The Acutely Unwell Patient Flashcards

1
Q

describe the ABCDE assessment?

A

focussed examination to detect life threatening problems in a sequential fashion. It allows for abnormalities to be addressed before moving on with the assessment. Re-assessment is needed.

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2
Q

why is ABCDE assessment important?

A
  • allows us to identify the deteriorating patient and treat abnormal physiology and perform life threatening interventions whilst buying time for deciding on further investigations and treatment.
  • ABCDE should be structured with clear communication with colleagues in stressful situations.
  • Decreases cognitive overload with framework to fall back on
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3
Q

when should an ABCDE assessment be carried out?

A

anyone who looks unwell, has altered conscious level, sudden deterioration or high NEWS score

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4
Q

what are the components of the ABCDE assessment?

A
Airway
Breathing
Circulation
Disability
Exposure
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5
Q

AIRWAY

  1. what signifies a patent airway?
  2. what are the consequences of obstructed airway
A
  1. patient alert/talking

2. can become fatal if not treated ASAP due to poor perfusion to organs

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6
Q

what are some of the causes of airway obstruction?

A
  • reduced conscious level so loss of soft tissue tone
  • foreign body (aspirated food, blood, vomit)
  • oedema (swelling and narrowing eg infection, burns, anaphalaxis)
  • tumour or abscess.
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7
Q

AIRWAY?
1. what are the signs of partial airway obstruction?

  1. what are the compensatory features of partial airway obstruction?
  2. what are the signs of complete airway obstruction?
A
  1. – snoring, gurgling (liquid), stridor (inspiration, obstruction at level of pharynx)
  2. Sitting up, leaning forwards (tripod position), reluctant to speak or cough, Nasal flaring, Accessory muscle use, Pursed lips, Paradoxical chest movements
  3. silent, ‘see-saw’ movement of chest and abdomen
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8
Q

what are the steps involved in airway support?

A
  • Manoeuvres: Head tilt and chin lift, Suction (if liquid in airway)
  • Airway adjuncts – nasopharyngeal, oropharyngeal airways
  • Anaesthetist for advanced airway
  • Apply oxygen
  • Re-assess
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9
Q

how can breathing be assessed as part of the ABCDE assessment?

A

look
feel
listen

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10
Q

BREATHING
1. what would you LOOK for to assess breathing?

  1. what would you FEEL for to assess breathing?
  2. what would you LISTEN for to assess breathing?
A
  1. colour of patient, resp rate (12-20), oxygen saturations, inspired oxygen
  2. tracheal deviation, chest wall movement, percuss
  3. equal air entry, absent breath sounds, added sounds
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11
Q

what are some of the causes of acute shortness of breath?

A
pneumothorax
pneumonia
anaphylaxis
asthma exacerbation
COPD
PE
acute pulmonary oedema
trauma
anaemia
sepsis
metabolic
overdose
poisoning
mental health conditions
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12
Q

what are the steps involved in management of breathing?

A
  • Oxygen 15L/min via mask with reservoir bag
  • Target sats 94-98%
  • All criticaly ill patients should be given oxygen
  • Aim for 88-92% in patients with COPD at risk of hypercarbic respiratory failure
  • ABG and CXR if indicated
  • Re-assess
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13
Q

what would you look for when assessing circulation as part of a ABCDE assessment?

A
  • Colour and temperature of hands
  • Peripheral and central pulse rate, rhythm, quality (weak, difficult to find = hypotension / bounding pulse = sepsis)
  • Capillary refill time (<2 seconds)
  • BP (systolic >100mmHg)
  • JVP
  • Heart sounds
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14
Q
  1. what is the equation for mean arterial pressure?

2. what are the causes of hypotension?

A
  1. MAP = CO X SVR
  2. pump (arrythmias, ACS, acute LVF)
    pipes (sepsis, anaphalaxis)
    fluid (hypovolaemia eg dehydration, haemorrhage)
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15
Q

what steps would be taking in management of circulation?

A
  • IV action
  • Take bloods
  • 12 lead ECG
  • Measure urine output (0.5ml/kg/h)
  • Commonest cause: hypovolaemia: 500ml fluid bolus (caution in cardiac, renal failure)
  • Tachy/bradyarrhymias – resus council guidelines
  • ACS: follow guidelines
  • Acute haemorrhage: stop the bleeding (pressure, contact surgeon), replace like with like – give packed red blood cells
  • Re-assess
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16
Q

what are the important things to consider when assessing disability as part of an ABCDE assessment?

