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Biomedical subjects

J L Caddell

Publications and source records attributed to J L Caddell.

At least 19 recordsLinked to original sources
PubMed1992

Hypothesis: new concepts concerning the pathophysiology of the sudden infant death syndrome due to magnesium deficiency shock.

There appear to be many contributing factors to sudden infant death syndrome (SIDS). One final common pathway that may explain some cases of SIDS is presented as a hypothesis: SIDS occurs as a shock-like event in a stressed infant with congenital or acquired magnesium deficiency with respect to calcium, or with genetically determined high magnesium requirements. Increased calcium and stress-related catecholamines favour platelet aggregation and release of mediators, chief of which appears to be thromboxane A2 (TXA2). TXA2, a major vasoconstrictor, bronchoconstrictor, and platelet aggregator is relatively unopposed during shock by prostacyclin, a vasodilator, bronchodilator, and platelet disaggregator which normally counterbalances its effects. The shock episode is self-limited. Infants who recover have suffered an apparent life threatening event (ALTE); those who die have insufficient pathology to explain the cause of death; the diagnosis is SIDS.

Humans↗
PubMed1989

Unreliability of plasma magnesium values in asphyxiated neonates.

The severely asphyxiated neonate usually shows a decreased blood pH and, if measured, a normal plasma Mg value. This is a retrospective review of the changes in these two parameters measured 2 or 3 times in 16 asphyxiated neonates as homeostasis was reestablished. The group was comprised of all asphyxiated neonates with 2 or 3 blood pH determinations, each with a plasma Mg determination within 6 h. Repeating these two tests had been prompted by poor clinical courses that suggested acid-base imbalance and Mg deficiency. The blood pH found on first sampling (day 0.42, with 0 the first day of life) was 7.24 +/- 0.02 (normal 7.35-7.45). This increased to 7.40 +/- 0.02 a mean of 2 days later (p less than 0.001 compared to first value by t test) and was still normal 4 days later (NS, compared to second value). The plasma Mg showed an opposing trend, with the first value 1.76 +/- 0.1 mEq/l (hospital normal 1.6-2.2 mEq/l); the second value 1.38 +/- 0.06 (p less than 0.004, compared to the first value), and the third, 1.30 +/- 0.11 (NS compared with the second value). It is concluded that plasma Mg determined during acidosis may give a falsely elevated value and may mask a true Mg deficiency which can be diagnosed only after homeostasis is reestablished, as when the blood pH is normal. While some asphyxiated infants were found to be hypomagnesemic, this study does not implicate Mg deficiency in meconium aspiration or any other cause of asphyxia.

Acidosis↗
PubMed1989

Validity of the parenteral magnesium load test for mature mammals.

Because of the difficulty in accurately assessing the Mg status of a hospitalized patient, the parenteral Mg retention test may be a valuable diagnostic tool. In former studies in animal models, this test has reliably identified adult rats fed two extremes of dietary Mg, but we found no tests of intermediate levels of Mg in adult animals. As a means of assessing the validity of the parenteral Mg retention tests in adult rats, the present study was conducted to learn (1) the relationship between Mg in plasma and bone in adult mammals that had optimal nutrition at the onset of the experiment, and (2) the relationship between Mg retention and Mg in plasma and bone in those animals. Animals were fed five levels of dietary Mg from 0 to 150 mg/100 g purified diet. Parenteral Mg retention tests were conducted after 2 weeks of dietary treatment, and 18 h after the completion of the tests, plasma and bone were analyzed for Mg. We found that plasma and femur levels of Mg varied linearly under conditions of Mg deficit, indicated by a high retention of the Mg load. As the deficit diminished, both plasma and femur levels approached a limit and the slope of the curve tends to zero. Mg retention and plasma or femur Mg level was approximated by a negative exponential curve. Stated another way, the logarithmic values of Mg retention decreased approximately linearly with increase in bone or plasma Mg. It was concluded that the parenteral Mg retention test is a valid test to evaluate Mg deficiency and to identify Mg sufficiency in adult mammals.

Animals↗
PubMed1988

Magnesium therapy in premature neonates with apnea neonatorum.

