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PubMed2004

Recent advances in the monitoring and management of diabetic ketoacidosis.

Diabetic ketoacidosis (DKA) is still a major contributor to morbidity and mortality in diabetes. The triad of hyperglycaemia, ketosis and acidosis can be diagnosed within a few minutes of the patient presenting, by measuring blood glucose and ketones using a meter, and venous blood pH on a blood gas analyser. Quantifying ketosis allows accurate distinction between simple hyperglycaemia and metabolic decompensation. We review the management of DKA, and the emerging role of near-patient testing in diagnosing ketosis and monitoring its resolution.

Blood Glucose↗
PubMed2006

Rapid and sensitive real-time polymerase chain reaction method for detection and quantification of 3243A>G mitochondrial point mutation.

Maternally inherited diabetes and deafness and mitochondrial encephalomyopathy, lactic acidosis with stroke-like episodes result from the 3243A>G mitochondrial point mutation. Current methods to detect the presence of the mutation have limited sensitivity and may lead to potential misclassification of patients with low levels of heteroplasmy. Here, we describe development and validation of a rapid real-time polymerase chain reaction (PCR) method for detection and quantification of levels of heteroplasmy in a single assay. Standard curve analysis indicated that the sensitivity of detection was less than 0.1%. Time from sample loading to data analysis was 110 minutes. We tested 293 samples including 23 known positives, 40 known negatives, and 230 samples from patients clinically classified as having type 2 diabetes. All positive samples were correctly detected, and of those samples previously quantified, heteroplasmy levels determined using the real-time assay correlated well (r(2) = 0.88 and 0.93) with results from fluorescently labeled PCR-restriction fragment length polymorphism and pyrosequencing methods. Screening of 230 patients classified as having type 2 diabetes revealed one patient with 0.6% heteroplasmy who had previously tested negative by PCR-restriction fragment length polymorphism. Real-time PCR provides rapid simultaneous detection and quantification of the 3243A>G mutation to a detection limit of less than 0.1%, without post-PCR manipulation.

Adenosine↗
PubMed1992

Antithrombin III, C1 inhibitor, methylglyoxal, and polymorphonuclear leukocytes in the development of vascular complications in diabetes mellitus.

Under conditions closely approximating those in vivo (100 mM sodium carbonate pH 7.3 with 0.9% NaCl, 37 degrees C), antithrombin III (AT III) and the C1 inhibitor (C1-INH) are inactivated by methylglyoxal (MG) with pseudofirst-order kinetics and second-order rate constants of 25.2 and 7.8 M-1 min-1, respectively. A study of the functional status of neutrophils from patients with diabetes mellitus (DM) prompts an idea that under hyperglycemia in the diabetic organism the polymorphonuclear leukocytes (PML) endure 'arousal' that is identical or analogous to their activation. Indeed, nonstimulated PML from DM patients display (i) an almost sixfold higher luminol-dependent chemiluminescence and (ii) a double rate of oxygen uptake as compared with those from healthy donors, and (iii) are capable of MG formation in the presence of acetoacetate, which in vivo may be an additional source of this inactivator of AT III and C1-INH in diabetic patients. Conditions leading to ketosis or lactic acidosis are discussed, and a probable scenario is proposed for the organismic deterioration in DM.

Acetoacetates↗
PubMed1975

[Lactacidaemia and disseminated intravascular coagulation associated with phenformin medication (author's transl)].

A patient with chronic active hepatitis developed vomiting, dyspnoea, tachycardia, diarrhoea and diffuse pains. For several years she had been treated with azathioprine and for a few weeks before admission with phenformin for mild diabetes. Laboratory examination revealed acute disseminated intravascular coagulation and lactacidaemia. Despite intensive treatment the patient died a few hours after admission, the post-mortem examination revealing diffuse pulmonary haemorrhages. The present case report and those published in the literature suggest that phenformin should not be given to diabetics who also have renal or hepatic disease. In any case, if phenformin is given, it should be stopped if hepatic, renal, infectious or thrombotic complications occur. In these cases and those of sudden unexplained deterioration in diabetics, hospitalisation is essential and lactic acid levels should be determined and coagulation tests performed.

