Trauma Basics: Shock!
29th July 2020
The term Shock is one of those words which triggers a pathological killer response in me every time I hear it. It is used indiscriminately and without rationale.
“Oh my god, I think they’re in Shock!”
Why are you saying that?
“I don’t know, I just think now is the right time to say it!”
But why do you think they’re in shock?
“I don’t know, they look a bit…shocky”
It is that it is a broad term with different meanings to different people. Most people will typically use the phrase “They’re in shock!” when the casualty is reacting badly to an emotionally traumatic experience. This emotional shock, pale skin, fast breathing and pulse, appearing confused, distracted, agitated or hyperactive is a common response to adrenaline. This will not kill you.
This article is about clinical shock. And that will kill everyone. Even you.
What is clinical Shock?
There is no established definition of the term but commonly it will relate to:
“A reduction in perfusion of oxygen to the vital organs”
This definition focuses on the outcome: For one reason or other, the casualty’s vital organs are no longer receiving sufficient oxygen.
It is for this reason that everyone in the world, regardless of cause, will die of shock. Even you.
Another, simpler, definition is:
“A failure of the circulatory system”
This definition focuses of the cause; there is a problem with either the heart, large vessels or blood, which inevitably leads to the first definition.
Types of Shock.
Depending how pedantic we want to be the classifications of Shock can be divided into many types, yet each one fundamentally relates to one of the components of the circulatory system.
For the responder this table makes for excellent revision practice but it’s application in the field is limited – does understanding all of the categories help achieve a more accurate diagnosis and will it affect your treatment in a pre-hospital environment?
Focusing on incidence rates, ease of diagnosis and our ability to treat, in this article we will consider five common categories of shock:
Hypovolaemic
Cardiogenic
Neurogenic
Anaphylactic
Septic (commonly referred to as “Sepsis”)
Hypovolaemic Shock
Blood loss as a result of injury is the leading cause of death for trauma casualties between from 1 to 46 years old (1) and hypovolaemic shock has the highest relative incidence rates of clinical shock at 16-22% compared to neurogenic shock of 4% (2, 3).
Hypovolaemic shock can be defined as a reduction of circulating blood volume. The key word in this definition is volume, not blood. This reminds us that as well as blood loss, other causes of fluid loss such as burns and dehydration can result in a reduction of blood volume leading to Hypovolaemic shock (4).
Recognition:
Response: Reduced
Breathing: Fast and weak
Pulse: Fast and weak
Colour: Pale
Temperature: Low
Capillary Refill: Slow
SpO2: Low
Blood Pressure: Low - due to reduced blood volume
Classification of Hypovolaemic Shock
For the initial evaluation of hypovolaemic casualties, the American College of Surgeons in 2008 defined in its training program Advanced Trauma Life Support (ATLS) four classes of Hypovolaemic shock (5). This classification was based upon an estimated percentage blood loss combined with corresponding vital signs such as the heart rate, systolic blood pressure and level of response to allocate each patient to the respective shock class. This table will be familiar to anyone who has received trauma training in thw last 10 years although the clinical validity of the ATLS classification of hypovolemic shock was questioned as early as 2010 (6-9) and was removed from the 10th edition ATLS and 9th edition PHTLS course materials in 2018 (10, 11) yet it is still commonly taught.
Shock Index
Although the heart rate and systolic blood pressure considered separately have been shown unreliable in determining the presence of Hypovolemic shock (6-8, 12-16), the ratio between them – known as the Shock Index - is a capable measure for hemodynamic instability. If a casualty’s heart rate (bpm) divided by their systolic blood pressure (mmHg) is a value of greater than 1.0 this is considered a reliable indicator of Hypovolaemic Shock (17-23) and Septic Shock (24). Utilizing the Shock Index clearly requires the ability to reliably and accurately take a casualty’s blood pressure and pulse rate.
Further reading - Blood Pressure
Treatment
Stop the bleed
Arrange urgent transport to hospital
Keep the casualty warm
Encourage the casualty to adopt a comfortable position
Provide supplemental Oxygen if available
Do not give the casualty food or drink beyond small sips if tolerated.
Cardiogenic Shock
Cardiogenic shock is primarily a disorder of cardiac function in the form of a critical reduction of the heart’s ability to pump (3). The most common incidences of Cardiogenic shock a responder will attend are Cardiac Arrest, Heart Attack or Angina.
