metabolic acidosis
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2022 ◽  
Vol 21 (1) ◽  
pp. 160-184
Author(s):  
F.G. Habasha ◽  
K, Michael ◽  
K.O. Al-Jebouril

The experimental design of this study was included (12) Friesian calves aged between 3-5 weeks. Calves were divided into two groups. Group I consisted of (8) calves were infected experimentally with 1.5 x 10“ of Salmonella typhimurium and often that treatment with chloramphenicol and electrolytes fluid were takes place. Group II consisted of (4) calves were infected with organisms but without treatment. The clinical findings of the disease were characterized by two forms which includes the septicemic and enteric forms. Haematological changes revealed a variable number of the total and differential leukocytic count, increased PCV, fibnnogen and decreased of the total plasma protein. . The changes in the acid-based balance indicate the development of metabolic acidosis.


Author(s):  
Jun-Ya Kaimori ◽  
Yusuke Sakaguchi ◽  
Sachio Kajimoto ◽  
Yuta Asahina ◽  
Tatsufumi Oka ◽  
...  

2022 ◽  
Vol 10 (1) ◽  
Author(s):  
Kentaro Ukita ◽  
Kanako Otomune ◽  
Ryo Fujimoto ◽  
Kanako Hasegawa ◽  
Koichi Izumikawa ◽  
...  

2022 ◽  
Vol 226 (1) ◽  
pp. S652-S653
Author(s):  
Natalie E. Taylor ◽  
Kent Heyborne ◽  
Patricia Hagan ◽  
Karilynn Rockhill

2022 ◽  
Vol 10 ◽  
pp. 2050313X2110685
Author(s):  
Lee Connolly ◽  
Ed Briggs

Pyroglutamic acid is an endogenous organic acid and a metabolite in the γ-glutamyl cycle, involved in glutathione metabolism. Accumulation of pyroglutamic acid is a rare cause of high anion gap metabolic acidosis. There are multiple risk factors for pyroglutamic acid accumulation, such as chronic paracetamol use and sepsis. In this case report, we discuss how we came to this diagnosis, how it was subsequently managed and why it is an important consideration for critically ill patients with risk factors who are likely to end up in an intensive care setting. Pyroglutamic acid recognition and treatment could benefit patients in the critically ill population as pyroglutamic acid is a rare cause of high anion gap metabolic acidosis, which is likely under-recognised and easily treated. Inappropriate management of metabolic disorders can contribute to patient morbidity and mortality. Therefore, the recognition and appropriate management of pyroglutamic acidaemia could benefit patients with risk factors for its development in a critical care setting.


Critical Care ◽  
2021 ◽  
pp. 30-31
Author(s):  
Steven Mensack
Keyword(s):  

2021 ◽  
Vol 50 (1) ◽  
pp. 666-666
Author(s):  
Patrick Jenkinson ◽  
Michelle Kirk ◽  
Bo Liu ◽  
Maria huaringa ◽  
Wajdi Al-Shweiat ◽  
...  

2021 ◽  
pp. 0271678X2110659
Author(s):  
Hannah G Caldwell ◽  
Ryan L Hoiland ◽  
Kurt J Smith ◽  
Patrice Brassard ◽  
Anthony R Bain ◽  
...  

This study investigated trans-cerebral internal jugular venous-arterial bicarbonate ([HCO3−]) and carbon dioxide tension (PCO2) exchange utilizing two separate interventions to induce acidosis: 1) acute respiratory acidosis via elevations in arterial PCO2 (PaCO2) (n = 39); and 2) metabolic acidosis via incremental cycling exercise to exhaustion (n = 24). During respiratory acidosis, arterial [HCO3−] increased by 0.15 ± 0.05 mmol ⋅ l−1 per mmHg elevation in PaCO2 across a wide physiological range (35 to 60 mmHg PaCO2; P < 0.001). The narrowing of the venous-arterial [HCO3−] and PCO2 differences with respiratory acidosis were both related to the hypercapnia-induced elevations in cerebral blood flow (CBF) (both P < 0.001; subset n = 27); thus, trans-cerebral [HCO3−] exchange (CBF × venous-arterial [HCO3−] difference) was reduced indicating a shift from net release toward net uptake of [HCO3−] (P = 0.004). Arterial [HCO3−] was reduced by −0.48 ± 0.15 mmol ⋅ l−1 per nmol ⋅ l−1 increase in arterial [H+] with exercise-induced acidosis (P < 0.001). There was no relationship between the venous-arterial [HCO3−] difference and arterial [H+] with exercise-induced acidosis or CBF; therefore, trans-cerebral [HCO3−] exchange was unaltered throughout exercise when indexed against arterial [H+] or pH (P = 0.933 and P = 0.896, respectively). These results indicate that increases and decreases in systemic [HCO3−] – during acute respiratory/exercise-induced metabolic acidosis, respectively – differentially affect cerebrovascular acid-base balance (via trans-cerebral [HCO3−] exchange).


2021 ◽  
Vol 14 (12) ◽  
pp. e245065
Author(s):  
Angela Heulwen Boal ◽  
Maurizio Panarelli ◽  
Caroline Millar

Starvation ketoacidosis (SKA) is a rarer cause of ketoacidosis. Most patients will only have a mild acidosis, but if exacerbated by stress can result in a severe acidosis. We describe a 66-year-old man admitted with reduced consciousness and found to have a severe metabolic acidosis with raised anion gap. His body mass index (BMI) was noted to be within the healthy range at 23 kg/m2; however, it was last documented 1 year previously at 28 kg/m2 with no clear timeframe of weight loss. While his acidosis improved with intravenous fluids, he subsequently developed severe electrolyte imbalance consistent with refeeding during his admission. Awareness of SKA as a cause for high anion gap metabolic acidosis is important and knowledge of management including intravenous fluids, thiamine, dietetic input and electrolyte replacement is vital.


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