Hypovolemic Shock Treatment & Management

  • Author: Paul Kolecki, MD, FACEP; Chief Editor: David FM Brown, MD   more...
 
Updated: Mar 21, 2012
 

Prehospital Care

The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field. Direct pressure should be applied to external bleeding vessels to prevent further blood loss.

  • Prevention of further injury applies mostly to the patient with trauma. The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss.
  • Although in selected cases stabilization may be beneficial, rapid transport of sick patients to the hospital remains the most important aspect of prehospital care. Definitive care of the hypovolemic patient usually requires hospital, and sometimes surgical, intervention. Any delay in definitive care, eg, such as delayed transport, is potentially harmful.
  • Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation.
    • In the setting of hypovolemic shock, positive-pressure ventilation may diminish venous return, diminish cardiac outcome, and worsen the shock state. While oxygenation and ventilation are necessary, excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock.
    • Appropriate treatment usually can be initiated without delaying transport. Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated. However, procedures in the field that prolong transportation should be delayed. Benefits to giving IV fluids prior to departure from the scene are not clear; however, IV lines and fluid resuscitation should be started and continued once the patient is en route to definitive care.
  • In recent years, there has been considerable debate regarding the use of military antishock trousers (MAST). MAST were introduced in the 1960s and, based mostly on anecdotal reports of success, their use became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970s. By the 1980s, the American College of Surgeons Committee on Trauma included their use in the standard of care for all patients with trauma and signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. The American College of Surgeons Committee on Trauma no longer recommends the use of MAST.
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Emergency Department Care

Three goals exist in the emergency department treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen delivery - completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood loss, and (3) fluid resuscitation. Also, the patient's disposition should be rapidly and appropriately determined.

Maximizing oxygen delivery

The patient's airway should be assessed immediately upon arrival and stabilized if necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be addressed immediately. High-flow supplemental oxygen should be administered to all patients, and ventilatory support should be given, if needed. Excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock and should be avoided.

Two large-bore IV lines should be started. The Poiseuille law states that flow is inversely related to the length of the IV catheter and directly related to its radius to the fourth power. Thus, a short large-caliber IV catheter is ideal; the caliber is much more significant than the length. IV access may be obtained by means of percutaneous access in the antecubital veins, cutdown of saphenous or arm veins, or access in the central veins by using the Seldinger technique. If central lines are obtained, a large-bore single-lumen catheter should be used. Intraosseous access has and continues to be used for hypotensive children younger than 6 years. Intraosseous access has also been used in hypotensive adults.[1] The most important factor in determining the route of access is the practitioner's skill and experience.

Placement of an arterial line should be considered for patients with severe hemorrhage. For these patients, the arterial line will provide continuous blood pressure monitoring and also ease arterial blood gas testing.

Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient), and the patient's response is assessed.

If vital signs return to normal, the patient may be monitored to ensure stability, and blood should be sent for typed and cross-matched. If vital signs transiently improve, crystalloid infusion should continue and type-specific blood obtained. If little or no improvement is seen, crystalloid infusion should continue, and type O blood should be given (type O Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications).

If a patient is moribund and markedly hypotensive (class IV shock), both crystalloid and type O blood should be started initially. These guidelines for crystalloid and blood infusion are not rules; therapy should be based on the condition of the patient.

The position of the patient can be used to improve circulation; one example is raising the hypotensive patient's legs while fluid is being given. Another example of useful positioning is rolling a hypotensive gravid patient with trauma onto her left side, which displaces the fetus from the inferior vena cava and increases circulation. The Trendelenburg position is no longer recommended for hypotensive patients, as the patient is predisposed to aspiration. In addition, the Trendelenburg position does not improve cardiopulmonary performance and may worsen gas exchange.

Autotransfusion may be a possibility in some patients with trauma. Several devices that allow for the sterile collection, anticoagulation, filtration, and retransfusion of blood are available. In the trauma setting, this blood almost always is from a hemothorax collected by means of tube thoracostomy.

Controlling further blood loss

Control of further hemorrhage depends on the source of bleeding and often requires surgical intervention. In the patient with trauma, external bleeding should be controlled with direct pressure; internal bleeding requires surgical intervention. Long-bone fractures should be treated with traction to decrease blood loss.

