Trauma Flashcards

1
Q

Pathophys of hemorrhagic shock?

A
  • imbalance occurs between systemic O2 delivery and O2 consumption
  • hemodynamic instability, coagulopathy, decreased O2 delivery, decreased tissue perfusion, and cellular hypoxia
  • initial response: macrocirculatory & mediated by neuroendocrine systemHormones release:
    • renin,
    • angiotensin,
    • vasopressin,
    • antidiuretic hormone,
    • growth hormone,
    • glucagon, cortisol,
    • epinephrine, and
    • norepinephrine
  • sets stage for microcirculatory response
  • Renal and adrenal system produce renin, angiotensin, aldosterone, cortisol, erythropoietin, catecholamines
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2
Q

What is the shock cascade?

A
  • ischemia of any area of the body triggers an inflammatory response that impacts non-ischemic organs even after adequate perfusion restored
  • individual ischemic cells respond to hemorrhage by taking up ISF, which further depletes intravascular fluid.cellular edema may choke off adjacent capillaries and result in no-reflow phenonmenon
    • this prevents reversal of ischemia even with adequate macroperfusion
  • Ischemic cells produce lactate and free radicals and inflammatory factors–> causes direct damage to cell and washes back to central circulation when flow reestablished
  • sets up for SIRA/MOF
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3
Q

What arethe CNS and cardiac response to hemorrhagic shock?

A
  • CNS: prime trigger of neuroendocrine response
    • controls selective perfusion to heart, kidney, brain
    • reflexes and cortical electrical activity are both depressed; reversible with mild hypoperfusion
    • someone obtunded/poor neuro exam following trauma- bad sign of injury. typically reversible
  • Cardiac: preserved from ischemia
    • lactate, free radicals, and other humoral factors released by ischemic cells all act as negative inotropes
    • Cardiac dysfunction is LATE SIGN and often a terminal event
    • patient with cardiac dx/direct cardiac trauma is great risk for decompensation d/t fixed SV, which inhibits the body’s ability to increase blood flow
    • in healthy person, blood flow to heart preserved
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4
Q

Pulmonary response to hemorrhagic shock

A
  • Pulmonary: filter of the inflammatory byproducts of ischemia
  • immune complex and cellular factors accumulate in pulm capillaries and lead to neutrophil and PLT aggregationwhich cause
    • increases capillary permeability
    • destruction lung architecture
    • ARDS
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5
Q

What is the renal response to hemorrhagic shock?

A
  • Renal/ adrenal: neuroendocrine response
    • GFR maintained with selective vasoconstriction
  • prolonged hypotension leads to decreased cellular energy and inability to concentrate urine (renal cell hibernation)
  • followed by patchy cell death, tubular epithelial necrosis, renal failure
  • blood flow concentrated to medulla and cortical areas
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6
Q

What is the gut, liver, and skeletal muscle response to hemorrhagic shock?

A
  • Gut: one of the earliest organs affected by hypoperfusion; may be the prime trigger of MSOF
    • intestinal cell death causes breakdown in barrier function of cut
    • causes increased translocation of bacteria to liver and lungs
      • can potentiate ARDS
  • Liver: failure of synthetic function of the liver after shock-> lethal
    • if you see liver failure after shock, poor prognosis for patient
  • Skeletal muscles: release lactic acid and free radicals; tolerate ischemia better than other organs
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7
Q

What encompasses the initial trauma assessment?

A
    1. Initial rapid assessment: (out in field) stable vs unstable
      * are they dying? dead?
  1. Primary survey: ABCDE: airway, breathing, circulation, disability, exposure
  • ABCs of airway patency, breathing and circulation
    • Airway- obstruction? airway maneuver? intubate?
    • Breathing- high flow o2? trachea ML? flail chest (3 or more fx segments of ribs) tension pneumo? massive hemothorax= 1500 cc blood
    • Circulation- skin temp, color, 2 large bore IVs, fluid, uncrossmatched blood
    • D- disability
      • Brief neuroexam
    • E- exposure
      • undress and inspect ventral and dorsal for all external injuries overlooked

decision made to proceed immediately to sx or continue on to secondary survey

  1. Secondary survey: detailed multi-system exam an history; further dx eval

​more about what happened, detailed exam, dx eval, medical hx

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8
Q

Steps in initial airway survey in trauma?

