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Punit S. Ramrakha

, Kevin P. Moore

, and Amir H. Sam

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date: 04 August 2020


Shock is defined as inadequate perfusion of vital organs. Concurrent hypotension need not necessarily be present. Unwell patients with a lactate >2mmol/L may have inadequate perfusion. The drop in BP is a late finding, particularly in young, fit people, so resuscitation should ideally commence before this point is reached.


  • If the BP is unrecordable, call the cardiac arrest team. Begin basic life support with chest compressions; attach a defibrillator, and establish venous access.

  • If the BP (MAP <60mmHg) is low or falling, call for urgent support and/or specialist help, e.g. intensive care unit.

  • The cause of hypotension is often apparent. If it is not, then one can usually make a rapid clinical assessment of likely causes:

    • Hypovolaemia.

    • Cardiac failure.

    • Systemic vasodilatation, e.g. sepsis, anaphylaxis, neurogenic.

    • Obstruction (e.g. PE, tension pneumothorax, tamponade).

    • Combined causes.

Differential diagnosis of shock

Cardiac pump failure

  • MI (Shock ST elevation myocardial infarction (STEMI), pp. [link][link]).

  • Dissection of the thoracic aorta (Shock Aortic dissection: assessment, pp. [link][link]).

  • Cardiac arrhythmias (Shock Arrhythmias: general approach, p. [link]).

  • Acute valvular failure or acute VSD (Shock Ventricular septal defect post-myocardial infarction (MI), pp. [link][link]).

  • Drug overdose (cardiac depressants; Shock Overdoses: general approach, pp. [link][link]).

  • Myocarditis.


  • Haemorrhage (GIT) (Shock Acute upper gastrointestinal bleeding 1, pp. [link][link]), aortic dissection or leaking AAA, trauma (fractures, liver or spleen injury, haemothorax, occult).

  • Fluid losses (diarrhoea, vomiting, polyuria, or burns).

  • ‘Third space’ fluid losses (acute pancreatitis; Shock Acute pancreatitis: assessment, pp. [link][link]).

  • Adrenal failure (Shock Addisonian crisis: assessment, pp. [link][link]).

Systemic vasodilatation

  • Sepsis.

  • Liver failure (Shock Acute liver failure: assessment and investigations, pp. [link][link]).

  • Drug overdose (calcium antagonists or other vasodilators, drugs causing multi-organ failure, e.g. paracetamol, paraquat).

  • Adrenal failure (may be both hypovolaemic and vasodilated).

  • Neurogenic shock (bradycardia and hypotension, autonomic failure).

Systemic vasodilatation: anaphylaxis

  • Recent drug therapy.

  • Food allergy (e.g. peanut).

  • Insect stings.


  • Cardiac tamponade (Shock Cardiac tamponade: presentation, pp. [link][link]).

  • PE (Shock Pulmonary embolism (PE): assessment, p. [link]).

  • Tension pneumothorax (Shock Tension pneumothorax, p. [link]).

Shock: assessment

If the BP is unrecordable, then call the cardiac arrest team. Begin basic life support (Airway, Breathing, Circulation, Disability/neurology, Exposure/environment), with emphasis on good-quality CPR, and establish venous access. If the cause of hypotension is not obvious, perform a rapid clinical examination, looking specifically for the following:

  • Check the airway is unobstructed. Give high-flow (60–100%) O2 by face mask. If airway is unprotected or breathing inadequate, ETT. A laryngeal mask airway (LMA) can be used to help oxygenation but does not protect the airway like ETT. Check both lungs are ventilated (? tension pneumothorax).

  • Note the respiratory rate (Shock in acidosis, pneumothorax, embolus, and cardiac failure, but often Shock regardless of cause).

