Predisposing factors
Precipitating factors
Dementia
Other cognitive impairment
History of delirium
Functional impairment
Visual impairment
Hearing impairment
Comorbidity or severity of illness
Depression
History of transients ischemia or stroke
Alcohol
Older age
Drugs
Physical restraints
Urinary catheter
Infection
Electrolyte imbalance
Metabolic acidosis
Iatrogenic event
Surgery
Trauma
Coma
Indeed the development of delirium is very often contingent on a complex interrelationship between these predisposing risks and precipitating factors, where those already vulnerable, perhaps because of having a number of predisposing factors, are exposed to a single (or multiple) precipitating factor(s). For example, a patient with dementia or other cognitive impairment may only develop delirium if they or when they are physically restrained to stop them wandering, are given a sedative agent at night-time or develop a urinary infection. It is extremely important to distinguish the predisposing elements here, often which we cannot control, from the much more controllable precipitating factors in order to provide adequate care and treatment.
14.6 Pathophysiology
Given the complex multifactorial causation and the probability that each individual episode of delirium has, a unique set of contributors, to isolate a single mechanism of delirium, is practically impossible. There is evidence amassing however highlighting how different sets of biological factors interacting can lead to acute cognitive dysfunction by interfering with large-scale neuronal networks. These include inflammation, metabolic imbalance, neurotransmitter derangement, physiological stressors, electrolyte imbalance and genetic abnormalities (Watt et al. 2013). We know that although delirium can occur at any age, children and older people are particularly vulnerable (Inouye et al. 2014); children obviously have less developed neuronal networks, and in older people they are more likely to have age-related damage to these networks, and so this further points favourably to the hypotheses that neuronal networks play a key role in the pathophysiology of delirium.
14.7 Diagnosis
The high prevalence and complex presentation of delirium means it is important that appropriate tools are used to aid in its diagnosis. Delirium is often unrecognised and easy to overlook (Inouye et al. 2014), and as mentioned above it is important not to class all confused or inappropriate behaviour as delirium, as much as it is important not to excuse delirious behaviour because the patient has an underlying cognitive impairment, psychiatric history or dementia. While some potential has been explored for the use of EEG of CT/MRI neuroimaging for the diagnosis of delirium, it shows low yield in unselected patients (Agency for Healthcare research and Quality 2013). There are a number of validated tools which can be applied to diagnose delirium. The NICE guidelines (2010) recommend using the DSM criteria as a basis for clinical assessment or alternatively using the Confusion Assessment Method (CAM) (Inouye et al. 1990). CAM is a 5-min questionnaire by which the present severity and fluctuation of nine delirium features are identified (Wong et al. 2010). The features tested are acute onset, inattention, disorganised thinking, altered level of consciousness, disorientation, memory impairment, perception disturbances, psychomotor agitation or retardation and altered sleep wake cycle. Based on the DSM criteria for delirium, the questionnaire is in the form of the algorithm and is quick and easy to administer. The step-by-step process first establishes the essential features which are sudden onset and fluctuating course as well as inattention. The latter part features a test to establish either disorganised thinking or altered level of consciousness. So essentially if you have the first two features and either (or both) of the latter, you are diagnosed as CAM positive and delirious. CAM is by far the most widely used assessment tool for delirium (Inouye et al. 2014) and has been adapted for use in several specialist settings such as ICU and emergency departments. CAM has also been adapted for use in nursing home patients (Dosa et al. 2007). The NH-CAM rearranges the minimum data set items which were previously used to identify delirium in nursing homes into a similar structure as the original CAM (Fig. 14.1). Other tools used include the Clinical Assessment of Confusion (Vermeersch 1990), the Global Attentiveness Rating (O’keefe and Gosney 1997) and the Delirium Observation Screening Scale (Schuurmans et al. 2003); however given its simplicity, efficiency, adaptability and efficacy, the best evidence supports the use of CAM (Wong et al. 2010). As with any tool, the quality of outcome is dependent on the ability of the user, and so it is important that adequate training is engaged to use such tools. Another important factor, especially in those with pre-existing cognitive impairment or dementia, is establishing their baseline cognitive ability. Families and carers can play a vital role in the diagnosis of delirium, and in fact the CAM has further been adapted to allow for families and carers to assess for signs of delirium CAM-ICU (Steis et al. 2012).
