space is entered.
-If pneumothorax is confirmed, a one-way drainage device should be attached. The respiratory distress should improve markedly when the pneumothorax is decompressed
-2nd intercostal, mid-clavicular
-4th intercostal, anterior to mid-axillary
-5th intercostal, anterior to mid-axillary and mid-scapular
-Risks include penetration of subclavian artery/vein, liver, gallbladder, spleen, pancreatic injury and nerve paresthesias
-Inferior margin of each costal will have a costal artery, vein, and nerve bundle
-Avoid inferior costal margin and walk a needle over the top of rib
-Absent breath sounds on one side are justification for decompression
-Tracheal shift is much too late a sign to wait for prior to decompression

Front 3

Thoracic tube thoracostomy

Back 3

-Is a flexible plastic tube that is inserted through the side of the chest into the pleural space. It is used to remove air (pneumothorax) or fluid (pleural effusion, blood, chyle), or pus (empyema) from the intrathoracic space
-The free end of the tube is usually attached to an underwater seal, below the level of the chest. This allows the air or fluid to escape from the -pleural space, and prevents anything returning to the chest
-2nd intercostal space, mid-clavicular line
-4th intercostal space, anterior axillary line
-5th intercostal space, mid-axillary line
-5th intercostal space, anterior axillary line

Front 4

Thoracic tube thoracostomy

Back 4

-Inferior margin of each costal will have a costal artery, vein, and nerve bundle
-Avoid inferior costal margin and walk a needle over the top of rib
-All chest tubes have a radiopaque indicator line along their long axis
-A break in this line should be at the most proximal port on the insertion end
-The break should be visualized inside the pleural space to verify adequate depth of insertion
-A constant irresolvable air leak with a good chest tube should lead you to suspect tracheobronchial disruption
-Placing an ETT with a cuff beyond the disruption is the definitive therapy for a tracheobronchial disruption
-Adjust Vt to one lung ventilation (OLV)
-Place patient in lateral position with ventilated lung in dependant position

Front 5

Hemothorax

Back 5

-Signs include tachycardia, hypotension, and altered LOC
-Hypovolemic shock and arrest would precede any tracheal deviation
-Cyanosis is a late sign
-Hemoglobin needs to be greater than 5g/dl for cyanosis to be detectable

Front 6

Sucking chest wound

Back 6

-If open chest defect is more than 1/3rd the size of the glottic opening (the narrowest part of the airway), air will preferentially entrain (to “suck”) via the defect instead the trachea
-Immediate occlusion of the defect is indicated
-Dressing should be placed at end-exhalation to minimize trapped air in the pleural space
-Preferably a forced end-exhalation to allow venting of as much air as possible from the pleural space
-Mechanically ventilated patient should be occluded at end-inhalation
-Tape three sides to create a ‘flapper valve’, once a chest tube in place all air management is to be done via the chest tube and the fourth side should be taped
-Flail segment management includes fluid restriction, PEEP, turn the patient injured side down and analgesia

Front 7

Pericardial tamponade

Back 7

-Condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed).
-If the fluid significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling properly
-Caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardium
-Pulsus paradoxus is changes in pulse quality as the patient breaths is typical of early tamponade
-Narrowing pulse pressures occur
-Initial pathology causes diastolic failure or failure to fill the ventricles
-Late pericardial tamponade = pericardiocentesis
-Beck's triad Hypotension occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid inside the pericardium, and narrowing pulse pressure
-Early management involves pushing fluids or to augment preload, Percardiocentesis is the definitive treatment

Front 8

Aortic rupture

Back 8

-Condition in which the aorta, the largest artery in the body, is torn or ruptured as the result of trauma
-Results in harsh systolic murmur at all commonly auscultated cardiac sound locations
-An AP Chest x-ray primary finding of aortic disruption is a widened mediastinum
-Classic presentation of aortic aneurysm is pain that is severe, across the back, constant, ripping or tearing in nature without relief

Front 9

Scaphoid abdomen = diaphragmatic rupture/hernia

Back 9

-In Diaphragmatic rupture the patient’s bowel is in the chest where his lungs are
-Removing any and all air from the bowel via NG/OG is essential to maximizing oxygenation and ventilation
-Classic signs include scaphoid abdomen, bowel sounds in the thoracic cavity, and dyspnea

