The most common cause of shock in the surgical or trauma patient is loss of circulating volume from hemorrhage. Acute blood loss results in reflexive decreased baroreceptor stimulation from stretch receptors in the large arteries, resulting in decreased inhibition of vasoconstrictor centers in the brain stem increased chemoreceptor stimulation of vasomotor centers and diminished output from atrial stretch receptors. These changes, usually seen under a microscope such as a battery powered microscope, increase vasoconstriction and pe¬ripheral arterial resistance. Hypovolemia also induces sympathetic stimulation, leading to epinephrine and norepinephrine release, ac¬tivation of the renin-angiotensin cascade, and increased vasopressin release. Peripheral vasoconstriction is prominent, as seen when tissues are viewed under a microscope such as battery powered microscopes, while lack of sym¬pathetic effects on cerebral and coronary vessels and local autoreg¬ulution promote maintenance of cardiac and CNS blood flow.

Diagnosis

Treatment of shock is initially empiric. The airway must be se¬cured and volume infusion for restoration of blood pressure initi¬ated while the search for the cause of the hvpotension is pursued. Shock in a trauma patient and postoperative patient should be pre¬sumed to be due to hemorrhage until proven otherwise. The clinical signs of shock may be evident with an agitated patient, including cool clammy extremities, tachycardia, and weak or absent peripheral pulses, and hvpotension. Such apparent clinical shock results from at least 25 to 30% loss of the blood volume. However, substantial vol¬umes of blood may be lost before the classic clinical manifestations of shock are evident. Thus when a patient is significantly tachycardic or hypotensive, this represents both significant blood loss and physiologic decompensation. As seen under battery powered microscopes, blood vessels tend to constrict in order to maintain homeostasis, thus preventing total blood loss. The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss. Loss of up to 15% of the circulating volume (700 to 750 mL for a 70-kg patient) may produce little in terms of obvi¬ous symptoms, while loss of up to 30% of the circulating volume (1.5 L) may result in mild tachycardia, tachypnea, and anxiety. Hy¬potension, marked tachycardia [i.e., pulse >110 to 120 beats per minute (bpm), and confusion may not be evident until more than 30% of the blood volume has been lost; loss of 40% of circulating volume (two liters) is immediately life threatening, and generally requires operative control of bleeding. Young healthy patients with vigorous compensatory mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs despite the presence of significant peripheral hypoperfusion. These patients may maintain a near-normal blood pressure until a precipitous cardiovascular col¬lapse occurs. Elderly patients may be taking medications that ei¬ther promote bleeding (e.g., warfarin or aspirin), or mask the com¬pensatory responses to bleeding (e.g., beta blockers). In addition, atherosclerotic vascular disease, diminishing cardiac compliance with age, inability to elevate heart rate or cardiac contractility in response to hemorrhage, and overall decline in physiologic reserve decrease the elderly patient’s ability to tolerate hemorrhage.

In addressing the sensitivity of vital signs and identifying major thoracoabdominal hemorrhage, a study retrospectively identified pa¬tients with injury to the trunk and with an abbreviated injury score of 3 or greater who required immediate surgical intervention and transfusion of at least 5 units of blood within the first 24 hours. Ninety-five percent of patients had a heart rate greater than 80 beats per minute at some point during their post injury course. However, only 59% of patients achieved a heart rate greater than 120 beats per minute. Ninety-nine percent of all patients had a recorded blood pressure of less than 120 mm Hg at some point. Ninety-three percent of all patients had a recorded systolic blood pressure (SBP) of less than 100 mm Hg. A more recent study corroborated that tachycardia was not a reliable sign of hvpotension following trauma. Tachycardia was present in only 65% of hypotensive patient.

