Puneet Kumar

ACUTE MANAGEMENT OF TRAUMATIC BRAIN INJURY
Trauma is a common cause of hospitalization in children, constituting about 15% of all pediatric admissions. More than half of these children have at least some degree of head injury. However, only a fraction of these children need neurosurgical intervention and it is critical that these children receive most appropriate medical interventions to minimize morbidity and mortality associated with this medical emergency. This is crucial as it is now well known that it is the secondary brain injury (due to hypoxia, hypercapnia, hypotension, seizures, metabolic derangements, increased intracranial tension, etc.) which is more damaging than the primary brain injury. This article summarizes the approach followed by me in these patients.

Initial assessment
The details of the accident and the probable mechanism of injury are ascertained. This helps in determining the possibilities of other injuries, for which the patient is then assessed. This is essential as failure to recognize injuries in a case of poly-trauma can prove dangerous.

Primary survey
Assessment and management of the Airway, Breathing and Circulation takes priority over further management of the injured child.

Airway: Patency of the airway is ascertained and any obstruction is cleared. Care is taken to stabilize the neck to protect the cervical spine from yet undiagnosed spinal injury. The chin-lift jaw-thrust maneuver is sufficient in most cases. Aspiration of secretions and/or vomitus is often required. Any solid foreign body in mouth/pharynx is also removed. Oropharyngeal airway is placed, if required to keep the airway patent. Endotracheal intubation is done if the patient is unconscious (GCS < 8) or if artificial respiration is likely to be required for a long period. Orotracheal route is preferred as there is risk of the tube entering the calvarium in case of fracture of cribiform plate. Emergency tracheostomy is done in cases where intubation is impossible because of facial/laryngeal trauma.

Breathing: Supplemental oxygen is administered to all children with moderate or severe head injury, until it is clear that it is not required. Assessment of adequacy of ventilation is the next step. Orogastric tube is inserted to decompress the stomach. Pneumothorax, tension pneumothorax, flail chest, hemothorax is ruled out/managed promptly as per the situation. Mechanical ventilation is needed in an occasional patient.

Circulation: Prompt assessment is made regarding presence and degree of hypovolemia. Pallor with without sweating, prolonged capillary refill time, low-volume pulses (narrow pulse pressure), tachycardia, tachypnea, lethargy, hypotonia and hypotension are important clues. As the assessment is progressing, intravenous access is obtained. Fluid is infused according to the degree of hypovolemia. Crystalloid (Ringer’s lactate) is the initial fluid of my choice in hypovolemia/shock. Intraosseus infusion and venous cut-down are occasionally required in a hypotensive child. Fresh whole blood transfusion is sometimes required in case of major hemorrhage. Though desirable, I have hardly used CVP line in these patients. It is essential to maintain blood pressure (BP) in high-normal range. Care is taken to prevent/treat hypothermia as it can affect circulatory dynamics adversely.

Secondary survey
Thorough clinical examination is done to rule out other injuries. Blood sample for hemoglobin, hematocrit, grouping and cross-matching is sent. ABG is occasionally required. X-rays are done on case-to case basis. Sonography of abdomen is done if intra-abdominal injury is suspected. Reference is sent for neurosurgeon, general surgeon and/or orthopaedician, as required.

Further management
In patients where cervical spine injury is a possibility, neck is immobilized appropriately. These patients are nursed in supine position with head in midline. This has an added advantage of maintaining jugular blood flow.

Wounds are cleaned and dressed; lacerations are sutured. Tetanus prophylaxis is given as per the standard guidelines.

Neurological assessment is essential for detecting the extent of brain damage. Glasgow Coma Score (GCS) or its modified form for children, pupils (size and reaction), and planter reflexes are noted. Quick neurological examination follows. I admit and closely monitor even the patients with apparently mild head injury with normal GCS and no neurological deficit. Those with moderate to severe injury need intensive care management and brain-specific therapies to prevent secondary brain injury and ensuring optimal outcome. Repeated neurological assessment at regular intervals is crucial for early detection of deterioration in these patients. No investigation can serve as a good substitute for this.

CT scan of head is planned. I request CT scan of head in almost all cases of head injury. The goal of CT scan is usually to identify the injury and also any space occupying lesion requiring neuro-surgical intervention. CT scan of cervical spine is also done where such an injury is a possibility. Repeat CT scan of head is only occasionally required in cases where the patient is deteriorating and an evolving intracranial lesion is suspected.

