Management of Dysphagia Following Traumatic Brain Injury

Alison A. Howle 0 1 Ian J. Baguley 0 1 Louise Brown 0 1 0 L. Brown School of Public Health, Tropical Medicine and Rehabilitation Sciences, James Cook University , Townsville, Australia 1 A. A. Howle I. J. Baguley (&) Brain Injury Rehabilitation Service, Westmead Hospital, University of Sydney , PO Box 533, Wentworthville, Sydney, NSW 2145, Australia Dysphagia is a common morbidity and cause of mortality following traumatic brain injury (TBI). Despite this, there is a paucity of evidence demonstrating the efficacy of dysphagia management strategies and treatments in this population. Typically, subjects with dysphagia following TBI are placed into non-specific 'neurogenic' dysphagia subject groups, which include subjects with degenerative neurological diseases, neurological cancers, and cerebrovascular accident. However, dysphagia following TBI has a multifactorial presentation, with causative and contributory factors including cognitivecommunication, behavioral, neurological, and mechanical issues. As such, the management for dysphagia post-TBI must be multifactorial, team-based and involve the patients' families and carers. Much of the research regarding the management and treatment of dysphagia in general is in its infancy: larger and more rigorous studies are required to demonstrate treatment efficacy. More studies specifically examining dysphagia and its management in the TBI population are required to ensure the future efficacy and accuracy of treatment. - Traumatic brain injury (TBI) and its complications contribute significantly to mortality and morbidity worldwide. In developed countries, the annual incidence rates are approximately 200 per 100,000 [1]. The greater the severity of TBI, the greater the economic burden on healthcare providers [2, 3], particularly acute care and rehabilitation services. Dysphagia is a common complication following TBI, with an incidence as high as 93 % in patients admitted to brain injury rehabilitation [4]. Dysphagia following TBI can be multifactorial, but mainly occurs because of neurological impairment to any or all of the three phases of swallowing (the oral preparatory, the oral and pharyngeal phases) and cognitive-communication and behavioral dysfunction [59]. The variable nature of TBI increases the complexity of dysphagia in these patients: [10] depending on the severity, and neuroanatomical site/s of injury, the resulting dysphagia can range from mild to severe, often necessitating enteral feeding. The complications from dysphagia are varied, costly and potentially fatal. Patients with TBI and dysphagia have longer average hospital admissions compared to those without dysphagia [11] and are at risk of weight loss, malnutrition and dehydration [12]. Dysphagia is causally linked with an increased risk of aspiration pneumonia; [1316] the incidence of which can be as high as 12 % following severe TBI [14]. The social and psychological impacts of dysphagia can reduce patients quality of life [17]. Post-discharge from rehabilitation, patients with TBI can be 79 times more likely to die from aspiration pneumonia compared to the general population [18]. Few studies have specifically assessed dysphagia following TBI. Studies of neurogenic dysphagia typically include heterogeneous subject groups, including subjects with cerebrovascular accident (CVA), progressive neurological diseases, brain tumors as well as TBI [19, 20]. Some studies involving TBI subjects even include other subjects with head and neck cancers [21] and dysphagia due to other structural/anatomical issues [22]., The majority of research into neurogenic dysphagia has, however, focused on subjects with CVA [23, 2427]. However, CVA and TBI populations are quite different. First, the pathophysiology of injury is dissimilar: CVArelated damage is usually focal whereas lesions in TBI represent a complex mixture of focal injury combined with diffuse axonal injury (DAI), with or without hypoxic injury. Thus, quite different neuromuscular and sensory deficits may present in each population [23]. Second, population demographics are different, with CVA more common in older patients with degenerative co-morbidities. In contrast, TBI is frequently sustained by healthy, young males [28]. Third, post-TBI cognitive-communication and behavioral deficits contribute to or cause dysphagia [5, 6, 29]. This is particularly the case with patients with severe DAI who experience abnormal arousal, attention and cognitive issues [10]. Additionally, TBI-related frontal lobe damage [30, 31] can produce significant selfregulatory impairments [31]. Fourth, it has been suggested that post-stroke oromotor features of dysphagia differ from those following TBI [23, 32]. Finally, patients with TBI may have concomitant injuries to the head and neck areas and/or necessitate prolonged endotracheal ventilation. All of these potential differences suggest that TBI-specific assessment and management of dysphagia should be recognized, along with the influence of these factors on the clinical management of such patients. Dysphagia Resulting from TBI Post-TBI dysphagia is caused and influenced by a number of factors. These include oropharyngeal neuromuscular and sensory deficits, cognitive-communication, and behavioral impairments, [5, 8, 9, 29, 33] physical injury to the head and neck regions [12], medications [5, 34], other concomitant injuries and prolonged endotracheal ventilation [12, 3439]. Tracheostomies, while not causing dysphagia on their own [3739], are common in this population and will also be discussed. Cognitive-Communication and Behavioral Issues Early TBI studies revealed that the most prevalent issue interfering with swallowing function was reduced cognition, followed by motor-control impairments [6]. In patients with normal or near normal swallowing physiology, these cognitive-communication and behavioral issues actually cause or worsen the dysphagia [40]. The strong relationship between cognition and safe oral feeding is reported frequently. [6, 8, 9, 33, 41, 42] For example, lower admission scores on the Ranchos Los Amigos (RLA) scale are a risk factor for dysphagia [41, 42] and that as cognitive function improves, so do functional oral feeding skills, [6, 29, 41, 42] such that RLA scores represent the most significant independent predictor of the time to return to full oral feeding [29]. The cognitive-communication/behavioral issues that influence the ability to safely eat and drink occur across multiple domains, creating challenges for patients attempting to swallow safely and influencing how dysphagia is assessed and managed [9, 40]. For example, postTBI attentional impairments mean that some patients may be so impaired that they are unaware of food in front of them [8, 9]. Low alertness levels can slow the triggering of the pharyngeal swallow [40]. Highly distractible patients may slow their rate of intake so they eat and drink less [40], placing them at risk of malnutrition (...truncated)