A
  • Stabilize C-spine
  • Provide oxygen (100% until ABG)
  • Initial steps for obstruction if spontaneously breathing:
    • chin lift
    • jaw thrust
    • suction
    • place OPA or NPA (+/-)
      • NO nasal airway or nasal ETT if possible basilar/ cranial base skull fx or maxillofacial injury- can enter cranial vault or orbit symptoms: battle sign, raccoon eyes, or bleeding from the ear or the nose…signs may not be immediately apparent
  • Symptoms of airway obstruction:
    • Notable Airway edema/direct airway injury
    • Cervical deformity
    • Cervical hematoma
    • Foreign bodies
    • Dyspnea, hoarseness, stridor, dysphonia
    • Subcutaneous emphysema & crepitation
    • Hemoptysis/active oral bleeding/copious secretions
    • Tracheal deviation
    • Jugular vein distention
    • Hemodynamic condition
  • Still inadequate? Consider BMV to assist spontaneous breathing
  • Consider SGA (short term)
  • Proceed to intubation: awake vs. RSI vs. cricothyroidotomy
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9
Q

What are some modifications to difficult airway algorithm in trauma?

Max amount of DL when establishing AW in trauma?

A
  • safety first! no option to awaken the patient as in ASA emergency airway algorithm
  • if something doesn’t work, change something!
  • Best choice: RSI with cricoid pressure for patient without serious airway problems VERSUS awake intubaiton with sedation and topical anesthesia, if possible, for those with anticipated difficult airways
    • Topicalization may be impossible for awake intubation- many of these patients are uncooperative or unstable- awake FOB may not be possible
      • locate cricothyroid membrane (consider marking),
      • pre-oxygenate,
      • perform RSI
      • then take a look with video laryngoscopy and attempt intubation (+/-bougie attempt)
      • consider SGA but do not delay
      • proceed to cricothyrotomy if no view
  • Max amount: 2 DL
    • cant wake up patient
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10
Q

Considerations for cricothyroidotomy in trauma patient?

A
  • with cspine stabilization, not able to get prime visualization of cricoidthyroid membrane
    • palpate thyoid/adam’s apple and go just below cartilage
    • go through lower 1/3 cricothyroid membrane to avoid thyroid/VC
    • Go in with 45 degree angle with angiocath
  • Possible contraindications to cricothyroidotomy
    • age younger 12 yo
    • suspected larngeal trauma/fracture
  • conversion to tracheostomy considered later (within 72 hours)
  • cric is not definitive airway
  • traheostomy not a great option initially because it takes longer than cric and requires neck extension
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11
Q

What are some considerations with the use of the jet ventilator?

A
  • Jet ventilator. Black triangle shows the high-pressure ventilation tubing that attaches to standard wall oxygen outlet 50 psi working pressure.
    • potential for barotrauma!
  • Ventilation block (white arrow) is used to control oxygen flow through tubing to a catheter, which is inserted in the airway.
  • Employs Venturi effect: the jet stream of fresh gas creates a pressure gradient and the pressure gradient generates a negative pressure entrainingflow.
    • will get good oxygenation but not good exchange.
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12
Q

What are some strong indicators for ETT intubation upon arrival with traumas?

A
  • Airway obstruction
  • hypoventilation
  • persistent hypoxemia (Sao2 <90%) despite supplemental oxygen
  • severe cognitive impairment (GCS <8)
  • Severe hemorrhagic shock
  • cardiac arrest
  • smoke inhalation with any of the following
    • airway obstruction
    • severe cognitive impairment (GCS <8)
    • major burn (>40%)
    • major burns and/or smoke inhalation with prolonged transport time
    • impending airway obstruction
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13
Q

What are some discretionary indications for ETT in trauma patient?

