Intraoperative Use of External Fixator Attachments for Reduction of Lower Extremity Fractures and Dislocations.

The mainstay of complex open lower extremity fractures and dislocations is the temporizing external fixator. We propose the use of external fixator attachments that allow for the reduction of fractures and dislocations intraoperatively. By using external fixator carbon fiber rods, the surgeon is able to create a capital "T" (sweet T) shaped attachment and connect this to a Schanz pin. Simultaneously, the external fixator carbon fiber rods can be configured into the shape of a capital Greek letter pi (Cherry II) and applied to an external fixator pin. When both of these configurations are used, multi-directional forces can be applied across the fracture fragments with the added benefit of using extrinsic hand muscle power for force generation and manipulation of fracture fragments to facilitate reduction.

Immediate, irreversible, posttraumatic coma: a review indicating that bilateral brainstem injury rather than widespread hemispheric damage is essential for its production.

Traumatic brain injury may result in immediate long-lasting coma. Much attention has been given to predicting this outcome from the initial examination because these predictions can guide future treatment and interactions with the patient's family. Reports of diffuse axonal injury in these cases have ascribed the coma to widespread damage in the deep white matter that disconnects the hemispheres from the ascending arousal system (AAS). However, brainstem lesions are also present in such cases, and the AAS may be interrupted at the brainstem level. This review examines autopsy and imaging literature that assesses the presence, extent, and predictive value of lesions in both sites. The evidence suggests that diffuse injury to the deep white matter is not the usual cause of immediate long-lasting posttraumatic coma. Instead, brainstem lesions in the rostral pons or midbrain are almost always the cause but only if the lesions are bilateral. Moreover, recovery is possible if critical brainstem inputs to the AAS are spared. The precise localization of the latter is subject to ongoing investigation with advanced imaging techniques using magnets of very high magnetic gradients. Limited availability of this equipment plus the need to verify the findings continue to require meticulous autopsy examination.

Why Alzheimer trials fail: removing soluble oligomeric beta amyloid is essential, inconsistent, and difficult.

Before amyloid formation, peptides cleaved from the amyloid precursor protein (APP) exist as soluble oligomers. These are extremely neurotoxic. Their concentration is strongly correlated with synaptic impairment in animals and parallel cognitive decline in animals and humans. Clinical trials have largely been aimed at removing insoluble beta amyloid in senile plaques and have not reduced soluble load. Even treatment that should remove soluble oligomers has not consistently reduced the load. Failure to significantly improve cognition has frequently been attributed to failure of the amyloid hypothesis or to irreversible alteration in the brain. Instead, trial failures may be because of failure to significantly reduce load of toxic Aß oligomers. Moreover, targeting only synthesis of Aß peptides, only the oligomers themselves, or only the final insoluble amyloid may fail to significantly reduce soluble load because of the interrelationship between these 3 points in the amyloid cascade. Thus, treatments may fail unless trials target simultaneously all 3 points in the equation-"triple therapy". Cerebrospinal fluid analysis and other monitoring tools may in the future provide reliable measurement of soluble load. But currently, only analysis of autopsied brains can provide this data and thus enable proper evaluation and explanation of the outcome of clinical trials. These data are essential before attributing trial failures to the advanced nature of the disease or asserting that failures prove that the theory linking Alzheimer's disease to products of amyloid precursor protein is incorrect.

Fibrinoid necrosis of small brain arteries and arterioles and miliary aneurysms as causes of hypertensive hemorrhage: a critical reappraisal.

Cerebral hemorrhage in hypertensive patients is still an important source of morbidity and death. Understanding its underlying pathological basis is essential for the development of fact-based attempts to prevent the hemorrhage. Fibrinoid necrosis and miliary aneurysms are associated with and are the probable underlying causative lesions. Unfortunately much misunderstanding and confusion surrounds understanding of both lesions. This review clarifies several points. These include the following: the nature of fibrinoid necrosis and the susceptibility of small brain arteries and arterioles to this lesion even in the so-called benign hypertension; the relationship of fibrinoid necrosis to lipohyalinosis and the reasons for preferring the term fibrinoid; the existence of miliary aneurysms; the distinction between these aneurysms and pseudo-aneurysms or fibrin globes; the importance of, and basis for, recognizing healed miliary aneurysms; the relationship of fibrinoid necrosis to these aneurysms.

