357 exam Flashcards

1
Q

Epidemiology / Demographics of posionings

A

Pharmaceutical
….Most common poisonings by pharmaceuticals differ between genders:
+ Females - non-opioid analgesics, antipyretics, antirheumatics
+ Males - anti-epileptic, sedative hypnotic, antiparkisons

Most poisonings in adult are deliberate

Most poisonings in children are accidental

Non-pharmaceutical poisoning e.g. envenomation

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2
Q

Non-pharmaceutical poisoning examples

A

Envenomation
Alcohol
Carbon monoxide
Pesticides

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3
Q

what type of drugs are likely to be abused

A

Act fast
Make you feel good
Stop you feeling bad

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4
Q

examples of drugs of abuse

A

CNS stimulants - amphetamines, nicotine , cocaine, caffeine,

CNS depressants - alcohol, opioids, benzodiazepines

Psychomimetics - cannabis, LSD, designer drugs

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5
Q

what type of drug is methamphetamine?

A

CNS stimulant

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6
Q

Pharmacodynamics of methamphetamine

A

Chemically similar to adrenaline, dopamine

Increases alertness, mental and physical capabilities, surprises appetite.

Induces psychosis, aggression

‘Fall off’ effect - hunger, lethargy, depression

Causes intense craving - high risk of addiction

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7
Q

Treatment of methamphetamine poisoning

A

support of symptoms including sedation

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8
Q

other names for mathamphetamine

A

meth, ice

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9
Q

other names for Methylenedioxymethamphetamine

A

(MDMA / Ecstacy / E / Pingers)

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10
Q

(MDMA / Ecstacy / E / Pingers) what does it do?

A

Original designed in 1914 as an appetite surpressant

Similar to Methamphetamine - with subtle changes to molecules - fewer effects of aggression, irritability and ‘fall off effect’

Triggers sense of confidence, friendliness, paranoia.

Can lead to hyperthermia, hypertension, tachycardia, thirst and over hydration

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11
Q

MDMA treatment

A

Treatment: supportive control of symptoms - no antidote

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12
Q

what does heroine do

A

Central nervous system depressant - opiate

Similar to codeine, morphine, fentanyl, oxycodone

Medical version - diamorphine

Causes sense or euphoria and well being

May lead to - rest. depression, pulmonary oedema, convulsions, hypotension, bradycardia

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13
Q

heroine overdose treatment

A

support of symptoms & naloxone

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14
Q

how can a paracetamol/ acetaminophen cause overdose

A

Commonly used drug

Readily available with no restriction on sales - responsible for 50% of all toxic ingestions in Australia

Majority (97-98%) of paracetamol readily metabolised in liver.

Small amount metabolised to NAPQI - highly hepatotoxic

NAPQI easily removed by Glutathione.

Limited amount of Glutathione produced

Overdose uses up all Glutathione - leaving NAPQI to cause liver injury

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15
Q

paracetamol overdose treatment

A

N-Acteylcysteine -

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16
Q

What is trauma?

A

the transference of energy to the body

Kinetic -
…..Blunt - falls, motor vehicle accidents…
…..Penetrating - bullet wound, stabbing..

Chemical - chemical burn, deprivation of oxygen

Thermal - scalds, burns…

Radiation - UV burns…

Electrical - electrocution..

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17
Q

is Trauma…an epidemic?

A

Epidemic - an illness, injury or disease that affects a large number of the population in a region…with apparent growth

Road fatalities in developed countries has fallen
Violence against the person and injury from falls has increased

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18
Q

describe the burden of injury from trauma

A

970 million people suffer injury globally p.a.

4.8 million die from those injuries

Total number of deaths did not decrease between 2005 - 2015

Leading cause of death ages 1 - 44 yrs

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19
Q

describe trauma from the australian context

A

Trauma responsible for 500,000 hospitalisations nationally p.a.

12,000 die due to trauma

Potential years lost = 1,207

This is greater loss of potential life than cancer and heart disease combined

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20
Q

common injuries that we should try prevent

A

Falls

Cycle injury

Motor vehicle injury

Risk taking prevention

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21
Q

what are the determinants of trauma

A

Age

Gender

Indigenous populations - more than twice the incidence of non-indigenous populations

Alcohol and drug use
Geography - remoteness and terrain

Driver behavioural factors

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22
Q

what is involved prehospital in the patient journey

A
Self care?
Bystander - first aid
First  Responders
Road ambulance
Helicopter Emergency Service
Royal Flying Doctor Service
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23
Q

what is involved in the emergency part of the patient journey

A

Not all patients arrive by ambulance

Triage works!

Remember the psychological effect of injury / illness on behaviour
- Anxiety or anger?

Jack of all trades - Master of…..

Key to success:

  • Organisation
  • Communication
  • Education
  • Empathy
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24
Q

what is involved in the intensive care unit part of the patient journey?

A

Patients may be sedated / anaesthetised but aware
Consider the impact on family
Patients may be conscious and ventilated

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25
Q

what happens in the operating room/ xray part of the patient journey ?

A

In some cases - direct to theatre

In theatre pt. cannot advocate for themselves - a key nursing role is advocacy

Transport to OT or to xray is hazardous for the critically ill patient - how would you manage the following in a lift:

  • Airway obstruction e.g. vomit
  • Haemorrhage
  • Cardiac arrest
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26
Q

What happens in the ward part of the patients journey?

A

Patients and their families leaving ICU are often very fearful
Higher ratio of patients to nurses
Holistic care is key
No less acute in some cases

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27
Q

what happens in the rehabilitation part of the patient journey?

A

For some patients this can be lifelong

In injury this can often involve young patients compared to stroke rehab for example

Application of clinical reasoning is just as valid here as ED or the ward

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28
Q

What is a trauma system

A

An integrated and organised approach to care of the
injured person from the site of injury to rehab and ideal
restoration of normal functioning

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29
Q

key factors of the prehospital phase of trauma systems

A

Ambulance call taker

Ambulance dispatch

On scene care - paramedic, doctor, nurse, first responder

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30
Q

key factors of transport phase of trauma systems

A

Contingent on - distance from hospital, condition of patien

Reception - early alert, clear standard
communication

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31
Q

trauma systems ongoing care considerations

A

Evidence based care
Integrated - hospital - rehab -
community - home

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32
Q

primary survey abbreviation

A
  • Control of catastrophic haemorrhage

Ac – Airway with c-spine control

B – Breathing

C – Circulation

D – Disability

E - Exposure

F farenheit

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33
Q

key points of consideration for primary survey

A

Find a life threatening problem - fix it -
move on

✤ A always trumps c (Airway over cervical
spine)

✤ Don’t get distracted by OMG injuries

✤ Don’t cause hypothermi

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34
Q

what is involved in the secondary survey

A

A detailed examination of each system
✤ Head to toe
✤ Every orifice - blood, CSF etc.
✤ Includes ECG, bloods, x-ray

Head to toe detailed examination

Look for ‘occult’ injuries
Difficult in unconscious patients

Followed by imaging e.g. POCUS, FAST scan, CT, x-ray

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35
Q

what is tertiary survey

A
Later in care
✤ Looking for development of problems:
✤ E.g. ARDS, infection, acute kidney 
injury
✤ Detailed scan
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36
Q

considerations of nursing care during trauma

A

Communication with patient

✤ Vital sign measurement

✤ Assist with interventions e.g. chest drain

✤ Record keeping

✤ Liaison with family / other

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37
Q

examples of different trauma pathophysiology

A

Coagulopathy

Hypothermia

Chest trauma

Abdo trauma

Pelvic injury

Skeletal injury

Penetrating trauma

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38
Q

what is coagulopathy

A

✤ This disease process of abnormal blot clotting
✤ Most trauma patients will have some form of bleed
✤ One the trauma triad - acidosis, hypothermia &
coagulopathy

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39
Q

causes of coagulopathy in trauma

A

✤ Causes:
✤ Hypothermia
✤ Haemodilution
✤ Acidosis

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40
Q

why is hypothermia considered trauma

A

Leads to vasoconstriction - reduced circulation
✤ Can cause:
✤ Arrhythmias
✤ Coagulopathy
✤ Can be caused by pre-hospital environment / within hospital
✤ Prevention is better than cur

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41
Q

hypothermia management

A

✤ Warmed IV fluids inc. blood
✤ Blankets reduce exposure
✤ Bair hugger

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42
Q

what are examples of thoracic trauma

A
✤ ATOM - FC
✤ Airway obstruction
✤ Tension pneumothorax
✤ Open pneumothorax 
✤ Massive haemothorax
✤ Flail chest
✤ Cardiac tamponade
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43
Q

