ANCC CONTACT HOURS Traumatic hypovolemic · PDF file · 2011-01-24ruptured ectopic pregnancy. ... Traumatic hypovolemic shock By Jeff Strickler, MA, RN, CEN, CFRN, EMT-P ... Case

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A VOICE on the EMS radio interrupts your thoughts: “Med 2 en route with 21-year-old male involved in motorcycle crash. Patient was wear-ing helmet and had no loss of consciousness. At present he is conscious, alert, and oriented, but complaining of abdominal pain. Heart rate 110 bpm with BP 120/90. ETA 5 minutes.”

You rush to assist with setting up the trauma room. Moments later, your patient arrives, ap-pearing anxious and complaining of severe ab-dominal pain, which he rates at 8 on a 0-to-10 pain intensity scale. You note his skin is pale and diaphoretic. He’s tachypneic, and a quick radial pulse check shows that he’s tachycardic. As you call for the ED physician, you realize that you’re seeing signs of impending shock. This man could die from unresolved hypovolemic shock unless the team responds quickly.

Hypovolemia is the most common cause of shock.1,2 (For other shock types, see What’s shock?) Although it’s often due to injury and massive blood loss, it can also have nontrau-matic causes, such as a gastrointestinal bleed or ruptured ectopic pregnancy. Hypovolemia can also be caused by fl uid losses and third-spacing from burn injuries, or dehydration from frequent vomiting or diarrhea.

This article discusses the causes, treatments, and nursing care for patients with traumatic hypovolemic shock. For a refresher on pathophysi-ology, see Pathophys particulars.

Compensated or not?One classifi cation system categorizes hypovole-mic shock into three stages: compensated, un-compensated, and irreversible.3 The value of this method is that the name of each phase describes what’s seen clinically.

Early compensated shock occurs when the body’s compensatory mechanisms are adequate to maintain cardiac output. Signs and symptoms of the compensatory response include tachy-cardia, tachypnea, oliguria, and anxiety due to sympathetic nervous system (SNS) stimulation; and skin changes (pallor, decreased capillary refi ll time, cool temperature, and diaphoresis) secondary to peripheral vasoconstriction, also

Traumatic hypovolemic

shock

By Jeff Strickler, MA, RN, CEN, CFRN, EMT-P

Halt the downward

spiral

Copyright © 2010 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

www.Nursing2010.com October l Nursing2010 l 35



due to SNS stimulation. Decreased cardiac output leads to decreased renal perfusion, which activates the renin-angiotensin-aldosterone sys-tem, leading to oliguria and further SNS activation. BP is often normal in early stages of shock, but progres-sion of shock leads to orthostatic or postural hypotension.

Uncompensated shock occurs when compensatory mechanisms start to fail and can no longer main-tain adequate cardiac output, caus-ing hypotension. Because a decrease in systolic BP doesn’t occur until at least 20% of blood volume is lost, it’s important to note that hypotension is a late sign.4

Irreversible shock is often associ-ated with losses of more than 25% of total blood volume. Unchecked, shock leads to cellular ischemia and subsequent acidosis, cellular necrosis, and organ failure that can’t be resolved, even if cardiac output increases.2 Once cellular breakdown and acidosis reach critical levels, reperfusion may lead to reperfusion injury, during which oxygen-free radicals overwhelm remaining cellular activity and cause neutrophil infi l-tration, microvascular damage, and impairment of the microcirculation.

Case study progressionBack to our patient… As the team begins assessment, you note that he’s becoming increasingly confused.

His abdomen is markedly distended and tender to light palpation. De-spite receiving 100% oxygen via a nonrebreather mask, he remains tachypneic. After placing him on a cardiac monitor, you see sinus tachycardia at 120 bpm. An indwell-ing urinary catheter is inserted with minimal initial output. His BP is now 90/70. You realize that your patient is now decompensating.

You recognize that an alteration in level of consciousness (LOC), tachypnea, tachycardia, peripheral vascular changes, and oliguria are signs of shock. The drop in BP is an ominous sign that shock is progressing.

As always, your nursing assess-ment starts with the ABCs (assess and support airway, breathing, and circulation) followed by determining the patient’s pertinent medical histo-ry and the mechanism of traumatic injury. When a patient is still ad-equately compensating for the fl uid loss, this history may provide the fi rst clue to the injury’s real extent and nature. Also perform a complete head-to-toe assessment to determine locations of pain, ecchymoses, or distension that could point to occult bleeding.

