The management of "asymptomatic" epidural hematomas. A prospective study

Standard neurosurgical management mandates prompt evacuation of all epidural hematomas to obtain a low incidence of mortality and morbidity. This dogma has recently been challenged. A number of authors have suggested that in selected cases small and moderate epidural hematomas may be managed conservatively with a normal outcome and without risk to the patient. The goal of this study was to define the clinical parameters that may aide in the management of patients with small epidural hematomas who were clinically asymptomatic at initial presentation because there was no clinical evidence of raised intracranial pressure or focal compression. A prospective study was conducted of 22 patients (17 males and five females) aged from 1 to 71 years, who had a small epidural hematoma diagnosed within 24 hours of trauma and were managed expectantly. Of these, 32% subsequently required evacuation of the epidural hematoma 1 to 10 days after the initial trauma. Analysis of the patients revealed that age, sex, Glasgow Coma Scale score, and initial size of the hematoma are not risk factors for deterioration. However, deterioration was seen in 55% of patients with a skull fracture transversing a meningeal artery, vein, or major sinus, and in 43% of those undergoing computerized tomography (CT) within 6 hours of trauma. In contrast, only 13% of patients in whom the diagnosis of a small epidural hematoma was delayed over 6 hours subsequently required evacuation of the epidural collection. Of patients with both risk factors, 71% required evacuation of the epidural hematoma. None of the patients suffered neurological sequelae attributable to this management protocol. It was concluded that patients with a small epidural hematoma, a fracture overlaying a major vessel or major sinus, and/or who are diagnosed less than 6 hours after trauma are at risk of subsequent deterioration and may require evacuation. Conversely, patients without these risk factors may be managed conservatively with repeat CT and careful neurological observation, because of the low risk of delayed deterioration.     

Risk of postoperative hemorrhage after intracranial surgery after early nadroparin administration: results of a prospective study

OBJECTIVE: Early postoperative pharmacological prophylaxis of deep vein thrombosis after intracranial surgery is still a matter of debate because of concerns regarding the formation of postoperative hematoma. The objective of this study was to prospectively analyze the rate of postoperative hemorrhage during a 3-year period of early postoperative administration of the low molecular weight heparin nadroparin (Fraxiparin) plus compression stockings in a large cohort of patients undergoing intracranial surgery. METHODS: A total of 2823 intracranial neurosurgical procedures, performed between June 1999 and 2002, were studied. Of these operations, 1319 (46.7%) were major intracranial surgical procedures (Group 1). Group 2 comprised 1504 operations (53.3%) considered to be minor surgical procedures (e.g., shunt procedures, biopsies). All patients except those with transnasal transsphenoidal removal of pituitary tumors underwent early postoperative imaging (computed tomography or magnetic resonance imaging) to determine postoperative hemorrhage. All significant postoperative hematomas (defined as those requiring surgical evacuation because of relevant space occupation and/or neurological deterioration) were treated surgically. Prophylaxis of venous thromboembolic events included early (<24 h) postoperative administration of 0.3 ml nadroparin subcutaneously plus intra- and postoperative compression stockings until discharge. RESULTS: Forty-three major postoperative hemorrhages (1.5%) were observed after 2823 intracranial procedures (95% confidence interval, 1.1-2.05). Forty-two (3.2%) of 1319 postoperative hematomas occurred in patients undergoing major intracranial procedures (Group 1). There was only 1 (0.07%) significant hemorrhage after 1504 minor intracranial procedures (Group 2). A subgroup analysis of patients who needed preoperative anticoagulation because of medical comorbidity did not reveal an increased frequency of postoperative hematoma when anticoagulation was stopped 24 hours before surgery P = 0.1, chi(2) test; 95% confidence interval, 0.89-3.0). CONCLUSION: This report describes the largest prospective study conducted to date to determine the hemorrhage rate after early postoperative anticoagulation. The results support the concept of postoperative pharmacological thromboembolic prophylaxis in patients undergoing intracranial surgery.     

