The kidney allocation system does not appropriately stratify risk of pediatric donor kidneys: Implications for pediatric recipients.

Kidney Allocation System (KAS) was enacted in 2014 to improve graft utility, while facilitating transplantation of highly-sensitized patients and preserving pediatric access to high-quality kidneys. Central to this system is the Kidney Donor Profile Index (KDPI), a metric intended to predict transplant outcomes based on donor characteristics but derived using only adult donors. We posited that KAS had inadvertently altered the profile and quantity of kidneys made available to pediatric recipients. This question arose from our observation that most pediatric donors carry a KDPI over 35 and have therefore been rendered relatively inaccessible to pediatric recipients under KAS. Here we explore early trends in pediatric transplantation following KAS, including: (i) use of pediatric donors, (ii) use of Public Health System (PHS) high infectious risk donors, (iii) wait time, and (iv) living donor transplantation. We note some concerning preliminary changes following KAS implementation, including the allocation of fewer deceased donor pediatric kidneys to children and stagnation in pediatric wait times. Moreover, the poor predictive power of the KDPI for adult donors appears to be even worse when applied to pediatric donors. These early trends warrant further observation and consideration of changes in pediatric kidney allocation if they persist.

Eculizumab prevents recurrent antiphospholipid antibody syndrome and enables successful renal transplantation.

Renal transplantation in patients with antiphospholipid antibodies has historically proven challenging due to increased risk for thrombosis and allograft failure. This is especially true for patients with antiphospholipid antibody syndrome (APS) and its rare subtype, the catastrophic antiphospholipid antibody syndrome (CAPS). Since a critical mechanism of thrombosis in APS/CAPS is one mediated by complement activation, we hypothesized that preemptive treatment with the terminal complement inhibitor, eculizumab, would reduce the extent of vascular injury and thrombosis, enabling renal transplantation for patients in whom it would otherwise be contraindicated. Three patients with APS, two with a history of CAPS, were treated with continuous systemic anticoagulation together with eculizumab prior to and following live donor renal transplantation. Two patients were also sensitized to human leukocyte antigens (HLA) and required plasmapheresis for reduction of donor-specific antibodies. After follow-up ranging from 4 months to 4 years, all patients have functioning renal allografts. No systemic thrombotic events or early graft losses were observed. While the appropriate duration of treatment remains to be determined, this case series suggests that complement inhibitors such as eculizumab may prove to be effective in preventing the recurrence of APS after renal transplantation.

Posterior internal fixation with screw plates in traumatic lesions of the cervical spine.

Posterior internal fixation associated with bone fusion is indicated in those traumatic cervical spines in which an additional posterior direct action is required to achieve reduction and/or decompression. The internal fixation device is represented by screw plates allowing strong anchorage, short fixation, and light postoperative immobilization. Twenty-three cases of posterior internal fixation in traumatic cervical spines are presented. In selected cases, the results can be estimated as very good with respect to instability, spinal balance involvement, canal stenosis, and reversible neurologic involvement.

Frontal intermittent rhythmic delta activity (FIRDA) in pial-dural arteriovenous malformation.

We report a case of FIRDA associated with a pial-dural arteriovenous malformation (AVM). The patient presented with headaches, papilledema and partial oculomotor nerve palsy. CT scan had failed to discover the AVM. After partial embolization of the AVM, the patient's symptoms and signs resolved, and the FIRDA disappeared. FIRDA has been thought to be caused by frontal lobe ischemia or periventricular edema. It has not been reported in benign intracranial hypertension (BIH). We postulate that the FIRDA in this case was due to the circulatory "steal" effect of the AVM, and not to the intracranial hypertension. Five percent of patients with dural AVM's present with a picture consistent with BIH. We recommend a diligent search for additional pathology if FIRDA is seen in association with presumed BIH.

Is testing for inherited coagulation inhibitor deficiencies in young stroke patients worthwhile?

OBJECTIVE: To test the hypothesis that in patients under age 50, with a first, arterial, ischemic cerebral infarct, whose family history and medical history do not suggest an inherited coagulation inhibitor deficiency, the yield of a laboratory search for these disorders will be low. MATERIALS AND METHODS: In 55 such patients under age 50, we systematically searched for deficiencies of protein C, protein S, and antithrombin III. RESULTS: No abnormalities of protein C or antithrombin III were found. One patient had a deficiency of protein S, which was most likely acquired rather than inherited. CONCLUSIONS: In patients who lack clinical features of a prothrombotic state, the yield of testing for protein C, S and AT III deficiency is likely to be low.