An adequate assessment includes evaluation of the chest, abdomen, and pelvis. Evaluation of the abdo-men is conducted initially through a focused assessment sonography for trauma (FAST) scan, which can identify pericardial fl uid in the chest as well as intraperitoneal fl uid in the abdomen. If the patient is hemo-dynamically stable, then a CT scan is indicated for more defi nitive evalua-tion of any injuries.

Long-bone fractures such as femur fractures can also cause signifi cant hypovolemia, so prepare to obtain extremity fi lms as appropriate.

A central venous pressure reading of less than 4 mm Hg (<5 cm H2O) indicates hypovolemia.5 Lab analysis shows decreased levels of hemoglo-bin and hematocrit, elevated lactate levels, and the presence of an arterial base defi cit greater than –2 mmol/L.

Serum lactate and arterial base defi cits are considered proxies for oxygen debt. Serum lactate levels that remain high signal that the body is attempting to produce en-ergy through anaerobic metabolism.

Base defi cit is considered a sur-rogate marker of metabolic acidosis. Patients with a signifi cant arterial base defi cit are more likely to die from the oxygen debt and poor metabolic state.2

Normalization of both lactate lev-els and base defi cit are considered resuscitation endpoints for deter-mining the degree of oxygen debt and the patient’s response to resus-citation. These are more signifi cant indicators than normotension.6

Many current efforts are leading to more direct measurements of cel-lular perfusion, such as measuring gastric pH or oxygenation in the tissues (StO2). Via infrared spec-trometry, StO2 noninvasively mea-sures hemoglobin oxygen saturation in subcutaneous tissue or skeletal muscles.7

Be aware of special considerations for certain age groups and patient populations. For example, pediat-ric patients may not exhibit classic signs and symptoms of hypovole-mic shock before loss of more than 25% blood volume.3 Because com-pensatory mechanisms in a child are particularly robust, BP may be maintained until about 30% of blood volume has been lost.

These other patient groups may also have atypical signs and symp-toms:• Older adults may not exhibit clas-sic signs due to inadequate physi-ologic reserves and an inability to initiate compensatory mechanisms—for example, because of reduced alpha-1 adrenergic receptor respon-siveness in older adults.• Patients on beta-adrenergic antag-onists may not be able to initiate the expected tachycardiac response.• Pregnant patients may be able to lose up to 1500 mL of blood without a change in BP, secondary to alterations in blood volume and

What’s shock?1,2,13

A clinical syndrome of inadequate tissue perfusion, shock results in a decreased supply of oxygen and nutrients to cells. The body responds initially by activating numerous com-pensatory mechanisms to improve cellular perfusion. If these fail, shock leads to widespread cellular necrosis, multiple organ dysfunction and failure, and death.

Although there are various types of shock, including hypovolemic, cardio-genic, neurogenic, anaphylactic, and septic, the fi nal common pathway in all types of shock is impaired cellular metabolism.



hemodynamics related to pregnancy. During the third trimester of preg-nancy, compression of the vena cava can reduce venous return to the heart. Placing these patients on their left side or manual displacement of the uterus to the left can dramatically increase cardiac output.3

Treatment prioritiesManagement of patients with hypovo-lemic shock has three primary goals:• Maximize oxygen delivery by en-suring an adequate airway (which may have been impacted as the LOC decreases) and by improving oxygenation through administra-tion of high-fl ow oxygen via a

nonrebreather mask or mechanical ventilation.• Control hemorrhage through basic means, such as direct manual pres-sure, interventional angiography, or surgical intervention.• Restore and maintain adequate cardiac output. To meet this goal, I.V. fl uid replacement is a top prior-ity. (In early shock from dehydra-tion, oral fl uid replacement may be adequate.) The I.V. fl uid of choice is an isotonic crystalloid, such as 0.9% sodium chloride solution or Ringer’s lactate solution.

The type of fl uids used to treat hypovolemia is still controversial. Crystalloids are generally recom-

mended, but colloids are often used to expand the intravascular space. However, most recent studies fail to demonstrate improved survival with colloids to offset the expense of their use.8

Additionally, hypertonic crystal-loid solutions are sometimes ad-ministered to shift fl uids from the intracellular and interstitial spaces into the intravascular space. But re-search has produced confl icting evi-dence about the effectiveness of this strategy except as a means to manage increased intracranial pressure.9

Generally, every 1 mL of blood loss requires 3 mL of fl uid to restore adequate cardiac output. Patients

Pathophys particulars



will need two large-bore venous access devices (at least 16-gauge) or a central venous access device for volume replacement. Give older adults smaller fl uid boluses while assessing for signs and symptoms of fl uid volume overload. For pe-diatric patients, the fl uid bolus amount is 20 mL/kg.3

Patients with ongoing blood loss may need blood component therapy, so obtain specimens for type and crossmatch. These blood products may be crossmatched packed cells or the more rapidly available un-crossmatched or type-specifi c units. Autotransfusion (collection and re-transfusion of the patient’s blood) is another option in some cases.

