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juniperpublishersanatomy-blog · 1 year ago

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Class Attendance and the Performances in Physiology Board Examinations: A Study in a Caribbean Medical School-Juniper Publishers

Abstract

Objective: Many faculty members in medical schools encourage their students to attend classes regularly emphasizing that some studies have reported strong positive correlation between the performances in the National Board of Medical Examiners (NBME) examination with their class attendance. The objective of our study was to assess the association of the physiology class attendance and NBME physiology scaled score.

Methods: For this study, 93 medical students who completed two terms of medical physiology at Trinity School of Medicine (TSOM) wereselected. They had their first attempt of NBME physiology examination from summer 2014 to fall 2015. Their physiology class attendance andNBME physiology scaled score were tabulated in Microsoft Excel. The correlation of the percentage of physiology class attendance and NBME physiology scaled score was determined by a Pearson correlation coefficient and regression analysis, using the SPSS version 24.

Results: The class attendance was a significant predictor of performance in physiology NBME subject examination (R2 (91) = 0.295, p = .000). A significant positive correlation was found between the class attendance (%) and NBME physiology score (r(91) = .543, p < 0.001).

Conclusion: The class attendance (%) was significantly correlated with the NBME physiology score. The physiology class attendance appears to be related to NBME physiology scaled score. However, the impacts of other factors such as study habits, environment, cultural habits, gender difference, and personal, familial, and socioeconomic stresses need to be assessed in further studies.

Keywords: NBME; Physiology; Scaled Scores; Class Attendance; Caribbean Medical School

Abbreviations: NBME: National Board of Medical Examiners; TSOM: Trinity School of Medicine; SAT: Scholastic Assessment Test; HSGPA: High School Grade Point Average; USMLE: United States Medical Licensing Examination

Introduction

Many faculty members in medical schools encourage their students to attend classes regularly emphasizing that regular class attendance facilitates learning and enhances their performance in examinations. Class attendance appears to be a better predictor of college grades than any other known predictor of college grades - including Scholastic Assessment Test (SAT) scores, High School Grade Point Average (HSGPA), studying skills, and the amount of time spent studying [1]. The efforts to increase the class attendance rates among college students helped to achieve dramatic improvements in average grades [2].

The National Board of Medical Examiners (NBME) provides subject examinations in the basic and clinical sciences to medical schools and other institutions that educate physicians or other health professionals. The NBME subject examinations assess the educational achievement of medical students in specific subject areas. These examinations are used at virtually all allopathic medical schools and many osteopathic medical schools in the United States and Canada, and approximately 25 international schools in the Caribbean, Mexico, Europe, Middle East, and Asia. The NBME examinations are primarily used as final examinations after courses, clerkships, or other units of instruction. However, the scores achieved on NBME examinations cannot be used by examinees for credit toward the United States Medical Licensing Examination (USMLE) [3]. Some studies reported that the NBME performance has a strong positive correlation with the class attendance [4-6]. Hence, we aimed to assess the correlation of physiology class attendance (%) with the NBME physiology scaled score.

Material and Methods

The present study is an analytical comparative study. The study was conducted in Trinity School of Medicine (TSOM), St. Vincent and the Grenadines, West Indies. At Trinity, Medical Physiology is taught to students in their first and second terms each of which comprises 15 weeks. The two terms of medical physiology are designed to give the students sufficient mastery over basic physiology and its application in clinical contexts to prepare them for the physiology sections of the USMLE Step 1. The students take part in NBME physiology at the end of their second term.

The medical students who studied two terms of medical physiology and took their NBME physiology subject examination from summer 2014 to fall 2015 at TSOM were included into this study. The students who dropped their physiology course before taking the NBME physiology and continued the same next term, those who did not study their two terms of medical physiology at TSOM, those transferred from other schools to TSOM, and those with low levels of attendance due to medical leave of absence and other extenuating circumstances were excluded from the study. Ethical clearance for the study was obtained from the research ethical committee of TSOM.

Three physiology faculty members utilized sign-in sheets, which were passed out in each class period to record the class attendance. Students were informed that the class attendance was being recorded for informational purposes and that there were no consequences regarding their absences. The students’ cooperation was good. At the end of the second term, their first attempt of NBME physiology scaled score and class attendance were tabulated in the Microsoft Excel. The correlation between the class attendance and NBME physiology scaled score was determined by a Pearson correlation coefficient and regression analysis, using the SPSS version 24. A p value of 0.05 or less was considered as statistically significant.

Results

A total of 93 students were included into the study of whom 42 were female and 51 were male. The students’ physiologyclass attendance was measured by the overall attendance percent (mean = 85.1%, SD = 11.9%) (Table 1). The students’ performance was assessed by the NBME physiology scaled score (mean = 45.9, SD = 9.1) (Table 1). There was wide variation in the class attendance (%) and NBME physiology scaled score of individual students.