A

conscious level
pupil size and reactivity
glucose

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17
Q

DISABILITY
1. what is the common scale used when assessing consciousness?

  1. what are the causes of loss of consciousness?
A
  1. AVPU - alert, verbal stimulation, pain, unresponsive
  2. : collapse secondary to CVD, hypoxaemia, shock, diabetic emergencies, endocrine emergencies, hypothermia, hepatic encephalopathy, uraemic encephalopathy, poisoning and overdose, seizures, epilepsy, head injury, acute stroke, cerebral tumour or infection, intracranial bleeds, alcohol or substance misuse, mental health problems
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18
Q

DISABILITY

whilst undertaking an ABCDE a patient has pin point pupils. what does this suggest and what would be the management?

A

overdose

antidote ie naloxone

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19
Q

DISABILITY

whilst undertaking an ABCDE a patient has unequal pupils. what does this suggest and what would be the next steps?

A

intracranial event

head CT

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20
Q

DISABILITY
whilst undertaking an ABCDE a patient is found to have glucose of 3mmol/L. what does this suggest and what would be the next steps?

A

hypoglycaemic (<4mmol/L)

100mL 20% dextrose IV

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21
Q

DISABILITY

what are the possible consequences of reduced conscious level and how can this be prevented?

A

risk of airway obstruction and aspiration, left lateral position, protect airway if GCS <8)

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22
Q

EXPOSURE

describe assessment of exposure as part of ABCDE assessment?

A
  • Focused examination of rest of patient, screen for other abnormal findings
  • Temperature, rash, calf swelling, bleeding, palpation
  • Collateral history, full examination
  • Re-assess
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23
Q

iSBAR

what is I?

A

identify self - name, position, location and who you are talking to
identify patient - name, age, sex, location

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24
Q

iSBAR

what is S?

A

SITUATION
state purpose “the reason I am calling is…”
if urgent say so

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25
Q

iSBAR

what is B?

A

BACKGROUND
tell the story
current problem
relevant history, examination, test results
management
if urgent give relevant vital signs, current management

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26
Q

iSBAR

what is A?

A

ASSESSMENT
state what you think is going on
“the patient is febrile and I can’t find the source of infection”

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27
Q

iSBAR

what is R?

A

REQUEST

eg “i’d like your opinion on…” or “i need help urgently, are you able to come”

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28
Q

how can causes of acute airway failure be classified?

A

extramural
mural
intraluminal

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29
Q

give examples of extramural causes of acute airway failure?

A
trauma
burns to face, head or neck
oedema
neck haematoma
thyroid cartilage
fat
abscess
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30
Q

give examples of mural causes of acute airway failure?

A

angioedema
burns to mouth
infection
neoplasm

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31
Q

give examples of intraluminal causes of acute airway failure?

A

foreign body
laryngospasm
tongue obstruction
bilateral recurrent laryngeal nerve palsy

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32
Q
  1. define sepsis

2. define septic shock

A
  1. life threatening organ dysfunction due to a dysregulated host immune response to infection
  2. sepsis unresponsive to adequate fluid resuscitation (remain hypotensive)
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33
Q

give examples of infections leading to sepsis?

A

common to less common

  • Pneumonia (streptococcus pneumoniae)
  • UTI (e. coli)
  • Intra-abdominal infections (gram negatives/ anaerobes)
  • Skin and soft tissue (staphylococcus aureus)
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34
Q

how would you identify a patient with sepsis?

A
  • NEWS score >5 (or 3 in one parameter / gut feeling)
  • Could this be due to infection?
  • Red flags?
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35
Q

what is the role of the sepsis red flags?

A
  • Signs to detect high risk patient
  • Bedside indication of organ dysfunction
  • Patient at high risk of severe illness and death
  • Prompts initiation of the sepsis 6
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36
Q

what are the sepsis red flags?

A
  • New or altered mental state/ confusion
  • Respiratory rate >25
  • Systolic BP <90 (20% less than normal)
  • O2 sats <94% (not copd) or supplemental O2 >40% to maintain sats
  • Oliguria/anuria or AKI
  • Lactate >2mmol/L
  • Coagulopathy/purpuric rash/ mottled/ashen /cyanotic
  • Heart rate >130bpm
  • Recent chemotherapy (2-3 weeks)
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37
Q

what are the sepsis 6?

