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Furtado C, Nayak S, Jadun C, Srivastava S, Hashim Z. Radiological Appearance and Imaging Techniques in the Diagnosis of Advanced Central Pontine Myelinolysis. Cureus 2022; 14:e30328. [DOI: 10.7759/cureus.30328] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 10/15/2022] [Indexed: 11/06/2022] Open
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Di Agostino S, Costanzo AA, Andreone P, Maurantonio M. Central pontine myelinolysis secondary to glycemic variability in type 1 diabetes: a case report and a systematic review of the literature. EXPLORATION OF MEDICINE 2021. [DOI: 10.37349/emed.2021.00050] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/08/2021] [Accepted: 06/24/2021] [Indexed: 02/09/2025] Open
Abstract
Central pontine myelinolysis (CPM) is a rare manifestation of osmotic demyelination syndrome (ODS) which involves the pons and causes significant morbidity and mortality. CPM usually occurs in the setting of rapid correction of severe chronic hyponatremia. A rare case of CPM due to hyperglycemia in a 27-year-old man with type 1 diabetes is reported. During the patient’s hospitalization, his plasma glucose level showed a wide variability ranging from 38 mg/dL to 530 mg/dL, while plasma sodium level was constantly normal. At computed tomography (CT) scans, areas of hypodensity with a hyperdense ring were identified in the anterior part of the pons. At magnetic resonance imaging (MRI) scan, pontine abnormalities compatible with CPM were observed. According to laboratory tests, we concluded that CPM resulted from rapid and wide shifts in osmolar gradient owing to variability in plasma glucose levels. While universally recognized in several clinical settings, CPM is rarely observed in diabetic patients. Our report supports the notion that hyperosmolarity per se plays a key role in the pathogenesis of CPM, which may occur independently of sodium abnormalities.
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Affiliation(s)
- Stefania Di Agostino
- Division of Metabolic Internal Medicine, University of Modena and Reggio Emilia, 41126 Modena, Italy
| | - Arianna A.C. Costanzo
- Division of Metabolic Internal Medicine, University of Modena and Reggio Emilia, 41126 Modena, Italy
| | - Pietro Andreone
- Department of Internal Medicine, General, Emergency and Post-Acute, Division of Metabolic Internal Medicine, University Hospital of Modena, 41126 Modena, Italy
| | - Mauro Maurantonio
- Department of Internal Medicine, General, Emergency and Post-Acute, Division of Metabolic Internal Medicine, University Hospital of Modena, 41126 Modena, Italy
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Niida S, Ogawa F, Nakajima K, Sakai K, Uchiyama M, Abe T, Takeuchi I. A Case of Central Pontine Myelinolysis Occurred During Treatment of Hyperosmolar Hyperglycemic Syndrome. Int Med Case Rep J 2021; 14:407-412. [PMID: 34177275 PMCID: PMC8219389 DOI: 10.2147/imcrj.s316943] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/25/2021] [Accepted: 06/04/2021] [Indexed: 12/05/2022] Open
Abstract
Central pontine myelinolysis (CPM) is a rare demyelinating condition which has been reported to occur in a variety of clinical settings, but most commonly in association with a rapid rise in plasma osmolality during correction of chronic hyponatremia. The clinical consequences can vary from a mild motor weakness that resolves completely over time to the devastating locked-in syndrome. In this presentation, we report a case of hyperosmolar hyperglycemic syndrome (HHS) with ponto-occipital disintegration. A 71-year-old female was transferred to our ER by an ambulance due to consciousness disorder and continuous fever for 10 days. We diagnosed septic shock caused by urinary tract infection (UTI), cerebral multiple infarctions, acute kidney injury (AKI) and HHS without treatment for diabetes. Then, we started therapeutic interventions for them based on the guideline with severe control for blood sugar (BS; primary 1635 mg/dl) under insulin therapy and hypernatremia (primary 153 mEq/l) under crystal infusion control in advanced care unit, apparently on routine lab data. However, the initial serum sodium value of 153 mEq/l was slowly compensated to 148 mEq/l in 60 hours under guideline on routine lab data, the initial compensated sodium value with osmolality was changed from 178 mEq/l to 150 mEq/l in the period. She recovered from her primary diagnosis and unconsciousness. After stabilized sepsis and HHS, we detected CPM on brain MRI due to following up multiple cerebral infarctions with left leg paralysis and verbal disorder. She gradually recovered over several months with intensive rehabilitation and eventually regained near normal functional capacity with stabilized BS. When we consider HHS with hypernatremia, it may be necessary to pay attention to not only to BS control and sodium control according to the guideline but also to osmolality changes to prevent CPM.
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Affiliation(s)
- Shoko Niida
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
| | - Fumihiro Ogawa
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
| | - Kento Nakajima
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
| | - Kazuya Sakai
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
| | - Munehito Uchiyama
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
| | - Takeru Abe
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
| | - Ichiro Takeuchi
- Department of Emergency Medicine, Yokohama City University School of Medicine, Yokohama, Kanagawa, 236-0004, Japan
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Weiss N, Thabut D. Neurological Complications Occurring After Liver Transplantation: Role of Risk Factors, Hepatic Encephalopathy, and Acute (on Chronic) Brain Injury. Liver Transpl 2019; 25:469-487. [PMID: 30697911 DOI: 10.1002/lt.25420] [Citation(s) in RCA: 47] [Impact Index Per Article: 7.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/30/2018] [Accepted: 12/19/2018] [Indexed: 02/06/2023]
Abstract
Orthotopic liver transplantation (LT) remains the only way to definitively cure patients with the most severe liver diseases. Because the survival rate is now fairly high, important questions about neurological sequelae or quality of life after LT have emerged. Indeed, LT represents a peculiar situation because up to 30% of patients present with neurological symptoms after LT compared with only 4% after cardiac transplant and 0.5% after renal transplant. These postoperative neurological symptoms have long been interpreted as sequelae of hepatic encephalopathy (HE). However, postoperative decompensation of an unknown cerebral condition due to the pathophysiology of cirrhosis or undiagnosed neurodegenerative disorders or aging constitute other possibilities that are underrecognized. Some patients who undergo LT for acute liver failure and patients with cirrhosis without episodes of HE and without any previous cerebral alteration also display post-LT neurological symptoms. This latter situation speaks in favor of a direct adverse effect of either general anesthesia, the surgical procedure, or factors related to the postoperative intensive care unit (ICU) environment. The role of inflammation, which has been described in the ICU setting, could also be a crucial determinant. In this review, we will discuss the neurological complications associated with LT, the neurocognitive complications after LT, and how to assess the LT-related neurological or neurocognitive complications. Furthermore, we will review the various hypotheses surrounding post-LT neurocognitive impairment and will conclude with recommendations for future directions.