Cytotoxic edema: monitoring its magnitude and contribution to brain swelling.

Cytotoxic edema (CytE) is an increment in total brain water produced when the excess water swells cells rather than expanding the extracellular space. CytE contributes to brain swelling with a resultant increase of intracranial pressure (ICP). However, questions remain concerning the magnitude of the contribution made by CytE to raised ICP and the ability of CytE by itself to produce lethal levels of ICP that result in brainstem herniation. These questions exist because there are pitfalls in estimating the magnitude of CytE and hence its contribution to ICP using either electron microscopy or in vivo surrogates for CytE such as impedance measurements or the apparent diffusion coefficient. Correlation of these measures has been made during CytE. However, the literature provides reasons to question whether any of these surrogates for CytE can give accurate quantitative measures of CytE. At present, there is little evidence to indicate that CytE can, by itself, raise ICP to lethal levels. However, because CytE can raise ICP, it is of interest to develop treatments to prevent or reduce CytE even though currently available data do not yet provide an established mechanistic basis upon which to base such therapy.

Intraoperative use of the pelvic c-clamp as an aid in reduction for posterior sacroiliac fixation.

Posterior pelvic ring injuries with dissociation of the sacroiliac joint can be a therapeutic challenge. Open procedures for reduction have a significant risk for wound complications although inadequate reductions using percutaneous methods can have poor long-term outcomes. Several indirect reduction methods have been previously described for closed reduction of the sacroiliac joint. We present our technique for the intraoperative use of the pelvic c-clamp as a reduction aid for the posterior pelvis in conjunction with percutaneous iliosacral screw fixation. This technique has been used routinely in our patients who sustain injuries to the sacroiliac joint and are candidates for closed reduction and percutaneous fixation. Our objective is to provide orthopedic surgeons an additional means by which to reduce sacroiliac disruptions by percutaneous means.

The acetabular reamer: a unique tool for anterior iliac crest bone graft harvesting.

Bone grafting is often required in craniofacial reconstruction. Morselized corticocancellous bone grafts are particularly useful in applications such as filling and contouring irregular bony defects. Obtaining grafts of this consistency by traditional methods is difficult. An efficient harvesting method that can produce such grafting material in clinically useful quantities is needed. We report the use of a mechanical acetabular reamer for the purpose of harvesting a bone graft from the iliac crest.

Reconstruction of limited soft-tissue defect with open tibial fracture in the distal third of the leg: a cost and outcome study.

This study was conducted to analyze the cost and outcome of free-tissue transfers versus local muscle flaps for reconstruction of limited soft-tissue defects associated with tibial fractures in the distal third of the leg. Twelve adult patients underwent either free (n = 6) or local muscle (n = 6) flap reconstruction were retrospectively reviewed. Total operative time for local muscle flap reconstruction was 215 +/- 47 minutes compared with 450 +/- 90 minutes (P < 0.0002) for free-muscle transfer. Median length of hospital stay after reconstruction was 7 days for local muscle flap compared with 9 days for free-muscle transfer. Total cost of the local muscle flap procedure was US dollars 11,729 +/- US dollars 4460 compared with US dollars 19,989 +/- US dollars 3295 (P < 0.0004) for free-flap reconstruction. Five of 6 patients in each group had excellent soft-tissue contours. Fracture healing was evident in all patients of each group. Thus, a local muscle flap for reconstruction of a limited distal tibial wound appears to be more cost-effective than free-tissue transfer because of equivocal outcomes achieved but at approximately half of the cost.

Exchange reamed nailing for aseptic nonunion of the tibia.

BACKGROUND: Exchange reamed nailing of the tibia is a common procedure in the treatment of an aseptic tibial nonunion. However, reports in the literature supporting this technique are limited. METHODS: Forty patients with a tibial nonunion after initial unreamed intramedullary nailing were retrospectively assessed after an exchange reamed nailing. The main outcome measurements included radiographic and clinical union as well as time from exchange reamed nailing to union. RESULTS: Thirty-eight patients achieved union of their fracture (95%). The average time from exchange nailing to union was 29 +/- 21 weeks. Complications included one deep vein thrombosis (2.5%) and two hardware failures (5%). CONCLUSION: Exchange reamed nailing for nonunions of the tibia results in a high union rate and is associated with a low complication rate. This technique is recommended as a standard procedure for aseptic tibial nonunions after initial unreamed intramedullary nailing.

