Earlier prediction of anastomotic insufficiency after thoracic esophagectomy by intramucosal pH.

OBJECTIVES: To assess the value of using intramucosal pH (pHi) measurements to evaluate the viability of the gastric tube after thoracic esophagectomy, and to determine whether these measurements may be used for early prediction of anastomotic insufficiency. DESIGN: Prospective, observational study. SETTING: University hospital in Japan. PATIENTS: Thirty-nine patients who had undergone thoracic esophagectomy as a treatment for esophageal cancer. INTERVENTIONS: The blood flow within the gastric tube was measured using a laser Doppler flowmeter during surgery. Periodic measurement of the pHi within the gastric tube (gastric pHi) began during surgery and continued until the second postoperative day. In 30 patients, the pHi within the rectum (rectal pHi) was measured simultaneously with the gastric pHi. The patients were divided into two groups: those patients who experienced anastomotic insufficiency constituted the leakage(+) group (n = 13); those patients who did not experience these complications were designated the leakage(-) group (n = 26). MEASUREMENTS AND MAIN RESULTS: The gastric pHi values correlated significantly with simultaneous measurements of the blood flow at the anastomotic site (p < .01). The postoperative gastric pHi values increased gradually in the leakage(-) group but stopped increasing after surgery in the leakage(+) group. The rectal pHi values increased gradually after surgery in both groups. Furthermore, there was a significant difference between the two groups when their gastric pHi values were subtracted from their rectal pHi values from the morning of the first postoperative day until the morning of the second postoperative day (p < .05). CONCLUSIONS: The gastric pHi values well reflected the viability of the gastric tube, especially when combined with the rectal pHi values. By measuring pHi, we can more accurately predict the risk of anastomotic insufficiency earlier after surgery and therefore give those patients who need it additional care to improve the viability of the gastric tube.     

Reduced adenosine receptor stimulation as a pathogenic factor in hyperhomocysteinemia.

In this review we discuss the hypothesis, and current evidence, that a decreased concentration of the endogenous purine-nucleoside adenosine contributes to the increased cardiovascular risk of patients with hyperhomocysteinemia. In hyperhomocysteinemia, the reaction equilibrium of the reaction catalysed by S-adenosylhomocysteine hydrolase will shift towards synthesis of S-adenosylhomocysteine, at the expense of free adenosine. Adenosine receptor stimulation induces several cardiovascular protective effects, such as vasodilation, inhibition of thrombocyte aggregation, of inflammation and of vascular smooth muscle cell proliferation. A decreased adenosine concentration could, therefore, well contribute to the cardiovascular complications of hyperhomocysteinemia. Previous animal studies have shown that administration of homocysteine decreases extracellular adenosine, associated with increased synthesis of S-adenosylhomocysteine. Recently, we showed that in patients with classical homocystinuria, cellular adenosine uptake is enhanced, thus limiting adenosine-induced vasodilation. These observations provide us with additional pharmacological targets, such as adenosine uptake inhibition, to reduce cardiovascular risk in patients with hyperhomocysteinemia.     

Adrenocortical insufficiency: a medical emergency.

Adrenal insufficiency is a deceptive disorder. Insidious in onset, chronic in nature, it can suddenly progress into an acute life-threatening condition that may mimic disorders of vastly different etiologies. The result can be a lethal delay in diagnosis. Prompt diagnosis and replacement of glucocorticoids and fluids are essential for survival. Acute adrenal insufficiency is frequently an exacerbation of an underlying chronic disorder of the adrenal cortex or pituitary gland. Yet any patient who has been treated with suppressive doses of glucocorticoids (e.g., cortisol, prednisone), experienced overwhelming sepsis, has received anticoagulant therapy, or has endstage metastatic carcinoma may suddenly develop adrenal insufficiency along with its deadly sequela of hypovolemic shock, hyperkalemia, hyponatremia, and hypoglycemia. Successful management of this condition requires not only a heightened clinical awareness of adrenal insufficiency, but effective stress reduction interventions and a thorough patient and family teaching program to support lifelong control of the disease.     

