Gambaran Radiografi Paru-Paru Babi Setelah Terapi Resusitasi Cairan Pasca Kondisi Syok Septik

Abstract

Sepsis memicu disfungsi endotel dan kebocoran kapiler yang berisiko diperburuk oleh resusitasi cairan agresif. Penelitian ini bertujuan menganalisis perubahan pola radiografi paru-paru babi setelah resusitasi cairan kristaloid pasca syok septik. Empat ekor babi diinduksi syok septik menggunakan lipopolisakarida Escherichia coli, kemudian diberikan resusitasi Ringer laktat 30 ml/kg. Evaluasi radiografi arah ventrodorsal dan laterolateral dilakukan menggunakan perangkat lunak ImageJ untuk membandingkan kondisi prasepsis dan pascaresusitasi. Hasil menunjukkan peningkatan dominan pada pola interstisial (34,5%), diikuti pola bronkial (20,5%) dan munculnya pola alveolar (14,2%) yang terlokalisasi di lobus kaudal. Tidak adanya perubahan signifikan pada pola vaskular mengonfirmasi bahwa edema dipicu oleh peningkatan permeabilitas kapiler, bukan tekanan hidrostatik vaskular murni. Meskipun resusitasi dilakukan, target mean arterial pressure (MAP) gagal tercapai (48,7 ± 3,7 mmHg), sementara progresi edema paru tetap terjadi. Temuan ini mengimplikasikan risiko fluid overload dari resusitasi seragam yang dapat memperburuk fungsi respirasi.

Sepsis triggers endothelial dysfunction and capillary leakage, which risks being exacerbated by aggressive fluid therapy. This study aims to analyze changes in pulmonary radiographic patterns in pigs following crystalloid fluid resuscitation after septic shock. Four pigs were induced into septic shock using Escherichia coli lipopolysaccharide and then administered 30 ml/kg of Ringer's lactate resuscitation. Ventrodorsal and laterolateral radiographic evaluations were performed using ImageJ software to compare pre-sepsis and post-resuscitation conditions. Results showed a dominant increase in the interstitial pattern (34.5%), followed by the bronchial pattern (20.5%) and the emergence of an alveolar pattern (14.2%) localized in the caudal lobes. The lack of significant changes in the vascular pattern confirms that the edema was triggered by increased capillary permeability rather than pure vascular hydrostatic pressure. Despite resuscitation, the target mean arterial pressure (MAP) failed to be achieved (48.7 ± 3.7 mmHg), while pulmonary edema progression persisted. These findings imply a risk of fluid overload from a uniform resuscitation approaches, which could worsen respiratory conditions.