Apnea, bradycardia, and neuromuscular hyperirritability have been associated with magnesium (Mg) deficiency in young human infants and weanling animals. This is a retrospective review of a clinical experience of Mg therapy among 200 premature neonates who showed physical and clinical chemical changes compatible with Mg deficiency. The 200 infants all had idiopathic apnea neonatorum, and 93% also had the respiratory distress syndrome (RDS). This review was conducted to learn whether Mg therapy was associated with a significant reduction in apnea. The author suggested that the dose of Mg be 0.4 mEq/kg body weight/day, as 50% MgSO4.7H2O intramuscularly (IM) for 5 days; or as 1.0 mEq/kg/day, as 10% MgCl2.6H2O by mouth for 2 or more weeks, with appropriate monitoring of plasma Mg values in all infants. Sixty-one infants received a minimum of 5 days of Mg by either route (mean, 11.4 +/- 0.9, Group A); five received 3-4 doses IM (mean, 3.6 +/- 0.2, Group B); and 134 received 0-2 doses IM (0.5 +/- 0.1, Group C). Group A infants Mg-treated before Day 20 showed earlier cessation of apnea and bradycardia than those treated after Day 20. In Group A patients, 7 dose-days [corrected] of Mg therapy was associated with continuation of apnea; 14 dose-days [corrected], with cessation of apnea. Compared with Group A, Group C continued to develop apnea (P less than .003) and bradycardia (P less than 0.03) over longer periods of time. Group A infants showed no record of death or of hospital readmission for recurrent apnea, while 32 of 134 Group C infants had one or both of those unfavorable outcomes (P less than 0.001), with four of the five deaths in Group C (NS) as the sudden infant death syndrome (SIDS). In conclusion, Mg was associated with a reduction of apnea in this population. Emphasis was placed on the need to closely observe infants receiving supplementary Mg, with monitoring of plasma Mg levels.

Apnea↗
PubMed1988

Structural changes in lungs of magnesium-deficient weanling rats dying spontaneously or after spontaneous recovery from the seizure-shock episode. Possible methods for sudden infant death syndromes.

A light and electron microscopic study of Mg-deficient weanling rats showed structural changes of the lungs associated with the audiogenic seizure-shock episode, and with sudden, spontaneous death or spontaneous recovery after the shock episode. Pathogen-free weanling males were fed a Mg-deficient (Mg-0) or Mg-sufficient (Mg-100) diet and were raised in a gnotobiotic environment. Mg-100 rats (n = 16), unstressed or stressed with noise or strychnine, showed normal lungs. Mg-0 rats (n = 20) experienced audiogenic seizure-shock, followed by hyperventilation with tonic-clonic hyperextension of the back and extremities. The lungs of Mg-0 rats sacrificed during shock showed marked hemorrhage, including petechiae; edema; and atelectasis. Eight that died after a post-shock period of hyperventilation and hyperextension of the spine showed partial recovery of the pulmonary lesion; they showed well-expanded lungs, pleural petechiae, persistent congestion, with mild to moderate pathology. Mg-0 rats killed for study 2 days after the seizure-shock episode showed few small areas of residual lung pathology. Ultrastructural changes after Mg-O shock included aggregated platelets, leukocytes, and occasional reticulocytes in congested capillaries. Surfactant was disrupted during Mg-0 seizure-shock, but a layer closely applied to the surface of the epithelium was evident 2 days after shock. Mg-0 rats dying spontaneously showed nonspecific structural changes of the lung similar to changes reported in the sudden infant death syndrome (SIDS).

Acoustic Stimulation↗
PubMed1988

Magnesium therapy in infants with postneonatal apnea.

Idiopathic postneonatal apnea is defined here as a sudden, unexpected attack of apnea that first occurs after the infant has been discharged from the neonatal nursery to his home. Little has been published concerning the patient's physical and clinical laboratory findings during the acute episode. The present report of 20 infants with postneonatal apnea retrospectively addressed these parameters, including all investigations conducted for magnesium deficiency. The first episode of apnea occurred at 48 +/- 12.5 days of age and was unpredicted, transient, and self-limited. In the sickest infants, the apneic attack was a form of shock, with apnea, bradycardia, and often with acute respiratory distress, and/or neuromuscular hyperirritability. Laboratory findings in such infants were compatible with shock, including: acidosis, hemoconcentration, and hyperkalemia. Some infants showed high retention of parenteral Mg loads and received Mg therapy. Those receiving 5 or more days of Mg supplements were called 'Mg-treated'. Seven such patients were treated for 20.4 +/- 3.7 days. They were compared with 13 'Mg-untreated' patients who received less than 5 days of Mg therapy, 0.9 +/- 0.2 days. There was no known recurrence of apnea requiring resuscitation, or any rehospitalization for an apneic attack among the Mg-treated infants. Of the 13 Mg-untreated infants, 6 were readmitted for apnea at 90 +/- 37 days of age; 2 of these had a third admission for apnea. In conclusion, in its most severe form, postneonatal apnea is a shock-like episode that is self-limited, with a propensity to recur. Mg therapy appears to be associated with a reduction in recurrent apnea. This conclusion is corroborated by the significant reduction in recurrent apnea in the follow-up of a parallel study of 61 Mg-treated versus 139 Mg-untreated premature infants with idiopathic postneonatal apnea (p less than 0.001). Further study can be recommended.

