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Block 43 Acute Care > Acutely Unwell > Flashcards

Acutely Unwell Flashcards

1
Q

Obstructive airway risks:

A

hypoxic injury to the brain, heart, kidneys and can lead to cardiac arrest and death

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2
Q

Partial airway obstruction - 3x added sounds and indications

A

Snoring - indicates a loss of tone
Gargling - indicates fluid such as secretion, blood or vomit
Stridor (inspiratory wheeze) indicates larynx obstruction

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3
Q

Signs of complete airway obstruction

A

Silent see saw movement of the chest

A paradoxical movement of abdomen and chest as the body tries to force oxygen past the obstruction

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4
Q

What is imminent with see saw chest?

A

Cardiac arrest

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5
Q

Most common cause of airway obstruction:

A

reduced / loss of consciousness
This causes a loss of soft tissue tone in the upper airway most notably the soft palate
Causes a snoring sound

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6
Q

3 further causes of airway obstruction (not LOC)

A

Foregin body - food, vomit, or blood
Oedema - Infection, Burn, Anaphylaxis
Tumor or abscess

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7
Q

Most common cause of airway obstruction in childre

A

foreign body

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8
Q

When to avoid head tilt chin lift manoeuvre

A

suspected head or neck trauma

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9
Q

Which airway is used in conscious patient?

A

Nasopharyngeal

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10
Q

When is nasopharyngeal airway contraindicated

A

Basal skull fracture - insertion -> risk of epistaxis

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11
Q

Signs of basal skull fracture

A 
CSF rhinorrhea is a sign of this
Battle sign (bruising over mastoid process from posterior auricular artery) and racoon eyes are signs of this
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12
Q

They are only for use in deeply unconscious patients as they can cause gag

A

Oropharyngeal airway

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13
Q

How to measure oropharyngeal airway

A

from mandibular angle to incisor.

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14
Q

3 things to look for to assess breathing

A

Colour of the patient - are they cyanosed
Resp rate - is this normal?
O2 sats and if they’re on supplemental oxygen

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15
Q

3 things to feel for to assess breathing

A

Tracheal deviation - this is uncomfortable and not the most reliable
Chest wall movements - equal and full
Percuss anterior and posterior

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16
Q

3 things to listen for to assess breathing

A

Equal air entry
Added sounds
Reduced sound

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17
Q

O2 sats target (usual) and type of O2

A

Get sats to targets of 94-98 using high flow oxygen via a non rebreather mask

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18
Q

O2 sats target t2rf

A

Target in patients of hypercapnic resp failure (COPD) is 88-92
Hypoxia kills before hypercapnia so aim for 94-98 unless 100% they are a retainer

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19
Q

Other steps to take action for breathing

A

Request ABG (pre and post oxygen) and CXR
Re asses and move on
Are their sats coming up?

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20
Q

2 things to look for to assess circulation

A

Colour of the patient centrally and peripherally

Do they look dehydrated or sweaty

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21
Q

5 things to feel for/measure to assess circulation

A

Temperature - central and peripheral
Pulse - peripheral and centrally, weak peripheral pulse - hypotension. Bounding pulse - early sepsis sign.
Capillary refill time >2 seconds is abnormal
Blood pressure
JVP

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22
Q

Listen for to assess circulation

A

Heart sounds for arrhythmias

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23
Q

3 potential areas which can cause hypotension and causes

A

Heart - arrhythmias, ACS and acute LVF
Pipes - sepsis and anaphylaxis giving systemic vasodilation
Fluid - hypovolemia from dehydration of haemorrhage

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24
Q

4 steps to manage acute haemorhhage

A

Stop the bleeding
Apply pressure
Contact a surgeon
Give packed red cells as crystalloid can’t carry oxygen

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25
Q

3 parts of disability

A

Conscious level _ AVPU
Pupil size and reactivity
Glucose - abcDEFG - don’t ever forget glucose

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26
Q

How to assess consciousness

A 
AVPU
Alert and talking
Responds to verbal stimulus
Responds to Painful stimulus (supraorbital pressure)
Unresponsive
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27
Q

Pupils findings

A

Pinpoint - think opiate OD - Naloxone

Uneven response - IC event so urgent CT head

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28
Q

Blood glucose below 4

A

Administer 100ml 20% dextrose IV

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29
Q

Steps for reduced consciousness

A

Anyway with reduced conscious level is at risk of obstruction
Place in left lateral position
Protect airway with a GCS below 8

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30
Q

Anaphylaxis definition

A

a severe systemic hypersensitivity reaction characterized by rapidly developing life threatening airway/breathing/circulation problems as well as skin/mucosal changes.

