Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Macroglossia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed2002

Epigenetic alterations of H19 and LIT1 distinguish patients with Beckwith-Wiedemann syndrome with cancer and birth defects.

Beckwith-Wiedemann syndrome (BWS) is a congenital cancer-predisposition syndrome associated with embryonal cancers, macroglossia, macrosomia, ear pits or ear creases, and midline abdominal-wall defects. The most common constitutional abnormalities in BWS are epigenetic, involving abnormal methylation of either H19 or LIT1, which encode untranslated RNAs on 11p15. We hypothesized that different epigenetic alterations would be associated with specific phenotypes in BWS. To test this hypothesis, we performed a case-cohort study, using the BWS Registry. The cohort consisted of 92 patients with BWS and molecular analysis of both H19 and LIT1, and these patients showed the same frequency of clinical phenotypes as those patients in the Registry from whom biological samples were not available. The frequency of altered DNA methylation of H19 in patients with cancer was significantly higher, 56% (9/16), than the frequency in patients without cancer, 17% (13/76; P=.002), and cancer was not associated with LIT1 alterations. Furthermore, the frequency of altered DNA methylation of LIT1 in patients with midline abdominal-wall defects and macrosomia was significantly higher, 65% (41/63) and 60% (46/77), respectively, than in patients without such defects, 34% (10/29) and 18% (2/11), respectively (P=.012 and P=.02, respectively). Additionally, paternal uniparental disomy (UPD) of 11p15 was associated with hemihypertrophy (P=.003), cancer (P=.03), and hypoglycemia (P=.05). These results define an epigenotype-phenotype relationship in BWS, in which aberrant methylation of H19 and LIT1 and UPD are strongly associated with cancer risk and specific birth defects.

Abdomen↗
PubMed2004

Paradoxical NSD1 mutations in Beckwith-Wiedemann syndrome and 11p15 anomalies in Sotos syndrome.

Sotos syndrome is an overgrowth syndrome characterized by pre- and postnatal overgrowth, macrocephaly, advanced bone age, variable degrees of mental retardation, and typical facial features. Defects of the NSD1 gene account for >or=60% of cases of Sotos syndrome, whereas the disease-causing mechanism of other cases remains unknown. Beckwith-Wiedemann syndrome (BWS) is a distinct overgrowth condition characterized by macroglossia, abdominal-wall defects, visceromegaly, embryonic tumors, hemihyperplasia, ear anomalies, renal anomalies, and neonatal hypoglycemia. Deregulation of imprinted growth-regulatory genes within the 11p15 region is the major cause of BWS, whereas the molecular defect underlying a significant proportion of sporadic BWS cases remains unknown. Owing to clinical overlaps between the two syndromes, we investigated whether unexplained cases of Sotos syndrome could be related to 11p15 anomalies and, conversely, whether unexplained BWS cases could be related to NSD1 deletions or mutations. Two 11p15 anomalies were identified in a series of 20 patients with Sotos syndrome, and two NSD1 mutations were identified in a series of 52 patients with BWS. These results suggest that the two disorders may have more similarities than previously thought and that NSD1 could be involved in imprinting of the chromosome 11p15 region.

Beckwith-Wiedemann Syndrome↗
PubMed2004

Microdeletion of LIT1 in familial Beckwith-Wiedemann syndrome.

Beckwith-Wiedemann syndrome (BWS), which causes prenatal overgrowth, midline abdominal wall defects, macroglossia, and embryonal tumors, is a model for understanding the relationship between genomic imprinting, human development, and cancer. The causes are heterogeneous, involving multiple genes on 11p15 and including infrequent mutation of p57(KIP2) or loss of imprinting of either of two imprinted gene domains on 11p15: LIT1, which is near p57(KIP2), or H19/IGF2. Unlike Prader-Willi and Angelman syndromes, no chromosomal deletions have yet been identified. Here we report a microdeletion including the entire LIT1 gene, providing genetic confirmation of the importance of this gene region in BWS. When inherited maternally, the deletion causes BWS with silencing of p57(KIP2), indicating deletion of an element important for the regulation of p57(KIP2) expression. When inherited paternally, there is no phenotype, suggesting that the LIT1 RNA itself is not necessary for normal development in humans.

