D-lactic acidosis - Revision history

Danbot: Strip excess bold

2026-03-22T09:29:45Z

Strip excess bold

Danbot: Formatting: removed excessive bold

2026-03-19T16:08:27Z

Formatting: removed excessive bold

Show changes

Ostermayer: Created page with "==Background== D-lactic acidosis (D-lactate encephalopathy) is a rare cause of '''anion gap metabolic acidosis with neurologic symptoms''' that occurs primarily in patients with '''short bowel syndrome (SBS)''' and an intact colonKowlgi NG, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. ''Gastroenterol Res Pract''. 2015;2015:476215. PMID 25977687. '''Pathophysiology:''' **Humans produce almost exclusively..."

2026-03-13T21:50:53Z

Created page with "==Background== *D-lactic acidosis (D-lactate encephalopathy) is a rare cause of '''anion gap metabolic acidosis with neurologic symptoms''' that occurs primarily in patients with '''short bowel syndrome (SBS)''' and an intact colon<ref name="kowlgi">Kowlgi NG, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. ''Gastroenterol Res Pract''. 2015;2015:476215. PMID 25977687.</ref> *'''Pathophysiology:''' **Humans produce almost exclusively..."

New page

==Background==
*D-lactic acidosis (D-lactate encephalopathy) is a rare cause of '''anion gap metabolic acidosis with neurologic symptoms''' that occurs primarily in patients with '''short bowel syndrome (SBS)''' and an intact colon<ref name="kowlgi">Kowlgi NG, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. ''Gastroenterol Res Pract''. 2015;2015:476215. PMID 25977687.</ref>
*'''Pathophysiology:'''
**Humans produce almost exclusively '''L-lactate'''; '''D-lactate''' is the mirror-image (enantiomer) produced by bacterial metabolism
**In SBS, unabsorbed carbohydrates reach the colon where they are fermented by colonic bacteria (''Lactobacillus'', ''Streptococcus bovis'', and other acid-resistant organisms) into organic acids including '''D-lactic acid'''
**The resulting acidic colonic environment further favors overgrowth of D-lactate-producing organisms → '''vicious cycle''' of escalating D-lactate production<ref name="kowlgi"/>
**Humans metabolize D-lactate much more slowly than L-lactate (via D-2-hydroxy acid dehydrogenase), so D-lactate accumulates in the blood
**D-lactate crosses the blood-brain barrier and causes neurologic dysfunction<ref name="petersen">Petersen C. D-lactic acidosis. ''Nutr Clin Pract''. 2005;20(6):634-645. PMID 16306300.</ref>
*'''Conditions associated with D-lactic acidosis:'''
**'''Short bowel syndrome''' (most common) — from surgical resection (Crohn's disease, mesenteric ischemia, volvulus, NEC, trauma), congenital abnormalities, or historical jejunoileal bypass for obesity<ref name="kowlgi"/>
**Small intestinal bacterial overgrowth (SIBO)
**Rarely: diabetes mellitus with intestinal dysmotility, chronic antibiotic use altering gut flora
*Episodes are typically precipitated by '''high carbohydrate meals''' (provides substrate for bacterial fermentation)<ref name="uribarri">Uribarri J, Oh MS, Carroll HJ. D-lactic acidosis: a review of clinical presentation, biochemical features, and pathophysiologic mechanisms. ''Medicine (Baltimore)''. 1998;77(2):73-82. PMID 9556700.</ref>
*'''The key diagnostic challenge:''' Standard laboratory L-lactate assays '''do NOT detect D-lactate''' — a normal reported "lactic acid" does not exclude D-lactic acidosis<ref name="bustos">Bustos D, Pernas JC, Perez-Ayuso E, et al. D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics. ''J Pediatr Surg''. 2004;39(2):e5. PMID 15065046.</ref>

