Moderate-to-Severe Traumatic Brain Injury in Children
Moderate-to-Severe Traumatic Brain Injury in Children
Dysautonomia is estimated to affect about one third of patients after moderate to severe TBI in the first few weeks after brain injury. The constellation of symptoms includes tachycardia, hyperthermia, diaphoresis, muscle over-reactivity, increased respiratory effort or rate, hypertension, and pupillary dilatation. This response is commonly referred to by numerous names such as brain or thalamic storming, autonomic dysreflexia, and, more recently, paroxysmal sympathetic hyperactivity (Perkes, Baguley, Nott, & Menon, 2010). These symptoms may be incorrectly identified as narcotic withdrawal. The incidence of a triad of symptoms, namely hypertension, dystonia, and diaphoresis, has been studied and found to be associated with poorer outcomes, possibly from secondary brain injury from the hypermetabolic state or elevated sympathetic tone. These symptoms reflect increased sympathetic nervous system activity resulting from hypothalamic-pituitary dysfunction and are more likely to occur after hypoxic/ischemic events. Compared with injured children who do not have dysautonomia, children with dysautonomia required longer rehabilitation and had less improvement in WeeFIM motor skills scores (Kirk et al., 2012). Therefore, effective management of dysautonomia is especially critical. In addition to strategies such as environmental controls to reduce noxious stimuli, pharmacologic management includes the use of benzodiazepines, opioid antagonists, beta-blockers (e.g., propranolol), central dopamine agonists (e.g., bromocriptine), dopamine antagonists (e.g., chlorpromazine), and alpha-agonists (e.g., clonidine; Kirk et al., 2012, Perkes et al., 2010). Eventual resolution of the symptoms typically occurs, and medications are tapered as tolerated.
After TBI, children are at increased risk for posttraumatic seizures. Early posttraumatic seizures may occur in the first 7 days, whereas late seizures occur after 1 week. Prophylaxis antiepileptic drug (AED) therapy is often prescribed for a minimum of 7 days. In the literature, there appears to be a debate as to which AED is most effective (Bansal et al., 2014, Chung and O'Brien, 2014, Liesemer et al., 2011). Levetiracetam and phenytoin are frequently used for early AED prophylaxis. Levetiracetam is well tolerated and eliminates the need for obtaining serum drug levels, although phenytoin is less costly. More studies are needed to determine the most effective AED for prevention of posttraumatic seizures. Regardless of prophylaxis, monitoring for seizures to prevent secondary injury from further trauma, hypoxemia, or increased metabolic demand is imperative.
Dysphagia related to cerebellar dysfunction may result in impaired oral motor skills of injured children. The four stages of swallowing (oral preparatory, oral, pharyngeal, and esophageal) must work in concert to transition a bolus of food from the anterior to the posterior oropharynx and prevent airway aspiration. Aspiration may be silent or chronic, resulting in pulmonary issues such as pneumonia or wheezing with respiratory compromise. Under the guidance of a speech language pathologist, radiographic imaging via a rehabilitation swallow study should assess oral motor transit of a food bolus, as well as thick to thin fluids. The results of the assessment determine strategies to facilitate advancement in oral feedings. Compensatory strategies are often utilized, such as texture modification of thick liquids or solids with honey or nectar, in addition to maneuvers such as head position or tucking the chin. Research has shown that these functional modifications will improve swallowing biomechanics for the short term (Miller, 2011). In addition to traditional compensatory techniques, recent approaches to treatment of swallow dysfunction have included use of electrical stimulation for modulation of neuronal systems affecting swallowing function. Trained speech language pathologists apply electrodes to the skin at the oropharyngeal neuromuscular junctions to deliver pulses of electrical stimulation to the muscles needed for swallowing in conjunction with ingestion of food or liquids (Doeltgen and Huckabee, 2012, Miller, 2011). Oral motor integrity plays an integral part in the ability to manage oral secretions as well. Until adequate oral nutrition is provided, alternative tube feeding options, such as nasogastric, nasojejunal, or gastrostomy feeding, are maintained to meet nutritional and caloric requirements and provide daily maintenance of fluid volumes.