Beckwith-Wiedemann Syndrome↗
PubMed2006

Loss-of-function mutations in euchromatin histone methyl transferase 1 (EHMT1) cause the 9q34 subtelomeric deletion syndrome.

A clinically recognizable 9q subtelomeric deletion syndrome has recently been established. Common features seen in these patients are severe mental retardation, hypotonia, brachycephaly, flat face with hypertelorism, synophrys, anteverted nares, cupid bow or tented upper lip, everted lower lip, prognathism, macroglossia, conotruncal heart defects, and behavioral problems. The minimal critical region responsible for this 9q subtelomeric deletion (9q-) syndrome has been estimated to be <1 Mb and comprises the euchromatin histone methyl transferase 1 gene (EHMT1). Previous studies suggested that haploinsufficiency for EHMT1 is causative for 9q subtelomeric deletion syndrome. We have performed a comprehensive mutation analysis of the EHMT1 gene in 23 patients with clinical presentations reminiscent of 9q subtelomeric deletion syndrome. This analysis revealed three additional microdeletions that comprise the EHMT1 gene, including one interstitial deletion that reduces the critical region for this syndrome. Most importantly, we identified two de novo mutations--a nonsense mutation and a frameshift mutation--in the EHMT1 gene in patients with a typical 9q- phenotype. These results establish that haploinsufficiency of EHMT1 is causative for 9q subtelomeric deletion syndrome.

Abnormalities, Multiple↗
PubMed2001

A longitudinal evaluation of craniofacial growth in a patient with Kabuki make-up syndrome: a case report.

The purpose of this investigation was to evaluate the craniofacial growth of a patient diagnosed with Kabuki make-up syndrome (KMS). Craniofacial growth was assessed by analysing lateral cephalometric radiographs with an interval of 12-15 months. They were taken from 6 years 9 months to 14 years 2 months. Angular and linear measurement analyses of the craniofacial complex showed a hypoplastic maxilla and a constricted maxillary basal arch width. The mandibular size was relatively large and had started to increase from 13 years 4 months. This resulted in a prognathic face caused by forward growth of the mandible and insufficient growth of the maxilla. The skeletal pattern was Class III. Open bite morphology with a steep mandibular plane (SN-MP), a relatively short ramus, and a large gonial angle were also observed. In this subject, the facial dysmorphism found in the maxilla and mandible may have been influenced by several factors. Connective tissue disorder, macroglossia, lower tongue posture, and tongue thrust swallowing have been identified as possible aetiological factors that may determine dysmorphism in the craniofacial complex in this KMS patient.

Cephalometry↗
PubMed2002

Discordant KCNQ1OT1 imprinting in sets of monozygotic twins discordant for Beckwith-Wiedemann syndrome.

Beckwith-Wiedemann syndrome (BWS) presents with visceromegaly, macroglossia, tumor predisposition and other congenital abnormalities, and is usually associated with abnormalities of chromosome 11p15. A number of identical twin pairs, mostly female, have been reported to be discordant for BWS. We show here that the incidence of female monozygotic twins among patients with BWS is dramatically increased over that of the general population. A cluster of imprinted genes within 11p15 is thought to be coordinately regulated via the imprinted expression of KCNQ1OT1, which encodes an untranslated RNA. In skin fibroblasts from five monozygotic twin pairs discordant for BWS, each affected twin had an imprinting defect at KCNQ1OT1 on 11p15, whereas the unaffected twin did not. Five additional monozygotic twin pairs, for whom only blood was available, also displayed an imprinting defect at KCNQ1OT1. It is possible that discordance for BWS in MZ twins is due to unequal splitting of the inner cell mass during twinning, thereby causing differential maintenance of imprinting at KCNQ1OT1. Alternatively, we propose that KCNQ1OT1 is especially vulnerable to a loss of imprinting event, caused by a lack of maintenance DNA methylation at a critical stage of preimplantation development, and that this loss of imprinting predisposes to twinning as well as to discordance for BWS. These data underscore the importance of continued surveillance of children born following assisted reproductive technologies that impact the preimplantation embryo.

Beckwith-Wiedemann Syndrome↗
PubMed2001

Perinatal outcome of pregnancy after GnRH antagonist (ganirelix) treatment during ovarian stimulation for conventional IVF or ICSI: a preliminary report.

