Cryopreserved cadaveric allografts for treatment of unexcised partial thickness flame burns: clinical experience with 12 patients

Partial thickness burns (PTB) usually heal within 3 weeks. Prevention of infection and desiccation of the wounds are crucial for optimal healing. Early tangential excision of the burn eschar and allografting prevent deepening of the burns, and are therefore advocated for treatment with the best functional and aesthetic results. For superficial partial thickness burns (SPTB) conservative use of topical antimicrobial agents with frequent dressing changes are implemented. We compared the conservarive treatment for PTBs and SPTBs to grafting cryopreserved cadaveric allografts with no prior excision.

Twelve patients with flame PTB areas were allografted after mechanical debridement without excision of the burn wounds. The allografts were cadaveric skin cryopreserved by programmed freezing and stored at −180°C for 30–48 months. Matching burns for depth and area were treated with silver sulfadiazine (SSD) one to two times daily until healing or debridement and grafting were required.

It was found that 80 per cent of the cryopreserved allografts adhered well and 76 per cent of the treated areas healed within 21 days, whereas only 40 per cent of the SSD-treated burns healed within 21 days.

Partial thickness burns can be treated successfully with viable human allografts (cryopreserved cadaveric skin) with no prior surgical excision. The burn wounds heal well within 3 weeks. For deep partial thickness burns (DPTB) treatment with allografts has no advantage if they have not been previously excised.     

Quadrivalvular rheumatic heart disease

Three cases of chronic rheumatic heart disease with involvement of all four valves are presented. The involvement of tricuspid and pulmonary valves was suspected clinically and was confirmed by two-dimensional echo, Doppler, hemodynamic and angiographic findings. These findings were also verified surgically and histopathologically in 2 cases. One of the cases died after cardiac catheterization; the other 2 cases were treated surgically with success.     

Should the patella be resurfaced in total knee arthroplasty? Efficacy of patellar resurfacing

To assess the long-term efficacy of patellar resurfacing, 100 knees were evaluated in 84 patients. The operations were performed between 1978 and 1982. The follow-up period ranged from 60 to 103 months. The diagnosis was degenerative joint disease (DJD) in 83%, rheumatoid arthritis in 12%, and miscellaneous in 5% of the knees. The implant (47 knees) and nonimplant (53 knees) groups were comparable with respect to age, body size, and length of follow-up period. The analysis revealed equivocal results. Considering all diagnostic categories combined, rest pain was marginally better in the resurfaced group (p = 0.04), but this difference resulted from an unequal distribution of subjects between mild and zero pain categories. Pain with walking, maximum walking distance, ability to climb stairs and rise from a chair, active arc of motion, extensor lag, and quadriceps strength were similar in the two groups. When the DJD group was considered separately, no significant difference emerged. There was little evidence to support a recommendation for routine patellar resurfacing in total knee arthroplasty.     

Chronic recurrent multifocal osteomyelitis and psoriasis—A report of a new association and review of related disorders

In summary, we have described two patients with CRMO and psoriasis, and have reviewed the musculoskeletal manifestations associated with pustular eruptions of the palms and soles. In view of the frequent occurrence of PPP in patients with CRMO, we suggest that the occurrence of psoriasis in our two patients is more than coincidence, and that noninfectious, inflammatory lesions of bone may be another musculoskeletal manifestation of psoriasis. This rare association, as well as the association of PPP with disorders associated with new bone formation, may shed new insights on the relatively common finding of periosteal elevation associated with psoriatic arthritis and the occasional severe juxta-articular osteolytic destructive bone lesions seen in psoriatic arthritis.     

Activity-induced weakness in recessive myotonia congenita with a novel (696+1G>A) mutation.

OBJECTIVE: To investigate the cause of the transient weakness that occurs in recessive myotonia congenita (RMC) following sustained muscle contraction. METHODS: Nerve excitability studies were performed on a 35-year-old male with RMC due to a novel 696+1G>A CLCN1 mutation. The median nerve was stimulated at the wrist and compound muscle action potentials (CMAPs) were recorded from abductor pollicis brevis (APB). Stimulus-response behaviour using two stimulus durations, threshold electrotonus to 100-ms polarizing currents, a current threshold relationship and the recovery of excitability following supramaximal stimulation were recorded at rest. Excitability parameters were also recorded before and after maximal voluntary contraction (MVC) of APB against resistance for 60s. Results were compared to data obtained from 12 normal controls. RESULTS: Baseline axonal excitability parameters were all normal, indicating that axonal function was normal at the point of stimulation. Following one minute of MVC, excitability parameters demonstrated a significant increase in threshold when compared to controls (RMC 54.9%; controls 15.5+/-3.1%). In the RMC patient, this increase in threshold was associated with a 39% reduction in the amplitude of the maximal CMAP, which remained unaffected in controls. CONCLUSIONS: The reduction in maximal CMAP is likely to represent muscle activation failure due to depolarization block, with the increase in threshold possibly reflecting a compensatory attempt by motor axons to overcome prolonged contraction-induced changes in the muscle membrane. SIGNIFICANCE: The prolonged recovery of excitability following sustained muscle contraction is likely to be a contributing factor to symptoms of weakness and fatigue experienced by RMC patients.     

