Mild Traumatic Brain Injury, Anatomy and Assessment of the Paediatric Airway - Assignment Example

Management of Conditions Student’s Name Institutional Affiliation Question One A “mild traumatic brain injury [MTBI]” or a concussion is defined as a physiological disruption in the functionality of the brain that presents with focal neurological deficits, loss of consciousness, altered personality or mental state as a result of a traumatic injury to the brain (Bernhardt, 2014). Other possible symptoms of a concussion include difficulties concentrating, memory lapses, blurred vision, noise or light sensitivity, drowsiness, insomnia, fatigue, nausea and vomiting, and headache, symptoms that can easily interfere with the social and school life of adolescents (Doolan, Day, Maerlender, Goforth, & Brolinson, 2011). Adolescents are particularly vulnerable to concussion due to their young developing brains with relatively larger subarachnoid space and thinner cranial bones (Jamault & Duff, 2013). After a concussion, an adolescent athlete may or may not be fit to return to play (RTP), and the decision lies with the health professional managing the athlete. A RTP decision is an agreement made by the medical team attending to an individual who has experienced a concussion with the regard to whether the individual is safe to resume their previous sporting activity. Such a decision is of significant to the health and safety of the athlete since the decision to RTP can be risked by major concerns such as post-concussion syndrome (PCS), second impact syndrome (SIS) and chronic traumatic encephalopathy (CTE) (Doolan et al., 2012). SIS is a condition that occurs after a sequential concussion characterised by a prolonged recovery. It is a severe injury with an estimated morbidity rate of about100% and a minimum mortality rate of 50% (Cantu, 2009). It is thought to be as a result of the trauma causing a swift cerebral auto-regulation loss coupled with substantial intracerebral swelling (Doolan et al., 2012). It occurs in athletes who sustain a concussion while still exhibiting symptoms of a previous concussion. PCS syndrome is characterised by a prolonged recovery after a single or subsequent concussion. It is postulated that symptoms such as confusion and amnesia are more likely to be exhibited by an on-field athlete who has a history of concussions (Doolan et al., 2012). The symptoms are commonly associated with a longer duration of recovery and may result in side-lining of an adolescent athlete from a season of competition or even a complete exclusion from the sport entirely (Doolan et al., 2012). CTE often occurs as a result of the cumulative impact of repeated concussions. The risk of CTE increase with the number of concussions sustained and for adolescents actively participating in sporting events, the risk is quite high if concussion preventive measures are not incorporated timely (Doolan et al., 2012). However, the symptoms of CTE only present much later in life. Initially, RTP was defined by a set timeline based on the severity of a concussion as classified at the time of occurrence (Giza et al., 2013). However, Giza et al. (2013) noted that the classification was less predictive of an individual’s length of recovery allowing some individuals, especially adolescents who naturally take longer to recover fully compared to adults, to resume their sporting activities too early. Therefore, new recommendation for RTP were structured that emphasized on removing the athlete from play immediately, individualised conservative management of adolescent athletes and a RTP only after assessment by a licenced healthcare professional (Giza et al., 2013). The guideline recommended by Giza et al. (2013) were in support of those posited in the “2008 Zurich Consensus Statement” that suggested a progressive, graded step by step approach to rehabilitation before an adolescent is deemed fit for RTP (Doolan et al., 2012). The basic recommendations are in six steps of at least 24 hours each. First, the athlete should not indulge in any activity after the concussion but should rest both physically and cognitively until asymptomatic; second the athlete can engage in light aerobic activity such as stationary cycling, swimming or walking to enhance heart rate; third is engagement in sport-specific exercise such as drills to enhance movement but avoiding head impact; Fourth, is using non-contact training drills such as passing drills that are more advanced to enhance resistance training with the aim of fortifying coordination and cognitive load during exercise; Fifth, is participation in full-contact practice or normal training exercise to allow functional skills assessment and restore the athlete's confidence; and fifth is when the athlete is permitted to return fully to normal playing after been certified ready to do so by the relevant health professionals (Doolan et al., 2012; Giza et al., 2013). The development of symptoms in any of the phases will result in a reversion back to the first step and a repeat of all the six steps. References Bernhardt, D.T. (2014). Concussion. Retrieved from http://emedicine.medscape.com/article/92095-overview Cantu, R. (2009). Second-Impact syndrome. Clinical Sports Medicine, 7, 37-44. Doolan, A.W., Dat, D.D., Maerlender, A.C., Goforth, M. & Gunnar, B. (2012). A review of return to play issues and sport-related concussion. Annals of Biomedical Engineering, 40(1), 