  • Check cardiac rhythm, and treat if abnormal (Shock Tachyarrhythmias heart rate >120bpm, pp. [link][link]; Shock Treatment options in tachyarrhythmias, p. [link]; Shock Broad complex tachycardia: diagnosis, p. [link]; Shock Monomorphic ventricular tachycardia (MVT), pp. [link][link]; Shock Polymorphic ventricular tachycardia, pp. [link][link]; Shock Ventricular tachycardia: drugs, p. [link]; Shock Narrow complex tachyarrhythmias (SVT), pp. [link][link]; Shock Dosages of selected antiarrhythmics for SVT, p. [link]; Shock Atrial fibrillation: assessment, pp. [link][link]; Shock Atrial fibrillation: management, pp. [link][link]; Shock Atrial fibrillation: rate control, p. [link]; Shock Atrial flutter, p. [link]; Shock Multifocal atrial tachycardia, p. [link]; Shock Accessory pathway tachycardia (AV re-entrant tachycardia), p. [link]; Shock Atrioventricular nodal re-entry tachycardia, p. [link]; Shock Bradyarrhythmias: general approach, pp. [link][link]; Shock Sinus bradycardia or junctional rhythm, p. [link]; Shock Intraventricular conduction disturbances, p. [link]; Shock Types of atrioventricular conduction block, p. [link]).

  • Is the JVP elevated (see Box 5.1)?

  • Is the BP the same in both arms (thoracic aortic dissection)?

  • Are there any unusual cardiac murmurs? (Acute valvular lesion, flow murmurs, including an S3, are often heard in vasodilated patients.)

  • Is the patient cold and clammy? This suggests cardiac failure or hypovolaemia. NB Patients with septic shock may also be peripherally shut down. Check for fever (temperature may be subnormal, especially in the elderly and children).

  • Is the patient warm and systemically vasodilated (capillary refill time). Palpate for bounding pulses.

  • Is the patient clinically dehydrated or hypovolaemic (skin turgor, mucous membranes, postural fall in BP)?

  • Any evidence of haematemesis (blood around the mouth) or melaena [per rectum (PR) examination]?

  • Is there any evidence of anaphylaxis, including urticaria, wheeze, or soft tissue swelling (e.g. eyelids or lips)?

  • Examine the abdomen. Is there fullness or a pulsatile mass in the abdomen (ruptured aneurysm)? Is there evidence of an acute abdomen [aneurysm (mottled legs), pancreatitis, perforated viscus]?

  • Is conscious level impaired [AVPU (Alert, Voice, Pain, Unresponsive), Glasgow Coma Scale (GCS)]?

  • Is there evidence of trauma or fractures?



  • NSTEMI, STEMI, Q waves, arrhythmias, PE (tachycardia, right heart strain, S1, Q3, T3), pericarditis (global ST elevation with PR depression).


  • Pneumothorax, PE (oligaemia), dissection (wide mediastinum), tamponade (globular cardiomegaly), pleural effusion (blunted costophrenic angles).

Blood tests

  • FBC (haemorrhage, Shock platelets in liver disease and sepsis), U&Es (renal impairment, adrenal failure), glucose, coagulation screen (liver disease, DIC), LFTs, troponin, CK, group and screen/cross-match.


  • Acidaemia, renal, lactate, ketoacidosis.

Septic screen

  • Culture of blood, urine, sputum, and viral swabs.


  • Echo (suspected tamponade, dissection, valve dysfunction), FAST scan, LP, USS, CT abdomen and head.

Shock: management

General measures

  • Check the airway patency; give O2 (60–100%) by face mask to optimize O2 saturation. If conscious level is impaired (GCS <8), or airway is compromised, or oxygenation is inadequate, consider airway adjuncts (nasopharyngeal, Guedel) and subsequent intubation (or supraglottic device, such as LMA, if ETT is not possible).

  • Lie the patient flat; elevate the legs to improve venous return and demonstrate hypovolaemia.

  • Insert two large-bore IV cannulae, and commence infusion of a crystalloid (Ringer’s lactate/Hartmann’s solution, Plasma-Lyte; 0.9% saline if hyperkalaemia or hypercalcaemia suspected). In most cases of shock, including cardiac causes, it is usually beneficial and safe to give a crystalloid (250mL boluses over 5–10min), while a more detailed assessment is being carried out. If the fluid challenge brings improvement, give a further fluid challenge while assessing the situation. If large volumes of crystalloid are needed, it is best to avoid exclusive use of 0.9% saline, which may cause hyperchloraemia and metabolic acidosis. Aim for 30mL/kg of crystalloid if septic shock.

