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Shock

Extracted from Survival Guide to Midwifery, 2nd Edition (2012) Diane M. Fraser and Margaret A. Cooper, Oxford; Churchill Livingstone: 2012. Courtesy Elsevier

Shock can be classified as follows:

Hypovolaemic - the result of a reduction in intravascular volume.

Cardiogenic - impaired ability of the heart to pump blood.

Distributive - an abnormality in the vascular system that produces a maldistribution of the circulatory system; this includes septic shock and anaphylactic shock.

Hypovolaemic shock

This is caused by any loss of circulating fluid volume that is not compensated for, as in haemorrhage, but may also occur when there is severe vomiting. The body reacts to the loss of circulating fluid in stages.

Initial stage The reduction in fluid or blood decreases the venous return to the heart. The ventricles of the heart are inadequately filled, causing a reduction in stroke volume and cardiac output. As cardiac output and venous return fall, the blood pressure is reduced. The drop in blood pressure decreases the supply of oxygen to the tissues and cell function is affected.

Compensatory stage The drop in cardiac output produces a response from the sympathetic nervous system through the activation of receptors in the aorta and carotid arteries. Blood is redistributed to the vital organs. Vessels in the gastrointestinal tract, kidneys, skin and lungs constrict. This response is seen as the skin becomes pale and cool. Peristalsis slows, urinary output is reduced and exchange of gas in the lungs is impaired as blood flow diminishes. The heart rate increases in an attempt to improve cardiac output and blood pressure. The pupils of the eyes dilate. The sweat glands are stimulated and the skin becomes moist and clammy. Adrenaline (epinephrine) is released from the adrenal medulla and aldosterone from the adrenal cortex. Antidiuretic hormone (ADH) is secreted from the posterior lobe of the pituitary. Their combined effect is to cause vasoconstriction, an increased cardiac output and a decrease in urinary output. Venous return to the heart will increase but, unless the fluid loss is replaced, will not be sustained.

Progressive stage This stage leads to multisystem failure. Compensatory mechanisms begin to fail, with vital organs lacking adequate perfusion. Volume depletion causes a further fall in blood pressure and cardiac output. The coronary arteries suffer lack of supply. Peripheral circulation is poor, with weak or absent pulses.

Final, irreversible stage of shock  Multisystem failure and cell destruction are irreparable. Death ensues.

Management

Priorities in the management of hypovolaemic shock:

  • Call for help

Shock is a progressive condition and delay in correcting hypovolaemia can ultimately lead to maternal death.

  • Maintain the airway

If the mother is severely collapsed, she should be turned on to her side and 40% oxygen administered at a rate of 4-6 l per minute If she is unconscious, an airway should be inserted.

  • Replace fluids

Two wide-bore intravenous cannulae should be inserted to enable fluids and drugs to be administered swiftly Blood should be taken for cross-matching prior to commencing intravenous fluids A crystalloid solution such as Hartmann's or Ringer's lactate is given until the woman's condition has improved To maintain intravascular volume, colloids (e.g. Gelofusine, Haemaccel) are recommended

  • Ensure warmth

It is important to keep the woman warm, but not overwarmed or warmed too quickly, as this will cause peripheral vasodilatation and result in hypotension

  • Arrest haemorrhage

The source of the bleeding needs to be identified and stopped

  • Monitor vital signs

Septic shock

The most common form of sepsis in childbearing in the UK is reported to be that caused by beta-haemolytic Streptococcus pyogenes (Lancefield group A). This is a Gram-positive organism, responding to intravenous antibiotics, specifically those that are penicillin based. In the general population, infections from Gram-negative organisms such as Escherichia coli, Proteus or Pseudomonas pyocyaneus are predominant; these are common pathogens in the female genital tract. The placental site is the main point of entry for an infection associated with pregnancy and childbirth. This may occur following prolonged rupture of fetal membranes, obstetric trauma or septic abortion, or in the presence of retained placental tissue. Endotoxins present in the organisms release components that trigger the body's immune response, culminating in multiple organ failure.

Clinical presentation 

The mother may present with a sudden onset of tachycardia, pyrexia, rigors and tachypnoea. She may also exhibit a change in her mental state. Signs of shock, including hypotension, develop as the condition takes hold. Haemorrhage may develop as a result of disseminated intravascular coagulation.

Management

This is based on preventing further deterioration by restoring circulatory volume and eradication of the infection.

  • Replacement of fluid volume will restore perfusion of the vital organs
  • Satisfactory oxygenation is also needed
  • Rigorous treatment with intravenous antibiotics, after blood cultures have been taken, is necessary to halt the illness
  • If retained products of conception can be detected on ultrasound, they should be removed.

     

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