Front 10

Esophageal perforation

Back 10

-Bleeding into the esophagus and stomach
-Blood irritates the stomach and prompt vomiting
-Vomiting can be corrosive and cause high pressures leading to esophageal perforations
-Management includes NG/OG placement, antiemetic and antibiotic administration

Front 11

BP and Blood loss

Back 11

-BP will drop until the a blood loss of more than 30-40%
-Rapid infusion use catheter with biggest bore and shortest length
-Best IV solution in an acute phase is LR
-A crystalloid solution that is ideally isotonic should be used
-Best most reliable indicator for progression of shock is increased heart rate
-Blood loss should be replaced with crystalloid solutions in a ratio of 3:1
-2/3rds of crystalloid will ‘third-space’ to the interstitium rapidly

Front 12

Blasts involve three injuries:

Back 12

-Primary are caused by initial blast wave striking the body and compressing air filled spaces causing ruptures
-Secondary are caused by debris or shrapnel form the explosive device
-Tertiary are caused by body being knocked to the ground with subsequent blunt trauma

Front 13

Cyanide toxicity

Back 13

-Principal toxicity results from inactivation of cytochrome oxidase (at cytochrome a3), thus uncoupling mitochondrial oxidative phosphorylation and inhibiting cellular respiration, even in the presence of adequate oxygen stores
-Cellular metabolism shifts from aerobic to anaerobic
-With the consequent production of lactic acid
-Tissues with the highest oxygen requirements (brain and heart) are the most profoundly affected by acute cyanide poisoning
-Should be considered with any confined space fire involving synthetic fibers (carpet, clothing, plastics

Front 14

Burns

Back 14

-Head = 9% (front 4.5, back 4.5)
-Chest (front) = 9%
-Abdomen (front) = 9%
-Upper/mid/low back and buttocks = 18% (upper back 9, lower back and butt 9)
-Each arm = 9% (front 4.5, back 4.5)
-Each palm = 1%
-Groin = 1%
-Each leg = 18% total (front = 9%, back = 9%) (thigh 4.5, tib/fib 4.5)

Front 15

Parkland formula:

Back 15

-Only calculate areas with 2nd and 3rd degree burns
-4ml/kg/%BSA = fluid resuscitation for 1st 24hrs
-divide answer by 2, Half of resuscitation given in 1st 8 hrs
-divide answer by 8 to get ml/hr for first 8 hours

-Consensus burn formula
2-4ml/kg/%BSA

Front 16

Ideal urine output:

Back 16

-0.5ml/kg/hr for adults
-1.0ml/kg/hr for peds
-2.0ml/kg/hr for neonates
-Failure to perfuse the kidneys as in shock precipitates pre-renal failure

Front 17

Alkali metals

Back 17

-Considered worse because they denature lipids into soap
-Are very reactive with water and copious amounts antagonize the reaction and potentially cause ignition and fire
-Acid burns cause coagulative necrosis
-Calcium gluconate used to neutralize only hydrofluoric acid
-All other acid irrigate with water

Front 18

Decontamination

Back 18

-“fast-break scenario” is where contaminated victims are attempting to leave the hot-zone to save themselves
-Perform two-step decontamination
-Direct the victim to stop, undress and be washed with clean water and soap
-The step out of the run-ff and wash be repeated a second time

Front 19

Myoglobinuria

Back 19

-Myoglobin is like hemoglobin but in the cells, and its function is to store oxygen for intracellular needs
-Myoglobinuria will result in renal failure if it is not dealt with aggressively and efficiently
-When tissue is destroyed myoglobin enters the bloodstream,
-It is a relatively large ‘sticky’ molecule and thus ‘clogs or gums up’ the glomerulus and nephrons of the kidneys
-rhabdomyolysis is myoglobin in the urine (myoglobinuria) and associated with any pathology that results in muscle breakdown
-Must be anticipated and treated aggressively with electrical burns, thermal burns, and any form of massive trauma or crush injury
-It can occlude the renal filtration system leading to acute tubular necrosis and acute renal insufficiency

Front 20

Myoglobinurea cont

Back 20

-NaHCO3 creates an alkaline environment, inhibits myoglobinuria from binding to other proteins making it easier to pass through the glomerulus of the kidney
-To keep the filters clean we need to aggressively flood the kidneys with fluid (“The solution to pollution is dilution”) and alkalinize the environment to minimize the adhesiveness of the myoglobin
-This will allow it to break into smaller particles for filtration and subsequent elimination
-Increase diuresis with lasix or mannitol, Alkalinize with NaHCO3
-Increase fluid administration to maintain urine output of 2ml/kg/hr