However 20% of patients have no redness, rash or swelling

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31
Q

Biphasic anaphylaxis

A

is a recurrence of symptoms within 72 hours of full recovery without any additional exposure to the allergen. The faster they respond to initial treatment the less likely this is

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32
Q

Suspected anaphylaxis

A

is the term used to describe patients presenting to the ED with anaphylactic-like symptoms and it is treated as anaphylaxis but is not diagnosed as this until the patient has seen a specialist allergist.

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33
Q

5 common triggers of anaphylaxis

A 
Food most common - nuts and shellfish 
Insect venom
Latex - this is common in healthcare workers or patients who are in the hosp alot having lots of procedures
Idiopathic
Drugs
34
Q

5 common drug triggers of anaphylaxis

A

Antibiotics
Anesthetic
Contrast
NSAID - cox 1 inhibition causing mast cell independent angioedema and bronchospasm
Vancomycin - calcium phosphate mechanism of non allergic mast cell activation

35
Q

3 ways in which anaphylaxis is triggered

A

Immunologically mediated (allergic), Non immunological (non allergic), Idiopathic

36
Q

Anaphylaxis pathophys. allergic

A

Sensitization (clinically silent):
first exposure -> mature B cells to produce IgE antibodies -> bind to mast cells and basophil receptors

2nd exposure:
Allergen cross links to the IgE receptors -> mast cells to degranulate -> releases preformed (histamine and tryptase) and newly formed (prostaglandin D2, leukotrienes and thromboxane )
Resulting in anaphylaxis

37
Q

Mast cell activated anaphylaxis pathophys

A

Direct non specific activation of histamine releasing agent
Calcium phospholipase mechanism seen in vancomycin and red man syndrome
Mastocytosis
MRGPRX2 model NMBA which is yet to be proven in humans

38
Q

Mast cell independent anaphylaxis pathophys

A

Cox 1 inhibition causing bronchospasm and or angioedema

NSAID

39
Q

The Big 3 criteria of anaphylaxis

A
  1. Sudden onset and rapid progression of symptoms
  2. Life threatening ABC symptoms
  3. Skin and mucosal changes - red, rashy and puffy
    Only 80% have these changes
40
Q

Adrenaline is dosed on weight in children but a good framework is

A

Above 12 - adult dose = 500 micrograms
6-12 - 0.3mg at 1 in 1000 = 300micograms
<6 - 0.15mg at 1 in 1000 = 150 micrograms

41
Q

5 steps to Managing anaphylaxis

A 
A-E
IM Adrenaline per dose
IV fluid bolus challenge:  Adult 500ml to 1L, Child at 20ml/kg
Chlorpheniramine
hydrocortisone
42
Q

Define Bacteraemia -

A

viable bacteria in the blood

43
Q

Define sepsis

A

a life threatening organ dysfunction due to a dysregulated host immune response to infection. The patient will die without treatment

44
Q

Define septic shock

A

This is when the arterial blood pressure drops resulting in hypoperfusion of organs despite fluid resus. This will lead to a high lactate as the organs enter anaerobic respiration. This can be measured with either a BP or <90 systolic despite fluid resus or lactate above 4.

45
Q

Define multiple organ dysfunction syndrome

A
  • severe septic shock and organ failure beyond possible recovery.
46
Q

Pathophysiology vasodilation in sepsis

A

Macrophage, lymphocytes and mast cells identify the pathogen and They release cytokines such as interleukins and TNF to active immune system
The cytokines activate further immune system cells which eventually lead to NO being released - vasodilation throughout the body

47
Q

Pathophysiology oedema in sepsis

A

Many cytokines cause endothelial lining permeability to increase meaning that fluids leak into the extracellular space and oedema as well as a reduction in IV volume. The oedema creates a space between blood and tissue so less oxygen reaches the tissue.

