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Biomedical subjects

B Chernow

Publications and source records attributed to B Chernow.

At least 145 records · Page 8Linked to original sources

Gastroesophageal fundoplication improves symptoms in refractory asthma.

Gastroesophageal (GE) reflux has been etiologically linked to a number of pulmonary diseases. Subclinical pulmonary aspiration from nocturnal GE reflux has been proposed as a cause of asthma. A patient with severe asthma, refractory to conventional medical therapy, is presented. The asthma was presumed to be secondary to gastroesophageal reflux and indeed the patient became asymptomatic following a Nissen fundoplication procedure. This case report documents that surgical correction of GE reflux may be an appropriate therapeutic maneuver in asthmatics who subclinically aspirate as a consequence of GE reflux.

Adult↗

Gentamicin-induced hypomagnesemia.

There have been several case reports of hypomagnesemia associated with gentamicin therapy. A cause and effect relationship between gentamicin and hypomagnesemia has been difficult to establish in these cases due to: 1) large doses of gentamicin; 2) concomitant administration of other antibiotics and cytotoxic agents; 3) failure to monitor drug levels; and 4) poor oral intake. To test for a direct cause and effect relationship and to determine the frequency of gentamicin-induced hypomagnesemia, we administered the drug for 10 days to six healthy, well-fed, subhuman primates. Five of the six animals developed a mean decrease in serum magnesium of 0.34 mg/dl (P = 0.03) after 10 days of therapy. Four of the five had levels in the frankly hypomagnesemic range (less than 1.4 mg/dl). Urine magnesium values were inappropriately elevated in relation to serum magnesium concentrations. It is concluded that gentamicin-induced hypomagnesemia may occur more commonly than has been previously appreciated. Serial monitoring of serum magnesium in patients receiving gentamicin is recommended.

Animals↗

Fenfluramine lowers plasma norepinephrine in overweight subjects.

The effect of fenfluramine on sympathetic nervous system activity was determined in 12 normotensive, obese men. Supine plasma norepinephrine (NE) concentrations decreased (p less than 0.001) from pretherapy levels (298 +/- 39 pg/ml) after one (166 +/- 30 pg/ml) and four weeks (171 +/- 28 pg/ml) of fenfluramine (60 mg daily). Fenfluramine did not alter the sympathetic nervous system responses to orthostasis or exercise. Fenfluramine-induced decreases in heart rate (72 +/- 3 to 67 +/- 4 beats/min, p less than 0.01) and mean arterial blood pressure (90 +/- 2 to 81 +/- 2 mmHg; p less than 0.005) were observed after only one week of therapy despite no significant change in body weight. We conclude that fenfluramine may be a useful agent in the treatment of patients with sympathetic hyperactivity. The effects of fenfluramine on given subsets of patients and control subjects are also defined.

Adult↗

Effect of clonidine on sympathetic nervous system activity in patients with essential hypertension.

This study analysed the effects of both seven and 30 days of treatment with clonidine on heart rate, blood pressure (BP), plasma norepinephrine (NE) levels and dopamine-beta-hydroxylase (DBH) activity at rest and after standing in seven patients with essential hypertension. The patients and 10 age-matched normotensive control subjects were evaluated under medication-free baseline conditions; the hypertensive patients were then given clonidine 0.1 mg twice daily. Baseline plasma NE and DBH levels were similar between the groups. Seven and 30 days of clonidine therapy reduced blood pressure (p less than 0.001) and NE concentrations (p less than 0.05) significantly. Clonidine did not effect the percent increase in NE induced by standing and was not associated with orthostatic hypotension. The blood pressure lowering effects of clonidine appear related to the centrally mediated and/or direct suppression of peripheral noradrenergic activity, indicating the utility of clonidine in cases of hypertension were the sympathetic nervous system (SNS) is hyperactive. Clonidine may also prove especially useful in cases where the initial pharmacotherapy (such as a diuretic) causes activation of the SNS.