A
  • Facial or neck injury with potential for airway obstruction
  • moderate cognitive impairment (GCS >9-12)
  • Persistent combativeness refractory to pharmacologic agents
  • Respiratory distress (without hypoxia or hyperventilation)
  • perioperative mgmt (pain control, painful preoperative procedures)
  • SCI (complete cervical injury at C5 level of above) with any evidence of respiratory depression
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14
Q

Airway mgmt with c-spine injury?

A
  • All airway maneuvers cause c-spine movement
    • Rigid collar is not enough
    • Manual inline stabilization (MILS) is preferred
  • Caution: unopposed vagal tone during airway manipulation
    • severe bradycardia and dyrrhythmias may result from the unopposed vagal activity during trahceal intubation or suctioning
      • preoxygenate and premedicate
  • there is NO airway manipulation technique that prevents movement of c-spine
    • anytime you do laryngoscopy, you will cause c-spine movmenet
    • still need MILS, collar etc
      • remember airway manipulation causing c-spine injury is incredibly rare.
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15
Q

What is manual inline stabilization technique?

A
  • two people optimally in addition to anesthesia provider
  • first assistant stabilizes and aligns the head in neutral position without applying cephalad traction
  • second person stabilizes both shoulders by holding them against the table or stretcher (prevents rotational mvmt)
  • anterior portion of the hard collar may be removed after immobilization to improve mouth opening
  • MILS can obstruct glottic view
  • some relaxation of the MILS to improve the glottic view when visualization of the larynx is restricted
    • mention submental intubation in maxillofacial injuries
  • even with video laryngoscope causes cervical spine mvmt
    • ​has not benes statistically sig in studies comparing DL to VL
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16
Q

S/S of blunt airway injuries?

Managmeent of blunt airway injuries?

A
  • symptoms:
    • hoarseness
    • muffled voice
    • dyspnea
    • stridor
    • dysphagia
    • odynophagia
    • cervical pain and tenderness
    • ecchymosis
    • subcutaneous emphysema
    • flattening of the Adam’s apple
  • Considerations:
    • DL can worsen; may enter false passage
    • CT before airway intervention if stable
    • Preferred airway management: FOB or surgical airway
    • 70% of blunt airway injuries also have C-spine injuries
    • can also have vascular injury, may cause hematomas which may obstruct the airway.
  • Blunt airway injuries can be missed
  • Blunt thoracic trauma that arrives pulseless has <1% survival
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17
Q

S/S of penetrating airway injury?

management?

A
  • Symptoms (more overt)
    • air bubbling through wound
    • hemoptysis,
    • coughing
  • management varies:
    • ETT inserted in wound
    • tracheostomy distal to wound
    • oral intubation (if injury high in the airway)
  • Penetrating thoracic trauma with signs of life has decent survival
  • ED thoractomy usually done for penetrating airway but NOT blunt
  • allows for external cardiac massage, emergency drainage of pericardial blood, clamping of great vessel bleeding
  • can resuscitate with catheter directly in right atrium
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18
Q

S/S tension pneumothorax?

Treatment?

A
  • Symptoms:
    • cyanosis
    • tachypnea
    • hypotension
    • neck vein distention
      • may be absent in hypovolemic patients
    • tracheal deviation
      • may be difficult to appreciate
    • diminished breath sounds affected side
  • No time for xray/CT to confirm
  • Treatment: needle decompression vs chest tube
    • Needle decompression=2nd ICS MCL- walk off third rib to do decompression in order to miss artery/nerve that run on superior portion of 2nd ICS
    • CT= Mid-axillary line 5th intercostal space
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19
Q

What is a flail chest? Anesthetic considerations?

A
  • two or more sites of at least three adjacent ribs
    • rib fractures associated with costochondral separation or sternal fracture
  • Deterioration due to flail chest develops over 3-6 hours
  • ARDS likely is lung contusion >20%
  • Automatic intubation not recommendedbetter to focus on analgesia to maintainadequate excursion and ventilation/ oxygenation
    • epidural or thoracic paravertebral blocks preferred along with O2 supp and non-invasive PPV.
  • Consider co-existing trauma in flail chest (hemo/pneumothorax)
20
Q

Treatment for hemorrhagic shock?

When should you suspect hemorrhagic shock?