==Clinical Features==
*Presentation is characterized by '''recurrent episodic encephalopathy''' and '''metabolic acidosis''' — typically following carbohydrate-rich meals
*'''Neurologic symptoms predominate''' (present in virtually all reported cases):<ref name="kowlgi"/>
**Altered mental status (confusion, disorientation, lethargy → stupor → coma)
**'''Slurred speech'''
**'''Ataxia and gait disturbance''' (often described as appearing "intoxicated")
**Impaired motor coordination
**Nystagmus
**Irritability, hostile/aggressive/bizarre behavior
**Weakness
**Headache
*'''GI symptoms:'''
**Nausea, vomiting
**Abdominal pain/distension (often chronic from underlying SBS)
**Diarrhea
*'''Classic pattern:''' Symptoms develop '''hours after a high-carbohydrate meal''' in a patient with known SBS, and resolve with fasting and correction of acidosis
*Neurologic symptoms may occur '''without significant acidosis''' in some cases, suggesting direct neurotoxicity of D-lactate beyond its contribution to acidosis<ref name="kowlgi"/>
*Episodes are '''recurrent''' — patients often present repeatedly before the diagnosis is made

==Differential Diagnosis==
*'''Other causes of anion gap metabolic acidosis''' (see [[Anion Gap Acidosis]]):
**[[Lactic Acidosis]] (L-lactic acid — sepsis, shock, mesenteric ischemia, seizures)
**[[Diabetic Ketoacidosis]]
**[[Toxic Alcohols]] (methanol, ethylene glycol)
**[[Salicylate Toxicity]]
**Uremia
*'''Other causes of encephalopathy in SBS patients:'''
**Thiamine deficiency ([[Wernicke encephalopathy]])
**[[Hepatic Encephalopathy]] (especially if intestinal failure–associated liver disease)
**[[Hypoglycemia]]
**Electrolyte derangements (hyponatremia, hyperammonemia)
**Medication toxicity
**[[Sepsis]] / bacteremia (SBS patients are at risk for catheter-related bloodstream infections)
**[[Mesenteric Ischemia]] (recurrent in SBS)
*'''Intoxication:''' Presentation mimics alcohol intoxication — patients may be dismissed as inebriated; '''serum ethanol level will be negative'''
*[[Ethanol Toxicity|Alcoholic ketoacidosis]]

==Evaluation==
===Workup===
*'''BMP/CMP:''' Anion gap metabolic acidosis (elevated anion gap); electrolytes, bicarbonate, BUN/creatinine, glucose
*'''ABG/VBG:''' Confirm metabolic acidosis; calculate anion gap
*'''Standard L-lactate level:''' May be normal or mildly elevated — '''a normal L-lactate in the setting of unexplained AGMA in a SBS patient should raise suspicion for D-lactic acidosis'''<ref name="kowlgi"/>
*'''D-lactate level:''' '''This is the confirmatory test'''
**Normal: < 0.25 mmol/L
**Diagnostic: > 3 mmol/L<ref name="bustos"/>
**'''This is a send-out test''' — NOT available on routine chemistry panels or point-of-care testing; results may take days
**Diagnosis must often be made clinically before results return
*'''Serum ketones:''' To exclude DKA and alcoholic ketoacidosis
*'''Serum ethanol, acetaminophen, salicylate levels:''' Exclude co-ingestants and toxic alcohols
*'''Serum osmolality and osmolar gap:''' Exclude toxic alcohol ingestion
*'''CBC:''' Leukocytosis may suggest alternative diagnosis (sepsis, ischemia)
*'''LFTs, ammonia:''' Exclude hepatic encephalopathy
*'''Thiamine level:''' Consider in malnourished SBS patients (Wernicke can coexist)
*'''Blood cultures:''' If febrile or concern for line sepsis
*'''CT abdomen:''' Consider to exclude bowel obstruction, bowel dilatation, or ischemia as alternative/contributing diagnoses

