Criteria of Prognostication of Comatose States in an Acute Period of Severe Craniocerebral Trauma

M.D. Blagodatsky, O.V. Onysko, A.V. Semenov

Irkutsk State Medical University, Irkutsk, Russia


Despite achievements in studying pathophysiology of severe craniocerebral trauma (SCCT) and introducton of new methods of diagnosis and treatment, mortality is still high and exhibits no tendency to reduction. The last years are characterized by a considerable growth of a number of comatose and vegetative patients. We studied correlation between clinical data and results of CT- and transcranial neurosonographic examinations with the purpose of prognostication of outcomes in comatose patients.

There were 126 cases, watched in an acute period of SCCT. Their age varied from 16 up to 85 years. Interventions were performed in 69 of them. All the cases had severe consciousness disorders on admission: sopor - 17 patients (Glasgow Coma Scale score of 7-9), coma of the 1-2 stage - 67 patients and coma of the 2-3 stage - 42 patients (Glasgow Coma Scale score of 3-5). A volume of examination was dependent on a state severity and indications for an urgent operation. All the cases had brain contusions of various localization. They were single (68), multiple (37) or associated with epi- and subdural hematomas (93), intracerebral hematomas or ventricular hemorrhage (34). Signs of diffuse axonal injury and brain stem contusion were present in 9 cases. Fatal outcomes were watched in 89 patients (76%). Diagnosis was verified with the help of transcranial neurosonography (37 cases) and CT (48 cases), intraoperatively (29 cases) and during post mortem examination (89 cases). There was no dynamics in 31 patients with coma of the 2-3 stage and 29 cases with coma of the 1-2 stage. A vegetative state and consciousness restoration were observed in 27 and 29 cases respectively. Fatal outcomes in a vegetative state were watched in 12 patients; there were 15 survivors and 5 cases, who recovered from a vegetative state in 0.5-3 years.

Cranioventricular indices (Evans index) of the anterior horns of lateral ventricles, areas of the third and fourth ventricles were measured. A state of the ambient cistern and a volume of a parenchymal hemorrhage focus were estimated. It was done with the purpose of studying objective criteria of prognosticating comatose states. A volume of parenchymal hemorrhage varied from 1 to 76 cm3. It was equal to 250 cm3 in subdural and epidural hemorrhages. There was correlation between a hemorrhage volume, a level of consciousness disturbances, Evans index and an outcome. Patients with subdural hemorrhage volume of 45 cm3 and less and parenchymal hemorhage volume of 25 cm3 had Evans index, which did not exceed 30%; the mortality rate reached 56%. When this index was more than 30% and there was deformity of the ambient cistern, the mortality rate in comatose patients increased up to 90%; there was no consciousness gain. These cases developed a vegetative state in 7-14 days of coma. Edema, brain dislocation and subdural hemorrhage were watched in 27 patients (31.5% of fatal outcomes). Evans index was more than 40%. All the patients had protective inhibition coma, signs of temporal-tentorial hemorrhage and herniation into the great occipital infundibulum. There was correlaton between a survival period and a hemorrhage volume: the more volume, the deeper coma and the bigger a minimum period of survival. This fact allowed to make a supposition, that a more reliable criterion of prognosticating a trauma outcome and a survival period is a combination of the following parameters: a certain volume of hemorrhage and a value of Evans index. Autopsy revealed hemorrhages into brain parenchyma in 55 cases. Their volume varied from 1.7 up to 65 cm3, being 25 cm3 on the average. Hemorrhage into ventricles was watched in 13 patients, into frontal lobes in 12 cases, into temporal lobes in 9 cases, into occipital lobes in 18 patients, into brain stem in 3 cases. A combination of contusion foci was observed in 8 patients. Petechial periventricular hemorrhages on the border of the cortex and white matter and into corpus callosum were diagnosed in 5 cases. Widening of the ventricular system and atrophy of frontal lobes were revealed during autopsy in 7 casualties.

There was correlation between an outcome and a degree of compression of the third and fourth ventricles. This sign was ascertained with the help of CT and transcranial neurosonographic examinations of patients with deep coma. It was watched in 94% of fatalities. Deformity of the ambient cistern was one more important sign of the second priority, present in 65% of cases. Besides, there was correlation between a volume of parenchymal hemorrhage and a trauma outcome. The mortality rate was as high as 96% in patients with multiple hemorrhagic foci. It did not exceed 54% in a single contusion focus with a volume of 15 cm3 and less.


  1. The most reliable CT and neurosonographic criteria, used for prognosticating an outcome of SCCT in epidural, subdural and parenchymal hemorrhages include a hemorrhage volume and Evans index, which are characterized by certain relationship. In case of Evans index of more than 30% and deformity of the ambient cistern, the mortality rate in comatose patients increased up to 90%. There was no consciousness gain and a vegetative state developed in 7-14 days of coma.
  2. Correlation between data of transcranial neurosonography, CT findings and autopsy results is the most reliable factor, which can be used during estimation of patients with deep coma and SCCT.
  3. Estimation of coma in patients with SCCT resulted in differentiated application of methods of conservative management; a considerable volume of hemorrhage and a comatose state against a background of unstable vital functions were not contraindications for surgical treatment.
  4. Compression of the third and fourth ventricles with deformity of the ambient cistern in comatose patients, confirmed by CT and TNS, was an unfavorable factor. Smoothing of the ambient cistern in vegetative patients was not a reliable sign. It was explained by an increase of intracranial space due to traumatic atrophic changes.