Deep vein thrombosis, which is less common in the uninjured pediatric population (O'Brien, 2012), is a frequent complication of TBI. Risk increases for multi-trauma patients, who are more likely to have hemodynamic instability resulting in vascular stasis, coagulopathic states, infections, and the use of invasive hemodynamic monitoring catheters such as central venous access. Comorbidities of extremity fractures and prolonged immobilization also contribute to such events. Early detection via clinical examination and venous Doppler ultrasound documentation of perfusion deficits should be followed by initiation of therapeutic anticoagulants as soon as the patient is considered not to be at risk for intracranial bleeding. Ongoing clinical observation is imperative to detect any signs of pulmonary embolism, including dyspnea, anxiety, cough, tachypnea, or tachycardia. Anticoagulant therapy may begin with subcutaneous low-molecular-weight heparin (LMWH) and transition to oral warfarin with bridging doses of LMWH until an international normalized ratio of 2-3 is achieved (O'Brien, 2012). Although LMWH eliminates the need for frequent prothrombin/international normalized ratio monitoring, intermittent laboratory draws are sometimes better tolerated than twice-daily subcutaneous injections for 3 to 6 months. Daily clinical monitoring of the affected extremity is recommended with documentation of initial circumferential measurements, as well as the presence and location of any pain, edema, or erythematous areas. Repeat imaging is performed to verify resolution and adequate perfusion of the affected limb prior to discontinuation of medication. Placement of a removable inferior vena cava filter may be appropriate as well.
Dyspraxia is a sensory processing disorder of frontoparietal brain injury that results in impaired performance of motor skill tasks. Postural control through the activation of core muscle groups is needed to perform functional motor movements from reintegration of vestibular, visual, and proprioceptive feedback through physical and occupational therapy. Through upright positioning and other neurodevelopmental techniques, therapists deliver specific sensory input for neuromuscular re-education to develop muscle tone, coordination, balance, and motor planning.
Spasticity and elevated muscle tone commonly evolve after brain injury because of dysfunction of sensorimotor control in the upper motor neurons (Kheder & Nair, 2012). Although a child requires a degree of tone for postural control during sitting and transfers, increased flexor tone and spasticity can become disabling and interfere with function. Spastic dystonia leads to discomfort, contractures, or other deformities, such as talipes equinovarus or scoliosis. In rehabilitation, it is prudent for the medical, nursing, and therapy team members to monitor the spasticity for a short interval, such as 2 weeks, for natural improvement, while maximizing physical therapy with therapeutic stretching exercises and medications. Evaluation of pain and spasticity is assessed daily by the rehabilitation team in relation to interference with functional gains, as well as caregiver tasks such as personal hygiene. This information is used to guide medication management by the medical staff. Spasms may interfere with bowel and bladder function and result in alterations in skin integrity from vulnerable tissue pressure or sheering injury. The Modified Ashworth Scale grades degree of spasticity in muscle tone on an ordinal scale (Bohannon & Smith, 1987).
Medications to manage tone are started at "low and slow" doses. Baclofen, a gamma aminobutyric acid B receptor agonist, is most widely used initially and is titrated to tolerance and effect. Associated fatigue may require a larger dose to be given initially at night. Over time the child should accommodate to the medication with fewer signs of fatigue symptoms. Clonidine, a central alpha agonist, is also frequently used and may be transitioned from every-8-hour dosing to transdermal delivery with a 24-hour enteral bridge until the patch is effective. This method permits a more even distribution and medication effect without variability in blood pressure levels. Gabapentin, a modulator of excitatory neurotransmitter release, may be useful as well with additional benefit of pain relief. Tizanidine, an alpha-2 receptor agonist, acts as a central muscle relaxant as well; however, tizanidine requires monitoring of liver enzymes for risk of acute hepatitis, which may limit its use in children. Benzodiazepines may be used, but sedative effects may interfere in daytime use, yielding undesired fatigue and a decreased level of alertness. The goal of single or combined medications is to optimize spasm relief and minimize adverse effects, which impede neurocognitive recovery.
If contractures evolve or spasticity is unrelieved after maximizing pharmacologic management and therapeutic exercises, a skilled medical provider may evaluate the child for focal treatment with botulinum toxin serotype A, which targets a specific skeletal muscle group by binding with acetylcholine receptors. The injections may be performed with use of conscious sedation for comfort if needed and provide temporary focal relief without generalized effects. The effects are evident within 2 weeks and may last up to 3 months. Serial casting or splinting may be implemented in addition to ongoing therapy to maximize the beneficial effect of the botulinum toxin injections (Intiso, 2012, Kheder and Nair, 2012, Lubsch et al., 2006, Van Rhijn et al., 2005). If focal treatment is ineffective and more general relief is indicated, insertion of a baclofen pump may be instituted for continuous intrathecal medication infusion. However, the inserted pump may interfere with the ability to ambulate and has inherent risks associated with placement (Gooch, Oberg, Grams, Ward, & Walker, 2004). Surgical interventions such as selective rhizotomy, tenotomy, or myotomy are reserved for failure of pharmacologic and physiotherapy management to achieve patient goals.