===Diagnosis===
*Diagnosis is primarily '''clinical''' — suspect D-lactic acidosis when:
**'''Anion gap metabolic acidosis''' PLUS '''encephalopathy/neurologic symptoms''' PLUS '''history of SBS or intestinal malabsorption''' PLUS '''normal or mildly elevated L-lactate'''
*The '''"lactate gap"''' — unexplained anion gap metabolic acidosis with normal L-lactate — is the hallmark laboratory clue<ref name="petersen"/>
*Confirmed by serum D-lactate > 3 mmol/L, but treatment should '''not be delayed''' pending this result
*Other organic acids (D-2-hydroxyisovaleric acid, D-2-hydroxyisocaproic acid) may contribute to the anion gap but are not routinely measured

==Management==
===Acute Treatment===
*'''NPO / fasting:''' Eliminates carbohydrate substrate for bacterial D-lactate production — '''this is the single most important acute intervention'''<ref name="kowlgi"/>
**IV fluids for hydration during fasting period
**Typically 24 hours of fasting followed by slow reintroduction of a '''low-carbohydrate diet'''
*'''IV sodium bicarbonate:''' For significant metabolic acidosis (pH < 7.2 or hemodynamically significant); correct acidosis gradually
*'''IV thiamine:''' 100 mg IV — administer empirically in all malnourished SBS patients (thiamine deficiency may coexist and mimics/worsens encephalopathy; thiamine is also a cofactor in D-lactate metabolism)<ref name="petersen"/>
*'''Enteral antibiotics:''' Target D-lactate-producing colonic flora<ref name="kowlgi"/>
**Metronidazole (oral)
**Oral vancomycin
**Oral neomycin or kanamycin
**Choice is often empiric; rotation may be needed for recurrent episodes
*'''Correct electrolyte abnormalities'''
*'''Avoid Lactated Ringer's solution''' — while LR contains only L-lactate and should not worsen D-lactic acidosis, normal saline is preferred to avoid any confusion

===Prevention of Recurrence===
*'''Low-carbohydrate diet:''' Reduce simple sugars and refined carbohydrates to limit substrate for bacterial fermentation — '''cornerstone of long-term management'''<ref name="uribarri"/>
*'''Probiotics:''' Non-D-lactate-producing strains (e.g. ''Lactobacillus rhamnosus GG'', ''Saccharomyces boulardii'') to recolonize with favorable flora — evidence is limited but promising<ref name="bustos"/>
*'''Intermittent or cycling enteral antibiotics:''' Reduce bacterial overgrowth
*'''Optimize SBS management:''' GI/nutrition consultation for intestinal rehabilitation, dietary counseling, parenteral nutrition adjustment
*'''Surgical options (refractory cases):''' Intestinal lengthening procedures, small bowel transplant, or colectomy (eliminates the site of D-lactate production — last resort)<ref name="kowlgi"/>

==Disposition==
*'''Admit:'''
**All patients with suspected or confirmed D-lactic acidosis
**Significant metabolic acidosis requiring IV bicarbonate
**Altered mental status (monitor for airway compromise)
**Inability to tolerate oral intake
**Need for IV hydration and serial lab monitoring
*'''ICU admission:'''
**Severe encephalopathy (GCS significantly depressed, inability to protect airway)
**Hemodynamic instability
**Severe acidosis (pH < 7.1)
*'''Consultations:'''
**'''GI / nutrition:''' For long-term SBS management, dietary counseling, and prevention of recurrence
**'''Medical toxicology:''' If diagnostic uncertainty regarding anion gap etiology
**'''Surgery:''' If bowel obstruction, ischemia, or surgical SBS management is being considered
*'''Discharge:'''
**Once neurologic symptoms have fully resolved, acidosis has corrected, and patient tolerates oral low-carbohydrate diet
**Arrange close GI follow-up
**Provide dietary counseling: avoid high-sugar/high-carbohydrate meals
**Educate patient/family on recognition of recurrent episodes and need for early ED presentation
*'''Prognosis:''' With appropriate treatment, acute episodes typically resolve within '''24–48 hours''' of fasting and supportive care; long-term prognosis depends on the underlying SBS and dietary adherence<ref name="kowlgi"/>