Free tissue transfer to a difficult wound of the lower extremity.

Amputation is still recommended to patients with a difficult wound of the lower extremity because limb salvage after free tissue transfer in these patients remains uncertain. During the past 3 years, the authors studied 15 patients (11 men, 4 women; age range, 17-71 years) with difficult wounds of the lower extremities who had free tissue transfers for limb salvage. Eleven patients had an extensive soft-tissue defect (nearly the entire length) of the legs or feet, and 4 had a composite-tissue defect of the legs or feet that required bony reconstruction. A total of 16 free tissue transfers (13 free muscle flaps, 2 osteomusculocutaneous flaps, and 1 adipofascial flap) were performed in 15 patients (1 patient had bilateral transfers). A saphenous vein loop or graft was used in 3 patients and a subsequent bone graft was done in 2 patients. Free tissue transfer was accomplished successfully in 14 patients (93%). Limb salvage was achieved ultimately in 12 patients (80%) who were able to ambulate during a 36-month follow-up. The authors believe that free tissue transfer for limb salvage in any patient with a difficult wound of the lower extremity is still a worthwhile procedure and should be attempted if possible. Meticulous preoperative preparation and intraoperative execution combined with the use of innovative microsurgical techniques are the keys for success.

Fracture of the femoral tunnel after an anterior cruciate ligament reconstruction.

Fractures after anterior cruciate ligament (ACL) reconstructive surgery are rare. Patella fractures can occur as a complication after bone-patellar tendon-bone autografts, and few case reports of tibia fractures have been published. Although reports of femur fractures have been published, the causes are attributed to stress risers other than the femoral tunnel. To our knowledge, this is the first case report of a femoral tunnel serving as a stress riser after an ACL reconstruction with bone-patellar tendon-bone autograft. The patient's fracture resulted from minimal trauma and required surgical fixation.

Vasodilation of brain surface arterioles by blockade of Na-H+ antiport and its inhibition by inhibitors of KATP channel openers.

Pial artrioles of rats were monitored in vivo and found to dilate in dose-dependent fashion upon application of either benzamil or ethyl isopropyl amiloride, both of which are inhibitors of the sodium-hydrogen antiport. Antiport blockade is known to decrease the internal pH of vascular smooth muscle (VSM). The dilation was blocked by 1 microm glibenclamide, which in that dose is a selective inhibitor of ATP sensitive potassium channels (K(ATP)). The nitric oxide synthase inhibitor nitro-l arginine (l-NNA) also blocked the response. Previous studies of this preparation under the same experimental conditions showed that l-NNA inhibited dilation by K(ATP) openers and that nitric oxide had no permissive action in this setting. Moreover, one study by others has demonstrated a pH sensitive site on the internal surface of K(ATP) while another study by others has demonstrated that sodium propionate, a direct acidifier of the cell, dilates rat basilar artery in K(ATP)-dependent fashion. Therefore, the present data support the following conclusions: decrease of internal pH dilates brain arterioles; the response is K(ATP) dependent; in some situations, inhibitors of nitric oxide synthase can inhibit K(ATP) and K(ATP)-dependent dilations including those produced by decrease of internal pH.

Cerebral hemorrhage produced by ruptured dissecting aneurysm in miliary aneurysm.

This report describes, for what may be only the second time, a ruptured miliary aneurysm within a cerebral hemorrhage. The report is unique in that the aneurysm has arisen at the site of a dissection within the wall of an arteriole at a site of fibrinoid necrosis. The case not only is a unique illustration of this pathogenetic pathway to miliary aneurysm formation, but also reemphasizes the relationship between fibrinoid and miliary aneurysm formation.

ATP-sensitive potassium channels in the cerebral circulation.

