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However, in 12 (25.5%) of those patients, during the periods from 3 to 6 months were observed repeated conditions of paroxysmal hypertension. The result observed was that the more is the size of the tumor, the less was the EDGA effect. Thus, in 2 patients with the tumor size more than 1 centimeter, the effect of hypertension remained only 3 months. In repeatedcheckup ofpatients with recurrence of paroxysmal hypertension on CT was detected hyperplasia adrenal gland or the existence of tumor. In 5 of those patients operated with LA lead to the achievement of normotension in 3 and the elimination of paroxysmal hypertension in 3 of the patients.
Conclusion. As has shown the comparative analysis of different methods of treating genesis of AH through medical intervention, today adrenalectomy is an operation that lets the marked reduction ofAP in it, and the elimination of its paroxysmal hypertension. We consider that the preferred way of operation is the one with small in-vasiveness-laparoscopic.
Undeniable advantages of LA are the decrease ofhospital stay as a result of its causing small amount physical injury, early recovery of working capacity, cosmetic effect. At the same, time the number of complications during and after the operation period do not exceed the ones had in traditional adrenalectomy. Nevertheless, the results mentioned are observed with tumors with the size up to 6 centimeters.
Naturally, the bigger is the size of tumor, the more technical issues are there in performing adrenalectomy. Therefore, in situations with tumors exceeding 6 centimeters, we gave our preference to traditional medical intervention. However, taking into account the advantages of adrenalectomy with its small invasiveness, in recent years we accomplished laparoscopic adrenalectomy with the technology called "hand-assist", in tumors with the size from 7 to 10 centimeters.
Considerable reduction of AP and the avoidance of its paroxysmal hypertension can also be achieved by EDGA in tumor in the size of up to 1 centimeter. In tumors of bigger size, this method is not effective. Nevertheless, despite the small invasiveness of the method, in the long-term period, in 25% of the patients the effect of reduction ofAP is temporary. In our observations, from periods from 3 to 6 in those patients was seen recurrence ofAH. Therefore, our point of view is that the EDGA is can be applied in cases with tumors up to 1 centimeter and high risk of anesthesia and surgery.
This way, LA nowadays is the preferred in most of the situations with adrenal gland tumors. Following the principles of adequate behavior of patients on all of the stages of treatment allows the reduction of risk of complications, which contributes to the safety and reliability of operations.
References:
1. Arabidze G. G., Arabidze Gr. G. Diagnosis of arterial hepertension//Angiology and vascular surgery. - Moscow, 1999. № 3. - P. 116-18.
2. Kalinin A. P., Maystrenco N. A. Surgery of adrenal glands. M: Medicine 2000; 179.
3. Emelyanov S. I., Kurganov I. A., Bogdanov D. Yu., Matveev N. L., Sadovnikov S. V. Possibility laparoscopic adrenalectomy in patients with big sizes adrenal tumors. Endoscopic surgery. 2011; 4: 3-9.
4. Karimov Sh. I., Tursunov B. Z., Sunnatov R. D., Temirov S. N. Arterial hypertension in hyperaldesteronizms: diagnosis and treatment. Diagnostic interventional radiology. 2008; 2: 67-73.
5. Hokotate H., Inoue H., Baba Y., Aldosteronomas: experience with superselective adrenal arterial embolization in 33 cases. Radiology. 2003; 227: 401-406.
6. Poulose B. K., Holzman M. D., Lao O. B. et al. Laparoscopic adrenalectomy. 100 resections with clinical long-term follow-up. Surg Endosc 2005; 19: 379-385.
7. Zacharias M., Ilaese A., Jurczok A. el al. Transperitoneal laparoscopic adrenalectomy: outline of the preoperative management, surgical approach, and outcome. Eur Urol 2006: 49: 448-459.
Kuzibaev Jamshid Muminovich, MD, Doctor of philosophy Republican Research center of emergency medicine, Neurosurgery department Senior researcher E-mail: [email protected] Makhkamov Kozim Ergashevich, MD, Doctor of medicine Republican Research center of emergency medicine, Neurosurgery department Chief of the department
Secondary brain damage due to progressive traumatic subdural hematoma
Abstract: We studied the clinical data of traumatic subdural hematoma patients to determine the risk factors of progression of traumatic subdural hematoma and its role in the development of secondary brain damage. Our study showed that progressive subdural hematoma happens more in the cases with low Glasgow coma scale score at presentation and intra-parenchymal contusion. However the incidence of progressive subdural hematoma after acute head injury was low (11.9%), it causes often increasing of brain ischemia volume (70.5%).
