Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACIDOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed2006

Impact of chloride balance in acidosis control: the Stewart approach in hemodialysis critically ill patients.

BACKGROUND: Metabolic acidosis is highly prevalent in critically ill patients with acute renal failure. Little is known about the mechanisms by which renal replacement therapy intervenes in such cases. The objective of this study is to analyze the role of hemodialysis in acidosis correction in intensive care unit patients, with an emphasis on chloride levels in plasma and dialysate. METHODS: We studied 19 intermittent hemodialysis procedures in 17 acidotic patients. The patients were grouped by procedure type (conventional or sustained low-efficiency dialysis) and by predialysis plasma chloride level (higher or lower than the dialysate chloride concentration). Immediately before and after each procedure, blood samples were collected for biochemical analysis. The Stewart method was used to calculate the strong ion difference and strong ion gap. RESULTS: The patients presented acidosis related to hyperchloremia, hyperphosphatemia, and high unmeasured anions. Hypoalbuminemia had an alkalinizing effect. Hemodialysis corrected acidosis mainly by reducing phosphate and unmeasured anions. In the group as a whole, chloride levels did not change after dialysis. However, when analyzed according to predialysis plasma chloride, the high-chloride group presented a reduction in plasma chloride, resulting in better base excess improvement (Delta standard base excess) than in the low-chloride group. Among the determinants of acid-base status, the only factors correlating with Delta SBE were Delta strong ion gap and Delta chloride. CONCLUSION: The serum chloride/dialysate chloride relationship during hemodialysis has an important impact on acidosis control.

Acidosis↗
PubMed2005

Lactic acidosis stimulates ganglioside and ceramide generation without sphingomyelin hydrolysis in rat cortical astrocytes.

Acidosis is a ubiquitous feature of cerebral ischemia, and triggers a cascade of biochemical events that results in neuronal injury. The purpose of this study was to evaluate the effects of lactic acidosis on the ganglioside composition, the ceramide and sphingomyelin (SM) levels in rat cortical astrocytes. Primary astrocyte cultures were exposed to lactic acid (pH 5.5) for 2, 5 and 17 h, and cell death was evaluated at each time point. Gangliosides, ceramides and SM were analyzed by high-performance thin layer chromatography. Lactic acidosis caused a progressive increase of both GM3 and GD3 gangliosides up to 5 h of treatment. However, at 17 h of acidosis, GM3 tented to return to the normal level whereas GD3 accumulated. Additionally, ceramides were gradually generated, whereas no significant decrease of SM occured for 17 h of acidosis. These results suggest that ceramides were not produced by the breakdown of SM and may be served as metabolic precursor for the biosynthesis of GM3 and GD3. Since these lipids are important messengers of the adaptative responses to stress, accumulation of sphingolipids triggered by lactic acid exposure of astrocytes might play an important role in determining the outcomes of injurious processes.

Acidosis, Lactic↗
PubMed1981

The probability of fetal metabolic acidosis during labor in a population at risk as determined by clinical factors.

The clinical data derived from 2,772 pregnancies managed in an intrapartum intensive care unit have been analyzed to establish which criteria will indicate in a more definite manner the probability that fetal metabolic acidosis will occur during labor and delivery. All antepartum and intrapartum clinical factors indicate a pregnancy and fetus with an increased probability of fetal metabolic acidosis. However, there is a remarkably consistent relationship between decreasing fetal weight in each week of gestational age and in increasing probability of fetal metabolic acidosis that will permit the magnitude of the risk to be determined with greater precision. The following clinical guidelines are proposed: (1) Current antepartum and intrapartum risk factors are appropriate for the selection of patients for intrapartum intensive care. (2) An accurate gestational age and an estimate of fetal weight within 200 gm will provide an indication of the probability of fetal metabolic acidosis in the individual fetus ranging from 15% to 50%. (3) The presence of meconium in the amniotic fluid increases the probability of metabolic acidosis as defined by fetal weight in relation to gestational age.

Acidosis↗
PubMed1998

Fetal oxygen saturation and fractional extraction at birth and the relationship to measures of acidosis.

