Reoperative Experience with Papillary Thyroid Cancer

Background

Intense postoperative monitoring has resulted in increasing detection of patients with recurrent papillary thyroid cancer (PTC). Our goals included quantifying successful reoperation, and analyzing surgical complications and reasons for relapse.

Methods

From 1999 to 2008, a total of 410 patients underwent reoperation for PTC relapse. We analyzed post-reoperative disease outcomes, reasons for relapse, and complications.

Results

Bilateral reoperative thyroidectomy was performed in 13 (3 %) patients; lobectomy, 34 (8 %); central neck (VI) soft tissue local recurrence excision, 47 (11.5 %); bilateral VI node dissection, 107 (26 %); unilateral VI dissection, 112 (27 %); levels II–V dissection, 93 (23 %); levels III–V, 86 (21 %); lateral single- or two-compartment dissection, 51 (12 %); and node picking, 20 (5 %) of level VI and 53 (13 %) lateral neck. Complications occurred in 6 %; including hypoparathyroidism, 3 %; unintentional recurrent laryngeal nerve (RLN) paralysis, 3 %; phrenic nerve injury, 0.5 %; spinal accessory nerve injury, 0.5 %; and chyle leak in 1.6 %. Of 380 (93 %) patients with follow-up (mean 5.2 years); 274 (72 %) patients are alive with no structural evidence of disease, 38 % developed disease relapse (mean 2.1 years), 42 (11 %) died from PTC, and 55 (14 %) are alive with disease. The reason for relapse was a false negative pre-reoperative ultrasound (US) in 18 (5 %), nodal recurrence in the operative field in 37 (10 %), a combination of these two reasons in 10 (3 %), and disease virulence (local or systemic recurrence) in 81 (21 %).

Conclusions

Although 72 % of patients were rendered structurally disease free after reoperation, nearly 40 % suffered additional relapse. Improved surgical technique or preoperative localization might positively affect 15–20 %; at least 20 % reflect the biologic aggressiveness of the disease.     

Futility and the Care of Surgical Patients: Ethical Dilemmas

Futility has been a contentious topic in medicine for several decades. Surgery in critical or end-of-life situations often raises difficult questions about futility. In this article, we discuss the definition of futility, methods for resolving futility disputes, and some ways to reframe the futility debate to a more fruitful discussion about the goals of care, better communication between surgeon and patient/surrogate, and palliative surgical care. Many definitions of futile therapy have been discussed. The most controversial of these is “qualitative futility” which describes a situation in which the treatment provided is likely to result in an unacceptable quality of life. This is an area of continued controversy because it has been impossible to identify universally held beliefs about acceptable quality of life. Many authors have described methods for resolving futility disputes, including community standards and legalistic multi-step due process protocols. Others, however, have abandoned the concept of futility altogether as an unhelpful term. Reframing the issue of futility as one of inadequate physician–patient communication, these authors have advocated for methods of improving communication and strengthening the patient–physician relationship. Finally, we discuss the utilization of consultants who may be of use in resolving futility disputes: ethics committees, palliative care specialists, pastoral care teams, and dedicated patient advocates. Involving these specialists in a futility conflict can help improve communication and provide invaluable assistance in arriving at the appropriate treatment decision.     

Myeloid cell microsomal prostaglandin E synthase-1 fosters atherogenesis in mice

Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1–derived PGE₂ in these cell types on discrete cellular components of the vasculature. The cell selective roles of mPGES-1 in atherogenesis are unknown. Mice lacking mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPGES-1-KOs), or endothelial cells (EC-mPGES-1-KOs) were crossed into hyperlipidemic low-density lipoprotein receptor-deficient animals. En face aortic lesion analysis revealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant with a reduction in oxidative stress, reflective of reduced macrophage infiltration, less lesional expression of inducible nitric oxide synthase (iNOS), and lower aortic expression of NADPH oxidases and proinflammatory cytokines. Reduced oxidative stress was reflected systemically by a decline in urinary 8,12-iso-iPF_2α-VI. In contrast to exaggeration of the response to vascular injury, deletion of mPGES-1 in VSMCs, ECs, or both had no detectable phenotypic impact on atherogenesis. Macrophage foam cell formation and cholesterol efflux, together with plasma cholesterol and triglycerides, were unchanged as a function of genotype. In conclusion, myeloid cell mPGES-1 promotes atherogenesis in hyperlipidemic mice, coincident with iNOS-mediated oxidative stress. By contrast, mPGES-1 in vascular cells does not detectably influence atherogenesis in mice. This strengthens the therapeutic rationale for targeting macrophage mPGES-1 in inflammatory cardiovascular diseases.Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce pain and inflammation by suppressing the formation of proinflammatory prostaglandins (PGs), particularly prostaglandin E₂ (PGE₂) formed by cyclooxygenase-2 (COX-2) (1). However, the development of NSAIDs specific for inhibition of COX-2 revealed a cardiovascular hazard attributable to suppression of cardioprotective PGs, especially prostacyclin (PGI₂) (2). This risk appears to extend to some of the older NSAIDs, like diclofenac, that also inhibit specifically COX-2 (3, 4). These developments prompted interest in microsomal PGE synthase (mPGES)-1 as a downstream alternative drug target to COX-2 (5): it is the dominant source among PGES enzymes in the biosynthesis of PGE₂ (6). Unlike NSAIDs, inhibitors of mPGES-1 would spare PGI₂ from suppression. Indeed, blockade or deletion of mPGES-1 results in accumulation of its PGH₂ substrate, rendering it available for metabolism by other PG synthases, including PGI₂ synthase (PGIS) (7).Consistent with these observations, we have found that whereas deletion of COX-2 in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) renders mice susceptible to thrombosis and hypertension (2), deletion of mPGES-1 in vascular cells has no such effect (8). Indeed, global deficiency of mPGES-1 restrains atherogenesis (9), the proliferative response to vascular injury (10) and angiotensin-induced aortic aneurysm formation (11) in mice.Despite this attractive cardiovascular profile, mPGES-1 is a complex drug target. The dominant prostanoid products of substrate rediversion differ among cell types. For example, whereas PGI₂ might be augmented in vascular cells, the consequence of mPGES-1 blockade in other cells might be an increase in thromboxane (Tx)A₂, a PG that promotes platelet activation, vasoconstriction, and atherogenesis (9). Even if an increase in PGI₂ afforded a desirable cardiovascular profile, it might undermine the analgesic efficacy of mPGES-1 inhibitors. Although the impacts of global deletion of mPGES-1 and COX-2 in many mouse models of analgesia are indistinguishable (12, 13), in some, PGI₂ rather than PGE₂ predominates (14) and thus may be the dominant mediator in certain subtypes of human pain. Finally, the consequences of PGE₂ suppression might differ between cell types. PGE₂ activates four E prostanoid (EP) receptors with contrasting intracellular signaling and consequent biology (15, 16). Indeed, the contrasting effect of mPGES-1 deletion in myeloid vs. vascular cells on the proliferative response to vascular injury reflects the differential consequences of EP activation rather than substrate rediversion (8).A potentially discriminating feature among inhibitors of COX-2 and mPGES-1 is their effect on atherosclerosis. Global postnatal deletion of COX-2 accelerates atherogenesis in hyperlipidemic mice (17), an observation that accords with a similar effect of deleting the PGI₂ receptor (the IP) (18, 19) and with the delayed detection of a cardiovascular hazard in randomized trials of COX-2 inhibitors in patients initially selected for being at low cardiovascular risk (20). By contrast, global deletion of mPGES-1 restrains atherogenesis in mice; in this case suppression of PGE₂ coincides with an increase in biosynthesis of PGI₂ (9). Here, we wished to segregate the effects on atherosclerosis of mPGES-1 depletion in myeloid from vascular cells. Our results strengthen the rationale for targeting macrophage mPGES-1 in the treatment of inflammatory cardiovascular disease.     

