Guest guest Posted May 9, 2007 Report Share Posted May 9, 2007 My 8YO does not have any GI problems. I tried to keep her SCD just to make things simpler, but she got extreme hypoglycemia, so I am supplementing her SCD meals that the younger 2 get with complex carbs here and there. She is doing much better now. Does anybody here manage hypoglycemia and still do SCD successfully? No matter how many times/day I fed her SCD she kept getting nauseated, weak, shakey, etc. - --------------------------------- Ahhh...imagining that irresistible " new car " smell? Check outnew cars at Yahoo! Autos. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 9, 2007 Report Share Posted May 9, 2007 These articles below show the link between hypoglycemia and microorganisms. This gives us a hint that doing SCD would be helpful for hypoglycemia since SCD starves out the pathogens. Could your daughter be displaying symptoms of a die off reaction? Or might she be sneaking illegal foods at school or with friends thus producing a continuous die off reaction? Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=10505722&query_hl=20&itool=pubmed_DocSum 1: Dig Dis Sci. 1999 Sep;44(9):1837-42. Related Articles, Links Click here to read Helicobacter pylori-induced gastritis may contribute to occurrence of postprandial symptomatic hypoglycemia. Acbay O, Celik AF, Kadioglu P, Goksel S, Gundogdu S. Department of Internal Medicine, Cerrahpasa Medical School Hospital, University of Istanbul, Turkey. In our clinical experience, postprandial symptomatic hypoglycemic (PSH) patients with H. pylori gastritis showed a substantial improvement in their hypoglycemic symptoms after the eradication of H. pylori. Therefore, in this study we have investigated whether H. pylori gastritis may contribute to the occurrence of PSH. For this purpose, we have evaluated the following parameters in 12 PSH patients with H. pylori gastritis before and one month after the eradication therapy: (1) the number and severity of PSH attacks that occurred in a one-month period using a 30-day diary, (2) the total symptom score following a mixed meal using a visual analog scale questionnaire (VASQ), and (3) the glucose and insulin responses to the mixed meal. After the eradication of H. pylori, the serum insulin responses at 30 and 60 min decreased (P < 0.001 in both), whereas the plasma glucose levels at 150, 180 and 210 min increased significantly (P < 0.001 for 180 min and P < 0.01 in others) following the mixed meal. The number and severity score of PSH attacks that occurred in a one-month period and the area under curve for symptom score in VASQ decreased significantly (P < 0.001 in all). These results suggest that H. pylori gastritis may contribute to the occurrence of PSH. PMID: 10505722 [PubMed - indexed for MEDLINE] 1: Dig Dis Sci. 1999 Sep;44(9):1837-42. Related Articles, Links Click here to read Helicobacter pylori-induced gastritis may contribute to occurrence of postprandial symptomatic hypoglycemia. Acbay O, Celik AF, Kadioglu P, Goksel S, Gundogdu S. Department of Internal Medicine, Cerrahpasa Medical School Hospital, University of Istanbul, Turkey. In our clinical experience, postprandial symptomatic hypoglycemic (PSH) patients with H. pylori gastritis showed a substantial improvement in their hypoglycemic symptoms after the eradication of H. pylori. Therefore, in this study we have investigated whether H. pylori gastritis may contribute to the occurrence of PSH. For this purpose, we have evaluated the following parameters in 12 PSH patients with H. pylori gastritis before and one month after the eradication therapy: (1) the number and severity of PSH attacks that occurred in a one-month period using a 30-day diary, (2) the total symptom score following a mixed meal using a visual analog scale questionnaire (VASQ), and (3) the glucose and insulin responses to the mixed meal. After the eradication of H. pylori, the serum insulin responses at 30 and 60 min decreased (P < 0.001 in both), whereas the plasma glucose levels at 150, 180 and 210 min increased significantly (P < 0.001 for 180 min and P < 0.01 in others) following the mixed meal. The number and severity score of PSH attacks that occurred in a one-month period and the area under curve for symptom score in VASQ decreased significantly (P < 0.001 in all). These results suggest that H. pylori gastritis may contribute to the occurrence of PSH. PMID: 10505722 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=11419494&query_hl=20&itool=pubmed_DocSum 1: Pediatr Infect Dis J. 2001 Jun;20(6):557-60. Related Articles, Links Click here to read Late onset infection in very low birth weight infants in Malaysian Level 3 neonatal nurseries. Malaysian Very Low Birth Weight Study Group. Ho JJ. Perak Medical College, Greentown, Ipoh, Malaysia. jackie@... BACKGROUND: The purpose of this study was to examine the