Delayed Bleeds from Head Trauma =============================== þ Delayed bleeds are a significant problem: - "Concussion" has 1-10% delayed bleed afterward. - Multi-trauma: 7-10% delayed bleed. [Diaz FG, et al. J Neurosurg 1989;50:217.; Gudeman SK, et al. Neurosugery 1979;5:309. Lopper MG, et al. Radiology 1979;133:645. þ Review of the subject, related to minor GSW to the head, by Harvey Louzon: The question of delayed ICH has arisen on several occasions in the past. Most recently when I suggested admitting patients who were anticoagulated with head trauma and negative initial head CT for 'observation'. Most people on the list felt, at the time, that this option is too agressive, so I'm surprised to see that some are advocating this policy for patients with graze GSW to the scalp who must certainly be at lower risk for delayed sequlae than the patient on warfarin who has sustained a good blow to the head. It certainly appears to be the case that a normal initial CT has good predictive value in excluding short-term morbidity. Nevertheless a literature review reveals a substantial incidence of delayed hemorrhage secondary to blunt trauma. This has been described with subdural (1), epidural (2) and intracerebral bleeds (3). The average incidence of delayed hemorrhage appears to be about 10% which is much higher than I had previously estimated. A substantial number of cases of delayed ICH start out with evidence of cerebral contusion (4). Incidentally, the presence of anticoagulation does indeed appear to place the patient at substantially greater risk for delayed bleed (5). In light of the above it has been my policy to re-scan ALL patients with even recent head trauma who present several days or weeks later with unrelenting symptoms in spite of an initial normal head CT. In answer to your second question, in light of the possible sequlae of cerebral contusion, I would indeed admit these patients if this is identified (4). You ask whether bleeds that are evident subsequently were present initially or not. Often they were not (probably the injury was below the limit of detection of the scanner). On the other hand SDH have been missed in their isodense phase (subacute: 3-14 days old) but that is another matter altogether. H. Louzon MD (1) Snoey ER, Levitt MA Delayed diagnosis of subdural hematoma following normal computed tomography scan. Ann Emerg Med 1994 May;23(5):1127-31 We report the cases of three patients with subdural hematoma following minor closed-head trauma in whom the initial neurologic examinations and cranial computed tomography (CT) scans were normal. In each case, the patient was re-evaluated clinically several times (average of four times) due to persistence of post-traumatic symptoms. The development of focal neurologic signs, which eventually led to a correct diagnosis, was significantly delayed in all three cases (average of 47 days). All three patients had large subdural hematomas requiring surgical drainage. The timely diagnosis of subdural hematoma may be difficult despite the appropriate use of CT scan in the immediate post-traumatic period. Repeat CT scan may be indicated in patients suffering minor head trauma with persistent symptoms. These patients seem to recover without deficit following neurosurgical treatment despite a significant delay in diagnosis. (2) Domenicucci M, Signorini P, Strzelecki J, Delfini R Delayed post-traumatic epidural hematoma. A review. Neurosurg Rev 1995;18(2):109-22 Post-traumatic acute epidural hematoma (EDH) is generally visible on the CT scan done immediately after admission: occasionally, it only comes to light at a later scan and is then termed delayed (DEDH). Since the introduction of CT, the frequency of this occurrence has gone up from 6-13% to 30%. The mechanisms responsible for the delayed appearance of the epidural hematoma a "tamponade" effect are usually increased endocranial pressure and post-traumatic arterial hypotension as well as, in a limited number of cases, coagulopathy, CSF drainage, and arterio-venous shunt. The authors report 5 of their own cases and 45 published cases and discuss the characteristics of this particular form of hematoma and its outcome. (3) Borthne A, Sortland O, Blikra G [Head injuries with delayed intracranial hemorrhage] Tidsskr Nor Laegeforen 1992 Nov 10;112(27):3425-8 Nine cases of delayed intracranial haematomas were found among 300 patients with head injuries during a two-year period. Six of the nine patients developed delayed traumatic intracerebral haematoma, two epidural haematoma and one subdural haematoma. Delayed intracerebral haematoma was diagnosed from 12 hours to six days after the trauma. The primary CT showed brain contusion in the majority of the patients. The outcome was poor. One patient died and two were severely disabled. The clinical course was more rapid in the two patients with epidural