T. Medical / Nursing Management

Individuals with traumatic brain injury (TBI) present with a number of medical and nursing complications whose management has a significant impact on outcomes.

Medications should be considered in the context of the identified impairments while taking into account the concurrent advantage of the medication for other impairments (e.g. Epival for seizure prophylaxis and need for mood stabilization), as well as the potential for adverse effects.

Bladder and bowel incontinence is a common complication in as many as 62% of individuals with moderate to severe TBI but can be managed with a carefully planned program. Incontinence has a negative impact on quality of life and can influence caregiver burden.

Post-traumatic seizure is defined as an initial or recurrent episode not attributable to another obvious cause after TBI; they can be further defined as immediate (occurring within the first 24 hours), early (within the first week of injury) and late (after the first week). Prophylactic anti-seizure medications are helpful in preventing early seizures (first week) but are not indicated after one week. Anti-convulsants can routinely result in significant cognitive side effects, and so their use must be carefully monitored.

Deep venous thromboembolism is common in the context of immobility, lower limb paresis and multi-trauma. Deep vein thrombosis (DVT) and pulmonary emboli (PE) can contribute to a significant amount of morbidity and mortality, and prophylaxis, especially with low-molecular weight heparin (LMWH), can be safe and effective. The risk of developing a DVT in the absence of prophylaxis is estimated to be approximately 20% post TBI.

Neuroendocrine disorders, particularly hypopituitarism and growth hormone deficiencies are common particularly following moderate to severe injuries with 27-40% of patients having at least one deficiency and 10-15% with more than one deficiency. Endocrine abnormalities may not appear until 3-6 months post TBI and the gold standard for diagnosis is serum tests assessing hormonal function. Abnormalities of antidiuretic hormone and adrenal insufficiency are the most commonly reported abnormalities.

Heterotopic ossification (HO) is the formation of pathological bone within soft tissues, often muscles, where bone formation does not usually occur. It can symptomatically occur in 10-15% of patients and can be quite painful and limit joint mobility thereby impeding rehabilitation progress. Once developed, treatment of HO (usually surgical) can be challenging.

• JFK Coma Recovery Scale – Revised (CRS-R)
• Patient Health Questionnaire (PHQ-9)
• Generalized anxiety Disorder 7-item (GAD-7)
• Agitated Behaviour Scale
• Galveston Orientation and Amnesia test (GOAT)
• Deep Vein Thrombosis: Diagnostic (Clinical Guide) – Thrombosis Canada
• Guidelines for Management of Neurogenic Bowel Dysfunction in Individuals with Central Neurological Conditions
• Provincial guidelines for the management of epilepsy in adults and children – Critical Care Services Ontario Guideline 2015
• American Association of Clinical Endocrinologists – Guideline
• American Epilepsy Society Algorithm: Proposed Algorithm for convulsive Status Epilepticus from treatment of convulsive Status Epilepticus in children and adults (2016) Epilepsy currents. 16-1
• Example of Passive and Assistive Range of Motion Exercises
• Standardized urinary function retraining program
• Indications of use (Health Canada) and insurance coverage (for Quebec only) for the Pharmacological Management of TBI related Impairments

• Venous Thromboembolism (VTE) Pocket Cards
• Heterotopic Ossification – Craig Hospital

• Bladder re-education basic Information – Patient
• Mild Traumatic Brain Injury: Neuroendocrine Dysfunction – Defense Centers or Excellence

Some individuals acquire secondary medical complications post TBI. The management of excretory systems, seizure prevention, thrombosis, and heterotopic ossification requires extensive co-ordination between rehabilitation teams, caregivers and the patient. Treatments should be administered as soon as appropriate and should be given prophylactically, if possible.

Bladder and bowel function should be assessed shortly after admission. As many as 62% of patients with TBI experience incontinence on admission to rehabilitation (Chua, Chuo, & Kong, 2003). Urinary disturbances are associated with impaired cognitive functioning and motor difficulties (Moiyadi, Devi, & Nair, 2007). Fecal incontinence frequency has been shown to be correlated with the severity of brain injury (Foxx-Orenstein et al., 2003). Promisingly, a case series found that recovery of bowel and bladder function could predict favourable functional outcomes following a TBI (Kushner & Johnson-Greene, 2014). In general, antibiotic treatment of asymptomatic bacteriuria is not recommended but cognitive or physical deterioration could be considered as a complication of urinary tract infection (Colgan et al., 2006; Lin & Fajardo, 2008).

