scholarly journals Serious acid-base disorder or life-threatening arrhythmia in patients with ABO-incompatible liver transplantation who received therapeutic plasma exchange : A report of two cases

2021 ◽  
Author(s):  
Sangho Lee ◽  
Kyoung-Sun Kim ◽  
Bo-Hyun Sang ◽  
Gyu-Sam Hwang
Keyword(s):  
Plasma Exchange ◽  
Metabolic Alkalosis ◽  
Therapeutic Plasma Exchange ◽  
Acid Base ◽  
Metabolic Derangement ◽  
Surgical Incision ◽  
Electrolyte Disturbance ◽  
Electrolyte Disturbances ◽  
Base Disorder ◽  
Life Threatening

Background: Excessive citrate load during therapeutic plasma exchange (TPE) can cause metabolic alkalosis with compensatory hypercarbia and electrolyte disturbances. If TPE is required immediately before ABO-incompatible (ABOi) liver transplant (LT) surgery, metabolic derangement and severe electrolyte disturbance could worsen during LT anesthesia.Case: We report two ABOi LT cases who received TPE on the day of surgery because isoagglutinin titers did not be dropped below 1:8. One case had a surprisingly high metabolic alkalosis with a pH of 7.73 immediately after tracheal intubation because of hyperventilation during mask bagging. The other experienced sudden ventricular tachycardia and blood pressure drop after surgical incision accompanied with severe hypokalemia of 1.8 mmol/L despite supplementation with potassium.Conclusions: Special attention should be paid to patients who just completed TPE the operative day morning as they are vulnerable to severe acid-base disturbances and life-threatening ventricular arrhythmias in ABOi LT.

scholarly journals Therapeutic plasma exchange in adult critically ill patients with life-threatening SARS-CoV-2 disease: A pilot study

2020 ◽  
Vol 60 ◽  
pp. 328-333 ◽  
Author(s):  
Fahad Faqihi ◽  
Abdulrahman Alharthy ◽  
Mohammed Alodat ◽  
Demetrios J. Kutsogiannis ◽  
Peter G. Brindley ◽  
...  
Keyword(s):  
Pilot Study ◽  
Plasma Exchange ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Therapeutic Plasma Exchange ◽  
Life Threatening

scholarly journals Life-threatening COVID-19 presenting as stroke with antiphospholipid antibodies and low ADAMTS-13 activity, and the role of therapeutic plasma exchange: A case series

2020 ◽  
Vol 8 ◽  
pp. 2050313X2096408
Author(s):  
Abdulrahman Alharthy ◽  
Fahad Faqihi ◽  
Abdullah Balhamar ◽  
Ziad A Memish ◽  
Dimitrios Karakitsos
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Plasma Exchange ◽  
Plasma Volume ◽  
Antiphospholipid Antibodies ◽  
Rescue Therapy ◽  
Antiviral Treatment ◽  
Case Series ◽  
Therapeutic Plasma Exchange ◽  
Life Threatening

We present a case series of three patients with COVID-19 who were admitted to our intensive care unit due to acute respiratory distress syndrome, brain infarction, pulmonary embolism, and antiphospholipid antibodies. We applied therapeutic plasma exchange on all cases. On intensive care unit admission, all patients had low (<10) Glasgow Coma Scale, and central nervous imaging showed multiple brain infarctions. COVID-19 was confirmed by reverse transcriptase polymerase chain reaction assays. Patients underwent rescue therapeutic plasma exchange using the Spectra OptiaTM Apheresis System (Terumo BCT Inc., USA), which operates with acid-citrate dextrose anticoagulant as per Kidney Disease Improving Global Outcomes 2019 guidelines. A dose of 1.5 plasma volume was used for the first dose and then 1 plasma volume daily for a total of five doses. Plasma was replaced with Octaplas LG® (Octapharma AG, USA), which is an artificial fresh frozen plasma product that has undergone viral inactivation by prion reduction technology. We administered ARDS-net/prone positioning ventilation, empiric antiviral treatment, therapeutic anticoagulation, and intensive care unit supportive care. Laboratory tests showed lymphocytopenia; elevated levels of D-dimer, fibrinogen, total bilirubin, C-reactive protein, lactate dehydrogenase, and ferritin; as well as low levels of ADAMTS-13 activity and antibody. Serology tests depicted positive IgM and IgG antiphospholipid antibodies (anti-cardiolipin and anti-β2-glycoprotein I antibodies). No side effects of therapeutic plasma exchange were recorded. After the completion of therapeutic plasma exchange, patients improved clinically and gradually recovered neurologically (after 27–32 days). To conclude, in life-threatening COVID-19, especially when immune dysregulation features such as antiphospholipid antibodies exist, therapeutic plasma exchange could be an effective rescue therapy.

