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Arterial ammonia levels in the management of fulminant liver failure  [cached]
Raschke R,Curry S,Remke S,Little E
Southwest Journal of Pulmonary and Critical Care , 2011,
Abstract: Previous studies have suggested that an arterial ammonia level greater than 150 mmol/L is highly sensitive for predicting subsequent development of cerebral edema in patients with fulminant liver failure. We performed a prospective cohort study to confirm this relationship. We enrolled 22 consecutive patients who presented to our transplant hepatology service with grade 3-4 encephalopathy associated with fulminant liver failure. All patients underwent placement of an intraparenchymal ICP monitor, and every 12 hourly arterial ammonia levels. The prevalence of intracranial hypertension (IHTN) in our population was 95% (21/22 patients), with 82 discrete episodes recorded. The sensitivity of arterial ammonia levels to predict the onset of IHTN was 62% (95% CI: 40.8 to 79.3) at a cut point of 150 mmol/L. Arterial ammonia levels preceding the first intracranial hypertension event were less than 150 mmol/L in 8 of 21 patients (39%). Fifty nine of 82 episodes of IHTN (73%) occurred when arterial ammonia levels were less than 150 mmol/L. We conclude that the arterial ammonia level is not useful in making decisions regarding management related to cerebral edema in patients with fulminant liver failure. In fact, since almost all our study patients with grade III or IV encephalopathy secondary to fulminant liver failure went on to develop intracranial hypertension, our study supports the contention that all such patients might benefit from ICP monitoring regardless of arterial ammonia levels.
Hypertonic saline solution increases cerebral perfusion pressure during clinical orthotopic liver transplantation for fulminant hepatic failure: preliminary results
Rocha Filho, Joel Avancini;Machado, Marcel Autran C.;Nani, Ricardo Souza;Rocha, Jo?o Plínio S.;Figueira, Estela R. R.;Bacchella, Telesforo;Rocha-e-Silva, Maurício;Auler Jr., José Otávio C.;Machado, Marcel C. C.;
Clinics , 2006, DOI: 10.1590/S1807-59322006000300008
Abstract: during orthotopic liver transplantation for fulminant hepatic failure, some patients may develop sudden deterioration of cerebral perfusion and oxygenation, mainly due to increased intracranial pressure and hypotension, which are likely responsible for postoperative neurological morbidity and mortality. in the present study, we hypothesized that the favorable effects of hypertonic saline solution (nacl 7.5%, 4 ml/kg) infusion on both systemic and cerebral hemodynamics, demonstrated in laboratory and clinical settings of intracranial hypertension and hemorrhagic shock resuscitation, may attenuate the decrease in cerebral perfusion pressure that often occurs during orthotopic liver transplantation for fulminant hepatic failure. methods: 10 patients with fulminant hepatic failure in grade iv encephalopathy undergoing orthotopic liver transplantation with intracranial pressure monitoring were included in this study. the effect on cerebral and systemic hemodynamics in 3 patients who received hypertonic saline solution during anhepatic phase (hss group) was examined, comparing their data with historical controls obtained from surgical procedure recordings in 7 patients (control group). the maximal intracranial pressure and the corresponding mean arterial pressure values were collected in 4 time periods: (t1) the last 10 min of the dissection phase, (t2) the first 10 minutes at the beginning of anhepatic phase, (t3) at the end of the anhepatic phase, and (t4) the first 5 minutes after graft reperfusion. results: immediately after hypertonic saline solution infusion, intracranial pressure decreased 50.4%. during the first 5 min of reperfusion, the intracranial pressure remained stable in the hss group, and all these patients presented an intracranial pressure lower than 20 mm hg, while in the control group, the intracranial pressure increased 46.5% (p < 0.001). the hss group was the most hemodynamically stable; the mean arterial pressure during the first 5 min of reperfusio
Hipotermia intravascular inducida en el manejo de la hipertensión intracraneana en insuficiencia hepática aguda: Caso clínico Intravascular hypothermia for the management of Intracranial hypertension in acute liver failure: Case report  [cached]
Luis Castillo F,Cristian Pérez R,Carolina Ruiz B,Guillermo Bugedo T
Revista médica de Chile , 2009,
Abstract: Acute liver failure has a mortality rate in excess of 80%. Most deaths are attributed to brain edema with intracranial hypertension and herniation of structures, where ammonium plays a major role in its generation. We report an 18 year-old female with a fulminant hepatic failure caused by virus A infection. The patient developed a profound sopor and required mechanical ventilation. A CT scan showed the presence of brain edema and intracranial hypertension. A Raudemic catheter was inserted to measure intracranial pressure and brain temperature. Intracranial hypertension became refractory and intravascular hypothermia was started, reducing brain temperature to 33°C. Seventy two hours later, a liver transplantation was performed. After testing graft perfusion, rewarming was started, completing 122 hours of hypothermia at 33°C. The patient was discharged in good conditions after 69 days of hospitalization.