In the patient whose pulse is lost in the ED or just prior to arrival, an emergency thoracotomy with cross-clamping of the aorta may be indicated to preserve blood flow to the brain. This procedure is palliative at best and requires immediate transfer to the operating room.

In the patient with GI bleeding, intravenous vasopressin and H2 blockers have been used. Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias, gangrene, and myocardial or splanchnic ischemia. Therefore, it should be considered secondary to more definitive measures. H2 blockers are relatively safe but have no proven benefit.

Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding from varices and peptic ulcer disease. These agents possess the advantages of vasopressin without the significant side effects.

In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered. These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated first, and then the esophageal one is inflated if bleeding continues. The use of this tube has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For this reason, its use should be considered only as a temporary measure in extreme circumstances.

Virtually all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical intervention.

Early consultation and definitive care are the keys. The goal in the ED is to stabilize the hypovolemic patient, determine the cause of bleeding, and provide definitive care as quickly as possible. If transfer to another hospital is necessary, resources should be mobilized early.

In patients with trauma, if the emergency medical services personnel indicate potential serious injury, the surgeon (or trauma team) should be notified prior to the patient's arrival. In a 55-year-old patient with abdominal pain, for example, emergency ultrasonography of the abdomen may be necessary to identify an abdominal aortic aneurysm before the vascular surgeon is notified. Every patient should be individually evaluated, because delaying definitive care can increase morbidity and mortality.

Resuscitation

Whether crystalloids or colloids are best for resuscitation continues to be a matter for discussion and research. Many fluids have been studied for use in resuscitation; these include isotonic sodium chloride solution, lactated Ringer solution,[2] hypertonic saline, albumin, purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70.

Proponents of colloid resuscitation argue that the increased oncotic pressure produced with these substances decreases pulmonary edema. However, the pulmonary vasculature allows considerable flow of material, including proteins, between the intravascular space and interstitium. Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears to be a more important factor in preventing pulmonary edema.

Another argument is that less colloid is needed to increase the intravascular volume. Studies have shown this to be true. However, they still have not demonstrated any difference in outcome with colloids compared with crystalloids.

Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, have some advantages compared with natural colloids such as purified protein fraction, fresh frozen plasma, and albumin. They have the same volume-expanding properties, but because of their structures and high molecular weights, they remain mostly in the intravascular space, reducing the occurrence of interstitial edema. Although theoretic advantages exist, studies have failed to show a difference in ventilatory parameters, pulmonary function test results, days using a ventilator, total hospital days, or survival.

The European Society of Intensive Care Medicine (ESICM) advises against the use of colloids-hydroxyethyl starches (HES) in patients with severe sepsis or risk of acute kidney injury. Physicians should also avoid using colloids in patients with head injury and refrain from administering gelatins and HES in organ donors.[3]

The combination of hypertonic saline and dextran also has been studied because of previous evidence that it may improve cardiac contractility and circulation. Studies in the US and Japan have failed to show any difference when this combination was compared with isotonic sodium chloride solution or lactated Ringer solution. Thus, despite the many available resuscitation fluids, current recommendations still advocate the use of normal saline or lactated Ringer solution. In the US, one reason for the predominant use of crystalloids over the other resuscitative fluids is cost.

Recent literature suggests that the early administration of FFP and platelets improves survival and decreases overall PRBC need in patients undergoing a massive transfusion.[4]

Restoring normal circulating volume and BP prior to definitive control of bleeding

During World War I, Cannon observed and characterized patients in clinical shock. He later suggested a model of permissive hypotension in the treatment of torso wounds, with the intent of minimizing further bleeding.

Findings from early studies showed that animals that were bled had increased survival if they received fluid resuscitation. However, in these studies, bleeding was well controlled with ligation after the animals were bled.

During the Korean and Vietnam wars, much more aggressive fluid resuscitation, as well as rapid access to definitive care, was emphasized. It was noted that patients who were aggressively resuscitated tended to have better outcomes, and in the 1970s, these principles were widely adopted in civilian patients.

Since then, many studies have been conducted to determine if these principles are valid in patients with uncontrolled hemorrhage. Most of these studies revealed increased survival in the permissive hypotension or delayed treatment arms. The theory is that increased pressure causes more bleeding and disrupts initial clots, whereas extreme hypotension may increase the risk of cerebral perfusion.

