Persistent Acidosis Research Articles

The OPTIMIST-A trial: evaluation of minimally-invasive surfactant therapy in preterm infants 25-28 weeks gestation.

BackgroundIt is now recognized that preterm infants ≤28 weeks gestation can be effectively supported from the outset with nasal continuous positive airway pressure. However, this form of respiratory therapy may fail to adequately support those infants with significant surfactant deficiency, with the result that intubation and delayed surfactant therapy are then required. Infants following this path are known to have a higher risk of adverse outcomes, including death, bronchopulmonary dysplasia and other morbidities. In an effort to circumvent this problem, techniques of minimally-invasive surfactant therapy have been developed, in which exogenous surfactant is administered to a spontaneously breathing infant who can then remain on continuous positive airway pressure. A method of surfactant delivery using a semi-rigid surfactant instillation catheter briefly passed into the trachea (the “Hobart method”) has been shown to be feasible and potentially effective, and now requires evaluation in a randomised controlled trial.Methods/designThis is a multicentre, randomised, masked, controlled trial in preterm infants 25–28 weeks gestation. Infants are eligible if managed on continuous positive airway pressure without prior intubation, and requiring FiO2 ≥ 0.30 at an age ≤6 hours. Randomisation will be to receive exogenous surfactant (200 mg/kg poractant alfa) via the Hobart method, or sham treatment. Infants in both groups will thereafter remain on continuous positive airway pressure unless intubation criteria are reached (FiO2 ≥ 0.45, unremitting apnoea or persistent acidosis). Primary outcome is the composite of death or physiological bronchopulmonary dysplasia, with secondary outcomes including incidence of death; major neonatal morbidities; durations of all modes of respiratory support and hospitalisation; safety of the Hobart method; and outcome at 2 years. A total of 606 infants will be enrolled. The trial will be conducted in >30 centres worldwide, and is expected to be completed by end-2017.DiscussionMinimally-invasive surfactant therapy has the potential to ease the burden of respiratory morbidity in preterm infants. The trial will provide definitive evidence on the effectiveness of this approach in the care of preterm infants born at 25–28 weeks gestation.Trial registrationAustralia and New Zealand Clinical Trial Registry: ACTRN12611000916943; ClinicalTrials.gov: NCT02140580.

PC.110 Hypothermia for Encephalopathy in Low and Middle-Income Countries (HELIX): A Feasibility Study

BackgroundTherapeutic hypothermia improves outcomes after neonatal encephalopathy in high-income countries, however the safety and efficacy of cooling in low- and middle-income countries (LMIC) is not known.ObjectiveTo examine the feasibility of...

P40: A case report of persistent near-fatal anion gap acidosis due to a massive gamma-butyrolactone (GBL)/ethanol intoxication

Case We report a case of an intentional massive gamma-butyrolactone (GBL) intoxication, the precursor of the recreational drug gamma-hydroxybutyric acid (GHB), resulting in life-threatening metabolic acidosis (pH 6.5) with a highly increased anion- and osmolal gap. Rapid analysis using gas chromatography revealed no methanol nor ethylene glycol but a GHB plasma concentration of 4398 mg/L, far above the upper limit concentration found in fatalities attributed to GBL. Full recovery was established following supportive treatment including hemodialysis. This is the first report of GBL intoxication as a cause of high serum anion- and osmolal gap metabolic acidosis. Conclusions GHB/GBL is not a substance classically associated with high anion gap metabolic acidosis (HAGMA), but the finding of the massive GHB concentration was a direct result of the method used in this lab, allowing the simultaneous detection of several substances potentially causing HAGMA (P. Van Hee et al. , Clin. Chem. Lab. Med. 2004; 42(11):1341-1345). Classical ethylene glycol methods would not measure GHB and suitable GC-MS techniques for rapid detection of this illicit drug are not widely available. Here, we propose that GBL/GHB intoxication should be considered in the differential diagnosis of this acid-base disorder. In view of the persistent acidosis, hemodialysis was life-saving.