Fig. 14.1
Comparison of CAM and NH-CAM
14.8 Outcomes
Independently both dementia and delirium have a large impact effecting length of stay in hospital, healthcare costs, morbidity, mortality and loss of functional independence. These effects are amplified when DSD is considered; however, unfortunately the consequences of DSD remain a relatively neglected research area (Fick et al. 2005). While there is conflicting evidence in the data around DSD and mortality, there are strong suggestions that it can significantly add to risk of death (Bellelli et al. 2007). It has however been well established that delirium, as a stand-alone factor, has a significant impact on mortality (McCusker et al. 2002). DSD also has been found to have a significant impact on rehabilitation, mobility and functional independence. Morandi et al. (2014) have signified that DSD needs to be recognised by clinicians as a prognostic factor in rehab, reporting a significant negative effect on functional outcomes, as well as leading to institutionalisation of patients. A further study by Morandi et al. (2015a) considered the psychological and emotional impact of DSD on patients. The study reported increased anxiety, depression and low mood amongst people who had experienced DSD. O’Malley et al. (2008) found that the experiences of patients who had delirium could be grouped into three main themes, incomprehension and feelings of discomfort, the need to keep distance and to protect oneself, and interventions which diminish suffering. Delirium and DSD can also have a profound effect on family, caregivers and healthcare staff; an important note to take from Morandi et al. (2015b) is that while there were elements of distress in both the informal caregivers and healthcare staff, it was substantially higher in the informal carers.
14.9 Management of DSD
Determining and correcting the underlying cause of delirium is the primary intervention in managing DSD, but the symptoms of delirium must be managed until the delirium is resolved. In general, the management of DSD can be classified into the two categories of non-pharmacologic and pharmacologic interventions. Non-pharmacologic interventions are preferred as first-line approaches because the medications used to treat the symptoms of delirium may actually exacerbate or prolong its course.
14.9.1 Non-pharmacological Interventions
Non-pharmacologic interventions are aimed at eliminating and/or decreasing the extrinsic risk factors associated with the development of delirium as well as decreasing the intensity and length of delirium symptoms and focus on modifications of the environment and interactions with the patient. Adequate night-time sleep needs to be assured and can be optimised through minimal frequency of vital sign assessment overnight in stable patients, early morning phlebotomy scheduled for later morning and reduction of noise, light and staff activities during the night. Sensory deficits must be accommodated, and associated modifications include the use of large clocks and posting of orientation boards with current date and names of assigned staff, adjusting approaches to the patient to accommodate type of visual and/or hearing impairment (e.g. approach from unaffected side if unilateral deficit) and communicating with a slow, calming voice at appropriate loudness level and facing the patient at eye level. Although there is little documented research examining these interventions, their use has become standard practice due to experience, common sense and lack of adverse effects (American Psychiatric Association 2010). As noted in the NICE guidelines (2010) regarding the prevention of delirium, the issues of hydration, nutrition, oxygenation, pain, mobility and/or immobility, infection, and the effects of medications must also be addressed in the management of delirium.
The interactions of all staff and family members with the patient are of paramount importance, and it is vital that all are educated regarding the risks, signs, symptoms and management of delirium. It is equally important that family members be supported and involved in the interdisciplinary plan of care from the outset (NICE 2010). Reassurance of safety, validation, redirection of attention to nonthreatening topics, engaging in pleasant conversations or activities and maintaining interactions with the resident throughout the day to minimise under-stimulation or overstimulation are necessary. If the presence of family members is calming, it may minimise symptoms and improve sleep quality and should be encouraged; but, if the presence of family members causes or increases agitation, it will only exacerbate symptoms and should be discouraged and/or minimised.
The use of physical restraints is contraindicated due to association with increased agitation, increased risk of injury, increased risk of death and prolongation of delirium (Evans et al., 2003). If absolutely necessary, physical restraints should be used only for a very short term in only the most severe cases of psychomotor agitation where there is significant risk of injury to the resident or staff and only after all other alternatives have been exhausted (Salzman et al. 2008).