Simple Mechanical Obstruction Research Articles

Schistosomiasis and the pulmonary vasculature (2013 Grover Conference series).

Inflammation is associated with multiple forms of pulmonary arterial hypertension (PAH), including autoimmune (scleroderma) and infectious (HIV, schistosomiasis) etiologies. More than 200 million people worldwide are infected with Schistosoma, predominantly in Brazil, Africa, the Middle East, and South Asia. Schistosomiasis causes PAH in about 6.1% of those chronically infected and is particularly associated with the species Schistosoma mansoni. Treatment for schistosomiasis-associated PAH includes antihelminthic treatment, if active infection is present (although associated with little immediate benefit to the pulmonary hypertension), and then pharmacologic treatment with targeted pulmonary vascular therapies, including phosphodiesterase type 5 inhibitors and endothelin receptor antagonists. The pathophysiological mechanism by which this parasitic infection causes pulmonary hypertension is unknown but is unlikely to be simple mechanical obstruction of the pulmonary vasculature by parasite eggs. Preexisting hepatosplenic disease due to Schistosoma infection is likely important because of portopulmonary hypertension and/or because it allows egg embolization to the lung by portocaval shunts. Potential immune signaling originating in the periegg granulomas causing the pulmonary vascular disease includes the cytokines interleukin (IL)-4, IL-6, IL-13, and transforming growth factor β. Modulating these pathways may be possible targets for future therapy of schistosomiasis-associated PAH specifically, and study of this disease may provide novel insights into other inflammatory causes of PAH.

Intra-abdominal adhesions in ultrasound. Parts I and II.

The peritoneal adhesions and their clinical consequences, such as bowel obstruction, infertility in women and increased risk of extrauterine pregnancy, still remain an unsolved problem in contemporary intra-abdominal surgery. The frequency of occurrence of adhesions following laparotomies is estimated to reach 67–97%(1, 2). The most common causes encompass a physical trauma (including surgical or thermal one, e.g. electrocoagulation), infection, ischemia and the presence of a foreign body (stitches, talc, gauze, intestinal contents). Peritoneal adhesions are the most common cause of intestinal obstruction. The presence of adhesions increases the risk of each surgery and extends its duration, in particular, the stage of opening the abdominal cavity. Adhesions increase the probability of damaging the intestine while opening the abdominal cavity by 20%(3–5). Adhesive obstruction of the bowels may occur in 5% of patients who underwent a surgery(6). The adhesions which cause intestinal obstruction most frequently form after surgeries involving the large intestine as well as urologic and gynecological procedures. After laparoscopic procedures, adhesions appear more rarely and their preparation is easier(7–9). The methods that help decrease the risk of intra-abdominal adhesions include: non-traumatic surgeries, minimally invasive surgery, usage of gloves without talc, removal of drains and remains of dead tissues from the peritoneal cavity, restraining from suturing the defects in the peritoneum as well as administering pharmacological agents such as non-steroidal anti-inflammatory drugs, anticoagulants, vitamin E, statin, medicines with topical anesthetizing effect, dextran derivatives (Adept – 4% icodextrin solution) and Seprafilm (a biological barrier that prevents adhesions; composed of two polysaccharides: hyaluronic acid, carboxymethylcellulose). Seprafilm is very hydrophilic and does not require suturing. The differentiation between simple mechanical obstruction and strangulation obstruction constitutes a difficult clinical problem. Strangulation and necrosis of the bowel are the cause of a high perioperative mortality rate which in these cases equals 8–28%(7, 10). When diagnosing adhesive obstruction, the most valuable methods comprise: repeated physical examinations, plain abdominal x-ray, computed tomography and bowel passage with water soluble contrast agent (gastrografin). Gastrografin is a hyperosmolar agent (1900 mOsm/L) which increases the amount of water in the bowel and stimulates its peristalsis. The bowel passage of gastrografin is then both a diagnostic and therapeutic method(11–13). To prevent adhesive obstruction, it is proposed to perform internal intestinal splinting for the period of 7–14 days(14). The relevant literature relatively seldom mentions the value of ultrasound examination (US) in assessing the number and localization of intra-abdominal adhesions. It is a shame since there are more and more specialists in clinical sonography who use more and more advanced US equipment. Therefore, abdominal examinations performed to assess adhesive disease of the peritoneal cavity should be encouraged. In 1994, Duffy and diZerega proposed the application of abdominal US examination prior to laparoscopic management of adhesive obstruction in order to localize the first trocar(15). I know Professor Andrzej Smereczynski personally. I have always admired him for his stubbornness in research, consistent actions, enthusiasm and motivation. The Professor has vast experience in clinical sonography. He constantly verifies his studies and findings in the operation theatre. He checks himself and his actions. This is a rare and exceptional feature among diagnosticians. I have read both papers with huge interest(16, 17). Despite my limited, not to say, scarce knowledge and experience in the field of sonography, I recognize the diagnostic significance and value of the examination that is performed well and properly. I can think of numerous clinical situations in which sonographic assessment of adhesions would be of enormous significance, namely: The selection of the best site to perform a surgical cut or insert the first trocar in the patients with the history of surgeries (laparotomies). Such a procedure would surely reduce the risk of damaging the bowel when opening the abdomen. The help to differentiate between simple intestinal obstruction and strangulation of the mesentery that may cause bowel necrosis and requires urgent surgical intervention. Diagnosis of so-called aggressive fibromatosis of the peritoneum in the course of multiple, familial polyposis of the large intestine. The more common application of US examination in intra-abdominal adhesions would reduce the number of computed tomography examinations which are expensive and burden the patient with a high dosage of radiation. I can imagine that learning sonographic diagnosis of intraabdominal adhesions requires a long training. Nonetheless, with such a distinguished center, where Professor Smereczynski works, we might hope that more and more radiologists and other specialists, necessarily including surgeons, will take an interest in this diagnostic method. With all my heart, I wish you all the best and many successes in developing intra-abdominal adhesion sonography.

