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Shock / CPR > Trauma / surgery > Flashcards

Trauma / surgery Flashcards

1
Q

What is REBOA, the different zones where it can be used, and the time of use

A

REBOA = resuscitative endovascular balloon occlusion of the aorta

Zone 1 = very proximal (before coeliac artery), used to prioritize cerebral and coronary perfusion in unstable patients.
Max 30-45 min

Zone 2 = between coeliac and renal artery, for intra-abdominal hemorrhage

Zone 3 = between renal artery and aortic trifurcation, for pelvic hemorrhage.
Max 60 min

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2
Q

What are the results of the CRASH-2 study on the use of TXA in bleeding human trauma patients

A

TXA improved mortality when given within 3h of trauma (without increased risk of thrombosis), but increased mortality when given past 3h
(benefit decreases by 10% for every 15 min delay)

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3
Q

What is the mechanism of TXA?

A

Lysine derivative that blocks the lysine site on plasminogen –> prevents binding of TPA –> prevents fibrinolysis

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4
Q

What is the survival to discharge rate following trauma in dogs and cats

A

Dogs: 90%
Cats: 75%

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5
Q

Where are injuries located most often following gunshot wounds in civilian dogs

A

Appendicular skeleton > thorax > head / neck > abdomen

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6
Q

What volume of blood loss does it take to start having severe signs of shock

A

> 15% total blood volume

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7
Q

What parameters have been found to predict need for blood transfusion in dogs with trauma

A
  • PCV/TS (PCV<39 with TS<4.5)
  • Base excess (<-6.6)
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8
Q

What proportion of dogs with a traumatic hemoperitoneum require surgery

A

6%

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9
Q

What is a contra-indication to hypotensive resuscitation

A

Traumatic brain injury

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10
Q

How is the severity of injuries related to the number of stories of the fall in high-rise syndrome in dogs and cats

A
  • Dogs: injury severity proportional to height of fall
  • Cats: severity increases until 7 stories then remains constant due to adjustments in their surface area. They have more limb injuries under 5 stories and more trunk injuries after 5-7 stories.
    Maximal speed reached by cats = 100 km/h
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11
Q

Where are injuries most commonly located in high rise syndrome

A

Head (facial injuries&raquo_space; TBI), thorax (pulmonary contusions, pneumothorax&raquo_space;diaphragmatic hernia), extremities

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12
Q

What is a hallmark of high-rise syndrome in cats and a complication if left untreated?

A

Hard palate fractures

Oronasal fistula is a complication of untreated and medically managed hard palate fractures

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13
Q

What is a rare but severe abdominal complication of high-rise syndrome in cats

A

Pancreatic rupture / traumatic pancreatitis

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14
Q

What is the mortality associated with high-rise syndrome? What is a negative prognostic factor in cats?

A

6-17%

Presence of abdominal injuries increases mortality by 2.5 times in cats

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15
Q

What are the 4 classes of hemorrhage (from humans)

A

Class I = loss up to 15% of blood volume -> minimal clinical symptoms except tachycardia

Class II = loss of 15-30% -> tachycardia, tachypnea, decrease in pulse pressure

Class III = loss of 30-40% -> pale MM, prolonged CRT, depression, hypotension

Class V = loss of > 40% -> life-threatening, signs of shock

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16
Q

List some predictors of mortality in dogs with trauma

A
  • Head trauma
  • Arrhythmias
  • Body wall hernias
  • Recumbency at the time of admission
  • MODS, ARDS, DIC, requirement for ventilation, requirement for vasopressors (no kidding)
  • Elevated lactate and creatinine but use of a comprehensive score is recommended
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17
Q

What causes hyperglycemia following trauma

A
  • Catecholamines
  • Glucagon
  • Cortisol
  • Growth hormone
18
Q

What is the difference between a penetrating and a perforating injury

A

A perforating injury passes completely through the body cavity

19
Q

Define a flail chest and a pseudo flail chest

A

Flail chest: Fractures of 3 or more adjacent ribs at 2 or more locations causing a segment to move independently from the chest wall and have paradoxical movements with the breathing