Stroke education by utility bill inserts.

To assess the usefulness of utility bill inserts in stroke education, a stroke fact sheet was included in the bills of 13,000 customers of a rural electric cooperative in eastern Arkansas. Recipients were asked to return their responses to four questions based on the fact sheet via a postage-paid postcard. Two hundred eleven people responded, for an overall 1.65% response rate. Seventy-seven percent responded correctly with all four "S" stroke symptoms. Hypertension was correctly identified by 88% and smoking by 72%. Fifty-seven percent said they would immediately dial 911 at the onset of symptoms, while 36% said they would contact their doctor.

Relative importance of patient, procedural and anatomic risk factors for early vein graft thrombosis after coronary artery bypass graft surgery.

AIM: The aim of the present study was to investigate the relative importance of a wide array of patient demographic, procedural, anatomic and perioperative variables as potential risk factors for early saphenous vein graft (SVG) thrombosis after coronary artery bypass graft (CABG) surgery. METHODS: The patency of 611 SVGs in 291 patients operated on at four different hospitals enrolled in the Reduction in Graft Occlusion Rates (RIGOR) study was assessed six months after CABG surgery by multidetector computed tomography coronary angiography or clinically-indicated coronary angiography. The odds of graft occlusion versus patency were analyzed using multilevel multivariate logistic regression with clustering on patient. RESULTS: SVG failure within six months of CABG surgery was predominantly an all-or-none phenomenon with 126 (20.1%) SVGs totally occluded, 485 (77.3%) widely patent and only 16 (2.5%) containing high-grade stenoses. Target vessel diameter ≤ 1.5 mm (adjusted OR 2.37, P=0.003) and female gender (adjusted OR 2.46, P=0.01) were strongly associated with early SVG occlusion. In a subgroup analysis of 354 SVGs in which intraoperative graft blood flow was measured, lower mean flow was also significantly associated with SVG occlusion when analyzed as a continuous variable (adjusted OR 0.984, P=0.006) though not when analyzed dichotomously, <40 mL/min versus ≥ 40 mL/min (adjusted OR 1.86, P=0.08). CONCLUSION: Small target vessel diameter, female gender and low mean graft blood flow are significant risk factors for SVG thrombosis within six months of CABG surgery in patients on postoperative aspirin therapy. This information may be useful in guiding revascularization strategies in selected patients.

Bilateral sixth nerve pareses with temporal arteritis and diabetes.

A 78-year-old white woman presented with a 1-month history of neck and right shoulder pain and a 12-day history of acute horizontal diplopia. On examination, bilateral sixth nerve pareses were present, right greater than left. On evaluation, the patient was noted to have normal fasting blood sugars, but moderately elevated blood sugars after a glucose load. A temporal artery biopsy was performed which was positive. Whether diabetic or arteritic, bilateral sixth nerve pareses resulted in our patient seeking medical attention. By considering temporal arteritis, it is possible that blindness was avoided.

Intermittent unidirectional nystagmus.

A 38-year-old woman developed intermittent oscillopsia occurring every 45 to 90 minutes and lasting 20 to 40 seconds. She had a right-beating jerk nystagmus during these episodes. At other times, her neurologic examination was normal, and no nystagmus could be elicited. The nystagmus resolved when her classic migraine headaches were controlled with medical therapy. This intermittent unidirectional nystagmus may represent dormant periodic alternating nystagmus or another type of dormant nystagmus appearing intermittently due to episodic migrainous brainstem ischemia.

Bilateral optic neuropathy associated with amiodarone therapy.

Amiodarone, an antiarrhythmic agent, has been associated with mild visual loss secondary to papillopathy and papilledema. We report a patient who developed bilateral optic neuropathy 4 weeks after initiation of amiodarone therapy. Nine months later, his vision was 20/50 in the right eye and 20/200 in the left. This report provides additional evidence that amiodarone may cause toxic optic neuropathy.

Pseudo-internuclear ophthalmoplegia with downshoot in myasthenia gravis.

Internuclear ophthalmoplegia is characterized by an adduction deficit on lateral gaze with dissociated nystagmus of the abducting eye. It is seen with lesions of the medial longitudinal fasciculus. In myasthenia gravis, extraocular muscle weakness can cause the same oculomotor pattern, which has been referred to as pseudo-internuclear ophthalmoplegia. We report the additional finding of downshoot in the adducting eye in two patients with pseudo-internuclear ophthalmoplegia and positive Tensilon tests.