The correlation coefficient (adjusted r2) of our study was 0.287 (Table 2) and significance F was <0.001. A significant positive correlation was found between the class attendance (%) and NBME physiology scaled score (r(91) = .543, p < 0.001) (Table 2). The regression model significantly predicted 29.5% (R2 = 0.295) of the NBME physiology scaled score of the students (Table 2).

Simple linear regression analysis between the class attendance (%) and NBME physiology scaled score showed that the class attendance contributed 26.9% (confidence interval 0.283, 0.552) of the variation in NBME physiology scaled score (Table 3). The regression model showed that for each 1.0% increase in class attendance, the NBME physiology scaled score is expected to increase by 0.417 (Table 3). The equation obtained from the regression model is: NBME physiology scaled score = 10.423 + 0.417 x class attendance (%). Hence, according to regression model equation, a student is expected to have 94.9% of class attendance to achieve a scaled score of 50, which is the national average in physiology NBME subject examination (Figure 1).

Discussion

The principal result of our study was a significant positive correlation between the class attendance (%) and NBME physiology scaled score (r = .543, p < 0.001). The result of our study is in line with the meta-analytical review done by Crede et al. [2] who found a strong relationship between the class attendance and college grades. Hence, they suggested increasing class attendance rates among college students to achieve dramatic improvements in average grades [2]. In a study of relationship between class attendance and NBME part I examination done by Fogleman et al. [4] analysed the results of survey via a 2 X 2 chi-square for each item and scores on the NBME examination. It showed that only class attendance were significantly different between students scoring above the mean (511.2) and those below the mean on the NBME part I examination (chi-square = 4.766; p <0.05) [4].

Similarly, Hammnen et al. [7] indicated a negative correlation between grades and number of absences from class. However, their correlation was weak, indicating that other factors were involved as most of the studies, including theirs, did not have matched experimental and control groups. Hence, it is impossible to state whether regular attendance caused slightly higher scores or whether the better students attend the classes more frequently [7]. Millis et al. [8] demonstrated that a significant correlation (r = 0.203, P < 0.05) between the attendance and students’ grade averages at the end of their second year. They found increased grade averages as attendance increased. Students may assume that the self-directed study and distance learning are equivalent to the class activities. The risk of poor performance in a significant number of first-year medical students may be because of their belief that the internet- and classroom-based instructions in basic medical science courses are equivalent [8].

In a study done by Subramaniam et al. [9] in a medical college, they found a significant correlation between the attendance and the students who passed the University examinations. The number of students passing the examination was maximum (>90%) compared to those getting distinction and failing the exam after they made attendance mandatory for the medical course [9]. A moderate to strong negative correlation between absenteeism and academic achievement suggested that the class attendance is very critical for learning and important in improving the knowledge and academic achievement [10]. Bamuhair et al. [11] reported the positive effect of attendance on the academic performances with a stronger effect for lectures compared to other teaching modalities. They suggested that the lecture attendance is critical for learning even in nontraditional methods of education [11].

In a study of association between lecture attendance and grade outcomes done by Horton et al. [12] they reported the positive correlation of exam grades with the lecture attendance in male students (r = 0.29, P < 0.04) and overall (r = 0.21, P < 0.02) but not for female students considered separately (r = 0.10, NS). They also found that the overall grades were correlated positively with lecture attendance in male students (r = 0.35, P < 0.01) and overall (r = 0.31, P < 0.001) but not when female students were considered separately (r = 0.20, NS) [12].

However, Cohall et al. [13] in their study found no significant association between the improvement in attendance and improved academic performances in the examinations. Their findings suggested that the other factors are more critical to academic success [13]. Therefore, even though the present study suggests that the higher percentage of class attendance add value to academic performance in board examinations, the other factors such as quality of lectures and the study habits may also have an equal impact in academic performance of the students in board examinations.

Conclusion and Recommendation

According to our study, the physiology class attendance (%) has a strong positive correlation with the scaled score in physiology NBME subject examination. It means that the performance of students in physiology NBME subject examination improves with increase in their class attendance (%). Therefore, we recommend that the faculty members should encourage the students to attend the classes regularly by implementing incentives such as points for class attendance or by applying academic activities during the class such as discussing comprehensive questions at the end of the lecture. Implementation of class attendance policies might enhance the performance of medical students in board examinations too.

We conducted this study only in the subject of Physiology. The study that includes a larger sample size from multiple basic medical science subjects and study samples from more than one medical school might further strengthen the results. Further studies should address the quality of lectures, other ways to increase intrinsic motivation for attending lectures, whether the relationship is causal, and whether the improvement in attendance percentage can improve the NBME physiology performances. In addition, the impacts of other factors such as study habit, environment, cultural habit, gender difference, and personal, familial, and socioeconomic stresses need to be assessed in further studies.

