Sepsis and septic shock

• Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection; it is not just "infection plus inflammation".^[1]
• Septic shock is the subset in which circulatory and metabolic abnormalities are profound enough to push mortality above 40 percent. It is identified by needing vasopressors to keep the mean arterial pressure at 65 mm Hg or more together with a lactate above 2 mmol per litre after adequate fluid.^{[1] [2]}
• The commonest infections leading to sepsis are pneumonia, urinary tract infection, intra-abdominal infection and skin or soft tissue infection; Escherichia coli and Staphylococcus species are frequent blood culture isolates.^[4]
• Management is an emergency: blood cultures, lactate, broad-spectrum antibiotics within 1 hour for those with possible shock, 30 mL per kilogram of crystalloid within 3 hours, norepinephrine first for hypotension, and early source control.^[2]
• Even with good care, sepsis kills between one in three and one in six of those it affects, so recognition and the first hour matter more than any later intervention.^[2]

By the end of this page you should be able to:

1. State the Sepsis-3 definitions of sepsis and septic shock and use SOFA and qSOFA.
2. Explain the pathophysiology from trigger to organ dysfunction, including cytokines, endothelial injury, vasodilation and coagulopathy.
3. Recognise sepsis early from clinical signs and lactate and distinguish infection from septic shock.
4. Apply the hour-1 bundle: cultures, antibiotics, fluids, vasopressors and source control.
5. Choose empiric antibiotics by likely source and adjust for neutropenia, MRSA risk and fungal risk.
6. Outline monitoring, complications, and care in children and in low-resource settings.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection.^[1] Infection alone is common and usually self-limiting or controlled by the immune system; sepsis is what happens when the host response injures its own tissues and organs. The older term "severe sepsis" is now redundant because any sepsis already implies organ dysfunction.^[1]

Operationally, organ dysfunction is an acute increase in the total Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score of 2 points or more from baseline as a result of infection, which carries an overall mortality risk of approximately 10 percent in a general hospital population with suspected infection.^[1] The SOFA score grades six organ systems (respiration, coagulation, liver, cardiovascular, central nervous system, renal) and requires laboratory values that are usually available in hospital care. The baseline SOFA score can be assumed to be zero when organ dysfunction was not known before the infection.^[1]

Because SOFA is cumbersome at the bedside, the task force also defined qSOFA (quick SOFA) to flag adults outside the intensive care unit who are likely to have poor outcomes. Any two of three of the following are enough: respiratory rate 22 breaths per minute or more, altered mentation (Glasgow Coma Scale below 15), or systolic blood pressure 100 mm Hg or less.^[1] qSOFA is not a definition of sepsis and should not be used as a single screening tool; it is a prompt to look harder for organ dysfunction and to escalate care.^[2]

Septic shock is a subset of sepsis in which circulatory and cellular or metabolic abnormalities are profound enough to substantially increase mortality. Clinically it is identified by persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or more and a serum lactate above 2 mmol per litre (above 18 mg per dL) despite adequate fluid resuscitation.^[1] When both are present, hospital mortality exceeds 40 percent.^[1]

Classification by source is also practical (discussed under antibiotic choices): community versus healthcare-associated, and by anatomical site (pneumonia, urinary tract, intra-abdominal, skin and soft tissue, central nervous system, unknown). Severity in the first hours is stratified by the presence of shock, lactate level and degree of organ failure.

Sepsis is a major health problem: the Surviving Sepsis Campaign authors estimate that it affects millions of people each year worldwide and kills between one in three and one in six of those it affects.^[2] A review of immune pathophysiology cites approximately 49 million cases and 11 million deaths in 2017, around one fifth of all deaths worldwide.^[3]

In the United States, sepsis costs more than 20 billion dollars in hospital care annually, making it one of the most expensive conditions treated in hospital. Reported incidence is increasing, probably reflecting older populations with more comorbidities, better recognition and coding practices.^[1][4]

A United States Centers for Disease Control and Prevention (CDC) review of patients with sepsis in four acute care hospitals found median age 69 years and at least one comorbidity in 97 percent of adult patients. The commonest illnesses leading to sepsis were pneumonia (35 percent), urinary tract infections (25 percent), gastrointestinal infections (11 percent) and skin or soft tissue infections (11 percent); 13 percent had no identified source.^[4] Respiratory infections preceded sepsis in 29 percent of paediatric patients, followed by gastrointestinal infections in 24 percent.^[4] Among adults, 58 percent of cases were healthcare-associated and 25 percent of patients died.^[4] No pathogen was identified in 31 percent of patients despite thorough investigation.^[4]