Oculomotor palsy and papilledema with pial-dural arteriovenous malformation.

A 62-year-old man presented with papilledema, a cranial bruit, and a partial left oculomotor nerve palsy. Arteriography revealed a large mixed pial-dural arteriovenous malformation involving the superior sagittal and both transverse sinuses. After the superior part of the malformation was embolized, the patient's papilledema and ocular motility disturbance resolved. The oculomotor disturbance may have been a nonspecific sign of increased intracranial pressure. Cranial auscultation should be performed in all cases of papilledema and cranial nerve palsy.

Silent cerebral infarction in patients with nonrheumatic atrial fibrillation. The Veterans Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators.

BACKGROUND: Cerebral infarction in patients with atrial fibrillation may vary from being clinically silent to catastrophic. The prevalence of silent cerebral infarction and its effect as a risk factor for symptomatic stroke are important considerations for the evaluation of patients with atrial fibrillation. METHODS AND RESULTS: This Veterans Affairs cooperative study was a double-blind controlled trial designed primarily to determine the efficacy of warfarin for the prevention of stroke in neurologically normal patients with nonrheumatic atrial fibrillation. It also was designed to evaluate patients with silent cerebral infarction. Computed tomography scans of the head were performed at entry, at the time of any subsequent stroke, and at termination of follow-up on all patients who completed the study without a neurological event. Of 516 evaluable scans performed at entry, 76 (14.7%) had evidence of one or more silent cerebral infarcts. Age (P = .011), a history of hypertension (P = .003), active angina (P = .012), and elevated mean systolic blood pressure (P < .001) were associated with the presence of this finding. Silent cerebral infarction occurred during the study at rates of 1.01% and 1.57% per year for the placebo and warfarin treatment groups, respectively (NS). Silent cerebral infarction at entry was not an independent predictor of later symptomatic stroke, but active angina was a significant predictor; 15% of the placebo-assigned patients with angina developed a stroke compared with 5% of the placebo-assigned patients without angina. CONCLUSIONS: Silent cerebral infarction is frequently seen in asymptomatic patients with atrial fibrillation. Age, history of hypertension, active angina, and elevated mean systolic blood pressure were associated with silent infarction at entry. The sample size was too small to determine whether warfarin had an effect on the incidence of silent infarction during the trial. Active angina at baseline was the only significant independent predictor for the later development of symptomatic stroke.

Warfarin in the prevention of stroke associated with nonrheumatic atrial fibrillation. Veterans Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators.

BACKGROUND: Nonrheumatic atrial fibrillation is common among the elderly and is associated with an increased risk of stroke. We investigated whether anticoagulation with warfarin would reduce this risk. METHODS: We conducted a randomized, double-blind, placebo-controlled study to evaluate low-intensity anticoagulation with warfarin (prothrombin-time ratio, 1.2 to 1.5) in 571 men with chronic nonrheumatic atrial fibrillation; 525 patients had not previously had a cerebral infarction, whereas 46 patients had previously had such an event. The primary end point was cerebral infarction; secondary end points were cerebral hemorrhage and death. RESULTS: Among the patients with no history of stroke, cerebral infarction occurred in 19 of the 265 patients in the placebo group during an average follow-up of 1.7 years (4.3 percent per year) and in 4 of the 260 patients in the warfarin group during an average follow-up of 1.8 years (0.9 percent per year). The reduction in risk with warfarin therapy was 0.79 (95 percent confidence interval, 0.52 to 0.90; P = 0.001). The annual event rate among the 228 patients over 70 years of age was 4.8 percent in the placebo group and 0.9 percent in the warfarin group (risk reduction, 0.79; P = 0.02). The only cerebral hemorrhage occurred in a 73-year-old patient in the warfarin group. Other major hemorrhages, all gastrointestinal, occurred in 10 patients: 4 in the placebo group, for a rate of 0.9 percent per year, and 6 in the warfarin group, for a rate of 1.3 percent per year. There were 37 deaths that were not preceded by a cerebral end point--22 in the placebo group and 15 in the warfarin group (risk reduction, 0.31; P = 0.19). Cerebral infarction was more common among patients with a history of cerebral infarction (9.3 percent per year in the placebo group and 6.1 percent per year in the warfarin group) than among those without such a history. CONCLUSIONS: Low-intensity anticoagulation with warfarin prevented cerebral infarction in patients with nonrheumatic atrial fibrillation without producing an excess risk of major hemorrhage. This benefit extended to patients over 70 years of age.