Managing Crush Injuries on Arrival
Kajal Jain, Nidhi Bhatia in Acute Trauma Care in Developing Countries, 2023
Management of crush syndrome consists of adequate rehydration of the patient and alkalinization of urine. The condition of the patient can deteriorate quickly due to acute kidney injury from crush syndrome, and requires immediate and vigorous fluid replacement in the short window period to increase their chances of survival. Fluid replacement should be continued till myoglobinuria has disappeared. Forced alkaline diuresis can prevent dialysis even if fluid resuscitation is delayed. Sodium bicarbonate is administered to help correct metabolic acidosis and reduce myoglobulin precipitation, thus decreasing injury to kidneys and risk of kidney failure. Urine pH should be maintained at > 6.5 to prevent ARF. Overaggressive use of bicarbonate can cause metabolic alkalosis and metastatic calcification. Acetazolamide can help counter metabolic alkalosis while alkalizing urine. It can be given in metabolic alkalosis if urine pH < 6.5. The use of acetazolamide/bicarbonate should be according to urine output, urine pH and serum pH (Figure 27.3).
Medical evaluation and management of pregnant patients undergoing non-obstetrical surgery
Hung N. Winn, Frank A. Chervenak, Roberto Romero in Clinical Maternal-Fetal Medicine Online, 2021
Progesterone has a direct effect on the hypothalamic apneustic center, altering its CO2 sensitivity. The hypothalamic response to a lower level of CO2 drives an increased tidal volume and respiratory rate. This reduces CO2, and pH begins to rise. The kidney secretes bicarbonate equalizing the system and acid–base balance. The pregnant woman is in a chronic state of compensated respiratory alkalosis. The normal blood gases of pregnancy are compensated respiratory alkalosis (11). The normal pH is 7.44 and bicarbonate levels decrease by 4meg/L. This loss of bicarbonate buffer renders the pregnant women more susceptible to metabolic acidosis. Arterial PO2 rises by approximately 5 to 10mm of mercury. However, in the supine position, arterial PO2 decreases by at least 6 to 10mm of mercury. Positioning the pregnant women with the uterus displaced to the left reduces this positional effect on oxygenation in the blood. Vital capacity and maximum voluntary ventilation are not altered. Functional residual capacity is reduced as the diaphragm is elevated by the rising uterus (11,12).
Biochemistry of Buffering Capacity and Ingestion of Buffers In Exercise and Athletic Performance
Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse in The Routledge Handbook on Biochemistry of Exercise, 2020
There is a perceived lower risk of GI discomfort compared to sodium bicarbonate (91, 95), although side effects still occur with sodium citrate. The most common symptoms include stomach cramps, bloating, nausea, vomiting, urge to defecate, diarrhoea, thirst, and headache (84, 109, 110); essentially the same side effects as sodium bicarbonate. Early studies reported no side effects from sodium citrate doses ranging from 0.1 to 0.5 g·kg−1BM (62, 74, 89), although these investigations failed to adequately record the incidence and severity of side effects, meaning that mild symptoms went unnoticed. Later studies reported side effects with doses of 0.5 g·kg−1BM (83, 84, 110), but GI distress was not experienced by volunteers in all studies (125). Symptom prevalence and severity increase in a dose-dependent manner for intakes of 0.5, 0.7, and 0.9 g·kg−1BM (124). Key moderators of these effects appear to be the volume of fluid supplied with the supplement and the time permitted to consume the fluid; concentrated solutions with a higher osmolality are more likely to result in GI distress (65). Higher doses potentiate these symptoms (124), and lower or staggered doses may reduce symptom prevalence and/or severity (74). Side effects may also have an ergolytic effect on exercise, particularly if sodium citrate is ingested 60–90 minutes pre-exercise, which means that individuals would perform exercise at the moment of the highest risk of GI distress and without reaching peak blood alkalosis (124).
