Cause Of Decompensation Research Articles

Special considerations for the stabilization and resuscitation of patients with cardiac disease in the Neonatal Intensive Care Unit

Effective resuscitation of neonates with congenital heart disease (CHD) depends on comprehensive planning, thorough understanding of physiology, vigilant monitoring, and interdisciplinary collaboration to achieve the best outcomes. Neonatal heart disease can affect cardiac structure, rhythm, or ventricular function, and may be either congenital or acquired. Critical congenital heart disease (CCHD) can result in inadequate pulmonary blood flow, impaired intracardiac mixing, airway obstruction, or insufficient cardiac output. Tailored resuscitation strategies are important as early as the delivery room, where some CHD lesions may cause immediate cardiovascular instability during the transition from fetal to postnatal circulation. Premature infants with CHD are at higher risk due to their small size and the complications associated with prematurity, affecting both CHD management and overall clinical stability. Addressing both cardiac and non-cardiac causes of decompensation requires a precise understanding of each patient's unique physiology and trajectory from delivery through postintervention intensive care.

Adherence to the Clinical Practice Guidelines for the hospital management of patients with decompensated heart failure in a Coronary Care Unit in Colombia

To assess adherence to the recommendations for the diagnosis and management of hospitalized patients with Decompensated Heart Failure issued by the European Society of Cardiology in 2021 at a Coronary Care Unit at a fourth-level hospital in the city of Bogotá. A descriptive cross-sectional study was conducted, including hospitalized patients in the Coronary Care Unit at Hospital San José in Bogotá, with a primary diagnosis of Decompensated Heart Failure, from September 2021 to January 2023. Patient data were collected from medical records. Adherence to the Decompensated Heart Failure guidelines was described in the study. High adherence was observed for laboratory tests and medication prescriptions recommended by the 2021 European Society of Cardiology guidelines. However, there was low adherence to the request for thyroid function tests, troponin, and iron studies. The cause of heart failure and decompensation was adequately recorded. The most common cause of decompensation was acute coronary syndrome. Regarding the hemodynamic profile on admission, the majority presented as Stevenson B. Pharmacological adherence to Class I recommendations showed high compliance in prescribing beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and Angiotensin Receptor-Neprilysin Inhibitors. However, lower adherence was observed for Sodium-glucose co-transporter two inhibitors and Mineralocorticoid receptor antagonists. Variable adherence rates were recorded, emphasizing satisfactory compliance with class I recommendations for certain medications and laboratory tests. It is necessary to improve adherence in the request for paraclinicals, especially in thyroid function tests and ferrokinetic profiles.

Efficiency and safety of total plasma exchange in critically ill cirrhotic patients with acute on chronic liver failure: a pilot study.

Treatment of patients with acute on chronic liver failure (ACLF) admitted to the ICU is very limited. The aim of this pilot study was to evaluate the efficiency on liver function and safety of therapeutic plasma exchange (TPE) in critically ill cirrhotic patients admitted with ACLF in a liver ICU. This is a prospective cohort of patients with ACLF grade > 2 treated by TPE admitted to the ICU that was matched to a control group. TPE was performed using a plasma filter (TPE2000, BAXTER®) on a CRRT machine (Prismaflex®, Baxter®). Ratio and type of fluid replacement were 50% with 5% albumin solution followed by 50% with fresh frozen plasma. Seven patients with a mean age of 50.6 ± 7.8 years (all males) and 14 controls matched to age, sex, etiology and cause of decompensation were recruited. At ICU admission, mean MELD score was 39.1 ± 2.7, mean SOFA score was 11.6 ± 5.2 and mean CLIF SOFA score was 12.9 ± 2.6. The grade of ACLF was 3 for 3 patients (42.9%) and 2 for 4 patients (57.1%). The TPE group had significantly higher levels of bilirubin (392.3 ± 117.1 vs. 219 ± 185, p = 0.04), and INR values (5.7 ± 3.4 vs. 3.5 ± 0.9, p < 0.005) compared to the control group. Patient survival was respectively 28.6% and 14.3% at 30 and 90 days in the TPE group and 35.7% and 7.14% in the control group respectively (HR: 1 (95% CI 0.19- 5.2; p = 1). One patient in the TPE group had a liver transplantation 13 days after admission to ICU and is still alive and none in the control group. Two (28.6%) patients died from complications related to the double lumen catheter used for TPE. This pilot study of TPE in patients with ACLF grade 2 and 3 showed a marked but transient improvement in liver function tests. TPE worth to be evaluated in large trials in ACLF patients, with a liver transplant project, and less organ failure.