Tension pneumothora Signs and symptoms

A

✤ Rapid resp rate
✤ Tracheal tug
✤ Absence of lung sounds

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44
Q

treatment of tension pneumothorax

A

✤ Needle decompression
✤ Intercostal chest drain
✤ Definitive treatment of cause

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45
Q

Open pneumothorax

(sucking chest wound) signs and symptoms

A

✤ Wound on chest wall (anterior or posterior)
✤ Tachypnoea
✤ Low SaO2
✤ Reduced chest movement / unilateral movement

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46
Q

management of open pneumothorac

A

Management
✤ Three sided dressing (acts as a flap valve)
✤ Intercostal chest drain

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47
Q

Massive haemothorax

Signs and symptoms

A

✤ Tachypnoea
✤ Low SAO2
✤ Reduced air entry
✤ Differenciated on x-ray from pneumothorax

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48
Q

management of massive haemothorax

A

✤ Supplemental oxygen (if indicated)
✤ Intercostal drainage
✤ Fluid resuscitation

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49
Q

flail chest signs and symptoms

A

✤ Rib pain +++
✤ Tachypnoea, Low SaO2
✤ Segment of ribs - paradoxical movement
✤ Fracture of 2 or more adjacent ribs in two or more place

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50
Q

flail chest management

A

Analgesia +++
✤ May require tracheal intubation
✤ Physiotherapy and breathing exercise

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51
Q

Cardiac Tamponade signs and symptoms

A

(Becks Triad)
✤ Reduced heart sounds
✤ Engorged neck veins
✤ Low BP

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52
Q

management of cardiac tamponade

A

Management

✤ Pericardiocentesis

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53
Q

common presentations of abdominal trauma

A

✤ Splenic rupture
✤ Liver rupture
✤ Rupture bowel
✤ Kidney injury

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54
Q

diagnostic aids for abdominal trauma

A

✤ F.A.S.T. - Focused Abdominal Sonography for
Trauma (now available pre-hospital)
✤ CT Scanning
✤ Diagnostic Peritoneal Lavage (DPL)

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55
Q

why is pelvic trauma so bad

A

✤ Pelvis forms a ring that is extremely strong
✤ Potentially life threatening on its own
✤ Can contain at least 3 litres of blood

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56
Q

signs and symptoms of pelvic trauma

A

Pelvic pain
✤ Mechanism and history
✤ Haematuria
✤ Leg discrepancy / groin pain

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57
Q

management of pelvic trauma

A

Pelvic binder
✤ Fluid resuscitation
✤ Analgesia
✤ External fixation

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58
Q

Skeletal trauma signs and symptoms:

A

Assess with - Look, Feel, Move
✤ Swelling, bruising deformity
✤ Pain
✤ Neurovascular assessment

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59
Q

complications of skeletal trauma

A

Compartment syndrome
✤ Infection in open fractures (osteomyelitis)
✤ Loss of function (or limb)

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60
Q

describe penetrating injury

A

✤ Low velocity
✤ E.g. stabbing, impalements
✤ Low energy - minimal damage to surrounding tissue
✤ Site and depth of injury dictates severity

✤ High velocity
E.g. gunshot
-High energy
- Dispersed wide spread from site of injury
- Caliber of gun (pistol v rifle) - severity of energy

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61
Q

key nursing issues in trauma care

A

Psychological factors
✤ Trauma has a life long impact for patients and
their family
✤ It affects healthcare workers

Pain relief
✤ Be the patient’s advocate

Communication
✤ The patient will remember more of what you say
than what you do

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62
Q

What is Multi Organ Dysfunction Syndrome?

A

Previously called multi-organ failure

Continuum of abnormal physiological changes and changes in organ function that occur in critical illness

Not only affects organs e.g. acute kidney injury but also immune, blood and endocrine systems

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63
Q

Pathophysiology of MODS

+
Equation

A

Similar to sepsis

Abnormal cellular responses involving several organ systems

Usually has a trigger

eg.
Increased inflamation, coagulation + decreased fibrinolysis = endothelial dysfunction and microvascular thrombosis = hypoperfusion ischaemia

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64
Q

Causes of MODS

A
Trauma
Gut failure e.g. bowel obstruction, paralytic ileum
Infection
Ventilator induced lung injury
Burns
Pancreatitis
Multiple blood transfusions
Cardiac bypass
Heat induced illness
Poisoning / toxicity …
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65
Q

Describe development of MODS/ worsening stages

A

Usually occurs in worsening stages:

  1. Increasing fluid requirement, mild resp. Alkalosis, oliguria, hyperglycaemia
  2. Tachypnoea, hypocapnia, hypoxaemia, moderate liver dysfunction, possible blood abnormalities
  3. Shock with increasing Azotemia (nitrogen containing compounds e.g. urea), acid based disturbance, coagulopathy
  4. Dependence on vasopressors with oliguria, lactic acidosis
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66
Q

review MODS/ sepsis flow chart

A

review MODS/ sepsis flow chart

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67
Q

How does MODS affect the cell aposis v necrosis

A

Apoptosis v Necrosis

Cells ‘self-destruct’ normally - damaged or aged cells - Apoptosis

Prevents abnormal function or mutations

In MODS - this process is altered - may be slowed down (in neutrophils) or sped up gut lining

This causes tissue / organ damage

Necrosis is cell death caused by hypoxia or trauma

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68
Q

Apoptosis v necrosis

A

Apoptosis does not need pro-inflammatory chemicals e.g. histamine to work
Necrosis is often caused by pro-inflammatory chemicals - and is often unregulated

Cells rupture and leak contents causing collateral damage
This then starts the surrounding cells breaking down - cascade
Necrosis caused significant and widespread tissue and organ damage

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69
Q

describe how MODS causes cell dysfunction

A

Every cell has a function

MODS causes the cell to dysfunction

For example liver, renal and cardiac cells make proteins

MODS inhibits this production

These cells stop functioning correctly

  • Cardiac cells contract weaker
  • Liver cells slow down metabolisation
  • Renal cells cease filtering
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70
Q

Why is MODS so bad?

A

MODS is systemic

The trigger e.g. trauma - causes a body wide reaction

For some reason multiple organs are affected by an enhanced immune, hormone and metabolic response

Homeostasis starts to fail

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71
Q

describe MODS and inflammation

A

Inflammation is normal part of healing process

In MODS and Sepsis - causes problems

Cytokines produced (e.g. histamine, prostaglandin, and nitric oxid) = vasodilation

Affects BP (lower)

Affects tissue perfusion

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72
Q

describe MODS and odema

A

Inflammatory response causes leaky vessels ‘capillary leak’

Fluid shifts:

  • Hypovolaemia
  • Pulmonary oedema
  • Acute kidney injury
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73
Q

describe coagulation as it relates to MODS

A

Coagulation is a normal process in response to tissue damage

Pro-coagulation occurs when:

  • Tissue damaged
  • Cytokines released from macrophages or endothelium

Normal anti-coagulation factors balance this

Procoagulants consume anti-clotting factors in MODS

This leads to abnormal clotting in areas not damaged

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74
Q

examples of how organs might be in dysfunction in MODS

Specific complications

A

Cardiovascular - Patient needs vasopressors (e.g. adrenaline) despite fluids

Respiratory - patient requires mechanical ventilation

Renal - urine output less thsn 0.5ml/kg/hr; raised creatinine

Haematological - low platelet count; abnormal clotting

Metabolic - low pH (<7.3); increased lactate

Hepatic - raised LFTs

CNS - Reduced GCS

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75
Q

key factors of management of organ dysfunction

A

Resuscitation

  • Fluid restoration
  • Control of hypothermia & acidosis

Early treatment of infection / injury
- Early anti-microbial therapy (broad spectrum)

Steroid therapy
- Coricosteroids ‘calm down’ immune system response

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76
Q

outline of mods

A

A complex syndrome

Abnormal host response to a trigger e.g. trauma

Early recognition is key

Similar process to sepsis

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77
Q

what is jacksons burn wound model

A

review diagram

jackson’s burn wound model is a model for understanding the local response of burns wounds.

Three zones of a burn wound :

Zone of coagulative necrosis - Area nearest to the heat source (or other injuring agent). Results in immediate coagulation of proteins leading to irreversible cellular death.

Zone of stasis - Damage in this area is less severe but there is compromised circulation. Untreated, this area undergoes necrosis as the injury progresses. Observed clinically as the progression of the depth of a burn over several days (3-5 days). The tissue in this zone is potentially salvageable.