Acidosis↗
PubMed1992

[Lactic acidosis, hyperamylasemia, and phenformin].

Phenformin is still used in the therapy of non-insulin dependent diabetes in association with sulphonylureas. The controindications to the use of this drug often are not kept in due consideration. It is therefore often possible to observe cases of irreversible lactic acidosis with lethal outcome. In this paper, three cases of lactic acidosis from phenformin administration are reported. Some characteristics of this clinical picture are underscored: accompanying ketoacidosis, hyperamylasemia. On the basis of their observation, the Authors conclude that those diabetic patients who can be treated with diet alone or with diet and sulphonylureas must not be treated with phenformin. Metformin is then proposed as a more flexible and safer drug.

Acidosis, Lactic↗
PubMed1999

Arteriovenous fistula in chronic renal failure patients: comparison between three different anesthetic techniques.

The creation of arteriovenous fistula is an established form of therapy for patients with chronic renal failure. Anesthetic management in such patients is governed by the presence of risk factors such as hypertension, ischemic heart disease, diabetes, chronic pulmonary disease, anemia, coagulopathy, metabolic acidosis and/or hyperkalemia. In an attempt to improve the quality of anesthetic care and outcome we designed the present study to compare the different anesthetic techniques which are used for creation of arteriovenous fistula. Retrospectively we reviewed 164 patients who underwent creation of arteriovenous fistula. We retrieved the data concerning the age, sex, ASA class, and coexisting diseases. The patients were classified into three groups depending on the anesthetic technique received. Group A (n = 48) patients received general anesthesia; group B (n = 39), patients received brachial plexus block and group C (n = 77), patients received local infiltration anesthesia. Chi-square test was used to compare between the percentages among the different groups. The percentages of cardiac patients showed significant differences between groups A and B and also between groups A and C. There was a significant difference between the groups A and B also between the groups A and C but not between groups B and C concerning age. ASA classes were not significantly different among the groups. Among the total number of patients, 34 were diabetics and 75 patients were cardiac. Axillary brachial plexus block was complete in 70% of patients and incomplete in 27% and failed in 3% of patients. We conclude that chronic renal failure patients are at increased risk during anesthesia. We conclude that brachial plexus blockade or local anesthetic infiltration are good alternatives to general anesthesia in these patients undergoing creation of arteriovenous fistula. Age, ASA class and cardiac status were the three determining factors for the choice of the anesthetic technique. Further multivariate prospective study are needed to confirm these results.

Adult↗
PubMed1987

Temporal profile of serum potassium concentration in nondiabetic and diabetic outpatients on chronic dialysis.

We analyzed routine serum potassium concentration measurements and conditions temporally associated with abnormalities in potassium concentration in outpatients on chronic hemodialysis (136 nondiabetics, 36 diabetics) and continuous ambulatory peritoneal dialysis (16 nondiabetics, 10 diabetics). The following potassium concentration frequencies were found: prehemodialysis, nondiabetics: normal 51.3%, severe hyperkalemia (greater than 6.0 mmol/l) 10%, severe hypokalemia (less than 3.0 mmol/l) 0.3%; diabetics: normal 57.8%, severe hyperkalemia 8.7%, severe hypokalemia 0.5%. Peritoneal dialysis, nondiabetics: normal 73.7%, severe hyperkalemia 0.6%, severe hypokalemia 4.9%; diabetics: normal 72.5%, severe hyperkalemia 0.9%, severe hypokalemia 2.9%. Normokalemia and severe hypokalemia were significantly (chi 2 test) more frequent in peritoneal dialysis than in prehemodialysis, whereas severe hyperkalemia was more frequent in prehemodialysis serum samples. No difference was found between nondiabetics and diabetics for either form of dialysis. 50% of prehemodialysis episodes of hyperkalemia were diet-induced. Hyperkalemic drugs and anuria were not associated with a higher risk of prehemodialysis hyperkalemia, but each one of 3 abnormalities, very high BUN (greater than 40 mmol/l), metabolic acidosis (TCO2 less than 15 mmol/l) and, in diabetics, severe hyperglycemia (serum glucose greater than 30 mmol/l), was associated with a statistically higher risk of hyperkalemia.