Transurethral incision of congenital obstructive lesions in the posterior urethra in boys and its effect on urinary incontinence and urodynamic study

Study Type--Therapy (case series) Level of Evidence 4. What's known on the subject? and What does the study add? We have clarified that there exist two types of voiding urodynamics (pressure-flow-study) for congenital urethral obstruction in boys; one is synergic pattern (SP) and the other is dyssynergic pattern (DP). In terms of daytime incontinence and nocturnal enuresis, the transurethral endoscopic incision of these obstructive lesions is only effective in the SP type, while never effective in the DP type. The synergic pattern (SP) seems to represent simple anatomical obstruction, while the dyssynergic pattern (DP) may represent anatomical obstruction complicated with functional obstruction. The efficacy of endoscopic incision to mild forms of congenital urethral obstruction has been controversial, especially in terms of nocturnal enuresis. One of the reasons for the controversy is due to the lack of pre-and post-operative urodynamic assessment with its linkage to symptomatic change. We have, for the first time in the world, systematically conducted voiding urodynamic study for those elusive lesions seen in enuretic boys. Conclusively, for simple mechanical obstruction (SP), we confirmed that some voiding urodynamic parameters improve after the endoscopic incision, parallel to symptomatic improvement, while in the rest (DP) endoscopic incision is never effective. The cause of this ineffectiveness seemed to be due to persistent functional obstruction having superimposed on mechanical obstruction. The result of the study urges us to be more keen to diagnose and treat the mild congenial urethral obstruction as well as the concomitant functional obstruction in boys with nocturnal enuresis. • To evaluate the clinical significance of congenital obstructive lesions of the posterior urethra in boys with refractory primary nocturnal enuresis. • VCUG was performed in 43 consecutive boys who visited our department from April 2004 to April 2009 who were unresponsive to conservative treatment. 20 patients of the 43 patients, underwent TUI. VCUG and UDS were performed before and 3-4 months after TUI. • In UDS, the maximum flow rate (Qmax), maximum bladder capacity, and post-voiding residual urine volume were determined using uroflowmetry (UFM), and the detrusor pressure (Pdet) at Qmax was determined in a pressure flow study (PFS). • Clinical outcome was evaluated 3-4 months and 6 months after TUI. • In VCUG performed 3-4 months after TUI, improvement was observed in urethral morphology in all patients. In preoperative PFS, two patterns were observed: 13 patients (65%) had a synergic pattern (SP) in which the Pdet increased with increasing urinary flow rate simultaneously with the initiation of voiding and seven (35%) had a dyssynergic pattern (DP) in which the Pdet was not coincident with the initiation of voiding, but was higher immediately before voiding than at Qmax. TUI was effective only in the SP group: symptomatic improvement was observed in 87.5% of patients with daytime incontinence and 77% of patients with nocturnal enuresis 6 months after TUI. • In the DP group, no effect was observed (0%). With regard to changes in UDS parameters, a significant decrease (P= 0.0004) was observed in the Pdet at Qmax and a significant increase (P= 0.036) was observed in the maximum bladder capacity in the SP group, whereas no significant differences were noted in any parameters in the DP group. • Two voiding urodynamic patterns with different clinical outcomes of TUI were detected among patients with congenital posterior urethral obstruction, the underlying disease of refractory primary nocturnal enuresis in boys.

