Sepsis and Septic Shock in Prehospital Emergency Medicine: Early Recognition, Early Action

Why the prehospital phase matters

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is the subset with circulatory and cellular-metabolic dysfunction. Clinically, it presents with a vasopressor requirement despite fluid administration and an elevated lactate. The exact thresholds should be taken from the current Surviving Sepsis Campaign (SSC) guidelines.

The prehospital emergency physician can rarely treat the underlying cause. They can, however, set the course: articulate the suspicion, stabilise organ function and transfer the patient to an appropriate hospital. Recognising sepsis in the prehospital setting often determines how quickly diagnostics, antibiotic therapy and source control begin in hospital.

Screening: think sepsis

Clinical warning signs

There is no single prehospital cardinal sign of sepsis. The combination of possible infection and new-onset organ dysfunction should raise suspicion:

• Breathing: raised respiratory rate, often the earliest and most frequently unmeasured sign; falling oxygen saturation
• Circulation: hypotension, tachycardia, prolonged capillary refill time, mottled or cool skin
• Consciousness: new confusion, drowsiness, agitation, which in older people is often the only sign
• Skin: petechiae or purpura, which should prompt consideration of meningococcal infection
• Kidneys: history of oliguria
• Temperature: fever or hypothermia; a normal temperature does not exclude sepsis

Risk profile from the history

The following constellations increase the pre-test probability:

• advanced age, dependency on care
• immunosuppression, ongoing chemotherapy (neutropenic fever)
• recent surgery or intervention
• indwelling catheters or ports
• diabetes mellitus, chronic kidney disease
• long-term glucocorticoid therapy or known adrenal insufficiency

qSOFA in prehospital emergency medicine: value and limitations

The qSOFA comprises three criteria: raised respiratory rate, altered mental status and low systolic blood pressure. The thresholds should be taken from the guideline currently in force. The following limitations apply to qSOFA in prehospital emergency medicine:

• The qSOFA is not a diagnostic criterion. It indicates an increased risk of an unfavourable course in suspected infection.
• According to the available data, it is relatively specific but has only limited sensitivity. A normal qSOFA does not exclude sepsis.
• Aggregated early warning scores with more parameters, such as NEWS2, are being discussed as an alternative or complement. Which instrument is best suited to the prehospital setting has not been conclusively established. The SSC guideline describes the current role of the scores.

In practice, this means that scores structure the assessment but do not replace the overall clinical impression. Where infection is suspected and vital signs are abnormal, the suspicion of "sepsis" should be actively stated and documented.

Prehospital diagnostics

On-scene diagnostics should capture organ dysfunction and narrow down the source. They must not delay transport.

• ABCDE assessment with complete vital signs. The respiratory rate is counted, not estimated.
• Blood glucose in any impairment of consciousness.
• Temperature, ideally stating the measurement method.
• 12-lead ECG, as tachyarrhythmias and ischaemia are common differential diagnoses or concomitant findings.
• Point-of-care lactate, where available. It serves as a parameter for trend and severity; however, elevated values are not specific to sepsis.
• Source identification: lungs (auscultation, breathing pattern), urinary tract, abdomen, skin and soft tissue (erysipelas, necrotising infection, pressure ulcers), catheters and ports, meningeal signs.
• Point-of-care ultrasound, if equipment and expertise are available. It helps to assess volume status and cardiac function, to look for free fluid and to exclude other causes of shock.

Important differential diagnoses include cardiogenic, hypovolaemic and obstructive shock, intoxication and adrenal crisis. Infection is a common trigger of adrenal crisis.

Haemodynamic management of septic shock in the emergency setting

Fluid therapy

Early fluid administration is standard in hypoperfusion. Volume, type and rate should follow the current SSC guideline. In the prehospital setting, a pragmatic approach has proven useful:

• Infuse crystalloids as boluses and reassess the effect after each bolus: heart rate, blood pressure, capillary refill, consciousness, work of breathing.
• Watch for signs of fluid overload, such as increasing dyspnoea, moist crackles or falling saturation. Patients with heart or kidney failure are at particular risk.
• Evidence: Whether a more restrictive or a more liberal fluid strategy is advantageous has not been conclusively established. Rigid formula-based administration without reassessment is not appropriate in the prehospital setting.