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Affiliation(s)
- Nicolas Weiss
- Brain Liver Pitié-Salpêtrière (BLIPS) Study Group, Assistance Publique - Hôpitaux de Paris, Groupement Hospitalier Pitié-Salpêtrière-Charles Foix, Département de Neurologie, Unité de Réanimation Neurologique, Sorbonne Université, Paris, France.,Centre de Recherche Saint-Antoine (CRSA), Sorbonne Université, INSERM, Paris, France
| | - Dominique Thabut
- Centre de Recherche Saint-Antoine (CRSA), Sorbonne Université, INSERM, Paris, France.,Brain Liver Pitié-Salpêtrière (BLIPS) Study Group, Assistance Publique - Hôpitaux de Paris, Groupement Hospitalier Pitié-Salpêtrière-Charles Foix, Service d'Hépato-Gastroentérologie, Unité de Soins Intensifs d'Hépato-Gastroentérologie, Sorbonne Université, Paris, France
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5
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Shah MK, Mandayam S, Adrogué HJ. Osmotic Demyelination Unrelated to Hyponatremia. Am J Kidney Dis 2018; 71:436-440. [DOI: 10.1053/j.ajkd.2017.10.010] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/13/2017] [Accepted: 10/06/2017] [Indexed: 02/07/2023]
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Savin AA, Trukhanov SA, Zyuzya YR, Sokolina IA, Malysheva EM, Bogomolov DV, Savina EB, Khodyachaya GV, Savin LA, Matrokhin NN, Bugun AV. [A case report of central pontine and extrapontine myelinolysis in the combination with spinal cord damage in a patient with tuberculosis in the lung]. Zh Nevrol Psikhiatr Im S S Korsakova 2017; 117:117-123. [PMID: 28374704 DOI: 10.17116/jnevro201711721117-123] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
A case report of central pontine and extrapontine myelinolysis in the combination with spinal cord damage is presented. The authors analyze literature data on this problem and discuss the pathogenesis and diagnostic issues of myelinolysis.
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Affiliation(s)
- A A Savin
- Evdokimov Moscow State Universuty of Medical Dentistry, Moscow, Russia
| | - S A Trukhanov
- Evdokimov Moscow State Universuty of Medical Dentistry, Moscow, Russia
| | - Yu R Zyuzya
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
| | - I A Sokolina
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
| | - E M Malysheva
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
| | - D V Bogomolov
- Federal state budgetary institution 'Russian Centre of Forensic Medical Expertise', Moscow, Russia
| | - E B Savina
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
| | - G V Khodyachaya
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
| | - L A Savin
- Evdokimov Moscow State Universuty of Medical Dentistry, Moscow, Russia
| | - N N Matrokhin
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
| | - A V Bugun
- City Scientific and Practical Center of Tuberculosis, Moscow, Russia
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Abstract
Major neurologic morbidity, such as seizures and encephalopathy, complicates 20-30% of organ and stem cell transplantation procedures. The majority of these disorders occur in the early posttransplant period, but recipients remain at risk for opportunistic infections and other nervous system disorders for many years. These long-term risks may be increasing as acute survival increases, and a greater number of "sicker" patients are exposed to long-term immunosuppression. Drug neurotoxicity accounts for a significant proportion of complications, with posterior reversible leukoencephalopathy syndrome, primarily associated with calcineurin inhibitors (i.e., cyclosporine and tacrolimus), being prominent as a cause of seizures and neurologic deficits. A thorough evaluation of any patient who develops neurologic symptoms after transplantation is mandatory, since reversible and treatable conditions could be found, and important prognostic information can be obtained.
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Affiliation(s)
- R Dhar
- Division of Neurocritical Care, Department of Neurology, Washington University, St. Louis, MO, USA.
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Shen ZY, Wu B, Liu T, Yang Y, Yin ML, Zheng WP, Zhang BY, Song HL. Immunomodulatory effects of bone marrow mesenchymal stem cells overexpressing heme oxygenase-1: Protective effects on acute rejection following reduced-size liver transplantation in a rat model. Cell Immunol 2016; 313:10-24. [PMID: 28069109 DOI: 10.1016/j.cellimm.2016.12.006] [Citation(s) in RCA: 22] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/22/2016] [Revised: 12/08/2016] [Accepted: 12/24/2016] [Indexed: 12/21/2022]
Abstract
Here we explore the T-lymphocyte suppressive and immunomodulatory effects of bone marrow mesenchymal stem cells (BMMSCs) overexpressing heme oxygenase-1 (HO-1) on acute rejection following reduced-size liver transplantation (RLT) in a rat model. The proliferation activity, cell cycle progression, secretion of proinflammatory cytokines, expression of CD25 and CD71 in lymphocytes, and activity of NK cells were found to be significantly lowered, and the proportion of regulatory T cells (Tregs) was found to be increased relative to BMMSCs when Adv-HO-1/BMMSCs were co-cultured with Con A ex vivo; secretion of anti-inflammatory cytokines was significantly higher. When treated with saline, BMMSCs or Adv-HO-1/BMMSCs, post-transplantation rats receiving Adv-HO-1/BMMSCs showed better median survival time, lower rejection activity index, higher anti-inflammatory cytokine levels, lower proinflammatory cytokine levels, more peripheral Tregs, and lower natural killer cell viability. These results suggest that HO-1 enhanced and prolonged the effects of BMMSCs on acute rejection following RLT, with immunomodulatory effects in which adaptive and innate immunity, as well as paracrine signaling, may play important roles.
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Affiliation(s)
- Zhong-Yang Shen
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China
| | - Bin Wu
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China
| | - Tao Liu
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China; Key Laboratory of Emergency and Care Medicine of Ministry of Health, Tianjin 300192, PR China
| | - Yang Yang
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China
| | - Ming-Li Yin
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China; Key Laboratory of Emergency and Care Medicine of Ministry of Health, Tianjin 300192, PR China
| | - Wei-Ping Zheng
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China
| | - Bo-Ya Zhang
- Key Laboratory of Emergency and Care Medicine of Ministry of Health, Tianjin 300192, PR China
| | - Hong-Li Song
- Department of Organ Transplantation, Tianjin First Central Hospital, Tianjin 300192, PR China; Tianjin Key Laboratory of Organ Transplantation, Tianjin 300192, PR China.
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Abstract
Anesthesia for liver transplantation pertains to a continuum of critical care of patients with end-stage liver disease. Hence, anesthesiologists, armed with a comprehensive understanding of pathophysiology and physiologic effects of liver transplantation on recipients, are expected to maintain homeostasis of all organ function. Specifically, patients with fulminant hepatic failure develop significant changes in cerebral function, and cerebral perfusion is maintained by monitoring cerebral blood flow and cerebral metabolic rate of oxygen, and intracranial pressure. Hyperdynamic circulation is challenged by the postreperfusion syndrome, which may lead to cardiovascular collapse. The goal of circulatory support is to maintain tissue perfusion via optimal preload, contractility, and heart rate using the guidance of right-heart catheterization and transesophageal echocardiography. Portopulmonary hypertension and hepatopulmonary syndrome have high morbidity and mortality, and they should be properly evaluated preoperatively. Major bleeding is a common occurrence, and euvolemia is maintained using a rapid infusion device. Pre-existing coagulopathy is compounded by dilution, fibrinolysis, heparin effect, and excessive activation. It is treated using selective component or pharmacologic therapy based on the viscoelastic properties of whole blood. Hypocalcemia and hyperkalemia from massive transfusion, lack of hepatic function, and the postreperfusion syndrome should be aggressively treated. Close communication between all parties involved in liver transplantation is also equally valuable in achieving a successful outcome.
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Rao PB, Azim A, Singh N, Baronia AK, Kumar A, Poddar B. Osmotic demyelination syndrome in Intensive Care Unit. Indian J Crit Care Med 2015; 19:166-9. [PMID: 25810613 PMCID: PMC4366916 DOI: 10.4103/0972-5229.152760] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/03/2022] Open
Abstract
Dyselectrolytemia, especially hyponatremia is a common occurrence in hospitalized patients, and a number of dreaded complications arise out of the disorder itself and its treatment. Osmotic demyelination syndrome develops secondary to rapid correction of hyponatremia. As the disease is rare and available literature from Intensive Care Units are limited, we report our retrospective observation over 5 years. Overall incidence was 2.5% with altered sensorium and hypokalemia as most common symptom and associated factor respectively. Isolated pontine involvement was in 41% and combined pontine, and extra-pontine lesions were found in 23% of cases. All patients received supportive therapy; out of which 2 died and complete neurological recovery was seen in 24% of patients. Our findings suggest that a well organized supportive therapy and multidisciplinary approach is of more concern than many available therapeutic modalities which are still to be proved.
