Treatment algorithm for adults with anaphylaxis [link]
Cardiac arrest [link]
In-hospital resuscitation algorithm [link]
Adult basic life support [link]
Cardiac arrest management [link]
Advanced life support algorithm [link]
Notes on using the advanced life support algorithm [link]
Post-resuscitation care [link]
Central venous access [link]
Severe sepsis and septic shock [link]
(Anaphylaxis in children is covered in [link])
Anaphylaxis is a generalized immunological condition of sudden onset, which develops after exposure to a foreign substance. The mechanism may:
• Involve an IgE-mediated reaction to a foreign protein (stings, foods, streptokinase), or to a protein–hapten conjugate (antibiotics) to which the patient has previously been exposed.
• Be complement mediated (human proteins eg γ-globulin, blood products).
• Be unknown (aspirin, ‘idiopathic’).
Irrespective of the mechanism, mast cells and basophils release mediators (eg histamine, prostaglandins, thromboxanes, platelet activating factors, leukotrienes) producing clinical manifestations. Angio-oedema caused by ACE inhibitors and hereditary angio-oedema may present in a similar way to anaphylaxis. Hereditary angio-oedema is not usually accompanied by urticaria and is treated with C1 esterase inhibitor.
• Drugs and vaccines (eg antibiotics, streptokinase, suxamethonium, aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), intravenous (IV) contrast agents).
• Hymenoptera (bee/wasp) stings.
• Foods (nuts, shellfish, strawberries, wheat).
The speed of onset and severity vary with the nature and amount of the stimulus, but the onset is usually in minutes/hours. A prodromal aura or a feeling of impending death may be present. Patients on β-blockers or with a history of ischaemic heart disease (IHD) or asthma may have especially severe features. Usually two or more systems are involved:
Swelling of lips, tongue, pharynx, and epiglottis may lead to complete upper airway occlusion. Lower airway involvement is similar to acute severe asthma—dyspnoea, wheeze, chest tightness, hypoxia, and hypercapnia.
Peripheral vasodilation and ↑ vascular permeability cause plasma leakage from the circulation, with ↓ intravascular volume, hypotension, and shock. Arrhythmias, ischaemic chest pain, and electrocardiogram (ECG) changes may be present.
• Discontinue further administration of suspected factor (eg drug). Remove stings by scraping them carefully away from skin.
• Give 100% oxygen (O2).
• Open and maintain airway. If upper airway oedema is present, get specialist senior help immediately. Emergency intubation or a surgical airway and ventilation may be required.
• In patients with shock, airway swelling, or respiratory difficulty give 0.5mg (0.5mL of 1:1000 solution) adrenaline intramuscular (IM). Repeat after 5min if there is no improvement. In adults treated with an adrenaline auto-injector (eg EpiPen®) the 300mcg dose is usually sufficient, but additional doses may be required. Give only 50% of the usual dose of adrenaline to patients taking tricyclic antidepressants, MAOIs, or β–blockers.
• In profound shock or immediately life-threatening situations, give CPR/ALS as necessary, and consider slow IV adrenaline 1:10,000 or 1:100,000 solution. This is recommended only for experienced clinicians who can also obtain immediate IV access. Note the different strength of adrenaline required for IV use. If there is no response to adrenaline, consider glucagon 1–2mg IM/IV every 5min (especially in patients taking β-blockers).
• Give a β2-agonist (eg salbutamol 5mg) nebulized with O2 for bronchospasm, possibly with the addition of nebulized ipratropium bromide 500mcg.
• Give IV fluid if hypotension does not rapidly respond to adrenaline. Rapid infusion of 1–2L IV 0.9% saline may be required, with further infusion according to the clinical state.
• Antihistamine H1 blockers (eg chlorphenamine 10–20mg slow IV) and H2 blockers (eg ranitidine 50mg IV) are commonly given. They are second line drugs that, with hydrocortisone 100–200mg slow IV, may reduce the severity/duration of symptoms.
• Admit/observe after initial treatment: prolonged reactions and biphasic responses may occur. Observe for at least 4–6hr after all symptoms have settled.
Report anaphylactic reactions related to drugs/vaccines to the Committee on Safety of Medicines. Further investigation of the cause (and possibly desensitization) may be indicated. Where identified, the patient and GP must be informed and the hospital records appropriately labelled. Medic-Alert bracelets are useful.