scholarly journals Effect of hypokalemia on renal expression of the ammonia transporter family members, Rh B Glycoprotein and Rh C Glycoprotein, in the rat kidney

2011 ◽  
Vol 301 (4) ◽  
pp. F823-F832 ◽  
Author(s):  
Ki-Hwan Han ◽  
Hyun-Wook Lee ◽  
Mary E. Handlogten ◽  
Jesse M. Bishop ◽  
Moshe Levi ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Metabolic Alkalosis ◽  
Collecting Duct ◽  
Family Members ◽  
Ammonia Excretion ◽  
Intercalated Cells ◽  
Acid Base ◽  
Ammonia Metabolism ◽  
Transporter Family ◽  
Base Disorder

Hypokalemia is a common electrolyte disorder that increases renal ammonia metabolism and can cause the development of an acid-base disorder, metabolic alkalosis. The ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg), are expressed in the distal nephron and collecting duct and mediate critical roles in acid-base homeostasis by facilitating ammonia secretion. In the current studies, the effect of hypokalemia on renal Rhbg and Rhcg expression was examined. Normal Sprague-Dawley rats received either K+-free or control diets for 2 wk. Rats receiving the K+-deficient diet developed hypokalemia and metabolic alkalosis associated with significant increases in both urinary ammonia excretion and urine pH. Rhcg expression increased in the outer medullary collecting duct (OMCD). In OMCD intercalated cells, hypokalemia resulted in more discrete apical Rhcg expression and a marked increase in apical plasma membrane immunolabel. In principal cells, in the OMCD, hypokalemia increased both apical and basolateral Rhcg immunolabel intensity. Cortical Rhcg expression was not detectably altered by immunohistochemistry, although there was a slight decrease in total expression by immunoblot analysis. Rhbg protein expression was decreased slightly in the cortex and not detectably altered in the outer medulla. We conclude that in rat OMCD, hypokalemia increases Rhcg expression, causes more polarized apical expression in intercalated cells, and increases both apical and basolateral expression in the principal cell. Increased plasma membrane Rhcg expression in response to hypokalemia in the rat, particularly in the OMCD, likely contributes to the increased ammonia excretion and thereby to the development of metabolic alkalosis.

scholarly journals Metabolic alkalosis is the most common acid–base disorder in ICU patients

Critical Care ◽  
2014 ◽  
Vol 18 (2) ◽  
pp. 420 ◽  
Author(s):  
Kjersti Mæhle ◽  
Bjørn Haug ◽  
Hans Flaatten ◽  
Erik Nielsen
Keyword(s):  
Metabolic Alkalosis ◽  
Acid Base ◽  
Icu Patients ◽  
Base Disorder

scholarly journals Critical Care COVID-19 Patient with a Picture of Thrombotic Thrombocytopenic Purpura

2020 ◽  
Author(s):  
Rehab AL-Ansari ◽  
Mohanad Bakkar ◽  
Leena Abdalla ◽  
Khaled Sewify
Keyword(s):  
Mechanical Ventilation ◽  
Critical Care ◽  
Plasma Exchange ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Kidney Injury ◽  
Therapeutic Plasma Exchange ◽  
Thrombocytopenic Purpura ◽  
Threatening Condition ◽  
Life Threatening

Background: Thrombotic thrombocytopenic purpura (TTP) is an uncommon haematological disease which can occur at any age and may present with COVID-19. This case describes a COVID-19 complication associated with a presentation resembling TTP. Case description: A 51-year-old man who had received a kidney transplant and was on immunosuppressant medication, was admitted to a critical care unit with severe COVID-19 pneumonia/acute respiratory distress syndrome (ARDS) which required intubation, mechanical ventilation and inotropic support. The course was complicated by the classic pentad of thrombocytopenia, intravascular haemolysis, acute kidney injury, neurological symptoms and fever, which prompted the diagnosis of probable TTP. After five sessions of therapeutic plasma exchange, the patient’s general status improved, he was weaned off mechanical ventilation and his renal panel and haemolytic markers normalized. Conclusion: TTP is a life-threatening condition which requires urgent management with therapeutic plasma exchange. This case highlights some possible complications of COVID-19 generally and in immunocompromised patients specifically. The potential role of plasma exchange in COVID-19 patients without a positive diagnosis of TTP (the so-called ‘TTP resembling presentation’) is an area of further research.