Role of myosin light chain kinase in intestinal epithelial barrier defects in a rat model of bowel obstruction

BackgroundBowel obstruction is a common cause of abdominal emergency, since the patients are at increased risk of septicemia resulting in high mortality rate. While the compartmentalized changes in enteric microfloral population and augmentation of bacterial translocation (BT) have already been reported using experimental obstruction models, alterations in epithelial permeability of the obstructed guts has not been studied in detail. Myosin light chain kinase (MLCK) is actively involved in the contraction of epithelial perijunctional actinomyosin ring and thereby increases paracellular permeability. In the current study we attempt to investigate the role of MLCK in epithelial barrier defects using a rat model of simple mechanical obstruction.MethodsWistar rats received intraperitoneal injection of ML-7 (a MLCK inhibitor) or vehicle at 24, 12 and 1 hrs before and 12 hrs after intestinal obstruction (IO). The distal small intestine was obstructed with a single ligature placed 10 cm proximal to the ileocecal junction in IO rats for 24 hrs. Sham-operated rats served as controls.ResultsMucosal injury, such as villous blunting and increased crypt/villus ratio, was observed in the distal small intestine of IO rats. Despite massive enterocyte shedding, intestinal villi were covered with a contiguous epithelial layer without cell apoptosis. Increased transmural macromolecular flux was noticed in the distal small intestine and the proximal colon after IO. The bacterial colony forming units in the spleen and liver of IO rats were significantly higher than those of sham controls. Addition of ML-7 ameliorated the IO-triggered epithelial MLC phosphorylation, mucosal injury and macromolecular flux, but not the level of BT.ConclusionsThe results suggest that IO-induced premature enterocytic sloughing and enhanced paracellular antigenic flux were mediated by epithelial MLCK activation. In addition, enteric bacteria may undergo transcytotic routes other than paracellular paths to cross the epithelium.

