Hukkelhoven et al. [105] |
134 monitored patients |
Single-centre, retrospective observational analysis of admission clinical predictors of ICP elevation |
Low |
No univariate predictors with p < 0.05. Model discrimination (AUC) = 0.50 (95 % CI 0.41–0.58) and calibration (Hosmer–Lemeshow goodness of fit) = 0.18 |
No admission CT data. No control for decision to monitor. Subjective classification of intracranial hypertension. Used only hourly ICP data |
Toutant et al. [6] |
218 |
Single-centre, retrospective analysis of prospective observational data on correlation of cisterns on admission CT and ICP |
Low |
74 % of monitored patients with absent cisterns had ICP > 30 mmHg |
Lack of rigorous definition and standardization of cisternal compression |
Mizutani et al. [7] |
100 |
Single-centre, retrospective analysis of correlation of admission CT parameters and initial ICP |
Low |
Admission CT findings that contributed to predicting initial degree of intracranial hypertension included (in order of predictive power) cisternal compression, subdural size, ventricular size (III and IV), intracerebral haematoma size, and subarachnoid haemorrhage |
ICP monitored by subarachnoid catheter. No data on later development of intracranial hypertension |
Eisenberg et al. [8] |
753 |
Multi-centre, retrospective analysis of prospective observational data on prediction of abnormal ICP |
Mod |
For first 72 h, strongest (p < 0.001) independent predictors of percent of monitored time that ICP > 20 mmHg were abnormal mesencephalic cisterns, midline shift, and subarachnoid blood. For ICP occurrences >20 mmHg, the strongest (p < 0.001) was cisternal compression, with age, midline shift, and intraventricular blood reaching p < 0.05 |
Used only end-hour ICP values |
Kishore et al. [9] |
137 (47 with normal admission CT) |
Single-centre, retrospective observational analysis of correlation of final Marshall CT classification with ICP course |
Low |
Elevated ICP was present in ≥55 % of patients with intra- or extra-axial haematomas. 17 % of patients with normal admission CT imaging had ICP > 20 mmHg |
Used only intermittent ICP measurements. Did not separate out patients with persistently normal CT imaging |
Narayan et al., 1982 [5] |
226 |
Single-centre retrospective observational study of predictors of intracranial hypertension |
Low |
Association with intracranial hypertension for abnormal admission CT = 53–63 %; for normal admission CT = 13 %. 2+ of predictive variables* with normal CT had 60 % incidence (*age > 40 years, systolic blood pressure ≤90 mmHg, or motor posturing) |
No magnitude for ICP elevation. No prospective verification of normal CT model. Examined only admission CT imaging. Used only end-hour ICP values |
Miller et al., 2004 [10] |
82 |
Single-centre retrospective observational study modeling CT characteristics as predictors of intracranial hypertension |
Low |
Initial CT ventricle size, basilar cisterns, sulcal size, transfalcine herniation, and gray/white differentiation were associated with, but not predictive of intracranial hypertension |
Non-standardised CT variable grading system. Small sample size for modeling. No magnitude for ICP elevation |
Lobato et al., 1983 [11] |
277 |
Single-centre, retrospective observational study of outcome of monitored patients |
Low |
Normal CT imaging post evacuation of extracerebral haematomas did not have ICP problems; normal, non-operative scans had 15 % incidence of intracranial hypertension, none severe (>35 mmHg). Other combinations of contusions or brain swelling had much higher incidences |
No multivariate statistics for ICP. Examined only admission CT imaging |
Poca et al. [12] |
94 |
Single-centre, retrospective analysis of prospective observational data on correlation of final Marshall CT classification with ICP course |
Low |
Development of intracranial hypertension by final Marshall Classification: DI I = 0 %; DI II = 28.6 % (10 % uncontrollable); DI III = 63.2 % (1/3 uncontrollable); DI IV = 100 % (all uncontrollable); EML = 65.2 % (1/2 uncontrollable); NEML = 84.6 % (1/2 uncontrollable) |
Did not separately report admission CT class as predictive of ICP course. Used only intermittent ICP measurements |
Miller et al. [59] |
225 |
Single-centre, retrospective observational study of ICP and outcome of consecutive sTBI patients |
Low |
Less than 25 % incidence of persistent ICP > 20 mmHg in patients with normal admission CT imaging |
Little detail on patients with normal admission CT |
Holliday et al. [106] |
17 |
Single-centre, retrospective observational study of ICP course of patients with normal admission CT imaging |
Low |
86 % of their patients with normal admission CT and ICP > 25 mmHg had associated pulmonary complications. Patients with “normal” admission CT did not develop intracranial hypertension |
Examined only admission CT imaging. Implications of “secondary” ICP elevation unclear. Normal CT could include cisternal compression, slit ventricles |
Lobato et al. [107] |
46 patients (39 monitored) |
Single-centre, retrospective observational study of ICP course of patients with repeatedly normal CT imaging |
Low |
No patient with persistently normal admission CT had sustained intracranial hypertension. Within the first 24 h, 10 % had transient ICP elevation below 25 mmHg |
Examined only admission CT imaging. |
O’Sullivan et al. [108] |
22 patients (8 with highresolution monitoring) |
Single-centre, retrospective observational analysis of ICP course in patients without signs of ICP elevation on admission CT |
Low |
88 % had intracranial hypertension (ICP > 20 mmHg), severe (protracted period ≥ 30 mmHg) in 62 % |
Primary ICP monitoring by subdural systems |
Lee et al. [13] |
36 |
Single-centre, retrospective observational analysis of ICP course in patients with CT diagnosis of DAI |
Low |
28 % had no ICP > 20 mmHg, 47 % had ICP values 21–30 mmHg and 25 % had ICP values >30 mmHg. Only 1 patient (3 %) underwent treatment |
Used only intermittent ICP measurements. Incomplete description of management methods |