Low Cerebrospinal Fluid Glucose Research Articles

Acute bacterial meningitis in children admitted to a rural Kenyan hospital: increasing antibiotic resistance and outcome.

Acute bacterial meningitis (ABM) is an important cause of mortality in Africa, but most studies are based in urban referral hospitals. Poor laboratory facilities make diagnosis difficult, and treatment is limited to inexpensive antibiotics. We retrospectively reviewed data from children admitted with ABM to a Kenyan district hospital from 1994 through 2000. We calculated the minimum incidence in children admitted from a defined area. We also examined the antibiotic susceptibility patterns. We identified 390 cases (1.3% of all admissions) of whom 88% were <5 years old. The apparent minimum annual incidence in children younger than 5 years of age increased from 120 to 202 per 100,000 between 1995 and 2000 (P < 0.001). Increasing the lumbar punctures performed by including prostrated or convulsing children significantly increased the number of cases detected (P < 0.005). The most common organisms in infants <3 months were streptococci and Enterobacteriaceae. Streptococcus pneumoniae (43.1%) and Haemophilus influenzae (41.9%) were predominant in the postneonatal period. The overall mortality was 30.1%, and 23.5% of survivors developed neurologic sequelae. Chloramphenicol resistance of H. influenzae rose from 8% in 1994 to 80% in 2000 (P < 0.0001) accompanied by an apparent increase in mortality. A short history, impaired consciousness and hypoglycemia were associated with death. Prolonged coma and low cerebrospinal fluid glucose were associated with neurologic sequelae. ABM in rural Kenya is a severe illness with substantial mortality and morbidity. Prognosis could be improved by broadening the criteria for lumbar puncture and use of appropriate antibiotics.

Diagnosis of adult tuberculous meningitis by use of clinical and laboratory features

The diagnosis of tuberculous meningitis is difficult. Discrimination of cases from those of bacterial meningitis by clinical features alone is often impossible, and current laboratory methods remain inadequate or inaccessible in developing countries. We aimed to create a simple diagnostic aid for tuberculous meningitis in adults on the basis of clinical and basic laboratory features. We compared the clinical and laboratory features on admission of 251 adults at an infectious disease hospital in Vietnam who satisfied diagnostic criteria for tuberculous (n=143) or bacterial (n=108) meningitis. Features independently predictive of tuberculous meningitis were modelled by multivariate logistic regression to create a diagnostic rule, and by a classification-tree method. The performance of both diagnostic aids was assessed by resubstitution and prospective test data methods. Five features were predictive of a diagnosis of tuberculous meningitis: age, length of history, white-blood-cell count, total cerebrospinal fluid white-cell count, and cerebrospinal fluid neutrophil proportion. A diagnostic rule developed from these features was 97% sensitive and 91% specific by resubstitution, and 86% sensitive and 79% specific when applied prospectively to a further 42 adults with tuberculous meningitis, and 33 with bacterial meningitis. The corresponding values for the classification tree were 99% and 93% by resubstitution, and 88% and 70% with prospective test data. This study suggests that simple clinical and laboratory data can help in the diagnosis of adults with tuberculous meningitis. Although the usefulness of the diagnostic rule will vary depending on the prevalence of tuberculosis and HIV-1 infection, we suggest it be applied to adults with meningitis and a low cerebrospinal fluid glucose, particularly in settings with limited microbiological resources.

Risk factors and prognostic indicators of bacterial meningitis in a cohort of 3580 postneurosurgical patients.