106-113. Giza, C.C., Kutcher, J.S., Ashwal, S., Barth, J., Getchius, T., Gioia, G., ... & Zafonte, R. (2010). Summary of evidence-based guideline update: Evaluation and management of concussion in sports. Neurology, 80(24), 2250-2257. Jamault, V. & Duff, E. (2013). Adolescent concussion. When to return to play. The Nurs Practioner, 38(2), 16-22. Question Two A paediatric patient has significant airways anatomical differences compared to an adult. These differences require that assessment and management approach of some conditions involving the paediatric airways be done slightly different compared to similar procedures if done on adult (Adewale, 2009). These differences are significant especially during management of conditions such as acute airway obstruction and during procedures such as tracheal intubation (Fladjoe & Stricker, 2009). The paediatric airway anatomy differs from that of an adult in that it is funnel-shaped while that of an adult is cylindrical (Wheeler, Spaeth, Mehta, Hariprakash & Cox, 2007). Other differences include a relatively large occiput compared to the body size that easily result in neck flexion that can possibly block the airways when the paediatric patient is in supine position; a smaller oral cavity space as result of the relatively larger paediatric tongue; the epiglottis is positioned horizontally and its shorter and narrower; the larynx is anterior and cephalad; and the diaphragm, which form the chief respiratory muscles, are not inset oblique to the ribs but horizontal such that the diaphragmatic function may be compromised creating a paradoxical movement of the chest if the child’s placement position is supine (Wheeler et al., 2007). The funnel shape anatomy of the paediatric airways slopes from the area around the thyroid cartilage and narrows towards the area around the cricoid ring at least when the glottis distensibility is considered (Adewale, 2009). The subglottic is the narrowest section of the paediatric airway. Due to this narrowness, partial airway obstruction at the subglottic such as after aspiration of foreign bodies, post-extubation subglottic edema and where mass lesions occur at the subglottis, is bound to be tolerated poorly in paediatric (Harless, Ramaiah & Bhananker, 2014). It is also salient to limit pressure exertion at the cricoid ring because of the narrowness of this region compared to the upper section of the airway (Harless, Ramaiah & Bhananker, 2014). This narrowness is also the basis of using uncuffed endotracheal tubes over the cuffed type for paediatric and neonatal patient. The uncuffed tracheal tubes are suitable for these patients since the ringlike cricoid cartilage and the tracheal tube form an area where an adequate seal can form (Adewale, 2009). On the contrary, an efficient seal will not be formed if uncuffed tracheal tubes are used in an adult due to the cylindricalness of the tracheal tube. The shorter length and smaller diameter of the paediatric airway has significant impact on air movement after a slight airway positional change. The tracheal length in neonates is as short as 4cm growing in length to a length of about 12 cm in adults while the diameter of the trachea ranges from about 5mm in neonates to 25 mm in adults (Wheeler et al., 2007). Based on the Hagen-Poiseuille’s law, the airflow resistance as a result of airway diameter reduction is directly proportional to the radius of the airways raised to power four (Wheeler et al., 2007). This means that for an infant who has an airway diameter of about 4mm, if the airway diameter is reduced by 2mm, it shall represents a cross-sectional area reduction of about 75% and a rise in airflow resistance by 32 times compared to a cross-sectional area reduction of about 44% and an increase in airflow resistance by five times in an adult (Adewale, 2009). This implies that paediatrics are at a higher risk of impaired airflow with minor obstruction compared to adults hence the need for precautionary measures to preclude the obstruction. Furthermore, paediatrics also have an exceptionally larger occiput compared to adults' that has the potential to interfere with the movement of air in the airways (Wheeler et al., 2007). In addition, in natural supine lying position, the paediatrics’ neck is usually flexed positioning the neck such that the airway is partially or even completely blocked. Therefore, paediatric patients placed in such a supine position may exhibit signs signifying obstructed airways such as stridor or snoring (Wheeler et al., 2007). Health professional handling paediatric patients should, therefore, be cautious when handling or performing various assessments on them. It is recommended that to maintain airway patency and neutrality, a small roll should be placed directly behind the upper thorax and the shoulder. This would move the occiput back and raise the thorax positioning the airway in a neither flexed nor extended position (Adewale, 2009). References Adewale, L. (2009). Anatomy and assessment of the paediatric airway. Pediatric Anesthesia, 19(Suppl. 