In-Hospital Management and Long-term Clinical Outcomes and Adherence in Patients With Acute Decompensated Heart Failure: Primary Results of the First Brazilian Registry of Heart Failure (BREATHE)

Heart failure (HF), a common cause of hospitalization, is associated with poor short-term clinical outcomes. Little is known about the long-term prognoses of patients with HF in Latin America. BREATHE was the first nationwide prospective observational study in Brazil that included patients hospitalized due to acute heart failure (HF). Patients were included during 2 time periods: February 2011-December 2012 and June 2016-July 2018 In-hospital management, 12-month clinical outcomes and adherence to evidence-based therapies were evaluated. A total of 3013 patients were enrolled at 71 centers in Brazil. At hospital admission, 83.8% had clear signs of pulmonary congestion. The main cause of decompensation was poor adherence to HF medications (27.8%). Among patients with reduced ejection fraction, concomitant use of beta-blockers, renin-angiotensin-aldosterone inhibitors and spironolactone decreased from 44.5% at hospital discharge to 35.2% at 3 months. The cumulative incidence of mortality at 12 months was 27.7%, with 24.3% readmission at 90 days and 44.4% at 12 months. In this large national prospective registry of patients hospitalized with acute HF, rates of mortality and readmission were higher than those reported globally. Poor adherence to evidence-based therapies was common at hospital discharge and at 12 months of follow-up.

Trends in Mortality and Health Care Burden of Cirrhotic Decompensation in Hospitalized Patients: A Nationwide Analysis.

Mortality caused by cirrhosis is now the 14th most common cause of death worldwide and 12th most common in the United States. We studied trends in inpatient mortality and hospitalization charges associated with cirrhotic decompensation from esophageal variceal bleeding, ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome from 2007 to 2017. Using the National Inpatient Sample databases, we first isolated patients 18 years or older with the diagnosis of cirrhosis using International Classification of Diseases, Ninth Revision (ICD-9) or International Classification of Diseases, Tenth Revision (ICD-10) codes. We then identified patients with the admission diagnosis of esophageal variceal bleeding, ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome. Time-series regression was used to determine whether a trend occurred over the study period. We also evaluated for patient-related demographic changes over the study period. A total of 259,897 cirrhotic patients with the studied decompensations were captured. During the study period, time-series regression confirmed downtrends in mortality rates and length of stay for all types of decompensations. Conversely, we found increases in hospitalization charges for all types of decompensations. Patient age increased over the study period. Patients were also more likely to be White and pay with. From 2007 to 2017, inpatient mortality rates and lengths of stay decreased for cirrhotic decompensations for all causes of decompensation. Total charges, conversely, increased for all causes.

The Role of the Vasculature in Heart Failure.

The contribution of the vasculature in the development and progression of heart failure (HF) syndromes is poorly understood and often neglected. Incorporating both arterial and venous systems, the vasculature plays a significant role in the regulation of blood flow throughout the body in meeting its metabolic requirements. A deterioration or imbalance between the cardiac and vascular interaction can precipitate acute decompensated HF in both preserved and reduced ejection fraction phenotypes. This is characterised by the increasingly recognised concept of ventricular-arterial coupling: a well-balanced relationship between ventricular and vascular stiffness, which has major implications in HF. Often, the cause of decompensation is unknown, with international guidelines mainly centred on arrhythmia, infection, acute coronary syndrome and its mechanical complications as common causes of decompensation; the vascular component is often underrecognised. A better understanding of the vascular contribution in cardiovascular failure can improve risk stratification, earlier diagnosis and facilitate earlier optimal treatment. This review focuses on the role of the vasculature by integrating the concepts of ventricular-arterial coupling, arterial stiffness and venous return in a failing heart.

Experience of successful laparoscopic sleeve resection of the stomach and treatment of morbid obesity in a patient with a classic form of congenital adrenal dysfunction

The article presents a clinical observation of a patient with congenital adrenal dysfunction (CHD), a salt-losing form of 21-hydroxylase enzyme deficiency (homozygous mutation I 172N), and also with morbid obesity, due to long-term use of high doses of glucocorticosteroids, who underwent bariatric surgery - laparoscopic sleeve resection of the stomach. A feature of the presented case is the elimination of one of the causes of decompensation of the disease, namely, overweight, as well as insulin resistance, which requires the intake of large doses of glucocorticoids, which in turn leads to a worsening of the course of obesity, thereby causing a vicious circle. 7 months after surgical treatment, the goal was achieved - a reduction in the dose of Prednisolone by 25%, with a decrease in body weight by 72.1% of overweight.The presented case clearly demonstrates the possibility of performing bariatric surgery for the treatment of morbid obesity in patients with CAH with the participation and control of a specialized multidisciplinary team. If there are indications for bariatric intervention, VDKN should not be an absolute contraindication to such operations, and the ratio of the safety profile and the efficacy profile testifies in favor of the need for their implementation.