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Affiliation(s)
- Parnandi Bhaskar Rao
- Department of Anesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
| | - Afzal Azim
- Department of Critical Care Medicine, SGPGI, Lucknow, Uttar Pradesh, India
| | - Neha Singh
- Department of Anesthesiology, Critical Care and Pain Medicine, Institute of Medical Sciences and SUM Hospital, SOA University, Bhubaneswar, Odisha, India
| | | | - Anand Kumar
- Department of Critical Care Medicine, SGPGI, Lucknow, Uttar Pradesh, India
| | - Banani Poddar
- Department of Critical Care Medicine, SGPGI, Lucknow, Uttar Pradesh, India
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Osmotic demyelination syndrome as the initial manifestation of a hyperosmolar hyperglycemic state. Case Rep Neurol Med 2014; 2014:652523. [PMID: 25431711 PMCID: PMC4241748 DOI: 10.1155/2014/652523] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/11/2014] [Accepted: 10/15/2014] [Indexed: 11/18/2022] Open
Abstract
Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported. The aim of this study was to present and discuss previous cases and the pathophysiological mechanisms involved in ODS secondary to HHS. A 47-year-old man arrived to the emergency room due to generalized tonic-clonic seizures and altered mental status. The patient was lethargic and had a Glasgow coma scale of 11/15, muscle strength was 4/5 in both lower extremities, and deep tendon reflexes were diminished. Glucose was 838 mg/dL; serum sodium and venous blood gas analyses were normal. Urinary and plasma ketones were negative. Brain magnetic resonance revealed increased signal intensity on T2-weighted FLAIR images with restricted diffusion on the medulla and central pons. Supportive therapy was started and during the next 3 weeks the patient progressively regained consciousness and muscle strength and was able to feed himself. At 6-month follow-up, the patient was asymptomatic and MRI showed no residual damage. In conclusion, the association of ODS with HHS is extremely rare. The exact mechanism by which HHS produces ODS still needs to be elucidated, but we favor a rapid hypertonic insult as the most plausible mechanism.
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Romanovsky A, Azevedo LC, Meeberg G, Zibdawi R, Bigam D, Bagshaw SM. Serum sodium shift in hyponatremic patients undergoing liver transplantation: a retrospective cohort study. Ren Fail 2014; 37:37-44. [DOI: 10.3109/0886022x.2014.975102] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
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Ahmed A, Tschetter PA, Krasowski MD, Engelman A. Massive Ethylene Glycol Poisoning Triggers Osmotic Demyelination Syndrome. J Emerg Med 2014; 46:e69-74. [DOI: 10.1016/j.jemermed.2013.08.068] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/27/2013] [Revised: 06/02/2013] [Accepted: 08/15/2013] [Indexed: 11/30/2022]
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Wadhwa J, Ananthakrishnan R, Sadashiv S, Hamide A. Extrapontine myelinolysis: rare manifestation of a well-known disorder. BMJ Case Rep 2013; 2013:bcr-2013-200808. [PMID: 24265340 DOI: 10.1136/bcr-2013-200808] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/03/2022] Open
Affiliation(s)
- Jyoti Wadhwa
- Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry, India
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Morard I, Gasche Y, Kneteman M, Toso C, Mentha A, Meeberg G, Mentha G, Kneteman N, Giostra E. Identifying Risk Factors for Central Pontine and Extrapontine Myelinolysis After Liver Transplantation: A Case–Control Study. Neurocrit Care 2013; 20:287-95. [DOI: 10.1007/s12028-013-9928-9] [Citation(s) in RCA: 29] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
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Cui R, Fayek S, Rand EB, Feygin T, Khrichenko D, Shaked A. Central pontine myelinolysis: a case report and clinical-pathological review. Pediatr Transplant 2012; 16:E251-6. [PMID: 22023701 DOI: 10.1111/j.1399-3046.2011.01591.x] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
An 11-yr-old child presented with acute mental status changes and spastic quadriplegia after orthotopic liver transplantation. Magnetic resonance (MR) imaging findings were consistent with central pontine and EPM. Initial immunosuppression included tacrolimus, mycophenolate mofetil, and corticosteroids. Given that neurotoxicity is a well-established side effect of CNI, the patient was converted to rapamycin and subsequently experienced significant neurologic recovery. The temporal resolution of the patient's symptoms suggests that prompt recognition of central pontine and EPM and conversion from tacrolimus to rapamycin during the early post-operative course may have therapeutic benefits for patients undergoing pediatric transplant with CNI-related neurotoxicity.
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Affiliation(s)
- Rosa Cui
- Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA, USA.
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Feltracco P, Barbieri S, Furnari M, Milevoj M, Rizzi S, Galligioni H, Salvaterra F, Zanus G, Cillo U, Ori C. Central nervous system infectious complications early after liver transplantation. Transplant Proc 2010; 42:1216-22. [PMID: 20534265 DOI: 10.1016/j.transproceed.2010.03.108] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
Infectious complications contribute to significant patient morbidity and mortality in orthotopic liver transplant (OLT) recipients. Early central nervous system (CNS) involvement (within the first month after OLT) by infectious disease is essentially set off by aggressive surgical procedures, severe morbid conditions of the pretransplant period, initial graft dysfunction, permanence of intravascular catheters, and prolonged mechanical ventilation. The type and severity of CNS infection may be determined by many factors, such as posttransplant adverse events; prolonged or repeated surgery with massive intraoperative transfusions, net state of immunosuppression, recurrence of infections by immunomodulating viruses, and retransplantation. Bacteria, viruses, and fungi can spread to the CNS just as they affect the abdomen, blood stream, respiratory tract, urine, drainages, etc. Because immunosuppressive drugs may modify the clinical presentation of CNS infections, it is very important to maintain vigilance and attend to minor neurologic symptoms. Special attention should therefore be given to cerebral investigation in patients with prolonged pulmonary contamination, unresponsive fever, and heavy corticosteroid therapy, primarily when they became disoriented, develop seizures, or exhibit focal neurologic signs. Clinical response to medical therapy may sometimes be poor because of chronic encapsulation of the pathogen, development of resistance, and/or catastrophic hemorrhagic complications.
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Affiliation(s)
- P Feltracco
- Department of Pharmacology and Anesthesiology, University Hospital of Padova, Italy.
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Abstract
The osmotic demyelination syndrome (ODS) has been a recognized complication of the rapid correction of hyponatremia for decades. However, in recent years, a variety of other medical conditions have been associated with the development of ODS, independent of changes in serum sodium. This finding suggests that the pathogenesis of ODS may be more complex and involve the inability of brain cells to respond to rapid changes in osmolality of the interstitial (extracellular) compartment of the brain, leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas. Features of the syndrome include quadriparesis and neurocognitive changes in the presence of characteristic lesions found on magnetic resonance imaging of the brain. Although slow correction of hyponatremia seems to be the best way to prevent development of the syndrome, there are new data that suggest reintroduction of hyponatremia in those patients who have undergone inadvertent rapid correction of the serum sodium and corticosteroids may play a role in prevention of ODS.