A
  • Give oxygen
  • Give IV antibiotics
  • Give IV fluids
  • Take blood
  • Check lactate
  • Monitor urine output
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38
Q

SEPSIS 6

describe the role of giving oxygen?

A
maintain >94% sats
Reduced supply (Hypovolaemia, leaky capillaries, tissue oedema, microthrombi) and increased demand (higher metabolic requirements) -> low oxygen saturation / high respiratory rate
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39
Q

SEPSIS 6

describe the role of taking blood cultures?

A

ideally take 2

allows for targeted antibiotic therapy

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40
Q

SEPSIS 6

describe the process of giving IV antibiotics?

A
  • Every hour delay in giving antibiotics increases mortality
  • Stat dose on front of drug chart
  • Where possible target antibiotics
  • Antibiotic guidelines differ from trust to trust
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41
Q

SEPSIS 6

describe the role of giving IV fluids?

A
  • Reduces organ dysfunction and multi organ failure
  • Optimise tissue organ delivery
  • Increases organ perfusion
  • Give even if BP not fallen
  • If hypotensive/lactate >2mmol/L give up to 30mls/kg of fluid stat
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42
Q

SEPSIS 6

describe the role of checking lactate?

A
  • Venous or arterial sample
  • Increased tissue hypoxia
  • Anaerobic metabolism
  • Sepsis is not the only cause of raised lactate
  • High lactate indicates poor prognosis
  • Lactate should improve with treatment
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43
Q

SEPSIS 6

describe the role of monitoring urine output?

A
  • Patient doesn’t have to have catheter
  • Need 0.5mls urine/kg/hr
  • Urine output reflects cardiac output
  • Measure BP but not CO on ward
  • A fall in urine output may be first indication that CO is falling even if BP is normal
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44
Q

SEPSIS PHYSIOLOGY

the heart?

A

inflammatory response to infection -> vasodilation and capillary leak -> decreased circulatory blood volume and decreased SVR ->drop in BP and decreased tissue perfusion

heart rate increases to try and compensate for drop in BP and in response to stress hormones

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45
Q

SEPSIS PHYSIOLOGY

the adrenal glands?

A

stress response -> release of adrenaline, noradrenaline and cortisol

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46
Q

SEPSIS PHYSIOLOGY

the kidneys?

A

decreased perfusion from low BP -> reduced urine output and AKI

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47
Q

SEPSIS PHYSIOLOGY

the skin?

A

reduced circulation to peripheries -> mottled discoloured skin and abnormal clotting -> purpuric rash

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48
Q

SEPSIS PHYSIOLOGY

the brain?

A

reduced blood flow to brain -> confusion, drowsiness, slurred speech, agitation, anxiety or altered conscious level
hypothalamus responds to infection with high or sometimes low body temp

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49
Q

SEPSIS PHYSIOLOGY

lungs?

A

fluid leaks into alveoli -> decreased gas exchange

tissue hypoxia -> acidosis->RR

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50
Q

SEPSIS PHYSIOLOGY

liver?

A

stress response alters gluconeogenesis and can lead to high or low blood sugars

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51
Q

SEPSIS PHYSIOLOGY

lactate?

A

tissue hypoperfusion and decreased clearance-> increased plasma lactate

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52
Q

describe how to review and escalate a patient with sepsis?

A
  • Once diagnosed you need to do sepsis 6 and done within hour of diagnosis
  • All patients with sepsis need to be reviewed by consultant or registrar ASAP
  • Review the patient
  • If no improvement with initial treatment refer to critical care
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53
Q

what are some of the complications of sepsis?

A
  • Death
  • Loss of fingers, toes, limbs
  • Impact on life and ability to work
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54
Q

what are the symptoms of post sepsis syndrome?

A
  • Sadness
  • Difficulty swallowing
  • Muscle weakness
  • Clouded thinking
  • Difficulty sleeping
  • Poor memory
  • Difficulty concentrating
  • Fatigue
  • Anxiety
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55
Q

define anaphylaxis?