Acute delirium as a form of presentation of a thalamic hemorrhagic stroke

Delirium is a frequent cause of decompensation in the elderly, especially with higher prevalence in highly dependent patients, in advanced ages and senile dementia. It is important to always look for the principal cause before treating only the symptom. This case describes a 79-year-old woman with an episode of agitation and disorientation lasting several days, underestimated by its mild nature, but which ends up being a thalamic hemorrhagic stroke. Hemorrhagic stroke is a less common pathology than ischemic stroke but with higher morbidity and mortality. Specifically focused on the thalamus produces behavioral and sensory alterations that can be confused with multiple pathologies. Early identification and approach influence recovery and the sequelae that are being worked with different physiotherapeutic therapies.

Hepatic Encephalopathy Confirmed by Magnetic Resonance Imaging in a Patient with Unobvious Cause of Chronic Liver Disease Decompensation

Fifty-four-year old male was admitted to the intensive care unit (ICU) due to impaired consciousness. Past medical history included alcohol dependence, liver cirrhosis, esophageal varices, 2 esophageal varices banding procedures in the past, pathological obesity. Computed tomography (CT) examination of the head performed in the referring hospital was normal. At admission the CT examination of the head was repeated and showed no abnormalities. Urgent esophagogastroduodenoscopy revealed presence of esophageal varices and scarification following previous banding procedures located in the middle and lower part of the esophagus. Gastrointestinal bleeding being the most likely cause of chronic liver decompensation was therefore excluded. Multimodal neurologic diagnostic assessment was negative. Finally magnetic resonance imaging (MRI) of the head was performed. Taking into account clinical picture and the MRI result, the differential diagnosis included chronic liver encephalopathy, exacerbated acquired hepatocerebral degeneration, and acute liver encephalopathy. Due to history of umbilical hernia CT of the abdomen and pelvis was performed and showed intussusception of the ileum, confirming hepatic encephalopathy. In this case report the MRI suggested the diagnosis of hepatic encephalopathy and prompted search for alternative causes of decompensation of chronic liver disease.

DISRUPTION OF THE UROTHELIAL BARRIER UNDER BENIGN PROSTATIC HYPERPLASIA AS A COMPONENT OF BLADDER DECOMPENSATION

Introduction. The urothelial barrier resists the aggressive effect of urine on the bladder tissues. Chronic retention of urine causes the development of an infectious and non-infectious inflammatory process with metaplasia and desquamation of the urothelial layer of the bladder. With long-term infravesical obstruction, the contact density between urothelial cells is disturbed, which leads to the loss of the barrier function of the mucous membrane of the urinary bladder.&#x0D; The purpose of the study is to investigate the role of urothelial barrier disruption in the development of urinary bladder decompensation in patients with BPH.&#x0D; Materials and methods. 70 patients with BPH were selected, their average age was 67.94±7.42 years. They underwent a bladder biopsy during the operation, followed by a pathomorphological examination.&#x0D; According to clinical manifestations, patients were divided into three groups: group I included 20 patients with bladder compensation (I-PSS – 16±4.5, Qmax – 15.8±2.4 ml/s, Qave – 12.8±2.8 ml/s, without post void residual); group II involved 20 patients with bladder subcompensation (I-PSS – 26±3.9, Qmax – 10.8±2.5 ml/s, Qave – 4.4±1.4 ml/s, post void residual – 150.1 ±80.8 ml.); and III group included 30 patients with bladder decompensation (before the cystostomy I-PSS – 33.1±1.88, post void residual – 1093.3±458.8 ml).&#x0D; Results. In the compensation stage of the bladder there is found multilayer transitional cell urothelium that often forms folds, causing pseudoepithelial outgrowths. The detrusor is represented by hypertrophied smooth muscle cells, with the phenomena of moderate hydropic dystrophy in individual myocytes, with isolated small foci of sclerosis. In the stage of bladder subcompensation we observe foci of desquamation of the surface layers of the urothelium and dystrophic changes in epitheliocytes. Areas of atrophy are combined with foci of hyperplasia of epitheliocytes with stratification of the epithelium (up to 14 - 18 layers or more). The lamina propria of the mucous membrane is swollen in most cases, the formation of lacuniform slits is seen. There are often foci of lymphoplasmacytic infiltration. The detrusor is mostly represented by hypertrophied smooth muscle cells, a significant number of which have signs of hydropic dystrophy.&#x0D; In the stage of bladder decompensation the foci of total desquamation of all layers of the urothelium can be observed; pronounced dystrophic changes of epitheliocytes also take place. The own plate of the mucous membrane is sharply thickened: due to the formation of numerous lacuniform slits it has a porous appearance. Erosive changes in the mucous membrane of the urinary bladder are accompanied by pronounced sclerosis of the stroma. In places of desquamation of the urothelium, submucosal foci of sclerosis are observed, which penetrate into the detrusor. The latter is represented by hypotrophied smooth muscle cells with signs of hydropic dystrophy. Due to the massive proliferation of connective tissue, muscle fibres are divided into separate bundles. Diffuse lymphoplasmacytic infiltration is observed in all layers of the bladder.&#x0D; Conclusion: The results of pathomorphological studies in the context of clinical and functional characteristics enables to distinguish three stages of SM remodelling in BPH: compensation, subcompensation and decompensation. Long-term chronic retention of urine causes a violation of the urothelial barrier, urine impregnation of all layers of the CM with the development of aseptic inflammation. A progressive increase in the specific weight of connective tissue, dystrophic changes in myocytes and nerve fibres become the cause of decompensation of the CM with a violation of the contractile ability of the detrusor.

