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Hypophosphatemia is a common disorder caused by decreased intake, increased loss or transcellular shift of phosphorus. Symptoms of severe hypophosphatemia include reversible depression of myocardial function, acute respiratory failure, coma, rhabdomyolysis, osteomalacia, renal tubular acidosis and hemolysis. This paper discusses common clinical disorders associated with hypophosphatemia and presents an approach to diagnosis and treatment.
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PMID:A clinical approach to common electrolyte problems: 3. Hypophosphatemia. 641 67

We evaluated the accuracy of a new device for continuous noninvasive measurement of cutaneous PCO2. The Hewlett-Packard capnometer (model 47210/HA) works by means of an infrared transducer applied to the forearm over an area of skin that has been stripped of the stratum corneum. Capnometer transcutaneous carbon dioxide pressure (CPCO2) was compared with arterial carbon dioxide pressure (PaCO2) during 60 simultaneously obtained measurements in 13 hemodynamically stable patients. Each patient was studied for 1 1/2 to 5 hours, and a wide range of PaCO2 values (21 to 82 mm Hg) was represented. The data show a clinically significant relationship whereby PaCO2 = CPCO2 - 4.13, with a SE of +/- 2.19 mm Hg. Clinical usefulness of noninvasive cutaneous CO2 monitoring can be foreseen in patients whose ventilatory support is being tapered, in those with respiratory depression caused by various neuromuscular disorders, and in patients with chronic obstructive pulmonary disease and acute respiratory failure. Our results indicate that continuous transcutaneous CPCO2 measurements are safe and accurate and strongly suggest that they can be of clinical usefulness in a select group of hemodynamically stable patients.
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PMID:Transcutaneous noninvasive monitoring of carbon dioxide tension. 679 84

Continuous positive pressure ventilation (CPPV) is an established therapy for treatment of acute respiratory failure (ARF). However, cardiac performance may be severely disturbed due to elevated intrathoracic pressure, inducing a decrease in cardiac output (CO) and oxygen delivery (DO2). Alternatively, mechanical ventilation with prolonged inspiratory to expiratory duration ratio (inversed ratio ventilation IRV) has been successfully used in ARF. No data are available about IRV in acute haemodynamic oedema. Thus, the cardiopulmonary effects of CPPV (positive end-expiratory pressure [PEEP] = 10 cm H2O) and IRV (inspiration to expiration duration ratio [I:E] = 3.0) were studied in nine dogs (body weight 29.9 +/- 4.3 kg) before and after induction of myocardial ischaemia. METHODS. Continuous intravenous anaesthesia and muscle paralysis were provided by 1.2 mg.kg-1 x h-1 piritramide and 0.08 mg.kg-1 x h-1 pancuronium, and the animals were ventilated with intermittent positive pressure ventilation (IPPV) as reference method. Cardiocirculatory performance was determined by means of heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and left ventricular end-diastolic pressure (LVEDP). Cardiac output (CO) was determined by thermodilution method. Systemic vascular resistance (SVR) was calculated. Pulmonary function was assessed by arterial and mixed venous blood gas tension for oxygen (PaO2, PvO2) and carbon dioxide (PaCO2). Functional residual lung capacity (FRC) was measured by means of the foreign gas wash-in method using helium as inert gas, and determination of extravascular lung water (EVLW) using the thermal-dye indicator technique. CPPV and IRV were studied in random sequence in the control phase and 60 min after induction of acute left ventricular ischaemia, which was achieved by occlusion of the ramus interventricularis anterior. RESULTS. During the control phase CPPV induced an increase in MPAP (P < 0.05), CVP (P < 0.05) and PAOP (P < 0.05). HR and MAP remained unchanged, whereas CO decreased by 16% (P < 0.05). FRC was elevated by 25 ml.kg-1 (P < 0.01), but not EVLW (9.1 +/- 3.5 ml.kg-1). There was no improvement in oxygenation; instead, oxygen delivery (DO2) decreased (P < 0.05). During inversed ratio ventilation MPAP, CVP, PAOP increased, but less than during CPPV. FRC was elevated mu 7.0 ml.kg-1 (P < 0.05), which was significantly less than during CPPV (P < 0.05). EVLW revealed no differences. During IPPV in the ischaemia phase cardiopulmonary performance deteriorated significantly. CO decreased by 19% (P < 0.05), whereas HR, MPAP, CVP and PAOP increased (P < 0.05). PaO2 was lower (P < 0.05) and alveolo-arterial PO2 gradient (PAaO2) increased (P < 0.05). All animals revealed moderate pulmonary oedema (EVLW = 15.1 +/- 8.4 ml.kg-1) (P < 0.01) and a lower FRC. Mechanical ventilation with PEEP significantly improved oxygenation and FRC; however, DO2 was slightly lower than during IPPV (not significant). IRV elevated PaO2, FRC and DO2, since CO was not depressed when compared with IPPV. CONCLUSIONS. CPPV and IRV may induce a recruitment of collapsed or hypoventilated lung areas, which is more pronounced during CPPV. During both modes of ventilation, oxygenation was improved without apparent changes in EVLW. Haemodynamic performance was more impaired during CPPV, and no improvement of left ventricular function secondary to an elevated intrathoracic pressure was observed. Occlusion of the RIVA coronary artery typically induces an infarction of 35% of left ventricular muscle mass; however, non-ischaemic myocardium reveals an unchanged or increased contractility. Thus, a reduction of left ventricular preload secondary to CPPV mainly contributes to haemodynamic depression, which is less pronounced during IRV due to a lower peak inspiratory airway pressure and mean airway pressure. IRV may be useful for mechanical ventCntCo
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PMID:[Cardiopulmonary effects of CPPV (continuous positive pressure ventilation) and IRV (inverse ratio ventilation) in experimental myocardial ischemia]. 848 92

