D-lactic acidosis with encephalopathy subsequent to “short bowel syndrome” in bariatric surgery. A case report in emergency room
Emergency Medicine Department, S. Andrea Hospital, Rome, Italy
We describe the case of a patient admitted in Emergency Department with D-lactic acidosis associated to encephalopathy secondary to “short bowel syndrome” following bariatric surgery.
D-lactic acidosis with encephalopathy is a severe complication of short bowel syndrome. It is characterized by metabolic acidosis due to increase of lactic acid determining neurological signs and symptoms of encephalopathy.
In short bowel syndrome’s patients there is a malabsorption or lack of absorption of carbohydrates; this causes an accumulation of lactic acid that reduces pH and promotes bacterial growth, mainly lactobacillus, which in turn produce D-lactic acid (1,2).
D-lactic acid is metabolized, and eliminated more difficult than L-lactic acid normally produced (2).
Patients with short bowel syndrome secondary to intestinal bariatric surgery can show D-lactic acidosis from few months to several years after the surgery (2).
Patients with D-lactic acidosis show neurological symptoms and signs as ataxia, difficulty speaking, nystagmus, asymmetry, memory loss, instability, irritability, sensorial alterations, stupor, and also coma.
Female, 31 years old, arrived in our Emergency Room (ER) (transported by public ambulance) for sudden onset of fatigue, stupor, difficulty speaking, ideomotor slowing. Sympthomathology began in the morning.
The patient underwent bariatric surgery in order to loose weight one year before presenting in ER. Her past history was negative.
She suffered of vomiting and fever four days before the admission in our ER. In that occasion she went in another Emergency Department where she was visited, physical examination did not show abnormal signs, and an abdominal CT scan was performed, which showed only the presence of kidney stones.
The patient was subjected to intravenous infusion of potassium chloride, and symptoms ameliorated, so she was discharged.
At admission in our ER, four days after the first visit, physical examination was again, negative; laboratory blood exams showed ipokaliemia. Arterial blood gas analysis showed a decompensated metabolic acidosis with normal lactates (pH 7.19, pCO2 29 mmHg, pO2 40 mmHg, HCO3- 11,1 mmol/L, lactates 0.9 mmol/L).
ECG and cerebral CT scan were performed and were within the limits of normality.
After intravenous bolus administration of 50 mEq Sodium Bicarbonate (NaHCO3) and intravenous slow infusion of other 50 mEq NaHCO3 in 400 cc of 0.9% Normal Saline (Sodium Chloride solution) and intravenous slow infusion of Potassium Chloride of 60 mEq in 250 cc of Normal Saline 0.9%, another arterial blood gas analysis was performed, and showed a slight increase of pH, but a reduction of bicarbonates (pH 7.29, pCO2 21 mmHg, pO2164 mmHg, HCO3- 10.1 mmol/L, lactates 0.9 mmol/L).
The persistence of metabolic acidosis together with neurological signs and symptoms allowed us to make diagnosis of metabolic acidosis due to D-lactates in bariatric surgery.
At the time there is no specific treatment for D-lactic acidosis, but its prompt and rapid diagnosis is of paramount importance to begin a correct therapy, mainly in patients with co-morbidities which can favor progression of acidosis, and worsening of general conditions with respiratory insufficiency, kidney failure, diabetes.
The therapeutic approach is the administration of intravenous bicarbonates, hydration, parenteral nutrition.
In some cases, it could be useful to administrate insulin to reduce fatty acid, and to promote the clearance of D-lactate; in unstable patients hemodialysis is indicated.
In few cases it is possible to use antibiotics in order to reduce the LAB, but their efficacy is not clear yet. Some antibiotics in fact could cause lactic acidosis. In some cases metronidazole has showed efficacy, but following its administration some lactobacilli developed resistance.
In order to prevent the symptoms it is fundamental to establish a correct diet by limiting ingestion of simple carbohydrates; small and frequent meals are advisable to avoid an excessive charge of glucose for intestinal flora, also fermented meals should be avoided (5,6).
- E Domann, F Fischer, F Glowazki, et al. Draft genome sequence of lactobacillus delbrueckii Strain #22 isolated froma patient with short bowel syndrome and previous D-lactic acidosis and encephalopathy. Genome Announc. 2016 Jul-Aug; 4(4): e00747-16.
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