Partial liquid ventilation improves lung function in ventilation-induced lung injury.

Disturbances in lung function and lung mechanics are present after ventilation with high peak inspiratory pressures (PIP) and low levels of positive end-expiratory pressure (PEEP). Therefore, the authors investigated whether partial liquid ventilation can re-establish lung function after ventilation-induced lung injury. Adult rats were exposed to high PIP without PEEP for 20 min. Thereafter, the animals were randomly divided into five groups. The first group was killed immediately after randomization and used as an untreated control. The second group received only sham treatment and ventilation, and three groups received treatment with perfluorocarbon (10 mL x kg(-1), 20 mL x kg(-1), and 20 ml x kg(-1) plus an additional 5 mL x kg(-1) after 1 h). The four groups were maintained on mechanical ventilation for a further 2-h observation period. Blood gases, lung mechanics, total protein concentration, minimal surface tension, and small/large surfactant aggregates ratio were determined. The results show that in ventilation-induced lung injury, partial liquid ventilation with different amounts of perflubron improves gas exchange and pulmonary function, when compared to a group of animals treated with standard respiratory care. These effects have been observed despite the presence of a high intra-alveolar protein concentration, especially in those groups treated with 10 and 20 mL of perflubron. The data suggest that replacement of perfluorocarbon, lost over time, is crucial to maintain the constant effects of partial liquid ventilation.

Treatment of ventilation-induced lung injury with exogenous surfactant.

OBJECTIVE: It has been demonstrated that pulmonary surfactant plays a role in the pathophysiology of ventilation-induced lung injury (VILI). Therefore, we investigated whether exogenous surfactant might restore lung function and lung mechanics in an established model of VILI. DESIGN: Prospective, randomized, animal study. SETTING: Experimental laboratory of a university. SUBJECTS: Twenty-four adult male Sprague-Dawley rats. INTERVENTIONS: First, a group of six animals were killed immediately after induction of anesthesia and used as healthy controls. Then, in 18 rats, VILI was induced by increasing peak inspiratory pressure (PIP) to 45 cmH2O without positive end-expiratory pressure (PEEP) for 20 min. Thereafter, animals were randomly divided into three groups of six animals each: one group was killed immediately after VILI and served as VILI-control. In the other two groups, ventilator settings were changed to a PIP of 30 cmH2O and a PEEP of 10 cmH2O, and a respiratory rate of 40 bpm. One group received a bolus of surfactant and the other group received no treatment. MEASUREMENTS AND RESULTS: Blood gas tension and arterial blood pressures were recorded every 30 min for 2 h. After the study period, a pressure-volume curve was recorded. Then, a broncho-alveolar lavage (BAL) was performed to determine protein content, minimal surface tension, and surfactant composition in the BAL fluid. Oxygenation, lung mechanics, surfactant function and composition were significantly improved in the surfactant-treated group compared to the ventilated and non-ventilated control groups. CONCLUSION: We conclude that exogenous surfactant can be used to treat VILI.

Treatment and prevention of acute respiratory failure: physiological basis.

Acute respiratory failure is caused by many factors and remains one of the most common reasons for admission to the intensive care unit (ICU). In all cases of acute respiratory failure, there is a shortage of surfactant at the alveolar level. This deficit of surfactant leads to an increase in alveolar surface tension that increases the retraction forces of the lung, leading to end-expiratory alveolar collapse, finally resulting in respiratory dysfunction, which includes hypoxemia, low lung compliance, increase of intrapulmonary shunts, low functional residual capacity, atelectasis, and pulmonary edema. The goal of the treatment and prevention of acute respiratory failure is therefore based on the following three main items: re-opening the collapsed alveolar units; preserving the active surfactant component in the remaining functional alveolar units, and preventing end-expiratory collapse. The following strategies can be used to prevent and/or treat acute respiratory failure: counterbalancing the retraction forces of the lung by applying sufficiently high external pressures; and/or decreasing the surface tension at the air-liquid interface by means of exogenous surfactant, and/or eliminating the air-liquid interface by filling the lung with perfluorocarbons. By applying these therapeutic strategies in routine clinical practice, we should achieve a reduction in the mortality rate of patients suffering from acute respiratory failure.