Notes on treatment algorithm on [link]
1 An inhaled β2-agonist such as salbutamol may be used as an adjunctive measure if bronchospasm is severe and does not respond rapidly to other treatment.
2 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.
3 If adults are treated with an EpiPen® the 300mcg will usually be sufficient. A second dose may be required. Half doses of adrenaline (epinephrine) may be safer for patients on amitriptyline, imipramine, or β-blocker.
4 A crystalloid may be safer than a colloid.
The management of choking is rightly taught as part of first aid. Recognition of the problem is the key to success. Clues include a person experiencing a sudden airway problem whilst eating, possibly combined with them clutching their neck.
Severity of airway obstruction
Victims with severe airway obstruction may be unable to speak or breathe and become unconscious (see Fig. 2.2).
Clinical features and recognition
Follow resuscitation algorithm (www.resus.org.uk) shown opposite. Cardiac arrest is a clinical diagnosis:
• Suspect cardiac arrest in any patient who is unconscious and who does not have signs of life. If you check a pulse, examine only for a major (carotid or femoral) one and take no longer than 10sec. Other ‘confirmatory’ clinical features (eg colour, pupil size/response) waste time and do not help. Note that some respiratory efforts, such as gasping, may persist for several minutes after the onset of cardiac arrest. Occasionally, an arrest may present as a grand mal fit of short duration.
• Most patients have had a sudden and unexpected out-of-hospital event.
Prior warning to the department is usually relayed by radio or direct telephone link from the Ambulance Service. While resuscitation is continued, ensure that accompanying relatives/friends are met and taken to an appropriate room, which has a telephone, facilities for making tea and coffee, and where privacy is possible. Arrange for a member of staff to stay with the relatives to act as a link with the Resuscitation Team.
Information to obtain from ambulance crew/relatives
• Patient details: including age, past medical history, current medication, chest pain before event
• Times of : collapse (often an approximation), 999 (or 112) call, arrival on scene, start of cardiopulmonary resuscitation (CPR), first defibrillating shock (if appropriate), other interventions (eg advanced airway management, drugs), restoration of spontaneous circulation (ROSC)
• Was there any bystander CPR?
Where a patient in cardiac arrest is brought to hospital by ambulance, the cardiac arrest team (ED staff, the hospital team, or a combination of both) should already be present in the resuscitation room with all equipment ready to receive the patient.
The team leader
The team leader controls, co-ordinates, organizes the team and makes treatment decisions. 4–6 team members are optimal. Each should know their role. Perform resuscitation in a calm, quiet, confident manner with minimal interruption to the performance of basic life support (BLS) or defibrillation.
Start the following procedures simultaneously:
• Continue BLS.
• Remove/cut clothing from the upper body to allow defibrillation, ECG monitoring, chest compression, and IV access.
• Obtain the ECG trace (through defibrillator pads or monitor leads). If already attached to an ECG monitor, note (print out if possible) the rhythm. Beware movement artefact, disconnected leads, electrical interference, etc.
• Follow the ALS algorithm ( [link]).
• Do not interrupt CPR except to perform defibrillation.
Airway and ventilation
Usually in the ED, advanced airway techniques will be used from the outset. If basic techniques are used (Fig. 2.4):
• With the patient on his/her back, open the airway by tilting the head and lifting the chin. (Use jaw thrust instead if neck trauma suspected.)
• Remove any visible obstructions from the mouth, but leave well-fitting dentures in place.
• Aim for each breath to last ≈1sec and 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.
Technique for chest compression (Fig. 2.5)
• Place the heel of one hand over the middle of the lower half of the patient's sternum, with the other hand on top. Extend or interlock the fingers of both hands and lift them to avoid applying pressure to the patient's ribs.
• Positioned above the patient's chest and with arms straight, press down to depress the sternum 5–6cm.
• Release all the pressure and repeat at a rate of 100–120/min.
• Compression and release phases should take the same time.
• Use a ratio of 30 chest compressions to 2 ventilations (30:2).
• Aim to change the person providing chest compressions every 2 min, but ensure that this is achieved without causing significant pauses.
• Most survivors have an initial rhythm of VF/VT. The treatment for this is defibrillation. With time, the chances of successful defibrillation and survival ↓ dramatically. Adhesive defibrillator pads have replaced manual paddles in most hospitals. Place one pad to the right of the upper sternum below the clavicle, the other in mid-axillary line level with V6 ECG electrode position. Avoid placement over the female breast. To avoid problems with pacemakers, keep pads >15cm away from them.