Posttraumatic pulmonary insufficiency: a treatable disease.

Posttraumatic pulmonary insufficiency was treated using positive end-expiratory pressure (PEEP), intermittent mandatory ventilation, and cardiovascular monitoring and support. These were begun when intrapulmonary shunt exceeded 15% and before development of hypoxemia despite high inspired oxygen fractions; or retention of CO2; or infiltrative changes on roentgenogram. Of 39 patients treated, 28 required aggressive intervention with levels of PEEP up to 40 cm H2O and support of cardiovascular function with fluids, blood, and ionitropic agents. Those sustaining blunt trauma required the same level of interventions as those with penetrating trauma, but for a significantly longer time. All had reversal of respiratory failure with reduction of shunt to 15%. There were no deaths from respiratory failure or the treatment modalities. Early aggressive treatment for all cases was successful and allowed differentiation of the severity of the original insult.     

Prediabetes as a risk factor for major adverse cardiovascular events

IntroductionType II diabetes mellitus (DM) is a proinflammatory process and a known risk factor for major adverse cardiac events (MACE). The same inflammatory markers may be present in prediabetes (pDM); however, the relationship between pDM by HbA1c and MACE is not well studied. We sought to see if pDM increases one’s risk for MACE.MethodsWe retrospectively studied patients at Beaumont Health, Michigan between 2006 and 2020. We divided patients into groups (G1–G5) based on haemoglobin A1c (HbA1c) trends over the study period as follows: G1: pDM patients who remained pDM; G2: pDM who progressed into DM; G3: pDM who normalized their HbA1c; G4: patients who maintained a normal HbA1c; and G5: patients with HbA1c persistently in the DM range. We compared MACE between the groups by univariate and multivariate regression analyses.ResultsA total of 119,271 patients were included in the study (G1: N = 13,520, G2: N = 6314, G3: N = 1585, G4: N = 15,018, G5: N = 82,834). Pairwise comparison revealed a statistically significant increase in the odds of MACE in all groups compared to those with normal HbA1c values (G4; p < .001). After adjusting for baseline characteristics, multivariate regression revealed elevated odds of MACE in patients with persistent pDM (G1; aOR = 1.087, p = .002) and diabetes (G2/G5; aOR = 1.25 and aOR = 1.18, p < .001) compared to individuals with normal HbA1c values.ConclusionPrediabetes is a risk factor for MACE. Normalization of HbA1c values appears to decrease the adjusted risk for MACE and should be the goal in patients with pDM.

KEY MESSAGES

• Patients with prediabetes (pDM) are at increased risk for major cardiovascular events.
• Normalization of HbA1c in pDM patients may have a clinically significant benefit, in terms of lowering the MACE risk.
• Prediabetes patients who progress into diabetes mellitus may represent a particularly high-risk group.

     

Tissue factor is a major stimulus for vegetation formation in enterococcal endocarditis in rabbits.

We examined the possible mechanisms of local initiation of coagulation in vegetation formation in enterococcal endocarditis by using a rabbit model. Contact activation and tissue factor expression by freshly excised aortic valves were assessed using assays developed for use with cultured cells. Bacteria alone lacked procoagulant activity and contact activation of plasma by excised valves did not occur. 4-d infected but not control valves expressed significant tissue factor activity (231 +/- 17 mU vs. 51 +/- 7 SE), which did not correlate with numbers of bacteria in vegetations. Tissue factor activity was also present in valves from rabbits infected for 1 and 2 d, as well as those from granulocytopenic and monocytopenic animals. Our findings suggest that tissue factor, expressed by host cells in response to infection, is a major stimulus for fibrin deposition in vegetation development.     

