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serotonin and other vasoactive substances are released. Anaphylactic reactions usually begin within 5–10 minutes of exposure to the trigger and the full reaction usually evolves within 30 minutes.
If anaphylaxis is suspected, samples for serial serum tryptase estimations should be taken. The enzyme tryptase is released from mast cells and it parallels histamine release. Peak concentrations well above 20 ng/ml indicate a true anaphylaxis/anaphylactic reaction. The peak value occurs anywhere between 30 minutes and 6 hours after exposure. Samples must be taken at the time of the acute event when the patient is stable, 1–2 hours later and a further sample at >24 hours.
Later investigation, after the acute event, involves skin testing to identify the presence of specific immunoglobulin E (IgE) antibodies. The value of skin tests, and especially the prick test, has been shown in extensive studies.
There are estimated to be 500 severe reactions in the UK each year. The estimated obstetric perioperative incidence of life‐threatening allergic reactions is 3.4 per 100 000 anaesthetics (from the Royal College of Anaesthetists National Audit 6 published in 2017 (Kemp et al., 2017) or 1.2 per 100 000 maternities. This is significantly lower than the incidence in non‐obstetric adult cases of 1 in 10 000 anaesthetics. The most frequent trigger agents perioperatively were antibiotics, neuromuscular blocking agents, chlorhexidine and patent blue dye. Anaphylaxis presented within 10 minutes of exposure to the triggering agent in 83% of cases; chlorhexidine and Patent Blue dye cases were slower to present. Hypotension was the presenting feature in 46% of the anaphylaxis cases and occurred during the reaction in all cases. Bronchospasm occurred in 49%. Urticaria and flushing were uncommon presenting features and skin signs were uncommon in the more severe reactions, sometimes only occurring after resuscitation. When the obstetric cases were examined the majority of patients were awake at the time of the reaction and complained of ‘feeling unwell’ before the onset of hypotension. Recognition of a critical event was prompt but recognition of anaphylaxis and starting anaphylaxis‐specific treatment was slower than in non‐obstetric cases. The report comments that this may have been because of the wider differential diagnosis for hypotension in the obstetric setting and that anaphylaxis was low on the list. Adrenaline was administered notably less often than in non‐obstetric settings, which may have reflected the availability of phenylephrine in the obstetric setting. Maternal and neonatal outcomes were good however and there were no cardiac arrests.
Burns
The direct effect of the burn causes fluid loss from the body leading to hypovolaemic shock. In addition, inflammatory mediators are released causing a massive leak of fluid into the tissues, resulting in a problem of distribution. This topic is discussed further in Chapter 22.
Obstructive shock
Obstructive shock can result from the following:
Massive pulmonary embolism (see Chapter 13)
Cardiac tamponade (see Chapter 17)
Tension pneumothorax (see Chapter 17)
This form of shock is due to a reduction in venous return to the heart. Patients, if conscious, are very dyspnoeic and struggle to sit upright, gasping for breath. Extreme tachycardia is a compensatory mechanism for compromised cardiac output. There will also be associated features of the pathology causing the obstruction of blood flow.
6.4 Symptoms and signs of shock
The signs and symptoms seen in the various forms of shock are primarily due to organ dysfunction resulting from inadequate tissue perfusion. The presentation is also partly influenced by the pathology causing the shock syndrome.
Hypovolaemic shock
This is the most common form of shock encountered on the labour ward. The signs of hypovolaemia are:
Fetal heart rate abnormalities
Increase in maternal heart rate
Cold, pale, sweaty, cyanosed skin with delayed capillary refill
Alteration of mental state
Tachypnoea
Fall in urine output
Narrowed pulse pressure
Hypotension (late sign)
Increase in heart rate
An increase in the heart rate occurs in compensation for hypovolaemia (1000–1500 ml blood loss) or vasodilatation, both of which can cause hypotension and shock. A maternal heart rate of more than 100 beats/min should be considered sinister, until proven otherwise. Most, but not all, women will become tachycardic if bleeding significantly, but paradoxical bradycardia also occurs. Vagal stimulation caused by cervical stimulation (e.g. products in the os) or peritoneal irritation can produce bradycardia profound enough to cause shock. Medications such a beta‐blockers and labetalol (alpha‐ and beta‐blocker) will prevent a tachycardic response to hypovolaemia and this may be falsely reassuring in the assessment of the bleeding patient.
Skin, capillary refill, mental state and urine output
The skin, kidneys and brain can be thought of as ‘end organs’ that reflect the adequacy of perfusion to tissues.
Capillary refill time (CRT)
This is an indication of skin perfusion. It can be assessed by compressing a fingernail, or pressing on the sternum, for 5 seconds. The test is normal if colour returns within 2 seconds of releasing compression (i.e. a CRT of less than 2 seconds – the time taken to say the words ‘capillary refill’). If the patient is in a cold environment, CRT, especially peripherally, will be unreliable.
Mental state
If the woman is conscious and talking sensibly, she is not only breathing through an open airway, she is perfusing her cerebral cortex with sufficient oxygenated blood (50% of the normal cardiac output). Increasing hypovolaemia and subsequent cerebral hypoperfusion cause alterations in the level of consciousness. These alterations may begin with agitation and, if untreated, may proceed through confusion and aggression to eventual unresponsiveness and death.
Narrowed pulse pressure
This is caused by an increase in diastolic blood pressure, that reflects vasoconstriction occurring due to endogenous catecholamine release as a compensation for hypovolaemia.
Systolic hypotension
The sign most commonly referred to in the context of shock, hypotension, is a very late sign in the obstetric population, developing only when significant blood loss has occurred. A successful outcome for the patient depends on the early recognition of shock, restoration of volume and control of haemorrhage.
Recognition of hypovolaemia
Maternal blood loss can be categorised into four classes of severity, as shown in Table 6.1 and graphically in Figure 6.2.
To