Early liver biopsy, intraparenchymal cholestasis, and prognosis in patients with alcoholic steatohepatitis
Laurent Spahr, Laura Rubbia-Brandt, Muriel Genevay, Antoine Hadengue, Emiliano Giostra
BMC Gastroenterology , 2011, DOI: 10.1186/1471-230x-11-115
Abstract: We studied 163 patients (age 55 yrs [35-78], male/female 102/61) with recent, heavy (> 80 gr/day) alcohol intake, histologically-proven ASH (97% with underlying cirrhosis, Maddrey's score 39 [13-200], no sepsis), who had a liver biopsy performed 3 days [0-10] after hospital admission for clinical decompensation. A semi-quantitative evaluation of steatosis, hepatocellular damage, neutrophilic infiltration, periportal ductular reaction, intraparenchymal cholestasis, and iron deposits was performed by two pathologists. All patients with a Maddrey's score ≥ 32 received steroids. The outcome at 3 months was determined. Statistical analysis was performed using the Wilcoxon and Fisher's exact tests, Kaplan-Meier method, and the Cox proportional hazard model.43 patients died after 31 days [5-85] following biopsy. The 3-month survival rate was 74%. Mean kappa value for histological assessment by the two pathologists was excellent (0.92). Univariate analysis identified age, the Maddrey's score, the Pugh's score, the MELD score and parenchymal cholestasis, but not other histological features, as factors associated with 3-month mortality. At multivariate analysis, age (p = 0.029, OR 2.83 [1.11-7.2], intraparenchymal cholestasis (p = 0.001, OR 3.9 [1.96-7.8], and the Maddrey's score (p = 0.027, OR 3.93 [1.17-13.23] were independent predictors of outcome. Intraparenchymal cholestasis was more frequent in non survivors compared to survivors (70% versus 25%, p < 0.001). Serum bilirubin was higher in patients with severe compared to those with no or mild intraparenchymal cholestasis (238 [27-636] versus 69 [22-640] umol/l, p < 0.001).In this large cohort of patients with histologically documented ASH early after admission and no sepsis, liver biopsy identified marked intraparenchymal cholestasis as an independent predictor of poor short term outcome together with age and the Maddrey's score. It may be hypothesized that incorporation of this particular variable into existing disease
Liver lobation and intraparenchymal distribution of the portal vein in Brazilian guinea pig (Galea spixii Wagler, 1831)
Gleidson Benevides de Oliveira,Márcio Nogueira Rodrigues,Roberto Sávio Bessa Silva,José Fernando Gomes de Albuquerque
Biotemas , 2011,
Abstract: Liver lobation and intraparenchymal distribution of the portal vein was described according to studies performed in 10 specimens of Brazilian guinea pigs. The portal vein was cannulated and perfusedwith a vinyl acetate solution and the liver immersed in sulfuric acid solution to obtain vascular casts. The liver presented five lobes, which were named left lateral, left medial, square, right lateral, right medial, and caudate lobes with caudate and papillary processes. The portal vein, entering the portal fissure, divided into two branches, the right and left ones, as it entered the portal fissure. The right branch emitted isolated or common trunk branches to the right lateral lobe and to the caudate process of caudate lobe. On its turn, the left main branch of portal vein divided into two other branches. One of them formed a common trunk for the left lateral, left medial, and square lobes, being the two last ones in a common way. The second branch coursed towards to the right medial branch. Just after its formation, the common trunk of the left main branch emits small vascular branches to the papillary process of caudate lobe.
