Complement

• A cascade activated by injury, shock, and severe infection, and contributes

to host defense and proinflammatory activation.
• In trauma, degree of activation is proportional to the magnitude of injury
and may serve as a marker for severity.
• In septic shock, elevations of C3a and C5a can contribute to the
development of organ dysfunction.
• C3a, C4a and C5a are potent mediators of increased vascular permeability,
smooth muscle cell contraction, histamine and arachidonic acid by-
product release, and adherence of neutrophils to vascular endothelium.
• Correlate with mortality in multiply injured patients.
 Neutrophils
• Activation is an early event in the upregulation of the inflammatory
response.
• The first cells to be recruited to the site of injury and acts through
phagocytosis.
• May also produce cell injury and organ dysfunction by generating and
releasing a number of substances that may induce cell or tissue injury,
such as; reactive O2 species, lipidperoxidation products, proteolytic
enzymes and vasoactive mediators.
• Ischemia-reperfusion activates PMNs and causes PMN-induced organ
injury.
 Cell Signaling
• Mediators produced during shock interact with cell surface receptors on
target cells to alter target cell metabolism by changes in cellular
oxygenation, redox state, high-energy phosphate concentration, gene
expression, or intracellular electrolyte concentration.
• Through cell surface receptors, which, once bound by a ligand, transmit
their information to the interior of the cell through a variety of signaling
cascades.
• Intracellular calcium (Ca2+) homeostasis and regulation represent one
such pathway that alterations in regulation may lead to direct cell injury,
changes in transcription factor activation & alterations in the expression
of genes important in homeostasis.
FORMS OF SHOCK
 Hypovolemic/Hemorrhagic
• Most common cause of shock in the surgery or trauma.
• Results in reflexive decreased baroreceptor stimulation from stretch
receptors in the large arteries, decreased inhibition of vasoconstrictor
centers in the brain stem, increased chemoreceptor stimulation of
vasomotor centers, and diminished output from atrial stretch receptors
 increase vasoconstriction and peripheral arterial resistance.
• Induces sympathetic stimulation, leading to epinephrine and
norepinephrine release, activation of the renin-angiotensin cascade, and
increased vasopressin release peripheral vasoconstriction &
vasodilation on cerebral & coronary vessels.
 Hypovolemic/Hemorrhagic
Diagnosis.
• Presumed in a trauma patient or postoperative patient until proven
otherwise.
• Signs may include agitation, cool clammy extremities, tachycardia,
weak or absent peripheral pulses, and hypotension.
• Results from at least 25% to 30% loss of the blood volume. However,
substantial volumes 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.
 Hypovolemic/Hemorrhagic
Diagnosis.
Clinical and physiologic response to hemorrhage has been classified
according to the magnitude of volume loss.
 Hypovolemic/Hemorrhagic
Diagnosis.
• Young healthy patients with vigorous compensatory mechanisms may
tolerate larger volumes of blood loss while manifesting fewer clinical signs.
• Elderly patients may be taking medications that either promote bleeding
(e.g., warfarin or aspirin) or mask the compensatory responses to bleeding
(e.g., β-blockers).
• Elderly patients may also have 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.
 Hypovolemic/Hemorrhagic
Diagnosis.
• Recent data in trauma patients suggest that a systolic blood pressure (SBP)
of less than 110 mmHg is a clinically relevant definition of hypotension and
hypoperfusion.
• A more recent study corroborated that tachycardia was not a reliable sign of
hemorrhage following trauma and was present in only 65% of hypotensive
patients.
• Serum lactate and base deficit derived from arterial blood gas are helpful to
estimate and monitor the extent of bleeding and shock. The amount
produced by anaerobic respiration is an indirect marker of tissue
hypoperfusion, cellular O2 debt, and the severity of hemorrhagic shock.
 Hypovolemic/Hemorrhagic
Diagnosis.
• Hematocrit changes may not rapidly reflect the total volume of blood loss,
however, it is associated with 24-hour fluid and transfusion requirements
and more strongly associated with packed red blood cell transfusion than
tachycardia, hypotension, or acidosis. Depression in the initial hematocrit
does not rule out substantial blood loss or ongoing bleeding.
• Understanding the patterns & sources of blood loss of the patient in shock
will help direct the evaluation and management.
• In the non-trauma patient, the GI tract must always be considered as a site
for blood loss.
 Hypovolemic/Hemorrhagic
Diagnosis.
• Injuries to major arteries or veins with associated open wounds may cause
massive blood loss rapidly, direct pressure must be applied.
• 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, and chest radiograph in stable patients.
• Intraperitoneal hemorrhage is probably the most common source of blood
loss inducing shock, with findings like abdominal distension, abdominal
tenderness, or visible abdominal wounds, and dentified by diagnostic
ultrasound or diagnostic peritoneal lavage.
 Hypovolemic/Hemorrhagic
Diagnosis.
• Patients who sustained high-energy blunt trauma should undergo
computed tomography scans to assess for head, chest, and/or
abdominal bleeding.