Fenomeno de Raynaud / Raynauds phenomenon

Raynauds phenomenos is a common paroxysmal vasomotor disorder. It must be distinguised between those with a functional character- primary phenomenon or Raynauds disease and secondary Raynauds phenomenon or syndrome. In our study the highest incidence (81 por ciento) corresponds to patients with secondary Raynauds syndrome; 58 por ciento of these patients showed capillary microscopy alterations and 64 por ciento were ANA test positive, showing those numbers their sensibility and specificity since primary Raynaud´s and healthy control patients did not show these figures. The clear prevalencxe of specific capillary microscopy alterations in secondary Raynauds patients schow that this technique is very useful in the differential diagnosis between primary and secondary Raynauds phenomenon. Serial capillaroscopy studies must then be performed to diagnose connective tissue diseases. Nailfold capillary microscopy is a very usefuld and easy complementary technique; it offers great help and also is of prognostic value in patient with Raynauds phenomenon or connwctive tissue diseases, together with the clinical and laboratory studies contributes for the early diagnosis of these disorders(AU)

Fenomeno de Raynaud / Raynaud's phenomenon

Raynaud's phenomenos is a common paroxysmal vasomotor disorder. It must be distinguised between those with a functional character- primary phenomenon or Raynaud's disease and secondary Raynaud's phenomenon or syndrome. In our study the highest incidence (81 por ciento) corresponds to patients with secondary Raynaud's syndrome; 58 por ciento of these patients showed capillary microscopy alterations and 64 por ciento were ANA test positive, showing those numbers their sensibility and specificity since primary Raynaudïs and healthy control patients did not show these figures. The clear prevalencxe of specific capillary microscopy alterations in secondary Raynaud's patients schow that this technique is very useful in the differential diagnosis between primary and secondary Raynaud's phenomenon. Serial capillaroscopy studies must then be performed to diagnose connective tissue diseases. Nailfold capillary microscopy is a very usefuld and easy complementary technique; it offers great help and also is of prognostic value in patient with Raynaud's phenomenon or connwctive tissue diseases, together with the clinical and laboratory studies contributes for the early diagnosis of these disorders

Mechanical ventilation with high positive end-expiratory pressure and small driving pressure amplitude is as effective as high-frequency oscillatory ventilation to preserve the function of exogenous surfactant in lung-lavaged rats.

OBJECTIVE: To demonstrate that under well-defined conditions, pressure-controlled ventilators (PCV) allow settings that are as good as high-frequency oscillatory ventilators (HFOV) at preserving the function of exogenous surfactant in lung-lavaged rats. DESIGN: Experimental, comparative study. SETTING: Research laboratory of a large university. SUBJECTS: Sixteen adult male Sprague-Dawley rats (280-310 g). INTERVENTIONS: Lung injury was induced by repeated lavage. After last lavage, all animals received exogenous surfactant and were then randomly assigned to two groups (n = 8 per group). The first group received PCV with small pressure amplitudes and high positive end-expiratory pressure. The second group received HFOV. In both groups, an opening maneuver was performed by increasing airway pressure to improve PaO2/F(IO2) to > or =500 torr. MEASUREMENTS AND MAIN RESULTS: Blood gases were measured every 30 mins for 3 hrs. Airway pressures were measured with a tip catheter pressure transducer. At the end of the study period, a pressure-volume curve was recorded and a broncho-alveolar lavage was performed to determine protein content and surfactant composition. The results showed that arterial oxygenation in both groups could be kept >500 torr during the 3-hr study period by using a mean airway pressure of 13+/-3 cm H2O in PCV and 13+/-2 cm H2O in HFOV. Further, there were no differences in the Gruenwald index, protein influx, or ratio of small to large aggregates between the study groups. CONCLUSION: PCV with sufficient level of positive end-expiratory pressure and small driving pressure amplitudes is as effective as HFOV to maintain optimal gas exchange, to improve lung mechanics, and to prevent protein influx and conversion of large into small aggregates after exogenous surfactant therapy in lung-lavaged rats.

