ATLS--essential training for Naval medical officers? Advanced Trauma Life Support.
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A 69-year-old woman was admitted to our hospital because of leucocytosis and systemic lymphadenopathy. On admission, white blood cell count was 163,000/microliters, most of which consisted of flower-like cells with convoluted nuclei in the peripheral blood. In the abnormal lymphocyte cells surface-marker test by flow cytometry showed that they expressed CD2, CD3, CD4, CD29, CD45RA, and CD38, but not CD8, CD16, and CD25. Serum anti-Human T-lymphotropic virus type-I (HTLV-I) antibody was negative in particle agglutination, enzyme-linked immunosorbent assay (ELISA) and western-blotting assay. HTLV-I proviral DNA in the abnormal lymphocyte cells was not detected by southern blotting hybridization technique. Moreover, HTLV-I provirus was not detected using a polymerase-chain-reaction (PCR). A monoclonal rearrangement of the TCR-beta chain gene was evident by using DNA probe in southern blot hybridization. Because of the rapid progress of the disease, chemotherapy was started immediately after admission. Though, this patient became refractory, and she died about 1 year after admission.
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To establish a desirable preventive measure against mother-to-child transmission of HTLV-I through breast milk, we conducted a prospective study to investigate the seroconversion rate among children born to HTLV-I carrier mothers on two highly HTLV-I-endemic islands where 8% of pregnant women carry HTLV-I. Between 1985 to 1991, 428 pregnant women were found to be positive against anti-HTLV-I antibody and were advised not to breast-feed their newborn babies. Among them, 212 women (50%) accepted this advice and the other mothers proceeded to breast-feed. Results were obtained from 277 children born to HTLV-I carrier mothers and were followed up until more than 30 months of age. When the seroconversion rate was analyzed by feeding manner, short-term breast-feeders (< or = 6 months) showed a statistically significant lower seroconversion rate than long-term breast-feeders (2/51; 3.9% vs. 13/64; 20.3%, p < 0.05). On the other hand, four out of 162 bottle-fed children (2.5%) became positive. It is hypothesized that maternal HTLV-I antibody may protect babies from HTLV-I infection through breast milk during the first 6 months.
Although the Advanced Trauma Life Support (ATLS) course is now taught internationally, its teaching effectiveness still requires confirmation. The Objective Structured Clinical Examination (OSCE) reliably assesses clinical performance by utilizing standardized patients. An OSCE of eight 15 minute trauma patient stations and two 40 item MCQ tests were used to test the teaching effectiveness of the ATLS program in 32 practicing physicians who applied for an ATLS program in Trinidad and Tobago. The physicians were randomly assigned to an ATLS group (n = 16) that completed the ATLS course and a non-ATLS group (n = 16). Before and after the ATLS course, all physicians completed MCQ tests and trauma OSCE. Mean (+/- SD) OSCE scores (standardized to 20) ranged from 9.8 +/- 1.7 to 10.0 +/- 1.7 and 9.5 +/- 1.8 to 10.8 +/- 1.3 in the ATLS and non-ATLS groups, respectively, prior to the ATLS course (NS). Post-ATLS OSCE scores ranged from 15.9 +/- 1.7 to 17.6 +/- 1.7 in the ATLS group (p < 0.05 compared to pre-ATLS) and 9.5 +/- 1.4 to 10.1 +/- 1.3 in the non-ATLS group, which did not improve their OSCE scores. Adherence to priorities was graded 1 to 7 with the pre-ATLS grades of 1.7 +/- 0.6 (ATLS) and 1.8 +/- 0.7 (non-ATLS) and post-ATLS grades of 6.4 +/- 1.1 (ATLS) and 2.1 +/- 0.6 (non-ATLS). Organized approach to trauma was graded 1 to 5 with pre-ATLS grades of 1.6 +/- 0.5 (ATLS) and 1.7 +/- 0.6 (non-ATLS) and post-ATLS grades of 4.5 +/- 0.6 (ATLS) and 1.9 +/- 0.6 (non-ATLS). Pre-ATLS MCQ scores (%) were similar: 53.1 +/- 8.4 (ATLS) and 57.3 +/- 5.4 (non-ATLS), but post-ATLS scores were greater in the ATLS group: 85.8 +/- 7.1 (ATLS) and 64.2 +/- 3.6 (non-ATLS). Our data support the teaching effectiveness of the ATLS program among practicing physicians as measured by improvement in OSCE scores, adherence to trauma priorities, maintenance of an organized approach to trauma care, and cognitive performance in MCQ examinations.
