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CHAPTER 15: Long-Term Outcomes After Critical Illness 111

Posttraumatic stress disorder is the development of characteristic years after hospital discharge. To date, 15 cohorts 9,30,128-134 comprising
symptoms that occur following a traumatic event(s) where triggers more than 950 patients have examined neurocognitive outcomes fol-
include a serious personal threat experienced with helplessness and lowing critical illness. The neurocognitive domains that are impaired
intense fear. The diagnostic criteria include a history of traumatic in ICU survivors may depend on the nature of the insults experienced
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event(s) accompanied by symptoms from each of three symptom clusters: during critical illness and its treatment, as well as the presence of pre-
hyperarousal symptoms, intrusive recollections, and avoidant/numbing existing neurologic abnormalities, and individual vulnerabilities such
symptoms. A number of studies have examined relationships between as older age, or comorbid disorders that might render specific domains
life-threatening critical illnesses and its treatment and the development more vulnerable to critical illness–induced brain injury. Neurocognitive
of PTSD. Schelling and colleagues were the first to introduce the concept impairments in survivors of critical illness occurred in 100% of patients
of PTSD resulting from critical illness and ICU treatment to the critical at hospital discharge and persisted in large numbers of patients at
care community. These authors evaluated HRQoL and PTSD in a cohort 2 months, 6 months, 135,136 9 months, 1 year, 9,137,138 2 years, and
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of 80 ARDS survivors 4 years following discharge from the ICU. Almost 6 years. 139,140 Neurocognitive impairments appear to improve during
one-third of the ARDS survivors reported impaired memory, bad dreams, the first 6 to 12 months posthospital discharge. The neurocognitive
anxiety, and sleeping difficulties after ICU discharge, with a prevalence impairments are often long lasting and quite severe, and many patients
rate of PTSD of 28%. PTSD was related to the number of adverse ICU- continue to experience significant chronic neurocognitive impair-
related memories recalled by patients. Kapfhammer and colleagues found ments, years after ICU discharge. For example, ARDS patients with
2,30
that 44% of critically ill patients developed PTSD at hospital discharge and neurocognitive sequelae all fell below the 6th percentile of the normal
24% had PTSD symptoms 8 or more years later. Further, 14% of medical distribution of neurocognitive functioning, with significant deficits in
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ICU patients with mechanical ventilation developed symptoms of PTSD. wide-ranging cognitive domains including memory, executive function-
A review by Davydow and colleagues found the median point prevalence ing, and mental processing abilities. 28
of questionnaire-ascertained “clinically significant” PTSD symptoms was While the majority of studies to date have excluded patients with
22%, and the median point prevalence of clinician-diagnosed PTSD was prior neurocognitive impairments using chart review and administra-
19% in populations of general critically ill patients. Prior psychopathol- tion of dementia screening instruments, it is not clear whether critical
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ogy, greater ICU benzodiazepine administration and post-ICU memories illness and/or its treatment is the cause of the observed neurocognitive
of in-ICU frightening and/or psychotic experiences were consistent pre- impairments or if it merely worsens preexisting comorbid disorders.
dictors of post-ICU PTSD. They noted from their review that female sex A recent longitudinal cohort study in older adults who did not
and younger age were less consistent predictors, and severity of critical ill- have premorbid neurocognitive impairments or premorbid dementia
ness was consistently not a predictor. Post-ICU PTSD was associated with assessed neurocognitive function prior to and following an acute care
substantially lower HRQoL. The prevalence in ARDS patients appears to or ICU hospitalization. Individuals who underwent acute care or
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be higher with psychiatrist-diagnosed PTSD prevalence at hospital dis- critical illness hospitalization had a greater decline in neurocognitive
charge, 5 and 8 years were 44%, 25% and 24% respectively. Memory for function and new incident dementia compared to individuals who
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nightmares or delusions while in ICU as well as a complete absence of any were not hospitalized. This finding suggests that the acute or critical
ICU memories have also been perceived as traumatic events. 119 illness may cause an abrupt decline in neurocognitive function that is
The etiology of psychiatric disorders following critical illness may not due to premorbid neurocognitive problems. A second study in sep-
be due to sequelae of brain injury sustained from critical illness and/ sis patients confirms these findings. The Health and Retirement Study
or its treatments, a psychological reaction to the emotional and physi- followed more than 27,000 older Americans, for whom neurocogni-
ological stress of critical illness, or both. Factors such as medications, tive function was assessed both before and after sepsis. Patients with
5
physiological changes, pain, altered sensory inputs, and an unfamiliar severe sepsis developed new, substantial, and persistent neurocogni-
environment are all potential contributors to the development of psychi- tive impairment. Thus, factors associated with acute or critical illness
atric sequelae. 120-122 A recent review article found an association between may be causally related to neurocognitive decline in older critically
recall of delusional memories after ICU discharge and PTSD-related ill patients. 5,142 An important addition to this literature comes from
symptoms, depression, and anxiety. Factual memories do not seem Pandharipande and colleagues which clearly showed that a broad case
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to protect survivors from experiencing symptoms of PTSD. A study by mix of ICU survivors had important neurocognitive dysfunction com-
Myhren et al, which evaluated 194 patients, found that 27% had symp- parable to that of mild dementia or moderate traumatic brain injury at
toms of posttraumatic stress and predictors of PTSD were higher educa- 1 year after their critical illness. This cognitive disability was present
tion level, optimism, factual recall, and memory of pain. 124 in all age groups. 6
While we are just beginning to appreciate how longstanding and
debilitating psychiatric disorders are following critical illness and the Pathophysiologic Mechanisms of Neurocognitive Impairments: Data
important contribution they have to decreased HRQoL and functional regarding potential mechanisms of neurocognitive impairments
outcomes, recent studies are beginning to investigate potential inter- are increasing as we conduct more long-term outcome studies that
ventions to prevent or reduce psychiatric sequelae. One review paper inform linkages to ICU or patient level risk factors. The etiology of
suggests that corticosteroid administration may be protective post-ICU neurocognitive impairments is undoubtedly multifactorial and due
PTSD. A novel study that used ICU diaries in critically ill patients to a spectrum of factors that interact dynamically with premorbid
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suggests the diaries may reduce the incidence of PTSD. Jones and col- and genetic variables to produce adverse outcomes. Current data
leagues conducted a randomized, controlled trial, where patients were suggest that unfavorable neurocognitive sequelae are not related
provided with an ICU diary that contained information and photo- to illness severity scores, medical data, age, smoking, or alcohol
graphs from their ICU stays. Of the patients who received the diary abuse. For example, neither ICU length of stay, Acute Physiology
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only 5% had clinically significant PTSD symptoms, compared to 13% and Chronic Health Evaluation II (APACHE II) scores, duration
of controls. Further, the patients who experienced the greatest benefit of mechanical ventilation, tidal volume, or days receiving sedative,
from the ICU diary intervention were those who had substantial early narcotic, or paralytic medications are associated with neurocogni-
PTSD symptoms. 126 tive impairments in critically ill patients. 28,136 Thus, the neurocogni-
tive impairments experienced by ICU survivors cannot simply be
■ NEUROCOGNITIVE IMPAIRMENTS explained in terms of the degree of acute illness severity. Possible
pathophysiologic mechanisms include hypoxemia, sedatives or
9
Critical illnesses and their associated treatments can and frequently do analgesics, hypotension, delirium, hyperglycemia, and sep-
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result in de novo neurocognitive impairments 1,28,127 that may persist for sis and inflammation. 145

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