At surfactant deficiency, application of "the open lung concept" prevents protein leakage and attenuates changes in lung mechanics.

OBJECTIVE: To evaluate whether mechanical ventilation using "the open lung concept" during surfactant depletion can attenuate the deterioration in pulmonary function. DESIGN: Experimental, comparative study. SETTING: Research laboratory of a large university. SUBJECTS: Eighteen adult male Sprague-Dawley rats, weighing 280-340 g. INTERVENTIONS: Twelve rats were anesthetized, mechanically ventilated with 100% oxygen, and randomly divided into two groups (n = 6 each). The open lung group underwent six saline lavages at different ventilator settings that prevented alveolar collapse. The settings (expressed as frequency/peak inspiratory pressure/positive end-expiratory pressure/inspiratory:expiratory ratio) were 30/26/6/1:2 during the first lavage, 100/27/10/1:1 during the next two lavages, and 100/33/15/1:1 during the last three lavages and during the remaining ventilation period. The ventilated control group underwent six saline lavages with settings at 30/26/6/1:2. After the lavages, peak inspiratory pressure and positive end-expiratory pressure were increased in this group by 2 cm H2O each for the remaining study period. An additional group of six animals were killed immediately after induction of anesthesia and served as healthy controls. Blood gases were measured before lavage, immediately after the last lavage, and thereafter hourly. At the end of the 4-hr study period, we constructed pressure-volume curves from which we determined total lung capacity at a distending pressure of 35 cm H2O (TLC35). Subsequently, total lung volume at a distending pressure of 5 cm H2O (V5) was determined, followed by bronchoalveolar lavage. RESULTS: In the ventilated control group, PaO2, V5, and TLC35 were significantly decreased and protein concentration of bronchoalveolar lavage was significantly increased compared with the healthy control group. In the open lung group, PaO2 did not decrease after the lavage procedure, and V5, TLC35, and the protein concentration of bronchoalveolar lavage were comparable with the healthy controls. CONCLUSION: We conclude that application of the open lung concept during surfactant depletion attenuates deterioration in pulmonary function.

Regional pressure volume curves by electrical impedance tomography in a model of acute lung injury.

OBJECTIVE: A new noninvasive method, electrical impedance tomography (EIT), was used to make pressure-impedance (PI) curves in a lung lavage model of acute lung injury in pigs. The lower inflection point (LIP) and the upper deflection point (UDP) were determined from these curves and from the traditional pressure-volume (PV) curves to determine whether the PI curves resemble the traditional PV curves. Furthermore, regional differences in the mentioned determinants were investigated. DESIGN: Prospective, experimental study. SETTING: Animal research laboratory. INTERVENTIONS: In nine anesthetized pigs, repeated lung lavage was performed until a Pao2 <80 torr was reached. Thereafter, an inspiratory PV curve was made using a constant flow of oxygen. During the intervention, EIT measurements were performed. MEASUREMENTS AND MAIN RESULTS: In this study, the LIP(EIT) was within 2 cm H2O of the LIP(PV). Furthermore, it was possible to visualize regional PI curves by EIT. No significant difference was found between the LIP(PV) (21.3+/-3.0 cm H2O) and the LIP(EIT) of the total lung (21.5+/-3.0 cm H2O) or the anterior parts of the lung (21.5+/-2.9 cm H2O). A significantly higher LIP (29.5+/-4.9 cm H2O) was found in the posterior parts of the lung. A UDP(PV) could be found in three animals only, whereas in all animals a UDP(EIT) could be determined from the anterior part of the lung. CONCLUSIONS: Using EIT, determination of LIP and UDP from the regional PI curves is possible. The obtained information from the regional PI curves may help in understanding alveolar recruitment. The use of this new bedside technique for clinical decision making remains to be examined.

Monitoring of recruitment and derecruitment by electrical impedance tomography in a model of acute lung injury.