Nutrition and vasoactive substances in the critically ill patient
Published in South African Journal of Clinical Nutrition, 2022
HC Spies, MA Frey, B Karstens
To emphasise, it is important to monitor haemodynamic stability in conjunction with vasoactive substance dose. Continuous monitoring of physiological parameters (also known as shock endpoints) signals improvement or worsening in tissue perfusion and oxygenation.8 Heart rate, blood pressure and urine output are considered basic endpoints, where a resolution of tachycardia, a mean arterial blood pressure (MAP) of >60–65 mmHg4 and a normal urine output may indicate an improvement.8,13 In the presence of anaerobic metabolism, increased lactic acid is produced.8 If the production of lactic acid exceeds the ability of the liver to excrete excess lactic acid, the serum lactate level will increase.8 The stabilisation or decrease4 of serum lactate levels will indicate an improvement; a lactate level of <2 mmol/l is considered normal.8 The arterial base deficit (calculated from pH, partial pressure of arterial oxygen tension and serum bicarbonate) reflects the use of bicarbonate to buffer acidosis.8 A reduction of base deficit reflects the successful restoration of tissue perfusion and oxygenation; a base deficit of −2 to 2 mmol/l is considered normal.8
Comparison of Centrifugal and Pulsatile Perfusion to Preserve Donor Kidneys Using Ex Vivo Subnormothermic Perfusion
Published in Journal of Investigative Surgery, 2022
Patrick P. W. Luke, Larry Jiang, Aushanth Ruthirakanthan, Daniel Lee, Qizhi Sun, Mahms Richard-Mohamed, Justin Kwong, Shahid Aquil, Rafid Alogaili, Aaron Haig, Alp Sener, Rabindra N. Bhattacharjee
Under general anesthesia, kidneys were subjected to 30 min warm ischemia in situ by cross-clamping the renal pedicles. After retrieval and flush with HTK solution, the paired kidneys were randomly assigned to undergo either: a) pulsatile perfusion or b) centrifugal perfusion with a hemoglobin oxygen carrier, HBOC-201, containing no vasodilators and nutrients at 22 °C. Oxygenation was achieved by an oxygenator and was set at 40%. Bicarbonate was added to adjust pH to physiologic levels. Urinary loss was replenished by equivalent volumes of PlasmaLyte solution (Baxter Corporation, USA) every half hour. A mean pressure of 70 mmHg was maintained during perfusion and perfusate oxygenation. Pump parameters such as flow rate and pressure were recorded every hour during preservation stage as well as reperfusion stage. After 4 hr perfusion with HBOC-201 at 22 °C, the function of both kidneys was assessed by reperfusion with autologous blood on pulsatile pump at 37 °C for another 4 hr to mimic post-storage transplantation conditions. Pump pressure, pH and oxygenation were maintained as if in perfusion. Blood pO2, pH and osmolality were monitored during reperfusion. To evaluate renal function, creatinine (10 mg/L) was added to the circuit. Figure 1B is a summary of the experimental procedure for our pump comparison.
Anion inhibition studies of the α-carbonic anhydrases from Neisseria gonorrhoeae
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Alessio Nocentini, Chad S. Hewitt, Margaret D. Mastrolorenzo, Daniel P. Flaherty, Claudiu T. Supuran
Inhibition constants in the range of 1.3–9.6 mM were measured for the following anions: all the halides, azide, bicarbonate, carbonate, stannate, perosmate, diphosphate, divanadate, perruthenate, and trifluoromethanesulfonate. The last anion is an interesting case, as it does not considerably inhibits hCA I and II (KIs > 100 mM) being thus an NgCA-selective (although weak) inhibitor. Among the halides, fluoride and iodide were weaker inhibitors than chloride and bromide (which was the most effective one among the halides). Bicarbonate, with a KI of 1.3 mM is a rather effective inhibitor (and this substrate of the enzyme is a much weaker hCA I and especially hCA II inhibitor, see Table 1), which presumably may constitute a way to inhibit the activity of this highly effective enzyme by one of the reaction products, which might be physiologically significant. This hypothesis needs to be checked, but it is known for example that in the case of V. cholerae, bicarbonate, generated by the activity of the various CAs present in this pathogen, induces virulence gene expression1;
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