Intracranial hematomas following aneurysmal rupture: experience with 309 cases

Three hundred and nine consecutive cases of intracranial hematomas due to aneurysmal rupture--representing 34% of the total number of patients with aneurysms observed in a 12-year period--were evaluated; of these, 211 were submitted to computed tomography scan. Hematomas were present on admission in 71% of patients and occurred at rebleeding in 29%. Ruptured middle cerebral artery aneurysms caused an intracranial hematoma more frequently than aneurysms in other locations. Ventricular hematomas were frequently observed--especially at rebleeding--in cases with anterior communicating artery aneurysms. Basal ganglia hematomas were detected in eight cases with internal carotid bifurcation aneurysms and in three with middle cerebral artery aneurysms. Subdural hematomas were observed in 32 cases, mainly due to ruptured middle-cerebral-artery and internal-carotid-artery aneurysms. As for clinical evolution, a rapid deterioration was observed in 39% of cases and a chronic course in 46%; a subacute deterioration was far less frequent. Delayed deterioration from vasospasm was observed in 8% of cases, and appeared to be related to the amount of subarachnoid bleeding associated with the hematoma. One hundred and forty-two patients were submitted to surgical treatment (evacuation of hematoma together with exclusion of aneurysm); deep coma, poor medical condition, stabilized neurological disability, or combinations of these factors accounted for the high number of patients not operated upon. Regardless of treatment, 24% of patients showed good results and 58% died. Presence of a large hematoma, ventricular hemorrhage, and shift of the ventricles represented significant risk factors, associated with a poor prognosis. A comparison between two groups of patients admitted within 3 days of hemorrhage--47 operated on early, and 149 with delayed treatment--showed that better results were achieved by early operations, especially for cases in Hunt's grades IV and V.     

Acute brain swelling during evacuation of subdural hematoma caused by delayed contralateral extradural hematoma: report of two cases

Two patients experienced severe brain swelling during the evacuation of acute subdural hematomas. Postoperative computed tomographic (CT) scans revealed delayed extradural hematomas on the sides opposite the subdural hematomas. Extradural bleeding occurred in the area of the fractured skull. One patient improved neurologically after evacuation of the extradural hematoma, and the other was not operated because he was moribund. Drilling exploratory burr holes in the fractured area may have been a better strategy than awaiting a postoperative CT scan. The reduction of intracranial pressure after the removal of subdural hematoma was postulated to be the most important factor contributing to the formation of the extradural hematoma.     

The significance of thrombocytopenia in the development of postoperative intracranial hematoma

A group of 35 patients undergoing intracranial surgery who exhibited perioperative thrombocytopenia (platelet count less than 150,000/microliters) was studied retrospectively. Of the 35 patients, 14 (40%) developed postoperative intracranial hematomas requiring reoperation and seven (20%) died within 2 weeks after the operation. Analysis revealed that a perioperative platelet count below 100,000/microliters in a patient who failed to respond to platelet transfusions was associated with a higher risk of postoperative hematoma formation. All six patients with this profile developed postoperative hematomas. If the platelet count rose promptly from below 100,000/microliters to a normal level after platelet transfusions, the incidence of hematoma formation decreased dramatically. None of the three patients with this response developed postoperative hematoma. In patients in whom an acute drop in platelet count from the normal range to between 100,000 and 124,000/microliters occurred in the immediate perioperative period, there was a significantly higher change of hematoma formation; this finding has not hitherto been described. Of the 14 patients with this clinical course, eight developed postoperative hematoma after craniotomy for tumors and vascular lesions. This latter observation was substantiated by the fact that thrombocytopenic patients with postoperative hematomas had a greater reduction in platelet count than thrombocytopenic patients with no postoperative hematomas (p = 0.0004).     