OBJECTIVE: We sought to determine umbilical cord oxygen saturation and fractional oxygen extraction values as measured at birth for a large tertiary hospital population and their predictive value for measures of acidosis. STUDY DESIGN: The computerized perinatal database of St. Joseph's Health Centre, London, Ontario, was used to obtain the umbilical cord gases, pH, mode of delivery, gestational age at delivery, and nuchal cord status for all live-born infants >500 gm between January 1991 and December 1995 (n = 22,134). Oxygen saturation values were calculated from the umbilical cord PO2 and pH data with a previously derived empirical equation, the accuracy of which was rechecked with 100 consecutive cord blood samples where oxygen saturation values were both calculated and measured with a hemoximeter (r = 0.99, p = 0.001). Fractional oxygen extraction values were calculated from the umbilical cord oxygen saturation data. RESULTS: There were 18,250 "validated" paired umbilical vein and artery blood gas and pH results available for analysis after patient case exclusions for missing, unreliable, or "unphysiologic" data. For all validated patient cases, mean umbilical vein oxygen saturation was 63% +/- 16% (SD), mean umbilical artery oxygen saturation was 24% +/- 15%, and mean fractional oxygen extraction was 0.62 +/- 0.20, with all three of these parameters significantly affected by mode of delivery, gestational age at delivery, and nuchal cord status. Umbilical vein and artery oxygen saturation and fractional oxygen extraction values showed significant relationships with umbilical artery base excess, albeit weak (r = 0.18 to 0.22), and pH (r = 0.46), which were best described using cubic regression models. Receiver-operator characteristic curve statistics for the prediction of acidosis at birth were also significant for all three of these parameters but lower when predicting metabolic versus mixed acidosis. However, all showed a poor positive predictive value for significant acidosis at birth, whether metabolic or mixed and regardless of the cutoff values used. CONCLUSION: Umbilical cord oxygen saturation and fractional oxygen extraction values as measured at birth for a large tertiary hospital population indicate a decreased oxygen margin of safety for infants born postterm, by cesarean section after labor, and with a nuchal cord. However, these values have a limited relationship to measures of acidosis, which may have clinical implications for the usefulness of intrapartum pulse oximetry.

Acidosis↗
PubMed2000

Effects of acidosis on the post-hypoxic recovery of synaptic transmission in gerbil hippocampal slices.

We investigated the effects of acidosis on the hypoxic neuronal damage using gerbil hippocampal slices. Acidosis has delayed the onset of harmful hypoxic depolarization, resulting in a decrease in the total hypoxic period and the hypoxic depolarization. This effect has been considered to be protective. However, the synaptic recovery after reoxygenation was attenuated when acidosis (pH: 6.2-6.9) was sustained. Conversely, the synaptic recovery was potentiated when the acidosis was restored to the physiological milieu during the reoxygenation period. These results suggest that acidosis plays a protective effect against the hypoxic neuronal damage only when rapid appreciable pH recovery is achieved during reoxygenation.

Acidosis↗
PubMed1998

The cardiac adrenergic system in ischaemia: differential role of acidosis and energy depletion.

OBJECTIVE: Acute myocardial ischaemia has been shown to modulate the beta-adrenergic system and to activate protein kinase C. The aim of this study was to investigate if two important components of ischaemia, i.e. energy depletion or acidosis, may contribute to these changes. METHODS: Isolated rat hearts were perfused either with anoxia (in the absence of oxygen) or with cyanide in the absence of glucose as models of energy depletion with a loss of high energy phosphates. Alternatively, isolated hearts were perfused with acidic modified Krebs-Henseleit solution to induce acidosis. RESULTS: Energy depletion induced by cyanide perfusion leads to an increase of beta-adrenergic receptors (81 +/- 7 vs. 50 +/- 3 fmol/mg protein, p < or = 0.05) comparable to the changes observed in ischaemia, yet without any change of total adenylyl cyclase activity or protein kinase C activity. Similar, yet less pronounced changes were induced by anoxic perfusion. Acidic perfusion, in contrast, promotes a translocation of protein kinase C to the plasma membranes, suggesting its rapid activation. Additionally, an increased total forskolin-stimulated activity of adenylyl cyclase (515 +/- 16 vs. 428 +/- 17 pmol/min/mg, p < or = 0.05) was observed. Both were comparable to the sensitization observed in early ischaemia. In acidosis, the density of beta-adrenergic receptors remained unaltered. CONCLUSIONS: These data suggest that the regulation of cardiac beta-adrenergic receptors is susceptible to energy depletion, but not to acidosis, whereas the intracellular enzymes both adenylyl cyclase and protein kinase C may be regulated by intracellular acidosis. This is the first differentiation of distinct components of ischaemia modulating the beta-adrenergic signal transduction pathway. Both components may be operative in concert in acute myocardial ischaemia and may contribute to the regulation of these components of signal transduction observed in acute ischaemia.