rate and mortality from late onset infection occurring in very low birth weight infants admitted to Malaysian nurseries. METHODS: Data on all infants 1500 g or below admitted to the 20 participating Level 3 nurseries were analyzed for late onset infection (clinical infection and positive blood or cerebrospinal fluid culture occurring after 48 h of life). RESULTS: The overall survival of the 962 study infants was 69%. The rate of late onset infection was 19.3%. The mortality in those with late onset infection was 30.8%. The most common infecting organism was Klebsiella pneumoniae, accounting for 38.3% of infections and 46.9% of deaths in infants with infection, followed by coagulase-negative staphylocci, 17.6 and 12.2%, respectively. On logistic regression analysis risk factors for late onset gram-negative compared with gram-positive infection were endotracheal intubation at birth and blood transfusion. Hypoglycemia was associated with gram-positive infection. CONCLUSION: The late onset infection rate in Malaysian very low birth weight infants does not differ from that reported from developed countries, but the mortality is higher. This could be because of an excess of gram-negative infections. PMID: 11419494 [PubMed - indexed for MEDLINE] 1: J Health Popul Nutr. 2005 Sep;23(3):259-65. Related Articles, Links Risk factors for mortality due to shigellosis: a case-control study among severely-malnourished children in Bangladesh. van den Broek JM, Roy SK, Khan WA, Ara G, Chakraborty B, Islam S, Banu B. Academical Medical Centre, University of Amsterdam, The Netherlands. To determine the risk factors for death of severely-malnourished Bangladeshi children with shigellosis, a case-control study was conducted at the Clinical Research and Service Centre of ICDDR,B: Centre for Health and Population Research in Dhaka, Bangladesh. One hundred severely-malnourished children (weight-for-age <60% of median of the National Center for Health Statistics), with a positive stool culture for Shigella dysenteriae type 1 or S. flexneri, who died during hospitalization, were compared with another 100 similar children (weight-for-age <60% and with S. dysenteriae type 1 or S. flexneri-associated infection) discharged alive. Children aged less than four years were admitted during December 1993-January 1999. The median age of the cases who died or recovered was 9 months and 12 months respectively. Bronchopneumonia, abdominal distension, absent or sluggish bowel sound, clinical anaemia, altered consciousness, hypothermia, clinical sepsis, low or imperceptible pulse, dehydration, hypoglycaemia, high creatinine, and hyperkalaemia were all significantly more frequent in cases than in controls. In multivariate regression analysis, altered consciousness (odds ratio [OR]=2.6, 95% confidence interval [CI] 1.0-6.8), hypoglycaemia (blood glucose <3 mmol/L (OR=7.8, 95% CI 2.9-19.6), hypothermia (temperature <36 degrees C) (OR=5.7, 95% CI 1.5-22.1), and bronchopneumonia (OR=2.5, 95% CI 1.1-5.5) were identified as significant risk factors for mortality. Severely-malnourished children with shigellosis having hypoglycaemia, hypothermia, altered consciousness and/or bronchopneumonia were at high risk of death. Based on the findings, the study recommends that early diagnosis of shigellosis in severely-malnourished children and assertive therapy for proper management to prevent development of hypothermia, hypoglycaemia, bronchopneumonia, or altered consciousness and its immediate treatment are likely to reduce Shigella-related mortality in severely-malnourished children. PMID: 16262023 [PubMed - indexed for MEDLINE] Display http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15962230&query_hl=20&itool=pubmed_docsum 1: J Infect Dis. 2005 Jul 15;192(2):336-43. Epub 2005 Jun 3. Related Articles, Links Click here to read Mice with disseminated candidiasis die of progressive sepsis. Spellberg B, Ibrahim AS, JE Jr, Filler SG. Los Angeles Biomedical Research Institute, Division of Infectious Diseases at Harbor-University of California at Los Angeles Medical Center, Torrance 90502, USA. bspellberg@... BACKGROUND: Candida species are among the most common etiologies of nosocomial bloodstream infections, causing a mortality of >40%. The murine model of hematogenously disseminated candidiasis is the standard for investigating both the activity of antifungal agents and the pathogenesis of this disease. However, despite decades of use, little is known about the physiological characteristics of the host in this model, and the cause of death remains unclear. METHODS: Using i-STAT technology, we measured blood chemistry and hemodynamic parameters to define host physiological characteristics during murine disseminated candidiasis. RESULTS: Mice with hematogenously disseminated candidiasis died of progressive sepsis, as manifested by worsening