• With biphasic defibrillators, use shock energy of 150J, for (mostly older) monophasic defibrillators, select 360J energy.
• Plan for chest compressions to be as continuous as possible, with minimal delays. Having paused briefly to assess the rhythm, recommence compressions until the defibrillator is charged. Pause briefly to deliver a shock (removing O2 sources and transdermal glycerol trinitrate (GTN) patches), then immediately restart CPR with 30:2 compressions: ventilation, and continue for 2min before reassessing the rhythm or feeling for a pulse.
• In monitored patients with pulseless ventricular tachycardia/fibrillation (VT/VF) where defibrillation is not immediately available, give a single precordial thump. With a tightly clenched fist, deliver one direct blow from a height of ≈20cm to the lower half of the sternum.
Techniques for securing the airway, providing oxygenation and ventilation are covered in Airway obstruction: basic measures, [link]. Although tracheal intubation has long been considered to be the gold standard definitive airway, only attempt this if suitably experienced. Laryngeal mask airway is a readily available, rapid alternative, which is easy to insert. Whatever method is used, aim to ventilate (preferably with 100% O2) using an inspiratory time of 1sec, a volume sufficient to produce a normal rise of the chest, at a rate of 10/min. For patients with tracheal tubes or laryngeal mask airways, ventilate without interrupting chest compressions, which should be continuous (except for defibrillation or pulse checks as appropriate).
There is little evidence that any drug improves outcome. Central venous cannulation is difficult, has risks and interrupts CPR. Peripheral access is easy and quick. Having given a peripheral IV drug, give a 20mL saline bolus and elevate the limb for 10–20sec. If IV access is impossible, consider intraosseous route ( [link]). It is no longer recommended for any drugs to be given by tracheal tube. Similarly, do not attempt intracardiac injections.
The first drug used in cardiac arrest (after oxygen) is adrenaline. In the case of VF/VT, administer adrenaline after three shocks, whereas in asystole/PEA, give it as soon as possible (see Adult life support algorithm, [link]).
Pulseless electrical activity (PEA)
is the clinical situation of cardiac arrest with an ECG trace compatible with cardiac output. PEA may be caused by:
• Failure of the normal cardiac pumping mechanism (eg massive MI, drugs such as β-blockers, Ca2+ antagonists or electrolyte disturbance, eg hypokalaemia, hyperkalaemia).
• Obstruction to cardiac filling or output (eg tension pneumothorax, pericardial tamponade, myocardial rupture, pulmonary embolism (PE), prosthetic heart valve occlusion, and hypovolaemia).
Prompt and appropriate correction of these can result in survival. Remember potentially reversible causes as the 4H's and 4T's (see Table 2.1).
Toxic substances (eg overdose)
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 changing pad position or defibrillator.
Asystole unresponsive to treatment and arrests which last >1hr are rarely associated with survival. However, exceptions occur—particularly in younger patients, hypothermia, near drowning, and drug overdose.
There are several devices available that can provide mechanical CPR. These include the ‘AutoPulse’ circumferential load-distributing band chest compression device (comprising a pneumatically actuated constricting band and backboard) and the ‘LUCAS’ gas-driven sternal compression device (with accompanying suction cup to provide active decompression). Widespread use of these devices may develop if early encouraging results are confirmed by larger studies. Mechanical CPR is potentially very useful in situations where the resuscitation attempt is prolonged (eg cardiac arrest associated with hypothermia, poisoning or following fibrinolytic treatment for PE), ensuring consistent CPR over a long period of time and freeing up an additional member of the team.
• Establish the underlying cardiac rhythm as quickly as possible in order to determine which ‘loop’ to follow to provide appropriate treatment—for VF/pulseless VT, the initial focus is defibrillation and good CPR; for asystole/PEA, the initial focus is good CPR, IV adrenaline, and searching for potentially reversible causes.
• Do not interrupt CPR except to perform defibrillation.
• Search for and correct potentially reversible causes of the arrest.
• Give IV adrenaline 1mg and amiodarone 300mg for VF/pulseless VT refractory to three shocks, followed by 1mg adrenaline every 3–5min. A further dose of 150mg IV amiodarone may be given for recurrent or refractory VF/VT. Lidocaine (1mg/kg) IV is an alternative to amiodarone, but do not give it if amiodarone has already been given.
