scholarly journals FC 025ACID BASE DISORDERS IN COVID-19

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Gaetano Alfano ◽  
Annachiara Ferrari ◽  
Francesco Fontana ◽  
Giacomo Mori ◽  
Riccardo Magistroni ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Kidney Injury ◽  
Respiratory Alkalosis ◽  
Fatality Rate ◽  
Acid Base ◽  
Study Population ◽  
The Impact ◽  
Acid Base Disturbance ◽  
Base Disturbance

Abstract Background and Aims Acid-base disorders are common in severely ill patients and reflect the severity of the underlying pathologic process. The incidence and effects of acid-base derangement in COVID-19 patients have been poorly evaluated until now. Tropism of the virus for the lungs and kidneys may theoretically lead to frequent acid-base alterations due to pneumonia and kidney injury, respectively. To verify the derangement of acid-base disorders in COVID-19, we investigated the distribution and the impact of acid-base disorders on the survival of symptomatic patients with a diagnosis of COVID-19. Method We retrospectively collected data from electronic charts of all COVID-19 patients hospitalized at the University Hospital of Modena from 4 March to 20 June 2020. Arterial blood gas (ABG) analysis was required to monitor pulmonary gas exchange and acid-base status. A pH of less than 7.37 was categorized as acidemia and a pH of more than 7.42 was categorized as alkalemia. 211 patients were included in the study population. In patients with multiple ABG analyses, we selected only the first measurement. Results The estimated mean age of the population was 64.7 ±15,3 years with a high predominance of males (71.6%). Half of the population referred dyspnea and 61.4% at physical examination. Most patients (82.6%) were on oxygen therapy when ABG analysis was performed. Overall, ABG analyses revealed acute respiratory compromise manifesting with a low arterial partial pressure of oxygen (P02, 70.2±25.1 mmHg), oxygen saturation (SO2, 92%) and a mild reduction of PO2/FiO2 ratio (231±129). Acid-base disturbance was found in the 79.7% of the patients, and contrary to our expectation, metabolic alkalosis (33.6%) was the main alteration followed by respiratory alkalosis (30.3%), combined alkalosis (9.4%) respiratory acidosis (3.3%) metabolic acidosis (2.8%) and other compensated acid-base disturbances (3.6%). ANOVA with post hoc Tukey, revealed statistically significant differences in age, sex, serum level of K, Na, bicarbonate, creatinine of PCO2, PO2/FiO2 ratio, CKD, symptoms (caught, diarrhea) and fatality rate among groups. Metabolic acidosis was associated with death (HR=8.2; CI 95%, 1,93-32,39; P<0.004), after adjustment for lung injury (PaO2/FiO2 ratio) tissue hypoperfusion (lactate) and renal involvement (estimated as GFR< 60 ml/min or development of acute kidney injury), Pathological pH (alkalosis or acidosis), variations of PCO2 or hypobicarbonatemia were not associated with mortality in our study population. Metabolic acidosis occurred in patients with a mean creatinine of 4.5±4.5 mg/dl. Notably, 33.3% of patients were on hemodialysis, 33.3% developed COVID-19-associated acute kidney injury and 33.3% had a GFR <60 ml/min. Patients with metabolic acidosis had the highest death-fatality rate (100%) after 7±5.6 days from admission, 50% died of acute respiratory distress syndrome and 50% of septic shock. Conclusion In conclusion, all kinds of acid-base alterations were found in patients with COVID-19. Metabolic and respiratory alkalosis were the most common acid-base disorders, whereas metabolic acidosis was the only acid-base disturbance associate with poor outcome in our cohort of patients.

scholarly journals Targeting acute kidney injury in COVID-19

2020 ◽  
Vol 35 (10) ◽  
pp. 1652-1662 ◽  
Author(s):  
John A Kellum ◽  
J W Olivier van Till ◽  
George Mulligan
Keyword(s):  
Acute Kidney Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Perfusion ◽  
Endothelial Damage ◽  
Acid Oxidation ◽  
Acid Base ◽  
The Impact ◽  
Pathophysiologic Mechanisms