Vasopressor

If hypotension persists despite fluid administration, norepinephrine is the vasopressor of choice. The blood pressure target for septic shock should be taken from the current SSC guideline and individualised, for example in pre-existing hypertension. Whether norepinephrine is given via a peripheral vein in the prehospital setting depends on local standards. In this case, a secure, well-running peripheral venous cannula is a prerequisite and the insertion site must be monitored closely.

Calculation aid for norepinephrine syringe driver (5 mg / 50 ml = 100 µg/ml). The table is purely a conversion and not a dosing recommendation. It is taken from the compendium, chapter on post-resuscitation care.

The dose is titrated to effect. Local dilution standards must be observed.

Hydrocortisone: usually in hospital, rarely prehospital

• Septic shock with ongoing vasopressor requirement (adults): hydrocortisone 200 mg/24 h i.v., as 50 mg every 6 h or as a continuous infusion (SSC 2026). The SSC 2026 suggests i.v. corticosteroids in septic shock, but as a weak recommendation with low-quality evidence and without a fixed norepinephrine threshold. The earlier orientation of the SSC 2021 was norepinephrine ≥ 0.25 µg/kg/min for ≥ 4 h. National guidelines may differ. This therapy is usually started in hospital.
• Special case of adrenal crisis: In known adrenal insufficiency or chronic glucocorticoid therapy, an infection can trigger an adrenal crisis. In adults, give hydrocortisone 100 mg i.v. (or i.m.) as a bolus without waiting for laboratory results (Beuschlein et al. 2024). If possible without delay, draw blood for cortisol and ACTH beforehand. In addition, give isotonic saline and, in hypoglycaemia, glucose. Take note of the patient's emergency card and any emergency kit they carry.

Airway and oxygenation

Oxygen is given as required. Airway management should be considered in impending respiratory exhaustion or reduced consciousness. Induction of anaesthesia in septic shock carries a risk of circulatory collapse. Vasopressor and fluids should therefore be prepared and the induction agents adjusted to the haemodynamic situation.

Prehospital antibiotics?

The evidence for routine prehospital antibiotic administration is limited. A survival benefit has not been demonstrated for the general prehospital emergency physician setting. More important is a short time to hospital, followed there by rapid, targeted therapy after blood cultures have been taken. Local protocols may provide for exceptions, for example in suspected fulminant meningococcal infection or with long transport times. Agent and dose are then determined by the local SOP and the summary of product characteristics.

Hospital allocation strategy

The receiving hospital should be selected not only by distance but also by treatment capability:

• Intensive care capacity must be available in septic shock or a relevant vasopressor requirement.
• Source control must be possible, for example through surgery, urology, gynaecology or interventional radiology, depending on the suspected source.
• Pre-alert with the explicit statement "suspected sepsis" or "septic shock", so that diagnostics and antibiotic therapy can begin without delay.
• Structured handover: suspected source, time of symptom onset, vital sign trends, lactate (if measured), fluid volume given, vasopressor dose, relevant comorbidities and immune status.
• Clarify treatment goals early, for example in very elderly patients or those receiving palliative care. Existing advance directives must be taken into account.

Practical summary

• In suspected infection with organ dysfunction, actively think of sepsis and communicate the suspicion.
• The qSOFA is a guide, not an exclusion criterion.
• Give fluids as boluses with continuous reassessment; titrate norepinephrine in persistent hypotension.
• Consider adrenal crisis in known adrenal insufficiency or long-term steroid therapy.
• Choose the receiving hospital according to intensive care capacity and the ability to achieve source control, and pre-alert early.

References

• Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026. Intensive Care Med 2026;52:863–936 / Crit Care Med 2026.
• Beuschlein F et al. European Society of Endocrinology and Endocrine Society Joint Clinical Guideline: Diagnosis and therapy of glucocorticoid-induced adrenal insufficiency. Eur J Endocrinol 2024;190:G25–G51.
• Nolan JP, Sandroni C et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2025 Post-Resuscitation Care. Resuscitation 2025 / Intensive Care Med 2025;51:2213–2288.

This article does not replace clinical judgement in the individual case or the current summary of product characteristics and guidelines.