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Biomedical subjects

S Ashwal

Publications and source records attributed to S Ashwal.

At least 109 records · Page 6Linked to original sources
PubMed1982

The choice of sedation for computed tomography in children: a prospective evaluation.

A prospective study of 582 pediatric cranial computed tomographic (CT) examinations was made in order to determine the efficacy and safety of two sedation regimens and general anesthesia. Two hundred seventy-nine outpatients were randomly given oral chloral hydrate (80 mg/kg) or an intramuscular preparation composed of atropine, meperidine, promethazine, and secobarbital (AMPS). Three hundred three inpatients were randomly administered chloral hydrate, the AMPS, or endotracheal anesthesia. Intravenous supplementation of the sedation was limited by the protocol to a maximum secobarbital dosage of 2 mg/kg. An additional retrospective analysis was made of 316 scan attempts obtained outside the study during the same period. A failed CT examination was defined as one that could not be completed or one that showed motion artifacts on two or more scan pairs after two scan pair repeats. The failure rate was 15% for the chloral hydrate group and 12% for the AMPS group. No motion artifacts were present on 94% of the completed studies. There was no mortality, but major and minor complications occurred in 3.5% of the randomized group. It was concluded that each of the methods had proved acceptably safe and effective and that measures can be taken to decrease complications and sedation failures further.

Administration, Oral↗
PubMed1981

Patterns of fetal lamb regional cerebral blood flow during and after prolonged hypoxia: studies during the posthypoxic recovery period.

In an effort to determine to what extent cerebral blood flow (CBF) varies in different parts of the brain after prolonged fetal hypoxia, we measured flow to 34 regions. In seven chronically catheterized fetal lambs at 130 to 140 days' gestation, flow was measured by means of radioactive labeled microspheres during a control period, during hypoxia, and at 4, 24, and 48 hours after hypoxia. Control blood flow to cortical, subcortical, and brain stem structures respectively equaled 221, 237 and 275 ml . min-1 . 100 gm-1. After 90 minutes of hypoxia, flows respectively increased 67%, 93%, and 160% to these areas, suggesting preferential shunting of flow to critical brain stem regions. By 4, 24, and 48 hours after hypoxia the regional flows ahd returned to values not significantly different from control values. We conclude that: (1) significant fetal regional cerebral blood flow differences occurred in utero, with brain stem and subcortical flows being greater than flows to other regions of the brain; (2) during prolonged intrauterine hypoxia, total cerebral blood flow increased about 95%, with evidence of preferential shunting to critical brain stem regions; (3) during the posthypoxic recovery period at 4, 24, and 48 hours, flows returned to normal, indicating no evidence of a post-ischemic hypoperfusion syndrome or impairment of the microcirculation.

Animals↗
PubMed1980

Computed tomography of tuberculous meningitis in infants and children.

Three cases are used to illustrate the computed tomography (CT) findings of tuberculous meningitis in infants and children. The clinical and laboratory findings of these patients are presented, and the differential diagnosis of viral, bacterial and fungal meningitis is reviewed. Tuberculous meningitis should be suspected, even in the infant or child with a negative tuberculin skin test, when a chronically ill patient presents with the acute signs of meningismus, the cerebrospinal fluid analysis demonstrates a low glucose and monocytosis, and cranial CT shows ventricular enlargement with prominent basal and sylvian fissure enhancement after intravenous contrast medium injection. The ease and safety of serial CT examinations make this procedure the ideal radiological method to follow the patient's course in order to evaluate the response to treatment.

Brain↗
PubMed1980

Patterns of fetal lamb regional cerebral blood flow during and after prolonged hypoxia.

In an effort to determine to what extent cerebral blood flow (CBF) varies in different parts of the brain during prolonged fetal hypoxia, we measured flow to 34 regions in 12 chronically catheterized fetal lambs 130 to 140 days gestation. Control values of PO2, PCO2 pH, heart rate, and blood pressure were obtained, and CBF was measured by use of radioactive labeled microspheres during a control period, during (15-, 30-, and 90-min) reduction of maternal inspired O2 concentration (fetal arterial PO2 was maintained at 12 to 15 torr), and 60 min after returning the ewe to room air. control blood flow to cortical, subcortical, and brainstem structures equaled 134, 186, and 254 ml x min-1 x 100 g-1, respectively. During hypoxia, CBF increased 92%, and 60 min after fetal oxygenation was restored, it remained 50% above control values. We noted a similar response in regional CBF to the cortex, subcortex, and brainstem during and after hypoxia. Blood flow to smaller areas within the three major regions were quite homogenous and had a similar pattern of response to hypoxia. We conclude that: (1) significant fetal regional CBF differences occurred in utero with brainstem and subcortical flows being substantially greater than flows to other regions of the brain; (2) during prolonged intrauterine hypoxia, total regional CBF increased 92%; (3) 1 hr after fetal oxygenation was restored, CBF still remained 50% above control values; and finally, (4) there was no significant preferential shunting of regional CBF during prolonged hypoxia in utero.

Animals↗
PubMed1979

Failure of electroencephalography to diagnose brain death in comatose children.