OBJECTIVE: To evaluate a noninvasive system for obtaining information about alveolar recruitment and derecruitment in a model of acute lung injury. DESIGN: Prospective experimental study. SETTING: Animal research laboratory. SUBJECTS: Nine anesthetized pigs. INTERVENTIONS: Electrical impedance tomography measurements were performed. Electrical impedance tomography is an imaging technique that can register the ventilation-induced impedance changes in different parts of the lung. In nine anesthetized pigs, repeated lung lavages were performed until a PaO2 of <80 mm Hg was reached. Thereafter, the lungs were recruited according to two different recruitment protocols: the open lung approach and the open lung concept. Five time points for measurements were chosen: healthy (reference), lavage (atelectasis), recruitment, derecruitment, and maintain recruited (final). MEASUREMENTS AND MAIN RESULTS: After lavage, there was a significant increase in the impedance ratio, defined as the ventilation-induced impedance changes of the anterior part of the lung divided by that of the posterior part (from 1.75 +/- 0.63 to 4.51 +/- 2.22; p < .05). The impedance ratio decreased significantly after performing the recruitment protocol (from 4.51 +/- 2.22 to 1.18 +/- 0.51). During both recruitment procedures, a steep increase in baseline impedance change was seen. Furthermore, during derecruitment, a decrease in the slope in baseline impedance change was seen in the posterior part of the lung, whereas the anterior part showed no change. CONCLUSION: Electrical impedance tomography is a technique that can show impedance changes resembling recruitment and derecruitment of alveoli in the anterior and posterior parts of the lung. Therefore, electrical impedance tomography may help in determining the optimal mechanical ventilation in a patient with acute lung injury.

The open lung concept: pressure-controlled ventilation is as effective as high-frequency oscillatory ventilation in improving gas exchange and lung mechanics in surfactant-deficient animals.

OBJECTIVE: To demonstrate in experimental animals with respiratory insufficiency that under well-defined conditions, commercially available ventilators allow settings which are as effective as high-frequency oscillatory ventilators (HFOV), with respect to the levels of gas exchange, protein infiltration, and lung stability. DESIGN: Prospective, randomized, animal study. SETTING: Experimental laboratory of a university. SUBJECTS: 18 adult male Sprague-Dawley rats. INTERVENTIONS: Lung injury was induced by repeated whole-lung lavage. Thereafter, the animals were assigned to pressure-controlled ventilation (PCV) plus The Open Lung Concept (OLC) or HFOV plus OLC (HFO(OLC)). In both groups, an opening maneuver was performed by increasing airway pressures to improve the arterial oxygen tension/fractional inspired oxygen (PaO(2)/FIO(2)) ratio to L 500 mm Hg; thereafter, airway pressures were reduced to minimal values, which kept PaO(2)/FIO(2) L 500 mm Hg. Pressure amplitude was adjusted to keep CO(2) as close as possible in the normal range. MEASUREMENTS AND RESULTS: Airway pressure, blood gas tension, and arterial blood pressure were recorded every 30 min. At the end of the 3-h study period, a pressure-volume curve was recorded and bronchoalveolar lavage was performed to determine protein content. After the recruitment maneuver, the resulting mean airway pressure to keep a PaO(2)/FIO(2) L 500 mm Hg was 25 +/- 1.3 cm H(2)O during PCV(OLC) and 25 +/- 0.5 cm H(2)O during HFOV(OLC). Arterial oxygenation in both groups was above L 500 mm Hg and arterial carbon dioxide tension was kept close to the normal range. No differences in mean arterial pressure, lung mechanics and protein influx were found between the two groups. CONCLUSIONS: This study shows that in surfactant-deficient animals, PCV, in combination with a recruitment maneuver, opens atelectatic lung areas and keeps them open as effectively as HFOV.

'Alveolar recruitment strategy' improves arterial oxygenation during general anaesthesia.

