Neurological injury and patterns of sacral fractures

1990 ◽  
Vol 72 (6) ◽  
pp. 889-893 ◽  
Author(s):  
Kevin J. Gibbons ◽  
Donald S. Soloniuk ◽  
Nizam Razack

✓ To evaluate the morphological and neurological findings in sacral spine injuries, a retrospective study was conducted of all patients admitted to Erie County Medical Center over a 2-year period with the diagnosis of pelvic or sacral injury. Of these 253 patients, 44 were found to have sacral fractures and form the basis of this study. The type of fracture, neurological deficit, treatment, and outcome in these patients were analyzed. The patient population consisted of 25 males and 19 females, with a mean age of 34 years (range 15 to 80 years). The fractures were classified by the degree of involvement of the foramina and central canal. Fractures through the ala sacralis only (Zone I, 25 cases) or involving the foramina but not the central canal (Zone II, seven cases) were less likely to cause nerve injury (24% and 29%, respectively). Fractures involving the central canal (Zone III), both vertical (five cases) and transverse (seven cases), were more likely to cause neurological injury (60% and 57%, respectively). Neurological deficits in Zone I and II injuries were usually unilateral lumbar and sacral radiculopathies. Zone III deficits were usually bilateral and severe; bowel and/or bladder incontinence was present in six of the 12 patients in this group. Deficits generally improved with time; however, operative reduction and internal fixation may have been useful, particularly in patients with unilateral root symptoms. The treatment options are discussed, and previously published series of sacral fractures are reviewed. The authors conclude that the classification of sacral fractures described is useful in predicting the incidence and severity of neurological deficit.

1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher

✓ The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 µl blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.


1997 ◽  
Vol 87 (3) ◽  
pp. 403-408 ◽  
Author(s):  
Kimberly S. Harbaugh ◽  
Robert L. Tiel ◽  
David G. Kline

✓ Despite their benign histological appearance and the current literature composed primarily of case reports with favorable outcomes, ganglion cysts involving peripheral nerves (GCPNs) can cause permanent neurological deficits. The authors present a 27-year Louisiana State University Medical Center (LSUMC) experience with the surgical management of GCPNs. From 1968 to 1995, 27 patients were surgically treated for 27 cysts that involved nerves at nine locations. Cysts of the peroneal nerve were the most common, comprising 52% of the cases. Motor deficit, pain, and sensory changes were present in 83%, 78%, and 48% of cases, respectively. A history of acute trauma was noted in 22%. The mean follow-up duration in these cases was 61 months. Motor recovery was good in only 58% of cases and was related to the severity of the preoperative motor deficit. Pain resolved or was significantly improved in 89% of cases. Five patients underwent nine procedures before referral to LSUMC for treatment of recurrence of their ganglion cysts. None of these patients suffered recurrence after undergoing surgery at LSUMC. However, four additional patients (17%) experienced a total of six recurrences after undergoing their initial procedure. The mean time to recurrence for the patient group as a whole was 16 months. On the basis of their experience, the authors conclude that GCPNs can behave in an aggressive fashion. Patients should be counseled preoperatively about the potential for limited motor recovery and a significant chance for recurrence.


2020 ◽  
Vol 6 (3) ◽  
pp. 20190133
Author(s):  
Alex Kiu ◽  
Tiffany Fung ◽  
Pranav Chowdhary ◽  
Sungmi Jung ◽  
Tom Powell ◽  
...  

Aneurysmal bone cysts (ABC) are rare, benign primary bone tumors. Although benign, they can be locally aggressive resulting in erosion of bone and surrounding tissues over time. In later stages, depending on the clinical urgency, immunotherapy or surgical resection remain treatment options. This report illustrates a case of a 32-year-old female who presented with chronic worsening low back pain without neurological deficits. Radiological imaging revealed a large destructive mass arising from the thoracic spine invading into the central canal, causing critical central stenosis and cord compression. Histopathology revealed ABC. This case highlights the importance of including ABCs and other ‘benign’/locally aggressive lesions in the differential of patients with insidious musculoskeletal complaints. This case also demonstrates that one can be neurologically asymptomatic despite having critical central canal stenosis and cord compression if the causative lesion is slow growing. Understanding this allows us to arrange for most appropriate management.


1998 ◽  
Vol 88 (4) ◽  
pp. 634-640 ◽  
Author(s):  
Neill M. Wright ◽  
Carl Lauryssen

Object. The 847 active members of the American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) Section on Disorders of the Spine and Peripheral Nerves were surveyed to quantitate the risk of vertebral artery (VA) injury during C1–2 transarticular screw placement. Methods. This retrospective study elicited the number of patients treated with transarticular screws, the number of screws placed, the incidence of VA injury and subsequent neurological deficit, and the management of known or suspected VA injury. Two hundred thirteen (25.1%) of the 847 surgeons responded. One hundred one respondents (47.4%) had placed a total of 2492 C1–2 transarticular screws in 1318 patients. Thirty-one patients (2.4%) had known VA injuries and an additional 23 patients (1.7%) were suspected of having injuries. However, only two (3.7%) of the 54 patients with known or suspected VA injuries exhibited subsequent neurological deficits and only one (1.9%) died of bilateral VA injury. Other iatrogenic complications included dural tears, screw fractures, screw breakout, fusion failure, infection, and suboccipital numbness. Conclusions. Including both known and suspected cases, the risk of VA injury was 4.1% per patient or 2.2% per screw inserted. The risk of neurological deficit from VA injury was 0.2% per patient or 0.1% per screw, and the mortality rate was 0.1%. The choice of management of intraoperative VA injuries was evenly divided between placing the patient under observation and initiating immediate postoperative angiography with possible balloon occlusion.


