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Paramedicine > HFB 2005 Management of Trauma > Flashcards

HFB 2005 Management of Trauma Flashcards

1
Q

Closed Fracture

A

A break within the body that doesn’t break the skin

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2
Q

Open Fracture/Compound Fracture

A

A complete break in which the bone breaks the skin.

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3
Q

Transverse Fracture

A

A break straight line across the bone

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4
Q

Spiral Fracture

A

It is a spiral shape fracture

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5
Q

Comminuted Fracture

A

Broken into two or more pieces

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6
Q

Impacted Fracture

A

It is an incomplete fracture which the end jam together

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7
Q

Greenstick Fracture

A

Fracture in a young, soft bone in which the bone bends and break

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8
Q

Oblique Fracture

A

Break at an angle

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9
Q

Common Mechanism of Injury of a fracture

A

A direct blow, fall, or motor vehicle accident can cause a fracture.
Twisting motion

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10
Q

Common Signs and Symptoms for a fracture

A

Pain
Swelling
Deformity
Bruising
Tenderness
Broken skin
Unable to bear weight
Trouble using or moving the injured area or nearby joints

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11
Q

Common Complications fracture

A

Haemorrhage (Blood loss)
Infection
Nerve damage
Compartment syndrome
Bone growth issue (greenstick)

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12
Q

Definitive / specialist care / treatment

A

Pain relief
Immobilisation
Splint
Clean an open wounds
surgery

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13
Q

Flail Chest

A

Three or more rib that have been fracture in two or more place

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14
Q

Signs and Symptoms for Flail Chest

A

Paradoxical motion of a chest wall

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15
Q

Contusions

A

Haematoma of the tissue where the capillaries are damage and leak into the tissue

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16
Q

Sprains

A

ligament in a joint is stretched too far or torn

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17
Q

Tendonitis

A

Tendon becomes inflamed and stiffness of the joint

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18
Q

Bursitis

A

Bursa, a fluid-filled sac that cushions joints, becomes inflamed

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19
Q

Hypothermia

A

It is when your core body temperature accidentally drops below 35°C.

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20
Q

Hypothermia Classifications

A

Mild 34°C-32°C (conscious shivering core temperature greater than 32°C)

Moderate 28°C-32°C (impaired consciousness may or may not be shivering and core temperature has fallen 28°C to 32°C)

Severe <28°C(unconscious vital signs present cool temperature has dropped below 28°C)

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21
Q

Define coagulopathy; in the setting of hypothermia, at what temperature does coagulopathy become a concern?

A

As body temperature drops, the enzymes and proteins responsible for blood clotting become less effective

Coagulopathy becomes a concern when body temperature falls below 34°C
That this point, platelet function diminishes, and the coagulation cascade slows down, impairing the formation of blood clots.

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22
Q

Discuss foundational hypothermia management / care plans / rationalise:

A

Protect patient from further heat loss

Ensure ambulance heaters are on

Remove wet clothing cover patient with a thermal blanket or an activation device if available.

If IV fluids are indicated for pt with poor perfusion ensure that Ivy fluids are warmed by using a hot water bottle.

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23
Q

Outline the metabolic response to hypothermia

A

Increase to try and maintain body temp

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24
Q

Pathophysiology: How does the body attempt to preserve normothermia?

A

The body tries to preserve homeostasis by increasing metabolic rate peripheral vasoconstriction increasing for preshivering muscle time or shivering.

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25
Q

At what core temperature does the body stop being able to ‘shiver?’

A

Between 30°C and 32°C

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26
Q

Explain Mechanisms of Heat Loss:

A

Radiation, If you stand outside on a cold day, heat radiates from your warm body into the cooler air, even if you are not in direct contact with anything.

Conduction, Sitting on a cold metal bench will cause heat to transfer from your body to the metal.

Convection, Standing in a cold wind (wind chill) or being in moving water accelerates heat loss.