Although hypophosphatemia is relatively uncommon, it may be seen in anywhere from 20% to 80% of patients who present to the ED with alcoholic emergencies, diabetic ketoacidosis (DKA), and sepsis. Severe hypophosphatemia, as defined by a serum level below 1.0 mg/dL, may cause acute respiratory failure, myocardial depression, or seizures. Because hypophosphatemia is not as often treated by ED physicians, becoming familiar with a single intravenous phosphate solution and specific guidelines for phosphate repletion are essential. One mL of the most commonly available phosphate solution (K2PO4) contains 4.4 meq of potassium and 3 mmol (93 mgs) of phosphate. Administering K2PO4 at a rate of 1 mL per hour is almost always a very safe and appropriate treatment for hypophosphatemia. This article provides guidelines for phosphate therapy in hypophosphatemic ED patients including those in DKA, those presenting with alcohol-related complaints including alcoholic ketoacidosis and patients with acute exacerbation of asthma and chronic obstructive pulmonary disease.
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PMID:Hypophosphatemia in the emergency department therapeutics. 1091 39

We report 6 patients in whom diffuse alveolar damage (DAD) was found on 1 or more lung biopsy specimens and who experienced recurrent episodes of acute respiratory failure. The patients ranged in age from 43 to 55 years. Two to five episodes of respiratory failure occurred in each over a period of 4 months to 2 years. One patient developed evidence of chronic lung disease; while the others remained well between episodes. Lung biopsies showed the acute stage of DAD in 3, overlapping acute and organizing stages in 3, and the organizing stage in 2. A definite cause was not identifiable in any. However, 4 had been treated with narcotics for chronic pain before the first episode, and 1 received this treatment before the recurrent episode. Three also were receiving psychotropic drugs for anxiety and depression. Five patients had evidence of gastroesophageal reflux disease (GERD) and/or hiatal hernia, 2 of whom underwent Nissen fundoplication in hopes of preventing future recurrences. Although a definite cause of the recurrent DAD was not identified, the findings suggest the possibility of a reaction to narcotics and/or psychotropic drugs in some patients, with a possible additional effect of GERD. A drug history should be carefully elicited in patients with recurrent DAD, and all potentially toxic drugs should be stopped.
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PMID:Diffuse alveolar damage and recurrent respiratory failure: report of 6 cases. 1177 76

The effects of acute renal failure on the impeded (IER) and unimpeded (UER) eruption dental rate and attrition rate (AR) were investigated. Adult female Wistar rats were injected with 125 mg/kg b.w of human methemoglobin (M-Hb) in order to induce a first episode of hemodynamically-mediated acute renal failure (H-ARF). Ten days after the injection of M-Hb, other groups of rats received another equal dose of the drug in order to induce a second episode of H-ARF. A group of six animals was pair-fed daily and individually with rats of M-Hb groups. Evaluation of renal function, histopathology studies, IER, UER, food intake (FI), AR and body weight gains was performed at different times after the first and second injections, of M-Hb. Treatment induced transient increases in plasma urea concentration and urine volume, and significant depression in urine osmolality, body weight gains, IER, UER and AR. In every case, the maximal effect of the first injection of M-Hb on the individual parameters was always greater than that of the second injection. Histologic sections showed interstitial cellular infiltration, desquamation of the proximal tubular epithelium and collapse or dilation of the tubular lumen. The functional values of kidney, histologic findings, IER, UER and AR of the pair-fed rats were not significantly different from control values. The results of the present study indicate that dental eruption rate (IER and UER) is relatively low in uremic rats with kidney tubule lesions and that both parameters are related.
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PMID:Depressed eruption dental rate in rats with hemodynamically-mediated acute renal failure. 1188 31