  • Send blood for U&Es, Mg2+, bone profile, glucose, CRP, FBC, coagulation screen, X-match, blood cultures, and blood gas (venous and/or arterial).

  • Insert an arterial line for more accurate assessment of the BP and arterial sampling. Catheterize the bladder to monitor the urine output. Metaraminol and ephedrine can be given through a peripheral line to temporarily improve the BP.

  • Titrate fluid replacement according to appropriate available dynamic parameters: stroke volume (variation <10%), central venous SpO2 (>75mmHg), venous–arterial CO2 gap (≤0.5mmHg), HR, BP, peripheral tissue perfusion, and urine output (>0.5mL/kg/h). Overenthusiastic fluid administration in patients with cardiac pump failure will precipitate pulmonary oedema.

  • Persistent hypotension, despite adequate filling, is an indication for inotropic support, assuming that tension pneumothorax and PE have been excluded. Insert a central venous line for inotrope infusions. The choice of first-line agent varies to some extent, depending upon the underlying diagnosis, but NA is a reasonable choice supported by RCTs.

  • Treat the underlying condition, and enlist specialist help early.

  • Ensure someone takes time to talk to the relatives to explain the patient is seriously ill and may die. Discuss the resuscitation status.

See Box 5.2.

Cardiogenic shock (cardiac pump failure)

  • Manage cardiac ischaemia, arrhythmias, and electrolyte disturbances.

  • Possible concurrent hypovolaemia? Consider cautious IV fluid challenges, rather than infusions. Optimize filling, guided by physical signs and response in filling pressures and stroke volume to fluid challenges (100–250mL of crystalloid).

  • If BP allows (aim for SBP >100mmHg), start a nitrate infusion (e.g. GTN 1–10mg/h).

  • If very hypotensive, start an IV inotrope infusion. NA should be commenced. The addition of levosimendan or dobutamine should be considered, as per local protocols.

  • Milronone and/or sildenafil may help in the presence of severe pulmonary hypertension, but expert assistance is advised.

  • Low-dose diamorphine (e.g. 2.5mg) is beneficial, as it vasodilates, reduces anxiety, and lowers the metabolic rate.

  • Consider non-invasive (CPAP) or invasive ventilation in patients with severe heart failure, as this decreases the work of breathing and benefits both LV afterload and preload.

  • If there is a potentially reversible cause for cardiogenic shock, consider intra-aortic balloon counterpulsation with heparin anticoagulation as an option, but this does not improve survival in RCTs (Shock Intra-aortic balloon counterpulsation 1, p. [link]).

  • TTE would be helpful in assessing cardiac function and response to fluid and vasopressors.

Hypovolaemic shock

  • Fluid replacement with crystalloids; colloids do not offer a survival advantage but achieve a more rapid haemodynamic response.

  • Give blood to maintain Hb 70–90g/L; 90–100g/L in ACS or sepsis.

  • Na+ and K+ abnormalities should be treated. Metabolic acidosis often responds to fluid replacement alone.

  • If the patient remains hypotensive in spite of fluids, consider other causes of shock (sepsis, tamponade, tension pneumothorax, etc.). Reperfusion injury may occasionally manifest itself as a hypotensive and vasodilated circulation. If fluid-replete, commence inotropes–NA, perhaps with the addition of levosimendan or dobutamine if a low cardiac output state is suspected.

  • If oliguria persists in an overloaded, resuscitated patient, furosemide (0.5–1.0mg/kg IV bolus, followed by an infusion of 1–10mg/h IV) may be given to try and maintain a urine output, as this may make fluid management easier. There is no evidence that furosemide improves outcome.


1. Patel A, Laffan MA, Waheed U, Brett SJ.Randomised trials of human albumin for adults with sepsis: systematic review and meta-analysis with trial sequential analysis of all-cause mortality. BMJ 2014;349:g4561.Find this resource:

2. Patel A, Brett SJ. Gelatin solutions for critically unwell septic adults. Br J Hosp Med (Lond) 2013;74:657.Find this resource:

3. Patel A, Waheed U, Brett SJ. Randomised trials of 6 % tetrastarch (hydroxyethyl starch 130/0.4 or 0.42) for severe sepsis reporting mortality: systematic review and meta-analysis. Intensive Care Med 2013;39:811–22.Find this resource:

Sepsis syndrome and septic shock


  • Bacteraemia

Positive blood cultures.

