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A 61-year-old diabetic woman was admitted with high fever, dehydration and acidosis caused by fasciitis necroticans of the forehead. The electrolytes and blood sugar level were corrected, broad spectrum antibiotics started and extensive débridement performed, followed by a second-look operation the next day. After the bacterial culture was known, the antibiotics were adapted. A split-skin graft gave an acceptable result.
PURPOSE: The object of this study was to evaluate the effect of betamethasone therapy on maternal glucose levels, to observe the incidence of ketoacidosis and gestational diabetes as well as to judge fetal outcome. METHODS: 26 patients underwent measurement with the CGMS for at least 72-hour. Morning urine was examined for ketones and glucose, venous blood was drawn from a hand vein for blood gas measurements. At a minimum of seven days after the last betamethasone treatment, an oral glucose tolerance test was performed to exclude gestational diabetes. For fetal outcome weight, body length, head circumference, APGAR and pH of umbilical cord blood were determined. RESULTS: All patients showed transient hyperglycaemia from day 1 to day 2 with normoglycaemia on day 3 (mean +/- SD: 129.6 +/- 20 mg/dL on day 1, 127.1 +/- 17.7 mg/dL on day 2, 96.7 +/- 12.9 mg/dL on day 3, and 91.3 +/- 17.8 mg/dL on day 4). There was a significant fall (p < 0.01) of the mean glucose levels between day 1/3, day 1/4, day 2/3, day 2/4. Neither acidosis (pH < 7.35) nor clinically relevant BE/lactate shifts were seen. Ketonuria was detected in 30 % of the patients before betamethasone, rose to 50 % (on day 1), fell to 24 % (on day 2), and 6 % (on day 3). One week later one patient (4 %) was diagnosed as having gestational diabetes, while four (17 %) showed impaired glucose tolerance. Fetal outcome showed no significant difference compared to the average of the Virchow Klinikum. CONCLUSION AND DISCUSSION: Pregnant patients have high glucose measurements for two days during betamethasone therapy. No maternal acidosis and no diabetic delayed metabolic effects were seen, and fetal outcome showed good results. A prophylactic use of insulin is not generally needed in healthy women.
Insulin is the cornerstone of therapy for diabetic ketoacidosis because it causes the rate of ketoacid production to fall; this action takes several hours to occur. Insulin also causes H+ to be transported from the intracellular fluid to the extracellular fluid in vitro. The purpose of this study was to determine if insulin led to the acute export of H+ from the intracellular fluid in vivo. If so, we wished to determine if this also occurred during chronic metabolic acidosis, to quantitate the magnitude of the H+ shift, and to evaluate the mechanisms involved. The administration of low- or high-dose insulin to normal dogs and high-dose insulin to dogs with chronic metabolic acidosis caused the concentration of bicarbonate in plasma to decline by close to 3 mmol/l. The PCO2 fell by close to 15% in all three groups of dogs, so one component of the fall was due to hyperventilation. As the pH of blood did not change, a primary metabolic acidosis also occurred. The fall in bicarbonataemia was not due to net accumulation of organic acids or to a loss of bicarbonate or organic anions in the urine. Taken together, insulin, when given at doses used to treat diabetic ketoacidosis, might induce a significantly greater degree of acidaemia in the extracellular fluid acutely after it is given.
Diabetic emergencies include diabetic ketoacidosis, insulin-induced hypoglycemia, hyperosmolar coma and lactic acidosis. By determining the blood pressure, observing for evidence of dehydration or sweating and making a rapid qualitative assessment of blood glucose and ketonemia, the physician can usually identify the condition promptly. When adequate facilities are available, continuous intravenous insulin infusion is preferred for treatment of diabetic ketoacidosis. The nonketotic hyperosmolar state should be corrected gradually, not rapidly, in order to avoid cerebral edema.