BACKGROUND: Gonadotrophin-releasing hormone (GnRH) antagonists have been proven safe and effective, with no adverse effects on offspring in animal studies. Careful study of pregnancy outcome in humans is mandatory. METHODS AND RESULTS: This preliminary report includes follow-up data of patients treated with the GnRH antagonist, ganirelix, during ovarian stimulation for IVF or ICSI. In total, 333 patients were randomized in a multicentre, double-blind, dose-finding study of ganirelix, at six different doses ranging from 0.0625 to 2 mg. In total, 68 vital intrauterine pregnancies were established that resulted in the birth of 46 singletons, 12 twins and one triplet. Follow-up of the 67 pregnant patients (one subject was lost to follow-up) revealed six miscarriages (9%). Of the 61 subjects with an ongoing pregnancy, two with a singleton pregnancy did not give birth to a live-born infant (one spontaneous abortion in week 19, and one intrauterine death in week 27). The mean gestational age was 39.4 weeks for singleton pregnancies, and 36.6 weeks for multiple pregnancies. In total, 73 infants (33 boys, 40 girls) were born. A birth weight <2500 g was reported for 8.7% and 54.2% of the infants resulting from singleton and twins delivery respectively. One major congenital malformation was diagnosed; a boy with Beckwith-Wiedemann syndrome (exomphalos and macroglossia). Seven minor malformations were reported among five infants. CONCLUSIONS: In this first follow-up study, the incidence of adverse obstetrical and neonatal outcome was comparable with reported incidences for IVF-embryo transfer pregnancies.

Adult↗
PubMed1998

Difficult tracheal intubation in patients with retinoblastoma caused by 13q deficiency.

Anesthetic management of retinoblastoma patients is unremarkable in most cases. Patients are most often babies and laryngoscopic procedures for intubation are usually easy. However, we recently experienced two cases with retinoblastoma with whom tracheal intubation was accomplished with difficulty. We report the two cases with a review of all 5-year records of retinoblastoma (rbl) in our institution. The cases we experienced recently were all patients with rbl with deletion of the long arm of thirteenth chromosome (13q-). In the 5-year review, the incidence of the difficult intubation was significantly higher (P < 0.05) in rbl with 13q- (4/11) than in rbl without 13q- (0/147). In our experience macroglossia was noted for the difficulty in the intubation. We assume that some patients with rbl will be cases of difficult intubation even to cannot ventilate-cannot intubate level when the results of their chromosomal analysis show a deletion on the thirteenth chromosome.

Anesthesia↗
PubMed1991

Biotin deficiency per se is teratogenic in mice.

We examined whether maternal biotin deficiency would potentiate the latent teratogenicity of relatively low doses of vitamin A in mice. The incidence and the type of gross congenital malformations (cleft palate, micrognathia, and micromelia) induced by biotin deficiency were similar among the groups given three different concentrations of vitamin A (4000, 12,000 and 60,000 IU) in the diet. Also, the type of these malformations was different from those (exencephaly, cleft palate and macroglossia) induced by a known teratogenic dose of vitamin A (1,200,000 IU). We conclude that in mice concentrations of vitamin A in the range of 4-10 times the level recommended by the National Research Council and biotin deficiency do not interfere with one another; also, biotin deficiency per se is teratogenic in mice.

Abnormalities, Drug-Induced↗
PubMed2004

Bigenic Cre/loxP, puDeltatk conditional genetic ablation.

Genetic ablation experiments are used to resolve problems regarding cell lineages and the in vivo function of certain groups of cells. We describe a two-component conditional ablation technology using a mouse carrying an X-linked puDeltatk transgene, which is only activated in cells expressing Cre. Ablation of the Cre-expressing cells can be temporally regulated by the time of ganciclovir (GCV) administration. This strategy was demonstrated using a Col2Cre transgenic line. Differentiating chondrocytes in bigenic animals could be ablated at different developmental stages resulting in disorganized growth plates and dwarfism. Macrocephaly, macroglossia and umbilical hernia were also observed in ablated 18.5 dpc embryos. Crosses between the puDeltatk selector transgenic line and existing cre lines will facilitate numerous temporally regulated tissue-specific ablation experiments.

Acetyltransferases↗
PubMed2003

Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children.