Main results of the first Brazilian Registry of Heart Failure (BREATHE)

Abstract Background Heart failure represents a common cause of hospitalization associated with poor short-term clinical outcomes. Little is known about the long-term prognosis of these patients in Latin America. Methods The rationale and design of the study were previously published (1). Briefly, BREATHE was the first nation-wide prospective observational study that included patients hospitalized due to acute heart failure in Brazil. In-hospital management as well as 12-month clinical outcomes were assessed. Patients were included during two time periods: from February 2011 to December 2012 (BREATHE I) and from June 2016 to July 2018 (BREATHE Extension). Adherence to evidence-based therapies was also evaluated. Results A total of 3,013 patients were included in 71 centers in Brazil. The median follow-up was 346 days. The BREATHE population included 39.3% of women, had a mean age of 65.2 (± 15.6) with a mean ejection fraction of 39.7% (± 17.5). Among the comorbidities, systemic arterial hypertension was the most common, present in almost 75% of the sample. At hospital admission, 83.8% of patients had clear signs of pulmonary congestion and the main cause of decompensation was poor adherence to heart failure medications, representing 27.8% of cases. Among patients with reduced ejection fraction, the concomitant use of renin-angiotensin-aldosterone inhibitors, beta-blocker and spironolactone at hospital discharge was 44.5% and decreased to 35.2% after 3 months (p&amp;lt;0.01). Mortality rate at 12 months was 28.9 for every 100 patient years with 26.2% readmission at 90 days and 46.4% at 365 days. The most common etiology of heart failure was ischemic disease (Figure 1) but the worst prognosis was associated with Chagas disease (Figure 2) including an analysis of a composite outcome encompassing death, myocardial infarction, stroke or cardiac arrest after discharge. Conclusions In this large national prospective registry of patients hospitalized with acute heart failure, mortality and readmission were higher than what have been reported globally. Poor adherence to evidence-based therapies was a common both at hospital discharge and 1-year of follow-up. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): Brazilian Society of Cardiology

Role of precipitants in transition of acute decompensation to acute-on-chronic liver failure in patients with HBV-related cirrhosis

Background & AimsPre-acute-on-chronic liver failure (ACLF) is a distinct intermediate stage between acute decompensation (AD) and ACLF. However, identifying patients with pre-ACLF and predicting progression from AD to ACLF is difficult. This study aimed to identify pre-ACLF within 28 days, and to develop and validate a prediction model for ACLF in patients with HBV-related decompensated cirrhosis.MethodsIn total, 1,736 patients with HBV-related cirrhosis and AD were enrolled from 2 large-scale, multicenter, prospective cohorts. ACLF occurrence within 28 days, readmission, and 3-month and 1-year outcomes were collected.ResultsAmong 970 patients with AD without ACLF in the derivation cohort, the 94 (9.6%) patients with pre-ACLF had the highest 3-month and 1-year LT-free mortality (61.6% and 70.9%, respectively), which was comparable to those with ACLF at enrollment (57.1% and 67.1%); the 251 (25.9%) patients with unstable decompensated cirrhosis had mortality rates of 22.4% and 32.1%, respectively; while the 507 (57.9%) patients with stable decompensated cirrhosis had the best outcomes (1-year mortality rate of 2.6%). Through Cox proportional hazard regression, specific precipitants, including hepatitis B flare with HBV reactivation, spontaneous hepatitis B flare with high viral load, superimposed infection on HBV, and bacterial infection, were identified to be significantly associated with ACLF occurrence in the derivation cohort. A model that incorporated precipitants, indicators of systemic inflammation and organ injuries reached a high C-index of 0.90 and 0.86 in derivation and validation cohorts, respectively. The optimal cut-off value (0.22) differentiated high-risk and low-risk patients, with a negative predictive value of 0.95.ConclusionsThree distinct clinical courses of patients with AD are validated in the HBV-etiology population. The precipitants significantly impact on AD-ACLF transition. A model developed by the precipitant–systemic inflammation–organ injury framework could be a useful tool for predicting ACLF occurrence.Clinical trial numberNCT02457637 and NCT03641872.Lay summaryIt was previously shown that patients with decompensated cirrhosis could be stratified into 3 groups based on their short-term clinical prognoses. Herein, we showed that this stratification applies to patients who develop cirrhosis as a result of hepatitis B virus infection. We also developed a precipitant-based model (i.e. a model that incorporated information about the exact cause of decompensation) that could predict the likelihood of these patients developing a very severe liver disease called acute-on-chronic liver failure (or ACLF).