Pseudo flail chest: Paradoxical movement of a portion of the chest due to severe intercostal muscle injury without rib fractures around

20
Q

What are the 3 main components of splenic vascularization? Where do they originate from?
What artery should be preserved when doing a splenecomty

A
  • Splenic artery and vein
  • Short gastric arteries and veins
  • Left gastroepiploic artery and vein

All originate from celiac artery (from abdominal aorta)

Must be careful to preserve pancreatic arteries (coming from the splenic artery) when ligating vessels

21
Q

What are the 4 abdominal muscles that constitute the abdominal wall? What layer holds sutures?

A

From out to in:

  • Rectus abdominis (parallel to linea alba)
  • Internal abdominal oblique (runs cranioventrally)
  • External abdominal oblique (runs caudoventrally)
  • Transversus abdominis (transverse to linea alba)

The external rectus sheath holds sutures

22
Q

What are common locations of abdominal wall hernias

A
  • Paracostal
  • Inguinal
  • Umbilical
  • Scrotal
  • Cranial pubic ligament rupture
  • Ventral / subxiphoid
  • Femoral
  • Dorso-lateral
23
Q

Describe some of the characteristics of the systemic response to severe injury

A
  • Extracellular release of DAMPs or alarming from activated neutrophile or necrotic cells –> activation of innate immune system and complement –> production and release of inflammatory mediators (IL-6, IL-8) –> SIRS
  • Platelets activated by trauma can also contribute to release of proinflammatory mediators
  • Neutrophils migrate across the damaged vascular endothelium, become sequestered by “bystanders” organs –> organ dysfunction
  • Simultaneously, a compensatory anti-inflammatory response occurs –> IL-10 and TGF-beta
24
Q

Name 3 bacterias commonly isolated from bite wounds

A
  • Pasteurella spp
  • Staph spp
  • Strep spp
25
Q

What are the 3 categories evaluated in the MGCS?

A
  • Motor activity
  • Brainstem reflexes
  • Level of consciousness
26
Q

What are the 2 components of trauma associated coagulopathy (TAC)?

A
  • Endogenous coagulopathy with concurrent tissue hypoperfusion (acute coagulopathy pf trauma shock)
  • Syndrome that occurs later and is exacerbated by resuscitation practices (resuscitation associated coagulopathy)
27
Q

What are the 3 phases of healing?

A
  1. Inflammatory phase (first 5 days):
    - PLT activated by hemorrhage and endothelial injury –> attract neutrophils (6h after injury) + monocytes (12h) (debridement phase begins)
    - Vasodilation from PGs, histamines, kindness allow leukocyte migration to the wound bed
    - Neuts remove extracellular debris / monocytes stimulate fibroblastic activity, collagen synthesis, angiogenesis / macrophages remove necrotic tissue, bacteria, foreign material
  2. Prolific phase (begin day 4, lasts 2-3 wks):
    - angiogenesis, granulation tissue, epithelialization
  3. Maturation phase (day 17-20 up to years):
    - wound contraction and remodeling of fibre bundles
    - Scar is only 80% as strong as original tissue
28
Q

Describe the pathophysiology of acute coagulopathy of trauma-shock

A

Characterized by hyaocoagulability with hyperfibrinolysis

Severe trauma and widespread tissue injury –> recessive plasma catecholamine –> generalized endothelial activation –> release of thrombomodulin, systemic coagulation activation, consumption of clotting factors and platelets –> pro coagulable thrombin activates protein C (potent endogenous anticoagulant) –> inhibits factor Va and VIIIa, as well as plasminogen activator inhibitor 1 and thrombin activatable fibrinolytic concurrently –> hyperfibrinolysis

catecholamine surge also damages endothelial glycocalyx –> shedding and release of endogenous anticoagulants (heparin) and profibrinolytic agents

29
Q

Briefly, how does platelet dysfunction occur in TAC?

