357 exam Flashcards
Epidemiology / Demographics of posionings
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
Non-pharmaceutical poisoning examples
Envenomation
Alcohol
Carbon monoxide
Pesticides
what type of drugs are likely to be abused
Act fast
Make you feel good
Stop you feeling bad
examples of drugs of abuse
CNS stimulants - amphetamines, nicotine , cocaine, caffeine,
CNS depressants - alcohol, opioids, benzodiazepines
Psychomimetics - cannabis, LSD, designer drugs
what type of drug is methamphetamine?
CNS stimulant
Pharmacodynamics of methamphetamine
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
Treatment of methamphetamine poisoning
support of symptoms including sedation
other names for mathamphetamine
meth, ice
other names for Methylenedioxymethamphetamine
(MDMA / Ecstacy / E / Pingers)
(MDMA / Ecstacy / E / Pingers) what does it do?
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
MDMA treatment
Treatment: supportive control of symptoms - no antidote
what does heroine do
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
heroine overdose treatment
support of symptoms & naloxone
how can a paracetamol/ acetaminophen cause overdose
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
paracetamol overdose treatment
N-Acteylcysteine -
What is trauma?
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..
is Trauma…an epidemic?
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
describe the burden of injury from trauma
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
describe trauma from the australian context
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
common injuries that we should try prevent
Falls
Cycle injury
Motor vehicle injury
Risk taking prevention
what are the determinants of trauma
Age
Gender
Indigenous populations - more than twice the incidence of non-indigenous populations
Alcohol and drug use
Geography - remoteness and terrain
Driver behavioural factors
what is involved prehospital in the patient journey
Self care? Bystander - first aid First Responders Road ambulance Helicopter Emergency Service Royal Flying Doctor Service
what is involved in the emergency part of the patient journey
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
what is involved in the intensive care unit part of the patient journey?
Patients may be sedated / anaesthetised but aware
Consider the impact on family
Patients may be conscious and ventilated
what happens in the operating room/ xray part of the patient journey ?
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
What happens in the ward part of the patients journey?
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
what happens in the rehabilitation part of the patient journey?
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
What is a trauma system
An integrated and organised approach to care of the
injured person from the site of injury to rehab and ideal
restoration of normal functioning
key factors of the prehospital phase of trauma systems
Ambulance call taker
Ambulance dispatch
On scene care - paramedic, doctor, nurse, first responder
key factors of transport phase of trauma systems
Contingent on - distance from hospital, condition of patien
Reception - early alert, clear standard
communication
trauma systems ongoing care considerations
Evidence based care
Integrated - hospital - rehab -
community - home
primary survey abbreviation
- Control of catastrophic haemorrhage
Ac – Airway with c-spine control
B – Breathing
C – Circulation
D – Disability
E - Exposure
F farenheit
key points of consideration for primary survey
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
what is involved in the secondary survey
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
what is tertiary survey
Later in care ✤ Looking for development of problems: ✤ E.g. ARDS, infection, acute kidney injury ✤ Detailed scan
considerations of nursing care during trauma
Communication with patient
✤ Vital sign measurement
✤ Assist with interventions e.g. chest drain
✤ Record keeping
✤ Liaison with family / other
examples of different trauma pathophysiology
Coagulopathy
Hypothermia
Chest trauma
Abdo trauma
Pelvic injury
Skeletal injury
Penetrating trauma
what is coagulopathy
✤ This disease process of abnormal blot clotting
✤ Most trauma patients will have some form of bleed
✤ One the trauma triad - acidosis, hypothermia &
coagulopathy
causes of coagulopathy in trauma
✤ Causes:
✤ Hypothermia
✤ Haemodilution
✤ Acidosis
why is hypothermia considered trauma
Leads to vasoconstriction - reduced circulation
✤ Can cause:
✤ Arrhythmias
✤ Coagulopathy
✤ Can be caused by pre-hospital environment / within hospital
✤ Prevention is better than cur
hypothermia management
✤ Warmed IV fluids inc. blood
✤ Blankets reduce exposure
✤ Bair hugger
what are examples of thoracic trauma