Triggers for de-compensation of Chronic Liver Disease in South of Lahore

Background: Cirrhosis is a leading cause of mortality and morbidity across the world with cases number estimated to be as high as 1.5 Billion. Pakistan is one of the countries where the burden of disease is significantly high. Aim: To understand potential causative factors contributing towards decompensation of liver disease and report it for the benefit of other units providing service to similar population. Study design: Prospective observational study Methods: Common complications of portal hypertension resulting from chronic liver disease include development of ascites, encephalopathy, GI bleeding and hepato-renal syndrome. Decompensation of cirrhosis can be transient with full recovery (re-compensation), or it can be chronic. During an event of acute decompensation, clinicians strive to treat the underlying trigger which may have resulted in decompensation alongside the supportive treatment. Several of such potential factors have been reported in the literature. New infection, dehydration, consumption of alcohol and new medications are a few to mention. Many a times the cause of decompensation remains unclear. Results: The patients with established cirrhosis can develop such complications of the disease resulting in what is known as decompensation at any point during disease. It is imperative for a liver unit to know the relevant causes of hepatic decompensation in its own patients so that the treatment is based on the evidence from local population; the data which is scarce. Conclusion: Non-compliance with medical advice was the commonest factor as opposed to the available data most of which reports infection as the commonest factor, although infection was the second most common factor, and the commonest concomitant factor in this subset of patients. Cause of decompensation remains unidentified in over one fourth of cases. Keywords: Decompensation, trigger, chronic liver disease

A Novel Approach Using Continuous Monitoring Of Peripheral Edema In Heart Failure Patients Allows Recognition Of Acute Decompensation Early In The Window Of Intervention

<h3>Introduction</h3> Peripheral edema is a common clinical sign along with weight gain, dyspnea, jugular distention, and elevated brain natriuretic peptides (BNP) of cardiac insufficiency associated with impending decompensation and hospitalization. Pitting edema is used in the clinical setting to classify edema severity. And patients occasionally use various subjective measures such as visibility of foot tendons, depth of sandal strap depression, and watch band tension to assess the degree of fluid retention. A better method is needed. A continuous, reliable, quantitative measurement of peripheral edema in the patient setting provides the early recognition necessary for diagnosis and treatment of the underlying causes of decompensation required to prevent the unnecessary cycle of crisis hospitalization. <h3>Hypotheses</h3> Continuous monitoring of ankle circumference will establish a normal baseline and allow detection of "ankle swelling" (peripheral edema) associated with fluid retention. We hypothesize that fluid retention presents as deviations from a normal baseline or "dry state" and can be characterized to distinguish between compensated events and decompensation trends. <h3>Methods</h3> A method of continuously measuring ankle circumference with 1 mm accuracy in the patient setting was employed, allowing us to test the feasibility of detecting changes in ankle swelling (peripheral edema) associated with fluid retention. An open pilot study was performed which collected ankle circumference and orientation data from both healthy normal and heart failure subjects. This data was enhanced using Subject Information Logs which tracked medication adherence, activity, salt intake, and daily weight. Continuous monitoring of the Daily Swelling Profile (DSP) allows definition of a Normal Baseline for each subject. Changes in fluid retention is identified as the difference between the Ankle Circumference Daily Rolling Average (DRA) compared to the Normal Baseline. Events from the Subject Information Logs were mapped to the Ankle Circumference Data. <h3>Results</h3> The following results were documented. Well-managed heart failure subjects present a DSP and Normal Baseline substantially equivalent to healthy normal subjects. Each subject's DSP represented as the change in ankle circumference from a horizontal position (sleeping) to standing or sitting throughout the day is 5-8 mm. Fluid retention or loss presents as a shift in the Ankle Circumference DRA. Compensated fluid retention such as missed medication or isolated high salt intake are observed as an increase in the Ankle Circumference DRA and return to normal after the subject corrects the anomalous behavior. Decompensated fluid retention is observed as an increasing trend in Ankle Circumference DRA and indicates a medical assessment and intervention may be needed. <h3>Conclusion</h3> A continuous, reliable, quantitative measurement of peripheral edema in the patient setting is a feasible method to recognize acute decompensation early in the window of intervention.

