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Introduction
Shock is defines defined as tissue hypoperfusion leading to inadequate delivery of
oxygen and nutrients to maintain normal tissue and cellular function and maintain
normal aerobic metabolism The resultant cellular injury is initially reversible; if the
hypoperfusion is severe enough and prolonged, the cellular injury becomes
irreversible, with end-organ dysfunction, cell death, and death of the patient .
The clinical manifestations of shock are the result of:
1. Stimulation of the sympathetic and neuroendocrine stress responses,
2. Inadequate oxygen delivery and end-organ dysfunction.
CLINICAL DILLEMMA OF SHOCK
1. Blood pressure alone is an insensitive measure of shock; significant
hypoperfusion and cellular death may be ongoing, despite normal blood
pressure. Inadequate oxygen delivery is presumed to be the pathologic defect in
shock.
2. The clinical dilemma faced in a patient with trauma shock is that the etiology
may not be immediately apparent. Inadequate treatment results in ongoing
hypoperfusion and activation of inflammatory mediators. Thus, treatment of the
patient in shock is initially empiric, while the underlying etiology of the shock state
is investigated.
TYPES OF SHOCK
1. Hypovolemic shock, the most common type, results from loss of circulating blood
volume. This may result from loss of whole blood (hemorrhagic shock), third space
fluid loss or a combination of both.
2. Vasogenic shock ( vasidilatory) results from decreased resistance within capacitance
vessels. Resulting from spinal shock, anaphylactic shock and initial stage of septic shock
3. Neurogenic shock is a form of vasogenic shock in which spinal cord injury or spinal
anesthesia causes vasodilatation due to acute loss of sympathetic vascular tone.
4. Cardiogenic shock results from failure of the heart as a pump (the heart itself is
impaired as a pump) as in severe arrhythmias or acute myocardial infarction. In trauma it
results from rupture of one of the heart champers or valves, cardiac contusion, or
coronary artery injury
5. Obstructive shock, which results from mechanical impediment to heart and circulation
rather than a primary cardiac failure. It is caused by pulmonary embolism, cardiac
tamponade or tension pneumothorax, results in depressed cardiac output,
6. Traumatic shock, the soft tissue injury and long bone fractures that occur in
association with blood loss yield an upregulation of proinflammatory mediators that is
more complex than simple hemorrhagic shock resulting in third space loss.
INITIAL MANAGEMENT OF SHOCK
(1) Definitive control of the airway must be secured,
(2) Control of active hemorrhage must occur promptly (generally in the operating room,
as delay in control of ongoing bleeding increases mortality),
(3) Adequate volume resuscitation with red blood cells and crystalloid solution
(4) Excessive fluid resuscitation may exacerbate bleeding.
Thus, both inadequate and uncontrolled volume resuscitation is harmful.
PHASES OF SHOCK
Cardiovascular Response
1. Hemorrhage results in diminished venous return to the heart and decreased
cardiac output.
2. This is compensated by increased cardiac heart rate and contractility in an
attempt to increase cardiac output.
3. Venous and arterial vasoconstriction is not uniform. Blood is shunted away from
less essential organ such as the intestine, kidney, and skin. In contrast, the brain and
heart preserve their blood flow despite decrease in cardiac output.
4. The majority of the blood volume is within the venous system. In shock there is
contraction of the capacitant veins increasing venous return to the heart and
maintaining ventricular filling.
HORMONAL RESPONSE
1. Increased sympathetic output induces catecholamine release from the
adrenal medulla. Catecholamine effects on peripheral tissues include stimulation
of hepatic glycogenolysis and gluconeogenesis to increase circulating glucose
availability to peripheral tissues, an increase in skeletal muscle glycogenolysis,
suppression of insulin release, and increased glucagon release.
2. Activation of the hypothalamic-pituitary-adrenal axis Shock stimulates the
hypothalamus to release corticotropin-releasing hormone that results in the release
of adrenocorticotropic hormone (ACTH) by the pituitary. ACTH subsequently
stimulates the adrenal cortex to release cortisol. Cortisol acts synergistically
with epinephrine and glucagon to induce a catabolic state. Cortisol stimulates
gluconeogenesis and insulin resistance, resulting in hyperglycemia as well as
muscle cell protein breakdown and lipolysis to provide substrates for hepatic
gluconeogenesis. Cortisol causes retention of sodium and water by the nephrons
of the kidney.
3. The renin-angiotensin system is activated in shock. This result in release of
aldosterone, ACTH, and antidiuretic hormone (ADH). Aldosterone, a mineralocorticoid,
acts on the nephron to promote reabsorption of sodium. ADH acts on the distal tubule and
collecting duct of the nephron to decrease water and sodium losses, and preserve
intravascular volume.
MANAGEMENT OF SHOCK
1. Recognition of shock.
The clinical manifestations of shock are related to tissue hypoperfusion and the
body response to shock by neuroendocrine response.
a. Due to compensatory mechanisms, (including preservation of venous return)
hypotension is noted only in stage III (loss of >30% of blood volume).
b. Tachycardia is an early sign of shock; it is an attempt to increase cardiac output.
Elderly patients however may not exhibit tachycardia because: (1) Limited
cardiac response to catecholamines stimulation. (2)Use of drugs as beta blockers
and (3) Presence of cardiac bacemaker.
c. Release of endogenous catecholamines increase peripheral vascular resistance
increasing diastolic pressure (decrease pulse pressure which is the difference
between systolic and diastolic blood pressure). So decrease pulse pressure is seen
in stage II and before decrease systolic blood pressure which is seen in stageIII.
d. Vasoconstriction of cutaneous circulation leads to pallor and cold skin.
e. Renal hypoperfusion and kidney attempts to preserve fluids would lead to
decreased urine output.
f. Due to cerebral hypoperfusion patient is irritable initially and later has altered
level of consciousness and coma.
g. Hemoglobin level or hematocrit concentration is not reliable to estimate
blood loss and diagnose shock.
Hemorrhagic shock
In adults, blood= 7% of ideal body weight= 5 liters
1. Identify patients whose blood loss was greater than initially estimated.
This avoids unnecessary fluid and blood transfusion
2. Identify patients with ongoing bleeding who need operative control of
hemorrhage.
3. Operating room resuscitation go hand in hand with operative control of
bleeding.
1. Rapid response: Patients respond rapidly to the initial fluid bolus
and remain hemodynamically stable. These patients have lost less
than 20% of their blood. No further boluses or blood transfusion is
needed. These patients should be maintained on fluid maintenance
rate. Typed and cross-matched blood should be prepared, operative
intervention is still a possibility.
2. Transient response: These patients have lost 20%-40% of their
blood. They respond initially to initial fluid therapy, but deteriorate
when I.V. fluids is lowered to the maintenance rate. This indicates
inadequate resuscitation or continued blood loss. They need
further Fluids and initiation of blood transfusion. In this group of
Hypothermia.
1. Patients with shock and hypothermia dont respond normally to
fluid resuscitation.
2. They may develop coagulopathy.
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