Possible cannabinoid-induced lactic acidosis requiring emergent dialysis.

Lactic acidosis is a common finding in the intensive care unit and is associated with increased mortality. We present the case of a 42-year-old male with alcohol use disorder and cirrhosis who developed sudden onset shortness of breath while smoking marijuana. He was found to have a lactic acid level of 25.6 mmol/L with a significant anion gap metabolic acidosis requiring emergent dialysis. He was hypertensive without evidence of tissue hypoperfusion. His profound type B lactic acidosis was primarily attributed to a rare manifestation of cannabinoid toxicity. At a clinic visit 3 months later, he was doing well and had not smoked marijuana since his discharge.

Unmasking the Rarity: A Case Report on Type B Lactic Acidosis in Pediatric Acute Lymphoblastic Leukemia.

Acute lymphoblastic leukemia (ALL) is the most prevalent pediatric malignancy, accounting for approximately 25% of childhood cancers. Despite significant advancements in treatment protocols, ALL remains a complex disease, often presenting with various complications, including the rare metabolic disturbance of type B lactic acidosis. This case report details the clinical journey of a 14-year-old female with ALL who developed type B lactic acidosis during treatment. The patient presented with intermittent fever, abdominal pain, jaundice, and hepatosplenomegaly, accompanied by severe anemia and thrombocytopenia. Initial management included supportive care and chemotherapy initiation. Despite aggressive interventions, the patient's condition deteriorated, with escalating lactic acidosis and respiratory distress, leading to a critical need for tailored management strategies. This report underscores the importance of early recognition and comprehensive management of type B lactic acidosis in pediatric ALL, highlighting its multifactorial etiology and potentially life-threatening consequences. Enhanced clinical awareness and a multidisciplinary approach are crucial for improving outcomes in such complex cases.

Type B Lactic Acidosis: A Very Rare but Fatal Complication of Gastrointestinal Solid Tumor.

Type B lactic acidosis, secondary to solid cancer, is very rare. It is mostly seen in patients with hematological malignancies. Although its exact pathogenesis is unknown, it is believed to be caused by overproduction and the inability of tumor cells to remove lactate. In the last 26 years, a systematic review of the literature only identified two previous reports of colorectal cancer-related type B lactic acidosis. Here, we report the third case of severe type B lactic acidosis due to stage IV colorectal with liver metastasis. Besides, this case is unique in that serum lactate levels reaching as high as 24 mmol/L were not reported in association with colorectal cancer. In most cases, the prognosis is still very poor because there are no standardized treatment recommendations. Early chemotherapy is still the only intervention that provides some survival benefits.

Malignancy Associated Type B Lactic Acidosis: A Rare, yet Fascinating Oncological Emergency.

Type B lactic acidosis has been described infrequently in hematologic malignancies, but even less often in solid tumors. Since 1978, there have been only 58 cases of solid tumor associated Type B lactic acidosis described in the literature. Lung cancer (neuroendocrine) is the most common tumor; others frequently have a poorly/undifferentiated histology. The prognosis is dismal. Malignancy associated type B lactic acidosis is not associated with hypoxemia. The most highlighted pathogenetic mechanism is the Warburg effect (aerobic glycolysis of tumor cells causing excess lactate). We describe a patient with metastatic GI neuroendocrine carcinoma with profound lactic acidosis, who died within 24 hours. When extremely ill cancer patients present with lactic acidosis, sepsis is usually a primary concern. This case highlights the need for providers to consider malignancy associated lactic acidosis (MA-LA) in the differential diagnosis, particularly in patients with advanced malignancies, of lung origin, of neuroendocrine or poorly/undifferentiated histologic subtypes. The implications and approach are distinct from Type A/D lactic acidosis, and would involve treatment of the underlying malignancy at the earliest.

Treatment of severe metformin-associated lactic acidosis with renal replacement therapy and tris-hydroxymethyl aminomethane: a case report.