In order to identify the incidence, risk factors and prognostic indicators of postneurosurgical bacterial meningitis, a 9-y retrospective cohort study was performed. The cohort comprised 3580 individuals who underwent neurosurgical operations at the Department of Neurosurgery of Catholic University, Rome, a 1,700-bed university hospital. We observed 52 episodes of postneurosurgical meningitis, with infection rates of 1.4/100 patients, 0.8/100 operations for craniotomies and 2.6/100 operations for internal cerebrospinal fluid (CSF) shunt or ventriculostomy with external drainage. The overall infection rate decreased from 2.5/100 operations in 1989 to 0.9/100 in 1997 (p = 0.03). Logistic regression analysis indicated that duration of ventriculostomy with external drainage [p < 0.01; odds ratio (OR) = 9.67; 95% confidence interval (CI) = 2.44-38.321 and increasing value of the APACHE III score (p <0.01; OR = 8.51; 95% CI = 2.15-33.68) were independent risk factors for development of meningitis. The overall case fatality rate was 8%. Predictors of mortality were low ( < 1.66 mmol/l) CSF glucose concentration (p = 0.001), increasing value of the APACHE IIl score (p = 0.002) and Gram-negative aetiology (p = 0.003).

The prognostic factors of cryptococcal meningitis in HIV-negative patients

Seventy-one patients with cryptococcal meningitis, 46 males and 25 females, aged 15–83 years, were included in this study. Their initial clinical manifestations, cerebrospinal fluid (CSF) features, and therapeutic results were analysed. Patients were treated with three different regimens: amphotericin B, fluconazole, and combination therapy. Based on the therapeutic results, the 71 patients were also divided into cured, improved, and failed groups. For statistical comparison, the clinical manifestations and CSF features, were compared according to therapeutic outcome. There was no statistical difference in outcome among the three different antifungal regimens. However, patients treated with fluconazole required 36% fewer days of hospitalization compared with those receiving amphotericin B. Significant prognostic factors, included low CSF glucose, high CSF lactate, high CSF cryptococcal antigen titre (≥1: 1024), initial level of consciousness, the presence of seizure, hydrocephalus, and central nervous system vasculitis. Multiple logistic regression analysis showed that only initial level of consciousness, and CSF antigen titre were strongly associated with therapeutic failure after other potentially confounding factors were adjusted for. Because some of the prognostic factors in cryptococcal meningitis can be corrected, early diagnosis, early use of appropriate antifungal treatment, and the correction of the underlying metabolic derangements are important in management.

Pronóstico de la meningitis bacteriana

To review the literature on the risk factors for bacterial meningitis (BM) and evaluate these factors in children diagnosed as having BM in the Paediatric Department of the University Hospital of Maracaibo between 1996 and 1998. We made a retrospective study of children diagnosed as having BM in the University of Maracaibo. We evaluated different factors related to BM. From 1 January 1996 to 31 December 1998 a total of 152 children were diagnosed as having bacterial meningitis; 69.7% were boys and 30.3% were girls. The commonest causal germ was Haemophilus influenzae. Disorders of sensation (42.7%) and signs of meningism (32.8%) were the most frequent neurological alterations. The main laboratory findings were leucocytosis (51.3%), thrombocytosis (49.3%), pleocytosis (70.3%), cerebrospinal fluid protein (49.3%) and low cerebrospinal fluid glucose (72.8%). Twelve patients (7.5%) died. Of this group, 10 were under one year of age and had septic shock. BM represents a major group of hospital admissions in everyday paediatric practice. Although the mortality has decreased, an increased risk of sequelas must be borne in mind. Clinico-neurological examination on admission and simultaneous analysis of laboratory investigations allows identification of prognostic indicators of morbidity and mortality.

GLUT-1 deficiency syndrome caused by haploinsufficiency of the blood-brain barrier hexose carrier.

The high metabolic requirements of the mammalian central nervous system require specialized structures for the facilitated transport of nutrients across the blood-brain barrier. Stereospecific high-capacity carriers, including those that recognize glucose, are key components of this barrier, which also protects the brain against noxious substances. Facilitated glucose transport in vertebrates is catalyzed by a family of carriers consisting of at least five functional isoforms with distinct tissue distributions, subcellular localizations and transport kinetics. Several of these transporters are expressed in the mammalian brain. GLUT-1, whose sequence was originally deduced from cDNAs cloned from human hepatoma and rat brain, is present at high levels in primate erythrocytes and brain endothelial cells. GLUT1 has been cloned and positionally mapped to the short arm of chromosome 1 (1p35-p31.3; refs 6-8). Despite substantial metabolic requirements of the central nervous system, no genetic disease caused by dysfunctional blood-brain barrier transport has been identified. Several years ago, we described two patients with infantile seizures, delayed development and acquired microcephaly who have normal circulating blood glucose, low-to-normal cerebrospinal fluid (CSF) lactate, but persistent hypoglycorrachia (low CSF glucose) and diminished transport of hexose into isolated red blood cells (RBC). These symptoms suggested the existence of a defect in glucose transport across the blood brain barrier. We now report two distinct classes of mutations as the molecular basis for the functional defect of glucose transport: hemizygosity of GLUT1 and nonsense mutations resulting in truncation of the GLUT-1 protein.

