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At least 811 records · Page 45Linked to original sources
PubMed2006

Introduction and evaluation of a computerised insulin protocol.

OBJECTIVE: To lower glucose levels in all patients in the intensive care unit (ICU) to the target range of 4.5-7.5 mmol/l using a nurse-driven computerised insulin protocol in combination with bedside glucose measurement. DESIGN: Cohort study. SETTING: Mixed adult ICU. PATIENTS AND PARTICIPANTS: All 182 patients admitted to the ICU during a 3-month period were studied, except for 3 patients admitted for diabetic keto-acidosis. INTERVENTIONS: Five steps were taken to improve glucose regulation: (1) Nurses were authorised to adjust insulin dosage using a protocol. (2) Glucose was measured more often. (3) Glucose was measured at the bedside. (4) Consecutive protocols aimed for successively lower glucose levels; the final protocol had a target range of 4.5-7.5 mmol/l. (5) The protocol was computerised. MEASUREMENTS AND RESULT: Mean glucose decreased from 9.23 mmol/l without protocol to 7.68 mmol/l with the final protocol. This final protocol with the target of 4.5-7.5 mmol/l was evaluated more extensively. Glucose levels were measured a total of 1854 times in 179 ICU admissions during 552 ICU treatment days. The median glucose level was 7.0 mmol/l, and 53.1% of glucose measurements were within the target range of 4.5-7.5 mmol/l. One episode of hypoglycaemia (glucose </= 2.2 mmol/l) occurred, representing 0.5% of patients or 0.05% of glucose measurements. CONCLUSIONS: The combined strategy of successively more ambitious nurse-driven (computerised) insulin protocols and bedside glucose measurement resulted in acceptably low glucose levels with very few episodes of hypoglycaemia.

APACHE↗
PubMed1983

Variability of the electrophoretic mobility of low density lipoprotein. Comparison of interstitial fluid from human aortic intima and serum.

Interstitial fluid was collected from human aortic intima and the low density lipoprotein (LDL) was compared with serum LDL by two-dimensional immunoelectrophoresis. In half the samples derived from normal intima the migration rate was within +/- 10% of migration of LDL in serum, but in the remaining samples it was higher, indicating an increase in net negative charge on the molecule. By contrast, in most samples of interstitial fluid from gelatinous thickenings the migration rate of LDL was lower than in serum, indicating reduction in net negative charge. To test for the effect of different electrolyte concentrations in interstitial fluid and serum, migration of alpha 2-macroglobulin (alpha 2-M) was measured simultaneously in both. This showed no significant difference between interstitial fluid and serum, and varied by less than 2% between different serum samples. However, the mobility of LDL relative to alpha 2-M showed a remarkable variation, ranging from 80.9 to 127.1% of alpha 2-M mobility in interstitial fluid and from 58.6 to 115.9% in 23 serum samples. In serum, LDL relative mobility showed no correlation with general acid-base status, as indicated by serum bicarbonate levels, with fatty meals or diabetic keto-acidosis, or with extent of glycosylation of haemoglobin. This suggested that the variation in surface charge is intrinsic to the molecule and not a transient reflection of the plasma environment. Experimental alterations in the surface charge of LDL change its interaction with smooth muscle cells and macrophages in vitro, and its mitogenic properties. This raises the possibility that physiological variation in the surface charge of LDL in different subjects could alter its atherogenic potential.

Adult↗
PubMed2006

Obstructive uropathy.

Routine second trimester ultrasound screening has resulted in more infants diagnosed with antenatal hydronephrosis. Current recommendations suggest postnatal evaluation of all infants with a renal pelvic diameter >5 mm with ultrasound and voiding cystourethrogram (VCUG.) There are many etiologies of obstructive uropathy including ureteropelvic junction (UPJ) obstruction, ureterovesical junction (UVJ) obstruction, posterior urethral valves (PUV), prune belly syndrome, and vesicoureteral reflux (VUR). Obstructive uropathy can result in tubular damage and decreased nephron number. Tubular damage can result in sodium wasting, hyperkalemic acidosis, and nephrogenic diabetes insipidus. Most patients do not require renal replacement therapy in the neonatal period; however, chronic renal insufficiency can occur if the neonate has a significant reduction in nephron number or progressive renal damage from obstruction or infection.