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Norenberg MD. Central pontine myelinolysis: historical and mechanistic considerations. Metab Brain Dis 2010; 25:97-106. [PMID: 20182780 DOI: 10.1007/s11011-010-9175-0] [Citation(s) in RCA: 58] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/18/2009] [Accepted: 01/28/2010] [Indexed: 02/06/2023]
Abstract
Central pontine myelinolysis (CPM) is a demyelinating condition affecting not only the pontine base, but also involving other brain areas. It usually occurs on a background of chronic systemic illness, and is commonly observed in individuals with alcoholism, malnutrition and liver disease. Studies carried out 25-30 years ago established that the principal etiological factor was the rapid correction of hyponatremia resulting in osmotic stress. This article reviews progress achieved since that time on its pathogenesis, focusing on the role of organic osmolytes, the blood-brain, barrier, endothelial cells, myelinotoxic factors triggered by osmotic stress, and the role of various factors that predispose to the development of CPM. These advances show great promise in providing novel therapeutic options for the management of patients afflicted with CPM.
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Affiliation(s)
- Michael D Norenberg
- Departments of Pathology, University of Miami School of Medicine, PO Box 016960, Miami, FL 33101, USA.
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21
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Infections associated with neutropenia and transplantation. ANTIBIOTIC AND CHEMOTHERAPY 2010. [PMCID: PMC7148738 DOI: 10.1016/b978-0-7020-4064-1.00040-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
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An JY, Park SK, Han SR, Song IU. Central pontine and extrapontine myelinolysis that developed during alcohol withdrawal, without hyponatremia, in a chronic alcoholic. Intern Med 2010; 49:615-8. [PMID: 20228603 DOI: 10.2169/internalmedicine.49.3069] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open
Abstract
Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are osmotic demyelination syndrome. A 45-year-old man with a history of alcoholism visited the ER with dysarthria and dysphagia for 2 days. These symptoms occurred 3 days after he had stopped drinking alcohol. The neurological symptoms progressed to anarthria, pseudobulbar palsy and gait disturbance. During admission, the electrolyte studies were within the normal range. Diffusion-weighted images revealed high signal intensities in the pons, thalamus and basal ganglia. Apparent diffusion coefficient image showed low signal intensities in the pontine lesion, but isosignal intensities in the extrapontine lesion. The symptoms gradually improved after 1 month with only conservative treatment. The 1 month-follow-up MRI showed significant reduction of the previous extrapontine lesions. These findings suggest that cytotoxic edema is central to the pathogenesis of CPM, but vasogenic edema plays an important role in the pathogenesis of EPM occurring during alcohol withdrawal.
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Affiliation(s)
- Jae Young An
- Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
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23
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Donmez FY, Guvenc Z, Emiroglu FK, Coskun M, Haberal M. Evaluation of neurological complications in pediatric liver transplant recipients: MRI versus CT. J Child Neurol 2009; 24:656-63. [PMID: 19168829 DOI: 10.1177/0883073808329531] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/17/2022]
Abstract
With the aim of guiding choice of the best imaging modality for specific clinical conditions, we retrospectively evaluated neuroradiological findings in pediatric liver transplant recipients with neurological complications. Computed tomography (CT) was used to examine 31 patients with acute neurological symptoms after liver transplantation, and magnetic resonance imaging (MRI) was used for 35 such patients. A total of 16 patients belonged to both groups. Headache was the most common symptom in patients with computed tomography; seizure was most common among patients with magnetic resonance imaging. Magnetic resonance imaging detected additional abnormalities in 5 patients presenting with seizures whose computed tomography results were normal or insufficient to explain the clinical picture. In conclusion, liver transplant recipients with seizure should undergo magnetic resonance imaging emergently when possible; omitting computed tomography. Choice of imaging modality should be directed by nature of symptoms and time interval between transplantation and symptom onset.
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24
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O'Malley G, Moran C, Draman MS, King T, Smith D, Thompson CJ, Agha A. Central pontine myelinolysis complicating treatment of the hyperglycaemic hyperosmolar state. Ann Clin Biochem 2008; 45:440-3. [PMID: 18583636 DOI: 10.1258/acb.2008.007171] [Citation(s) in RCA: 41] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022]
Abstract
Central pontine myelinolysis (CPM) is well recognized to occur in a variety of clinical settings, but particularly following rapid correction of severe hyponatraemia. The development of CPM as a result of rapid shifts in plasma osmolality during the treatment of the hyperglycaemic hyperosmolar state (HHS) has hitherto been described in only one case. We report a second case in which this complication occurred in association with treatment of the HHS. The patient was a 49-year-old woman who presented to another hospital with drowsiness and a plasma glucose of 106 mmol/L. Her admission plasma sodium was 135 mmol/L. She received treatment with intravenous insulin and 0.9% normal saline, and there was a rapid drop in plasma glucose by 60 mmol/L within 6 h, which was associated with a rebound rise of plasma sodium to 159 mmol/L. Her plasma glucose and sodium were later stabilized. When the patient was transferred to our hospital a few days later, she was noted to have flaccid quadraparesis and pseudobulbar palsy. A magnetic resonance imaging scan revealed a pontine lesion consistent with CPM. She made a gradual recovery over several months with intensive rehabilitation and eventually returned to near normal functional capacity. This is the second case report in the literature of CPM complicating the management of HHS and highlights the importance of the judicious and measured correction of hyperglycaemia and the appropriate management of fluid replacement and electrolyte balance when treating this condition.
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Affiliation(s)
- Grainne O'Malley
- Division of Endocrinology and Diabetes, Beaumont Hospital, Dublin, Ireland
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25
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Lim KH, Kim S, Lee YS, Kim KH, Kim J, Rhee JY, Kim HJ, Yi HG, Oh SY, Lim JH, Han SW, Lee S, Kim I, Yoon SS, Park S, Kim BK. Central pontine myelinolysis in a patient with acute lymphoblastic leukemia after hematopoietic stem cell transplantation: a case report. J Korean Med Sci 2008; 23:324-7. [PMID: 18437020 PMCID: PMC2526450 DOI: 10.3346/jkms.2008.23.2.324] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
Abstract
We describe a 37-yr-old man who developed central pontine myelinolysis (CPM) after allogeneic hematopoietic stem cell transplantation (HSCT) for acute lymphoblastic leukemia. After HSCT, desquamation developed on the whole body accompanied by hyperbilirubinemia. The liver biopsy of the patient indicated graft-versus-host disease- related liver disease, and the dose of methylprednisolone was increased. Then, the patient developed altered mentality with eye ball deviation to the left, for which electroencephalogram and magnetic resonance imaging (MRI) scans were done. Brain MRI scan demonstrated the imaging findings consistent with central pontine myelinolysis and extrapontine myelinolysis. He did not have any hyponatremia episode during hospitalization prior to the MRI scan. To the best of our knowledge, presentation of CPM after allogeneic HSCT is extremely rare in cases where patients have not exhibited any episodes of significant hyponatremia. We report a rare case in which hepatic dysfunction due to graft-versus-host disease has a strong association with CPM after HSCT.