Zone of hyperaemia - In the outermost zone inflammatory mediators cause widespread dilatation of blood vessels. Provided there is resolution of hyper-dynamic response, tissues will recover.

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78
Q

how do burns cause damage twice

A

Initial destruction of tissue

Inflammatory response causes further problems

> 30% TBSA causes release of inflammatory mediators

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79
Q

how burns can affect around the body

resp, metabolic, immunological, cardiov

A

resp- bronchoconstriction, ARDS

Metabolic- increased BMR threschhold

Immunological- reduced immune response

Cardiov- reduce myocardial contractility, increased capilary permiability, peripheral and splanatic vasoconstriction

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80
Q

discuss burns impact of fluid loss

A

Fluid shifts reduce intravascular volume.

Onset often takes 6 to 8 hours.

Results in hypovolaemic shock

Rhabdomyolysis may begin…..

Renal failure

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81
Q

What makes cells live?

A

Life needs energy
Energy = ATP (Adenosine triphosphate)
The production of energy = respiration
This occurs in the mitochondria

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82
Q

What keeps cells alive?…

A

Cells need glucose to make ATP

ATP can be made without Oxygen
…BUT…only makes 8 ATP – Anaerobic respiration

With Oxygen – makes 30 ATP - Aerobic respiration

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83
Q

discuss Cellular effects of shock

A

Mitochondrial damage begins

Lysosomes rupture – begins cell lysis

Release of cytokines, lactic acid, complement, kinins, prostaglandins…..

Metabolic acidosis

Multiple organ failure begins

Reperfusion may exacerbate toxic mediator release (may lead to SIRS)

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84
Q

review coagulopathy in burns

A

review coagulopathy in burns

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85
Q

what is involved in the assessment and management of burns

A
  1. Immediate care
  2. Assessment of severity of burn
  3. Fluid resuscitation
  4. Patient flow chart
  5. Vital sign assessment
  6. Referral and specialist management
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86
Q

what is the impact of airway burns

A

Swelling due to burns in the upper airway can be fatal.

Swelling of the vocal cords can obstruct the airway completely.

Consider early intubation

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87
Q

Indicators of poss. inhalation injury

A

Hx of fire / explosion in enclosed space

Collapse / confusion at any time

Hoarseness / change of voice

Insp. stridor / exsp. wheeze

Facial burn – singed nasal hair

Soot in sputum

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88
Q

how do burns affect breathing

A

Inhalation of hot gases to bronhcial tree:

  • Damage to alveoli
  • Altered gas exchange
  • Pulmonary oedema

ALL cases should receive high conc. humidified O2

Senior anaesthetic help required

Tracheal tubes should be left uncut

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89
Q

what does smoke inhalation do

A

Smoke contains many harmful chemicals.

Inhalation of smoke can cause these poisons to enter the body.

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90
Q

why is carbon monoxide an issue

A

Carbon monoxide is present in almost all forms of combustion.

It attaches with great affinity to red blood cells. hb binds to CO blocking out normal oxygen

Don’t expect a “cherry red” appearance.

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91
Q

circulation issues with burns

A

Hypovolaemia due to fluid loss

Can result in acute kidney injury and widespread organ damage

Need to estimate extent of burn…

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92
Q

Assessment of severity of burn

A

Burn Severity is determined by:
Extent of burn – described as percentage of Total Body Surface Area (%TBSA)

Depth of burn.

Burn location.

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93
Q

Estimating the extent of burn

A

Serial halving

Palm of patient’s hand = 1 % (includes fingers)

Rule of nines

Lund & Browder charts

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94
Q

what s the burn Rule of nines

A

review chart

“Rule of Nines” is a methid of calculating total body surface area thst divides the body surface into areas of nine percent (%) or multiples of nine (%)

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95
Q

what is the lund bowder chart

A

review chart

used to assess the burned body surface area. Different percentages are used because the ratio of the combined surface area of the head and neck to the surface area of the limbs is typically larger in children than that of an adult.

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96
Q

describe erythema/ superficial burn like

A

Very painful – sensation throughout

Redness – good capillary refill

Skin often intact

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97
Q

describe partial thickness burn

A

Deeper than epidermis
Often blistered
Very painful
Sensation intact

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98
Q

describe full thickness burn

A

No sensation
May not be painful
Hard leathery
eschar

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99
Q

what are the catergories looked at for refferals for burns

A

extensive burns (SA), full thickness (cm), Inhalation injury, Associated problems, extremes of age, special types of burns eg. electrical, critical areas, non accidental burns, psychiatric illness

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100
Q

Primary management of burns

A

Commence fluid resuscitation

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101
Q

describe parkland formula

A

Parkland Formula
Crystalloid resuscitation with Hartmanns solution.
Volume (mls)required in first 24 hours:

4 x %TBSA x body weight in (kg)
Half the fluid given in first 8 hours
Other half given over remaining 16 hours
Time since incident (may mean ‘catch up’)

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102
Q

describe hypothermia

A

Temp less than 36.0deg C

One of the trauma triad

Can be caused by injury – skin is a thermoregulator

Can be caused by first aid – running water

Can be iatrogenic – cold hospital environment

Prevent – blankets, environment

Treat – warmed IV fluids (inc. blood), warmed blankets, Bair Hugger

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103
Q

systemic complications and management of burns

A

Renal failure may occur as a complication of renal hypoperfusion (inadequate resuscitation), septicaemia or haemoglobinuria/myoglobinuria.

Haematology Intravascular haemolysis along with wound losses will increase blood transfusion requirements.

Nutrition Patients are profoundly catabolic with a BMR peaking at 4 days. These patients require early and aggressive feeding preferably enterally to maintain intestinal mucosal integrity.

Cerebral Hyponatraemia complicating resuscitation may result in the burn encephalopathy syndrome. This is seen as cerebral irritability.

Sepsis Burn injury is associated with a generalised loss of immunocompetence, and sepsis remains a major cause of death in burns.

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104
Q

interventions other than fluid resus for burns patients

A

Analgesia
Sedation
Tetanus status?
Escharotomy?

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105
Q

pathophys of shock

A

Cells need perfusion with oxygen and glucose

Perfusion is provided by blood pressure

Where blood pressure is normal the cell is able to function normally

Mitochondria within the cell produce ATP + H2O + CO2 (Aerobic respiration)

When perfusion fails = shock

Cell switches metabolism to Anaerobic respiration = much less ATP + H2O + CO2 + Lactic acid

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106
Q

what does metabolic acidosis do (shock)

A

Metabolic acidosis causes mitochondria to fail

Cell lysis occurs

Lactic acid enters blood + inflammatory cytokines

Unless compensated – leads to metabolic acidosis systemically

Eventual multi organ involvement and dysfunction

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107
Q

Initial management of shock (hypov)

A

Catastrophic haemorrhage control

  • Direct pressure / elevation
  • Indirect pressure
  • Tourniquet
  • Haemostats

IV access – two large cannula – peripheral venous

Initial fluid bolus crystalloid 250ml and determine response

Consider blood transfusion

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108
Q

class 1 of shock

A

less than 15% blood loss, HR over 100, normal systolic, normal/ increased pulse pressure, 14-20 RR, slightly anvious

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109
Q

class 2 of shock

A

15-30% blood loss, HR over 100, normal systolic, decreased pulse pressure, 20-30 RR, mildly anxious

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110
Q

class 3 of shock

A

30-40% blood loss, HR over 120, decreased systolic, decreased pulse pressure, 30-40 RR, anxious/ confsed

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111
Q

class 4 of shock

A

over 40% blood loss, HR over 140, decreased systolic, decreased pulse pressure, over 35 RR, confused/ lethargic

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112
Q

what are the 3 possible response for shock treatment

A

rapid response, transient response, no response

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113
Q

rapid response to trauma characteristics

A

vitals return to normal. minimal fluid loss, low need for crystalloid and blood, type x- match blood prep, possible need for operative intervention,

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114
Q

transient response to trauma characteristics

A

vitals have transient improvvement , recurrence of low BP/ high HR, moderate and ongong fluid loss, high need for crystalloid, moderate to high need for blood, type specific bloo prep, likley need for operative intervention

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115
Q

no response to trauma characteristics

A

vitals remain abnormal, severe blood loss, high need for crystalloid, immediate need for blood, o neg blood prep, highly likely need for operative intervention

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116
Q

vascular access in shocked patients

A

Peripheral venous access difficult

Central access – needs skilled clinicians and takes time

options. ..
1. peripheral venous access
2. central venous cannulation ( skilled operaters needed,
3. intraosseous access

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117
Q

benefits of intraosseous access

A

Useful in difficult venous access

Landmarks easy to find

Can deliver fluids and most drugs rapidly and easily

Painful in conscious patients

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118
Q

examples of 2 catergories of life threatening circulation problems

A

External haemorrhage
- Wounds, traumatic amputations

Internal haemorrhage

  • Penetrating trauma e.g stab / gunshot
  • Fractures e.g. pelvis
  • Abdominal e.g. liver rupture, spleen, small bowel
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119
Q

symptoms of life threatening circulation problems

A
Tachycardia
Pale
Oliguria
Tachypnoea
Diaphoresis
BP……?
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120
Q

as we loose blood vessels….