Ventriculoperitoneal shunt infections with gram-negative bacteria.

Infection causes major morbidity and mortality in patients with cerebrospinal fluid (CSF) shunts. The prognosis of CSF shunt infections caused by Gram-negative bacteria (GNB) has been thought to be particularly poor. The authors reviewed all GNB shunt infections treated at Children's Memorial Hospital from January 1986 to January 1990 (n = 23). Of these infections 20 (87%) occurred within 4 weeks after shunt revision (median, 10 days). The most frequent symptoms were fever, lethargy, and irritability; the illness was not severe in the majority of these patients. Escherichia coli was isolated from 12 of 23 patients (52%), Klebsiella pneumoniae from 5 (22%), and mixed GNB from 3 (13%) patients. Initial treatment always included immediate shunt removal, externalized ventricular drainage, and intravenous antibiotics. Extraventricular drainage revision and/or intraventricular antibiotics were required in four patients whose CSF cultures were persistently positive for GNB. At admission, these patients had CSF glucose levels of < 10 mg/dl and CSF positive for GNB by Gram's stain. The overall cure rate was 100%, and no recurrence was observed; however, a subsequent infection with a different organism developed in four patients. Only 2 of 19 patients (11%) who were followed up suffered apparent CNS damage. One patient died of unrelated causes shortly after treatment. Our findings indicate that 1) patients with GNB CSF shunt infections often appear relatively well at presentation; 2) CSF positive for GNB by Gram's stain and very low CSF glucose levels predict continued positive CSF cultures, despite appropriate antibiotic therapy; and 3) GNB CSF shunt infections can be successfully treated by prompt shunt removal, extraventricular drainage, and intravenous antibiotics.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunocytological diagnosis of primary cerebral non-Hodgkin's lymphoma.

Four men with primary cerebral non-Hodgkin's lymphoma diagnosed by immunocytological analysis of cerebrospinal fluid (CSF) presented with cranial nerve palsies. All had CSF lymphocytoses and low CSF glucose. The cell phenotypes were two T cell tumours, one B cell, and one null. A review of 13 previously recorded cases of immunocytologically diagnosed CNS non-Hodgkin's lymphoma showed that there were 10 B cell, two T cell, and one null tumour. Overall (17 cases) the cell phenotype distribution was 65% B cell, 24% T cell, and 11% null. High CSF lymphocyte counts were found in 94%, proteinosis in 85%, and low CSF glucose in 87%. In contrast to the B cell tumours, all of the T cell tumours were diagnosed by CSF cytology before being visualised radiologically. It is suggested that all CSF lymphocytes (greater than 5 x 10(6)/ml) should be immunohistochemically typed to permit earlier diagnosis of CNS non-Hodgkin's lymphoma.

Omentum graft for intractable subdural empyema

A subdural empyema developed in a young man after craniotomy for evacuation of a hematoma in a sylvian fissure arachnoid cyst and the subdural space. Despite prolonged systemic and subdural antibiotic administration and a debridement of the subdural space, infection persisted, as evidenced by persistent fever, an elevated white blood cell count, and an extremely low cerebrospinal fluid glucose level. The infection was cured after a second debridement operation where microsurgically revascularized free omentum was used to obliterate the cyst and to cover the cerebral hemisphere in the craniotomy defect. The use of vascularized free omentum may prove useful in cases of refractory cranial wound infection and cerebrospinal fluid fistulas.