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Affiliation(s)
- Kyu-Hyoung Lim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Sunyoung Kim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Yoon-Su Lee
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Ki Hwan Kim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Jinwon Kim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Ji young Rhee
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Hye Jin Kim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Hyeon Gyu Yi
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - So Yeon Oh
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Joo Han Lim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Sae-Won Han
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Sangyoon Lee
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Inho Kim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Sung-Soo Yoon
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Seonyang Park
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Byoung Kook Kim
- Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
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26
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Snell DM, Bartley C. Osmotic demyelination syndrome following rapid correction of hyponatraemia. Anaesthesia 2007; 63:92-5. [DOI: 10.1111/j.1365-2044.2007.05341.x] [Citation(s) in RCA: 32] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
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27
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Dawwas MF, Lewsey JD, Neuberger JM, Gimson AE. The impact of serum sodium concentration on mortality after liver transplantation: a cohort multicenter study. Liver Transpl 2007; 13:1115-24. [PMID: 17663412 DOI: 10.1002/lt.21154] [Citation(s) in RCA: 90] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
Abstract
Modification of the current allocation system for donor livers in the United States to incorporate recipient serum sodium concentration ([Na]) has recently been proposed. However, the impact of this parameter on posttransplantation mortality has not been previously examined in a large risk-adjusted analysis. We assessed the effect of recipient [Na] on the survival of all adults with chronic liver disease who received a first single organ liver transplant in the UK and Ireland during the period March 1, 1994 to March 31, 2005 (n=5,152) at 3 years, during the first 90 days, and beyond the first 90 days, adjusting for a wide range of recipient, donor, and graft characteristics. Compared to those with normal [Na] (135-145 meq/L; n=3,066), severely hyponatremic recipients ([Na]<130 meq/L, n=541), had a higher risk-adjusted mortality at 3 years (hazard ratio [HR] 1.28; 95% confidence interval [CI], 1.04-1.59; P<0.02). The excess mortality was, however, confined to the first 90 days (HR 1.55; 95% CI, 1.18-2.04; P<0.002) with no significant difference thereafter. This was also true for hypernatremic recipients ([Na]>45 meq/L, n=81), who had an even greater risk-adjusted mortality compared to normonatremic recipients (overall: HR 1.85; 95% CI, 1.25-2.73; P<0.002; <or=90 days: HR 2.29; 95% CI, 1.42-3.70; P<0.001; >90 days: HR 1.12; 95% CI, 0.55-2.29; P=0.8), whereas mildly hyponatremic recipients ([Na] 130-134 meq/L, n=1,127) had similar risk-adjusted mortality to those with normal [Na] at the same time points. In conclusion, recipient [Na] is an independent predictor of death following liver transplantation. Attempts to correct the [Na] toward the normal reference range are an important aspect of pretransplantation management.
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Affiliation(s)
- Muhammad F Dawwas
- Hepatobiliary and Liver Transplant Unit, Addenbrooke's Hospital, Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK.
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28
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Huq S, Wong M, Chan H, Crimmins D. Osmotic demyelination syndromes: Central and extrapontine myelinolysis. J Clin Neurosci 2007; 14:684-8. [PMID: 17462902 DOI: 10.1016/j.jocn.2006.02.015] [Citation(s) in RCA: 38] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2005] [Revised: 02/17/2006] [Accepted: 02/21/2006] [Indexed: 11/16/2022]
Abstract
Osmotic demyelination syndromes are often progressive disorders, with clinical features ranging from a mild tremor or dysarthria to a progressive quadraparesis. Although rapid correction of serum sodium is known to be a potent causative factor, additional pathogenic factors exist, which appear critical in predisposing pontine and extrapontine glia to osmotic stress. Interestingly, several cases of osmotic demyelination have emerged where serum sodium was found to be within normal limits and minimal or no correction of a hypo or hypernatraemic state was implemented. We describe two cases--one of extra pontine and another of central-pontine myelinolysis, both of which have occurred in the context of relatively normal serum sodium. The first case illustrates the association of extrapontine myelinolysis with the traditional risk factor of alcoholic cirrhosis and intravenous fluid resuscitation, while the second, more unusual case, describes a patient who developed central pontine myelinolysis possibly in association with alpha interferon therapy.
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Affiliation(s)
- S Huq
- Department of Neurology, Gosford District Hospital and Royal North Shore Hospitals, Pacific Highway, St Leonards, NSW 2065, Australia.
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29
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Rossi M, Mennini G, Lai Q, Ginanni Corradini S, Drudi F, Pugliese F, Berloco P. Liver transplantation(). J Ultrasound 2007; 10:28-45. [PMID: 23396075 PMCID: PMC3478701 DOI: 10.1016/j.jus.2007.02.006] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
Orthotopic liver transplantation (OLT) involves the substitution of a diseased native liver with a normal liver (or part of one) taken from a deceased or living donor. Considered an experimental procedure through the 1980s, OLT is now regarded as the treatment of choice for a number of otherwise irreversible forms of acute and chronic liver disease.The first human liver transplantation was performed in the United States in 1963 by Prof. T.E. Starzl of the University of Colorado. The first OLT to be performed in Italy was done in 1982 by Prof. R. Cortesini. The procedure was successfully performed at the Policlinico Umberto I of the University of Rome (La Sapienza).The paper reports the indications for liver transplantation, donor selection and organ allocation in our experience, surgical technique, immunosuppression, complications and results of liver transplantation in our center.
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Affiliation(s)
- M. Rossi
- Department of General Surgery and Transplantation “P. Stefanini”, University “La Sapienza”, Rome, Italy
| | - G. Mennini
- Department of General Surgery and Transplantation “P. Stefanini”, University “La Sapienza”, Rome, Italy
| | - Q. Lai
- Department of General Surgery and Transplantation “P. Stefanini”, University “La Sapienza”, Rome, Italy
| | - S. Ginanni Corradini
- Department of Clinical Medicine, Division of Gastroenterology, University “La Sapienza”, Rome, Italy
| | - F.M. Drudi
- Department of Radiology, University “La Sapienza”, Rome, Italy
| | - F. Pugliese
- Department of Anesthesiology, Critical Care Medicine, and the Treatment of Pain, University “La Sapienza”, Rome, Italy
| | - P.B. Berloco
- Department of General Surgery and Transplantation “P. Stefanini”, University “La Sapienza”, Rome, Italy
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30
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Diagnosis: Osmotic myelinolysis (central pontine myelinolysis and extrapontine myelinolysis). Ann Saudi Med 2007; 27:308-311. [PMCID: PMC6074296 DOI: 10.5144/0256-4947.2007.308] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 02/01/2007] [Indexed: 12/01/2023] Open
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31
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Guarino M, Benito-Leon J, Decruyenaere J, Schmutzhard E, Weissenborn K, Stracciari A. EFNS guidelines on management of neurological problems in liver transplantation. Eur J Neurol 2006; 13:2-9. [PMID: 16420387 DOI: 10.1111/j.1468-1331.2006.01353.x] [Citation(s) in RCA: 47] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
Neurological impairment after orthotopic liver transplantation (OLT) is common and represents a major source of morbidity and mortality. The diagnosis and management of neurological problems occurring after OLT are difficult and evidence-based guidelines for this task are currently lacking. A Task Force was set up under the auspices of the European Federation of Neurological Societies to devise guidelines to prevent and manage neurological problems in OLT. We selected six major neurological problems and approached them combining an evidence-based scientific literature analysis with a search of consensus by means of a Delphi process. Search results were translated into a series of recommendations constituting a basis for better care of patients with neurological complications after OLT.
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Affiliation(s)
- M Guarino
- Neurology Unit, S. Orsola-Malpighi University Hospital, Bologna, Italy
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32
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Kleinschmidt-Demasters BK, Rojiani AM, Filley CM. Central and Extrapontine Myelinolysis: Then…and Now. J Neuropathol Exp Neurol 2006; 65:1-11. [PMID: 16410743 DOI: 10.1097/01.jnen.0000196131.72302.68] [Citation(s) in RCA: 106] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022] Open
Abstract
In this review, we emphasize neuropathologic and neurobehavioral aspects of central pontine and extrapontine myelinolysis (CPM/EPM), also known as the osmotic demyelination syndrome. The literature is reviewed from the time of the initial report in 1959 and from key developments that have occurred more recently. Particular consideration is given to pathogenic mechanisms as revealed by recent animal studies. The role of white matter pathology in neurobehavioral dysfunction is also considered. The "then" and "now" of CPM and EPM tell 2 different stories. Yet, in many respects, this expansion of information over the past nearly 50 years simply represents a continuum, as well as recognition, of the vast gaps that still persist in our understanding of this disorder.