The most commonly identified blood culture pathogens in adults were Staphylococcus species (including coagulase-negative staphylococci and Staphylococcus aureus), Escherichia coli and Streptococcus species; in infants Enterococcus species predominated and in children over one year Klebsiella species.^[4] Sepsis is usually caused by bacteria but may result from viruses, parasites or fungi. People living with HIV, tuberculosis, malaria or other chronic infections are at higher risk, and sepsis acquired in healthcare settings is one of the commonest serious adverse events in care delivery.^[4]

Prevention is a large part of sepsis control: most infections leading to sepsis are preventable through vaccination, infection control and good management of chronic disease. Pneumococcal and influenza vaccination in particular have prevented many sepsis deaths, and suboptimal coverage leaves avoidable cases.^[4]

The trigger is always an infection, which may be confirmed or only suspected at presentation. The likely source and organism vary with where the infection was acquired, comorbid illness, devices, recent antibiotics, neutropenia and local resistance patterns. Risk factors for sepsis itself are largely the risk factors for severe infection: older age, diabetes, chronic kidney, heart, lung or liver disease, malignancy, immunosuppression from any cause (including corticosteroids, cytotoxics, HIV), indwelling vascular or urinary devices, recent surgery, malnutrition, pregnancy and extremes of age.^[4]

Specific populations deserve emphasis:

• Older adults. Most sepsis in high-income settings occurs in people over 65. Atypical presentation (confusion, falls, anorexia) is common and makes recognition late.^[4]
• Immunocompromised and neutropenic. Fever in a neutropenic patient is an emergency, and empiric antibiotics should be given within 1 hour of triage.^[7] Pseudomonas and other Gram-negative organisms, as well as mucosal organisms, are the usual threats; prolonged neutropenia and mucosal injury increase risk.
• Children. Paediatric sepsis differs in presentation: blood pressure is maintained until late, so perfusion markers (heart rate, capillary refill, skin temperature, mental state, urine output) matter more than blood pressure, and fluid is given in smaller aliquots.^[6]
• Pregnancy and the puerperium. Genital tract infection, pyelonephritis and (in endemic areas) malaria are common sources; the physiological changes of pregnancy mask early deterioration, so thresholds are applied with care.

Sepsis is a multifaceted disruption of the finely tuned immunological balance between inflammation and anti-inflammation. The upregulation of pro- and anti-inflammatory pathways leads to a system-wide release of cytokines, mediators and pathogen-related molecules, activating coagulation and complement cascades.^[3]

Recognition of pathogen-derived molecular patterns (PAMPs) or endogenous host-derived danger signals (damage-associated molecular patterns, DAMPs) is the starting signal. These molecules activate toll-like receptors on antigen-presenting cells and monocytes, initiating transcription of genes involved in inflammation, cell metabolism and adaptive immunity.^[3] Binding of PAMPs and DAMPs to these receptors leads to nuclear translocation of nuclear factor-kappa B, and expression of early activation genes including interleukin-1, interleukin-12, interleukin-18, tumour necrosis factor alpha and interferons. These in turn activate further cytokines (interferon-gamma, interleukin-6, interleukin-8), complement and coagulation pathways and, by negative feedback, downregulation of the adaptive immune system.^[3]

Both pro- and anti-inflammatory responses are upregulated; the net effect differs between patients. The resulting inflammation produces progressive tissue damage and multiple organ dysfunction, while a later immunosuppressive phase ("immunoparalysis") renders survivors susceptible to nosocomial and opportunistic infection.^[3]

Endothelial injury is central. The endothelium is both a victim and a driver: it suffers microvascular injury and activates the coagulation and complement cascades, producing capillary leak, tissue oedema and organ hypoperfusion. Endothelial cells lose their anticoagulant function and promote coagulation through decreased expression of thrombomodulin and heparan sulphate and increased expression of tissue factor. Pro-inflammatory stimulation of the endothelium increases permeability, adhesion molecule expression and cytokine production.^[3]