1986 ◽  
Vol 65 (1) ◽  
pp. 48-62 ◽  
Author(s):  
S. Sam Finn ◽  
Sigurdur A. Stephensen ◽  
Carole A. Miller ◽  
Laura Drobnich ◽  
William E. Hunt

✓ Thirty-two patients with aneurysmal subarachnoid hemorrhage (SAH) were managed according to a protocol based on pain control and hemodynamic manipulation, monitored by an arterial line and Swan-Ganz catheter. Hemodynamic parameters were adjusted to four clinical situations. 1) For the unoperated patient with no neurological deficit, the regimen aims to maintain pulmonary wedge pressure (PWP) at 10 to 12 mm Hg, and the cardiac index (CI) and blood pressure (BP) at normal levels. 2) For the unoperated patient presenting with or developing neurological deficit, the PWP is increased until the deficit is reversed or the CI falls; the CI is high, and the BP normal. 3) For the postoperative patient with no neurological deficit, the PWP is maintained at 12 to 14 mm Hg, the CI is a high normal, and the BP is normal. 4) For the postoperative patient developing neurological deficit but showing no surgical complication on the computerized tomography scan, the PWP is increased until the deficit is reversed or the CI falls; the CI is high and the BP is increased with vasopressors if necessary. Fourteen patients developed neurological deficits either preoperatively, postoperatively, or both. Neurological deficits were repeatedly reversed by increasing the PWP, as measured hourly. In several patients an optimal wedge pressure was determined, below which deficits would reappear. In one patient whose neurological deficit was reversed on several occasions by increasing the PWP, the optimal PWP rose after each episode until it reached 22 mm Hg. Detailed event-related analysis of these patients' course illustrates these phenomena well. The optimal PWP varied from patient to patient, but ranged most frequently from 14 to 16 mm Hg. Meticulous monitoring of the patients' neurological status coupled with prompt correction of low PWP (assuming an adequate CI) has proven to be an effective way to prevent and reverse neurological deficits following aneurysmal SAH.


2016 ◽  
Vol 60 (11) ◽  
pp. 6774-6779 ◽  
Author(s):  
Seongman Bae ◽  
Min-Chul Kim ◽  
Su-Jin Park ◽  
Hee Sueng Kim ◽  
Heungsup Sung ◽  
...  

ABSTRACTEmerging resistance to colistin in clinicalAcinetobacter baumanniiisolates is of growing concern. Since current treatment options for these strains are extremely limited, we investigated thein vitroactivities of various antimicrobial combinations against colistin-resistantA. baumannii. Nine clinical isolates (8 from bacteremia cases and 1 from a pneumonia case) of colistin-resistantA. baumanniiwere collected in Asan Medical Center, Seoul, South Korea, between January 2010 and December 2012. To screen for potential synergistic effects, multiple combinations of two antimicrobials among 12 commercially available agents were tested using the multiple-combination bactericidal test (MCBT). Checkerboard tests were performed to validate these results. Among the 9 colistin-resistant strains, 6 were pandrug resistant and 3 were extensively drug resistant. With MCBT, the most effective combinations were colistin-rifampin and colistin-teicoplanin; both combinations showed synergistic effect against 8 of 9 strains. Colistin-aztreonam, colistin-meropenem, and colistin-vancomycin combinations showed synergy against seven strains. Colistin was the most common constituent of antimicrobial combinations that were active against colistin-resistantA. baumannii. Checkerboard tests were then conducted in colistin-based combinations. Notably, colistin-rifampin showed synergism against all nine strains (100%). Both colistin-vancomycin and colistin-teicoplanin showed either synergy or partial synergy. Colistin combined with another β-lactam agent (aztreonam, ceftazidime, or meropenem) showed a relatively moderate effect. Colistin combined with ampicillin-sulbactam, tigecycline, amikacin, azithromycin, or trimethoprim-sulfamethoxazole demonstrated limited synergism. Using MCBT and checkerboard tests, we found that only colistin-based combinations, particularly those with rifampin, glycopeptides, or β-lactams, may confer therapeutic benefits against colistin-resistantA. baumannii.


