Major Haemorrhage in Trauma

Reviewed and revised 5 August 2015

OVERVIEW

Goals of management

• “FIND the bleeding, STOP the bleeding”
• Rapid and effective restoration of blood volume
• Maintain functional blood composition to preserve blood function:
  — haemostasis, oxygen carrying capacity, oncotic pressure and biochemistry

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

SOURCE OF HAEMORRHAGE

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.

“Think SCALPeR when finding the bleeding”

APPROACH TO HAEMORRHAGE CONTROL

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

Approach to hemorrhage control:

• Get help early (e.g. surgeon, IR, anesthetics, ICU)
• 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

PULSE PALPATION AS A GUIDE TO BLOOD PRESSURE

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.

CLASSIFICATION OF STAGES OF HAEMORRHAGIC SHOCK

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:

• Class 1
  • Blood loss: up to 750 mL or 15% blood volume
  • Heart rate: <100/min
  • Blood pressure: normal
  • Pulse pressure (mmHg): normal/ increased
  • Respiratory rate: 14-20/min
  • Urine output: >30 mL/h
  • CNS: slightly anxious
  • Heart rate is minimally elevated or normal (<100)Typically, there is no change in blood pressure, pulse pressure, or respiratory rate.
• Class 2
  • Blood loss: 750-1500 mL or 15-30% blood volume
  • Heart rate: 100-120/min
  • Blood pressure: normal
  • Pulse pressure (mmHg): decreased
  • Respiratory rate: 20-30/min
  • Urine output: 20-30 mL/h
  • CNS: mildly anxious
• Class 3
  • Blood loss: 1500-2000 mL or 30-40% blood volume
  • Heart rate: 120-140/min
  • Blood pressure: decreased
  • Pulse pressure (mmHg): decreased
  • Respiratory rate: 30-40/min
  • Urine output: 5-15 mL/h
  • CNS: anxious, confused
• Class 4
  • Blood loss: >2000 mL or >40% blood volume
  • Heart rate: >140/min
  • Blood pressure: decreased
  • Pulse pressure (mmHg): decreased
  • Respiratory rate: >35/min
  • Urine output: negligible
  • CNS: confused, lethargic

Unfortunately, the classic stages of hemorrhagic shock (a la ATLS) are of limited clinical relevance in the real world, because of:

• 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 (rather than tachycardia) 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).

LETHAL TRIAD AND ACUTE COAGULOPATHY OF TRAUMA/ SHOCK

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).

HYPOTHERMIA PREVENTION AND TREATMENT

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

Damage control resuscitation (DCR) is a systematic approach to the management of the trauma patient with severe injuries that starts in the emergency room and continues through the operating room and the intensive care unit (ICU)

• DCR aims to maintain circulating volume, control haemorrhage and correct the ‘lethal triad’ of coagulopathy, acidosis and hypothermia until definitive intervention is appropriate
• DCR has 3 components:
  • permissive hypotension (aka minimal normotension) (this is controversial)
  • early haemostatic 
resuscitation
  • damage control surgery

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.

Haemostatic resuscitation

• aims to avoid or ameliorate acute coagulopathy of trauma and the complications of aggressive crystalloid fluid resuscitation while maintaining circulating volume
• involves early use of blood products in ratios resembling that of whole blood

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.

CRYSTALLOID RESUSCITATION

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

These downsides are part of the rationale for a haemostatic resuscitation approach to major haemorrhage in trauma.

References and Links

LITFL

• Trauma Tribulation 025 — Trauma! Major haemorrhage
• CCC — Haemostatic resuscitation
• CCC — Permissive hypotension
• CCC — Damage control surgery and damage control resuscitation

Journal articles and textbooks

• Bickell WH, Wall Jr MJ, et al. Immediate vs. Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Injuries. N Engl J Med. 1994; 331:1105 [Free fulltext]
• Deakin CD, Low JL. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study. BMJ. 2000 Sep 16;321(7262):673-4. PMC27481.
• Duchesne JC, et al. Damage control resuscitation: from emergency department to the operating room. Am Surg 2011; 2:201-6. PMID: 21337881
• Guly HR, Bouamra O, Little R, Dark P, Coats T, Driscoll P, Lecky FE. Testing the validity of the ATLS classification of hypovolaemic shock. Resuscitation. 2010 Sep;81(9):1142-7. PMID: 20619954.
• Poulton TJ. ATLS paradigm fails. Ann Emerg Med. 1988 Jan;17(1):107. PMID: 3337405.
• Thomas I, Dixon J. Bradycardia in acute haemorrhage. BMJ. 2004 Feb 21;328(7437):451-3. PMC344269.
• Thompson D, Adams SL, Barrett J. Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann Emerg Med. 1990 Mar;19(3):268-75. PMID: 2310066.

FOAM and web resources

• Broome Docs — Managing Traumatic bleeding: how can we apply the evidence in smaller hospitals?
• EMCrit Lecture: Haemostatic Resuscitation by Richard Dutton
• EMCrit Podcast 30 – Haemorrhagic Shock Resuscitation
• Resus.ME — Battlefield Resuscitation
• Resus.ME — European Trauma Bleeding Guidelines updated
• Resus.ME — Evidence refutes ATLS shock classification