Ringer's lactate/sodium chloride
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Ringer’s lactate/sodium chloride Acute pulmonary oedema, hyperchloraemic metabolic acidosis and other toxicities: case report
A 40-year-old woman developed acute pulmonary oedema, respiratory compromise and hyperchloraemic metabolic acidosis due to fluid overload following administration of sodium chloride and ringer’s lactate for uterine distension [time to reaction onsets not stated]. The woman presented to the early pregnancy clinic at 11 weeks of gestation because of light vaginal bleeding. An incomplete miscarriage was confirmed with ultrasonography. Initial medical and conservative management of the retained products was not successful. A repeat ultrasonography revealed presence of the retained products measuring 3cm. Hence, surgical evacuation of retained products of conception was scheduled. Prior to anaesthesia induction with midazolam, propofol and fentanyl, and IV infusion of ringer’s lactate [Hartmann’s solution] was initiated. Her airway was maintained with a laryngeal mask. She was also administered amoxicillin/clavulanic acid [coamoxiclav] and ondansetron, along with sevoflurane for maintenance of anaesthesia. To minimise the risk of incomplete removal, hysteroscopic approach was selected, and she was administered IV 0.9% sodium chloride solution. She was stable throughout the procedure, and a total 1500mL of final hysteroscopic fluid deficit was noted. Additionally, she had received 1000mL of the ringer’s lactate solution. Her RR increased from 12 to 24 breaths/minute with a drop in end-tidal carbon dioxide partial pressure from 5.5 to 3.0 kPa while she was still in the operating theatre. Her oxygen saturation also dropped from 99% to 93% despite an increased FIO2 of 1.0 for emergence, and HR increased from 80 to 120 beats/minute. To use a facemask connected to the anaesthetic machine circle system and allow continuous positive airway pressure (CPAP) ventilation, the laryngeal mask was removed. She had passed 200–300mL of blood per vagina, and was treated with tranexamic acid, oxytocin and misoprostol. Chest auscultation showed widespread crepitations indicative of an acute pulmonary oedema. The woman was kept on CPAP ventilation to maintain oxygen saturation. A dilutional anaemia and hyperchloraemic metabolic acidosis were noted in venous blood gas analysis. Based on all the findings, a diagnosis of acute pulmonary oedema and hyperchloraemic metabolic acidosis secondary to fluid overload caused by sodium chloride and ringer’s lactate was confirmed. She was treated with furosemide, and a radial arterial line was inserted. The widespread pulmonary oedema was confirmed on chest Xray. She was then shifted to the post-anaesthesia care unit on 15L of oxygen via a non-rebreather mask. Diuresis of 1500mL over 90 minutes was noted on furosemide therapy. One hour later, she was shifted to the high dependency unit, and received oxygen via high-flow nasal device. After 6h of the respiratory compromise, she was de-escalated onto standard nasal cannula. A mild tricuspid regurgitation was noted in a transth
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