haematoma than in the others. Marked elevation of intracranial pressure was monitored in both cases prior to the second CT examination. In spite of successful evacuation of the haematoma, one patient died and the other developed physical and mental retardation. In one patient a subdural haematoma was diagnosed three months after the trauma. The patient did well postoperatively. (4) Fukamachi A, Nagaseki Y, Kohno K, Wakao T The incidence and developmental process of delayed traumatic intracerebral haematomas. Acta Neurochir (Wien) 1985;74(1-2):35-9 Although delayed traumatic intracerebral haematomas (DTICH) have been frequently reported especially after the advent of computerized tomography (CT), the developmental processes of traumatic intracerebral haematomas and the incidence of DTICH have not been described precisely. Based on early sequential CT examinations of 84 intracerebral haematomas for which initial CT scans were performed as early as within 6 hours of injury, we could ascertain four types of the developmental processes: Type I (39%) included the haematomas which were already evident in the initial CT scans, Type II (11%) the haematomas which were small or medium initially and increased their sizes afterwards, Type III (24%) the haematomas of which admission CT scans could not demonstrate any changes at the sites of development of the haematomas, and Type IV (26%) the haematomas of which initial CT scans showed a salt and pepper or flecked high-density appearance. Types III and IV denoted the DTICH and accounted for 50% of all the haematomas. Therefore, DTICH are thought to be not as uncommon as previously reported. Aetiologies and changes in the concepts of the DTICH are discussed, and it is stressed that, in the cases with eventual extra- and intra-cerebral combined haematomas, any surgical treatment of an extracerebral haematoma plays an important role in the development of DTICH. (5) Stein SC, Young GS, Talucci RC, Greenbaum BH, Ross SE Delayed brain injury after head trauma: significance of coagulopathy. Neurosurgery 1992 Feb;30(2):160-5 We reviewed the records of 253 patients with head injury who required serial computed tomographic (CT) scans; 123 (48.6%) developed delayed brain injury as evidenced by new or progressive lesions after a CT scan. An abnormality in the prothrombin time, partial thromboplastin time, or platelet count at admission was present in 55% of the patients who showed evidence of delayed injury, and only 9% of those whose subsequent CT scans were unchanged or improved from the time of admission (P less than 0.001). Among patients developing delayed injury, mean prothrombin time at admission was significantly longer (14.6 vs. 12.6 s, P less than 0.001) and partial thromboplastin time was significantly longer (36.9 vs. 29.2 s, P less than 0.001) than patients who did not have delayed injury. If coagulation studies at admission were normal, a patient with head injury had a 31% risk of developing delayed insults. This risk rose to almost 85% if at least one clotting test at admission was abnormal (P less than 0.001). We conclude that clotting studies at admission are of value in predicting the occurrence of delayed injury. If coagulopathy is discovered in the patient with head injury early follow-up CT scanning is advocated to discover progressive and new intracranial lesions that are likely to occur. Another Reference: Stein SC, Young GS, Talucci RC, Greenbaum BH, Ross SE Delayed brain injury after head trauma: significance of coagulopathy. Neurosurgery 1992 Feb;30(2):160-5 ABSTRACT: We reviewed the records of 253 patients with head injury who required serial computed tomographic (CT) scans; 123 (48.6%) developed delayed brain injury as evidenced by new or progressive lesions after a CT scan. An abnormality in the prothrombin time, partial thromboplastin time, or platelet count at admission was present in 55% of the patients who showed evidence of delayed injury, and only 9% of those whose subsequent CT scans were unchanged or improved from the time of admission (P less than 0.001). Among patients developing delayed injury, mean prothrombin time at admission was significantly longer (14.6 vs. 12.6 s, P less than 0.001) and partial thromboplastin time was significantly longer (36.9 vs. 29.2 s, P less than 0.001) than patients who did not have delayed injury. If coagulation studies at admission were normal, a patient with head injury had a 31% risk of developing delayed insults. This risk rose to almost 85% if at least one clotting test at admission was abnormal (P less than 0.001). We conclude that clotting studies at admission are of value in predicting the occurrence of delayed injury. If coagulopathy is discovered in the patient with head injury early follow-up CT scanning is advocated to discover progressive and new intracranial lesions that are likely to occur.