Inflammatory response also leads to pulmonary edema bibasal crackles can be heard which means people often think a pneumonia is causing the sepsis when in reality it could be an infection from elsewhere

48
Q

Pathophysiology coagulation in sepsis

A

The coagulation system is activated and fibrin is deposited throughout the systemic circulation compromising perfusion more. It also consumes platelets and clotting factors as they are being used up. This will lead to a thrombocytopenia and hemorrhage with an inability to form clots to stop them. This is known as disseminated intravascular coagulation

49
Q

Lactate raised in sepsis because…

A

this is raised due to tissue hypoperfusion which switches the tissues into anaerobic - of which lactate is a product

50
Q

Hypotension and tachycardia is caused in sepsis by

A

the drop in systemic vascular resistance meaning the heart has to pump more to maintain cardiac output

51
Q

Infections predisposing to sepsis

A 
35% Pneumonia - strep pneumoniae
25% UTI E.Coli - most common in over 65’s
11% Abdominal infection gram neg
Ruptured viscus
Anastomotic leak
Pancreatitis, peritonitis and appendicitis
11% Skin, soft tissue - staph aureus
Endocarditis
Device related
Meningitis or encephalitis
52
Q

6 rf for sepsis

A

Extremes of age meaning under 1 and over 75
Chronic conditions such as COPD and diabetes
Chemotherapy, immunosuppression steroids
Surgery, recent trauma or burns
Pregnancy or peripartum
Any indwelling medical device such as a catheter or central line

53
Q

8 signs of sepsis on examination

A

Any sign of potential source of infection eg chest infection (cough), cellulitis, wound discharge or dysuria
Reduced urine output
Cyanosis
Non blanching rash - meningococcal septicaemia
New onset AF or arrhythmia
Warm skin due to dilation
Long septic shock will be cold as SNS over powers - bad sign
Short cap refill and bounding pulse

54
Q

4 key things to be aware of in sepsis

A

Tachypnoea is often a first sign of sepsis
Elderly patients often present with confusion or drowsiness
Neutropenic / immunosuppressed patients may have normal obs but be life threatening il
N+V and hyperglycaemia can also occur in septic patients

55
Q

8 sepsis red flags

A 
Altered mental state
RR above 35
Systolic BP below 90 or 20% lower than normal
O2 sats below 94 or needing 40l oxygen to maintain it
Lactate above 2
Coagulopathy and rash
HR above 130
Recent chemo within 2-3 weeks
56
Q

Sepsis 6

A

Lactate
Serial lactates
Good for seeing if they response to treatment
High - bad prognosis
Blood culture
Urine output - can respond to cardiac output faster than BP. minum 0.5ml/kg/Hr
Oxygen
Broad spec AB
Every 1 hour delay increases mortality by 7.6%
Fluid
500ml crystalloid in 15 mins
If severe hypotension or lactate above 2 they get fluid at 30ml/kg stat so a 75kg man gets 2.25 litres over an hour

57
Q

Septic shock management

A

Treat with aggressive IV fluids. If IV fluid bolus does not increase their BP and lactate then they should be educated to ICU where they can be started on Inotropes such as noradrenaline.

58
Q

Neutropenic sepsis

A

This is a medical emergency. It is sepsis in a person with a neutrophil count of less than 1x10 to the power of 9. Low neutrophils are usually the consequence of anticancer or immunosuppressants.

