Dysphagia

• Problems - Common oropharyngeal swallowing problems following TBI include delayed or absent pharyngeal swallow reflex, reduced tongue control, pharyngeal residue, and aspiration (Hoppers & Holm, 1999)

• Causes - Nervous system damage and related complications:
  • Decreased cognition, such an a decreased ability to follow instructions, impaired judgment as to the amount and rate of intake, and limited control of impulsivity
  • Motor control defects in the swallowing process from impaired reflexes and injury of nerves, nuclei, and/or receptors, that can cause disruption in the 4 swallowing phases: oral preparatory phase, oral phase, pharyngeal phase, and esophageal phase

• Incidence - Dysphagia is common after severe head injury (Schurr, et al 1999), between 27%-42% in the acute rehabilitation setting (Hoppers & Holm, 1999)

• Diagnosis (performed by or in conjunction with the speech-language pathologist)
  • Bedside swallowing assessment
    • Chart review for medical problems
    • History of swallowing problems
    • Observation of palate at rest; rise, if any, of the larynx on dry swallows; condition of the mucosa and dentition; and language and mental status
    • Detailed orofacial sensory and motor examination, particularly of cranial nerves V, VII, IX, X, and XII
    • Cursory voice and speech analysis
  • Video fluoroscopy (modified barium swallow study (MBS)), performed by a speech-language pathologist, is the objective method of choice (Hoppers & Holm, 1999), for abnormalities, such as:
    • Prolonged, delayed, or absent swallowing reflex
    • Bolus entering the hypopharynx before swallow was initiated
    • Pooling in the valleculae or piriform
    • Swallow mechanism triggered at the piriform sinus
    • Aspiration, including "silent" aspiration in which there is no cough
    • Reduced pharyngeal peristalsis
  • Fiberoptic endoscopic evaluation of swallowing (FEES) is particularly reliable for aspiration and pharyngeal residue and can be used in conjunction with MBS (Hoppers & Holm, 1999) and to make recommendations for oral or nonoral feeding in patients with acute TBI (Leder, 1999)
  • Ultrasound to visualize swallowing
  • Manometry to assess pressure dynamics of the pharynx, or manufluorography
  • Scintigraphy, electroglottography, and electrography

• Treatment involves a multidisciplinary team management program, and includes:
  • "Direct" therapy, in which food and liquids are used together with facilitation and compensation
  • "Indirect" therapy in which no food or liquid is used, such as oral desensitization, muscle reeducation, cognitive perceptual training, proper positioning, and/or adapted feeding devices

Stress Ulceration (gastritis or duodenitis) and gastrointestinal bleeding are common GI complications following TBI

• Causes - May occur, particularly following severe TBI and in minimally responsive patients, within 12 hours postinjury, due to increased vagal activity and increased ICP which results in increased acid secretion.  There is also a possible high prevalence of Helicobacter pylori infection following TBI which warrants screening (Shem & Englander, 1998)

• Treatment
  • Drugs which may increase susceptibility to mucosal damage should be prescribed with caution, such as nonsteroidal anti-inflammatory drugs, anticoagulants, steroids, and aspirin
  • Histamine-2 blockers, such as Zantac, Axid, or Pepcid, or antacids can prevent high acidity, but may increase susceptibility to infection
  • Sucralfates, a nonacid form of prophylaxis, and Omeprazole (Prilosec), which blocks acid production, are possible alternatives

Decreased Gut Motility is probably caused by damage to cranial nerve X, which causes decreased vagal tone and loss of pressure gradient, and by increased ICP, cytokines, interleukin-1, and certain medications following TBI. Decreased motility can lead to:

• Gastroesophageal Reflux, which is fairly common following TBI, and is:
  • Exacerbated by decreased consciousness and gastrostomy or nasogastric tubes
  • Treated with cisapride (Propulsid), preferably, or with metzclopramide (Reglan)

• Constipation, which is common following TBI due to lack of mobility, medications, and diet changes, and is treated with stool softeners, suppositories, and adequate hydration

• Gastroparesis, a delay in gastric emptying into the small bowel, can occur in minimally responsive patients at about 1 week postinjury
  • Signs include abdominal pain, nausea, vomiting, and intolerance of feedings
  • Treatment is traditionally with metzclopramide. However, cisapride may be preferred, due to the concern over the antagonism of central dopamine receptors with metzclopramide. Erythromycin may also facilitate gastric emptying, but cause upper abdominal pain, bloating, nausea, or diarrhea

Increased Gut Motility is less common that decreased motility, but can cause diarrhea, particularly in low-level brain-injured patients on enteral feedings, malnourished patients, and patients on certain medications or with bacterial, viral, or parasitic infections. Diarrhea requires:

• Diligence in monitoring skin integrity, electrolyte imbalances, malabsorption syndromes, and severe dehydration
• Supplemental fiber and possibly drugs such as codeine or Lomotid

Hepatic Complications, specifically increased values on liver function tests, are very common following TBI and are due, in almost all cases, to medications, particularly anticonvulsants and antispasmodics, but may be due to increased hepatic conjunctive metabolism or infection, such as hepatitis