Transfusion may be indicated if the patient is hemodynamically un-stable and shows little response to treatment with fl uids. The patient’s hemoglobin level may be used as a transfusion trigger: in general, 8 g/dL is a marker for initiating transfusion in patients experiencing blood loss. However, a higher value may be ap-propriate for older patients and those with signifi cant comorbities, such as coronary artery disease.2

Depending on the extent of bleed-ing, a patient may require transfusion of multiple units of blood products. Most institutions have a massive transfusion protocol for circumstanc-es in which total blood volume has been replaced with crystalloids, col-loids, and blood products in less than

24 hours. These protocols dictate the use of blood products in this setting and the addition of supplemental products such as platelets and cryo-precipitate.

During assessment and treatment, take care to maintain normothermia. Hypothermia leads to coagulopathy and a shift of the oxyhemoglobin dissociation curve to the left. This causes oxygen to have a greater affi n-ity for hemoglobin instead of being released to the cells. Keep the patient covered, ensure a warm ambient en-vironment, and administer warmed fl uid and blood products.

Other treatment optionsPermissive hypotension, also called hypotensive resuscitation, is an emerg-ing resuscitation strategy under investi-gation. It calls for fl uid administration to maintain an effective BP of approxi-mately 80 to 90 mm Hg, but not high-er until an expedited defi nitive surgical repair is accomplished. Aggressive fl uid resuscitation may be associated with hemodilution and disruption of the normal coagulation system, result-ing in further bleeding. Studies have shown improved outcomes with the use of hypotensive resuscitation, but its use isn’t indicated for closed head injury due to the likelihood of worsen-ing cerebral ischemia.2

In the past, pneumatic antishock trousers were considered part of standard therapy for the treatment of hypovolemic shock. But use of this

device hasn’t demonstrated improved patient outcomes, so it’s no longer recommended to treat shock. Its only application is immobilization of pelvic or lower extremity fractures.10

A recent large, randomized, placebo-controlled study demon-strated that I.V. tranexamic acid sig-nifi cantly reduced the risk of death from hemorrhage in bleeding trauma patients.1 1 For more on promising treatment advances for hypovolemic shock, see Lessons learned from recent military actions.

Diagnostic imaging and ongoing careAfter fl uid resuscitation, the priority becomes identifying the underly-ing cause of shock. Many patients with traumatic hypovolemic shock require diagnostic imaging studies, such as ultrasound or computed to-mography scanning. Severe internal injury and ongoing blood loss may require surgery to locate and stop bleeding.

Ongoing nursing assessment should target adequate response to treatments. Monitor for improv-ing LOC, increasing urine output (greater than 0.5 mL/kg/hour or at least 30 mL/hour in an average-sized adult), and hemodynamic stability. Continual monitoring of endpoints of resuscitation is critical. (As previ-ously mentioned, these endpoints are indicators of tissue perfusion, such as serum lactate levels and restoration of normal arterial base defi cits.)

Assess for and manage the trauma triad of hypothermia, coagulopathy, and acidosis, which predisposes the patient to a poor outcome. Coagu-lopathy can occur in patients who receive large amounts of volume resuscitation due to the dilution and consumption of platelets and clotting factors.2 This coagulopathy should be corrected by the administration of fresh frozen plasma, platelets, and cryoprecipitate.12

Case closedAs you continue to assess and support your patient, the ED team moves at

Lessons learned from recent military actions14-17

Many advances in the management of traumatic hypovolemic shock have been developed in the combat zones of Iraq and Afghanistan. Two changes are leading to the better control of bleeding following traumatic injury:• hemostatic granules/powders used as a foundation to initiate rapid clotting.• renewed use of tourniquets for control of external hemorrhage. Studies have shown that despite earlier fears, patients can tolerate prolonged tourniquet applica-tion without serious complications.

Recent experiences in combat medicine have also shown the value of whole blood over packed red cells. Administering whole blood or the supplement of packed red cells with plasma, platelets, or coagulation factors has reduced the inci-dence of the complications associated with severe hypovolemic shock. Although a conclusive recommendation for the ratio of red blood cells to plasma hasn’t been established, it’s much closer to 1:1 than originally believed.

