ee3 Abstract Neuroimaging is critical to the diagnosis and manage ment of many children in the intensive care unit (ICU) The most appropriate type of imaging study to perform will depend on the clinic[.]
ee3 Abstract: Neuroimaging is critical to the diagnosis and management of many children in the intensive care unit (ICU) The most appropriate type of imaging study to perform will depend on the clinical situation Close consultation with radiologists will improve selection and interpretation of imaging studies This chapter reviews the fundamentals of neuroimaging techniques and presents imaging examples of conditions seen in the ICU Key words: neuroimaging, computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, angiography, stroke, hemorrhage, demyelination, hydrocephalus 62 Coma and Depressed Sensorium NEETHI PINTO AND CASEY STULCE PEARLS • Coma is a state of unconsciousness with lack of awareness and loss of wakefulness • A Glasgow Coma Scale score of less than 15 in children should be taken seriously • Arousal may be depressed by either direct brainstem injury involving the reticular formation or bilateral cerebral hemispheric dysfunction • The ABCs (airway, breathing, and circulation) should be prioritized during management of a comatose child When in doubt, it is better to protect the airway in order to prevent hypoxemia and hypercarbia • Early measurement of blood glucose is important during initial stabilization of a comatose child • Abnormal pupillary reflexes and/or altered respirations may be signs of impending herniation • The goal of therapy should be the prevention of secondary brain injury • A combination of physical signs, electroencephalography, somatosensory evoked potentials, and magnetic resonance imaging can be helpful in predicting outcomes Coma refers to injury and impaired function of the brain due to structural central nervous system (CNS) and/or metabolic or systemic etiologies Coma may result from traumatic or nontraumatic brain injury; it is a life-threatening medical emergency prompting immediate methodical evaluation and treatment If not recognized and evaluated, secondary injury with resultant morbidity and mortality may occur Conversely, rapid treatment may improve prognosis.1 hallucinations; states of reduced alertness include lethargy, obtundation, and stupor Lethargy refers to drowsiness or decreased wakefulness but with a preserved ability to communicate when appropriately stimulated Obtundation refers to a deeper state of unresponsiveness, with loss of ability to respond to vigorous stimuli Stupor refers to decreased responsiveness with arousability only to noxious stimuli The subjective, examiner-dependent nature of these states and lack of uniformity in their definitions in the literature are problematic, rendering these terms less useful as specific descriptors of altered consciousness.1,3 Rather, the use of validated coma scales to gauge level of consciousness (LOC) allows for improved objectivity and uniformity in describing states of altered consciousness Ideally, these scales would have interrater reliability, ease of administration, applicability to both a wide range of ages and a variety of clinical scenarios resulting in altered consciousness, and an ability to differentiate levels of coma requiring intervention.4 Among the available instruments, the Glasgow Coma Scale (GCS) score is the most commonly used and widely accepted (Table 62.2).4–6 The GCS focuses on assessment of cortical function in three areas (motor response, verbal performance, and eye opening) and has been modified for use in children and infants.4,7,8 Total scores range from to 15, with categorization of scores from to 8, to 12, and 13 to 15, reflecting severe, moderate, and mild injury, respectively Definitions Consciousness is a spontaneous state of awareness of self and environment and wakefulness Coma is a pathologic state of unconsciousness, with lack of awareness of self and environment and loss of wakefulness Unlike states of transient unconsciousness, such as syncope and concussion, coma is a sustained state that requires the duration of unconsciousness to be at least hour Comatose patients present with their eyes closed; coma is distinct from normal sleep due to its deep unarousable state.1,2 Coma may result in a spectrum of outcomes ranging from recovery to brain death In between recovery and brain death are other disorders, including locked-in state, minimally conscious state, and the persistent vegetative state (Table 62.1) As noted in these other states of disordered consciousness, awareness requires wakefulness, but wakefulness (with intact sleep-wake cycles) does not require awareness.2 Aside from these altered states of consciousness, other terms are used to describe alterations in mental status that reference states of heightened or reduced alertness States of heightened alertness include delirium (see Chapter 134), delusions, and 756 Epidemiology Estimating the incidence of pediatric coma is complicated by the fact that studies use