Transfusions in burn patients with/without comorbidities.

Medical comorbidities such as renal, cardiac, and cerebrovascular disease are known risk factors for mortality in burn patients. Patients with large burns often require blood transfusions during excision and skin grafting. The purpose of this study was to determine if there was a difference in the transfusion requirements of burn patients with/without comorbidities. This was a retrospective review of burn patient data between March 1999 and May 2004. There were 1,615 admissions to the burn unit; comorbidity data was available on 1,490 patients. Of these, 383/1,490 (26%) had comorbid conditions upon admission: 85/383 (22%) were transfused; 52/85 (61%) also underwent skin grafting. Most patients (298/383) with comorbidities were not transfused; however, 108/298 (36%) were grafted. Transfused patients with comorbidities had a mean +/- SD age of 53 +/- 18 years old, a 19% +/- 22% TBSA burn, and a length of stay of 29 +/- 26 days compared with patients with comorbidities who did not require transfusion and were 48 +/- 19 years old, had 8 +/- 13% TBSA, and a length of stay of 8 +/- 8 days. Of patients with comorbidities, 31/54 (57%) were transfused in the <10% TBSA group and 26/44 (59%) in the 10 to 19% TBSA group. There was a 5-fold increase in mortality among the transfused patients with comorbidities compared with the nontransfused group. Patients with comorbidities were more likely to be transfused in the <20% TBSA patient group. The odds of receiving a transfusion were highest in patients with cardiac diseases, stroke, and other central nervous system and psychiatric disorders. Co-occurring conditions that increased the odds of receiving a transfusion were procedures and inhalation with burn injury.

Use of blood bank services in a burn unit.

Burn patients may need transfusions, especially during surgery. The purpose of the study was to determine blood bank services utilization at an urban burn center. This was a retrospective review (March 1999 to May 2004) of burn patient data on blood utilization. There were 1615 admissions; 800 (49.5%) of the patients had a type and screen (T and S); 180 of 1615 (11%) were transfused with 1691 red blood cell (RBC) units; 616 units of fresh- frozen plasma (FFP), 399 units of pooled platelets, and 38 units of apheresis platelets. Of the 180 transfused patients, 140 (79%) received RBCs, 11 (6%) received RBCs plus FFP, 23 (13%) received RBCs plus FFP plus platelets, and 3 (2%) each received RBCs plus platelets and FFP. Overall, 3393 red cell units were cross-matched, and 1691 units were transfused for a cross-match/transfused unit (C/T) ratio of 2.01. Seventy-three (5.7%) of 1282 of patients with 0% to 10% TBSA required transfusions; 42 (21%) of 193 with 11% to 20% TBSA; 24 (39%) of 61 with 21% to 30% TBSA; and 62% of patients with 31% or greater TBSA required transfusion (P = .001). As %TBSA increased, more of the cross-matched units were transfused: 37% in the 0% to 10% TBSA to 59% in the 30% or greater TBSA burn. The C/T ratio in the 0% to 10% TBSA was 2.69; only 18% of patients with a T&S received blood. Although most patients who underwent transfusion were in the less than 30% TBSA group, more of the red cell units were used in patients with a 30% or greater TBSA burn. Elimination of admission T&S and cross matches in burn patients with less than 20% TBSA may improve the C/T ratio in this cohort.

Molecular basis of two novel high-prevalence antigens in the Kell blood group system, KALT and KTIM.

BACKGROUND: The Kell blood group system consists of 25 antigens that result from single-nucleotide polymorphisms. Most polymorphic Kell antigens reside on the N-terminal domain of Kell before the zinc-binding catalytic motif, which is the major site for endothelin-3-converting enzyme activity. Kell antigens are important in transfusion medicine owing to their strong immunogenicity, and the corresponding antibodies are clinically significant. Two probands were studied whose serum samples contained antibodies to different high-prevalence Kell antigens. STUDY DESIGN AND METHODS: Standard hemagglutination methods were used for serologic testing of Proband 1 and Proband 2. DNA was prepared from both probands and family members. The 19 exons and the intron-exon regions of KEL from both probands were amplified by polymerase chain reaction, and the sequences were compared with that of common KEL. The identified substitutions were located on a three-dimensional model of Kell generated based on the crystal structure of neutral endopeptidase, a homolog of Kell. RESULTS: In Proband 1, a homozygous 1988G>A mutation (Arg623Lys) in Exon 17 was present. One sibling of Proband 1 was homozygous for 1988G>A. In Proband 2, a homozygous 1033G>A mutation (Asp305Asn) in Exon 8 was present. Three siblings of Proband 2 were heterozygous for 1033G>A. CONCLUSION: The identified KEL mutations of the two probands are novel and inherited. The antigen absent from the red blood cells (RBCs) of Probands 1 and 2 are named KALT and KTIM, respectively. KALT is unique in that it is the only Kell antigen sensitive to treatment of RBCs by trypsin.

Thrombotic microangiopathy syndrome as an AIDS-defining illness: the experience of J. Stroger Hospital of Cook County.

Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are severe life-threatening disseminated thrombotic microangiopathies (TMA). Although many cases are idiopathic, TMA can occur in association with pregnancy, malignancy, autoimmune diseases, and HIV infection. We retrospectively analyzed the cases of 17 patients with TMA coexistent with HIV infection admitted to our institution. Median T-cell count at presentation was 28 cells/mm3 Patients presented with severe thrombocytopenia (median platelet count 19 x 10(9)/L) and high lactate dehydrogenase levels (median 1,057 U/L). The majority of patients (82%) presented with renal dysfunction. Forty-one percent of patients had fever and 29% had neurological signs at presentation, which were associated with inferior outcome. Despite plasma exchange, inpatient mortality for the first TMA episode was 47%. Some patients relapsed following an initial TMA episode. However, there were responders with remissions lasting 5 years. We conclude that TMA, coexistent with an HIV-associated low CD4 count, is a treatable condition. Considering TMA as an AIDS-defining illness may help clinicians recognize this syndrome earlier, leading to prompter treatment and improved survival rates.