BACKGROUND: Type B lactic acidosis is a rare but serious side effect of metformin use. The risk of metformin-associated lactic acidosis is elevated in renal or liver impairment, heart failure and in metformin overdose. Metformin-associated lactic acidosis is treated with renal replacement therapy although this can be limited by metformin's large volume of distribution and a patient's hemodynamic instability. Tris-hydroxymethyl aminomethane is a buffer that rapidly equilibrates in liver cells and increases the intracellular pH of hepatocytes. Intracellular alkalosis increases lactate uptake by the liver and can promote gluconeogenesis which results in increased lactate metabolism and decreased lactate production. Unlike intravenous bicarbonate which can worsen acidosis due to carbon dioxide retention and hypocalcemia, tris-hydroxymethyl aminomethane does not generate large amounts of carbon dioxide and can improve cardiac contractility in experimental models. CASE PRESENTATION: We present a case of a 43-year-old African American male who intentionally ingested 480,000 g of metformin. He developed severe metformin-associated lactic acidosis that was refractory to 21 hours of high flux hemodialysis. This was followed by an additional 12 hours of high flux hemodialysis augmented by continuous intravenous infusion of tris-hydroxymethyl aminomethane. After initiating tris-hydroxymethyl aminomethane, the patient had rapid reversal of lactic acidosis and was weaned off vasopressors and mechanical ventilation. CONCLUSIONS: While metformin-associated lactic acidosis can be treated with renal replacement therapy, severe cases of lactic acidosis may not be amenable to renal replacement therapy alone. Through its unique buffer mechanisms, tris-hydroxymethyl aminomethane can be used in conjunction with dialysis to rapidly improve acidosis associated with metformin.

Unveiling of Type B Lactic Acidosis From Systemic Lupus Erythematosus-Associated B-cell Lymphoma: A Fatal Oncology Emergency.

Type B lactic acidosis is a rare oncological emergency usually associated with leukemia and lymphoma but also with solid malignancies. It can often go unrecognized as a possible source of lactic acidosis, leading to a delay in treatment. We review a 56-year-old woman with systemic lupus erythematosus and generalized lymphadenopathy being evaluated for underlying malignancy who presented with dyspnea, fatigue, and hematemesis. The patient was hemodynamically unstable and had severe lactic acidosis, leukocytosis, electrolyte derangements, multiple organ damage, and worsening diffuse lymphadenopathy. She was initially treated for septic shock due to acalculous cholecystitis on imaging with antibiotics and a cholecystostomy. The latter was complicated by a liver laceration requiring explorative laparotomy and open cholecystectomy, during which an excisional biopsy of the omental lymph node was done and confirmed B-cell lymphoma with marked plasmacytic differentiation. Her lactic acidosis never fully cleared despite surgery, and the refractory nature of it despite appropriate treatment of septic shock confirmed the diagnosis of type B lactic acidosis from underlying B-cell lymphoma. Chemotherapy was deferred due to the acuity of the condition. She continued to deteriorate despite aggressive management and was transitioned to comfort measures only per family request, following which she passed away. Type B lactic acidosis should be suspected in oncology patients without clinical evidence of ischemia who are not responding to fluid resuscitation and appropriate treatment of septic shock. Prompt recognition and early initiation of antineoplastic agents should be considered, when possible, to prevent adverse outcomes.

An Oncological Emergency: Severe Type B Lactic Acidosis From Warburg Effect in Diffuse Large B-cell Lymphoma.

Lactic acidosis is the most common anion gap metabolic acidosis in critically ill patients. Type B lactic acidosis is most commonly seen with hematological malignancies, especially lymphomas. It is considered an oncological emergency and is associated with high mortality and poor outcomes if not treated promptly. Here, we present the case of a 48-year-old male who developed Type B lactic acidosis secondary to newly diagnosed diffuse large B-cell lymphoma. This case highlights the importance of including Type B lactic acidosis in the differential diagnosis in a patient with unexplained lactic acidosis and hypoglycemia with otherwise vague symptoms and the need for a thorough search for quick diagnosis and early management.