different criteria for severity of brain injury Typically, studies of traumatic brain injury (TBI) include patients 757 CHAPTER 62 Coma and Depressed Sensorium TABLE Disorders of Consciousness and Other Conditions 62.1 Condition Awareness Wakefulness Physical Exam Outcome Brain death Absent Absent No reflexes or only spinal reflexes Absent respiratory function No recovery Coma Absent Absent No purposeful movement Variably depressed respiratory effort Death, persistent vegetative state, or recovery by wk Persistent vegetative state Absent Intact No purposeful movement Normal respiratory effort Dependent on etiology Minimally conscious state Very limited Intact Severe limitation of movement Variably depressed respiratory effort Recovery unknown Locked-in syndrome Present Intact Quadriplegia, pseudobulbar palsy; eye movements preserved Normal to variably depressed respiratory effort Recovery unlikely Modified from Ashwal S Medical aspects of the minimally conscious state in children Brain Dev 2003;25(8):535–545 TABLE Glasgow Coma Scale Scoring With Modification for Infants and Children 62.2 Activity Infant Child Adult Score Motor response Moves spontaneously, purposely Withdraws to touch Withdraws to pain Decorticate posturing to pain Decerebrate posturing None Obeys commands, spontaneous movements Localizes pain Withdraws to pain Flexion in response to pain Extension in response to pain None Follows commands Localizes pain Withdraws to pain Flexion in response to pain Extension in response to pain None Verbal response Coos and babbles Irritable, cries Cries in response to pain Moans in response to pain None Age-appropriate, oriented, smiles Confused, aware of environment Irritable, inconsistently consolable Inconsolable, unaware of environment, agitated None Oriented Confused Inappropriate words Nonspecific sounds None Eye opening Spontaneous To sound To pain None Spontaneous To sound To pain None Spontaneous To sound To pain None Data from Kirkham FJ, Newton CR, Whitehouse W Paediatric coma scales Developmental Medicine & Child Neurology 2008;50:267–274; Wong CP, Tay EL Childhood brain injury: a review Neurol Asia 2015;20:105–115 with GCS scores less than 12, whereas studies of nontraumatic brain injury include patients with GCS scores less than 8.8 With these criteria in mind, the incidence of pediatric TBI (see Chapter 118) ranges from 765 per 100,000 children aged to 15 years to 1188 per 100,000 children aged to years,8-10 but traumatic and nontraumatic coma appear to have approximately equal incidences of 30 per 100,000 children.3,11 Notably, the incidence of nontraumatic pediatric coma is highest among infants, with 160 per 100,000 children age to years affected.11 Relevance As a medical emergency, coma presents a challenge to intensivists because optimal care requires timely intervention However, information is frequently limited during the initial evaluation Assessment of LOC and knowledge of CNS anatomy and physiology may provide helpful clues in attempting to interpret patient history and physical findings and optimize care A careful general physical examination with a focused neurologic examination can suggest the diagnosis, aid in the location of lesions, guide therapeutic intervention, and determine prognosis Further adjunctive radiologic and laboratory evaluation may then confirm physical findings A timely, methodical approach to the management of the comatose child may affect prognosis and long-term outcomes Therefore, this chapter considers CNS anatomy, the pathophysiology of coma, historical and physical findings that aid in the localization of lesions and the etiology of coma, the emergent management and initial evaluation of patients with altered levels of consciousness, and the prognosis and outcomes of patients who present with coma Physiology/Pathophysiology Arousal is mediated by the ascending reticular activating system (ARAS) The ARAS is principally located in the brainstem in the paramedian tegmental gray matter immediately ventral to the pons (Fig 62.1) The ARAS is composed of two distinct anatomic pathways The first pathway consists of cholinergic neurons originating in the pedunculopontine tegmental and laterodorsal 758 S E C T I O N V I Pediatric Critical Care: Neurologic • BOX 62.1 Etiologies of Impaired Consciousness and Coma Cerebral cortex Metabolic-Toxic Hypoxia-Ischemia Cerebellum Thalamus Subthalamus and hypothalamus Midbrain Pons Bulb Ascending reticular activating system in brainstem Afferent collaterals • Fig 62.1 Ascending reticular activating system (ARAS) The ARAS is principally located in the brainstem and is composed of two distinct anatomic pathways These pathways mediate arousal through projections to the thalamus and cortex 12 Industrial toxins (e.g., heavy metals, organic phosphate, cyanide, volatile hydrocarbons) Substance abuse (e.g., alcohol, cocaine, heroin, amphetamine) Shock Cardiac or pulmonary failure Near drowning Carbon monoxide poisoning Strangulation Poisoning, Including in Cases of Munchausen by Proxy