Equations in Surgery

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LETTER TO EDITOR

Equations in Surgery Aman Jawwad 1 Received: 3 September 2020 / Accepted: 29 September 2020 # Association of Surgeons of India 2020

intake stimulates tubuloglomerular feedback that decreases sodium reabsorption in the tubules, reducing calcium absorption along with it. This precipitates calcium stones. Moderate dietary calcium binds to oxalate in the gut, and the trapped calcium oxalate is defecated. Low dietary calcium allows more oxalate to be absorbed, promotes oxaluria, and predisposes to oxalate stones. Urinary citrate binds ionized calcium. Hypocitraturia allows precipitation of calcium oxalate stones. Lower potassium intake prevents urinary excretion of citrate leading to an increased risk of calcium oxalate stones [3–5].

Sir, With great interest, readers learned from the article by Raj Kumar et al. [1] where the authors gave a concise account of the concepts of chemistry pertinent to surgery. Biomolecules in the living system are in a constant flux. “Equilibrium is death” hence the living state is a non-equilibrium steady state destined to work. Assessment of these chemical reactions by a surgeon is crucial to the understanding of the human body. A revisit to the basic science brought up a few more of its innumerable connections with surgery that could have been included by the authors: 1) Complications of massive transfusion: Blood stored for 2 weeks accumulates acid load due to its original sampling from venous blood, buffering of citrate with anticoagulant, and the generation of lactic acid during glycolysis while red blood cells (RBCs) are stored. Citrate chelates calcium and magnesium. Once transfused, preservative citrate is metabolized to bicarbonate in the liver. A faster rate of transfusion or impaired hepatic metabolism precipitates citrate toxicity leading to metabolic alkalosis, hypocalcaemia, and hypomagnesemia. Inactivated sodium-potassium ATPase pump on the membrane of stored RBCs accumulates extracellular potassium leading to hyperkalemia during initial transfusion of blood. After transfusion, the restored pump function promotes intracellular potassium uptake causing hypokalemia [2]. 2) Renal stones: Calcium is passively reabsorbed with sodium and water in the renal tubules. Increased dietary sodium

Authors of the original article aptly mentioned the use of urinary sodium level as a safer and cheaper investigation for differentiating pre-renal acute kidney injury (AKI) from renal causes of AKI. However, studies have shown that the accuracy of urinary sodium in determining the cause of AKI is limited, while the combined assessment of fractional excretion of sodium and fractional excretion of urea has a better accuracy [6]. The fact stated by the authors that interferon gamma is released by macrophages contradicts the existing literature that Interferon gamma is released by natural killer cells and CD4+ T cells, while macrophages release TNF alpha and interleukins [7]. To summarize, the readers agree with the authors that the evaluation of chemical reactions in the human b