Shock

What is Shock?

"Shock" is a clinical term to describe a condition in which:

• The body temperature is subnormal.
• Reflexes are subnormal.
• Respiration is shallow.
• There is a rapid thready pulse.

Causes of Shock

The cause of the clinical signs of shock is circulatory failure, which results in impaired perfusion of tissues and inadequate cellular oxygenation. There are several different circumstances that might lead to the development of shock, such as:

Hypovolaemia

This is caused by massive reduction in circulating blood volume; for example due to loss in severe haemorrhage or extensive body burns where there is excessive loss of tissue fluid from the injured area.

Trauma, pain and major surgery

These factors can affect the vasomotor control of the peripheral circulation; the capillaries become dilated and blood pools in the peripheral circulation. A secondary hypovolaemia then occurs.

Endotoxaemia

Endotoxaemia can occur in severe infections by Gram negative bacteria. The toxins produced by the bacteria are thought to induce blood clotting in very small vessels, occluding blood flow and resulting in blood pools in the peripheral tissues. Endotoxaemia is a risk factor for the development of disseminated intravascular coagulation (DIC).

Cardiac disruption

Acute cardiac malfunction such as myocardial infarction, severe arrhythmias or sudden failure of the valves can cause circulatory collapse.

Pathophysiology of Shock

In shock caused by haemorrhage or burns, there is reflex vasoconstriction of the peripheral and splanchnic blood vessels. The body becomes starved of oxygen but there is no constriction of the cerebral or coronary blood vessels - this protects the brain and the heart.

The fall in blood pressure stimulates the release of renin from the kidney; consequently angiotensin from the liver is activated which causes an increase in blood pressure. This in turn stimulates the adrenal cortex to secrete aldosterone, which causes the kidney to retain sodium and water.

The kidney is particularly vulnerable to shock; the flow of urine may cease and if the condition is prolonged, acute tubular necrosis can develop.

• After a sustained period of oxygen deficit, the vasomotor control over the blood vessels is lost. Blood becomes pooled in the capillary beds and this state is termed "irreversible shock" which is rapidly fatal.

Treatment of Shock

The aim of treatment is to recover full circulatory function and thus increase tissue perfusion to normal levels. The mainstay of treatment is fluid therapy to increase circulatory volume and drug therapy as required to counteract the predisposing cause of the condition. Oxygen therapy will be required if signs of hypoxia are present. Drug therapies may include antiprostaglandins, antibiotics, sympathomimetics, antiarrhythmics, vasodilators, bicarbonate and glucose, as indicated by the underlying cause and the diagnostic lab work.glucocorticosteriods, are contra-indicated unless a specific defciency is noted i.e hypoadrenocortism

Post-Mortem Findings

Post-mortem findings are non-specific for shock, and include:

• The lungs are wet and heavy, showing congestion and oedema. A degree of atelectasis (collapse) also develops. The alveolar capillaries are distended with blood and the alveoli are filled with haemorrhage and oedematous fluid.
• In the intestine, the blood vessels are congested and there is patchy haemorrhage of the mucosa due to localised anoxia. There is also a considerable amount of blood stained fluid within the lumen which can be mistaken for inflammation.
• The kidneys cortex appears pale due to tubular necrosis, while the medulla is darkened by congestion.
• Histologically, the tubular epithelial cells die and fall into the lumen, the basement membranes rupture and irritant material escapes into the interstitium.

Literature Search

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Nursing management of the hypovolemic shock patient. Davis, H.; The North American Veterinary Conference, Gainesville, USA, Veterinary technicians. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 19-22 - Full Text Article