• For torsade de pointes, and refractory VF in patients with suspected digoxin toxicity or hypomagnesaemia (eg on K+ losing diuretics), give IV magnesium sulphate 2g (= 8mmol = 4mL of 50% solution).
• In asystole and PEA, give IV 1mg adrenaline as soon as possible and thereafter every 3–5min.
• Exercise caution before using adrenaline in arrests associated with cocaine or other sympathomimetic drugs.
• Atropine is no longer routinely recommended in asystole or slow PEA.
• In PEA arrests associated with hyperkalaemia, hypocalcaemia, or Ca2+ channel blocking drug or magnesium overdose, give 10mL 10% IV calcium chloride (6.8mmol).
• With good quality CPR, acidosis develops slowly. Do not ‘routinely’ give an alkali. Give 50mL of sodium bicarbonate 8.4% solution (50mmol) if arrest is associated with tricyclic overdose ( [link]) or hyperkalaemia and consider it in patients with severe acidosis (arterial pH<7.1, base excess less than –10). Allow further administration to be guided by repeated arterial blood gas (ABG) results.
• 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.
Pacing and external cardiac percussion
Pacing may be of 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 there is a delay before pacing can be performed, external cardiac percussion can provide a cardiac output and ‘buy time’. Perform external cardiac percussion 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, and a detectable output, is not achieved restart conventional CPR.
Features such as coma or pupil reflexes are unreliable prognostic indicators in the early post-resuscitation phase. Accurate prognostication in an individual patient is rarely possible before 24–72hr. Involve the intensive care unit/critical care unit (ICU/CCU) team early.
Pending this and following ROSC
• Ensure that the airway is protected ( [link]).
• Maintain oxygenation and ventilation. Correct hypoxia and prevent hypercapnoea under ABG guidance (may require IPPV). Use pulse oximetry to monitor SpO2 non-invasively, titrating inspired oxygen concentration to achieve SpO2 of 94–98%.
• In intubated patients, insert an oro- or nasogastric tube to decompress the stomach.
• Obtain a 12-lead ECG and a CXR (check position of tracheal tube, central lines and presence of pneumothorax etc.).
• Optimize cardiac output: inotropes, vasodilators, fluids and/or diuretics may be needed under haemodynamic monitoring guidance. If the arrest is associated with an acute coronary syndrome, consider immediate thrombolysis and/or coronary revascularization.
• Cerebral blood flow autoregulation is deficient post-arrest. Maintaining arterial pressures ‘normal’ for the patient may prevent hypotensive hypoperfusion. ↑ BP above the normal for the patient may worsen cerebral oedema.
• Seizures aggravate brain injury by ↑ ICP and cerebral metabolic requirements. Treat with appropriate anticonvulsants (as [link]) and ensure adequate oxygenation and ventilation.
• Measure U&E, Ca2+, Mg2+, and correct abnormalities appropriately.
• Obtain full blood count (FBC) to exclude anaemia contributing to myocardial ischaemia and to provide an admission baseline.
• Both hypo- and hyperglycaemia compromise neurological outcome. Monitor plasma glucose concentration regularly and aim to avoid both hypo- and hyperglycaemia (keep the level ≤10mmol/L).
• No drug has been shown to improve cerebral outcome following cardiac arrest. The routine use of steroids, mannitol, Ca2+ channel blockers, etc., is unwarranted.
• When any drug is used, remember that pharmacokinetic profiles are often impaired post-resuscitation. Dose adjustment and careful monitoring are needed.
• Avoid/treat hyperthermia with antipyretic or active cooling.
• There is compelling data to support the early induction of mild therapeutic hypothermia (32–34°C) in patients who are comatose following out of hospital VF arrest. Mild hypothermia is believed to be neuroprotective in this situation (and pending more data, may be of benefit in other situations as well, eg other arrest rhythms, in-hospital arrests, paediatric patients). Cooling may be initiated by external techniques (cooling blankets, water or air circulating blankets) or internally by an infusion of 30mL/kg of 4°C 0.9% saline—liaise with ICU. Mild hypothermia is typically maintained for 12–24hr.