Mucormycosis Outbreak Associated With Hospital Linens

Mucormycosis is an invasive fungal infection with a high fatality rate. We investigated an outbreak of mucormycosis in a pediatric hospital to determine routes of pathogen transmission from the environment and prevent additional infections. A case was defined as a hospital-onset illness consistent with mucormycosis, confirmed by culture or histopathology. Case-patient medical records were reviewed for clinical course and exposure to items and locations within the hospital. Environmental samples were collected from air and surfaces. Fungal isolates collected from case-patients and the environmental samples were identified using DNA sequencing. Five case-patients had hospital-associated cutaneous mucormycosis over an 11-month period; all subsequently died. Three case-patients had conditions known to be associated with susceptibility to mucormycosis, while 2 had cardiac conditions with persistent acidosis. The cases occurred on several different wards throughout the hospital, and hospital linens were the only exposure identified as common to the case-patients. Rhizopus species were recovered from 26 (42%) of 62 environmental samples from clean linens and associated areas and from 1 (4%) of 25 samples from nonlinen-related items. Case-patients were infected with Rhizopus delemar, which was also isolated from cultures of clean linens and clean linen delivery bins from the off-site laundry facility. Hospital linens were identified as a vehicle that carried R. delemar into contact with susceptible patients. Fungal species identification using DNA-based methods is useful for corroborating epidemiologic links in hospital outbreak investigations. Hospital linens should be laundered, packaged, shipped and stored in a manner that minimizes exposure to environmental contaminants.

Spectrum of Etiologies Causing Hydrometrocolpos

Background: Hydrometrocolpos (HMC) develops as a result of vaginal outflow obstruction and the accumulation of secretions. It might be secondary to persistent cloaca, urogenital sinus, some syndromes, presence of the vaginal septum, vaginal atresia, and imperforate hymen. Each of them has different treatment options and follow-up protocols. This study was performed to identify the etiology and the related management of patients with HMC.Materials and Methods: A descriptive series of patients with HMC managed in our hospital between 2004 and 2011 is being presented. The medical record of these patients was analyzed for etiology, management, and outcome.Results: Eight patients with HMC were managed during 7 years at our department. Underlying etiologies included urogenital sinus (n=3), and 1 each of imperforate hymen, transverse vaginal septum, Herlyn-Werner-Wunderlich syndrome, persistent cloaca, and a variant of the cloaca. Four patients were prenatally diagnosed. The patient with imperforate hymen was managed successfully with incision and drainage. Abdominal vaginostomy was done in three patients with urogenital sinus as initial procedure. In patient with persistent cloaca, a colostomy and abdominal vaginostomy were performed. Patient with cloaca variant died due to persistent acidosis and salt wasting.Conclusion: HMC may have different etiological factors which may dictate different surgical management. Etiology of HMC can be as simple as imperforate hymen to the most severe cloacal malformations.

Spectrum of etiologies causing hydrometrocolpos.

Hydrometrocolpos (HMC) develops as a result of vaginal outflow obstruction and the accumulation of secretions. It might be secondary to persistent cloaca, urogenital sinus, some syndromes, presence of the vaginal septum, vaginal atresia, and imperforate hymen. Each of them has different treatment options and follow-up protocols. This study was performed to identify the etiology and the related management of patients with HMC. A descriptive series of patients with HMC managed in our hospital between 2004 and 2011 is being presented. The medical record of these patients was analyzed for etiology, management, and outcome. Eight patients with HMC were managed during 7 years at our department. Underlying etiologies included urogenital sinus (n=3), and 1 each of imperforate hymen, transverse vaginal septum, Herlyn-Werner-Wunderlich syndrome, persistent cloaca, and a variant of the cloaca. Four patients were prenatally diagnosed. The patient with imperforate hymen was managed successfully with incision and drainage. Abdominal vaginostomy was done in three patients with urogenital sinus as initial procedure. In patient with persistent cloaca, a colostomy and abdominal vaginostomy were performed. Patient with cloaca variant died due to persistent acidosis and salt wasting. HMC may have different etiological factors which may dictate different surgical management. Etiology of HMC can be as simple as imperforate hymen to the most severe cloacal malformations.

Regional citrate anticoagulation in CVVH: A new protocol combining citrate solution with a phosphate‐containing replacement fluid