Reagent strips in the evaluation of cerebrospinal fluid glucose levels

The value of Visidex IIR, Haemo-Glukotest 20-800RR, MultistixR and DextrostixR reagent strips--the latter alone or in combination with a glucometer--in the determination of cerebrospinal fluid (CSF) glucose levels has been evaluated and compared with the results of a standard glucose oxidase method (Beckman). Fifty-four CSF specimens were evaluated and the closest correlation (r = 0.8002) obtained by the use of DextrostixR in combination with a glucometer. All four methods detected two cases with very low CSF glucose values (less than 1.5 mmol/l) but confusing results were obtained in three cases having slightly reduced CSF glucose values (2.0-2.2 mmol/l).

Cerebrospinal fluid white cell, glucose and protein changes during the treatment of Haemophilus influenzae meningitis.

298 cerebrospinal fluid (CSF) samples obtained from 116 children with ongoing Haemophilus influenzae meningitis were analyzed in order to determine the kinetics of the white blood cell (WBC) count and the glucose and protein concentrations--parameters for which there are no "reference values" available for the convalescence period of meningitis. The values determined during the first 10 days of treatment are presented as percentile distribution graphs. CSF WBC counts increased slightly for the first 24 h but declined thereafter without reaching, however, the normal value (less than or equal to 5/microliter) within 10 days in the majority of cases. Low CSF glucose concentrations usually increased to a normal or almost normal level within 48 h. CSF protein concentrations declined steadily throughout the treatment. Extremely high CSF WBC or low CSF glucose concentrations suggested neurological complications or treatment failure. The value of sequentially determined CSF WBC, glucose and protein in monitoring recovery from H. influenzae meningitis is, however, so vague that routine spinal taps do not seem indicated after CSF has become sterilized.

Hypoglycorrhachia after subarachnoid hemorrhage.

The cerebrospinal fluid (CSF) of 33 patients with a nontraumatic subarachnoid hemorrhage was analyzed to determine whether hypoglycorrhachia occurred frequently after a subarachnoid hemorrhage. Twenty-three patients (70%) developed an abnormally low CSF glucose concentration or a lowered CSF-blood glucose ratio after their hemorrhage. Thus, hypoglycorrhachia seems to be a common spinal fluid subarachnoid hemorrhage.

External drainage for ventricular infection following cerebrospinal fluid shunts.

57 children with shunt-related ventricular infection were treated with external ventricular drainage and a combination of systemic and intraventricular antibiotics. For persistent infection or inadequate drainage volume the external ventricular drain was promptly changed. Cerebrospinal fluid cultures of 54 (95%) of the children became sterile within an average of 5.1 days. As soon as three consecutive 48-hour cultures of the cerebrospinal fluid were negative, the external ventricular drainage was removed and a new ventriculoperitoneal shunt was inserted. Provided that three consecutive 48-hour cultures of the cerebrospinal fluid were negative at the time of reinstitution of ventriculoperitoneal shunting, low cerebrospinal fluid glucose readings were not associated with any greater risk of recurrent infection than following primary ventriculoperitoneal shunting.

Hypoglycorrhachia in Pediatric Patients

Hypoglycorrhachia (abnormally low cerebro spinal fluid glucose content) eludes exact numerical definition, largely because of the dynamic equilibrium between blood and CSF glucose. A group of 181 pediatric patients with a CSF glucose less than 50 mg/100 ml or a CSF/blood glucose ratio less than 0.50 were studied. Hypoglycorrhachia was present in patients with bacterial meningitis, aseptic meningitis, meningeal carcinomatosis, subarachnoid hemmorrhage, and hypoglycemia. Markedly diminished CSF glucose values were seen primarily in patients with bacterial meningitis. Higher CSF/blood glucose ratios predominated in those with hypoglycemia and neonates with low-normal blood sugars. Following bacterial meningitis and hypoglycemia, aseptic meningitis (including five children with documented enterovirus meningitis and one with documented mumps meningitis) was the third most common cause of hypoglycorrhachia in children. When readily available, positive CSF viral cultures may allow early cessation of antibiotic therapy in two types of patients with meningitis and hypoglycorrhachia: (1) those receiving previous recent antibiotic therapy, and (2) those with CSF findings more typical of a bacterial meningitis.