Following a TBI, patients are susceptible to developing seizures. When managing seizures there are several pharmacological treatments available; however, these carry the risk of adverse effects. Intramuscular midazolam has been shown to be effective for acute seizure cessation (Wroblewski & Joseph, 1992). In terms of seizure prophylaxis, phenytoin is the most commonly studied medication. Numerous studies have found phenytoin to be only as effective as a placebo (McQueen, Blackwood, Harris, Kalbag, & Johnson, 1983; Temkin et al., 1990; Young et al., 1983). The use of anticonvulsants for treatment of late post traumatic seizures has been shown to increase seizure occurrence (Formisano et al., 2007), and have longer hospital stays and worse functional outcomes (Bhullar et al., 2014). Phenytoin and levetiracetam have comparable efficacies in terms of seizure rates (Inaba et al., 2013; Kruer et al., 2013), complications (Jones et al., 2008), mortality rates (Inaba et al., 2013) and length of stays (Kruer et al., 2013). A meta-analysis by (Zafar, Khan, Ghauri, & Shamim, 2012) also concluded that there was no superiority of either drug at preventing early seizures. However, phenytoin use is associated with greater days of fever (Gabriel & Rowe, 2014), adverse reactions (Inaba et al., 2013), and worse neurological status (Szaflarski, Sangha, Lindsell, & Shutter, 2010).

The reader is referred to the ERABI for more detailed review https://erabi.ca/modules/module-10/.

Deep vein thrombosis (DVT) is a common complication following TBI; the risk of developing a DVT in absence of prophylaxis is estimated to be 20% after a TBI (Haddad & Arabi, 2012). Low-molecular weight heparin (LMWH) has been shown to reduce the risk of DVTs and PEs within the first 48 hours after injury (Glassner et al., 2013; Norwood, Berne, Rowe, Villarreal, & Ledlie, 2008). LMWH medications are also popular because they can be injected subcutaneously allowing for ease of administration and dosage adjustment; however, these drugs are expensive (Watanabe TK & MO., 2001). When comparing LMWH to low-dose unfractionated heparin (LDUH) in a mixed trauma population, a study found that patients receiving LDUH were more likely to experience DVT compared to those receiving LMWH (Geerts et al., 1996). Physical methods for venous thromboprophylaxis are still limited. One study found that sequential compression devices are not that effective in reducing the risk of developing DVT or pulmonary embolism after a TBI (Gersin et al., 1994). However, the use of compression stockings combined with LMWH has been shown to be more effective in preventing venous thromboembolism than stockings alone (Agnelli et al., 1998).

Endocrine disorders such as hypopituitarism can evolve over time post ABI; therefore, screening should be conducted as soon as possible. During the acute stage of recovery, cortisol levels of less than 7.2 µg/dL may indicate adrenal insufficiency (Bernard, Outtrim, Menon, & Matta, 2006). Treatment should also be considered and initiated in those cases where hyponatremia, hypotension and hypoglycemia are present and cortisol levels are between 7.2 and 18 µg/dL (Schneider, Kreitschmann-Andermahr, Ghigo, Stalla, & Agha, 2007). In the acute stage of recovery it is not necessary to assess growth, gonadal or thyroid hormones as there is no evidence to suggest that supplementation of these hormones during this phase is beneficial (Ghigo et al., 2005; Schneider et al., 2007); however, during the post recovery stage, at 3-6 months, a clinical assessment for hypopituitarism should be completed (Powner & Boccalandro, 2008; Powner, Boccalandro, Alp, & Vollmer, 2006; Schneider et al., 2007). This is especially important if any of the following symptoms are noted: loss of secondary hair, impaired sexual function, weight changes, polydipsia, or amenorrhea. Hormonal screening should include 0900 AM serum cortisol, fT3, fT4, TSH, FSH, LH, testosterone in men and E2 in women, prolactin, and Insulin-like Growth Factor (IGF-I). In patients with polyuria or suspected diabetes insipidus, urine density, sodium and plasma osmolality should also be evaluated. Low IGF-I levels strongly predict severe GH deficiency (in the absence of malnutrition). Normal IGF-I levels may be found in patients with GH deficiency; therefore, provocative tests are necessary in patients with another identified pituitary hormone deficit. Provocative testing is recommended if IGF-I levels are below the 25th percentile of age related normal limits (Ghigo et al., 2005).