The renin-angiotensin-aldosterone system and the acidification capacity of the renal tubule were studied in 13 diabetic patients with chronic renal failure. As a whole, the group showed hyporeninaemic hypoaldosteronism (HH). Studied alone, 12 of the 13 patients presented the requirements for HH. This group showed hypercholaemic hyperkalaemic metabolic acidosis with a disturbance in renal acidification which may be classified as Type IV renal tubular acidosis. The results of this group were compared to those of another two groups; one of diabetic patients without chronic renal failure and the other with chronic renal failure (C Cr less than 40ml/min); both were seen to show different behaviour to that of the group affected by the two processes.
Diabetes exacerbates neuronal cell death induced by cerebral ischemia. One contributing factor is enhanced acidosis during ischemia. Astrocytes are vulnerable to hypoxia under acidic conditions in vitro and may be targets of ischemia under diabetic conditions. The objective of this study was to determine whether diabetes would cause damage to astrocytes after an ischemic brain injury in vivo. Diabetic and nondiabetic rats were subjected to 5 min of forebrain ischemia and followed by 30 min, 6 h, or 1 or 3 days of recovery. The results showed that ischemia caused activation of astrocytes in nondiabetic rats. In contrast, diabetes caused astrocyte activation in early stage of reperfusion and astrocyte death in late stage of reperfusion. Remarkable astrocyte death was preceded by increased DNA oxidation. Further studies revealed that increased astrocyte damage coincided with enhanced production of free radicals. These data suggest that hyperglycemic ischemia worsens outcome in astrocytes, as it does in neurons.
Macrovascular complications in diabetics create a high risk for cardiovascular disease (CVD). Generally, the main risk factors for CVD include age, men's sex, elevated LDL-cholesterol and reduced HDL-cholesterol, elevated fibrinogen, hypertension, smoking, and diabetes mellitus. Clinical manifestation of coronary disease is determined by number, area, and severity of coronary stenoses, myocardial function, and presence of induced ischemia. Routine pharmacological treatment of ISHD concentrates on risk factors and hasn't been yet focused on changes in energy metabolism during ischemic situation which are important factors contributing to ischemic damage. Substances able to optmize energy metabolism of heart muscle offer a very tempting way both for ISHD treatment and for treatment of following cardiovascular complications. Optimal use of energy source in heart muscle can favour heart activity so that comparable amount of contractile work requires less oxygen. The most beneficial way of getting energy for myocardium while low consumption of oxygen is oxidation of glucose. Because of a large amount of free fatty acids (FFAs) in diabetics a more demanding way of oxidation takes place in them, the oxidation of FFAs. Therefore myocardium of a diabetic needs under normal perfusion conditions more oxygen to provide energy. Besides increase in demand of oxygen, FFAs separate glycolysis from glucose oxidation and increase undesirable production of lactate and protons. An ischemic myocardium of a diabetic has primarily bigger demand of oxygen then myocardium of a non-diabetic. Development of cell ischemia, with all the known consequences in forms of lactate acidosis, calcium overload, and depletion of ATP, leads to considerable contractile disorder. Unfavourable position of metabolic activities in myocardium of diabetics and faster and more serious progression of atherosclerosis result in a big risk of CVD in diabetics. Incidence of coronary events in diabetics without history of ISHD is as big as in non-diabetics with history of coronary events.