Apnea↗
PubMed1987

Pulmonary lesion induced by stress in magnesium-deficient rats. A light- and electron-microscopic study.

A light- and electron-microscopic study was made of the lungs of magnesium (Mg)-sufficient and Mg-deficient pathogen-free weanling rats raised in a gnotobiotic environment. Mg-sufficient rats were studied unstressed, after mild auditory stress, or after strychnine seizures and showed essentially no pulmonary pathology. Mg-deficient rats were studied with no known seizures or immediately after audiogenic seizure-shock. Light microscopy of lung from Mg-deficient rats with audiogenic seizure-shock revealed atelectasis, generalized edema and hemorrhage, and pleural petechiae. Ultrastructural changes in lung alveoli of Mg-deficient rats with seizure-shock included gaps in capillary endothelium, swelling and separation of endothelial cells from the underlying basement membranes; Type I cell necrosis and separation from basement membranes; and intraalveolar red blood cells, fibrin, and precipitated plasma. The seizure-shock episode of acute Mg deficiency produces structural changes in the lung similar to changes produced by several forms of shock, early acute oxygen toxicity, and the respiratory distress syndrome (RDS) in human neonates.

Animals↗
PubMed1985

Protection by magnesium of renal calcinosis in furosemide-treated weanling rats with moderate magnesium deficiency.

Prolonged treatment of premature infants with the potent diuretic furosemide has resulted in hypercalciuria, sometimes with renal calcinosis and other complications. Furosemide was administered to weanling rats to explore its effect on magnesium and calcium metabolism. The animals were fed purified diets providing 40 mg magnesium/100 g diet or 10 mg magnesium/100 g. Half of each dietary group (40-F or 10-F) received 18 doses of furosemide, 20 mg/kg body weight, intraperitoneally between days 7 and 35, and half received normal saline intraperitoneally (40-O or 10-O). Furosemide had little effect on the magnesium-sufficient animals (40-F), but comparison of 10-O and 10-F data showed that it aggravated the magnesium-deficiency syndrome. Comparison of data from 40-F and 10-F animals showed the protective effect of magnesium in preserving calcium homeostasis in furosemide-treated animals: the elevation of calcium values in 10-F rats was greater in plasma (p less than 0.0005), heart (p less than 0.0025), and kidney (p less than 0.0005). Stated another way, furosemide was associated with severely disordered calcium metabolism only in animals fed suboptimal magnesium. Studies exploring the role of magnesium in furosemide-treated infants can be recommended.

Animals↗
PubMed1978

The postmortem diagnosis of magnesium deficiency: studies in an animal model for the human infant.

Weanling rats were studied as a model for the human infant to determine the optimal tissue in which to assess the status of magnesium after death. Control rats were fed laboratory chow or purified diets that provided a surfeit of magnesium and accommodated a normal rate of growth. Other rats were fed diets that resulted in two degrees of magnesium deficiency: one that might result in spontaneous death within one week, and the other, within two weeks. These times may correlate with six months and one year in the human infant, the period during which the sudden infant death syndrome usually occurs. There was no consistent difference between the magnesium concentration found in the vitreous humor, liver, heart, or skeletal muscle of magnesium-deficient and control rats. However, bone accurately reflected the level of dietary magnesium. There was a significant difference between the magnesium concentration of the anterior and posterior halves of the ribs, indicating irregular distribution of magnesium within the bone. Significant differences were found in the magnesium concentrations of different bones from the same animals. Therefore one entire bone, such as the sternum or the rib, should be studied. The need to match control and study subjects for age was apparent.

Animals↗
PubMed1975

Parenteral magnesium load tests in postpartum American women.

The magnesium status of 185 moderate income American mothers was assessed in the immediate postpartum period by the intravenous magnesium load test. Pre- and postload collections of urine were each made for approximately 24 hours because pilot studies revealed significant diurnal variation in magnesium excretion. The magnesium load provided 0.4 to 0.5 mEq of magnesium/kg of estimated lean body weight. The mean retention was 51% +/- 2.2 (SEM). Patients retaining more or less than an arbitrary limit of 40% of the magnesium load were compared. No differences in mean age, weight, or parity were found between the groups. The high retention group reported a diet lower in magnesium and had a significantly lower plasma magnesium value. Magnesium retention of over 90% of the load was found in biologically immature multiparas (less than 17 years) and in young mothers of twins. Among the multiparous patients, those with the longest interval since the previous pregnancy had the lowest retention values. Most of the primiparous patients had met the magnesium requirements of a singleton pregnancy and rejected most of the load, but 6 primiparous women whose active labor exceeded 18 hours had a retention of 77.91% of the load. This was significantly higher than the 45.0 +/- 3.52 (SEM) % retention in 70 primiparous mothers with shorter duration of active labor (P less than 0.005). No other symptoms or complications of pregnancy could be correlated with the magnesium load values. Further definition of the magnesium load test is indicated.