STUDY OBJECTIVES: To assess the prevalence of sleep-disordered breathing in a nonselected group of children with Down syndrome and to determine significant predisposing factors for this condition. DESIGN: Prospective study. SETTING: Tertiary care university hospital in Madrid, Spain. PATIENTS: The study population included 108 consecutive children with Down syndrome (mean [SD] age, 7.9 [4.5] years; range, 1-18 years) independently of whether or not suggestive clinical features of sleep-disordered breathing were present. INTERVENTIONS: In addition to history, physical examination, and lateral radiographs of the nasopharynx, all participants underwent an overnight cardiorespiratory polygraphy at the hospital using a portable ambulatory device (Apnoescreen II plus). An apnea-hypopnea index of at least 3 was required for defining the presence of sleep-disordered breathing. RESULTS: The prevalence of sleep-disordered breathing was 54.6%, with a significantly higher prevalence in boys (64.7%) than in girls (38.5%) (P < .05). The group with sleep-disordered breathing was significantly younger (6.4 [3.9] years) than those with normal polysomnographic recordings (9.6 [4.6] years) (P < .001). In the multivariate analysis, age (less than 8 years old) (odds ratio [OR], 3.36; 95% confidence interval [CI], 1.40, 8.06); male sex (OR, 3.32; 95% CI, 1.32, 8.12); and tonsillar hyperplasia (OR, 5.24; 95% CI, 1.52, 19.03) were significantly associated with sleep-disordered breathing. Body mass index, adenoid hyperplasia, previous tonsillectomy or adenoidectomy, congenital heart disease, malocclusion, and macroglossia did not affect the prevalence of sleep-disordered breathing. CONCLUSIONS: The prevalence of sleep-disordered breathing in children with Down syndrome is very high, particularly in boys. Tonsillar hyperplasia may play a role in the pathophysiology of sleep-disordered breathing in these patients. Adenoid hyperplasia, obesity, and congenital heart disease were not important risk factors for sleep-disordered breathing.

Adolescent↗
PubMed2000

Sudden death in an 8-week-old infant with Beckwith-Wiedemann syndrome.

The authors report a case of a 2-month-old girl diagnosed with Beckwith-Wiedemann syndrome (BWS) who was born prematurely and died suddenly in the hospital just before being discharged. BWS is a malformation syndrome associated with an increased risk of childhood tumors. The major features of BWS are macroglossia, abdominal wall defects, and visceromegaly, frequently leading to premature birth. Due to complex inheritance patterns, a predominance of nonfamilial cases, and the variability in expression of the features (termed incomplete penetrance), the risk of delayed diagnosis is evident. Secondary to hyperplastic pancreatic islands, hypoglycemia occurs frequently, and if not anticipated, adequate measures for prevention of hypoglycemic episodes may be delayed, resulting in possible intellectual deficits. The infant presented here died of natural causes: immaturity of the lungs resulting in marginal respiratory function and compounded by increased risk for asphyxia secondary to the enlarged tongue. The clinical history and findings in this infant are discussed in respect to the genetic syndrome with their relevance to medicolegal examination and the causes and manner of death.

Autopsy↗
PubMed2000

Prediction of difficult mask ventilation.

BACKGROUND: Maintenance of airway patency and oxygenation are the main objectives of face-mask ventilation. Because the incidence of difficult mask ventilation (DMV) and the factors associated with it are not well known, we undertook this prospective study. METHODS: Difficult mask ventilation was defined as the inability of an unassisted anesthesiologist to maintain the measured oxygen saturation as measured by pulse oximetry > 92% or to prevent or reverse signs of inadequate ventilation during positive-pressure mask ventilation under general anesthesia. A univariate analysis was performed to identify potential factors predicting DMV, followed by a multivariate analysis, and odds ratio and 95% confidence interval were calculated. RESULTS: A total of 1,502 patients were prospectively included. DMV was reported in 75 patients (5%; 95% confidence interval, 3.9-6.1%), with one case of impossible ventilation. DMV was anticipated by the anesthesiologist in only 13 patients (17% of the DMV cases). Body mass index, age, macroglossia, beard, lack of teeth, history of snoring, increased Mallampati grade, and lower thyromental distance were identified in the univariate analysis as potential DMV risk factors. Using a multivariate analysis, five criteria were recognized as independent factors for a DMV (age older than 55 yr, body mass index > 26 kg/m2, beard, lack of teeth, history of snoring), the presence of two indicating high likelihood of DMV (sensitivity, 0.72; specificity, 0.73). CONCLUSION: In a general adult population, DMV was reported in 5% of the patients. A simple DMV risk score was established. Being able to more accurately predict DMV may improve the safety of airway management.