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In previous studies we have shown stimulation of renal acid excretion in the proximal tubules of rats with diabetes of short duration, with no important alterations in glomerular hemodynamics; on the other hand, in thyroparathyroidectomized rats (TPTX model), a significant decrease in renal acid excretion, glomerular filtration rate (GFR) and renal plasma flow (RPF) was detected. Since important changes in the parathyroid hormone-vitamin D-Ca axis are observed in the diabetic state, the present study was undertaken to investigate the renal repercussions of thyroparathyroidectomy in rats previously made diabetic by streptozotocin (45 mg/kg). Four to 6 days after the induction of diabetes (DM), a group of rats were thyroparathyroidectomized (DM + TPTX). Renal functional parameters were evaluated by measuring the inulin and sodium para-aminohippurate clearance on the tenth day. The decrease in the GFR and RPF observed in TPTX was not reversed by diabetes since the same alterations were observed in DM + TPTX. Net acid (NA) excretion was unchanged in DM (6.19 +/- 0.54), decreased in TPTX (3.76 +/- 0.25) and returned to normal levels in DM + TPTX (5.54 +/- 0.72) when compared to the control group (6.34 +/- 0.14 mumol min-1 kg-1). The results suggest that PTH plays an important vasodilator role regarding glomerular hemodynamics, since in its absence the impairment in GFR and RPF was not reversed by the diabetic state. However, with respect to acid excretion, the presence of diabetes was able to overcome the negative stimulus represented by TPTX.
A variety of fatal complications are associated with diabetes mellitus. Among these, diabetic ketoacidosis (DKA) figures largely in fatalities in young diabetics. Although hyperosmotic diuresis in DKA causes extreme fluid loss, acute renal failure is less common than expected in DKA. We treated a case of severe DKA with associated coma, acute respiratory failure, and acute renal failure in a 24-year-old man who had been diagnosed with type 1 diabetes mellitus at age 19. The comatose patient had been intubated before transfer to our hospital for intensive care. Despite infusion with isotonic saline and insulin, metabolic acidosis was refractory. On day 2, urine output decreased and pulmonary congestion developed, so we started continuous veno-venous hemodiafiltration (CVVHDF), which was effective against the metabolic acidosis; urine output increased gradually. CVVHDF was withdrawn on day 7, and the patient's renal function recovered completely. He was discharged from the intensive care unit (ICU) on day 14.
Diabetes is associated with a fluctuating impairment in oxygen transport of the erythrocytes. This impairment is correlated with hyperglycemia by the formation of glycosylated hemoglobin (HbAIC) and with inhibitory factors of glycolysis i.e. hypophosphatemia and acidosis which lower the concentration of red cell 2,3-diphosphoglycerate. Diabetic angiopathy may be the ultimate result of innumerable microvascular responses to discrete hypoxic injuries associated with increased plasma permeation through the vessel walls. It is shown that two additional risk factors for atherosclerosis--smoking and hypertriglyceridemia may also lead to arterial wall hypoxia by changing the position of the oxyhemoglobin dissociation curve.
Long term experience with the use of sulfonylurea and/or biguanide oral hypoglycemic agents in patients under the age of 30 years shows the following results: 1) Oral treatment under 30 years of age is effective only for a limited period of time, in the large majority less than 24 months;--2) The success of oral treatment of diabetics and the period of effectiveness is increased if the subject is overweight at the time of discovery of the diabetes mellitus;--3) The type of antidiabetic treatment, i.e., insulin only, oral only, or oral and insulin, does not influence the susceptibility to the complications likely to appear in this age group, such as retinopathy, coronary disease, neuropathies and urinary and dental infections;--4) Poteinuria, peripheral vascular disease and various abnormalities of plasma lipids involving cholesterol and triglycerides, are significantly more common in patients under oral therapy than in those receiving insulin. These findings suggest the necessity for serious reconsideration of therapy as soon as any of these pathological events appear, especially the proteinuria or the lipid anomalies;--5) The duration of the oral treatment preceding therapeutic insulin does not have influence on the subsequent metabolic disturbance (hypoglycemia, deto-acidosis) and thus on the ultimate control of the diabetic state;--6) The somatic growth of the diabetic child is maintained regardless of the type of treatment as long as it is effective. Growth is interrupted however very early if oral treatment becomes ineffective with regard to control of the diabetes. Monitoring of somatic growth during oral antidiabetic treatment is of obvious importance. An interruption in growth is an indication for insulin therapy even if the diabetic control appears satisfactory;--7) The course and the outcome of pregnancy do not appear to be affected by the use of oral therapy at the time of conception. This holds true also for cases in which oral treatment precedes the use of insulin, the pregnancy having commenced during the course of insulin therapy.