Evaporation, Sweating during exercise leads to heat loss as sweat evaporates, cooling the body

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27
Q

Discuss the neurological, cardiovascular and respiratory responses to hypothermia:

A

Neurological, Cognitive and Behavioural Changes and CNS Depression
Cardiovascular, profound vasoconstriction and increase in heart rate and blood pressure however after time it will progress into progressive Brady cardia hypertension and myocardial irritability

Respiratory, Tachypnea it will begin to become Hypoventilation and final Apnea

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28
Q

Hyperthermia

A

It is when the core body temperature rise above 38°C

29
Q

Discuss foundational hyperthermia management / care plans / rationalise:

A

Position the patient prone or flat and avoid head up position to avoid hypertension collapse and arrhythmias

Strip/Spray/fan
○Remove excess clothing wet the skin and promote vigorous airflow
○Oral fluids to help rehydrate the patient
○IV fluids Cold IV fluids to be titrated to adequate perfusion and or temperature
○Ice bath or cold shower for rapid cooling of hyperthermia patients

30
Q

Define coagulopathy; in the setting of hyperthermia, at what temperature does coagulopathy become a concern?

A

Coagulopathy typically becomes a significant concern when body temperatures exceed 42°C

Proteins responsible for blood clotting become damaged.

Platelet dysfunction

Disseminated intravascular coagulation (DIC)

31
Q

What physiological mechanisms and biochemistry causes one to sweat?

A

Increased body temperature → Hypothalamus activates the sympathetic nervous system.

Sympathetic nerves release acetylcholine, which stimulates eccrine sweat glands.

Ions (Na⁺, Cl⁻) are released into the sweat duct → Water follows via osmosis, producing sweat.

Sweat is excreted on the skin surface → Evaporation cools the body.

32
Q

Excessive heat is toxic to cells. Briefly summarise what occurs when cells are damaged in the setting of hyperthermia

A

Hyperthermia damages cells by denaturing proteins, disrupting membranes, impairing mitochondria, causing calcium overload, and triggering inflammation. If unchecked, it leads to cell death, organ damage, and potentially life-threatening systemic effects.

33
Q

What are four primary physiological responses to heat stress?

A

Vasodilation of Skin Blood Vessels: This increases blood flow to the skin, allowing more heat to be transferred from the core of the body to the surface, where it can be dissipated into the environment.
Sweating: as sweat evaporates from the skin, it absorbs heat and cools the body.
Increased Respiratory Rate: expel more heat through evaporative cooling from the lungs and respiratory passages
Decreased Heat Production: decreasing energy expenditure and avoiding excessive muscular activity

34
Q

Hyperthermia Classifications

A

Heat Cramps, Painful muscle cramps or spasms, typically in the legs, arms, or abdomen, caused by excessive sweating and loss of electrolytes, particularly sodium
Heat Stress, A general condition caused by exposure to high temperatures, leading to stress on the body’s ability to regulate heat
Heat Exhaustion, A more serious condition than heat cramps, characterised by dehydration and the body’s inability to cool down effectively.
Heat Stroke the most severe and life-threatening heat illness, occurring when the body’s core temperature rises above 40°C and thermoregulation fails.

35
Q

Discuss the neurological, cardiovascular and respiratory responses to heat stress:

A

Neurological: Hypothalamic Activation, Heat-induced Cognitive Impairment , and Motor Coordination Changes.
Cardiovascular: Vasodilation, increased heart rate, and Increased Risk of Cardiovascular Strain
Respiratory: Increased respiratory rate, shifts in Oxygen Demand

36
Q

Discuss the neurological, cardiovascular and respiratory responses to heat stroke:

A

Neurological: CNS Dysfunction, LOC, and Seizures
Cardiovascular:Severe Vasodilation, Increased heart rate, cardiac arrhythmiasm, and Disseminated Intravascular Coagulation
Respiratory: Hyperventilation, Pulmonary Edema, and Hypoxemia

37
Q

Haemotoxin Exposure

A

Toxins that primarily affect the blood and blood vessels, leading to blood clotting disturbances, haemolysis (destruction of red blood cells), or damage to blood vessel walls.
Example: Tiger Snake and Mulga Snake (King Brown)

