Trauma! Major Haemorrhage

We have 3 main goals:

• Stop bleeding
• Rapid and effective restoration of blood volume
• Maintain functional blood composition to preserve blood function:
  — hemostasis, oxygen carrying capacity, oncotic pressure and biochemistry

Critical bleeding is major haemorrhage that is life threatening and may require massive transfusion.

—

When assessing the major trauma patient, remember the mantra:

“FIND the bleeding, STOP the bleeding”

It is convenient to consider injuries to 6 regions which may account for major blood loss:

• ‘Street’: scalp and external sources (especially small children)
• Chest
• Abdomen
• Long bones (especially femurs)
• Pelvis
• Retroperitoneum

Don’t search satisfice and settle for one site of bleeding… be thorough and systematic.

So here’s another mantra for you:

“Think SCALPeR when finding the bleeding”

—

Yet another handy tip:

Whenever you think ‘control hemorrhage’, think ‘correct coagulopathy’

Approach to hemorrhage control:

• Find the cause
• Initial measures, such as:
  — Direct pressure and elevation,
  — Adrenaline soaked gauze, hemostatic dressings
  — Reduce and splint long bone and pelvic fractures
  — Tourniquets
• Invasive measures, such as:
  — sutures
  — tamponade, by packing or foley catheter with balloon inflated
  — tie off vessels
  — cautery
  — interventional radiology
  — damage control surgery
• Correct coagulopathy

Learn more:

• Resus.ME — Simple emergency haemorrhage control (foley catheter technique for neck wounds)

—

Traditional ATLS teaching held that:

• If only the carotid pulse is palpable, the systolic blood pressure (SBP) is 60-70 mmHg
• If the carotid and femoral pulses are palpable, the SBP is 70-80 mmHg
• If the radial pulse is also palpable, the SBP is >80 mmHg

In reality, the pulses are lost in that order (radial, then femoral, then carotid) but the SBP at which they disappear varies and is often lower than what ATLS advises. Thus the ATLS guide will tend to overestimate blood pressure.

Remember that perfusion is more important than blood pressure anyway!

—

An easy way to remember the categories is to think of the scores in a game of tennis:

Love – 15 – 30 – 40 — game over (>40)

These stages are described in ATLS as follows:

—

Unfortunately, patients in the real world don’t tend to read ATLS manuals… or if they do they often choose to ignore them!

The classic stages of hemorrhagic shock (a la ATLS) don’t bear out in reality

The reasons for this include:

• Differences in compensation for different types of injuries (e.g. blunt versus penetrating trauma)
• Age (e.g. blunted physiological responses in the elderly)
• Comorbidities
• Medications (e.g. beta-blockade may conceal shock by preventing tachycardia)

Also, bradycardia is often seen in major haemorrhage:

• One theory is that there are 2 phases of response to bleeding:
  — inital catacholamine surge with tachycardia, followed by
  — subsequent bradycardia of uncertain mechanism (parasympathetically mediated?)
• But there also seems to be a group of patients who have relative bradycardia — they fail to mount the initial tachycardia. Some have also noted that bradycardia is more common in acute rapid blood loss (Thomas and Dixon, 2004).
• Some have explained the bradycardia as being due to vagal stimulation from peritoneal stimulation in intra-abdominal hemorrhage, but bradycardia has been seen in penetrating extremity trauma too (Thompson et al, 1990).

Learn more:

• Resus.ME — Evidence refutes ATLS shock classification

—

The lethal triad is:

• Hypothermia
• Coagulopathy
• Acidosis

These three factors both cause, and contribute to, acute coagulopathy of trauma/ shock (ACoTS) which leads to, and result from, major hemorrhage. They feed off one another, such that bleeding begets more bleeding. This is the theoretical rationale for damage control resuscitation (see below).

image courtesy of Scott Weingart at EMCrit.org

Image from: emcrit.com—

Prevent and treat hypothermia with the following:

• Aggressive resuscitation with blood products
• Use warmed fluids (e.g. Level 1 Fluid Warmer)
• Bair Hugger or warm blankets
• Minimise exposure
• Increase ambient temperature
• Continuous temperature monitoring

—

Damage control resuscitation has 3 components:

• permissive hypotension (aka minimal normotension)
• early hemostatic 
resuscitation
• damage control surgery

The underlying principles are to limit ongoing haemorrhage, identify and correct coagulopathy and restrict the use of 
crystalloids.

Permissive hypotension

• Permissive hypotension, or minimal normotension, seeks to avoid excessive fluid administration (and the associated problems of hemodilution, fluid overload and clot disruption). Classically a target SBP of 80 to 100 mmHg is advised.
• As perfusion is more important than blood pressure, an alternate strategy (a la EMCrit) is to target a MAP >65 mmHg together with a good radial pulse and pulse oximetry waveform. If the BP is too high, use titrated aliquots of fentanyl (e.g. 25 micrograms IV) to provide sympatholysis as well as analgesia.

Damage control surgery

Damage control surgery refers to limited surgical interventions that serve to control haemorrhage and minimize contamination until the patient has sufficient physiological reserve to undergo definitive interventions. The strategy aims to bring the ‘lethal triad’ under control, so that the patient will be able to tolerate further surgery once he or she improves.

Hemostatic resuscitation and massive transfusion protocols are discussed in the Trauma Tribulation 026 — Trauma! Massive Transfusion.

Learn more:

• EMCrit Lecture: Haemostatic Resuscitation by Richard Dutton
• EMCrit Podcast 30 – Haemorrhagic Shock Resuscitation
• Resus.ME — Battlefield Resuscitation
• Broome Docs — Managing Traumatic bleeding: how can we apply the evidence in smaller hospitals?

—

Traditional ATLS teaching is to initiate fluid resuscitation with 1-2 L of crystalloid such as normal saline or compound sodium lactate (Hartmann’s solution).

Potential downsides of this approach include:

• dilutional coagulopathy
• impaired oxygen delivery due to dilutional anaemia
• hypothermia
• worsening metabolic acidosis (especially hyperchloremic non-anion gap metabolic acidosis from normal saline administration)
• clot dislodgement and haemorrhage from blood pressure elevation

—