Image-guided endoscopic evacuation of spontaneous intracerebral hemorrhage

BACKGROUND: Spontaneous ICH is a devastating disease with high morbidity and mortality. Intracerebral hemorrhage lacks an effective medical or surgical treatment despite the acknowledged pathophysiologic benefits of achieved hemostasis and clot removal. Image-guided stereotactic endoscopic hematoma evacuation is a promising minimally invasive approach designed to limit operative injury and maximize hematoma removal. METHODS: A single-center randomized controlled trial was designed to assess the safety and efficacy of stereotactic hematoma evacuation compared to best medical management. Patients were randomized within 24 hours of hemorrhage in a 3:2 fashion to best medical management plus endoscopic hematoma evacuation or best medical management alone. Data were collected to assess efficacy and safety of hematoma evacuation and to identify procedural components requiring technical improvement. RESULTS: Ten patients have been enrolled and randomized to treatment. Six patients underwent endoscopic evacuation with a hematoma volume reduction of 80% +/- 13% at 24 hours post procedure. The medical arm demonstrated a hematoma enlargement of 78% +/- 142% during this same period. Rehemorrhage rates and deterioration rates were similar in the 2 groups. Mortality was 20% in the endoscopic group and 50% in the medical treatment cohort. The endoscopic technique was shown to be effective in identification and evacuation of hematomas, whereas reduction in the number of endoscopic passes and maintenance of hemostasis require further study. CONCLUSION: Image-guided stereotactic endoscopic hematoma removal is a promising minimally invasive technique that is effective in immediate hematoma evacuation. This technique deserves further investigation to determine its role in ICH management.     

Is computed tomographic scanning necessary in patients with tentorial herniation? Results of immediate surgical exploration without computed tomography in 100 patients

Computed tomographic (CT) scans are performed on virtually all patients with severe head injury at the time of admission. Because of the time involved in obtaining these studies, the evacuation of significant intracranial mass lesions is delayed. To avoid such delays, the authors performed burr-hole exploration for the diagnosis of intracranial hematomas before CT scans were obtained in 100 consecutive head-injured patients with clinical signs of tentorial herniation or upper brain stem dysfunction upon admission to the emergency room. Patients in whom a hematoma was discovered had a craniotomy for evacuation of the clot; those in whom the exploration was negative had a CT brain scan immediately after operation. Burr-hole exploration revealed extracerebral mass lesions in 56 patients. In 38 patients, the exploration was negative, and postoperative CT scanning showed no significant hematoma. Of 6 patients in whom the CT scan demonstrated extraaxial hematomas requiring surgical evacuation, 4 had subdural hematomas that were missed because the exploration was incomplete; 1 patient had an epidural hematoma and 1 had a subdural hematoma contralateral to a craniotomy on the side of a positive initial burr-hole exploration. Our results indicate that the relatively small subgroup of head-injured patients with early tentorial herniation or upper brain stem compression have a high incidence of immediate extraaxial hematomas and a low incidence of intracerebral hematomas. This is particularly true of patients over 30 years of age and those who suffer low speed trauma, such as falls and vehicle-pedestrian accidents.     

Acute nontraumatic spinal subdural hematomas in three patients.

