Treatment of severe diabetic acidosis with tris-hydroxymethyl aminomethane in a thirteen-year-old child

Diabetic ketoacidosis is a severe complication of type I diabetes. A 13-year-old female (40 kg) patient was admitted to our Intensive Care Unit with severe metabolic acidosis (pH: 6.8), hyperglycemia (835 mg/dL) and coma. Her hemodynamic conditions were unstable and, even though a large amount of plasma expanders, crystalloids, and inotropic support were supplied, the patient went into cardiac arrest in the first hour of treatment. After resuscitation, a better hemodynamic balance was achieved and metabolic acidosis was treated with fluid replacement therapy, continuous insulin infusion, and Tris-hydroxymethyl aminomethane (THAM) as a buffering agent. This therapy rapidly improved her metabolic conditions. The patient was discharged 5 days after Intensive Care Unit admission in good condition and without neurological sequelae.     

Rhabdomyolysis after liver transplantation: a case report

Our aim was to present the case of a pediatric biliary atresia patient who experienced rhabdomyolysis with severe cardiac arrhythmias associated with hyperkalemia, metabolic acidosis, and myoglobulinemia during liver transplantation. A 5-year-old girl, weighing 16.5 kg, with end-stage liver disease due to biliary atresia underwent living donor liver transplantation. A sudden onset of atrial fibrillation with rapid ventricular response was noted during the transplantation. The cardiac arrhythmia was associated with hyperkalemia, metabolic acidosis, and myoglobulinemia. Rhabdomyolysis was suspected. Hyperkalemia and metabolic acidosis were not corrected despite treatment with 10 mL of 50% glucose plus 6 U of regular insulin in 4 succeeding boluses and 110 mEq sodium bicarbonate before sending the patient to the intensive care unit. A corresponding decrease and normalization in serum potassium and correction of metabolic acidosis were noted as responses to a single dose of intravenous (20 mg) dantrolene. The patient was extubated 5 days after transplantation. The kidney function remained within normal limits during the rhabdomyolysis and the entire hospital stay. The patient was discharged 7 weeks later and is surviving with the original liver graft and satisfactory kidney function to date.     

Severe acidosis caused by starvation and stress

A 1-year-old boy had severe anoxic brain injury owing to a cardiorespiratory arrest. He had an initial metabolic acidosis, but this largely resolved by hospital day 2. He then had a persistent, profound metabolic acidosis. Evaluation on hospital day 6 found that the patient had ketonemia, ketonuria, and a normal serum glucose level; he had received no intravenous dextrose during his hospitalization. The dextrose-free fluids were given initially to protect his brain from the deleterious effects of hyperglycemia after brain injury. Continuation beyond 24 hours was inadvertent. The initiation of dextrose-containing intravenous fluids produced a rapid resolution of his metabolic acidosis. Starvation usually produces a mild metabolic acidosis, but when combined with physiologic stress, starvation may cause a severe metabolic acidosis. Among the few reports of severe starvation ketoacidosis, our case is unique because the patient was monitored closely in an intensive care unit, allowing us to describe the time course of the acidosis in detail.     

Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion.

The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 microg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's Glasgow Coma Scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.     

Metabolic acidosis during urinary retention in a patient with an enterovesical fistula

We report a patient known to have an enterovesical fistula who presented severe acute metabolic acidosis during an episode of urinary retention. The enterovesical fistula which had been intermittently symptomatic for 4 years, had developed after several intestinal surgical procedures and related intraperitoneal sepsis following resection of colon cancer 21 years previously. The patient who had a total colectomy and ileostomy, was admitted for hip replacement with the routine placement of a Foley bladder catheter. Three weeks post-operatively, the patient developed acute urinary retention following removal of the urinary catheter. The output from his ileostomy was immediately markedly increased, presumably from bladder urine diverted into the intestines through the enterovesical fistula. Within a few days he presented a normal anion gap metabolic acidosis with raised urea and stable creatinine; his clinical status deteriorated markedly with profound obtundation. These metabolic abnormalities were readily corrected by re-insertion of the Foley catheter with restoration of normal urine flow and immediate corresponding fall in the ileostomy output. Radiographic studies showed the presence of the enterovesical fistula originating from the jejunum. This is the first report of acute metabolic acidosis in association with an enterovesical fistula; the severe metabolic disturbances were triggered by the development of urinary retention resulting in the diversion of urine into the small bowel through the fistula.     