Pacient s jaterní cirhózou na interním oddělení, intervence případného abúzu alkoholu

Liver cirrhosis represents a common condition with substantial mortality. Manifestation and progression of ascites, hepatic encephalopathy or gastrointestinal bleeding are among main reasons for hospital admission. Infections represent another specific area in cirrhotic patients. Timely and correct diagnosis and therapy of these conditions are the mainstay of optimal outcome. Manifestation of complications of liver cirrhosis significantly deteriorates prognosis of the patient. Ascites in portal hypertension develops as a result of sodium and consequently water retention. Therapy comprises of restriction of sodium intake, diuretic therapy with combination of spironolactone and furosemide, alternatively large-volume paracentesis. Hepatic encephalopathy comprises a spectrum of neuropsychiatric abnormalities from subtle changes to overt desorientation and asterixis to hepatic coma. Treatment includes correcting of predisposing conditions, administering of non-absorbable disaccharides or rifaximin. The most common cause of bleeding in a cirrhotic patient is oesophageal bleeding. Therapy is complex including hemodynamic stabilisation, antibiotic prophylaxis, vasoactive and endoscopic treatment. Infections are common causes of decompensation and occurrence of complications of advanced chronic liver disease. Their unfavourable outcome is a result of a complex immune disorder in cirrhotic patients. Specific type of infection in cirrhosis is spontaneous bacterial peritonitis, which has to be always excluded with diagnostic paracentesis. The mainstay of successful therapy of infections is timely and vigorous broad spectrum antibiotic therapy which can significantly improve otherwise unfavourable outcome of these patients.

CAUSES OF DECOMPENSATION IN HOSPITALIZED CIRRHOTIC PATIENTS

Decompensation of liver cirrhosis represents a turning point in the prognosis of cirrhotic patients presenting more complex medical needs that can lead to a prolonged hospital stay and a significant risk of in-hospital death. Likewise, mean survival decreases from 12 years for compensated cirrhosis to almost two years for decompensated cirrhosis. Apica BS et al. (2013) reported ascites as the most frequent cause of decompensation in 95.3% cases in the African population. On the other hand, the Colombian study of Sanchez (2016) conducted with the Latin population indicates as the leading cause of decompensation ascites (36.1%), variceal bleeding (28.4%). Unfortunately, in Mexico, we do not have data indicating the most frequent cause of decompensation in hospitalized patients. Therefore, knowing the frequency and most common causes of decompensation will direct prevention and timely treatment strategies. Objective: To determine the cause and prevalence of liver cirrhosis decompensation in patients admitted to the Hospital General de México. Observational, descriptive, retrospective study, Inpatients, hospitalized in the Gastroenterology Service of the General Hospital of Mexico "Dr. Eduardo Liceaga" with a diagnosis of liver cirrhosis, during the period from March 2019 to March 2021. The results were analyzed by descriptive statistics, frequency measures, and measures of central tendency (to obtain percentages, mean and average). We reviewed 454 records of patients diagnosed with liver cirrhosis with an average age of 59 years with a range of 18-75 years, predominantly male 59.25%. The most frequent etiology was alcohol in 44.71%, followed by non-alcoholic steatohepatitis 9.91%, autoimmune causes 7%, and viral (hepatitis B and C) 3.30%; however, up to 31.7% the etiology cannot be determined. According to the Child-Pugh classification, the predominant one was C up to 53.96%. The most frequent decompensation was gastrointestinal bleeding with 52.64%, of which 47.57% were of variceal origin, acute kidney injury with 50%, hepatic encephalopathy 46.03%, and ascites 40.96%. It should be noted that 15.19% presented acute on chronic hepatic failure, and 11.23% toxic-alcoholic hepatitis: less frequently hyponatremia 8.37%, spontaneous bacterial peritonitis (SBP) 7.92%, hepatorenal syndrome 1.98%, and hepatopulmonary syndrome 1.10%. See table 1. In this study, the most frequent cause of decompensation was variceal bleeding, which differs from that reported in the literature in previous studies; however, this may be because the study population attends assessment in advanced stages of the disease and sometimes in the terminal phase to receive specialized care. The authors declare that there is no conflict of interest.