Abstract As of 15 August 2020, Coronavirus disease 2019 (COVID-19) has been reported in >21 million people world-wide and is responsible for more than 750,000 deaths. The occurrence of acute kidney injury (AKI) in patients hospitalized with COVID-19 has been reported to be as high as 43%. This is comparable to AKI in other forms of pneumonia requiring hospitalization, as well as in non-infectious conditions like cardiac surgery. The impact of AKI on COVID-19 outcomes is difficult to assess at present but, similar to other forms of sepsis, AKI is strongly associated with hospital mortality. Indeed, mortality is reported to be very low in COVID-19 patients without AKI. Given that AKI contributes to fluid and acid–base imbalances, compromises immune response and may impair resolution of inflammation, it seems likely that AKI contributes to mortality in these patients. The pathophysiologic mechanisms of AKI in COVID-19 are thought to be multifactorial including systemic immune and inflammatory responses induced by viral infection, systemic tissue hypoxia, reduced renal perfusion, endothelial damage and direct epithelial infection with Severe Acute Respiratory Syndrome Coronavirus 2. Mitochondria play a central role in the metabolic deregulation in the adaptive response to the systemic inflammation and are also found to be vital in response to both direct viral damage and tissue reperfusion. These stress conditions are associated with increased glycolysis and reduced fatty acid oxidation. Thus, there is a strong rationale to target AKI for therapy in COVID-19. Furthermore, many approaches that have been developed for other etiologies of AKI such as sepsis, inflammation and ischemia–reperfusion, have relevance in the treatment of COVID-19 AKI and could be rapidly pivoted to this new disease.

scholarly journals The impact of acute kidney injury on fatality of ischemic stroke from a hospital-based population in Joinville, Brazil

2019 ◽  
Vol 41 (3) ◽  
pp. 323-329
Author(s):  
Helbert do Nascimento Lima ◽  
Tais Saibel ◽  
Gisele Colato ◽  
Norberto Luiz Cabral
Keyword(s):  
Acute Kidney Injury ◽  
Ischemic Stroke ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Final Study ◽  
Study Population ◽  
Predictive Strength ◽  
The Impact ◽  
Brazilian Studies ◽  
Worse Prognosis

Abstract Introduction: The occurrence of acute kidney injury (AKI) after ischemic stroke has been associated to a worse prognosis. There is a lack of Brazilian studies evaluating this issue. This study aimed to describe the impact of AKI after a first-ever ischemic stroke in relation to fatality rate in 30 days. Methods: This was a retrospective hospital-based cohort. We included patients who had their first ischemic stroke between January to December 2015. AKI was defined by an increase of serum creatinine in relation to baseline value at admission ≥ 0.3 mg/dL or a rise in serum creatinine level by 1.5 times the baseline value at any point in the first week after admission. We performed a univariate and multivariate analysis to evaluate the presence of AKI with fatality in 30 days. Results: The final study population (n=214) had mean age of 66.46 ± 13.73 years, 48.1% were men, the mean NIHSS was 6.33 ± 6.27 and 20 (9.3%) presented AKI. Patients with AKI were older, had a higher score on the NIHSS, and had higher creatinine values on hospital discharge. The 30-day mortality was higher in the AKI subgroup compared to non-AKI (35% vs. 6.2%, p < 0.001). AKI was an independent predictor of fatality after an ischemic stroke but limited by severity of stroke (NIHSS). Conclusion: The presence of AKI is an important complication after ischemic stroke. Despite its impact on 30-day fatality, the predictive strength of AKI was limited by the severity of stroke.

scholarly journals Obesity, Anion Accumulation, and Anion Gap Metabolic Acidosis: A Cohort Study

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0003562021
Author(s):  
Douglas C. Lambert ◽  
Matthew K. Abramowitz
Keyword(s):  
Metabolic Acidosis ◽  
Proportional Hazards ◽  
Cox Proportional Hazards ◽  
Anion Gap ◽  
Acid Base ◽  
Unmeasured Anion ◽  
Cox Proportional Hazards Models ◽  
Increased Risk ◽  
Acid Base Disturbance ◽  
Base Disturbance