hypotension, tachycardia, and hypothermia. The mice developed metabolic acidosis, as well as profound acidemia and hypoglycemia. They also developed renal insufficiency, which became severe only shortly before death. Kidney fungal burden was correlated with severity of renal failure and systemic acidosis. The presence of significant weight loss, hypotension, or hypothermia was predictive of imminent death. CONCLUSIONS: These findings indicate that the murine model of hematogenously disseminated candidiasis accurately recapitulates the progressive sepsis seen during severe clinical cases. The results underscore the validity of the model for study of the pathophysiological aspects of this disease, as well as for the evaluation of antifungal drug efficacy. PMID: 15962230 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15570563&query_hl=20&itool=pubmed_docsum 1: Vet Clin Pathol. 2004;33(4):244-8. Related Articles, Links Artifactual hypoglycemia associated with hemotrophic mycoplasma infection in a lamb. Burkhard MJ, Garry F. Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort , CO, USA. burkhard.19@... BACKGROUND: A 35-day-old male lamb with Mycoplasma ovis infection (previously Eperythrozoon ovis) was evaluated because of severe hypoglycemia (serum glucose 4 mg/dL, Hitachi 704 automated chemistry analyzer) inconsistent with the animal's condition. Whole blood glucose concentration measured with a glucometer was 74 mg/dL. OBJECTIVE: The purpose of this study was to investigate this discrepancy through in vitro evaluation of the patient's blood. METHODS: Blood was incubated alone, with increasing concentrations of plasma, or with equine serum of known glucose concentration for 0, 15, 30, and 60 minutes at room temperature; end-point glucose concentrations were compared with blood from a control sheep handled similarly. RESULTS: A rapid decline in glucose concentration was observed in heparinized or EDTA anticoagulated whole blood from the infected lamb incubated alone or with the equine serum. Glucose concentrations in incubated samples from a control sheep remained stable. Incubation of increasing concentrations of heparinized blood with autologous plasma resulted in decreased glucose concentrations in patient, but not control, blood. As parasitemia decreased after treatment, serum glucose concentration increased, serum lactate concentration decreased, and in vitro glucose concentration stabilized. CONCLUSIONS: These findings are consistent with parasite-associated in vitro glucose consumption. An increase in the lamb's plasma glucose concentration associated with reduction of parasite load suggested excess glucose consumption also may have occurred in vivo. Publication Types: * Case Reports PMID: 15570563 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15188715&query_hl=20&itool=pubmed_docsum 1: Epidemiol Infect. 2004 Jun;132(3):455-65. Related Articles, Links Comment in: * Epidemiol Infect. 2005 Dec;133(6):1143-4; author reply 1144-6. An epidemic of gastroenteritis and mild necrotizing enterocolitis in two neonatal units of a University Hospital in Rome, Italy. Faustini A, Forastiere F, Giorgi Rossi P, Perucci CA. Department of Epidemiology Local Health Authority RME, Rome, Italy. In the summer of 1999 a cluster of 18 cases of necrotizing enterocolitis (NEC) occurred in a University Hospital in Rome, Italy. The cases presented with mild clinical and radiological signs, and none died. Seventy-two per cent had a birth weight of > 2500 g, 66.7% had a gestational age of > 37 weeks, 30% presented with respiratory diseases and/or hypoglycaemia. All cases occurred within 10 days of birth and between 5 and 7 days after two clusters of diarrhoea (14 cases). The NEC outbreak had two phases; most cases in the first phase occurred in the at-risk unit, whereas those in the second phase occurred in the full-term unit. In the multivariate analysis, invasive therapeutic procedures, pathological conditions and formula feeding were associated with NEC. Although no predominant common bacteria were isolated, we suggest an infective origin of this outbreak. PMID: 15188715 [PubMed - indexed for MEDLINE] Display Show http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15296272&query_hl=20&itool=pubmed_docsum 1: Rev Prat. 2004 May 15;54(9):957-62. Related Articles, Links [Meningococcal purpura fulminans in children] [Article in French] Leclerc F, Binoche A, Dubos F. Reanimation pediatrique, hopital Jeanne de Flandre, CHU de Lille, 59037 Lille Cedex. fleclerc@... In France, the incidence of meningococcal infections is increasing and the most severe presentation, called purpura fulminans, has still a death rate of 20-25%. Diagnosis of invasive meningococcal infection must be evoked in any child presenting with febrile purpura (vasculitic rash not disappearing with " tumbler test " ); a fulminating form must be suspected