Low CSF Glucose Level in Sarcoidosis Involving the Central Nervous System

Sarcoidosis, a systemic granulomatous disease of undetermined etiology and pathogenesis,¹may involve multiple organs and produce a wide spectrum of clinical manifestations.^2,3The nervous system is not commonly affected,^4-6but when it is, neurologic manifestations are protean. Recently Siltzbach outlined the clinical features observed in 311 cases of sarcoidosis diagnosed at the Sarcoidosis Clinic at the Mount Sinai Hospital in New York from 1946 to 1961.⁷Four of the patients experienced a mode of onset referable to the nervous system, and 13 (4%) had evidence of nervous system involvement sometime during the course of their disease. Although there are a number of publications which describe the neurologic manifestations of sarcoidosis,^6,8we were unable to find a review of the changes which occur in the cerebrospinal fluid (CSF) in this entity. Sarcoidosis is rarely considered in the differential diagnosis of low CSF glucose, probably because most

Mumps meningoencephalitis with low cerebrospinal-fluid glucose, prolonged pleocytosis and elevation of protein.

Abstract Four patients with mumps meningoencephalitis had prolonged lowering of the cerebrospinal-fluid glucose. Retrospective study of 45 other cases of mumps meningoencephalitis revealed 10 additional patients with at least one glucose value of less than 40 mg per 100 ml. Pleocytosis persisted for as long as five weeks; increases in pleocytosis and in protein content of the cerebrospinal fluid during the hospital course were frequently recorded. A consideration of known mechanisms that might be responsible for hypoglycorrhachia in mumps meningoencephalitis fails to account satisfactorily for the phenomenon.

REYE'S SYNDROME-Reply

<i>To the Editor</i>.—We do not share Dr. Winograd's belief that an abnormal blood or cerebrospinal fluid (CSF) glucose level is necessary to the diagnosis of Reye's syndrome. In accepting Reye's cases as a syndrome, Dr. Winograd must accept Reye's original data; a low blood or CSF glucose level was not uniformly present (CSF, 13/19; blood, 6/9). In Bradford and Latham's recent review article, a low blood glucose level was found in 27 out of 63 cases in which this determination was performed. A low CSF glucose level was found in 31 out of 59 cases. It is our view, as emphasized in the title of our report, that hepatocellular dysfunction is primary and encephalopathy is a consequence of this. Presumably, the hypoglycemia encountered in many cases is also a consequence of hepatic dysfunction. A laboratory hallmark of this syndrome, which to date has always been present when sought, is

HYPOGLYCORRHACHIA WITH MENINGEAL CARCINOMATOSIS. REPORT OF TWO CASES.

Article1 July 1965Hypoglycorrhachia with Meningeal CarcinomatosisReport of Two CasesYOUNG S. KIM, M.D., JEROME S. RESNICK, M.D.YOUNG S. KIM, M.D.Search for more papers by this author, JEROME S. RESNICK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-63-1-115 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn recent years attention has been called to the fact that cerebrospinal fluid glucose may be extremely low and of diagnostic importance in conditions other than the infectious meningitides. Although hypoglycorrhachia was described in 1904 in a case of carcinomatosis of the meninges without infection (1), this phenomenon received little or no attention in the English literature until 1952 when Dodge, Sayre, and Svien (2) reported four cases with metastatic carcinoma in which the metastases involved the meninges and there was associated low cerebrospinal fluid (CSF) glucose. Subsequently, Berg (3) reported five cases of his own, and at that time...

Low cerebrospinal fluid glucose associated with meningeal neoplasia

Summary A case of diffuse meningeal gliomatosis with hypoglycorrhachia in a 4-year-old child is presented. Inclusion of this syndrome in the differential diagnosis of central nervous system disease is emphasized.

Neoplastic involvement of the meninges with low cerebrospinal fluid glucose concentrations simulating tuberculous meningitis.

Neoplastic involvement of the meninges with low cerebrospinal fluid glucose concentrations simulating tuberculous meningitis.