Pancreas Divisum: Beyond the Apparent

Acute recurrent pancreatitis is a common clinical problem. The etiology and clinical management vary widely. Pancreas divisum is the most common congenital anomaly of the pancreas. However, only a small percentage of individuals with pancreas divisum develop acute or recurrent pancreatitis. Clinical manifestations range from isolated episodes of acute recurrent pancreatitis to chronic pancreatitis, and in some cases unexplained pain without any recognizable inflammation. The variations in clinical presentation, clinical progression of the disease, and responses to endoscopic or nonendoscopic treatments are not entirely predictable. 1 These facts have led to substantial controversy about the association of pancreas divisum with pancreatic disease. They lead us to believe that mere presence of an anatomic anomaly is not in itself sufficient and there have to be other disease modifiers or cofactors that are responsible for pancreatic injury. Environmental insults such as oxidative stresses could play a role, however, these do not seem to be universally reproducible. A key may lie in the genetic make up of the individual. In this issue of the journal, Garg and colleagues 2 have investigated the association of genetic mutations and acute recurrent pancreatitis in individuals with pancreas divisum. They have tested for genetic mutations known to be associated with pancreatitis: cystic fibrosis transmembrane conductance regulator gene (CFTR), cationic trypsinogen (PRSS1), and serine protease inhibitor Kazal type 1 (SPINK1) gene. This study was conducted in a tertiary referral center in Northern India. They studied 12 subjects with pancreas divisum and acute recurrent pancreatitis. Their control group included patients with acute recurrent pancreatitis but no pancreas divisum, patients with chronic pancreatitis due to other causes, and healthy volunteers. Mutations in individuals with asymptomatic pancreas divisum were not evaluated. Detailed work-up was carried out including analysis for the presence of microcrystals in the bile before considering etiology of pancreatitis to be idiopathic. All subjects with pancreas divisum and acute recurrent pancreatitis underwent endoscopic retrograde cholangiopancreatography with minor papillotomy and temporary stenting of the dorsal duct. Response to endoscopic therapy was defined as reduction in >50% of acute pancreatitis episodes/year. Prevalence of SPINK1 gene mutations was found to be similar in patients with recurrent acute pancreatitis with or without pancreas divisum and those with chronic pancreatitis. However, only 1 in 50 of the control group had SPINK1 gene mutation. Polymorphism in the CFTR gene was seen at a higher frequency in those with pancreas divisum. One could argue that the ideal control should be those with pancreas divisum but without symptoms. From clinical practice, we know that these controls would be hard to identify without the use of secretin-stimulated magnetic resonance cholangiopancreatography or other expensive noninvasive imaging. SPINK1 gene mutations along with mutations in CFTR have been previously shown to occur at a higher frequency in patients with idiopathic chronic and acute recurrent pancreatitis. 3,4 Some animal studies have demonstrated that genetic mutations in CFTR might be responsible for an increased inflammatory response in mice. 5 SPINK1 gene mutations were previously found in a Finnish study to occur at a higher rate in those with acute pancreatitis, suggesting that the SPINK1 gene mutation probably enhances the susceptibility to acute pancreatitis. 6 This study of Garg and colleagues raises a very thought-provoking question: is pancreatitis in patients with pancreas divisum related to the outflow obstruction at the minor papilla? From previous studies we know that only a minority of those with pancreas divisum are symptomatic and the responses to therapy are not uniformly the same despite minor papillotomy, which should relieve any obstruction. The findings of this and other studies suggest an etiology other than a simple mechanical obstruction alone. In this study, responses to endoscopic therapy were similar to those already reported, with significant improvement in approximately 70% of patients. 7 This study involved numbers that were too small to examine whether the response to therapy is predictable based on the genetic mutations. Despite the

Creatinine as the gold standard for kidney injury biomarker studies?

Before 2005, when the Acute Dialysis Quality Initiative proposed a consensus definition [1], acute kidney injury (formerly known as ‘acute renal failure’) was identified by most clinicians in the way that Justice Potter Stewart identified obscenity: they knew it when they saw it. Epidemiologists and clinical researchers, who needed an objective criterion, seemed to devise a different definition for every new study; indeed, over 35 definitions have been used to define AKI in the nephrology literature [2]. For Homer Smith, who introduced the term ‘acute renal failure’ in his textbook, The Kidney: Structure and Function in Disease and Health [3], a specific definition did not seem to matter: nowhere in his textbook does he propose a way to define AKI. We know that definitions do matter in modern clinical medicine. The consensus definition of acute myocardial infarction, which has evolved over the years and now requires biochemical evidence of myocardial tissue injury, has facilitated the design and execution of studies that have led to revolutionary changes in the treatment and outcome of patients with acute myocardial infarction around the world. The consensus definitions of sepsis and acute lung injury similarly permitted the critical care community to study and advance the clinical science and management of critically ill patients, with some clear success stories [4,5]. Within nephrology, the new consensus definition of chronic kidney disease, while controversial, has focused attention on early recognition and staging of the clinical syndrome, influenced clinical trial design as well as referral patterns to nephrologists [6], and hopefully will provide a tangible benefit for our patients. Defining AKI is clearly of paramount importance as nephrology struggles to translate a host of steady advances in the understanding of the pathobiology of AKI into clinical benefit for patients. Unfortunately, however, we face a challenge not faced by cardiologists and pulmonologists: the uncertain relationship between our ‘gold standard’ biomarkers [serum creatinine (SCr) and urine output] and our disease process. In cardiology, the relationship between the defining biomarker (troponin) and the disease process (myocardial infarction) is direct: injured myocardial cells release troponin into the circulation, where it can be measured and used to diagnose a clinical condition. In pulmonology, one of the biomarkers used is the partial pressure of oxygen: acute lung injury and acute respiratory distress syndrome are defined by the difference between the alveolar and arterial concentration of oxygen. This biomarker reflects the critical life sustaining function of the organ: delivery of oxygen to the circulation to support aerobic metabolism. What is curious about our universally used biomarker (SCr) is that we do not trust it; it is not an injury marker but rather a functional marker (and a poor one at that, especially in the acute setting). A rise in SCr may not define kidney injury at all: for example, the syndrome ‘pre-renal azotaemia’ may look biochemically just like ‘acute tubular necrosis’ by changes in SCr, but differs markedly in underlying pathophysiology, treatment implications and prognosis. All nephrologists know that SCr can be deceptively normal: consider lupus nephritis, in which severe parenchymal injury can coexist with preserved glomerular filtration rate and maintenance of a normal SCr. The ability of SCr to reliably identify AKI is particularly impaired when we try to define relatively milder forms of the disease. Using mathematical models of creatinine kinetics, we have argued [7] that the prevailing consensus definitions of AKI, which largely use percentage changes in SCr, are misinformed because they will lead to a delay in the diagnosis in patients with elevated baseline SCr levels—precisely the population in which AKI is most common. Any definition of AKI, however, which is based on SCr—whether absolute increases over a defined time period, as we have proposed, or percentage rises over baseline—will be bound to misclassify patients. (The inclusion of urine output criteria present in the RIFLE [1] and AKIN [8] definitions may add even more confusion: oliguria can be masked by diuretics, and can denote simple mechanical obstruction of Foley catheters.) It is interesting in this context to observe the evolution of the kidney injury biomarker field, where several proteins and urinary enzymes have been studied as potential

