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Ovid: Oxford Handbook of Accident and Emergency Medicine

Editors: Wyatt, Jonathan P.; Illingworth, Robin N.; Clancy, Michael J.; Munro, Philip T.; Robertson, Colin E. Title: Oxford Handbook of Accident and Emergency Medicine, 2nd Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 2 – Life-threatening emergencies Chapter 2 Life-threatening emergencies P.42
Anaphylaxis Management of anaphylaxis in children is covered on p622. Anaphylaxis is a generalized immunological condition of sudden onset which develops after exposure to a foreign substance in a previously sensitized person. The mechanism may involve:

  • an IgE mediated reaction to a foreign protein (stings, foods, streptokinase), or to a protein-hapten conjugate (antibiotics).
  • complement mediated: (human proteins eg γ-globulin, blood products)
  • unknown (aspirin, ‘idiopathic’)

Irrespective of the mechanism, chemical mediators (histamine, kallikreins/kinins, prostaglandins, platelet activating factors and leukotrienes) are released from mast cells and basophils, to produce clinical manifestations. Common causes of anaphylaxis

  • drugs (antibiotics, especially penicillins, streptokinase, aspirin, NSAIDs)
  • hymenoptera (bee/wasp) stings
  • foods (nuts, shellfish, strawberries)
  • vaccines

Clinical features The speed of onset and severity vary according to the nature and amount of the stimulus, but the onset is usually in mins/hrs. A prodromal aura, or a feeling of impending death may be present. Patients on ß-blockers or with a history of IHD or asthma may have especially severe features. Respiratory system Swelling of lips, tongue, pharynx and epiglottis may lead to complete upper airway occlusion. Lower airway involvement with features similar to acute severe asthma may develop—dyspnoea, wheeze, chest tightness, hypoxia and hypercapnia. Skin Pruritus, erythema, urticaria and angio-oedema. Cardiovascular Peripheral vasodilation and ↑vascular permeability cause plasma leakage from the circulation, with ↓intravascular volume, hypotension and shock. Arrhythmias, ischaemic chest pain and ECG changes may be present. GI tract Nausea, vomiting, diarrhoea, abdominal cramps. Treatments Follow the Resuscitation Council (UK) guidelines shown below. Additional notes

  • Discontinue further administration of suspected factor (eg drug). Remove stings using forceps or by scraping the sting carefully away from skin.
  • Give 100% O2. Open and maintain airway (if upper airway oedema is present, emergency tracheal intubation or a surgical airway and ventilation may be required).
  • If bronchospasm is present, give salbutamol 5mg nebulized with O2.
  • Give only 50% of the usual dose of adrenaline/epinephrine to patients who are taking tricyclic antidepressants or MAOIs.
  • Even slow dilute IV adrenaline/epinephrine may be hazardous and so is only considered for use by an expert in the presence of life-threatening features.
  • Admit and observe after initial treatment: prolonged reactions/relapses may occur.

Report anaphylactic reactions related to drugs or vaccines to the Committee on Safety of Medicines. Further investigation of the cause (and in some cases, desensitisation) may be indicated. Where identified, the patient and GP must be informed and the hospital records appropriately labelled. Medic-alert bracelets may be useful. P.43

Figure. Treatment algorithm for adults with anaphylaxis1
  • An inhaled beta2-agonist such as salbutamol may be used as an adjunctive measure if bronchospasm is severe and does not respond rapidly to other treatment.
  • If profound shock judged immediately life threatening give CPR/ALS if necessary. Consider slow IV adrenaline (epinephrine) 1:10,000 solution. This is hazardous and is recommended only for an experienced practitioner who can also obtain IV access without delay. Note the different strength of adrenaline (epinephrine) that may be required for IV use.
  • If adults are treated with an Epipen, the 300 micrograms will usually be sufficient. A second dose may be required. Half doses of adrenaline (epinephrine) may be safer for patients on amitriptyline, imipramine, or beta blocker.
  • A crystalloid may be safer than a colloid.