Abnormalities in gas exchange during general anaesthesia are caused partly by atelectasis. Inspiratory pressures of approximately 40 cm H2O are required to fully re-expand healthy but collapsed alveoli. However, without PEEP these re-expanded alveoli tend to collapse again. We hypothesized that an initial increase in pressure would open collapsed alveoli; if this inspiratory recruitment is combined with sufficient end-expiratory pressure, alveoli will remain open during general anaesthesia. We tested the effect of an 'alveolar recruitment strategy' on arterial oxygenation and lung mechanics in a prospective, controlled study of 30 ASA II or III patients aged more than 60 yr allocated to one of three groups. Group ZEEP received no PEEP. The second group received an initial control period without PEEP, and then PEEP 5 cm H2O was applied. The third group received an increase in PEEP and tidal volumes until a PEEP of 15 cm H2O and a tidal volume of 18 ml kg-1 or a peak inspiratory pressure of 40 cm H2O was reached. PEEP 5 cm H2O was then maintained. There was a significant increase in median PaO2 values obtained at baseline (20.4 kPa) and those obtained after the recruitment manoeuvre (24.4 kPa) at 40 min. This latter value was also significantly higher than PaO2 measured in the PEEP (16.2 kPa) and ZEEP (18.7 kPa) groups. Application of PEEP also had a significant effect on oxygenation; no such intra-group difference was observed in the ZEEP group. No complications occurred. We conclude that during general anaesthesia, the alveolar recruitment strategy was an efficient way to improve arterial oxygenation.

Comparison of exogenous surfactant therapy, mechanical ventilation with high end-expiratory pressure and partial liquid ventilation in a model of acute lung injury.

We have compared three treatment strategies, that aim to prevent repetitive alveolar collapse, for their effect on gas exchange, lung mechanics, lung injury, protein transfer into the alveoli and surfactant system, in a model of acute lung injury. In adult rats, the lungs were ventilated mechanically with 100% oxygen and a PEEP of 6 cm H2O, and acute lung injury was induced by repeated lung lavage to obtain a PaO2 value < 13 kPa. Animals were then allocated randomly (n = 12 in each group) to receive exogenous surfactant therapy, ventilation with high PEEP (18 cm H2O), partial liquid ventilation or ventilation with low PEEP (8 cm H2O) (ventilated controls). Blood-gas values were measured hourly. At the end of the 4-h study, in six animals per group, pressure-volume curves were constructed and bronchoalveolar lavage (BAL) was performed, whereas in the remaining animals lung injury was assessed. In the ventilated control group, arterial oxygenation did not improve and protein concentration of BAL and conversion of active to non-active surfactant components increased significantly. In the three treatment groups, PaO2 increased rapidly to > 50 kPa and remained stable over the next 4 h. The protein concentration of BAL fluid increased significantly only in the partial liquid ventilation group. Conversion of active to non-active surfactant components increased significantly in the partial liquid ventilation group and in the group ventilated with high PEEP. In the surfactant group and partial liquid ventilation groups, less lung injury was found compared with the ventilated control group and the group ventilated with high PEEP. We conclude that although all three strategies improved PaO2 to > 50 kPa, the impact on protein transfer into the alveoli, surfactant system and lung injury differed markedly.

Purine in bronchoalveolar lavage fluid as a marker of ventilation-induced lung injury.