Two isoelectric electroencephalograms obtained 24 hours apart support a clinical diagnosis of brain death in prolonged coma. Without documentation of electrocerebral silence, physicians are reluctant to discontinue vital support systems. A radionuclide bolus technique has been developed that documents the absence of cerebral blood flow in suspected brain death and supplements the flat EEG. In a recent review of this technique, all 27 adults who had EEG activity maintained the integrity of their cerebral blood flow. This contrasts to our studies of 5 children, all of whom demonstrated persistent EEG activity but had no evidence of cerebral blood flow by either the isotope bolus technique (5 patients) or cerebral angiography (4 patients). These children (mean age, 7 months) lacked cephalic reflexes and were maintained on assisted ventilation for an average of 15 days. Multiple electroencephalographic tracings persistently demonstrated low-voltage cortical activity over this time. Despite the lack of cerebral blood flow, all patients were continued on respiratory support. At autopsy, extensive brain liquefaction necrosis was noted. In comatose children, EEG monitoring may be of limited value while cerebral blood flow measurements can provide more practical and prognostic information.

Brain Death↗
PubMed1977

Radionuclide bolus angiography: a technique for verification of brain death in infants and children.

Fifteen infants and children, 11 of whom had clinical brain death and four of whom were comatose, were evaluated with the radionuclide bolus study and electroencephalography. Clinical criteria for brain death included: (1) absence of spontaneous respirations, (2) absence of cephalic reflexes, and (3) unresponsiveness. Results demonstrated complete correlation among clinical examination, EEG, and radionuclide study in 79% of cases. An approach to the evaluation of the infant or child with possible brain death is outlined utilizing serial examinations, radionuclide bolus study, and electroencephalography. The radionuclide bolus study appears to be a safe, rapid, portable technique which can be used for this purpose in infants and children.

Angiography↗
PubMedDate not supplied

Myoadenylate deaminase deficiency in children.

Myoadenylate deaminase (MADA) is an enzyme which participates in the purine nucleotide cycle necessary for energy production in human skeletal muscle. Approximately 35 patients with deficiency of this enzyme have been reported; one-half experienced their initial difficulties in childhood. Children with "primary" MADA deficiency typically have symptoms including muscle cramps, stiffness, and post-exercise myalgia and weakness. In "secondary" MADA deficiency, the clinical findings have been variable with delayed motor development, hypotonia, cardiomyopathy, delayed speech development, and generalized weakness. In most cases creatine kinase determinations, nerve conduction velocity studies, and routine muscle histopathology have been normal. Diagnosis has been established by demonstrating an absence of MADA activity by either direct muscle enzyme assay or histochemical staining. In this report we describe a 12-year-old boy with primary MADA deficiency and contrast his symptoms with those of previously described pediatric patients.

AMP Deaminase↗
PubMedDate not supplied

Infantile myositis: a case diagnosed in the neonatal period.

Infantile myositis is an inflammatory myopathy occurring in children under one year of age. This condition is extremely rare in the neonatal period and may be confused with other causes of generalized weakness. Creatine kinase activity is usually markedly elevated and electromyography demonstrates low amplitude, polyphasic motor unit activity. Muscle biopsy, necessary for diagnosis, documents characteristic findings of perifascicular atrophy and the presence of perivascular inflammatory cells. The diagnosis should be followed by corticosteroid treatment. The patient presented is the youngest biopsy-proved case of infantile myositis. In this report, his symptoms and clinical course are compared with those of previously described patients. The role of infectious agents and the immune state in the etiology of infantile myositis is considered.

Biopsy↗
PubMedDate not supplied

Brain death in children: Part II.

The determination of brain death in children has increasingly relied on a variety of neurodiagnostic studies to confirm the clinical diagnosis. This second article on brain death reviews the relevant pediatric electroencephalographic, evoked response, and cerebral blood flow studies, provides our recommendations and protocol for the determination of brain death in children, and considers some of the problems associated with physiologic stabilization of the brain dead child who is considered for organ donation.

Adolescent↗
PubMedDate not supplied

Brain death in children: Part I.

The determination of brain death during childhood has become increasingly important and in some ways controversial. This initial article reviews historical data and guidelines and provides a perspective for the recommendations which will be discussed in the second article (Part II).

Adolescent↗
PubMedDate not supplied

Reflex sympathetic dystrophy syndrome in children.

We report 3 children with reflex sympathetic dystrophy syndrome, review the literature, and discuss current concepts of diagnosis and management. In this disorder, pain, tenderness, swelling, vasomotor instability, and dystrophic skin changes frequently develop after minor injury. The clinical diagnosis is supported by osteopenia detected on radiographs and either increased or decreased radionuclide uptake on bone scan of the affected extremity. Treatment with a graduated program of physical therapy and transcutaneous electrical nerve stimulation is beneficial in almost all patients. In contrast to adults, the prognosis of childhood reflex sympathetic dystrophy syndrome is favorable; most children recover completely after one episode.

Adolescent↗
PubMedDate not supplied

Anencephaly: clinical determination of brain death and neuropathologic studies.