Intracranial pressure monitoring: Vital information ignored  [cached]
Joseph Mathew
Indian Journal of Critical Care Medicine , 2005,
Abstract: Though there is no Class I evidence for the benefit of intracranial pressure (ICP) monitoring, the bulk of the published literature supports its use when indicated. This review deals with the pathophysiology of raised ICP, evidence for and against monitoring, and basic guidelines for monitoring. It is unfortunate that ICP monitoring is not routinely performed in most of the centres in India due to the popular perception of it being risky, technologically complex and expensive. This article is an attempt to provide all the essential information on this complex topic without going into excessive detail, in the hope that ICP monitoring will be more widely used in India.
Prognostic significance of intracranial pressure monitoring and intracranial hypertension in severe brain trauma patients
Kosti? Aleksandar,Stefanovi? Ivan,Novak Vesna,Veselinovi? Dragan
Medicinski Pregled , 2011, DOI: 10.2298/mpns1110461k
Abstract: Since without prospective randomized studies it is not possible to have a clear attitude towards the importance of intracranial pressure monitoring, this study was aimed at examining the prognostic effect of the intracranial pressure monitoring and intracranial pressure oriented therapy in severe brain trauma patients, and at defining optimal intracranial pressure values for starting the treatment. Two groups of patients were treated in the study, one consisted of 32 patients undergoing intracranial pressure monitoring and the second group of 29 patients without intracranial pressure monitoring in the control group. The study was prospective with groups randomized. There were 53% survivals in the intracranial pressure monitored patients and 34% in the control group, with no significant difference in the survival rate between the two groups (χ2=2.11; p=0.15; p>0.05). The average intracranial pressure in the patients with intracranial hypertension who died was 27 mm Hg, while in the patients who survived the average intracranial pressure was significantly lower (Student’s t test: t=2.91; p=0.008; p<0.01) and it was 18 mm Hg. We recommend starting intracranial pressure oriented therapy when the patient’s intracranial pressure exceeds 18 mmHg during 2 hours of monitoring.
Evaluation of Encapsulated Liver Cell Spheroids in a Fluidised-Bed Bioartificial Liver for Treatment of Ischaemic Acute Liver Failure in Pigs in a Translational Setting  [PDF]
Clare Selden, Catherine Wendy Spearman, Delawir Kahn, Malcolm Miller, Anthony Figaji, Eloy Erro, James Bundy, Isobel Massie, Sherri-Ann Chalmers, Hiram Arendse, Aude Gautier, Peter Sharratt, Barry Fuller, Humphrey Hodgson
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0082312
Abstract: Liver failure is an increasing problem. Donor-organ shortage results in patients dying before receiving a transplant. Since the liver can regenerate, alternative therapies providing temporary liver-support are sought. A bioartificial-liver would temporarily substitute function in liver failure buying time for liver regeneration/organ-procurement. Our aim: to develop a prototype bioartificial-liver-machine (BAL) comprising a human liver-derived cell-line, cultured to phenotypic competence and deliverable in a clinical setting to sites distant from its preparation. The objective of this study was to determine whether its use would improve functional parameters of liver failure in pigs with acute liver failure, to provide proof-of-principle. HepG2cells encapsulated in alginate-beads, proliferated in a fluidised-bed-bioreactor providing a biomass of 4–6×1010cells, were transported from preparation-laboratory to point-of-use operating theatre (6000miles) under perfluorodecalin at ambient temperature. Irreversible ischaemic liver failure was induced in anaesthetised pigs, after portal-systemic-shunt, by hepatic-artery-ligation. Biochemical parameters, intracranial pressure, and functional-clotting were measured in animals connected in an extracorporeal bioartificial-liver circuit. Efficacy was demonstrated comparing outcomes between animals connected to a circuit containing alginate-encapsulated cells (Cell-bead BAL), and those connected to circuit containing alginate capsules without cells (Empty-bead BAL). Cells of the biomass met regulatory standards for sterility and provenance. All animals developed progressive liver-failure after ischaemia induction. Efficacy of BAL was demonstrated since animals connected to a functional biomass (+ cells) had significantly smaller rises in intracranial pressure, lower ammonia levels, more bilirubin conjugation, improved acidosis and clotting restoration compared to animals connected to the circuit without cells. In the +cell group, human proteins accumulated in pigs' plasma. Delivery of biomass using a short-term cold-chain enabled transport and use without loss of function over 3days. Thus, a fluidised-bed bioreactor containing alginate-encapsulated HepG2cell-spheroids improved important parameters of acute liver failure in pigs. The system can readily be up-scaled and transported to point-of-use justifying development at clinical scale.