Trauma outcome variables before and after the institution of the Advanced Trauma Life Support (ATLS) program were compared for the largest hospital in Trinidad and Tobago from July 1981 through December 1985 (pre-ATLS) and from January 1986 to June 1990 (post-ATLS). A total of 199 physicians were ATLS trained by June 1990. Outcome data were analyzed for all dead or severely injured patients (ISS > or = 16; n = 413 pre-ATLS and n = 400 post-ATLS). Trauma mortality decreased post-ATLS (134 of 400 vs. 279 of 413) throughout the hospital, including the ICU (13.6% post-ATLS ICU mortality vs. 55.2% pre-ATLS). The odds of dying from trauma increased with age (1.02 for each year), ISS score (1.24 for each ISS increment), and blunt injury, both pre-ATLS and post-ATLS. Post-ATLS mortality was associated with a higher ISS (31.6 vs. 28.8). Although there was a higher percentage of blunt injury pre-ATLS (84.0%) versus post-ATLS (68.3%), the mortality rates for both blunt and penetrating injuries were higher in the pre-ATLS group (19.7% pre-ATLS vs. 6.3% post-ATLS for penetrating and 76.6% pre-ATLS versus 46.2% post-ATLS for blunt). For each ISS category, mortality was greater in the pre-ATLS group (ISS > or = 24 pre-ATLS mortality 47.9% vs. 16.7% post-ATLS; ISS 25-40 pre-ATLS mortality 91.0% vs. 71.0% post-ATLS). The overall ratio of observed to expected mortality based on the MTOS data base was lower for the post-ATLS period (pre-ATLS ratio 3.16; post-ATLS ratio 1.94).(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: We tested the effectiveness of Advanced Trauma Life Support (ATLS) training among surgical residents using a specially designed mannequin. MATERIALS AND METHODS: Thirty-two Postgraduate Year I surgical residents were randomly assigned to two groups of 16 each. By use of a trauma mannequin, the 32 residents' performances were scored using four trauma scenarios before 16 residents (ATLS group) completed a standard ATLS course. Performances were also scored after the ATLS course on another four trauma scenarios. The scores were standardized to a maximum of 20 for each scenario. Organized Approach scores with a range of 1 to 5, Priority scores ranging from 1 to 7, and global ratings of Honors, Pass, Borderline, or Fail were assigned for each clinical scenario. RESULTS: The pre-ATLS assessment scores were similar for both groups ranging between 9.4 +/- 3.5 and 11.4 +/- 2.9 for the ATLS group and between 10.2 +/- 3.8 and 11.4 +/- 3.9 for the non-ATLS group. The ATLS group scores ranged from 16.0 +/- 1.3 to 17.4 +/- 3.1 after the course and the non-ATLS group scores ranged from 11.4 +/- 4.2 to 12.9 +/- 4.0 (P < 0.05). Pre-ATLS Organized Approach scores were 2.9 +/- 1.0 and 2.7 +/- 1.1 (NS) for the ATLS and non-ATLS groups, respectively, with post-ATLS scores being significantly higher in the ATLS group (4.9 +/- 1.2 compared with 2.8 +/- 1.2 for the non-ATLS group, P < 0. 05). Initial Priority scores were also similar for both groups (3.2 +/- 1.4 for the ATLS group and 3.3 +/- 2.0 for the non-ATLS group). Post-ATLS Priority scores were significantly higher (6.4 +/- 1.4) in the ATLS group compared with 4.2 +/- 1.9 for the non-ATLS group (P < 0.05). The pre-ATLS global ratings were similar for both groups and post-ATLS there were 10 Honors ratings in the ATLS group and none for the control group. CONCLUSIONS: Using a trauma mannequin, for assessment, surgical residents completing the ATLS course demonstrated superior resuscitation skills compared with a non-ATLS group.
