Safety of epidural analgesia in an orthotopic liver transplantation

In the literature devoted to the problems of liver transplantation, there is no clearly indicated attitude of the authors to intraoperative epidural blocks, although theoretically the benefits of a sympathetic block are considered. Some sources recommend prophylactic sodium bicarbonate infusion to alleviate post-reperfusion syndrome, but its effectiveness is questionable.Purpose: to present the physiological, biochemical and hematological characteristics of recipients at the stages of orthotopic liver transplantation with an assessment of the feasibility of using sodium bicarbonate for the prevention of reperfusion complications.Materials and methods. An observational study, contains an analysis of data from 39 participants operated on in 2020 in the volume of: hepatectomy, an orthotopic liver transplantation, with an initial assessment on the Child- Turcott- Pugh scale of 11 points. All participants were operated on under general inhalation anesthesia with sevoflurane and thoracic epidural three- component anesthesia according to the Breivik- Niemi method. There are 3 stages of data registration: the beginning of the anhepatic stage; the beginning of the neohepatic stage; the end of the operation.Results and discussion. Significant fluctuations in hemodynamics, violations of the acid-base state and energy metabolism were not revealed; a decrease in hepatic protein synthesis, a shift of the P50 point to the left, and moderate metabolic acidosis did not exceed the levels described in the literature. The dynamics of acidosis, РСО2 and natremia did not depend on the infusion of soda. There was no close correlation between arterial blood pH and lactate concentration.Conclusion. The benefits and safety of epidural anesthesia in orthotopic liver transplants are obvious and make it possible to recommend this component as a routine element of anesthesia during these operations. The indications for sodium bicarbonate infusion should be narrowed and consensus is needed to determine the critical pH value for sodium bicarbonate infusion.

Flecainide toxicity with high pacemaker capture thresholds and associated takotsubo syndrome

We describe a case of a woman in her 80s with persistent atrial fibrillation (AF) despite being on flecainide who was admitted for AF with rapid ventricular response. Attempts with direct-current cardioversions were unsuccessful despite increased doses of the antiarrhythmic therapy. At atrioventricular (AV) nodal ablation, very high right ventricular capture thresholds resulted in abortion of the procedure as back-up ventricular pacing could not be assured with adequate margin for safety. Shortly following the electrophysiology (EP) study, the patient developed cardiogenic shock with new apical left ventricular regional wall motion abnormality suggestive of apical ballooning and a toxic-appearing wide QRS complex electrocardiogram (EKG). The patient was successfully treated with sodium bicarbonate infusion for presumed flecainide toxicity. The regional wall motion abnormality and EKG changes resolved along with normalisation of capture thresholds after 2 days of treatment. The patient underwent an uncomplicated successful AV nodal ablation several weeks later.

Metformin-associated lactic acidosis: reinforcing learning points

Metformin-associated lactic acidosis (MALA) carries a high mortality rate. It is seen in patients with type 2 diabetes on metformin or patients who attempt suicide with metformin overdose. We present the case of a man in his early 20s with type 2 diabetes, hypertension and hypothyroidism who presented with agitation, abdominal pain and vomiting after ingesting 50–60 g of metformin; he developed severe lactic acidosis (blood pH 6.93, bicarbonate 7.8 mEq/L, lactate 28.0 mEq/L). He was managed with intravenous 8.4% bicarbonate infusion and continuous venovenous haemodiafiltration. He also developed acute renal failure (ARF) requiring intermittent haemodialysis and continuous haemodiafiltration. MALA is uncommon and causes changes in different vital organs and even death. The primary goals of therapy are restoration of acid-base status and removal of metformin. Early renal replacement therapy for ARF can result in rapid reversal of the acidosis and good recovery, even with levels of lactate normally considered to be incompatible with survival.

