PubMed · 8634052
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F A Frizelle, M P Dunkely, A Cuschieri. 1996. Port attachment without capacitive coupling.. https://doi.org/10.1111/j.1445-2197.1996.tb01195.x
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The pathogenesis and pathophysiologic features of electrical injury are more complex than once thought. The relative contributions of thermal and pure electrical damage depend on the duration of electric current passage, the orientation of the cells in the current path, their location, and other factors. If the contact time is brief, nonthermal mechanisms of cell damage will be most important and the damage is relatively restricted to the cell membrane. When contact time is much longer, however, heat damage predominates and the whole cell is affected directly. These parameters also determine the anatomic tissue distribution of injury. Damage by Joule heating is not known to be dependent on cell size, whereas larger cells are more vulnerable to membrane breakdown by electroporation. Cells do survive transient plasma membrane rupture under appropriate circumstances or if therapy is instituted quickly. If membrane permeabilization is the primary cellular pathologic condition, then injured tissue may be salvageable and the challenge for the future is to identify a technique to reseal the damaged membranes promptly. Present standards of care for electrical injury require a fully staffed and well-equipped intensive care unit, available operating suites, and the availability of the full range of medical specialists. Major teaching hospitals with burn centers may be the ideal setting for the treatment of an electrical trauma victim. After the initial resuscitation, efforts are directed primarily towards preventing additional tissue loss mediated through the compartment syndrome, compressive neuropathies, or the presence of necrotic tissue. Renal and cardiac failure caused by the release of intracellular muscle contents into the circulation must be prevented. Attention can then be directed towards maximizing tissue salvage and preventing late skeletal and neuromuscular complications. Reconstructive procedures that transfer healthy tissue from a distance are necessary to optimize the functional value of the remaining tissue. Finally, unless the patient is rehabilitated psychologically, the real benefit from other sophisticated care will not be fully realized. These goals are important throughout the acute care of the patient. In the future, new guidelines for treating electrical trauma will be based on a clearer understanding of the relevant pathophysiologic features. These strategies will rely on improved diagnostic imaging and on reversing the fundamental problem of cell membrane damage. Moreover, complex biochemical and organ system pathophysiologic interactions will require careful management. If successful, research efforts presently underway should improve the prognosis of victims after electrical trauma.
A free flap used for face and neck reconstruction usually results in tissue bulking and needs several debulking procedures to match the contour of the face and neck. In this paper we report an experience with a patient who underwent tissue expansion of a transplanted musculocutaneous free flap in the face for debulking of the flap and four further aesthetic reconstructions of the face and neck. The result shows that a transplanted free flap tolerates tissue expansion well. The versatile use of tissue expansion shows obvious advantages in that the transplanted flap is not only enlarged substantially by means of tissue expansion, but it is also debulked at the same time of achieve a desired thin flap for further reconstruction of the face and neck.
A patient with a dual chamber pacemaker received two transthoracic (anterior-anterior paddle position) shocks for VF. Subsequent analysis of stimulation thresholds revealed a marked rise in the ventricular threshold only. Later, she received three additional shocks (anterior-posterior paddle position) during electrophysiological study to terminate episodes of induced VT. Following these, the ventricular stimulation threshold was > 10 V at 2.0 ms. The selective damage at the ventricular site in this patient led us to carry out in vitro studies that revealed a preferential shunting of high electrical energy into the ventricular lead, as compared to the atrial lead, following a DC shock. These observations may explain the selective pacing malfunction observed in out patient.