Adult↗
PubMed1989

Cleft palate in the Beckwith-Wiedemann syndrome.

Patients with the Beckwith-Wiedemann syndrome have numerous anomalies, varying somewhat from case to case. The most common presentation is exomphalos, macroglossia, and somatic gigantism. Although cleft palate in association with this syndrome has been rarely reported, we have observed 6 patients with cleft palate in 10 patients who were diagnosed with the Beckwith-Wiedemann syndrome. The literature is reviewed and discussed.

Beckwith-Wiedemann Syndrome↗
PubMed1997

Midline glossectomy and epiglottidectomy for obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome is caused by narrowing of the pharyngeal airway and loss of dilator tone during sleep. In patients with severe apnea surgical correction often requires attention to both the oropharynx and hypopharynx. Tongue reduction surgery has been described for persistent apnea after failure of palatal surgery. We describe our experience with midline glossectomy with epiglottidectomy in 12 patients with a mean age of 48.8 +/- 14.2 years and body mass index of 36.0 +/- 8.8 kg/m2. Response to treatment was defined as a postoperative respiratory disturbance index (RDI) below 20. Three patients (25%) responded to treatment. The mean apnea index decreased from 48.9 to 35.7, RDI decreased from 73.3 to 46.6, and lowest oxygen saturation increased from 65.9 to 77.9%. RDI in responders decreased from 69.7 to 10. Midline glossectomy with epiglottidectomy has variable results, yet is effective in selected patients with hypopharyngeal narrowing related to macroglossia.

Adult↗
PubMed1975

Amyloidosis: review of 236 cases.

From 1960 through 1972, 236 cases of amyloidosis with histologic proof were found. The amyloidosis was primary (without evidence of preceding or coexisting disease) in 132 cases (group 1) and associated with multiple myeloma in 61 (group 2). Secondary amyloidosis appeared in 19 cases (associated with rheumatoid arthritis or osteomyelitis in two-thirds of them). There were 22 patients with amyloid localized to a single organ (bladder, lung, skin, or larynx in more than half of them). Two patients had familial amyloidosis. In group 1 and group 2, the most common presenting symptoms were fatigue, weight loss, edema, dyspnea, light-headedness or syncope, and paresthesias. Symptoms of the carpal-tunnel syndrome were frequent. The liver was palpable in almost 50% of the series, but splenomegaly was an initial finding in less than 10%. Macroglossia was recorded in 26% of group 2 and in 12% of group 1. Enlargement of submandibular structures was noted in about 10% of cases; and purpura, particularly around the eyes, was a significant feature. Substantial numbers of the patients had carpal-tunnel syndrome, nephrotic syndrome, congestive heart failure, sprue, peripheral neuropathy, or orthostatic hypotension. Approximately 50% of patients had renal insufficiency at the time of diagnosis. Proteinuria was found in more than 90%. A monoclonal protein was found in the serum of 49% of group 1 and in 74% of group 2. Monoclonal proteins were found in the urine of 35% and 81%, respectively. Only 12% of patients in group 1 had no monoclonal protein when both serum and urine were analyzed, and all patients of group 2 had a monoclonal protein in the serum or urine when both were analyzed. Lambda light chains were more common than kappa. None of the patients in group 1 had more than 15% plasma cells in the marrow, whereas more than half of group 2 had more than 15% plasma cells. Roentgenograms showed no evidence of skeletal disease in 94% of group 1, but 50% of group 2 had skeletal abnormalities. Rectal biopsy was positive for amyloid in 84% of cases. Kidney, liver, and carpal-tunnel biopsies were positive in 90% or more. Follow-up of all 193 patients in groups 1 and 2 revealed that 80% of group 1 and 97% of group 2 had died. The median survival was 14.7 months in group 1 and 4 months in group 2. Cardiac failure was the most common cause of death, accounting for 30% of the fatalities. We also reclassified all cases by the method of Isobe and Osserman (105), which is based on clinical patterns: pattern I--principal involvement of tongue, heart, gastrointestinal tract, muscle, nerves, skin, and carpal ligaments; pattern II--principal involvement of liver, spleen, kidneys, and adrenals; and mixed pattern I and II. This analysis failed to reveal predictive value in the clinical pattern classification, and did not discern the survival differences between primary amyloidosis (group 1) and amyloidosis with myeloma (group 2). Consequently, for the present we prefer the classification used in this study.

