Acute lactic acidosis as a complication of thiamine-free parenteral nutrition in two neutropenic children (original) (raw)
Related papers
JPEN. Journal of parenteral and enteral nutrition, 2015
Thiamine is a water-soluble vitamin implicated in several metabolic processes. Its deficiency, due to prolonged parenteral nutrition without adequate vitamin supplementation, can lead to multiorgan failure characterized by cardiovascular impairment and metabolic acidosis refractory to bicarbonate administration. Only thiamine administration allows the remission of symptoms. We report 2 preterm infants with acute thiamine deficiency due to prolonged parenteral nutrition without adequate vitamin supplementation.
Severe lactic acidosis in an extremely low birth weight infant due to thiamine deficiency
Journal of pediatric endocrinology & metabolism : JPEM, 2018
In this case report, we present a preterm newborn with persistent lactic acidosis who received total parenteral nutrition (TPN) that lacked thiamine. A 28-week-old, 750 g female infant was born with an Apgar score of 8 at the 5th minute. Umbilical cord blood gas levels, including lactate level, were normal, and she was admitted to our neonatal intensive care unit (NICU). Achieving full enteral feeding was not possible due to gastric residues and abdominal distention, making the patient dependent on TPN during the first 2 weeks of life. An insidious increase in lactic acid levels and uncompensated metabolic acidosis were apparent from the 23rd day of life. Severe metabolic acidosis was persistent despite massive doses of bicarbonate. The acidosis resolved dramatically within 6 h when the patient was administered with thiamine. Although TPN is life saving in the NICU, meticulous attention must be paid to provide all essential macro- and micro-nutrients.
Thiamine-Responsive Lactic Acidosis, Encephalopathy, and Shock
Journal of Pharmacy Technology, 1998
Objective: To report a case of severe lactic acidosis, encephalopathy, and hypotension in a patient receiving total parenteral nutrition without multivitamin supplementation and the dramatic response to intravenous administration of thiamine. Case Summary: A 15-year-old African-American girl undergoing treatment for chronic myelogenous leukemia with allogenic bone marrow transplantation and requiring total parenteral nutrition was admitted to our intensive care unit for management of life-threatening lactic acidosis, encephalopathy, and hemodynamic instability. Because of the manufacturing shortage of parenteral multivitamin preparations, oral multivitamins were prescribed; however, the patient was unable to swallow the oral multivitamins because of oral mucositis. Intravenous administration of thiamine promptly reversed the profound metabolic, neurologic, and hemodynamic abnormalities. Discussion: Carbohydrate loading associated with inadequate thiamine intake may result in potenti...
Lactic acidosis in thiamine deficiency
Clinical Nutrition, 1993
Two chronically ill patients with limited nutritional intake during several weeks developed prolonged lactic acidosis. As no other causes of hyperlactaemia could be identified, thiamine deficiency was suspected. Supplementation of 600 mg thiamine resulted in a rapid normalisation of serum lactate levels (in patient 1 from 10.9-2.4 mmol/l; in patient 2 from 11.8-2.0 mmol/l) and acid base status (patient 1: pH from 7.11-7.30, bicarbonate from 8.6-21.2 mmol/l; patient 2: pH from 7.24-7.46, bicarbonate from 16-28 mmol/l; before and after treatment, respectively). Thiamine deficiency was confirmed by the degree of stimulation of erythrocyte transketolase activation by adding thiamine pyrophosphate, evaluated before and after thiamine replacement therapy. Stimulation decreased in patient 1 from 170% to 17% and in patient 2 from 20% to 0%, respectively. In addition to the metabolic derangement right ventricular heart failure was confirmed by echocardiography in both patients and again this was rapidly reversible by thiamine supplementation. We conclude that in malnourished patients unexplained prolonged lactic acidosis may result from thiamine deficiency, which is rapidly reversible by thiamine replacement therapy.