OBJECTIVE: To investigate in a rat model of ventilation-induced lung injury whether metabolic changes in the lung are reflected by an increased purine concentration (adenosine, inosine, hypoxanthine, xanthine, and urate; an index of adenosine-triphosphate breakdown) of the bronchoalveolar lavage fluid and whether purine can, thus, indirectly serve as a marker of ventilation-induced lung injury. DESIGN: Prospective, randomized, controlled trial. SETTING: Research laboratory. SUBJECTS: Forty-two male Sprague-Dawley rats. INTERVENTIONS: Five groups of Sprague-Dawley rats were subjected to 6 mins of mechanical ventilation. One group was ventilated at a peak inspiratory pressure of 7 cm H2O and a positive end-expiratory pressure of 0 cm H2O. A second group was ventilated at a peak inspiratory pressure of 45 cm H2O and a positive end-expiratory pressure of 10 cm H2O. Three groups of Sprague-Dawley rats were ventilated at a peak inspiratory pressure of 45 cm H2O without positive end-expiratory pressure. Before mechanical ventilation, two of these groups received intratracheal administration of saline or exogenous surfactant at a dose of 100 mg/kg and one group received no intratracheal administration. A sixth group served as the nonventilated controls. MEASUREMENTS AND MAIN RESULTS: Bronchoalveolar lavage fluid was collected in which both purine concentration (microM; mean +/- SD) and protein concentration (mg/mL; mean +/- SD) were determined. Statistical differences were analyzed using the one-way analysis of variance (ANOVA) with a Student-Newman-Keul's post hoc test. Purine and protein concentrations were different between groups (ANOVA p value for purine and protein, <.0001). Both purine and protein concentrations in bronchoalveolar lavage fluid were increased in Group 45/0 (3.2 +/- 1.9 and 4.2 +/- 1.6, respectively) compared with Group 7/0 (0.4 +/- 0.1 [p < .05] and 0.4 +/- 0.2 [p < .001]) and controls (0.2 +/- 0.2 [p < .01] and 0.2 +/- 0.1 [p < .001]) and in Group 45/Na (5.8 +/- 2.5 and 4.2 +/- 0.5) compared with Group 7/0 (purine and protein, p < .001) and the controls (purine and protein, p < .001). Positive end-expiratory pressure prevented an increase in purine and protein concentrations in bronchoalveolar lavage fluid (0.4 +/- 0.3 and 0.4 +/- 0.2, respectively) compared with Group 45/0 (purine, p < .01; protein, p < .001) and Group 45/Na (purine and protein, p < .001). Surfactant instillation preceding lung overinflation reduced purine and protein concentration in bronchoalveolar lavage fluid (2.1 +/- 1.6 and 2.7 +/- 1.0) compared with Group 45/Na (purine, p < .001; protein (p < .01). Surfactant instillation reduced protein concentration compared with Group 45/0 (p < .01). CONCLUSIONS: This study shows that metabolic changes in the lung as a result of ventilation-induced lung injury are reflected by an increased level of purine in the bronchoalveolar lavage fluid and that purine may, thus, serve as an early marker for ventilation-induced lung injury. Moreover, the study shows that both exogenous surfactant and positive end-expiratory pressure reduce protein infiltration and that positive end-expiratory pressure decreases the purine level in bronchoalveolar lavage fluid after lung overinflation.

Exogenous surfactant preserves lung function and reduces alveolar Evans blue dye influx in a rat model of ventilation-induced lung injury.

BACKGROUND: Changes in pulmonary edema infiltration and surfactant after intermittent positive pressure ventilation with high peak inspiratory lung volumes have been well described. To further elucidate the role of surfactant changes, the authors tested the effect of different doses of exogenous surfactant preceding high peak inspiratory lung volumes on lung function and lung permeability. METHODS: Five groups of Sprague-Dawley rats (n = 6 per group) were subjected to 20 min of high peak inspiratory lung volumes. Before high peak inspiratory lung volumes, four of these groups received intratracheal administration of saline or 50, 100, or 200 mg/kg body weight surfactant; one group received no intratracheal administration. Gas exchange was measured during mechanical ventilation. A sixth group served as nontreated, nonventilated controls. After death, all lungs were excised, and static pressure-volume curves and total lung volume at a transpulmonary pressure of 5 cm H2O were recorded. The Gruenwald index and the steepest part of the compliance curve (Cmax) were calculated. A bronchoalveolar lavage was performed; surfactant small and large aggregate total phosphorus and minimal surface tension were measured. In a second experiment in five groups of rats (n = 6 per group), lung permeability for Evans blue dye was measured. Before 20 min of high peak inspiratory lung volumes, three groups received intratracheal administration of 100, 200, or 400 mg/ kg body weight surfactant; one group received no intratracheal administration. A fifth group served as nontreated, nonventilated controls. RESULTS: Exogenous surfactant at a dose of 200 mg/kg preserved total lung volume at a pressure of 5 cm H2O, maximum compliance, the Gruenwald Index, and oxygenation after 20 min of mechanical ventilation. The most active surfactant was recovered in the group that received 200 mg/kg surfactant, and this dose reduced minimal surface tension of bronchoalveolar lavage to control values. Alveolar influx of Evans blue dye was reduced in the groups that received 200 and 400 mg/kg exogenous surfactant. CONCLUSIONS: Exogenous surfactant preceding high peak inspiratory lung volumes prevents impairment of oxygenation, lung mechanics, and minimal surface tension of bronchoalveolar lavage fluid and reduces alveolar influx of Evans blue dye. These data indicate that surfactant has a beneficial effect on ventilation-induced lung injury.