Caffeine Intoxication: Unregulated, Over-the-Counter Sale of Potentially Deadly Supplements.

Caffeine is an integral part of beverages, food, and medications. Severe intoxication of caffeine is rare, and reports are even scarcer. However, over-the-counter, unregulated sale of performance-enhancing compounds, such as caffeine, turns high-dose consumption into a real concern. Severe intoxication may be fatal, usually by malignant cardiac arrhythmia. We report a case of a 23-year-old university student who accidentally consumed about 100 times the amount present in an expresso of anhydrous caffeine.

Type B lactic acidosis associated with diffuse large B-cell lymphoma and the Warburg effect.

Type B lactic acidosis is a rare complication of non-tissue perfusion abnormalities caused by solid tumors or hematologic malignancies. Herein, we present the case of a 42-year-old man with type B lactic acidosis and hypoglycemia who was found to have a diffuse large B-cell lymphoma. The cause of lactic acidosis and/or hypoglycemia is thought to be the Warburg effect, which is when the metabolic rate of a rapidly growing malignant tumor is very high and dominated by glycolysis. Systemic damage from type B lactic acidosis can occur when the increased rate of glycolysis exceeds the normal muscle and liver lactic acid clearance rate. The Warburg effect is a rare but serious condition that needs to be recognized, not only in diffuse large B-cell lymphoma, but also in other malignancies. The prognosis of lactic acidosis in patients with malignant tumors is very poor. Currently, effective chemotherapy seems to be the only hope for survival.

Albuterol-Induced Type B Lactic Acidosis: Not an Uncommon Finding.

Lactic acidosis (LA) is usually a medical emergency diagnosed by laboratory evaluation in emergency rooms (ERs) and hospital settings in critically ill patients. LA is classified into two major types based on pathophysiology; type A results from tissue hypoxia and/or hypoperfusion and type B results from deranged metabolic activity in the cells in the absence of hypoxia/hypoperfusion. Prompt evaluation and treatment are essential to prevent morbidity and mortality, especially in patients with type A LA. Most cases of LA are due to type A (hypoperfusion/hypoxia). However, with increased testing of lactic acid levels in ERs and hospitals, we are encountering a few cases of type B LA as well. Diagnosing the exact type is crucial because of differences in management. We here describe a patient with albuterol-induced type B LA, which resolved after discontinuing the albuterol breathing treatments.

A Challenging Case of Coexisting Type A and Type B Lactic Acidosis: A Case Report.

The etiology of lactic acidosis can potentially be misleading, especially in a critically ill patient with malignancy. Type B lactic acidosis represents a rare and often lethal complication of malignancy. When differentiating the types of lactic acidosis, Type A is due to marked tissue hypoperfusion and Type B is due to causes in the setting of a normal perfused state. We report the case of a 56-year-old male with newly diagnosed poorly differentiated neuroendocrine metastatic carcinoma and renal cell carcinoma who presented with a decreased level of consciousness and appetite. The patient was started on a sepsis protocol from an initial intensive care unit (ICU) admission. Broad spectrum antibiotics were initiated, and despite management, his mentation and respiratory status worsened, leading to intubation and mechanical ventilation. The patient continued to have elevated lactic acid and white count levels throughout the hospital course. After extensive workup and an ICU stay of 16 days, a decision was made to pursue comfort care measures and the patient passed away shortly thereafter. The patient's persistently elevated lactic acidosis may have resulted from the inherent malignancy. The literature mentions glycolysis with enhanced metabolism as a proposed mechanism. One theory states that these changes enable cancer cells to acquire and metabolize nutrients in a way that favors proliferation over efficient adenosine triphosphate (ATP) production, resulting in elevations of lactate production. Patients presenting to the ICU with elevated lactic acid levels need to be thoroughly worked up for all potential causes. In our case, the underlying malignancies likely caused the persistently elevated lactic acidosis, despite subtherapeutic treatment and resuscitative measures.

