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*Members: Drs. Dorothi' M. Anna Jarvis (chairman), Emergencv Medicine, Hospital for Sick Children, Toronto; Marilvn Li
(vice-chairman), head, Emergency Services, Children 's Hospital of Eastern Ontario, Ottawa; Donald K. Clogg (past chairman), director,
Emergency Department, Alberta Children's Hospital, Calgarv; Robert Thivierge (secretarvy), Emergencv Departmnent, h6pital
Sainte-Justine, Montreal; and Niranjan Kissoon (member-at-large and principal author), director, Emergency Department, Children's
Hospital of Western Ontario, London. Canadian Paediatric Society Accident Prevention Committee representative: Dr. Heather Onvett,
Department ofPediatrics, Queen 's Universitv, Kingston, Ont.
Reprint requests to: Emergencv Paediatrics Section, Canadian Paediatric Societv, Children's Hospital of Eastern Ontario, 401 Smnvth Rd.,
Ottawa, Ont. KJH 8LI
- For prescribing information see page 1007 CAN MED ASSOC J 1990; 142 (9) 949
.M
Control of increased intracranial pressure children will vomit two to three times after even a
minor head injury.7 However, protracted vomiting
Table 1 outlines the emergency therapy for and retching associated with other symptoms or
increased intracranial pressure, which is common signs indicate a more severe head injury. Amnesia,
among children who have severe head injury with or irritability, lethargy, pallor or agitation may also
without a mass lesion. Since the risk of death indicate severe injury.
increases with an intracranial pressure greater than The child's medical history must be obtained;
20 mm Hg prompt, aggressive treatment in suspect- evidence of such conditions as a predisposition to
ed cases is warranted. seizures or a bleeding diathesis is important and
would further dictate clinical management.
History-taking and physical and neurologic Table 2 outlines the salient points in a physical
assessment and neurologic examination. Bradycardia with hy-
pertension (a Cushing response) is usually a late
These procedures are invaluable to (a) deter- response in children with increased intracranial pres-
mine the severity of the intracranial injury and sure and therefore not very reliable.4 Early clues to
identify those at risk for secondary injury and (b) increased intracranial pressure include a decrease in
identify injuries to other regions that may contribute the Glasgow Coma Scale score of 2 points or more,
to illness and death. abnormality or changes in pupillary size and reaction
Events surrounding the injury, such as the to light, respiratory abnormalities and development
mechanism of injury, the time and the loss or of paresis in absence of shock, hypoxia or seizures.
presence of consciousness, should be obtained. How- Because a rapid pulse often signifies blood loss,
ever, reports may be inconsistent and hence unreli- other injuries should be sought. The child with
able. Fortunately the progression of symptoms pro- severe head injury should be kept in a normothermic
vides invaluable information to assist the physician state since increased cerebral metabolism may cause
in clinical decision-making. A brief seizure at the secondary brain injury.
time of injury may not be clinically significant and The Glasgow Coma Scale (Table 3) is an impor-
may not necessitate therapy. However, one or more tant tool that influences treatment decisions and
prolonged seizures associated with cardiorespiratory outcome.6" Although coma scales for children have
compromise necessitates prompt treatment. Many not been validated, the Glasgow scale may be used
for children less than 2 years of age, who have
limited verbal skills, by assigning a full verbal score
.. . .. - if the child cries after stimulation.9 The rest of the
neurologic examination helps to determine the pres-
ence of focal neurologic signs that may signify an
intracranial mass lesion or impending cerebral her-
niation from increased pressure.
11 :.. .. ..
f' ;.!
952 CAN MED ASSOC J 1990; 142 (9) For prescribing information see page 972