A

a severe, life threatening, generalised or systemic hypersensitivity reaction. Characterised by rapidly developing, life threatening airway and/or breathing and/or circulation problems usually with skin and or mucosal changes

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56
Q

what is biphasic anaphylaxis?

A

after complete recovery of anaphylaxis, a recurrence of symptoms within 72 hours with no further exposure to the allergen

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57
Q

give examples of common triggers for anaphylaxis?

A
insect venom
food (nuts)
latex
drugs (antibiotics, anaesthetic drugs,NSAIDs, contrast media)
idiopathic
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58
Q

describe the IgE mediated allergic mechanism of anaphylaxis?

A
  • mature B cells produce specific IgE antibodies to the allergen
  • IgE antibodies bind to mast cells and basophils receptors
  • this initial phase of sensitisation is clinically silent
  • on re-exposure, the allergen cross links the 2 specific IgE receptors creating a bridge and resulting in mast cell degranulation
  • release of histamine, tryptase etc, followed by newly formed mediators eg prostoglandin D2, leukotrienes, thromboxane A2 results in clinical manifestation of IgE mediated anaphylaxis
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59
Q

describe non allergic mechanisms of anaphylaxis?

A

MAST CELL ACTIVATION

  • direct non specific activation - histamine releasing agents
  • calcium and phospholipase dependent mechanism eg vancomycin and red man syndrome
  • MRGPRX2 activation
  • mastocytosis

MAST CELL INDEPENDENT MECHANISM
- COX-1 inhibition - NSAIDs (bronchospasm, angioedema)

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60
Q

what cofactors may modulate the onset of allergic and non allergic immediate hypersensitivity?

A
stress
infection
dose of allergen
rate of drug infection
chemical property and molecular weight of drugs
host factors
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61
Q

what grading system can be used to assess severity of anaphylactic reactions?

A

Ring and Messmer grading

62
Q
RING AND MESSMER GRADING (ANAPHYLAXIS)
grade 1 signs and symptoms
1. skin
2. abdo
3. resp tract
4. cardiovascular
A
  1. itching, flush, uricaria, angioedema
  2. -
  3. -
  4. -
63
Q
RING AND MESSMER GRADING (ANAPHYLAXIS)
grade 2 signs and symptoms
1. skin
2. abdo
3. resp tract
4. cardiovascular
A
  1. itching, flush, uricaria, angioedema
  2. nausea, cramps
  3. rhinorrhea, hoarseness, dyspnea
  4. tachycardia, hypotension, arrhythmia
64
Q
RING AND MESSMER GRADING (ANAPHYLAXIS)
grade 3 signs and symptoms
1. skin
2. abdo
3. resp tract
4. cardiovascular
A
  1. itching, flush, uricaria, angioedema
  2. vomiting, defecation
  3. laryngeal oedema, bronchospasm, cyanosis
  4. shock
65
Q
RING AND MESSMER GRADING (ANAPHYLAXIS)
grade 4 signs and symptoms
1. skin
2. abdo
3. resp tract
4. cardiovascular
A
  1. itching, flush, uricaria, angioedema
  2. vomitin, defecation
  3. respiratory arrest
  4. cardiac arrest
66
Q

what is the criteria of anaphylaxis?

A
  • Sudden onset and rapid progression of symptoms
  • Life threatening ABC problems
  • Skin and/or mucosal changes (flushing, urticaria, angioedema)
  • Exposure to known allergen/trigger for patient supports diagnosis
  • GI symptoms
67
Q

ANAPHYLAXIS

describe what you may see during airway assessment?

A
  • Swelling (tongue/throat)
  • Difficulty breathing and swallowing
  • Sensation throat is closing up
  • Hoarse voice
  • Stridor
68
Q

ANAPHYLAXIS

describe what you may see on breathing assessment?

A
  • SOB
  • Increased respiratory rate
  • Wheeze
  • Patient becomes tired
  • Confusion caused by hypoxia
  • Cyanosis (late sign)
  • Respiratory arrest
69
Q

ANAPHYLAXIS

describe what you may bee on circulation assessment?

A
  • Signs of shock – pale/clammy
  • Increased pulse rate
  • Low BP (hypotension)
  • Decrease conscious level
  • Myocardia ischaemia/angina
  • Cardiac arrest
70
Q

ANAPHYLAXIS

describe what you may see on disability assessment?