Regional citrate anticoagulation (RCA) is a valid anticoagulation method in continuous renal replacement therapies (CRRT) and different combination of citrate and CRRT solutions can affect acid-base balance. Regardless of the anticoagulation protocol, hypophosphatemia occurs frequently in CRRT. In this case report, we evaluated safety and effects on acid-base balance of a new RCA- continuous veno-venous hemofiltration (CVVH) protocol using an 18 mmol/L citrate solution combined with a phosphate-containing replacement fluid. In our center, RCA-CVVH is routinely performed with a 12 mmol/L citrate solution and a postdilution replacement fluid with bicarbonate (protocol A). In case of persistent acidosis, not related to citrate accumulation, bicarbonate infusion is scheduled. In order to optimize buffers balance, a new protocol has been designed using recently introduced solutions: 18 mmol/L citrate solution, phosphate-containing postdilution replacement fluid with bicarbonate (protocol B). In a cardiac surgery patient with acute kidney injury, acid-base status and electrolytes have been evaluated comparing protocol A (five circuits, 301 hours) vs. protocol B (two circuits, 97 hours): pH 7.39 ± 0.03 vs. 7.44 ± 0.03 (P < 0.0001), bicarbonate 22.3 ± 1.8 vs. 22.6 ± 1.4 mmol/L (NS), Base excess −2.8 ± 2.1 vs. −1.6 ± 1.2 (P = 0.007), phosphate 0.85 ± 0.2 vs. 1.3 ± 0.5 mmol/L (P = 0.027). Protocol A required bicarbonate and sodium phosphate infusion (8.9 ± 2.8 mmol/h and 5 g/day, respectively) while protocol B allowed to stop both supplementations. In comparison to protocol A, protocol B allowed to adequately control acid-base status without additional bicarbonate infusion and in absence of alkalosis, despite the use of a standard bicarbonate concentration replacement solution. Furthermore, the combination of a phosphate-containing replacement fluid appeared effective to prevent hypophosphatemia.

Persistent acidosis at presentation in a patient with type 1 diabetes: Concomitant diagnosis of type 1 distal renal tubular acidosis

We present a rare case of a 7-year-old boy who was diagnosed with type 1 diabetes mellitus and type 1 distal renal tubular acidosis concomitantly. The proband presented with history of polyuria, polydipsia and lethargy. He was found to be severely dehydrated. Initial pH value was 7.025 with bicarbonate level of 5.3 mmol/L, and serum glucose of 23 mmol/L. Despite adequate rehydration and insulin therapy (0.1 U/kg/hr), he continued to have persistent metabolic acidosis with normal bicarbonate. Other causes for acidosis were thought off, and with further inquiry, the parents revealed that the father and two other siblings are treated for renal tubular acidosis. Our patient had urine pH of 8, serum potassium 2.9 - 3.7 (3.5 - 5.4 mmol/L), chloride 110 - 116 (98 - 110 mmol/L). The diagnosis of type 1 renal tubular acidosis was made, and the acidosis was corrected with oral sodium bicarbonate and potassium chloride. The patient was discharged on subcutaneous multiple daily insulin injections.

Acidosis with hyperuricemia and renal tubular damage in viral gastroenteritis

Acidosis with hyperuricemia and renal tubular damage in viral gastroenteritis

Glomerular basement membrane lipidosis in Alagille syndrome

Alagille syndrome is characterized by a paucity of interlobular bile ducts with chronic cholestasis, cardiac, skeletal, and eye abnormalities and is associated predominantly with JAG1 mutations. Various renal abnormalities have been sporadically described. The classic renal histopathology described in Alagille syndrome is mesangiolipidosis, with lipid deposits predominately confined to the mesangium and minimal deposition within the glomerular basement membrane (GBM). We report a 5-year-old girl with Alagille syndrome who presented with persistent subnephrotic proteinuria and renal tubular acidosis. A renal biopsy showed GBM irregularities (mimicking membranous glomerulonephritis), mesangial sclerosis, and focal segmental glomerulosclerosis (FSGS) on light microscopy. Electron microscopy revealed few lipid inclusions within the mesangium but extensive inclusions along the GBM. These findings are mostly consistent with those reported previously in Alagille syndrome. However, the histologic distribution of lipid vacuoles is seemingly reversed in this patient and is uniquely accompanied by FSGS, emphasizing the spectrum of renal histopathology seen in Alagille syndrome. The proteinuria observed in this patient is likely attributed to significant GBM lipid deposition, which over time may contribute to the development of FSGS.

Disproportionate Acidosis After Traumatic Bladder Rupture: A Case-Control Study.