The Advanced Trauma Life Support (ATLS) course sponsored by the American College of Surgeons Committee On Trauma (ACSCOT) presents a standardized method of initial trauma care. This study attempted to measure any changes in morbidity and mortality in trauma patients after the introduction of ATLS training. Over a 3-year period (May 1996 to September 1997-pre-ATLS period; December 1997 to April 1999-post-ATLS period), 63 trauma patients with an Injury Severity Scale (ISS) > or =16 (n = 31, pre-ATLS and n = 32, post-ATLS) were prospectively studied in two community teaching hospitals. There was no significant difference in mortality rate between groups (48% [15 of 31] pre-ATLS vs. 30% [10 of 32] post-ATLS; P = .203, Fisher exact test). Mortality rates within the ISS range of 16 to 25 were 64% (nine of 14 pre-ATLS) versus 29% (five of 17 post-ATLS), and for the ISS 26 to 35 subgroup, 40% (four of 10 pre-ATLS) versus 25% (two of eight post-ATLS), and within the ISS 36 to 75 subgroup, 29% (two of seven pre-ATLS) versus 43% (three of seven post-ATLS). There was a significant difference in mortality during the first 60 minutes after admission: 0.0% post-ATLS versus 24.2% pre-ATLS (P = .002, Fisher exact test (95% confidence interval ranged from 12-45% in the pre-ATLS group and 0-11% in the post-ATLS group). According to the TRISS methodology (a worldwide-accepted mathematical method to calculate chances of survival through logistical regression),ATLS improved outcome from sub-"Major Trauma Outcome Study" (MTOS) standard results (z = -2.9 to a MTOS standard result z = -0.49). Our data demonstrate that introduction of the ATLS program significantly improved trauma patient outcome in the first hour after admission, as well as improvement from sub-MTOS standard to MTOS standard levels.
UNLABELLED: Hypercalcemia is observed in >80% of ATL. Serum MIP-1alpha levels were elevated in all 24 ATL with hypercalcemia but undetectable in all 10 patients with humoral hypercalcemia of malignancy with solid tumors and in 34 of 37 ATL without hypercalcemia. We propose that serum MIP-1alpha is a clinical hallmark for hypercalcemia in ATL. INTRODUCTION: High serum cytokines levels are not always associated with hypercalcemia in patients with adult T-cell leukemia (ATL), suggesting that other factors are involved in the pathogenesis of ATL patients with hypercalcemia. This study was designed to determine the role of macrophage inflammatory protein-1alpha (MIP-1alpha), a chemokine recently described as an osteoclast stimulatory factor, in ATL-associated hypercalcemia. MATERIALS AND METHODS: We measured serum interleukin (IL)-1beta, IL-6, TNF-alpha, parathyroid hormone-related protein (PTHrP), and MIP-1alpha levels in ATL patients by enzyme-linked immunosorbent assays. FACScan was used to measure the expression of RANKL on ATL cells. Osteoclast formation in cocultures of ATL cells and peripheral blood mononuclear cells (PBMCs) was evaluated by TRACP staining. RESULTS: High serum MIP-1alpha levels were noted in all 24 ATL patients with hypercalcemia and in 3 of 37 ATL patients without hypercalcemia. The elevated levels of MIP-1alpha and calcium in ATL patients decreased after effective chemotherapy, emphasizing the role of MIP-1alpha in ATL hypercalcemia. ATL cells spontaneously produced MIP-1alpha. MIP-1alpha significantly enhanced human monocyte (precursor cells of osteoclasts) migration and induced RANKL expression on ATL cells. ATL cell-induced osteoclast formation from PBMCs was inhibited by anti-MIP-1alpha antibody and osteoprotegerin. CONCLUSION: Our results suggest that MIP-1alpha can induce RANKL on ATL cells in autocrine fashion and that RANKL seems to mediate the hypercalcemic effect of MIP-1alpha in ATL. We propose that MIP-1alpha is the clinical hallmark of hypercalcemia in ATL and could be a potentially useful therapeutic target.