Background: Obesity is associated with low serum bicarbonate, an indicator of metabolic acidosis and a CKD risk factor. To further characterize acid-base disturbance and subclinical metabolic acidosis in this population, we examined prospective associations of body mass index (BMI) with elevated anion gap, and whether anion gap values in obesity associate with low bicarbonate. Methods: Data from adult outpatients (n = 94,448) in the Bronx, NY were collected from 2010-2018. Mixed effects models and Cox proportional hazards models were used to examine associations of BMI with elevated anion gap and anion gap metabolic acidosis, and of baseline anion gap with incident low bicarbonate and anion gap metabolic acidosis. Anion gap was defined using traditional and albumin-corrected calculations. Results: Greater BMI was associated with higher anion gap over time, and with progressively greater risk of developing an elevated anion gap (HRs for BMI ≥ 40 vs. 18-<25 kg/m2: 1.32 [95% CI: 1.23 - 1.42] for traditional and 1.74 [95% CI: 1.63 - 1.85] for corrected). Higher BMI was also associated with increased risk of developing anion gap metabolic acidosis (HR for BMI ≥ 40: 1.53 [95% CI: 1.39 - 1.69]). Among patients with obesity, higher anion gap was associated with increased risk of incident low bicarbonate (HRs for 4th vs 1st quartile: 1.29 [95% CI: 1.23 - 1.44] for traditional and 1.36 [95% CI: 1.26 - 1.48] for corrected); and higher risk of anion gap metabolic acidosis (HR for 4th vs 1st quartile 1.78 [1.59 - 1.99]). Conclusions: Obesity is characterized by unmeasured anion accumulation and acid retention or overproduction. Modest elevations in anion gap among patients with obesity are associated with previously unrecognized anion gap metabolic acidosis.

Electrolyte and acid–base disorders in AKI

2015 ◽  
Author(s):  
Achim Jörres ◽  
Dietrich Hasper ◽  
Michael Oppert
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Sodium Bicarbonate ◽  
Kidney Injury ◽  
Medical Emergency ◽  
Acid Base ◽  
Compensatory Mechanisms ◽  
Electrolyte Disturbances ◽  
Underlying Pathology

Electrolyte disturbances are common in patients with acute kidney injury (AKI) and should be corrected. In particular, hyperkalaemia above 6–6.5 mmol/L (especially with electrocardiogram changes) constitutes a medical emergency and warrants immediate intervention. Both hypo- and hypernatraemia may occur during AKI. Chronic changes in serum sodium need to be corrected bearing in mind the underlying pathology; however, when severe and evolving rapidly they should be corrected faster, irrespective of the cause. Acid–base disorders are also common in AKI and need to be treated in the context of underlying problems and physiological compensatory mechanisms. In metabolic acidosis, a bicarbonate deficit may be corrected by sodium bicarbonate administration. Of note, whilst patients with AKI tend to retain electrolytes such as potassium and phosphate, this might be reversed during renal replacement therapy and even substitution of these losses may be required.

scholarly journals Assessment of Cardiopulmonary Bypass Duration Improves Novel Biomarker Detection for Predicting Postoperative Acute Kidney Injury after Cardiovascular Surgery

2021 ◽  
Vol 10 (13) ◽  
pp. 2741
Author(s):  
Tao Han Lee ◽  
Cheng-Chia Lee ◽  
Jia-Jin Chen ◽  
Pei-Chun Fan ◽  
Yi-Ran Tu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiopulmonary Bypass ◽  
Fatty Acid Binding Protein ◽  
Cardiovascular Surgery ◽  
Kidney Injury ◽  
Fatty Acid Binding ◽  
Discriminatory Ability ◽  
Postoperative Risk ◽  
Study Population ◽  
Postoperative Aki

Urinary liver-type fatty acid binding protein (L-FABP) is a novel biomarker with promising performance in detecting kidney injury. Previous studies reported that L-FABP showed moderate discrimination in patients that underwent cardiac surgery, and other studies revealed that longer duration of cardiopulmonary bypass (CPB) was associated with a higher risk of postoperative acute kidney injury (AKI). This study aims to examine assessing CPB duration first, then examining L-FABP can improve the discriminatory ability of L-FABP in postoperative AKI. A total of 144 patients who received cardiovascular surgery were enrolled. Urinary L-FABP levels were examined at 4 to 6 and 16 to 18 h postoperatively. In the whole study population, the AUROC of urinary L-FABP in predicting postoperative AKI within 7 days was 0.720 at 16 to 18 h postoperatively. By assessing patients according to CPB duration, the urinary L-FABP at 16 to 18 h showed more favorable discriminating ability with AUROC of 0.742. Urinary L-FABP exhibited good performance in discriminating the onset of AKI within 7 days after cardiovascular surgery. Assessing postoperative risk of AKI through CPB duration first and then using urinary L-FABP examination can provide more accurate and satisfactory performance in predicting postoperative AKI.

scholarly journals Does deeper hypothermia reduce the risk of acute kidney injury after circulatory arrest for aortic arch surgery?

