JEMS Clinical Review
>> Understand the definition of shock.
>> Know the pathophysiology and signs of shock.
>> List the basic and unique treatment tenets for hemorrhagic shock.
>> Understand the application and use of the tourniquet.
Cavitary: Denoting the presence of one or more cavities.
Hemostatic: Arresting the flow of blood within the vessels or hemorrhage.
Hypovolemic shock: A state of physical collapse and prostration caused by massive blood loss, about one-fifth or more of total blood volume.
Hypotensive resuscitation: Limiting fluid resuscitation—at least until hemorrhage is controlled—by natural hemostasis, external pressure, angiography or surgery.
Types of Shock
>> Pulmonary embolism
>> Pericardial tamponade
>> Tension pneumothorax
>> Constrictive pericarditis
>> Adrenal insufficiency
Source: Zimmerman J: Fundamental Critical Care Support, Fourth Edition. Society of Critical Care Medicine: Mount Prospect, Ill., 7–3, 2007.
It’s an uncommonly quiet Saturday night when you get dispatched to a high-speed motor vehicle crash. You arrive on scene to see a mangled car at rest against the side of a house. An inspection of the vehicle shows heavy damage, and you see multiple patients. As you and your partner move in to begin triage, you note the absence of movement from inside the car.
Five patients are identified, but only one seems to be alive. A prolonged extrication yields a young, female patient, who’s removed by the rescue team on a backboard with a C-collar. Your initial and rapid exam reveals an obtunded but breathing patient with active bleeding from a traumatic amputation of her left lower extremity at the knee level. Her heart rate is in the 140s, with a blood pressure of 110/90 mmHg. You orotracheally intubate her for airway protection due to a diminished level of consciousness and transport her without delay to a trauma center.
Two large-bore IV lines are initiated, and a compression dressing is placed over her bleeding stump. After updating the trauma center, you notice the patient’s blood pressure has dropped to 100/90, and your compression dressing has become saturated with blood. You infuse 1 L of normal saline and apply a new pressure dressing, but it’s becoming clear that this standard approach isn’t going to be effective.
You apply a tourniquet at the thigh just a few minutes before arriving at the hospital, significantly reducing the bleeding. On arrival, the patient has a heart rate of 136 and systolic blood pressure (SBP) of 98 mmHg, with a moderately saturated dressing.
In 1872, Samuel Gross described shock as the “rude unhinging of the machinery of life.”(1) Although Gross’s definition is elegant, a more precise description of shock is a condition characterized by the inadequate delivery of oxygen and the nutrients necessary for normal cellular and tissue function.
Hemorrhagic shock, a form of hypovolemic shock, is most commonly encountered in trauma patients, but it’s important to recognize that several types of shock exist (see Figure 1). Hemorrhagic shock can be categorized into a system based on physiologic parameters that roughly correlate to the volume of blood loss. No hard lines distinguish one category from another, and blood pressure alone can’t be the determinant for shock.
As previously mentioned, shock is the inadequate delivery of nutrients to tissues. Essentially, it’s a supply-and-demand problem. The condition can result in a change of aerobic to anaerobic metabolism with the extent of metabolic derangement depending on the length of time and severity of the insult. Although some differences between the various types of shock exist, changes will occur in the function of most body systems, including cardiovascular, neuroendocrine and immunologic.
Stimulation of the sympathetic system results in an increased heart rate and contractility with the initial insult. Further, peripheral vasoconstriction occurs, resulting in an elevated diastolic blood pressure as the body attempts to maintain normotension. Peripheral vasoconstriction also leads to preferential shunting of blood from non-essential organs (e.g., small bowel and skin). The complicated system of response is regulated in many ways by the hypothalamic-pituitary-adrenal axis.
Through multiple pathways, cortisol is released and acts in conjunction with epinephrine and glucagon to induce a catabolic state. Catabolism results in insulin resistance and muscle breakdown. Additionally, hypovolemia results in the release of anti-diuretic hormone (ADH) and aldosterone. This release results in mesenteric vasoconstriction and retention of sodium and water in efforts to maintain intravascular volume.
Many proteins are activated in shock-like states. Pro-inflammatory mediators (e.g., TNF, IL-1 and IL-6) have a role in the hemodynamic instability, vasodilation, fevers, lung disease and multi-organ failure that can result from shock.
As the needs of the cell exceed that which can be delivered, metabolism changes from aerobic (use of oxygen) to anaerobic. Anaerobic metabolism affects cellular function, physiology and morphology. Ultimately, this results in cell death and organ dysfunction.
As always, your assessment should begin with evaluation of the airway, breathing, circulation (ABC) and disability. Address any problems with any of these components as soon as they’re identified.