A

vasoconstrict until cant and plateu

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121
Q

as we loose blood heart rate ….

A

HR increases unitil plateaus

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122
Q

as we loose blood bp …

A

stays constant due to compensation then falls rapidly

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123
Q

describe Trauma induced coagulopathy, what makes it worse?

A

Systemic anticoagulation

Fibrinolysis

Made worse by:

  • Hypothermia
  • Acidosis
  • Haemodilution

Imbalance of procoagulant / anticoagulant / platelets and fibrinolysis

Occurs in approx. 25% of all major trauma patients

4 times more likely to die than those without the condition

Likelihood reduced by:

  • Prevention of hypothermia
  • Haemorrhage control
  • Appropriate blood / fluid management
124
Q

components of the vertebral column (cross section)

A

review image in word

  • intravertebral foramen
  • vertebral body
  • intervertebral disc

intervertebral disc can become compressed in a weight bearing situation

125
Q

what is c1 to c7 of the spine

A

cervical curvature (concave)

126
Q

what is t1 to t12 of the spine?

A

thoracic curvature (convex)

127
Q

what is l1 to l5 of the spine?

A

lumbar curvature (concave)

128
Q

what is sacrum of the spine like

A

belove lumar spine above coccyx, fused, convex

129
Q

what is the coccyx of the spine like

A

4 fused vertebrae

130
Q

where is the normal weight bearing line on the spine

A

on the concave right side

131
Q

what is kyphosis

A

An increased front-to-back curve of the upper spine is called kyphosis.

132
Q

what is scoliosis

A

abnormal lateral curvature of the spine.

133
Q

vertebral anatomy. what are the 3 main parts of the vertebrae

A

Body
Arch
Articular processes

134
Q

describe body of vertebrae

A

Transfers weight along axis of column

Connected by ligaments

Separated by intervertebral discs

135
Q

describe the vertebral arch of the vertebrae

A

Forms posterior margin of vertebral foramen (foramen – opening)

Walls – pedicles

Roof – laminae

All together form – vertebral canal

136
Q

describe the lumbar vertebrae

A

Largest vertebrae

Vertebra is thicker

Bear the most weight

Spinous process – surface attachment for lower back muscles

137
Q

describe joints of the vertabrae

A

No intervertebral disc between C1 / C2

Nucleus Pulposus – soft, elastic, gelatinous core – surrounded by Anulus Fibrosus – effectively a shock absorber

Aging process – less water content in Nucleus Pulposus

  • reduced shock absorbency
  • Length of vertebral column shortens
138
Q

review diagram labeling joints of the spine

A

review diagram labeling joints of the spine

The bottom picture shows a disc prolapsing and impinging on the spinal cord – this is very common in lumbar spine area and is usually known as a slipped disc.

139
Q

breifly describe physiology of the spinal cord

A

Different parts of the cord have different functions

Some parts are ascending – travelling from receptors to brain
Some descending - from brain to effectors

140
Q

describe neurogenic shock

A

Caused by interruption of sympathetic stimulation at or above T6

Shock = inadequate perfusion of the vital organs

Low BP
BP = C.O. x Peripheral Resistance

Sympathethic stimulation lost due to cord injury

Results in loss of muscle tone and loss of normal vaso constriction
Reduced vasoconstriction = reduced peripheral resistance = reduced BP

Signs and symptoms:
- Hypotension, bradycardia, flushed warm extremeties…but urine output remains within normal range

It is possible to have hypovolaemic shock AND neurogenic shock

141
Q

what is spinal shock

A

This is a temporary state – lasts days to weeks

Loss of motor and sensory function below level of cord injury.

Loss of all spinal reflexes below injury

Flaccid paralysis (including bladder and bowel)

Priapism may be present

Ends when reflex arcs
below level of injury start to return.

Different as it is related to neurological function rather than blood pressure

142
Q

what is Poikilothermia

A

Inability to maintain core body temperature

Temperature usually regulated by hypothalamus

Results in vasodilation and loss of heat through this mechanism

143
Q

Classification of spinal cord injuries

A

tetraplegia

paraplegia

144
Q

tetraplegia vs paraplegia

A

Tetraplegia
- Impairment or loss of motor and / or sensory function in cervical segments of spinal cord as a result of damage to neural elements of cord
Decreased function to arms, trunk, legs and pelvic organs

Paraplegia
- Impairment or loss of motor and / or sensory function in thoracic, lumbar or sacral segments of cord as a result of damage to neural elements of cord
Arm function remains intact
Trunk, legs and pelvic organs may be involved.

145
Q

breifly describe cellular respiration

A

Life comes from Energy = ATP

What does a cell need to make energy (ATP)?
- Oxygen and Glucose

Inadequate perfusion of Oxygen and Glucose = cell dysfunction or cell death

ATP – produced in mitochondria (internal respiration)

With normal perfusion of Oxygen = Aerobic respiration

Inadequate perfusion or no Oxygen = AnAerobic respiration

146
Q

aerobic respiration vs anarobic respiration

A

Aerobic respiration produces:
Sufficient ATP for cell to function and survive
Waste products – water and CO2

Anaerobic respiration produces:
Much less ATP
Cell dysfunction or death
Waste products – water, CO2 and Lactic acid

147
Q

3 components of the cardiovascular system

A

blood, vessels and heart

148
Q

t or f

Provides cell with oxygen and glucose – removes waste

149
Q

How does Oxygen and Glucose get to the cell?

A

Carried in Blood – which is carried in Blood vessels

150
Q

How does the Blood move to the cells and perfuse them?

A

pushed by the heart

this push is what we know as blood pressure

151
Q

t or f the body doesnt need bp to be normal

152
Q

BP equation

A

Blood pressure = Cardiac Output (CO) x Peripheral Resistance (PR)

153
Q

how is CO and BP changed when trying to stabalise low bp

A

If a drop in B.P. is detected the body will try to bring it back to normal by altering CO and PR

154
Q

review physiology of the immune system

A

Inflammation is normal – 1st stage of healing

Caused by release of cytokines (chemicals released by the immune system that have an affect on other cells)

Cytokines include:
+Histamine from mast cells - powerful vasodilator
+Nitric oxide – powerful vasodilator
+Tumour Necrosis Factor, Interleukin1 and many others

Vasoldilation
Also triggers change in core temperature – pyrexia or hypothermia

155
Q

define sepsis

A

“Sepsis is life threatening organ dysfunction caused by a dysregulated host response to infection”
(Singer, et al 2016)

In plain English:
Life threatening organ failure caused by an abnormal response to infection

156
Q

Sepsis pathophysiology

A

In Sepsis release of pro-inflammatory cytokines systemically (throughout the body) – which cause:

+ Vasodilation:
- decreased Peripheral Vasc. Resistance = decreased B.P.
- Compensatory mechanisms fail (Angtiotension II & Noradrenaline)
- Causes blood vessels to become leaky
…..Causes widespread oedema
……Fluid from oedema comes from systemic circulation = relative hypovolaemia

+Drop in B.P. (if not managed) causes:

  • Anaerobic respiration / Mitochonrial dysfunction
  • Lactic acid production = Metabolic Acidosis
  • Metabolic Acidosis – leads to cell death and further inflammatory reaction
157
Q

patient assessment considerations for sepsis

A
A- E assessment essential
 Sepsis is a medical emergency
 Early recognition is key
 A, B, C, D, E assessment
 YOU could be the first person to spot that something is wrong
158
Q

breathing signs of sepsis

A

Resp Rate >20
21 – 24 = Moderate risk
>24 = High risk
Or new need for >40% oxygen to maintain SaO2 more than 92% = High risk

ANY ONE HIGH RISK– INITIATE SEPSIS BUNDLE
TWO OR MORE MODERATE RISK INITIATE SEPSIS BUNDLE
(NICE, 2016)

159
Q

circulation signs of sepsis (ranges)