A
  • Sense of impending doom
  • Anxiety/panic
  • Decreased consciousness caused by ABC
71
Q

ANAPHYLAXIS

describe what you may see on exposure assessment?

A

Skin changes: often first feature, in 80% of cases, skin, mucosal or both, erythema (patchy, generalised, rash), urticaria (hives, weals, welts), angioedema (similar to urticaria but involves swelling of deeper tissue (eyelids, lips, throat, mouth)

72
Q

ANAPHYLAXIS

how is airway managed?

A

oxygen 15 Litre non rebreathe mask

73
Q

ANAPHYLAXIS

how is breathing managed?

A

O2 sats probe

74
Q

ANAPHYLAXIS

how is circulation managed?

A

BP cuff
ECG
iv access
adrenaline (IM 0.5ml 1:1000 repeat as required after 5 mins) and fluids

75
Q

ANAPHYLAXIS

describe the use of fluids in its management?

A
  • IV access
  • 500ml-1000ml IV bolus in adults, 20-30mls/kg may be required
  • Monitor response – further boluses required
  • Crystalloid only
  • Avoid colloids and stop if already up (may be cause of reaction)
76
Q

ANAPHYLAXIS

describe the use of drugs in management?

A
antihistamine and steroids
• Chlorphenamine and hydrocortisone
• Second line drugs
• After initial resus
• Do not delay ABC
• Can wait until transferred to hospital
77
Q

ANAPHYLAXIS

differentials

A
  • Life threatening: asthma, sepsis

* Non-life threatening: vasovagal, panic attack, idiopathic non allergic urticaria or angioedema

78
Q

what is the acute investigation for a patient with anaphylaxis?

A

Mast cell tryptase testing
- Ideal sample timing
• After initial resus started when feasible to do so
• 1-2 hours after onset of symptoms (no later than 4 hours after)
• 24 hours or in convalescence/at follow up

79
Q

ANAPHYLAXIS

what are auto injectors?

A
  • Used by patient or carer: severe reactions, difficult to avoid trigger
  • Prescribed/taught to use after suspected attack and prescribed by allergy specialist
  • Patient/carer needs to be trained to use it
80
Q

what is the management of anaphylaxis once the patient is stabilised?

A
  • Adult and young people over 16 should be observed for 6-12 hours from onset
  • Those whose reactions were controlled promptly and easily may be observed for shorter period
  • Children under 16 years should be admitted to hospital under care of a paediatric medical team
81
Q

ANAPHYLAXIS

what information should be given to patient before discharge?

A
  • Anaphylaxis, including signs, symptoms of anaphylactic reaction, risk of biphasic reaction, what to do if anaphylactic reaction occurs
  • Demonstrate use of adrenaline injector and when to use it
  • Advice regarding avoidance of suspected trigger
  • Information about need for referral to specialist allergy service and referral process
  • Information about patient support groups
82
Q

how can you identify patients with haemorrhage?

A
  • Pallor, cool peripheries, clammy skin
  • Obvious signs of bleeding
  • PR bleeding, vaginal area (pregnancy)
  • Cullens/grey turner sign = intra abdominal bleeding
  • If trauma assess long bones and pelvis
  • Tachycardia and low BP common yet younger patients may compensate
  • Elderly patients may have preexisting chronic anaemia exacerbating a bleed, pharmacology could mask clinical signs off bleed (beta blockers masking tachycardia)
83
Q

what happens if bleeding occurs in an area with plenty of spaces?

A

eg abdomen, long bones, pelvis, externally – prone to heavy bleeds – hypotension, tachycardia, low Hb, unstable quickly, aggressive haemostatic resuscitation

84
Q

what happens if bleeding occurs in an area with limited space?

A

pressure affects from bleed eg intracraniam (low GCS, neurological deficit, high risk of airway compromise) and pericardium sac (constrictive, heart failure, low CO, masked by acute bleed)

85
Q

describe a class I bleed?

A
<750ml
<15% blood loss
<100 HR
BP normal
resp rate 14-20
urine output >30
86
Q

describe class II bleed?

A
750-1500ml
15-30% blood loss
HR 100-120
BP normal
Resp rate 20-30
urine output 20-30
87
Q

describe class III bleed?

A
1500-2000ml
30-40% blood loss
HR 120-140
BP decreased
resp rate 30-40
urine output 5-20ml/hr
88
Q

describe class IV bleed?