Vasodilation and distributive shock. Loss of vascular tone through arterial vasodilation is one of the main causes of haemodynamic instability in sepsis. Cytokine-triggered nitric oxide, kinins and other mediators dilate resistance vessels, lower systemic vascular resistance, and maldistribute flow between and within organs. The resulting distributive shock is hyperdynamic: high or normal cardiac output with low filling pressures and falling perfusion pressure. The heart itself suffers sepsis-induced cardiomyopathy through beta-adrenergic downregulation and nitric oxide; interleukin-1 and tumour necrosis factor alpha have direct depressant effects in vitro.^[3]

Coagulopathy and disseminated intravascular coagulation. Sepsis is frequently associated with coagulopathy. Tissue factor-driven activation of the extrinsic pathway, platelet activation and impaired endogenous anticoagulants (protein C, antithrombin) promote microvascular fibrin deposition, while fibrinolysis is suppressed. In a large analysis, 29 percent of critically ill patients with sepsis met criteria for sepsis-induced coagulopathy, which is synonymous with disseminated intravascular coagulation in this context.^[3] Disseminated intravascular coagulation is defined by the International Society on Thrombosis and Haemostasis as an acquired syndrome of intravascular coagulation with loss of localisation that can damage the microvasculature and cause organ dysfunction. In sepsis it presents with systemic activation of coagulation and suppressed fibrinolysis, leading to consumption of platelets and clotting factors, bleeding as well as thrombosis, and increased mortality.^[3]

Organ-specific consequences. In septic shock, severe acute respiratory distress syndrome is reported in up to 40 percent of cases, more often with a pulmonary source. Acute kidney injury arises less from simple hypoperfusion than from inflammation, microcirculatory failure, endothelial and glycocalyx injury, and tubular epithelial cell stress. Neutrophil extracellular traps, complement activation products (C3a, C5a) and leukocyte plugging of capillaries contribute to microvascular occlusion and tissue damage.^[3]

The important clinical takeaway is that sepsis is a dynamic condition. Early on the dominant problem is often hyperinflammation and organ dysfunction; later, immunosuppression and catabolism predispose to secondary infection and poor recovery.

Sepsis is diagnosed at the bedside before any laboratory result returns, because every hour of delay worsens outcome. Look for a presumed or confirmed infection plus evidence of organ dysfunction.

History (in the patient's words). Fever, chills or rigors, feeling suddenly much worse, confusion, breathlessness, fainting, severe malaise, severe diarrhoea or abdominal pain, burning on urination, or a wound that has become painful and red. Patients may describe a "different" illness from their usual infections. Elderly patients may present only with confusion, falls or anorexia.^[4]

Examination. Fever or hypothermia, tachycardia, tachypnoea, hypotension, altered consciousness or agitation, warm or cool peripheries, mottled skin, delayed capillary refill, poor urine output, focal signs of source (crackles, dysuria, abdominal tenderness, cellulitis, meningism).

Red flags. Altered mental status; systolic blood pressure 100 mm Hg or less; respiratory rate 22 per minute or more; lactate above 2 mmol per litre; hypoxaemia; oliguria; mottling; fever with neutropenia or immunosuppression; pregnancy; extremes of age. These mark out patients who need immediate action rather than watchful waiting.^[1][2]

Sources in practice. Think of pneumonia first (crackles, hypoxia, chest X-ray changes), urinary tract infection (dysuria, frequency, flank pain, positive urinalysis), intra-abdominal infection (pain, guarding, ileus, recent surgery), skin and soft tissue infection (erythema, warmth, pain out of proportion in necrotising fasciitis), device-related bacteraemia, and, when the source is not obvious, occult abscess or endocarditis.^[4][5]

Sepsis must be separated both from uncomplicated infection and from non-infectious conditions that mimic it. The mimics include acute pancreatitis, massive haemorrhage, cardiogenic or hypovolaemic shock, pulmonary embolism, adrenal crisis, thyrotoxic or myxoedema crisis, drug reaction or toxin, haematological malignancy, vasculitis and cytokine release syndromes. Fever is not required; sepsis can present with hypothermia. SIRS criteria remain useful for recognising infection but are neither specific nor sufficient, and many hospitalised patients meet them without sepsis.^[1]