Thiamine responsive acute life threatening metabolic acidosis in exclusively breast-fed infants
Nutrition, 2016
Background: Acute life threatening metabolic acidosis in exclusively breast fed infants due to thiamine deficiency is not described. Kashmir valley, a north Indian state has a population that largely consumes polished rice. Methods: A six months prospective descriptive study of infants who presented with acute life threatening metabolic acidosis (Blood pH 7.0) due to thiamine deficiency. Results: Twenty three infants (Eleven male; Twelve female) in the age range of 32 days to 4 months had a pH of 7 at admission. Onset of moaning was immediate (2À24 hours). Blood lactate levels were more than 15mmol/L. Blood thiamine levels of six infants in whom it was done ranged from 11À69 nmol/L (control 78À185 nmol/L). All infants were exclusively breast fed. Maternal staple diet consisted of polished rice. All mothers consumed rice after washing it thrice. Twelve lactating mothers were on customary dietary restrictions. Practice of straining rice after cooking was observed in thirteen. The commonest symptoms were irritability (82%) and reflux (56%). Commonest signs were tachycardia (100%) and moaning (73%). At presentation 52% were in cardiogenic shock. Response to thiamine was dramatic with moaning and irritability subsiding in two hours and tachycardia in four hours. Adequate perfusion was achieved in one hour. Eighteen patients seen at six months follow up had normal neurodevelopment. Conclusions: Thiamine deficiency in an infant can present as sudden onset metabolic acidosis. If treated early, metabolic acidosis due to thiamine deficiency is associated with good immediate and long term prognosis even if pH is less than 7 at presentation.
Consideration of alternative causes of lactic acidosis: Thiamine deficiency in malignancy
The American journal of emergency medicine, 2017
Lactic acidosis is a common metabolic acidosis characterized by increased serum lactate and is usually associated with a decreased blood pH. Lactic acidosis has many different causes but has been differentiated into type A, hypoxic causes, and type B, non-hypoxic causes. Tissue hypoxia, type A, is the most common cause, usually secondary to processes such as sepsis and multi-organ failure. Type A must be differentiated from type B in the correct clinical setting as treatments are vastly different. Type B causes may include drug side-effects, toxins, enzymatic defects, inherited or acquired, any of which may lead to overproduction or underutilization of lactate. However, as most clinicians are more familiar, and likely more initially concerned with hypoxic etiologies, evaluation is directed toward finding the source of hypoperfusion or hypoxia, and thus generally leading to a delay in discovering a type B cause (or mixed type A and type B). Here we describe a case of lactic acidosis ...
Unexplained Severe Lactic Acidosis in Young Patient
Albanian Journal of Trauma and Emergency Surgery
Case report: A 27-year-old previously healthy man was admitted to the ICU complaining nausea, vomiting and disorientation, after he ingested 1500 mg paracetamol, but its relatives explained that they possess in the house only metformin (maybe he ingested metformin instead of paracetamol). First blood gas showed moderate, and hours later severe lactic acidosis Ph 7,01, Lac 25 m mol/L, BE -26,4. Aggressive rehydration and hemofiltration was started, until full recovery after 24 hours of hospital admission. He was discharged after three days in healthy condition. Discussion: Lactic acidosis is a common cause of metabolic acidosis at the ICU. Type A is most common and caused by hypoperfusion or hypoxia, whilst type B has other causes including use of the antidiabetic drug metformin. Metformin associated lactic acidosis (MALA) is an important treatment-associated condition, and although rare, it is very serious. Conclusion: MALA should be strongly suspected in patients presenting with wi...
Severe lactic acidosis and thiamine administration in an HIV-infected patient on HAART
International Journal of STD & AIDS, 2001
Severe lactic acidosis has been increasingly reported as a potentially fatal complication of HIV treatment. We report on an asymptomatic HIV-infected woman treated with stavudine, lamivudine and indinavir for one year. She was hospitalized because of progressive dispnoea, oedema, cyanosis and severe lactic acidosis. Arterial blood pH was 6.98, bicarbonate 4.4 mmol/l (normal value 22-26), blood lactate: 29.7 mmol/l (normal value <2.2). Hepatic function was normal. She had an impressively rapid response (within a few hours) to empirical treatment with thiamine (100 mg i.v.). No evidence of sepsis or malabsorption were identified and vitamin B1 level was not tested before thiamine infusion. Three months later she was re-started successfully on nelfinavir plus nevirapine. The rapid response to thiamine infusion deserves a careful attention and such an approach should be considered in similar cases as a support treatment of this potentially life-threatening complication of HIV therapy.
Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences in these assays, especially in the case of ethylene glycol poisoning.
A Report of Two Cases: Unlearning Lactic Acidosis
Clinical Practice and Cases in Emergency Medicine, 2021
Introduction The term “lactic acidosis” reinforces the misconception that lactate contributes to acidemia. Although it is common to discover an anion gap acidosis with a concomitant elevated lactate concentration, the two are not mutually dependent. Case Report Here we describe two patients exhibiting high lactate concentrations in the setting of metabolic alkalemia. Conclusion Lactate is not necessarily the direct cause of acid-base disturbances, and there is no fixed relationship between lactate and the anion gap or between lactate and pH. The term “metabolic acidosis with hyperlactatemia” is more specific than “lactic acidosis” and thus more appropriate.