Traumatic bladder injury is rare and often missed on initial evaluation. We sought to identify early markers of bladder injury with a high sensitivity. A retrospective review from 1999 to 2008. There were 28 patients diagnosed with traumatic bladder injury. The most common mechanism was car accidents with pelvic fractures. 93% (26) of the patients presented with significant metabolic acidosis, without evidence of hemorrhagic shock. For intra- and extraperitioneal bladder ruptures, the mean hemoglobin level on arrival was 12.4 + 2.0 (range 9.0-16.0) and 11.4 + 1.9 (range 8.2-14.7). The average pH on arrival for intraperitoneal ruptures was 7.22 + 0.16 (range 6.86-7.37) and for extraperitoneal ruptures, 7.22 + 0.16 (range 6.85-7.37). The pH improved in all patients with intraperitoneal rupture after surgical repair, up to a mean of 7.27 + 0.11 (range 7.06-7.36, p = 0.5) within 12 h. Extraperitoneal ruptures recovered more quickly with a pH after catheter drainage of 7.34 + 0.04 (range 7.27-7.37, p = 0.1) within 12 h. The ISS for intraperitoneal and extraperitoneal ruptures were similar, 30 + 12 (range 13-57) and 32 + 13 (range 13-57, p = 0.7). A cohort of trauma patients, matched by ISS, age, and pelvic fracture, but without bladder rupture, was used for comparison. Their mean ISS was 30 + 10 (range 14-57). The average pH for this group on arrival was 7.33 + 0.11 (range 7.16-7.42), and 47% of these patients had a normal pH. There was a significant difference between the pH on arrival in the ruptured compared to the nonruptured cohort (intraperitoneal pH 7.22, p = 0.008, extraperitoneal pH 7.22, p = 0.02). Three patients died (mortality 10.7%). Disproportionate acidosis in the trauma patient is a sensitive indicator of bladder injury, especially with a pelvic fracture or hematuria. Fully resuscitated patients with persistent acidosis and an appropriate mechanism should be evaluated for bladder injury.

Survival after extracorporeal cardiopulmonary resuscitation in infants and children with heart disease

We investigated survival and predictors of mortality for infants and children with heart disease treated with extracorporeal membrane oxygenation as an aid to cardiopulmonary resuscitation. Children (<18 years) with heart disease who received extracorporeal cardiopulmonary resuscitation and were reported to the Extracorporeal Life Support Organization database were evaluated. Patients were classified into one of 3 groups based on underlying cardiac physiology: single ventricle, 2 ventricles, and cardiac muscle disease. Patients with eligible procedure codes were assigned a Risk Adjustment for Congenital Heart Surgery-1 classification. Four hundred ninety-two patients were eligible for analysis, and 279 (57%) were assigned a Risk Adjustment for Congenital Heart Surgery-1 category. Overall survival was 42%. In a multivariable logistic regression analysis, significant pre-extracorporeal predictors for mortality included single-ventricle physiology (odds ratio, 1.6; 95% confidence interval, 1.05-2.4), a history of a stage 1-type procedure (odds ratio, 2.7; 95% confidence interval, 1.2-6.2), and extreme acidosis (arterial blood gas pH < 7.01; odds ratio, 2.2; 95% confidence interval, 1.3-3.7). Right carotid artery cannulation was associated with decreased mortality risk (odds ratio, 0.6; 95% confidence interval, 0.4-0.9). During extracorporeal support, complications, including renal injury, evidence of neurologic injury, and persistent acidosis, were associated with an increased risk of hospital mortality. Use of extracorporeal membrane oxygenation as an adjunct to cardiopulmonary resuscitation resulted in hospital survival in 42% of infants and children with heart disease. Underlying cardiac physiology and associated cardiac surgical procedures influenced mortality, as did pre-extracorporeal resuscitation status and extracorporeal membrane oxygenation-associated complications.

Alkalemia during continuous renal replacement therapy and mortality in critically ill patients*

Acid-base disorders are common in critically ill patients. Once continuous renal replacement therapy (CRRT) is initiated, it becomes a major determinant of acid-base status. We hypothesized that therapy-induced alkalemia and alkalosis is associated with increased mortality. The CCF-ARF Registry (1995-01) was used to identify 405 patients supported with bicarbonate based continuous hemodialysis. Proportion of days with an elevated pH to the number of days with normal pH was used to assess the association of alkalemia and the number of days with alkalemia, and mortality. Multivariable analyses were used to adjust for days with acidosis, and other relevant covariates. Serum bicarbonate and pH levels plateau after 48 hrs of CRRT. Study subjects had on average 1.5 +/- 2.9 days where pH was greater than 7.45, and .4 days where serum bicarbonate level was greater than 28 mmol/L, during a median of 9 days of CRRT. Daily dialysis dose was inversely associated with the number of days with a low serum bicarbonate level, but was not associated with increased frequency of an elevated pH or serum bicarbonate level. Increasing proportion of days with elevated pH or serum bicarbonate was not associated with increased mortality in multivariable analysis. Alkalemia and alkalosis occur frequently during CRRT, but they are not associated with increased mortality. Persistent acidosis and acidemia while on CRRT was a strong predictor of poor outcome.

Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis

Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca(2+) responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca(2+) levels and Ca(2+) transient amplitude. Recent experimental evidence indicates that activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca(2+) transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca(2+) handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca(2+) uptake and SR Ca(2+) load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.

The exceptionally rare (sic) Common Scoter

A 1-month-old infant with congenital heart disease underwent initial cardiac surgery (Mee Shunt) at day 20 but was later readmitted because of poor shunt flow and hypoxemia. Despite therapy, the infant deteriorated and suffered a cardiopulmonary arrest. After 40 minutes of resuscitation, spontaneous cardiac output was reestablished, and subsequently, the child was placed on extracorporeal circulation membrane oxygen (ECMO) support. The infant deteriorated further over the next 3 days with persistent acidosis, marked abdominal distension associated with significant nasogastric aspirates, and the passage of small amounts of bloodstained stool. The presumed diagnosis was necrotizing enterocolitis, and despite the grave prognostic indicators, the decision was taken to undertake laparotomy. At surgery, there was 350 mL of unclotted venous blood in the peritoneal cavity. The bowel was grossly normal. A ruptured, infarcted, hemorrhagic spleen was discovered to be the cause of the bleeding. A splenectomy was performed, and the child made rapid recovery, sufficiently well to undergo redo Mee shunt 2 days later. A splenic infarct was confirmed at pathological examination. The cause of the splenic infarct and rupture is uncertain in this baby but may have been related to either cardiopulmonary resuscitation and/or ECMO. The importance of this case is the similarity in presentation in a baby with congenital heart disease between necrotizing enterocolitis (which is relatively common) and hemoperitoneum secondary to splenic rupture (which is very rare). Medical practice contains many useful maxims such as, “What walks like a duck, talks like a duck, is often a duck.” This case demonstrates that not all ducks are the common Mallard ( Anas platyrhynchos) but occasionally the exceptionally rare (sic) Common Scoter ( Melanitta nigra). The management of neonatal cardiac patients on ECMO therapy continues to be a challenge, and particular diagnostic rigor should be applied in their care.

Pitfalls in the management of newborn cloacas

Clinicians caring for newborns with persistent cloaca face significant challenges in the newborn period. Avoiding key pitfalls during this time can have dramatic implications. We reviewed the medical records of 361 patients with cloaca operated on at our institution and analyzed sequelae that resulted from incorrect management in the newborn period. Of 361 patients, 282 underwent primary operations at our institution, and 79 patients were referred to us after a failed repair at other institutions. Pitfalls in management during the newborn period included the following: (1) Failure to recognize and manage hydrocolpos, which occurred in 46 patients. Of these, three patients developed pyocolpos (two progressed to vaginal perforation), and 43 suffered from persistent bilateral hydronephrosis, megaureters, recurrent urinary tract infections, persistent acidosis, or failure to thrive due to undrained hydrocolpos. They underwent unnecessary urinary drainage procedures (nephrostomy, ureterostomy, cystostomy, or vesicostomy) in the newborn period. When the vagina was finally decompressed, all of these symptoms disappeared. (2) Colostomy or vesicostomy problems, which occurred in 50 patients. These included incorrect placement of the colostomy (too distal, which interfered with the pull-through) in 24 and colostomy prolapse in 23. Incompletely diverting loop colostomies led to urinary tract infections in 49 patients. Vesicostomy prolapse occurred in three patients. (3) Clinical misdiagnosis, which occurred in 42 patients. Six were incorrectly diagnosed as "intersex" and 36 as "rectovaginal fistula." In this group only the rectum was repaired, and the patients were left with a urogenital sinus that required reoperation. Proper management of a newborn with cloaca includes drainage of a hydrocolpos, which avoids unnecessary urinary diversions and pyocolpos. Our preferred colostomy is one with separated stomas, adequate distal bowel for the pull-through, and use of a proper technique to avoid prolapse. Correct clinical diagnosis of cloaca avoids problems during the definitive repair.