Theoretical knowledge is important, but many of the skills required during the management of a cardiac arrest need expert teaching and supervised practice. Attend an approved Resuscitation Council (UK) Advanced Life Support course (see www.resus.org.uk)—preferably before starting in the ED.
Central venous access may be required for:
• Administration of emergency drugs.
• Central venous pressure measurement.
• Administration of IV fluids, especially when peripheral veins are collapsed or thrombosed. Note: other routes (eg femoral vein) are generally preferable for giving large volumes rapidly.
• Transvenous cardiac pacing.
Choice of vein
The external jugular vein
is often readily visible and can be cannulated easily with a standard IV cannula.
The internal jugular and subclavian veins
are generally used for central venous access in the ED. Subclavian vein cannulation has a relatively high risk of pneumothorax, so the internal jugular vein is usually preferable, via a ‘high’ approach. When possible, use ultrasound (USS) guidance and the right side of the neck (↓ risk of thoracic duct damage). If, however, a chest drain is already in situ, use the same side for central venous cannulation.
Seldinger technique for central venous access
The method of choice, because the relatively fine needle ↓ 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 cannula are inserted over the guidewire and advanced into the vein. The guidewire and dilator are removed, and the cannula secured. Once the cannula is in place, check that venous blood can be freely aspirated and secure the cannula.
Precautions and problems
Central venous access is a specialized technique with potentially life-threatening complications, including: pneumothorax, haemothorax, arterial puncture, thoracic duct damage, air embolism, and infection.
• Expert supervision is essential. Cannulation is particularly difficult and hazardous in hypovolaemic, shocked, or agitated patients. In such situations, consider whether it is possible to defer the procedure.
• USS has become widely available and is increasingly used by suitably trained ED specialists. It ↓ complications and failure rates by clarifying the relative positions of needle, vein, and surrounding structures. Variant anatomy and vein patency can also be assessed by USS.
• 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 technique. If possible, tilt the trolley 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 chest X-ray (CXR) to check for pneumothorax and the position of the cannula.
External jugular vein
The vein can be seen and felt as it crosses superficially over the sternomastoid muscle and runs obliquely towards the clavicle. Gentle 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 may be difficult because of valves and the angle at which the vein joins the subclavian vein.
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. The high approach described has less risk of pneumothorax than lower approaches (Fig. 2.7).
• 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.
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 (Fig. 2.8).
Septic patients have a systemic inflammatory response syndrome (SIRS) as a consequence of infection. Severe sepsis refers to septic patients with evidence of organ hypoperfusion. Septic shock is present when septic patients exhibit hypotension unresponsive to intravenous fluid resuscitation.
Systemic inflammatory response syndrome
This requires 2 or more of:
• Body temperature of >38°C or <36°C
• Heart rate >90/min
• Respiratory rate >20 breaths/min or PaCO2 < 4.3kPa
• WCC >12 × 109/L or <4 × 109/L or >10% immature (band) forms
Severely septic patients have SIRS with evidence of hypoperfusion (eg systolic BP <90mmHg and/or lactate >3mmol/L). Obtain senior/ICU help early. Intensive therapy of severely septic patients focuses upon certain
• CVP of 8–12mmHg.
• mean arterial pressure >65mmHg.
• urine output >0.5mL/kg/hr.
• central venous saturation >65%.
Adopt the following approach:
• Obtain senior/ICU assistance now.
• Assess and manage airway, breathing, circulation (ABC)—in particular, provide high flow oxygen, secure good IV access and give an initial IV fluid bolus of 20mL/kg of 0.9% saline. Some patients may require early tracheal intubation and IPPV.
• Look for obvious sources of infection.
• Check BMG (and treat if hypoglycaemic).
• Take blood cultures before starting antibiotics (the choice of antibiotics will depend upon the likely cause and is considered on [link]).
• Patients who remain hypotensive and/or have a lactate >3mmol/L require central venous and arterial catheterization in an intensive care/resuscitation setting, with IVI noradrenaline to maintain mean arterial pressure >65mmHg and IV 0.9% saline 500mL boluses every 20mins to achieve CVP 8–12mmHg (12–15mmHg in mechanically ventilated patients).
Shock is a clinical condition characterized by failure to adequately perfuse and oxygenate vital organs. Clinically, shock is recognized by:
• Hypotension Generally considered to be systolic BP <90mmHg (in adults), but values may be higher in young, fit or previously hypertensive patients. Associated tachycardia (>100/min) is common, but may not be present in patients with cardiac or neurological causes or in those taking β-blockers. A few patients with haemorrhagic shock have a paradoxical bradycardia.
