Thomas A. Gennarelli

A revision of the Trauma Score.

The Trauma Score (TS) has been revised. The revision includes Glasgow Coma Scale (GCS), systolic blood pressure (SBP), and respiratory rate (RR) and excludes capillary refill and respiratory expansion, which were difficult to assess in the field. Two versions of the revised score have been developed, one for triage (T-RTS) and another for use in outcome evaluations and to control for injury severity (RTS). T-RTS, the sum of coded values of GCS, SBP, and RR, demonstrated increased sensitivity and some loss in specificity when compared with a triage criterion based on TS and GCS values. T-RTS correctly identified more than 97% of nonsurvivors as requiring trauma center care. The T-RTS triage criterion does not require summing of the coded values and is more easily implemented than the TS criterion. RTS is a weighted sum of coded variable values. The RTS demonstrated substantially improved reliability in outcome predictions compared to the TS. The RTS also yielded more accurate outcome predictions for patients with serious head injuries than the TS.

Diffuse axonal injury in head injury: Definition, diagnosis and grading

Diffuse axonal injury is one of the most important types of brain damage that can occur as a result of non‐missile head injury, and it may be very difficult to diagnose post mortem unless the pathologist knows precisely what he is looking for. Increasing experience with fatal non‐missile head injury in man has allowed the identification of three grades of diffuse axonal injury. In grade 1 there is histological evidence of axonal injury in the white matter of the cerebral hemispheres, the corpus callosum, the brain stem and, less commonly, the cerebellum; in grade 2 there is also a focal lesion in the corpus callosum; and in grade 3 there is in addition a focal lesion in the dorsolateral quadrant or quadrants of the rostral brain stem. The focal lesions can often only be identified microscopically. Diffuse axonal injury was identified in 122 of a series of 434 fatal non‐missile head injuries–‐10 grade 1, 29 grade 2 and 83 grade 3. In 24 of these cases the diagnosis could not have been made without microscopical examination, while in a further 31 microscopical examination was required to establish its severity.

Organ injury scaling: spleen, liver, and kidney.

The Organ Injury Scaling (O.I.S.) Committee of the American Association for the Surgery of Trauma (A.A.S.T.) was appointed by President Trunkey at the 1987 Annual Meeting. The principal charge was to devise injury severity scores for individual organs to facilitate clinical research. The resultant classification scheme is fundamentally an anatomic description, scaled from 1 to 5, representing the least to the most severe injury. A number of similar scales have been developed in the past, but none has been uniformly adopted. In fact, this concept was introduced at the A.A.S.T. in 1979 as the Abdominal Trauma Index (A.T.I.) and has proved useful in several areas of clinical research. The enclosed O.I.S.s for spleen, liver, and kidney represent an amalgamation of previous scales applied for these organs, and a consensus of the O.I.S. Committee as well as the A.A.S.T. Board of Managers. The O.I.S. differs from the Abbreviated Injury Score (A.I.S.), which is also based on an anatomic scale but designed to reflect the impact of a specific organ injury on ultimate patient outcome. The individual A.I.S.s are, of course, the basic elements used to calculate the Injury Severity Score (I.S.S.) as well as T.R.I.S.S. methodology. To ensure that the O.I.S. interdiffuses with the A.I.S. and I.C.D.-9 codes, these are listed alongside the respective O.I.S. Both the currently used A.I.S. 85 and proposed A.I.S. 90 are provided because of the obligatory transition period. Indeed, A.I.S. 90 contains the identical descriptive text as the current O.I.S.s. The Abdominal Trauma Index and other similar indices using organ injury scoring can be easily modified by replacing older scores with the O.I.S.s.(ABSTRACT TRUNCATED AT 250 WORDS)

Organ injury scaling, II: Pancreas, duodenum, small bowel, colon, and rectum.

The Organ Injury Scaling (O.I.S.) Committee of the American Association for the Surgery of Trauma (A.A.S.T.) has been charged to devise injury severity scores for individual organs to facilitate clinical research. Our first report (1) addressed O.I.S.s for the Spleen, Liver, and Kidney; the following are proposed O.I.S.s for Pancreas (Table I), Duodenum (Table II), Small Bowel (Table III), Colon (Table IV), and Rectum (Table V). The grading scheme is fundamentally an anatomic description, scaled from 1 to 5, representing the least to the most severe injury. We emphasize that these O.I.S.s represent an initial classification system which must undergo continued refinement as clinical experience dictates.

Biomechanics of Acute Subdural Hematoma

Acute subdural hematoma (ASDH) due to ruptured bridging veins occurs under acceleration conditions associated with rates of acceleration onset. That this is due to the strain-rate sensitivity of these veins was confirmed in an experimental model of ASDH. The results of this model were consistent with the clinical causes of ASDH, where 72% are due to high-strain falls and assaults and 24% are due to lower strain-rate vehicular injuries. A mathematical model embodying the known mechanical properties of subdural veins was used to develop tolerance criteria for the occurrence of ASDH. This tolerance curve was consistent with the clinical and experimental data but differed from tolerances previously proposed for head injury.