Footnote 1 Resuscitation Council (UK) guideline, 2002. See: http://www.resus.org.uk P.44
Cardiac arrest Background The appropriate and timely management of a patient in cardiac arrest is one of the most challenging events to confront the A&E doctor. Training Theoretical knowledge is important, but many of the skills required during the management of a cardiac arrest need expert teaching and supervised practice. Attendance at an approved Resuscitation Council (UK) Advanced Life Support course (see http://www.resus.org.uk) is strongly recommended—preferably before starting in A&E. Most cardiac arrest patients treated in A&E have sustained a sudden and unexpected out-of-hospital event. Prior warning to the department should be relayed by radio or direct telephone link from the Ambulance Service. In such cases, while the resuscitation attempt is continued, ensure that accompanying relatives or friends are met and taken to an appropriate room which has a telephone, facilities for making tea, coffee, and where privacy is possible. A member of nursing staff must stay with the relatives and act as a link with the Resuscitation Team (p24). Obtain the following information from ambulance crew/relatives:

  • times of: collapse (often an approximation) 999 (or 112) call arrival on scene start of CPR first defibrillating shock (if appropriate) other interventions (eg advanced airway management, drugs) restoration of spontaneous circulation (ROSC)
  • was there any bystander CPR?
  • patient details, including age, past medical history, current medication, chest pain before event

Clinical features and recognition Cardiac arrest is a clinical diagnosis: Any patient who is unconscious and who does not have a major (carotid or femoral) pulse is in cardiac arrest. The time taken to check for a pulse or other signs of a circulation should not exceed 10secs. Other ‘confirmatory’ clinical features (eg colour, pupil size/response) waste time and do not contribute to the diagnosis. Note that some respiratory efforts, such as gasping, may persist for several mins after the onset of cardiac arrest. Occasionally, an arrest may present as a grand mal fit of short duration. P.45
Cardiac arrest: general management Call for help Where a patient in cardiac arrest is being brought to hospital by ambulance, the members of the cardiac arrest team (either A&E staff, the hospital team, or a combination of both) should already be present with all equipment ready to receive the patient. One doctor, usually the most senior, must act as team leader The team leader’s role is to control, co-ordinate and organize the team and make treatment decisions. The optimal number of team members is 5-6. Each member should know his own role. Resuscitation is performed in a calm, quiet, confident manner with minimal interruption to the performance of basic life support or defibrillation. Start the following procedures simultaneously:

  • continue basic life support (p46).
  • remove clothing from the upper body to allow defibrillation, ECG monitoring, chest compressions and IV access
  • obtain an ECG trace using the defibrillator paddles or by attaching monitor leads. If the patient is already attached to an ECG monitor, note (print out if possible) the rhythm. Beware movement artefact, disconnected leads, electrical interference etc.
  • follow the universal ALS algorithm.
  • do not interrupt CPR except to perform defibrillation.

Adult basic life support (BLS) Even the best BLS cannot reverse the myocardial and cerebral deterioration associated with cardiac arrest—therefore do not waste time. Airway and ventilation Usually in the A&E department, advanced airway techniques will be used from the outset. Where basic techniques are used, remember:

  • With the patient on his back, open the airway by tilting the patient’s head and lifting the chin. (Avoid head tilt if trauma to the neck issuspected).
  • Remove any visible obstructions from the mouth, but leave well-fitting dentures in place.
  • Give breaths lasting ≈2secs. Each should make the chest rise. After each breath, maintain the head tilt/chin lift, take your mouth away from the patient’s and watch for the chest to fall as the air comes out.
  • Use a ratio of 15 chest compressions to 2 ventilations (15:2).

Chest compression

  • Place the heel of one hand over the lower half of the patient’s sternum, with the other hand on top of the first. Extend or interlock the fingers of both hands and lift them to avoid applying pressure to the patient’s ribs.
  • With yourself above the patient’s chest and your arms straight, press down to depress the sternum 4-5cm.
  • Release all the pressure and repeat at a rate of 100/min.
  • Compression and release phases should take the same time.


Figure. Basic life support algorithm1

Footnote 1 See Resuscitation Council (UK) guidelines, 2000 (http://www.resus.org.uk) P.48