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lupine-publishers-juns · 2 years ago

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Lupine Publishers | The TUR Syndrome Re-Incarnating as ARDS after Saline use as Irrigating Fluid in Endoscopic Surgery

Abstract

Objective: To demonstrate the TUR syndrome characterized with hyponatraemia (HN) will no longer be seen after using saline as irrigating fluid in urology, but it has re-incarnated as the acute respiratory distress syndrome (ARDS) presenting with the same clinical picture of the multiple organ dysfunction syndrome (MODS). Material and Methods: A focused objective and relevant narrative review of other eminent authors’ work and mine are used here. Results: The TUR syndrome characterized with HN will no longer occur in urology after the use of saline as irrigating fluid in endoscopic surgery. It has reincarnated as ARDS presenting with the same MODS clinical picture. It is induced by VO caused by iv fluid infusions. This induces cardiovascular shock (VOS) that cause ARDS. The latter is already common in clinical practice due to the excessive us of iv fluids in the management of shock, acutely ill patients, and prolonged major surgery as iatrogenic complication of fluid therapy. The wrong Starling’s law dictates the current faulty rules on fluid management of shock that mislead physicians into giving too much fluid. The correct replacement is the hydrodynamics of the porous orifice (G) tube which should be the new scientific basis for fluid therapy in shock management. The currently available hypertonic sodium therapy of 5%NaCl and/ or 8.4%NaCo3 is lifesaving therapy for HN, the TUR syndrome and ARDS. Conclusion: The TUR syndrome may seem to have been eradicated in urology with the use of saline as irrigating fluid in endoscopic surgery. However, it has reincarnated as ARDS with the same clinical picture of MODS. It is an iatrogenic complication of fluid therapy dictated by the wrong Starling’s law for which the hydrodynamic of the G tube is the correct replacement that should be the new scientific basis for a new policy on fluid management of shock.

Keywords: The TUR syndrome; Endoscopic Surgery; ARDS; Shock; Fluid Therapy; Starling’s law, Capillary-ISF transfer

Introduction

My beginning with the transurethral resection of the prostate (TUR) syndrome started in 1981 after I attended post-mortem (PM) examinations on 3 patients who died after the TURP surgery. I was only an SHO in urology working for the late Mr. KC Perry and JP Ward at DGH in Eastbourne. At the PM examination it was clear and obvious to me that these patients died of internal drowning as result of massive volumetric overload (VO) of fluids used for resuscitation of a cardiovascular shock they suffered, and the fluid was retained in their bodies. When I asked the pathologist why doesn’t he mention that retained VO in his report? He replied: “because it offends treating physicians”? The word offends hit me right hard on my head like a hammer. My next question to myself was if it offends them why do physicians do it? This had led me to immediately replace the term fluid overload with the new and original Volumetric Overload (VO) after adding the cardiovascular hypotension Shock to it to become (VOS) that was introduced to avoid the word offends but it has proved to be a new scientific medical discovery. Another few questions such as: “What is misleading physicians into giving too much fluid during the resuscitation of shock? What shock is it? I communicated with Richard Harrison III (who may be late now) who is the originator of the hyponatraemic shock of the TUR syndrome and the use of 5%NaCl therapy in clinical practice for years during his retirement [1]. I reported later the true pioneer originators of this shock and the hypertonic sodium therapy (HST) were Danowski et al who induced it experimentally in dogs by massive 5%Glucose infusion [2]. Harrison advised me to “put the poison in the honey” that I could not accept. After the PM examination I suspected and incriminated Starling’s law being the scientific basis of fluid therapy in shock that dictates the wrong rules on fluid therapy for shock management documented in articles and books [3-7], for which the hydrodynamics of the porous orifice (G) tube is the correct replacement (Figures 1a&b) [8,9]. I felt so strongly about it that I wrote a letter to the late great professor of physiology Eric Neil and author of Sampson Wright Textbook of Physiology later in 1983 [10,11]. He nicely replied in handwritten letter as he was in retirement asking: Why and how may Starling’s law cause death of patients? The answer is there now after 40 years of hard scientific research and investigations [12]. The inflow pressure pushes fluid through the orifice. Creating fluid jet in the lumen of the G tube**. The fluid jet creates negative side pressure gradient causing suction maximal over the proximal part of the G tube near the inlet that sucks fluid into lumen. The side pressure gradient turns positive pushing fluid out of lumen over the distal part maximally near the outlet. Thus, the fluid around G tube inside C moves in magnetic field-like circulation (5) taking an opposite direction to lumen flow of G tube. The inflow pressure 1 and orifice 2 induce the negative side pressure creating the dynamic G-C circulation phenomenon that is rapid, autonomous, and efficient in moving fluid and particles out from the G tube lumen at 4, irrigating C at 5, then sucking it back again at 3, Maintaining net negative energy pressure inside chamber C. **Note the shape of the fluid jet inside the G tube (Cone shaped), having a diameter of the inlet on right hand side and the diameter of the exit at left hand side (G tube diameter). I lost the photo on which the fluid jet was drawn, using tea leaves of fine and coarse sizes that run in the centre of G tube leaving the outer zone near the wall of G tube clear. This may explain the finding in real capillary of the protein-free (and erythrocyte-free) sub-endothelial zone in the Glycocalyx paradigm. It was also noted that fine tea leaves exit the distal pores in small amount maintaining a higher concentration in the circulatory system than that in the C chamber- akin to plasma proteins.

