A newborn girl with watery diarrhea, weight loss, and severe metabolic acidosis

1994 ◽  
Vol 6 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Victor Nizet ◽  
Cedric j. Priebe

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.



2021 ◽  
Vol 12 ◽  
Author(s):  
Aurelio Negro ◽  
Ignazio Verzicco ◽  
Stefano Tedeschi ◽  
Nicoletta Campanini ◽  
Magda Zanelli ◽  
...  

BackgroundPheochromocytoma (PHEO) clinical manifestations generally mirror excessive catecholamines secretion; rarely the clinical picture may reflect secretion of other hormones. Watery diarrhea, hypokalemia and achlorhydria (WDHA) is a rare syndrome related to excessive secretion of vasoactive intestinal peptide (VIP).Clinical CaseA 73-year-old hypotensive man affected by adrenal PHEO presented with weight loss and watery diarrhea associated with hypokalemia, hyperchloremic metabolic acidosis (anion gap 15 mmol/l) and a negative urinary anion gap. Abdominal computed tomography scan showed a right adrenal PHEO, 8.1 cm in maximum diameter, with tracer uptake on 68GaDOTA-octreotate positron emission tomography. Metastasis in lumbar region and lung were present. Both chromogranin A and VIP levels were high (more than10 times the normal value) with slightly elevated urine normetanephrine and metanephrine excretion. Right adrenalectomy was performed and a somatostatin analogue therapy with lanreotide started. Immunostaining showed chromogranin A and VIP co-expression, with weak somatostatin-receptor-2A positivity. In two months, patient clinical conditions deteriorated with severe WDHA and multiple liver and lung metastasis. Metabolic acidosis and hypokalemia worsened, leading to hemodynamic shock and exitus.ConclusionsA rare case of WDHA syndrome caused by malignant VIP-secreting PHEO was diagnosed. High levels of circulating VIP were responsible of the rapidly evolving clinical picture with massive dehydration and weight loss along with severe hyperchloremic metabolic acidosis and hypokalemia due to the profuse untreatable diarrhea. The rescue treatment with lanreotide was unsuccessful because of the paucity of somatostatin-receptor-2A on VIP-secreting PHEO chromaffin cells.



2020 ◽  
pp. 000313482095692
Author(s):  
Marina L. Reppucci ◽  
Eliza H. Hersh ◽  
Prerna Khetan ◽  
Brian A. Coakley

Background Gastrointestinal (GI) perforation is a risk factor for mortality in very low birth weight (VLBW) infants. Little data exist regarding pretreatment factors and patient characteristics known to independently correlate with risk of death. Materials and Methods A retrospective review of all VLBW infants who sustained GI perforation between 2011 and 2018 was conducted. Birth, laboratory, and disease-related factors of infants who died were compared to those who survived. Results 42 VLBW infants who sustained GI perforations were identified. Eleven (26.19%) died. There were no significant differences in birth-related factors, hematological lab levels at diagnosis, presence of pneumatosis, or bacteremia. Portal venous gas ( P = .03), severe metabolic acidosis ( P < .01), and elevated lactate at diagnosis ( P < .01) were statistically more likely to occur among infants who died. Discussion Portal venous gas, severe metabolic acidosis, and elevated lactate were associated with an increased risk of mortality among VLBW infants who develop a GI perforation. Further research is required to better identify risk factors.



2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Grace Mzumara ◽  
Stije Leopold ◽  
Kevin Marsh ◽  
Arjen Dondorp ◽  
Eric O. Ohuma ◽  
...  

Abstract Background Severe metabolic acidosis and acute kidney injury are major causes of mortality in children with severe malaria but are often underdiagnosed in low resource settings. Methods A retrospective analysis of the ‘Artesunate versus quinine in the treatment of severe falciparum malaria in African children’ (AQUAMAT) trial was conducted to identify clinical features of severe metabolic acidosis and uraemia in 5425 children from nine African countries. Separate models were fitted for uraemia and severe metabolic acidosis. Separate univariable and multivariable logistic regression were performed to identify prognostic factors for severe metabolic acidosis and uraemia. Both analyses adjusted for the trial arm. A forward selection approach was used for model building of the logistic models and a threshold of 5% statistical significance was used for inclusion of variables into the final logistic model. Model performance was assessed through calibration, discrimination, and internal validation with bootstrapping. Results There were 2296 children identified with severe metabolic acidosis and 1110 with uraemia. Prognostic features of severe metabolic acidosis among them were deep breathing (OR: 3.94, CI 2.51–6.2), hypoglycaemia (OR: 5.16, CI 2.74–9.75), coma (OR: 1.72 CI 1.17–2.51), respiratory distress (OR: 1.46, CI 1.02–2.1) and prostration (OR: 1.88 CI 1.35–2.59). Features associated with uraemia were coma (3.18, CI 2.36–4.27), Prostration (OR: 1.78 CI 1.37–2.30), decompensated shock (OR: 1.89, CI 1.31–2.74), black water fever (CI 1.58. CI 1.09–2.27), jaundice (OR: 3.46 CI 2.21–5.43), severe anaemia (OR: 1.77, CI 1.36–2.29) and hypoglycaemia (OR: 2.77, CI 2.22–3.46) Conclusion Clinical and laboratory parameters representing contributors and consequences of severe metabolic acidosis and uraemia were independently associated with these outcomes. The model can be useful for identifying patients at high risk of these complications where laboratory assessments are not routinely available.





1989 ◽  
Vol 8 (3) ◽  
pp. 243-245 ◽  
Author(s):  
F.P. Gijsenbergh ◽  
M. Jenco ◽  
H. Veulemans ◽  
D. Groeseneken ◽  
R. Verberckmoes ◽  
...  

A rare case of butylglycol intoxication in a suicide attempt is reported. Coma and hypotension were present on admission and severe metabolic acidosis arose subsequently. Forced diuresis and haemodialysis led to an uneventful outcome.





2010 ◽  
Vol 48 (2) ◽  
pp. 160-161 ◽  
Author(s):  
Wouter Van Moerkercke ◽  
Mathias Leys ◽  
Philippe Meersseman


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