==See Also==
*[[Lactic Acidosis]]
*[[Anion gap acidosis]]
*[[Metabolic Acidosis]]
*[[Altered mental status]]
*[[Wernicke encephalopathy]]
*[[Short bowel syndrome]]
*[[Acid-Base Disorders]]

==External Links==
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC4421027/ D-lactic acidosis: an underrecognized complication of short bowel syndrome - Gastroenterol Res Pract 2015]
*[https://pubmed.ncbi.nlm.nih.gov/9556700/ D-lactic acidosis: review of clinical presentation, biochemical features, and pathophysiologic mechanisms - Medicine 1998]
*[https://pubmed.ncbi.nlm.nih.gov/16306300/ D-lactic acidosis - Nutr Clin Pract 2005]
*[https://pubmed.ncbi.nlm.nih.gov/15065046/ D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics - J Pediatr Surg 2004]
*[https://www.mayoclinicproceedings.org/article/S0025-6196(11)63729-4/fulltext D-lactic acidosis: pathologic consequence of saprophytism - Mayo Clin Proc 1998]

==References==
<references/>

[[Category:FEN]] [[Category:GI]] [[Category:Heme/Onc]]

← Older revision		Revision as of 09:29, 22 March 2026
Line 1:		Line 1:
	==Background==		==Background==
	*D-lactic acidosis (D-lactate encephalopathy) is a rare cause of ~~'''~~anion gap metabolic acidosis with neurologic symptoms~~'''~~ that occurs primarily in patients with ~~'''~~short bowel syndrome (SBS)~~'''~~ and an intact colon<ref name="kowlgi">Kowlgi NG, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. ''Gastroenterol Res Pract''. 2015;2015:476215. PMID 25977687.</ref>		*D-lactic acidosis (D-lactate encephalopathy) is a rare cause of anion gap metabolic acidosis with neurologic symptoms that occurs primarily in patients with short bowel syndrome (SBS) and an intact colon<ref name="kowlgi">Kowlgi NG, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. ''Gastroenterol Res Pract''. 2015;2015:476215. PMID 25977687.</ref>
	*Pathophysiology:		*Pathophysiology:
	**Humans produce almost exclusively ~~'''~~L-lactate~~'''~~; ~~'''~~D-lactate~~'''~~ is the mirror-image (enantiomer) produced by bacterial metabolism		**Humans produce almost exclusively L-lactate; D-lactate is the mirror-image (enantiomer) produced by bacterial metabolism
	**In SBS, unabsorbed carbohydrates reach the colon where they are fermented by colonic bacteria (''Lactobacillus'', ''Streptococcus bovis'', and other acid-resistant organisms) into organic acids including ~~'''~~D-lactic acid~~'''~~		**In SBS, unabsorbed carbohydrates reach the colon where they are fermented by colonic bacteria (''Lactobacillus'', ''Streptococcus bovis'', and other acid-resistant organisms) into organic acids including D-lactic acid
	**The resulting acidic colonic environment further favors overgrowth of D-lactate-producing organisms → ~~'''~~vicious cycle~~'''~~ of escalating D-lactate production<ref name="kowlgi"/>		**The resulting acidic colonic environment further favors overgrowth of D-lactate-producing organisms → vicious cycle of escalating D-lactate production<ref name="kowlgi"/>
	**Humans metabolize D-lactate much more slowly than L-lactate (via D-2-hydroxy acid dehydrogenase), so D-lactate accumulates in the blood		**Humans metabolize D-lactate much more slowly than L-lactate (via D-2-hydroxy acid dehydrogenase), so D-lactate accumulates in the blood
	**D-lactate crosses the blood-brain barrier and causes neurologic dysfunction<ref name="petersen">Petersen C. D-lactic acidosis. ''Nutr Clin Pract''. 2005;20(6):634-645. PMID 16306300.</ref>		**D-lactate crosses the blood-brain barrier and causes neurologic dysfunction<ref name="petersen">Petersen C. D-lactic acidosis. ''Nutr Clin Pract''. 2005;20(6):634-645. PMID 16306300.</ref>
Line 11:		Line 11:
	**Small intestinal bacterial overgrowth (SIBO)		**Small intestinal bacterial overgrowth (SIBO)
	**Rarely: diabetes mellitus with intestinal dysmotility, chronic antibiotic use altering gut flora		**Rarely: diabetes mellitus with intestinal dysmotility, chronic antibiotic use altering gut flora
	*Episodes are typically precipitated by ~~'''~~high carbohydrate meals~~'''~~ (provides substrate for bacterial fermentation)<ref name="uribarri">Uribarri J, Oh MS, Carroll HJ. D-lactic acidosis: a review of clinical presentation, biochemical features, and pathophysiologic mechanisms. ''Medicine (Baltimore)''. 1998;77(2):73-82. PMID 9556700.</ref>		*Episodes are typically precipitated by high carbohydrate meals (provides substrate for bacterial fermentation)<ref name="uribarri">Uribarri J, Oh MS, Carroll HJ. D-lactic acidosis: a review of clinical presentation, biochemical features, and pathophysiologic mechanisms. ''Medicine (Baltimore)''. 1998;77(2):73-82. PMID 9556700.</ref>
	*The key diagnostic challenge: Standard laboratory L-lactate assays '''do NOT detect D-lactate''' — a normal reported "lactic acid" does not exclude D-lactic acidosis<ref name="bustos">Bustos D, Pernas JC, Perez-Ayuso E, et al. D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics. ''J Pediatr Surg''. 2004;39(2):e5. PMID 15065046.</ref>		*The key diagnostic challenge: Standard laboratory L-lactate assays '''do NOT detect D-lactate''' — a normal reported "lactic acid" does not exclude D-lactic acidosis<ref name="bustos">Bustos D, Pernas JC, Perez-Ayuso E, et al. D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics. ''J Pediatr Surg''. 2004;39(2):e5. PMID 15065046.</ref>