What is the TUR Syndrome? And what is causing the “Understanding Gap”? Our prospective cohort study on the TUR syndrome was conducted in 1987-8, a letter to the editor of BJU was reported in 1988 [13], MD Thesis was accepted November 1988 [14], and the article reported in 1990 [15]. The TURP syndrome is a condition induced by gaining large volume of sodium-free fluid overloading the cardiovascular system and spelling over into the interstitial fluid (ISF) space of vital organs and subcutaneous. The fluid of 1.5%Glycine used as irrigating fluid gets absorbed, or rather infused through peri-prostatic veins, during the TURP surgery as well as all endoscopic surgeries performed under sodium-free fluid irrigation of any type such as Mannitol, Sorbitol, Glucose and Cytal. Also, intravenous (iv) infusion of 5% Glucose considerably and significantly contributes to it- as well as saline. What is more, excessive infusion of saline or any sodium-based fluid such as Saline, Hartman, Ringer, plasma, and plasma substitutes, and blood worsens it transferring the shock being treated from VOS 1 into VOS 2 [16] and causing ARDS 1 and 2 [17,18] with apparent correction of HN, and has high morbidity and mortality later. The TUR syndrome has a characteristic severe drop of serum sodium level causing acute dilutional hyponatraemia (HN) induced by VO 1 (Figures 2 & 3) with severe clinical symptoms affecting all vital organs causing the multiple organ dysfunction syndromes (MODS) (Table 1) or ARDS [17,18] with recognizable clinical picture but one system may predominate such as acute kidney injury (AKI). The HN of <120 mmol/l has 2 paradoxes and 2 nadirs that have eluded authorities and physicians on HN, and that has made the TUR syndrome most elusive and invisible making it though obvious it has remained invisible even to authorities on HN. Professors and consultant urologists who are such swift good resection experts have testified that the TUR syndrome does not exist as no fluid absorption occurs, with a negative prospective study of 100 patients [19]. Off course no such hyponatraemia occurs when the irrigating fluid is saline whatever the volume absorbed and infused. Another important reason that prevents massive 1.5% glycine absorption and the TUR syndrome is for the Urologist not to breach the prostate capsule and not to open the venous sinuses where the irrigating fluid is directly injected intravenously (iv) into the periprostatic veins. There was also another good swift urologist who reported >1000 consecutive TURP surgeries without seeing the TUR syndrome. The risk of VO during endoscopic surgery will continue to occur as long as there are registrars in training and even with the experienced consultants who occasionally and inadvertently breach the prostatic capsule and open the venous sinuses. However, the TUR syndrome due to 1.5% Glycine VO with its characteristic HN has an undoubted reality [13-15] and [20-22]. Our study reported 10% incidence of the TUR syndrome with one near death case that was saved [14] and a similar study done a year earlier in the same department reported 7% incidence of morbidity with 1% mortality [22]. Before the TUR syndrome disappears into oblivion and is totally replaced by ARDS a most comprehensive literature review on the subject was reported in 2018 after the wide use of saline as irrigating fluid in the TURP surgery [23]. Here a distinction between a physiological VO of <2 L infused in less than one hour that is extensively studied by Hahn in volunteers and patients is known as Volume Kinetic (VK) (20) and the pathological VO of 3.5-5 L gained in < 1 h that causes the TUR syndrome [15] is highlighted. This has been a cause of serious misunderstanding gap in the pathogenesis of the TUR syndrome. The physiological response of VK is remarkably different from the pathological response of VO which is paradoxical: VK elevates blood pressure and induces diuresis while VO causes hypotension with bradycardia and causes acute renal failure.

The TURP syndrome starts by presenting with cardiovascular hypotension shock to anaesthetists and surgeons in theatre [24,25] and at times by cardiac or cardiopulmonary arrest [26] and sudden death. By next morning the surviving patients present with coma, convulsion and bizarre paralysis to physicians, neurologists, and ICU specialists [15]. It has the characteristic serum hypo-osmolality. BUT other solute contents dilutions seem to be apparently spontaneously improving due to water shift into cells [Table 2, Figures 1 and 2]. The HN of <120 mmol/l causes cardiovascular hypotension shock. Volumetric overload (VO) is the most highly significant factor causing its patho-aetiology with a (p=0.0007). Osmolality was also significantly low (p=0.02) while all other serum solute changes including the most remarkable drop in serum sodium and huge elevation in serum glycine did not reach statistical significance in the multiple regression analysis, yet it did alone when pre- and post-operative levels are compared!? [Table 2 and 3]. This cardiovascular shock of VOS is easily confused with and mistaken for haemorrhagic or septicaemia shock and is wrongly treated with further massive volume expansion that usually kills the patient as happened in the 3 patients mentioned above!?