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33
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Deleu D, Salim K, Mesraoua B, El Siddig A, Al Hail H, Hanssens Y. “Man-in-the-barrel” syndrome as delayed manifestation of extrapontine and central pontine myelinolysis: Beneficial effect of intravenous immunoglobulin. J Neurol Sci 2005; 237:103-6. [PMID: 15975595 DOI: 10.1016/j.jns.2005.05.012] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/14/2005] [Accepted: 05/23/2005] [Indexed: 01/18/2023]
Abstract
"Man-in-the-barrel" syndrome has been rarely described following osmotic myelinolysis. We report a case of a 45-year-old woman admitted with septicemia and severe hyponatremia. She presented with a "man-in-the-barrel" syndrome which developed more than 10 days after rapid correction of the hyponatremia. There was radiological evidence of central pontine and extrapontine myelinolysis. Three days after completing a course of intravenous immunoglobulin therapy (0.4 g/kg body weight/day for 5 days) there was considerable improvement (Expanded Disability Status Scale score improved 30%). This case, reported for its peculiar mode of development, unusual presentation and challenging therapeutic response to intravenous immunoglobulin, highlights the enigmatic and unpredictable aspects of osmotic myelinolysis.
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Affiliation(s)
- Dirk Deleu
- Department of Medicine (Neurology), Hamad Medical Corporation, P.O. Box 3050, Doha, State of Qatar.
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34
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Fraser C, Charnas L, Orchard P. Central pontine myelinolysis following bone marrow transplantation complicated by severe hepatic veno-occlusive disease. Bone Marrow Transplant 2005; 36:733-4. [PMID: 16044132 DOI: 10.1038/sj.bmt.1705115] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]
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35
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Marchiori PE, Lino AM, Britto N, Bacchella T, Machado MC, Mies S, Massarollo P, Scaff M. Neuropsychiatric complications due to organ transplantation: a survey of 1499 Brazilian patients at a single center in São Paulo, Brazil. Transplant Rev (Orlando) 2005. [DOI: 10.1016/j.trre.2005.06.002] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]
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36
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Yu J, Zheng SS, Liang TB, Shen Y, Wang WL, Ke QH. Possible causes of central pontine myelinolysis after liver transplantation. World J Gastroenterol 2004; 10:2540-3. [PMID: 15300900 PMCID: PMC4572157 DOI: 10.3748/wjg.v10.i17.2540] [Citation(s) in RCA: 59] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
AIM: To sum up the clinical characteristics of patients with central pontine myelinolysis (CPM) after orthotopic liver transplantation (OLT) and to document the possible causes of CPM.
METHODS: Data of 142 patients undergoing OLT between January 1999 to May 2003 were analyzed retrospectively. Following risk factors during perioperation were analyzed in patients with and without CPM: primary liver disease, preoperative serum sodium level, magnesium level and plasma osmolality, fluctuation degree of serum sodium concentration, and immunosuppressive drug level, etc.
RESULTS: A total of 13 (9.2%) neurologic symptoms appeared in 142 patients post-operation including 5 cases (3.5%) with CPM and 8 cases (5.6%) with cerebral hemorrhage or infarct. Two patients developing CPM after OLT had a hyponatremia history before operation (serum sodium < 130 mmol/L), their mean serum sodium level was 130.6 ± 5.54 mmol/L. The serum sodium level was significantly lower in CPM patients than in patients without neurologic complications or with cerebral hemorrhage/infarct (P < 0.05).The increase in serum sodiumduring perioperative 48 h after OLT in patients with CPM was significantly greater than that in patients with cerebral hemorrhage/infarct but without neurologic complications (19.5 ± 6.54 mmol/L, 10.1 ± 6.43 mmol/L, 4.5 ± 4.34 mmol/L, respectively, P < 0.05). Plasma osmolality was greatly increased postoperation in patients with CPM. Hypomagnesemia was noted in all patients perioperation, but there were no significant differences between groups. The duration of operation on patients with CPM was longer than that on others (492 ± 190.05 min, P < 0.05). Cyclosporin A (CsA) levels were normal in all patients, but there were significant differences between patients with or without neurologic complications (P < 0.05).
CONCLUSION: CPM may be more prevalent following liver transplantation. Although the diagnosis of CPM after OLT can be made by overall neurologic evaluations including magnetic resonance imaging (MRI) of the head, the mortality is still very high. The occurance of CPM may be associated with such factors as hyponatremia, rapid rise of serum sodium concentration, plasma osmolality increase postoperation, the duration of operation, and high CsA levels.
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Affiliation(s)
- Jun Yu
- Department of Hepatobiliary Surgery, the First Affiliated Hospital, Medical School of Zhejiang University,Hangzhou 310003, Zhejiang Province, China
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37
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Baddley JW, Salzman D, Pappas PG. Fungal brain abscess in transplant recipients: epidemiologic, microbiologic, and clinical features. Clin Transplant 2002; 16:419-24. [PMID: 12437621 DOI: 10.1034/j.1399-0012.2002.02033.x] [Citation(s) in RCA: 64] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
Fungal brain abscess is an unusual but serious complication associated with solid organ and hematopoietic stem cell transplantation. To examine the epidemiology and clinical features of fungal brain abscess in transplant recipients, we reviewed retrospectively all cases of fungal brain abscess diagnosed during a 3-yr period among 1,620 adult patients who underwent allogeneic or autologous stem cell, liver, heart, lung, or renal transplantation at one institution. Seventeen cases of fungal brain abscess were identified and occurred a median of 140 d post-transplantation. Fungal brain abscess was more common among allogeneic stem cell transplant recipients (p < 0.01). Aspergillus species were most commonly isolated, but unusual, opportunistic molds were also identified. Altered mental status was present in 65% of patients, and multiple brain lesions were commonly seen on imaging studies. Although fungal brain abscess is an uncommon disease in this population, outcome was poor, suggesting that early recognition of this disease might be helpful.
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Affiliation(s)
- John W Baddley
- Department of Medicine, Division of Infectious Diseases, University of Alabama at Birmingham, 35294-0006, USA.
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38
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Germiniani FMB, Roriz M, Nabhan SK, Teive HAG, Werneck LC. [Central pontine and extra-pontine myelinolysis in an alcoholic patient without hydro-electrolyte disturbances: case report]. ARQUIVOS DE NEURO-PSIQUIATRIA 2002; 60:1030-3. [PMID: 12563402 DOI: 10.1590/s0004-282x2002000600028] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
Central pontine myelinolysis (CPM) and extra-pontine myelinolysis (EPM) are different presentations of a demyelinating disorder of the brain more commonly associated with rapid correction of hyponatremia, spastic tetraparesia and pseudo-bulbar palsy. There are in the literature a few cases of CPM/EPM in patients without electrolyte disturbances. We report the case of a 39 year-old man with severe alcoholism, who presented with spastic tetraparesis and palsy of several cranial nerves, associated with lesions in the magnetic resonance compatible with CPM/EPM. The patient had a good follow-up after pulse therapy with corticosteroids.
