Shock and resuscitation

Published on 11/04/2015 by admin

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Last modified 11/04/2015

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Shock and resuscitation

The pathophysiology of shock

The term ‘shock’ can be defined as acute circulatory failure of sufficient magnitude to compromise tissue perfusion, which if untreated, proceeds rapidly to irreversible organ damage and death of the patient.

Hypoxia in the shocked patient compounds the problem of cellular oxygen delivery. It may be caused by mechanical airways obstruction, impaired gas exchange (e.g. pneumonia or pulmonary embolism) or hypoventilation (e.g. respiratory depression due to opioids) for example.

There are several mechanisms of shock:

The classical symptoms and signs of shock include hypotension, hyperventilation, a rapid weak pulse, cold clammy cyanotic skin and oliguria. Mental changes also occur, most commonly anxiety, confusion and combativeness. Investigations reveal metabolic acidosis, low oxygen saturation and low central venous pressure. Notably, in septic shock there is peripheral vasodilatation rather than vasoconstriction.

Shock has been described as progressing through three stages. In stage I, there are attempts at compensation with skin and splanchnic vasoconstriction. Symptoms and signs are minimal but recognisable. In stage II, decompensation occurs, with body mechanisms unable to sustain tissue perfusion despite working at full capacity. Urgent intervention is needed at this stage. By stage III the changes are essentially irreversible, with prolonged shock having caused severe damage to major organs. Successful treatment depends crucially on early recognition of shock and its precursors, prompt diagnosis and treatment of the underlying cause and effective support of vital organ function.

Early recognition of shock

When surgical patients deteriorate catastrophically, it is often found on retrospective examination of charts that vital signs had been deteriorating for some time, but that clinical staff had failed to respond. Early recognition and intervention is crucial because failure of one organ leads to synergistic failure of other organs and an escalating risk of irreversible damage and death.

To help recognise these patients early, structured scoring systems have been developed, seeking to emulate the simplicity, reliability and clinical value of the Glasgow Coma Scale (Table 16.1, p. 219). These generally employ routinely recorded physiological data and most are modifications of the Early Warning Score (Table 4.1). These have proved extremely useful for spotting those at risk of deterioration needing urgent medical attention and have become part of standard care for surgical patients.

Types of shock

Hypovolaemic shock (preload insufficiency): Preload is defined as the rate of venous return of blood to the heart. Preload insufficiency reduces the diastolic filling pressure and volume and leads to low cardiac output. The underlying problem may be inadequate total blood volume and underfilling of the venous compartment, i.e. absolute hypovolaemia (hypovolaemic shock) or else may be relative hypovolaemia (distributive shock) caused by an increase in capacity of the venous compartment or capillary beds relative to blood volume. Hypovolaemia is responsible for the majority of cases of shock encountered in hospital. Figure 15.1 (p. 200) shows the changes in vital signs associated with increasing amounts of blood loss.

The main causes of fluid loss leading to hypovolaemic shock are:

• ‘Revealed’ haemorrhage, e.g. massive haematemesis from peptic ulcer, deep lacerations, large haematemeses (vomiting of blood), continued loss from a wound drain indicating internal bleeding

• ‘Concealed’ haemorrhage, e.g. intra-abdominal bleeding from ruptured spleen or aortic aneurysm, haemorrhage from a duodenal ulcer into small intestine, intramuscular blood loss from fractures

• Extensive burns, resulting in massive loss of serum into blisters or from the skin surface

• Severe vomiting or diarrhoea, or prolonged fluid loss from a small bowel fistula or ileostomy

• Excessive urinary fluid loss, e.g. diabetic ketoacidosis, recovering acute tubular necrosis

• Sequestration of fluid in bowel caused by bowel obstruction

• Massive loss of fluid into interstitial tissues (‘third space losses’) as occurs in sepsis

• Major accumulation of fluid in the peritoneal cavity, e.g. acute pancreatitis

Septic shock: Septic shock is impaired tissue perfusion in the context of an inflammatory response. The aetiology is frequently infective but not always; it may be traumatic or surgical, or it may involve local inflammation, infection, severe burns or the presence of necrotic tissue, e.g. a gangrenous leg. If immune responses escape local control, this spill over provokes a complex cellular response and mediator cascade that leads to progressive clinical manifestations including the systemic inflammatory response syndrome (SIRS) and, later, multiple organ dysfunction (MODS). Mediator responses involve the complement system, acute phase proteins and cytokines (particularly TNF-alpha and the interleukins IL1-beta and IL6); once triggered, the inflammatory response cascade is difficult to control or suppress.

Septic shock is a combination of distributive shock and organ dysfunction induced by mediators of the host inflammatory response (e.g. cytokines, complement) and sometimes directly by bacterial toxins, especially certain staphylococci or Gram-negative bacilli, e.g. from a colonic anastomotic leak. Bacterial toxins and cell wall components activate defensive mechanisms and the net result of this immune burst is that oxygen usage declines, metabolic acidosis develops and multiple organ dysfunction ensues. Failure of oxygen usage is the result of cardiorespiratory impairment, microcirculatory imbalance and, at cellular level, mitochondrial dysfunction.

Septic shock itself can be thought of in three phases. Initially there is extensive vasodilatation, causing relative hypovolaemia. In phase 2 there is widespread endothelial damage causing greatly increased capillary permeability and massive fluid leakage into the interstitial space. This manifests clinically as inadequate blood pressure in the presence of normal or increased cardiac output; until phase 3, when depression of myocardial contractility ensues.

The inflammatory burst also upsets normal blood coagulation by downregulating normal anticoagulants such as alpha-1-antitrypsin, and stimulating procoagulants such as tissue factor as well as inhibiting fibrinolysis. The result may be disseminated intravascular coagulation with microvascular occlusion, large vessel thrombosis and ischaemia, all contributing to organ dysfunction.

Toxic shock syndrome is a particular form of septic shock associated with staphylococcal or streptococcal infection associated with the use of super-absorbent tampons.