Studies have found that following a TBI disruptions to salt and water levels can lead to inappropriate secretion of antidiuretic hormone (Doczi, Tarjanyi, Huszka, & Kiss, 1982; Makulski, Taber, & Chiou-Tan, 2008). Restricting fluid intake has proven effective, but studies are conflicting about the amount of fluid that should be limited; Doczi et al. (1982) suggest limiting daily fluid intake to less than 600 to 800 mL, whereas Born, Hans, Smitz, Legros, and Kay (1985)suggest limiting intake to 250 to 500 ml.

A review by Estes and Urban (2005) notes that for those who sustain a mild TBI, growth hormone deficiency has been identified during regular blood work, but no other symptoms have appeared. The authors suggest waiting 3 years post trauma before beginning treatment in attempt for the endocrine system to correct itself. However, if there is a clear indication of anterior or posterior pituitary dysfunction, consulting an endocrinologist is strongly recommended.

Heterotopic ossification (HO) is another common complication following TBI. Among individuals with TBI the most commonly sites of HO are the soft tissues around the hip, elbow, shoulder and knee (Garland, 1991; Garland, Blum, & Waters, 1980; van Kampen, Martina, Vos, Hoedemaekers, & Hendricks, 2011; Vanden Bossche & Vanderstraeten, 2005). The hip is the most frequent site of ossification (Dizdar et al., 2013; Vanden Bossche & Vanderstraeten, 2005), with total ankylosis of the joint occurring in 5-16% of affected hips (Stover, Niemann, & Tulloss, 1991). HO of the shoulder has been found to affect 5% of individuals with a brain injury (Cipriano, Pill, & Keenan, 2009), while the knee is a less common site for HO following a head injury (Sarafis, Karatzas, & Yotis, 1999). Of the joints affected by HO after head injury, ankylosis is most likely to occur in the posterior elbow (Garland et al., 1980). Triple phase technicium-99 bone scan is gold standard for diagnosing HO (Freed, Hahn, Menter, & Dillon, 1982).

Etidronate has been used as a prophylaxis for HO in other disease populations, but its use in TBI is understudied. A study found that Etidronate usage did significantly lower incidence of HO when compared to a control (Spielman, Gennarelli, & Rogers, 1983). Similar to Etidronate, the effects of nonsteroidal anti-inflammatory drugs (NSAIDS) as a prophylaxis are not well studied in the TBI literature.

There are few treatments for HO post ABI. Range of motion exercises are beneficial for treating HO post TBI. Studies have found that forceful manipulation is not only useful in maintaining motion but also aids in the prevention of bony ankylosis and does not appear to exacerbate the ossification process (Ellerin et al., 1999; Garland, Razza, & Waters, 1982; Garland & Varpetian, 2003). Anaesthesia may be needed to help differentiate between spasticity and ankylosis and to allow sufficient muscle relaxation to perform the joint manipulation (Garland & Varpetian 2003).

Surgical excision is also a treatment option for HO post ABI. A systematic review by Lee, Namdari, Hosalkar, Keenan, and Baldwin (2013) focused specifically on the surgical excision of HO in the elbow and found it resulted in improvements in range of motion with low levels of recurrence (14.3%). However, complications such as fracture, infection, nerve palsies, wound complications and loss of motion without recurrence were found in 27.5% of cases (Lee et al., 2013). In many studies, the recurrence of HO was evaluated months following the initial operation, with rates ranging from 0 to 27% (Fuller, Mani, & Keenan, 2013; Fuller, Mark, & Keenan, 2005; Ippolito, Formisano, Caterini, Farsetti, & Penta, 1999; Ippolito, Formisano, Farsetti, Caterini, & Penta, 1999; Moore, 1993). The majority of the studies did not specify what qualified as recurrence; however, a study by Kolessar, Katz, and Keenan (1996) found recurrence rates differed based on the classification system utilized (23.8% versus 4.8% using the Brooker classification and the Stover and colleagues classification, respectively). Overall, the surgical excision of HO resulted in improved range of motion, although, one study noted a decrease in range of motion for a small portion of participants (Ippolito, Formisano, Farsetti, et al., 1999). Improvements in activities of daily living and ambulation were also reported (Fuller et al., 2005; Ippolito, Formisano, Caterini, et al., 1999; Ippolito, Formisano, Farsetti, et al., 1999; Melamed et al., 2002). Although therapy was provided after the surgery in many of the studies, only one study formally evaluated its effectiveness; (Lazarus, Guttmann, Rich, & Keenan, 1999) found that patients who had continuous passive range of motion exercises post operatively made significantly greater gains compared to those individuals who did not (57.9° versus 24.1°, p=0.04).

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