Common Problems in TBI Management
Dysautonomia is estimated to affect about one third of patients after moderate to severe TBI in the first few weeks after brain injury. The constellation of symptoms includes tachycardia, hyperthermia, diaphoresis, muscle over-reactivity, increased respiratory effort or rate, hypertension, and pupillary dilatation. This response is commonly referred to by numerous names such as brain or thalamic storming, autonomic dysreflexia, and, more recently, paroxysmal sympathetic hyperactivity (Perkes, Baguley, Nott, & Menon, 2010). These symptoms may be incorrectly identified as narcotic withdrawal. The incidence of a triad of symptoms, namely hypertension, dystonia, and diaphoresis, has been studied and found to be associated with poorer outcomes, possibly from secondary brain injury from the hypermetabolic state or elevated sympathetic tone. These symptoms reflect increased sympathetic nervous system activity resulting from hypothalamic-pituitary dysfunction and are more likely to occur after hypoxic/ischemic events. Compared with injured children who do not have dysautonomia, children with dysautonomia required longer rehabilitation and had less improvement in WeeFIM motor skills scores (Kirk et al., 2012). Therefore, effective management of dysautonomia is especially critical. In addition to strategies such as environmental controls to reduce noxious stimuli, pharmacologic management includes the use of benzodiazepines, opioid antagonists, beta-blockers (e.g., propranolol), central dopamine agonists (e.g., bromocriptine), dopamine antagonists (e.g., chlorpromazine), and alpha-agonists (e.g., clonidine; Kirk et al., 2012, Perkes et al., 2010). Eventual resolution of the symptoms typically occurs, and medications are tapered as tolerated.
After TBI, children are at increased risk for posttraumatic seizures. Early posttraumatic seizures may occur in the first 7 days, whereas late seizures occur after 1 week. Prophylaxis antiepileptic drug (AED) therapy is often prescribed for a minimum of 7 days. In the literature, there appears to be a debate as to which AED is most effective (Bansal et al., 2014, Chung and O'Brien, 2014, Liesemer et al., 2011). Levetiracetam and phenytoin are frequently used for early AED prophylaxis. Levetiracetam is well tolerated and eliminates the need for obtaining serum drug levels, although phenytoin is less costly. More studies are needed to determine the most effective AED for prevention of posttraumatic seizures. Regardless of prophylaxis, monitoring for seizures to prevent secondary injury from further trauma, hypoxemia, or increased metabolic demand is imperative.
Dysphagia related to cerebellar dysfunction may result in impaired oral motor skills of injured children. The four stages of swallowing (oral preparatory, oral, pharyngeal, and esophageal) must work in concert to transition a bolus of food from the anterior to the posterior oropharynx and prevent airway aspiration. Aspiration may be silent or chronic, resulting in pulmonary issues such as pneumonia or wheezing with respiratory compromise. Under the guidance of a speech language pathologist, radiographic imaging via a rehabilitation swallow study should assess oral motor transit of a food bolus, as well as thick to thin fluids. The results of the assessment determine strategies to facilitate advancement in oral feedings. Compensatory strategies are often utilized, such as texture modification of thick liquids or solids with honey or nectar, in addition to maneuvers such as head position or tucking the chin. Research has shown that these functional modifications will improve swallowing biomechanics for the short term (Miller, 2011). In addition to traditional compensatory techniques, recent approaches to treatment of swallow dysfunction have included use of electrical stimulation for modulation of neuronal systems affecting swallowing function. Trained speech language pathologists apply electrodes to the skin at the oropharyngeal neuromuscular junctions to deliver pulses of electrical stimulation to the muscles needed for swallowing in conjunction with ingestion of food or liquids (Doeltgen and Huckabee, 2012, Miller, 2011). Oral motor integrity plays an integral part in the ability to manage oral secretions as well. Until adequate oral nutrition is provided, alternative tube feeding options, such as nasogastric, nasojejunal, or gastrostomy feeding, are maintained to meet nutritional and caloric requirements and provide daily maintenance of fluid volumes.
