# 10 - SECTION 3 Neurologic Critical Care

## SECTION 3 Neurologic Critical Care

function and HF are at substantially elevated SCD risk, only ~20% of 
all SCDs occur in patients with poor left ventricular function. Most 
SCDs occur in individuals with preserved ventricular function who 
would not qualify for a primary prevention ICD. Although SCD rates 
are elevated compared to the general population, the absolute SCD 
risk in patients with CHD or HF who have an LVEF >35% is not high 
enough to warrant consideration of ICD therapy. While the incidence 
of SCD is lower in patients with preserved LVEF, SCD accounts for 
a greater proportion of cardiac deaths, and active efforts are being 
made to advance SCD risk stratification in this segment of the 
population. However, at present, SCD prevention primarily involves 
cardiac risk factor modification and standard medical therapy for the 
underlying condition.

Preventing Sudden Death in the General Population 
Only 
about one-half of men and one-third of women who suffer SCA are 
recognized to have heart disease prior to the event, and only half 
have warning symptoms prior to the event. SCD often occurs with­
out warning as the first manifestation of cardiac disease. In order 
to prevent these SCDs, preventive interventions would need to be 
employed broadly to the general population. Although several risk 
scores have recently been developed with the intent to stratify SCD 
risk in low-risk populations, the clinical utility to date is limited by 
the low absolute incidence of SCD, which is estimated to be only 
50–90 per 100,000 in the general adult population. Therefore, cur­
rent efforts aimed at preventing SCD in general populations primar­
ily focus on modification of the SCD risk factors outlined previously. 
Individuals who adhere to a low-risk, healthy lifestyle that includes 
avoidance of smoking, maintaining a healthy body weight, par­
ticipating in moderate exercise, and a Mediterranean-type dietary 
pattern have markedly lower rates of SCD. A substantial number of 
SCDs are likely to be preventable through lifestyle modifications and 
treatment of risk factors.
PART 8
Critical Care Medicine
■
■FURTHER READING
Al-Khatib SM et al: 2017 AHA/ACC/HRS guideline for management 
of patients with ventricular arrhythmias and the prevention of sud­
den cardiac death: a report of the American College of Cardiology/
American Heart Association Task Force on Clinical Practice Guide­
lines and the Heart Rhythm Society. J Am Coll Cardiol 72:e91, 2018.
Callaway CW et al: Part 8: Post-cardiac arrest care: 2015 American 
Heart Association guidelines update for cardiopulmonary resus­
citation and emergency cardiovascular care. Circulation 132:S465, 

2015.
Dankiewicz J et al: Hypothermia versus normothermia after out-ofhospital cardiac arrest. N Engl J Med 384:2283, 2021.
Deo R, Albert CM: Epidemiology and genetics of sudden cardiac 
death. Circulation 125:620, 2012.
Marijon E et al: Lancet Commission to reduce the global burden 
of sudden cardiac death: A call for multidisciplinary action. Lancet 
402:883, 2023.
Merchant RM et al: Part 1: Executive summary: 2020 American 
Heart Association guidelines for cardiopulmonary resuscitation and 
emergency cardiovascular care. Circulation 142:S337, 2020.
Myerburg RJ et al: Pulseless electric activity: Definition, causes, 
mechanisms, management, and research priorities for the next 
decade: Report from a National Heart, Lung, and Blood Institute 
workshop. Circulation 128:2532, 2013.
Perman SM et al: 2023 American Heart Association focused update on 
adult advanced cardiovascular life support: An update to the Ameri­
can Heart Association Guidelines for cardiopulmonary resuscitation 
and emergency cardiovascular care. Circulation 149:e254, 2024.
Zeppenfeld K et al: 2022 ESC guidelines for the management of 
patients with ventricular arrhythmias and the prevention of sudden 
cardiac death. Eur Heart J 43:3997, 2022.

Section 3	 Neurologic Critical Care
J. Claude Hemphill, III, Wade S. Smith, 

S. Andrew Josephson, Daryl R. Gress

Nervous System 

Disorders in Critical Care
Life-threatening neurologic illness may be caused by a primary 
disorder affecting any region of the neuraxis or may occur as a con­
sequence of a systemic disorder such as hepatic failure, multisystem 
organ failure, or cardiac arrest (Table 318-1). Neurologic critical care 
focuses on preservation of neurologic tissue and prevention of second­
ary brain injury caused by ischemia, hemorrhage, edema, herniation, 
and elevated intracranial pressure (ICP). Encephalopathy is a general 
term describing brain dysfunction that is diffuse, global, or multifocal. 
Severe acute encephalopathies represent a group of various disorders 
due to different neurologic or systemic etiologies but that share the 
common themes of primary and secondary brain injury.
■
■PATHOPHYSIOLOGY
Brain Edema 
Swelling, or edema, of brain tissue occurs with many 
types of brain injury. The two principal types of edema are vasogenic 
and cytotoxic. Vasogenic edema refers to the influx of fluid and solutes 
into the brain through an incompetent blood-brain barrier (BBB). In 
the normal cerebral vasculature, endothelial tight junctions associated 
with astrocytes create an impermeable barrier (the BBB), through 
which access into the brain interstitium is dependent upon specific 
transport mechanisms. The BBB may be compromised in ischemia, 
trauma, infection, and metabolic derangements, and typically devel­
ops rapidly following injury. Cytotoxic edema results from cellular 
swelling, membrane breakdown, and ultimately cell death. Clinically 
significant brain edema usually represents a combination of vasogenic 
and cytotoxic components. Edema can lead to increased ICP as well as 
tissue shifts and brain displacement or herniation from focal processes 
(Chap. 30). These tissue shifts can cause injury by mechanical disten­
tion and compression in addition to the ischemia of impaired perfusion 
consequent to the elevated ICP.
Ischemic Cascade and Cellular Injury 
When delivery of sub­
strates, principally oxygen and glucose, is inadequate to sustain cel­
lular function, a series of interrelated biochemical reactions known 
as the ischemic cascade is initiated (see Fig. 437-2). The release of 
excitatory amino acids, especially glutamate, leads to influx of calcium 
and sodium ions, which disrupt cellular homeostasis. An increased 
intracellular calcium concentration may activate proteases and lipases, 
which then lead to lipid peroxidation and free radical–mediated cell 
membrane injury. Cytotoxic edema ensues, and ultimately necrotic 
cell death and tissue infarction occur. This pathway to irreversible cell 
death is common to ischemic stroke, global cerebral ischemia, and 
traumatic brain injury.
Penumbra refers to areas of ischemic brain tissue that have not 
yet undergone irreversible infarction, implying that these regions are 
potentially salvageable if ischemia can be reversed. Factors that may 
exacerbate ischemic brain injury include systemic hypotension and 
hypoxia, which further reduce substrate delivery to vulnerable brain 
tissue, and fever, seizures, and hyperglycemia, which can increase cellu­
lar metabolism, outstripping compensatory processes. Clinically, these 
events are known as secondary brain insults because they lead to exacer­
bation of the primary brain injury. Prevention, identification, and treat­
ment of secondary brain insults are fundamental goals of management.
An alternative pathway of cellular injury is apoptosis. This process 
implies programmed cell death, which may occur in the setting of 
ischemic stroke, global cerebral ischemia, traumatic brain injury, and