Acidosis↗
PubMed1984

Renal tubular acidosis does not alter circulating values of calcitriol.

In 10 patients with renal tubular acidosis, seven with type I and three with Fanconi syndrome, simultaneous measurements of vitamin D metabolites and electrolytes were made. No marked abnormalities of calcidiol2, calcidiol3, 24,25(OH)2D, or calcitriol were found in these patients, whose mean serum HCO3 was 18 +/- 3 mM/L (SD). Further, no relationship between serum HCO3 and calcitriol could be found. These results suggest that either vitamin D deficiency may be required before any alterations in the production of calcitriol are seen, or that the effects of acidosis in animals may not be reflected in humans. Further, it appears less likely that the bone disease found in renal tubular acidosis is related to abnormalities in vitamin D metabolism resulting from systemic acidosis, but that bone disease is more likely related to the acidosis and hypercalcuria prevalent in this disorder.

Acidosis, Renal Tubular↗
PubMed1987

Effects of bicarbonate on arterial and brain intracellular pH in neonatal rabbits recovering from hypoxic lactic acidosis.

We used 31P spectroscopy to determine whether administration of a neutralizing dose of bicarbonate in rabbits with lactic acidosis caused a paradoxical brain intracellular acidosis. Ten 10- to 16-day-old rabbits were anesthetized with 0.75% halothane/oxygen and their lungs mechanically ventilated. Metabolic acidosis was induced by decreasing PaO2 to 25 to 35 mm Hg for 1 to 2 hours until the base deficit was 10 to 15 mEq/L. Cerebral ischemia was prevented by maintaining arterial blood pressure at +/- 20% of control value with a venous infusion of epinephrine. Hypoxia was then terminated by administration of 100% oxygen, which was continued for the remainder of the study. After 15 minutes 100% oxygen, 5 mEq/kg 4.2% bicarbonate was administered to five animals; 5 minutes later the same dose was repeated. Control rabbits were given equal volumes of saline solution. In all animals, arterial pH decreased from 7.43 +/- 0.06 to 7.25 +/- 0.08 (SE) during hypoxia, and brain intracellular pH from 7.22 +/- 0.06 to 7.09 +/- 0.09 (SE). Both pH values remained low during reoxygenation. Bicarbonate administration normalized arterial pH (7.41 +/- 0.03), whereas treatment with saline solution did not (7.23 +/- 0.01, P less than 0.05). PaCO2 rapidly increased by 10 mm Hg in the bicarbonate group, and remained elevated; it was unaffected by saline solution administration. Brain intracellular pH in the bicarbonate group increased by 0.12 U over 40 minutes, but intracellular pH in the saline solution group decreased 0.05 pH U (P less than 0.05) over the same period. We conclude that administering a total dose of 10 mEq/kg sodium bicarbonate to neonatal rabbits recovering from hypoxic lactic acidosis increases arterial pH, brain intracellular pH, and PaCO2; it does not produce paradoxical intracellular acidosis in the brain.

Acidosis, Lactic↗
PubMed2003

Increased tissue oxygen extraction and acidosis with progressive severity of sepsis.

