eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Shock, Hemorrhagic

William P Bozeman, MD, Associate Professor, Associate Director of Research, Department of Emergency Medicine, Wake Forest University School of Medicine

Updated: Sep 18, 2008

Introduction

Background

Shock is a state of inadequate perfusion, which does not sustain the physiologic needs of organ tissues. Many conditions, including blood loss but also including nonhemorrhagic states such as dehydration, sepsis, impaired autoregulation, obstruction, decreased myocardial function, and loss of autonomic tone, may produce shock or shocklike states.

Pathophysiology

In hemorrhagic shock, blood loss exceeds the body's ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes.

Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic conditions with subacute blood loss.

Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen delivery (ie, DO₂), and increased oxygen consumption (ie, VO₂) by tissues. Lactate levels, acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and comorbid factors all may affect a patient's response to hemorrhagic shock.

Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure.

Frequency

United States

Accidental injuries remain the leading cause of death in individuals aged 1-44 years.¹ Hemorrhagic shock is a leading cause of death among trauma patients.²

Clinical

History

History taking should address the following:

• Specific details of the mechanism of trauma or other cause of hemorrhage are essential.
• Inquire about a history of bleeding disorders and surgery.
• Prehospital interventions, especially the administration of fluids, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information.

Physical

Findings at physical examination may include the following:

• Head, ears, eyes, nose, and throat
  • Sources of hemorrhage usually are apparent.
  • The blood supply of the scalp is rich and can produce significant hemorrhage.
  • Intracranial hemorrhage usually is insufficient to produce shock, except possibly in very young individuals.
• Chest
  • Hemorrhage into the thoracic cavities (pleural, mediastinal, pericardial) may be discerned at physical examination. Ancillary studies often are required for confirmation.
  • Signs of hemothorax may include respiratory distress, decreased breath sounds, and dullness to percussion.
  • Tension hemothorax, or hemothorax with cardiac and contralateral lung compression, produces jugular venous distention and hemodynamic and respiratory decompensation.
  • With pericardial tamponade, the classic triad of muffled heart sounds, jugular venous distention, and hypotension often is present, but these signs may be difficult to appreciate in the setting of an acute resuscitation.
• Abdomen
  • Injuries to the liver or spleen are common causes of hemorrhagic shock. Spontaneous rupture of abdominal aortic aneurysm (AAA) may also cause severe intra-abdominal hemorrhage and shock.
  • Blood irritates the peritoneal cavity; diffuse tenderness and peritonitis are common when blood is present. However, the patient with altered mental status or multiple concomitant injuries may not have the classic signs and symptoms at physical examination.
  • Progressive abdominal distention in hemorrhagic shock is highly suggestive of intra-abdominal hemorrhage.
• Pelvis
  • Fractures can produce massive bleeding. Retroperitoneal bleeding must be suspected.
  • Flank ecchymosis may indicate retroperitoneal hemorrhage.
• Extremities
  • Hemorrhage from extremity injuries may be apparent, or tissues may obscure significant bleeding.
  • Femoral fractures may produce significant blood loss.
• Nervous system
  • Agitation and combativeness may be seen in the initial stages of hemorrhagic shock.
  • These signs are followed by a progressive decline in level of consciousness due to cerebral hypoperfusion or concomitant head injury.

Differential Diagnoses

Other Problems to Be Considered

Cardiac tamponade
Knife wounds

Workup

Laboratory Studies

• Laboratory studies are essential in management of many forms of hemorrhagic shock. Baseline levels are determined frequently, but these infrequently change the initial management after trauma. Serial evaluations of the following can help guide ongoing therapy.
  • CBC
  • Prothrombin time and/or activated partial thromboplastin time
  • Urine output rate can help guide adequacy of perfusion.
  • ABGs (Levels reflect acid-base and perfusion status.)
  • Lactate and base deficit are used in some centers to indicate the degree of metabolic debt. Clearance of these markers over time can reflect the adequacy of resuscitation.
• Typed and crossmatched packed red blood cells should be ordered immediately based on clinical suspicion of hemorrhagic shock. Fresh frozen plasma and platelets also may be required to correct or prevent coagulopathies that develop in severe hemorrhagic shock.