Diabetes Mellitus, Type 1↗
PubMed2000

Complications of chronic renal insufficiency: beyond cardiovascular disease.

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.

Acidosis↗
PubMed1980

[Influence of insulinfree rehydration on diabetic derangements (author's transl)].

In two groups of pts with diabetic derangements the effect of infusion therapy was investigated with regard to metabolic and endocrine functions. The rate of infusion was adapted to the height of the central venous pressure and the administration of electrolytes to their serum concentration. Insulin was withheld until no further decrease of blood glucose was noted. Group A consisted of 8 pts with severe diabetic ketoacidosis (blood glucose higher than 25 mmol/l, pH below 7.0 and/or bicarbonate below 10 mmol/l). The duration of insulinfree rehydration was 8.8 +/- 1.3 (x +/- SE) hrs and the fluid retention 4060 +/- 3 633 ml. The osmolality in serum decreased from 356 +/- 12 to 340 +/- 8 mosm/kg H2O and the blood glucose from 37.9 +/- 2.9 to 28.6 +/- 3.4 mmol/l. No correlation existed between the decrease of blood glucose and the expansion of the intravascular volume. Therefore, the decrease of blood glucose was not caused by a simple dilution effect. High renal glucose excreation was observed (408 +/- 83 mmol) but could not explain the decrease of blood glucose. The glucose clearance fell from 25.9 +/- 6.9 to 21.5 +/- 3.8 ml/min/1.73 m2 body surface from the first to the last 2-hr periods. It must be concluded that the initial rehydration deminished gluconeogeneses and/or increased tissue glucose utilization without exogenous insulin administration. This conclusion is supported by the decrease in the plasma concentration of the contrainsular hormons. Glucagon decreased 579 +/- 209 to 319 +/- 88 pg/ml (n.s.). Cortisol from 49.9 +/- 4.6 to 35.8 +/- 6.7 micrograms/100 ml (p < 0.05) and Adrenalin from 2.43 +/- 1.03 to 0.4 +/- 0.22 ng/ml (p < 0.05). Blood gas analysis revealed only minimal and ketobodies in serum no changes. Therefore, it can be concluded that rehydration and decrease of plasma concentration of contrainsular hormones do not influence the enhenced lipolyses in diabetic ketoacidosis. Group B consisted of 8 pts with nonacidotic diabetic derangements (blood glucose higher than 25 mmol/l, pH above 7.3 and/or bicarbonate above 18 mmol/l) and an acute weightloss of more than 3 kg. The insulinfree rehydration lasted 13 +/- 1.6 hrs and the fluid retention was 4620 +/- 380 ml. The serum osmolality decreased from 317 +/- 5.3 to 288 +/- 1.9 mmol/l. The decrease of blood glucose could not be explained by delution effect. The renal glucose excreation was 370 +/- 120 mmol/l in total and the glucose clearance decreased from 15.3 +/- 8.4 to 8.0 +/- 2.8 ml/min/1.73 m2 body surface (p < 0.01). Decrease of gluconeogenese and/or increase of glucose assimilation of the tissues can also be expected for the pts with nonacidotic diabetic derangements during plain rehydration.

Acidosis↗
PubMed1975

Insulin therapy in phenformin-associated lactic acidosis; a case report, biochemical considerations and review of the literature.

A patient with phenformin-associated lactic acidosis was treated with insulin and showed marked improvement coincident with the expected onset of action of the insulin administered. Relative insulin deficiency was demonstrated although several phenomena characteristic of phenformin-associated lactic acidosis obscured its reflection in the usual indices. From data presented and a review of the literature the following pathogenesis is proposed for the observed metabolic derangement. A background of relative insulin deficiency would permit enhanced pyruvate (and hence lactate) formation from protein sources. Insulin deficiency would also lead to inhibition of pyruvate dehydrogenase which slows pyruvate removal. Phenformin accumulation (cf impaired renal function) further reduces pyruvate removal by decreasing its conversion to glucose, but in addition alters the redox state. For the lactic acidosis which results, insulin administration may thus constitute specific therapy. Diabetes 24:28-35, January, 1975.