BACKGROUND: Lactic acidosis and increased production of CO(2) are common in septic shock. Presumably, both acidosis and CO(2) enhance the release of oxygen from hemoglobin. The purpose of this study was to assess the relationship of oxygen utilization, CO(2) production, acidosis, and hemoglobin oxygen (Hgb-O(2)) dissociation with progressive severity of sepsis to shock. MATERIALS AND METHODS: Femoral arterial and vein, hepatic vein, portal vein, and pulmonary artery catheters were placed in 16 anesthetized swine. Organ blood flow was determined by timed injections of colored microspheres. After baseline measurements, Pseudomonas aeruginosa was infused in eight animals. This bacterial slurry was continued inciting a progression of sepsis to shock. Eight animals served as instrumented controls. RESULTS: With sepsis and shock, there was a progressive decrease in pH and an increase in pCO(2) in plasma with all sampling sites (P < 0.01 septic shock versus baseline versus control). Blood flow to the liver and intestines increased with sepsis (P < 0.01) but then returned to near baseline control values during shock. VO(2) and/or percent O(2) extraction increased with sepsis and septic shock for the whole body and for the liver, intestine and leg (P < 0.01). There was a strong correlation between venous O(2) saturation, acidosis, and pCO(2) to percent O(2) extraction (r > 60; P < 0.0001). However, calculated P(50) values for Hgb-O(2) dissociation remained unchanged. CONCLUSIONS: This study demonstrates that increased oxygen extraction in severe sepsis is related to a fall in tissue oxygen availability and not related to any allosteric change in Hgb-O(2) dissociation. Therefore, acidosis and hypercapnia do not have a demonstrable effect on altering oxygen availability during sepsis.

Acid-Base Equilibrium↗
PubMed1988

Metabolic acidosis after bladder replacement: comparison of severity and reversibility in ileal and colonic reservoirs.

Metabolic acidosis developed frequently after ureterosigmoidostomy and rectosigmoid bladder construction but has been reported rarely after the newer methods of continent urinary diversion which also employ intestinal reservoirs. We created an animal model in which to compare the metabolic effects of bladder replacement with segments of ileum or colon and the potential for reversing these derangements with nicotinic acid and chlorpromazine. One year after six dogs' bladders were replaced by colon (three) or ileum (three), all dogs appeared in excellent health and were free of urinary tract obstruction and clinical infection. Both groups of dogs were severely acidotic with diminished arterial pH and arterial and venous total CO2 concentrations although normal serum electrolytes and creatinine concentrations were maintained. Both groups of dogs absorbed approximately one half the urinary sodium, chloride and urea presented to their intestinal reservoirs. After treatment with nicotinic acid and chlorpromazine, the metabolic status of both groups of animals improved. Although nicotinic acid reduced urinary excretion of electrolytes more effectively than chlorpromazine, nicotinic acid was not more effective for reversing metabolic acidosis. When nicotinic acid was provided as an adjunct to sodium bicarbonate therapy in two animals acidosis was corrected at reduced doses of sodium bicarbonate. Based upon this work in an animal model, there does not appear to be a metabolic advantage to intestinal reservoirs which incorporate ileum versus colon. However, asymptomatic patients with normal serum electrolytes and creatinine concentrations may be acidotic. The effects of long term mild acidosis are unknown. However, if therapy is required to prevent diminution of whole body buffers or changes in bone density specific therapy with nicotinic acid or chlorpromazine may reduce the requirement for alkali for correction of metabolic acidosis.

Acidosis↗
PubMed1980

A case of incomplete renal tubular acidosis (type 1) associated with medullary sponge kidney followed by nephrocalcinosis.

A case is reported of incomplete renal tubular acidosis (type 1) associated with medullary sponge kidney followed by nephrocalcinosis. Although several cases of classic renal tubular acidosis associated with medullary sponge kidney have been documented a case of incomplete renal tubular acidosis associated with medullary sponge kidney seems to be rare. We recommend examination for incomplete renal tubular acidosis in patients with medullary sponge kidney and nephrocalcinosis without systemic acidosis.

Acidosis, Renal Tubular↗
PubMed1983

The acidosis of chronic renal failure.

The acidosis of chronic renal failure is not due to bicarbonate wastage per se; rather, bicarbonate reabsorption per nephron is markedly enhanced. The ability to lower the urine pH is preserved. While overall ammonium production may be decreased in chronic renal failure, both ammonium production and excretion are markedly increased when expressed per remaining nephron. Titratable acid excretion in chronic renal failure is essentially maximal, owing to the effect of parathyroid hormone on phosphate excretion by the kidney. Thus, it appears that the acidosis of chronic renal failure is solely the consequence of the reduction in functional renal mass. Extrarenal buffering may contribute substantially to the maintenance of a near normal acid-base status in patients with marked reduction in glomerular filtration rate. That homeostasis is so well preserved until glomerular filtration rate falls to approximately 10 per cent of normal is remarkable; the price, however, may be considerable. Prolonged acidosis may magnify the tendency of renal failure to cause osteodystrophy. An obvious treatment for the acidosis of renal failure is exogenous alkali therapy. Most clinicians withhold alkali therapy until the bicarbonate concentration falls below 20 mEq per L. If the acidosis cannot be safely corrected with exogenous therapy, dialysis should be initiated.