The toxic theory of the TUR syndrome and septic theory of ARDS.

Sepsis and septic shock in the pathogenesis of ARDS is as innocent as the wolf in Josef story [18], so is glycine in the aetiology of the TUR syndrome [15], particularly as correctly mentioned that the TUR syndrome occurs with Mannitol, Sorbitol, and Glucose. Professor Alan Arieff has clearly reported the morbidity and mortality of hyponatraemia (HN) of the TUR syndrome induced by 1.5%Glycine as well as the excessive 5%Glucose infused intravenously during prolonged surgery in healthy women [27]. That does not mean that I deny the toxicity of glycine and the seriousness of sepsis. I am just saying they are misleading like a mirage to someone thirsty and lost in the desert. While thinking about it please, try to attend the PM examination of some patients who died from the TUR syndrome and ARDS. Every anaesthetist should examine own practice when he embarks on Bolus Fluid Therapy (BFT) during anaesthetic induction and watch out how much fluid is given during prolonged major surgery. Review the scientific basis of fluid therapy in the management of septic and all other types of shock on which bases the current practice is implemented.

Fluid therapy Regimen and Iatrogenic complications

The TUR syndrome occurs because of combination of fluid absorption and direct iv infusion of the irrigating fluid when the prostatic capsule is breached, and venous sinuses are open. In clinical practice all ARDS cases occur as result of iv infusion of fluids. In our study 7 cases of capsule breaching occurred among the 10 TUR syndrome cases as observed by the surgeon. The iv infusion occurs with both the liberal regimen of Early Goal-Directed Therapy (EGDT) and Bolus fluid therapy (BFT) of the conservative regimen. Hahn is a professor and consultant of anaesthesia and intensive care. He is also a leader and world authority on fluid therapy and the editor of a book on the same subject. I would and have recommended him as the head of a committee to write the new guidelines on fluid therapy in shock management. He has my new book that will help him for >8 months now, please read it if you’ve not done so already. Like all anaesthetists, Intensive care therapists, surgeons, and physicians of the whole world who remain to practice the liberal fluid therapy regimen also well known as EGDT in the management of shock, don’t you? Go to any ICU near you and observe the swollen-up ARDS patients mostly with trunk oedema comparing their body weight on hospital admission with their current weight while suffering from ARDS. Try to attend the PM examination of the TURP patients and ARDS patients. Allow me to reproduce this section from my article later that is most recommended reading to all physicians interested in the subject of fluid therapy, the TUR syndrome, HN, VOS and ARDS [18].

The role of Starling’s law

Starling’s law [28,29] dictates the current faulty rules on fluid therapy in the management of shock. It thus misleads physicians into giving too much fluid during shock resuscitation [30]. More than 21 reasons were reported to show that Starling’s law is wrong [31], none of it can be denied or refuted. The correct replacement is the hydrodynamic of the porous orifice (G) tube [8,9] (Figure 1 a & b) that was built on capillary ultrastructure anatomy of having precapillary sphincter [32] and a porous wall [33] that allow the passage of plasma proteins-hence nullify the oncotic pressure. It follows that the extended Starling Principle is wrong and a misnomer [34,35] and all the equations are also wrong.

Two types of VO inducing VOS and causing ARDS of type 1 and 2

There are two types of VO: Type 1 induced by sodium-free fluid and Type 2 induced by sodium-based fluid. These in turn induce VOS 1 and VOS 2 which cause ARDS 1 and ARDS 2, respectively. The clinical picture is the same for both types (Table 1). Type 1 is characterized with HN of the TUR syndrome with which the cerebral neurological manifestations of coma, convulsions, and bizarre paralysis predominate while type 2 may have moderate hypoproteinemia if induced by crystalloids and none when plasma, plasma substitutes and blood are used. Type 2 may complicate Type 1 or may occur do novo. Manifestations of the multiple organ dysfunction syndrome (MODS) are the same and appear in every case, but one system may predominate. When Hahn sent me his article on Revised Starling Principle calling for revalidation [34] I immediately responded with an article: Revised Starling’s Principle (RSP): a misnomer as Starling’s law is proved wrong. I considered research on validating RSP is a total waste of money, time, and efforts.