Metformin-associated lactic acidosis precipitated by acute renal failure

In type II diabetes treated with metformin, lactic acidosis is a rare but severe complication. Commonly patients with lactic acidosis show signs of shock, tissue hypoxia, acute hepatic or renal failure and the link between metformin therapy and lactic acidosis may be coincidental, associated or causal. Excessive plasma metformin concentrations show that lactic acidosis is due to a toxicological mechanism. The case of a 65-year-old woman with type II diabetes, in whom severe type B2 lactic acidosis secondary to metformin was precipitated by acute renal failure, is presented. The association of diuretics with non-steroidal anti-inflammatory drugs and colchicine was responsible for a volume depletion and an acute renal failure. Initial serum creatinine was 643 micromol x l(-1) and arterial blood gas analysis revealed a pH of 7.01. Aggressive volume expansion and correction of the acidosis with intravenous bicarbonate therapy failed. At the intensive care unit, calculated anion gap was 35 mmol x l(-1) (normal range 10-18) and lactate concentration was 12.4 mmol x l(-1), liver profile was normal. Prolonged haemodialysis using bicarbonate dialysate resulted in a favourable outcome. Toxicology confirmed retrospectively the presence of a plasma concentration of metformine of 20 mg x l(-1) (normal <2). One month after this episode she has made a recovery of tubular necrosis, although no longer prescribed metformin. Metformin should be temporally stopped when acute renal failure occurs or is anticipated; patient with acute renal failure and high calculated anion gap should benefit from lactate measurements. Early bicarbonate haemodialysis is an adequate treatment of lactic acidosis caused by accumulation of metformin associated with acute renal failure     

Metformin-associated lactic acidosis: incidence, diagnosis, prognostic factors and treatment

We describe the case of a patient with severe lactic acidosis, as well as presenting some data on its incidence, diagnosis, prognostic factors, and the most appropriate treatment. A 76 year-old male patient with diabetes on treatment with metformin, hypertension, dyslipaemia, and with mild cognitive impairment, was admitted to the Intensive Care Unit in a state of circulatory shock, requiring aggressive treatment with vasopressors and volume. The patient had acute kidney injury with an anuria of 3 days, probably secondary to dehydration to vomiting and to NSAIDs. As a result of the acute renal damage, the patient suffered a severe metformin-associated lactic acidosis. The rest of the causes of metabolic acidosis with an increased anion gap were ruled out, as well as a possible sepsis or rhabdomyolysis. Metformin-associated lactic acidosis is an uncommon metabolic condition, but with a high mortality. To reduce the mortality of these patients, it is important to make an early diagnosis using the clinical records, physical examination, and laboratory tests, with an early resuscitation with volume, vasopressors, bicarbonate, and renal replacement therapy.     

Intradialytic hypercapnic respiratory failure managed by noninvasive assisted ventilation.

We report a hemodialysis patient with acute hypercapnic respiratory failure managed on noninvasive intermittent positive pressure ventilation and progressive metabolic acidosis. Dialysate bicarbonate concentration of 25 mEq/l was associated with exacerbation of metabolic acidosis, while higher dialysate bicarbonate concentration of 30 mEq/l induced a dangerous increase in PCO(2) level. Excessive bicarbonate buffering and CO(2) production induced by severe metabolic acidosis, malnourishment and tissue hypoxia, could explain inadequate correction of metabolic acidosis and worsening of hypercapnia in this patient. Our findings suggest the need for close monitoring of blood gases and cautious modulation of dialysate bicarbonate concentration in the presence of progressive metabolic acidosis in hypercapnic hemodialysis patients.     

Unexpected metabolic acidosis during rectal surgery

A case is reported in which severe metabolic acidosis developed during rectal surgery in a patient who was normal in all other respects. The possible connection of pre-operative whole gut irrigation with the development of the acidosis is discussed.     