Acidosis↗
PubMed1989

Diabetic emergencies.

Diabetic emergencies continue to be a significant cause of premature death in patients with diabetes. They include the diabetic comas (hypoglycaemia, severe diabetic ketoacidosis, hyperosmolar hyperglycaemic non-ketotic coma, lactic acidosis), emergency surgery and myocardial infarction. There is still considerable avoidable morbidity and mortality during treatment, and as a result of misdiagnosis. Simple guidelines are thus needed for the general practitioner and admitting physician to improve management. Hypoglycaemia is far the commonest diabetic emergency, and is relatively easy to diagnose and treat. Delays in treatment are potentially damaging and largely unnecessary. Diabetic ketoacidosis is still relatively common but is often preventable. Initial treatment for this and hyperosmolar nonketotic coma is rehydration. This is followed by IM or IV infusion of moderate amounts of insulin, early potassium replacement, and alkali only if the acidaemia is severe. Lactic acidosis requires mainly rigorous alkalinisation but is very rare. The metabolic derangements in emergency surgery and myocardial infarction are best treated by combined glucose, potassium and insulin infusions. In all cases treatment is easiest and probably more successful if consistent simple guidelines are provided.

Diabetes Complications↗
PubMed2000

Complement activation products in the urine from proteinuric patients.

The presence of plasma proteins in the tubular lumen has variety of adverse effects on the tubular cells. Among various plasma proteins filtered through glomerular barrier, complement has been proven as the possible candidate inducing tubulointerstitial injury. To study the role of intratubular complement activation in proteinuric patients, complement activation products (CAP) at C3 level (iC3b and Bb) and C9 level (membrane attack complex) were measured in both plasma and urine of patients with minimal change nephrotic syndrome (MCNS), focal glomerular sclerosis, IgA nephropathy, membranous nephropathy, and diabetic nephropathy. For evaluation of the effect of metabolic acidosis on the intratubular complement activation, urinary CAP were measured before and after sodium bicarbonate administration in patients with renal insufficiency. The following results were obtained: (1) Patients with focal glomerular sclerosis and diabetic nephropathy showed the highest level of urinary CAP excretion rate (unit/creatinine), while MCNS revealed no increase. (2) Patients with membranous nephropathy showed a unique finding, i.e., isolated increase of membrane attack complex excretion. (3) There was no significant correlation between urine and plasma levels of CAP. (4) Except for MCNS patients, the urinary excretion rate of CAP significantly increased when the level of proteinuria exceeded the nephrotic range, and it was significantly correlated with the serum creatinine level. (5) Urinary CAP excretion rate significantly decreased 2 wk after sodium bicarbonate administration without affecting the level of proteinuria or plasma CAP. These results suggest that the degree of intratubular complement activation correlates with the level of proteinuria, type of glomerular disease, impairment of renal function, and metabolic acidosis.

Adolescent↗
PubMed2004

[Lactic acidosis and acute abdomen from biguanide intoxication].

Metformin, an anti-hyperglycaemic drug, reduces mortality in obese patients with a non-insulin-dependent diabetes mellitus type II (United Kingdom Prospective Diabetes Study) and is therefore recommended as the first line therapy. A metformin-associated lactic acidosis due to accumulation or intoxication is a rare but severe complication with a mortality rate of up to 50%. The main clinical symptoms are unspecific and the patient may present with acute abdominal pain and reduced consciousness. This can easily be misinterpreted and may lead to a wrong diagnosis. Only a thorough clinical examination and exact analysis of laboratory values in combination with the medical history and chronic medication will allow a correct diagnosis. We report a case of a 79-year-old female patient whose clinical symptoms were initially interpreted as an acute intestinal ischemia. A progressively deteriorating haemodynamic state led to an exploratory laparotomy. Postoperatively, the correct diagnosis of a metformin-associated lactic acidosis due to acute renal failure was made. In the course of the ICU stay the condition improved after bicarbonate haemodialysis and the patient was discharged 11 days after admission.