Neurogenic diabetes insipidus presenting in a patient with subacute liver failure: a case report
Manu Shankar Hari, Anthony K Parsons, Andy K Burroughs, Steve Shaw, James O'Beirne, Banwari Agarwal
Journal of Medical Case Reports , 2010, DOI: 10.1186/1752-1947-4-232
Abstract: A 25-year-old man presented with subacute liver failure. While awaiting a liver transplant, the patient developed cerebral edema, which resulted in neurogenic diabetes insipidus secondary to cerebral edema. The patient died before the liver transplantation could be carried out.Neurogenic diabetes insipidus is well recognized in the neurosurgical population as a consequence of cerebral edema and increased intracranial pressure, both of which occur commonly in patients with subacute liver failure.Cerebral edema occurs in patients presenting with fulminant liver failure, resulting in increased intracranial pressure (ICP). The incidence and severity of cerebral edema increases as the onset of liver failure becomes rapid. It occurs in up to 80% of patients with acute and hyperacute fulminant liver failure but less frequently (20%) in those with subacute fulminant liver failure. There is a significant association between the presence of cerebral edema and the development of central diabetes insipidus in patients with traumatic brain injury [1] and in postoperative neurosurgical patients. We present a case of neurogenic diabetes insipidus that developed during the course of subacute fulminant liver failure.A 25-year-old Nigerian man was admitted to our hospital's intensive care unit (ICU), after emergency tracheal intubation and ventilation for worsening encephalopathy and a deteriorating Glasgow Coma Scale score. The working diagnosis was seronegative hepatitis leading to subacute fulminant liver failure and grade three hepatic encephalopathy.His admission to our hospital was preceded by an admission to a local hospital with a ten day history of painless jaundice and malaise, progressing to three days of nausea and vomiting. The patient had no history of encephalopathy or coagulopathy. Liver function tests on admission were abnormal (bilirubin, 381 μmol/L, alanine transferase [ALT], 684 U/L), but an ultrasound scan showed a normal liver. Autoimmune and viral screen result
Standardized intensive care unit management in an anhepatic pig model: new standards for analyzing liver support systems
Christian Thiel, Karolin Thiel, Alexander Etspueler, Thomas Schenk, Matthias H Morgalla, Alfred Koenigsrainer, Martin Schenk
Critical Care , 2010, DOI: 10.1186/cc9196
Abstract: Eight pigs underwent total hepatectomy after Y-graft interposition between the infrahepatic vena cava and the portal vein to the suprahepatic vena cava. An intracranial probe was inserted for intracranial pressure (ICP) monitoring. Animals received pressure-controlled ventilation under deep narcosis. Vital parameters were continuously recorded. Urinary output, blood gas analysis, haemoglobin, hematocrit, serum electrolytes, lactate, and glucose were monitored hourly, and creatinine, prothrombin time, international normalised ratio, and serum albumin were monitored every 8 hours. Sodium chloride solution 0.9%, hydroxyethyl starch 6%, fresh frozen plasma, and erythrocyte units were used for volume substitution, and norepinephrine was used to prevent severe hypotension. Serum electrolytes and acid-base balance were corrected as required. Antibiotic prophylaxis with ceftriaxon was given daily, as well as furosemide, to maintain diuresis.Postoperative survival was 100% after 24 hours, with a maximum survival of 73 (mean, 58 ± 4) hours. Haemodynamic parameters such as heart rate, mean arterial pressure, and pulse oximetry remained stable during surgical procedures and following anhepatic status due to ICU therapy until escalating at time of death. Deteriorating pulmonary function could be stabilized by increasing oxygen concentration, positive end-expiratory pressure, and maximal airway pressure. Furosemide was used to maintain diuresis until renal failure occurred. ICP started at 15-17 mmHg and increased continuously up to levels of 41-43 mmHg at time of death. All animals died as a result of multiple-organ failure.Using standardized intensive care management after total hepatectomy, we were able to prolong anhepatic survival over 58 hours without the use of liver support systems. The survival benefit of liver support systems in previous animal studies should be reevaluated against our model.Several models of acute hepatic failure have been investigated in animal studies
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