Proof by eminent authors on the VO role in the aetiology of the TUR syndrome and ARDS

Professor Robert Hahn from Sweden has done lots of research infusing various types of fluid used in clinical practice to normal adult volunteers and patients, as well as animal research and clinical studies and reported >340 articles on the TURP syndrome alone (PubMed 2017) and 532 articles in total (PubMed search 2021): Here is what Robert Hahn said: in the abstract of an article reported in 2017 [36]:

Abstract [36]:

“Adverse effects of crystalloid fluids are related to their preferential distribution to the interstitium of the subcutis, the gut, and the lungs. The gastrointestinal recovery time is prolonged by 2 days when more than 2 liters is administered. Infusion of 6-7 liters during open abdominal surgery results in poor wound healing, pulmonary oedema, and pneumonia. There is also a risk of fatal postoperative pulmonary oedema that might develop several days after the surgery. Even larger amounts cause organ dysfunction by breaking up the interstitial matrix and allowing the formation of lacunae of fluid in the skin and central organs, such as the heart.” Thank you, Professor Hahn for a most impressive work indeed. New guidelines based on currently available evidence on fluid therapy for resuscitation of sepsis, septic shock, trauma patients, critically ill patients, ARDS and patients undergoing prolonged major surgery are badly needed. Professor Hahn is the expert witness on fluid therapy. Why does not Hahn believe his own results? Why doesn’t he make the most obvious conclusion based on what he said in the abstract above? What and how much more evidence and years that he needs to believe that the pathological VO of massive fluid infusions induces cardiovascular shock that is VOS of both types and causes ARDS? If my articles referenced here and the books [3- 7] particularly the one Hahn has now for 8 months and being held in the press awaiting his introduction, then allow me most sincerely and humbly to give you a helping hand to lift you up to where I stand and clearly see the picture on the real issues discussed here. Hahn does not need to do any more research studies. Just report a re-analysis of data from previously reported articles he has done and reported before, based on his previous published articles on the TUR syndrome and saline-based fluid infusions. Please, reexamine and re-analyse your own research work in a manner and method identical to your article reported here [20]. Please, Hahn don’t bother with equations that are hard to understand and are meaningless and perhaps misleading or even wrong. Do not use fancy sophisticated graphs that does not impress me. I would love, most sincerely and humbly, to give you a hand to get you out of the huge maze you have been lost inside it for >3 decades. All you need to do my friend now is to liberate yourself from the illusive and misleading concepts of the toxic/septic hypotheses of glycine and sepsis!? One must unlearn old bad habits to be able to receive and acquire the new correct ones.

Evidence for the VO Theory causing VOS and ARDS

“The prevalence of “liberal fluid infusion” in resuscitation of all types of shocks not only septic shock in clinical practice all over the world is attributed to an impactful article by Rivers et al, reported at The N Engl J Med 2001 [37]. Dr Rivers’ investigation reported EGDT in the treatment of severe sepsis and septic shock. In this singlecenter study published more than 20 years ago involving patients presenting to the emergency department with severe sepsis and septic shock, the conclusion was: “mortality was markedly lower among those who were treated according to a 6-hour protocol of EGDT, in which intravenous fluids, vasopressors, inotropes, and blood transfusions were adjusted to reach central hemodynamic targets, than among those receiving usual care” Usual care means conservative fluid regime. There is something grossly wrong with this conclusion, but I cannot tell what is it? Not yet. Let us see what other author investigators have said first. The EGDT of liberal fluid infusion has been termed “aggressive” by some authors. However, it has been adopted all over the world not only for the therapy of septic shock but also whenever fluid therapy is required for the management of all types of shocks. “In another article by Dr Rivers 11 years later in 2012 [38] he compared the liberal to the conservative approach concluding in his last statement: “In contrast to what is true in politics, in fluid management of acute lung injury, it is OK to be both liberal and conservative.” So, Dr Rivers says it is OK to have it both ways: “one for the ebb and one for the flow”! Sorry, sir, I disagree. It is not OK. It is not politics either. No, you cannot have it both ways. The right way is only one. The issue here is how much fluid should be infused during the ebb phase of shock and does it have a maximum limit? Replace the loss but do not overdo it. Since the cardiovascular system (CVS)’ maximum capacity of an adult is 7 L and the normal blood volume is 5 L, the maximum infused volume of fluid should be limited by the maximum capacitance of the CVS. What do you expect when you try to fit 10-15 L of fluid into a 7 L capacity container? Simple physics and common sense indicate that it must spell over if it is open system or burst if closed! The cardiovascular system is no exception. Dr Rivers should re-examine his own data and tell us where and why he went so grossly wrong.” The EGDT has spread like fire in a haystack, and it remains operative in current clinical practice all over the world that is why ARDS is so common yet remains under recognized and underestimated affecting and killing hundreds of thousands of patients per year.” Other authors have confirmed the significant role of VO of crystalloids in causing the morbidity and mortality of ARDS both in adult and children of trauma patients [39,40]. All authors have stopped short of recognizing VOS as Cause of ARDS or MODS morbidity and mortality. Quoting also from this article [18] I mention here the remarkable multicenter study by Rowan et al. [41] Like Hahn they reported results that demonstrate the massive VO retained in the body of surviving ARDS patients. After sending 3 emails to Rowan commending the authors on their results and asking about the dead patients retained fluid VO, none of the 40+ authors replied. “The PRISM Investigators reported its Trial by Rowan et al at NEJM 2017 [41] concluded: “In this meta-analysis of individual patient data, EGDT did not result in better outcomes than usual care and was associated with higher hospitalization costs across a broad range of patient and hospital characteristics.” Thank you, Dr Rowan and colleagues for the excellent research and report. This is good evidence-based medicine, but more is needed, from you, and you have the data to provide it. Based on this conclusion that agrees with other multicenter trials I wonder is time to say goodbye Dr Rivers? The aggressive and deleterious liberal approach of EGDT is no longer wanted. It should be abandoned immediately. Even when the nasty liberal approach goes away, hopefully soon, it remains bad enough with the conservative regime as it is now that must be sorted out! I wonder what Dr Rivers has to say about this, particularly as authors of 3 other huge prospective multicenter trials of The ProCESS/ARISE/ProMISe reported similar conclusion by Huang et al. [42]. So, Rowan gave the results of: The cumulative VO was -136 ml in the conservative-strategy group, as compared with 6992 ml in the liberal-strategy group (P<0.001). For patients who were in shock at baseline, the cumulative seven-day VO was 2904 ml in the conservative-strategy group and 10,138 ml in the liberal strategy group (P<0.001). For patients who were not in shock at baseline, the cumulative VO was −1576 ml in the conservative-strategy group and 5287 ml in the liberal-strategy group (P<0.001)”. “First, the negative sign (-) indicating negative fluid balance has appeared in the data above and is very important. It characterizes the nonsymptomatic patients among the conservative-strategy group. These patients should be used as the controls for the statistical analysis of the data. I have been waiting for 40 years to see these VO results. I am still waiting to see VO data with statistical significance in mortality patients. I plead with and urge the respected authors of major randomized Trials of FACCT, PRISM, ProCESS, ARISE, and ProMISe to come forward with these data, please,