Figure. Mouth to mouth ventilation1

Footnote 1 MC Colquhoun et al. ABC of Resuscitation, BMJ Publishing. P.49

Figure. Chest compressions1

Footnote 1 MC Colquhoun et al. ABC of Resuscitation, BMJ Publishing. P.50
Cardiac arrest management: specific interventions Defibrillation The vast majority of survivors will have an initial rhythm of VF/VT. The treatment for this is defibrillation. With the passage of time, the chances of successful defibrillation and ultimate survival ↓ dramatically. Correct defibrillation technique is crucial to ↓ transthoracic impedance and ↑ the chances of success. Remove O2 and transdermal GTN patches. Use gel pads to aid current passage. Place one paddle to the right of the upper part of the sternum below the clavicle, the other just outside the position of the cardiac apex (V4-5 position). Avoid placement over the breast in female patients. To avoid problems with implanted pacemakers, keep pads/paddles at least 15cm away from the device. With older defibrillators (which are monophasic and use a damped sinusoidal waveform), select 200J energy for the first two shocks. If unsuccessful, give the third and subsequent shocks at 360J. Newer (biphasic) defibrillators use shocks of different (reduced) energy. Use of some biphasic machines does not involve escalation of shock energy, but the biphasic machines deliver shocks (usually 150J) which are equivalent in efficacy. The information regarding these aspects is displayed on modern defibrillators: ensure that you know how to use the machines in your department. Note that after a shock is given, there is often a delay before an ECG trace of diagnostic quality is obtained. Also, the first few cardiac cycles may be associated with a weak pulse. Allow for these features before rushing to diagnose PEA (EMD). It is not necessary to check for a pulse after a defibrillating shock unless a rhythm compatible with cardiac output is obtained. Drugs There is little evidence that any drug improves outcome in cardiac arrest. If a drug is to be given, the best route of administration is via a central vein. However, this technique is not simple and carries its own risks. Therefore, if you are inexperienced, unsure or this cannot be achieved promptly and safely, secure IV access via a peripheral route. Having given a drug by a peripheral IV route, give a 20mL bolus of 0.9% saline and elevate the limb for 10-20secs to aid entry to the circulation. If venous access is not possible, some drugs (epinephrine/adrenaline, atropine, lidocaine) can be given via the tracheal tube at twice the standard IV dose. Do not give sodium bicarbonate, calcium salts or amiodarone via the tracheal route. Do not attempt intracardiac injections: they interrupt CPR, can cause lethal complications and rarely reach their intended site. With good quality CPR, acidosis is slow to develop. Do not ‘routinely’ give an alkalizing agent such as sodium bicarbonate. Small amounts, eg 50mL of 8.4% solution (50mmol) can be given to patients with severe acidosis (arterial pH < 7.1, base excess < -10). Further administration should be guided by repeated ABG results. In situations where ABG analysis is not possible, it is reasonable to consider using an alkalizing agent after 20-25mins, particularly if resuscitation has been sub-optimal or delayed. End-tidal CO2 monitoring may be useful to confirm correct tracheal tube placement and indirectly measure cardiac output during CPR. P.51
Length of resuscitation The duration of the resuscitation attempt depends upon the nature of the event, the time since the onset and the estimated prospects for a successful outcome. In general, continue resuscitation while VF/pulseless VT persists, always provided that it was initially appropriate to commence resuscitation. If VF persists despite repeated defibrillation, try a change of paddle position or defibrillator. Asystole unresponsive to treatment is unlikely to be associated with survival, as are arrest situations which have lasted >1h. However, exceptions can occur—in particular in younger patients, hypothermia, near drowning and drug overdose. Pulseless electrical activity (PEA) PEA (previously termed electromechanical dissociation—EMD) is the clinical situation of cardiac arrest in a patient who has an ECG trace which is compatible with cardiac output. PEA (EMD) may be caused by:

  • failure of the normal cardiac pumping mechanism (eg massive MI, drugs such as ß-blockers or calcium antagonists or electrolyte disturbance, such as hypocalcaemia, hyperkalaemia).
  • obstruction to cardiac filling or output (eg tension pneumothorax, pericardial tamponade, myocardial rupture, PE, prosthetic heart valve occlusion and hypovolaemia).

Prompt and appropriate correction of these underlying causes can result in survival. Potentially reversible causes are easily remembered as 4H’s and 4T’s according to their initial letter as follows: 4H’s

  • Hypoxia
  • Hypovolaemia
  • Hyper/hypokalaemia/metabolic disorders
  • Hypothermia


  • Tension pneumothorax
  • Tamponade (cardiac)
  • Toxic substances (eg overdose)
  • Thromboembolic/mechanical obstruction


Figure. Advanced life support universal algorithm1

Footnote 1 See Resuscitation Council (UK) guidelines, 2000 (http://www.resus.org.uk) P.53
Notes on using the ALS algorithm