A helpful bedside distinction is: if a patient has organ dysfunction and infection is only one of several possible explanations, treat as sepsis until infection is excluded, but simultaneously re-evaluate for non-infectious mimics.^[2]

• Blood cultures. At least two sets, ideally one from a peripheral vein and one from a central line if present, before antibiotics whenever this does not substantially delay treatment. The acceptable delay is less than 45 minutes. Do not let culture collection delay antibiotics in shock.^[2]
• Lactate. Serum or point-of-care lactate, repeated; an elevated level increases and a normal level decreases the likelihood of sepsis, but lactate is neither sensitive nor specific enough to rule sepsis in or out alone.^[1][2]
• Routine labs. Full blood count and differential, urea and electrolytes (creatinine), liver function tests, coagulation screen including platelets and fibrinogen, glucose, arterial or venous blood gas, procalcitonin is not recommended to decide when to start antibiotics.^[2]
• Source localisation. Urinalysis and culture, chest X-ray, focused ultrasound of abdomen or heart, computed tomography of abdomen or pelvis when intra-abdominal infection is possible. Drainable collections should be identified early.
• Organ dysfunction monitoring. Arterial blood gas for PaO2/FiO2, bilirubin, urine output, Glasgow Coma Scale, echocardiography when cardiac dysfunction is suspected.
• Special tests. Lumbar puncture when meningitis is suspected and not contraindicated; imaging of sinuses, joints or spine based on presentation; pregnancy test when relevant; HIV and tuberculosis testing in endemic settings or when risk factors exist.

Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection; operationally, suspected or documented infection with an acute increase of 2 or more SOFA points.^[1]

qSOFA (bedside screening): any two of respiratory rate 22 or more per minute, altered mentation, systolic blood pressure 100 mm Hg or less.^[1]

Septic shock: sepsis plus vasopressors to maintain mean arterial pressure 65 mm Hg or more and lactate above 2 mmol per litre despite adequate volume resuscitation.^[1]

Sepsis-3 discarded: "severe sepsis", SIRS as a requirement, and sepsis as infection plus 2 of 4 SIRS criteria alone. SIRS is retained as a useful aid to recognising infection but not as a marker of severity.^[1]

Paediatric note. Formal Sepsis-3 definitions for children were not adopted by the 2020 paediatric guidelines; children are identified by sepsis-associated organ dysfunction, and septic shock by cardiovascular dysfunction (hypotension, need for a vasoactive drug, or impaired perfusion). The adult qSOFA and SOFA cutoffs do not map onto childhood physiology.^[6]

Sepsis and septic shock are medical emergencies; treatment and resuscitation begin immediately on recognition.^[2] The practical bundle for the first hour is:

1. Measure lactate, and remeasure if it is above 2 mmol per litre.^[2]
2. Obtain blood cultures before antibiotics, provided this does not add a substantial delay (less than 45 minutes).^[2]
3. Administer broad-spectrum antibiotics immediately, ideally within 1 hour of recognition, for possible septic shock or a high likelihood of sepsis; for possible sepsis without shock, reassess rapidly and give antibiotics within 3 hours if concern persists.^[2]
4. Give at least 30 mL per kilogram of intravenous crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock.^[2]
5. Start vasopressors if hypotension persists despite fluids, targeting a mean arterial pressure of 65 mm Hg, with norepinephrine first line.^[2]
6. Identify source and begin source control early, including removing lines that may be the source.^[2]

The sequence in practice is not always tidy; antibiotics should not wait for central access or for all investigations when shock is suspected.

Empiric antibiotic choice follows the likely source, local resistance, prior cultures, devices and host risk. Where the source is unclear, a regimen with broad Gram-negative and, when indicated, anti-MRSA coverage is used; the beta-lactam is given first. Antipseudomonal coverage is reserved for risk factors for multidrug-resistant organisms. Blood cultures guide later de-escalation, which should be reconsidered daily.^[5][2]

The table below summarises guideline-based site-directed regimens.^[5]

Source control must be begun promptly and revisited daily. Infected catheters should be removed once alternative vascular access is secured; abscesses drained; necrotic tissue debrided; obstructed ureters or bowel decompressed. Antibiotics cannot sterilise an undrained collection, and patients with an uncontrolled source have higher mortality.^[5][2]