Adult↗

Postprandial hypoglycemia after Nissen fundoplication for reflux esophagitis.

The motility of the stomach is modulated by the complex interplay of muscular, humoral, and neuronal factors. Rapid gastric emptying has been described after gastrectomy, gastrojejunostomy, vagotomy with pyloroplasty, and with active peptic ulcer disease. Rapid emptying may result in "dumping" syndrome and in postprandial hypoglycemia. We report a patient who developed postprandial hypoglycemia after a Nissen fundoplication for reflux esophagitis. This is the first report of this complication after this surgical procedure. The hypoglycemia was secondary to a combination of rapid gastric emptying, rapid absorption of glucose causing hyperglycemia, and excessive insulin secretion. This syndrome should be considered in patients who develop hypoglycemic symptoms after fundoplication. Treatment with a low carbohydrate diet and anticholinergic agents may offer symptomatic relief.

Adult↗

Development of a primate model of exposure hypothermia.

A nonhuman primate model of exposure-induced hypothermia was developed and the hemodynamic effects of hypothermia were evaluated in five animals. With decreasing core temperature from 37 degrees C to 33 degrees C there was a 47% increase in heart rate, a 23% increase in mean arterial pressure, a 48% increase in cardiac output, a 260% increase in oxygen consumption, and a 237% increase in minute ventilation. As the core temperature decreased from 33 degrees C to 29 degrees C there were decreases in the heart rate, blood pressure, and cardiac output such that at 29 degrees C these values were not significantly different from the values obtained at 37 degrees C. However, the oxygen consumption was still 180% increased and the minute ventilation 40% higher at 29 degrees C than at 37 degrees C. This model will allow the evaluation of the physiology of hypothermia and the effectiveness of different rewarming techniques.

Animals↗

Postcraniotomy diabetes insipidus. Who's at risk?

Diabetes insipidus (DI) is thought to be a relatively common complication after craniotomy procedures. To identify subsets of patients at risk for this problem, the postoperative courses of 135 consecutive patients undergoing craniotomy were scrutinized retrospectively. All patients received similar anesthetic management and all were hospitalized in the ICU postoperatively. DI developed in 9 (5 transient, 4 permanent) of 135 patients (6.7%). All 9 patients developing DI had undergone craniotomy for treatment of a pituitary disorder. It is concluded that postcraniotomy DI is a problem almost exclusively observed in patients with pituitary/hypothalamic disease and that DI rarely occurs in patients with other types of intracranial pathology.

Adult↗

Bedside blood glucose determinations in critical care medicine: a comparative analysis of two techniques.

The accuracy of a new reagent test strip (Chemstrip BG) for the quantitative estimation of whole blood glucose concentration was compared to that of a widely used test strip (Dextrostix). To perform the comparative study, venous blood specimens were obtained from 133 patients. Interpretations of reagent strip glucose readings were made by three observers who separately recorded their impressions from the two strips on each patient. These estimated levels were compared to quantitative (glucose oxidase) concentrations measured from the same specimen. Although there were significant correlations (p less than 0.001) between both reagent strips and the measured values, the Chemstrip BG results more closely approximately measured values for the range of glucose concentrations encountered (10-600 mg/dl). In addition, Chemstrip BG was easier to read and measured a wider range of values than Dextrostix and, unlike Dextrostix, Chemstrip BG strips could be stored for review at a later time. This new glucose test strip accurately and rapidly determines whole blood glucose concentration at the bedside.

Blood Glucose↗

Plasma, urine, and CSF catecholamine concentrations during and after ketamine anesthesia.