Acidosis↗
PubMed2000

Low fetal oxygen saturation at birth and acidosis.

OBJECTIVE: To measure umbilical cord blood oxygen saturation, to calculate preductal oxygen saturation at birth, and to assess its predictive value for acidosis. METHODS: Umbilical cord blood samples of 1537 live-born singleton neonates were analyzed. Oxygen saturation was measured by spectrophotometry; pH and base excess were measured by a pH and blood gas analyzer. Preductal oxygen saturation was calculated with an empirical equation. Acidosis was defined as 2 standard deviations (SDs) below the mean of umbilical artery (UA) pH or base excess (7.09 and -10.50 mmol/L, respectively). The predictive value for acidosis of UA and umbilical vein (UV) oxygen saturation and calculated preductal oxygen saturation was determined with receiver operating characteristic curves. RESULTS: The mean values (+/-SD) of UV, UA, and calculated preductal oxygen saturation were 52 +/- 18%, 26 +/- 17%, and 31 +/- 16%, respectively. Forty-seven neonates had UA pH less than 7.09 and 60 had UA base excess less than -10.50 mmol/L. The UV, UA, and calculated preductal oxygen saturation showed considerably weaker relations to UA base excess (multiple r(2) =.056,.003, and.017, respectively; P <.001) than to UA pH (multiple r(2) =.112,.126, and.148, respectively; P <. 001). Receiver operating characteristic areas under the curve were higher when predicting low pH compared with low base excess (for UV, UA, and calculated preductal oxygen saturation: 0.716 versus 0.699, 0.747 versus 0.586, and 0.765 versus 0.628, respectively). The difference was significant for UA oxygen saturation (P <.05). All tests showed high sensitivity and negative predictive values, but low specificity and positive predictive values. CONCLUSION: Low fetal oxygen saturation measured at birth seemed to be associated with low fetal pH and base excess values, but its predictive value for acidosis in an unselected population was limited, particularly if acidosis was metabolic.

Acidosis↗
PubMed2001

Ventilatory response in metabolic acidosis and cerebral blood volume in humans.

The relationship between alterations in cerebral blood volume (CBV) and central chemosensitivity regulation was studied under neutral metabolic conditions and during metabolic acidosis. Fifteen healthy subjects (56+/-10 years) were investigated. To induce metabolic acidosis, ammonium chloride (NH(4)Cl) was given orally. CBV was measured using Near Infrared Spectroscopy during normo- and hypercapnia and related to inspired ventilation (V(i)). A mean acute metabolic acidosis of Delta pH - 0.04 was realized with a mean decreased arterialized capillary PCO(2) (P(c)CO(2)) of 0.20 kPa (1.5 mmHg) (both P<0.001). During normocapnia, CBV was 3.51+/-0.71 and 3.65+/-0.56 ml 100 g(-1) (mean+/-S.D.), measured under neutral metabolic conditions and during acute metabolic acidosis, respectively (ns). Corresponding values of V(i) were 7.6+/-1.4 and 10.0+/-2.4 l min(-1) (P<0.01), respectively. The slopes of the CO(2)-responsiveness (DeltaCBV/DeltaP(c)CO(2) and DeltaV(i)/DeltaP(c)CO(2)), were not significantly different during both metabolic conditions. A significant correlation between DeltaCBV/DeltaP(c)CO(2) and DeltaV(i)/DeltaP(c)CO(2) was found during metabolic acidosis (P<0.01), but not under neutral metabolic conditions. CBV does not contribute in a predictable way to the regulation of central chemoreceptors.

Acidosis↗
PubMed2001

Acidosis modifies metabolic functions but does not affect vascular resistances in perfused rat livers.