38
Q

Haemotoxin effects on each system

A

Neurological: Nil
Cardiovascular: Haemorrhage, coagulation disorders, disseminated intravascular coagulation (DIC), and this can lead to shock
Respiratory: hypoxia
Renal: Acute kidney injury, due blockage of renal tubules.
Gastrointestinal: Internal bleeding, and vomiting
Integumentary: Bruising and necrosis may occur around the bite site due to local haemorrhage

39
Q

Neurotoxin Exposure

A

It disrupt normal nerve function by interfering with synaptic transmission, often leading to paralysis or abnormal nerve activity.
Example: Eastern Brown Snake and Redback Spider (Latrodectus hasselti)

40
Q

Neurotoxin effects on each system

A

Neurological: paralysis, severe pain, muscle spasms, and seizures. due to block or overactive nerve signals
Cardiovascular: tachycardia, hypotension, or arrhythmias
Respiratory: Paralysis leading to respiratory failure
Renal: Neurotoxins don’t directly affect the kidneys but can lead to AKI
Gastrointestinal: nausea, vomiting, or abdominal pain
Integumentary: Muscle fasciculations (involuntary twitches) or local sweating at the bite or sting site

41
Q

Cytotoxin Exposure

A

Cytotoxins are toxins that cause cell destruction or damage, often leading to tissue necrosis (death) at the site of the bite or sting.
Example: Death Adder and the Box Jellyfish (Chironex fleckeri)

42
Q

Cytotoxin effects on each system

A

Neurological: Nil
Cardiovascular: tissue damage, which can trigger a strong inflammatory response. Leading hypotension and shock.
Respiratory: NIl
Renal: rhabdomyolysis and thus causing AKI
Gastrointestinal: nausea, vomiting, and abdominal pain
Integumentary: Local necrosis

43
Q

What is a burn

A

It is damage to the skin and deeper tissue, cause by Thermal (heat and cold), radiation, chemical and electrical.

44
Q

Unpack Jackson’s Burn Wound Model:

A

Zone of coagulation: This occurs at the point of maximum damage and this zone is characterised by irreversible tissue damage due to coagulation of the constituent proteins that occurs because of the damage.
Zone of stasis or zone of ischemia: This zone lies adjacent to the zone of coagulation and it is subject to a moderate degree of damage associated with vascular leakage, elevated concentration of vasoconstrictors, and local inflammatory reactions resulting in compromised tissue perfusion. But the integrity of the tissue in this zone can be saved with proper wound care
Zone of hyperemia: This is the outermost zone. It is characterised by the eased blood supply and inflammatory vasodilation. The tissue here will recover unless there is severe sepsis or prolong hypoperfusion.

45
Q

Outline Electrical Burns:

A

Electrical burns occur when electricity passes through the body, causing damage to tissues, organs, and skin.
S/S:
Entry and exit wounds
Localized pain, swelling, and blistering
Muscle pain and weakness
Heart irregularities

46
Q

Outline Chemical Burns:

A

Chemical burns occur when the skin, eyes, or internal tissues come into contact with corrosive substances such as acids, alkalis, or other toxic chemicals.
S/S
Redness, pain, blistering, swelling, or blackened skin (depending on the chemical)
Immediate or delayed onset, depending on the chemical’s nature
Eye exposure can result in vision changes, pain, or blindness

47
Q

Outline Thermal Burns:

A

Thermal burns are caused by exposure to heat sources such as fire, hot liquids, steam, or hot objects. it can also be cold.
S/S:
Pain, redness, swelling, blistering
Shock: Rapid heart rate, low blood pressure, confusion (Hypovolemia)

48
Q

Outline Radiation Burns:

A

Radiation burns occur when the skin or other tissues are exposed to radiation, which damages cells and tissues.
S/S
Redness, dryness, pain, and peeling (similar to sunburn)

49
Q

Classify Burns by Depth and outline their clinical features: Superficial

A

Affect the epidermis only
Characterised by redness, pain, dryness, and with no blisters.
Mild sunburn is an example of a superficial thickness burn.

50
Q

Classify Burns by Depth and outline their clinical features: Partial-thickness or second-degree burns

A

Involve the epidermis and a portion of the dermis
Become inflamed and when pressure is applied to the reddened area. The area will blanch, but will demonstrate rapid capillary refill upon release of the pressure.
Painful to pressure, form blisters, are wet, waxy, or dry, and may appear ivory or pearly white.