STUDY DESIGN: The clinical data, magnetic resonance imaging, intraoperative findings, and functional outcome were reviewed for three patients under anticoagulant therapy who experienced acute nontraumatic spinal subdural hematoma. OBJECTIVES: To draw attention to this rare complication of anticoagulant therapy and to assess the magnetic resonance findings and clinical outcome of patients with spinal subdural hematoma after surgical evacuation. SUMMARY OF BACKGROUND DATA: Among intraspinal hematomas, spinal subdural hematomas are by far the least common. Magnetic resonance findings have been demonstrated in only a few cases of spinal subdural hematomas. The timing of the operation and the anatomic location of the hematoma essentially determine the functional outcome. METHODS: Three case reports of spinal subdural hematomas in patients receiving anticoagulant therapy are presented. Particular interest was given to the clinical and magnetic resonance data, the intraoperative findings, and the functional outcome. RESULTS: The three patients each had a complete preoperative neurologic deficit. Sagittal T1- and T2-weighted magnetic resonance images of the spine proved to have high sensitivity for defining the type of bleeding and delineating the craniocaudal extension of the hematoma. Surgical evacuation was performed within 26 hours after the onset of symptoms. Intraoperative findings showed the hematoma to be confined between the dura and the arachnoid in two patients, and to be associated with rupture into the subarachnoid space in one patient. Postoperative recovery was incomplete in two patients, and did not improve in the remaining patient. CONCLUSIONS: Spinal subdural hematoma must be considered in patients under anticoagulant therapy with spontaneous signs of acute spinal cord or cauda equina compression. Magnetic resonance imaging with sagittal T1- and T2-weighted images were adequate and reliable for diagnosis of spinal subdural hematoma. On the basis of previous studies and the authors' intraoperative findings, spinal subdural hematomas could be viewed as spinal dural border hematomas. The level of preoperative neurologic deficit seemed to be critical for recovery despite prompt surgical evacuation.     

Post-thyroidectomy cervical hematoma

AIM: Postoperative hematoma is a complications of thyroid surgery uncommon but potentially life threatening. It has implications for the trend toward outpatient procedures. METHODS: Retrospective review of 1.221 thyroidectomies performed at our institution over a 6-years period, to identify patients with hematomas requiring reoperation. Symptoms, treatment and findings at reoperation were evaluated. A control group (n=120) was compared for perioperative risk factors and outcome. RESULTS: Eighteen patients (1.5%) developed a postoperative hematoma. Symptoms included neck pain/pressure in 10 patients, respiratory distress in 9, wound drainage in 2, dysphagia in 1, agitation and sweating in 1. Mean time to symptom onset was 12 hours (range: 1.3-40 hours). Six hematomas presented between 7 and 24 hours, and 3 beyond 24 hours. Six patients required bedside hematoma evacuation. The bleeding source was identified in 15 patients. All patients recovered well, but one required a temporary tracheostomy. Case/controls comparison yielded in the study group a higher prevalence of hyperthyroidism (55.6% vs 25.8%, P=0.022) and intrathoracic goiter (50% vs 22.5%, P=0.029), and a longer mean hospital stay (5.22 vs 4.1, P=0.012); morbidity was not increased. CONCLUSIONS: Postoperative hematoma is an uncommon complication of thyroid surgery. If treated promptly, serious consequences can be avoided. The relatively long interval between the initial operation and the hematoma development needs to be considered when establishing outpatient practice guidelines.     

Acute epidural hematoma: an analysis of factors influencing the outcome of patients undergoing surgery in coma

Mortality due to epidural hematoma is virtually restricted to patients who undergo surgery for that condition while in coma. The authors have analyzed the factors influencing the outcome of 64 patients who underwent epidural hematoma evacuation while in coma. These patients represented 41% of the 156 patients operated on for epidural hematoma at their centers after the introduction of computerized tomography (CT). Eighteen patients (28.1%) died, two (3.1%) became severely disabled, and 44 (68.8%) made a functional recovery. The mortality rate for the entire series was 12%, significantly lower than the 30% rate observed when only angiographic studies were available. A significant correlation was found between the final result and the mechanism of injury, the interval between trauma and surgery, the motor score at operation, the hematoma CT density (homogeneous vs. heterogeneous), and the hematoma volume. The patient's age, the course of consciousness before operation (whether there was a lucid interval), and the clot location did not correlate with the final outcome. The mortality rate was significantly higher in patients operated on within 6 hours or between 6 and 12 hours after injury than in those undergoing surgery 12 to 48 hours after injury. Compared with the patients operated on later, the patients undergoing surgery in the early period were, on the average, older and had more rapidly developing symptoms, more pupillary changes, lower motor scores at surgery, larger hematomas, a higher incidence of mixed CT density clots, more severe associated intracranial lesions, and higher postoperative intracranial pressure (ICP). The mechanism of trauma seems to influence the course of consciousness before and after surgery. Passengers injured in traffic accidents had a lower incidence of a lucid interval and longer postoperative coma than patients with low-speed trauma, suggesting more frequent association of diffuse white matter-shearing injury. The duration of postoperative coma correlated with the morbidity rate in survivors. Forty-eight patients (75%) had one or more associated intracranial lesions, and 70% of these required treatment for elevation of ICP after hematoma evacuation. An ICP of over 35 mm Hg strongly correlated with poor outcome; administration of high-dose barbiturates was the only effective means for lowering ICP in nine of 15 patients who developed severe intracranial hypertension after surgery. This study attempts to identify patients at greater risk for presenting postoperative complications and to define a strategy for control CT scanning and ICP monitoring.     