Animals↗
PubMed1998

Primary cutaneous mucormycosis in a premature infant: case report and review of the literature.

Mucormycosis is an uncommon infection caused by fungi of the order Mucorales, family Mucoraceae, and almost always occurs in individuals with predisposing factors such as diabetes mellitus, metabolic acidosis, or immunodeficiency states. Although mucormycosis is a rare infection in childhood, sporadic cases of skin infections have been described in young infants and older children; primary skin infection has been associated with multiple nosocomial outbreaks caused by contaminated elastic bandages. In all reported cases involving premature infants, the elimination of the infection involved surgical debridement. We report for the first time successful conservative treatment with intravenous amphotericin B in a premature infant with primary cutaneous infection caused by Rhizopus oryzae.

Amphotericin B↗
PubMed2001

What do we really know about the ubiquitin-proteasome pathway in muscle atrophy?

Studies of many different rodent models of muscle wasting have indicated that accelerated proteolysis via the ubiquitin-proteasome pathway is the principal cause of muscle atrophy induced by fasting, cancer cachexia, metabolic acidosis, denervation, disuse, diabetes, sepsis, burns, hyperthyroidism and excess glucocorticoids. However, our understanding about how muscle proteins are degraded, and how the ubiquitin-proteasome pathway is activated in muscle under these conditions, is still very limited. The identities of the important ubiquitin-protein ligases in skeletal muscle, and the ways in which they recognize substrates are still largely unknown. Recent in-vitro studies have suggested that one set of ubquitination enzymes, E2(14K) and E3(alpha), which are responsible for the 'N-end rule' system of ubiquitination, plays an important role in muscle, especially in catabolic states. However, their functional significance in degrading different muscle proteins is still unclear. This review focuses on the many gaps in our understanding of the functioning of the ubiquitin-proteasome pathway in muscle atrophy, and highlights the strengths and limitations of the different experimental approaches used in such studies.

Animals↗
PubMed1989

Education for practice: the role of practical experience in undergraduate and general clinical training.

A questionnaire and interview study in two London medical schools reviewed the undergraduate curricula and house year from the perspectives of graduates one year after qualification. Data from 113 house officers (44%), obtained by questionnaire and interview, showed general satisfaction with training. However, they also saw undergraduate preparation as deficient in exposure to some practical procedures and common conditions, and several difficult communication skills were not taught. Graduates reported that they would have liked more experience as undergraduates in resuscitation, lumbar puncture, inserting nasogastric tubes, endotracheal intubation, and in managing diabetic keto-acidosis, asthmatic attacks, myocardial infarcts and respiratory failure. The purposes of the house year and the articulation between it and the undergraduate years require clarification.

Attitude of Health Personnel↗
PubMed1995

[A case of sepsis due to Escherichia coli isolated from blood, transtracheal aspiration and urine].

We reported a 53-year-old female who was admitted due to partial loss of consciousness. She had been diagnosed as old pulmonary tuberculosis and diabetes mellitus. She was diagnosed as diabetic keto-acidosis on admission. We isolated Escherichia coli in the blood, transtracheal aspiration (TTA) and from the urine. We have experienced 6 cases where the same bacteria was isolated from the blood and TTA at the same time. In all 6 cases, we have found single bacteria in the blood and a few other bacteria in TTA. Blood culture is the most certain method to detect the origin of infectious diseases. But the compromised host, as in this case, has multifocal infections in many cases. In order to understand the pathological aspects of the infection, we must obtain many kinds of samples and as many as possible.

Blood↗
PubMed1984

Endocrine physiology of electrolyte metabolism.

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.