A

HR >90bpm

  • 91 – 130 = Moderate risk
  • > 131 = High risk

Systolic B.P. <100mmHg

  • 91 – 100 = Moderate risk
  • <90mmHg = High Risk

Not passed urine in past 12 – 18 hours = Moderate risk

Not passed urine > 18hrs = High risk

ANY ONE HIGH RISK– INITIATE SEPSIS BUNDLE
TWO OR MORE MODERATE RISK INITIATE SEPSIS BUNDLE
(NICE, 2016)

160
Q

disablility/ neurological signs of septic shock

A

GCS< 15 (of new onset)

ANY ONE HIGH RISK– INITIATE SEPSIS BUNDLE
TWO OR MORE MODERATE RISK INITIATE SEPSIS BUNDLE
NICE, 2016

161
Q

exposure signs of septic shock

A
  • Raised white cell count
  • Temp - Pyrexia>38C or Hypothermia <36 C = Moderate Risk
  • Mottled / ashen appearance / non blanching rash = High Risk
  • Signs of infection – redness / swelling / discharge
  • Cyanosis = High Risk

ANY ONE HIGH RISK– INITIATE SEPSIS BUNDLE
TWO OR MORE MODERATE RISK INITIATE SEPSIS BUNDLE
(NICE, 2016)

162
Q

considerations when using sepsis care bundle

A

Recently became one single bundle

Within first hour of arrival:

  1. Measure lactate – remeasure if >2mmol/l
  2. Obtain blood cultures before administering antibiotics
  3. Administer broad spectrum antibiotics
  4. Rapid administration 30ml/kg crystalloid fluid if hypotensive / Lactate > 4mmol/l
  5. Give vasopressors if hypotensive during or after fluid – keep MAP >65mmHg

Time zero = time of triage

163
Q

priorities of care in sepsis - airway

A

Airway

+ Ensure patency (esp. GCS< 8)

164
Q

what are the functions of the skin

A

Also known as the integumentary system

Function:

  • Protection
  • Temperature regulation
  • Water regulation
  • Sensory reception

How would the loss of any of these functions affect the person?

165
Q

what are the different layers of the skin?

A

Epidermis

Dermis

  • Nerve endings
  • Blood vessels
  • Hair follicles
  • Sebaceous glands
  • Sweat glands

Subcutaneous
-Adipose tissue

166
Q

review layers of the skin diagram

A

review layers of the skin diagram

hair
pore
germinal layer of epid.
sebaceous g;and
sensory nerve
sweat gland
hair follicle
blood vessel
subcut fat
fascia
muscle
167
Q

What is a burn?

A

Comes from Old English word ‘Baernan

An injury caused by heat, or a chemical, radiological or mechanical force that simulates the action of heat

168
Q

what are the types of thermal burns

A
Flame
Scald
Contact
Steam
Flash
169
Q

types of burns

A

Thermal
Chemical
Electrical
Radiation

170
Q

Sources of Chemical Burns

A
Acids
Alkalines (bases)
Oxidisers
Phosphorous
Vesicants
171
Q

Chemical Burns mechanisms

A

Reduction

Oxidation

Corrosion

Desiccation (drying out)

Vesication (causing blister e.g. mustard gas)

172
Q

types of electrical burns

A

Contact burns
Flash burns
Flame burns

But can travel along muscle and nerve fibres

173
Q

how do lightning strikes affect people, prevention of injury strategies?

A

50 per year injured

10 per year die

Prevention is a priority

  • Don’t be the tallest object
  • Don’t stand under tall objects
  • Take shelter in a substantial structure
174
Q

Electrical Burn Complications

A
Asphyxia
Cardiac arrest
Neurological
Convulsions
Kidney damage
175
Q

what are radiation burns

A

Radiation burns can be caused by X-rays or radiation therapy to treat cancer.

176
Q

treatment of radiation burns

A

May be contaminated
- Decontaminate before transport

Irrigate open wounds gently to avoid further damage
- Internal radiation absorption

Contact radiation burns

  • Decontaminate the wound.
  • Treat it as a burn.
177
Q

assessment and management of burns

A
  1. Immediate care
  2. Assessment of severity of burn
  3. Fluid resuscitation
  4. Patient flow chart
  5. Vital sign assessment
  6. Referral and specialist management
178
Q

describe immediate care of the burn

A

Stop the burning process:
- Remove the heat – water / cooling pad (Water-jel)

  • Remove the burning agent e.g. Chemical burns – irrigation
  • Begin ABCDE approach
179
Q

considerations for treatment of airway burnt patients

A

Swelling due to burns in the upper airway can be fatal.

Swelling of the vocal cords can obstruct the airway completely.

Consider early intubation

180
Q

What is critical care nursing?

A

Nursing care of patients who have…Manifest or potential disturbances of vital organ functions and who need assistance, support and restoration to health or the delivery of pain management preparation for a dignified death.’
World Federation of Critical Care Nurses (2016)

181
Q

Essential care of the critically ill patient- 2 factors

A

reducing risk to patients

provision of quality care

182
Q

how to reduce risk to the critically ill patient

A
  • recognise specific need, particlarly sedate/ unconcious or immobile pta
  • recognise specific complications that may req. special obs or treatment
  • vigilant monitoring
  • ADPIE
    manage environemntal factors affectig the pt
183
Q

how to provide quality care to the critically ill pt

A
  • developmemt of skills and knowledge for practice
  • EBP
  • Optimal use of protocol driven therapy
  • competent, efficient and safe practice, ADPIE, monitoring consequence of nursing interventions
  • continuity of care
184
Q

read chap 5 of critical care text

A

read chap 5 of critical care text

185
Q

what is Invasive Positive Pressure Ventilation

A

mechanical ventilation
Over half of all admissions to ICU require invasive (also called mechanical) ventilation

(invasive positive pressure ventilation, which requires delivering breaths either through an endotracheal tube or a tracheostomy tube.)

186
Q

IPPV indications

A

Apnoea

Inability to protect airway e.g. loss of gag reflex, low GCS

Clinical signs of rest failure - such as … SOB, productive coughing,
wheezing, cyanosis

Inability to sustain oxygenation to meet metabolic demands

187
Q

review phases of normal breathing and vetilator respiratory components diagrams

A

review phases of normal breathing and vetilator respiratory components diagrams

188
Q

How does mechanical ventilation work?

A

Patient intubated with endotracheal tube

Modern ventilators - able to detect, respond and control pressure and gas flow

Respiratory cycle - inspiration and expiration

A ventilator ‘breath’ can be classified by:
+ The mechanism that starts inspiration - patient or ventilator
+ The parameter that is limited / controlled during inspiration
+ The parameter that cycles the breath from inspiration to expiration

For example the ventilator could be set as:

  1. Ventilatior initiated inspiration
  2. The duration of inspiration may be the controlled phase
  3. A tidal volume may be set and this will trigger the expiratory phase
189
Q

A ventilator ‘breath’ can be classified by:

A

ventilator ‘breath’ can be classified by:
+ The mechanism that starts inspiration - patient or ventilator
+ The parameter that is limited / controlled during inspiration
+ The parameter that cycles the breath from inspiration to expiration
For example the ventilator could be set as:
1. Ventilatior initiated inspiration
2. The duration of inspiration may be the controlled phase
3. A tidal volume may be set and this will trigger the expiratory phase

190
Q

complications of mechanical ventilation

A

complications related to intubation, mechanical complications related to presence of ETT, ventilator induced lung injury, complications related to oxygen, complications of mechanical ventilation

191
Q

describe venous access in critical care?

A

difficult to cannulate shocked pt eg. veins collapsed

192
Q

venous vein accsess routes

A

Peripheral

Central
- Jugular or subclavian

Peripherally Inserted Central Cannulaton

193
Q

-Indications for PICC line insertion

A

parenteral delivery of nutrition, antibiotics, and analgesics, as well as chemotherapy and repeated blood transfusions.

194
Q

how is picc line inserted and where does it go?

A

PICCs are placed in a vein of the upper arm. The right basilic vein is the vein of choice due to its larger size and superficial location.

Once a suitable vein is identified in your arm, the skin around the area is cleaned and prepared. Numbing medicine is injected into the skin to minimize pain. To place the PICC line, a needle is inserted through your skin and into the vein in your arm. Ultrasound or an X-ray might be used to confirm the placement.

small incision is made in the vein so that a catheter can be inserted.

Once the catheter is in your arm, it’s carefully advanced along the vein. The catheter continues up your arm and toward your heart.

195
Q

What care does picc line need - daily and weekly

A
keep dressing dry and in tact
bp on other arm
flush befor eand after meds
change dressing and ports every 7 days
watch for contamination
watch for signs of local infection
196
Q

What possible complications are there for picc line?