Delayed postoperative spinal epidural hematomas.

BACKGROUND CONTEXT: Symptomatic epidural hematomas after spinal surgery are uncommon and are usually diagnosed within 24 hours after surgery. PURPOSE: We report a series of delayed epidural hematomas in a subset of patients who awoke from surgery neurologically unchanged and then deteriorated more than 3 days after their index procedure. The goals of this report are to outline the clinical presentation, radiological characteristics and outcome of this uncommon entity. STUDY DESIGN/SETTING: We retrospectively reviewed the database of six spine surgeons over a 4-year period, looking for presence of epidural hematomas as a cause of clinical deterioration after an asymptomatic postoperative period of at least 3 days. PATIENT SAMPLE: We identified a subset of patients who awoke from surgery neurologically unchanged and then deteriorated more than 3 days after spinal surgery. A total of 4,018 patients were identified over the 4-year period of review. OUTCOME MEASURES: Presence of spinal epidural hematoma as a cause of clinical deterioration after an asymptomatic period of at least 3 days. The medical records, including the history, physical, preoperative and postoperative neurological examinations, as well as plain radiographs and magnetic resonance images, were reviewed. METHODS: We retrospectively reviewed the database of six spine surgeons over a 4-year period. We looked for delayed spinal epidural hematomas as a cause of clinical deterioration after an asymptomatic postoperative period of at least 3 days. We examined potential risk factors for spinal extradural hematomas. RESULTS: Of 4,018 patients, we identified seven with spinal epidural hematoma who presented more than 3 days after their index procedure. The initial presenting symptom, which heralded the subsequent onset of neurological deterioration, consisted of severe sharp pain with radiation to the extremities. The average time to neurological deterioration was 5.3 days. Fifty-seven percent of the patients had multiple previous spinal surgeries at the site of the epidural hematoma. Surgical evacuation of the epidural hematomas resulted in neurological improvement in five patients. Persistent neurological deficits were observed in two patients. CONCLUSION: Delayed spinal epidural hematomas are an uncommon cause of delayed deterioration after spinal surgery. Previous surgery with attendant scarring that results in impairment of clot resorption may be a contributing factor in the development of the condition.     

Intraoperative development of contralateral epidural hematoma during evacuation of traumatic extraaxial hematoma

Intraoperative development of an epidural hematoma contralateral to a craniotomy for acute traumatic extraaxial hematoma has been previously reported. This entity, however, has never been distinctly defined and differentiated from either the delayed or the bilateral acute epidural hematoma. We present 3 new cases of intraoperative contralateral acute epidural hematoma and review the 14 previously reported cases. The typical clinical presentation is a severe head injury with an acute extraaxial hematoma and severe ipsilateral brain displacement during craniotomy. If brain displacement is not noted at craniotomy, then the contralateral hematoma is manifested by immediate postoperative neurological deterioration or intractable elevated intracranial pressure. The presence of any of these signs makes an immediate postoperative CT scan or burr holes contralateral to the original craniotomy mandatory for early diagnosis. In addition to defining "intraoperative contralateral epidural hematoma," stricter definitions of the terms "delayed epidural hematoma" (no hematoma present on the initial CT scan but one present on a later scan) and "bilateral epidural hematomas" (present on the initial scan) are proposed.     