Ketamine has been reported to increase plasma catecholamine concentrations. Prior investigations have only studied plasma catecholamine levels for short periods after iv ketamine. Because ketamine is one of the most frequently used anesthetic agents in critical care research, we evaluated ketamine's effect on catecholamines over a longer period of time. Plasma, urine, and CSF epinephrine (E) and norepinephrine (NE) concentrations were serially measured during a 2-h ketamine infusion and a subsequent 2-h "wake-up" period. No changes in heart rate, mean arterial blood pressure or urine, plasma, and CSF NE concentrations were noted during the 4-h study period, whereas there were significant (p less than 0.005) increases in urine, plasma, and CSF E levels during ketamine infusion but not during the wake-up period. An unexpected finding was that the baboons have very high basal plasma E levels versus those in humans. It is concluded that ketamine is a useful anesthetic agent for critical care research involving measurements of sympathetic nervous system activity. The interesting observation of high plasma levels in the baboon warrants further investigation.

Anesthesia↗

Marked stress hyperglycemia in a child.

A 16-month-old child is presented who developed severe "stress hyperglycemia" with the onset of a respiratory distress syndrome. The serum glucose rose from 74 mg/dl to 520 mg/dl and returned to 52 mg/dl all within 24 h. These variations in serum glucose were paralleled by a similar marked increase in plasma cortisol concentration (from 41 to 90 to 36 micrograms/dl). The patient was receiving no iv dextrose and required no exogenous insulin. These data are consistent with a diagnosis of stress hyperglycemia. This report is unique in that, to our knowledge, stress hyperglycemia to levels greater than 350 mg/dl have not been previously reported in either adults or children.

Humans↗

Hypocalcemia in critically ill patients.

Hypocalcemia is an important metabolic problem in critical care medicine. To determine the frequency of this problem and the patient subsets at risk, a retrospective study of a large series of ICU patients was performed. During the study period, 259 patients were admitted to the ICU, of whom 210 (81%) had a serum calcium (Ca++) measured. Of these 210 patients, 135 (64%) were hypocalcemic (serum Ca++ less than 8.5 mg/dl) and 75 (36%) were normocalcemic. Serum albumin concentration was less than 3.5 g/dl in 70% of the hypocalcemic patients who hd albumin measured, suggesting that the ionized Ca++ concentration may have been normal in many of these patients. On the other hand, 32% of the hypocalcemic patients were alkalotic (pH greater than or equal to 7.45) which indicates that ionized Ca++ levels may have been low because Ca++ binding to protein increases with alkalosis. Gastrointestinal bleeders and postabdominal surgery patients were more likely to have low total serum Ca++ whereas cardiac and neurosurgical patients were more likely to have a normal total serum Ca++ (p less than 0.05). Ionized Ca++ was calculated in 36 of the normocalcemic and 80 of the hypocalcemic patients. The hypocalcemic group had significantly lower ionized Ca++ levels when compared to those of the normocalcemic group (p less than 0.001). Patients with low serum Ca++ values spent a longer time in the ICU (p less than 0.01), had an increased incidence of renal failure and sepsis (p less than 0.01), had an increased mortality rate (p less than 0.001), and received a greater number of blood transfusions (p less than 0.001) than patients in the normocalcemic group. It is concluded that: (1) hypocalcemia is a frequent finding in critically ill patients; (2) determining ionized Ca++ levels is useful because many ICU patients have alterations in both arterial pH and serum albumin levels; (3) hypoalbuminemia, sepsis, red cell transfusions, and renal failure are predisposing factors for hypocalcemia; and (4) hypocalcemic patients do less well clinically than normocalcepatientsmic patients.

Calcium↗

Secondary adrenal insufficiency after intrathecal steroid administration.

A 38-year-old man developed secondary adrenal insufficiency as a consequence of intrathecal methylprednisolone administration. Evidence in support of this diagnosis included an absent plasma cortisol response to insulin-induced hypoglycemia, an inadequate adrenal response to exogenous corticotropin stimulation, a typical delayed response to prolonged corticotropin infusion over 3 days, and the findings of an elevated level of prednisolone in the cerebrospinal fluid a full 2 months after its administration. It is therefore recommended that patients receiving intrathecal steroids be carefully observed for the possible development of secondary adrenal insufficiency.

Adrenal Insufficiency↗