Adult↗
PubMed2001

Facial infiltrating lipomatosis.

Facial infiltrating lipomatosis is a rare congenital disorder in which mature lipocytes invade adjacent tissue. The phenotypic features include soft-tissue and skeletal hypertrophy, premature dental eruption, and regional macrodontia. There is a high risk for regrowth after resection that is, perforce, subtotal. The etiology, natural history, optimal management, and relationship to other disorders of fatty overgrowth are unclear. In this study, the clinical features, radiographic findings, histopathology, and postoperative results were analyzed in 13 patients with facial infiltrating lipomatosis. The condition was diagnosed in infancy (eight male subjects, five female subjects) and characterized by enlargement of the cheek (n = 12) or chin (n = 1). Other findings included cutaneous capillary blush (n = 9), ipsilateral macroglossia (n = 8), and mucosal neuromas (n = 6). Most patients had early eruption of ipsilateral deciduous and permanent teeth (n = 12). Computed tomography and magnetic resonance imaging showed an infiltrated soft-tissue mass of fatty density (n = 13) and skeletal overgrowth (n = 9). Multiple resection was performed on six patients (mean number of operations per patient, 2.5; range, one to six operations); regrowth and/or worsening of the capillary stain occurred in all six patients. Because surgical removal of the mass is usually unsuccessful, specific management of this condition will require insight into its etiopathogenesis. Given the presence of mucosal neuromas and lipomatosis, this study included testing for the known mutations in three entities that are associated with these soft-tissue findings (Cowden syndrome, Bannayan-Riley-Ruvalcava syndrome, and multiple endocrine neoplasia type 2B). Results of DNA analyses for these germline mutations were negative. It is more likely that this disorder is caused by a somatic mutation involving a local increase in growth factor(s).

Adipose Tissue↗
PubMed1999

End-tidal carbon dioxide monitoring during sedation with a combination of midazolam and ketamine for children undergoing painful, invasive procedures.

BACKGROUND: Previous studies evaluating the respiratory effects of sedation regimens have focused on events such as a decline in O2 saturation or apnea. The current study used both end-tidal carbon dioxide (ETCO2) monitoring and pulse oximetry to evaluate the respiratory effects of midazolam and ketamine. METHODS: Fifty children who required sedation during invasive procedures formed the cohort for the study. During sedation, ETCO2 was sampled from nasal cannulae of spontaneously breathing patients and measured by a side-stream aspirating infrared device. RESULTS: During the procedure, O2 saturation decreased by 3% or more in three patients. Supplemental oxygen at 2 liters per minute was administered to these patients. The lowest oxygen saturation was 84%. During the total of 767 minutes of monitoring, there were 3068 ETCO2 values recorded. The high ETCO2 values ranged from 37 to 53 mmHg (40.5 +/- 3.3 mmHg). Ninety percent, or 2760, of the values were 40 mmHg or less, 7% or 214 were between 41 and 45 mmHg, 3% or 92 were between 46 and 49 mmHg, and 2 isolated values were greater than 50 mmHg. One episode of airway obstruction was identified by noting cessation of the ETCO2 waveform. This was relieved by repositioning the patient's airway. The three episodes of O2 desaturation, two ETCO2 values greater than 50 mmHg, and the episode of upper airway obstruction all occurred in three patients. Two of these patients had trisomy 21 with macroglossia, and the third had had a recent upper respiratory infection and a history of tonsillar hypertrophy. CONCLUSION: The incidence of adverse cardiorespiratory events associated with the current sedation regimen of midazolam-ketamine is lower than that reported with other commonly used regimens. The addition of ETCO2 monitoring provides an additional monitor to allow for early detection of airway obstruction or subclinical degrees of respiratory depression.

Capnography↗