Imaging Studies

• Standard radiography
  • Cervical spine, chest, and pelvis radiographs are the standard screening images for severe trauma.
  • Other radiographs may be indicated for orthopedic injuries.
• Computed tomography
  • Image the appropriate region of suspected injury.
  • CT scanning frequently is the method of choice for evaluating possible intra-abdominal and/or retroperitoneal sources of hemorrhage in stable patients.
  • Oral contrast material may not increase the diagnostic yield of abdominal CT scanning in blunt trauma. Scanning should not be delayed to administer oral contrast material.³
• Ultrasonography
  • Bedside abdominal ultrasonography can be very useful for the rapid detection of AAA and free intra-abdominal fluid.
  • Thoracic ultrasonographic findings can immediately confirm hemothorax or pericardial tamponade.
• Directed angiography may be diagnostic and therapeutic. Interventional radiologists have had good success achieving hemostasis in hemorrhage caused by a variety of vessels and organs.

Other Tests

• An ECG can be useful for detecting dysrhythmias and cardiac sequelae of shock.
• Tissue oximetry using Near Infrared Spectroscopy (NIRS) shows promise for continuous noninvasive measurement of perfusion in hemorrhagic shock and other conditions.⁴

Procedures

• Tube thoracostomy is necessary in significant hemothorax with or without pneumothorax.
• Central venous access facilitates fluid resuscitation and monitoring of central venous pressure and is necessary if peripheral intravenous access is inadequate or impossible to obtain.
• Diagnostic peritoneal lavage is used to detect intra-abdominal blood, fluid, and intestinal contents. It is sensitive but not specific for abdominal injury. It is not used to evaluate the retroperitoneum, which can hold significant hemorrhage, and does not identify the source of hemorrhage.

Treatment

Prehospital Care

• The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care.
• Intravenous access and fluid resuscitation are standard. However, this practice has become controversial.
  • For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question.⁵
  • Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled.
  • These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet.

Emergency Department Care

• Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs.
• Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock.
• Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access), should be initiated.
  • Intravascular volume and oxygen-carrying capacity should be optimized.
  • In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock.
  • Blood products are often required in severe hemorrhagic shock. Replacement of lost components using red blood cells (RBCs), fresh frozen plasma (FFP), and platelets may be essential. The ideal ratio of RBCs to FFP remains undetermined. Recent combat experience has suggested that aggressive use of FFP may reduce coagulopathies and improve outcomes.⁶
• Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care.
• Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions.

Consultations

Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, interventional radiologist, and others as required.

Medication

Achievement of hemostasis, fluid resuscitation, and use of blood products are the mainstays of treatment. Pressor agents may be useful in some settings (eg, spinal shock), but these agents should not be substitutes for adequate volume resuscitation and blood product replacement.

Vasopressors

These agents augment both coronary and cerebral blood flow during the low-flow state associated with shock.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and renal vasodilation

Dosing

Adult

1-5 mcg/kg/min IV; not to exceed 50 mcg/kg/min IV; after initiating therapy, increase dose by 1-4 mcg/kg/min IV q10-30min until optimal response is obtained; in more than 50% of patients, satisfactory maintenance is achieve with doses <20 mcg/kg/min IV

Pediatric

Administer as in adults

Interactions

Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects

Contraindications

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Closely monitor urine flow, cardiac output, pulmonary wedge pressure, and BP during infusion; prior to infusion, correct hypovolemia with whole blood or plasma, as indicated; monitoring of central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia

Norepinephrine (Levophed)

Used in protracted hypotension following adequate fluid-volume replacement. Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increase cardiac muscle contractility and heart rate, as well as vasoconstriction; result is increased systemic BP and coronary blood flow.

Dosing

Adult

2 mcg/kg/min IV; titrate to effect (low normal BP, eg, 80-100 mm Hg systolic, which is sufficient to perfuse vital organs)

Pediatric

0.1 mcg/kg/min IV; titrate to effect

Interactions

Atropine may enhance the pressor response by blocking reflex bradycardia

Contraindications

Documented hypersensitivity; peripheral or mesenteric vascular thrombosis because ischemia may be increased and area of infarct may be extended

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Correct blood-volume depletion, if possible, before therapy; administer into a large vein (extravasation may cause severe tissue necrosis); caution in occlusive vascular disease

Vasopressin (Pitressin)

Has vasopressor and ADH activity. Increases water resorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects); however, vasoconstriction also is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

Dosing

Adult

0.1-0.5 U/min IV, titrate as needed; after bleeding stops, continue at same dose for 12 h and taper over 24-48 h

Pediatric

Initial dose: 0.002-0.005 U/kg/min IV, titrate dose to a maximum 0.01 U/kg/min IV