1976 ◽  
Vol 45 (3) ◽  
pp. 348-351 ◽  
Author(s):  
Laurance J. Guido ◽  
Russel H. Patterson

✓ Two cases of focal neurological deficit secondary to intraoperative cerebrospinal fluid drainage are presented. Successful resolution was achieved by use of an epidural blood patch. Possible etiological mechanisms and prevention of the complication are discussed.


2014 ◽  
Vol 37 (1) ◽  
pp. E12 ◽  
Author(s):  
Mohamad Bydon ◽  
Vance Fredrickson ◽  
Rafael De la Garza-Ramos ◽  
Yiping Li ◽  
Ronald A. Lehman ◽  
...  

Sacral fractures are uncommon lesions and most often the result of high-energy trauma. Depending on the fracture location, neurological injury may be present in over 50% of cases. In this article, the authors conducted a comprehensive literature review on the epidemiology of sacral fractures, relevant anatomy of the sacral and pelvic region, common sacral injuries and fractures, classification systems of sacral fractures, and current management strategies. Due to the complex nature of these injuries, surgical management remains a challenge for the attending surgeon. Few large-scale studies have addressed postoperative complications or long-term results, but current evidence suggests that although fusion rates are high, long-term morbidity, such as residual pain and neurological deficits, persists for many patients.


2017 ◽  
Vol 61 (9) ◽  
Author(s):  
James A. Karlowsky ◽  
Krystyna M. Kazmierczak ◽  
Boudewijn L. M. de Jonge ◽  
Meredith A. Hackel ◽  
Daniel F. Sahm ◽  
...  

ABSTRACT The combination of the monobactam aztreonam and the non-β-lactam β-lactamase inhibitor avibactam is currently in clinical development for the treatment of serious infections caused by metallo-β-lactamase (MBL)-producing Enterobacteriaceae, a difficult-to-treat subtype of carbapenem-resistant Enterobacteriaceae for which therapeutic options are currently very limited. The present study tested clinically significant isolates of Enterobacteriaceae (n = 51,352) and Pseudomonas aeruginosa (n = 11,842) collected from hospitalized patients in 208 medical center laboratories from 40 countries from 2012 to 2015 for in vitro susceptibility to aztreonam-avibactam, aztreonam, and comparator antimicrobial agents using a standard broth microdilution methodology. Avibactam was tested at a fixed concentration of 4 μg/ml in combination with 2-fold dilutions of aztreonam. The MIC90s of aztreonam-avibactam and aztreonam were 0.12 and 64 μg/ml, respectively, for all Enterobacteriaceae isolates; >99.9% of all isolates and 99.8% of meropenem-nonsusceptible isolates (n = 1,498) were inhibited by aztreonam-avibactam at a concentration of ≤8 μg/ml. PCR and DNA sequencing identified 267 Enterobacteriaceae isolates positive for MBL genes (NDM, VIM, IMP); all Enterobacteriaceae carrying MBLs demonstrated aztreonam-avibactam MICs of ≤8 μg/ml and a MIC90 of 1 μg/ml. Against all P. aeruginosa isolates tested, the MIC90 of both aztreonam-avibactam and aztreonam was 32 μg/ml; against MBL-positive P. aeruginosa isolates (n = 452), MIC90 values for aztreonam-avibactam and aztreonam were 32 and 64 μg/ml, respectively. The current study demonstrated that aztreonam-avibactam possesses potent in vitro activity against a recent, sizeable global collection of Enterobacteriaceae clinical isolates, including isolates that were meropenem nonsusceptible, and against MBL-positive isolates of Enterobacteriaceae, for which there are few treatment options.


1993 ◽  
Vol 78 (2) ◽  
pp. 274-279 ◽  
Author(s):  
Thomas H. Milhorat ◽  
Fariborz Nobandegani ◽  
John I. Miller ◽  
Chandrakant Rao

✓ This report describes a new and reliable technique for producing experimental noncommunicating syringomyelia. In 30 rats, 1.2 to 1.6 µl of kaolin was microinjected into the dorsal columns and central gray matter of the spinal cord at C-6. The inoculations caused transient neurological deficits in four animals and no deficits in 26 animals. Within 24 hours, kaolin and polymorphonuclear leukocytes entered the central canal and drained rostrally. The clearance of inflammatory products induced a proliferation of ependymal cells and periependymal fibrous astrocytes, which formed synechiae and obstructed the canal at the level of injection and at one or more levels up to C-1. In 22 animals followed for 48 hours or longer, the upper end of the central canal became acutely dilated and formed an ependyma-lined syrinx that enlarged to massive dimensions within 6 weeks. The rostral syrinxes did not communicate with the fourth ventricle and were not associated with hydrocephalus. The histological findings in acute noncommunicating syringomyelia were characterized by progressive stretching and thinning of the ependyma, elongation of intracanalicular septae, and the formation of periependymal edema. After 3 weeks, there was progressive compression of the periependymal tissues associated with stretching of axons, fragmentation of myelin sheaths, and the formation of myelin droplets. These findings and the sequence in which they evolved were identical in most respects to those occurring in acute and subacute noncommunicating hydrocephalus.


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