Adolescent↗
PubMed1975

The magnesium load test: I. A design for infants.

The purpose of this study was to design the shortest suitable magnesium load test for infants up to six months of age. A 56-hour test was used to study cation and creatinine excretion before and after an intramuscular load of 0.49 mEq of magnesium/kg of body weight. No diurnal excretion pattern for magnesium was found, and most of the magnesium rejected by the kidney was excreted by neonates within 32 hours, and by infants from one to six months of age within 24 hours. The postload urinary magnesium value usually stabilized at a slightlyhigher level than the preload level. The mean plasma magnesium level increased about 0.65 mEq/liter one hour after the load, and at the end of the test was 0.25 mEq/liter higher than the initial value; abnormally low plasma values were normalized. Renal excretion of creatinine and potassium was not affected by the magnesium load, but the 24-hour postload excretion was higher than the 24-hour preload excretion of calcium for all patients, and of sodium for some full-term neonates. Because of slow excretion of magnesium and concomitant caocium loss, special precautions are required for testing and repletion of young infants to avoid magnesium overload and calcium depletion. A suitable test would have an eight-hour preload period, a load of 0.49 mEq of magnesium (0.12 ml of 50 per cent MgSO4.7H20) per kg of body weight, and a postload collection of 32 hours for neonates and 24 hours for infants from one to six months of age.

Age Factors↗
PubMed1975

The magnesium load test: II. Correlation of clinical and laboratory data in neonates.

Parenteral magnesium load tests were conducted on 91 infants less than one month of age, most of whom had marked hyperirritability and symptoms compatible with the diagnosis of electrolyte imbalance with relative or absolute magnesium deficiency. Most of the patients studied had a 40-hour test, with an eight-hour preload and a 32-hour postload collection of urine. Of 43 premature infants studied, only three retained less than 40 per cent of the load: one was untreated, one had low retention of a second load following a course of therapy, and the mother of the third had received magnesium within 24 hours of delivery. Of 48 full-term infants studied, ten retained less than 40 per cent of the load. These were asymptomatic or had minor problems. Irritability was common in both high and low retention groups. Ten per cent of the low retention group and 50 per cent of the high retention group manifested two or more of the nonspecific signs compatible with the diagnosis of magnesium deficiency; the difference was significant (P smaller than 0.025). Eleven premature and six full-term infants with very high initial retention received five or six intramuscular injections of magnesium, after which the magnesium retention was about 30 per cent lower than the initial value. For most patients, repletion therapy was given orally. Although low plasma magnesium values related to high magnesium retention, correlation on an individual basis was poor. The plasma calcium levels of three patients with combined hypomagnesmia and hypocalcemia failed to respond to calcium therapy and remained low until the plasma magnesium value was corrected. Magnesium appeared to be specific therapy for symptomatic infants found to be deficient. More males than females had sufficient symptoms to warrant study.

Calcium↗
PubMed1975

The magnesium load test: III. correlation of clinical and laboratory data in infants from one to six months of age.

A study of 64 infants from one to six months of age was made using the 32-hour parenteral magnesium load test. Most of the infants were studied for neuromuscular hyperirritability or other signs compatible with magnesium deficiency; some with unrelated problems served as controls. Magnesium retention below 40 per cent was found in 26 infants who presented with minor sign or signs that were otherwise explained, as by infection. Twelve who retained 72 per cent of the load were normal or small at birth, amply fed on demand, and grew at accelerated rates, increasing from the 50th to the 88th mean percentile by ten weeks, when they were "fat, hungry, jumpy babies," exemplifying the Mg deficiency syndrome of growth. Seven infants of 8.2 plus or minus 1 weeks had had one or more sudden, transient episodes that included: apnea, gasping, tonic or tonic-clonic fits, and flaccidity, often with pallor, cyanosis, eye signs, sweating, or tearing. Despite preload Mg in two, the group retained 88 per cent of the load. Mg appeared to be specific therapy in high retention groups. The signs are nonspecific but resemble premonitory signs and the type of episode that may occur in the sudden infant death syndrome (SIDS), suggesting a possible link between magnesium depletion and SIDS.

Black or African American↗