The effects of heparin and dietary fish oil on embolic events and the microcirculation downstream from a small-artery repair.

In recent studies we demonstrated that platelet emboli induced by arterial injury impair the microcirculation. The present study was performed to determine if heparin or dietary cod liver oil reduces the incidence of emboli following the same arterial injury and, in turn, whether these agents prevent the associated decrease in microcirculatory blood flow. The cremaster muscle of 29 male Sprague-Dawley rats was isolated on a single neurovascular bundle consisting of the iliac artery and vein and the genitofemoral nerve. Emboli were generated by a thrombogenic injury of the iliac artery, and their number and their subsequent effect on capillary perfusion in the downstream microcirculation were measured. Nine animals received heparin (10-unit IV bolus plus 10 units/hour IV infusion), 10 were fed cod liver oil (10 percent by weight of food) for 3 weeks prior to the experiment, and 9 animals receiving no treatment served as controls. The number of emboli was significantly reduced in the heparin group, but there was no accompanying improvement in capillary perfusion. In contrast, in the cod liver oil group, the number of emboli was not reduced, but there was significant improvement in capillary perfusion. These findings suggest that the harmful effect that platelet emboli have on the microcirculation is probably biochemical in nature (vasoconstriction) rather than related to simple mechanical obstruction to flow.

Obstructed intestine as a reservoir for systemic infection

Intestinal motility, absorption, and secretion are altered after intestinal obstruction, but at what point the normal bacterial barrier function of the viable gut fails after intestinal obstruction is unclear. Thus, we tested whether after simple intestinal obstruction bacteria would translocate across the viable intestinal wall to cause systemic infection. Within 6 hours of intestinal ligation 1 cm proximal or distal to the ileocecal valve, bacteria had translocated to the mesenteric lymph nodes, and by 24 hours after intestinal obstruction, bacteria had spread to the liver, spleen, and blood stream. Bacterial translocation rarely occurred in the animals undergoing laparotomy and sham intestinal ligation, indicating that bacterial translocation was not due to surgical stress. Based on the results of these studies, bacterial translocation induced by intestinal obstruction appears to be due to disruption of the ecology of the normal gut microflora, leading to intestinal overgrowth with certain enteric bacilli and mucosal damage. Although the exact mechanism(s) by which simple mechanical obstruction injures the intestine is not known, the fact that mucosal injury did not occur in germ-free mice suggests that bacteria may play a role in the pathogenesis of obstruction-induced intestinal injury.

Improvement of Collateral Circulation after Arterial Thrombosis with Indomethacin Therapy