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Affiliation(s)
- Francisco Manoel B Germiniani
- Serviço de Neurologia, Departamento de Clinica Medica, Hospital de Clinicas da Universidade Federal do Parana, Curitiba, PR, Brasil
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39
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Abstract
One of the well recognized stimuli for central pontine myelinosis (CPM) is the rapid correction of chronic hyponatraemia. Conventionally this has been perceived to lead to pontine glial cell swelling through osmosis and eventually to cell death. However, although a purely osmotic argument has been central to any patho-physiological understanding of CPM, there are deficiencies in this approach that do not account for why certain individuals develop CPM with relatively mild osmotic insults. Here we review the varying aetiologies of CPM and propose a novel hypothesis for CPM causation by suggesting that individuals predisposed to CPM have inadequate energy provision as well as other factors that result in a pro-apoptotic drive, which renders them susceptible to brain injury from diverse causes. In CPM, the precipitant of brain injury appears to be osmotic stress. Furthermore, this model suggests a number of therapeutic interventions that may prevent or at least mitigate the consequences of CPM.
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Affiliation(s)
- H Ashrafian
- Nuffield Department of Medicine, Oxford University, The John Radcliffe Hospital, Headington, UK
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40
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Abstract
Central nervous system (CNS) infections, accounting for 4-29% of CNS lesions in transplant recipients, are a significant post-transplant complication. Focal CNS infectious lesions or brain abscesses have been documented in 0.36-1% of the transplant recipients. Mycelial fungi, particularly Aspergillus, are by far the most frequent etiologies of post-transplant brain abscesses. Bacteria, with the exception of Nocardia, are rarely associated with brain abscesses in transplant recipients. Time of onset and concurrent extraneural lesions have implications relevant towards invasive diagnostic procedures in transplant recipients with brain abscesses. Meningoencephalitis in transplant recipients is predominantly due to viruses, e.g., herpesviruses, and less frequently due to Listeria monocytogenes, Toxoplasma gondii, and Cryptococcus. Despite a wide, and at times perplexing array of opportunistic pathogens that can cause CNS infections, the temporal association of the infection with the time elapsed since transplantation, risk factors, clinical manifestations, and neuroimaging characteristics of the lesion can allow a reasoned and rational approach towards the recognition, diagnosis, and appropriate management of CNS infections in transplant recipients.
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Affiliation(s)
- N Singh
- VA Medical Center and University of Pittsburgh, Thomas E. Starzl Transplantation Institute, Pittsburgh, Pennsylvania 15240, USA. nis5+@pitt.edu
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41
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Abstract
Many liver transplant recipients are now reaching survival beyond 5 years from the liver transplant procedure, and many others are alive more than a decade from acquiring their new liver. Orthotopic liver transplant recipients enjoy the benefits of normal liver function, but a variety of metabolic and other medical problems often develop that require diagnosis and adequate management. These problems include hyperlipidemia, obesity, diabetes mellitus, renal disfunction, arterial hypertension, bone disease and neuropsychiatric syndromes. The gastroenterologist, internist, or local family physician is frequently called on to identify and treat these postoperative complications in conjunction with physicians at the transplant center.
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Affiliation(s)
- S J Munoz
- Division of Hepatology, Department of Medicine, Albert Einstein Medical Center Philadelphia, Pennsylvania, USA.
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42
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Singh N, Paterson DL. Encephalitis caused by human herpesvirus-6 in transplant recipients: relevance of a novel neurotropic virus. Transplantation 2000; 69:2474-9. [PMID: 10910264 DOI: 10.1097/00007890-200006270-00002] [Citation(s) in RCA: 105] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
BACKGROUND Human herpesvirus-6 (HHV-6) is a neurotropic virus. Encephalitis is a significant clinical manifestation of HHV-6; however, sparse data on this entity exist in transplant recipients. METHODS Cases of HHV-6 encephalitis reported in the literature (13 bone marrow transplant recipients and 1 liver transplant recipient) were reviewed. The diagnosis was established in all by viral isolation and/or detection of HHV-6 DNA in the cerebrospinal fluid by polymerase chain reaction or histopathologic method. RESULTS HHV-6 encephalitis occurred a median of 45 days (range 10 days to 15 months) after transplantation. Mental status changes, ranging from confusion to coma (92%), seizures (25%), and headache (25%) were the predominant clinical presentations. Focal neurologic findings occurred in only 17% of the patients. Twenty-five percent of the patients had fever; however, the height of fever (< or =40 degrees C) in febrile patients was striking. Cerebrospinal fluid pleocytosis was generally lacking. Abnormal neuroimaging findings, characterized by low-attenuation lesions in the posterior cerebral lobes, were present only in 17% of the patients. Overall mortality in patients with HHV-6 encephalitis was 58% (7 of 12); 42% (5 of 12) of the deaths were caused by HHV-6. Cure was documented in 7 of 8 patients who received ganciclovir or foscarnet for > or =7 days, compared with 0% (0 of 4) in those who did not receive these drugs or received them for < 7 days (P=.01). CONCLUSIONS HHV-6 may be associated with encephalitis after transplantation and warrants consideration in transplant recipients with encephalitis of unidentifiable etiology.
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Affiliation(s)
- N Singh
- Veterans Affairs Medical Center and University of Pittsburgh, Thomas E Starzl Transplantation Center, Pennsylvania, USA. nis5+@pitt.edu
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Vecino MC, Cantisani G, Zanotelli ML, Marroni CA, Brandão AB, Cassal AP, Perla AD, Freitas DM. [Neurologic disorders in patients submitted to liver transplantation: analysis of 30 consecutive cases]. ARQUIVOS DE NEURO-PSIQUIATRIA 2000; 58:304-9. [PMID: 10849632 DOI: 10.1590/s0004-282x2000000200017] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
Neurologic complications are important source of morbi-mortality, in liver transplantation. They result from previous factors, alterations during the surgical procedure, effects from immunosuppressor drugs, coagulopathy and infections. We analyzed, retrospectively, the chronology, causes, and frequencies of neurologic alterations in thirty adult patients submitted to liver transplantation, and our results differ slightly from those registered in other series.
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Affiliation(s)
- M C Vecino
- Equipe de Transplante Hepático, Hospital São Francisco, Irmandade da Santa Casa de Misericórdia de Porto Alegre, RS, Brasil.
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Bronster DJ, Emre S, Boccagni P, Sheiner PA, Schwartz ME, Miller CM. Central nervous system complications in liver transplant recipients--incidence, timing, and long-term follow-up. Clin Transplant 2000; 14:1-7. [PMID: 10693627 DOI: 10.1034/j.1399-0012.2000.140101.x] [Citation(s) in RCA: 150] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
BACKGROUND Neurological impairment is a major source of morbidity and mortality following orthotopic liver transplantation (OLT). We reviewed our experience with neurologic complications among our first 463 consecutive adult OLT recipients. METHODS Between September 1988 and October 1993, 463 adult patients underwent OLT. Data on incidence, time of onset, and outcome of central nervous system (CNS) complications was obtained from patient charts, including autopsy results when available. CNS complications were classified by clinical presentation and by etiology. RESULTS 93 patients (20.1%) had CNS complications following OLT. Encephalopathy (11.8%) and seizure (8.2%) were the leading complications. The incidence of immunosuppressive drug-related complications was 5.6%; coma, 1.7%; cerebral hemorrhage, 1.5%; central pontine myelinolysis (CPM), 1.2%; stroke, 0.6%; and primary CNS lymphoma, 0.2%. Most CNS events (80%) were encountered in the first month after OLT. In the majority of cases, encephalopathy (70%) and seizure (50%) presented in the first 2 wk. Although most CNS infections occurred early, 2 patients developed tuberculous meningitis more than 1 yr post-OLT. In 12 patients, death was directly related to CNS complications (2.6%). CONCLUSIONS Most CNS complications occur early following OLT but may be seen even after 1 yr. Patients may survive serious neurologic events, such as cerebral hemorrhage, CPM, and meningitis.