Most important in preventing secondary brain injury is maintenance of normal intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Care is taken to prevent/ manage hypotension in all such children. BP is maintained in high-normal range. Though desirable, most centers (including mine) do not have the facilities of ICP monitoring in cases of moderate and severe head injury. In the absence of such monitoring, close clinical monitoring is a must. Clinical signs of raised ICP appear late and any omission here will have devastating consequences. All patients with moderate/severe injury are nursed with head in neutral position, 15-30º above horizontal. However, raising of head is avoided in hypotensive patients. Appropriate analgesia is given. Fever is managed aggressively. Supplemental oxygen is guided by pulse oximetery/ABG. The room is not brightly lit; the staff is instructed to avoid unnecessary noise, unnecessary handling and unnecessary/vigorous suctioning. Proper care of endotracheal tube in mechanically ventilated patients is important to prevent tube blockade. Very agitated/restless child is sedated. However, sedation should be as minimum as possible. In mechanically ventilated patients, a high PEEP is avoided. All these measures tend to reduce spikes in ICP. In any child with sudden neurological deterioration, I use mannitol (0.5 gm/kg) intravenously over 20 minutes empirically. Mannitol is, however, avoided in hypotensive patients and in those with documented evidence of intracranial hemorrhage. In such patients and in those with impending herniation (papillary signs, bradycardia) hyperventilation is the best way to reduce ICP quickly. Hyperventilation is done with bag-and-mask or bag-and-tube for not more than 2-5 minutes. Prolonged hyperventilation is known to lose its effectiveness. Most authors caution against reducing PaCO2 below 30 mmHg for prolonged periods, for fear of cerebral vasoconstriction and poor outcome. Those who do not respond to hyperventilation generally have poor prognosis for survival. Recently, there is increasing evidence in favour of hypertonic saline for management of raised ICP. It is infused as intravenous bolus followed by maintenance drip @ 1.1 ml/kg/min. It can be used in hypotensive patients also and can raise BP (and thus CPP) in addition to lowering of ICP. I haven’t used this, but intend to do so in future. I do not use steroids, loop diuretics and barbiturates for reducing ICP, as they can adversely affect the outcome.

Seizures can also cause/ aggravate secondary brain damage in these patients. Patients having seizures are managed as per standard protocol. For prophylaxis, I use loading dose of phenytoin (15 kg/kg) intravenously over 30 minutes in all patients with moderate/severe head injury. Further use (maintenance therapy) and duration of seizure prophylaxis is individualized. In most patients, it is discontinued at the time of discharge. In survivors of severe head injury and those who remained stable but have multiple intracranial hematomas, I use long term phenytoin for another 2-4 weeks.

Hyperglycemia, if present, is managed with insulin (on sliding scale).

Intravenous antibiotics are used in all cases of penetrating head trauma/ CSF leak.


Mild Traumatic Brain Injuries May Cause Transient, Persistent Symptoms After Injury

March 9, 2009 — Mild traumatic brain injuries (TBIs), particularly those that are more severe, may cause transient or persistent symptoms in the first year after injury, according to the results of a prospective and longitudinal cohort study reported in the March issue of Pediatrics.

"This study provides reassurance for parents of kids who suffer first-time concussions because we can see that more often than not they recover fully within a short amount of time," lead author Keith Owen Yeates, PhD, from Nationwide Children's Hospital and Ohio State University College of Medicine in Columbus, said in a news release. "However, the study also shows that kids who are at risk because their concussions are more severe need to be monitored for a longer period of time as their symptoms may last longer."

The goal of this study was to assess whether mild TBIs in children and adolescents, especially when associated with acute clinical features reflecting more severe injury, result in different postinjury trajectories of postconcussive symptoms (PCSs) vs mild orthopaedic injuries (OIs).

At 2 large children's hospitals, 186 children with mild TBI and 99 with mild OI were recruited from consecutive admissions to emergency departments. Age range was 8 to 15 years. Current PCSs were rated by parents within 3 weeks of injury and at 1, 3, and 12 months after the injury. At the first evaluation, parents retrospectively rated preinjury symptoms, and children with mild TBI underwent brain magnetic resonance imaging.

Clinical characteristics evaluated for their ability to predict PCSs were loss of consciousness, Glasgow Coma Scale score less than 15, accompanying injuries, acute symptoms of concussion, and intracranial abnormalities on magnetic resonance imaging.

Four longitudinal trajectories of PCSs were determined based on finite mixture modeling; these were no PCSs, moderate persistent postconcussive symptoms, high acute/resolved PCSs, and high acute/persistent PCSs.

