Long-term economic impact of coiling vs clipping for unruptured intracranial aneurysms.

BACKGROUND: : Treatment of unruptured intracranial aneurysms (UIAs) involves endovascular coiling or aneurysm clipping. While many studies have compared these treatment modalities with respect to various clinical outcomes, few studies have investigated the economic costs associated with each procedure. OBJECTIVE: : To determine the reoperation rate, postoperative complications, and inpatient and outpatient costs associated with surgical or endovascular treatment of patients with UIAs in the United States. METHODS: : We utilized the MarketScan database to examine patients who underwent surgical clipping or endovascular coiling procedures for UIAs from 2000 to 2009, comparing reoperation rates, complications, and angiogram and healthcare resource use. Propensity score matching techniques were used to match patients. RESULTS: : We identified 4,504 patients with surgically treated UIAs, with propensity score matching of 3,436 patients. Reoperation rates were significantly lower in the clipping group compared to the coiling group at 1- (P < .001), 2- (P < .001), and 5 years (P < .001) following the procedure. However, postoperative complications (immediate, 30 and 90 days) were significantly higher in those undergoing surgical clipping. Although hospital length of stay and costs were higher in the clipping group for the index procedure, the number of postoperative angiograms and outpatient services used at 1, 2, and 5 years were significantly higher in the coiling group. CONCLUSION: : Though surgical clipping resulted in lower reoperation rates, it was associated with higher complication rates and initial costs. However, overall costs at 2 and 5 years were similar to endovascular coiling due to the significantly higher number of follow-up angiograms and outpatient costs in these patients. ABBREVIATIONS: : SAH, subarachnoid hemorrhageUIAs, unruptured intracranial aneurysms.

Complications of transforaminal cervical epidural steroid injections.

STUDY DESIGN: A comprehensive literature review. OBJECTIVES: To review and critically evaluate the past literature focusing on incidence and clinical presentation of complications associated with transforaminal cervical epidural steroid injection (TFCESI) and techniques employed to avoid them. The overall goal is to guide the direction of future research and improve clinical care by increasing awareness of complications and measures that may be undertaken to increase safety. SUMMARY OF BACKGROUND DATA: TFCESI is a component in the diagnosis and management of cervical radicular syndromes in patients who have failed conservative management. There has been much discussion and also controversy in the recent literature. Considerable attention has been paid to reports of catastrophic complications and proposed measures to avoid them. METHODS: Medical databases were searched for studies of TFCESI. The bibliographies of these articles were then searched as well. Thoracic and lumbar articles were discarded as were any non-transforaminal cervical procedures or those that did not involve injection into the epidural space. Particular attention was paid to serious neurologic sequelae after TFCESI and its mechanism, as well as techniques being employed to avoid complications. RESULTS: There are a limited number of studies looking at complications of TFCESI. One retrospective study reported an overall rate of complications of 1.64%. There are reports of serious neurologic sequelae in the literature including brain and spinal cord infarction due to embolic phenomenon of particulate steroids. Cadaveric dissection revealed ascending and deep cervical arterial branches entering the external opening of the posterior intervertebral foramen, the classic target site for TFCESI. Measures to avoid complications mentioned in the literature include the use of nonparticulate steroids, test dose of local anesthetic before injection of steroids, live fluoroscopy, digital subtraction, no to light sedation, use of true lateral view to supplement frontal and oblique views in fluoroscopy, use of blunt needles, and computed tomography guidance. CONCLUSION: The literature reveals a number of rare, potentially catastrophic neurologic sequelae including brain and spinal cord infarction. Most of these are thought to be due to intravascular uptake of particulate steroids. The true overall incidence remains obscure due to the lack of blinded controlled studies. Injectionists, referring physicians, and patients should be aware of the nature and potential consequences of these complications. Additionally, it is imperative for injectionists to standardize techniques to minimize complications, especially by using a test dose of local anesthetic before injection of preferably nonparticulate corticosteroid.

Dexamethasone treatment causes resistance to insulin-stimulated cellular potassium uptake in the rat.

Patients treated with glucocorticoids have elevated skeletal muscle ouabain binding sites. The major Na(+)-K(+)-ATPase (NKA) isoform proteins found in muscle, alpha2 and beta1, are increased by 50% in rats treated for 14 days with the synthetic glucocorticoid dexamethasone (DEX). This study addressed whether the DEX-induced increase in the muscle NKA pool leads to increased insulin-stimulated cellular K+ uptake that could precipitate hypokalemia. Rats were treated with DEX or vehicle via osmotic minipumps at one of two doses: 0.02 mg.kg(-1).day(-1) for 14 days (low DEX; n = 5 pairs) or 0.1 mg.kg(-1).day(-1) for 7 days (high DEX; n = 6 pairs). Insulin was infused at a rate of 5 mU.kg(-1).min(-1) over 2.5 h in conscious rats. Insulin-stimulated cellular K+ and glucose uptake rates were assessed in vivo by measuring the exogenous K+ infusion (K+(inf)) and glucose infusion (Ginf) rates needed to maintain constant plasma K+ and glucose concentrations during insulin infusion. DEX at both doses decreased insulin-stimulated glucose uptake as previously reported. Ginf (in mmol.kg(-1).h(-1)) was 10.2 +/- 0.6 in vehicle-treated rats, 5.8 +/- 0.8 in low-DEX-treated rats, and 5.2 +/- 0.6 in high-DEX-treated rats. High DEX treatment also reduced insulin-stimulated K+) uptake. K+(inf) (in mmol.kg(-1).h(-1)) was 0.53 +/- 0.08 in vehicle-treated rats, 0.49 +/- 0.14 in low-DEX-treated rats, and 0.27 +/- 0.08 in high-DEX-treated rats. DEX treatment did not alter urinary K+ excretion. NKA alpha2-isoform levels in the low-DEX-treated group, measured by immunoblotting, were unchanged, but they increased by 38 +/- 15% (soleus) and by 67 +/- 3% (gastrocnemius) in the high-DEX treatment group. The NKA alpha1-isoform level was unchanged. These results provide novel evidence for the insulin resistance of K+ clearance during chronic DEX treatment. Insulin-stimulated cellular K+ uptake was significantly depressed despite increased muscle sodium pump pool size.