SummaryWe compared development of feline hindlimb collateral circulation and coagulation changes 3 hours following aortic thrombosis in five non-treated and five indomethacin treated (20 mg/kg) cats. Coagulation changes were monitored with the one stage prothrombin time (OSPT), partial thromboplastin time (PTT), protamine sulfate dilution test for fibrin monomer (PSD), and platelet counts. Collateral circulation was assessed with aortograms. Significant changes in coagulation parameters with the exception of platelet counts were not observed in either group. Platelet counts of non-treated cats were reduced to 63 ± 5% of control while platelet counts of treated cats were 96 ± 3% of control. Aortograms of non-treated cats indicated poor hindlimb perfusion around the thrombus, while aortograms of indomethacin treated animals indicated significant blood flow to the hindlimbs through collateral channels. These results support a role for the platelet in post thrombosis vasospasms and suggest that anti-platelet therapy could have positive effects in reducing the extent of ischemic damage which follows arterial thrombosis.Several studies, using cat and dog models, have demonstrated a significant reduction of collateral blood flow can occur following formation of an occlusive arterial thrombus (1–5). The collateral flow which developed after thrombosis was significantly less than when occlusion was accomplished with mechanical methods such as ligation (1, 3, 4). This suggested the presence of a thrombus produced effects on blood vessels more complex than simple mechanical obstruction. Imhoff originally suggested that the inhibition of collateral flow which followed thrombosis was related to the release or formation of a vasoactive substance which would induce constriction of collateral source or re-entry vessels (1). Butler, in later studies, suggested that it was serotonin which was responsible for the post thrombosis inhibition of collateral blood flow (2). The involvement of serotonin would seem logical, since the majority of blood serotonin is found in the platelet (6), is released upon platelet activation (7-9), and is a potent vasoconstrictor (10). A mechanism for serotonin involvement has proposed that the platelets in the flowing blood come into contact with the thrombus, are activated and release serotonin (2–4). Consideration of the biochemistry of platelet activation makes it apparent that serotonin is neither the only nor the most powerful vasoactive substance released by the platelet. Thromboxane A2 (TxA) is a critical substance in the activation, release, and aggregation of platelets (11, 12, 13). Thromboxane A2 is a particularly powerful vasoconstrictor which would be a more likely candidate to produce the type of long lasting vasospasm necessary to reduce collateral flow in the post thrombosis state (11, 12, 13). The relationship between thromboxane A2 and serotonin is suggested by recent studies which demonstrate that serotonin can initiate thromboxane A2 release from canine and feline platelets (14). Therefore, serotonin could be an intermediate mechanism in the process of collateral inhibition.If this hypothesis is correct, then inhibition of TxA synthesis should prove as beneficial in improving collateral flow after thrombosis as serotonin antagonists. To test this hypothesis we examined the effect of indomethacin treatment on development of collateral circulation following aortic thrombosis. Indomethacin is a non-steroidal, anti-inflammatory drug which inhibits cyclooxygenase, the major enzyme in the PG and TxA synthetic pathway (15–19).

Postoperative ascending cholangitis following portoenterostomy for biliary atresia: measures for control.

AbstractTwenty‐five patients with biliary atresia were treated by a modification of Kasai's hepatic portoenterostomy operation. The midportion of the Roux‐en‐Y bilioenteric conduit was exteriorized as a Mikulicz anastomosis. This type of biliary reconstruction permitted precise analysis of the biliary drainage, including determinations of the concentrations and types of microorganisms infecting the bilioenteric conduit before, during, and after episodes of cholangitis.Cholangitis was a universal complication in all patients having sustained bile drainage and, paradoxically, was a hallmark of a successful operation. Attacks of infection were frequent for the first 6 to 9 months. There was no correlation between types and amounts of bacteria in the bile drainage and episodes of cholangitis. Therefore, bile culture data were of no use in selection of specific antibiotic treatment. Nevertheless, antibiotics effective against enteric microorganisms usually cured the infection promptly. Maneuvers that may be helpful in lessening the incidence and severity of cholangitis during this early period consist of exteriorization of the bilioenteric conduit to ensure unimpeded flow of bile, use of choleretic agents, and preventive use of antibiotics.A second period in which patients were at risk occurred 1–2 years after operation. In this instance, cholangitis was almost invariably a consequence of simple mechanical obstruction of the bilioenteric conduit. Early crushing of the Mikulicz spur and postponement of closure of the bilioenteric conduit were found to be important in prevention of cholangitis during this period.