The questions that have not been answered adequately are as follows: Which mechanisms and injury patterns are more amenable to the restoration of circulating blood volume? What BP is adequate but not excessive?

Although some data indicate that a systolic BP of 80-90 mm Hg may be adequate in penetrating truncal trauma without head injury, further studies are needed.

Current recommendations are for aggressive fluid resuscitation with lactated Ringer solution or normal saline in all patients with signs and symptoms of shock, regardless of underlying cause.

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Contributor Information and Disclosures
Author

Paul Kolecki, MD, FACEP  Associate Professor, Department of Emergency Medicine, Thomas Jefferson University Hospital, Director of Undergraduate Emergency Medicine Student Education, Jefferson Medical College, Philadelphia, PA, Consultant, Philadelphia Poison Control Center, Philadelphia, PA

Paul Kolecki, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Carl R Menckhoff, MD, FACEP  Associate Professor, Department of Emergency Medicine, Medical College of Georgia; Medical Director and Chairman, Medical Center of Lewisville; Regional Ultrasound Director, Questcare Partners

Carl R Menckhoff, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel J Dire, MD, FACEP, FAAP, FAAEM  Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

A Antoine Kazzi  MD, Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

A Antoine Kazzi is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Sarkar D, Philbeck T. The use of multiple intraosseous catheters in combat casualty resuscitation. Mil Med. Feb 2009;174(2):106-8. [Medline].

  2. Ghafari MH, Moosavizadeh SA, Moharari RS, Khashayar P. Hypertonic saline 5% vs. lactated ringer for resuscitating patients in hemorrhagic shock. Middle East J Anesthesiol. Oct 2008;19(6):1337-47. [Medline].

  3. Reinhart K, Perner A, Sprung CL, Jaeschke R, Schortgen F, Johan Groeneveld AB, et al. Consensus statement of the ESICM task force on colloid volume therapy in critically ill patients. Intensive Care Med. Mar 2012;38(3):368-83. [Medline].

  4. Zink KA, Sambasivan CN, Holcomb JB, Chisholm G, Schreiber MA. A high ratio of plasma and platelets to packed red blood cells in the first 6 hours of massive transfusion improves outcomes in a large multicenter study. Am J Surg. May 2009;197(5):565-70; discussion 570. [Medline].

  5. Burns B, Gentilello L, Elliot A, Shafi S. Prehospital hypotension redefined. J Trauma-Injury Infection and Crit Care. Dec 2008;65(6):1217-21. [Medline].

  6. Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma. Jun 2002;52(6):1141-6. [Medline].

  7. Graham CA, Parke TR. Critical care in the emergency department: shock and circulatory support. Emerg Med J. Jan 2005;22(1):17-21. [Medline].

  8. Langley DM, Moran M. Intraosseous needles: they're not just for kids anymore. J Emerg Nurs. Aug 2008;34(4):318-9. [Medline].

  9. Ogino R, Suzuki K, Kohno M, et al. Effects of hypertonic saline and dextran 70 on cardiac contractility after hemorrhagic shock. J Trauma. Jan 1998;44(1):59-69. [Medline].

  10. Silbergleit R, Satz W, McNamara RM, et al. Effect of permissive hypotension in continuous uncontrolled intra-abdominal hemorrhage. Acad Emerg Med. Oct 1996;3(10):922-6. [Medline].

  11. Skagius E, Siegbahn A, Bergqvist D, Henriksson A. Activated coagulation in patients with shock due to ruptured abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. Jan 2008;35(1):37-40. [Medline].

  12. Smith K, Deimling DL, Hinckley WR. Transporting the pregnant patient in shock; case report and review. Air Medical J. Jan-Feb 2009;28(1):37-9. [Medline].

  13. Stern SA. Low-volume fluid resuscitation for presumed hemorrhagic shock: helpful or harmful?. Curr Opin Crit Care. Dec 2001;7(6):422-30. [Medline].

  14. Yajima D, Motani H, Hayakawa M, Sato Y, Iwase H. A fatal case of hypovolemic shock after cesarean section. Am J Forensic Med Pathol. Sep 2007;28(3):212-5. [Medline].

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