Intensive care treatment of severe mixed metabolic acidosis

We report a case of severe metabolic acidosis associated with acute renal failure and septicaemia following treatment with maximal therapeutic doses of metformin and diclofenac. On the second day of intensive care the patient deteriorated with respiratory insufficiency and abdominal pain during continuous renal replacement therapy. A laparoscopy revealed a perforated cholecystitis with abscess formation. The patient regained renal function and recovered. Intake of diclofenac 5 days before this episode could have been the main cause of renal insufficiency and metabolic acidosis in this patient and could also have delayed surgical treatment by masking early clinical signs of perforated cholecystitis. The renal failure may also have caused metformin and lactate to accumulate, contributing to the mixed pattern of metabolic acidosis. This case report describes a mixed organic and non-organic metabolic acidosis associated with acute renal failure, presumably resulting from a combination of drugs and diseases often found in the elderly - metformin for diabetes mellitus and a non-steroidal anti-inflammatory drug for cholecystolithiasis. Acid-base balance and electrolyte changes were rapidly normalized by continuous renal replacement therapy.     

Lactate- or bicarbonate-buffered solutions in continuous extracorporeal renal replacement therapies

BACKGROUND: Continuous renal replacement therapies (CRRTs) are well accepted for critically ill patients with acute renal failure (ARF). Today, daily fluid exchange in CRRT reaches 30 to 40 liter and more. Therefore, the composition of the substitution/dialysate fluid, often primarily developed either for intermittent treatment or for peritoneal dialysis, becomes more relevant. Lactate (30 to 45 mmol/liter) is frequently used as the buffer because of the high stability of this substance. However, lactate is thought to have negative effects on metabolic and hemodynamic parameters. METHODS: Published data for different substitution fluids are presented with respect to acidosis and lactate concentration, uremia, and hemodynamic and metabolic alterations. RESULTS: Only a few studies compare substitution fluids with different buffers. Uremia and acidosis (pH, base excess) were sufficiently controlled during CRRT with an exchange volume of in average 30 liters using either buffer. If patients with severe liver failure and lactic acidosis were excluded, no difference in hemodynamic and metabolic parameters between the solutions occurred. The plasma lactate concentration was elevated during lactate use in some cases, but lactate levels remained within normal limits in patients without liver impairment. The bicarbonate concentration in the solutions should exceed 35 to 40 mmol/liter, as in some cases the buffer capacity of the solutions was inadequate. In patients with severe liver failure or lactic acidosis, solutions with lactate buffer were shown not to be indicated. CONCLUSION: In patients with reduced lactate metabolism, for example, concomitant severe liver failure, after liver transplantation or in lactic acidosis, bicarbonate-buffered solutions should be used. In nearly all other cases of critically ill patients with ARF, lactate-buffered solutions may be used as well as bicarbonate solutions.     

A case of lupus nephritis with hyporeninemic hypoaldosteronism]

We report a case of 67-year-old woman with systemic lupus erythematosus presenting hyporeninemic hypoaldosteronism. She admitted because of anasarca in March, 1990. She manifested nephrotic syndrome, and hyperkalemia and hyperchloremic metabolic acidosis. The hyperkalemia was disproportionate to the degree of renal insufficiency. Basal levels of plasma renin activity and plasma aldosterone concentration were low. Renal tubular function studies revealed normal hydrogen ion secretion. Renal biopsy demonstrated diffuse proliferative lupus nephritis and prominent interstitial cell infiltration. There was no vasculitis of glomerular vascular poles. After treatment of lupus nephritis with prednisolone, levels of plasma renin activity and plasma aldosterone concentration were elevated. Hyperkalemia and metabolic acidosis were normalized and renal function improved. We conclude that the heperkalemia and metabolic acidosis could be attributed to hyporeninemic hypoaldosteronism.     