A
>2000ml
>40% blood loss
HR >140
BP decreased
resp rate >40
urine output <5ml/hr
89
Q

what is major haemorrhage?

A
  • 50% blood loss within 3 hours or at a rate >150ml/min
  • Approximately 2500ml in 70kg male (normal blood volume 65-70ml/kg)
  • Haemorrhage protocol can vary from trust to trust
90
Q

what is the lethal triad?

A

Coagulopathy, hypothermia and acidosis

will cause and worsen acute haemorrhage

Aim for damage control resuscitation; haemostatic resuscitation, permissive hypotension, damage control surgery

91
Q

describe the components of managing a haemorrhaging patient?

A
  • Oxygen-hypoperfusion
  • IV access – wide bore cannulae x2
  • FBC, renal profile (hypocalcaemia linked with worsening bleeds / deranged renal profile suggest underlying metabolic acidosis making coagulopathy worse), electrolyte profile, liver profile, clotting factors (INR), group and save
  • CT angiography – identify where bleeding is coming from
  • Warmed IV fluids/blood products if necessary
92
Q

describe how bleeding can be controlled in an acutely haemorrhaging patient?

A

aim for haemostasis
• Direct pressure
• Red cell concentrate – major haemorrhage protocol
• Tranexamic acid (crash 2 crash 3 trials – disputed benefits)
• Permissive hypotension (systolic of 90 – prevent blood clots being diluted)/ minimal volume normotensive approach (mean arterial pressure of 65, if above this phentonyl, if hypotensive use fluid bolus) – don’t give too much crystalloid, prevent haemorrhaging
• Correction of clotting defects or deficits

93
Q

give examples of potential source of bleeding?

A
trauma
GI
intracranial
dissecting aortic aneurysm
obstetric
94
Q

how can bleeding due to trauma be managed?

A

Direct pressure/stabiliation (pelvic binder)

relieve secondary effects of major bleeding (hamorrhagic pleural effusions and cardiac tamponade)

95
Q

what are the next steps in a patient with bleeding due to GI cause?

A
  • Endoscopy
  • Sengstaken / Minnesota tube
  • Surgical intervention
96
Q

what is the management of a patient with bleeding due to intracranial bleed?

A

Neurosurgical decompression

97
Q

what is the management of a patient with bleeding due to dissecting aortic aneurysm?

A

vascular surgery

endovascular repair

98
Q

give examples of blood products?

A
fresh frozen plasma
cryoprecipitate
prothrombin complex concentrate
platelets
idarucizumab
99
Q

what is fresh frozen plasma

A

contains all factors (low concentrations), liver failure, malnutrition, trauma

100
Q

what is cryoprecipitate used for?

A

fibrinogen von Willebrand, factor VIII, XIII fibronectin. Haemophilia A, fibrinogen deficiency <1.5g/l

101
Q

describe the use of prothrobin complex concentrate?

A

replace vitamin k dependent factors 2,7,9 10. Warfarin anticoagulation. Best treatment for bleeding in factor Xa inhibitors but does not directly inhibit or effect the mechanism of Xa inhibiors

102
Q

describe the use of platelets?

A

thrombocytopenia <30 x10^9 or severe bleeding max of 100x 10^9

103
Q

what can be used for dabigatran reversal?

A

idarucizumab

104
Q

what is the significance of lactate >4mmol/L in haemorrhaging patients?

A

associated with increased mortality

105
Q

THE LETHAL TRIAD

describe issues with hypothermia?

A

impair platelet function and enzymatic function within clotting cascade

106
Q

THE LETHAL TRIAD

describe the issues of acidosis?

A

inadequate tissue perfusion leading to lactic acidosis impairing clotting (exacerbated by crysalloid administration) maximise oxygenation and minimise causes of hypoventilation to avoid respiratory acidosis

107
Q

THE LETHAL TRIAD

describe the issues with coagulopathy

A

aggrevated by hypothermia and acidosis. Avoid large volumes of crystalloid or unbalanced blood products. Acute coagulopathy of trauma = independent of lethal triad, recognised in severely injured patients characterised by systemic anticoagulation mediated by protein C and hyperfibrinolysis

108
Q

what is meant by permissive hypotension?