Distribution of trajectories differed between mild TBI and OI. Compared with the OI group, the mild TBI group was more likely to have high acute/resolved and high acute/persistent trajectories vs no PCSs. Children with mild TBI in whom the acute clinical presentation reflected more severe injury were especially likely to have high acute/resolved and high acute/persistent trajectories of symptoms.

"Parents should pay particular attention to these symptoms when they last more than a month or two and report all ongoing symptoms to their child's doctor so they can intervene appropriately," Dr. Yeates said.

Limitations of this study include recruitment rates below 50% for the mild TBI and OI groups, possible recruitment bias, and all clinical features weighted equally in the cumulative severity index and multiple symptoms summed in the measure of PCSs.

"Mild traumatic brain injuries, particularly those that are more severe, are more likely than orthopedic injuries to result in transient or persistent increases in PCSs in the first year after injury," the study authors write. "Additional research is needed to elucidate the range of factors, both injury related and non–injury related, that place some children with mild traumatic brain injuries at risk for PCSs."
Available from: http://www.medscape.com/viewarticle/589322?src=mp&spon=9&uac=107013PN 

The National Institutes of Health supported this study. The study authors have disclosed no relevant financial relationships. (Pediatrics. 2009;123:735-743.)

The changing “epidemiology” of pediatric head injury and its impact on the daily clinical practice

Aim This article focuses on the developments that occurred during the last two decades in the management of pediatric head injury. It describes the changes in incidence, various advancements in diagnosis, management, prognosis, prevention and strategies required for better outcome, and control of head injury.

Materials and methods Thorough evaluation of various papers, research, and our experience revealed that in developed countries, there has been a decreasing trend in head trauma incidence and trauma-related deaths as compared to developing countries.

Results This is mainly attributed to the widespread implementation of preventive measures. The development in imaging facilities, better characterization and grading of severe trauma (see, for example, diffuse axonal injury), an advanced understanding of the pathophysiology of secondary brain injury, endocrinological disturbances, predictive factors of outcome, development in neurophysiological monitoring, management advances in critical care units, implementation of safely measures, etc. have brought a significant change in overall outcome and profile of pediatric head injury

Conclusion The further developments in field of brain plasticity, stem cell, rehabilitation, evolution of new drugs, preventive community measures, and global policies to deal with head trauma are expected to play a major role in days to come. The development of future pediatric trauma centers based on current evolutions (in order to achieve a good outcome), global and emphatic preventions of trauma will be required to establish equilibrium between developed and developing countries. (Kumar R, Mahapatra, AK. Journal Child's Nervous System; February 12, 2009)

Intracerebral Hemorrhage Volume Predicts Poor Neurologic Outcome in Children
Background and Purpose—Although intracerebral hemorrhage (ICH) volume and location are important predictors of outcome in adults, few data exist in children.

Methods—A consecutive cohort of children, including full-term newborns to those younger than 18 years of age with nontraumatic, acute ICH and head CT available for analysis were studied. Clinical information was abstracted via chart review. Hemorrhage volume was expressed as percentage of total brain volume (TBV) with large hemorrhage defined as 4% of TBV. Hemorrhages were manually traced on each head CT slice and volumes were calculated by multiplying by slice thickness. Location was classified as supratentorial or infratentorial. Logistic regression was used to identify predictors of poor neurological outcome, defined as a Glasgow outcome scale 2 (death or persistent vegetative state).

Results—Thirty children were included, median age 6 years. Median ICH volume was 20.4 cm3 and median ICH size as a percentage of TBV was 1.9%. Only 4 of 22 children with ICH <4% of TBV had poor outcomes, vs 5 of 8 children with ICH 4% of TBV (P=0.03). In multivariate analysis, hemorrhage 4% of TBV (OR, 22.5; 95% CI, 1.4–354; P=0.03) independently predicted poor outcome 30 days after ICH. In this small sample, infratentorial hemorrhage location and the presence of intraventricular hemorrhage did not predict poor outcome.

Conclusions—ICH volume predicts neurological outcome at 30 days in children, with worst outcome when hemorrhage is 4% of TBV. Location and ICH etiology may also be important. These findings identify children with ICH who are candidates for aggressive management and may influence counseling regarding prognosis. (Lori C. Jordan , Jonathan T. Kleinman, et al In Stroke. 2009 Published online before print March 12, 2009, doi: 10.1161/STROKEAHA.108.541383)