Research news and notes

1. Almost all surgical residents experience needlestick injuries 

It should not surprise anyone that injuries with “sharps” occur in medical practice and that surgeons are at a high risk. Nevertheless, I was shocked to learn how high the incidence of needlestick injuries really is. In the June 28 issue of the New England Journal of Medicine, Makary et al [3] presented the results of a survey of surgical trainees in 17 medical centers. The response rate was excellent at 95%, for a total of 699 responders. An amazing 83% had had a needlestick injury by the time of the survey. The survey included residents at all stages of training, and there were more responders from PGY-1 (221) than PGY-5 (78). Among the PGY-5 patients, 77 (99%) had had a needlestick during their training. Most had multiple needlesticks—a mean of 7.7 in the PGY-5 group. A majority (53%) of the responders had at least 1 needlestick involving a high-risk patient, defined as someone with a history of HIV, hepatitis B or C, or intravenous drug use. Only about half of the responders reported an injury to the health service; the nonreporters usually cited futility or lack of time. Even more appalling, many of the residents who did not report to the employee health service did not tell anyone else about their injury. Most of the injuries occurred in the operating room and involved a solid-bore needle.

The article raises the awareness of the problem of needlestick injuries in surgeons, particularly residents. The underreporting is a potentially serious problem. The authors propose system-level changes that could increase reporting, including special curricula of training for safe techniques, peer education to encourage reporting, and routine postoperative checklists that include a question about injuries to personnel.

In a recent study from Britain [11], 763 questionnaires were posted to orthopedic surgeons; 261 (34.2%) surgeons responded. Of respondents, 117 (47%) had sustained sharps injuries in the previous 12 months. Only 82 (33%) surgeons always reported such injuries, although 208 (84%) expressed concerns of occupationally acquired hepatitis C viral transmission. The annual incidence of needlesticks appears to be even higher and reporting rate lower than in the New England Journal of Medicine study.

I doubt that the efforts to increase reporting will be very successful. There is already a strong incentive to report—the surgeons are concerned about viral transmission, and not reporting the injury in a timely fashion may result in the denial of future compensation. Why, then, are the injuries underreported? Maybe the surgeons are not really concerned about infection after all. There is no epidemic of hepatitis C and HIV among surgeons. The rate of transmission is very small, 0.001% to 0.032% per annum (0.035%-1.12% risk over a 35-year professional career, even in an area with an extremely high prevalence of hepatitis C virus (HCV) among its injecting drug-using population) [9]. Among all surgeons, those performing liver transplantation are the most likely to be exposed to HCV. In a study on 117 liver transplant surgeons, 2 (1.7%) surgeons had antibodies to HCV, and 1 (0.8%) of them had detectable HCV RNA. Assuming that both infections were acquired during surgery, the estimated maximum rate of HCV transmission is 1 per 449 to 683 years of liver transplant practice [10]. I assume that the risk would be lower for surgeons who do not operate on patients with a particularly high prevalence of HCV, such as liver transplant recipients and intravenous drug users. A study in a general health care worker population [7] found HCV seroconversion only in patients who had hollow-bore needlestick injuries, rather than solid-bore needles or other sharp objects.

2. Carotid stenting—reducing risk of emboli with flow reversal 

The risk of embolic infarction is a serious limitation of carotid artery stenting. One approach has been to produce temporary flow reversal in the internal carotid artery (ICA). Matas et al [5] present their experience with 62 patients who were deemed to be at high risk for surgery and had severe carotid artery stenosis. They used transcervical access, created a temporary fistula that reversed the flow in the internal carotid, and only then crossed the lesion with the stent. Immediately after the procedure, 1 patient had a transient ischemic attack in the anterior cerebral artery territory, and another had a stroke, with contralateral hemiplegia. A third patient had a delayed severe cerebral hemorrhage that required surgical drainage, for a total neurologic morbidity of 3 of 62.

Evidently, they had few or no patients with poor collateral circulation. Because flow reversal may produce a “steal” phenomenon, it could require better collateral than simply occluding the ICA. If the lesion to be treated with carotid artery stenting is hemodynamically significant, and the patient really needs that ICA, I suspect that the patient would not tolerate the procedure. How did the authors study the collateral circulation before the procedure? In addition, opening the neck for access and creation of a fistula does approach the invasiveness of open surgery.

3. What does neurogenesis after stroke mean? 

The brain possesses intrinsic repair mechanisms. A growing body of research demonstrates the presence of proliferating neural stem cells in adult brains. A recent study by Zhang et al [12] in the Journal of Neuroscience describes the properties of the subventricular zone (SVZ) cells and their behavior in a rat model of stroke. In normal brains, SVZ stem cells give rise to cells that migrate dorsally and ventrally along the lateral ventricular surface and ultimately in the direction of the olfactory bulbs. In stroke, the SVZ cells migrated mostly laterally toward the stroke and exhibited greater migration distance. The cells divided during migration. This work demonstrates an intrinsic brain response to injury, directing new cells in the direction of the injury and the cell loss. The intuitive response is to see this as a mechanism of brain repair, but it is not necessarily so. In a study by Nygren et al [6], more newborn cells were found in the SVZ of stroke-injured mice but not in injured mice exposed to an enriched environment. In mice kept in an enriched environment, the number of newborn astrocytes, neuroblasts, and reactive astrocytes in the striatum ipsilateral to the ischemic injury was markedly attenuated, and new adult neurons were not found. An enriched environment is known to enhance neural function and recovery. The enriched environment after experimental stroke did increase neurogenesis in the hippocampus. It is possible that increased neurogenesis and migration from the SVZ are maladaptive. An enriched environment more closely resembles the natural conditions for animals compared with bare cages of a “regular” environment. Increased neurogenesis and migration from the SVZ may be an anomaly related to keeping the animals in bare cages or serve no function. We can make no assumptions before the physiology of brain injury and repair is better understood.

4. Reherniation after lumbar discectomy 

How much disc material to remove when performing a discectomy? Knowing when to stop is never easy. A team of orthopedic surgeons from Stanford [1] tried subtotal discectomy in 30 prospectively collected patients and compared their outcomes with a historic cohort of 46 patients treated with discectomy alone. Reherniation rates and clinical outcomes were determined by independent evaluation at 6, 12, and 24 months after surgery. Although aggressive discectomy decreased the reherniation rate from 18% to 9%, patient satisfaction decreased, and both back pain and Oswestry scores were worse. Reherniation was unusually common in the historic control group in this study. Reherniation rates are commonly estimated at between 5% to 15% [8], [9]. A variety of methods have been tried to prevent reherniation—from fusion [2] to packing the disc space with oxidized cellulose [4]. So far, no superior method exists. Patients often ask me when I describe the procedure: “Will you put something there instead of the disc? Will you close the defect through which the disc herniated?” These are reasonable questions. In the future, I hope to be able to replace the resected nucleus pulposus with a polymer that has similar properties and then close the defect that allowed the herniation to occur.