  • Systemic inflammatory response syndrome (SIRS)

SIRS not thought to be due to infection. Two or more of: temperature >38.3°C or <36°C, RR 20min or PaCO2 <32mmHg (4.3kPa), HR 90bpm, total WCC >12 × 109/L or <4.

  • Sepsis

Evidence of infection plus systemic inflammatory response.

  • Severe sepsis

Sepsis plus evidence of organ dysfunction: confusion, hypoxia, oliguria, metabolic acidosis.

  • Septic shock

Severe sepsis with hypotension refractory despite adequate fluid resuscitation, or lactic acidosis (lactate >4mmol/L).

NB These definitions are in the process of being redefined, with an emphasis on criteria being present in critically unwell patients.


General symptoms

Sweats, chills, or rigors. Breathlessness. Headache. Confusion in 10–30% of patients, especially the elderly. Nausea, vomiting, or diarrhoea may occur.


Hypotension (SBP <90mmHg or a 40mmHg fall from baseline) and tachycardia, with peripheral vasodilatation (warm peripheries, bounding peripheral pulse, bounding pulses in forearm muscles) are the hallmarks of early sepsis, but patients do become shut down eventually. SVR is reduced and cardiac output is Shock initially, but severe myocardial depression may occur. Other features include fever >38°C or hypothermia <35.6°C (immunocompromised or elderly patients may not be able to mount a febrile response), tachypnoea and hypoxia, metabolic acidosis, and oliguria. Focal physical signs may help to localize the site of infection.


  • Blood tests

Blood cultures, U&Es, blood sugar, FBC, coagulation studies, LFTs, CRP, group and save, serum lactate, ABGs. Amylase, CK, and serology. Procalcitonin which is more specific for bacterial sepsis.

  • Culture

Blood, sputum, urine, lines and tips, wound swabs, throat swab, drain fluid, stool, nasopharyngeal aspirate for viral PCR, MRSA swabs, CSF (as indicated), blood films (if recent travel).

  • Imaging

CXR, USS, or CT brain, chest, abdomen, and pelvis for collections. Echo if endocarditis suspected.

Continuous assessments in ICU/HDU

Patients should be monitored in either an ICU or HDU. An arterial line should be inserted for continuous BP monitoring and intermittent blood sampling. It is important in the management of such critically ill patients not to lose sight of the needs of the patient. It is easy in an ICU setting not to examine patients but to look at charts. Always examine the patient at least twice a day and determine whether the clinical parameters match those on the ICU chart.

Ask yourself twice a day

  • Is gas exchange satisfactory? Watch for developing ARDS (Shock Adult respiratory distress syndrome 1, p. [link]) or ventilator-associated pneumonia. Examine the chest daily for deterioration that may be masked on ABG by adjustments of mechanical ventilation and do a CXR if needed.

  • Is the circulation adequate? Note the BP (and MAP), filling pressures, and cardiac output. Examine the peripheries (are they cool and shut down, or warm?). Is the urine output satisfactory? Is there a swing on the arterial trace, suggestive of hypovolaemia? Is there a developing metabolic acidosis, or rising lactate, which may indicate tissue hypoperfusion?

  • Fluid requirements. (What is the fluid balance? Is the patient clinically dry, euvolaemic, or oedematous?)

  • Is the patient receiving adequate nutrition (TPN or enteral)? Give enteral nutrition, if possible; even 10mL/h will benefit the gut mucosa. Give with TPN if the gut function is not adequate, but ensure regular aspiration of any unabsorbed feed.

  • What do the tests show [U&Es, LFTs, Ca2+, PO43–, Mg2+, CRP, cultures (blood, urine, sputum, lines and tips, etc.)]?

  • Are there signs of sepsis? Is there a new focus of infection?


The incidence of bacteraemia is 7/1000 admissions to hospital. Of these, 20% develop septic shock and ~50% of these die (see Table 5.1; also see Box 5.3).

Table 5.1 Mortality in sepsis

Mortality (%)



Bacteraemia plus septic shock


Septic shock plus ARDS


Septic shock: management

Patients with established shock require adequate haemodynamic monitoring and high-dependency facilities.