Post-surgical pain syndromes: a review for the non-pain specialist

Purpose

This is a selective narrative review of the latest information about the epidemiology, impact, and prevention of chronic post-surgical pain (CPSP), intended primarily for those without a special interest in pain medicine.

Principal findings

Chronic post-surgical pain is an important problem in terms of personal impact. It has staggering economic implications, exerts powerful negative effects on the quality of life of many of those it afflicts, and places a significant burden on chronic pain treatment services in general. It is well known that surgery at certain body sites is apt to cause CPSP, but emerging evidence shows a strong correlation between CPSP and demographic (young age, obesity, and female sex) and psychological characteristics (anxiety, depression, stress, and catastrophizing). Severe acute pain is a strong risk factor for CPSP, and this adds yet more weight to the argument that acute pain should be controlled effectively. In specific circumstances, CPSP can be reduced by regional anesthetic techniques, infiltration of local anesthetic, or preoperative use of gabapentin. The ability of other known interrupters of afferent nociceptive transmission—commonly used to reduce CPSP when administered at the time of surgery—is currently unproven, as is the hypothesis that the use of remifentanil during surgery worsens CPSP.

Conclusions

Reduction of CPSP is a worthy long-term outcome for anesthesia providers to consider as they plan the perioperative care of their patients. More evidence is needed about the effect of currently used analgesics and other perioperative techniques on CPSP.     

Perceived professional support and the use of blocking behaviours by hospice nurses

A prospective study of the impact of training 41 hospice nurses in assessment skills was used to test hypotheses that blocking behaviours would be used more when patients disclosed feelings and used less when nurses perceived that they had satisfactory professional support Each nurse was asked to assess a patient's current problems before and after feedback training and 8 months later Audiotape recordings of these interviews were rated by trained raters They determined the frequency of nurses' responses which had the function of blocking patient disclosure and the emotional level of patient disclosure Before each patient assessment each nurse was interviewed and questionnaires administered to measure her perceptions of the support she received Blocking behaviours were most evident when patients disclosed their feelings (Kendalls r=0 36, P < 0 001) In interviews containing most patient disclosure of feeling, blocking was significantly less (r= - 0 24, P < 0 5) when the nurse felt that practical help would be available if needed and when the nurse felt that her direct supervisor was concerned about the nurse's own welfare (r= -0 37, P < 0 005)     

Robotic gastric electrical stimulator placement: technique and literature review

Gastroparesis in a chronic setting is a disorder that results in diminished quality of life. Laparoscopic gastric electrical stimulator (GES) placement is now being performed in patients with medically refractory gastroparesis. During this procedure, a significant amount of suturing is required to anchor the electrodes to the gastric wall. Robotic surgery may provide surgeons with several technical and ergonomic advantages during this procedure, when compared with a standard laparoscopic approach. The aim of this study is to present a case and review the technique and literature for robotic placement of GES. This report demonstrates the safety and feasibility of robotic GES placement.     

Pancreatic pseudotumors associated with multifocal idiopathic fibrosclerosis

Two patients with multifocal idiopathic fibrosclerosis and sclerosing cholangitis developed biliary obstruction due to a fibrotic pancreatic pseudotumor. The masslike fibrosis mimicked pancreatic carcinoma on sonography and cholangiopancreatography. In one patient sonography was successfully used to assess the response of the pseudotumor to corticosteroid therapy.