Recognition
Response: Reduced
Breathing: Typically faster and /or difficult
Colour: Pale
Temperature: Low
Capillary Refill: Slow
SpO2: Low
Blood Pressure: Low - due to reduced cardiac output
The recognition features of Cardiogenic and Hypovolaemic are similar as the same issue has occurred: a failure of the circulatory system causing reduced perfusion although the mechanisms are different - reduced cardiac output versus reduced volume. The key difference is that your Hypovolaemic casualty will almost certainly be due to trauma whilst your Cardiogenic casualty could also, but is most likely to be, a medical casualty without a mechanism of injury, rather a history or leading events.
Further reading - SAMPLE - the art of Casualty Questioning
Treatment
Recognise the difference between heart attack and angina and treat accordingly
Encourage the casualty to adopt a comfortable position
Provide supplemental Oxygen if available titrated to their SpO2
Neurogenic Shock
Neurogenic shock is a state of imbalance between sympathetic and parasympathetic regulation of cardiac action and vascular smooth muscle resulting in uncontrolled vasodilation (3). i.e. involuntary vasodilation leading to reduced blood pressure. Whilst a relatively low incidence of less than 4% (3) the most common cause of Neurogenic shock in the pre-hospital setting is spinal cord injury accounting for 15-20% of all cases (25) followed by surgical intervention (26). Neurogenic shock can also occur due to traumatic brain injury, meningitis, or, more rarely, during or after epileptic seizures (3).
Recognition
Response: Reduced
Breathing: Slower, deeper or irregular
Colour: Flushed
Temperature: Warm
Capillary Refill: Fast
SpO2: Low
Blood Pressure: Low - due to vasodilation (note: this is sometimes seen with a widening pulse pressure)
Whilst neurogenic shock is most commonly associated with spinal cord injury, the classic vital signs above are most likely seen following traumatic brain injury and can be absent or slow to appear with spinal cord injury (27).
Treatment
The key issue is to recognise the condition and manage the cause.
Further reading - Spinal Injury in Remote Environments
Anaphylactic & Septic Shock
Anaphylactic and Septic shock are both similar in mechanism; vasodilation with a shift of fluid from the intravascular to the extravascular space (3) leading to low blood pressure.
Anaphylaxis is triggered by unregulated production of histamine in response to an allergen. Sepsis is triggered by an unregulated response to infection. As such, the signs can be expected to be similar:
Recognition
Response: Reduced
Breathing: Faster. (often difficult with anaphylaxis)
Colour: Flushed due to vasodilation (possible rash with anaphylaxis)
Temperature: Warm
Capillary Refill: Fast
SpO2: Low
Blood Pressure: Low - due to vasodilation
The key differentiator is the cause – allergen or infection.
Further reading - Understanding Anaphylaxis
Sepsis education has experienced a renaissance recently with a much more focus placed on identifying sepsis early on, especially in vulnerable casualties. As such, there are now many diagnostic and recognition tools for clinicians, some more accurate and easier to apply than others.
The Quick SOFA” (qSOFA) score can be used for screening, requiring only a preliminary examination of state of consciousness, respiration rate, and blood pressure. If the casualty meets two or more of the following criteria together with a history of infection - there is a high likelihood of sepsis (28-30).
Reduced response
Breathing over 22 breaths per minute
Systolic blood pressure below 100mmHg
Summary
Assessment of the casualti’s vital signs alone are reasonable for identifying clinical shock in a broad sense but are not strong indicators alone for identifying which type of shock. To challenge or confirm one’s suspicion of any type of clinical shock a history is needed in the first instance.
All causes of clinical shock will lead to a reduced level of response - this is usually the first signs to manifest as a result of hypoxia.
All causes of clinical shock will also display low Sp02 and low blood pressure.
Most types of shock are mechanistic in their nature so the vital signs deteriorate predictably:
In Hypovolaemic and Cardiogenic shock the casualty does not have enough warm, red stuff inside them or it is not being pumped around, they will become cold, pale, with poor capillary refill.
Neurogenic, Anaphylactic and Spetic shock cause vasodilation, causing the casualty to appear warmer, more flushed and with a fast capillary refill.
In Hypovolaemic, Cardiogenic, Anaphylactic and Septic shock, the body will attempt to compensate against the hypoxia with faster, weaker breathing. Low blood pressure will typically be compensated by a faster, weaker pulse.
Neurogenic shock is less intuitive - the problem is at the neurological level and so the breathing and pulse become slower, deeper or irregular, which appears counter-intuitive to hypoxia.
Next article: Trauma and hypothermia
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