Initial resuscitation targets restoration of perfusion, not a single number. For sepsis-induced hypoperfusion or septic shock, give at least 30 mL per kilogram of crystalloid within the first 3 hours.^[2] Crystalloids are first-line, with balanced crystalloids preferred to normal saline and albumin considered after large volumes. Starches and gelatins should not be used.^[2] Colloid-sparing dynamic measures (passive leg raising with stroke volume or pulse pressure, or echocardiography) guide further fluids more safely than static pressures or clinical examination alone, although in low-resource settings peripheral perfusion, mottling and capillary refill are reasonable surrogates.^[2]

If hypotension persists, norepinephrine is the first-line vasopressor over dopamine, vasopressin, epinephrine and angiotensin II, with a strong recommendation.^[2] The initial mean arterial pressure target is 65 mm Hg. Vasopressin is usually added when norepinephrine reaches 0.25 to 0.5 micrograms per kilogram per minute, and epinephrine added if pressure remains inadequate. Norepinephrine may be started peripherally to avoid delay, but only briefly and into a proximal vein. Where norepinephrine is unavailable, epinephrine or dopamine can be used, and improving its availability should be a priority.^[2] For adults aged 65 or over, a lower target range may be considered in very frail or hypertensive patients, but 65 mm Hg remains the standard initial target.^[2]

When the patient has cardiac dysfunction with persistent hypoperfusion despite adequate volume and pressure, either dobutamine added to norepinephrine or epinephrine alone may be used. Invasive arterial pressure monitoring and balanced reassessment beat protocolised Rivers-style early goal-directed therapy, which is no longer recommended as a fixed bundle.^[2]

For adults with septic shock and an ongoing requirement for vasopressors, intravenous corticosteroids are suggested. The typical regimen is hydrocortisone 200 mg per day, given as 50 mg intravenously every 6 hours or as a continuous infusion, usually started when norepinephrine or epinephrine reaches at least 0.25 micrograms per kilogram per minute for 4 hours or more.^[2] Steroids reduce vasopressor requirement and accelerate shock resolution, but have not shown a clear mortality benefit and they increase the risk of neuromuscular weakness.^[2] They are not recommended for sepsis without shock, nor for uncomplicated infection.^[2]

For sepsis-induced acute respiratory distress syndrome, prevention of further lung injury is as important as treating infection: low tidal volume ventilation at 6 mL per kilogram, an inspiratory plateau pressure not above 30 cm H2O, higher positive end-expiratory pressure for moderate or severe disease, and prone positioning for more than 12 hours a day for moderate to severe cases. High-flow nasal oxygen is preferred over non-invasive ventilation for sepsis-induced hypoxaemic respiratory failure.^[2]

For acute kidney injury, fluid stewardship and early recognition come first; when renal replacement therapy is needed, either continuous or intermittent modalities are acceptable, but renal replacement should not be initiated without a definitive indication.^[2] In sepsis-induced acidosis with severe metabolic acidaemia (pH at or below 7.2) and acute kidney injury, sodium bicarbonate therapy is suggested, whereas bicarbonate is not recommended to improve haemodynamics or reduce vasopressor requirement in lactic acidosis alone.^[2]

Monitoring should be serial and combined: clinical perfusion, urine output appropriate for body weight and context, lactate trend, mental status, respiratory rate and work of breathing, and invasive pressure if available. Serum lactate should be interpreted in context and trended rather than treated as a perfusion target in isolation.^[2] Culture results are reviewed daily to de-escalate antibiotics; procalcitonin plus clinical evaluation may be used to decide when to stop antibiotics when the best duration is unclear.^[2] Goals of care, prognosis and palliative needs should be addressed early with patients and families, ideally within 72 hours.^[2]

• Acute respiratory distress syndrome, with diffuse alveolar damage, hypoxaemia and high ventilatory requirements.^[3]
• Acute kidney injury, common and often non-oliguric, driven by inflammation and microcirculatory dysfunction.^[3]
• Disseminated intravascular coagulation and thrombocytopenia, with both bleeding and thrombosis risk.^[3]
• Septic cardiomyopathy and arrhythmias (especially atrial fibrillation), which may mimic hypovolaemia.
• Metabolic: hyperglycaemia (insulin is usually started when glucose reaches or exceeds 180 mg per dL, targeting 144 to 180 mg per dL), severe acidosis, adrenal dysfunction. ^[2]
• Neuromuscular weakness related to illness and to corticosteroids.
• Secondary infections and immunosuppression after recovery.
• Post-sepsis syndrome: physical deconditioning, cognitive impairment and psychological sequelae in survivors, with recommended screening and rehabilitation follow-up.^[2]

