Shock is what occurs when we have insufficient tissue perfusion. There are different forms of shock:
- Septic shock
- Haemorrhagic shock
- Neurogenic shock
- Cardiogenic shock
- Anaphylactic shock
We can also classify it as:
- Cardiogenic shock
- Distributive shock
- Hypovolaemic shock
- Obstructive shock
The most common clinical features/labs which are suggestive of shock include hypotension tachycardia, tachypnoea reduced consciousness or abnormal mental status, cold, clammy extremities, mottled skin, oliguria metabolic acidosis, and hyperlactatemia.
Septic shock is a risk of patients with severe sepsis. It’s mortality is >40%.
We’ve discussed sepsis in it’s corresponding CCC.
Patients with infection + 2+ elements of SIRS are diagnosed as having sepsis. Those with organ failure have severe sepsis and those with refractory hypotension have septic shock.
This is characterised by:
Temperature - 36ºC - 38ºC (either hypothermic or hyperthermic) HR - >90 beats/min
RR - >20/min
WBC count - >12,000 or < 4,000
Excessive cytokine release causes an excessive vasodilatory response and extravasation of neutrophils.
Average adult volume of blood is about 7% of body weight. Haemorrhagic shock occurs when we see excessive blood loss:
There are 4 classes to haemorrhagic shock:
Parameter | Class I | Class II | Class III | Class IV |
Blood loss ml | <750ml | 750-1500ml | 1500-2000ml | >2000ml |
Blood loss % | <15% | 15-30% | 30-40% | >40% |
Pulse rate | <100 | >100 | >120 | >140ml |
Blood pressure | Normal | Normal | Decreased | Decreased |
Respiratory rate | 14-20 | 20-30 | 30-40 | >35 |
Urine output | >30ml | 20-30ml | 5-15ml | <5ml |
Symptoms | Normal | Anxious | Confused | Lethargic |
It is most likely in patients suffering from trauma. However may also occur in patients with:
- Tension pneumothorax
- Spinal cord injury
- Myocardial contusion
- Cardiac tamponade
Occurs after spinal cord transaction (usually at a higher level) → autonomic interruption → decreased sympathetic tone/increased parasympathetic tone → decreased PVR → decreased preload and CO → decreased tissue perfusion and shock.
We may use IV fluids to raise the BP and vasopressors to return PVR to normal.
The main cause for cardiogenic shock is IHD and MI. However, in the traumatic setting it can be due to myocardial trauma or myocardial contusion. This should be suspected in patients with sternal fractures or chest contusions. It is most commonly to the RHS of the heart due to blunt force trauma → chamber or valve rupture.
A transthoracic echo should assess for pericardial fluid or direct injury to the myocardium.
Treatment is supportive but if there is trauma to the chamber or valve we need to treat the defects surgically.
Inotropes such as dobutamine help.
Once again, more information on anaphylactic shock can be found in the CCC on anaphylaxis.
We treat anaphylaxis using IM adrenaline over the anterolateral aspect of the middle 1/3rd of thigh (but any IM injection site will suffice).
🔢 Classification
We can also classify shock according to 4 distinct types:
- Hypovolaemic - this is characterised by decreased intravascular volume. Some causes include:
- Haemorrhage
- GI losses - vomiting, diarrhoea, NG suction, drain.
- Renal losses - diuretics, hypoaldosteronism.
- Skin losses - burns, Stevens-Johnson syndrome, heatstroke, pyrexia.
- Third-space losses - pancreatitis, cirrhosis, intestinal obstruction, trauma.
- Cardiogenic - due to intracardiac causes the result in decreased CO and systemic hypoperfusion. Some causes include:
- Cardiomyopathies
- Arrhythmias
- MI
- Distributive - this is characterised by warm peripheries and peripheral vasodilation. It is the most common. Some causes include:
- Sepsis/SIRS
- Anaphylaxis
- Neurogenic shock
- Addisonian crisis
- Obstructive - due to extra Adrian causes that lead to decreased left ventricular cardiac output. Causes can be pulmonary vascular or mechanical in origin. It is relatively less common compared to the other 3 types. Some causes include:
- Pulmonary embolism
- Pulmonary hypertension
- Tension pneumothorax
- Cardiac tamponade
- Constrictive pericarditis
🧰 Management
- A - Ensure airway is patent
- B - Administer O2 if hypoxaemic - evidence actually shows that a target saturation of 88% - 92% is better than >96% as it is associated with lower mortality.
- C - Establish IV access early with 2 wide-bore cannulas. An initial MAP of 65mmHg is targeted if we do not know the cause of shock.
- IV fluid challenge - a bolus of 500ml saline or Hartmann’s solution over <15 minutes.
- If it is haemorrhagic in origin then activate and follow the local major haemorrhage protocol which involves using blood products.
- Vasopressors/inotropes can be used if unresponsive to IV fluids or blood products.
- Dobutamine is an inotrope frequently used.
- D - Treat underlying cause
- Sepsis - follow sepsis pathway and begin the sepsis 6.
- Anaphylaxis - administer adrenaline to the outer 1/3rd of the thigh, repeating every 5 minutes if there is no improvement.
- Cardiogenic
- STEMI - 300mg aspirin (loading dose).
- Hypovolaemic
- Haemorrhage - identify and aim to stop source of bleeding and activate the major haemorrhage protocol.
- Blood products not clear fluids (unless blood products are unavailable)
- Target Hb of 70-90g/L
- Reverse anticoagulation
- Warfarin - prothrombin complex
- Dabigatran - idarucizumab
- Apixaban/Ricardo a an - andexanet alfa
- IV tranexamic acid if the haemorrhage is due to trauma.
- Burns - fluid resuscitation according to the Parkalnd crystalloid estimate.
- DKA - IV insulin infusion according to local protocols.
- Obstructive
- Cardiac tamponade - pericardiocentesis.
- PE - anticoagulation and thrombolysis (shock is the only indication for thrombolysis in PE).
- Tension pneumothorax - local protocols differ but urgent decompression is needed via thoracocentesis, chest drain, thoracostomy.
- E - examine the patient properly while exposing the body/maintaining dignity and minimising heat loss.