A
Bleeding.
Nerve injury.
Irregular heartbeat.
Damage to veins in your arm.
Blood clots.
Infection.
A blocked or broken PICC line.
197
Q

why do we need BP

A

Perfusion
- Circulation of blood within an organ or tissue
…..Adequate amounts to meet the cells current needs for oxygen, nutrients and waste removal

198
Q

what do cells do with blood

A

receive needs and expel wastes, transport system

needs used to maintain organs so the body can function efficiently

199
Q

Organs perfusion requirements?

A

The heart requires constant perfusion

Brain and spinal cord cannot go for more than 4 to 6 minutes

Kidneys will be permanently damaged after 45 minutes

Skeletal muscles cannot tolerate more than 4 hours

200
Q

3 elements of the cardiovascular system

A

3 elements:
Heart
Blood and its components
Blood vessels

201
Q

components of Cardiac output

A

Stroke volume

  • Pre-load
  • Myocardial contractility

Heart Rate

After load / Peripheral Vascular resistance have big impact

202
Q

what is cardiac output

A

Amount of blood pumped through the circulatory system in 1 minute

Expressed in litres per minute

Cardiac Output = Stroke Volume × Heart Rate

203
Q

components of stroke volume

A

Preload…
- Starlings law
“the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return…”

  • Myocardial contractility
204
Q

describe the sympathetic nervous system

A

Prepares the body to respond to various stresses

  • Increases heart rate
  • Strengthens the force of cardiac muscle contractions

Noradrenaline

Adrenaline

205
Q

what triggers the sympathetic and parasympathetic stimulation

A

Cardiac centre in medulla

  • Sympathetic stimulation
  • Parasympathetic stimulation

Baro and chemo-receptors in Carotid and Aortic arteries

206
Q

what is afterload/ peripheral vascular restatance

A

the force a chamber of the heart has to generate to eject blood

Usually refers to left ventricle

207
Q

what is normal blood volume

A

Normal adult blood volume – 7% of body weight

70kg - 5,000mls

208
Q

equation for oxygen delivery and influences on arterial oxygen concentration

A

Oxygen delivery = Cardiac output x Arterial oxygen conc.

Arterial oxygen concentration

  • quantity of haemoglobin
  • saturation of haemoglobin
209
Q

what does hb do to o2

A

Once oxygen has entered the blood from the lungs, it is taken up by haemoglobin (Hb) in the red blood cells

oxygen bonded with Hb molecules travel to organs and oxygen is released to tissue cells

210
Q

types of blood vessels

A
Arteries
Arterioles and capillaries
- Diffusion
Veins
Venules

75% of blood capacitance is within venous system – “Venous reserve”

211
Q

What is blood pressure equation

A

Blood pressure = Peripheral resistance x Cardiac output

212
Q

how is blood pressure maintained

A

BP = CO x PR

Maintain BP at all costs

Change CO
- Heart rate
- Stroke volume 
...Force of contraction
...Increased pre-load

Change Periph. Resist

213
Q

what causes change in PVR

A

Baro-receptors – Carotid and Aortic

Release of Adrenaline - Noradrenaline

  • Vasoconstriction
  • Increased afterload

Renin – Angiotensin- Aldosterone pathway

Anti-diuretic hormone

214
Q

Pathophysiology of shock - What is shock?

A

“Shock is the manifestation of the rude unhinging of the machinery of life”
Samuel V. Gross 1872
OR

“Shock is an inadequate delivery of oxygen and nutritive substrates to the tissues”

215
Q

what are the Metabolic effects of shock

A

Reduction in oxygen – anaerobic respiration

Much less energy produced

Lactic acid produced as a by-product

Cellular breakdown begins

216
Q

Cellular effects of shock

A

Mitochondria damage begins

Lysosomes rupture – begins cell lysis

Release of cytokines, lactic acid, complement, kinins, prostaglandins…..

Metabolic acidosis

Multiple organ failure begins

Reperfusion may exacerbate toxic mediator release (may lead to SIRS)

217
Q

how might the body try compensate for shock

A

Neurogenic
- Baroreceptors

Endocrine

  • Vasopressors – Adrenaline, Noradrenaline
  • Renin – Angiotensin
  • Aldosterone
  • ADH

Inflammatory
- Nitric Oxide

218
Q

Definition of hypovolaemic shock, what fluids can be lost

A

Shock caused by loss of fluid volume:

Whole blood – haemorrhage

Plasma – burns

Interstitial – diaphoresis, vomiting, diarrhoea

219
Q

primary survey in relation to shock

A
Some suggestion of change to 
 AcBCDE in massive haemorrhage
Ac
B – RR, Sa02, IPPA
C – Pulse, BP, Cap refill, urine output
D – AVPU
E – Any obvious bleeding
220
Q

basics of management of shock

A

Control of obvious external bleeding
Splinting of long bone fractures
Supplemental oxygen
Fluid resuscitation

221
Q

what is splinting

A

secure (a broken limb) with a splint or splints

222
Q

where may massive blood loss occur leading to shock

A

Massive haemothorax 1500 – 2000ml

Fractured Femur 1000 – 1200 ml

Fractured pelvis - >2000ml

223
Q

principles of fluid resuscitation in shock

A
IV Fluids...
- Don’t carry oxygen (yet!)
- Don’t clot
MUST be warmed
Dilutional coagulopathy...
224
Q

principles of fluid resusitation (Blood)

A

Type specific takes time

Transfused blood does not initially coagulate well

Potential for transfusion reaction

Potential for TRALI – Transfusion Related Acute Lung Injury

225
Q

fluid resus methods

A

Fluid challenge v hypotensive resuscitation

226
Q

what is fluid challenge

A

The principle behind the fluid challenge technique is that by giving a small amount of fluid in a short period of time, the clinician can assess whether the patient has a preload reserve that can be used to increase the stroke volume with further fluids.

227
Q

what is hypotensive resusitation

A

“Permissive hypotension”

Increased mortality assoc. with rapid fluid challenge (Geoghegan et al, 2010)

Evidence recommends withholding fluids

  • Where a radial pulse is palpable
  • Where a central pulse if palpable in penetrating torso trauma
  • This referred to the pre-hospital setting…

Sapsford (2008) argues insufficient evidence to alter algorithm in hospital at present
Head injuries…

strategy that uses limited fluids and blood products during the early stages of treatment for hemorrhagic shock. A lower-than-normal blood pressure is maintained until operative control of the bleeding can occur.

228
Q

What is Aggressive fluid challenge (ATLS)

A

Initial warmed IV bolus of up to 2,000ml (20ml/kg in a child) as rapidly as possible

Observe patients response…

229
Q

what is the non average patient for which consideration should be taken during shock care

A

Athletes

Pregnancy

Extremes of age

Complicating factors:
Medicines
Pacemaker
Anaemia

Hypothermia

230
Q

crystalloid or colloid for resus during shock

A

Crystalloid require at least 3:1 ratio of replacement

Colloids much more expensive

…what is the evidence

231
Q

What is Tranexamic acid used for in shock

A

Anti-fibrinolytic agent i.e. blocks the action of clot dissolving enymes.

Used off label in the UK – up to the clinicians judgement as to indication

CRASH 2 trial (2011) – increased survival without increased risk of adverse events.

Recommended administration within 3 hrs

Cost +/- £6.80 per dose.

232
Q

What is Tranexamic acid used for in shock

A

Anti-fibrinolytic agent i.e. blocks the action of clot dissolving enymes.

Used to reduce haemorrhage

Used off label in the UK – up to the clinicians judgement as to indication

CRASH 2 trial (2011) – increased survival without increased risk of adverse events.

Recommended administration within 3 hrs

Cost +/- £6.80 per dose.

233
Q

the primary survey for trauma

A

Similar to A- E assessment
AcBCDEF

Fix a life threatening problem at each step before moving on

Can be done simultaneously with other members of the trauma team

234
Q

What is involved in Catastrophic haemorrage part of the primary survey? types/ possible causes?

A

Relatively uncommon in hospital

Bleeding that if not stopped will lead to death rapidly

Arterial external haemorrhage

Traumatic amputations

Penetrating trauma e.g. stabbing / shooting

Rapid treatment:

  • External direct pressure
  • Tourniquet
  • Haemostatic agents
235
Q

What is catastrophic haemorrhage?
what is involved in Catastrophic haemorrage part of the primary survey?
what situations can cause it?

