Shock, Hemorrhagic

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

  • 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:
 

Imaging Studies:
 

Other Tests:
 

Procedures:
 

Prehospital Care:

Emergency Department Care:

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

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.

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:
 

Transfer:
 

Complications:
 

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Bibliography

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Constructed by Dr N.A. Nematallah Consultant in perioperative medicine and intensive therapy, Al Razi Orthopedic Hospital , State of Kuwait, email : razianesth@freeservers.com