in the presence of only one ecchymosis and signs of infection, remembering that recognition of shock is difficult in children. The Health Authority recommend to administer a third generation cephalosporin promptly for any child with signs of infection and an ecchymotic purpura (>3 mm of diameter), and then to refer the patient to the hospital. Children with purpura fulminans should be referred to a paediatric intensive care unit. Management includes antibiotics, steroids, fluid resuscitation and catecholamines (be aware of hypoglycaemia, particularly in infants, and hypocalcaemia). Treatment of cutaneous necrosis and distal ischemia is difficult and still controversial: antithrombin, protein C, tissue plasminogen activator and vasodilator infusion have no proved efficacy. Cases must be rapidly notified to the Public Health Service who will institute chemoprophylaxis for close contacts. Given the predominance of serogroup B in France, we hope that an efficient vaccine will soon become available. PMID: 15296272 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=12793713&query_hl=20&itool=pubmed_DocSum 1: Intern Med. 2003 May;42(5):421-3. Related Articles, Links Click here to read Streptococcal toxic shock syndrome presenting with spontaneous hypoglycemia in a chronic hemodialysis patient: pathophysiological mechanisms. Igaki N, Matsuda T, Hirota Y, Kawaguchi T, Tamada F, Goto T. Department of Internal Medicine, Takasago Municipal Hospital, Takasago. Hypoglycemia is fatal if associated with sepsis in end-stage renal disease (ESRD) patients. We report a hemodialysis patient of streptococcal toxic shock syndrome presenting with hypoglycemia. She was found to be severely hypoglycemic with a plasma glucose level of 16 mg/dl. Immunoreactive insulin levels were undetectable throughout the clinical course. Several factors including reduced renal gluconeogenesis, reduced hepatic glucose output and excessive peripheral glucose utilization may account for the hypoglycemia in this patient. In conclusion, we would like to draw attention to the fact that septic ESRD patients without diabetes are prone to develop profound hypoglycemia with serious consequences. Publication Types: * Case Reports PMID: 12793713 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=12442027&query_hl=20&itool=pubmed_DocSum Pediatr Infect Dis J. 2002 Nov;21(11):1042-8. Related Articles, Links Click here to read Acute bacterial meningitis in children admitted to a rural Kenyan hospital: increasing antibiotic resistance and outcome. Mwangi I, Berkley J, Lowe B, Peshu N, Marsh K, Newton CR. Kenya Medical Research Institute, Center for Geographic Medicine Research-Coast, Kilifi, Kenya. BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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. PMID: 12442027 [PubMed - indexed for MEDLINE] > My 8YO does not have any GI problems. I tried to keep her SCD just to make > things simpler, but she got extreme hypoglycemia, so I am supplementing her > SCD meals that the younger 2 get with complex carbs here and there. She is > doing much better now. Does anybody here manage hypoglycemia and still do > SCD successfully? No matter how many times/day I fed her SCD she kept > getting nauseated, weak, shakey, etc. > > - > > > --------------------------------- > Ahhh...imagining that irresistible " new car " smell? > Check outnew cars at Yahoo! Autos. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 9, 2007 Report Share Posted May 9, 2007 I don't know what to think. Is bacteria the ONLY reason she could have low blood sugar? Previously, she had very little problem with this. It only reared it's head if she decided to skip dinner (just not hungry) and go to bed. This was a rare occassion in the first place. If that happened, she would wake up hypoglycemic and I would need to give her breakfast in bed. On SCD, she gets this way 1-2 times/day and almost every morning even though I make her eat a bedtime snack, and have been giving her breakfast in bed. She was vomitting after breakfast in bed and then okay with breakfast #2. This happened 3X in a row, and then I started her on some starch/carb snacks & it went away. There were previously no illegals as she is homeschooled and honest to a fault. I gave her a piece of whole grain toast with cheese or nutbutter as a snack 1-2 times/day and she is now fine. I don't know what to think. She has never really had the signs of bacterial/yeast overgrowth (never had the bloated belly, no constipation or diarrhea & never taken antibiotics), but I thought she would do fine eating SCD along with us. She is not one to fuss over food, so she doesn't really fight me over diet. She just wants to hurry up and eat so she can go be a kid! I think once the little ones ( -- ASD and Hope -- 2 abdominal surgeries to correct a GI birth defect) are veteran SCDers (like in a year), I