A

Relatively uncommon in hospital

Bleeding that if not stopped will lead to death rapidly

Arterial external haemorrhage

Traumatic amputations

Penetrating trauma e.g. stabbing / shooting

Rapid treatment:

  • External direct pressure
  • Tourniquet
  • Haemostatic agents
236
Q

What is involved in Airway with restriction of c-spine motion part of the primary survey

A

Airway take priority over all other elements

All unconscious patient suspected of having c-spine injury

All injuries above clavicles should be suspected of having c-spine injury

Collar v self-splinting (we will cover in more detail in Topic 7 - Spinal Injury)

Ability to speak?

What indicates possible airway obstruction?

Manual manoeuvres - head tilt or jaw thrust?

If moving patient - have suction available

237
Q

What is involved in Breathing part of the primary survey

A
Remember RIPPA from Year 1?
Resp rate
Inspect
Palpate
Percuss 
Auscultate

What observations tell you about this? O2, RR

What immediate interventions?
BVM, ventilation

238
Q

What is involved in circulation part of the primary survey

A

What observations tell you about the patient’s circulatory state?

oliguria- low urine output… indicates decreased renal blood flow,

What possible immediate interventions?
fluids

239
Q

What is involved in disability part of the primary survey, things affecting LOC?

A

What are we actually assessing at this step?
LOC

What would a GCS of less than 8 mean?
intubate

List 4 things that can affect conscious state:
drugs./substance abuse.
medications.
epilepsy.
low blood sugar.
240
Q

What is involved in exposure part of the primary survey

A

Look for any ‘OMG’ injuries

Any obvious wounds, deformed limbs, bruising

241
Q

What is involved in farenheit part of the primary survey

A

Hypothermia results in poor outcomes for trauma patients

Blood coagulates poorly at lower temperatures
- Trauma triad - acidosis, hypothermia, coagulopathy
What does iatrogenic mean?

Hypothermia in trauma is commonly iatrogenic

It must be prevented:

  • Bair hugger
  • Warmed IV fluids
242
Q

pharmacology used in major trauma

A

Tranexamic acid
- Used to reduce haemorrhage

Analgesia

Anaesthesia / sedation

eg. Fentanyl , propofol- general anaesthetic agent, rocuronium - neuro-muscular blocker

243
Q
  • What type of drug is Fentanyl and How is it different to morphine?
    contraindications?
A

Fentanyl has an analgesic and sedative effect on the human body. it is an opioid analgesic

Although Morphine Sulphate and fentanyl are both opiate analgesic medications there are
some differences between the medications.

Fentanyl is considered 50 to 100 times more
potent than morphine and fentanyl is a synthetic
opioid where as morphine is pure and comes from opium. (Trescot et al., 2008).

244
Q

Rapid sequence induction - what is it? example

A

Rapid sequence induction (RSI) is a method of achieving rapid control of the airway whilst minimising the risk of regurgitation and aspiration of gastric contents.

airway management technique that produces inducing immediate unresponsiveness (induction agent) and muscular relaxation (neuromuscular blocking agent) and is the fastest and most effective means of controlling the emergency airway

eg. Fentanyl , propofol- general anaesthetic agent, rocuronium - neuro-muscular blocker

245
Q

Psychological factors following major trauma

A

Post –traumatic stress disorder may be common not just to trauma (injury) but to critical illness

Severity of injury does not predict a PTSD reaction

Important to follow up with patient in the long term – liaison with primary care

Consider your words
patients will remember what you say for a lot longer than what you do

246
Q

Anatomy of the spine

A

Bony structures
- Vertebral column – cervical, thoracic, lumbar, sacral and coccyx

  • Spinal Cord
  • Joints
  • Muscle groups
247
Q

function of the spine

A
- Support
Weight bearing (anterior -Vertebral Body)

Movement

  • Muscle attachments
  • Joint articulations

Nerve distribution & protection (posterior Vertebral Arch)

248
Q

describe the cervical spine

A

The cervical spine
C1 – is called Atlas – it carries the world (head) on it’s shoulders
C2 – is called the axis – this is the bone on which the head pivots (like an axle on a car wheel)

C2 has a peg (Dens or ‘tooth’) – this stops C1 from slipping forward.
The xray shows a fracture of c1 and c2
This is usually fatal and referred to as Hangmans fracture

249
Q

describe the lumbar vertebrae

A

Largest vertebrae
Vertebra is thicker
Bear the most weight
Spinous process – surface attachment for lower back muscles

250
Q

describe the joints of the spine

A

No intervertebral disc between C1 / C2

Nucleus Pulposus – soft, elastic, gelatinous core – surrounded by Anulus Fibrosus – effectively a shock absorber

Aging process – less water content in Nucleus Pulposus

  • reduced shock absorbency
  • Length of vertebral column shortens
251
Q

Common spinal cord injuries

A

Approx 180000 cases of spinal cord injury globally p.a.

Leading causes – Motor vehicles – followed by falls, snowboarding, rugby and diving

51% are tetraplegic – all 4 limbs

Main risk factors:
Age
Gender
Alcohol / drug use

Most common vertebra involved – C5 – 7, T12 and L1

252
Q

primary spinal cord injury?

A

Mechanical – bone fragments, direct trauma

Damage to axons, blood vessels, cell membranes of cord

253
Q

secondary spinal cord injuries?

A

Occurs minutes to years after primary injury

Changes in blood supply

Electrical activity

254
Q

immediate assessment process following spinal cord injury

A
- Catastrophic haemorrhage
Ac – Airway with restriction of spinal movement
B - Breathing
C – Circulation 
D - Disability
E - Exposure
F - Fahrenheit
255
Q

immediate care following spinal cord injury

A

Application of cervical collar

Indications

  • Alteration in sensory or motor function
  • Unconscious
  • Can have adverse effects e.g. increased ICP
  • In line spinal control
  • Observe airway – especially when moving patient

What would you do if patient vomits on route to x-ray for example?
bring suctioning and equipment along

256
Q

aim of immediate care following spinal injury

A

Aim is to prevent secondary injury

  • Observe for neurogenic shock
  • Further movement causing further damage
  • Reduce inflammation – swelling
  • Assessment and stabilise patient
  • CT / MRI scan with xray
  • Consider patient pressure areas!
257
Q

possible ongoing care needs following spinal injury

A
  • May require Halo frame
  • Gastrointestinal dysfunction
    …..May require nasogastric tube for first 48 hra
    …..Distension and inability to empty bowel
    ……Slow digestive processes
- Genito urinary dysfunction
....Urinary catheter required
....Loss of voluntary bladder control
....Priapism in men 
Impotence in men
  • Pressure care crucial
258
Q

how a cervical collar should be fitted and its’ purpose

A

Measure the distance from the top of the patient’s shoulder to the angle of the jaw with your hand (image 1)
On the collar, measure from the bottom of the rigid plastic to the “measuring post”. This should correspond to the above measurement (image 2)
Check that the collar fits correctly
The neck should not be overextended
The mouth should not be able to be fully opened

purpose - to support your neck and spinal cord, and to limit the movement of your neck and head.

259
Q

Explain what a log roll is and its’ purpose

A

Logrolling is a common patient care procedure performed by many health care workers. The purpose of logrolling is to maintain alignment of the spine while turning and moving the patient who has had spinal surgery or suspected or documented spinal injury.

260
Q

what is autonomic dysreflexia

A

Autonomic dysreflexia is a syndrome in which there is a sudden onset of excessively high blood pressure. It is more common in people with spinal cord injuries that involve the thoracic nerves of the spine or above (T6 or above).

signs of AD include high blood pressure, pounding headache, flushed face, sweating above the level of injury, goose flesh below the level of injury, nasal stuffiness, nausea, and a slow pulse

261
Q

4 signs or symptoms that would lead you to suspect your patient has a spinal cord injury

A
  • extreme back pain
  • numbness
  • weakness
  • loss of bladder/ bowel function
262
Q

What is poisoning / intoxication?

A

Poisoning can be defined as an interaction between a foreign chemical (toxin) and a biological system that results in damage to a living organism.

263
Q

risk assessment for poisoning/ intoxication?

A

Not all overdoses are deliberate / not all accidents are accidental

  1. What agent & formulation (e.g. tablet, slow release etc.)
  2. Dose (if known)
  3. Time since ingestion
  4. Clinical features and progress
  5. Patient factors (weight / comorbidities / ingestion of others substance e.g. alcohol
264
Q

initial assessmet of poisoning/ intox

A

primary survey

265
Q

factors to consider when caring for poisoning/ intox./ care- treatment options

A

Supportive care and monitoring

Investigations
- Screening and specific investigations

Decontamination

Enhanced elimination

Antidotes

Disposition

266
Q

Management of common presentations of poisoning/ intox

A
Very few specific antidotes
- Specific antidotes include:
Naloxone
Flumazenil for benzodiazepines
N-Acetylcysteine for paracetamol

supportive care

267
Q

What is ‘supportive’ care?