Localized myofibroblastic proliferation in the neck of a patient with an IgG myeloma.

We describe a myofibroblastic proliferation in the neck and lower part of the face involving skin and muscle of a 68-year-old female patient with an IgG kappa myeloma. Biopsies showed a fusocellular proliferation with scarce pseudoganglion cells involving the superficial fascia and the cutaneous muscle of the neck. The proliferative cells showed immunohistochemical and ultrastructural features characteristic of myofibrobasts with a proliferating cell nuclear antigen index of 48%; 42% of the cells displayed HLADR-positive membrane staining. Cellular proliferation subsided following the use of immunosuppressive drugs. Eight months after initial consultation, the patient developed polymyositis without a proliferative component and died of aplastic anemia.

[Acute fatty liver of pregnancy complicated by pancreatitis]. / Hígado graso agudo del embarazo complicado con pancreatitis.

A woman with acute fatty liver of pregnancy developed fulminant hepatic failure after delivery, a time when spontaneous recovery was expected. Pancreatitis and multiple organ failure was documented and intensive treatment in a critical care unit was needed to support organ function. She underwent plasmapheresis due to extreme hyperbilirubinemia and coma. She recovered completely.

Rápida eficacia de terbinafina oral en onicomicosis de los pies: experiencia clínica multicéntrica / Rapid efficacy of oral terbinafine in foot onychomycoses: multicentric clinical experience

Se presenta la experiencia clínica multicéntrica Chile-Uruguay en el tratamiento de la onicomicosis de los pies con Terbinafina oral administrada por 3 meses y en un período de observación postratamiento de 6 meses. Se incluyen 102 pacientes, 43 hombre y 59 mujeres, con una edad promedio de 50 años, que presentaban un cuadro clínico de onicomicosis de los pies, el que fue confirmado por la presencia de dermatofitos en el cultivo micológico inicial (73,5 por ciento trichophyton rubrum). Se seleccionó la uña más comprometida, en la que se evaluaron onicólisis, engrosamiento ungueal, cambio de coloración e inflamación paroniqueal como parámetros clínicos y la evaluación micológica se hizo por examen directo y cultivo. La uña seleccionada tuvo un crecimiento estadísticamente significativo tanto en la fase de tratamiento como la de postratamiento. Los signos clínicos mejoraron durante todo el seguimiento y el 73 por ciento a 86 por ciento de los pacientes alcanzó mejoría total de estos parámetros a los 9 meses de seguimiento. Los exámenes micológicos se fueron negativizando progresivamente, alcanzando en la evaluación final a los 9 meses un 85,9 por ciento y un 90,5 por ciento para exámenes directos y cultivos negativos, respectivamente. Recaídas con cultivos micológicos positivos fueron observadas en 3 pacientes (5 por ciento ). El medicamento fue bien tolerado y los efectos adversos mas frecuentes fueron los gastrointestinales en 11 pacientes. No hubo alteraciones de los parámetros bioquímicos hepáticos. En conclusión, la terbinafina aparece como un nuevo antimicótico de alta eficacia en un corto período de tratamiento

[Fibrous hamartoma in childhood]. / Hamartoma fibroso de la infancia.

A new case of fibrous hamartoma of infancy is described as a benign but persistent soft-tissue tumor that appears during the first 2 years of life, as a rare condition. The histopathological study shows the three characteristic elements: fibrous, uni-locular adipose tissue and mixoid mesenchymal tissue. The histogenesis of this peculiar tumor is discussed.

Adenocarcinoma mucinoso primario del piel / Primary mucious adenocarcinma of skin

Se presenta el caso de un adenocarcinoma mucionoso primitivo de piel, ubicado en la mejilla, con historia de 9 años de evolución signada por la recidiva lesional. Se hace una consideración y análisis de la literatura. La negatividad del antígeno carcino embrionario sugiere una línea de diferenciación más primitiva, quizás de una etapa precoz del germen epitelial (AU)