Case of distal renal tubular acidosis complicated with renal diabetes insipidus, showing aggravation of symptoms with occurrence of diabetes mellitus

We report herein a 27-year-old male case of inherited distal renal tubular acidosis complicated with renal diabetes insipidus, the symptoms of which were aggravated by the occurrence of diabetes mellitus. At 2 months after birth, he was diagnosed as having inherited distal renal tubular acidosis and thereafter supplementation of both potassium and alkali was started to treat his hypokalemia and metabolic acidosis. At the age of 4 years, calcification of the bilateral renal medulla was detected by computed tomography. Subsequently his urinary volume gradually increased and polyuria of approximately 4 L/day persisted. At the age of 27 years, he became fond of sugar-sweetened drinks and also often forgot to take the medicine. He was admitted to our hospital due to polyuria of more than 10 L day, muscle weakness and gait disturbance. Laboratory tests disclosed worsening of both hypokalemia and metabolic acidosis in addition to severe hyperglycemia. It seemed likely that occurrence of diabetes mellitus and cessation of medications can induce osmotic diuresis and aggravate hypokalemia and metabolic acidosis. Consequently, severe dehydration, hypokalemia-induced damage of his urinary concentration ability and enhancement of the renin angiotensin system occurred and thereby possibly worsened his hypokalemia and metabolic acidosis. As normalization of hyperglycemia and metabolic acidosis might have exacerbated hypokalemia further, dehydration and hypokalemia were treated first. Following intensive treatment, these abnormalities were improved, but polyuria persisted. Elevated plasma antidiuretic hormone (12.0 pg/mL) and deficit of renal responses to antidiuretic hormone suggested that the polyuria was attributable to the preexisting renal diabetes insipidus possibly caused by bilateral renal medulla calcification. Thiazide diuretic or nonsteroidal anti-inflammatory drugs were not effective for the treatment of diabetes insipidus in the present case.     

Severe metabolic acidosis and hypokalemia in a patient with enterovesical fistula

We report a case of a 59-year-old woman who had severe metabolic acidosis and hypokalemia due to an enterovesical fistula. The patient came to our hospital complaining of systemic weakness and numbness of the fingers. She was found to have hyperchloremic metabolic acidosis (arterial bicarbonate, 2.8 mEq/l) and hypokalemia (serum potassium, 1.9 mEq/l) and was admitted for treatment. Following the correction of metabolic acidosis and hypokalemia, the patient was examined for the underlying cause of these electrolyte and acid-base disorders. She had a history of total hysterectomy followed by radiotherapy due to uterine cancer 30 years previously. After the surgery, she had suffered postoperative neurogenic bladder dysfunction, necessitating intermittent self-catheterization. Two years before admission, she had begun to experience watery diarrhea. A radiographic study after recovery from the acid-base and electrolyte disorders revealed the presence of an enterovesical fistula. The fistula was surgically resected and the metabolic acidosis completely cleared. Unexplained hyperchloremic metabolic acidosis with hypokalemia may suggest the presence of an enterovesical fistula in patients with a surgical history of malignant pelvic tumor and neurogenic bladder dysfunction.     

An unsuspected cause for metabolic acidosis in chronic renal failure: sorbent system hemodialysis

A severe metabolic acidosis was produced in a patient with chronic renal failure by hemodialysis using a sorbent system to regenerate bicarbonate dialysate with an initial bicarbonate concentration of 60 mEq/L. The acidosis resolved with standard single-pass hemodialysis. In five additional patients, the bicarbonate concentration of the dialysate with the sorbent system was noted to be low and quite variable (mean +/- SD, 16.5 +/- 8.3 mEq/L, range 5 mEq/L to 39 mEq/L). The low dialysate bicarbonate failed to correct metabolic acidosis and, in fact, was capable of further lowering the serum bicarbonate. The capacity of the regenerating cartridge to release protons makes this form of dialysis a potential cause for metabolic acidosis. The safety of the sorbent system dialysis, at least in the bicarbonate mode, requires further evaluation.     