Twelve liveborn anencephalic infants were serially examined to determine if they would meet our clinical criteria for whole brain death within a 7-day period: Protocol 1 infants (6) received intensive care including intubation from birth; and Protocol 2 infants (6) received intensive care during the period in which death was imminent. Brain death was determined by absence of brainstem function, including loss of all cranial nerve responses and sustained apnea (PCO2 greater than 60 torr) for 48 hours with confirmation of findings by an outside consulting child neurologist. The initial examinations of these 12 infants revealed spontaneous movements and startle myoclonus (12), suck, root, and gag responses (7), increased tone (8), deep tendon reflexes (9), absent pupillary responses (9), absent oculocephalic and corneal responses (6), absent auditory/Moro responses (7), and nonvisualization of the optic nerve (8). Mild depression of neurologic function occurred during the first several days of life; subsequently, the infants' responses were easier to elicit and more sustained. Only 2 infants met the clinical criteria for brain death. Neuropathologic findings indicated that observed complex motor responses were not based upon cortical activity because no infant had a normally-formed cerebrum. Brainstem neuronal activity may have accounted for these motor responses in some patients but even at this level neurons were scanty or absent. Our findings suggest that, although rare, clinical brain death can be determined in liveborn anencephalic infants; ophthalmologic and otologic developmental abnormalities may confound examination of cranial nerve function; and absence of cortical neurons supports the widely held opinion that these infants do not experience sensation.

Anencephaly↗
PubMedDate not supplied

CBF and CBF/PCO2 reactivity in childhood strangulation.

Four children with self-inflicted strangulation injuries had cerebral blood flow determined by stable xenon computed tomography (XeCTCBF) within 24 hours of admission. All had suffered a severe hypoxic-ischemic cerebral injury; 3 initially had fixed pupils, all were apneic with varying bradyarrhythmias, and the initial mean arterial pH was 7.26 (+/- 0.18). The initial blood glucose values were greater than 300 mg/dl (334 and 351 mg/dl) in the 2 patients who died compared to the 2 who survived (104 and 295 mg/dl). The cardiac index was depressed during the first several days of hospitalization in the 2 patients who died (less than 2.0 L/min/m2) compared to the 2 who survived. Total CBF was normal (63 +/- 8 ml/min/100 gm) and local variations in CBF were present. PCO2 reactivity was determined by hyperventilating the 4 patients for 20 min from an end tidal PCO2 of 39 +/- 3 torr to 29 +/- 1 torr and then repeating the XeCTCBF study. Marked regional variability in the CBF/PCO2 response was observed, ranging from 0.5-5.5 ml/min/100 gm/torr PCO2. In the 2 patients who died, the CBF/PCO2 was decreased (1.2 ml/min/100 gm/torr PCO2) compared to the 2 patients who survived (2.1 ml/min/100 gm/torr PCO2). Although CBF was normal in these 4 children, the hyperventilation response was depressed, variable, and even paradoxical which may be important in the evolution of further brain injury and is a critical factor in deciding whether hyperventilation may be of clinical benefit.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Guillain-Barré syndrome in childhood: natural course and efficacy of plasmapheresis.

Eight children with Guillain-Barré syndrome were treated with plasmapheresis. Retrospective comparisons were made with 11 historic control patients. Eight children required mechanical ventilation, 4 of whom were in the plasmapheresis group. One week after the last plasmapheresis treatment, patients receiving plasmapheresis within 7 days of symptom onset had improved by one Guillain-Barré syndrome score. Discharge Guillain-Barré syndrome scores were significantly lower for those receiving plasmapheresis (P < .05). Patients in the plasmapheresis group had a decrease in the number of days of mechanical ventilation, time until motor recovery, and overall cost. Our results are consistent with published literature and indicate that plasmapheresis for childhood Guillain-Barré syndrome is a safe and effective treatment to shorten the time to recovery.

Adolescent↗
PubMedDate not supplied

End of life care in Duchenne muscular dystrophy.

End of life care for patients with Duchenne muscular dystrophy (DMD) has become increasingly complex because of new technologies, changes in medical personnel over periods of time, emergence of home health care systems, and increasing patient and family autonomy in decision-making. In this review, we discuss the medical problems, particularly respiratory and cardiac failure, faced by DMD patients. Current concepts concerning the evaluation and options for treatment of these problems are presented as well as the ethical issues involved in the care of the DMD patient. These issues include the medical indications for treatment, patient preferences, quality-of-life issues, and contextual features related to legal, institutional, religious, geographic, cultural, social, and financial factors. We also present our experience at Loma Linda University Medical Center over the past 10 years in the development of a home mechanical ventilation program for DMD patients and an algorithm for the evaluation of these patients. Many patients with DMD do well on long-term ventilation, but some find that their quality of life is less than desirable and choose to discontinue this method of life-prolongation. Many of these new options are very expensive, making the decision to use them a difficult one. Ultimately, these are societal issues that require clear reflection on matters of resource allocation that should be performed by health care professionals, citizens, and health planners.

Adolescent↗