Interactions

Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects

Contraindications

Documented hypersensitivity; coronary artery disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine headache; excessive doses may result in hyponatremia

Epinephrine (Adrenalin, Bronitin)

Used for hypotension refractory to dopamine. Alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Dosing

Adult

1 mcg/min IV titrated according to hemodynamic response; typical dosage range is 1-10 mcg/min

Pediatric

0.1-1 mcg/kg/min IV titrated according to hemodynamic response

Interactions

Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics

Contraindications

Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly person and in prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

Follow-up

Further Inpatient Care

• Admit the patient to an ICU, surgical ICU, or pediatric ICU.
• Patients with hemorrhagic shock should be admitted to an intensive care or monitored setting appropriate for the underlying condition and physiologic state.

Transfer

• In hospitals without facilities to provide definitive care, patients should be stabilized as much as possible and transferred to a facility with a higher level of care.

Complications

• Coagulopathies may occur in severe hemorrhage. Fluid resuscitation, while necessary, may exacerbate coagulopathies.
• Sepsis and multiple organ system failure occur days after acute hemorrhagic shock.
• Death is a possible complication.

Patient Education

• For excellent patient education resources, visit eMedicine's Shock Center. Also, see eMedicine's patient education article Shock.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize occult hemorrhage
• Assumption that hypotension after trauma is due to head injury
• Failure to perform a rectal examination
• Failure to diagnose the cause(s) of hemorrhage
• Inadequate resuscitation (Therapy for hemorrhagic shock should be rapidly initiated and aggressively pursued.)
• Failure to make appropriate consultations in a timely fashion

Special Concerns

• Pregnancy: Optimization of perfusion in the mother is the treatment of choice for the fetus.
• Pediatric: Compensatory mechanisms may be effective in children. Hypotension is a late finding and represents significant hemorrhage.
• Geriatric: Medications and underlying diseases may modify responses to hemorrhage.

References

1. National Center for Injury Control and Prevention. Ten Leading Causes of Death by age group. 2004. Center for Disease Control and Prevention; [Full Text].

2. Cocchi MN, Kimlin E, Walsh M, Donnino MW. Identification and resuscitation of the trauma patient in shock. Emerg Med Clin North Am. Aug 2007;25(3):623-42, vii. [Medline].

3. Tsang BD, Panacek EA, Brant WE, Wisner DH. Effect of oral contrast administration for abdominal computed tomography in the evaluation of acute blunt trauma. Ann Emerg Med. Jul 1997;30(1):7-13. [Medline].

4. Ward KR, Ivatury RR, Barbee RW, Terner J, Pittman R, Filho IP. Near infrared spectroscopy for evaluation of the trauma patient: a technology review. Resuscitation. Jan 2006;68(1):27-44. [Medline].

5. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. Oct 27 1994;331(17):1105-9. [Medline].

6. Gonzalez EA, Moore FA, Holcomb JB, Miller CC, Kozar RA, Todd SR. Fresh frozen plasma should be given earlier to patients requiring massive transfusion. J Trauma. Jan 2007;62(1):112-9. [Medline].

7. Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: hemorrhagic shock. Crit Care. Oct 2004;8(5):373-81. [Medline]. [Full Text].

8. Wilson M, Davis DP, Coimbra R. Diagnosis and monitoring of hemorrhagic shock during the initial resuscitation of multiple trauma patients: a review. J Emerg Med. May 2003;24(4):413-22. [Medline].

Keywords

blood loss, hemorrhage, shock, shocklike state, hemorrhagic shock, spontaneous hemorrhage, trauma, clinical hemorrhagic shock, acute bleeding, severe hemorrhagic shock, sepsis, bleeding disorders, intracranial hemorrhage, abdominal aortic aneurysm, AAA, intra-abdominal hemorrhage, retroperitoneal hemorrhage, retroperitoneal bleeding, abdominal bleeding, organ failure

Contributor Information and Disclosures

Author

William P Bozeman, MD, Associate Professor, Associate Director of Research, Department of Emergency Medicine, Wake Forest University School of Medicine
William P Bozeman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and National Association of EMS Physicians
Disclosure: Nothing to disclose.

Medical Editor

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Associate Professor, Department of Emergency Medicine, University of Texas-Houston
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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Tom Scaletta, MD, Past-President, American Academy of Emergency Medicine; Chairperson, Department of Emergency Medicine, Edward Hospital; Assistant Professor of Emergency Medicine, Rush Medical College and Cook County Hospital
Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

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

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

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