BACKGROUND: In brain blood vessels, electrophysiological studies proving the existence of ATP-sensitive potassium channels (KATP) are scarce. However, numerous pharmacological studies establish the importance of KATP channels in these blood vessels. This review emphasizes the data supporting the importance of vascular KATP in the responses of brain blood vessels. SUMMARY OF REVIEW: Electrophysiological data show the existence of KATP in smooth muscle and endothelium of brain vessels. A much larger number of studies in virtually all experimental species have shown that classic openers of KATP dilate brain arteries and arterioles. This response can by blocked by glibenclamide, a selective inhibitor of KATP opening. Several physiological or pathophysiological responses are also blocked by glibenclamide. KATP contains a multiplicity of potential sites of interaction with drugs of diverse, sometimes unrelated, structures. Drugs with imidazole or guanidinium groups are particularly likely to have effects on KATP. This complicates interpretation of the actions of such drugs when used as supposedly selective pharmacological probes for other putative targets. A pH-sensitive site on the internal surface of cloned channels may explain the glibenclamide-inhibitable dilation produced by intracellular acidosis and perhaps by CO2. In some situations KATP appears to be involved in either the synthesis/release or action of endothelium-derived mediators of cerebrovascular tone. The importance of KATP may be dependent on the portion of the cerebrovascular tree being studied and on diverse experimental conditions, age, species, and the presence of disease. CONCLUSIONS: KATP have been shown to mediate a wide range of cerebrovascular response in physiologic or pathologic circumstances in a variety of experimental conditions. Their relevance to cerebrovascular responses in humans remains to be explored.

Dilation of rat brain arterioles by hypercapnia in vivo can occur even after blockade of guanylate cyclase by ODQ.

1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ) is an inhibitor of guanylate cyclase and has been reported to inhibit dilation of cerebral blood vessels by hypercapnia. This supports the hypothesis that this dilation is dependent upon guanylate cyclase, activated by nitric oxide (NO) released from neural tissue. However, there are conflicting reports concerning the role of guanylate cyclase in response to hypercapnia. Therefore, we tested the effect of topically applied ODQ (10 microM) on rat pial arterioles observed with a microscope through a closed cranial window. In one study, we tested ODQ ability to inhibit both the dilation produced by hypercapnia (3% and 5% inspired CO(2)) and, in the same rats, the dilation produced by N-methyl-D-aspartate (NMDA). In another experiment, we tested the ability of ODQ to inhibit dilation produced by hypercapnia and the dilation produced by 3-morpholinosydnonimine (SIN-1), a donor of NO. The responses to NMDA and to NO are known to depend upon activation of guanylate cyclase and were both blocked in the present study. However, the response to hypercapnia was not affected. These findings provide evidence that hypercapnic dilation can occur independently of guanylate cyclase activation.

Structure and location of amyloid beta peptide chains and arrays in Alzheimer's disease: new findings require reevaluation of the amyloid hypothesis and of tests of the hypothesis.

New in situ high resolution electronmicroscopic examination of amyloid fibrils in situ indicate that in Alzheimer's disease these fibrils are not simply long chains of self aggregated amyloid beta peptide. The amyloid beta is not only associated with P protein and glycans, as was well known from previous immunohistologic studies, but is arranged in the form of short chains at right angles to a P protein backbone with the glycans wrapped around that backbone. These findings suggest that the hypothesis causally relating simple, fibrillar amyloid beta to Alzheimer's disease must be reevaluated since such simple fibrils may be absent, or not the major form of the amyloid beta in the brain. Other data shows that shorter multimers, so-called protofibrils, or dimers of amyloid beta or molecules cleaved from it can be highly toxic. Some of these may be in the soluble amyloid beta fraction. Shorter multimers or dimers of amyloid beta, either extra or intracellular, may be the real links between amyloid beta production and Alzheimer's disease. Toxicity studies employing fibrillar amyloid beta may not be relevant, even if they produce lesions, because they do not employ amyloid beta in the form in which it actually exists in the Alzheimer brain. Studies of treatments designed to remove fibrils or to prevent their formation may be ineffective or suboptimal in effectiveness because they do not reduce the relevant amyloid burden and/or fail to alter the arrangement of shorter multimers of amyloid beta around its P-protein and glycan core.