1), 1-8. Fladjoe, J. & Stricker, P. (2009). Pediatric difficult airway management: Current devices and techniques. Anesthesiology Clinics, 27(2), 185-195. Harless, J., Ramaiah, R. & Bhananker, S.M. (2014). Pediatric airway management. International Journal of Critical Illness & Injury Science, 4(1), 65-70. Wheeler, D.S., Spaeth, J.P., Mehta, R., Hariprakash, S,P. & Cox, P.N. (2007). Assessment and management of the pediatric airway. In Pediatric Critical Care Medicine. Basic science and Clinical Evidence (pp. 223-252). New York, NY: Springer Publishing. Question Three The guidelines changed in 2007 with the development of new evidence against the use of diuretics and hyperventilation in the management of traumatic brain injury (TBI) (Helmy, Vizcaychipi & Gupta, 2007). Initially diuretics and hyperventilation were routinely used in the management of increased intracranial pressure (ICP) but current evidence suggest the side –effects of hyperventilation and diuretics make it riskier to apply them as first-line management in TBI (Kochanek et al., 2012). In head injury patients, the intracranial volume comprises any mass lesions in the brain, volume of blood in the blood vessels, the cerebrospinal fluid volume, and the total volume of the brain (Brain Trauma Foundation [BTF], 2007). Therefore, to reduce ICP and enhance intracranial compliance a volume reduction in one of the highlighted components is essential. The blood volume component is affected by carbondioxide (CO2) concentrations such that for a mmHg decrease in carbon dioxide partial pressure, blood flow decrease of about 4% can occur hence the effect of ventilation in decreasing ICP (Ainsworth, 2015). Hyperventilation which can reduce the carbon dioxide partial pressure to about 30-35 or even much lower depending on the intensity of the hyperventilation, results in arteriole vasoconstriction, blood volume and ICP decrease (Helmy, Vizcaychpi, Gupta, 2007). However, the vasoconstriction can be extreme to cause brain tissues to undergo ischemia and hypoxemia. The limitation of hyperventilation stems from its mechanisms of ICP volume control highlighted above. One of the controversies in the use of hyperventilation is because subarachnoid haemorrhage, a common manifestation in TBI may be accompanied by cerebral vasospasm. Hence, additional hyperventilation induced vasoconstriction during an attempt to decrease ICP may easily lead to ischaemia and hypoxia (Ainsworth, 2015). Second, while unaffected brain blood vessels respond to hypocapnia by vasoconstricting, damaged ones may have lost their autoregulatory capacity and may vasodilate after a decrease in blood flow to the brain. This can divert most blood and nutrients into the damaged brain areas limiting the availability of the same for other brain areas causing more harm to the latter (Helmy, Vizcaychpi, Gupta, 2007; Ainsworth, 2015). Besides, this diversion may paradoxically increase ICP due to increased capillary permeability of damaged tissues. Third is the rebound vasodilation after used hyperventilation that can increase the ICP again (Ainsworth, 2015). This is because in the course of hyperventilation when cerebral CO2 is maintained at low levels, bicarbonate ions in the brain usually adjust to buffer the pH within normal limits. A sudden increase in CO2 after hyperventilation result in massive molecules of CO2 that cross the blood-brain-barrier resulting in cerebral acidosis that induces dilation of cerebral blood vessels allowing more blood into brain areas culminating in an elevation in ICP that is refractory to hyperventilation (Ainsworth, 2015). Also, hyperventilation was initially used especially in paediatric management of severe TBI to facilitate a rapid decrease in ICP under assumptions that the patients commonly presented with hyperaemia after TBI (Kochanek et al., 2012). Through reducing ICP and enhancement in perfusion to regions of the brain experiencing ischemia, hyperventilation was thought to be of benefit to the brain after TBI, especially in paediatric patients. However, recent research suggest that hyperaemia is actually not common in children and coupled with the concerns over the side-effects associated with hyperventilation making this form of therapy not to be recommended as a first line management of TBI (Kochanek et al., 2012). Before 2007, diuretics especially the osmotic diuretic mannitol were applicable in lowering ICP even though there was not sufficient evidence to support their use for this purpose (BTC, 2007). No randomised controlled trials existed to support the utilization of these diuretics as first line management of TBI even though they were initially been used in hyperosmolar therapy (BTC, 2007; Ainsworth, 2015). Mannitol can cause a rapid loss of body fluids through diuresis that may consequently deplete the intravascular volume. With a depleted intravascular volume, haematocrit rises with a possible rise in blood viscosity (Ainsworth, 2015). The latter increases the damaged brain area’s susceptibility to stroke. In addition the increase in plasma osmolarity above 320 mOsm/L as a result of diuresis may be associated with renal and neurological side-effects that may aggravate the brain injury (Helmy, Vizcaychipi & Gupta, 2007). References Ainsworth, C.R. (2015). Head trauma treatment & Management. Retrieved from http://emedicine.medscape.com/article/433855-treatment Brain Trauma Foundation. (2007). Guidelines for the management of severe traumatic brain injury. New York, NY: Brain Traum Foundation. Helmy, A., vizcaychipi, M. & Gupta, A.K. (2007). Traumatic brain injury: intensive care management. British Journal of Anaesthesia, 99(1), 32-42. Kochanek, P.M., Carney, N., Ashwal, S. (2012). Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescent- second edition. Pediatric Critical Care Medicine, 13(1), S1-S82. Read More