Keywords: brain injury, secondary brain damage, progression, subdural hematoma, risk factors.
Introduction The lethal nature of TSH is largely explained by its frequent as-
Traumatic subdural hematoma (TSH) represents a challenge sociation with primary brain damage, consisting of contusion and for neurosurgeons due to its high mortality and morbidity rates. brain swelling [5; 9; 10; 13]. The most severe lesion associated
with TSH is secondary brain damage. However, the nature and the causes of brain damage that occurs after traumatic brain injury (TBI) are multiple and poorly understood [4].
Moreover, a hypoxaemic secondary insult contributes to marked brain swelling. The pathophysiology of TBI may develop from the complex interaction of the hematoma volume, the severity and distribution of the primary traumatic insult, and the presence of secondary insults [5, 10].
Secondary brain damage is an important factor that influences the outcome of TSH. However, only a few studies have discussed the pathophysiology of TSH from the standpoint of secondary brain damage.
In our study, the clinical data of TSH patients were analyzed to determine the risk factor of progression of TSH and its role in the development of secondary brain damage.
Materials and Methods
142 patients with TBI who had CT scan more than twice in our hospital from 2011 to 2015 were subject of this study, who have acute subdural hematoma on initial CT scan. The management for acute subdural hematoma is divided into two groups; emergent surgery and conservative management. Emergent surgery was performed if subdural hematoma causes mass effect. If the condition of a patient and the amount of hematoma did not meet surgery based on clinical judgment, the patient's status was observed closely with follow-up CT and conservatively managed.
Progressive subdural hematoma (PSH) was defined as more than 25% of increase of hematoma on the second CT taken within 24 hours after the first CT. The cases with surgery for subdural hematoma were excluded in spite of the increase of hematoma postoperatively.
Out of 142 patients with subdural hematoma the incidence of PSH was 11.9%. The group of 17 with PSH and the group of 125 without PSH were compared. Based on the medical record and brain CT, general medical condition, trauma, and factors associated with evaluation and outcome were investigated. General condition is specified into sex, age, past medical history, coagulation status such as number of platelet. The trauma-related factors were the initial Glasgow Coma Scale (GCS) score, the time from trauma to the first brain CT, and the time interval between the first and the second CT.
Statistical analysis. Statistical analyses were performed using the MedCalc software package (Version 11.4.2.0). A variate logistic analysis was used to determine the predictors of PSH. Predictors were defined as being significant if P value is lower than 0.05. Chi-square statistics were calculated for categorical comparisons. Values for the continuous parameters are given as the mean±SD.
Illustration of case
63-year-old male who had an altered mentality when brought to the emergency room due to head injury 30 minutes ago. He was with GCS score of 10. The initial CT scans obtained 30 minutes postinjury showed small amount of acute subdural hematoma and small contusion in the left frontal area of the brain (Figure 1). The patient's neurological status was observed closely with follow-up CT scan, 20 hours after the first scan. On the second CT, progression of the acute subdural hematoma and hemorrhagic contusion in the left frontal area of the brain were revealed (Figure 2). The patient underwent emergency craniectomy and hematoma removal. However, his mental status did not improve due to secondary brain damage, and the outcome was lethal.
Figure 1. Initial CT scans obtained 30 minutes postinjury, demonstrating small amount of acute subdural hematoma and small contusion in the left frontal area of the brain
Figure 2. Second CT scans revealing progression of the acute subdural hematoma and hemorrhagic contusion in the left frontal area of the brain
Results
The mean age of total 142 patients was 51.2 years while the mean age of patients with PSH was 36.7±11.8, and the mean age of patients without PSH was 46.7±13.3. The mean age was lower in the group with PSH (P=0.003). However, considering that PSH occurred more in males (14 males, 3 females), the gender and the occurrence of PSH are not associated with P-value of 0.98 (Table 1).