Adrenal Cortex Hormones↗
PubMed1998

Guidelines for the treatment of acidaemia with THAM.

THAM (trometamol; tris-hydroxymethyl aminomethane) is a biologically inert amino alcohol of low toxicity, which buffers carbon dioxide and acids in vitro and in vivo. At 37 degrees C, the pK (the pH at which the weak conjugate acid or base in the solution is 50% ionised) of THAM is 7.8, making it a more effective buffer than bicarbonate in the physiological range of blood pH. THAM is a proton acceptor with a stoichiometric equivalence of titrating 1 proton per molecule. In vivo, THAM supplements the buffering capacity of the blood bicarbonate system, accepting a proton, generating bicarbonate and decreasing the partial pressure of carbon dioxide in arterial blood (paCO2). It rapidly distributes through the extracellular space and slowly penetrates the intracellular space, except for erythrocytes and hepatocytes, and it is excreted by the kidney in its protonated form at a rate that slightly exceeds creatinine clearance. Unlike bicarbonate, which requires an open system for carbon dioxide elimination in order to exert its buffering effect, THAM is effective in a closed or semiclosed system, and maintains its buffering power in the presence of hypothermia. THAM rapidly restores pH and acid-base regulation in acidaemia caused by carbon dioxide retention or metabolic acid accumulation, which have the potential to impair organ function. Tissue irritation and venous thrombosis at the site of administration occurs with THAM base (pH 10.4) administered through a peripheral or umbilical vein: THAM acetate 0.3 mol/L (pH 8.6) is well tolerated, does not cause tissue or venous irritation and is the only formulation available in the US. In large doses, THAM may induce respiratory depression and hypoglycaemia, which will require ventilatory assistance and glucose administration. The initial loading dose of THAM acetate 0.3 mol/L in the treatment of acidaemia may be estimated as follows: THAM (ml of 0.3 mol/L solution) = lean body-weight (kg) x base deficit (mmol/L). The maximum daily dose is 15 mmol/kg for an adult (3.5L of a 0.3 mol/L solution in a 70kg patient). When disturbances result in severe hypercapnic or metabolic acidaemia, which overwhelms the capacity of normal pH homeostatic mechanisms (pH < or = 7.20), the use of THAM within a 'therapeutic window' is an effective therapy. It may restore the pH of the internal milieu, thus permitting the homeostatic mechanisms of acid-base regulation to assume their normal function. In the treatment of respiratory failure, THAM has been used in conjunction with hypothermia and controlled hypercapnia. Other indications are diabetic or renal acidosis, salicylate or barbiturate intoxication, and increased intracranial pressure associated with cerebral trauma. THAM is also used in cardioplegic solutions, during liver transplantation and for chemolysis of renal calculi. THAM administration must follow established guidelines, along with concurrent monitoring of acid-base status (blood gas analysis), ventilation, and plasma electrolytes and glucose.

Acidosis↗
PubMed2001

IgA-kappa type multiple myeloma affecting proximal and distal renal tubules.

A 45-year-old male was admitted because of chest pain, lumbago, and bilateral ankle pain. Examination disclosed hypophosphatemic osteomalacia, acquired Fanconi syndrome, and abnormalities in distal nephron such as distal renal tubular acidosis and renal diabetes insipidus. Further exploration revealed IgA kappa multiple myeloma excreting urinary Bence Jones protein (kappa-light chain). Renal biopsy revealed thick basement membranes and elec-tron-dense crystals in proximal tubular epithelial cells. Immunofluorescent studies revealed deposition of kappa-light chain in renal tubular epithelial cells that caused the renal tubular damage. Although the osteomalacia was relieved by medical treatment, the urinary Bence Jones protein and the renal tubular defects were not improved by the chemotherapy for the myeloma. The patient died of exacerbation of multiple myeloma at 50 years of age.

Biopsy↗
PubMed1992

[Male osteoporosis, an unrecognised etiology: moderate idiopathic proximal tubulopathy (MIPT)].

