will generally receive EEG testing and CT or MR imaging of the brain Consultation with a neurologist who treats children is important to coordinate this workup (see Chapters 72 Seizures and 97 Neurologic Emergencies ) The new onset of focal seizures, with or without the presence of fever, should be evaluated with a head CT scan to determine the presence of a focal lesion such as a tumor, abscess, or hemorrhage Only after the results of this study are known should a lumbar puncture be performed if no lesion predisposing to herniation is found If neuroimaging is unavailable and meningitis or encephalitis is a concern, or if the patient is unstable, empiric treatment for bacterial meningitis or herpetic encephalitis may be administered and lumbar puncture deferred (see Chapter 94 Infectious Disease Emergencies ) History of Toxic Ingestions If no history or physical examination findings suggestive of head trauma or seizures are present, a toxic ingestion should be considered, especially in toddlers and adolescents The availability of any substances capable of depressing CNS function should be thoroughly explored In general, coma from toxic ingestions is of slower onset than that from trauma and may be preceded by delirium or other abnormal behaviors Chapter 102 Toxicologic Emergencies lists major toxidromes that result from ingestions that produce CNS depression The pupils of a poisoned comatose patient are a particularly valuable source of information Miosis occurs with ingestions of narcotics, clonidine, organophosphates, gamma-hydroxybutyrate (GHB), phencyclidine, phenothiazines, and occasionally, barbiturates and ethanol Mydriasis is produced by ingestions of anticholinergic agents (e.g., atropine, antihistamines, and tricyclic antidepressants) and sympathomimetic compounds (e.g., amphetamines, caffeine, cocaine, LSD, and nicotine) Nystagmus may indicate the ingestion of barbiturates, ketamine, phencyclidine, or phenytoin Pupillary responses are likely to be preserved in toxic or metabolic comas Systemic toxins not cause unequal pupils; anisocoria in the setting of ALOC should be pursued with neuroimaging TABLE 17.5 POISONS UNDETECTED BY TYPICAL DRUG SCREENING THAT CAUSE COMA/ALTERED LEVEL OF CONSCIOUSNESS Miosis present Bromide Chloral hydrate Clonidine Gamma-hydroxybutyrate (GHB) Methadone, buprenorphine Organophosphates Phenobarbital Pilocarpine and tetrahydrozoline eye drops Phenothiazines Valproic acid Mydriasis present Anoxia caused by cyanide, carbon monoxide, or methemoglobinemia LSD A toxicologic screen of blood and urine should be considered in all children with coma of unknown origin The growing legality and popularity of edible marijuana preparations has produced a rise in pediatric cannabis ingestions causing ALOC Table 17.5 lists compounds capable of causing coma that are not typically detected by routine drug screening, grouped by pupillary effects The poisoned patient with depressed consciousness should be intubated with a cuffed endotracheal tube for airway protection Naloxone may be administered as empiric antidotal therapy for coma-producing toxic ingestions involving unknown medications Flumazenil should not be given routinely to these patients because seizures may result Its use is limited to pure benzodiazepine overdoses in patients with no history of seizures or drug habituation Increased Intracranial Pressure or Focal Neurologic Defect Nontraumatic causes of increased ICP or focal neurologic deficits include neoplasms, CSF shunt malfunction, cerebral abscess, and hemorrhage (see Chapters 97 Neurologic Emergencies and 122 Neurosurgical Emergencies ) These patients may present with a history of headache, vomiting, confusion, lethargy, meningismus, focal neurologic dysfunction, or seizure activity, or may present with sudden onset of deep coma Initial physical signs of increased ICP include sluggishly reactive pupils and, in infants, a bulging fontanelle More severe and prolonged increases in ICP produce a unilaterally enlarged pupil, other cranial nerve palsies (III, IV, VI), papilledema, and Cushing triad of hypertension, bradycardia, and irregular breathing All may signal impending or progressive herniation From the standpoint of the emergency physician, which type of herniation is present is unimportant; all are life-threatening, and the initial treatment is identical for all Endotracheal intubation using rapid sequence induction is performed to gain airway and breathing control Evaluation should parallel that for traumatic head injury, bearing in mind the increased desirability of using IV contrast for CT imaging Comatose patients with a CSF shunt may need their shunt reservoir or ventricle tapped emergently to treat increased ICP Fever Coma accompanied by