Behandlungsmöglichkeiten bei traumatischen Epiduralhämatomen

The authors report 118 consecutive cases of patients with traumatic extradural hematoma (EDH) which were analyzed according to different clinical parameters and treatment modalities. Patients, treated for EDH between 1992 and 1998 in our department were distributed into 5 treatment groups depending on their clinical and neuroradiological findings on admission and during the hospitalization. Group I consisted of 75 patients (64%) who required immediate surgical evacuation of the hematoma after admission. Group II included 12 patients (10%) with initially conservative treatment despite visible EDH on the first CT-scan, which had to be operated on in the course because of neurological deterioration or increase of hematoma size. The 14 patients (12%) forming group III developed an acute EDH after the initial CT-scan revealed no extradural blood; 7 patients (6%) out of group IV showed a chronic EDH (delay trauma/diagnosis > 72 h), which required operative evacuation. All 10 patients (8%) comprising group V were treated conservatively. In each group the following parameters were analyzed: patient age, size and location of hematoma, trauma mechanism, additional intracranial lesions or skull fractures, intraoperative findings and neurostatus on admittance and during the hospitalization. The decision for non-operative treatment of EDH and the timing of a delayed intervention has to be made individually in each case in dependence of parameters like patient age, hematoma-size and -location and neurological status and course. Chronic EDH should be operated immediately, as well as hematomas presenting with an increase in size. Delayed developing EDH imply worse outcome and make adequate surveillance of high-risk patients mandatory.     

Rapid resolution of acute epidural hematoma: case report and review of the literature

Acute epidural hematomas present a serious and urgent condition. Standard management is early diagnosis and immediate surgical evacuation. Otherwise, there is a high risk of quick deterioration and death. Only patients with small asymptomatic epidural hematomas can be managed conservatively with close observation. We present a case of traumatic right temporal epidural hematoma. This is one of the rare cases of rapid spontaneous resolution of epidural hematomas within hours. Various possible mechanisms to explain the rapid resolution are discussed together with a review of the literature regarding the conservative treatment of epidural hematoma.     

Delayed evolution of post-traumatic contralateral extracerebral hematoma after evacuation of initial hematoma]

105 patients over a 5-year period underwent emergency evacuation of traumatic intracranial hematomas. Seven (6.7%) developed delayed contralateral extracerebral hematomas (5 epidural and 2 subdural hematomas). These hematomas were insignificant or not present on initial computed tomography (CT) scan, but repeat CT scan after craniotomy showed sizable hemorrhage. In one patient, neurological deterioration heralded the delayed onset. In one case, intraoperative ultrasound imaging disclosed an epidural hematoma. Ultrasound examination is recommended in cases with a skull fracture contralateral to the initial hemorrhage.     

Implications of systemic hypotension for the neurological examination in patients with severe head injury

