Hematoma and distraction arthroplasty for thumb basal joint osteoarthritis: a prospective,single-surgeon study including outcomes measures

PURPOSE: Many surgeons have abandoned the simple trapeziectomy as a surgical treatment option for thumb basal joint arthritis secondary to reports of postoperative weakness. The thumb metacarpal subsiding into the trapezial void has been proposed as the causative factor. The goal of the present study was to evaluate the results of trapeziectomy and postoperative K-wire immobilization of the thumb metacarpal in a distracted position without the use of ligament reconstruction or tendon interposition. METHODS: Twenty-six thumbs in 26 patients from a single surgeon's practice were entered into a prospective single-arm study for surgical treatment of peritrapezial arthritis. Treatment consisted of piecemeal excision of the entire trapezium and 5 weeks of K-wire immobilization of the first metacarpal in slight distraction and opposition. No ligament reconstruction or tendon interposition was used. Motion, strength, stress radiographs, standardized dexterity tests, and outcomes questionnaires including the Arthritis Impact Measurement Scales 2 (AIMS2) were evaluated before surgery and 6 and 24 months after surgery. RESULTS: At 6 months 19 of 26 patients (73%) reported complete relief of pain and at 24 months 92% were entirely pain free. Range of motion evaluation showed 24 of 26 thumbs adducted fully into the plane of the palm and 25 of 26 opposed to the fifth metacarpal head. Comparisons between preoperative and 24-month postoperative strength measurements showed an average 47% increase in grip strength, 33% increase in key pinch strength, and a 23% increase in tip pinch strength over preoperative values. AIMS2 data showed postoperative improvement in "hand and finger function" and "arthritis pain" scales. CONCLUSIONS: After trapezial excision K-wire immobilization in a slightly overcorrected position without tissue interposition or ligament reconstruction restores a stable, pain-free thumb that has superior strength and motion compared with published reports of the more complicated interventions.     

Dysfunctional LAD-1 neutrophils and colitis

Leukocyte adhesion deficiency 1 (LAD-1) is characterized by absent or dysfunctional beta2 integrin (CD18), leading to defective chemotaxis, adherence, phagocytosis, and bacterial killing. Colitis, except for rare intestinal necrotizing events, is not a well-recognized feature of this immunodeficiency. A case of nonspecific colitis clinically resembling Crohn's disease in a patient with the severe form of LAD-1 (0.5% < CD18) has been previously reported. We describe an adult patient with the moderate form of LAD-1 and chronic colitis characterized by extensive inflammation and ulceration of the right colon and terminal ileum, leading to adhesions and strictures. The chronic colitis described in this article associated with the dysfunctional neutrophils of LAD-1 represents a distinct pathology from the commonly encountered forms of inflammatory bowel disease (IBD). The existence of active IBD in the presence of dysfunctional CD18/CD11(a-b) intercellular adhesion molecules (ICAM-1) interaction is relevant to the proposed targeting of ICAM-1 for the treatment of Crohn's disease.     

Ultrasound examination of ankle injuries in children

Fourteen children with ankle injuries, an open tibia and fibula physis, and negative radiographs had ultrasonography of their injured ankles. Five had an anterior talofibular ligament injury and five had an anterior tibiofibular ligament injury. Four had normal ultrasound examinations. Only two had a physeal injury, both of which were associated with a ligament injury. Eleven children had only lateral ankle tenderness. Ultrasound of these 11 revealed ligamentous injuries, normal examinations, and the two physeal injuries. Ligamentous injury was not associated with other tenderness patterns.     

Mechanism of endotracheal tube movement with change of head position in the neonate

The mechanism of alteration of endotracheal tube position with movement of the head and neck in the neonate was studied in a term newborn cadaver. The infant was intubated and serial radiographs were obtained with the head and neck in different positions. We propose that the skull acts as a lever arm from the anterior end of the maxilla to the first cervical vertebra. The fulcrum for movement of this lever arm is the upper cervical spine. Movement of the endotracheal tube in the trachea is directed by the maxillocervical lever arm when the skull and upper cervical spine are flexed, extended, or rotated.     

Rapid detection of neonatal intracranial hemorrhage by transillumination

Using transillumination and a sensitive cadmium sulfide light meter, 145 newborns were screened for the presence of intracranial hemorrhage. Intracranial hemorrhage (ICH) was suspected when the light meter could not detect any light passing through the anterior fontanel when the light beam was directed through the frontal eminence. ICH was confirmed by branial computed tomography or postmortem examination in all 17 infants not transmitting light. Spectrophotometry was performed on samples of cerebrospinal fluid (CSF) to demonstrate the mechanism through which blood in the CSF blocks light transmission.     

Failure of serial chest radiographs to predict recovery from respiratory distress syndrome.

Chest radiographs of 29 patients with the clinical and radiographic diagnosis of RDS during the 5 days of the illness were graded according to a modification of the classification of Bomsel. There was no significant difference between the radiographs of surviving neonates and those who died of RDS. Mean L/S ratios were also collected from 26 of the 29 patients. Those who survived had significantly more mean L/S ratios greater than 2.5 than did the nonsurvivors (p less than 0.01). This difference did not correlate with the staging of the chest radiographs. The mean L/S ratio is a better predictor of survival than chest radiographs during the first 5 days of RDS.     