A

compromise between ensuring adequate tissue perfusion whilst reducing risk of dilutional coagulopathy and clot disruption

109
Q

what is haemostatic resuscitation?

A

initiate and coordinate safe and rapid transfusion 2:1:1 packed RBCs: fresh frozen plasma: platelets
• Monitor every 30-60mins for; temp, acid base, ionised calcium, PT/APTT, fibrinogen, platelets, FBC.
• Consider tranexamic acid (1g bolus followed by 1g over 8 hours)
• Consider Calcium chloride 10mls 10% over 10 minitues if ionised Ca<1.1
• Consider vitamin K and prothrombin complex in patients warfarinised

110
Q

what are the different sources of haemorrhage?

A
SCALPeR
• scalp and external sources
• Chest
• Abdomen
• Long Bones
• Pelvis
• Retroperitoneum
111
Q

what are the different sources of haemorrhage?

A
SCALPeR
• scalp and external sources
• Chest
• Abdomen
• Long Bones
• Pelvis
• Retroperitoneum
112
Q

name some invasive measures of haemorrhage control?

A
  • Sutures
  • Tamponade
  • Tie off vessels
  • Cautery
  • Interventional radiology
  • Damage control surgery
113
Q

name some invasive measures of haemorrhage control?

A
  • Sutures
  • Tamponade
  • Tie off vessels
  • Cautery
  • Interventional radiology
  • Damage control surgery
114
Q

PULSE PALPATION BP

systolic BP if only carotid pulse palpable

A

60-70

115
Q

PULSE PALPATION BP

systolic BP if carotid, femoral and radial pulses are palpable

A

> 80

116
Q

PULSE PALPATION BP

systolic BP if carotid, femoral and radial pulses are palpable

A

> 80

117
Q

describe a class I haemorrhagic stroke

A
  • Blood loss upto 750ml or 15% blood loss
  • HR <100
  • BP – normal
  • Pulse pressure – normal/increased
  • Resp rate – 14-20
  • Urine output - >30
  • CNS – slightly anxious
118
Q

describe a class II haemorrhagic stroke?

A
  • Blood loss: 750-1500 mL or 15-30% blood volume
  • Heart rate: 100-120/min
  • Blood pressure: normal
  • Pulse pressure (mmHg): decreased
  • Respiratory rate: 20-30/min
  • Urine output: 20-30 mL/h
  • CNS: mildly anxious
119
Q

describe a class IV haemorrhagic stroke?

A
  • Blood loss: >2000 mL or >40% blood volume
  • Heart rate: >140/min
  • Blood pressure: decreased
  • Pulse pressure (mmHg): decreased
  • Respiratory rate: >35/min
  • Urine output: negligible
  • CNS: confused, lethargic
120
Q

describe a class IV haemorrhagic stroke?

A
  • Blood loss: >2000 mL or >40% blood volume
  • Heart rate: >140/min
  • Blood pressure: decreased
  • Pulse pressure (mmHg): decreased
  • Respiratory rate: >35/min
  • Urine output: negligible
  • CNS: confused, lethargic
121
Q

describe crystalloid resuscitation?

A

Initiate fluid resuscitation with 1-2L of crystalloid such as normal saline or compound sodium lactate (hartmanns solution)

122
Q

what are the downsides to crystalloid resuscitation?

A
  • Dilutional coagulopathy
  • Impaired oxygen delivery sue to dilutional anaemia
  • Hypothermia
  • Worsening metabolic acidosis
  • Clot dislodgement and haemorrhage from BP elevation
123
Q

how is dabigatran reversed?

A

Idarucizumab (works within minutes)

Activated charcoal – within 2 hours of administration

124
Q

how is apixaban reversed?

A

Activated charcoal within 2 hours of administration

Andexanet alfa – not yet licensed

125
Q

how is apixaban reversed?

A

Activated charcoal within 2 hours of administration

Andexanet alfa – not yet licensed

126
Q

COMPONENTS OF BLOOD

red cells

A

1 unit = 250-350mls
Preserved with glucose and mannitol
Lasts 35 days
Must be completed within 4 hours from time removed from blood bank

127
Q

what are the indications for red cells

A

Anaemia
Solid tumours
Myelodysplasia anaemia
Avoid transfusions in patients with B12 and folate deficiencies

128
Q

COMPONENTS OF BLOOD

platelets

A
Straw coloured
Kept at room temperature in agitator
Start within 30 mins of removal from lab
Complete within 20-30mins
Doesn’t have to be ABO compatible
129
Q

what are the indications of platelets?