Check the airway is clear. Give high-flow O2—if there is refractory hypoxia, intubate and ventilate. Insert a large-bore peripheral venous cannula to begin fluid resuscitation. Insert a central line and an arterial line.

Key recommendations from the updated Surviving Sepsis Campaign guidelines (2012)4 for management of severe sepsis and septic shock are summarized here:

  • Early goal-directed resuscitation: during the first 6h after recognition (in patients with hypotension or serum lactate >4mmol/L) is current practice but not supported by multiple RCTs.

  • Resuscitation goals include:

    • MAP ≥65mmHg.

    • Central venous O2 saturation ≥70%.

    • Urine output ≥0.5mL/kg/h.

  • Source identification:

    • Within first 6h of presentation.

    • Blood cultures before antibiotic therapy.

    • Culture all sites as clinically indicated.

    • Imaging studies performed promptly to confirm potential source of infection.

  • Broad-spectrum antibiotics:

    • Within 1h of diagnosis of severe sepsis/septic shock (give first dose of antibiotics yourself).

    • Daily reassessment of antimicrobial therapy with microbiology and clinical data.

    • Antibiotic therapy guided by clinical response; normally 7–10 days, but longer if response is slow or if there are undrainable foci of infection or immunologic deficiencies.

  • Source control: abscess drainage, tissue debridement, or removal of IV access devices if potentially infected as soon as possible, following successful initial resuscitation (exception: infected pancreatic necrosis where surgical intervention is best delayed).

  • IV fluids:

    • Crystalloid fluid challenge (e.g. 1L of crystalloids over 30min) to restore circulating volume; aim for 30mL/kg.

    • Rate of fluid administration should be reduced if cardiac filling pressures increase without concurrent haemodynamic improvement.

  • Vasopressors:

    • NA or dobutamine (administered centrally) are first line.

    • Vasopressin infusion (or long-acting terlipressin bolus) may be added to NA.

  • Inotropic therapy: consider dobutamine when cardiac output remains low, despite fluid resuscitation and vasopressor therapy.

  • Steroids: hydrocortisone (50mg 6-hourly), after adequate fluid resuscitation, may be considered in refractory shock but does not improve survival.

  • Blood products:

    • Target Hb of 70–90g/dL. Aim for a higher target in the presence of tissue hypoperfusion, CAD, intracerebral pathology, or acute haemorrhage.

    • Do not use FFP to correct laboratory clotting abnormalities, unless there is bleeding or planned invasive procedures.

    • Administer platelets when platelet counts are <20 × 109/L and there is significant bleeding risk.

    • Liaise closely with haematology, especially if DIC is suspected.

  • Ventilation:

    • A strategy of low tidal volume, driving pressure, and inspiratory plateau pressure to prevent ARDS.

    • Positive end-expiratory pressure (PEEP).

    • Head of bed elevation in mechanically ventilated patients, unless contraindicated.

  • Glucose control: use IV insulin to control hyperglycaemia, targeting a blood glucose <10mmol/L after initial stabilization.

  • Renal replacement: continuous haemofiltration is the preferred method.

  • DVT prophylaxis: low-dose UFH (renal impairment) or LMWH, unless contraindicated, with dynamic compression (e.g. Flowtron®) of the legs, unless contraindicated.

  • Stress ulcer prophylaxis: H2 blockers or PPIs.

  • Consideration of limitation of support (where appropriate): discuss advance care planning with patients and families. Describe likely outcomes and set realistic expectations.


4. Dellinger RP, Levy MM, Rhodes A, et al. (2012). Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock. Intensive Care Med 39:165–228.Find this resource:

Sepsis syndrome/septic shock: antibiotics

Antibiotic choice is dictated by the suspected site of infection, probable organism, host factors (e.g. age, immunosuppression, hospitalization, and local antibiotic resistance patterns), and local sensitivities. A suggested empiric regimen is presented by source of sepsis:

  • Pneumonia—community-acquired: co-amoxiclav + clarithromycin or azithromycin or doxycycline.

  • Pneumonia—hospital-acquired: piperacillin and tazobactam + gentamicin or amikacin. NB If Staphylococcus aureus suspected, add teicoplanin or vancomycin (if MRSA) or flucloxacillin (if MSSA).