Metabolic Disorders Infection Hypoglycemia Acidosis Diabetic ketoacidosis Organic and aminoacidemias Hyperammonemia Hepatic encephalopathy Reye syndrome Urea cycle disorder Disorders of fatty acid metabolism Valproic acid encephalopathy Uremia Bacterial Viral Rickettsial Paroxysmal Disorders Epilepsy Migraine Structural-Intrinsic Trauma Dehydration Hyponatremia Calcium and magnesium imbalance Concussion Cerebral contusion Epidural hematoma Subdural hematoma/effusion Intracerebral hematoma Diffuse axonal injury Endocrine Disorders Neoplasms Fluid and Electrolyte Imbalance Thyroid dysfunction Adrenal insufficiency Hypoparathyroidism tegmental nuclei of the mesopontine tegmentum These cholinergic neurons send excitatory signals through the thalamus to the cortex The second pathway consists of noradrenergic and serotonergic neurons originating in the upper brainstem and caudal hypothalamus This second pathway bypasses the thalamus and activates neurons in the lateral hypothalamic area, basal forebrain, and cerebral cortex This second pathway includes the locus coeruleus, the periaqueductal gray matter, and the raphe nuclei.12 Because the ARAS receives collaterals from and is stimulated by every major somatic and sensory pathway directly or indirectly, it is best regarded as a physiologic rather than an anatomic entity This partly explains why patients with very large discrete lesions (e.g., brain tumors) may be entirely alert, whereas patients with anatomically undetectable but biochemically widespread lesions (e.g., hepatic encephalopathy) may be deeply comatose Primarily, two types of lesions depress the level of arousal: direct brainstem– diencephalic injury involving the reticular formation and nuclei or bilateral cerebral hemisphere dysfunction Consequently, conscious behavior depends on the interplay between the cerebral cortex and the ARAS because these neural components are required for arousal and to maintain awareness.13,14 The differential diagnosis is age related (Table 62.3) Hypoxemia and ischemia/reperfusion injury are important causes of coma in all ages of pediatric patients These entities are thoroughly discussed in Chapter 62 Etiology Initial Treatment of the Comatose Child Coma is a nonspecific consequence of various CNS insults.3 Coma may present as part of the progression of a known illness, as an unpredictable consequence of a known systemic disease, or as a result of a totally unexpected event or illness.15 As discussed earlier, unilateral cortical lesions not typically cause coma because the ARAS is widely distributed in the cortical region However, a small brainstem lesion can cause immediate coma because of the close proximity to the ARAS Lesions in the brainstem may be due to demyelinating diseases, vascular disease, neoplasm, or head trauma Common etiologies of coma in the pediatric population include metabolic, toxic, structural, and intrinsic causes (Box 62.1) The approach to the comatose child necessitates immediate, ongoing resuscitation while simultaneously undertaking elements of the physical examination, seeking historical details, and initiating diagnostic evaluation Hypertensive Encephalopathy Vitamin Deficiency Thiamine Pyridoxine Niacin Mitochondrial Disorders Exogenous Toxins and Poisons Narcotics, neuroleptics, antidepressants, antiepileptic drugs, stimulants Over-the-counter drugs, acetaminophen, mushrooms Vascular Disease Cerebral infarction Thrombosis, embolism Cerebral hemorrhage Arteriovenous malformation Aneurysm Vasculitis Trauma to carotid or vertebral artery in the neck Focal Infection Cerebritis Abscess Hydrocephalus Prehospital Care Survival and outcome depend on delivery of high-quality care as soon as possible after injury Recommendations for prehospital trauma life support follow.1,16 Airway: Endotracheal intubation if GCS is or less CHAPTER 62 Coma and Depressed Sensorium TABLE Common Considerations of Altered Mental 62.3 Status at Various Ages Infant Child Adolescent Infection Ingestion Ingestion Inborn error of metabolism Infection Trauma Metabolic Trauma, including inflicted Infection Trauma, including inflicted Metabolic Psychological Congenital abnormality Seizure Seizure Hypoxic ischemic injury Hypoxic ischemic injury Hypoxic ischemic injury Intussusception Breathing: Maintaining adequate oxygenation and normal ventilation Circulation: Control of external hemorrhage and intravenous fluid resuscitation to maintain systolic blood pressure appropriate for age Assessment of blood glucose levels Cervical spine precautions Recognition and treatment of increased intracranial pressure (ICP; see Chapter 63) Treatment of seizures (see Chapter 64) Safe transportation to a pediatric hospital with a high-level trauma center and neuroimaging and neurosurgical capacity if due to TBI Initial Stabilization Upon arrival to the hospital setting, continued attention to airway, breathing, and circulation are paramount in the initial management and stabilization of the comatose child to ensure adequate oxygenation, ventilation, and