Therapeutic Plasma Exchange in Neonates and Infants: Successful Use of a Miniaturized Machine

2017 ◽  
Vol 44 (2) ◽  
pp. 100-105 ◽  
Author(s):  
Enrico Vidal ◽  
Francesco Garzotto ◽  
Mattia Parolin ◽  
Chiara Manenti ◽  
Anna Zanin ◽  
...  
Keyword(s):  
Plasma Exchange ◽  
Pediatric Population ◽  
Treatment Method ◽  
Therapeutic Plasma Exchange ◽  
Life Saving ◽  
Blood Exchange ◽  
Blood Exchange Transfusion ◽  
Life Threatening ◽  
Technical Issues ◽  
Neonates And Infants

Therapeutic plasma exchange (TPE) in neonates and small infants is a treatment method at the forefront that may become a potentially life-saving procedure in a wide array of severe conditions. Indications for TPE in the pediatric population have been mainly derived from adult literature, with neonatal hyperbilirubinemia being the most notable exception. The only alternative to TPE in small pediatric patients is manual blood exchange transfusion, which, however, bears an unacceptably high risk of severe complications. Still, technical issues due to extracorporeal circulation in neonates have burdened TPE so far, since machines developed for adults require a relatively large blood volume to operate. We in this study, describe our preliminary experience of TPE for treating 2 potentially life-threatening conditions in neonatal age. To overcome the aforementioned limitations, plasmapheresis was performed in both cases using a machine specifically designed for patients weighing less than 10 kg.

scholarly journals Acid-Base Correction: A Case Report and Review of the Literature

2010 ◽  
Vol 11 (2) ◽  
pp. 126-129
Author(s):  
Mike Ward Jones ◽  
Matthew Williams
Keyword(s):  
Case Report ◽  
Hydrochloric Acid ◽  
Colorectal Surgery ◽  
Metabolic Alkalosis ◽  
Review Of The Literature ◽  
Acid Base ◽  
Risks And Benefits ◽  
Hospitalised Patients ◽  
Life Threatening

Metabolic alkalosis is a common acid-base abnormality in hospitalised patients, though not frequently life-threatening. We present a case of severe metabolic alkalosis complicating colorectal surgery, which necessitated treatment with intravenous hydrochloric acid. The pathophysiology and treatment of severe metabolic alkalosis are reviewed, with an emphasis on the risks and benefits of hydrochloric acid use.

scholarly journals Opiate Withdrawal Complicated by Tetany and Cardiac Arrest

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Irfanali R. Kugasia ◽  
Nehad Shabarek
Keyword(s):  
Cardiac Arrest ◽  
Withdrawal Symptom ◽  
Respiratory Alkalosis ◽  
Withdrawal Symptoms ◽  
Opiate Withdrawal ◽  
Acid Base ◽  
Severe Withdrawal ◽  
Base Disorder ◽  
Life Threatening ◽  
Acid Base Status

Patients with symptoms of opiate withdrawal, after the administration of opiate antagonist by paramedics, are a common presentation in the emergency department of hospitals. Though most of opiate withdrawal symptoms are benign, rarely they can become life threatening. This case highlights how a benign opiate withdrawal symptom of hyperventilation led to severe respiratory alkalosis that degenerated into tetany and cardiac arrest. Though this patient was successfully resuscitated, it is imperative that severe withdrawal symptoms are timely identified and immediate steps are taken to prevent catastrophes. An easier way to reverse the severe opiate withdrawal symptom would be with either low dose methadone or partial opiate agonists like buprenorphine. However, if severe acid-base disorder is identified, it would be safer to electively intubate these patients for better control of their respiratory and acid-base status.

scholarly journals Life-threatening metabolic alkalosis in Pendred syndrome

2011 ◽  
Vol 165 (1) ◽  
pp. 167-170 ◽  
Author(s):  
Narayanan Kandasamy ◽  
Laura Fugazzola ◽  
Mark Evans ◽  
Krishna Chatterjee ◽  
Fiona Karet
Keyword(s):  
Metabolic Alkalosis ◽  
Collecting Duct ◽  
Sensorineural Deafness ◽  
Apical Plasma Membrane ◽  
Cortical Collecting Duct ◽  
Loss Of Function ◽  
Pendred Syndrome ◽  
Acid Base ◽  
Life Threatening ◽  
Acid Base Status

IntroductionPendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Recently, pendrin has also been identified in the kidneys, where it is found in the apical plasma membrane of non-α-type intercalated cells of the cortical collecting duct. Here, it functions as a chloride–bicarbonate exchanger, capable of secreting bicarbonate into the urine. Despite this function, patients with Pendred syndrome have not been reported to develop any significant acid–base disturbances, except a single previous reported case of metabolic alkalosis in the context of Pendred syndrome in a child started on a diuretic.Case reportWe describe a 46-year-old female with sensorineural deafness and hypothyroidism, who presented with severe hypokalaemic metabolic alkalosis during inter-current illnesses on two occasions, and who was found to be homozygous for a loss-of-function mutation (V138F) in SLC26A4. Her acid–base status and electrolytes were unremarkable when she was well.ConclusionThis case illustrates that, although pendrin is not usually required to maintain acid–base homeostasis under ambient condition, loss of renal bicarbonate excretion by pendrin during a metabolic alkalotic challenge may contribute to life-threatening acid–base disturbances in patients with Pendred syndrome.

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