51
Q

Classify Burns by Depth and outline their clinical features: Full-thickness or third-degree burns

A

Burns extend through the full dermis and often affect the underlying subcutaneous tissue
Skin appearance can vary from waxy white to leathery grey to charred and black
Does not blanch to pressure, it is not typically painful due to the damage to the nerve endings

52
Q

Classify Burns by Depth and outline their clinical features: Subdermal

A

Involve injury to the deeper tissues, such as muscle or bone.
They are often blackened and it frequently leads to loss of the burned part.

53
Q

Hypovolaemic Shock

A

It is caused by a sudden drop in the circulating blood volume leading to cell ischemic. It caused by either trauma or burns

54
Q

Compensatory shock S&S:

A

It is the Early Stage of shock
Tachycardia, Pale, cool, clammy skin, Delayed capillary refill, Normal to slightly decreased blood pressure, Tachypnea, Anxiety, and restlessness

55
Q

Decompensatory Shock S&S

A

It is the Progressive Stage
Hypotension, Tachycardia, but weakening pulse, Altered mental status, Cold, mottled, cyanotic skin, Labored, shallow breathing, and Weakness and fatigue

56
Q

Irreversible Shock S&S

A

It is the Late Stage.
Severe hypotension, Bradycardia or very weak, irregular pulse, Coma or unresponsiveness, and Respiratory failure.

57
Q

Absolute fluid loss:

A

It is where the fluid has left the body e.g. Haemorrhage

58
Q

Relative fluid loss/third spacing:

A

The fluid has move outside the blood vessel and into the third space, so is no long in circulation. e.g. During inflammation

59
Q

What causes hypovolaemic shock in the person who has burns injuries?

A

Hypovolemic shock in burn injuries occurs due to fluid loss and inflammation. Burns damage the skin, causing plasma to leak from vessels. Inflammation makes blood vessels more permeable, worsening fluid loss. thus less fluid and lower oxygen delivery to organs.

59
Q

Trauma Lethal Triad, or Triad of Death

A

Refers to three critical conditions that often lead to death if not managed promptly. These are:

Hypothermia, Acidosis, Coagulopathy

60
Q

What is hypoperfusion? Define end - organ hypoperfusion.

A

condition where there is insufficient blood flow to tissues and organs, preventing them from receiving adequate oxygen and nutrients necessary for normal function.
MAP is (65mmg) and SBP is (90mmg)

61
Q

Neurogenic shock definition:

A

Its is a type of distributive shock that is caused by a disruption to the autonomic pathways, typically a spinal cord injury’s at T6 or high. Resulting in a loss of sympathetic stimulation and unopposed parasympathetic response.

62
Q

Explain what happens to the autonomic system in neurogenic shock:

A

In neurogenic shock, the sympathetic nervous system (SNS) is disrupted, leading to vasodilation (widening of blood vessels) and bradycardia (slow heart rate) due to unopposed parasympathetic activity. This causes low blood pressure (hypotension) and inadequate blood flow to organs, resulting in shock.

63
Q

Benefits vs complications of fluid provision?

A

Benefits; Supports Cardiac Output and Restores Blood Volume which counteract the hypotension
Complication; Fluid Overload and Peripheral oedema

64
Q

Spinal shock definition:

A

It is a transient loss of motor, sensory and autonomic function below an spinal cord injury. Only the spinal cord is affected

65
Q

Explain the local inflammatory response that occurs in spinal shock:

A

The local inflammatory response involves the release of pro-inflammatory cytokines and immune cells at the injury site, leading to swelling and tissue damage. This inflammation exacerbates the initial spinal cord injury, contributing to further nerve cell death,

66
Q

What are the four phase of spinal shock

A

Phase 1- Hyporeflexia
Phase 2 - Return of Reflexes
Phase 3 - Hyperreflexia
Phase 4 - Resolution of spinal shock

67
Q

Signs and symptoms of neurogenic shock

A

Hypotension
Bradycardia
Altered Level of Consciousness

Paramedicine (2 decks)

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