INITIAL EVALUATION OF KIDNEY FUNCTION IN PATIENTS WITH LIVER CIRRHOSIS OF CEIHET, HIDALGO

Kidney injury has become one of the main causes of decompensation in cirrhotic patients. There are few studies in our country that compare various methods to assess kidney function in these patients. Objective: To evaluate the initial renal function in patients with liver cirrhosis from CEIHET, Hidalgo. Observational, cross-sectional, retrospective and analytical study, selecting 186 files with a diagnosis of liver cirrhosis, from January 2020 to June 2021, evaluating renal function (MDRD-6, 24-hour urine creatinine clearance, KDIGO / CKD and Serum cystatin C) at the initial check-up appointment. Statistical analysis was performed through measures of central tendency, dispersion and correlation. 186 files were analyzed, 53.2% (n = 99) women; mean age of 63 years and a mean time since the diagnosis of cirrhosis of 2.2 years. 117 patients (63%) Child Pugh A. The main etiology of cirrhosis was metabolic fatty liver in 110 patients (53.8%). At the time of the first visit, 140 patients (75.3%) had serum creatinine levels between 1 and 2 mg/dl, with a mean of 1.3. Regarding 24-hour urine creatinine clearance, 93 patients (50%) showed levels greater than 90ml / min, and 47 (25.2%) had levels less than 45ml / min. When measuring filtration rate by MDRD-6, 86 (46.4%) showed levels higher than 90ml / min, and 40 (21.5%) had levels lower than 45ml / min. Regarding KDIGO / CKD, 100 individuals (53.8%) showed rates greater than 90ml / min, and only 27 (14.5%) rates less than 45ml / min. In serum Cystatin C, 103 (55.5%) had levels between 1 and 1.5mg / L, and 50 (27%) showed levels greater than 1.5mg / L. When comparing the various measurements, there was only a statistical difference between KDIGO / CKD and the other scales, showing a lower rate of detection of initial kidney injury (p 0.008, 0.07 and 0.04). In total, 89 (48%) of the patients had creatinine clearance less than 60ml / min at the initial consultation. Discussion. In our study, almost half of the patients with cirrhosis present a degree of kidney damage from the first visit to Hepatology. It was impossible to determine whether it is acute, exacerbated chronic, or definitive chronic disease. The use of 24-hour urine creatinine clearance, serum cystatin C, and MDRD-6 is helpful since serum creatinine levels alone erroneously estimate the degree of kidney injury in these patients. We essentially consider the initial kidney function evaluation in all cirrhotic patients to identify probable causes and treat them. We found that up to 48% of patients with liver cirrhosis present some degree of kidney injury at the time of their first consultation with Hepatology. 24-hour urine creatinine clearance, serum cystatin C, and MDRD-6 appear useful in evaluating renal function in these patients. The authors declare that there is no conflict of interest

Impact of COVID-19 Pandemic Lockdown in Decompensated Heart Failure Hospitalizations

Background and ObjectivesCoronavirus disease 2019 (COVID-19) pandemic lockdown may have collaterally affected the care of patients with acute decompensated heart failure (ADHF). We aimed to evaluate the impact of lockdown pandemic on hospitalizations for ADHF.MethodsWe conducted a single-center study, performing a retrospective analysis of prospectively collected data. We included consecutive adult patients with a primary diagnosis of ADHF admitted to a cardiovascular disease specialized hospital. We compared those patients admitted between March–June of 2019 (before COVID-19 [BC]) and 2020 (after COVID-19 [AC]), during mandatory lockdown.ResultsA total 79 corresponding to BC period and 60 to AC period were included, representing a decrease of 25% (interquartile range [IQR], 11–33). During the BC period, 31.6% of patients were referred from other centers compared to 15% during the pandemic (p=0.02). In the AC period patients were older (median age, 81[IQR, 73–87] years vs. 77 [IQR, 64–84] years, p=0.014). The etiology of HF, cause of decompensation, left ventricular function, and laboratory parameters were similar in both periods. The use of mechanical ventilation (13.9% vs. 3.3%, p=0.03) and circulatory support (7.6% vs. 0%, p=0.02) was higher in the BC period. During the BC period, 5 emergency heart transplants were performed, and none in AC, (p=0.004). In-hospital mortality was similar in both periods (3.8% vs. 3.3%; p=0.80).ConclusionsWe observed a reduction in the number of hospitalizations and referral of patients for ADHF during COVID-19 pandemic.

