Sepsis and Shock

Question 1

What is sepsis?

Answer 1

An overwhelming global response to infection

Question 2

What haemodynamic changes are there in sepsis and what sort of clinical signs do these lead to?

Answer 2

In sepsis there is peripheral vasodilation and maldistribution of flow
This leads to HYPOTENSION - this activates baroreceptors which then lead to an increase in heart rate and contractility leading to TACHYCARDIA

Question 3

What other key clinical signs are there in sepsis beyond haemodynamics?

Answer 3

Elevated respiratory rate
TEMPERATURE (usually of >38 but can also be <36)
WCC >12 or <4
Altered mental state (drowsy, confused etc.)
Not passed urine in a while (12-18h)
They might have CLINICAL SIGNS OF SHOCK (mottled, low CRT)

Question 4

What type of shock is septic shock and how does this occur?

Answer 4

In septic shock the peripheral vasodilation is profound and there is lack of blood flow to peripheral organs and other structures - this poor distribution of blood flow classifies septic shock as an example of DISTRIBUTIVE SHOCK

Question 5

How should we initially manage sepsis when it is first identified?

Answer 5

Initiate the SEPSIS6 or BUFALO

• Blood cultures - put in two wide bore IV cannulas an get some bloods including (FBC, U&E, glucose, VBG, cultures)
• Urine output - important to monitor this to get an idea of how well perfused the kidneys are. Put in a catheter if necessary
• Fluids - correct hypotension with fluid challenges (500mL 0.9% NaCl over 10-15mins). Repeat this if necessary
• Antibiotics - attempt to identify a source of infection and treat with the right abx according to trust guidelines. If no source identified then go broad spectrum
• Lactate - good measurement of the level of tissue hypo perfusion - get this with a blood gas. Concerning if >3
• Oxygen - Resp rate will usually be high and they might be hypoxic. Correct this with O2 therapy

Question 6

What would make you consider elevating to a senior after your initial management? How might they then be managed?

Answer 6

Concerning features include:

• Only TRANSIENTLY RESPONDING TO FLUID CHALLENGES (their BP is peaking after each challenge but then dropping again)
• PERSISTENTLY HIGH LACTATE - this suggests ongoing tissue hypoxia

***will need ICU input - consider central venous catheterisation and arterial line insertion - they might need to be managed with IV ADRENALINE to maintain their mean arterial pressure

Question 7

What is a possible complication of sepsis? What causes it?

Answer 7

SIRS - systemic inflammatory response syndrome

It is simply caused by the large and overwhelming release of cytokines and inflammatory mediators

Question 8

What are the criteria for SIRS?

Answer 8

Must have 2 of the following:

• Temp >38 or <36
• HR >96
• WCC <4 or >12
• Resp rate >20
• Blood glucose >7.7 (in non-diabetic). An early response to infection is to release sugars into the blood

Question 9

What is the difference between SIRS and SEPSIS?

Answer 9

Technically SEPSIS is just SIRS secondary to an identified source of infection.

Question 10

What is shock?

Answer 10

The life-threatening hypo perfusion and resulting hypoxia of organs

Question 11

What mnemonic can be used to identify the clinical signs of shock?

Answer 11

HEP B
Hands - Cool, clammy, reduced CRT, sweating
End-organ perfusion - Low consciousness, poor urine output
Pulses - weak, thready
Blood Pressure - low due to vasodilation

Question 12

What are the different types of shock?

Answer 12

Distributive (inc septic)
Cardiogenic 
Hypovolaemic 
Neurogenic 
Anaphylactic
Obstructive

Question 13

What is meant by preload and afterload?

Answer 13

These are important terms in shock.
Preload is the amount of the blood in the heart at the end of diastole (how much blood the hearts primed with before contraction)
Afterload is the resistance to outflow (the systemic vascular resistance)

Question 14

In the early stages of shock how does the body attempt to compensate and what effect does this have?

Answer 14

At perfusion to tissues begins to drop the body compensated by constricting blood vessels (VASOCONSTRICTION) to try and preserve blood flow. This has the effect of increasing afterload.