Thirty-six patients admitted with severe head injury and various degrees of systemic hypotension were studied to determine the effect of hypotension on the validity of the neurological examination in reflecting mechanical brain compression. All patients had clinical signs of transtentorial herniation or upper brainstem compression and underwent immediate bilateral placement of exploratory burr holes for the diagnosis and removal of intracranial hematomas. All patients were initially hypotensive: 10 were in cardiac arrest, 7 had a systolic blood pressure (SBP) < 60 torr, and 19 had SBP of 60–90 torr. The median score on the Glascow coma scale was 3 (range 3–8). Although 4 of the 10 cardiac arrest patients had anisocoria, only one (10%) had an intracranial hematoma. Among the seven patients with severe hypotension, only two had anisocoria and neither had an intracranial hematoma; one patient in this group (14%) had a hematoma that was diagnosed at autopsy. In contrast, intracranial hematomas were discovered by burr-hole placement and evacuated in 13 (68%) of 19 patients with initially moderate hypotension, including seven (78%) of nine patients with anisocoria. Anisocoria was associated with mechanical brain compression from an intracranial hematoma significantly more often in patients with an initial SBP of 60–90 torr than in those with initial cardiac arrest or SBP < 60 torr (chi-square p < 0.05). Intracranial hematomas were significantly more frequent among patients with SBP of 60–90 torr than among those with a lower SBP or initial cardiac arrest (p < 0.01). Thirty-three of 36 patients died; each of the three survivors had an initial SBP of 60–90 torr, and hematomas were removed in two. In head-injured patients with SBP > 60 torr, clinical signs of tentorial herniation or upper brainstem dysfunction remain valid indicators of possible mechanical compression; the high percentage of patients with acute intracranial hematomas in this group warrants immediate diagnostic burr-hole exploration. In patients with severe initial hypotension (SBP < 60 torr) or cardiac arrest, clinical findings of brainstem dysfunction cannot be relied upon to indicate mechanical compression, and computed tomography scanning should be done immediately after resuscitation to determine the need for surgical exploration.     

Cardiopulmonary hemodynamic changes during acute subdural hematoma evacuation

The aim of this study was to clarify the mechanism of hemodynamic changes leading to intraoperative hypotension during evacuation of acute subdural hematoma. To our knowledge, little data is available about the mechanism of hemodynamic changes during surgical interventions to decrease intracranial pressure after severe head injury. The influence of preoperative hypotension on intraoperative hypotension was examined. Hemodynamic studies (pulmonary artery catheterization) were carried out in 15 patients before and after acute subdural hematoma evacuation. All patients were assessed for hemodynamic parameters, evacuated hematoma volume, and intracranial pressure measurements. Comparison between just before and after evacuation of the hematoma showed that the mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, pulmonary vascular resistance, central venous pressure, and pulmonary capillary wedge pressure all decreased after hematoma evacuation. However, the cardiac index was unchanged after hematoma evacuation. Mean arterial blood pressure is dependent on the cardiac index and vascular resistance, so the decrease in arterial blood pressure during hematoma evacuation was the result of a decline in vascular resistance. The influence of preoperative blood pressure on intraoperative hemodynamic changes was analyzed by dividing the patients into two groups, the preoperative hypotension group and preoperative nonhypotension group. The decrease in mean arterial blood pressure was more marked in the preoperative hypotension group than in the preoperative nonhypotension group. Intraoperative hypotension during evacuation of acute subdural hematoma is caused by a decrease in vascular resistance. Preoperative hypotension is a also risk factor for intraoperative hypotension.     

Use of intraoperative ultrasonography to improve the diagnostic accuracy of exploratory burr holes in patients with traumatic tentorial herniation

Seventeen head-injured patients with signs of brain stem compression at admission underwent emergency bilateral burr-hole exploration before computerized tomographic (CT) scanning. After exploration of the epidural and subdural spaces, real-time ultrasonography was performed intraoperatively to identify intraaxial hematomas. Epidural or subdural hematomas were identified surgically in 11 patients (65%) and immediately evacuated through a craniotomy; in 2 patients, bilateral subdural hematomas were removed. Ultrasonography showed no evidence of intracerebral mass lesions in 14 (82%) of the 17 patients, demonstrated extensive contusions of the temporal lobe in 2 patients (prompting partial lobectomy in both cases), and revealed a small intraparenchymal hematoma deep within the dominant hemisphere, which was not removed, in 1 patient. The sensitivity of ultrasound images for identifying intraparenchymal lesions was evaluated postoperatively by CT or autopsy. In 15 patients (88%), the results of ultrasonography were confirmed. In 2 (12%), CT scans showed small but significant lesions at the frontal pole missed by ultrasonography; one patient had a residual subdural hematoma, and the other a small intraparenchymal hemorrhage. These results confirm that patients with clinical evidence of brain stem compression soon after head injury often have extraaxial hematomas that can be readily identified by burr-hole exploration. Although intraparenchymal hematomas are rare immediately after head injury, they can usually be identified by intraoperative ultrasonography. This simple technique can reduce the risk of missing intracranial hematomas during emergency burr-hole exploration and improve intraoperative decision making in this population of severely head-injured patients.     