will play around with my healthy child and see if she can benefit from 100% SCD. She has never eaten junk food, so I don't feel any urgency & am more concerned about making her miserable now when we are not doing this diet to help her in the first place! BTW, I used to feel the same as she did (hypoglycemic) when I cut the starches. This time I'm not having such a problem & I don't know why. If I do eat an occassional starch, I also feel fine. For me removing dairy is making the bigger difference & I'm glad I did that. It feels much better to be non-dairy plus low starch or no starch than starches and dairy all day long. - pecan post wrote: These articles below show the link between hypoglycemia and microorganisms. This gives us a hint that doing SCD would be helpful for hypoglycemia since SCD starves out the pathogens. Could your daughter be displaying symptoms of a die off reaction? Or might she be sneaking illegal foods at school or with friends thus producing a continuous die off reaction? Mimi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=10505722&query_hl=20&itool=pubmed_DocSum 1: Dig Dis Sci. 1999 Sep;44(9):1837-42. Related Articles, Links Click here to read Helicobacter pylori-induced gastritis may contribute to occurrence of postprandial symptomatic hypoglycemia. Acbay O, Celik AF, Kadioglu P, Goksel S, Gundogdu S. Department of Internal Medicine, Cerrahpasa Medical School Hospital, University of Istanbul, Turkey. In our clinical experience, postprandial symptomatic hypoglycemic (PSH) patients with H. pylori gastritis showed a substantial improvement in their hypoglycemic symptoms after the eradication of H. pylori. Therefore, in this study we have investigated whether H. pylori gastritis may contribute to the occurrence of PSH. For this purpose, we have evaluated the following parameters in 12 PSH patients with H. pylori gastritis before and one month after the eradication therapy: (1) the number and severity of PSH attacks that occurred in a one-month period using a 30-day diary, (2) the total symptom score following a mixed meal using a visual analog scale questionnaire (VASQ), and (3) the glucose and insulin responses to the mixed meal. After the eradication of H. pylori, the serum insulin responses at 30 and 60 min decreased (P < 0.001 in both), whereas the plasma glucose levels at 150, 180 and 210 min increased significantly (P < 0.001 for 180 min and P < 0.01 in others) following the mixed meal. The number and severity score of PSH attacks that occurred in a one-month period and the area under curve for symptom score in VASQ decreased significantly (P < 0.001 in all). These results suggest that H. pylori gastritis may contribute to the occurrence of PSH. PMID: 10505722 [PubMed - indexed for MEDLINE] 1: Dig Dis Sci. 1999 Sep;44(9):1837-42. Related Articles, Links Click here to read Helicobacter pylori-induced gastritis may contribute to occurrence of postprandial symptomatic hypoglycemia. Acbay O, Celik AF, Kadioglu P, Goksel S, Gundogdu S. Department of Internal Medicine, Cerrahpasa Medical School Hospital, University of Istanbul, Turkey. In our clinical experience, postprandial symptomatic hypoglycemic (PSH) patients with H. pylori gastritis showed a substantial improvement in their hypoglycemic symptoms after the eradication of H. pylori. Therefore, in this study we have investigated whether H. pylori gastritis may contribute to the occurrence of PSH. For this purpose, we have evaluated the following parameters in 12 PSH patients with H. pylori gastritis before and one month after the eradication therapy: (1) the number and severity of PSH attacks that occurred in a one-month period using a 30-day diary, (2) the total symptom score following a mixed meal using a visual analog scale questionnaire (VASQ), and (3) the glucose and insulin responses to the mixed meal. After the eradication of H. pylori, the serum insulin responses at 30 and 60 min decreased (P < 0.001 in both), whereas the plasma glucose levels at 150, 180 and 210 min increased significantly (P < 0.001 for 180 min and P < 0.01 in others) following the mixed meal. The number and severity score of PSH attacks that occurred in a one-month period and the area under curve for symptom score in VASQ decreased significantly (P < 0.001 in all). These results suggest that H. pylori gastritis may contribute to the occurrence of PSH. PMID: 10505722 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=11419494&query_hl=20&itool=pubmed_DocSum 1: Pediatr Infect Dis J. 2001 Jun;20(6):557-60. Related Articles, Links Click here to read Late onset infection in very low birth weight infants in Malaysian Level 3 neonatal nurseries. Malaysian Very Low Birth Weight Study Group. Ho JJ. Perak Medical College, Greentown, Ipoh, Malaysia. jackie@... BACKGROUND: The purpose of this study was to examine the rate and mortality from late onset