Search PubMed⌕ Search

Biomedical subjects

Clifford T Pereira

Publications and source records attributed to Clifford T Pereira.

5 recordsLinked to original sources
PubMed2007

Blood transfusions are associated with increased risk for development of sepsis in severely burned pediatric patients.

OBJECTIVE: To determine the risk of developing sepsis following transfusion of blood products in severely burned pediatric patients. DESIGN: Retrospective, cohort study. SETTING: Shriners Hospital for Children and University Hospital. PATIENTS: Severely burned pediatric patients with >30% total body surface area (TBSA) burn. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Two hundred seventy-seven pediatric burn patients over a period of 7 yrs (1997-2004) were included in the study, with 25 patients being septic at admission and therefore excluded. Patients were stratified according to TBSA burn and presence or absence of inhalation injury. The amounts of packed red blood cells (RBCs) and fresh frozen plasma (FFP) were recorded during hospital stay before the development of sepsis. Blood product administration was normalized for the number of surgeries and divided into two groups: high (RBCs>20/FFP>5) or low (RBCs<20/FFP<5) amount of blood products. Sepsis was diagnosed based on the criteria set by the Society of Critical Care Medicine in conjunction with positive blood culture or presence of organisms in the organs at autopsy. By stratifying the groups into low and high blood transfusion, we found that patients with >60% TBSA burn with inhalation injury have an 8% risk of developing sepsis in the low RBC group, which increases to 58% in the high RBC group (p<.05). Similar results were found for RBCs per operation, FFP, and FFP per operation (p<.05). There were no differences in age and gender between groups. CONCLUSIONS: Pediatric burn suffering from a 60% TBSA burn with concomitant inhalation injury are more likely to develop sepsis if they are given high amounts of blood products, indicating an immunocompromised state following blood transfusion.

Burns↗
PubMed2006

Cytokine expression profile over time in severely burned pediatric patients.

A severe burn leads to hypermetabolism and catabolism resulting in compromised function and structure of essential organs. The massive release of cytokines is implicated in this hypermetabolic response. The aim of the present study was to compare cytokine expression profiles from severely burned children without signs of infections or inhalation injury (n = 19) to the cytokine profiles from normal, noninfected, nonburned children (n = 14). The Bio-Plex suspension array system was used to measure the concentration of 17 cytokines. The expression of proinflammatory and anti-inflammatory cytokines was maximal during the first week after thermal injury. Significant increases were measured for 15 mediators during the first week after thermal injury: interleukin (IL) 1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 p70, IL-13, IL-17, interferon gamma, monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta, and granulocyte colony-stimulating factor (P < 0.05). Granulocyte-macrophage colony-stimulating factor was significantly increased during the second week after burn (P < 0.05). Within 5 weeks, the serum concentrations of most cytokines decreased, approaching normal levels. When compared with the cytokine levels measured in normal children, a total of 16 cytokines were significantly altered (P < 0.05). After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis. The cytokine concentrations decrease during 5 weeks after burn but remain elevated over nonburned values. Furthermore, the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.

Adolescent↗
PubMed2005

The pharmacologic modulation of the hypermetabolic response to burns.

Patients with burns less than 40% TBSA do not have catabolism unless sepsis develops. Those with burns more than 40% TBSA always experience catabolism, which causes metabolic derangements that persist for at least 1 year after the injury in most body tissues. The accomplishments of the past decade have placed us in the midst of an exciting paradigm shift from what used to be a primary concern (ie, mortality) to areas that are more likely to enhance the quality of life of burn survivors. Modulating postburn hypermetabolism for the burned patient is of overwhelming importance in both the immediate care stage and the rehabilitative stage. Postburn hypermetabolism cannot be completely reversed but may be manipulated by nonpharmacologic and pharmacologic means. Early burn wound excision and complete wound closure, prevention of sepsis, the maintenance of thermal neutrality for the patient by elevation of the ambient temperature, and graded resistance exercises during convalescence are simple, highly effective primary treatment goals. Although the initial burn injury and sepsis-related complications principally determine the extent of the metabolic response in burn victims, obligatory activity, background- and procedural-related pain, and anxiety also greatly increase metabolic rates. Judicious maximal narcotic support, appropriate sedation, and supportive psychotherapy are mandatory if their effects are to be minimized. Several anabolic and anticatabolic agents are available for use during immediate care and rehabilitation. Exogenous, continuous low-dose insulin infusion, beta-blockade with propranolol, and the use of the synthetic testosterone analogue oxandrolone are the most cost-effective and least toxic therapies to date. These greatly assist therapeutic minimization of the loss of lean body mass and linear growth delay and are effective in burned patients with and without sepsis. Adverse effects, cost benefits, and the ease of administration and monitoring must be examined when considering the possibility of their use.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Altering metabolism.

A significant proportion of the mortality and morbidity of severe burns is attributable to the ensuing hypermetabolic response. This response can last for as long as 1 year after injury and is associated with impaired wound healing, increased infection risks, erosion of lean body mass, hampered rehabilitation, and delayed reintegration of burn survivors into society. Pharmacologic and nonpharmacologic strategies may be used to reverse the catabolic effect of thermal injury. Nonpharmacologic strategies include early excision and wound closure of burn wound, aggressive treatment of sepsis, elevation of the environmental temperature to thermal neutrality (31.5 +/- 0.7 degrees C), high carbohydrate, high protein continuous enteral feeding, and early institution of resistive exercise programs. Pharmacologic modulators of the postburn hypermetabolic response may be achieved through the administration of recombinant human growth hormone, low-dose insulin infusion, use of the synthetic testosterone analog, oxandrolone, and beta blockade with propranolol. This review article discusses these modulators of postburn metabolism.

Adrenergic beta-Antagonists↗