The selection of patients for mitral commissurotomy

<h2>Abstract</h2> Mitral commissurotomy has its place among methods currently useful in the treatment of rheumatic heart disease. The operation should be restricted to patients with significant and progressive disability due to mitral stenosis. Its use in asymptomatic patients is not justified in view of the present surgical risk. The technical success of mitral commissurotomy depends greatly on the surgeon's experience with this procedure. Granting perfect technic, a given patient can be improved only to the degree that his cardiovascular disability is caused by simple mechanical obstruction at the mitral valve. This means that patients with disability due primarily to causes other than mitral stenosis must be recognized and excluded from operation. With good surgery and proper medical evaluation many patients have been improved, at least on a short term basis. No one can predict with certainty the long term results or the eventual place of surgery in the treatment of mitral stenosis. It seems likely that some form of surgery will be used to relieve mechanical mitral obstruction until the successful prevention of rheumatic fever eradicates mitral stenosis and renders such surgery obsolete. Until then, proper selection of patients will be a matter of great importance.

EARLY RECOGNITION AND MANAGEMENT OF INTESTINAL STRANGULATION

Although improvements in therapy have resulted in a decided reduction in mortality in simple mechanical obstruction of the small bowel, the mortality in strangulation obstruction is still high. In a recentreport by McKittrick and Sarris,159 per cent of the deaths in their patients with intestinal obstruction occurred in the strangulation group. In the hospitals of the Medical College of Virginia, strangulation of the small bowel has been responsible for more deaths in the years 1941 to 1946 than appendicitis with rupture and peritonitis. Most authors agree that the most important factor influencing a favorable outcome in strangulation of the small bowel is early surgical intervention. A study of the patients seen by us during the past five years has impressed us with the likelihood that if close attention is paid to the clinical history and to the physical observations early and correct diagnosis of intestinal strangulation is usually

GALLSTONE OBSTRUCTION

The recognition of the specific nature of an obstructing lesion of the bowel is a vastly important expedient in the proper management of intestinal obstruction. With the introduction of suction therapy for the treatment of acute obstruction by Wangensteen and Paine,¹the need for exact diagnosis has become even more pressing. While it is clear that in certain cases simple mechanical obstruction of the small bowel can be treated successfully without recourse to surgery, the management of obstruction of the small bowel by decompression is not without danger, especially when the exact nature of the lesion has not been ascertained. In certain instances of diagnostic uncertainty, suction decompression of the bowel postpones the inevitable train of events and creates a false sense of security. Gallstone ileus is one of the conditions in which temporizing procedures are not indicated; once this diagnosis is established, the hazard of any procedure other

Histological Changes Observed in the Intestinal Wall Following Simple Mechanical Obstruction in Rabbits

Due to the almost miraculous recovery of the intestinal wall in cases of ileus after surgical relief of mechanical obstruction as well as the recovery of the intestinal wall in certain forms of mesenteric thrombosis after simple enterostomy, this investigation was undertaken to demonstrate what changes, if any, may occur following simple mechanical obstruction in the various tissues of the intestinal wall.Simple mechanical ileus of the terminal ileum was produced in 11 rabbits. At varying postoperative intervals (12, 24, 36, 48, and 72 hours), the rabbits were sacrificed, and sections from 3 different levels of the ileum were removed—1 cm., 10 cm., and 20 cm. proximal to the obstructing ligature. Sufficient intestine was removed from each level to obtain 10 specimens for immediate fixation, making a total of 30 gross sections from each animal. For controls, sections were removed also from a normal rabbit corresponding to the different levels mentioned above.Gross lesions observed postoperatively were: Aft...

Intestinal obstruction: Application of some of the newer principles evolved from experimental and clinical experience