Mgmt?

A
  • Definitive treatment: operative control of bleeding at source
    • Expect major bleeding:
      • Falls >6 feet,
      • high energy deceleration injury, and
      • high velocity GSW
  • Free fluid on X-ray, FAST, or CT warrants immediate intervention
  • MGMT
    • Ideal SBP 100-110mmHg
      • ​appreciate that you can have 1500-2000 blood loss before you see decrease in SBP
      • in elderly patient, important to maintain 100-110. 90 still ok in younger/healthier pt
    • Tachycardia not always a reliable indicator
      • ​absent in up to 30% of traumas
      • cofounder is Bezold-Jarisch reflex, chronic cocaine, vagal stimulation
        • injury without compensation of tachycardia increases mortality
    • Follow lactate, base deficit
      • Intraop endpoints of resuscitation
    • Goal hgb 7-9g/dL
21
Q

What does base defiict tell us?

A
  • more reliable than pH
  • reflects
    • severity of shock
    • oxygen debt
    • changes in o2 delivery
    • adequacy of fluid resus.
    • likelihood of MOF
  • Severity of base deficit
    • mild= 2-5
    • moderate 6-9
    • severe >10
22
Q

Normal lactate?

A

0.5-1.5mmol/L

>5mmol/L indicates significant lactic acidosis

23
Q

What are damage control principles in trauma?

A
  • 1st phase (arrival): recognition of severity of injury; control of bleeding; rapid transport to the OR
    • Limiting crystalloids,
    • permissive hypotension,
    • active rewarming,
    • early administration of FFP and platelets at high ratios with PRBCs
  • 2nd phase (in OR)
    • surgeons rapidly control bleeding; leave abdominal cavity open
    • goals-
    • maintain intravascular volume
    • temperature
    • acid-base status
    • coagulation
  • 3rd phase: ICU management with same goals as 2nd phase
  • 4th phase: multiple returns to the OR at 24- to 48-hour intervals for organ repair, abdominal washout, and debridement
24
Q

How is fluid resuscitation managed in the damage control phase of trauma?

A
  • DAMAGE CONTROL:
    • brief permissive hypotension
      • not possible in TBI, SCI, or in elderly with chronic HTN
    • rapid control of any bleeding source- abbreviated surgery
    • definitive sx held off until physiologically stable
    • AVOID large volume crystalloid infusion
    • early administration of plasma and other blood products in a balanced ratio (preferably 1:1:1) of packed red blood cells (PRBCs), plasma, and platelets
      • sometimes 2:1:1, 3:1:1:, 4:1:1 depending on center
    • tranexamic acid (+/-)
      • helpful ​first 3 hours
    • New PRBC’s preferred (<14 days old)
      • fewer complications like TRALI with newer blood
    • No crossmatch & severe hemorrhage: O Rh-positive PRBCs and AB-negative FFP
25
Q

Why are cyrstalloids so bad in trauma?

A
  • elevate lactate
  • normal saline- increases base deficit
  • crystalloids used as carriers for blood
  • large volume crystalloid found to be independent cause of ARDS and abdominal compartment syndrome
  • cyrstalloids dilute clotting factors and can disrupt hemostatic plugs
  • worsen endothelial dysfunction in glycocalyx
    • massive hemorrhage damages soluble network of plasma components-the glycocalyx- on the endothelium that stabilize membrane integrity-
    • plasma is able to reconstitute syndecan-1, the main component of glycocalyx
26
Q

What are some treatment goals for Traumatic Brain injury?