  • Intra-abdominal sepsis: piperacillin and tazobactam + metronidazole + gentamicin or amikacin.

  • Biliary tract: piperacillin and tazobactam + gentamicin or amikacin.

  • Urinary tract—community-acquired: co-amoxiclav or ciprofloxacin or fosfomycin.

  • Urinary tract—hospital-acquired: piperacillin and tazobactam or gentamicin or amikacin or ciprofloxacin.

  • Skin and soft tissue: co-amoxiclav + flucloxacillin and clindamycin.

  • Sore throat: benzylpenicillin.

  • Multiple organisms (anaerobes, Escherichia coli, Streptococcus): meropenem + vancomycin or teicoplanin + gentamicin or amikacin + metronidazole.

  • Meningitis: ceftriaxone and amoxicillin or (if pen. and cef. allergic) vancomycin or rifampicin or chloramphenicol.

NB Consult your microbiologists for local antibiotic policy.

Remove infective foci

It is essential to identify and drain focal sites, e.g. obstructed urinary tract or biliary tree, drain abscesses, and to resect dead tissue.

Causes of treatment failure

  • Resistant or unusual infecting organism.

  • Undrained abscess/ongoing source of sepsis.

  • Inflammatory response (raised CRP, raised WCC) may persist, despite adequate antimicrobial therapy.

  • Advanced disease.

  • Ongoing immunosuppression/neutropenia.

  • Incorrect diagnosis.

Toxic shock syndrome

  • Distinct clinical illness caused by toxin-producing Gram-positive bacteria, usually staphylococci or streptococci.

  • Infection is often localized, and illness is manifest by toxins (e.g. superantigens).

  • 85% of cases are ♀.

  • Association with use of tampons and postpartum in ♀ or following nasal packing (either sex).

  • May occur with any focal infections due to a toxin-producing strain, including post-operative wound infections.

Clinical features

  • Fever: >38.9°C.

  • Rash: diffuse macular (seen in ≥95%), mucous membrane involvement common. Desquamation 1–2 weeks later, palms and soles (non-specific: consider drug reaction in differential diagnosis).

  • Hypotension: SBP <90mmHg, or postural hypotension; often fluid-unresponsive.

  • Diarrhoea and vomiting are common.

  • NSAIDs may mask symptoms.

  • DIC and petechial rash.

  • Multi-organ failure may rapidly follow.

Laboratory findings

  • Normochromic normocytic anaemia (50%) and leucocytosis (>80%).

  • Renal/hepatic failure (20–30%).

  • Myalgia and elevated CK are common.

  • DIC.

  • Pyuria.

  • CSF pleiocytosis (sterile).

  • Blood cultures rarely positive.

  • Vaginal swabs, throat swab, and wound swabs.

  • Toxin-producing S. aureus in 98% of menses-associated cases.

  • Sometimes positive ASO titres or anti-staphylococcal antibodies.


  • Limit toxin production/release.

  • Drain any focal collections and remove foreign bodies.

  • Anti-staphylococcal antibiotics (high-dose flucloxacillin, teicoplanin, or clindamycin IV).

  • Supportive care, as for any patient with shock.


Anaphylaxis is a severe, life-threatening generalized or systemic hypersensitivity reaction, characterized by rapidly developing life-threatening airway and/or breathing and/or circulation problems, usually associated with skin and mucosal changes. The UK incidence of anaphylactic reactions is increasing.

Atopic individuals are particularly at risk, but it may occur in the absence of a past history. Urticarial disease may also present with anaphylaxis. Precipitants include:

  • Insect bites (especially wasp and bee stings).

  • Foods and food additives (e.g. peanuts, fish, eggs).

  • Drugs and IV infusions (blood products and IV immunoglobulin, vaccines, antibiotics, aspirin and other NSAIDs, iron injections, heparin, monoclonal antibodies, e.g. rituximab).


Cutaneous features include skin redness, pruritus, urticaria, conjunctival injection, angio-oedema, and rhinitis. More severe manifestations include laryngeal obstruction (choking sensation, cough, stridor), bronchospasm, tachycardia, hypotension, and shock.