Monitoring vital signs frequently will allow you to identify trends and help identify shock. Subtle clues of early hemorrhagic shock—such as narrowed pulse pressure (difference between systolic and diastolic) and cool, pale extremities—can provide significant insight into the patient’s condition and subsequent treatment. Unless masked by medication, such as a beta blocker, a patient will exhibit signs of shock first by mounting tachycardia.
Specifically, you should examine your patient for the absence or presence of pulses in the extremities. Remember that the presence of pulses in particular locations will give you a clue to the patient’s SBP:
Note that automated blood pressure cuffs can give erroneous values, so providers should also use manual BP measurements in patients found to be hypotensive.(2) In addition to palpating pulses when evaluating circulation, it’s important to identify sites of active or potentially active bleeding. Address any active bleeding as it’s found. Wounds that are hemostatic should be periodically evaluated to ensure the site hasn’t converted to active bleeding, which can happen with ongoing resuscitation.
Once you identify a shock state, begin treatment as soon as possible. Administer high-flow oxygen and attempt endotracheal intubation if the patient’s condition warrants and won’t delay transport to the hospital. Correct any other causes of shock (e.g., tension pneumothorax).
Immediately initiate hemorrhage control by applying direct pressure over the wound. Standard sterile gauze can be used the majority of time. Avoid adding more gauze to a soaked dressing because this can actually reduce the direct pressure needed to stop bleeding. Should gauze soak through on a wound, it may be necessary to check whether the dressing is actually in the appropriate place and the correct amount of pressure is being applied.
If soaked, remove all but the first layer of gauze and reapply a clean dressing. It may also be beneficial to elevate the affected region above the level of the heart. Although some recent literature has called into question the efficacy of proximal pressure points as a means to control distal hemorrhage, it can still be considered part of the hemorrhage control toolkit.(3)
Next, obtain IV access via large-bore catheters (14 or 16 gauge). If IV access isn’t possible, use an intraosseous route. Ideally, volume replacement for hemorrhage is in the form of blood products, but Advanced Trauma Life Support (ATLS) recommendations are for isotonic fluid replacement in the form of either warmed lactated Ringer’s or normal saline.(4) Current recommendations call for the infusion of 1–2 L of isotonic solution, noting the response. The patient may show permanent response, transient response or non-response, based on the amount of blood loss and ongoing process. Although not a protocol for prehospital providers, it’s useful to understand the concept of hypotensive resuscitation.
Historically, the goal of active resuscitation of the patient in hemorrhagic shock was the restoration of a “normal” blood pressure. A more complete understanding of the pathophysiology of shock has potentially changed this paradigm to hypotensive resuscitation or permissive hypotension. Restoring blood pressure in uncontrolled environments to presumed normal levels may have the unintended effect of worsening the bleeding.
Aggressive resuscitation attempts at increasing blood pressure may result in “popping the clot” off a wound that may have formed in the face of hypotension.(5) Therefore, targeting an SBP of 90 mmHg in hemorrhagic shock until definitive control of bleeding results in improved outcomes in the penetrating trauma patient.(6)
Although this concept has taken hold in the trauma community for all types of patients in hemorrhagic shock, hypotension can result in secondary insult in the patient with traumatic brain injury (TBI). In general, prehospital resuscitation should be guided by end-organ perfusion (i.e., clear mentation) and preservation of vital functions without increasing risk of further bleeding. A general proposal is to target fluid administration to a goal of a palpable radial pulse.(7)
Recent changes have also affected the recommended fluid for resuscitation. Armed conflict has frequently advanced trauma care, and the current conflicts are no different. Early transfusion of blood and blood products in fairly even ratios, called hemostatic resuscitation, has been shown to have a positive outcome on mortality. Once active bleeding or hemorrhagic shock is recognized, transfusion is the preferred method for volume resuscitation. Although not totally validated, in the U.S.—where component therapy is the norm—the goal is to transfuse in a 1:1:1 ratio of packed red blood cells to fresh frozen plasma and platelets.
Due to problems with banked blood that include storage, portability and infectious disease, numerous attempts have been made over the years to create blood product substitutes that would enable their use in a variety of situations, including the prehospital environment. Several trials have been undertaken, but none have yet shown significant positive results.(8)
Many hemostatic agents have been introduced to the field over the past five years. These have been developed to help staunch active bleeding with a goal of being well tolerated—stable both at room temperature and under extreme conditions—and easy to use with minimal training. The agents comprise several different materials, have been approved for external wounds and have found their way into the prehospital environment. The most common products are HemCon, Celox and Quickclot/Quickclot Combat Gauze. Each has different properties that help achieve hemostasis.(9)
Although all seem to provide a baseline capability for hemostasis, none are 100% effective, and some variability in their efficacy exists.(10,11) It’s important to remember that whatever product is used, that product’s application instructions should be followed. Most information about these products has come from animal models and the military. But currently, there haven’t been any randomized, prospective studies on hemostatic agents’ efficacy in the non-combat prehospital environment. Ongoing research with different materials and impregnations will need proper evaluation before coming to practical use.