Sustained Gastric Mucosal Acidosis After Hemorrhage in Spite of Rapid Hemodynamic Restoration With Blood or Hypertonic/Hyperoncotic Solution

Splanchnic hypoperfusion has been implicated as the motor of multiple organ dysfunction. Hypertonic saline has shown to benefit microcirculatory blood flow. In hemorrhaged animals, we tested the hypothesis that small-volume 3% NaCl/10% dextran 40 (3%HSD) promotes global and regional improvements, including gastric mucosal acidosis reversal. Seventeen dogs (18.8 ± 1.2 kg) were bled (20 mL/min) to a mean arterial pressure of 40–45 mm Hg, which was maintained at these levels for 15 min. They were randomly assigned to two groups: Blood (n = 9), total shed blood retransfused at 40 mL/min; or a 4-min bolus injection of 3%HSD (n = 8), in a volume equivalent to 25% of total shed blood. All animals were followed for 30 min thereafter. Gastric mucosal PCO2 (gas tonometry), portal vein PCO2, superior mesenteric artery blood flow (SMA, ultrasonic flowprobes), and systemic and regional O2-derived variables were evaluated throughout the protocol. Hemorrhage induced significant reductions of arterial pressure, cardiac output, and SMA blood flow, while portal–arterial and gastric–arterial PCO2 gradients increased. Total shed blood transfusion, as well as 3%HSD bolus injection, promptly restored all parameters, except for the increased gastric–arterial PCO2 gradient. We conclude that persistent gastric mucosal acidosis cannot be adequately predicted by global and splanchnic O2 derived variables in following hemorrhage and resuscitation with total shed blood transfusion or small-volume hypertonic–hyperoncotic solution.

Distal renal tubular acidosis.

Research in the past several years has led to the understanding of numerous genetic mutations that lead to inheritable forms of distal renal tubular acidosis (dRTA). Most of these mutations affect the physiology of the A-intercalated cells of the renal cortical collecting duct. These include mutations of genes encoding carbonic anhydrase II, kidney anion exchanger 1, and different subunits of the H+-ATPase proton pump. Genetic defects in any one of these components may impair renal acidification and thereby result in persistent acidosis, failure to thrive, and nephrocalcinosis. The present review provides a summary of the most recently identified genetic mutations resulting in a dRTA phenotype and, when possible, describes a mechanism. Most causes of dRTA are due to loss of function or inappropriate targeting of transporters. The collaboration of clinicians, geneticists, and renal physiologists has enabled us to better understand at the cellular level the different mechanisms leading to dRTA. Such information should lead to earlier diagnosis and treatment, thereby minimizing the irreversible complications affecting patients with this or similar diseases.

Child abuse by intentional iron poisoning presenting as shock and persistent acidosis.

A case of intentional iron poisoning presented to our hospital. The patient's persistent acidosis and the team's observation of maternal indifference indicated the diagnosis. This case should alert physicians to a potential source for intentional poisoning that is present in most homes with young infants.

Diverse patterns of acid-base abnormalities associated with a modified sigmoid neobladder

In this study, we analyzed the pattern of metabolic acidosis in patients following the construction of a sigmoid neobladder and then search for the risk factors which affecting this. In 23 men aged 43-73 years and nine women aged 49-74 years who underwent sigmoid neobladder surgery, we performed physical examinations and blood tests every 3 months for 13-75 months (38.7+/-16.6: mean+/-SD). We monitored acid-base balance, serum electrolytes, creatinine, lipid and liver function in patients for up to 6 years postoperatively. Creatinine clearance over 24 h was determined preoperatively. According to pH and base excess measured during follow-up, patients were classified into three groups (normal, 17 patients; temporary acidosis, eight patients; persistent acidosis, seven patients). Patients with temporary acidosis could compensate spontaneously by 1 year without being given sodium bicarbonate; those with persistent acidosis could not compensate spontaneously and five of them required medication with sodium bicarbonate after 1 year. Serum creatinine in patients with persistent acidosis was consistently higher during follow-up than in the other two groups. Preoperative creatinine clearances in the normal, temporary, and persistent groups were 94.25+/-27.47, 95.19+/-18.63, and 69.18+/-16.18 ml/min/1.73 m(2), respectively, being significantly lower in the persistent group ( P<0.05). In this group, patients with creatinine clearances less than 70 ml/min/1.73 m(2) could not compensate for metabolic acidosis. Normal and temporary groups showed different changes of serum chloride and bicarbonate during follow-up (respectively higher and lower) although the renal functions of the two groups were similar. Chloride and bicarbonate varied reciprocally with pH and base excess. Temporal hyperchloremic metabolic acidosis was observed until a year after surgery. In conclusion, temporary acidosis can be caused in some patients in spite of normal renal function, although it is difficult to predict it. In addition, careful follow-up is required, especially in patients with a creatinine clearance <70 ml/min/1.73 m(2) who can encounter persistent acidosis.