Identification of the CD4+ T cell as a major pathogenic factor in ischemic acute renal failure

Leukocytes have been implicated in the pathogenesis of ischemic acute renal failure (ARF), but the roles of the individual cell types involved are largely unknown. Recent indirect evidence suggests that T cells may play an important role in a murine model of ARF. In the current study, we found that mice deficient in T cells (nu/nu mice) are both functionally and structurally protected from postischemic renal injury. Reconstitution of nu/nu mice with wild-type T cells restored postischemic injury. We then analyzed the contribution of the individual T cell subsets to postischemic injury and found that mice deficient in CD4(+) T cells, but not mice deficient in CD8(+) T cells, were significantly protected from ARF. Direct evidence for a pathophysiologic role of the CD4(+) T cell was obtained when reconstitution of CD4-deficient mice with wild-type CD4(+) T cells restored postischemic injury. In addition, adoptive transfers of CD4(+) T cells lacking either the costimulatory molecule CD28 or the ability to produce IFN-gamma were inadequate to restore injury phenotype. These results demonstrate that the CD4(+) T cell is an important mediator of ischemic ARF, and targeting this cell may yield novel therapies.     

Palatal insufficiency: a surgical technique for reconstruction

Nasal regurgitation and hypernasality are the major complications after extirpation of the soft palate, retromolar trigone, and tonsillar areas. The surgical procedure described herein provides satisfactory correction of the defect. The combined approach of advancement-rotation palatoplasty and an advanced lateral pharyngeal wall flap appears to be an alternative solution to the use of an obturator or inferiorly based pharyngeal flap.     

Surgery for chronic vein insufficiency.

1. Although varicose veins are the most prevalent form of venous insufficiency, obstruction or valvular incompetence of the deep system produces the most severe forms of lower extremity venous insufficiency and is responsible for most cases of leg ulceration of venous etiology. 2. With careful patient selection, surgery for varicose veins can be successful. Deep venous surgery, however, has limited indications and still carries a high failure rate; it should only be indicated in selected patients after conservative therapy has failed. 3. The main causes for failure of deep venous surgery are the low pressure and low velocity flow characteristics of the venous system that favor thrombosis.     

Immobility--a major risk factor for development of pressure ulcers among adult hospitalized patients: a prospective study

OBJECTIVE: To identify risk factors associated with pressure ulcer development among adult hospitalized medical and surgical patients. DESIGN: A prospective comparative study including 530 adult patients from medical and surgical wards. Registered Nurses made the data collection on admission and once a week for up to 12 weeks. The risk assessment scale used was the Risk Assessment Pressure Sore (RAPS) scale, including the following variables; general physical condition, activity, mobility, moisture, food intake, fluid intake, sensory perception, friction and shear, body temperature and serum albumin. RESULTS: Sixty-two (11.7%) patients developed 85 pressure ulcers. The most common pressure ulcer was that of nonblanchable erythema. Patients who developed pressure ulcers were significantly older, hospitalized for a longer time, had lower scores on the total RAPS scale, had lower weight and lower diastolic blood pressure than nonpressure ulcer patients did. In the multiple logistic regression analyses using variables included in the RAPS scale immobility emerged as a strong risk factor. When adding remaining significant variables in the analyses, mobility, time of hospitalization, age, surgical treatment and weight were found to be risk factors for pressure ulcer development. CONCLUSION: It is confirmed that immobility is a risk factor of major importance for pressure ulcer development among adult hospitalized patients. The results also indicate that the RAPS scale may be useful for prediction of pressure ulcer development in clinical practice.     

A focus on inflammation as a major risk factor for atherosclerotic cardiovascular diseases

Atherosclerosis is a dynamic, pathogenic process in the artery wall, with potential adverse outcome for the host. Acute events such as myocardial infarction and ischemic stroke often result from rupture of unstable atherosclerotic lesions. Understanding the underlying pathology of such lesions and why and when they rupture, is therefore of great interest for the development of new diagnostics and treatment. Inflammation is one of the key drivers of atherosclerotic plaque development and the interplay between inflammation and lipids constitutes the hallmark of atherosclerotic disease. This review summarizes the role of inflammation in atherosclerosis and presents some of the latest discoveries as well as unmet needs regarding the role of inflammation as major risk factor in atherosclerotic disease.