Abdomen, Acute↗
PubMedDate not supplied

Ocular and orbital phycomycosis.

Cerebro-rhino-orbital phycomycosis (CROP) occurs predominantly in individuals with diabetes mellitus in a state of metabolic acidosis. Other forms of metabolic acidosis, especially in infants, may predispose to phycomycotic infections. CROP has also been reported in patients with leukemia or lymphoma. CROP usually begins in the palate or paranasal sinuses and rapidly spreads to the orbital contents. Proptosis, loss of vision, and ophthalmoplegia occur and death from cerebral involvement commonly ensues. The fungus tends to invade arteries and cause thrombosis and tissue infarction. Rhizopus is the most commonly isolated genus in CROP, accounting for almost all cases. The diagnosis can be strongly suspected by the characteristic clinical manifestations. Therapy includes treatment of the underlying disease, surgical excision of the necrotic tissue containing fungal elements and the systemic administration of amphotericin-B. The effect of treatment has improved since the disease was first described, but the condition still has a high mortality, especially if it is not diagnosed early.

Adolescent↗
PubMed2001

Clinical and pathologic features of focal segmental glomerulosclerosis with mitochondrial tRNALeu(UUR) gene mutation.

BACKGROUND: Several families have been described in which an A to G transition mutation at position 3243 (A3243G) of the mitochondrial DNA (mtDNA) is associated with focal and segmental glomerulosclerosis (FSGS). However, the prevalence, clinical features, and pathophysiology of FSGS carrying mtDNA mutations are largely undefined. METHODS: Among 11 biopsy-proven primary FSGS patients of unknown etiology, we examined seven FSGS patients to determine whether any of the clinical and pathological features of FSGS were associated with an A3243G mtDNA mutation. In four subjects in whom the A3243G mtDNA mutation was discovered in blood leukocytes, as well as in urine sediments, we retrospectively reviewed the medical records and re-evaluated the renal biopsy specimen using light and electron microscopy. We further screened the patient's family members for the presence and degree of heteroplasmy for this mtDNA mutation and obtained medical histories that were consistent with mitochondrial cytopathy. RESULTS: The four individuals identified with the A3243G mtDNA mutation were female. Proteinuria was diagnosed in these individuals during a routine annual health checkup in their teenage years. None of the patients showed any symptoms related to mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode, whereas diabetes mellitus in two of the patients and a hearing disturbance in one patient became manifest within a 3- to 13-year follow-up period. Strict maternal transmitted inheritance was confirmed by pedigree studies in all of these patients. Steroid therapy was ineffective in all four patients. In two of these patients, renal function declined slowly to end-stage renal failure. Histologic examination of biopsy specimens revealed that glomeruli were not hypertrophied, while electron microscopic examination identified severely damaged, multinucleated podocytes containing extremely dysmorphic abnormal mitochondria in all patients. CONCLUSIONS: FSGS may belong to the spectrum of renal involvement in A3243G mtDNA mutation in humans. Severely injured podocytic changes containing abnormal mitochondria may explain the pathogenesis of FSGS in association with the A3243G mtDNA mutation.

DNA, Mitochondrial↗
PubMed1984

Lithium intoxication associated with acute renal failure.

Lithium can produce transient natriuresis, nephrogenic diabetes insipidus, and partial distal renal tubular acidosis. Lithium intoxication is commonly associated with mild renal insufficiency and may produce acute renal failure. We have described a case of acute renal failure in a patient with severe lithium intoxication, as well as cardiac arrhythmias and hypothyroidism, both of which have been reported to occur with lithium toxicity. Treatment with daily hemodialysis eventually produced complete recovery. Lithium clearance occurs quickly with hemodialysis, but a rebound effect occurs as lithium in intracellular water equilibrates with extracellular fluid. Prolonged dialysis may be required to reduce the blood lithium level to the therapeutic range. We conclude that lithium intoxication may produce severe reversible renal failure as a result of direct tubular epithelial damage.

Acute Kidney Injury↗