The mechanism of IL-2-mediated protection against GVHD in mice. II. Protection occurs independently of NK/LAK cells.

We have recently demonstrated that high-dose IL-2, when begun on the day of bone marrow transplantation, has a potent protective effect against graft-vs.-host disease mortality, especially when coadministered with T cell-depleted syngeneic bone marrow cells. Because several groups of investigators have demonstrated that lymphokine-activated killer cells can mediate GVHD protection, we hypothesized that the mechanism of protection by IL-2 administration might involve the in vivo activation of natural killer and/or LAK cells. In order to test this hypothesis, we evaluated the effect of IL-2 administration on the number of NK1+ cells and on NK-mediated cytotoxic activity in recipients of GVHD-producing inocula. Furthermore, we evaluated the effects on IL-2-induced GVHD protection of depleting NK cells and LAK precursor cells in vivo with mAb against NK1.1 or antiserum against asialo GM1. The results demonstrate that: (1) The number of NK1+ cells is not increased in spleens of IL-2-treated compared with control recipients of GVHD-producing inocula; (2) NK activity is not increased in IL-2-treated compared with control recipients of GVHD-producing inocula during or immediately following the period of IL-2 administration; (3) depletion of NK cells and LAK precursors from the donor and host influenced the time course of GVHD-related mortality in a complex fashion; and (4) IL-2-induced GVHD protection is largely independent of the activity of an NK or LAK cell population of donor or host origin. IL-2-induced GVHD protection therefore reflects primarily the activity of non-LAK protective cell populations, or it may be a direct inhibitory effect on responding donor cell populations as they encounter host antigen.     

Right ventricular-pulmonary arterial interactions

The application of pulsatile models to hemodynamic data has made possible a more complete understanding of the relationship of pulmonary pressure and flow. To review the genesis of these concepts, the unique characteristics of the pulmonary artery and right ventricle are outlined as a basis for understanding why differences in their pulsatile properties from the systemic circuit must exist. The pulmonary impedance spectrum is introduced and the concept of optimal right ventricular-pulmonary artery coupling is explored based on a review of extensive experimental data. Finally, available studies of normal pulmonary impedance in man and abnormal impedance in human disease states are reviewed, with emphasis on disturbances in optimal ventricular-vascular coupling. The important implications of these concepts for understanding and treatment of cardiovascular disease are developed.     

Immunocytochemical demonstration of neural cell adhesion molecule (NCAM) along the migration route of luteinizing hormone-releasing hormone (LHRH) neurons in mice.

Contact between the developing forebrain and the ingrowing central processes of the olfactory, vomeronasal and terminal nerves is preceded by a migration of neural cell adhesion molecule (NCAM)-immunoreactive cells from the epithelium of the olfactory pit and the formation of an NCAM-immunoreactive cellular aggregate in the mesenchyme between the olfactory pit and the forebrain. The axons of the olfactory, vomeronasal, and terminal nerves, also NCAM-immunoreactive, grow into the cellular aggregate, which as development proceeds, becomes continuous with the rostral tip of the forebrain. The lateral and more rostral part of the cellular aggregate receives the ingrowing axons of the olfactory nerves and becomes the olfactory nerve layer of the olfactory bulb. The medial, more caudal part receives the central processes of the vomeronasal and terminal nerves. The vomeronasal nerve ends in the accessory olfactory bulb. The central processes of the terminal nerve end in the medial forebrain. Luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons, like the vomeronasal and terminal nerves, originate from the medial part of the olfactory pit. These LHRH cells migrate into the brain along and within a scaffolding formed by the NCAM-immunoreactive axons of the vomeronasal and terminal nerves, and they are never seen independent of this NCAM scaffold as they cross the nasal lamina propria. The results suggest that: (1) NCAM is likely to be necessary for scaffold formation, and (2) the scaffold may be essential for the subsequent migration of LHRH neurons into the brain. Because they aggregate, migrating LHRH-immunoreactive neurons, on which we did not detect NCAM immunoreactivity, may interact via other cell adhesion molecules (CAM). Inasmuch as the interaction between the LHRH-immunoreactive neurons and the NCAM-immunoreactive scaffold is heterotypic, the possibility of a heterophilic (NCAM to other CAM) interaction is not ruled out. These findings focus our attention on the functional role of NCAM in this migratory system.