The expression of activated cell antigens (Ags) on adult T cell leukemia (ATL) cells at different clinical stages (acute, chronic, and smoldering), and ATL cells from enlarged lymph nodes were studied using monoclonal antibodies (MoAbs). The expressions of CD25 (Tac), CD28, T9 (transferrin receptor), and Ki-67 (proliferating cell nuclear antigen) Ags were high, and that of CD7 Ag was low in both acute and chronic ATL cells compared with that in normal T cells. The expressions of T9 and Ki-67 Ags were higher in acute ATL cells than in chronic ATL cells. The expression of CD38 Ag was higher in acute ATL cells but not in chronic ATL cells compared with normal T cells. On the contrary, the expression of HLA-DR Ag on the cell surface and the transcript of the HLA-DR Ag gene were high in chronic ATL cells, but not in acute ATL cells. A high percentage of lymph node ATL cells expressed T9, CD38, and Ki-67 Ags, although the peripheral blood ATL cells of the same patients showed significantly lower levels of expression of the same Ags. Interestingly, CD7 and HLA-DR Ags were detected on the majority of lymph node ATL cells. Moderately high percentage of smoldering ATL cells expressed CD25, CD28, and HLA-DR Ags, though a few numbers of leukemic cells were present in the samples. These findings confirm that the modes of activation of ATL cells in different clinical stages differ, and suggest that the differences might be reflected in the clinical features. The low expression of HLA-DR Ag in acute ATL cells, despite high expression of the Ag in chronic ATL cells, suggests that successive events that suppress HLA-DR Ag expression are necessary for the transformation of chronic ATL cells into acute ATL cells. Moreover, the high expressions of T9, CD38, Ki-67, CD7, and HLA-DR Ags on lymph node ATL cells indicate that ATL cells preferentially proliferate in lymph nodes.
An important disease entity distinct from cutaneous T-cell lymphoma (CTCL) in Japan is adult T-cell leukemia/lymphoma (ATL), which usually shows the same phenotype as CTCL, i.e., a helper/inducer T-cell phenotype (CD4+CD8-), and usually involves the skin. Clinically, both CTCL and ATL are heterogeneous in nature. In this study, we demonstrated differences between CTCL and ATL in terms of clinical and immunopathologic cell surface features. In patients with ATL, the predominant clinical findings were peripheral lymph node involvement, skin lesions, hepatosplenomegaly, leukemic manifestations, and an aggressive course. In patients with CTCL, by contrast, only skin lesions predominated at the onset of the disease and a relatively good prognosis was demonstrated. Phenotypic heterogeneity of ATL in the skin, i.e., CD4-CD8-, CD4+CD8-, and CD4-CD8+, was demonstrated. Expression of Leu8, CD7 (Leu9), and CD45RA (2H4) was high in both the skin-infiltrating ATL cells and peripheral blood and lymph node ATL cells compared with that in the skin-infiltrating CTCL cells. Expression of CD25 (IL-2R), CD71 (OKT9), HLA-DR, and HLA-DQ was higher in the skin-infiltrating ATL cells than in CTCL cells. Expression of CD29 (4B4) was high, and that of CD45RA (2H4) was low in both the skin-infiltrating ATL and CTCL cells compared with the peripheral blood and lymph node ATL cells. Expression of CD45RO (UCHL-1) was not significantly high in the skin-infiltrating CTCL cells compared with that in ATL cells. The most significant phenotypic difference between ATL cells and CTCL cells was the expression of Leu8 (lymph node homing receptor), CD7 and CD25 antigens on the cell surface, and the main phenotypic difference between skin-infiltrating ATL and CTCL cells and peripheral blood and lymph node ATL cells was the expression of CD29 and CD45RA. These findings confirm that the difference in antigen expression on the cell surface might reflect the clinical features of ATL and CTCL, and suggest that the predominant phenotype of peripheral blood and lymph node ATL cells is that of naive, relatively immature or activated T-cells, and that CTCL cells are previously activated (memory) T-cells. In other words, CTCL cells do not share the same origin as ATL cells. These observations support the concept that ATL is a disease distinct from CTCL.