2021 ◽  
Author(s):  
Andrew M Vekstein ◽  
Babtunde A Yerokun ◽  
Oliver K Jawitz ◽  
Julie W Doberne ◽  
Jatin Anand ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Circulatory Arrest ◽  
Aortic Surgery ◽  
Multivariable Analysis ◽  
Kidney Injury ◽  
Deep Hypothermia ◽  
Moderate Hypothermia ◽  
Bladder Temperature ◽  
Increased Risk ◽  
The Impact

Abstract OBJECTIVES The impact of hypothermic circulatory arrest (HCA) temperature on postoperative acute kidney injury (AKI) has not been evaluated. This study examined the association between circulatory arrest temperatures and AKI in patients undergoing proximal aortic surgery with HCA. METHODS A total of 759 consecutive patients who underwent proximal aortic surgery (ascending ± valve ± root) including arch replacement requiring HCA between July 2005 and December 2016 were identified from a prospectively maintained institutional aortic surgery database. The primary outcome was AKI as defined by Risk, Injury, Failure, Loss, End Stage Renal Disease (ESRD) criteria. The association between minimum nasopharyngeal (NP) and bladder temperatures during HCA and postoperative AKI was assessed, adjusting for patient-level factors using multivariable logistic regression. RESULTS A total of 85% (n = 645) of patients underwent deep hypothermia (14.1–20.0°C), 11% (n = 83) low-moderate hypothermia (20.1–24.0°C) and 4% (n = 31) high-moderate hypothermia (24.1–28.0°C) as classified by NP temperature. When analysed by bladder temperature, 59% (n = 447) underwent deep hypothermia, 22% (n = 170) low-moderate, 16% (n = 118) high-moderate and 3% mild (n = 24) (28.1–34.0°C) hypothermia. The median systemic circulatory arrest time was 17 min. The incidence of AKI did not differ between hypothermia groups, whether analysed using minimum NP or bladder temperature. In the multivariable analysis, the association between degree of hypothermia and AKI remained non-significant whether analysed as a categorical variable (hypothermia group) or as a continuous variable (minimum NP or bladder temperature) (all P &gt; 0.05). CONCLUSIONS In patients undergoing proximal aortic surgery including arch replacement requiring HCA, degree of systemic hypothermia was not associated with the risk of AKI. These data suggest that moderate hypothermia does not confer increased risk of AKI for patients requiring circulatory arrest, although additional prospective data are needed.

Cerebral acid-base and gas metabolism in brain injury

1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping
Keyword(s):  
Metabolic Acidosis ◽  
Brain Injury ◽  
Brain Damage ◽  
Close Correlation ◽  
Respiratory Alkalosis ◽  
Acid Base ◽  
Content Type ◽  
Arterial Blood ◽  
Gas Metabolism ◽  
Permanent Brain Damage

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.

Metabolic Alkalosis Secondary to Baking Soda Treatment of a Diaper Rash

PEDIATRICS ◽  
1981 ◽  
Vol 67 (6) ◽  
pp. 820-822
Author(s):  
Jose Gonzalez ◽  
Ronald J. Hogg
Keyword(s):  
Case Report ◽  
Side Effects ◽  
Sodium Bicarbonate ◽  
Complete Resolution ◽  
Metabolic Alkalosis ◽  
Acid Base ◽  
Prior Application ◽  
Acid Base Disturbance ◽  
Base Disturbance

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

Respiratory Acidosis and Alkalosis

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Carbonic Acid ◽  
Clinical Manifestations ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Body Fluids ◽  
The Body ◽  
Acid Base ◽  
Acid Base Equilibrium ◽  
Therapeutic Principles ◽  
The Impact

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis.  This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis

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