Cetoacidosis no diabética en una mujer embarazada,debido a inanición aguda con gripe A (H1N1) concomitante e insuficiencia respiratoria

Threatening refractory metabolic acidosis due to short-term starvation nondiabetic ketoacidosis is rarely reported. Severe ketoacidosis due to starvation itself is a rare occurrence, and more so in pregnancy with a concomitant stressful clinical situation.This case report presents a nondiabetic woman admitted in intensive care for respiratory failure type 1 during the third trimester of pregnancy with a severe metabolic acidosis refractory to medical treatment.We diagnosed the patient with acute starvation ketoacidosis based on her history and the absence of other causes of high anion gap metabolic acidosis after doing a rigorous analysis of her acid-base disorder.     

Metformin-associated lactic acidosis: case reports and literature review

BACKGROUND: Lactic acidosis is a widely recognized, though rare, side effect of metformin. This paper describes five patients admitted to Chang Gung Memorial Hospital from 1 September 1998 to 31 May 2001 suffering severe lactic acidosis caused by metformin, and reviews the literature. PATIENTS: Five cases diagnosed as having meftormin-associated lactic acidosis (MALA) were discovered during the study period. Three had normal renal function before the onset of MALA and two had attempted suicide bytaking large amounts of metformin. One patient with end-stage renal disease developed MALA despite regularhemodialysis three times a week. One of the patients who had taken metformin to attempt suicide was not diabetic. RESULTS: All patients suffered severe metabolic acidosis with a high anion gap and blood lactate level. Four developed profound hypotension, and three of these also suffered acute respiratory failure. Three patients received conventional hemodialysis and two continuous renal replacement therapy. A young non-diabetic female who had taken a large dose of metformin to commit suicide died from multiple organ failure despite aggressive treatment. CONCLUSIONS: Lactic acidosis is a serious reaction to metformin, and hemodialysis (the treatment of choice) should be done urgently to prevent serious complications. MALA should be suspected in patients presenting with wide anion gap metabolic acidosis and high blood lactate, even when they are non-diabetic.     

Acute valproic acid intoxication: interest of a treatment by extracoporeal elimination combined with L-carnitine

We present the case of a 24-year-old-female patient, who made an attempt to autolysis with valproic acid, benzodiazepines and neuroleptic. The valproic acid plasma level was very high (1437 μg/mL), confirming it was a severe intoxication. She presents an acute encephalopathy with prolonged status epilepticus, a lactic metabolic acidosis and hematologic disorders such as bicytopenia. Treatment including L-carnintine and continuous veno-venous haemodialysis (CVVHD) was rapidly introduced to prevent the occurrence of cerebral oedema. The evolution was favourable despite the occurrence of a nosocomial ventilation acute lung injury. The patient had motor sequelae of cranial nerves following status epilepticus extended, which disappeared spontaneously after several days.     

Life threatening hypokalemia and quadriparesis in a patient with ureterosigmoidostomy

We report quadriparesis as a result of severe hypokalemia and acidosis in a 15-years-old young man who had undergone ureterosigmoidostomy for bladder extrophy 3 months earlier. The patient was initially mistakenly diagnosed to be a case of Guillain–Barre syndrome. On investigations acidosis and profound hypokalemia were present. Dramatic improvement occurred after correction of hypokalemia and acidosis with intravenous potassium and bicarbonate. The underlying mechanism as well as the treatment of hyperchloremic metabolic acidosis and hypokalemia after ureterosigmoidostomy are hereby discussed.     

Hyperammonemia in distal renal tubular acidosis: is it more common than we think?

The hyperammonemia in distal renal tubular acidosis, previously only described in two cases, is considered an unusual occurrence. After the report published in 2005, we observed plasma ammonia levels above normal range during metabolic decompensation in two other consecutive pediatric patients suffering from distal renal tubular acidosis. The ammonia plasma levels returned to normal range after treatment with sodium bicarbonate and potassium salt. In distal renal tubular acidosis, hyperammonemia is probably the result of an imbalance between the increased ammonia synthesis, in response to metabolic acidosis, and the impaired ammonia excretion, typical of distal renal tubular acidosis. According to this physiopathological mechanism, our observation shows that hyperammonemia is not an uncommon finding in distal renal tubular acidosis, and should be included among differential diagnosis of hyperammonemia in infants and children.