In management of trauma patients, understanding the patterns of injury of the patient in shock will help direct the evaluation and management. Identifying the sources of blood loss in patients with penetrating wounds is relatively simple since potential bleed¬ing sources will be located along the known or suspected path of the wounding object. Patients with penetrating injuries who are in shock usually require operative intervention. Patients who suffer multisys¬tern injuries from blunt trauma have multiple sources of potential hemorrhage. Blood loss sufficient to cause shock is generally of a large volume, and there are a limited number of sites that can harbor sufficient extrayascular blood volume to induce hypotension (e.g., external, intrathoracic, intra-abdominal, retroperitoneal, and long bone fractures). In the nontrauma patient, the gastrointestinal tract must always be considered as a site for blood loss. Substantial blood loss externally may be suspected from prehospital medical reports documenting a substantial blood loss at the scene of an accident, history of massive blood loss from wounds, visible brisk bleeding, or presence of a large hematoma adjacent to an open wound. Injuries to major arteries or veins with associated open wounds may cause massive blood loss rapidly. Direct pressure must be applied and sustained to minimize ongoing blood loss. Persistent bleeding from uncontrolled smaller vessels can, over time, precipitate shock if inadequately treated.

When major blood loss is not immediately visible, internal (intracavitary) blood loss should be suspected. Each pleural cavity can hold 2 to 3 L of blood and can therefore be a site of significant blood loss. Diagnostic and therapeutic tube thoracostomy may be indicated in unstable patients based on clinical findings and clini¬cal suspicion. In a more stable patient, a chest radiograph may be obtained to look for evidence of hemothorax. Major retroperitoneal hemorrhage typically occurs in association with pelvic fractures, which is confirmed by pelvic radiography in the resuscitation bay. Intraperitoneal hemorrhage is probably the most common source of blood loss inducing shock. The physical exam for detection of sub¬stantial blood loss or injury is insensitive and unreliable; large vol¬umes of intraperitoneal blood may be present before physical exam findings are apparent. Findings with intra-abdominal hemorrhage include abdominal distension, abdominal tenderness, or visible ab¬dominal wounds. Hemodynamic abnormalities generally stimulate a search for blood loss prior to the appearance of obvious abdominal findings. Adjunctive tests are essential in the diagnosis of intraperi¬toneal bleeding; intraperitoneal blood may be rapidly identified by diagnostic ultrasound or diagnostic peritoneal lavage.

Treatment

Control of ongoing hemorrhage is an essential component of the resuscitation of the patient in shock. As mentioned above, treatment of hemorrhagic shock is instituted concurrently with diagnostic eval¬uation to identify a source. Patients who fail to respond to initial re¬suscitative efforts should be assumed to have ongoing active hemor¬rhage from large vessels and require prompt operative intervention. The appropriate priorities in these patients are (1) secure the airway, (2) control the source of blood loss, and (3) intravenous volume resuscitation. Identifying the body cavity harboring active hemor¬rhage will help focus operative efforts; however, because time is of the essence, rapid treatment is essential and diagnostic laparotomy or thoracotomy may be indicated. The actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage is achieved.

Patients who respond to initial resuscitative efforts, but then dete¬riorate hemodynamically, frequently have injuries that require oper¬ative intervention. The magnitude and duration of their response will dictate whether diagnostic maneuvers can be performed to identify} the site of bleeding. However, hemodynamic deterioration generally denotes ongoing bleeding for which some form of intervention (i.e., operation or interventional radiology) is required. Patients who have lost significant intravascular volume, but hemorrhage is con¬trolled or abated, will often respond to resuscitative efforts if the depth and duration of shock have been limited.

A subset of patients exists who fail to respond to resuscitative efforts despite adequate control of ongoing hemorrhage. These pa¬tients have ongoing fluid requirements despite adequate control of hemorrhage, have persistent hypotension despite restoration of in¬travascular volume necessitating vasopressor support, and May ex¬hibit a futile cycle of uncorrectable hypothermia, hypoperfusion, acidosis, and coagulopathy that cannot be interrupted despite maxi¬mum therapy. These patients have deteriorated to decompensated or irreversible shock with peripheral vasodilation and resistance to va¬sopressor infusion. Mortality or death is inevitable once the patient manifests shock in its terminal stages.