Before discharge, educate patients and families about sepsis and its sequelae, reconcile medications, and arrange follow-up for new impairments; after discharge screen for physical, cognitive and emotional problems and refer to rehabilitation or follow-up programmes where available.^[2]

Newborns before 37 weeks gestation are excluded from the 2020 paediatric guidelines; term neonates and children up to 18 years are included, but formal Sepsis-3 adoption in paediatrics is pending. Septic shock in children is severe infection leading to cardiovascular dysfunction (hypotension, need for vasoactive drugs, or impaired perfusion). Because children maintain blood pressure until late, perfusion markers take priority. Fluids are given as 10 to 20 mL per kilogram boluses, up to 40 to 60 mL per kilogram over the first hour when intensive care is available and up to 40 mL per kilogram if not, with reassessment after each bolus and care to avoid fluid overload.^[6] Antimicrobials should ideally be given within 1 hour of recognition of septic shock, and lactate above 2 mmol per litre (and especially above 4) predicts higher mortality.^[6] A 40 mL per kilogram total may be exceeded in warm shock if carefully titrated, but expertise is required.

Febrile neutropenia should be treated as potential sepsis: empiric antipseudomonal therapy started within 1 hour of triage, preceded by blood cultures. First-line options include monotherapy with an antipseudomonal beta-lactam such as piperacillin-tazobactam, cefepime or a carbapenem; add vancomycin for suspected MRSA, catheter infection or severe mucositis. Add mould-active antifungal cover when prolonged neutropenia, persistent fever or computed tomography suggest fungal disease. Mucositis, neutropenic colitis, and uncontrolled sources (including typhlitis or perianal infection) are common complications.^[7][5]

Atypical presentation is common. An early, inclusive definition of probable sepsis is wise, with a low threshold for antibiotics in shock. Renal, hepatic and volume-overload considerations modify fluid and drug dosing.

Uterine infection, pyelonephritis and endemic malaria are common sources. Physiological leukocytosis and tachycardia complicate detection; lower thresholds for evaluation and multidisciplinary care are appropriate.

Sepsis is commonest and most deadly where diagnostic and therapeutic resources are scarcest. The practical adaptations supported by current guidance are:

• When blood gas or lactate testing is unavailable, clinical perfusion (capillary refill, mottling, skin temperature, urine output, mental status) and simple repeated vital signs are the main monitoring tools.^[2]
• Where qSOFA and SIRS are the only bedside options, either can prompt reassessment, but neither is an adequate single screen.^[1][2]
• If broad-spectrum beta-lactams are unavailable, any effective antibacterial coverage that matches local organisms and resistance patterns is better than delay.^[2]
• Where norepinephrine is unavailable, epinephrine or dopamine can substitute temporarily while efforts are made to obtain norepinephrine.^[2]
• Invasive arterial monitoring, central lines, vasopressin and renal replacement may be unavailable; vasopressors can be started peripherally briefly, fluids titrated carefully to perfusion, and transfer arranged early if possible.^[2]
• In paediatric settings without intensive care, give bolus fluids only when hypotension is present and limit the total to 40 mL per kilogram.^[6]
• Source control by bedside procedures (central line removal, bladder catheter change, abscess drainage by available specialists) is often the intervention that saves lives.^[5]
• Vaccination, water sanitation, maternal and neonatal care, malaria and HIV control and careful infection prevention do more to reduce sepsis deaths than any resuscitation bundle.^[4]

• Acute respiratory distress syndrome
• Acute kidney injury
• Disseminated intravascular coagulation
• Pneumonia (community-acquired and hospital-acquired)
• Urinary tract infection and pyelonephritis
• Intra-abdominal infections
• Febrile neutropenia
• Cardiogenic and hypovolaemic shock
• Antimicrobial stewardship
• Paediatric resuscitation and advanced life support