  • When assessing the patient’s rhythm, if (fine) VF cannot be excluded, treat as for VF.
  • Carry out a pulse check if an ECG rhythm compatible with a cardiac output is present. A pulse check after a defibrillating shock is unnecessary unless a rhythm compatible with output is produced.
  • The energies used (for a monophasic defibrillator) for the first three shocks are: 200J, 200J and 360J. If VF/VT persists, give subsequent shocks at 360J. If a shock is successful in converting VF/VT to another rhythm (perfusing or not) and then VF recommences, restart at 200J again. If using a biphasic defibrillator, give shocks of equivalent energy (typically 150J).
  • The commonest cause for failure to achieve defibrillation is poortechnique (see p50).
  • The timing and role of anti-arrhythmic drugs is still debatable and to date, no agent has been shown to improve rates of survival to hospital discharge. Consider amiodarone for VF/pulseless VT refractory to three shocks. The initial dose is 300mg (from a prefilled syringe or made up to 20mL with 5% dextrose). In refractory cases, consider giving a further 150mg, followed by an IVI of 1mg/min.
  • Give epinephrine/adrenaline 1mg IV every 3mins. For patients in VF/VT, the process of assessing rhythm ± pulse check, three DC shocks (if needed) and 1min of CPR will take ≈3mins, therefore epinephrine/adrenaline should generally be given every loop. For non-VF/VT rhythms, each loop lasts 3mins—likewise, give epinephrine/adrenaline every loop, but do not give it in the first min after defibrillation in case a pulse reappears after a period of ‘myocardial stunning’.
  • Exercise caution before using epinephrine/adrenaline in patients whose cardiac arrest is associated with cocaine or other sympathomimetic drugs.
  • Do not use ‘high dose’ epinephrine/adrenaline.
  • Give atropine in a single dose of 3mg IV for asystole.
  • Pacing may be of some value in patients with extreme bradyarrhythmias, but its value in asystole is unproven (except for rare cases of trifascicular block with P waves present).
  • If pacing is deemed desirable, but there is a delay before it can be performed, external cardiac percussion can provide a cardiac output and ‘buy time’. External cardiac percussion is performed using a clenched fist:
    • over the heart at a rate of 100/min
    • with a blow more gentle than a precordial thump
  • Each blow should generate a QRS complex. If this is not achieved with a detectable output, restart conventional CPR.
  • During the periods of CPR, search for and correct potentially reversible causes of cardiac arrest.
  • Follow loops of the algorithm for as long as it is considered appropriate for the resuscitation to continue. Provided that the attempt was commenced appropriately, it should not normally be stopped if the rhythm is still VF.

Post-resuscitation care Features such as coma or absent pupil reflexes can be misleading if used as prognostic indicators in the immediate post-resuscitation phase. Accurate prognostication in an individual patient is rarely possible until 24-72h after the event. The early involvement of senior members of the ITU/CCU team is crucial. All patients should be treated in one of these units when they leave the A&E department. Pending this and following restoration of spontaneous circulation:

  • Ensure that the airway remains adequate.
  • Maintain oxygenation and ventilation under ABG guidance. Correct hypoxia and prevent hypercapnoea (some patients require IPPV). Use pulse oximetry to assess O2 saturation non-invasively.
  • Obtain an ECG and a CXR.
  • Optimise cardiac output to minimize the chance of reperfusion injury. Invasive haemodynamic monitoring may be required.
  • Cerebral blood flow autoregulation is poor in the post-arrest phase. Maintaining arterial pressures which are ‘normal’ for the patient may prevent hypotensive hypoperfusion. Similarly, artificially elevating the BP above the normal for the patient may aggravate cerebral oedema.
  • Seizures aggravate brain injury by increasing ↑ ICP and cerebral metabolic requirements. Treat seizures with appropriate anti-convulsants (p144) while ensuring adequacy of ventilation.
  • Measure U&E, Ca2+, Mg2+ and correct electrolyte abnormalities appropriately.
  • Obtain FBC to exclude anaemia as a contributing factor to myocardial ischaemia and to provide an admission baseline.
  • Monitor plasma glucose concentration and keep it within the normal range.
  • Body temperature control is important. Aim to avoid/treathyperthermia. Mild hypothermia (33-37°C) in some haemodynamically stable patients may be beneficial, but do not attempt to actively induce this without consulting ITU.
  • No drug or other agent has been shown to improve cerebral outcome following cardiac arrest. The routine use of agents such as steroids, mannitol, calcium channel blockers etc is at present unwarranted.
  • Obtain relevant information from the patient’s family/friends and provide support for them as appropriate.

Anti-arrhythmic drugs The routine use of anti-arrhythmic drugs to prevent further malignant ventricular arrhythmias is controversial. They can have significant -ve inotropic and proarrhythmic effects. If used, remember that pharmacokinetic profiles are impaired in the immediate post-resuscitation phase and adjust the dosages appropriately. Team considerations Complete relevant audit forms and provide feedback to staff. On occasions staff require counselling and support. P.55
Central venous access 1 Indications In A&E, central venous access may be useful for several reasons:

  • administration of emergency drugs, especially in cardiac arrest
  • central venous pressure measurement
  • administration of IV fluids, especially when peripheral veins are collapsed or thrombosed (however, other routes are generally preferable for rapidly giving large volumes IV)
  • transvenous cardiac pacing

