This patient’s clinical presentation indicates an infection of the central nervous system (CNS) and systemic compromise, as signs of sepsis and septic shock are evident by the initial assessment performed in the ED. The initial evaluation of patients with a suspected CNS infection should include a detailed clinical history, assessment of epidemiologic fac-tors, risk factors for infection, and medical comorbidities. Initial neurologic assessment provides important prognostic information and allows for comparison of serial neurologic examinations. This patient should be isolated in the ED, and droplet precautions should be maintained until a final etiologic diagnosis is made. Following initial assessment and determination of a potential CNS infection, initial steps in the management of this patient should include an evaluation of the ABCs (airway, breathing, and circulation), assessment of the hemodynamic status, collection of blood and cerebrospinal fluid (CSF) samples, and initiation of appropriate antimicrobial therapy. Patients with suspected meningitis who present with abnormal mental status or neurologic deficits, especially those with a GCS of 12 or less, require intensive care unit (ICU) admission for observation (Table 7-1).
Airway
Rapid neurologic deterioration and ensuing loss of consciousness with impairment of reflexes that maintain the airway mandate permanent airway control (Table 7-2).1 Failure to recognize imminent airway loss may result in complications such as aspiration, hypox-emia, and hypercapnia. Preferred induction agents for rapid sequence intubation (RSI)
C h a p t e r
care
in the setting of suspected brain injury with high intracranial pressure (ICP) include propofol2 and etomidate,3 both of which are short-acting agents that will not obscure the neurologic examination for a prolonged period of time. Adverse effects of propofol include drug-induced hypotension that usually responds to fluid infusion.3 Adverse effects of etomidate include nausea, vomiting, myoclonic movements, seizures (by lowering of seizure threshold),3 and adrenal suppression.4 Midazolam may be an alternative, but unfavorable effects on the ICP have been reported with the use of this agent.2,5 Succinylcholine is the most commonly administered muscle relaxant for RSI owing to its rapidity of onset (30 to 60 seconds) and short duration (5 to 15 minutes).6 However, side effects of succinyl-choline include hyperkalemia, cardiac arrhythmias, exacerbation of neuropathy or myopathy, malig-nant hyperthermia, and elevation of ICP in patients with intracranial mass lesions.3,7 For this reason, in neurologic patients, a nondepolarizing neuromuscular blocking agent such as cis-atracurium,8 rocuronium,3 or vecuronium is preferred if needed.9 In patients with increased ICP, premedication with intravenous lidocaine for RSI is of questionable use but sometimes has been suggested.10
reathing
The goal of treatment is to ensure oxygenation and ventilation at an adequate oxygen level and main-tenance of normocarbia, as this is associated with good effects on the cerebral blood flow (CBF). Both hypoxia and hyercarbia are detrimental for the CBF and have the potential for increasing cerebral edema and development of high ICP (Figure 7-1).11
circulation
Isotonic fluid resuscitation and vasopressors are indicated for brain-injured patients in shock.12,13 Dextrose-containing solutions should be avoided as hyperglycemia may be detrimental to the table -1. ndications for C admission
e de n e
n e n en de e ed
n d e den e n ede nd d ne d e
e ne de de e n de e e e en
e e e n
e nd e e need e n en n
Abbreviation: GCS, Glasgow Coma Scale.
table -2. ndications for ntubation (permanent air ay)
In e
e e
In n e e n e en
xe nd ed en n e e
In e ed e n
eed e e e d n e ed ne e n n e n n e
injured brain.14 Initial assessment of the volume status by placement of a central venous catheter for measurement of central venous pressure (CVP) is recommended by current Surviving Sepsis Cam-paign Guidelines to achieve a CVP of 8 to 10 mm Hg and a goal mean arterial pressure (MAP) of 65 mm Hg or more with crystalloids, colloids, or vasopressors.13 The influence of such treatment on the CBF of these patients is unknown. In the healthy person, cerebral autoregulation maintains a con-stant CBF with MAP ranging from 60 to 130 mm Hg. However, when autoregulation is impaired, as it may in severe CNS infections, there is a risk of cerebral hypoperfusion as well as ischemia when MAP decreases, and a risk of hyperperfusion leading to vasogenic edema when MAP increases. An associa-tion between cerebral ischemia and poor neurologic outcome or death has been demonstrated in vari-ous studies of bacterial meningitis.15,16 Cerebral perfusion pressures (CPPs) less than 30 mm Hg were strongly correlated with death or major neurologic sequelae in infants and children with meningitis.17 Taken together, these findings suggest that maintenance of an adequate CPP, primarily by manipulat-ing MAP, would prevent cerebral ischemia, attenuate brain damage, and improve the prognosis.
Dopamine, norepinephrine, and phenylephrine are frequently used to restore CPP by increasing the MAP in the ICU. Selection of the initial vasopressor is frequently guided by the clinical character-istics of the patient as well as the goals of therapy. Consideration should be given to the effect of vaso-pressors on cerebral hemodynamics (Table 7-3). The disruption of the blood-brain barrier (BBB) in Figure -1. Effect of blood gases on cerebral blood flow (CBF) and intracranial pressure (ICP). (Adapted from Miller RD, et al. Miller’s Anesthesia, 7th ed, page 308.)
0 50 100
Pao2, Paco2, MAP (mm Hg)
CBF (mL/100 g/min)
100
75
50
25
0
150 200
PaO2 PaCO2 MAP
table -3. hemodynamic effects of asopressors on Cerebral Circulation
Drug Mechanism CBF Cp CMrO pbto
en e ne e e n
e ne ne xed e e e n
ne ne xed e n
ne e de enden n d e
e n e e n
Abbreviations: CBF, cerebral blood flow; ICP, intracranial pressure; CMRO2, cerebral metabolic rate of oxygen; PbtO2, brain tissue oxygen tension. (Adapted with premission from Muzevich KM and Voils SA. Role of vasopressor administration in patients with acute neurologic injury. Neurocrit Care 2009;11:112-119.)
care CNS infections may allow for these agents to have direct effects on the cerebral vasculature, although this may be theoretical. Several studies have demonstrated that norepinephrine may increase the CBF with no net effect on ICP, global cerebral metabolism, and oxygen consumption, suggesting that the net effect on CBF is related to abnormal autoregulation (Table 7-3).18 Both norepinephrine and dopa- mine have been recommended as first-line vasopressors in patients with septic shock; however, a recent study showed less side effects when using norepinephrine, making this the agent of choice in septic shock.19