How to encounter the child in coma

Introduction
Comatose child almost always refers to the pediatric emergency unit (1). Many reports showed that encounter with these situations need good level of critical care knowledge and good level of professional clinical practice (2,3).
 Level of consciousness in children is a very important question with difficult answer (4). Coma refers to a state of complete unawareness and unresponsiveness (5). One of the most important scales for the assessment of neurologic conditions is the Glasgow Coma Scale (Table 1) (6). Some etiologies and diagnosis of acute childhood comatose are listed in Table 2 and 3 (5).
Differential diagnosis for children presenting with coma or altered level of consciousness is very important for any pediatrician (7-9).

Pathophysiology of coma
Brainstem and pons have important role in our consciousness; they modulate cortical signals for other downstream targets of central nervous system (CNS) (10).
Ascending reticular activating system (ARAS) is responsible for awareness. Good function of the ARAS and brain hemispheres depends on many factors, including the presence of substrates needed for energy production, adequate blood flow to deliver these substrates, maintenance of normal body temperature, absence of abnormal serum concentrations of metabolic wastes elements or exogenous toxins, and the absence of CNS infection or seizure with abnormal neuronal activity (11).

Non-traumatic Coma
CNS infection
Meningitis, encephalitis, or other types of CNS infection may cause coma in a child (12,13). Inflammation of the brain might be due to infections and this condition should be seriously considered because of unexpected results (14). Despite the fact that Haemophilus influenza and Streptococcus pneumoniae vaccines are available, bacterial infection is still a common cause of loss of consciousness (LOC), but other microorganisms can involve in LOC (15). Enteroviruses and Herpes viruses could cause viral encephalitis. Most of the time, fungal infections or parasitic infections (toxoplasmosis, etc.) have a slower onset of symptoms (16). Focal infections (brain abscess, subdural empyema, epidural abscess) could induce focal seizure and may lead to LOC (17).

Malignancy
Direct invasion of the ARAS by the malignancies such as hematologic malignancy with CNS involvement may cause LOC (18) which may be due to increase in intracranial pressure, seizure (19) or brain hemorrhage. Lethargy and vomiting are some of the signs and symptoms in brain malignancy involvement (20).
Vascular cause
Cerebrovascular origin of coma is important for patient’s management. Three types of etiology interrupt cerebral blood flow including brain hemorrhage, thrombosis and embolism (21). Arteriovenous malformation (AVM), aneurysm, and cavernous hemangioma are structural abnormalities which cause brain hemorrhage (22,23). They may lead to the spontaneous intracranialhemorrhage and LOC (23).

 Ischemic stroke occurs due to thrombosis or embolism. Stroke usually may cause focal neurological deficit, not coma (24). Brain hemorrhage and parenchymal swelling could lead to raised ICP (25) and make ARAS blood flow deficiency. Consequently, this deficiency leads to LOC (26).

Toxic Ingestions
Pediatric toxic ingestion or accidental poisoning is a very common chief complaint in pediatric emergency unit (27,28). Toxin ingestion could be unintentional or intentional (29).Body packing is one of the child abuses and may be a cause of coma that should be considered (30). Special epidemiological surveillance in any region is important and necessary (28). Some toxin may cause coma or LOC due to several pathophysiology.

Serum metabolites and substrate
Abnormal serum levels of substrates or metabolites could lead to the LOC and coma. Hypoglycemia, metabolic acidosis or alkalosis, abnormal serum electrolyte levels (Na, K, Ca, P and Mg) are some of the main causes of serum substrate abnormalities which may lead to LOC (31,32). Renal and hepatic failure may result in progressive apathy, confusion and coma (33).
Urea cycle deficiency could present with ALOC and hyperammonemia in neonates or young children. Hyperammonemic coma is a result of total enzyme insufficiency (34).
Reye’s syndrome is very rare but could induce liver failure and could predispose the patient to delirium that progresses to coma (35).

Acknowledgement
We would like to thank Clinical Research Development Center of Ghaem Hospital for their assistant in this manuscript. This study was supported by a grant from the Vice Chancellor for Research of the Mashhad University of Medical Sciences for the research project as a medical student thesis with approval number of 901043.

Conflict of Interest
 The authors declare no conflict of interest.