59
Q

5 Clinical features of acute haemorrhage

A

Pallor
Cool peripheries
Clammy skin
Hypotensive and tachycardic
Be aware young patients may not be because they have vascular tone to compensate
Some old patients may be on drugs to stop the physiology eg beta blockers would stop a tachycardia

60
Q

3 things to look for (when stable) in acute haemorrhage

A

Check for bleeding in rectum, vagina and PR and any other places
Check abdomen for things like cullens and grey turner’s sign
Cullens is umbilical discolouration to intra abdominal bleed of any kind
Grey turners is along the flanks often associated with hemorrhagic pancreatitis
Assess long bones and the pelvis

61
Q

5 areas prone to heavy bleeds

A

skull, chest, abdomen, pelvis and retroperitoneum

62
Q

Classification of bleeding

A
  1. Physiology is normal but are bleeding (<15% blood loss)
  2. Slight changes in physiology but remain normotensive however slightly tachy (30%)
  3. Becoming hypotensive and v tach. On edge of severe haemorrhage. (40%)
  4. Severe hypo and tacchy. (>40% = dead)
63
Q

Major haemorrhage is defined as

A

a 50% blood loss in 3 hours or >150ml per minute. That works out to 2500 ml in a 70kg male. Normal circulating blood volume is 65/70ml/kg.

64
Q

Which 3 areas are found on CT polytauma

A

intrathoracic, abdominal and cranial trauma

65
Q

What is the lethal triad of bleeding

A

Hypothermia, acidosis, coagulopathy

66
Q

Why is hypothermia a major problem in haemorrhage

A

impairs platelet and enzymatic function within the clotting cascade

67
Q

Why is acidosis a major problem in haemorrhage

A

tissue hypoperfusion leads to lactic acidosis which impairs clotting

68
Q

What 4 steps should be taken with hypothermia in haemorrhage

A

Limit exposure, remove wet clothing and ensure good temperature
Continually monitor temperature via rectal probe
Use warming blankets forced air if available
Rapid transfusion of warmed blood products

69
Q

What 2 steps should be taken with acidosis in haemorrhage

A

Restore perfusion ASAP with haemostatic resuscitation ignoring traditional 1-2L of crystalloid
Maximise oxygenation and minimise hypoventilation to remove any potential for additional respiratory acidosis

70
Q

What should be avoided in acidosis with haemorrhage and why

A

Worsened by administration of crystalloid due to a delusional anaemia effect

71
Q

What 3 steps should be taken with coagulopathy in haemorrhage

A

Liaise with haematology from the outset as initial clotting screen is inaccurate in acute haemorrhage
Manage major haemorrhage patients as if they are coagulopathic don’t wait for lab results
Thromboelastography can provide good information if available

72
Q

Which 4 things are part of damage control resuscitation is done to prevent the lethal triad occurring in haemorrhage

A

haemostatic resuscitation, permissive hypotension and early damage control surgery

73
Q

Permissive hypotension is…

A

the act of maintaining a blood pressure lower than physiologic levels in a patient that has suffered from hemorrhagic blood loss.

A compromise between ensuring adequate tissue perfusion and reducing the risk of delusional coagulopathy and clot disruption

74
Q

5 features of Managing hemorrhage

A 
Oxygen 15/L reservoir
2 wide bore cannula peripheral access
Bloods - FBC, Us and Es, Liver screen, CLotting screen and group and save
CT angiography
Warmed fluid/blood products
75
Q

what reverses dabigatran

A

Idaruciamab

76
Q

4 ways to reverse warfarin and timings

A

stop warfarin
vitamin K (4-24h)
Fresh frozen plasma (less common now)
Human prothrombin complex (<1 hour but under 6h half life so give vit K also)

77
Q

Reversing warfarin in emergency major bleed - 3 steps

A

Stop warfarin
Give phytomenadione which is a vitamin K1 slow IV
Give prothrombin complex - factor 2,7,9 and 10

78
Q

Reversing warfarin with Inr above 8 and a minor bleed (3 steps)

A

Stop warfarin
Give phytomenadione which is a vitamin K1 slow IV
Give prothrombin complex - factor 2,7,9 and 10

79
Q

Reversing warfarin with Inr above 8 no bleed

A

Give phytomenadione by mouth

80
Q

Reversing warfarin with Inr 5-8 minor bleed

A

Phyomenadione slow IV

81
Q

Reversing warfarin with Inr 5-8 no bleed

A

Withhold 1-2 dose of warfarin and reduce maintenance at lower dose

82
Q

When is warfarin restarted

A

INR < 5

Block 43 Acute Care (5 decks)

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