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STUDY DESIGN: A case of metformin-associated lactic acidosis after elective spinal surgery is reported. OBJECTIVE: To inform spinal surgeons of this potentially fatal side effect and make them aware that metformin should be stopped 48 hours before surgery. SUMMARY OF BACKGROUND DATA: Metformin is a commonly used oral hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus. A rare side effect of metformin is lactic acidosis, which has a 50% mortality rate. Risk factors for metformin-associated lactic acidosis include renal, hepatic, and cardiac failure. Two cases have been reported in postsurgical patients. No cases of this disorder have been reported after orthopedic procedures. METHODS: A patient who developed metformin-associated lactic acidosis after cervical spinal fusion is presented. RESULTS: Recognition of the cause and aggressive medical management led to resolution of the lactic acidosis. Subsequent surgery was uneventful when metformin was discontinued more than 48 hours before surgery. CONCLUSION: Spinal surgeons should be aware of this preventable, potentially fatal side effect and stop metformin 48 hours before surgery.
The binding of insulin to a specific receptor on IM-9-cultured human lymphocytes was studied in vitro under conditions simulating diabetic ketoacidosis. Compared with control incubations at pH 7.4, binding was reduced by 19 per cent at pH 7.1 and by 48 per cent at pH 6.8. Addition of beta-hydroxybutyrate, at concentrations similar to those seen clinically, "restored" insulin binding toward normal. We suggest that, by counteracting the effects of acidosis, ketoacids themselves maintain normal insulin-receptor binding in diabetic ketoacidosis. These data also illustrate that small molecules, present in vivo, can significantly alter the interactions between a hormone and its receptor in vitro.
Lactic acidosis is a serious clinical situation associated with a high case fatality rate. Lactic acidosis is particularly found in conditions with an insufficient supply of oxigen in the tissue. Other causes for lactic acidosis can be hepatic or renal insufficiency. For the therapy of overweight patients with type 2 diabetes metformin is the first choice if diet and physical training have been ineffective. Metformin, however, has the potential to increase serumlactate. Therefore its ability to cause lactic acidosis is controversely discussed. We present a 64-year-old female patient with metformin-associated lactic acidosis. She had several pre-existing risk factors to develop a lactic acidosis. On her referral to the hospital she suffered from acute renal failure which is considered to be a contraindication for the use of metformin.
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OBJECTIVES: To review diabetic ketoacidosis, including the "two bags system", a method of administering liquids in order to provide a smoother correction of the hyperglycemic and ketotic states. METHODS: Review of recent publications (last 7 years) from a Medline search and chapters published in pediatric textbooks that discuss the etiology, therapy, and complications of diabetic ketoacidosis. The management approach incorporates the findings of these publications as well as the clinical experience at the Childreńs Hospital of Philadelphia and Duke University Medical Center. RESULTS: The pathology of the type 1 Diabetes Mellitus involves the progressive destruction of the ss cells of the pancreas, causing insulin deficiency. Insulin is essential in the metabolism of carbohydrates, protein and fat. Insulin deficiency may lead to diabetic ketoacidosis which has three components: 1) hyperglycemia, which causes glycosuria and consequently dehydration; 2) lipolysis which, causes ketonemia/ketonuria; and 3) acidosis, that is caused by the dehydration and the high serum levels of ketones. Diabetic ketoacidosis is a serious condition and, if not treated appropriately, can cause coma and death. In children cerebral edema is the major complication of the therapy for diabetic ketoacidosis. Careful replacement of insulin, fluids, glucose and electrolytes is essential. CONCLUSIONS: The literature presents different ways to manage DKA in pediatrics, without a consensus on the cause of the most important complication (cerebral edema), and consequently without a consensus on the best approach. The use of the two saline bags in patients in DKA allows fast adjustments in the dextrose concentration of the infusion fluids, simplifying and reducing the costs of the treatment of diabetic ketoacidosis.