The use of tourniquets has gone in and out of fashion for intractable hemorrhage of an extremity. Until recently, they had been viewed as dangerous tools and their use discouraged unless as a last resort. The morbidities associated with their use have traditionally included nerve palsy, amputation and fasciotomies.
With the predominance of extremity wounding in the most recent armed conflicts, along with its safe use in orthopedic surgery, the tourniquet has come back into vogue. Multiple studies have demonstrated the safety of tourniquet use.(12–15) As with many other modalities, continued study is needed to establish best practices. But in general, the tourniquet should be at least two inches wide. Studies have
demonstrated that narrow tourniquets aren’t as effective and may, in fact, result in the complications that removed the tourniquet from treatment options in the past.(13,16)
Although the tourniquet is probably safe if on for less than two hours, it’s not truly known how long it can be safely applied. The armed services recommend the tourniquet be applied proximal to the wound and tightened until bleeding stops and distal pulses are no longer present. The time of application should be noted, a “T” placed on the patient’s forehead and its presence communicated with any turnover of care.(16) Finally, tourniquet time should be minimized, and repeated exams should take place to monitor necessity and effectiveness of its use.
Hemorrhagic shock, a form of hypovolemic shock, is the most common cause of shock in the trauma patient. Understanding the pathophysiology of shock allows the provider to expect its various presentations. The team can begin appropriate therapy when faced with early signs, such as narrowed pulse pressure and tachycardia. Urgent transport to a trauma center should not be delayed. Undertake the standard ABC evaluation with a focus on circulation and hemorrhage control.
Ultimately, the place for the patient in hemorrhagic shock is the operating room. After a rapid initial evaluation, which should include cavitary triage and identification of the most likely cause for shock, the ongoing shock state should prompt packaging the patient for travel to the operating room for definitive hemorrhage control. JEMS
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3.Swan KG, Wright DS, Barbagiovanni SS, et al. Tourniquets revisited. J Trauma. 2009; 66(3):672–
4. American College of Surgeons: ATLS: Advanced Trauma Life Support for Doctors (Student Course Manual), Eighth Edition. American College of Surgeons: Chicago, 63, 2008.
5. Pepe PE, Dutton RP, Fowler RL. Preoperative resuscitation of the trauma patient. Curr Opin Anaesthesiol. 2008; 21(2):216–221.
6. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994; 331(17):1105–1109.
7. Revell M, Greaves I, Porter K. Endpoints for fluid resuscitation in hemorrhagic shock. J Trauma. 2003; 54(5 Suppl):S63–S67.
8. Chen JY, Scerbo M, Kramer G. A review of blood substitutes: examining history, clinical trial results and ethics of hemoglobin-based oxygen carriers. Clinics. 2009; 64(8):803–813.
9. Zeller J, Fox AD, Pryor JP. Beyond the battlefield: Use of hemostatic dressings in civilian EMS. JEMS. March 2008; 33(3):102–109.
10. Arnaud F, Teranishi K, Tomori T, et al. Comparison of 10 hemostatic dressings in a groin puncture model in swine. J Vasc Surg. 2009; 50(3):632–639.
11. Kheirabadi BS, Scherer MR, Estep J, et al. Determination of efficacy of new hemostatic dressings in a model of extremity arterial hemorrhage in swine. J Trauma. 2009; 67(3):450–460.
12. Kragh JF, Baer DG, Walters TJ. Extended (16 hour) tourniquet application after combat wounds: A case report and review of the current literature. J Orthop Trauma. 2007; 21(4):274–278.
13. Kragh JF, Walters TJ, Baer DG, et al. Practical use of emergency tourniquets to stop bleeding in major limb trauma. J Trauma. 2008; 64(2 Suppl):S38–S50.
14. Sambasivan CN, Schreiber MA. Emerging therapies in traumatic hemorrhage control. Curr Opin Crit Care. 2009; 15(6):560–568.
15. Doyle GS, Taillac PP. Tourniquets: A review of current use with proposals for expanded prehospital use. Prehosp Emerg Care. 2008; 12(2): 241–256.
16. Welling DR, Burris DG, Hutton JE, et al. A balanced approach to tourniquet use: Lessons learned and relearned. J Am Coll Surg. 2006; 203(1):106–115.
This article originally appeared in April 2011 JEMS as “Shock Sense: Detecting & correcting hemorrhagic shock in trauma patients.”