	==Clinical Features==		==Clinical Features==
	*Presentation is characterized by ~~'''~~recurrent episodic encephalopathy~~'''~~ and ~~'''~~metabolic acidosis~~'''~~ — typically following carbohydrate-rich meals		*Presentation is characterized by recurrent episodic encephalopathy and metabolic acidosis — typically following carbohydrate-rich meals
	*Neurologic symptoms predominate (present in virtually all reported cases):<ref name="kowlgi"/>		*Neurologic symptoms predominate (present in virtually all reported cases):<ref name="kowlgi"/>
	**Altered mental status (confusion, disorientation, lethargy → stupor → coma)		**Altered mental status (confusion, disorientation, lethargy → stupor → coma)
Line 29:		Line 29:
	**Abdominal pain/distension (often chronic from underlying SBS)		**Abdominal pain/distension (often chronic from underlying SBS)
	**Diarrhea		**Diarrhea
	*Classic pattern: Symptoms develop ~~'''~~hours after a high-carbohydrate meal~~'''~~ in a patient with known SBS, and resolve with fasting and correction of acidosis		*Classic pattern: Symptoms develop hours after a high-carbohydrate meal in a patient with known SBS, and resolve with fasting and correction of acidosis
	*Neurologic symptoms may occur ~~'''~~without significant acidosis~~'''~~ in some cases, suggesting direct neurotoxicity of D-lactate beyond its contribution to acidosis<ref name="kowlgi"/>		*Neurologic symptoms may occur without significant acidosis in some cases, suggesting direct neurotoxicity of D-lactate beyond its contribution to acidosis<ref name="kowlgi"/>
	*Episodes are ~~'''~~recurrent~~'''~~ — patients often present repeatedly before the diagnosis is made		*Episodes are recurrent — patients often present repeatedly before the diagnosis is made