✤ ATOM - FC ✤ Airway obstruction ✤ Tension pneumothorax ✤ Open pneumothorax ✤ Massive haemothorax ✤ Flail chest ✤ Cardiac tamponade
Tension pneumothora Signs and symptoms
✤ Rapid resp rate
✤ Tracheal tug
✤ Absence of lung sounds
treatment of tension pneumothorax
✤ Needle decompression
✤ Intercostal chest drain
✤ Definitive treatment of cause
Open pneumothorax
(sucking chest wound) signs and symptoms
✤ Wound on chest wall (anterior or posterior)
✤ Tachypnoea
✤ Low SaO2
✤ Reduced chest movement / unilateral movement
management of open pneumothorac
Management
✤ Three sided dressing (acts as a flap valve)
✤ Intercostal chest drain
Massive haemothorax
Signs and symptoms
✤ Tachypnoea
✤ Low SAO2
✤ Reduced air entry
✤ Differenciated on x-ray from pneumothorax
management of massive haemothorax
✤ Supplemental oxygen (if indicated)
✤ Intercostal drainage
✤ Fluid resuscitation
flail chest signs and symptoms
✤ Rib pain +++
✤ Tachypnoea, Low SaO2
✤ Segment of ribs - paradoxical movement
✤ Fracture of 2 or more adjacent ribs in two or more place
flail chest management
Analgesia +++
✤ May require tracheal intubation
✤ Physiotherapy and breathing exercise
Cardiac Tamponade signs and symptoms
(Becks Triad)
✤ Reduced heart sounds
✤ Engorged neck veins
✤ Low BP
management of cardiac tamponade
Management
✤ Pericardiocentesis
common presentations of abdominal trauma
✤ Splenic rupture
✤ Liver rupture
✤ Rupture bowel
✤ Kidney injury
diagnostic aids for abdominal trauma
✤ F.A.S.T. - Focused Abdominal Sonography for
Trauma (now available pre-hospital)
✤ CT Scanning
✤ Diagnostic Peritoneal Lavage (DPL)
why is pelvic trauma so bad
✤ Pelvis forms a ring that is extremely strong
✤ Potentially life threatening on its own
✤ Can contain at least 3 litres of blood
signs and symptoms of pelvic trauma
Pelvic pain
✤ Mechanism and history
✤ Haematuria
✤ Leg discrepancy / groin pain
management of pelvic trauma
Pelvic binder
✤ Fluid resuscitation
✤ Analgesia
✤ External fixation
Skeletal trauma signs and symptoms:
Assess with - Look, Feel, Move
✤ Swelling, bruising deformity
✤ Pain
✤ Neurovascular assessment
complications of skeletal trauma
Compartment syndrome
✤ Infection in open fractures (osteomyelitis)
✤ Loss of function (or limb)
describe penetrating injury
✤ 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
key nursing issues in trauma care
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
What is Multi Organ Dysfunction Syndrome?
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
Pathophysiology of MODS
+
Equation
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
Causes of MODS
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 …
Describe development of MODS/ worsening stages
Usually occurs in worsening stages:
- Increasing fluid requirement, mild resp. Alkalosis, oliguria, hyperglycaemia
- Tachypnoea, hypocapnia, hypoxaemia, moderate liver dysfunction, possible blood abnormalities
- Shock with increasing Azotemia (nitrogen containing compounds e.g. urea), acid based disturbance, coagulopathy
- Dependence on vasopressors with oliguria, lactic acidosis
review MODS/ sepsis flow chart
review MODS/ sepsis flow chart
How does MODS affect the cell aposis v necrosis
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
Apoptosis v necrosis
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
describe how MODS causes cell dysfunction
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
Why is MODS so bad?
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
describe MODS and inflammation
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
describe MODS and odema
Inflammatory response causes leaky vessels ‘capillary leak’
Fluid shifts:
- Hypovolaemia
- Pulmonary oedema
- Acute kidney injury
describe coagulation as it relates to MODS
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
examples of how organs might be in dysfunction in MODS
Specific complications
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
key factors of management of organ dysfunction
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
outline of mods
A complex syndrome
Abnormal host response to a trigger e.g. trauma
Early recognition is key
Similar process to sepsis
what is jacksons burn wound model
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.
how do burns cause damage twice
Initial destruction of tissue
Inflammatory response causes further problems
> 30% TBSA causes release of inflammatory mediators
how burns can affect around the body
resp, metabolic, immunological, cardiov
resp- bronchoconstriction, ARDS
Metabolic- increased BMR threschhold
Immunological- reduced immune response
Cardiov- reduce myocardial contractility, increased capilary permiability, peripheral and splanatic vasoconstriction
discuss burns impact of fluid loss
Fluid shifts reduce intravascular volume.