A New Characterization of Injury Severity

ASCOT (A Severity Characterization of Trauma) is a physiologic and anatomic characterization of injury severity which combines emergency department admission values of Glasgow Coma Scale, systolic blood pressure, respiratory rate, patient age, and AIS-85 anatomic injury scores in a way that obviates ISS shortcomings. ASCOT values are related to survival probability using the logistic function and regression weights reaffirm the importance of head injury and coma to the prediction of patient outcome. The ability of TRISS and ASCOT to discriminate survivors from non-survivors and the reliability of their predictions, as measured by the Hosmer-Lemeshow statistic, were compared using Major Trauma Outcome Study (MTOS) patient data. ASCOT performance matched or exceeded TRISSs for blunt-injured patients and for penetrating-injured patients. ASCOT performance gains were modest for blunt-injured patients. The Hosmer-Lemeshow statistics suggest that ASCOT reliably predicts patient outcome for penetrating-injured patients and nearly so for blunt-injured patients. Statistically reliable predictions were not achieved by TRISS for either set. ASCOT provides a more precise description of patient physiologic status and injury number, location, and severity than TRISS. The ASCOT patient description may be useful in relating to other important outcomes not highly correlated with TRISS or the Injury Severity Score (ISS) such as disability, length of stay, and resources required for treatment.

Physical model simulations of brain injury in the primate

Diffuse brain injuries resulting from non-impact rotational acceleration are investigated with the aid of physical models of the skull-brain structure. These models provide a unique insight into the relationship between the kinematics of head motion and the associated deformation of the surrogate brain material. Human and baboon skulls filled with optically transparent surrogate brain tissue are subjected to lateral rotations like those shown to produce diffuse injury to the deep white matter in the brain of the baboon. High-speed cinematography captures the deformations of the grids embedded within the surrogate brain tissue during the applied load. The overall deformation pattern is compared to the pathological portrait of diffuse brain injury as determined from animal studies and autopsy reports. Shear strain and pathology spatial distributions mirror each other. Load levels and resulting surrogate brain tissue deformations are related from one species to the other. Increased primate brain mass magnified the strain amplified without significantly altering the spatial distribution. An empirically-derived value for a critical shear strain associated with the onset of severe diffuse axonal injury in primates is determined, assuming constitutive similarity between baboon and human brain tissue. The primate skull physical model data and the critical shear strain associated with the threshold for severe diffuse axonal injury were used to scale data obtained from previous studies to man, and thus derive a diffuse axonal injury tolerance for rotational acceleration for humans.

Mortality of patients with head injury and extracranial injury treated in trauma centers.

The types and severity of injuries of 49,143 patients from 95 trauma centers were coded according to the 1985 version of the Abbreviated Injury Scale (AIS). This paper analyzes the causes, incidence, and mortality in 16,524 patients (33.6% of the trauma center patients) with injury to the brain or skull and compares them to patients without head injury. Relative to its incidence, patients with head injury composed a disproportionately high percentage (60%) of all the deaths. This was due to the high mortality rate for head-injured patients. Overall mortality of patients with head injury (18.2%) was three times higher than if no head injury occurred (6.1%). This mortality was little influenced by extracranial injuries except when minor and moderate head injuries were accompanied by very severe (AIS levels 4 to 6) injuries elsewhere. The cause of death in head-injured patients was approximated and it was found that 67.8% were due to head injury, 6.6% to extracranial injury, and 25.6% to both. Head injury is thus associated with more deaths (3,010 vs. 1,972) than all other injuries and causes almost as many deaths (2,040 vs. 2,170) as extracranial injuries. Because of its high mortality, head injury is the single largest contributor to trauma center deaths.

Axonal injury: a universal consequence of fatal closed head injury?

Abstractβ-Amyloid precursor protein immunostaining has recently been shown to be a reliable method for detecting the damage to axons associated with fatal head injury. In an attempt to compare the efficacy of this technique with conventional histological detection of axonal damage, we have reanalysed sections from a large well-characterised series of head-injured and control patients. The results indicate that the frequency of axonal injury has been vastly underestimated using conventional silver techniques, and that axonal injury may in fact be an almost universal consequence of fatal head injury.

Head Injury in Man and Experimental Animals: Clinical Aspects

Clinical studies have demonstrated that, with regard to death, the two worst types of head injury are subdural haematoma (SDH) and diffuse axonal injury (DAI). These two have different mechanisms of causation; SDH occurs much more commonly in non-vehicular injuries, especially falls, while DAI is caused, almost exclusively by vehicular mechanisms. The production of these two types of injury in non-impact acceleration models helps to explain these causal differences, but also shows that both injuries share a common mechanical cause, differing only in degree. SDH is due to vascular injury that is caused by relatively short duration angular acceleration loading at high rates of acceleration. These are the circumstances that occur in falls where the head rapidly decelerates because of impact to firm, unyielding surfaces. DAI is also due to angular acceleration of the head, but occurs most readily when the head moves coronally and it only occurs when the acceleration duration is longer and the rate of acceleration lower than conditions that produce SDH. These conditions are met in vehicle occupants where impact to deformable or padded surfaces lengthens the deceleration and decreases its rate. In DAI the principal mechanical damage is to the brain itself (mainly to axons) while in SDH the primary damage occurs to surface blood vessels. Now that models of the two most important types of head injury have been created in the laboratory, it is hoped that a better understanding of their pathophysiology will result in new strategies to affect protection from their occurrence and in improved treatment when they do occur.