Problems Central venous access is a specialized technique with potentially life-threatening complications, including:

  • pneumothorax
  • haemothorax
  • arterial puncture
  • thoracic duct damage
  • air embolism
  • infection


  • Expert supervision is essential. Central venous cannulation is particularly difficult and hazardous in hypovolaemic, shocked or agitated patients. In these situations, consider deferring the procedure until the situation has improved.
  • Bleeding dyscrasias and anticoagulant treatment are contraindications to internal jugular and subclavian vein access.
  • Severe pulmonary disease is a relative contraindication to central venous access, especially by the subclavian route, because a pneumothorax would be particularly dangerous.
  • Use aseptic techniques throughout.
  • If possible, tilt the trolley 5-10° head down to fill the internal jugular and subclavian veins and ↓ risk of air embolus.
  • After successful or attempted subclavian or internal jugular cannulation, take a CXR to check for pneumothorax and the position of the catheter.

Choice of vein The external jugular vein is often readily visible and can be cannulated easily with a standard IV cannula during resuscitation for cardiac arrest. The internal jugular and subclavian veins are generally used for central venous access in A&E. Subclavian vein cannulation has a relatively high risk of pneumothorax and so the internal jugular vein is usually preferable, using a ‘high’ or ‘middle’ approach. Use the right side of the neck when possible, to avoid the risk of damage to the thoracic duct. If, however, a chest drain is already in place, use the same side for central venous cannulation. The femoral vein is infrequently used, because of concern about introducing infection, but it is useful for temporary venous access in cardiac arrest, in severe trauma (especially burns) and in drug addicts with many thrombosed veins. P.57
Equipment for central venous access Seldinger technique This is usually the method of choice, because the relatively small needle minimizes the risk of complications such as pneumothorax. The technique involves inserting a hollow metal needle into the vein—a flexible guidewire is threaded through the needle which is then removed. A tapered dilator and plastic catheter are inserted over the guidewire and advanced into the vein. The guidewire and dilator are removed and the cannula secured. Cannula over needle These devices are routinely used for peripheral venous access. Longer versions can be used for central venous access, especially in emergencies such as cardiac arrest: for internal jugular access in an adult a 15cm 16G cannula is suitable, preferably with an integral sliding tap to minimize bleeding and the risk of air embolism when the needle is removed. P.58
Central venous access 2 Internal jugular vein The internal jugular vein runs antero-laterally in the carotid sheath, parallel to the carotid artery and deep to the sternocleidomastoid muscle. Many approaches to this vein have been described. The high approaches (as described here) have less risk of pneumothorax than low approaches.

  • Turn the patient’s head away from the side to be cannulated.
  • Identify the carotid pulse at the level of the thyroid cartilage.
  • Insert the needle 0.5cm lateral to the artery, at the medial border of sternomastoid muscle.
  • Advance the needle at an angle of 45° parallel to the sagittal plane, pointing towards the ipsilateral nipple. The vein should be entered at a depth of 2-4cm and blood aspirated freely. If it is not, try again slightly more laterally.
  • Introduce the cannula, check for free aspiration of venous blood, connect and secure it.

Subclavian vein (infraclavicular approach)

  • Turn the patient’s head away from the side of cannulation.
  • Identify the mid-clavicular point and the sternal notch.
  • Insert the needle 1cm below the mid-clavicular point and advance it horizontally below and behind the clavicle, aiming at a finger in the suprasternal notch. The vein is usually entered at a depth of 4-6cm.
  • Introduce the cannula, confirm free aspiration of venous blood, connect and secure it.
  • Examine the chest and obtain a CXR.

External jugular vein The vein can be seen and felt as it crosses superficially over the sternomastoid muscle and runs obliquely towards the clavicle. Pressure on the lower end of the vein will distend it. A standard IV cannula can easily be inserted into the external jugular vein, but passing a catheter centrally into the superior vena cava may be difficult or impossible because of valves and the angle at which the vein joins the subclavian vein. Femoral vein Insert the needle ≈1cm medial to the femoral artery and just below the inguinal ligament, pointing slightly medially and with the needle at 20-30° to the skin. Use a Seldinger technique or cannula over needle device. P.59

Figure. Internal jugular cannulation1

Footnote 1 M Rosen et al. Handbook of Percutaneous Central Venous Catheterisation, W.B. Saunders, London.

Figure. Subclavian vein cannulation2

Footnote 2 JH Cosgriff. An Atlas of Diagnostic and Therapeutic Procedures for Emergency Personnel, J.B. Lippincott, Philadelphia.

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