Repression of telomerase in the somatic tissues of humans, and probably other long-lived mammals, appears to have evolved as a powerful protective barrier against cancer. Immortalization in vitro of normal human cells that lack telomerase involves the reactivation of telomerase or, rarely, an alternative (ALT) mechanism for maintaining telomeres. Inactivation of the effectors of replicative senescence, i.e. genes encoding one or more elements of the p16/pRB and/or ARF/p53/p21 anti-proliferative pathways, is required for telomerase depression leading to immortalization. Regulation of telomerase in normal human cells is mediated primarily by transcriptional repression of hTERT, the gene encoding the catalytic subunit of telomerase. Rodent cells do not possess stringent controls on telomerase activity in the soma and this explains why they are so readily immortalized and transformed in culture compared with their human counterparts. Because active telomerase has been found to exist in the proliferative compartments of self-renewing tissues, it is not yet clear whether the telomerase present in 90% of human cancers exists as a consequence of selection of pre-existing telomerase-positive cells during carcinogenesis or through induction of hTERT expression in cells in which it is normally tightly repressed. In support of the latter, chromosome transfer techniques have revealed the presence of genes on normal human chromosomes that are able to extinguish hTERT transcription in cancer cells and induce them to undergo senescence. It is clear that telomerase is obligatory for continuous tumour cell proliferation, clonal evolution and malignant progression. Telomerase therefore represents an attractive target at which to aim new anti-cancer drugs. Results with a variety of telomerase inhibitory strategies in human cancer cells have confirmed that its functional inactivation results in progressive telomere shortening, leading to growth arrest and/or cell death through apoptosis. Promising candidate small molecule inhibitors are beginning to emerge that will form the basis for anti-telomerase drug development.
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PMID:The significance of telomerase activation and cellular immortalization in human cancer. 1243 51

In the period from 1990 to 2002, 201 patients with suicidal antihypertensive drugs poisoning were treated, including 138 women and 63 men from 15 to 84 (mean 36) years old. The main causes of suicides were various kinds of depression (63%) as well as psychopathy and/or sociopathy (16%) and schizophrenia (10%). Twenty eight patients attempted repeatedly to commit suicide. Thirty six persons were poisoned by only antihypertensive drugs, in 165 remaining cases intoxications were mixed including antihypertensive and other different medications. beta-blockers (38.3%), calcium channel blockers (34.8%), angiotensin converting enzyme inhibitors (24.3%) and diuretics (2.5%) were used in suicidal attempts. There were no suicidal poisonings with angiotensin II AT1 receptor antagonists, alpha 1-blockers and imidazole receptor agonists. In the examined group three patients died of cardiogenic shock, electromechanical dissociation and secondary acute respiratory failure resistant to therapy. The drugs used in these cases were propranolol, amlodipine, theophylline, captopril, doxepine, propafenone, furosemide, methimazole and alcohol. Mortality rate in antihypertensive drug poisonings was 1.5%.
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PMID:[Suicidal poisoning with antihypertensive drugs]. 1456 90

Acute respiratory failure is a common complication of drug abuse. It is more likely to develop in the setting of chronic lung disease or debility in those with limited respiratory reserve. Drugs may acutely precipitate respiratory failure by compromising respiratory pump function and/or by causing pulmonary pathology. Polysubstance overdoses are common, and clinicians should anticipate complications related to multiple drugs. Impairment of respiratory pump function may develop from central nervous system (CNS) depression (suppression of the medulla oblongata, stroke or seizures) or respiratory muscle fatigue (increased respiratory workload, metabolic acidosis). Drug-related respiratory pathology may result from parenchymal (aspiration-related events, pulmonary edema, hemorrhage, pneumothorax, infectious and non-infectious pneumonitides), airway (bronchospasm and hemorrhage), or pulmonary vascular insults (endovascular infections, hemorrhage, and vasoconstrictive events). Alcohol, cocaine, amphetamines, opiates, and benzodiazepines are the most commonly abused drugs that may induce events leading to acute respiratory failure. While decontamination and aggressive supportive measures are indicated, specific therapies to correct seizures, metabolic acidosis, pneumothorax, infections, bronchospasm, and agitation should be considered. Drug-related respiratory failure when due to CNS depression alone may portend well, but in patients with drug-related significant pulmonary pathology, a protracted course of illness may be anticipated.
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PMID:Acute respiratory failure from abused substances. 1529 19

A subgroup of patients infected with the Hantavirus develops a pulmonary syndrome (HPS) characterized by severe acute respiratory failure and myocardial depression, that has a high mortality rate. Extracorporeal life support (ECLS) could be a valuable therapeutic tool in such patients. We report a 24 years old male with HPS that was successfully managed when an arterio-venous shunt was added to a conventional veno-arterial ECLS technique. Precise criteria have been developed to predict which patients should be considered for this treatment.
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PMID:[Addition of an arterio-venous shunt during veno-arterial extracorporeal life support in a patient with Hantavirus pulmonary syndrome]. 1634 89


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