Biosynthesis of O-glycans in leukocytes from normal donors and from patients with leukemia: increase in O-glycan core 2 UDP-GlcNAc:Gal beta 3 GalNAc alpha-R (GlcNAc to GalNAc) beta(1-6)-N-acetylglucosaminyltransferase in leukemic cells

We have studied the biosynthesis of altered O-glycan structures on leukocytes from patients with chronic myelogenous leukemia and with acute myeloblastic leukemia (AML). It has been shown previously that the activity of CMP-NeuAc:Gal beta 1-3GalNAc alpha-R (sialic acid to galactose) alpha(2-3)-sialytransferase (EC 2.4.99.4) is increased in leukocytes from patients with chronic myelogenous leukemia (M. A. Baker, A. Kanani, I. Brockhausen, H. Schachter, A. Hindenburg, and R. N. Taub, Cancer Res., 47: 2763-2766, 1987) and with AML (A. Kanani, D. R. Sutherland, E. Fibach, K. L. Matta, A. Hindenburg, I. Brockhausen, W. Kuhns, R. N. Taub, D. van den Eijnden and M. A. Baker, Cancer Res., 50: 5003-5007, 1990). This increased activity may in part be responsible for the hypersialylation observed in leukemic leukocytes; however, hypersialylation may also be due to changes in underlying O-glycan structures. To test this hypothesis, we have assayed in normal human granulocytes and leukemic leukocytes several glycosyltransferases involved in the synthesis and elongation of the four common O-glycan cores. UDP-GlcNAc:Gal beta 1-3GalNAc-R (GlcNAc to GalNAc) beta(1-6)-GlcNAc transferase (EC 2.4.1.102), which synthesizes O-glycan core 2 (GlcNAc beta 1-6[Gal beta 1-3]GalNAc alpha), is significantly elevated in chronic myelogenous leukemia (4-fold) and AML (18-fold) leukocytes relative to normal human granulocytes. Neither normal nor leukemic cells show detectable activities of GlcNAc transferases which synthesize O-glycan core 3 (GlcNAc beta 1-3GalNAc-R) and core 4 (GlcNAc beta 1-6[GlcNAc beta 1-3] GalNAc-R) or the blood group I structure. The beta 3-GlcNAc transferase which elongates core 1 and core 2 was found at low levels in normal granulocytes but was not detectable in leukemic cells. The beta 3-GlcNAc transferase and beta 4-Gal transferase involved in poly-N-acetyllactosamine synthesis, as well as the beta 3-Gal transferase synthesizing core 1 (Gal beta 3 GalNAc), were present in all samples but were significantly increased in patients with AML. The observed changes are consistent with hypersialylation in leukemia.     

Human leukemic myeloblasts and myeloblastoid cells contain the enzyme cytidine 5'-monophosphate-N-acetylneuraminic acid:Gal beta 1-3GalNAc alpha (2-3)-sialyltransferase

We have examined the role of CMP-NeuAc:Gal beta 1-3GalNAc-R alpha(2-3)-sialyltransferase in fresh leukemia cells and leukemia-derived cell lines. Enzyme activity in normal granulocytes using Gal beta 1-3GalNAc alpha-o-nitrophenyl as substrate was 1.5 +/- 0.7 nmol/mg/h whereas activity in morphologically mature granulocytes from 6 patients with chronic myelogenous leukemia (CML) was 4.2 +/- 1.6 nmol/mg/h (P less than 0.05). Myeloblasts from 5 patients with CML in blast crisis showed enzyme activity levels of 6.5 +/- 2.5 nmol/mg/h. From 2 patients with CML, both blasts and granulocytes were obtained, with higher enzyme activity in the patients' blasts (7.1 nmol/mg/h) than in their granulocytes (4.9 nmol/mg/h) in both cases, suggesting that the increase in enzyme activity is related to the differentiation or proliferation status of the CML cells. However, similarly high enzyme levels were also seen in myeloblasts from acute myeloblastic leukemia patients (5.6 +/- 1.4 nmol/mg/h) and in some acute myeloblastic leukemia-derived cell lines (KG1a and HL60), suggesting that increased levels of this enzyme are not directly correlated with the presence of the Ph1 chromosome. This alpha(2-3)-sialyltransferase activity can also be detected in normal peripheral blood lymphocytes and exhibits increased activity in chronic lymphocytic leukemia cells and acute lymphoblastic leukemia. These data suggest that the level of enzyme activity may vary with growth rate and maturation status in myeloid and lymphoid hemopoietic cells. Finally, we have identified a glycoprotein in acute myeloblastic leukemia cells that serves as a substrate for the alpha(2-3)-sialyltransferase. The desialylated form of the glycoprotein was resialylated in vitro by the purified placental form of this alpha(2-3)-sialyltransferase and exhibits a molecular weight of about 150,000.