Blood substitutes have been studied extensively, but despite some promising research, no clinically viable product is currently available.



an accelerated pace. As prescribed, you administer a bolus infusion of Ringer’s lactate through the periph-eral venous access established by the EMTs while a coworker establishes a second large-bore venous access. Us-ing the fl uid warmer helps prevent hypothermia. Specimens are taken for initial lab tests and a call is placed to the blood bank requesting type- specifi c units of RBCs. A stat portable chest X-ray reveals no pneumothora-ces, traumatic hemomediastinum, or hemothorax.

A bedside FAST scan shows a sig-nifi cant amount of free intraperitoneal fl uid. The on-call surgeon decides to operate immediately due to the ongo-ing internal bleeding and hemody-namic instability.

After surgical repair of a lacerated mesenteric artery and normalization of his fl uid status, the patient recov-ers uneventfully.

Being prepared saves livesDespite aggressive resuscitative efforts, a patient in traumatic hypovolemic shock is at high risk for signifi cant

morbidity and mortality. Your knowl-edge, preparation, and rapid inter-ventions support the patient’s survival and optimal recovery from this life-threatening disorder. ■

REFERENCES1. Blackbourne, LH. Advanced Surgical Recall. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.

2. Emergency Nurses Association. Shock. In: Trauma Nursing Core Course Provider Manual. 6th ed. 2007; 75-91.

3. Emergency Nurses Association. Emergency Nurs-ing Core Curriculum. 6th ed. Philadelphia, PA: WB Saunders; 2007.

4. O’Shea, RA, ed. Principles & Practice of Trauma Nursing. United Kingdom: Elsevier Health Sciences; 2005.

5. Intravenous fluid resuscitation. In: Shock. The Merck Manuals Online Medical Library. http://www.merck.com/mmpe/sec06/ch067/ch067c.html .

6. Klabunde, RE. Frank Starling mechanism. http://www.cvphysiology.com/Cardiac%20Function/CF003.htm.

7. McKinley BA, Marvin RG, Cocanour CS, Moore FA. Tissue hemoglobin O2 saturation during resus-citation of traumatic shock monitored using near infrared spectometry. J Trauma. 2000;48(4):637-642.

8. Perel P, Roberts I, Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Sys Rev. 2007;(4):CD000567.

9. Tyagi R, Donaldson K, Loftus CM, Jallo J. Hy-pertonic saline: a clinical review. Neurosurg Rev. 2007;30(4):277-289.

10. Mattox KL, Bickell W, Pepe PE, Burch J, Feli-ciano D. Prospective MAST study in 911 patients. J Trauma. 1989;29(8):1104-1112.

11. Shakur H, Roberts I, Bautista R., et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376(9734):23-32.

12. Fakhry SM, Michetti CP. Bleeding and coagula-tion complications. In: Moore EE, Feliciano DV, Mattox KL. Trauma. New York, NY: McGraw Hill; 2004: 1251-1275.

13. Brandler ES, Sinett RH. Shock, cardiogenic. Emedicine. Updated January 26, 2010. http://emedi-cine.medscape.com/article/759992-overview.

14. Kheirabadi, BS, Edens JW, Terrazas B, et al. Comparison of new hemostatic granules/powders with currently deployed hemostatic products in a lethal model of extremity arterial hemorrhage in swine. J Trauma. 2009; 66 (2) 316-326.

15. Kragh, J, Walters TJ, Baer DG, et al. Practical use of emergency tourniquets to stop bleeding in major limb trauma. J Trauma. 2008; 64(2 supp): S38-S50.

16. Spinella PC, Holcomb JB. Resuscitation and transfusion principles for traumatic hemorrhagic shock. Blood Rev. 2009;23(6):231-240.

17. Eastman AL, Minei JP. Comparison of hemo-globin-based oxygen carriers to stored human red blood cells. Crit Care Clinics.2009;25(2):303-310.

RESOURCE

Kolecki P, Menckhoff CR. Shock, hypovolemic. Emedicine. Updated March 11, 2010. http://emedicine.medscape.com/article/760145-print.

Jeff Strickler is the director of emergency services at University of North Carolina Hospitals, Chapel Hill, N.C.

The author has disclosed that he has no fi nancial relationships related to this article.

DOI-10.1097/01.NURSE.0000388308.45275.3e

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Traumatic hypovolemic shock: Halt the downward spiral

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ANCC CONTACT HOURS Traumatic hypovolemic · PDF file · 2011-01-24ruptured ectopic pregnancy. ... Traumatic hypovolemic shock By Jeff Strickler, MA, RN, CEN, CFRN, EMT-P ... Case