eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Shock, Hemorrhagic: Treatment & Medication

Author: William P Bozeman, MD, Associate Professor, Associate Director of Research, Department of Emergency Medicine, Wake Forest University School of Medicine
Contributor Information and Disclosures

Updated: Sep 18, 2008

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

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

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

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

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.

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

Atropine may enhance the pressor response by blocking reflex bradycardia

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

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.

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

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

Documented hypersensitivity; coronary artery disease

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.

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

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

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)

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

More on Shock, Hemorrhagic

Overview: Shock, Hemorrhagic
Differential Diagnoses & Workup: Shock, Hemorrhagic
Treatment & Medication: Shock, Hemorrhagic
Follow-up: Shock, Hemorrhagic
References

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].

Further Reading

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 Professor, Department of Emergency Medicine, University of Texas-Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center, San Antonio, Texas
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: Talecris Biotherapeutics Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Tom Scaletta, MD, President, Emergency Excellence (EmEx) (www.emergencyexcellence.com); Assistant Professor of Emergency Medicine, Rush Medical College, Cook County Hospital; Chairperson, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine
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, 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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