Clinical picture of (VOS, The TUR syndrome, ARDS and MODS)

The clinical picture of ARDS is that of the multiple organ dysfunction syndrome (MODS) (Table 1) reported previously by Khadarow and Marshal in 2002 [43]. Another remarkable article was reported by Schrier in 2010 [44]. Demonstrating the link of the TUR syndrome with ARDS by having identical clinical picture with minor variations was reported by Ghanem as complications of VO covering the cardiovascular/hematological that appear first under general Anaesthesia with bradycardia [45], the cerebral/ neurological with coma appear first under spinal/epidural Anaesthesia and convulsions and bizarre paralysis predominate in the TUR syndrome, not in ARDS [46], the respiratory of ARDS and hepatic/gastrointestinal manifestations [47] and AKI predominate later were documented recently in individual specific reports. Excessive bleeding and leukocytosis in the absence of sepsis also occur.

Therapy of VOS, the TUR syndrome and ARDS [17] Prevention

Based on the above discussion, ARDS is an iatrogenic complication of fluid therapy in hospital, never in community, that is overlooked and underestimated. Being iatrogenic; means it is preventable. In order to prevent VOS and ARDS a limit to the maximum amount of fluid used during shock resuscitation or major surgery must be agreed upon. Professor Hahn [36] found that infusing 2 L of saline to human volunteers produces symptoms. Infusing >3 L is pathological. More than 5 L is associated with deleterious morbidity [38,39]. So, the maximum volume of fluids that can be infused safely to an adult patient is 3 L which is the daily fluid requirement, and no more fluid of any kind is given for 24 hours except replacing the actual loss that does not include urine loss. The patient should be put on a weighing scale every day from hospital admission till discharge or death. Any retained volume of fluid above his body weight on admission is pathological. On using CVP for monitoring fluid therapy, please refrain from persisting to elevate CVP to levels above 12 and up to 18-22 cm saline [48]. This is a major cause for inducing VO and VOS and ARDS during shock resuscitation, particularly septic shock [37]. Look up any physiology textbook to find out that the normal CVP is 0 and it swings between -7 and +7 cm saline which is the level that should be aimed at in monitoring fluid replacement in shock of sepsis, trauma, and bleeding, acutely ill and during major surgery. Elevating CVP is not synonymous with elevating arterial pressure. If hypotension develops later during ICU stay, inotropic drugs, hydrocortisone 200 mg and HST should be used. The latter restores the pre-capillary sphincter tone (peripheral resistance) so that the capillary works as normal G tube again [9], but no isotonic crystalloids or colloids infusions of above the daily fluid requirement should be given. If persistence with the current liberal regimen of Early Goal-Directed Therapy (EGDT) and conservative Bolus Fluid Therapy regime continues, then more reports on ARDS will continue. Future authors will be hopefully taking into consideration the mentioned above data concerning VO/Time, or the retained fluid VO at the time of inducing ARDS or death on reporting new trials or case reports.