A
  • Primary goal: prevent secondary injury
    • Avoid:
      • hypotension,
      • hypoxemia,
      • anemia,
      • raised ICP,
      • acidosis, &
      • glucose >200 mg/dL
  • Normalize bp (mean >80 mmHg), PaO2 >95, ICP <20 to 25 mmHg, & CPP at ~70 mmHg (CPP= MAP-ICP)
  • General management:
    • HOB 30 degrees, sedation & paralysis PRN, NS preferred over LR;mannitol & hypertonic Na+ PRN
      • in areas where BBB is not intact, mannitol and hyptertonic saline can lead to increased edema!
    • NS preferred d/t LR being slightly hypotnoic (osm 255, Na 130), which can promote brian swelling
    • Smooth/ rapid intubation; avoid desaturation
      • need deep anesthesia and muscle relaxation before airway manipulation if hemodynamically stable
      • severe hypotension may necessitate omission/reduciton of IV anesthetic
    • Hyperventilation: wait 24 hours after injury;
      • only for short periods;
      • only as emergency intervention when osmotic agents ineffective;
      • guided by ICP monitoring
    • Avoid hypoxia, hypercarbia, hyperthermia
27
Q

What can ICP/IOP elevation lead to in TBI or open globe injury?

Mgmt to prevent elevation in ICP/IOP?

A
  • Leads to herniation or extrusion of eye contents
  • If hemodynamically stable: proceed with opioid, generous dose IV anesthetic, and MR
    • Succinylcholine(+/-) curriont opinion says defasciculating dose of roc precedes and won’t see elevation in ICP/IOP
    • Intubating doses of Roc for RSI higher
    • Ketamine (+/-)- current opinion says no appreciable increase in ICP or IOP. traditionally a no
    • Roc- 1.2-1.5 mg/kg; higher dose equals longer duration
    • Vasopressor of choice in TBI is phenylephrine- does not cause cerebra vasoconstriciton
28
Q

What comprises a GCS score?

Treatment guideliens based on GCS score?

A
  • Scores obtained for eye opening, verbal response, and motor activity correlates with severity of injury and prognosis
  • Assessment of motor function should be performed on the extremity that responds best. The limb affected by neurologic injury is examined, but the result is not considered in the GCS
  • Maximally dilated and unresponsive “blown” pupil suggests uncal herniation under the falx cerebri
  • Mild TBI (GCS score of 13 to 15) who maintain a stable GCS score for 24 hours after injury are very unlikely to deteriorate further; need a short period of observation
  • Moderate TBI (GCS score of 9 to 12) may be accompanied byintracranial lesions that require surgical evacuation;
  • early CT is needed.
    • Early tracheal intubation, mechanical ventilation, and close observation may be required in the management of patients with moderate TBI because of combative or agitated behavior and the potentially catastrophic consequences of respiratory depression or pulmonary aspiration occurring during diagnostic evaluation
  • Severe TBI is classified as a GCS score of 8 or less at the time of admission and carries a significant risk for mortality.
    • Patients with GCS <8 have a 40% likelihood of an intracranial hematoma
29
Q

What is a complete vs incomplete spinal cord injury?

What is spinal shock?

Ventilatory considerations for spinal cord injury?

What is brown-sequard syndrome?

A
  • Complete vs. incomplete
    • actual level of injury can be several segments below area of symptoms
    • cannot differentiate at admission
      • complete- virtually no chance of recovery
      • incomplete- anal sphincter tone maintained
  • Spinal shock: flaccidity and loss of reflexes
    • subsides days to weeks
    • can make incomplete SCI look like complete
  • C4 & above- ventilator
    • must not give succinylcholine after 24 horus
  • Partial cord transection: Brown-Séquard syndrome
    • ipsilateral motor and contralateral sensory deficit below the injury
30
Q

What is involved in evaluation in blunt cardiac injury?

S/S?

Most commonly injured area?

What is commotion cordis?

A
  • Evaluation- ECG, Troponin, TEE
  • RV most commonly injured
  • s/s
    • angina
    • dypspnea
    • chest wall bruising
    • dysrhythmias
    • CHF
  • Commotio cordis
    • blow to chest in young people
    • s/s- VF/TV
    • Txmt- defib
31
Q

Anesthetic mgmt of pt with blunt cardiac injury?

A
  • Want to maintain cardiac contractility but also lower elevated pulmonary vascular resistance
  • anesthetics given only after restoration of intravascular volume and titrated to maintain BP
  • Inotropes (milrinone) to gain some pulmonary vasodilation
  • consider maintenance with IV anesthetics and opioids to avoid the myocardial Depression from inhalational anesthetics
  • patient with myocardial contusion and increased risk for perioperative arrhythmias and hypotension
32
Q

S/S pericardial tamponade?