• Altered consciousness and/or fainting (especially on standing or sitting up) may result from ↓ cerebral perfusion.
• Poor peripheral perfusion Cool peripheries, clammy/sweaty skin, pallor, ↓ capillary return, but note that in the early phase of endotoxic septic shock there may be vasodilatation with warm peripheries.
• Oliguria ↓ renal perfusion with urine output <50mL/hr (in adults).
Classification of shock
Traditional classification of types of shock is artificial—mixed aetiologies are common.
• Blood loss: trauma, gastrointestinal (GI) bleed (haematemesis, melaena), ruptured abdominal aortic aneurysm, ruptured ectopic pregnancy.
• Fluid loss/redistribution (‘third spacing’): burns, GI losses (vomiting, diarrhoea), pancreatitis, sepsis.
• Primary: myocardial infarction (MI), arrhythmias, valve dysfunction, myocarditis.
• Secondary: cardiac tamponade, massive pulmonary embolus, tension pneumothorax.
Septic shock (see [link])
More common at the extremes of age, in patients with diabetes mellitus, renal/hepatic failure and the immunocompromised (eg HIV infection, underlying malignancy, post-splenectomy, steroid therapy). Note that fever, rigors and ↑ white cell count (WCC) may not be present.
• Organisms responsible include Gram +ve and –ve, especially Staph. aureus, Strep. pneumoniae, N meningitidis, coliforms including enterococci and Bacteroides (especially in patients with intra-abdominal emergencies, such as ruptured diverticular abscess). In the immunocompromised, Pseudomonas, viruses, and fungi may cause septic shock.
Anaphylactic shock: see [link].
Neurogenic shock: see [link].
Investigation and treatment should occur simultaneously. Get senior help immediately.
• Address the priorities—ABC.
• Give high flow O2 by mask.
• Secure adequate venous access and take blood for FBC, U&E, glucose, liver function tests (LFTs), lactate, coagulation screen, and if appropriate, blood cultures.
• Monitor vital signs, including pulse, BP, SpO2, respiratory rate.
• Check ABG.
• Monitor ECG and obtain 12 lead ECG and CXR.
• Insert a urinary catheter and monitor urine output hourly.
• For shock associated with ↓ effective circulating blood volume, give IV crystalloid (0.9% saline) 20mL/kg as bolus. Give further IV fluids including colloid ± blood (aim for haematocrit (Hct) >30%) according to aetiology and clinical response (and in particular, pulse, BP, central venous pressure (CVP), and urine output). Use caution with IV fluid infusion in shock related to cardiogenic causes, and in ruptured or dissecting aortic aneurysm.
• Look for, and treat specifically, the cause(s) of the shock. Echocardiography, USS, CT, and/or surgical intervention may be required. Specific treatments include:
• Laparotomy: ruptured abdominal aortic aneurysm, splenic and/or liver trauma, ruptured ectopic pregnancy, intra-abdominal sepsis.
• Thrombolysis/angioplasty: MI.
• Thrombolysis: PE.
• Pericardiocentesis/cardiac surgery: cardiac tamponade, aortic valve dysfunction.
• Antidotes: for certain poisons.
• Antibiotics: sepsis. The choice of antibiotic will depend upon the perceived cause and local policies (eg ceftriaxone for meningococcal disease). Where there is no obvious source, empirical combination therapy is advised (eg co-amoxiclav + gentamicin + metronidazole). Obtain specialist microbiological advice early, especially in neutropaenic/immunocompromised patients.
• Inotropic and vasoactive therapy, assisted ventilation, and invasive monitoring (including arterial and CVP lines) are often needed as part of goal directed therapy. Get specialist ICU help early.
1 Colquhoun MC et al. (1999). ABC of Resuscitation, 4th edition. BMJ Books, London.
1 Colquhoun MC et al. (1999). ABC of Resuscitation, 4th edition. BMJ Books, London.
1 Rosen M et al. Handbook of Percutaneous Central Venous Catheterization. W.B. Saunders, London.
2 Cosgriff JH. An Atlas of Diagnostic and Therapeutic Procedures for Emergency Personnel. J.B. Lippincott, Philadelphia.