A

Widespread release of ADP following tissue trauma may prematurely activate platelets leading to their exhaustion and retention into circulation.

29
Q

List metabolic consequences of trauma

A
  • Sympathoadrenal activation
  • Neuroendocrine activation
  • Hyperglycemia
  • Hyperlactatemia
  • Metabolic acidosis
  • Hypothermia
  • GI injury +/- translocation
  • Systemic inflammation
  • Acute traumatic coagulopathy
30
Q

Why do patients develop hyperglycemias after trauma?

A

Release of counter regulatory hormones (glucagon, growth hormone, cortisol, catecholamine)
- Epinephrine –> proteolysis, glycogenolysis (glycogen –> glu), inhibition of insulin mediated glucose uptake by muscle
- Cortisol –> gluconeogenesis (amino acid –> glu), inhibits insulin activity, exacerbates effects of glucagon and epinephrine

31
Q

How are open fractures classified according to the Gustily-Anderson classification scheme?

A

I - open fracture with wound < 1cm; mild to moderate soft tissue bruising
II - open fracture with wound > 1cm without extensive soft tissue damage
III - Open fractures with extensive soft tissue damage
IIIa - Extensive trauma with adequate tissue covering remaining, irrespective of wound size
IIIb Extensive trauma with soft tissue loss, perinatal stripping and bone exposure
IIIb - Extensive trauma associated with arterial blood supply injury

32
Q

What are indications for open reduction after traumatic joint luxation?

A
  • Unsuccessful attempts at closed reduction
  • Joint reluxation
  • Chronic luxation
  • Concurrent intra-articular fractures
  • Internal stabilization is necessary fr adjacent long bone fractures
  • Neurologica injury suspected and exploration warranted
33
Q

Wounds classification:

A
  • Clean: atraumatic, surgically created under aseptic conditions
  • Clean contaminated: minor break in aseptic surgical technique
  • Contaminated: Recent traumatic wound with bacterial contamination vs major break in surgical asepsis
  • Dirty or infected: older wound with exudate or obvious infection –> >10^5 organisms/g of tissue
34
Q

Name a few factors that can delay wound healing

A
  • Poor O2 delivery (anemia, severe trauma, hypovolemia)
  • Hypoproteinemia (<2g/L –> decreases fibrous tissue deposition)
  • Chemotherapy/radiation therapy
  • Diabetess, uremia, liver disease
  • Steroids
34
Q

What are the burn degrees?

A
  • 1st degree: superficial epidermis only
  • 2nd degree: epidermis and superficial dermis
  • 3rd degree: full thickness (entire epidermis and dermis)
  • 4th degree: full thickness with extension to muscle, tendon and bone
35
Q

How is the total surface body area (TBSA) burned estimated?

A
  • Head –> 9%
  • Each forelimb –> 9%
  • Each hind limb –> 18%
  • Dorsal trunk –> 18%
  • Ventral trunk –> 18%

> 20% of TBSA –> serious CV, metabolic and pulmonary derangements

> 50% of TBSA –> poor prognosis

36
Q

Why can hypovolemic shock occur in burn patients?

A

As a result of capillary thrombosis leading to leakage of plasma. Most dramatic loss of fluids and electrolytes occurs within the first 12 hours.

37
Q

What volume of blood is held by a 22 gauze, 44 gauze, lap sponge

A
  • 2*2 gauze holds 3.25 +/- 1.25 mL
  • 4*4 gauze holds 10 +/- 2 mL
  • lap sponge holds about 150 mL
38
Q

A pneumomediastinum can lead to air in which other cavities?

A
  • Pneumothorax
  • SC emphysema
  • Pneumoperitoneum
39
Q

Explain the Macklin effect

A

Alveolus ruptures –> air dissects through peribronchovascular sheaths into pulmonary interstitium –> tracks along the perivascular space into the pulmonary hill and mediastinum –> pleural space

Shock / CPR (5 decks)

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