Onset often takes 6 to 8 hours.
Results in hypovolaemic shock
Rhabdomyolysis may begin…..
Renal failure
What makes cells live?
Life needs energy
Energy = ATP (Adenosine triphosphate)
The production of energy = respiration
This occurs in the mitochondria
What keeps cells alive?…
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
discuss Cellular effects of shock
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)
review coagulopathy in burns
review coagulopathy in burns
what is involved in the assessment and management of burns
- Immediate care
- Assessment of severity of burn
- Fluid resuscitation
- Patient flow chart
- Vital sign assessment
- Referral and specialist management
what is the impact of airway burns
Swelling due to burns in the upper airway can be fatal.
Swelling of the vocal cords can obstruct the airway completely.
Consider early intubation
Indicators of poss. inhalation injury
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
how do burns affect breathing
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
what does smoke inhalation do
Smoke contains many harmful chemicals.
Inhalation of smoke can cause these poisons to enter the body.
why is carbon monoxide an issue
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.
circulation issues with burns
Hypovolaemia due to fluid loss
Can result in acute kidney injury and widespread organ damage
Need to estimate extent of burn…
Assessment of severity of burn
Burn Severity is determined by:
Extent of burn – described as percentage of Total Body Surface Area (%TBSA)
Depth of burn.
Burn location.
Estimating the extent of burn
Serial halving
Palm of patient’s hand = 1 % (includes fingers)
Rule of nines
Lund & Browder charts
what s the burn Rule of nines
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 (%)
what is the lund bowder chart
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.
describe erythema/ superficial burn like
Very painful – sensation throughout
Redness – good capillary refill
Skin often intact
describe partial thickness burn
Deeper than epidermis
Often blistered
Very painful
Sensation intact
describe full thickness burn
No sensation
May not be painful
Hard leathery
eschar
what are the catergories looked at for refferals for burns
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
Primary management of burns
Commence fluid resuscitation
describe parkland formula
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’)
describe hypothermia
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
systemic complications and management of burns
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.
interventions other than fluid resus for burns patients
Analgesia
Sedation
Tetanus status?
Escharotomy?
pathophys of shock
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
what does metabolic acidosis do (shock)
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
Initial management of shock (hypov)
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
class 1 of shock
less than 15% blood loss, HR over 100, normal systolic, normal/ increased pulse pressure, 14-20 RR, slightly anvious
class 2 of shock
15-30% blood loss, HR over 100, normal systolic, decreased pulse pressure, 20-30 RR, mildly anxious
class 3 of shock
30-40% blood loss, HR over 120, decreased systolic, decreased pulse pressure, 30-40 RR, anxious/ confsed
class 4 of shock
over 40% blood loss, HR over 140, decreased systolic, decreased pulse pressure, over 35 RR, confused/ lethargic
what are the 3 possible response for shock treatment
rapid response, transient response, no response
rapid response to trauma characteristics
vitals return to normal. minimal fluid loss, low need for crystalloid and blood, type x- match blood prep, possible need for operative intervention,
transient response to trauma characteristics
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
no response to trauma characteristics
vitals remain abnormal, severe blood loss, high need for crystalloid, immediate need for blood, o neg blood prep, highly likely need for operative intervention
vascular access in shocked patients
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
benefits of intraosseous access
Useful in difficult venous access
Landmarks easy to find
Can deliver fluids and most drugs rapidly and easily
Painful in conscious patients
examples of 2 catergories of life threatening circulation problems
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
symptoms of life threatening circulation problems
Tachycardia Pale Oliguria Tachypnoea Diaphoresis BP……?
as we loose blood vessels….
vasoconstrict until cant and plateu
as we loose blood heart rate ….
HR increases unitil plateaus
as we loose blood bp …
stays constant due to compensation then falls rapidly