infection occurring in very low birth weight infants admitted to Malaysian nurseries. METHODS: Data on all infants 1500 g or below admitted to the 20 participating Level 3 nurseries were analyzed for late onset infection (clinical infection and positive blood or cerebrospinal fluid culture occurring after 48 h of life). RESULTS: The overall survival of the 962 study infants was 69%. The rate of late onset infection was 19.3%. The mortality in those with late onset infection was 30.8%. The most common infecting organism was Klebsiella pneumoniae, accounting for 38.3% of infections and 46.9% of deaths in infants with infection, followed by coagulase-negative staphylocci, 17.6 and 12.2%, respectively. On logistic regression analysis risk factors for late onset gram-negative compared with gram-positive infection were endotracheal intubation at birth and blood transfusion. Hypoglycemia was associated with gram-positive infection. CONCLUSION: The late onset infection rate in Malaysian very low birth weight infants does not differ from that reported from developed countries, but the mortality is higher. This could be because of an excess of gram-negative infections. PMID: 11419494 [PubMed - indexed for MEDLINE] 1: J Health Popul Nutr. 2005 Sep;23(3):259-65. Related Articles, Links Risk factors for mortality due to shigellosis: a case-control study among severely-malnourished children in Bangladesh. van den Broek JM, Roy SK, Khan WA, Ara G, Chakraborty B, Islam S, Banu B. Academical Medical Centre, University of Amsterdam, The Netherlands. To determine the risk factors for death of severely-malnourished Bangladeshi children with shigellosis, a case-control study was conducted at the Clinical Research and Service Centre of ICDDR,B: Centre for Health and Population Research in Dhaka, Bangladesh. One hundred severely-malnourished children (weight-for-age <60% of median of the National Center for Health Statistics), with a positive stool culture for Shigella dysenteriae type 1 or S. flexneri, who died during hospitalization, were compared with another 100 similar children (weight-for-age <60% and with S. dysenteriae type 1 or S. flexneri-associated infection) discharged alive. Children aged less than four years were admitted during December 1993-January 1999. The median age of the cases who died or recovered was 9 months and 12 months respectively. Bronchopneumonia, abdominal distension, absent or sluggish bowel sound, clinical anaemia, altered consciousness, hypothermia, clinical sepsis, low or imperceptible pulse, dehydration, hypoglycaemia, high creatinine, and hyperkalaemia were all significantly more frequent in cases than in controls. In multivariate regression analysis, altered consciousness (odds ratio [OR]=2.6, 95% confidence interval [CI] 1.0-6.8), hypoglycaemia (blood glucose <3 mmol/L (OR=7.8, 95% CI 2.9-19.6), hypothermia (temperature <36 degrees C) (OR=5.7, 95% CI 1.5-22.1), and bronchopneumonia (OR=2.5, 95% CI 1.1-5.5) were identified as significant risk factors for mortality. Severely-malnourished children with shigellosis having hypoglycaemia, hypothermia, altered consciousness and/or bronchopneumonia were at high risk of death. Based on the findings, the study recommends that early diagnosis of shigellosis in severely-malnourished children and assertive therapy for proper management to prevent development of hypothermia, hypoglycaemia, bronchopneumonia, or altered consciousness and its immediate treatment are likely to reduce Shigella-related mortality in severely-malnourished children. PMID: 16262023 [PubMed - indexed for MEDLINE] Display http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15962230&query_hl=20&itool=pubmed_docsum 1: J Infect Dis. 2005 Jul 15;192(2):336-43. Epub 2005 Jun 3. Related Articles, Links Click here to read Mice with disseminated candidiasis die of progressive sepsis. Spellberg B, Ibrahim AS, JE Jr, Filler SG. Los Angeles Biomedical Research Institute, Division of Infectious Diseases at Harbor-University of California at Los Angeles Medical Center, Torrance 90502, USA. bspellberg@... BACKGROUND: Candida species are among the most common etiologies of nosocomial bloodstream infections, causing a mortality of >40%. The murine model of hematogenously disseminated candidiasis is the standard for investigating both the activity of antifungal agents and the pathogenesis of this disease. However, despite decades of use, little is known about the physiological characteristics of the host in this model, and the cause of death remains unclear. METHODS: Using i-STAT technology, we measured blood chemistry and hemodynamic parameters to define host physiological characteristics during murine disseminated candidiasis. RESULTS: Mice with hematogenously disseminated candidiasis died of progressive sepsis, as manifested by worsening hypotension, tachycardia, and hypothermia. The