fever may indicate CNS infection (see Chapters 31 Fever and 94 Infectious Disease Emergencies ) Resistance to neck flexion is the most important physical finding in meningitis, the most common infection of this type, although children younger than years of age may lack this finding Historical data may also include a steadily increasing headache, irritability, vomiting, and worsening oral intake Kernig and Brudzinski signs may be present Infants may exhibit paradoxic irritability, in which crying is worsened by picking up the baby Other useful physical clues to CNS infection are the rashes that accompany meningococcemia, varicella, and Rocky Mountain spotted fever The historical and physical findings in encephalitis are similar to those in meningitis; meningismus may be absent, however Seizures are particularly common if herpes simplex is the causative agent A history of localized CNS dysfunction, seizures, or a focal infection (e.g sinusitis, dental abscess) before the onset of febrile coma or the presence of concomitant focal neurologic signs may indicate the presence of a focal cerebral infection such as an abscess or subdural empyema In addition, either diffuse or focal infections may present with signs of increased ICP secondary to cerebral edema or blockage of CSF flow If this is the case, a head CT scan should be obtained before lumbar puncture is performed A contrast-enhanced study is desirable if concern about focal infection is present The ill-appearing patient should receive antibiotics before neuroimaging is performed CSF analysis remains the key to establishing the diagnosis of CNS infection Abnormalities of CSF white blood cell count (pleocytosis), glucose, and protein occur in roughly predictable patterns with bacterial or viral meningitis, and pathogens may be visible using Gram and other stains (see Chapter 94 Infectious Disease Emergencies ) Rapid testing with agglutination studies or polymerase chain reaction tests might also be used to identify pathogens CSF pleocytosis in encephalitis is variable and, if present, is usually mild (less than 500 cells/mm3), with normal levels of glucose and protein being common In the absence of signs of infection, bloody or xanthochromic CSF under increased pressure indicates subarachnoid hemorrhage Metabolic Abnormalities The presence of a metabolic disorder leading to coma is usually apparent once the results of routine laboratory tests are available These values for glucose, sodium, potassium, bicarbonate, calcium, magnesium, and phosphorus make any deficiency or excess of these serum components readily apparent and treatable Blood gas analysis for evaluation of acidosis or alkalosis from metabolic or respiratory causes may also be indicated Decreased consciousness caused by diabetic ketoacidosis may initially worsen because of a paradoxical temporary decrease in CSF pH and/or cerebral edema complicating the disease Renal and hepatic functions should be quantified with analysis of blood urea nitrogen, creatinine, and ammonia Markedly elevated serum blood urea nitrogen and creatinine, oliguria, hypertension, anemia, acidosis, and hypocalcemia indicate the presence of uremic coma as a result of renal failure Hyperammonemia with decreased mental status may be caused by hepatic failure, acetaminophen ingestion with resultant hepatotoxicity, valproic acid toxicity, Reye syndrome, or inborn metabolic errors The hyperammonemia of Reye syndrome is accompanied by a history of antecedent viral illness and likely treated with aspirin (see Chapter 97 Neurologic Emergencies ) Unremitting vomiting is soon accompanied by encephalopathy, in the absence of jaundice, scleral icterus, focal neurologic signs, or meningeal irritation Hyperammonemia without accompanying liver failure in the young infant may indicate the presence of a congenital urea cycle defect Coma of Unknown Origin Patients with coma of unknown origin not falling into any of the diagnostic categories discussed previously usually benefit from a noncontrast brain CT scan, CSF analysis, and neurologic consultation, in that order The emergence of new infectious diseases such as West Nile virus and eastern equine encephalitis virus means that diagnosis may require consultation with infectious disease experts and the Centers for Disease Control If meningeal irritation is present without fever or ... origin The growing legality and popularity of edible marijuana preparations has produced a rise in pediatric cannabis ingestions causing ALOC Table 17.5 lists compounds capable of causing coma that... irregular breathing All may signal impending or progressive herniation From the standpoint of the emergency physician, which type of herniation is present is unimportant; all are life-threatening,