Last Updated: July 16, 2002
Background: Shock is a state in which adequate perfusion to sustain the physiologic needs of organ tissues is not present. Many conditions, including sepsis, blood loss, impaired autoregulation, 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, the 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.
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 administered, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information.
Physical: Finidngs 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.
Blood irritates to 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 intraabdominal 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
Lab 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
ABGs (Levels reflect acid-base and perfusion status.)
Lactate and base deficit are used in some centers.
Typed and cross-match packed red blood cells should be obtained immediately.
Fresh frozen plasma and platelets also may be required to correct 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 for 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.
Ultrasonography
Bedside abdominal ultrasonography can be useful for the rapid detection of free intra-abdominal fluid and, sometimes, specific parenchymal injury.
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.
Procedures:
Tube thoracostomy is necessary in hemothorax and 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.
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.
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 may be required.
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, radiologist, and others as required
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.
Drug Category: Vasopressors -- These agents augment both coronary and cerebral blood flow during the low-flow state associated with shock.
Drug Name |
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 |
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Adult Dose |
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, satisfactorily maintenance is achieve with doses <20 mcg/kg/min IV |
Pediatric Dose |
Administer as in adults |
Contraindications |
Documented hypersensitivity; pheochromocytoma; ventricular fibrillation |
Interactions |
Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects |
Pregnancy |
C - Safety for use during pregnancy has not been established. |
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 |
Drug Name |
Norepinephrine (Levophed) and epinephrine (Adrenalin) -- 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 increases. |
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Adult Dose |
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 Dose |
0.1 mcg/kg/min IV; titrate to effect |
Contraindications |
Documented hypersensitivity; peripheral or mesenteric vascular thrombosis because (ischemia may be increased; area of infarct may be extended) |
Interactions |
Atropine may enhance the pressor response by blocking reflex bradycardia |
Pregnancy |
D - Unsafe in pregnancy |
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 |
Drug Name |
Vasopressin (Pitressin) -- Has vasopressor and ADH activity. Increases water resorption at the 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 Dose |
0.1-0.5 U/min IV, titrate as needed; after bleeding stops, continue at the same dose for 12 h and taper over 24-48 h |
Pediatric Dose |
Initial dose: 0.002-0.005 U/kg/min IV, titrate dose to a maximum 0.01 U/kg/min IV |
Contraindications |
Documented hypersensitivity; coronary artery disease |
Interactions |
Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects |
Pregnancy |
B - Usually safe but benefits must outweigh the risks. |
Precautions |
Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine headache; excessive doses may result in hyponatremia |
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.
Medical/Legal 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.
Bibliography
Bickell WH, Wall MJ Jr, Pepe PE: Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994 Oct 27; 331(17): 1105-9
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 1997 Jul; 30(1): 7-13
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