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Affiliation(s)
- D J Bronster
- Department of Neurology, The Mount Sinai Medical Center, New York, NY, USA
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Vecino MC, Cantisani G, Zanotelli ML, Marrone CA, Brandão AB, Cassal AP, Perla AS, Freitas DM. Neurological complications in liver transplantation. Transplant Proc 1999; 31:3048-9. [PMID: 10578388 DOI: 10.1016/s0041-1345(99)00665-x] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
Affiliation(s)
- M C Vecino
- Liver Transplantation Group, Hospital São Francisco, Irmandadeda Santa Casa de Misericórdia de Porto Alegre, Rio Grande do Sul, Brasil
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Mazariegos GV, Molmenti EP, Kramer DJ. Early complications after orthotopic liver transplantation. Surg Clin North Am 1999; 79:109-29. [PMID: 10073184 DOI: 10.1016/s0039-6109(05)70009-8] [Citation(s) in RCA: 44] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]
Abstract
The cost and impact of early post-transplant complications continue to be high. Diagnosis and management involves a high index of suspicion, rapid diagnostic and therapeutic interventions, and elimination of technical problems. Preoperative assessment of the donor and recipient medical condition and meticulous attention to detail during the technical performance of OLTx are the mainstays in achieving a good outcome.
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Affiliation(s)
- G V Mazariegos
- Thomas E. Starzl Transplantation Institute, Pittsburgh, Pennsylvania, USA.
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Bonham CA, Dominguez EA, Fukui MB, Paterson DL, Pankey GA, Wagener MM, Fung JJ, Singh N. Central nervous system lesions in liver transplant recipients: prospective assessment of indications for biopsy and implications for management. Transplantation 1998; 66:1596-604. [PMID: 9884245 DOI: 10.1097/00007890-199812270-00005] [Citation(s) in RCA: 69] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
BACKGROUND Precise diagnosis of central nervous system (CNS) lesions in liver transplant recipients remains problematic. Brain biopsies are often not feasible as a result of coagulopathy. We sought to determine whether selected clinical or radiologic characteristics can predict the likely etiology of CNS lesions in liver transplant recipients and thus obviate the need for diagnostic brain biopsies. METHODS A 4-year prospective, observational, cohort study was conducted at liver transplant centers at four geographically diverse medical institutions. A total of 1730 consecutive liver transplant recipients were evaluated for CNS lesions; 60 patients with radiologically documented CNS lesions comprised the study sample. RESULTS Vascular events (52%, 31/60), infections (181%, 11/60), immunosuppressive associated leukoencephalopathy (12%, 7/60), central pontine myelinolysis (8%, 5/60), and malignancy (3%, 2/60) were the predominant etiologies of CNS lesions. CNS lesions were most likely to occur within 30 days of transplantation (43%, 26/60); central pontine myelinolysis, subdural hematoma, acute infarcts, and Aspergillus brain abscesses were the predominant etiologies during this time. All brain abscesses were fungal; 73% (8/11) of these patients concurrently had documented extraneural (pulmonary) infection as a result of the same fungal pathogen. Thus, a diagnostic brain biopsy is not warranted in these patients. Patients on dialysis were more likely to have ischemic or infectious CNS lesions (P=0.03). Vascular events were more likely to occur in repeat transplant recipients (P=0.03). Twenty-five percent (15/60) of the CNS lesions occurred more than 1 year after transplantation; small vessel ischemic lesions, malignancy, or non-Aspergillus fungal brain abscesses accounted for all such lesions. CONCLUSIONS A presumptive etiologic diagnosis can be established in a vast majority of CNS lesions in liver transplant recipients based on identifiable presentation that includes time of onset, unique risk factors, and neuroimaging characteristics. Empiric therapy of brain abscesses in liver transplant recipients should include antifungal and not antibacterial agents.
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Affiliation(s)
- C A Bonham
- University of Pittsburgh, Thomas E. Starzl Transplantation Institute, Pennsylvania, USA
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Abstract
Hyponatremia is the most common electrolyte abnormality among hospitalized patients. Death or brain damage associated with hyponatremia has been described since 1935, and it is now evident that hyponatremia can lead to death in otherwise healthy individuals. In the past, it had been assumed that the likelihood of brain damage from hyponatremia was directly related to either a rapid decline in plasma sodium or a particularly low level of plasma sodium. Recent studies have demonstrated that other factors may be more important. These factors include the age and gender of the individual, with children and menstruant women the most susceptible. Although many clinical settings are associated with hyponatremia, those most often associated with brain damage are postoperative, polydipsia, pharmacological agents, and heart failure. Morbidity and mortality associated with hyponatremia are primarily a result of brain edema, hypoxemia, and associated hormonal factors. Management of hyponatremia is largely determined by symptomatology. If the patient is asymptomatic, discontinuation of drugs plus water restriction is often sufficient. If the patient is symptomatic, active therapy to increase the plasma sodium with hypertonic NaCl is usually indicated. Although inappropriate therapy of hyponatremia can lead to brain damage, such an occurrence is rare. Thus, the risk of not treating a symptomatic patient for exceeds that of improper therapy.
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Affiliation(s)
- C L Fraser
- Department of Medicine, San Francisco VA Medical Center, University of California School of Medicine 94121, USA
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Vaughn BV, Ali II, Olivier KN, Lackner RP, Robertson KR, Messenheimer JA, Paradowski LJ, Egan TM. Seizures in lung transplant recipients. Epilepsia 1996; 37:1175-9. [PMID: 8956848 DOI: 10.1111/j.1528-1157.1996.tb00549.x] [Citation(s) in RCA: 42] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
PURPOSE We wished to assess organ transplant recipients, who incur a significant risk for seizures. METHOD We reviewed 85 lung transplants performed in 81 patients at the University of North Carolina hospitals between 1991 and 1994. All patients were reviewed for age, reason for transplant, detailed description of seizures, neurological examination, medications, and laboratory results, including cyclosporine level, EEG, and brain imaging. RESULTS Eighteen of 81 (22%) patients experienced seizures. Patients aged < 25 years had the greatest risk of seizures and 15 of the 18 patients had cystic fibrosis. Sixteen of the 18 (89%) patients, by history, had partial-onset seizures. Eleven of the 18 (61%) patients had seizures < or = 10 days after initiation of intravenous methylprednisolone for allograft rejection. Two patients had seizures associated with sustained hypertension: 1 of these patients was simultaneously being treated for rejection. Four patients had strokes (1 before transplant) and seizures. Two patients were receiving imipenem. Magnetic resonance imaging (MRI) of the brain demonstrated areas of increased T2 signal in 8 of 9 patients. CONCLUSIONS Our findings demonstrate multiple etiologies for seizures in our transplant recipients. However, we believe that patients, especially those aged < 25 years, being treated with intravenous methylprednisolone for rejection may be at increased risk of seizures. We hypothesize that the focal loss of blood-brain barrier (BBB) may play a significant role in the development of partial seizures in lung transplant recipients.
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Affiliation(s)
- B V Vaughn
- Department of Neurology, University of North Carolina at Chapel Hill, 27599-7025, USA
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