Early Hypotension and Fever

1–2 liters of 0.9% NaCl (may add intermittent infusions of 250 cc of albumin 5%)Define resuscitation goal
A MAP goal higher than the usual 65 mmHg may be necessary in neurocritical patients with compromised cerebral perfusionStart vasopressor if MAP below target after fluid challenge
Norepinephrine, low dose vasopressin, epinephrine
Phenylephrine is not adequateObtain echocardiogram and assess systolic function
Start dobutamine if decreased left ventricular ejection fractionConservative fluid strategy after resuscitation goal is achieved
Can use diuretics if MAP stable and evidence of cerebral edema or raised ICPDiagnosis of infectious source
Panculture (blood cultures, urinalysis with culture and sensitivity, sputum sample)
Culture CSFStart broad-spectrum antibiotics as soon as possibleConsider hydrocortisone if vasopressor dependenceAvoid activated human recombinant protein C if increased risk of ICHBlood product administration
Consider red blood cell transfusion to keep hemoglobin > 9–10 g/dL if cerebral perfusion is compromised
Platelet transfusion to keep platelet count > 50,000 if recent ICH or neurosurgery
FFP to correct coagulopathy if recent ICH or neurosurgeryMechanical ventilation
Careful titration of PEEP if raised ICPSedation and analgesia
Sedation holidays
Minimize use of opiates if possibleGlucose control
Maintain blood sugars between 140–180 mg/dL

MAP, mean arterial pressure; CSF, cerebrospinal fluid; ICH, intracranial hemorrhage; FFP, fresh frozen plasma; PEEP, positive end expiratory pressure; ICP, intracranial pressure

Patients with refractory septic shock may be treated with corticosteroids (hydrocortisone 50 mg intravenously every 6 hours). Corticosteroids may reduce vasopressor dependency but do not appear to improve survival. Their use should not be a problem in critical neurological patients. However, recombinant human activated protein C must not be administered to patients with intracranial hemorrhage or recent neurosurgery, because there is an increased risk of hemorrhage associated with the use of this drug.

Early initiation of broad-spectrum antibiotics is crucially important. Ideally, they should be started within the first hour of the diagnosis of septic shock. Pancultures should be obtained before the first antibiotic dose if at all possible, but cannot delay the start of antibiotics. Nosocomial meningitis may be associated with early sepsis, and thus cultures should include a cerebrospinal fluid sample in any patient with cerebrospinal fluid diversion devices (ventriculostomy, lumbar drainage) or previous neurosurgical procedures.

Septic shock guidelines generally recommend transfusion of red blood cells only when the hemoglobin concentration is below 7 g/dL. While we still do not know the ideal hemoglobin target in patients with severe acute brain insults, such as severe traumatic head injury or poor-grade subarachnoid hemorrhage, improving oxygen carrying capacity may be particularly beneficial in these patients with compromised cerebral perfusion and recent or persistent hypotension. Until more information is available, we aim at a higher target of hemoglobin concentration of 9–10 g/dL in critically ill neurological patients who are septic and hypotensive.

Glucose management should also be more cautious in patients with acute brain injury. Cerebral microdialysis studies have shown that neuroglycopenia and anaerobic metabolism can occur with glycemias between 60–80 mg/dL, which are levels often considered acceptable in other patients. We use insulin infusions in hyperglycemic patients but cautiously. Our target is generally to keep serum glucose between 140–180 mg/dL avoiding too tight control.

High positive end expiratory pressure (PEEP) can improve oxygenation in patients with sepsis complicated by acute respiratory distress syndrome. High PEEP is not contraindicated in patients with raised intracranial pressure, but the effect of gradual increases in PEEP on the intracranial pressure need to be carefully monitored.

Sedation should be guided by a protocol with a clear goal (e.g., a sedation level defined by the Richmond Agitation Sedation Scale, RASS) and scheduled drug interruptions. These sedation holidays allow us to follow the neurological examination and also reduce the incidence of delirium (see chapter 17). We must remember that opiates are excellent analgesic agents but will greatly confound the neurological examination. The confounding effect of opiates may be quite prolonged in elderly patients and those with liver or renal failure.

Our patient was promptly resuscitated with fluids and norepinephrine. Broad-spectrum antibiotics were started within 30 minutes of the onset of hypotension. The source of sepsis was eventually recognized to be ventilator associated pneumonia. Despite rapid control of the hypotension and adequate treatment of the infection, the brief hypotension proved too much for our patient. He remained stuporous and a repeat head CT scan four days later showed multifocal brain infarctions. This case illustrates that the brain is exquisitely sensitive to ischemia, particularly after a major initial insult such as SAH in our case.

Fever is ubiquitous in critically ill patients and central fever is even more common in patients with acute brain injury. Pancultures should be obtained including CSF when appropriate (meningitis may cause severe sepsis) Yet, when fever is accompanied by hypotension, patients should be rapidly treated for early sepsis following a comprehensive protocol. Any delay in reversing the situation may cause additional brain injury.

KEY POINTS TO REMEMBER REGARDING EARLY HYPOTENSION AND FEVER

Although components of the systemic inflammatory response syndrome (e.g., persistent fever, tachycardia), can be attributed to the brain injury in acute neurological patients, the occurrence of sudden hypotension and high fever should always activate a septic shock protocol.
The general principles of septic shock management are generally appropriate in patients with acute brain injury, but there are notable differences.
Obtain samples for pancultures immediately including CSF.
The brain is at risk for additional injury from systemic complications, and rapid fluid resuscitation, administration of vasopressors and inotropes, broad coverage with antibiotics, blood transfusion, and glucose control are essential first measures.

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