Treatment of ARDS [6]

Hypertonic sodium therapy (HST) of 5%NaCl and/or 8.4%NaCo3 has truly proved lifesaving therapy for the TUR syndrome and acute dilution HN [17,18] as well as Secondary VOS 2 that complicates fluid therapy of VOS 1 causing ARDS. It works by inducing massive diuresis; being a potent suppressor of antidiuretic hormone. My experience in using it for treating established ARDS with sepsis and primary VOS 2 that causes ARDS is limited. However, evidence on HST suggests it will prove successful if given early, promptly, and adequately to ARDS patients while refraining from any further isotonic crystalloid or colloid fluid infusions using saline, Hydroxyethyle starch and/or plasma therapy- just give the normal daily fluid requirement and no more. After giving HST over one hour using the CVP catheter already inserted, the patient recovers from AKI and produces through a urinary catheter massive amount of urine of 4-5 L as you watch. This urine output should not be replaced. Just observe the patient recovering from his AKI, coma and ARDS and asks for a drink. This is done in addition to the cardiovascular, respiratory, and renal support on ICU. Patients with AKI on dialysis, the treating nephrologist should aim at and set the machine for inducing negative fluid balance. The HST of 5%NaCl and/or 8.4%NaCo3 is given in 200 ml doses over 10 minutes and repeated. I did not have to use more than 1000 ml during the successful treatment of 16 patients. Any other hypertonic sodium concentration is not recommended- I know Hahn tried 1.8%NaCl and it does not work. A dose of intravenous diuretic may be given but it does not work in a double or triple the normal dose. A dose of 200 mg of hydrocortisone is most useful. Antibiotic prophylactic therapy is given in appropriate and adequate doses to prevent sepsis and septic shock. No further fluid infusions of any kind of crystalloids, colloids and blood is given. The urinary loss should not be replaced as this represent a surplus in the body and must be discarded otherwise defeats the objective of treatment.

Addendum: Relevant articles on the history of the TUR syndrome and ARDS

This addendum is dedicated to important landmark articles on the history of the TUR syndrome and ARDS that could not be fitted directly on the above focused narrative review on how the TUR syndrome has been reincarnated into ARDS. It is optional reading for the interested reader, but it completes this review. The first part is dedicated to eminent authors on the TUR syndrome and ARDS whether directly or indirectly. The second part is a section on selfreferences by the author that report important issues that highlight aspects of the presentation.

A. Other Eminent Authors

Creevy was the first author to report the TUR syndrome as acute water Intoxication [49]. Ashbaugh et al were the first to report ARDS in the Lancet in 1967 [50]. Lessels et al. reported in a letter to the editor as the only article on death during prostatectomy [51]. Hendry was first to report that the osmotic pressure of various body fluid is the same as plasma [52]. Guyton and Coleman reported the negative pressure of the subcutaneous space of -7 cm water, a fact that cannot be explained by Starling’s law [53]. Calnan et al reported the negative pressure in lymphatic vessels [54]. Renkin was the first to call for reconsideration of Starling’s law [55]. The Coshran injuries Group, Finfer, Vincent and futier et al demonstrated that oncotic pressure does not work and the argument on albumin versus saline is obsolete [56-59].

B. Self-references

Articles 60 and 61 have educational and entertainment value. Articles 62 and 63 shows the relevance of my work on ARDS to Covid-19 pandemic ARDS. Article 64- 66 corrects other received misconceptions on capillary physiology to augment the discovery of the G tube hydrodynamics and its impact on the capillary- ISF transfer. Articles 67 and 68 report the two clinical studies on which the above article is based. Article 68 corrects some errors and misconceptions on fluid therapy. Article 70 is on preventing renal failure in the critically ill patients. Article 71 reports my Experience with cystoprostadenectomy with “prostatic capsule sparing” for orthotopic bladder replacement. Article 72 is on Features and Complications of Nephroptosis Causing the Loin Pain and Haematuria Syndrome. Article 73 reports “New Discoveries in Medicine and Physiology Originated in Urology”. Article 74 is on an Update on Ghanem’s new scientific discoveries in physics, Physiology, and Medicine, Article 75 is on Goodbye Starling’s law, hello G tube.

Conclusion

The TUR syndrome as defined and characterized with acute dilutional hyponatraemia will no longer be seen in urology after the use of saline as irrigating solution in endoscopic surgery. However, the ARDS will replace it with identical clinical picture of MODS that continue to occur with high morbidity and mortality that is underrecognized and underestimated. The ARDS is common in clinical practice and is induced by excessive sodium-based fluid infusion and is likely to occur in urology due to the added risk of irrigating fluid absorption and infusion through periprostatic veins. Neither the toxic theory nor the septic theory plays the significant assumed rule in the pathogenesis of the TUR syndrome and ARDS. Both are iatrogenic complications of fluid therapy, induced by VO of > 3 L in <1 h time and is severe at 7-10 L of retained fluid VO in surviving ARDS patients wile mortality occur with 12 L, and both have preventative and curative therapy of HST of 5%NaCl and/or 8.4%NaCo3.

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