Natural History of Cirrhosis: Changing Trends in Etiology Over the Years

Background and Goals: The aims of the present study were to investigate the natural history of cirrhosis and to determine trends in the etiology of cirrhosis. Methods: Between January 2001 and January 2018, a total of 1,341 patients had been diagnosed with cirrhosis and were included. Results: A total of 898 cirrhotic patients, who were followed up for at least 6 months were included into the analysis. The median age was 54 years. The median Child-Pugh and MELD scores were 7.5 and 11, respectively. Ascites (51%) was the most common causes of decompensation. Chronic viral hepatitis was the most frequent cause of cirrhosis (58%). Hepatitis B virus (HBV) infection was the main etiology (34%), followed by hepatitis C virus (HCV) infection (18%). Among 129 patients with cryptogenic cirrhosis (CC), 60 had metabolic abnormalities. If these 60 patients with CC were considered to have nonalcoholic fatty liver disease (NAFLD)-related cirrhosis, the proportion of NAFLD-related cirrhosis increased from 1.8 to 8.0%. At admission, 74 patients (8%) had been diagnosed with hepatocellular carcinoma (HCC). A new HCC developed in 80 patients during the follow-up period. The probability of developing HCC was 3.9% at 12 months. Logistic regression analysis showed that the development of HCC was significantly associated with older age (p < 0.001), male gender (p < 0.001), viral etiology (p = 0.026), and baseline high aspartate aminotransferase level (p = 0.01). Overall, 104 cirrhotic patients died. Conclusion: HBV and HCV remain the leading causes of etiology in cirrhosis and HCC. However, NAFLD-related cirrhosis is recognized as a growing burden.

Comparison of demographic features and prognosis between cardiogenic shock in patients with Chagas heart disease and other etiologies – Registry Of Acute Medical Emergencies in Brazil (ROAD)

Abstract Background Chagas disease is a chronic, systemic, parasitic infection caused by Trypanosoma cruzi, and a common cause of heart failure (HF) in Latin America. The incidence can be as high as 14% in endemic areas. The prognosis seems to be worse than other causes of HF, with mortality of up to 20%/year. Mortality and prognosis during the acute decompensation, however, are less studied. Purpose Compare differences between cardiogenic shock (CS) in patients with HF caused by chronic Chagas heart disease (ChHD) and those caused by other etiologies (non-ChHD). Methods We performed a multicentric, prospective, observational study of patients admitted with CS at 3 emergency departments in Brazil between January 2015 and December 2019. Baseline characteristics and intrahospital outcomes were obtained. Statistical analysis: The primary outcome was combined intra-hospital events (death, stroke, acute renal failure and bleeding). Comparison between groups was performed through Chi-squared and Student's T-test and the multivariate analysis by logistic regression, being p&amp;lt;0.05 considered significant. Results 856 patients with CS were included, 158 (18,5%) ChHD and 698 (81,5%) non-ChHD. Those with ChHD were younger (60.5±11.7 vs. 64.9±4.8 years old, p&amp;lt;0.0001), less often male (50.0 vs. 64.3%, p=0.001) and had lower prevalence of diabetes (20.9 vs. 36.2%, p&amp;lt;0.0001), hypertension (36.07 vs. 64.1%, p&amp;lt;0.0001), chronic obstructive pulmonary disease (1.9 vs. 7.8%, p=0.007) and dyslipidemia (14.6 vs. 36%, p&amp;lt;0.0001). The ejection fraction was lower in ChHD (26 + 7.3 vs. 30.4% + 11.4, p&amp;lt;0.0001) and they had more definitive pacemaker (17.3 vs. 6.8%, p&amp;lt;0.0001). At the admission, patients with ChHD had lower systolic blood pressure (91.3±20.6 vs. 98.8±25.9 mmHg, p=0.001) and were more symptomatic, with orthopnea (41.3 vs. 28.3%, p=0.004), dyspnea (75.3 vs. 57.3%, p&amp;lt;0.0001). Treatment in the first 24 hours was different, with less withdrawal of beta-blockers (51.2 vs. 63.9%, p=0.006) and more use dobutamine (80.4 vs. 66.2%, p&amp;lt;0.0001). Main cause of decompensation was progression of disease in 39.1% of ChHD versus 22.9% of non-ChHD (p&amp;lt;0.001). Decompensation seemed more severe with greater necessity of orotracheal intubation (30 vs. 14.5%, p&amp;lt;0.0001), intra-aortic balloon pump (27.9 vs. 7.5%, p&amp;lt;0.0001), bleeding (9.2 vs. 3.8%, p=0.012) and acute renal failure (46.7 vs. 35.8%, p=0.024). The primary outcome was observed in 57% of the non-ChHD and 71.5% of the ChHD (OR 0.578, 95% CI: 0.314–1.064, p=0.079). Also, there were no differences between intra-hospital mortality in patients with ChHD versus non-ChHD (37.3 vs. 32.7%, p=0.261). Conclusion To the best of our knowledge, this is the biggest registry with Chagasic patients in cardiogenic shock. They were younger and had less comorbidities, but were admitted with lower blood pressure, more symptoms and needed more inotropes in the first 24 hours. No difference in mortality or combined outcome was observed. Funding Acknowledgement Type of funding source: None