	==Differential Diagnosis==		==Differential Diagnosis==
Line 48:		Line 48:
	**[[Sepsis]] / bacteremia (SBS patients are at risk for catheter-related bloodstream infections)		**[[Sepsis]] / bacteremia (SBS patients are at risk for catheter-related bloodstream infections)
	**[[Mesenteric Ischemia]] (recurrent in SBS)		**[[Mesenteric Ischemia]] (recurrent in SBS)
	*Intoxication: Presentation mimics alcohol intoxication — patients may be dismissed as inebriated; ~~'''~~serum ethanol level will be negative~~'''~~		*Intoxication: Presentation mimics alcohol intoxication — patients may be dismissed as inebriated; serum ethanol level will be negative
	*[[Ethanol Toxicity\|Alcoholic ketoacidosis]]		*[[Ethanol Toxicity\|Alcoholic ketoacidosis]]

Line 55:		Line 55:
	*BMP/CMP: Anion gap metabolic acidosis (elevated anion gap); electrolytes, bicarbonate, BUN/creatinine, glucose		*BMP/CMP: Anion gap metabolic acidosis (elevated anion gap); electrolytes, bicarbonate, BUN/creatinine, glucose
	*ABG/VBG: Confirm metabolic acidosis; calculate anion gap		*ABG/VBG: Confirm metabolic acidosis; calculate anion gap
	*Standard L-lactate level: May be normal or mildly elevated — ~~'''~~a normal L-lactate in the setting of unexplained AGMA in a SBS patient should raise suspicion for D-lactic acidosis~~'''~~<ref name="kowlgi"/>		*Standard L-lactate level: May be normal or mildly elevated — a normal L-lactate in the setting of unexplained AGMA in a SBS patient should raise suspicion for D-lactic acidosis<ref name="kowlgi"/>
	*D-lactate level: ~~'''~~This is the confirmatory test~~'''~~		*D-lactate level: This is the confirmatory test
	**Normal: < 0.25 mmol/L		**Normal: < 0.25 mmol/L
	**Diagnostic: > 3 mmol/L<ref name="bustos"/>		**Diagnostic: > 3 mmol/L<ref name="bustos"/>
Line 71:		Line 71:

	===Diagnosis===		===Diagnosis===
	*Diagnosis is primarily ~~'''~~clinical~~'''~~ — suspect D-lactic acidosis when:		*Diagnosis is primarily clinical — suspect D-lactic acidosis when:
	**Anion gap metabolic acidosis PLUS ~~'''~~encephalopathy/neurologic symptoms~~'''~~ PLUS ~~'''~~history of SBS or intestinal malabsorption~~'''~~ PLUS ~~'''~~normal or mildly elevated L-lactate~~'''~~		**Anion gap metabolic acidosis PLUS encephalopathy/neurologic symptoms PLUS history of SBS or intestinal malabsorption PLUS normal or mildly elevated L-lactate
	*The ~~'''~~"lactate gap"~~'''~~ — unexplained anion gap metabolic acidosis with normal L-lactate — is the hallmark laboratory clue<ref name="petersen"/>		*The "lactate gap" — unexplained anion gap metabolic acidosis with normal L-lactate — is the hallmark laboratory clue<ref name="petersen"/>
	*Confirmed by serum D-lactate > 3 mmol/L, but treatment should ~~'''~~not be delayed~~'''~~ pending this result		*Confirmed by serum D-lactate > 3 mmol/L, but treatment should not be delayed pending this result
	*Other organic acids (D-2-hydroxyisovaleric acid, D-2-hydroxyisocaproic acid) may contribute to the anion gap but are not routinely measured		*Other organic acids (D-2-hydroxyisovaleric acid, D-2-hydroxyisocaproic acid) may contribute to the anion gap but are not routinely measured