A

The goal of supportive care is to prevent or treat as early as possible the symptoms of a disease, side effects caused by treatment of a disease, and psychological, social, and spiritual problems related to a disease or its treatment.

268
Q

Consider possible effects of poison, what systems?

A

Poisoning morbidity and mortality usually results from the acute effects of the toxin on the cardiovascular, central nervous or respiratory systems.

Monitoring is essential to detect the progress of the intoxication and to time the administration of supportive care.

269
Q

If the patient deteriorates more quickly than expected, …? (intox/ poisoning)

A

go back to the resuscitation phase, then revise the risk assessment.

To ensure ongoing assessment is comprehensive, the patient requires regular:

  • Vital signs, cardiac monitoring, neurological assessment
  • Haemodynamic monitoring, psychological assessment
  • General assessment for signs such as rashes, diaphoresis.
270
Q

what is decontamination

A

The principle of decontamination is that by reducing the dose absorbed the subsequent severity and duration of clinical toxicity will be reduced.

271
Q

risks of decontamination

A

Tendency to overestimate the potential benefits / underestimating potential hazards of gastrointestinal decontamination procedures

No longer routine, the decision to decontaminate is based on weighing up the benefits against the risks

Basic resuscitation and supportive care take precedence

272
Q

poisoning decontamination options

A
Options include:
Single dose activated charcoal
Induced emesis
Gastric lavage
Whole bowel irrigation.
273
Q

what is the aim of enhanced elimination

A

Aims:
- Reduce severity & duration of clinical intoxication by increasing the rate of removal of an agent.

  • Indicated if they reduce mortality, length of stay, compilations or the need for other invasive interventions
  • Used where agents are characterised by: severe toxicity, poor outcome despite good supportive care and antidote administration, slow endogenous rates of elimination, suitable pharmacokinetics
274
Q

enhanced elimination options

A

Multiple dose activated charcoal

Haemodialysis and haemofiltration

Urinary alkalinisation

Charcoal haemoperfusion.

275
Q

review alcohol poisoning

A

review alcohol poisoning

276
Q

review opioid poisoning

A

review opioid poisoning

277
Q

review methamphetamine poisoning

A

review methamphetamine poisoning

278
Q

review paracetamol poisoning

A

review paracetamol poisoning

279
Q

review snake bite poisoning

A

review snake bite poisoning

280
Q

Trauma in the older person?

A

Only 8% return to independent living 1 year post polytrauma.

  • Diminished vision, hearing and touch expose older people to increased risk of injury
  • Hospital separations increase exponentially, becoming extremely high in the 85+ age group.
281
Q

trauma and falls?

A
  • Falls are the main cause for injury-related hospital separations
  • The reason for the fall is likely to be complex, despite a simple explanation
  • There needs to be a falls assessment and referral programs for those who do not require immediate hospitalization.
282
Q

the aging process skin injury

A

Skin
Epidermis flattening and loss of papillae leads to decreased adhesion between layers of the skin

Loss of subcutaneous fat and wrinkling of the skin

Nails become thick and brittle.

283
Q

the aging process muscoskeletal injury

A

Atrophy of tissue extends to muscle and bone

Decreased muscle strength and movement

Bone mass decreases, resulting in more brittle bones.

284
Q

the aging process respiratory system injury

A

Respiratory system
•Trachea and rib cage become less flexible
•The number of alveoli reduces
•Reduction in the arterial partial-pressure of oxygen.

285
Q

the ageing process circulatory system injury

A

Circulatory system
•The myocardium loses contractility resulting in decreased cardiac output
•Vasculature thins and stiffens
•Arrhythmias and conduction disturbances are more prevalent, harder to diagnose and not tolerated as well.

286
Q

The ageing process renal system injury

A

Renal system
20% decrease in the size of the kidney by the age of 80

A decrease in glomerular filtration rate increases the chance of adverse drug reactions and drug-induced renal failure

Fluid overload is a real risk and fluid resuscitation must be titrated to central venous pressure and urine output.

287
Q

the ageing process gastrointestinal inury

A
  • Gastric emptying, splenic blood flow and gastrointestinal motility all decrease with age.
  • A difficult presenting complaint that brings older people to the ED is abdominal pain.
  • Mortality from abdominal symptoms is ten times higher in older persons when compared to young people.
288
Q

what is a common fracture in older person

A

Colles fracture

type of fracture of the distal forearm in which the broken end of the radius is bent backwards.

289
Q

describe fractured neck of femur

A

Major weight bearing bone

50% of body weight going through neck of femur

Blood supply to head of femur travels through neck of femur

High risk of avascular necrosis

290
Q

broad classifications for neck of femur fractures

A

Broad classifications:

  • Intracapsular - ‘true’ neck of femur fracture
  • Extracapsular
  • Each type requires a different management strategy
291
Q

assessment of the older adult trauma

A

Primary survey

Secondary survey
–What could we miss

292
Q

immediate nursing care following trauma in the older adult

A

Fluid balance and restoration - haemorrhage

Analgesia

Pressure assessment and care

What else do you think is an immediate priority?
- more at risk individuals

293
Q

review surgical management of the older adult (trauma)

A

review surgical management of the older adult (trauma) video on lms

294
Q

If a drop in B.P. is detected the body will try to bring it back to normal by …….?

A

If a drop in B.P. is detected the body will try to bring it back to normal by altering CO and PR

295
Q

Recognising Sepsis – high risk groups

A

Infants (under 1 year)

Elderly (over 75 years)

Impaired immune system:

  • Cancer patients – active treatment
  • Immuno-therapy – organ transplant or rheumatoid arthritis
  • AIDS
  • Diabetes Mellitis

Recent surgery (less than 6 weeks)

Pregnancy, recent birth / termination / miscarriage (within 6 weeks)

Any breach of the skin

IV drug users

Indwelling lines or catheters

(NICE, 2016)

296
Q

Recognising Sepsis - pitfalls

A

Young people compensate well for long periods…then crash rapidly

Beware underlying illnesses / drugs masking sepsis e.g. beta blockers masking tachycardia

Abusive behaviour could be caused by sepsis

297
Q

priorities of care during sepsis care - breathing?

A

Breathing
+ Maintain SaO2 > 94% (88-92% in COPD)
+ Consider if cause of infection is respiratory e.g. pneumonia
+ May require ventilation

298
Q

priorities of care during sepsis care - circulation?

A

Circulation
+ Maintain systolic B.P. >90mmHg

+ IV fluid resuscitation if hypotensive – 30ml/kg OR / AND Lactate >4mmol/litre

+ May require IV vasopressors if hypotensive despite fluids
e.g.
Adrenaline – increases force of myocardial contraction, heart rate and peripheral resistance (vaso-constrict)

Noradrenaline – increases heart rate and increases peripheral resistance

Dopamine – increases heart rate and increases peripheral resistance

Dobutamine – stimulates beta 1 adrenergic receptors in heart – increases force of myocardial contraction and heart rate

299
Q

priorities of care during sepsis care - disability?

A
Disability
\+  Decreased GCS = risk to airway
\+ Determine cause of altered conscious state:
-BGL?
- Trauma?
- Stroke?
- Hypoxia?
- Hypotension?
- Toxins?
- Medication?
300
Q

priorities of care during sepsis care - exposure?

A

Rashes may not appear OR may be a very late sign

Log roll patient and expose all of patient – check skin folds, soles of feet

Monitor temperature – may be hyperthermic – BUT – could also be hypothermic

301
Q

What is svt

A

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart.

302
Q

No.1 cause of CHD

A

Atherosclerosis

303
Q

What is the role of apoptosis in the pathophysiology of multiple organ dysfunction syndrome (MODS) in sepsis?

A

Apoptosis (programmed cell death) is the principal mechanism by which dysfunctional cells are normally eliminated. The proinflammatory cytokines may delay apoptosis in activated macrophages and neutrophils, but other tissues (eg, gut epithelium), may undergo accelerated apoptosis. Therefore, derangement of apoptosis plays a critical role in the tissue injury of sepsis.

304
Q

necrosis is caused by

A

Necrosis is cell death caused by hypoxia or trauma

305
Q

hypotensive resus…

Evidence recommends withholding fluids when?

A
  • Where a radial pulse is palpable
  • Where a central pulse if palpable in penetrating torso trauma
  • This referred to the pre-hospital setting…