P0008CASE REPORT: METABOLIC ALKALOSIS RESULTING IN RESPIRATORY COMPROMISE IN A PATIENT UNDERGOING HIGH DOSE METHOTREXATE THERAPY

Background and Aims High dose Methotrexate (HDMTX) is an important component of several modern oncological/haematological treatment protocols due to its central nervous system penetrance. Nephrotoxicity represents a significant adverse effect and can limit therapeutic options. Therefore, strategies to prevent this are paramount. Urinary alkalinisation and large volume resuscitation to maintain adequate hydration and urine output are the typical strategies. Urinary alkalinisation prevents tubular precipitation of methotrexate and therefore, a strict urinary pH target of 7 is maintained via a continuous bicarbonate infusion. Method We describe a case report, of Iatrogenic metabolic alkalosis leading to respiratory compromise in a patient receiving HDMTX from Mayo Clinic, Rochester. Results We present the case of a 76-year-old woman with a Diffuse Large B-Cell Lymphoma with CNS involvement who presented for elective admission for her 1st cycle of HDMTX. She received 7g of Methotrexate at dosing of 8 g/m2. She received the standard urinary alkalinisation with pre- and post-hydration. Her baseline HCO3- was 28 mEq/L. Her 48 hour MTX level was elevated at 1.2 so the urinary alkalinisation protocol was continued until <0.1 mcmol/L. On day 4, she developed frequent episodes of apnoea. Her ABG demonstrated a metabolic alkalaemia pH 7.54, pCO 53, pO2 91, HCO3 45. She was transferred to the ICU for close monitoring. Her bicarbonate infusion was discontinued and she received acetazolamide. Her bicarbonate improved to 31 after 12 hours. She had a significant improvement in her respiratory status with no further episodes of apnoea. Her bicarbonate infusion was restarted due to elevated MTX levels. She was discharged home with no further complications. Conclusion Iatrogenic Metabolic alkalosis leading to respiratory compromise represents a rare but important complication of urinary alkalinsation protocols for High-dose Methotrexate therapy.

Sodium Fate after Sodium Bicarbonate Infusion: Influence of Altered Acid-Base Status

Background: We have previously investigated the fate of administered bicarbonate infused as a hypertonic solution in animals with each of the 4 chronic acid-base disorders. Those studies did not address the fate of sodium, the coadministered cation. Methods: We examined baseline total body water (TBW), Na+ space, HCO3– space, and urinary sodium and bicarbonate excretion after acute hypertonic NaHCO3 infusion (1-N solution, 5 mmol/kg body weight) in dogs with each of the 4 chronic acid-base disorders. Observations were made at 30, 60, and 90 min postinfusion. Retained sodium that remains osmotically active distributes in an apparent space that approximates TBW. Na+ space that exceeds TBW uncovers nonosmotic sodium storage. Results: Na+ space approximated TBW at all times in normal and hyperbicarbonatemic animals (metabolic alkalosis and respiratory acidosis), but exceeded TBW by ~30% in hypobicarbonatemic animals (metabolic acidosis and respiratory alkalosis). Such osmotic inactivation was detected at 30 min and remained stable. The pooled data revealed that Na+ space corrected for TBW was independent of the initial blood pH but correlated with initial extracellular bicarbonate concentration (y = –0.01x + 1.4, p= 0.002). The fate of administered sodium and bicarbonate (internal distribution and urinary excretion) was closely linked. Conclusions: This study demonstrates that hypobicarbonatemic animals have a Na+ space that exceeds TBW after an acute infusion of hypertonic NaHCO3 indicating osmotic inactivation of a fraction of retained sodium. In addition to an expanded Na+ space, these animals have a larger HCO3– space compared with hyperbicarbonatemic animals. Both phenomena appear to reflect the wider range of titration of nonbicarbonate buffers (Δ pH) occurring during NaHCO3– loading whenever initial [HCO3–]e is low. The data indicate that the fate of administered bicarbonate drives the internal distribution and the external disposal of sodium, the co-administered cation, and is responsible for the early, but non-progressive, osmotic inactivation of a fraction of the retained sodium.