Management of spontaneous cerebellar hematomas: a prospective treatment protocol

OBJECTIVE: To identify easily applicable guidelines for the surgical and conservative management of spontaneous cerebellar hematomas. METHODS: A treatment protocol was developed and prospectively applied for the management of 50 consecutive cases of cerebellar hematomas. The appearance of the fourth ventricle, adjacent to the hematoma, on computed tomographic scans was divided into three grades (normal, compressed, or completely effaced). The degree of fourth ventricular compression was correlated with the size and volume of the hematoma and the presenting Glasgow Coma Scale (GCS) score. The hematoma was surgically evacuated for all patients with Grade III compression and for patients with Grade II compression when the GCS score deteriorated in the absence of untreated hydrocephalus. Patients with Grade I or II compression were initially treated with only ventricular drainage in the presence of hydrocephalus and clinical deterioration. RESULTS: The degree of fourth ventricular compression was classified as Grade I in 6 cases, Grade II in 26, and Grade III in 18. The degree of fourth ventricular compression was significantly correlated with the volume of the hematoma (r(s) = 0.67, P < 0.0001), hydrocephalus (r(s) = 0.44, P = 0.001), the preoperative GCS score (r(s) = 0.43, P = 0.001), the maximal diameter of the hematoma (r(s) = 0.43, P = 0.001), and a midline location of the hematoma (chi(2) = 6.84, P < 0.009). Acute deterioration in GCS scores occurred for 6 (43%) of 14 patients with Grade III ventricular compression who were conscious at presentation. Thirteen patients with Grade I or II ventricular compression and stable GCS scores of more than 13 were treated conservatively. Nine patients were treated with ventricular drainage only, and 28 underwent posterior fossa craniectomy and evacuation of the hematoma with ventricular drainage. The mortality rate at 3 months was 40%. None of the patients with Grade III fourth ventricular compression and GCS scores of less than 8 at the time of treatment experienced good outcomes. Overall, 15 (60%) of 25 patients with hematomas with maximal diameters of more than 3 cm and Grade I or II compression did not require clot evacuation. CONCLUSION: Conscious patients with Grade III fourth ventricular compression should undergo urgent clot evacuation before deterioration. Surgical evacuation of the clot may not be required for large hematomas (>3 cm) if the fourth ventricle is not totally obliterated at the level of the clot.     

Wound hematomas after carotid endarterectomy

Fifteen of 596 (2.5 percent) carotid endarterectomies performed at Brooke Army Medical Center were complicated by significant wound hematomas requiring reoperation and hematoma evacuation. The wound hematomas resulted from capillary oozing in 80 percent of the cases and arteriotomy bleeders in 20 percent of the cases. Antiplatelet therapy and postoperative hypertension appear to be significant factors predisposing to the development of wound hematomas. In eight cases, local anesthesia was utilized for the hematoma evacuation, and there were no complications. When general anesthesia was utilized for hematoma evacuation, there was considerable difficulty with airway management in six of seven patients. Complications developed in four of these patients. One patient had respiratory insufficiency secondary to laryngeal edema. Two of the patients sustained myocardial infarctions, one of whom died, and a dense neurologic deficit developed in the fourth patient who died as a result of this complication. Meticulous surgical technique in obtaining hemostasis, control of postoperative hypertension, and wound drainage when indicated will help reduce the incidence of postoperative wound hematoma. When a significant postoperative wound hematoma does complicate carotid endarterectomy, the hematoma should be promptly evacuated utilizing local anesthesia.