nutch_noindex
CANCEL
/nutch_noindex

Manuel Garcia, MD

  • No Image

Specialties

Gastroenterology

Work and Education

Professional Education

University of Puerto Rico, San Juan, Puerto Rico, 1983

Internship

University Of Puerto Rico, San Juan, PR, 1984

Residency

University Of Puerto Rico, San Juan, PR, 1988

Fellowship

Stanford University School of Medicine Registrar, Palo Alto, CA, 1991

Board Certifications

Pediatric Gastroenterology, American Board of Pediatrics

All Publications

Treatment of catheter occlusion in pediatric patients Conference on Evidence-Based Approach to Optimal Management of HPEN Access Kerner, J. A., Garcia-Careaga, M. G., Fisher, A. A., Poole, R. L. SAGE PUBLICATIONS INC. 2006: S73S81

Abstract

A proper initial assessment of catheter occlusion is the key to successful management. The assessment screens are for both thrombotic and nonthrombotic causes (including mechanical occlusion). If mechanical occlusion is excluded, thrombotic occlusion is treated with alteplase. Nonthrombotic occlusions are treated according to their primary etiologies: lipid occlusion is treated with 70% ethanol, mineral precipitates are treated with 0.1-N hydrochloric acid (HCl), drug precipitates are treated according to their pH-acidic drugs can be cleared with 0.1-N HCl, basic medications can be cleared with sodium bicarbonate or 0.1-N sodium hydroxide (NaOH). Prevention of occlusion of central venous access devices is also critical. To date, no data conclusively show heparin flushes to be superior to saline flushes. No prophylactic regimen, including low-dose warfarin, low-molecular-weight heparin, or 1 unit heparin/mL of parenteral nutrition has been endorsed by any major medical, nursing, or pharmacy group due to lack of scientific evidence. The most encouraging information on decreasing occlusion rate comes from experience with positive-pressure devices that attach to the hub of most catheter lumens and prevent retrograde blood flow and, consequently, decrease the risk of thrombus formation in the catheter lumen.

View details for Web of Science ID 000248557900013

View details for PubMedID 16387916

Gastrointestinal manifestations of food allergies in pediatric patients. Nutrition in clinical practice Garcia-Careaga, M., Kerner, J. A. 2005; 20 (5): 526-535

Abstract

Foods that account for 90% of allergic reactions in children are cow's milk protein, eggs, peanut, soy, tree nuts, fish, and wheat. Food allergy can manifest as urticaria/angioedema, anaphylaxis, atopic dermatitis, respiratory symptoms, or a gastrointestinal (GI) disorder. GI allergic manifestations can be classified as immunoglobulin E (IgE) mediated (immediate GI hypersensitivity and oral allergy syndrome); "mixed" GI allergy syndromes (involving some IgE components and some non-IgE or T-cell-mediated components) include eosinophilic esophagitis and eosinophilic gastroenteritis. Non-IgE-mediated or T-cell-mediated allergic GI disorders include dietary protein enteropathy, protein-induced enterocolitis, and proctitis. All these conditions share a common denominator: the response of the immune system to a specific protein leading to pathologic inflammatory changes in the GI tract. This immunological response can elicit symptoms such as diarrhea, vomiting, dysphagia, constipation, or GI blood loss, symptoms consistent with a GI disorder. The detection of food allergies can be accomplished by the use of radioallergosorbent (RAST) testing and skin prick tests in helping to assess the IgE-mediated disorders. Patch tests may help evaluate delayed hypersensitivity reactions. Treatment of GI allergic disorders ranges from strict dietary elimination of offending food(s), use of protein hydrolysates, and use of L-amino acid-based formula when protein hydrolysates fail. Treatment with topical (for eosinophilic esophagitis) or systemic steroids is used if all dietary measures are unsuccessful. Maternal breast feeding or the use from birth of hydrolysate formulas (extensive or partial hydrolysates) may be efficacious in the prevention of atopic disease in "high-risk" families (with at least 1 parent or sibling with a history of atopic disease).

View details for PubMedID 16207693

Gastrointestinal bleeding CLINICAL PEDIATRICS Nguyen, P. C., Garcia-Careaga, M., Bass, D. 2005; 44 (7): 641-643

View details for Web of Science ID 000231687200015

View details for PubMedID 16151574

A practical guideline for calculating parenteral nutrition cycles. Nutrition in clinical practice Longhurst, C., Naumovski, L., Garcia-Careaga, M., Kerner, J. 2003; 18 (6): 517-520

Abstract

Both physiologic and psychological reasons for cycling total parenteral nutrition (TPN) have been well established. Despite widespread acceptance of this practice, the only previously published method for calculating TPN cycle rates is inherently flawed.A mathematical formula was derived to facilitate reliable calculation of cyclic TPN flow rates as a function of total volume and cycle time. A publicly accessible website was subsequently developed to expedite rapid determination of TPN cycles.A fail-safe method of calculating TPN cycle flow rates can be expressed as F = V/(4T-10), where F is equal to the basal flow rate (mL/h), T is equal to the desired cycle time (hours), and V is equal to the total volume of TPN (mL) to be delivered in 24 hours. The basal flow rate and twice the basal flow rate are used for the first and last 2 hours of the TPN cycle, and the remainder of the cycle runs at 4 times the basal flow rate. TPN cycles may be easily calculated online using this formula at http://peds.stanford.edu/tpn.html.We have developed a fail-safe method of calculating TPN cycle flow rates that will consistently deliver the desired volume and have made an online implementation of this formula publicly available.

View details for PubMedID 16215087

Management of esophageal strictures in children with recessive dystrophic epidermolysis bullosa. Journal of pediatric gastroenterology and nutrition Castillo, R. O., Davies, Y. K., Lin, Y., Garcia, M., Young, H. 2002; 34 (5): 535-541

Abstract

Recessive dystrophic epidermolysis bullosa is a rare, genetically transmitted skin disorder characterized by blister formation and scarring in response to minor trauma. One of the most debilitating features of the disease is the development of esophageal strictures, which produces profound dysphagia, exacerbating an already highly compromised nutritional status common to these patients. Due to the extreme fragility of epithelial surfaces, the optimal therapeutic approach to esophageal strictures in this setting has not been established.We have developed an approach to treatment of esophageal strictures in children with epidermolysis bullosa combining upper endoscopy using small caliber endoscopes, endotracheal intubation, and fluoroscopically assisted balloon dilatation. We report our experience using this technique in 22 children who have undergone a total of 109 dilatations.Upper endoscopy, endotracheal intubation, and balloon dilatation were well tolerated by even very young children with epidermolysis bullosa. Dysphagia was markedly reduced post-procedure, permitting resumption of normal diet for age, including solids, within six hours of the procedure. Post-procedure recovery has been rapid and does not require admission to the hospital. Complications have been infrequent, minor, and limited to the first year of our experience. The mean interval between dilatations for all children is 11 months. All children have gained weight, and have not required steroids or phenytoin.Balloon dilatation is a safe and effective therapy for esophageal strictures in children with recessive dystrophic epidermolysis bullosa. Limited upper endoscopy and endotracheal intubation are well tolerated by these children. This approach should be considered as primary therapy in this clinical setting.

View details for PubMedID 12050581

Gastrointestinal dysfunction associated with syringomyelia and hydromyelia JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION Garcia-Careaga, M., Cox, K. M., Blankenberg, F., Cox, K. L. 2000; 31 (1): 71-75

View details for Web of Science ID 000087924200016

View details for PubMedID 10896075