Deep vein thrombosis, which is less common in the uninjured pediatric population (O'Brien, 2012), is a frequent complication of TBI. Risk increases for multi-trauma patients, who are more likely to have hemodynamic instability resulting in vascular stasis, coagulopathic states, infections, and the use of invasive hemodynamic monitoring catheters such as central venous access. Comorbidities of extremity fractures and prolonged immobilization also contribute to such events. Early detection via clinical examination and venous Doppler ultrasound documentation of perfusion deficits should be followed by initiation of therapeutic anticoagulants as soon as the patient is considered not to be at risk for intracranial bleeding. Ongoing clinical observation is imperative to detect any signs of pulmonary embolism, including dyspnea, anxiety, cough, tachypnea, or tachycardia. Anticoagulant therapy may begin with subcutaneous low-molecular-weight heparin (LMWH) and transition to oral warfarin with bridging doses of LMWH until an international normalized ratio of 2-3 is achieved (O'Brien, 2012). Although LMWH eliminates the need for frequent prothrombin/international normalized ratio monitoring, intermittent laboratory draws are sometimes better tolerated than twice-daily subcutaneous injections for 3 to 6 months. Daily clinical monitoring of the affected extremity is recommended with documentation of initial circumferential measurements, as well as the presence and location of any pain, edema, or erythematous areas. Repeat imaging is performed to verify resolution and adequate perfusion of the affected limb prior to discontinuation of medication. Placement of a removable inferior vena cava filter may be appropriate as well.
Dyspraxia is a sensory processing disorder of frontoparietal brain injury that results in impaired performance of motor skill tasks. Postural control through the activation of core muscle groups is needed to perform functional motor movements from reintegration of vestibular, visual, and proprioceptive feedback through physical and occupational therapy. Through upright positioning and other neurodevelopmental techniques, therapists deliver specific sensory input for neuromuscular re-education to develop muscle tone, coordination, balance, and motor planning.
Spasticity and elevated muscle tone commonly evolve after brain injury because of dysfunction of sensorimotor control in the upper motor neurons (Kheder & Nair, 2012). Although a child requires a degree of tone for postural control during sitting and transfers, increased flexor tone and spasticity can become disabling and interfere with function. Spastic dystonia leads to discomfort, contractures, or other deformities, such as talipes equinovarus or scoliosis. In rehabilitation, it is prudent for the medical, nursing, and therapy team members to monitor the spasticity for a short interval, such as 2 weeks, for natural improvement, while maximizing physical therapy with therapeutic stretching exercises and medications. Evaluation of pain and spasticity is assessed daily by the rehabilitation team in relation to interference with functional gains, as well as caregiver tasks such as personal hygiene. This information is used to guide medication management by the medical staff. Spasms may interfere with bowel and bladder function and result in alterations in skin integrity from vulnerable tissue pressure or sheering injury. The Modified Ashworth Scale grades degree of spasticity in muscle tone on an ordinal scale (Bohannon & Smith, 1987).
Medications to manage tone are started at "low and slow" doses. Baclofen, a gamma aminobutyric acid B receptor agonist, is most widely used initially and is titrated to tolerance and effect. Associated fatigue may require a larger dose to be given initially at night. Over time the child should accommodate to the medication with fewer signs of fatigue symptoms. Clonidine, a central alpha agonist, is also frequently used and may be transitioned from every-8-hour dosing to transdermal delivery with a 24-hour enteral bridge until the patch is effective. This method permits a more even distribution and medication effect without variability in blood pressure levels. Gabapentin, a modulator of excitatory neurotransmitter release, may be useful as well with additional benefit of pain relief. Tizanidine, an alpha-2 receptor agonist, acts as a central muscle relaxant as well; however, tizanidine requires monitoring of liver enzymes for risk of acute hepatitis, which may limit its use in children. Benzodiazepines may be used, but sedative effects may interfere in daytime use, yielding undesired fatigue and a decreased level of alertness. The goal of single or combined medications is to optimize spasm relief and minimize adverse effects, which impede neurocognitive recovery.
If contractures evolve or spasticity is unrelieved after maximizing pharmacologic management and therapeutic exercises, a skilled medical provider may evaluate the child for focal treatment with botulinum toxin serotype A, which targets a specific skeletal muscle group by binding with acetylcholine receptors. The injections may be performed with use of conscious sedation for comfort if needed and provide temporary focal relief without generalized effects. The effects are evident within 2 weeks and may last up to 3 months. Serial casting or splinting may be implemented in addition to ongoing therapy to maximize the beneficial effect of the botulinum toxin injections (Intiso, 2012, Kheder and Nair, 2012, Lubsch et al., 2006, Van Rhijn et al., 2005). If focal treatment is ineffective and more general relief is indicated, insertion of a baclofen pump may be instituted for continuous intrathecal medication infusion. However, the inserted pump may interfere with the ability to ambulate and has inherent risks associated with placement (Gooch, Oberg, Grams, Ward, & Walker, 2004). Surgical interventions such as selective rhizotomy, tenotomy, or myotomy are reserved for failure of pharmacologic and physiotherapy management to achieve patient goals.
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