A

Acute leukaemia
Chronic stable thrombocytopenia
Major haemorrhage
Normal platelet count is 15—400^9/l

130
Q

COMPONENTS OF BLOOD

fresh frozen plasma

A
Corrects coagulopathy 
Stored in freezer for 2 yrs
20-25 mins to defrost
150-300mls by blood giving set
30mins-1 hour transfused
Can be stored in blood bank for 24 hrs
Once removed from blood bank must be used in 4 hours
131
Q

what are the indications for cryoprecipitate transfusion?

A

During massive haemorrhage to maintain clotting

132
Q

what are the indications for cryoprecipitate transfusion?

A

During massive haemorrhage to maintain clotting

133
Q

describe the ABG findings for a patient with type 1 respiratory failure?

A

PaO2 less than 8, PaCO2 low or normal

134
Q

what are the potential causes of type 1 respiratory failure?

A

Pulmonary embolus
pneumonia
asthma
pulmonary oedema

135
Q

what are the ABG findings for a patient with type 2 respiratory failure?

A

PaO2 less than 8 and raised PaCO2

136
Q

how can the causes of type 2 respiratory failure be classified

A

pulmonary problems
mechanical problems
central problems

137
Q

what pulmonary problems can cause type 2 respiratory failure?

A

COPD
pulmonary oedema
pneumonia

138
Q

what mechanical problems can cause type 2 respiratory failure?

A

chest wall trauma
muscular dystrophies
motor neuron disease
myasthenia gravis

139
Q

what central problems can cause type 2 respiratory failure?

A

opiate overdose

acute CNS disease

140
Q

what equations are important to keep in mind when thinking about the physiology of stroke?

A
BP = CO X SVR
CO = HR X SV
141
Q

what equations are important to keep in mind when thinking about the physiology of stroke?

A
BP = CO X SVR
CO = HR X SV
142
Q

what can cause shock?

A
  • decrease in cardiac output – cardiogenic shock (MI, PE, tamponade, valve rupture). Low CO compensated with increase HR – tachycardia, cold, clammy peripheries
  • Alteration in systemic vascular resistance (sepsis, anaphylaxis, spinal shock)
  • Stroke volume - fluid loss – haemorrhage, bowel obstruction, diarhoea and vomiting, urinary loss
  • Addisonian crisis
143
Q

how can JVP be used to distinguish cause of shock?

A

Low and postural hypotension and cold = hypovolaemia

Low and bounding pulse and warm = septic

High and wet lungs and cold = cardiogenic

144
Q

what are the potential complications of shock?

A
  • Brain failure – confusion and coma, cortical necrosis
  • Heart failure
  • Lung failure – pulmonary oedema
  • Renal failure – oliguria, anuria, hyperkaleamia, fluid overload
  • Blood failure – DIC
  • Generalised tissue failure – acidosis
145
Q

describe the principles of shock management?

A
  • Evaluate and establish cause
  • General - ABC/ Investigation and support
  • Specific - Depends on cause Eg hypovolaemia – fluids, sepsis, antibiotics
146
Q

describe stage 2 hypovolaemia?

A
15-30% loss
partially compensated by SVR
mild tachycardia
postural drop
narrow pulse pressure
sweating
anxiety
147
Q

describe stage 2 hypovolaemia?

A
15-30% loss
partially compensated by SVR
mild tachycardia
postural drop
narrow pulse pressure
sweating
anxiety
148
Q

describe stage 4 hypovolaemia?

A

> 40% loss
very low BP
weak tachycardia
tachypnoea

149
Q

describe stage 4 hypovolaemia?

A

> 40% loss
very low BP
weak tachycardia
tachypnoea

150
Q

what is the criteria of systemic inflammatory response syndrome?

A
at least 2 of the following
• Temp <38
• Tachycardia >90
• Resp rate >20 PaCO2 <4.3
• White cells >12 <4
151
Q

what are the first line antibiotics in septic shock?

A

Cefuroxime

Gentamicin

152
Q

what is the management of cardiogenic shock?

A

Positive ionotropes – dopamine, debutamine