mice developed metabolic acidosis, as well as profound acidemia and hypoglycemia. They also developed renal insufficiency, which became severe only shortly before death. Kidney fungal burden was correlated with severity of renal failure and systemic acidosis. The presence of significant weight loss, hypotension, or hypothermia was predictive of imminent death. CONCLUSIONS: These findings indicate that the murine model of hematogenously disseminated candidiasis accurately recapitulates the progressive sepsis seen during severe clinical cases. The results underscore the validity of the model for study of the pathophysiological aspects of this disease, as well as for the evaluation of antifungal drug efficacy. PMID: 15962230 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15570563&query_hl=20&itool=pubmed_docsum 1: Vet Clin Pathol. 2004;33(4):244-8. Related Articles, Links Artifactual hypoglycemia associated with hemotrophic mycoplasma infection in a lamb. Burkhard MJ, Garry F. Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort , CO, USA. burkhard.19@... BACKGROUND: A 35-day-old male lamb with Mycoplasma ovis infection (previously Eperythrozoon ovis) was evaluated because of severe hypoglycemia (serum glucose 4 mg/dL, Hitachi 704 automated chemistry analyzer) inconsistent with the animal's condition. Whole blood glucose concentration measured with a glucometer was 74 mg/dL. OBJECTIVE: The purpose of this study was to investigate this discrepancy through in vitro evaluation of the patient's blood. METHODS: Blood was incubated alone, with increasing concentrations of plasma, or with equine serum of known glucose concentration for 0, 15, 30, and 60 minutes at room temperature; end-point glucose concentrations were compared with blood from a control sheep handled similarly. RESULTS: A rapid decline in glucose concentration was observed in heparinized or EDTA anticoagulated whole blood from the infected lamb incubated alone or with the equine serum. Glucose concentrations in incubated samples from a control sheep remained stable. Incubation of increasing concentrations of heparinized blood with autologous plasma resulted in decreased glucose concentrations in patient, but not control, blood. As parasitemia decreased after treatment, serum glucose concentration increased, serum lactate concentration decreased, and in vitro glucose concentration stabilized. CONCLUSIONS: These findings are consistent with parasite-associated in vitro glucose consumption. An increase in the lamb's plasma glucose concentration associated with reduction of parasite load suggested excess glucose consumption also may have occurred in vivo. Publication Types: * Case Reports PMID: 15570563 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15188715&query_hl=20&itool=pubmed_docsum 1: Epidemiol Infect. 2004 Jun;132(3):455-65. Related Articles, Links Comment in: * Epidemiol Infect. 2005 Dec;133(6):1143-4; author reply 1144-6. An epidemic of gastroenteritis and mild necrotizing enterocolitis in two neonatal units of a University Hospital in Rome, Italy. Faustini A, Forastiere F, Giorgi Rossi P, Perucci CA. Department of Epidemiology Local Health Authority RME, Rome, Italy. In the summer of 1999 a cluster of 18 cases of necrotizing enterocolitis (NEC) occurred in a University Hospital in Rome, Italy. The cases presented with mild clinical and radiological signs, and none died. Seventy-two per cent had a birth weight of > 2500 g, 66.7% had a gestational age of > 37 weeks, 30% presented with respiratory diseases and/or hypoglycaemia. All cases occurred within 10 days of birth and between 5 and 7 days after two clusters of diarrhoea (14 cases). The NEC outbreak had two phases; most cases in the first phase occurred in the at-risk unit, whereas those in the second phase occurred in the full-term unit. In the multivariate analysis, invasive therapeutic procedures, pathological conditions and formula feeding were associated with NEC. Although no predominant common bacteria were isolated, we suggest an infective origin of this outbreak. PMID: 15188715 [PubMed - indexed for MEDLINE] Display Show http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=15296272&query_hl=20&itool=pubmed_docsum 1: Rev Prat. 2004 May 15;54(9):957-62. Related Articles, Links [Meningococcal purpura fulminans in children] [Article in French] Leclerc F, Binoche A, Dubos F. Reanimation pediatrique, hopital Jeanne de Flandre, CHU de Lille, 59037 Lille Cedex. fleclerc@... In France, the incidence of meningococcal infections is increasing and the most severe presentation, called purpura fulminans, has still a death rate of 20-25%. Diagnosis of invasive meningococcal infection must be evoked in any child presenting with febrile purpura (vasculitic rash not disappearing with " tumbler test " ); a fulminating form must be suspected in the presence of only one