Treatment?

A

Sx: tachycardia, hypotension, distant heart sounds, distended neck veins, pulsus paradoxus, or pulsus alternans- these sx may be absent in hypovolemic patient

Must maintain preload & contractility

Preferred to evacuate pericardial blood under local

Induce with small doses of ketamine if necessary

Wait until prepped and draped to induce (if you need to go to sleep)

only very tiny doses at induciton

33
Q

Considerations with abdominal trauma?

What is abdominal compartment syndrome? s/s

A
  • laparoscopy/ laparotomy: required in most patients after gunshot wound to abdomen
  • FAST ultrasound vs. CT
  • Occult bleeding can be massive before abdominal distention appreciated
  • Unrecognized hypoperfusion: splanchnic ischemia
  • acidosis in the intestinal wall
  • translocation of microorganisms & inflammatory mediators, from intestines
  • intestines are the earliest organ affected by hypoperfusion
  • leads to sepsis and multi-organ failure

Abdominal compartment sydrome s/s:

  • a tense severely distended abdomen,
  • increased peak airway pressure,
  • CO2 retention, and
  • oliguria
  • Intra-abdominal pressure >20 to 25 mmHgsignals decreased perfusion and may require surgical decompression

Limiting crystalloids has had the most impact on reducing the incidence

34
Q

Orthopedic and soft tissue trauma considerations?

A
  • Early repair reduces complications
  • Vascular injuries: the P’s- pain, pulselessness, pallor, paresthesias, and paresis
  • Compartment syndrome: requires emergency fasciotomy
    • Pressure >30 cm of H2O needs immediate surgery
    • Caution with regional- masks pain of compartment syndrome
  • Delayed fracture repair is associated with an increased risk of DVT, pneumonia, sepsis, and the pulmonary and cerebral complications of fat embolism.
  • In open fractures, an additional important concern is infection. Wounds left unrepaired for more than 6 hours are likely to become septic.
35
Q

What is DO2 index?

What variables does it integrate?

A

oxygen delivery index

3 variables

  • Hgb concentration
  • arterial oxygen sat
  • cardiac output

Minimum value 500 mL/min/m2

36
Q

Coagulopathy in trauma?

A
  • Hemodilutional coagulopathies from fluid resuscitation
  • Rapid consumption of clotting factors
  • Activation of Protein C (inhibits clotting factors V and VIII, decreases the inhibition of TPA)
  • INR, aPTT, platelets, fibrinogen, and fibrin degradation products (FDPs)
  • TEG/ ROTEM: clot formation & dissolution
  • FDP >40 mg/mL, is suggestive of DIC
37
Q

Considerations regarding blood product administration?

A
  • PRBC’s “new blood” preferred <14 days old
    • ​TRALI is leading cause of death from blood product admin- primarily result of FFP and platelets as well as old blood
  • citrate- present in all blood products
    • chelates calcium
    • hypocalcemia: defective coagulation plus hypotension, decreased pulse pressure, arrhythmias, change in mental status, and tetany
  • FFP: all coagulation components
  • PRBC: FFP ratio currently preferred at 1:1 or 2:1
  • Platelets: infuse to goal >50k
  • Cryoprecipitate contains factor VIII, fibrinogen (I), von Willebrand factor, fibronectin, and factor XIII
  • Used primarily to replace fibrinogen\
  • TXA has value early in resuscitation, especially in 1st 3 hours
  • Prothrombin complex concentrates: Bebulin (factors II, IX, and X) and Kcentra(adds factor VII) for emergency reversal of warfarin; will not work for Pradaxa or Eliquis
  • `New drug for Pradaxa (Praxbind)
38
Q

Anesthetic pharmacology administration in trauma?