As the shock process becomes overwhelming the constriction will not be enough and the blood pressure will fall once more

Question 15

What are some causes of hypovolaemic shock and what is the process?

Answer 15

LOSSES - major haemorrhage, D&V, burns or pancreatitis.

Major loss decreases preload, afterload is increased to compensate but ultimately oxygen delivery is decreased

Question 16

What are some causes of cardiogenic shock and what is the process?

Answer 16

This can commonly happen post-MI or due to a malignant dysrhythmia
The heart stops pumping effectively and doesn’t empty its contents and so preload increases, afterload increases as response
Reduced CO leads to decreased oxygen delivery

Question 17

What are some examples of obstructive shock and what is the process?

Answer 17

Causes include tension pneumothorax or cardiac tamponade or PE
Obstruction to cardiac filling or emptying (preload might be increased or decreased) - RAISED JVP
Afterload is increased due to body’s vasoconstriction
Decreased CO leads to decreased oxygen delivery (similar to cardiogenic)

Question 18

What are some examples of distributive shock? What is unique about this type?

Answer 18

Anaphylactic, septic and neurogenic are all types of distributive shock
The difference is that in distributive the afterload is decreased - overwhelming vasodilation is the cause of poor perfusion rather than poor cardiac circulation

Question 19

What is anaphylactic shock and how does it affect haemodynamics?

Answer 19

Overwhelming type 1 hypersensitivity
IgE mediated mast cell degranulation leading to release of histamine which vasodilates
Occurs within 30 mins of exposure and responses can be global
- Cutaneous
- GI
- Respiratory
- Cardiovascular

Question 20

What are the classes of haemorrhagic shock?

Answer 20

(this is a type of hypovolaemic shock)
I - up to 750mL blood loss- 15% blood volume
II - 750-1500mL - 15-30% blood loss. RR increases and HR increases
III -1500-2000mL -30-40% - only now does BP drop
IV - >2000mL - >40%

Question 21

Describe the process of neurogenic shock - what are common causes?

Answer 21

This is a rare cause and most commonly due to anaesthetic incident or spinal cord trauma
- There is a loss of sympathetic tone meaning there is global vasodilation with no compensation. Hence why it is a form of distributive shock

Question 22

What is toxic shock syndrome?

Answer 22

A form of shock caused by EXOTOXINS (usually those produced by strep pyogenes or staph aureus)-SUPERANTIGENS
- These antigens can activate up to 20% of T cells at any one time and cause a very fast immune response. Profound vasodilation leads to form of distributive shock

Question 23

What is an Addisonian crisis?

Answer 23

Someone with Addison’s has destruction of adrenal cortex and so they have reduced amounts of mineralocorticoids and glucocorticoids. As a result they cannot activate the renin-angiotensin aldosterone response pathway meaning there is no water and sodium retention and there can be very low BP - SHOCK

Question 24

How should we treat shock?

Answer 24

ABCDE ASSESSMENT (Always remember signs like BP, HR, CRT, urine output, RR, O2 sats

IV ACCESS - two wide bore cannula (14G or 16G) into each of the ACFs
Get some bloods (FBC, U&E, Glucose, VBG, Crossmatch, CRP)

FLUID CHALLENGE (500mL NaCl 0.9% over 10-15mins or as short a time as possible). Giving too much fluid to a patient with cardiogenic shock can make situation worse 
BLOOD PRODUCTS IF HAEMORRHAGIC 

DRUGS - consider 1 in 10,000 adrenaline to vasoconstriction

Question 25

Why will people with shock have tachypnoea?

Answer 25

Due to hypoxia they will increase anaerobic respiration and increase production of lactic acid leading to a metabolic acidosis - the tachypnoea is compensatory

Question 26

What is a complication of systemic inflammation?

Answer 26

The inflammatory markers can activate the clotting cascade leading to widespread platelet aggregation and microvascular thrombosis formation (DIC)

In DIC so many of the platelets are used up in microvascular thrombi that the clotting ability of the blood is reduced so there is concurrent bruising and bleeding elsewhere - can be life-threatening