tissue perfusion Cervical spine injury and increased ICP should be suspected in comatose patients with TBI Compared with other organs, metabolic activity in the brain is relatively high The brain has little capacity to store glucose and accordingly depends on constant delivery of energy substrate and oxygen to maintain normal metabolic function Early management of blood glucose and appropriate treatment of hypoglycemia is crucial to treatment and prevention of secondary injury Comatose patients often are hypercapnic and hypoxemic Thus, supplemental oxygen should be provided to the patient with hypoxia during the initial evaluation Airway Upper airway obstruction as a result of decreased muscle tone of the pharyngeal soft tissue is a common problem in unresponsive patients, necessitating endotracheal intubation for airway protection It also is common practice to endotracheally intubate patients with hemodynamic instability or neurologic instability In most circumstances, it is safer to endotracheally intubate electively rather than emergently to protect an already compromised brain from further injury as a result of respiratory failure Endotracheal intubation (if not already done prior to hospital arrival) should be performed if the GCS is or less 759 Hyperextension of the neck must be avoided during intubation Rapid sequence intubation should be performed with careful selection of medications in order to avoid agents that may worsen intracranial hypertension and caution with the dosage of medication (e.g., benzodiazepines and barbiturates) to prevent compromise of mean arterial pressure and cerebral perfusion pressure During endotracheal intubation, special precautions should be taken to protect cerebral circulation and prevent further increases in ICP Pretreatment with lidocaine and thiopental may help to diminish elevation in ICP associated with airway manipulation and suctioning After intubation, careful attention to endotracheal tube position and suctioning of oropharyngeal secretions is warranted Once the patient’s airway is secured, adequacy of oxygenation and ventilation must be maintained by choosing appropriate ventilator settings and evaluating respiratory effort, continuous pulse oximetry, and end-tidal carbon dioxide monitoring Breathing Hyperventilation may facilitate reduction in ICP or hypercarbia due to hypoventilation from altered mental status (e.g., in the setting of intoxication) However, it is also important to maintain Paco2 between 35 and 40 mm Hg in order to avoid rapid fluctuations in cerebral blood flow from cerebral vasoconstriction (seen with excessive hyperventilation) and exacerbation of secondary injury An exception is in cases of brain herniation, where hyperventilation is often the most expeditious intervention As noted in the patient’s initial stabilization, continued prevention of hypoxia is essential to maintaining normal metabolic function and prevention of secondary brain injury Circulation Rapid assessment of circulation and tissue perfusion—including evaluation of central and peripheral pulses, capillary refill, and blood pressure—is important Hypotension must be corrected to reestablish adequate cerebral blood flow to ensure oxygen and substrate delivery Once hypotension is corrected, some evidence indicates that blood pressure should be maintained higher than the 75th percentile for age to maintain adequate cerebral perfusion pressure pending placement of ICP monitoring equipment.17 Vascular access may prove challenging—timely placement of intraosseous access must be considered Aggressive fluid resuscitation with isotonic fluids to restore normal circulatory status may be necessary Hypotonic fluids are not indicated and may exacerbate cerebral edema Management of blood pressure depends on suspected etiology of the comatose state On the one hand, maintenance of mean arterial pressure is necessary to ensure adequacy of cerebral perfusion pressure if increased ICP is suspected On the other hand, in cases of hypertensive encephalopathy or intracranial hemorrhage, judicious correction and/or prevention of hypertension may be warranted History Given the need to evaluate and treat the comatose child emergently, an abbreviated but targeted interview of the child’s parents or caregivers can provide insight into the etiology of the coma Important elements to elicit from the history, which may elucidate the cause of the coma, include the following ... brainstem and caudal hypothalamus This second pathway bypasses the thalamus and activates neurons in the lateral hypothalamic area, basal forebrain, and cerebral cortex This second pathway includes... involving the reticular formation or bilateral cerebral hemispheric dysfunction • The ABCs (airway, breathing, and circulation) should be prioritized during management of a comatose child When in doubt,... to the management of the comatose child may affect prognosis and long-term outcomes Therefore, this chapter considers CNS anatomy, the pathophysiology of coma, historical and physical findings