Routine renal tubular investigations in 8 osteoporotic men, in whom phosphorus/calcium balance studies were normal or almost normal revealed moderate phosphorus (PD) or bicarbonate (BD) diabetes possibly responsible for their decalcification. Osteoporosis affected the spine and lower limbs, resulting in clinical pictures of frequently recurrent spontaneous algodystrophy. Histomorphometric studies revealed an increase in surface areas of resorption, the diagnosis of PD being based upon the finding at several successive investigations, in the absence of any drug treatment, of a phosphorus clearance of greater than 20 ml/min and/or a phosphorus reabsorption level of less than 80%. Arterial HC03 levels of greater than 21 mEg/l and a fractional bicarbonate excretion (FBE) of greater than 15% enabled the diagnosis of bicarbonate diabetes (proximal tubular acidosis). These cases of PD and BD appeared to be secondary to proximal tubulopathies for which no known etiology was found.

Acidosis, Renal Tubular↗
PubMed1991

Endocrine crises. Hyperkalemia.

Clinical disorders causing hyperkalemia require a basic understanding of normal K homeostasis, which consists of external and internal K balances. The kidney is predominant in maintaining the external balance of K, and a number of mechanisms exist to provide a renal adaptation to defend against K excess. Likewise, several factors are known to modulate internal K balance--i.e., its distribution within the body. Some of these factors may provide defense against hyperkalemia before the kidneys have time to adapt. Potassium retention by the kidney causes hyperkalemia when renal failure is advanced, or earlier in the face of impaired tubular function in a variety of disorders. Hyperkalemia out of proportion to loss of renal function also occurs in the syndrome of hyporeninemic hypoaldosteronism. Drug-induced hyperkalemia is increasingly common and usually is caused by nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, cyclosporine, or K-sparing diuretics. Clinical disorders of internal K imbalance include diabetes mellitus, systemic acidosis, and use of beta-blockers. Hyperkalemia is usually asymptomatic, but the danger of cardiac arrest or arrhythmia in severe hyperkalemia forces prompt clinical attention. Available treatment choices include agents that antagonize the effect of K on membrane potentials, redistribute it internally into cells, and remove it altogether from the body. The diagnostic work-up can then proceed, first by distinguishing renal and extrarenal causes, then by examining the roles of specific factors outlined in the section on normal K homeostasis.

Aged↗
PubMed1988

Management of hypophosphatemia.

The etiology, clinical presentation, and management of hypophosphatemia are reviewed. Phosphorus is a major intracellular anion and plays an important role in many biochemical pathways relating to normal physiologic functions. Approximately 60 to 90% of the 1 to 1.5 g of daily dietary phosphorus intake is absorbed, and of that amount, about two thirds is excreted in the urine. The overall incidence of hypophosphatemia is about 2 to 3% of all hospitalized patients. Factors associated with hypophosphatemia include phosphate-binding antacid therapy, nasogastric suction, liver disease, sepsis, alcoholism, and acidosis associated with diabetic ketoacidosis. Patients receiving parenteral nutrient solutions were also at higher risk for hypophosphatemia before the routine supplementation of these formulations with phosphate. Patients with hypophosphatemia may be asymptomatic or may experience weakness, malaise, anorexia, bone pain, and respiratory arrest. The major systems involved include the neuromuscular, hematologic, and skeletal systems. Phosphorus-containing products used to treat hypophosphatemia are a combination of monobasic and dibasic phosphate salts. Therefore, it is essential to calculate doses in millimoles rather than milligrams or milliequivalents to more accurately reflect the phosphorus concentration and to avoid potentially serious dosage errors. Normal daily requirements are readily maintained by dietary sources of phosphorus such as milk products or may be supplemented by phosphate-containing products administered orally or intravenously. Since phosphorus is a key factor in many organ systems, it is essential to monitor serum phosphorus concentrations in patients at risk for hypophosphatemia.

Humans↗