Persistent Lactic Acidosis: Thinking Outside the Box.

A 54-year-old male presented with possible sepsis and elevated serum lactic acid (LA) of 18.7 mmol/L. Despite the sepsis treatment protocol and the management of other causes of type A lactic acidosis, his LA remained elevated. Herein, we present a case of type B lactic acidosis in the setting of a diffuse large B cell lymphoma. The proposed mechanisms of persistent lactic acidosis in malignancy are highlighted in this case report.

Consideration of alternative causes of lactic acidosis: Thiamine deficiency in malignancy.

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 in the setting of thiamine deficiency thought to be secondary to advanced lung cancer. The purpose of this paper is to bring awareness to the clinician to consider other causes of lactic acidosis when evaluating a patient.

Thiamine Deficiency in Tropical Pediatrics: New Insights into a Neglected but Vital Metabolic Challenge.

In humans, thiamine is a micronutrient prone to depletion that may result in severe clinical abnormalities. This narrative review summarizes current knowledge on thiamine deficiency (TD) and bridges the gap between pathophysiology and clinical presentation by integrating thiamine metabolism at subcellular level with its function to vital organs. The broad clinical spectrum of TD is outlined, with emphasis on conditions encountered in tropical pediatric practice. In particular, TD is associated with type B lactic acidosis and classic forms of beriberi in children, but it is often unrecognized. Other severe acute conditions are associated with hypermetabolism, inducing a functional TD. The crucial role of thiamine in infant cognitive development is also highlighted in this review, along with analysis of the potential impact of TD in refeeding syndrome during severe acute malnutrition (SAM). This review aims to increase clinical awareness of TD in tropical settings where access to diagnostic tests is poor, and advocates for an early therapeutic thiamine challenge in resource-limited settings. Moreover, it provides evidence for thiamine as treatment in critical conditions requiring metabolic resuscitation, and gives rationale to the consideration of increased thiamine supplementation in therapeutic foods for malnourished children.

A case series of clinically undiagnosed hematopoietic neoplasms discovered at autopsy.

OBJECTIVES: In the United States, autopsy rates have diminished to less than 5% during the last half of the 20th century and the beginning of the 21st century for a multitude of reasons. Many believe this results in unrecognized malignancies that could have explained a patient's death. METHODS: We describe six deaths in which hematopoietic neoplasms were identified at autopsy but were not diagnosed clinically. RESULTS: The six undiagnosed hematopoietic malignancy cases discovered at autopsy include four men and two women ranging from 50 to 78 years of age. One patient was African American and five patients were white, all with multiple comorbidities. The tumors included diffuse large B-cell lymphoma, activated B-cell type, intravascular large B-cell lymphoma, ALK-negative anaplastic large cell lymphoma arising in a setting of human immunodeficiency virus, and a myeloid sarcoma. CONCLUSIONS: These cases illustrate the importance of the traditional postmortem examination in not only confirming clinical diagnoses but also identifying previously unknown diagnoses. Hematologic malignancies may present with nonspecific clinical manifestations, and this series of cases also emphasizes the necessity for widening the differential diagnosis in patients with unexplained lactic acidosis and hepatic failure to include hematopoietic malignancies since prompt treatment may be lifesaving.

Lactic Acidosis Associated with Acute Lymphoblastic Leukemia / 대한신장학회잡지

Occurence of lactic acidosis with adequate tissue oxygenation(type B lactic acidosis) has been described in association with leukemia, lymphoma, small cell carcinoma and breast cancer. However, no such case has been reported in Korea. Therefore, we report a case of type B lactic acidosis in a man with rapidly progressing acute lymphoblastic leukemia which had been transformed from lymphoma.