ecchymosis and signs of infection, remembering that recognition of shock is difficult in children. The Health Authority recommend to administer a third generation cephalosporin promptly for any child with signs of infection and an ecchymotic purpura (>3 mm of diameter), and then to refer the patient to the hospital. Children with purpura fulminans should be referred to a paediatric intensive care unit. Management includes antibiotics, steroids, fluid resuscitation and catecholamines (be aware of hypoglycaemia, particularly in infants, and hypocalcaemia). Treatment of cutaneous necrosis and distal ischemia is difficult and still controversial: antithrombin, protein C, tissue plasminogen activator and vasodilator infusion have no proved efficacy. Cases must be rapidly notified to the Public Health Service who will institute chemoprophylaxis for close contacts. Given the predominance of serogroup B in France, we hope that an efficient vaccine will soon become available. PMID: 15296272 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=12793713&query_hl=20&itool=pubmed_DocSum 1: Intern Med. 2003 May;42(5):421-3. Related Articles, Links Click here to read Streptococcal toxic shock syndrome presenting with spontaneous hypoglycemia in a chronic hemodialysis patient: pathophysiological mechanisms. Igaki N, Matsuda T, Hirota Y, Kawaguchi T, Tamada F, Goto T. Department of Internal Medicine, Takasago Municipal Hospital, Takasago. Hypoglycemia is fatal if associated with sepsis in end-stage renal disease (ESRD) patients. We report a hemodialysis patient of streptococcal toxic shock syndrome presenting with hypoglycemia. She was found to be severely hypoglycemic with a plasma glucose level of 16 mg/dl. Immunoreactive insulin levels were undetectable throughout the clinical course. Several factors including reduced renal gluconeogenesis, reduced hepatic glucose output and excessive peripheral glucose utilization may account for the hypoglycemia in this patient. In conclusion, we would like to draw attention to the fact that septic ESRD patients without diabetes are prone to develop profound hypoglycemia with serious consequences. Publication Types: * Case Reports PMID: 12793713 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\ ct&list_uids=12442027&query_hl=20&itool=pubmed_DocSum Pediatr Infect Dis J. 2002 Nov;21(11):1042-8. Related Articles, Links Click here to read Acute bacterial meningitis in children admitted to a rural Kenyan hospital: increasing antibiotic resistance and outcome. Mwangi I, Berkley J, Lowe B, Peshu N, Marsh K, Newton CR. Kenya Medical Research Institute, Center for Geographic Medicine Research-Coast, Kilifi, Kenya. BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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. PMID: 12442027 [PubMed - indexed for MEDLINE] > My 8YO does not have any GI problems. I tried to keep her SCD just to make > things simpler, but she got extreme hypoglycemia, so I am supplementing her > SCD meals that the younger 2 get with complex carbs here and there. She is > doing much better now. Does anybody here manage hypoglycemia and still do > SCD successfully? No matter how many times/day I fed her SCD she kept > getting nauseated, weak, shakey, etc. > > - > > > --------------------------------- > Ahhh...imagining that irresistible " new car " smell? > Check outnew cars at Yahoo! Autos. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 10, 2007 Report Share Posted May 10, 2007 I have determined (long before we started SCD) that I have to include protein with every meal or I get weak and shaky too. If I'm feeling a bit shaky in the afternoon, I might eat a boiled egg for a snack. Seems to do the trick. HTH, White (SCD since 2/1/07 with my 7 yo daughter) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 10, 2007 Report Share Posted May 10, 2007 Hi , << My 8YO does not have any GI problems. I tried to keep her SCD just to make things simpler, but she got extreme hypoglycemia, so I am supplementing her SCD meals that the younger 2 get with complex carbs here and there. She is doing much better now. Does anybody here manage hypoglycemia and still do SCD successfully? No matter how many times/day I fed her SCD she kept getting nauseated, weak, shakey, etc. >> I have also suffered from hypoglcemia. It was much worse preSCD - I would frequently get waek, feel faint etc. if I was a little late with a meal or hadn't eaten much. I have found the diet has helped immensely - I still occasionally get a bit weak if I skip a meal but not to the same level as preSCD. Also I have found that if I try to have a snack that is either carbs or protein it doesn't sit well and usually makes it worse. Having a snack with both protein and carbs keeps the low blood sugar at bay for me. Sheila, SCD Feb. 2001, UC 23yrs mom of and Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.