Shock and its Management
A recent veterinary textbook defines shock as “the clinical state resulting from an inadequate supply of oxygen to the tissues or an inability of the tissues to properly use oxygen.” This deprives the organs and tissues of oxygen (carried in the blood) and allows the buildup of waste products.
Shock also known as Peripheral Circulatory Failure.
Shock can result in serious damage or even death. Many attempts have been made to define shock, but because it is such a complex disorder, no single definition has been successful.
Classification of Shock
There are four general categories of shock: hypovolemic, cardiogenic, septic and vasogenic shock-
Hypovolemic shock
Hypovolemic shock is the result of inadequate intravascular circulatory volume commonly resulting from Haemorrhage, fluid loss in excess of intake, or third spacing of body fluids.
- Acute blood loss: Major laceration, ruptured abdominal or thoracic organs, surgical procedures.
- Fluid loss: Severe vomiting, diarrhoea, burns
- Fluid sequestration: Massive tissue trauma, especially crushing injuries
Cardiogenic shock
Cardiogenic shock occurs from cardiac insufficiency with lowered cardiac output. It may result from-
- Inherent heart diseases such as arrhythmias, myocardial trauma etc.
- Extracardiac diseases such as cardiac tamponade, tension pneumothorax
- The circulatory failure is central in origin
Septic or endotoxic shock
Septic or endotoxic shock occurs from massive infection caused by gram negative microbes. Various diseases which can cause this type of shock are peritonitis, pyometra, haemorrhagic gastroenteritis, intestinal strangulation, or volvulus, pericarditis, mastitis, osteomyelitis etc.
Vasogenic shock
Vasogenic shock occurs either due to extensive vasoconstriction or extensive vasodilatation. Direct action of toxic substance on blood vessels produces dilatation of blood vessels. It leads to decreased resistance and increased capacity of vascular bed.
- Pain or extensive handling and traction of the viscera – massive vasoconstriction
- Deep anaesthesia or spinal injury – extensive vasodilatation
- Anaphylactic shock occurs due to antigen-antibody reaction and resultant histamine release. Histamine leads to increased permeability and massive vasodilatation.
Pathophysiology of Shock-
Although the nature of shock vary, the fundamental sequence of events is essentially the same in all forms of shock-
- Some precipitating cause decreases cardiac output and blood pressure
- Stimulation of sympathoadrenal system leads to peripheral vasoconstriction and shunting of blood away from the skin and intestinal viscera
- Heart rate and myocardial contractility increases, leading to cardiac output
- Simultaneously there is increased release of ADH, activation of rennin-angiotensin system and release of aldosterone which ultimately helps to conserve water and sodium through the kidneys
In micro vascular level certain compensatory changes become less reversible as shock persists and provide a positive feedback-
- There is lowered oxygen delivery to tissue due to sympathetic constriction of arteriole and pre-capillary sphincters.
- Development of cellular anoxia with release of lactic acid
- Permeability of cell membrane increases with release of lysozymesCapillary stasis and decreased capillary pH triggers vascular pulling and decreased venous return to heart
- Hypercoagulability also occurs, which may leads to disseminated intravascular coagulopathy (DIC).
The end result in all forms of shock is cardiac failure ultimately leading to death.
Symptoms of Shock-
It is easy to recognise fully established shock; but it is difficult in early or compensated shock. Shock is dynamic and not a static process.
Physical examination findings associated with hypovolemic and cardiogenic shock include-
- Tachycardia
- Tachypnea
- Pallor of mucous membrane
- Prolongation of the capillary refill time and decrease pulse quality
- Heart murmurs or arrhythmias (not absolute)
Laboratory findings during shock shows lowered red blood cells, haematocrit and plasma proteins; and elevated blood urea nitrogen (BUN).
Other signs include weakness, restlessness, and depression, reduced urine output, coma and dilation of pupils.
Treatment of Shock-
The most important goals in the treatment of shock in animals include-
- quickly diagnosing the patient’s state of shock
- quickly intervening to halt the underlying condition (stopping bleeding, re-starting the heart, giving antibiotics to combat an infection, etc.
- treating the effects of shock (low oxygen, increased acid in the blood, activation of the blood clotting system)
- and supporting vital functions (blood pressure, urine flow, heart function).
Patent airway should be ensured by intubating animal if collapsed or comatose. Oxygen should be delivered via musk, cannula or endotracheal tube.
Haemorrhage, if any, should be controlled by direct pressure, bandages, tourniquet or ligation.
Fluid therapy: A multi electrolyte, sodium containing crystalloid replacement solution is usually the fluid of choice; plasma and whole blood have obvious advantages.