1.1. In simple mechanical obstruction of the small bowel, particularly of the duodenum and jejunum, the earliest symptoms are due to dehydration and other chemical changes in the blood and tissues from loss of electrolytes and fixed bases due to vomiting and failure of reabsorption of digestive juices in the lower bowel. Shock-syndrome effects and some nervous factor connected with distention of the gut are important in the production of symptoms of intestinal obstruction. Toxemia ordinarily does not play a rôle in these cases until the intraintestinal pressure has increased to the extent of seriously impairing the circulation in the involved segment of bowel, thus producing gangrenous changes in the mucosa. 2.2. Paralytic ileus is most frequently due to peritonitis. The inhibition of function of the gut is due to excessive splanchnic irritation. As a result of the inhibition, the intestine distends from the accumulation of gas and liquids. Re-establishing the normal gradient by blocking the splanchnic stimulation, using hypertonic saline solution freely to stimulate peristalsis, and decompressing the distended intestine by a high enterostomy, are recommended. 3.3. In strangulation obstruction, the profound local circulatory changes result in an early and serious toxemia and shock. Whether the toxemia is due to an enterotoxin or to liberation of toxic substances from gangrenous patches in the gut, has not been settled. It is a clinical fact that the intestine immediately proximal to a simple mechanical obstruction, as well as the markedly distended loops in paralytic ileus, often shows serious damage to the gut wall as the result of the tremendous increase in intraintestinal pressure. Treatment then becomes the same as for strangulation obstruction, namely exteriorization when possible and decompression by enterostomy. 4.4. The possibility of gas-traps resulting from a primary, simple obstruction because of lengthening and twisting of the intestinal tube must be borne in mind and surgical treatment is to be directed toward overcoming these multiple obstructions. 5.5. The advantages of a high enterostomy with the introduction of a soft tube for a considerable distance and the production of slow decompression by means of suction from an electric pump are stressed. 6.6. Conservation of pancreatic juice, particularly when jejunostomies are performed, is desirable, and methods of accomplishing this are described. 7.7. Blood transfusions, hypertonic and normal saline, and dextrose solutions are definitely indicated in the treatment of various forms of ileus. The effect of hypertonic saline solution on peristalsis and the effect of the large amounts of water contained in normal saline and dextrose solutions upon intestinal secretion are to be borne in mind. They increase intraintestinal pressure and for that reason decompression should accompany the introduction of these solutions whenever conditions permit. 8.8. The unsatisfactory results that have followed the use of various drugs to stimulate peristalsis are probably due to the fact that they stimulate certain forms of intestinal contractions, but they do not increase propulsive movements. That hypertonic saline solution does increase these latter movements has been shown both experimentally and clinically. 9.9. The many disadvantages of ether and the advantages of spinal anesthesia are discussed. 10.10. The fall in blood pressure which occurs with spinal anesthesia, and which can usually be prevented, is due to a dilatation of the smaller vessels of the skin, muscles and splanchnic areas and is not due to a diminution in circulating blood volume as occurs in shock.

Value of X-Ray Evidence of Bowel Obstruction in Various States of Intestinal Stasis.

X-ray evidence of gas in the small intestine in experimental simple mechanical obstruction and in strangulation obstruction has been reported previously., It was found that definite evidence of gaseous distention of the bowel proximal to a simple obstruction was present as early as 4 or 5 hours after the establishment of the obstruction and in 20 to 24 hours the intestinal distention was fairly general in the proximal bowel. The X-ray was not found to be of the same value in detecting the presence of strangulation as it was in the early recognition of simple obstruction of the intestine. These X-ray observations have now been extended to include cases of isolated loop obstruction, mesenteric vein ligation and experimental peritonitis. In 23 dogs, segments of intestine from 10 inches to 3 feet in length were isolated from the rest of the intestinal tract (ileum, jejunum or duodenum) and the ends were turned in forming loops obstructed at both ends. Intestinal continuity was re-established by end-to-end or lateral anastomosis. The obstructed loop may be regarded as a form of strangulation obstruction because of the interference with the vascular supply as a result of the greatly increased intra-intestinal pressure. The intestinal anastomosis obviated the confusing factor of an additional simple obstruction which was found difficult of evaluation in the interpretation of the findings in a previous study even though lead shot were attached to the strangulated segment. These dogs lived from 21 hours to 13 days (average 3.5 days), and post mortem examination revealed discoloration and distention of the obstructed loop, and peritonitis. Perforation of the loop was the cause of the peritonitis in one-third of the cases.

Cause of Death in Simple Mechanical Obstruction of Upper Part of Intestine.

No other journal can match Anesthesia & Analgesia for its original and significant contributions to the anesthesiology field. Each monthly issue features peer-reviewed articles reporting on the latest advances in drugs, preoperative preparation, patient monitoring, pain management, pathophysiology, and many other timely topics. Backed by internationally-known authorities who serve on the Editorial Board and as Section Editors, Anesthesia &Analgesia is your gateway to everything that is happening in anesthesia and 14 related subspecialties: Analgesia; Ambulatory Anesthesia; Anesthetic Pharmacology; Cardiovascular Anesthesia; Critical Care and Trauma; Economics, Education, and Policy; Neurosurgical Anesthesia; Obstetric Anesthesia; Pain Mechanisms; Pain Medicine; Pediatric Anesthesia; Regional Anesthesia; Patient Safety; and Technology, Computing and Simulation.