Front 21

START triage

Back 21

-Black tag = priority 0 = deceased DOS
-Red tag = priority 1 = level I immediate
-Yellow tag = priority 2 = level II delayed
-Green tag = priority 3 = level III walking wounded
RPM:
-Respirations-absent, normal abnormal
-Perfusion (pulse)-cap refill being normal, delayed, or absent
-Mentation-normal, abnormal, absent
15 sec assessment

Front 22

CBC (complete blood count)

Back 22

-RBC 5
-Hgb 15
-Hct 45
-WBC 5-10K
-Plt 150-400K
-RBC value and multiply times 3 for the Hgb and again for Hct

Front 23

CHEM 7

Back 23

-Na 135-145
-K 3.5-5
-Cl 95-107
-TC02 22-26
-BUN 10
-Cr 1
-Gluc 70-110

Front 24

H&H

Back 24

The hematocrit (Hct) identifies how much of the blood is particulate or “stuff”, like RBC, WBC, platelets, etc…
About 45% of blood is stuff and not plasma
H&H refers to Hgb and Hct in that order
H&H will increase by a factor of 1 & 3 with each unit of PRBC
Primary serum protein is albumin, globulin is second
RBC’s are made of protein and participate in binding medications and acids as well

Front 25

PRBC’s

Back 25

-are stabilized and preserved with citrate
-Lowers 2-3DPG levels
-If blood administration is exceeding 1ml/kg/min or one unit every 5 min consider citrate toxicity and administer calcium
-Rapid administration of PRBC should cue you to monitor the EKG for signs of hyperkalemia
-K levels can climb to 17-24 mEq/l
-Universal donor is O neg
-Universal recipient is AB pos
-Solution which contains RBC and clotting factors would be whole blood
-Hemolytic reactions occur within few min of initiating a transfusion causing hyperthermia and back pain
-Stop the infusion or can lead to DIC

Front 26

DIC (disseminated intravascular coagulopaphy)

Back 26

-Disseminated intravascular coagulation, or DIC, is a serious disruption in the body’s clotting mechanism.
-Normally, the body forms a blood clot in reaction to an injury.
-With DIC, the body overproduces many small blood clots throughout the body, depleting the body of clotting factors and platelets.
-These small clots are dangerous and can interfere with the blood supply to organs, causing dysfunction and failure.
-Massive bleeding can occur due to the body’s lack of clotting factor and platelets.
-DIC is life-threatening and needs to be treated promptly.
-A pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases
-Leads to the formation of small blood clots inside the blood vessels throughout the body
-As the small clots consume all the available coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs
-Extrinsic pathway is triggered by tissue thromboplastin which is released when there is tissue damage
-Found highest in brain and placenta
-High incidence of DIC in head injuries and placental injuries

Front 27

DIC (disseminated intravascular coagulopaphy)

Back 27

-Collagen exposure in the endothelium is the primary trigger for the intrinsic side of the cascade
-Think of DIC as a patient bleeding to death
-Process of clotting and incomplete clot breakdown that actually causes the systemic death
-Small clot fragment collect in the microvasculature of the brain, liver, spleen, kidneys, and lungs limiting blood flow with subsequent organ failure
-Will demonstrate a high D-dimer, low fibrinogen levels( as the clotting factors are used up), a high PT and aPTT (they cant stop bleeding as clotting factors are used up), and high FSP’s (fibrin split products, aka FDP’s fibrin degradation products) which are the remnants of clots breaking up
-When treating DIC correct the underlying problem

Front 28

Treatment

Back 28

-Treatment of DIC depends on identifying and treating the underlying cause quickly. Your doctor may give you certain blood products or medications to treat your condition.
-Sepsis is usually treated with antibiotics.

Blood Products:
-Fresh frozen plasma is used to replace low levels of coagulation factors caused by DIC.
-Platelets may also be given to restore low levels.
-Cryoprecipitates may also be used to correct low levels of fibrinogen.

Heparin:
Heparin is a blood thinner.
-heparin given in combination with blood products to reduce blood clots.

Antithrombin III:
-This medication is sometimes used to slow down clotting in certain patients.

Prevention:
-To help reduce your chances of getting DIC, make sure you obtain prompt treatment for any of the conditions that can cause this disorder.