Multi-organ failure and critical illness

Question 1

Pathophysiological responses to haemorhage and reduced MAP (3)

Answer 1

Baroreceptor (immediate)- Increases SNS and reduces PNS, increasing HR and ionotropy and causing arteriolar and venous constriction
Endocrine- catecholamine and steroid release
Reduced renal perfusion (mins to hours)- RAA axis activation causing Na and water retention increasing circulatory volume

Question 2

ABC treatment in trauma

Answer 2

A-intubate
B-ventilate (increases oxygenation and decreases O2 requirement of patient)
C-IV access and fluid resuscitation

Question 3

Side effects of anaesthetic induction agents in trauma

Answer 3

Vasodilation and hypotension (vasoconstriction stops) - can lead to hypovolaemic cardiac arrest (responds to treatment)

Question 4

Treatment of hypovolaemic cardiac arrest

Answer 4

CPR, adrenaline, blood, resuscitation (reacts well to increased volume and adrenaline)

Question 5

5 sites of major blood loss in trauma

Answer 5

‘Blood on the floor and 4 more’

1) External
2) Chest
3) Abdomen
4) Pelvis and retro peritoneum
5) Around long bone fractures esp. femur

Question 6

Typical ABG result in trauma

Answer 6

Metabolic (lactic) acidosis with respiratory compensation if possible (Can’t if on ventilator)

Question 7

Effect of crush injuries on serum potassium

Answer 7

Rises as released by burst cells

Question 8

Does Hb level show blood loss?

Answer 8

Not immediately, concentration isn’t changed by bleeding, need to wait until after fluid resus.

Question 9

Fluid replacement in major haemorrhage

Answer 9

Don’t give too much clear fluid as dilutes Hb clotting factors and platelets so makes you bleed.
Give blood, FFP and platelets eraly
Major haemorrhage protocol

Question 10

Triad of death in major haemorrhage

Answer 10

Hypothermia from cold fluids and environment - decreases coagulation
Acidosis from anaerobic resp due to hypoperfusion - decreases heart performance
Coagulopathy from cold, bleed more, more acidotic etc. LOOK AT DIAGRAM

Question 11

Medications in major haemorrhage

Answer 11

Tranexamic acid and vasopressor

Question 12

Imaging to find source of bleeding

Answer 12

CT if stable enough, CXR and pelvic XR in resus if not

Question 13

Preferred type of imaging in spinal trauma

Answer 13

MRI

Question 14

Type of CT used

Answer 14

Dual bolus CT with contrast

Question 15

What are high density lesions in brain on CT caused by?

Answer 15

Blood - contrast doesn’t get to brain

Question 16

What kind of damage is found at post mortem in traumatic brain injuries?

Answer 16

Hypoxic-ischaemic damage

Question 17

Mechanism of hypoxic-ischaemic damage in traumatic brain injuries

Answer 17

Inflammation increases ICP causing inadequate cerebral blood flow and distortion of vital structures.

Question 18

Why does ABC need treating before can treat D (brain injury)?

Answer 18

Brain needs steady oxygen from cardiac output - need good cerebral oxygen supply before can treat brain injuries

Question 19

Perfusion rate of brain

Answer 19

750mls/min

Question 20

How is cerebral blood flow maintained as MAP changes?

Answer 20

Constricts as MAP increases and vice versa - fails at extremes though (<70 and >160)

Question 21

How does the brain initially cope with decrease in cerebral blood flow and what happens drops too low?

Answer 21

Initial it increases oxygen extraction from the blood. When flow is below 20ml/100g/min get failure of electrical function (symptoms) and below 10 you get failure of ionic pumps so K out and Na in (cell death)

Question 22

CPP(Cerebral Perfusion Pressure)=

Answer 22

MAP-ICP

Question 23

Ideal CPP

Answer 23

60-70mmHg

Question 24

How does brain compensate for increase in ICP (e.g a bleed)?

Answer 24

Loses CSF and Venous blood - can only lose a certain amount so becomes uncompensated after that

Question 25

What does uncal herniation do

Answer 25

Squashes pons and midbrain causing fixed dilated pupil on same side

Question 26

SIgns of raised ICP

Answer 26

Depressed level of consciousness, pressor (cushing’s) response, projectile vomiting, CN6 palsies

Question 27

What is the cushing’s triad in the pressor response?

Answer 27

Increased BP, irregular breathing and bradycardia

Question 28

Signs of brainstem herniation

Answer 28

CN3 palsy, motor posturing, lower extremity rigidity, hyperventilation

Question 29

Methods to control ICP

Answer 29

Remove mass lesion, reduce CSF volume (drain), reduce parenchymal volume, reduce cerebral blood volume

Question 30

How do you reduce parenchymal volume?

Answer 30

Osmotic therapy - give manatol

Question 31

How do you reduce cerebral blood volume? (arterial and venous)

Answer 31

Arterial- sedation, mech ventilation, CPP control, avoid fever, treat seizures
Venous- sitting head up, avoid jugular compression

Question 32

Effect of PaO2 and PaCO2 on cerebral blood flow

Answer 32

Hypoxemia and hypercapnia increase cerebral blood flow - balance effect of increased ICP vs ischaemia from decreased flow

Question 33

Last option for reducing ICP

Answer 33

Decompressive craniotomy

Question 34

Why is being unwell immunosuppressive?

Answer 34

Cortisol levels raised

Question 35

Sepsis 6

Answer 35

3 in 3 out within an hour
In: O2, fluids, antibiotics
Out: Urine output, cultures, lactate

Question 36

High risk sepsis defined on NEWS chart by…

Answer 36

Scoring over 5 or 3 in one parameter

Question 37

Sepsis red flags

Answer 37

Supplemental O2 requirement, RR>25, HR>130, lactate>2mmol, purpuric rash, SBP<90, V or less on AVPU