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A 45-year-old man is admitted to the intensive care unit (ICU) for head trauma related to a fall on the stairs after acute alcohol intoxication. He is found by neighbors lying on the ground and unconscious, with no idea on the delay since the fall. When the ambulance arrives on scene, the Glasgow Coma Scale (GCS) is 8/15, and the man is intubated. On admission to the emergency department (ED) his blood pressure (BP) is 150/90 mm Hg, heart rate 86 bpm, and temperature 35.9°C. His pupils are symmetric (2.5 mm) and reflective, and there is no obvious sign of lateralization. The patient localizes to pain, does not obey orders, and does not open his eyes. A CT scan performed at ED admission discloses several petechial lesions and moderate edema. The day after admission, the patient becomes febrile (temperature 38.6°C) with no obvious sign of infection. Neurologic examination is deteriorating, with the patient being unable to localizing pain (E1M4V1). A repeated CT scan shows an increase in the cerebral contusions but no increase in edema and no mass effect. Transcranial Doppler ultrasound does not show signs of intracranial hypertension. The neurosurgeon does not consider implantation of intracranial pressure (ICP) monitoring at this stage. During the night the patient develops progressive hypoxemia with a Pao2/Fio2, ratio of 180, hypotension (BP 85/40 mm Hg), tachycardia, fever (temperature 39.5°C), and oliguria (urine output 0.3 mL/kg/h at time of assessment). Clinical examination reveals mottled skin mostly around the knees, no heat murmur, and a few crackles predominant at the right lower lobe. The abdominal examination is without specificities. An arterial blood gas reveals pH at 7.33, Paco2 42, Pao2 72 mm Hg, Sao2 95%, hemoglobin concentration 8.6 g/dL, and lactate 2.9 mmol/L.

Does this patient have sepsis?

Sepsis is a major health problem, representing close to 10% of admissions in the ICU. Mortality is still quite high, depending on the criteria used to define it, but remains around 30% for sepsis without shock and 40% to 50% for septic shock. The definition of sepsis has been revised,1 but it can be defined as a dysregulated host response associated with organ dysfunction that is frequently observed in critically ill patients. Of note, the presence of systemic inflammation response (SIRS) criteria is not mandated, because up to 1 patient in every 12 patients presenting with sepsis can be missed when SIRS criteria are mandated.2

Shock is defined as a life-threatening, generalized form of acute circulatory failure, associated with inadequate oxygen utilization by the cells.3 Arterial hypotension (defined as systolic BP < 90 mm Hg, or mean arterial pressure [MAP] < 65 mm Hg, or a decrease by at least 40 mm Hg from baseline), although commonly present, should not be required to define shock.3

How can circulatory failure be assessed at bedside?

Hypotension was present in this patient, with a systolic arterial pressure < 90 mm Hg and a MAP at 55 mm Hg suggesting circulatory failure. However, hypotension without signs of tissue hypoperfusion is insufficient to qualify for septic shock. First, we should exclude some degree of hypovolemia and the impact of sedation. If hypotension persists after a fluid loading of 30 mL/kg of crystalloids, vasopressors should be used. A patient with sepsis treated with vasopressor agents and presenting signs of hypoperfusion qualifies for the definition of septic shock.

In addition to hypotension, we have three important clinical windows that can be ...

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