Platelet aggregability in relation to impaired consciousness after head injury.

Abstract

SYNOPSIS ADP-induced platelet aggregation was studied for up to six weeks in 34 patients with head injuries. The patients were divided into three groups according to the degree of impaired consciousness assessed by a clinical coma scale, and change in platelet aggregation was related to the coma score. Platelet aggregation was markedly reduced in all eight patients dying within 24 hours of injury. All 17 patients who remained unconscious for four days or more showed decreased platelet aggregation up to nine days after admission, the most marked effect being on the second day. Platelet function in this group returned to normal within 16 days. Nine patients with only slightly impaired consciousness also showed subnormal platelet aggregation during the first few days with a return to normal by the fourth day. Platelet counts remained within normal limits in all groups. We suggest that during coma following head injury brainstem dysfunction induces neurohumoral changes in the blood which are responsible for a decrease in platelet function.Several recent reports (Goodnight et al, 1974;Preston et al, 1974), have described coagulation abnormalities in relation to head trauma. In these studies platelet counts were done but no attention was given to platelet function. Platelet abnormalities are found in other neurological diseases; after cerebrovascular accidents decreased platelet aggregation has been described (Danta, 1973), and multiple sclerosis is associated with enhanced platelet stickiness (Caspary et al, 1965). In Down's syndrome platelet serotonin (5HT) uptake is found to be decreased (Bayer and McCoy, 1974). Functional disorders of the neutrophil granulocyte (which in several aspects is similar to the blood platelet (Stormorken, 1969)) are found after brain damage, anoxia (Dodsworth and Harris, 1971), and head injury (Van Woerkom et al, 1973). During general anaesthesia impaired phagocytosis is recognized (Lofstrom and Schildt, 1974) and during operations impaired platelet aggregability, possibly caused by general anaesthesia, has been described (O'Brien et al, 1971). In these conditions the changes in platelet and leucocyte function seem to be related to the state of consciousness. Therefore we aimed to study platelet function after severe head injury, particularly in relation to the degree of impaired con-

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

“…The methods used were TEG, Multiplate® (Roche Diagnostics, Basel, Switzerland) and spectrophotometry. All studies found that platelet function decreased after injury [ 22 , 24 , 29 , 36 – 38 ]. This appeared to be independent of platelet transfusion and pre-injury antithrombic therapy [ 36 , 37 ].…”

“…Five other studies reported a similar pattern of normal to below-normal platelet function on admission that then decreased over time in stimulation to collagen (COL) [ 24 ], ADP, thrombin receptor activating peptide (TRAP) and arachidonic acid (AA or ASPI) [ 22 , 37 ]. The lowest platelet function levels were observed 6–48 h after injury [ 24 , 29 , 37 , 38 ] and then returned to normal after 2–16 days [ 22 , 29 , 37 , 38 ]. In the two studies that observed patients for more than one week, platelet function increased to above-normal levels (i.e.…”

“…In this review, we observed that TBI was followed by a decrease in platelet count and function that appeared to be independent of platelet transfusions and antithrombic therapy [ 36 , 37 ]. Platelet count typically stayed within reference ranges [ 19 , 20 , 24 – 26 , 29 , 30 , 35 ] and returned to admission levels within two weeks [ 28 , 30 , 31 ], while platelet function decreased below reference levels about 6–48 h after injury [ 24 , 29 , 37 , 38 ]. The reason behind this is likely multifactorial.…”

Interplay between Platelet Dysfunction and Vascular Thrombosis in Traumatic Injury

“…Platelet count also follows similar pattern albeit slowly [80] though onset of recovery occurs earlier than platelet functions [128] that correlates with changes in ADAMTS-13 levels [130]. The trend of initial hypofunction followed by restoration and rebound hyperfunction has been observed in diverse conditions such as head injury [93,121,131], critical care units [24], and spinal cord injury [132]. In an animal model of TBI, the changes paralleled increase in pro inflammatory cytokines such as IL-6, KC (keratinocyte chemoattractant), and soluble p-selectin [133].…”

Coagulopathy following pediatric head injury and its importance in predicting outcome

“…The tissue factor-factor VII complex activates factor X and prothrombin, occasionally leading to DIC with consequent hemorrhage. Apart from DIC, other coagulation abnormalities like thrombocytopenia and platelet function disorders have been reported to occur commonly following head injury 13 .…”