A
  • most anesthetics are direct CV depressants; inhibit compensatory reflexes
    • hypovolemia leads to higher plasma concentrations and increased sensitivity
  • dilutional hypoproteinemia: increased free fraction of drugs
  • hypovolemia may be masked by catecholamine surge & revealed with administration of anesthetic
    • OVERALL: reduce administered doses of induction agents and opioids
  • Ketamine and Etomidate are frequent drugs of choice @ induction
    • Caution with Ketamine in catecholamine depleted patients
  • MAC reduced by ~25% in hemorrhagic shock
  • in acutely unstable pt- airway without aneshtesia- muscle relaxant and small dose opioid, etomidate, ketamine

high risk recall

39
Q

Hypothermia in trauma?

A
  • Core temperature < 35°C
    • main effects: acidosis, hypotension, and coagulopathy
  • cardiac depression & ischemia,
  • arrhythmias, peripheral vasoconstriction,
  • impaired tissue oxygen delivery,
  • elevated oxygen consumption during rewarming,
  • blunted response to catecholamines,
  • increased blood viscosity,
  • metabolic acidosis,
  • electrolyte imbalance,
  • reduced drug clearance, & infection
  • Coagulation factor function decreased ~10% for each 1°C drop in temperature
  • Aggressive rewarming is critical
40
Q

Ventilatory managment in trauma pt?

A

Lung protective strategies

VT no more than 6 mL/kg

appropriate level of PEEP

titration of FiO2 to lowest possible level

plateau airway pressures below 35 cm H2O

avoidance of auto-PEEP

41
Q

Correction of acidosis and use of Na Bicarb?

A
  • Monitor serial serum K+’s & treat hyperkalemia PRN
  • Correct the cause of metabolic acidosis rather than using liberal bicarbonate
  • Use only short term to prevent dysrhythmias when pH<7.2

Na Bicarb use –>

  • shift of the oxyhemoglobin dissociation curve causing decreased O2 unloading,
  • shift to left
  • a hyperosmolarity due to excessive sodium load,
  • hypokalemia, further
  • hemodynamic depression,
  • overshoot alkalosis a few hours after giving the drug, and
  • intracellular acidosis if adequate ventilation or pulmonary blood flow cannot be provided
42
Q

What is occult hypoperfusion syndrome?

A

common in postoperative trauma patients, particularly young ones.

-syndrome is characterized by a normal BP maintained by systemic vasoconstriction;

decreased intravascular volume and cardiac output; and organ system ischemia.

-risk for MOSF if the hypoperfusion is not promptly corrected

43
Q

Considerations for trauma in pregnancy?

A
  • Can cause spontaneous abortion, preterm labor, or premature delivery
  • Best treatment: resuscitation of mother
  • 2nd/3rd trimester: get usg to determine fetal age, size, and viability, have fetal heart rate monitored continuously if fetus is at age of viability
  • Immediate cesarean section: mother in extremis, uterus is hemorrhaging, or gravid uterus is impairing surgical control of abdominal or pelvic hemorrhage
  • Placental abruption: secondary to substance abuse or abdominal trauma
    • can lead to uterine hemorrhage; emergency cesarean section is necessary
  • Kleihauer-Betke blood test: has fetal blood entered mom’s circulation?
    • If yes, anti-Rh0 immune globulin administered if Rh(-) mom carrying Rh (+) fetus
  • 3rd trimester: aortocaval compression requires left uterine displacement
    • if on spine board, tilt entire board
  • consider HOB elevation to improve ventilation since and contents are displaced upward
44
Q

Trauma considerations in elderly?

A
  • More prone to morbidity
  • Decreased cardiopulmonary reserves
  • higher incidence of postoperative mechanical ventilation
  • greater risk for multi-system organ failure after hemorrhagic shock
  • Higher hct desired to optimize tissue oxygenation
  • High risk of post-traumatic cardiac dysfunction: monitor cardiac status (a-line, TEE, non-invasive hemodynamic monitors) to guide fluids/ inotropes
  • Decreased requirement for postop opioids
  • Potential agitation/ delirium with sedatives
  • High risk DVT due to immobilization
45
Q

Trauma consideration in jehovah’s witness?

A

May use deliberate hypotension

May need early surgical control of bleeding

Patient may consent to cell salvaging if one continuous system is used

Colloids (ask first), pressors, and inotropes to keep tissue O2 delivery optimized

Post-acute: consider erythropoietin to promote RBC regrowth