(See Fig. 5.1.)

  • Remove the suspected precipitant if still being received.

  • Maintain the airway: if respiratory obstruction is imminent, intubate and ventilate. Consider emergency cricothyroidotomy (Shock Percutaneous cricothyrotomy, p. [link]) with a 14G needle and jet insufflation with 100% O2 if intubation not possible.

  • Give 100% O2: if there is refractory hypoxaemia, intubate and ventilate.

  • Lie the patient flat with head-down tilt if hypotensive/legs raised.

  • Give IM adrenaline 0.5–1mg (0.5–1mL of 1 in 1000 adrenaline injection), and repeat every 10min according to BP and pulse.

  • If IV access is present, use small IV doses of adrenaline (0.1–0.2mg), then review response. SC adrenaline should not be given in anaphylactic shock due to variable absorption.

  • Establish venous access, and start IV crystalloid fluids (e.g. 500mL over 30min). Persistent hypotension requires a continuous adrenaline infusion, titrated to BP response.

  • Give IV hydrocortisone 200mg and chlorphenamine 10mg.

  • Continue H1 antagonist (e.g. chlorphenamine 4mg every 4–6h) for at least 24–48h longer if urticaria and pruritus persist.

  • If bronchospasm does not subside, treat as severe asthma (including salbutamol, nebulized or intratracheal adrenaline, aminophylline).

  • Once stable, consider investigations such as timed trypase levels, IgE level, complement.

Fig. 5.1 Treatment algorithm for anaphylaxis.

Fig. 5.1 Treatment algorithm for anaphylaxis.

Angioneurotic oedema (C1 esterase inhibitor deficiency)

See Shock C1 esterase inhibitor deficiency (angioneurotic oedema), p. [link].

Lactic acidosis

Lactic acidosis is a metabolic acidosis due to excess production, or reduced metabolism, of lactic acid. It may be divided into two types: type A (tissue hypoperfusion) and type B (non-hypoxic).


Patients are usually critically ill. Clinical features include:

  • Shock (often BP <80/40mmHg).

  • Kussmaul respiration.

  • Tachypnoea.

  • Deteriorating conscious level.

  • Multi-organ failure, including hepatic, cardiac, and renal failure.

  • Clinical signs of poor tissue perfusion (cold, cyanotic peripheries).


  • ABGs (pH <7.34, severe if pH <7.2).

  • Serum electrolytes, including bicarbonate and chloride to calculate the anion gap, if lactate unavailable. Raised anion gap >16mmol/L [anion gap = (Na+ + K+) – (bicarbonate + chloride)].

  • FBC (anaemia, neutrophilia).

  • Blood glucose.

  • Blood lactate level >4mmol/L (mainly done on ABG analysers).

  • Screen for sepsis (blood cultures, CRP, MSU, etc.).

  • Spot urine (50mL) for drug screen if cause unknown.

  • CXR looking for consolidation or signs of ARDS.

Assessment of severity

Severity is assessed by blood lactate concentration and the degree of acidaemia. This may be confounded by the presence of AKI. In the early stages, the arterial pH may be normal or even raised, as elevated lactate levels in the CNS cause hyperventilation, with compensatory respiratory alkalosis. The best predictor of survival is the arterial pH. Patients presenting with a lactate of >5mmol/L and a pH <7.35 have a mortality of >50%.


The principle of management is diagnosis and treatment of the cause (see Box 5.4). All patients should be managed in a high -dependency area.

  • Sepsis: start broad-spectrum antibiotics (e.g. cefotaxime + metronidazole).

  • Diabetic lactic acidosis: insulin and fluids, as needed (Shock Diabetic ketoacidosis: assessment, pp. [link][link]).

  • Shock: consider invasive haemodynamic monitoring (Shock Shock: management, pp. [link][link]).

  • Renal failure: treat by continuous haemo(dia)filtration. These patients are usually too unstable to tolerate haemodialysis.

  • Methanol: infuse ethanol or fomepizole (competitive metabolism; Shock Toxic alcohols, pp. [link][link]).

  • Acidaemia: the role of bicarbonate is controversial, as it may lower CSF pH. There is no benefit of bicarbonate over equimolar saline in controlled trials.