BACKGROUND: Few data exist concerning the consequences of acidosis on intrahepatic vascular resistances and hepatic functions. METHODS: The consequences of pH and PCO2 changes on the intrahepatic vascular reactivity to norepinephrine (NE, 10(-9) to 3 x 10(-5) M) have been investigated in isolated rat livers perfused with solutions bubbled with 5, 10, or 15% CO2 and in solutions in which pH was decreased by replacing HCO3- with NaCl while maintaining a normal PCO2. Hepatic O2 consumption (VO2) and urea release were also measured during these experiments. RESULTS: The NE-induced increase of portal pressure did not change during hypercarbic and normocarbic acidosis. In contrast, the NE-induced increase of urea release was higher when the solution of perfusion was bubbled with 10 and 15% CO2, while during normocarbic acidosis the NE-induced increase of urea release did not change with pH. In the absence of NE, acidosis decreased hepatic VO2 and urea release but portal pressure was not modified by changing % CO2 or pH in the Krebs-Henseleit-bicarbonate solution. CONCLUSIONS: This study clearly shows that, in the liver, the consequences of acidosis are far more important on the metabolism (VO2 and urea release) than on the intrahepatic vascular resistance.

Acidosis↗
PubMed1999

Zidovudine-induced mitochondrial disorder with massive liver steatosis, myopathy, lactic acidosis, and mitochondrial DNA depletion.

Zidovudine is known to be responsible for a mitochondrial myopathy with ragged-red fibres and mitochondrial DNA depletion in muscle. Lactic acidosis alone or associated with hepatic abnormalities has also been reported. A single report mentioned the concomitant occurrence of muscular and hepatic disturbances and lactic acidosis in a patient receiving zidovudine, but muscle and liver tissues were not studied. A 57-year-old man with AIDS, who had been treated with zidovudine for 3 years, developed fatigue and weight loss. Serum creatine kinase and hepatic enzyme levels were high. Lactic acidosis was present. Liver biopsy showed diffuse macrovacuolar and microvacuolar steatosis. After withdrawal of zidovudine, creatine kinase, aspartate aminotransferase, and alanine aminotransferase levels normalised within 5 days, and lactacidaemia decreased. Acidosis persisted. The patient became confused and febrile and died 8 days after detection of high blood lactic acid. A muscle sample obtained at autopsy showed mitochondrial abnormalities with ragged-red fibres and lipid droplet accumulation. Southern blot analysis showed depletion of mitochondrial DNA, affecting skeletal muscle and liver tissue. No depletion was found in myocardium and kidney. This case emphasises that zidovudine treatment can induce mitochondrial multisystem disease, as revealed in our case by myopathy, liver steatosis and lactic acidosis.

Acidosis, Lactic↗
PubMed1984

Effect of ethanol on lactic acidosis in experimental hemorrhagic shock.

Many trauma victims who have hemorrhagic shock are also intoxicated. Ethanol could worsen the severity of shock and decrease the amount of blood loss necessary to reach or maintain the shock state, perhaps by increasing lactic acidosis. We examined the effect of ethanol on lactic acidosis in a group of rats that were intoxicated, then put in a state of hemorrhagic shock (MAP = 40 mm Hg). These animals were compared to a control group that were in a similar state of hemorrhagic shock but not intoxicated. The volumes of blood necessary to reach and maintain the predetermined model state of shock for two hours in each group were also measured. The animals were paralyzed and placed on controlled ventilation. The ethanol produced an expected baseline lactic acidosis, and it took significantly less blood volume loss to keep the intoxicated group in shock. However, during shock there was no significant difference in the state of lactic acidosis. These results suggest that acute ethanol intoxication made the animals more sensitive to hemorrhage. This effect was not mediated by an increase in lactic acidosis in our model.

Acidosis↗
PubMed1999

Early metabolic acidosis and coma after acetaminophen ingestion.

Metabolic acidosis and coma may develop in patients who experience severe hepatic injury after acetaminophen poisoning. The onset of acidosis and coma soon after acetaminophen overdose, but preceding manifest hepatic injury, contrasts with the typical course of poisoning. This pattern has been reported in a limited number of cases. Coingestions and the rare occurrence of these findings after an overdose have engendered controversy as to whether acetaminophen alone is the cause of early coma and acidosis. We describe 4 separate overdoses among 3 patients who arrived at the emergency department comatose with a metabolic acidosis soon after ingesting large amounts of acetaminophen without evidence of toxic liver injury. Our cases support the view that early metabolic acidosis with coma does indeed occur after acetaminophen poisoning, independent of hepatic failure or its complications.

Acetaminophen↗