Platelet count dropped and prolonged coagulation time in severe brain injury showed the association with progressive intracra-
nial hemorrhage, but statistic significance was not observed with P-value of 0.18 (Table 1). It is considered as a result of small number of cases with abnormalities on laboratory data.
Initial GCS showed the significant relation with the incidence of PSH,. When it is divided into severe (GCS 3-8), moderate (GCS 9-12), and mild (GCS 13-15), the lower the GCS score seems more likely in patients with PSH with P-value of 0.007. Regarding the severity of brain injury, higher rate of PSH was occurred in patients with intraparenchymal contusion (64.7% versus 20.0%, P=0.002). (Table 1).
Table 1. - Clinical variables related to the development of PSH in the patients with head trauma
Clinical variables No. of patients with PSH P value
Gender 0.98
male 112 14 (12.5%)
female 30 3 (10%)
Initial GCS 0.007
13-15 42 2 (6.2%)
9-12 82 8 (9.7%)
3-8 18 7 (25.0%)
Intraparenchymal contusion 0.002
Yes 36 11 (37.9%)
No 106 6 (6.2%)
Coagulopathy 0.18
Yes 33 7 (39.4%)
No 109 10 (16.4%)
Secondary brain damage was diagnosed if patient's repeat CT scans show new brain ischemic area or increasing of the initial ischemia volume. Based on the repeat CT scan, increase of brain ischemia volume was not found in 12 (70.5%) patients with PSH and in 22 (17.6%) patients without PSH. 7 (41.1%) out of patients with PSH had no brain ischemia, 8 (47.1%) had local
brain ischemia, and 2 (11.7%) had hemispheric brain swelling. Among patients without PSH 85 (68%) had no brain ischemia, 36 (28.8%) had local brain ischemia, and 4 (3.2%) had hemispheric brain ischemia. Patients without PSH had significantly (P<0.0001) less increase of brain ischemia volume than those with PSH (Table 2).
Table 2. - Relations between the PSH and secondary brain damage
Repeat CT scan data PSH P value
+ (%) - (%)
Increase of brain ischemia volume 12 (70.5%) 22 (17.6%) <0.0001
No brain ischemia 7 (41.1%) 85 (68%) 0.05
Local brain ischemia 8 (47.1%) 36 (28.8%) 0.21
Hemispheric brain ischemia 2 (11.7%) 4 (3.2%) 0.32
GOS was lower in patients with PSH showingpoorprogno-sisA lethal outcome was seen in 41.1% of patients with PSH and in 12.8% of those without PSH, respectively (x2 test, P = 0.008).
Discussion
Progressive intracranial hemorrhage (PSH) which is continuous hemorrhage after trauma should be distinguished from delayed in-tracranial hemorrhage [11]. In this study, PSH is distinguished from delayed intracranial hemorrhage in previous studies [2; 6; 8; 12]. PSH was defined as the aggravation of mental status due to the rapid progression of subdural hemorrhage found on the initial CT [1]. The risk factors of PSH figured out on this study were the first brain CT scanning time detecting subdural hemorrhage and the GCS score at admission. The higher incidence of PSH was statistically significant in the cases that had brain CT scan within 3 hours after trauma, lower initial GCS, and presence of intraparenchymal contusion.
The incidence of PSH is reported as 23-48%, and it was 11.9% in this study [12]. However, it is expected to be higher since there
were cases which surgery had been performed right after the initial brain CT. It is also because the initial brain CT scan was delayed, so the large amount of intracranial hematoma was detected on the first brain CT scans. PSH is reported higher in the old age, due to low contractility of blood vessels and free space in skull [3; 7; 8]. The result from this study showed no statistical significance of the age. It is regarded as because of a small sample size. Regarding sex of patients, males tend to be more active and to work where heavier load is required so that they are more exposed to trauma. The absolute number of occurrence of PSH was significantly higher in males but it was not relative statistically considering the incidence of trauma.
Conclusion
Our study showed that PSH happens more in the cases with low GCS at presentation and intraparenchymal contusion. However the incidence of PSH after acute head injury was low (11.9%), it causes often increasing of brain ischemia volume (70.5%). A lethality rate was higher in patients with PSH then in ones without PSH (41.1% versus 12.8%).
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