	==Management==		==Management==
	===Acute Treatment===		===Acute Treatment===
	*NPO / fasting: Eliminates carbohydrate substrate for bacterial D-lactate production — ~~'''~~this is the single most important acute intervention~~'''~~<ref name="kowlgi"/>		*NPO / fasting: Eliminates carbohydrate substrate for bacterial D-lactate production — this is the single most important acute intervention<ref name="kowlgi"/>
	**IV fluids for hydration during fasting period		**IV fluids for hydration during fasting period
	**Typically 24 hours of fasting followed by slow reintroduction of a ~~'''~~low-carbohydrate diet~~'''~~		**Typically 24 hours of fasting followed by slow reintroduction of a low-carbohydrate diet
	*IV sodium bicarbonate: For significant metabolic acidosis (pH < 7.2 or hemodynamically significant); correct acidosis gradually		*IV sodium bicarbonate: For significant metabolic acidosis (pH < 7.2 or hemodynamically significant); correct acidosis gradually
	*IV thiamine: 100 mg IV — administer empirically in all malnourished SBS patients (thiamine deficiency may coexist and mimics/worsens encephalopathy; thiamine is also a cofactor in D-lactate metabolism)<ref name="petersen"/>		*IV thiamine: 100 mg IV — administer empirically in all malnourished SBS patients (thiamine deficiency may coexist and mimics/worsens encephalopathy; thiamine is also a cofactor in D-lactate metabolism)<ref name="petersen"/>
Line 90:		Line 90:
	**Choice is often empiric; rotation may be needed for recurrent episodes		**Choice is often empiric; rotation may be needed for recurrent episodes
	*Correct electrolyte abnormalities		*Correct electrolyte abnormalities
	*~~'''~~Avoid Lactated Ringer's solution~~'''~~ — while LR contains only L-lactate and should not worsen D-lactic acidosis, normal saline is preferred to avoid any confusion		*Avoid Lactated Ringer's solution — while LR contains only L-lactate and should not worsen D-lactic acidosis, normal saline is preferred to avoid any confusion

	===Prevention of Recurrence===		===Prevention of Recurrence===
	*Low-carbohydrate diet: Reduce simple sugars and refined carbohydrates to limit substrate for bacterial fermentation — ~~'''~~cornerstone of long-term management~~'''~~<ref name="uribarri"/>		*Low-carbohydrate diet: Reduce simple sugars and refined carbohydrates to limit substrate for bacterial fermentation — cornerstone of long-term management<ref name="uribarri"/>
	*Probiotics: Non-D-lactate-producing strains (e.g. ''Lactobacillus rhamnosus GG'', ''Saccharomyces boulardii'') to recolonize with favorable flora — evidence is limited but promising<ref name="bustos"/>		*Probiotics: Non-D-lactate-producing strains (e.g. ''Lactobacillus rhamnosus GG'', ''Saccharomyces boulardii'') to recolonize with favorable flora — evidence is limited but promising<ref name="bustos"/>
	*Intermittent or cycling enteral antibiotics: Reduce bacterial overgrowth		*Intermittent or cycling enteral antibiotics: Reduce bacterial overgrowth
Line 119:		Line 119:
	**Provide dietary counseling: avoid high-sugar/high-carbohydrate meals		**Provide dietary counseling: avoid high-sugar/high-carbohydrate meals
	**Educate patient/family on recognition of recurrent episodes and need for early ED presentation		**Educate patient/family on recognition of recurrent episodes and need for early ED presentation
	*Prognosis: With appropriate treatment, acute episodes typically resolve within ~~'''~~24–48 hours~~'''~~ of fasting and supportive care; long-term prognosis depends on the underlying SBS and dietary adherence<ref name="kowlgi"/>		*Prognosis: With appropriate treatment, acute episodes typically resolve within 24–48 hours of fasting and supportive care; long-term prognosis depends on the underlying SBS and dietary adherence<ref name="kowlgi"/>

	==See Also==		==See Also==